fibrin and Necrosis

Clinical features of COVID-19 range from mild respiratory symptoms to fatal outcomes. Autopsy findings are important for understanding COVID-19-related pathophysiology and clinical manifestations. This systematic study aims to evaluate autopsy findings in paediatric cases. We searched PubMed, EMBASE, and Cochrane Database Reviews. We included studies that reported autopsy findings in children with COVID-19. A total of 11 studies (24 subjects) were included. The mean age of patients was 5.9 ± 5.7 years. Grossly, there was pericardial and pleural effusion, hepatosplenomegaly, cardiomegaly, heavy soft lung, enlarged kidney, and enlarged brain. The autopsy findings of the lungs were diffuse alveolar damage (78.3%), fibrin thrombi (43.5%), haemorrhage (30.4%), pneumonia (26%), congestion and oedema (26%), angiomatoid pattern (17.4%), and alveolar megakaryocytes (17.4%). The heart showed interstitial oedema (80%), myocardial foci of band necrosis (60%), fibrin microthrombi (60%), interstitial and perivascular inflammation (40%), and pancarditis (30%). The liver showed centrilobular congestion (60%), micro/macrovesicular steatosis (30%), and arterial/venous thrombi (20%). The kidney showed acute tubular necrosis (75%), congestion (62.5%), fibrin thrombi in glomerular capillaries (37.5%), and nephrocalcinosis, mesangial cell hyperplasia, tubular hyaline/granular casts (25% each). The spleen showed splenitis (71.4%), haemorrhage (71.4%), lymphoid hypoplasia (57.1%), and haemophagocytosis (28.6%). The brain revealed oedema (87.5%), congestion (75%), reactive microglia (62.5%), neuronal ischaemic necrosis (62.5%), meningoencephalitis (37.5%), and fibrin thrombi (25%). SARS-CoV-2 and CD68 were positive by immunohistochemistry in 85.7% and 33.3% cases, respectively. Autopsy findings of COVID-19 in children are variable in all important organs. It may help in better understanding the pathogenesis of SARS-CoV-2.

Topics: Autopsy; Child; Child, Preschool; COVID-19; Fibrin; Humans; Infant; Lung; Necrosis; SARS-CoV-2; Thrombosis

Preeclampsia evolves in 2 stages: a placental problem that generates signals to the mother to cause a range of responses that comprise the second stage (preeclampsia syndrome). The first stage of early-onset preeclampsia is poor placentation, which we here call malplacentation. The spiral arteries are incompletely remodeled, leading to later placental malperfusion, relatively early in the second half of pregnancy. The long duration of the first stage (several months) is unsurprisingly associated with fetal growth restriction. The first stage of late-onset preeclampsia, approximately 80% of total cases, is shorter (several weeks) and part of a process that is common to all pregnancies. Placental function declines as it outgrows uterine capacity, with increasing chorionic villous packing, compression of the intervillous space, and fetal hypoxia, and causes late-onset clinical presentations such as "unexplained" stillbirths, late-onset fetal growth restriction, or preeclampsia. The second stages of early- and late-onset preeclampsia share syncytiotrophoblast stress as the most relevant feature that causes the maternal syndrome. Syncytiotrophoblast stress signals in the maternal circulation are probably the most specific biomarkers for preeclampsia. In addition, soluble fms-like tyrosine kinase-1 (mainly produced by syncytiotrophoblast) is the best-known biomarker and is routinely used in clinical practice in many locations. How the stress signals change over time in normal pregnancies indicates that syncytiotrophoblast stress begins on average at 30 to 32 weeks' gestation and progresses to term. At term, syncytiotrophoblast shows increasing markers of stress, including apoptosis, pyroptosis, autophagy, syncytial knots, and necrosis. We label this phenotype the "twilight placenta" and argue that it accounts for the clinical problems of postmature pregnancies. Senescence as a stress response differs in multinuclear syncytiotrophoblast from that of mononuclear cells. Syncytiotrophoblast irreversibly acquires part of the senescence phenotype (cell cycle arrest) when it is formed by cell fusion. The 2 pathways converge on the common pathologic endpoint, syncytiotrophoblast stress, and contribute to preeclampsia subtypes. We highlight that the well-known heterogeneity of the preeclampsia syndrome arises from different pathways to this common endpoint, influenced by maternal genetics, epigenetics, lifestyle, and environmental factors with different fetal and matern

Topics: Apoptosis; Autophagy; Cellular Senescence; Extracellular Vesicles; Female; Fibrin; Humans; Necrosis; Placentation; Pre-Eclampsia; Pregnancy; Stress, Physiological; Trophoblasts

Topics: Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis; Arteries; Capillaries; Endothelium, Vascular; Fibrin; Humans; Kidney Glomerulus; Necrosis; Neutrophils; Peripheral Nerves; Thrombosis; Vasculitis; Veins

The indications of the pathological examination of the placenta are mainly represented by uteroplacental vascular deficiency. The clinical context is often evocative, but it can sometimes be solely an intra-uterine growth retardation or an unexplained in utero fetal death. So, the pathological lesions of this uteroplacental vascular deficiency must be well-known to be correctly interpreted, for none of these lesions is truly specific. The pathological diagnosis is based on a group of macroscopic and microscopic arguments. Various physiopathological mechanisms, often imperfectly known, can be at the origin of an uteroplacental vascular insufficiency, but in the current position, the pathological examination does not allow etiopathogenic orientation. The development of the trophoblastic biopsies gives us access to a new material which, in parallel with the cytogenetic analysis, often allows us, in front of an unexplained intra-uterine growth retardation, to direct the diagnosis towards uteroplacental vascular insufficiency. The histological analysis of the chorionic villous sampling taken precociously during pathological pregnancies is thus a major diagnostic contribution. But especially, this analysis gives access to new information which, in the near future, will enable us to better define the pathological evolution of the lesions of hypoxic chorionic villous and to contribute to a better knowledge of this pathology which, under many aspects, still conceals many mysteries.

Topics: Chorionic Villi; Chorionic Villi Sampling; Cysts; Female; Fetal Death; Fetal Hypoxia; Fibrin; Gestational Age; Humans; Infarction; Necrosis; Organ Size; Placenta; Placenta Diseases; Placental Circulation; Pregnancy; Pregnancy Complications; Trophoblasts; Uterus

Although mortality rates from coronary heart disease in the western countries have declined in the last few decades, morbidity caused by this disease is increasing and a substantial number of patients still suffer acute coronary syndrome (ACS) and sudden cardiac death. Acute coronary syndrome occurs as a result of myocardial ischaemia and its manifestations include acute myocardial infarction and unstable angina. Culprit plaque morphology in these patients varies from thrombosis with or without coronary occlusion to sudden narrowing of the lumen from intraplaque haemorrhage. The coronary artery plaque morphologies primarily responsible for thrombosis are plaque rupture, and plaque erosion, with plaque rupture being the most common cause of acute myocardial infarction, especially in men. Autopsy data demonstrate that women <50 years of age more frequently have erosion, whereas in older women, the frequency of rupture increases with each decade. Ruptured plaques are associated with positive (expansive) remodelling and characterized by a large necrotic core and a thin fibrous cap that is disrupted and infiltrated by foamy macrophages. Plaque erosion lesions are often negatively remodelled with the plaque itself being rich in smooth muscle cells and proteoglycans with minimal to absence of inflammation. Plaque haemorrhage may expand the plaque rapidly, leading to the development of unstable angina. Plaque haemorrhage may occur from plaque rupture (fissure) or from neovascularization (angiogenesis). Atherosclerosis is now recognized as an inflammatory disease with macrophages and T-lymphocytes playing a dominant role. Recently at least two subtypes of macrophages have been identified. M1 is a pro-inflammatory macrophage while M2 seems to play a role in dampening inflammation and promoting tissue repair. A third type of macrophage, termed by us as haemoglobin associated macrophage or M(Hb) which is observed at site of haemorrhage also can be demonstrated in human atherosclerosis. In order to further our understanding of the specific biological events which trigger plaque instability and as well as to monitor the effects of novel anti-atherosclerotic therapies newer imaging modalities in vivo are needed.

Topics: Acute Coronary Syndrome; Cardiac Imaging Techniques; Chronic Disease; Coronary Artery Disease; Coronary Thrombosis; Female; Fibrin; Hemorrhage; Humans; Macrophages; Male; Necrosis; Plaque, Atherosclerotic; Platelet Aggregation; Risk Factors; Rupture, Spontaneous; Vascular Calcification

Baboons are susceptible to natural Ebola virus (EBOV) infection and share 96% genetic homology with humans. Despite these characteristics, baboons have rarely been utilized as experimental models of human EBOV infection to evaluate the efficacy of prophylactics and therapeutics in the United States. This review will summarize what is known about the pathogenesis of EBOV infection in baboons compared to EBOV infection in humans and other Old World nonhuman primates. In addition, we will discuss how closely the baboon model recapitulates human EBOV infection. We will also review some of the housing requirements and behavioral attributes of baboons compared to other Old World nonhuman primates. Due to the lack of data available on the pathogenesis of Marburg virus (MARV) infection in baboons, discussion of the pathogenesis of MARV infection in baboons will be limited.

Topics: Animals; Base Sequence; Blood Coagulation Factors; Disease Models, Animal; Ebolavirus; Fibrin; Hemorrhagic Fever, Ebola; Humans; Lymphatic Diseases; Marburg Virus Disease; Marburgvirus; Necrosis; Papio; Sequence Homology, Nucleic Acid; Species Specificity; Thrombocytopenia

The salient features of systemic vasculitis are endothelial swelling, inflammatory infiltrates, and fibrinoid necrosis of the arterial wall. Of these three, the concept of fibrinoid necrosis is undoubtedly the most elusive. Is it really necrosis, defined as unprogrammed cell death, that we are looking at? And does the adjective 'fibrinoid', meaning fibrin-like, cover its most important attribute? In early case reports on systemic vasculitis the term was used with caution, but over the years it has grown in status to become the most characteristic histopathological manifestation of systemic vasculitis in patients with anti-neutrophil cytoplasmic antibodies (ANCA), suggesting that the clue to the auto-immune mechanisms that damage the vessel wall lies in the necrotic lesion. But what is this assumption based on? This review discusses the history of fibrinoid necrosis in vasculitis, focusing on the ideas that have been postulated over the years regarding this lesion. Special attention will be paid to its occurrence in the kidney in systemic vasculitis.

Topics: Antibodies, Antineutrophil Cytoplasmic; Arteries; Autoimmunity; Fibrin; Humans; Kidney; Necrosis; Vasculitis

Pulmonary vascular inflammatory disorders may involve all components of the pulmonary vasculature, including capillaries. The principal histopathologic features of pulmonary capillaritis include capillary wall necrosis with infiltration by neutrophils, interstitial erythrocytes, and/or hemosiderin, and interalveolar septal capillary occlusion by fibrin thrombi. Immune complex deposition is variably present. Patients often present clinically with diffuse alveolar hemorrhage, which is characterized by dyspnea and hemoptysis; diffuse, bilateral, alveolar infiltrates on chest radiograph; and anemia. Pulmonary capillaritis has been reported with variable frequency and severity as a manifestation of Wegener's granulomatosis, microscopic polyarteritis, systemic lupus erythematosus, Goodpasture's syndrome, idiopathic pulmonary renal syndrome, Behçet's syndrome, Henoch-Schönlein purpura, IgA nephropathy, antiphospholipid syndrome, progressive systemic sclerosis, and diphenylhydantoin use. In addition to history, physical examination, and routine laboratory studies, certain ancillary laboratory tests, such as antineutrophil cytoplasmic antibodies, antinuclear antibodies, and antiglomerular basement membrane antibodies, may help diagnose an underlying disease. Diagnosis of pulmonary capillaritis can be made by fiberoptic bronchoscopy with transbronchial biopsy, but thoracoscopic biopsy is often employed. Since many disorders can result in pulmonary capillaritis with diffuse alveolar hemorrhage, it is crucial for clinicians and pathologists to work together when attempting to identify an underlying disease. Therapy depends on the disorder that gave rise to the pulmonary capillaritis and usually includes corticosteroids and cyclophosphamide or azathioprine. Since most diseases that result in pulmonary capillaritis are treated with immunosuppression, infection must be excluded aggressively.

Topics: Anemia; Bronchoscopy; Capillaries; Diagnosis, Differential; Dyspnea; Erythrocytes; Fibrin; Hemoptysis; Hemorrhage; Hemosiderin; Humans; Immunosuppressive Agents; Lung; Lung Diseases; Necrosis; Neutrophils; Pulmonary Alveoli; Pulmonary Embolism; Thoracoscopy; Vasculitis

Liver pathology is one of the main features of HELLP syndrome and develops on the basis of a generalised activation of intravascular coagulation. Fibrin deposits and haemorrhagic necrosis predominantly develop in the periportal areas and may eventually lead to subcapsular haematomas or even rupture of the liver. While the compensated form of activation of intravascular coagulation, which is diagnosed by a decrease in antithrombin III and an increase in thrombin-antithrombin III complex (TAT) and the appearance of fibrin, monomers and D-dimers, is found in almost all cases of HELLP syndrome, the decompensated form of intravascular coagulation with prolonged bleeding time (PT, PTT) and drop in fibrinogen is found only in the most severe forms. The development of a decompensation of coagulation correlates with the appearance of severe complications such as liver haematoma, abruptio placentae, renal failure and pulmonary oedema. The best prophylaxis against the development of life-threatening complications is early diagnosis and termination of pregnancy after stabilisation of the maternal condition, consisting of magnesium sulphate infusion, antihypertensive treatment with dihydralazine or calcium antagonists, steroids etc. Severe complications of HELLP syndrome have occasionally been observed in the postpartum period. As prophylaxis against postpartal worsening of HELLP syndrome, curettage of the uterus and continuation of the treatment with calcium antagonists and dexamethasone have been recommended.

Topics: Biopsy; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Female; Fibrin; HELLP Syndrome; Hemorrhage; Humans; Infant, Newborn; Liver; Necrosis; Pregnancy; Rupture, Spontaneous

The etiology of venous ulceration is far more complex than Homans' theory of stagnation and hypo-oxygenation. Indeed, studies have shown that flow in lipodermatosclerotic limbs is actually faster than normal. We suggest, therefore, that the terms "stasis dermatitis" and "stasis ulcer" be dropped from medical parlance. The term "lipodermatosclerosis with ulceration" as used by the British, or simply "venous ulcer," would seem more appropriate. Venous hypertension, produced by incompetence of deep and communicating vein valves and thrombosis of segments of the deep system, is closely correlated with the development of venous ulcers. Precisely how this venous hypertension translates into ulceration is unclear. Burnand et al showed that fibrin cuffs are deposited around the capillaries in lipodermatosclerotic limbs. These cuffs may serve as barriers to the diffusion of oxygen, leading to local ischemia and epidermal necrosis. Others suggest that trapped leukocytes in the microcirculation alter capillary permeability by releasing various inflammatory mediators that hasten the flow of fibrinogen across the capillary membrane and promote the formation of fibrin cuffs. Proof of this hypothesis is still lacking, but may eventually come from using radioactive WBC tagging procedures. A synthesis of these two theories may in fact explain the etiology of venous ulceration.

Topics: Capillary Permeability; Cell Hypoxia; Chronic Disease; Fibrin; Fibrinogen; Humans; Hypertension; Leg Ulcer; Leukocytes; Microcirculation; Necrosis; Terminology as Topic; Thrombosis; Venous Insufficiency; Venous Pressure

Topics: Fibrin; Hepatectomy; Humans; Kupffer Cells; Liver; Liver Diseases; Macrophage Activation; Macrophages; Necrosis

Topics: Arthritis, Rheumatoid; Connective Tissue; Fibrin; Humans; Necrosis; Rheumatoid Factor; Rheumatoid Nodule; Synovitis; Wounds and Injuries

Topics: Angina Pectoris; Coronary Artery Bypass; Coronary Circulation; Coronary Vessels; Fibrin; Humans; Myocardium; Necrosis; Postoperative Complications; Saphenous Vein; Thrombosis; Transplantation, Autologous

Topics: Animals; Anticoagulants; Antigens, Neoplasm; BCG Vaccine; Blood Coagulation; Cell Adhesion; Cell Line; Cell Survival; Endothelium; Fibrin; Fibrinolysis; Humans; Immunity; Liver Neoplasms; Lung Neoplasms; Lymph Nodes; Macrophages; Mycobacterium bovis; Necrosis; Neoplasm Metastasis; Neoplasms; Organ Specificity; Platelet Aggregation

Topics: Animals; Arteriosclerosis; Blood Platelets; Blood Vessels; Calcium; Cell Division; Cell Membrane Permeability; Collagen; Disease Models, Animal; Elastin; Endothelium; Fibrin; Glycosaminoglycans; Histocytochemistry; Humans; Lipid Metabolism; Microscopy, Electron; Necrosis; Platelet Adhesiveness

Topics: Acute Kidney Injury; Adolescent; Adult; Child; Child, Preschool; Diarrhea; Female; Fibrin; Humans; Hypocalcemia; Infant; Infant, Newborn; Kidney; Kidney Tubules; Male; Microscopy, Electron; Muscles; Muscular Diseases; Myofibrils; Myoglobinuria; Necrosis; Phosphorus; Respiratory Distress Syndrome, Newborn; Respiratory Tract Infections; Staining and Labeling; Tetany; Thrombosis

Topics: Animals; Aorta; Arteriosclerosis; Blood Platelets; Calcinosis; Child; Cholesterol; Collateral Circulation; Coronary Disease; Coronary Vessels; Erythrocytes; Female; Fibrin; Fibroblasts; Glycosaminoglycans; Hemorrhage; Histocytochemistry; Humans; Lipids; Macrophages; Male; Middle Aged; Muscle, Smooth; Necrosis; Rabbits; Rupture; Thrombosis

Topics: Animals; Antibodies; Arteries; Blood Platelets; Capillaries; Coronary Disease; Coronary Vessels; Cortisone; Dogs; Endocarditis; Fibrin; Graft Rejection; Heart Failure; Heart Transplantation; Hemorrhage; Humans; Immunosuppression Therapy; Immunosuppressive Agents; Infections; Kidney Transplantation; Male; Microscopy, Electron; Middle Aged; Myocarditis; Myocardium; Necrosis; Rabbits; Shwartzman Phenomenon; Time Factors; Transplantation Immunology; Transplantation, Homologous

Topics: Adult; Aged; Autopsy; Brain; Central Venous Pressure; Colitis; Colon; Enteritis; Female; Fibrin; Heart Ventricles; Hemorrhage; Humans; Kidney; Kidney Glomerulus; Kidney Tubules; Liver; Lung; Male; Middle Aged; Myocardium; Necrosis; Pancreas; Shock; Thrombosis

Regenerative endodontic procedures (REPs) using autologous platelet concentrates as scaffolds can improve the biologic outcome of treatment. This prospective, randomized trial compared the clinical and radiographic performance of REPs using platelet-rich plasma (PRP), platelet-rich fibrin (PRF), a platelet pellet (PP), and an induced blot clot (BC).. Sixty-seven healthy children (aged 8-11 years) with 88 immature necrotic incisors were included. After the root canal disinfection step, the teeth were randomly assigned into 1 of the following groups (n = 22/group) according to the scaffold used: PRP, PRF, PP, and BC. In the PRP, PRF, and PP groups, the platelet concentrates were introduced into the root canal without prior induction of apical bleeding. Treatment outcomes were assessed using a combined clinical and radiographic scoring system, whereas the changes in root dimensions were compared using linear measurements of root length and width with ImageJ (National Institutes of Health, Bethesda, MD) and Turboreg (Biomedical Imaging Group, Swiss Federal Institute of Technology, Lausanne, Switzerland) and planar measurements using the radiographic root area (RRA) and radiographic canal area (RCA) techniques. One-way analysis of variance, the Duncan multiple range test, the Kruskal-Wallis test, the Mann-Whitney U test, and chi-square dependency tests were used for statistical analysis of data (all P = .05).. Except for 2 teeth in the PRF and BC groups, all teeth showed similar and high success scores (periapical healing, radiographic root development, and positive response to sensitivity tests) after an average follow-up time of 28.25 ± 1.2 months. Of all teeth, 73.9% showed complete apical closure with similar closure rates among groups (P > .05) and a greater tendency for conical-shaped apical closure than a blunt apex. Although linear measurements indicated a similar increase in root length and width among all groups (P > .05), the RRA of the BC group was significantly greater than those of the PRF and PP groups, and the RCA of the BC group was significantly greater than PRP, PRF, and PP (all P < .05) when the follow-up time was not used as a factor. Eighty-six percent of the teeth showed a positive response to sensitivity tests with similar initial response times (P > .05).. PRP, PRF, and PP can yield similar clinical and radiographic outcomes to BC without the need for prior apical bleeding and with significantly less tendency for root canal obliteration. RRA and RCA may reveal minor differences that cannot be determined by linear measurements.

Topics: Child; Fibrin; Humans; Necrosis; Platelet-Rich Fibrin; Platelet-Rich Plasma; Prospective Studies; Regenerative Endodontics; Thrombosis; Tooth Diseases

Co-existence of vulnerable plaque and pro-thrombotic state may provoke acute coronary events. It was hypothesized that elevated serum levels of fibrin and fibrinogen degradation products (FDP) are associated with larger total plaque and necrotic core (NC) areas.. Seventy-five patients presenting with stable anginal symptoms (69%) or stabilized acute coronary syndrome (ACS; 31%), and found to have non-obstructive coronary artery disease (CAD) with a fractional flow reserve >0.8, were studied. Invasive virtual histology intravascular ultrasound (VH-IVUS) was performed in 68 LAD arteries, 6 circumflex arteries, and 1 right coronary artery. Serum FDP levels were measured using ELISA technique. Plaque volumetrics and composition were assessed in each VH-IVUS frame and averaged. The median age of patients was 56 (47-63) years; 52% were men and 23% had diabetes. The average length of coronary artery studied was 62 mm. After adjustment for systemic risk factors, medications, CRP levels and ACS, male gender (P<0.001) and serum FDP levels (P=0.02) were independent predictors of a larger NC area. Older age (P<0.001), male gender (P<0.0001) and increased serum FDP level (P=0.03) were associated with a larger plaque area.. In patients with CAD, a higher serum level of FDP is independently associated with larger plaques and greater plaque NC.

Topics: Angina, Stable; Coronary Artery Disease; Female; Fibrin; Fibrinogen; Humans; Male; Middle Aged; Necrosis; Plaque, Atherosclerotic; Ultrasonography, Interventional

Diagnostic laparoscopy is the ultimate diagnostic tool to evaluate the appendix. Still, according to the literature, this strategy results in a negative appendectomy rate of approximately 12-18 % and associated morbidity. Laparoscopic criteria for determining appendicitis are lacking. The goal of this study is to define clear and reliable criteria for appendicitis during diagnostic laparoscopy that eventually may safely reduce the negative appendectomy rate.. From December 2009 through April 2011, 134 patients were included and analysed in a single-centre prospective pilot study. Intraoperatively, the appendix was evaluated by the surgeon according to nine criteria for appendicitis. The operating surgeon decided whether it should be removed or not. Immediately after the operation the surgeon had to complete a questionnaire on nine criteria for appendicitis. All removed appendices were examined by a pathologist. In case the appendix was not removed, the clinical postoperative course was decisive for the (missed) presence of appendicitis.. In 109 cases an inflamed appendix was removed; in 25 patients the appendix was normal, 3 of which had been removed. After univariate analysis and clinical judgement six variables were included in the Laparoscopic APPendicitis score (LAPP score). In this study, use of the LAPP score would have led to a positive predictive value of 99 % and a negative predictive value of 100 %.. This study presents the LAPP score. The LAPP score is an easily applicable score that can be used by surgeons to evaluate the appendix during diagnostic laparoscopy. The score has high positive and negative predictive value. The LAPP score needs to be validated in a multicentre validation study.

Topics: Adolescent; Adult; Appendectomy; Appendicitis; Appendix; False Positive Reactions; Female; Fibrin; Humans; Intestinal Perforation; Laparoscopy; Male; Mesentery; Necrosis; Pilot Projects; Predictive Value of Tests; Prospective Studies; Severity of Illness Index; Suppuration; Surveys and Questionnaires; Unnecessary Procedures; Young Adult

Redon drains are still used to suction wounds for vacuum sealing. Vacuum-assisted closure (V.A.C.((R)); Kinetic Concepts Inc, San Antonio, TX) is a computer-controlled therapy system for delivering topical negative pressure therapy. The efficiency of V.A.C. in the treatment of pressure ulcers was prospectively studied in a randomised controlled trial in which patients with pressure ulcers were randomly assigned to negative pressure wound therapy (NPWT) using either V.A.C. or Redon bottles. The target parameters were absolute and relative proportion of wound area consists of granulation tissue, fibrin and necrosis. Other outcome measures were the number of dressing changes and time invested using each system. The study was terminated after a post hoc analysis after inclusion of ten patients because of the significantly better results when using V.A.C., and the substantially larger care effort needed in the Redon group compared with the V.A.C. group. An increase in surface granulation tissue of 54% was observed in the V.A.C. group, and a reduction in the Redon group (P = 0.001). The Redon group showed an increase in fibrin tissue at the wound base of 21.8%, whereas in the V.A.C group, a 27% reduction was observed (P = 0.035). Necrosis was reduced in the V.A.C. group, but this difference did not reach significance. Redon bottles are not a good alternative for V.A.C. therapy for delivering NPWT.

Topics: Aged; Aged, 80 and over; Austria; Debridement; Drainage; Equipment Design; Equipment Failure; Fibrin; Granulation Tissue; Humans; Necrosis; Negative-Pressure Wound Therapy; Nursing Evaluation Research; Pressure Ulcer; Severity of Illness Index; Therapy, Computer-Assisted; Time and Motion Studies; Treatment Outcome; Workload; Wound Healing

To evaluate the efficacy of hyaluronic acid to improve the healing of surgical incisions in the oral cavity.. Six Italian private practices participated in this trial, each centre provided 12 patients. After suturing, patients were randomised to receive either a single application of 0.8% hyaluronic acid or a placebo (the carrier). Outcome measures were: assessment of wound healing 10 days post-operatively on a Likert scale by the blind operators and by an independent and blinded outcome assessor on the photographs, adverse events and post-operative complications. Reproducibility was assessed by evaluating agreement between operators and the independent outcome assessor using the weighted Kappa statistic.. Thirty-six patients were evaluated in each group, at ten days none had dropped-out. No post-operative complications or adverse events occurred. There were no statistically significant differences for wound healing, assessed clinically by the blinded operators or on photographs evaluated by a blinded and independent outcomes assessor. There was a substantial agreement between operators and the independent outcome assessor in the wound scoring.. Hyaluronic acid placed over surgical incisions in the oral cavity does not appear to improve wound healing. Further trials are needed to better understand the potential role of hyalulonic acid in dental applications.

Topics: Adult; Aged; Female; Fibrin; Follow-Up Studies; Humans; Hyaluronic Acid; Male; Middle Aged; Mouth Mucosa; Necrosis; Periodontium; Photography, Dental; Pilot Projects; Placebos; Postoperative Complications; Single-Blind Method; Surgical Wound Dehiscence; Surgical Wound Infection; Suture Techniques; Treatment Outcome; Wound Healing

The aim of this prospective clinical study was to analyze graft-enhanced soft tissue healing during the initial phases after tooth extraction. Twenty patients in need of tooth extraction (incisors, canines, and premolars) and implant replacement were included. In patients with multiple extractions, one tooth was randomly selected for treatment. After administration of antibiotics, the selected tooth was gently removed. The socket was completely filled with deproteinized bovine bone mineral integrated in a 10% collagen matrix to fill out the space of the alveolus and support the soft tissue. A biopsy punch with a diameter corresponding to the socket orifice was chosen to harvest a free gingival graft of 2- to 3-mm thickness from the palate. The punched graft was carefully sutured to the deepithelialized soft tissue margins of the socket. One week after graft insertion, 64.3% of the mean graft area was fully integrated, 35.6% was fibrinoid, and 0.1% showed necrotic parts. Three and 6 weeks postsurgery, the mean integrated graft surface increased to 92.3% and 99.7%, respectively. After 6 weeks, a mean of 0.3% of the surface in four grafts showed incomplete wound closure, and no fibrin or necrosis was present. Colorimetry of the graft and adjacent tissue revealed a mean color match of deltaE = 2.91, lower than the critical threshold of 3.7 for intraoral visibility of different colors. This soft tissue punch technique led to successful biologic and esthetic integration of the transplanted graft into the local host tissues.

Topics: Adult; Animals; Biopsy; Bone Matrix; Bone Substitutes; Cattle; Collagen; Colorimetry; Female; Fibrin; Follow-Up Studies; Gingiva; Graft Survival; Humans; Male; Middle Aged; Necrosis; Prospective Studies; Tissue Adhesives; Tooth Extraction; Tooth Socket; Wound Healing

Regeneration of mineralized and soft connective tissue components of the attachment apparatus is the main goal in the treatment of periodontal diseases. Often, apical migration of epithelium (long junctional epithelium) effectively prevents the formation of bone and connective tissue attachment after periodontal surgery. The purpose of the present study was to compare conventional periodontal surgery combined with carbon dioxide laser and conventional periodontal surgery alone with respect to epithelial elimination and degree of necrosis of mucoperiosteal flaps. After signing a consent form, five patients with at least two comparable bilateral periodontal defects needing pocket elimination surgery participated in this study. The investigators randomly divided each side into test and control sites. Each patient received oral hygiene instruction and initial therapy prior to surgery. At surgery, the test site received a sulcular incision and carbon dioxide laser de-epithelialization of the outer and inner aspects of the flap. The control group received reverse bevel incision only. The surgeon performed open flap debridement on all teeth. At the time of surgery, the surgeon did a biopsy of each site and submitted specimens for histologic evaluation. A matched pairs t-test was used to analyze the data. The results show significant differences between the carbon dioxide laser and reverse bevel incision with respect to sulcular (P < or = 0.025) and gingival (external) (P < or = 0.01) flap surface epithelial elimination and tissue necrosis (P < or = 0.005). These results should be replicated with a larger number of subjects. The carbon dioxide laser eliminated sulcular and gingival (external) epithelium without disturbing underlying connective tissue. This finding supports the concept that the carbon dioxide wavelength has little or no effect on tissues beyond the target. However, neither laser nor blade eliminated all the epithelium. Researchers observed chronic inflammation in the control and test sites, with a predominance of plasma cells. Lining the sulcular and gingival (external) lased areas, investigators found coagulation necrosis covered by fibrin and coagulated blood. The laser appears to effectively remove epithelium at the time of surgery; however, future long-term, well-controlled quantitative histologic studies are needed to evaluate the effect of repeated carbon dioxide laser de-epithelialization of the gingival (external) surface of mucoperiosteal

Topics: Biopsy; Blood Coagulation; Carbon Dioxide; Cell Movement; Connective Tissue; Debridement; Epithelial Attachment; Epithelium; Female; Fibrin; Gingivectomy; Humans; Inflammation; Laser Therapy; Male; Matched-Pair Analysis; Necrosis; Oral Hygiene; Periodontal Diseases; Periodontal Pocket; Periodontium; Plasma Cells; Regeneration; Surgical Flaps; Wound Healing

Recent evidence supports the - rare - occurrence of vertical transplacental SARS-CoV-2 transmission. We previously determined that placental expression of angiotensin-converting enzyme 2 (ACE2), the SARS-CoV-2 receptor, and associated viral cell entry regulators is upregulated by hypoxia. In the present study, we utilized a clinically relevant model of SARS-CoV-2-associated chronic histiocytic intervillositis/massive perivillous fibrin deposition (CHIV/MPFVD) to test the hypothesis that placental hypoxia may facilitate placental SARS-CoV-2 infection.. We performed a comparative immunohistochemical and/or RNAscope in-situ hybridization analysis of carbonic anhydrase IX (CAIX, hypoxia marker), ACE2 and SARS-CoV-2 expression in free-floating versus fibrin-encased chorionic villi in a 20-weeks' gestation placenta with SARS-CoV-2-associated CHIV/MPVFD.. The levels of CAIX and ACE2 immunoreactivity were significantly higher in trophoblastic cells of fibrin-encased villi than in those of free-floating villi, consistent with hypoxia-induced ACE2 upregulation. SARS-CoV-2 showed a similar preferential localization to trophoblastic cells of fibrin-encased villi.. The localization of SARS-CoV-2 to hypoxic, fibrin-encased villi in this placenta with CHIV/MPVFD suggests placental infection and, therefore, transplacental SARS-CoV-2 transmission may be promoted by hypoxic conditions, mediated by ACE2 and similar hypoxia-sensitive viral cell entry mechanisms. Understanding of a causative link between placental hypoxia and SARS-CoV-2 transmittability may potentially lead to the development of alternative strategies for prevention of intrauterine COVID-19 transmission.

Topics: Adult; Angiotensin-Converting Enzyme 2; Carbonic Anhydrase IX; Chorionic Villi; COVID-19; Female; Fibrin; Gestational Age; Histiocytes; Humans; Hypoxia; Infectious Disease Transmission, Vertical; Necrosis; Placenta; Pregnancy; Pregnancy Complications, Infectious; SARS-CoV-2; Stillbirth; Trophoblasts

Background: Endotoxemia causes endothelial dysfunction and microthrombosis, which are pathogenic mechanisms of coagulopathy and organ failure during sepsis. Simvastatin has potential anti-thrombotic effects on liver endothelial cells. We investigated the hemostatic changes induced by lipopolysaccharide (LPS) and explored the protective effects of simvastatin against liver vascular microthrombosis. Methods and results: We compared male Wistar rats exposed to LPS (5 mg/kg one i.p. dose) or saline in two experimental protocols—placebo (vehicle) and simvastatin (25 mg/kg die, orally, for 3 days before LPS). Morphological studies were performed by light- and electron-microscopy analyses to show intravascular fibrin deposition, vascular endothelial structure and liver damage. Peripheral- and organ-hemostatic profiles were analyzed using whole blood viscoelastometry by ROTEM, liver biopsy and western-blot/immunohistochemistry of thrombomodulin (TM), as well as immunohistochemistry of the von Willebrand factor (VWF). LPS-induced fibrin deposition and liver vascular microthrombosis were combined with a loss of sinusoidal endothelial TM expression and VWF-release. These changes were associated with parenchymal eosinophilia and necrosis. ROTEM analyses displayed hypo-coagulability in the peripheral blood that correlated with the degree of intrahepatic fibrin deposition (p < 0.05). Simvastatin prevented LPS-induced fibrin deposition by preserving TM expression in sinusoidal cells and completely reverted the peripheral hypo-coagulability caused by endotoxemia. These changes were associated with a significant reduction of liver cell necrosis without any effect on eosinophilia. Conclusions: Simvastatin preserves the antithrombotic properties of sinusoidal endothelial cells disrupted by LPS, deserving pharmacological properties to contrast sepsis-associated coagulopathy and hepatic failure elicited by endotoxemia

Topics: Animals; Disease Models, Animal; Endothelial Cells; Endotoxemia; Fibrin; Hemostatics; Lipopolysaccharides; Liver Diseases; Male; Necrosis; Rats; Rats, Wistar; Sepsis; Simvastatin; Thrombosis; von Willebrand Factor

The objective of this study was to evaluate critically the nature and prevalence of histological pulmonary lesions in dogs and cats that had died or were euthanized because of tick paralysis. A retrospective and prospective case study of 11 cats and 23 dogs was carried out. Retrospective cases were gathered from the Veterinary Laboratory Services database at The University of Queensland (UQ). Prospective cases were provided by Veterinary Specialist Services and UQ VETs Small Animal Hospital. Lung and other tissue samples were collected for histopathological analysis. All tick intoxicated animals demonstrated evidence of pulmonary parenchymal changes: alveolar oedema, interstitial and alveolar congestion and alveolar fibrin exudation. Eleven of 23 (48%) dogs exhibited mild to severe bronchopneumonia. A lower rate (18%) of bronchopneumonia was found in cats, with one case of aspiration pneumonia. A novel pulmonary histological grading scheme was developed to evaluate the correlation between clinical presentation and histopathological changes. Novel extrapulmonary lesions in cats included hepatic necrosis and acute renal tubular necrosis attributed to hypoxia. We concluded that both dogs and cats with high clinical grade tick paralysis are extremely likely to have pulmonary pathology. High-protein oedema and fibrin exudation are predicted to be present in most cases of canine and feline tick paralysis.

Topics: Animals; Bronchopneumonia; Cat Diseases; Cats; Dog Diseases; Dogs; Fibrin; Lung; Necrosis; Retrospective Studies; Tick Paralysis

Topics: Bile Ducts; Fibrin; Humans; Liver; Necrosis; Perfusion; Plasma; Tissue Plasminogen Activator

The COVID-19 pandemic has provided many challenges in the field of thrombosis and hemostasis. Among these is a novel form of coagulopathy that includes exceptionally high levels of D-dimer. D-dimer is a marker of poor prognosis, but does this also imply a causal relationship? These spectacularly raised D-dimer levels may actually signify the failing attempt of the fibrinolytic system to remove fibrin and necrotic tissue from the lung parenchyma, being consumed or overwhelmed in the process. Indeed, recent studies suggest that increasing fibrinolytic activity might offer hope for patients with critical disease and severe respiratory failure. However, the fibrinolytic system can also be harnessed by coronavirus to promote infectivity and where antifibrinolytic measures would also seem appropriate. Hence, there is a clinical paradox where plasmin formation can be either deleterious or beneficial in COVID-19, but not at the same time. Hence, it all comes down to timing.

Topics: Acute Lung Injury; Animals; Antifibrinolytic Agents; COVID-19; COVID-19 Drug Treatment; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinolysin; Fibrinolysis; Humans; Immune System; Lung; Necrosis; Prognosis; Thrombolytic Therapy; Tissue Plasminogen Activator

Topics: Apoptosis; Behcet Syndrome; Extracellular Traps; Fibrin; Humans; Necrosis; Neutrophils; Protein-Arginine Deiminase Type 4; Reactive Oxygen Species; Thrombin; Thrombosis

Forensic imaging technology has rapidly advanced over the past several decades and is gaining increasing significance in medico-legal death investigations. Medical-grade computed tomography (CT) is now routinely used in post-mortem examinations at numerous institutions across the globe. However, the resolution of medical-grade CT is limited and unsuitable when used to depict some smaller anatomical structures or micro-trauma. High-resolution micro-CT offers up to 100× the resolution to overcome this problem but is a very recent addition to the field of forensic radiology. Few studies so far have attempted to validate the results which is an essential prerequisite for it to be used in the criminal justice process as demanded by regulatory bodies. This study directly compares micro-CT images with histology, the current gold standard. Three cases were examined: two larynges from suspected strangulations and one ribcage of a case of fatal child abuse. A strong correlation was observed between histology and micro-CT as the majority of skeletal injuries were identified correctly. This paper discusses the forensic implications of the results and how micro-CT is complementary to histology.

Topics: Adult; Female; Fibrin; Forensic Medicine; Fractures, Bone; Fractures, Cartilage; Hematoma; Humans; Hyoid Bone; Imaging, Three-Dimensional; Infant; Larynx; Necrosis; Osteoblasts; Osteoclasts; Osteocytes; Rib Fractures; Thyroid Cartilage; X-Ray Microtomography

Blood loss remains a major concern during surgery and can increase the morbidity of the intervention. The use of topical haemostatic agents to overcome this issue therefore becomes necessary. Fibrin sealants are promising haemostatic agents due to their capacity to promote coagulation, but their effectiveness and applicability need to be improved. We have compared the haemostatic efficacy of a novel nanostructured fibrin-agarose hydrogel patch, with (c-NFAH) or without cells (a-NFAH), against two commercially available haemostatic agents in a rat model of hepatic resection. Hepatic resections were performed by making short or long incisions (mild or severe model, respectively), and haemostatic agents were applied to evaluate time to haemostasis, presence of haematoma, post-operative adhesions to adjacent tissues, and inflammation factors. We found a significantly higher haemostatic success rate (time to haemostasis) with a-NFAH than with other commercial haemostatic agents. Furthermore, other relevant outcomes investigated were also improved in the a-NFAH group, including no presence of haematoma, lower adhesions, and lower grades of haemorrhage, inflammation, and necrosis in histological analysis. Overall, these findings identify a-NFAH as a promising haemostatic agent in liver resection and likely in a range of surgical procedures.

Topics: Animals; Fibrin; Hemorrhage; Hemostatics; Hydrogels; Inflammation; Liver; Male; Nanostructures; Necrosis; Rats, Wistar; Sepharose

The present study aimed to determine the impact of different sealant materials on histopathological changes to the liver surface after liver resection. Thirty-six landrace pigs underwent left anatomical hemihepatectomy and were assigned to a histopathological control group (HPC, n = 9) with no bleeding control, a clinically simulated control group (CSC, n = 9) with no sealant but bipolar cauterization and oversewing of the liver surface, and two treatment groups (n = 9 each) with a collagen-based sealant (CBS) or a fibrinogen-based sealant (FBS) on resection surface. After postoperative day 6, tissue samples were histologically examined. There were no significant differences in preoperative parameters between the groups. Fibrin production was higher in sealant groups compared with the HPC and CSC groups (both p < 0.001). Hepatocellular regeneration in sealant groups was higher than in both control groups. A significantly higher regeneration was seen in the FBS group. Use of sealants increased the degree of fibrin exudation at the resection plane. Increased hepatocellular necrosis was seen in the CBS group compared with the FBS group. The posthepatectomy hepatocellular regeneration rate was higher in the FBS group compared with the CBS group. Randomized studies are needed to assess the impact of sealants on posthepatectomy liver regeneration in the clinical setting.

Topics: Administration, Topical; Animals; Collagen; Drug Combinations; Fibrin; Fibrin Tissue Adhesive; Fibrinogen; Hemostatics; Hepatectomy; Liver; Liver Regeneration; Necrosis; Perioperative Period; Postoperative Hemorrhage; Swine; Thrombin; Treatment Outcome

Heart transplantation is the only cure for patients with terminal cardiac failure, but the supply of allogeneic donor organs falls far short of the clinical need

Topics: Animals; Antibodies; Complement System Proteins; Enzymes; Fibrin; Galactosyltransferases; Heart Transplantation; Heterografts; Humans; Liver; Male; Membrane Cofactor Protein; Myocardium; Necrosis; Papio; Perfusion; Platelet Count; Prothrombin Time; Swine; Thrombomodulin; Time Factors; Transplantation, Heterologous

The focus of this double-blind randomized study was on evaluating the effect of an aqueous extract of Mastruz (Chenopodium ambrosioides L.) on the bone repair process in vivo. In total, 36 male Wistar rats were randomly selected for this study, and divided into 3 groups (n = 12): Group HS (Hemostatic Sponge), Group SM (Hemostatic Sponge with Mastruz) and Group BC (Blood Clot). In each animal, bone defects measuring 2 mm in diameter were performed in both tibias for placement of the substances. After 3 and 10 days, the animals were sacrificed, and the tissues were analyzed under an optical microscope relative to the following events: inflammatory infiltrate; necrosis; young fibroblasts; osteoclastic and osteoblastic activity; endosteal and periosteal bone formation; and bone repair. The results were assessed by using Kruskal-Wallis and Mann-Whitney tests (p < .05). Inflammatory infiltrate demonstrated difference between Groups SM and BC in the time interval of 3 days (p = .004); an event related to the presence of the fibrin sponge and liquid of the extract, which induced a foreign body initial reaction. The presence of young fibroblasts (p = .003), osteoclastic (p = .003), and osteoblastic (p = .020) activity was statistically significant between Groups HS and BC in the time interval of 10 days; performance was related to the presence of the sponge within bone. As regards injured bone tissue repair, Group SM demonstrated a higher level of regenerative capacity (p = 0.004), due to a larger quantities of endosteal and periosteal bone formation, demonstrated in Group SM. The aqueous extract of mastruz stimulated bone neoformation, presenting wound closure with bone tissue at the end of 10 days.

Topics: Animals; Bone and Bones; Bone Regeneration; Chenopodium ambrosioides; Double-Blind Method; Fibrin; Inflammation; Male; Necrosis; Osteogenesis; Phytotherapy; Plant Extracts; Random Allocation; Rats; Rats, Wistar; Wound Healing

This report suggests a strong association between coagulase-negative Staphylococcus simulans and endocarditis in broiler chickens of a single flock. Clinical signs included increased mortality and lameness, and some dead chickens were found on their backs. Lesions included cauliflower-like, fibrinous vegetative lesions on the left atrioventricular valve; cream-coloured, necrotic foci of varying size in the liver; and necrosis of the femoral head. Histopathological examination of the heart revealed multifocal conglomerates of bacterial colonies attached to the valvular endocardium, threads of fibrin, and inflammatory cells with the presence of heterophils. S. simulans strains were first identified by API ID32, and then confirmed with Matrix-Assisted Laser Desorption Ionization Time-of-Flight Mass Spectrometry and by partial sequencing of the rpoB and dnaJ genes. These bacteria were resistant to methicillin but sensitive to vancomycin and characterized by slime production and protease activity.

Topics: Animals; Anti-Infective Agents; Chickens; Drug Resistance, Bacterial; Endocarditis; Fibrin; Methicillin; Necrosis; Staphylococcal Infections; Staphylococcus; Vancomycin; Virulence Factors

Coagulation cascade activation and fibrin deposits have been implicated or observed in diverse forms of liver damage. Given that fibrin amplifies pathological inflammation in several diseases through the integrin receptor αMβ2, we tested the hypothesis that disruption of the fibrin(ogen)-αMβ2 interaction in Fibγ(390-396A) mice would reduce hepatic inflammation and fibrosis in an experimental setting of chemical liver injury. Contrary to our hypothesis, α-naphthylisothiocyanate (ANIT)-induced liver fibrosis increased in Fibγ(390-396A) mice, whereas inflammatory cytokine expression and hepatic necrosis were similar to ANIT-challenged wild-type (WT) mice. Increased fibrosis in Fibγ(390-396A) mice appeared to be independent of coagulation factor 13 (FXIII) transglutaminase, as ANIT challenge in FXIII-deficient mice resulted in a distinct pathological phenotype characterized by increased hepatic necrosis. Rather, bile duct proliferation underpinned the increased fibrosis in ANIT-exposed Fibγ(390-396A) mice. The mechanism of fibrin-mediated fibrosis was linked to interferon (IFN)γ induction of inducible nitric oxide synthase (iNOS), a gene linked to bile duct hyperplasia and liver fibrosis. Expression of iNOS messenger RNA was significantly increased in livers of ANIT-exposed Fibγ(390-396A) mice. Fibrin(ogen)-αMβ2 interaction inhibited iNOS induction in macrophages stimulated with IFNγ in vitro and ANIT-challenged IFNγ-deficient mice had reduced iNOS induction, bile duct hyperplasia, and liver fibrosis. Further, ANIT-induced iNOS expression, liver fibrosis, and bile duct hyperplasia were significantly reduced in WT mice administered leukadherin-1, a small molecule that allosterically enhances αMβ2-dependent cell adhesion to fibrin. These studies characterize a novel mechanism whereby the fibrin(ogen)-integrin-αMβ2 interaction reduces biliary fibrosis and suggests a novel putative therapeutic target for this difficult-to-treat fibrotic disease.

Topics: 1-Naphthylisothiocyanate; Animals; Benzoates; Bile Ducts; Cell Adhesion; Female; Fibrin; Humans; Hyperplasia; Inflammation; Interferon-gamma; Liver Cirrhosis, Biliary; Macrophage-1 Antigen; Male; Mice; Mice, Knockout; Necrosis; Thiohydantoins

A well-known histopathological feature of diseased skin in Buruli ulcer (BU) is coagulative necrosis caused by the Mycobacterium ulcerans macrolide exotoxin mycolactone. Since the underlying mechanism is not known, we have investigated the effect of mycolactone on endothelial cells, focussing on the expression of surface anticoagulant molecules involved in the protein C anticoagulant pathway. Congenital deficiencies in this natural anticoagulant pathway are known to induce thrombotic complications such as purpura fulimans and spontaneous necrosis. Mycolactone profoundly decreased thrombomodulin (TM) expression on the surface of human dermal microvascular endothelial cells (HDMVEC) at doses as low as 2 ng/ml and as early as 8 hrs after exposure. TM activates protein C by altering thrombin's substrate specificity, and exposure of HDMVEC to mycolactone for 24 hours resulted in an almost complete loss of the cells' ability to produce activated protein C. Loss of TM was shown to be due to a previously described mechanism involving mycolactone-dependent blockade of Sec61 translocation that results in proteasome-dependent degradation of newly synthesised ER-transiting proteins. Indeed, depletion from cells determined by live-cell imaging of cells stably expressing a recombinant TM-GFP fusion protein occurred at the known turnover rate. In order to determine the relevance of these findings to BU disease, immunohistochemistry of punch biopsies from 40 BU lesions (31 ulcers, nine plaques) was performed. TM abundance was profoundly reduced in the subcutis of 78% of biopsies. Furthermore, it was confirmed that fibrin deposition is a common feature of BU lesions, particularly in the necrotic areas. These findings indicate that there is decreased ability to control thrombin generation in BU skin. Mycolactone's effects on normal endothelial cell function, including its ability to activate the protein C anticoagulant pathway are strongly associated with this. Fibrin-driven tissue ischemia could contribute to the development of the tissue necrosis seen in BU lesions.

Topics: Anti-Bacterial Agents; Buruli Ulcer; Endothelial Cells; Fibrin; Humans; Macrolides; Mycobacterium ulcerans; Necrosis; Skin; Thrombomodulin

The prognosis of gastric cancer during pregnancy is unfavorable because of delayed diagnosis and advanced stage. We present a case of gastric carcinoma metastasized to the placenta and uterus during pregnancy. Pathological examination revealed a poorly differentiated adenocarcinoma of the stomach with lymph node metastasis. After counseling, the patient decided to terminate the pregnancy and begin immediate treatment for gastric cancer. Hysterectomy and subtotal hysterectomy were performed because medical termination of the pregnancy was unsuccessful. Pathological examination of the placenta and uterus revealed metastases of gastric adenocarcinoma. All the uterine vessels were packed with tumor cells and the myometrium showed extensive coagulative necrosis. Moreover, microscopic findings of the placenta were consistent with massive perivillous fibrin deposition. Our case clearly suggests that massive perivillous fibrin deposition in the placenta can be associated with malignancy during pregnancy and that uterine metastasis of maternal malignancy may result in myometrial dysfunction unresponsive to uterotonics.

Topics: Adenocarcinoma; Adult; Chorionic Villi; Female; Fibrin; Humans; Necrosis; Neoplasm Proteins; Placenta; Placental Circulation; Pregnancy; Stomach Neoplasms; Trophoblastic Tumor, Placental Site; Up-Regulation; Uterine Neoplasms; Uterus

Protein kinase C epsilon (PKCε) has been shown to play a role in experimental steatosis by acute alcohol. The "two-hit" hypothesis implies that preventing steatosis should blunt more advanced liver damage (e.g., inflammation and necrosis). However, the role of PKCε in these pathologies is not yet known. The goal of this current work was to address this question in a model of chronic alcohol exposure using antisense oligonucleotides (ASO) against PKCε.. Accordingly, PKCε ASO- and saline-treated mice were fed high-fat control or ethanol (EtOH)-containing enteral diets for 4 weeks.. Chronic EtOH exposure significantly elevated hepatic lipid pools as well as activated PKCε. The PKCε ASO partially blunted the increases in hepatic lipids caused by EtOH. Administration of PKCε ASO also completely prevented the increase in the expression of fatty acid synthase, and tumor necrosis factor α caused by EtOH. Despite these protective effects, the PKCε ASO was unable to prevent the increases in inflammation and necrosis caused by chronic EtOH. These latter results correlated with an inability of the PKCε ASO to blunt the up-regulation of plasminogen activator inhibitor-1 (PAI-1) and the accumulation of fibrin. Importantly, PAI-1 has been previously shown to more robustly mediate inflammation and necrosis (vs. steatosis) after chronic EtOH exposure.. This study identifies a novel potential mechanism where EtOH, independent of steatosis, can contribute to liver damage. These results also suggest that PAI-1 and fibrin accumulation may be at the center of this PKCε-independent pathway.

Topics: Animals; Biomarkers; Body Weight; Central Nervous System Depressants; Diglycerides; Enzyme Activation; Ethanol; Fatty Liver, Alcoholic; Fibrin; Gene Expression; Hepatitis, Alcoholic; Lipid Metabolism; Liver; Male; Mice; Mice, Inbred C57BL; Necrosis; Protein Kinase C-epsilon

Emerging evidence indicates that various haemostatic components can regulate the progression of liver disease. Thrombin-activatable fibrinolysis inhibitor (TAFI) possesses anti-inflammatory properties besides its anti-fibrinolytic function. Here, we investigated the contribution of TAFI to the progression of disease in murine models of chronic and acute liver failure. Chronic carbon tetrachloride (CCL4) administration induced liver damage and fibrosis both in TAFI knockout (TAFI-/-) mice and wild-type controls. Smooth muscle actin-α (α-SMA) content of liver tissue was significantly increased after 1 and 3 weeks, and pro-collagen α1 expression was significantly increased after 3 and 6 weeks in TAFI-/- mice. TAFI-/- mice showed significantly elevated levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) after 3 weeks of CCL4. Neutrophil influx was significantly increased in TAFI-/- mice after 6 weeks of CCL4. No difference in hepatic fibrin deposition between TAFI-/- and wild-types was observed. After acetaminophen intoxication, necrosis was significantly increased in TAFI-/- mice at 24 hours (h) after injection. AST and ALT levels were decreased at 2 and 6 h after acetaminophen injection in TAFI-/- mice, but were significantly higher in the TAFI-/- mice at 24 h. Similarly, hepatic fibrin deposition was decreased at 6 h in TAFI-/- mice, but was comparable to wild-types at 24 h after injection. In conclusion, TAFI deficiency results in accelerated fibrogenesis and increased liver damage in murine models of chronic and acute liver disease, which may be related to increased inflammation.

Topics: Acetaminophen; Actins; Acute Disease; Alanine Transaminase; Animals; Aspartate Aminotransferases; Carbon Tetrachloride; Carboxypeptidase B2; Chemical and Drug Induced Liver Injury; Chronic Disease; Collagen Type I; Collagen Type I, alpha 1 Chain; Fibrin; Gene Expression Regulation; Liver; Liver Cirrhosis, Experimental; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Necrosis; Neutrophil Infiltration; RNA, Messenger; Time Factors

Concanavalin A (Con A) treatment induces severe hepatitis in mice in a manner dependent on T cells, interferon (IFN)-gamma, and tumor necrosis factor (TNF). Treatment with the anticoagulant heparin protects against hepatitis, despite healthy production of IFN-γ and TNF. Here, we investigated molecular and cellular mechanisms for hypercoagulation-mediated hepatitis. After Con A challenge, liver of wild-type (WT) mice showed prompt induction of Ifnγ and Tnf, followed by messenger RNA expression of tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1), which initiate blood coagulation and inhibit clot lysis, respectively. Mice developed dense intrahepatic fibrin deposition and massive liver necrosis. In contrast, Ifnγ(-/-) mice and Ifnγ(-/-) Tnf(-/-) mice neither induced Pai1 or Tf nor developed hepatitis. In WT mice TF blockade with an anti-TF monoclonal antibody protected against Con A-induced hepatitis, whereas Pai1(-/-) mice were not protected. Both hepatic macrophages and sinusoidal endothelial cells (ECs) expressed Tf after Con A challenge. Macrophage-depleted WT mice reconstituted with hematopoietic cells, including macrophages deficient in signal transducer and activator of transcription-1 (STAT1) essential for IFN-γ signaling, exhibited substantial reduction of hepatic Tf and of liver injuries. This was also true for macrophage-depleted Stat1(-/-) mice reconstituted with WT macrophages. Exogenous IFN-γ and TNF rendered T-cell-null, Con A-resistant mice deficient in recombination-activating gene 2, highly susceptible to Con A-induced liver injury involving TF.. Collectively, these results strongly suggest that proinflammatory signals elicited by IFN-γ, TNF, and Con A in both hepatic macrophages and sinusoidal ECs are necessary and sufficient for the development of hypercoagulation-mediated hepatitis.

Topics: Animals; Concanavalin A; Endothelial Cells; Fibrin; Hepatitis, Animal; Interferon-gamma; Liver; Macrophages; Mice; Mice, Knockout; Mitogens; Necrosis; Plasminogen Activator Inhibitor 1; Signal Transduction; STAT1 Transcription Factor; T-Lymphocytes; Thrombophilia; Thromboplastin; Tumor Necrosis Factor-alpha

Ischemia and infection of the distal part of the tracheobronchial anastomosis are the leading causes of bronchial anastomotic leakage with a high morbidity and mortality. To improve interpretation of healing of the anastomosis and the consequences, we have developed a classification scheme that allows quality control and defines early and standardized treatment of complications.. We conducted a retrospective analysis of the records of 202 patients treated in our institution between January 1, 2006 and December 31, 2010 after sleeve lobectomy. All patients received prophylactic inhalation with tobramycin 80 mg twice a day. Neoadjuvant treatment was given in 21% of the patients. Routine bronchoscopy on day 7 was performed with classification of the anastomosis as follows: X, unknown; 1, healing well with no fibrin deposits; 2, focal fibrin deposits and superficial (mucosal) necrosis; 3, circular fibrin deposits, superficial (mucosal) necrosis, and/or ischemia of the distal mucosa; 4, transmural necrosis with instability of the anastomosis; and 5, perforation, necrosis of the anastomosis, and insufficiency.. The anastomosis was graded as satisfactory (1 and 2) in 86% of the patients. In 14%, it was regarded as critical (≥3-5) leading to systemic antibiotic treatment and control bronchoscopy. The overall 30-day mortality was 1%.. Quality control of the tracheobronchial anastomosis comprised bronchoscopy performed before patients were dismissed. Inasmuch as postoperative bronchoscopy is not always performed by the operating surgeon, this classification is an aid to improve the description of endobronchial healing and to commence treatment of critical bronchial healing.

Topics: Adult; Aged; Aged, 80 and over; Anastomosis, Surgical; Bronchi; Bronchoscopy; Female; Fibrin; Germany; Humans; Male; Middle Aged; Necrosis; Pneumonectomy; Postoperative Complications; Quality Indicators, Health Care; Retrospective Studies; Time Factors; Trachea; Treatment Outcome; Wound Healing

To determine the fibrinoid necrosis and hyalinization extent in placenta observed in normal, diabetic and hypertensive pregnancies.. Comparative cross-sectional study.. Institute of Basic Medical Sciences, Dow University of Health Sciences, Karachi, from 2008-2010.. One hundred and fifty placentae were divided in three groups on the basis of their histories and clinical examination. Group A (control), Group B (Diabetic) and Group C (Hypertensive), each consisted of 50 samples. The samples were transferred to Dow Diagnostic Reference and Research Laboratory for histopathology and gross examination. The tissue samples were taken from different sites, processed and routine staining done. The slides were then examined under light microscope for hyalinization and fibrinoid necrosis. The data was analyzed by applying ANOVA and post-hoc Tukey at 95% confidence interval. Mean ± standard deviations (SD) were computed.. The mean number of hyalinized villi in control group was 0.54 ± 0.908, 1.18 ± 1.9540 in the diabetic group and 2.14 ± 1.863 in the hypertensive group. The difference in their average turned out to be statistically significant (p-value < 0.001). Mean number of villi having fibrinoid necrosis was statistically significant in both the diabetic and hypertensive groups as compared to the control group i.e. 13.98 vs. 4.02 and 10.08 vs. 4.02 respectively (p-value < 0.001).. There was significantly greater fibrinoid necrosis and hyalinization in placentae from mothers having diabetes and hypertension. The fibrinoid necrosis was seen more in diabetic group as compared to hypertensive and control, while hyalinization was observed more frequently in hypertensive group as compared to the other groups. Placental changes as seen in examination of delivered placentae will be helpful in preventing the adverse effects in successive pregnancies.

Topics: Analysis of Variance; Chorionic Villi; Cross-Sectional Studies; Diabetes, Gestational; Female; Fibrin; Gestational Age; Humans; Hypertension; Hypertension, Pregnancy-Induced; Microscopy; Necrosis; Organ Size; Pakistan; Placenta; Pregnancy; Pregnancy in Diabetics

Diabetes is associated with increased risk of cardiovascular disease. Advanced glycation end-products (AGEs) are considered to be a major pathogenic factor for diabetic vascular complications. The levels of AGEs are increased in diabetic patients. We have studied the presence of the major AGE methylglyoxal (MGO)-derived hydroimidazolone in human aorta and carotid arteries, using immunohistochemistry (IHC), western blotting and mass spectrometry. By IHC, MGO-derived modifications were detected mainly associated with cells in intimal thickenings and cells in microvessels in adventitia. In type V lesions MGO-derived AGE was also present, extracellular in the necrotic core and in cells at the border of the core. The highest degree of modification was probably associated with cell nuclei. By western blotting and mass spectrometry fibrin(ogen), the cytoskeleton-associated protein moesin and the nuclear proteins lamin A and C were identified as putative main targets for MGO-derived modification. LC-MS/MS studies of fibrin(ogen) modified in vitro with low concentrations of MGO identified the sites that were most prone to modification. These results indicate that AGE modifications occur preferentially on specific proteins. The modification of these proteins may play a role in vascular dysfunction and development of atherosclerosis in diabetes.

Topics: Aged; Aged, 80 and over; Amino Acid Sequence; Aorta; Blotting, Western; Carotid Artery, Common; Case-Control Studies; Chromatography, Liquid; Diabetic Angiopathies; Elasticity; Female; Fibrin; Fibrinogen; Glycation End Products, Advanced; Humans; Imidazoles; Immunohistochemistry; Male; Middle Aged; Molecular Sequence Data; Necrosis; Norway; Protein Processing, Post-Translational; Proteomics; Pyruvaldehyde; Tandem Mass Spectrometry

Intraplaque haemorrhage has been shown to be important in necrotic core enlargement. Immunolocalisation of fibrin within progressive stages of plaque progression has not been extensively studied.. Histological sections (n = 74) of human coronary arteries were stained immunohistochemically for fibrin II, red blood cell antigen (glycophorin A), and CD31. Plaques were chosen to represent a range of lesions [6 adaptive intimal thickening, AIT (AHA grade I); 4 intimal xanthomas (AHA grade II), 19 pathologic intimal thickening, PIT (AHA grade III, or pre-atheroma); 34 fibroatheromas, FA (AHA grade IV and V); and 11 thin cap fibroatheromas (TCFA, AHA grade IV)].. Fibrin was generally absent in the intima of AIT and PIT, with moderate staining in cores of early FA (2.6 +/- 0.3). All late FA and TCFA demonstrated intracore fibrin, with mean scores of 2.9 +/- 0.3 and 3.0 +/- 0.3, respectively. Intimal vasa vasorum counts increased with intimal fibrin score (p < 0.0001); in 68% of cores with fibrin staining, there was minimal or no evidence of red cell breakdown.. Fibrin in necrotic cores is present proportional to intraplaque vasa vasorum and before red cells, suggesting leakage of vessels before frank intraplaque haemorrhage. Fibrin may play a role in the bridge between pre-atheroma and atheroma.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Coronary Artery Disease; Coronary Vessels; Death, Sudden, Cardiac; Disease Progression; Fibrin; Humans; Male; Middle Aged; Necrosis; Prospective Studies; Tunica Intima

Clinical morphological investigations were carried out in a flock of 22,000 Ross 308 broiler chickens at the age of 38 days that experienced a sudden increase in mortality rates. Morbidity and mortality rates were followed and gross anatomical examination of 150 bodies (7%) of all 1541 dead chickens was performed. In all necropsied birds, without exception, the typical macroscopic lesions were observed only in the gizzard. Focal or diffuse pseudomembranous deposits were found subcuticularly and on the gizzard mucous coat. Microscopically, hyalinization, desquamated epithelial cells and single foci of microorganisms were present among the formed pseudomembranes. Among the fibrin networks of coagulated exudate, a single bacilli were detected. Clostridium perfringens was isolated from all gastric samples investigated. Polymerase chain reactions were positive for alpha-toxin and negative for beta-toxin and beta(2)-toxin.

Topics: Animal Husbandry; Animals; Bacterial Toxins; Calcium-Binding Proteins; Chickens; Clostridium Infections; Clostridium perfringens; Disease Outbreaks; Epithelial Cells; Exudates and Transudates; Fibrin; Gastritis; Gizzard, Avian; Necrosis; Poultry Diseases; Type C Phospholipases

Nanomaterials have been used to create new consumer products as well as applications for life sciences and biotechnology. The aim of this study was to evaluate the tissue response to implanted polyethylene tubes filled with fibrin sponge embedded with silver nanoparticles dispersion.. Thirty rats received individually 4 polyethylene tubes filled with sponge embedded in 47 ppm, 23 ppm silver nanoparticles dispersion, 2.5% sodium hypochlorite, or with no embedding as control. The observation periods were 7, 15, 30, 60, and 90 days. After each period of time, 6 animals were killed, and the tubes and surrounding tissue were removed, fixed, and prepared to be analyzed in light microscope with glycol methacrylate embedding, 3-μm serial cutting, and hematoxylin-eosin stain. Qualitative and quantitative evaluations of the reactions were performed.. Both materials caused moderate reactions at 7 days. The response was similar to the control on the 15th day with 23 ppm silver nanoparticles dispersion and 2.5% sodium hypochlorite and on the 30th day with 47 ppm silver nanoparticles dispersion.. It was possible to conclude that silver nanoparticles dispersion was biocompatible especially in a lower concentration.

Topics: Animals; Calcinosis; Connective Tissue; Drug Carriers; Fibrin; Male; Nanoparticles; Necrosis; Neutrophil Infiltration; Rats; Rats, Wistar; Root Canal Irrigants; Silver; Sodium Hypochlorite

Platelet-rich plasma (PRP) has been promoted as a surgical adjunct to enhance hard and soft tissue wound healing. Although anecdotally reported to be of value, the results of controlled studies examining the added effects of PRP on surgical procedures have been mixed. The purpose of this study was to test the effect of PRP on flap strength at various post-surgical time points in a minipig animal model.. Twelve Yucatan minipigs provided four sites per animal. PRP was prepared from each animal at the time of surgery. Following reflection of a mucoperiosteal flap in each quadrant, subgingival plaque and calculus were removed. Each surgical site was irrigated with sterile saline; prior to suturing, one randomly selected test quadrant in each arch was treated with PRP. Four animals were euthanized at day 14, and two animals were euthanized at 2, 7, 10, and 28 days. The flap strength in each quadrant was tested by attaching to a loop of 3-0 silk suture through the tissue; the force required to separate the flap from the tooth/bone interface was recorded for each site. A separate portion of each flap site was prepared for descriptive histologic examination, including inflammation, hemorrhage, and new bone growth.. Flap strength was significantly less on day 2 compared to later time points, and there were no significant differences between the test and control groups. No histologic differences in healing between test and control sites were seen at any time point.. PRP did not seem to contribute to greater flap strength at any post-surgical time point, nor was it associated with any histologic differences in wound healing in this Yucatan minipig model. The time points chosen for observation post-surgery, as well as the variability in the PRP platelet count, may have contributed to the lack of positive findings in this study.

Topics: Animals; Biomechanical Phenomena; Dental Calculus; Dental Plaque; Disease Models, Animal; Edema; Female; Fibrin; Gingiva; Gingivitis; Necrosis; Osteoblasts; Osteogenesis; Periodontium; Platelet-Rich Plasma; Postoperative Hemorrhage; Random Allocation; Stress, Mechanical; Subgingival Curettage; Surgical Flaps; Suture Techniques; Swine; Swine, Miniature; Tensile Strength; Time Factors; Wound Healing

Transgastric endoscopic necrosectomy has been recently introduced as the effective and alternative management of infected pancreatic necrosis and pancreatic abscess. However, up to 40% of patients who undergo endoscopic necrosectomy may need an additional percutaneous approach for subsequent peripancreatic fluid collection or non-resolution of pancreatic necrosis. This percutaneous approach may lead to persistent pancreatocutaneous fistula, which remains a serious problem and usually requires prolonged hospitalization, or even open-abdominal surgery. We describe the first case of pancreatocutaneous fistula and concomitant abdominal wall defect following transgastric endoscopic necrosectomy and percutaneous drainage, which were endoscopically closed with fibrin glue injection via the necrotic cavity.

Topics: Adhesives; Endoscopy, Gastrointestinal; Female; Fibrin; Humans; Middle Aged; Necrosis; Pancreas; Pancreatic Fistula

This paper presents color image processing methods for the analysis of dermatological images in the context of a content-based image retrieval (CBIR) system. Tests were conducted on the classification of tissue components in skin lesions, in terms of necrotic tissue, fibrin, granulation, and mixed composition. The images were classified based on color components by an expert dermatologist following a black-yellow-red model. Indexing and retrieval of images were performed based on texture information obtained from the red, green, blue, hue, and saturation components of the color images. The performance of the CBIR system was measured in terms of precision and recall. Initial results demonstrate the potential of the proposed methods with the best precision result of 70% obtained for the characterization of mixed tissue composition.

Topics: Color; Fibrin; Granulation Tissue; Humans; Image Processing, Computer-Assisted; Information Storage and Retrieval; Necrosis; Pattern Recognition, Automated; Skin; Skin Diseases

Pleomorphic hyalinizing angiectatic tumor (PHAT) of the soft tissue is a rare distinctive tumor listed as a benign neoplasm in the new World Health Organization classification. It may recur and most reported recurrent tumors retained the typical morphological appearance of PHAT; rare tumors recurred with the appearance of a sarcoma. Reported herein is an additional example of recurrent PHAT, but in contrast to the previously described cases the present tumor morphologically qualified as a sarcoma from the very beginning; it recurred as a high-grade myxofibrosarcoma. A 76-year-old woman presented with a solitary subcutaneous tumor in the axilla that was surgically removed. Seven months later, the patient experienced a local recurrence. Microscopically, the typical features of PHAT were identified in the initial lesion, namely hyalinized, fibrin-containing vessels and pleomorphic stromal cells; there were areas of hemorrhage and necrosis. Additionally, peripherally located areas of the tumor manifested highly pleomorphic cells with frequent atypical mitoses, producing a sarcomatous appearance. The mitotic index in the sarcomatous part was 1/10 high-power fields (HPF). Hyalinized, fibrin-containing vessels were absent in these sarcomatous areas, and the stroma was myxoid. The recurrent lesion was composed of large highly pleomorphic oval, round, spindled or bizarre cells with a high mitotic rate, ranging from 3/10 HPF to 7/10 HPF. The neoplastic cells were arranged haphazardly in a myxoid matrix. Hyalinized, fibrin-containing vessels typical for PHAT were absent. PHAT may be more aggressive than previously thought, and PHAT may encompass a morphological spectrum of the lesion ranging from benign to malignant.

Topics: Aged; Dermatofibrosarcoma; Female; Fibrin; Humans; Hyalin; Necrosis; Neoplasm Recurrence, Local; Sarcoma; Skin; Skin Neoplasms

Chronic wounds are a growing challenge for physicians and health insurance agencies. The burden of affected patients is enormous, because of pain but also because of long-lasting therapies and dependence on nursing services. In other areas of medicine, computer-based diagnostics is established, yet, accurate wound documentation is rarely conducted and is often limited to size measurement with a ruler and a rough photo documentation. Objective assessment of lesions by evaluation of granulation tissue, fibrin coverage and necrosis is not performed. The aim of this study was to investigate the spread and variety in judgement of a chronic wound. A diabetic ulcer was described by 16 wound therapists (eight physicians and eight nurses). Granulation tissue, fibrin coverage, necrosis, size and depth of the lesion, wound exudate and wound edges were judged, and the therapeutical consequences were determined. Study data show an extensive inhomogeneity and a wide spread of the results, like in no other field of medical diagnostics. This could be shown in the group of physicians, as well as in the group of nursing personnel. As the choice of treatment by a specialist is based upon the assessment of the wound, it is possible that in practice it can lead to suboptimal therapy. This is a consequence of varying treating physicians and subsequent changes in treatment regimens. This results in a prolongation of treatment and burden for the patient. Circumstances like this contribute to rising of costs in this area of the health care system. The goal is to apply objective wound diagnostic technologies in the field of chronic wounds to catch up with other diagnostic procedures.

Topics: Chronic Disease; Clinical Competence; Diabetic Foot; Fibrin; Granulation Tissue; Humans; Necrosis; Nurses; Observer Variation; Physicians; Reproducibility of Results; Wound Healing

Skin flap necrosis is one of the hazards encountered in plastic and reconstructive surgery. Angiogenic agents may be useful for treating it by increasing blood flow. The angiogenic effect of fibrin in vitro has been demonstrated, but little is known about its in vivo effect. Te authors tested the hypothesis that local application of fibrin can improve the survival of ischemic skin flaps.. A cranially based dorsal skin flap (3 x 7 cm) was made in each rat. Fibrin (8 mg suspended in 400 microl of phosphate-buffered saline) was applied to the subcutaneous side of elevated skin flaps in the experimental group (n = 15), and phosphate-buffered saline alone was delivered in the control group (n = 15). Tissue blood flow of the skin flaps was measured four times (before the operation and on days 1, 3, and 7) at 1, 3, and 5 cm distal to the baseline of the skin flap. The survival rate of the skin flaps was measured on day 7 and histologic assessments were performed.. The blood flow change rate at 5 cm in the experimental group was significantly higher than that in the control group on day 7 (60.9 +/- 5.7 percent versus 13.7 +/- 4.8 percent, p < 0.001). The survival rate of skin flaps was also significantly improved in the experimental group (77.0 +/- 2.0 percent) in comparison with the control group (54.7 +/- 2.2 percent, p < 0.01). Histologic analysis showed many more blood vessels in the experimental group in comparison with the control group.. The local application of fibrin could improve the blood flow and survival of ischemic skin flaps.

Topics: Animals; Endothelial Cells; Fibrin; Ischemia; Male; Necrosis; Rats; Rats, Wistar; Regional Blood Flow; Surgical Flaps; Tissue Survival

The conventional technique of microvascular anastomosis may cause trauma to the vessel wall. In addition, the technique is difficult for beginners and is time consuming. The duration of ischemia is an important limiting factor for muscle transfer. In the case of multiple-digit replantations, fatigue developed in the surgeon may also result in suboptimal results. This study was performed to establish an easier and shorter method of microvascular anastomosis using the Arista hemostatic agent.. In this study, 20 carotid arteries obtained from rats were equally divided into two groups. The arteries were then divided and repaired using three simple interrupted stay sutures with Arista powder. Evaluations were performed using the following three methods: (1) clamping time during the vessel anastomosis, (2) patency test (after 1 hour, 24 hours, and 28 days), and (3) light microscopic findings.. The clamping time in the conventional suture anastomosis group was 21+/-4 minutes, whereas that of the minimal suture in the Arista group was 12+/-2 minutes; the difference between the two groups was statistically significant (P<.001). There was no significant difference between the patency rates of the two groups (P= .474). It was observed that the Arista group showed qualitatively less perivascular foreign-body giant cell reaction than the control group. There was no evidence of vascular mural fibrinoid necrosis, indicating that Arista was nontoxic for the vessel walls.. The Arista-assisted microvascular anastomosis is an alternative to the conventional suture-only method because it reduces the anastomosis time significantly and does not cause narrowing of the vessel wall. We believe that this technique has the potential for improving the performance of microvascular anastomosis in clinical practice.

Topics: Anastomosis, Surgical; Animals; Carotid Arteries; Constriction; Fibrin; Foreign-Body Reaction; Giant Cells, Foreign-Body; Hemostatics; Male; Microspheres; Microsurgery; Necrosis; Rats; Rats, Wistar; Starch; Suture Techniques; Time Factors; Vascular Patency; Vascular Surgical Procedures

Varicella (chickenpox) is one of the most frequent highly infectious diseases in childhood. It is caused by varicella-zoster virus. Lethal complications are rare. Focused on histological findings, we present a case of a sudden unexpected death of an otherwise healthy 18-month-old girl due to varicella-induced pneumonia. The histological and immunohistochemical investigations of the lung tissue revealed typical findings of a varicella pneumonia: haemorrhagic and necrotic nodules, intra-alveolar fibrin, numerous neutrophilic granulocytes, lymphocytes, plasmacells, macrophages, multinucleated giant cells and hyaline membranes. Varicella-related deaths are preventable by vaccine. To prevent complications and lethal outcome of varicella as reported here, the recommendations concerning vaccination against varicella must be taken into account in paediatric practice.

Topics: Adolescent; Chickenpox; Death, Sudden; Female; Fibrin; Forensic Pathology; Hemorrhage; Humans; Lung; Lymphocytes; Macrophages, Alveolar; Necrosis; Neutrophils; Plasma Cells; Pneumonia, Viral

The factor V Leiden (FVL) mutation (Arg506Glu) results in the production of an FV protein that when activated is relatively resistant to inactivation by activated protein C and thereby leads to predisposition to thrombosis. The rather high prevalence of the FVL mutation in the general population prompted speculation about a potential survival benefit for individuals carrying the FVL allele. Indeed, both clinical and experimental animal data suggest that a heterozygous FVL genotype might protect against the lethal consequences of sepsis. We sought to confirm the survival advantage of heterozygous FVL mice in septic disease.. Controlled animal experiment.. Academic research laboratory.. Wild-type, heterozygous, and homozygous FVL mice subjected to 1 x 10 live bacteria as model for septic peritonitis.. None.. The intraperitoneal injection of E. coli led to growth and dissemination of bacteria and provoked an inflammatory response as evident from elevated cytokine levels (interleukin-6, interleukin-10, and tumor necrosis factor-alpha), induced thrombin-antithrombin complex levels, increased granulocyte influx into the peritoneal cavity, liver necrosis, and adhesion of leukocytes to the vessel wall, resulting in approximately 50% mortality after 72 hrs. The FVL genotype had no significant effect on bacterial outgrowth, markers of inflammation (i.e., tumor necrosis factor-alpha levels of 152 [96.2-200], 152 [99.7-1745], and 110 [99.7-177] pg/mL in peritoneal lavage fluid at t = 20 hrs for wild-type, heterozygous, and homozygous FVL mice, respectively), thrombin generation (i.e., thrombin-antithrombin complex levels of 19.9 [9.31-37.4], 10.4 [6.55-15.8], and 12.6 [8.24-29.0] ng/mL in peritoneal lavage fluid at t = 6 hrs for wild-type, heterozygous, and homozygous FVL mice, respectively), and/or survival (50%, 36%, and 50% for wild-type, heterozygous, and homozygous FVL mice, respectively).. The FVL allele has no beneficial effect in mouse septic peritonitis, and the general protective effect of FVL in sepsis needs further investigation.

Topics: Animals; Antithrombin III; Ascitic Fluid; Cell Adhesion; Cytokines; Disease Models, Animal; Escherichia coli; Factor V; Fibrin; Genotype; Granulocytes; Heterozygote; Homozygote; Kidney; Leukocytes; Liver; Lung; Mice; Mice, Transgenic; Necrosis; Peptide Hydrolases; Peritoneal Lavage; Peritonitis; Point Mutation; Sepsis; Thrombosis

Increased risk of thrombosis, with propitious conditions for fibrin deposition, along with upregulation of inflammation, are important factors that enhance plaque formation in atherosclerosis. Evidence supporting the role of anticoagulant protein C (PC) as an inflammatory agent has emerged, supplementing its well-known function as an anticoagulant. Thus, we sought to examine whether a PC deficiency would lead to an enhanced response to an acute arterial hyperplasic challenge. The presentation of early arterial inflammation was studied using a copper/silicone arterial cuff model of accelerated focal neointimal remodeling in mice with a heterozygous total deficiency of PC (PC+/-). Increased inflammation, cell proliferation, cell migration, fibrin elevation, and tissue necrosis were observed in the treated arteries of PC+/- mice, as compared to arteries of equally challenged age- and gender-matched WT mice. These results indicate that PC+/- mice subjected to this challenge displayed enhanced focal arterial inflammation and thrombosis, leading to larger neointimas and subsequent localized occlusion, as compared to their WT counterparts.

Topics: Animals; Arteritis; Carotid Arteries; Carotid Artery Diseases; Cell Movement; Cell Proliferation; Copper; Disease Models, Animal; Fibrin; Fibrinogen; Mice; Mice, Transgenic; Microscopy, Electron, Scanning; Microscopy, Electron, Transmission; Necrosis; Protein C; Protein C Deficiency; Time Factors; Tunica Intima

Topics: Brain; Brain Infarction; Brain Ischemia; Cerebral Arteries; Cerebrovascular Circulation; Corpus Striatum; Diagnosis, Differential; Endothelium, Vascular; Fibrin; Humans; Hypertension; Magnetic Resonance Imaging; Necrosis; Vasospasm, Intracranial

HBOC-201, a bovine polymerized hemoglobin, has been proposed as a novel oxygen-carrying resuscitative fluid for patients with hemorrhagic shock (HS). Herein, we evaluated the hemostatic effects of HBOC-201 in an animal model of HS. A 40% blood loss-controlled hemorrhage and soft tissue injury were performed in 24 invasively monitored Yucatan mini-pigs. Pigs were resuscitated with HBOC-201 (HBOC) or hydroxyethyl starch (HEX), or were not resuscitated (NON) based on cardiac parameters during a 4-h prehospital phase. Afterward, animals received simulated hospital care for 3 days with blood or saline transfusions. Hemostasis measurements included in vivo bleeding time (BT), thromboelastography (TEG), in vitro bleeding time (platelet function; PFA-CT), prothrombin time (PT), and partial thromboplastin time (PTT). Serum lactate was measured and lung sections were evaluated for microthrombi by electron microscopy. During the prehospital phase, BT remained unchanged in the HBOC group. TEG reaction time increased in HBOC pigs during the late prehospital phase and was greater than in NON or HEX pigs at 24 h (P = 0.03). TEG maximum amplitude was similar for the two fluid-resuscitated groups. PFA-CT increased in both resuscitated groups but less with HBOC (P = 0.02) in the prehospital phase; this effect was reversed by 24 h (P = 0.02). In the hospital phase, PT decreased (P < 0.02), whereas PTT increased above baseline (P < 0.01). Lactic acidosis in HBOC and HEX groups was similar. Aspartate aminotransferase was relatively elevated in the HBOC group at 24 h. Electron microscopy showed no evidence of platelet/fibrin clots or microthrombi in any of the animals. Twenty-four-hour group differences mainly reflected the fact that all HEX animals (8/8) received blood transfusions compared with only one HBOC animal (1/8). In swine with HS, HBOC resuscitation induced less thrombopathy than HEX during the prehospital phase. Mild delayed effects on platelet and clot formation during the hospital phase are transient and likely related to fewer blood transfusions. In swine with HS, HBOC resuscitation induced less thrombopathy than HEX during the prehospital phase but more thrombopathy in the hospital phase. The delayed effects on platelet and clot formation during the hospital phase are transient and may be related to the need for fewer blood transfusions.

Topics: Acidosis, Lactic; Animals; Bleeding Time; Blood Coagulation; Blood Platelets; Cattle; Fibrin; Hematocrit; Hemoglobins; Hemorrhage; Hemostasis; Hydrogen-Ion Concentration; Hydroxyethyl Starch Derivatives; Lactates; Lung; Microscopy, Electron; Myocardium; Necrosis; Oxygen; Partial Thromboplastin Time; Polymers; Prothrombin Time; Shock, Hemorrhagic; Sodium Chloride; Swine; Thrombelastography; Time Factors

The regeneration after liver injury is regulated by the release and activation of several growth factors. The role of the plasmin/alpha(2)-antiplasmin (alpha(2)-AP) system in liver regeneration was investigated.. CCl(4) was injected intraperitoneally into the mice deficient (-/-) in fibrinolytic factors: alpha(2)-AP-/-, plasminogen (Plg) -/-, and Plg-/-.alpha(2)-AP-/-, and wild-type (WT) mice. The liver tissue was examined for its microscopic appearance, fibrinolytic activity, and fibronectin levels.. In the gene deficient and WT mice, the livers exhibited the same extent of necrosis 2 days after the CCl(4) injection. The livers of the WT mice normalized after 7 days, and the alpha(2)-AP-/- mice normalized after 5 days. In contrast, the livers of the Plg-/- and Plg-/-.alpha(2)-AP-/- mice remained in the damaged state until 14 days after the liver injury. The injection of anti-alpha(2)-AP antibody in the WT mice improved the regeneration after the liver injury, and the injection of tranexamic acid in the alpha(2)-AP-/- mice reduced.. These results suggest that the plasmin/alpha(2)-AP system played an important role in hepatic repair via clearance from the injury area.

Topics: alpha-2-Antiplasmin; Animals; Carbon Tetrachloride; Cell Division; Chemical and Drug Induced Liver Injury; Extracellular Matrix Proteins; Fibrin; Fibrinolysin; Fibrinolysis; Fibronectins; Injections; Liver; Liver Diseases; Liver Regeneration; Mice; Mice, Knockout; Necrosis; Neutralization Tests; Plasminogen Activator Inhibitor 2; Tranexamic Acid

A 31-year-old man who underwent chemotherapy and bone marrow transplantation to treat acute myeloblastic leukemia was admitted to our department complaining of high fever and hypotension. His physical examination revealed warm shock state, eruptions resembling that seen in systemic lupus erythematosus on his face and cyanosis in his fingers. We diagnosed septic shock and idiopathic skin eruption on his face. Following treatment with blood transfusion, anticoagulant, antibiotics, respirator and continuous arteriovenous hemofiltration and dialysis, the patient's condition gradually improved. The eruptions on his face first observed at admission progressed with a worsening of his disseminated intravascular coagulation (DIC), and subsided with an improvement in his DIC. A biopsy of the eruption was taken and pathological findings of the eruption revealed multiple micro-fibrin depositions of the dermis. The skin necrosis in purpura fulminans often begins in the distal extremities. But our patient developed this uncommon skin eruption on his face. Patients with an idiopathic skin eruption resembling a butterfly rash in a septic patient should be considered to complicate DIC as in the present case.

Topics: Adult; Bone Marrow Transplantation; Disseminated Intravascular Coagulation; Exanthema; Face; Fibrin; Humans; IgA Vasculitis; Leukemia, Myeloid, Acute; Male; Necrosis; Sepsis

Antiphospholipid syndrome is characterized by recurrent pregnancy loss, thrombosis, and antiphospholipid antibodies. However, some women with clinical features of antiphospholipid syndrome test negative for antiphospholipid antibodies ("antiphospholipid-like syndrome"). Women with antiphospholipid and antiphospholipid-like syndromes have serum immunoglobulin G that harms murine pregnancy, suggesting that the mechanisms of fetal death may be similar in both groups. The objective of our study was to determine whether patients with antiphospholipid and antiphospholipid-like syndromes share pathophysiology by comparing the histology of gestational tissues from these groups.. Placenta and abortion specimens were obtained from 44 pregnancies in 26 women with antiphospholipid syndrome and 37 pregnancies in 21 women with antiphospholipid-like syndrome. Of these, 16 pregnancies with antiphospholipid syndrome and 8 with antiphospholipid-like syndrome were treated with a variety of medications intended to improve pregnancy outcome. Placentas from 31 elective pregnancy terminations and 40 pregnancies complicated by idiopathic preterm delivery served as an additional control group. Twenty histologic parameters were systematically assessed by a single investigator who was blinded to the clinical status of the specimens. Histopathologic findings were compared among groups using multivariate logistic regression analysis.. Antiphospholipid syndrome pregnancies included 15 spontaneous abortions, 13 fetal deaths, and 16 live births. Pregnancies in the antiphospholipid-like syndrome group resulted in 5 spontaneous abortions, 30 fetal deaths, and one live birth. Gestational tissues from antiphospholipid and antiphospholipid-like syndrome pregnancies were similar for every histologic feature tested. Decidua from women with both antiphospholipid and antiphospholipid-like syndromes had more necrosis, acute and chronic inflammation, and vascular thrombus compared to controls. Placental tissue from antiphospholipid and antiphospholipid-like syndrome pregnancies showed more infarction, intravascular fibrin deposition, syncytial knot formation, and fibrosis than controls. Histologic features were variable within groups. There were no histologic differences in tissues from live births and pregnancy losses, or in treated and untreated pregnancies.. Placental histopathology is similar in antiphospholipid and antiphospholipid-like syndrome pregnancies, suggesting that these disorders may share pathophysiology. Histologic findings in women with APS are non-specific and may not differentiate between women with APS and APS-like syndromes.

Topics: Abortion, Spontaneous; Adult; Antibodies, Antiphospholipid; Antiphospholipid Syndrome; Chorionic Villi; Decidua; Female; Fetal Death; Fibrin; Fibrosis; Humans; Inflammation; Logistic Models; Necrosis; Placenta; Pregnancy; Thrombosis; Trophoblasts

We postulated that skin metastases and cutaneous local recurrences from breast adenocarcinoma show different growth patterns with distinct angiogenic profiles.. Fifty-one surgically resected dermal breast cancer deposits were evaluated for growth pattern, E-cadherin expression, presence of necrosis and a fibrotic focus, fibrin deposition, carbonic anhydrase IX expression (CA IX), microvessel density, endothelial cell proliferation and blood vessel immaturity. Growth patterns were infiltrative, with carcinoma cells infiltrating the dermis without significant disturbance of the pre-existing architecture, expansive, meaning that a nodule of carcinoma cells and desmoplastic tissue pushed aside the pre-existing dermal structures, or mixed. All lobular carcinomas showed an infiltrative growth and lacked membranous E-cadherin expression. Different growth patterns in the ductal carcinomas were not correlated with differences in E-cadherin expression. The presence of necrosis and/or a fibrotic focus and the expression of the hypoxia marker CA IX were significantly associated with an expansive growth. Fibrin was present in all expansive deposits and less frequently in the other growth patterns. There was a positive association between fibrin deposition, CA IX expression and microvessel density. The latter was significantly higher in the expansive and mixed growth patterns than in the infiltrative pattern. Endothelial cell proliferation was highest in the expansive growth pattern and was positively correlated with the presence of a fibrotic focus and with fibrin deposition. The maximum percentage of immature blood vessels was higher in the expansive and mixed growth patterns than in the infiltrative one.. The recognition of different subgroups of cutaneous breast cancer deposits with different degrees of hypoxia-driven angiogenesis may have important implications for the usefulness of anti-angiogenic therapy.

Topics: Adenocarcinoma; Antigens, Neoplasm; Biomarkers, Tumor; Breast Neoplasms; Cadherins; Carbonic Anhydrase IX; Carbonic Anhydrases; Cell Hypoxia; Female; Fibrin; Fluorescent Antibody Technique, Indirect; Humans; Immunoenzyme Techniques; Microcirculation; Necrosis; Neoplasm Proteins; Neovascularization, Pathologic; Skin; Skin Neoplasms

Acute vascular or humoral rejection, a vexing outcome of organ transplantation, has been attributed by some to activation and by others to apoptosis of endothelial cells in the graft. We asked which of these processes causes acute vascular rejection by tracing the processes during the development of acute vascular rejection in porcine cardiac xenografts performed in baboons. Apoptosis, assayed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL), expression of activated caspase-3, and proapoptotic genes Bax and Bcl-x(L), was not detected until acute vascular rejection was well advanced, and even then, apoptosis was largely confined to myocytes. Activation of the endothelium, as evidenced by expansion of rough endoplasmic reticulum and increased ribosomal antigen and phospho-p70 S6 kinase, occurred early in the course of acute vascular rejection and progressed through the disease process. These findings suggest that acute vascular rejection is caused by an active metabolic process and not by apoptosis in the endothelium.

Topics: Acute Disease; Animals; Antibody Formation; Apoptosis; Blood Vessels; CD59 Antigens; Disease Models, Animal; Disease Progression; Endothelium, Vascular; Fibrin; Gene Expression; Graft Rejection; Guinea Pigs; Heart Transplantation; Humans; In Situ Nick-End Labeling; Myocardium; Necrosis; Papio; Rats; Rats, Inbred Lew; Swine; Transplantation, Heterologous

Monocrotaline (MCT) is a pyrrolizidine alkaloid (PA) plant toxin that produces hepatotoxicity in people and animals. Human exposure to PAs occurs through consumption of contaminated grains and herbal remedies. Injection (ip) of MCT in rats produced dose-dependent hepatic parenchymal cell injury that was significant at 200 mg/kg. Injection of 300 mg/kg MCT produced time-dependent hepatotoxicity with significant injury beginning by 12 h after treatment. Histopathologic examination of liver sections revealed coagulative hepatocellular necrosis, widening of sinusoids and hemorrhage in centrilobular regions. MCT-induced damage to central venular endothelial cells (CVECs) and sinusoidal endothelial cells (SECs) in the liver was quantified using immunohistochemical staining and by increased plasma hyaluronic acid concentration. MCT damaged CVECs and SECs in the liver by 8 h after treatment. Extensive endothelial cell injury was restricted to centrilobular regions. To determine if damage to endothelial cells in the liver stimulated activation of the coagulation system, fibrin deposition was quantified using immunohistochemistry. Extensive fibrin deposition occurred in the liver after MCT treatment and was restricted to centrilobular regions. Interestingly, both endothelial cell damage and fibrin deposition preceded the onset of hepatic parenchymal cell injury. These results suggest that endothelial cell damage and fibrin deposition in centrilobular regions of the liver are prominent features of MCT-induced liver injury.

Topics: Animals; Dose-Response Relationship, Drug; Endothelium, Vascular; Fibrin; Fluorescent Antibody Technique, Indirect; Hemorrhage; Hyaluronic Acid; Immunohistochemistry; Liver; Male; Microcirculation; Monocrotaline; Necrosis; Rats; Rats, Sprague-Dawley

The impact of clot stability affecting the vasculopathy and tissue necrosis in Shwartzman reaction was investigated using plasma Factor XIII A2-depleted rabbit (FXIII-DR). Plasma Factor XIIIA2 (FXIIIA2) was depleted by infusion of the mono-specific goat anti-rabbit FXIIIA2 IgG. Generalized Shwartzman reaction (GSR) was induced by priming and challenged by i.v. injection of LPS and local Shwartzman reaction (LSR) was primed by intradermal injection of LPS and challenged by i.v. injection of LPS. Histological examination of the GSR animals showed, extensive thrombi accumulation in renal tubules and bilateral cortical necrosis of kidney in 8 out of 10 rabbits but none in the FXIII-DR. Fibrinogen levels were elevated to 3 approximately 4 fold at 24 h and lowered at 48 h whereas a steady rise was seen in the FXIII-DR. FDP levels in GSR animals were significantly elevated at 24 h and further increased at 48 h but only slightly elevated in the FXIII-DR. Examination of the LSR tissues after 48 h showed an acute onset of progressive cutaneous vascular thrombosis, purpura, and secondary hemorrhagic necrosis whereas neither fibrin deposit nor necrosis of tissue were detected in FXIII-DR despite of an early edema formation. Fibrinogen levels were also increased two fold at 24 h but returned to basal levels at 48 h in control LSR animals but not affected at all in FXIII-DR. These results suggest that during the severe inflammatory conditions such as sepsis, the fibrinolytic system is functionally sufficient to dissipate the pathogenic accumulation of disseminated intravascular clots and exudated fibrin clots if those clots were prevented from getting crosslinked in plasma.

Topics: Animals; Antibodies, Monoclonal; Disease Models, Animal; Disseminated Intravascular Coagulation; Factor XIII; Factor XIII Deficiency; Fibrin; Fibrinogen; Kidney; Kidney Diseases; Lipopolysaccharides; Necrosis; Plasminogen; Rabbits; Sepsis; Shwartzman Phenomenon; Skin; Skin Diseases

Pseudoxanthoma elasticum (PXE) is a rare genetic disorder clinically characterized by skin, cardiovascular and eye manifestations, mainly due to calcification and fragmentation of elastic fibres. Although infrequent, complications during pregnancy in women affected by PXE have been reported. The aim of the present study was to compare structural features of placentae at term from 14 control and 15 PXE-affected women, in order to better understand if and how abnormal mineral and/or matrix accumulation might affect placental function in PXE. In all cases, pregnancy, fetus growth and delivery were normal. Both gross and light microscopy examination did not reveal dramatic differences between placentae of PXE patients and controls, with regard to weight, dimensions, infarcts, thrombi, inflammatory lesions or vessels. However, necrotic changes and mineralization appeared statistically more pronounced in PXE. By electron microscopy the most remarkable differences between PXE and control placentae were observed in the localization and morphology of mineral precipitates; a significant higher deposition of mineral precipitates was observed associated with the "matrix"-type fibrinoid and among collagen fibrils, especially on the maternal side. Immunocytochemistry revealed the presence of vitronectin and fibronectin associated with the PXE-specific mineralizations and the absence of mineralization on the small and scarce elastic fibres in either controls or in PXE.

Topics: Adult; Calcinosis; Chemical Precipitation; Female; Fibrin; Fibronectins; Gestational Age; Humans; Immunohistochemistry; Microscopy, Electron; Minerals; Necrosis; Organ Size; Placenta; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Pseudoxanthoma Elasticum; Vitronectin

Tissue necrosis following spider bites is a widespread problem. In the continental United States, the brown recluse (Loxosceles reclusa), hobo spider (Tegenaria agrestis), garden spider (Argiope aurantia) and Chiracanthium species, among others, reportedly cause such lesions. The exact mechanism producing such lesions is controversial. There is evidence for both venom sphingomyelinase and spider digestive collagenases. We have examined the role of spider digestive proteases in spider bite necrosis. The digestive fluid of A. aurantia was assayed for its ability to cleave a variety of connective tissue proteins, including collagen. Having confirmed that the fluid has collagenases, the digestive fluid was injected into the skin of rabbits to observe whether it would cause necrotic lesions. It did not. The data do not support the suggestions that spider digestive collagenases have a primary role in spider bite necrosis.

Topics: Animals; Collagen; Collagenases; Connective Tissue; Elastin; Endopeptidases; Extracellular Matrix Proteins; Female; Fibrin; Hemolymph; Molecular Weight; Necrosis; Rabbits; Skin; Spider Bites; Spider Venoms; Spiders

In the present studies, we report the cloning and structural characterization of the HFGL2 gene and its functional role in human fulminant hepatitis. The HFGL2 gene is approximately 7 kb in length with 2 exons. The putative promoter contains cis element consensus sequences that strongly suggest the inducibility of its expression. From the nucleotide sequence of the human gene, a 439-amino acid long protein is predicted. The overall identity between the murine fgl2 and hfgl2 coded proteins is over 70%. About 225 amino acids at the carboxyl end of these molecules are almost 90% identical, and correspond to a well-conserved fibrinogen-related domain. Both HFGL2 and FGL2 encode a type II transmembrane protein with a predicted catalytic domain toward the amino terminus of the protein. Transient transfection of Chinese hamster ovary (CHO) cells with a full-length cDNA of HFGL2 coding region resulted in high levels of prothrombinase activity. Livers from 8 patients transplanted for fulminant viral hepatitis were examined for extent of necrosis, inflammation, fibrin deposition, and HFGL2 induction. In situ hybridization showed positive staining of macrophages in areas of active hepatocellular necrosis. Fibrin stained positively in these areas and was confirmed by electron microscopy. These studies define a unique prothrombinase gene (HFGL2) and implicate its importance in the pathogenesis of fulminant viral hepatitis.

Topics: Adolescent; Adult; Amino Acid Sequence; Animals; Child, Preschool; CHO Cells; Cloning, Molecular; Consensus Sequence; Cricetinae; Female; Fibrin; Fibrinogen; Hepatitis, Viral, Human; Humans; Infant; Liver; Male; Middle Aged; Molecular Sequence Data; Necrosis; Promoter Regions, Genetic; Thromboplastin; Transfection

The assumption that fibrin and crosslinked fibrin impart irreversibility to arterial thrombi is explored with procedure developed for measuring changes in platelet function, morphology and fibrinogen metabolism in aging occlusive thrombi, in which the condition of stasis is imposed uniformly. Arterial thrombi containing autologous (111)In labeled platelets were generated in vivo by bilateral mechanical injury of porcine carotid arteries. Vessels containing the platelet-rich thrombi were harvested and incubated intact (37 degrees C) for intervals ranging from 30 min to 12 h. The isolated vessels were then bisected and agitated in culture medium containing tick anticoagulant and hirudin for 60 min. Disaggregated platelets were evaluated for yield (from (111)In radioactivity) viability (dense body ATP secretion) and morphology (electron microscopy). Western analysis of fibrin(ogen) in thrombus extracts was performed using anti-fibrinogen Bbeta- and gamma-chain monoclonal antibodies for thrombi at each time point. A stable recovery of nearly 50% of platelets was observed during 12 h of thrombus aging. As thrombi aged, viability of disaggregated platelets gradually decreased with platelet necrosis the predominant feature beyond 6 h. By western analysis of thrombus extracts, nearly 50% of fibrinogen was cleaved to fibrin and extensively crosslinked within 30 min of injury with no evidence of fibrinolysis. With the exception of a declining proportion of gamma-monomer, these features remain relatively constant during 12 h of thrombus maturation. It is concluded that neither fibrin nor crosslinked fibrin are dominant factors imparting cohesion within platelet thrombi. Furthermore, under conditions of complete arterial occlusion imposed by this experimental design, there is no evidence of endogenous fibrinolysis.

Topics: Adenosine Triphosphate; Animals; Arthropod Proteins; Blood Platelets; Carotid Artery Injuries; Carotid Artery Thrombosis; Cytoplasmic Granules; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Fibrinolytic Agents; Hirudins; Intercellular Signaling Peptides and Proteins; Necrosis; Peptides; Recombinant Proteins; Swine; Time Factors

Leukocytoclastic vasculitis is defined by histologic features and can be observed in a wide range of entities. Independent of the causative disease, extracutaneous complications are frequent, mainly in the kidneys and gastrointestinal tract. It has been suggested that the severity of histological changes could correlate with the clinical course of the disease. We have therefore compared the severity of histological changes of leukocytoclastic vasculitis to clinical and laboratory findings indicative of extracutaneous involvement in a large group of patients. Among 289 patients followed for cutaneous vasculitis, we included 184 patients with purpuric papules and proven leukocytoclastic vasculitis who all had standardized investigations. A cutaneous biopsy was performed early and standardized laboratory investigations were carried out. The slides were retrospectively randomized and the depth of vasculitis and severity of vascular necrosis were determined according to a semiquantitative scale. These data were compared to the renal, gastrointestinal and articular symptoms using Fischer's exact test, Chi-square test and variance analysis. The intensity of vascular necrosis and the depth of vasculitis were no more severe in patients having renal changes, gastrointestinal involvement or articular symptoms. Both variance analysis and Chi-square tests failed to show a significant increase in the severity score in patients having extracutaneous complications. In this study, the severity of histopathological changes was not predictive of extracutaneous involvement. Thus it appears that the degree of involvement of the cutaneous vessels probably does not correlate with that of vessels in visceral organs.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Child; Child, Preschool; Female; Fibrin; Gastrointestinal Diseases; Humans; Joint Diseases; Kidney Diseases; Male; Middle Aged; Necrosis; Prognosis; Random Allocation; Severity of Illness Index; Skin Diseases, Vascular; Vasculitis, Leukocytoclastic, Cutaneous

Ten thousand & thirty seven autopsies performed from the year 1982 to 1992 were studied retrospectively, to find out the number of deaths due to bleeding diathesis. Eighty-seven (0.87%) patients died due to bleeding diathesis, out of which haemolytic uraemic syndrome (HUS) was seen in 9 cases (10.34%), disseminated intravascular coagulation (DIC) in 67 cases (77.01%) & 11 cases were grouped as miscellaneous. Martius scarlet blue stain was carried out to demonstrate fibrin & depending on the number of thrombi in the glomerulus & blood vessels, the lesions were graded as mild, moderate or severe. Kidney was the most common organ involved in all groups of bleeding diathesis. In DIC kidney & lung involvement was almost equal.

Topics: Autopsy; Disseminated Intravascular Coagulation; Female; Fibrin; Hemolytic-Uremic Syndrome; Hemorrhagic Disorders; Humans; Kidney; Lung; Male; Necrosis; Retrospective Studies; Staining and Labeling; Thrombosis

Liver failure following major hepatectomy is characterized pathologically by massive hepatic necrosis, which is thought to begin with injury of sinusoidal endothelial cells (SECs). To examine the early events of SECs leading to hepatic damage, we performed time-course analyses of the morphological and functional perturbation of SECs after endotoxin administration to hepatectomized rats. At 1.5 h after endotoxin injection, when hepatocellular damage was not yet evident, SECs showed augmented expression of intercellular adhesion molecule-1, with frequent adherence of infiltrating leucocytes and ultrastructural features of defenestration and hypertrophied cytoplasm enriched with cell organelles. The serum level of hyaluronate, as an indicator of the functional state of SECs, was significantly elevated. At 3 h, SECs underwent necrosis and disruption, accompanied by fibrin deposits with concomitant hepatocellular necrosis. The morphological and functional alterations of SECs precede necrotic changes in hepatocytes and SECs in endotoxin-induced liver failure after partial hepatectomy.

Topics: Animals; Bilirubin; Cell Adhesion; Cytoplasm; Endothelium, Vascular; Endotoxins; Fibrin; Hepatectomy; Immunohistochemistry; Intercellular Adhesion Molecule-1; Leukocytes; Liver; Liver Failure; Male; Microscopy, Electron; Necrosis; Organelles; Rats; Rats, Sprague-Dawley; Transaminases; Tumor Necrosis Factor-alpha

A commercially available monoclonal antibody against human fibrin was used to detect fibrin in canine formalin-fixed, paraffin wax-embedded tissue by applying a slightly modified alkaline phosphatase anti-alkaline phosphatase (APAAP) technique. Twenty-eight mammary tumours from six bitches were examined for the presence of fibrin. Thrombi and extravascular fibrin deposits were detected in 15 tumours (12 complex adenocarcinomas, one adenocarcinoma, two solid carcinomas), and a single thrombus was detected in one adenoma; 12 tumours (three adenomas, one complex adenoma, four complex adenocarcinomas and four adenocarcinomas) did not show any staining reaction.

Topics: Adenocarcinoma; Adenoma; Animals; Antibodies, Monoclonal; Carcinoma; Dogs; Female; Fibrin; Immunohistochemistry; Mammary Neoplasms, Animal; Necrosis; Thrombosis

Cerebral amyloid angiopathy (CAA) is known to be associated with intracerebral hemorrhage in the elderly. In this study we demonstrated that, among 101 cases with intracerebral hemorrhages found in 1000 consecutive autopsied cases (average age, 82.9 years) at a geriatric hospital, CAA accounted for 10.9% of them (31.0% of lobar and 14.3% of cerebellar hemorrhages). Immunohistochemically, the cerebrovascular amyloid was positive for beta/A4 peptide, and less intensely for cystatin C. The CAA-related hemorrhages were characteristically located near the cortical surface and ruptured into the subarachnoid space. No mutation of the amyloid precursor protein gene or the cystatin C gene was detected in these cases. From the observation of 500 serial sections containing amyloid-laden vessels of a patient with CAA-related hemorrhage, it was suggested that the hemorrhage occurred at microaneurysms with fibrinoid necrosis, which were found in small arteries in the cerebral cortex. The spatial distribution of CAA was closely associated with that of subpial beta/A4 peptide deposits in the brain, raising the possibility that the cerebrovascular amyloid originates from the brain parenchyma. Finally, the severity of CAA did not seem to be influenced by the inheritance of the epsilon 4 allele of the apolipoprotein E gene, which is known as a risk factor for dementia of the Alzheimer type.

Topics: Aged; Aged, 80 and over; Alleles; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Aneurysm, Ruptured; Apolipoproteins E; Cerebellar Diseases; Cerebral Amyloid Angiopathy; Cerebral Arteries; Cerebral Cortex; Cerebral Hemorrhage; Cerebrospinal Fluid Proteins; Cystatin C; Cystatins; Cysteine Proteinase Inhibitors; Fibrin; Humans; Immunohistochemistry; Intracranial Aneurysm; Middle Aged; Mutation; Necrosis; Peptide Fragments; Pia Mater; Risk Factors; Subarachnoid Space

The spectrum of organisms causing native valve endocarditis is changing. Despite an increasing incidence of infections caused by gram-negative organisms, they remain a rare cause of native valve endocarditis. Escherichia coli is especially uncommon. We describe the case of a 47-year-old man with no previous history of cardiac problems, who presented with culture-positive E coli endocarditis of his native aortic valve. His complicated clinical course necessitated emergent valve replacement, emphasizing the virulence of this organism. The high mortality rate and significant morbidity associated with this entity necessitates aggressive medical management and early surgical intervention.

Topics: Aortic Valve; Echocardiography; Endocarditis, Bacterial; Escherichia coli; Escherichia coli Infections; Fibrin; Humans; Male; Middle Aged; Necrosis

We investigated the distribution and frequency of microthromboemboli (MTE) in acute infarcts in humans and determined whether MTE in the contralateral circulation resulted in histological changes.. Forty patients dying within the first month after unilateral infarct were investigated. Infarct etiology was determined mainly on the pathological findings. Whole brain sections from the region of maximal necrosis were stained for fibrin. Fibrin-containing MTE were transferred to a schematic drawing and counted. Sections from 20 patients without infarcts served as controls.. Infarct sections had significantly more MTE than controls. Infarcts of thrombotic (n=6) and thromboembolic (n=21) origin had more MTE than infarcts of embolic origin (n=13). Thromboembolic infarcts had the highest number of MTE within the region assumed to be the ischemic penumbra, other arterial territories, and the contralateral hemisphere. Patients with large infarcts and those with short clinical courses had a higher number of MTE. Sixteen patients had recent micronecroses in the contralateral hemisphere.. There seems to be a pattern of MTE in acute infarcts that is dependent on cause, size, and clinical duration. Our findings of contralateral micronecroses emphasize that acute infarcts may result in more widespread cerebral injury than clinically expected. Given the many variables influencing stroke and death in humans, the results have to be interpreted with caution.

Topics: Acute Disease; Aged; Autopsy; Brain; Cause of Death; Cerebral Arteries; Cerebral Infarction; Cerebrovascular Circulation; Cerebrovascular Disorders; Coloring Agents; Female; Fibrin; Humans; Intracranial Embolism and Thrombosis; Male; Necrosis

The present study was undertaken in rats to clarify the role of sinusoidal circulatory disturbances due to fibrin thrombi in the development of focal and random hepatocellular necrosis in endotoxemia. Sinusoidal circulation was examined microscopically in vivo in rats injected with endotoxin or heparin, or both. The sinusoids in places were occluded by adherent fibrin and neutrophils soon after endotoxin injection, and subsequently the sinusoidal blood flow stagnated, reversed, or detoured. Most of these sinusoidal circulatory disturbances recovered in a few hours. However, when the sinusoidal occlusion developed simultaneously in clusters of adjacent sinusoids, the sinusoidal circulatory disturbance persisted and induced ischemic foci and then hepatocellular coagulative necrosis. Pretreatment with heparin definitely prevented the adherence of fibrin and neutrophils to the sinusoidal walls, and focal hepatocellular necrosis did not appear. These results suggest that focal and random hepatocellular necrosis in endotoxemia is caused by circulatory disturbances due to fibrin thrombi in clusters of adjacent sinusoids.

Topics: Animals; Blood Circulation; Endotoxemia; Endotoxins; Fibrin; Heparin; Lipopolysaccharides; Liver; Male; Microscopy; Necrosis; Rats; Rats, Wistar; Thrombosis

Topics: Animals; Cat Diseases; Cats; Chronic Disease; Feline Infectious Peritonitis; Fibrin; Male; Necrosis; Orchitis; Testis

Arterial fibrinoid lesions in major salivary glands and lingual minor salivary glands from four autopsied patients with primary Sjögren's syndrome were studied histologically and immunohistochemically. On a morphological basis, the preceding arterial fibrinoid necrosis was regarded as medial damage, particularly of smooth muscle cells. The medial smooth muscle cells underwent vacuolated degeneration and disappeared, and resulted in full-blown fibrinoid arteritis. By means of the immunoperoxidase method the distribution of the immunoglobulins, fibrin, complement (C3), transferrin, ferritin, vimentin and lysozyme was studied. The normal arterial wall reacted with the lambda light chain of immunoglobulin, transferrin and vimentin Vacuolated degeneration of medial smooth muscle cells, regarded as the initial change in cases of vascular fibrinoid lesion, was positive for IgG, C3 and vimentin. We suggest that IgG antibody is a useful marker to detect the initial phase of arterial fibrinoid necrosis. In the foci of fibrinoid necrosis, fibrin, C3 and vimentin were detected. Among these three antibodies, only fibrin was negative in the normal arterial wall and vacuolated degenerates of medial smooth muscle cells. Mononuclear cells surrounding areas of fibrinoid necrosis stained strongly with antisera to immunoglobulins, transferrin, ferritin and vimentin, and negatively with fibrin, C3 and lysozyme antibodies.

Topics: Adult; Aged; Arteries; Complement C3; Female; Ferritins; Fibrin; Humans; Immunoglobulin G; Immunohistochemistry; Leukocytes, Mononuclear; Male; Middle Aged; Necrosis; Salivary Glands; Salivary Glands, Minor; Sjogren's Syndrome; Tongue; Transferrin; Vimentin

This investigation compared the ability of six Latin American antivenoms (monovalent antibothropic INS, Santafé de Bogotá; polyvalent INS; polyvalent probiol, Santafé de Bogotá; antibothropic Instituto Butantan, IB, São Paulo, Brazil; polyvalent Instituto Clodomiro Picado, ICP, San José, Costa Rica; polyvalent MYN, Mexico) to neutralize various pharmacological and enzymatic effects of Bothrops atrox venom from Antioquia and Chocó, north-west of Colombia. Our results demonstrated conspicuous differences in the ability of the six antivenoms. In terms of neutralization of lethality, the highest efficacy was observed in the polyvalent INS and the lowest in the polyvalent MYN antivenom. All antivenoms were highly effective in the neutralization of hemorrhage, polyvalent INS and probiol being the highest. In the neutralization of edema-forming activity, the most effective antivenom was the polyvalent (ICP); monovalent (INS) and polyvalent (MYN) were the least effective. All antivenoms were effective in the neutralization of the myotoxic activity of B. atrox venom, the most effective being the polyvalent (INS) and antibothropic (IB). Defibrinating activity was neutralized by all antivenoms; polyvalent (MYN) showed the lowest efficiency. Polyvalent (ICP) antivenom had the highest neutralizing ability against the indirect hemolytic effect of B. atrox venom; polyvalent (MYN) did not neutralize this enzymatic activity. Overall, the polyvalent antivenom (INS) showed the highest neutralizing ability.

Topics: Animals; Antivenins; Blood Coagulation; Colombia; Crotalid Venoms; Edema; Fibrin; Hemolysis; Hemorrhage; Lethal Dose 50; Mice; Necrosis; Neutralization Tests

During liver fibrosis, there is a putative pacemaker role of fibronectin. Fibrinogen is closely linked to fibronectin during clotting processes. The aim of this study was to show fibrinogen gene expression during liver damage.. Fibrinogen/fibrin deposition in damaged livers was studied by immunohistology. Fibrinogen gene expression was analyzed in vivo in a model of CCl4-induced rat liver damage and in vitro in isolated liver cells by means of Northern blot analysis and in situ hybridization.. Immunohistology showed striking amounts of fibrinogen and fibrin deposits in pericentral necrotic areas (short-term damage) and within fibrotic septa (long-term damage). Total RNA extracted from short-term-damaged livers contained an increased fibrinogen messenger RNA level. By in situ hybridization, fibrinogen transcripts were localized in cells of the nonnecrotic areas (short-term damage) and outside fibrotic septa (long-term damage). In vitro studies showed fibrinogen de novo synthesis restricted to hepatocytes.. The results show fibrinogen/fibrin deposition during short-term liver injury and liver fibrogenesis, which may suggest the involvement of a "clotting-like process" in short-term liver damage and liver fibrosis. The data might indicate that fibrin/fibronectin constitute a "provisional matrix," which affects the attraction and proliferation of inflammatory and matrix-producing cells.

Topics: Animals; Blotting, Northern; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury; Female; Fibrin; Fibrinogen; Gene Expression; Immunohistochemistry; In Situ Hybridization; Liver; Liver Cirrhosis, Experimental; Liver Diseases; Necrosis; Rats; Rats, Wistar; RNA, Messenger

We report here, a patient of systemic lupus erythematosus (SLE) with severe fibrinoid necrosis in the afferent arteriole of the glomerulus, in whom antiphospholipid antibody might have contributed to the pathogenesis. A 24-year-old female who was suffering from severe anemia with fragmented red blood cells, acute renal failure and thrombocytopenia, was admitted to our hospital. Further examinations revealed findings compatible with active lupus nephritis. Moreover, she was found to be positive for antiphospholipid antibody, and anticardiolipin antibody, as well as for lupus anticoagulant and syphilis test. Intensive treatment by methylprednisolone pulse therapy, hemodialysis, and double filtration plasmapheresis were performed. However, 13 days after admission she died suddenly because of intracranial hemorrhage. Pathological investigation of renal tissue revealed severe fibrinoid necrosis of the arterioles mainly in the glomerular afferent arteriole associated with diffuse proliferative lupus nephritis. In this case, hemolytic uremic syndrome (HUS) was associated with SLE. Antiphospholipid antibody was considered to be not only an accelerator in the arterial lesions of HUS, but also an initiator of HUS itself.

Topics: Adult; Arterioles; Female; Fibrin; Hemolytic-Uremic Syndrome; Humans; Kidney Glomerulus; Lupus Erythematosus, Systemic; Necrosis

The masseter and temporalis muscles were investigated ultrastructurally in 2 patients having fibrodysplasia ossificans progressiva (FOP). Results showed atrophy and necrosis of muscle fibres. Both cases contained cartilage which was calcified in the second case and was associated with degenerating chondrocytes. The blood vessels showed various changes, with haematoma formation and large fibrin deposits. Some of the fibrin deposits seen in the second case were surrounded with cartilage. This suggests that the cartilage probably forms as a reaction to an old haemorrhage. It is possible that the effect of the mutant gene found in FOP is on blood vessels rather than the normal regulatory mechanisms of the inducible osteogenic precursor cells. These degenerating blood vessels often result in haemorrhage and fibrin deposits; the fibrosis, cartilage or bone formation are probably secondary changes. Amianthoid fibres found in the tendon of the temporalis muscles of the second case, together with the other changes of fibrosis and cartilage formation, account for the severe restricted mouth opening suffered by these patients.

Topics: Adolescent; Adult; Arterioles; Calcinosis; Capillaries; Cartilage; Female; Fibrin; Fibrosis; Hematoma; Humans; Male; Masseter Muscle; Muscle Fibers, Skeletal; Muscular Atrophy; Mutation; Myositis Ossificans; Necrosis; Temporal Muscle; Tendons; Venules

Endothelial cell damage causes massive hepatic necrosis as a result of fibrin deposition in the hepatic sinusoids. When a stable analog of prostaglandin I2, beraprost sodium, was administered to rats given either dimethylnitrosamine, carbon tetrachloride, or endotoxin following Corynebacterium parvum administration, the hepatic necrosis produced in each was attenuated, but to a greater extent in the dimethylnitrosamine and endotoxin/Corynebacterium parvum models, where fibrin deposition in the hepatic sinusoids occurs, as compared to the carbon tetrachloride model, where such fibrin deposition does not occur. Beraprost sodium reduced the expected increase of portal venous pressure in the endotoxin/Corynebacterium parvum model without affecting plasma thrombin-antithrombin III complex levels. Beraprost sodium also significantly reduced cell killing of both isolated rat hepatocytes and hepatic sinusoidal endothelial cells exposed to tert-butyl hydroperoxide when compared to controls. Beraprost sodium could prove to be a therapeutic candidate for the treatment of hepatic necrosis, particularly in cases associated with fibrin deposition in the hepatic sinusoids because of its fibrin clot-clearing action.

Topics: Animals; Antithrombin III; Capillaries; Carbon Tetrachloride; Cells, Cultured; Dimethylnitrosamine; Endothelium, Vascular; Endotoxins; Epoprostenol; Fibrin; Liver; Liver Diseases; Male; Necrosis; Peptide Hydrolases; Portal Pressure; Propionibacterium acnes; Prothrombin Time; Rats; Rats, Inbred F344

The micromorphological alterations in chronic venous insufficiency are characterized by a patchlike distribution. At least in the initial stages, normal skin areas may alternate with regions containing severe alterations. The capillaries may be rarified, or elongated and dilated with formation of glomerulus-like clusters, or they may show proliferation within a granulomatous repair tissue. Pericapillary accumulation of fibrin may be observed only within necrotic tissue surrounding an ulcer. The pericapillary space which is enlarged and edematous in chronic venous insufficiency, cannot be anatomically defined. The interstitial tissue may contain a secondary chronic inflammation with repair function. Finally a hyaline scar tissue with so-called "avascular" fields and dystrophic calcification/ossification may result.

Topics: Capillaries; Collagen; Extracellular Space; Factor VIII; Fibrin; Humans; Immunoenzyme Techniques; Microscopy, Electron; Necrosis; Postphlebitic Syndrome; Skin; Venous Insufficiency

Endothelial cell activation and alterations of intravascular coagulation were investigated in 27 cases of Hodgkin's disease (HD), in five cases of anaplastic large cell lymphoma (ALCL), and in ten reactive lymph nodes. Lymph node sections were immunostained for E-selectin, a molecule present on cytokine-activated endothelial cells; for tissue factor (TF), a cellular initiator of the coagulation cascade; for glycoprotein (gp) II/III, a platelet-specific antigen; and for fibrin. In HD, vascular activation was particularly prominent in the nodular sclerosis subtype, as indicated by a larger number of E-selectin-positive blood vessels (72 +/- 49) compared with mixed cellularity (22 +/- 37). High expression of E-selectin was associated with alterations of intravascular coagulation, as indicated by immunostaining of some vascular endothelial cells for TF, by a higher incidence of intravascular thrombi, and by the extensive presence of areas of fibrin exudation and necrosis. In ALCL, the levels of endothelial cell activation and intravascular coagulation were comparable to those of HD nodular sclerosis. In reactive nodes, some E-selectin-positive blood vessels were observed only in 3/10 cases; immunostaining for TF was not detected on endothelial cells; and alterations of intravascular coagulation were rarely observed.

Topics: Adolescent; Adult; Aged; Cell Adhesion Molecules; E-Selectin; Endothelium, Vascular; Female; Fibrin; Hodgkin Disease; Humans; Lymph Nodes; Male; Middle Aged; Necrosis; Neoplasm Proteins; Regional Blood Flow; Thromboplastin; Thrombosis

Holmium-laser synovectomy was carried out to remove allergically inflamed synovial membranes in rabbit knee joints. The healing process was then investigated at different periods. Left knee joints of 12 rabbits were exposed to Ho:YAG-laser radiation at a wavelength of 2.1 microns, pulse energy of 600 mJ, pulse length of 1 ms, and repetition rate of 3 Hz. Twelve others were treated conventionally and 12 served as controls. After 1 day, 1 week, and 1 and 3 months, respectively, 3 animals from each group were sacrificed and the synovialis grossly and microscopically examined. Coagulation necrosis, inflammation, and edema resulted following laser therapy. After 1 week, the synovial layer consisted of a scarlike formation of fibers and within 1 month, its surface appeared smooth. The mechanical abrasion caused hemorrhage and necrosis. Fibrosis developed in the capsular layers, and after 3 months, the surface appeared coarse and villous. Based on these preliminary findings, holmium-laser synovectomy may offer an alternative method to existing therapeutic techniques.

Topics: Aluminum Silicates; Animals; Arthritis, Experimental; Collagen; Curettage; Edema; Fibrin; Granulocytes; Histiocytes; Holmium; Knee Joint; Light Coagulation; Macrophages; Necrosis; Rabbits; Synovectomy; Synovial Fluid; Synovial Membrane; Synovitis; Yttrium

Endoscopy reveals that the lesions of reflux esophagitis are red and white spots and streaks. The red lesions are thought to reflect local inflammatory alterations with or without partial necrosis of the squamous epithelium, while white lesions represent complete necroses of the squamous epithelium with fibrin deposits. Fifty-nine patients with reflux esophagitis and red lesions (n = 23) or white lesions (n = 36) underwent endoscopically controlled biopsy of selected particles. Histologic analysis confirmed the hypothesis that white lesions are nearly always necroses involving all layers of the squamous epithelium with fibrin deposits (and rarely epithelial hyperplasia), while red lesions are caused by local granulocytic inflammation or granulation tissue with partial reepithelialization. These results suggest that reflux esophagitis Savary Stages I and II can be rationally subclassified into reflux esophagitis with red spots (Stage Ia), white spots (Stage Ib), red streaks (Stage IIa), and white streaks (Stage IIb).

Topics: Biopsy; Epithelium; Esophagitis, Peptic; Esophagoscopy; Esophagus; Fibrin; Humans; Necrosis

When rats received endotoxin 48 hours after two-thirds liver resection, 50% of them died within 12 hours with massive hepatic necrosis at a dose that did not affect sham-operated rats. In the hepatic sinusoids, fibrin deposition and endothelial cell destruction occurred 5 hours after endotoxin administration. When antithrombin III concentrate was infused concomitantly with endotoxin administration, all rats survived 12 hours, and the extent of hepatic necrosis and the deranged serum glutamic pyruvic transaminase values were significantly attenuated at 5 hours compared with those in the control rats. Similar improvements in the incidence of mortality and liver injury were observed after treatment with gum arabic before hepatectomy. The stimulatory state of Kupffer cells based on the ability to produce superoxide anions estimated by formazan deposition after liver perfusion with nitro blue tetrazolium and phorbol myristate acetate was increased between 24 and 72 hours after operation. This increase disappeared after gum arabic treatment. It is concluded that massive hepatic necrosis can occur as a result of sinusoidal fibrin deposition provoked by endotoxin in partially hepatectomized rats. Activated Kupffer cells may contribute to this provocation.

Topics: Animals; Endotoxins; Fibrin; Formazans; Hepatectomy; Kupffer Cells; Liver; Liver Function Tests; Male; Necrosis; Rats; Rats, Inbred Strains

The stomach surgically removed from 38 patients because of chronic ulcers are studied. The fibrinoid necrosis zone observed at the bottom of 30 ulcers is formed of two layers out of which the superficial layer only is necrotic while the deep one represent a fibrinoid swelling. The latter consists of the network of collagen fibers and fibrin elements with surviving connective tissue cells. Two processes going into the opposite directions take place on the border between the fibrinoid zone and granulation tissue: the spread of the fibrinoid to the granulation tissue and its organization by the granulation tissue elements. Interrelationship between these processes as well as the intensity of the fibrinoid necrosis rejection from the surface determines the thickness of the zone. Fibrinoid prevents the stomach wall digestion but at the same time inhibits the ulcer healing.

Topics: Adult; Chronic Disease; Fibrin; Gastrectomy; Gastric Mucosa; Histocytochemistry; Humans; Microscopy, Electron; Middle Aged; Necrosis; Staining and Labeling; Stomach; Stomach Ulcer

Malignant renal hypertension was induced in male Wistar rats. In the early phase of the disease, ie. the 1st week, a transient and generalized activation of arterial cellular functions was observed, while later, on day 21 widespread intimal proliferations developed in the arteries. This early activation included an increase in transmural permeability, DNA-, protein, collagen, elastin and ground substance synthesis, a rise in mural PGI2 content and an increase in number of Weibel-Palade bodies. An activation of platelets and monocytes could also be detected during the 1st week. In a group of rats the development of malignant hypertension was interrupted following the early activation of arteries and the incidence of intimal proliferations was compared with that of rats with maintained hypertension. No intimal proliferation was observed on day 21 in the rats with interrupted hypertension. It is concluded that the early activation of the artery does not furnish enough stimulus for triggering intimal proliferations and intimal plaques are not direct sequelae of the early arterial reaction. Furthermore the entrance of plasma materials during transmural permeability increase can not induce smooth muscle proliferation if the hypertension is interrupted.

Topics: Animals; Aorta; Arteries; Arterioles; Cell Membrane Permeability; Endothelium; Fibrin; Hypertension, Renovascular; Hypertrophy; Iron; Male; Microscopy, Electron; Muscle, Smooth, Vascular; Necrosis; Rats; Rats, Inbred Strains; Renin

The brain stems from 52 corpses were microscopically examined. These cases died as a result of closed head injuries, which were clinically diagnosed and/or diagnosed postmortem as primary brain stem lesions. The morphological changes in these cases were compared with morphological changes in the brain stems of corpses who died from cerebral hemorrhage with additional secondary brain stem lesions. The examinations revealed acidophilic necrosis of the vessel walls in brain stem hemorrhages with fibrin impregnation of the vessel walls. Fibrin penetration to the perivascular space was the basic morphological marker that helped to differentiate between these two groups of cases.

Topics: Adolescent; Adult; Aged; Arteries; Brain Stem; Cerebral Hemorrhage; Child; Fibrin; Humans; Intracranial Pressure; Middle Aged; Muscle, Smooth, Vascular; Necrosis

Owing to special reactivity anchored in its structure the connective tissue responds to all kinds of injuries with tissue changes which in their completeness are designated as inflammation. An expressive carrier of mesodermal inflammation is the synovial membrane in which these tissue changes are manifested at first by the vessels and cells of the blood, and subsequently by all other constituents of the synovial membrane.

Topics: Collagen; Fibrin; Fibroblasts; Humans; Hypertrophy; Inflammation; Necrosis; Synovial Membrane; Synovitis; Time Factors

Atrophie blanche is an uncommon condition characterized by the development of white atrophic patches of skin on the lower extremities, which form as a result of fibrinoid vasculitis of superficial and mid-dermal vessels followed by necrosis and ulceration of the epidermis. We report four cases in which similar lesions developed on the legs and ankles of young Jewish Russian immigrants to Israel. Although the lesions share many features with atrophie blanche, they differ in their early age of onset, the male predilection, and the extension of the fibrinoid vasculitic process into the subcutaneous tissue. Additionally, the peculiar population clustering (Georgia, U.S.S.R.), common ethnic background, and a family history of similar lesions in close relatives seem to point to a familial or genetic predisposition underlying the development of the disease.

Topics: Adolescent; Adult; Atrophy; Biopsy; Capillaries; Female; Fibrin; Humans; Leg Ulcer; Male; Necrosis; Skin; Skin Ulcer; Vasculitis

This study reviews liver disease in toxemia of pregnancy based on 102 cases submitted to the Armed Forces Institute of Pathology. The common clinical features were right upper quadrant and epigastric pain, nausea, vomiting, and elevation of the serum transaminases. Jaundice occasionally developed. These occurred in severe preeclampsia or eclampsia and their cause was usually recognized. However, hepatic symptoms and signs did result in inappropriate diagnoses and misdirected therapy. Such confusion occurred when these were the initial problems confronting the clinician in women presenting with advanced toxemia due to poor prenatal care. They were also likely to be misleading when other more classic parameters, such as blood pressure and proteinuria, were only midly abnormal. Central nervous system complications were the common cause of death but liver disease could be partially or wholly responsible. Extensive periportal lesions, hepatic hematomas, spontaneous rupture, and infarction all contributed to hepatic injury and to morbidity. Fibrin deposition, hemorrhage, or both in the periportal areas was characteristic of the histopathology. Scanning electron microscopy validated this spectrum of change. A toxemic vasculopathy related to severe vasospasm in the hepatic arterial circulation may be responsible.

Topics: Eclampsia; Female; Fibrin; Hemorrhage; Humans; Infarction; Liver; Liver Diseases; Necrosis; Pre-Eclampsia; Pregnancy

Necrotizing fasciitis (NF) is a grave infection of the skin leading to gangrene of the integument and often having a complicated and prolonged course. Studies on blood coagulation and fibrinolysis were done in 15 patients with NF and compared with 5 cases of erysipelas (E). In both conditions local fibrin deposition occurred initially in their course, but it was quantitatively more pronounced in NF than in E. Fibrinolysis decreased and stayed low at the site of NF up to 5 months (median) after discharge from hospital. Fibrinogen and activities of several plasma serine proteinases modifying coagulation were increased during the course of both diseases and even at the follow-up. Factor XII was decreased during the first week in E but a transient drop was present in NF only on days 3 and 4. The treatment of NF consists of high doses of appropriate antibiotics instituted early in its course. A beneficial effect of 300-500 IU heparin/kg/day was suggested from this open study. The hard induration preceding the appearance of skin gangrene was inhibited, if heparin was given early in the course of NF. We conclude that the enhanced fibrin deposition and vascular occlusions in the skin are the basis for most complications present in NF.

Topics: Adult; Aged; Anti-Bacterial Agents; Blood Coagulation; Endopeptidases; Erysipelas; Factor VIII; Factor XII; Fasciitis; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Humans; Male; Middle Aged; Necrosis; Serine Endopeptidases; Staphylococcus aureus; Streptococcus

We have reviewed 74 cases of patients with permanent pacing, using different types of pacing leads in order to determine what morphological changes are produced by this therapy. Macroscopic examination of the heart was performed and slides at the implantation site reviewed when available. Severe chronic inflammation, scarring and a myocardial response were the prominent findings. From a strictly morphological aspect, the initial trauma at implantation time, the chronic foreign body reaction and myocardial response to chronic trauma, are both much less significant in endovenous than in epimyocardial pacing.

Topics: Abscess; Aged; Autopsy; Cardiomyopathies; Female; Fibrin; Humans; Male; Middle Aged; Myocardium; Necrosis; Pacemaker, Artificial

The presence and localization of fibrin and fibronectin in rheumatoid nodules were studied using an indirect immunoperoxidase technique on tissue specimens fixed in formaldehyde, embedded in paraffin and pretreated with pepsin and testicular hyaluronidase. Three zones characteristic for rheumatoid nodules was recognized. Central area with necrosis, containing at least in part fibrinogen-antigenic material and fibronectin especially in the peripheral part of the necrotic area. Around the necrosis a layer of mesenchymal cells in a palisade arrangement was found. Especially in the external part of this layer fibronectin was demonstrated around and between the cells, where fibrin was absent. Peripherally, a zone of non-specific granulation tissue containing moderate amount of fibronectin decreasing towards the surround mature connective tissue, was seen. In the border of the cellular layer vessels were found in variable amount. In some of the vessels vasculitis was demonstrated with the presence of inflammatory cell infiltration, fibrin deposition and occasionally thrombosis. The pathogenesis of the inflammatory reaction in rheumatoid nodules is discussed.

Topics: Adult; Aged; Female; Fibrin; Fibronectins; Humans; Immunoenzyme Techniques; Immunoglobulin G; Male; Middle Aged; Necrosis; Rheumatoid Nodule; Staining and Labeling

A 36-year-old man presented with IgA nephropathy (Berger's disease) and acute abdominal pain. Surgical biopsy of the ileum revealed deposits of IgA, C3, and fibrin in segments of the wall of submucosal arteries. The immune deposits appeared associated with areas of fibrinoid necrosis. These findings support the hypothesis that Berger's disease is a systemic disease, and provide a possible explanation for the abdominal pain associated with IgA nephropathy.

Topics: Abdomen; Adult; Arteries; Biopsy; Complement C3; Fibrin; Fluorescent Antibody Technique; Follow-Up Studies; Glomerular Mesangium; Glomerulonephritis, IGA; Histocytochemistry; Humans; Ileum; Immunoglobulin A; Male; Necrosis; Pain

Experimental studies of hemostasis of the traumatised spleen are reported. After experimental trauma, rapid intraoperative hemostasis and subsequent preservation of the spleen was achieved by the use of a homologous fibrin glue system. A collagen fleece or an autologous fascial flap was used as a carrier for the adhesive mixture. Moreover hemostasis was also attempted with an infrared contact coagulation device and a Neodym-YAG-Laser. After fibrin gluing all the substances used are quickly absorbed by the organism. This is one of the major advantages of the fibrin adhesive method. When the bleeding surface was covered with a collagen fleece or a fascial flap, hemostasis was attained quickly. The collagen fleece has an absorptive effect which improves the hemostatic quality. Hemostasis with infrared coagulation is based on infrared light and on mechanical tissue compression. Possible pools of blood can be managed by compressing the contact surface. With this method, too, hemostasis can quickly be achieved. It was impossible to attain equally positive results with the contact-free laser device. Hemostasis is caused by a burn necrosis with the coagulation methods. The tissue healing process lasts until the necrotic tissue has been absorbed.

Topics: Blood Coagulation; Fascia; Fibrin; Granulation Tissue; Hemostatic Techniques; Humans; Infrared Rays; Laser Therapy; Necrosis; Spleen; Time Factors; Tissue Adhesives

In a prospective study of erythema multiforme, forty-two cases were selected with the use of defined criteria. In thirty-three cases (79%), the erythema multiforme occurred following a lesion of recurrent herpes simplex; in four cases (10%), it was related to administration of a sulfonamide drug. Herpes-associated erythema multiforme (HEM) was largely recurrent erythema multiforme minor and was characterized histopathologically by inflammatory changes, such as spongiosis and exocytosis, and by focal liquefaction degeneration of the basal cell zone of the epidermis. Sulfa-associated erythema multiforme (SEM) was a nonrecurrent illness with widespread cutaneous and mucosal damage associated with prominent histologic necrosis of epidermal cells. The deposition of C3 and fibrin along the dermoepidermal junction and the deposition of IgM, C3, and fibrin around dermal blood vessels by immunofluorescence microscopy were similar in both groups. Although HEM and SEM may have somewhat different clinical and histologic features, there is significant overlap in the pattern of tissue damage.

Topics: Adolescent; Adult; Aged; Child; Child, Preschool; Complement C3; Epidermis; Erythema Multiforme; Female; Fibrin; Herpes Simplex; Humans; Immunoglobulin M; Male; Middle Aged; Necrosis; Prospective Studies; Recurrence; Sulfonamides

Experimental infection in mice with Dermatophilus (D.) congolensis-like microorganisms was carried out, intraperitoneally and subcutaneously. This strain had been isolated from porcine tonsil and reported to be different in some morphological and biological points from D. congolensis. Macroscopic examination revealed multiple abscesses in the peritoneal cavities, or subcutaneous abscesses after the intraperitoneal or subcutaneous injection respectively. Histopathologic examination revealed the characteristic arrangement of the neutrophils surrounding the bacterial colony and peripheral macrophages in the abscess lesions. The lesions contained many microorganisms which showed wide range of the characteristic morphologic variation such as: mycelial elements, coccoid elements and large coccoid elements with transverse or longitudinal septa. Chlamydospore-like elements were sometimes found in the microcolonies in early lesions. The morphology of the lesions and the microorganisms was compared with those of other bacteria including D. congolensis.

Topics: Abscess; Actinomycetales; Actinomycetales Infections; Animals; Fibrin; Granuloma; Inflammation; Liver Abscess; Macrophages; Mice; Necrosis; Neutrophils; Palatine Tonsil; Pancreatic Diseases; Peritoneal Cavity; Splenic Diseases; Swine

The occurrence of the Local Shwartzman Reaction (LSR) in equine species has not previously been reported. The molecular mechanism appears identical to that reported for the rabbit and other species. The immunopathologic and histopathologic similarities of the experimentally induced LSR in horses and ponies to that of the hoof-laminae (an extension of the skin) lesion in naturally-occurring and/or carbohydrate induced laminitis may offer insight into the pathogenesis of this complex disease.

Topics: Animals; Blood Platelets; Endotoxins; Female; Fibrin; Fluorescent Antibody Technique; Horses; Inflammation; Male; Necrosis; Neutrophils; Shwartzman Phenomenon; Skin

Fibrinoid necrosis which in previous investigations was demonstrated in the epithelial cells of the skin and of the liver in certain disorders, may also appear in the colloid bodies in lichen planus. Trichrome stainings were positive for fibrinoid, staining reactions with haematoxylin variants indicated the presence of keratin and precursors, and investigations in Wood's light permitted conclusions concerning the appearance of mixed proteins, of which keratofibrinoid seems to be the most important. Circulatory disturbances are emphasized as having an important role. The colloid bodies are extruded from the epidermis, according to the observations of Kerr et al., following the rules of apoptosis.

Topics: Epidermis; Epithelium; Fibrin; Histocytochemistry; Humans; Keratins; Lichen Planus; Microscopy, Fluorescence; Necrosis; Paraproteins; Staining and Labeling

In examination of 732 knee joints through the arthroscope since 1961, various types of debris were observed in 47. The debris was classified into four groups: precipitation of fibrin, degeneration and necrosis of villi, desquamation of articular cartilage, and metaplasia of villi. Diseases of the knee joint and their pathogenesis are discussed in the light of these findings.

Topics: Cartilage, Articular; Endoscopy; Fibrin; Humans; Joint Diseases; Knee Joint; Metaplasia; Necrosis

Coronary artery bypass graft surgery has been available and widely successful for the symptomatic treatment of ischemic heart disease. Despite its widespread use, there is little information available on the pathological consequences of this procedure on the human heart. In this article, morphological consequences of coronary artery bypass graft surgery is reviewed. Intimal changes occurring within the vein graft itself consist predominately of fibrous initimal proliferation, which in some patients may progress to from an occlusive plaque. Most occlusions, however, occur at the coronary artery bypass graft anastomosis site and the mechanisms of occlusion include compression of the vascular lumen, thrombosis, and dissection of the coronary artery. Most graft failure occurs in the setting of too small a native coronary artery lumen. The myocardium is also at risk for alterations as a result of the bypass operation. Contraction band or reperfusion necrosis is the type of injury most commonly seen, and it appears to occur most often in the distribution of patent grafts. Accelerated atherosclerosis in vein grafts and the myocardial injury associated with revascularization require further detailed morphological studies, but these are important areas for pathological exploration since they bear on important and yet unanswered questions about coronary bypass surgery: can it in the long run perserve myocardium and prolong life?

Topics: Adult; Aged; Coronary Artery Bypass; Coronary Vessels; Female; Fibrin; Humans; Male; Middle Aged; Myocardial Infarction; Myocardium; Necrosis; Postoperative Complications; Saphenous Vein; Thrombosis; Time Factors; Transplantation, Autologous

Plasmatic arterionecrosis, the causative lesion of hypertensive cerebral hemorrhage, follows upon medial muscle cell necrosis. The development of medial muscle cell necrosis, the earliest cerebral arterial change seen in hypertensive rats, was inhibited when these animals were fed a cholesterol and lard-supplemented diet. Insudation of fibrin was noted in the arterial intima of hypertensive rats with bilaterally constricted renal arteries. Removal of the constriction induced a fall in the elevated blood pressure and an increase of intimal muscle cells. These were responsible for the dissolution of the deposited fibrin, leading to arteriosclerosis. These myointimal cells may originate from the endothelium. Arterial contraction caused by methoxamine hydrochloride often induced the intrusion of one medial muscle cell into another and increased endothelial permeability. 12-24 h after contraction, the arterial segments showed medial muscle cell necrosis, endothelial desquamation with platelet adhesion, and blood plasma infiltration.

Topics: Animals; Arteriosclerosis; Cerebral Arteries; Cerebral Hemorrhage; Fibrin; Humans; Hypertension; Male; Mesenteric Arteries; Methoxamine; Muscle Contraction; Muscle, Smooth; Necrosis; Rats; Renal Artery

Twenty cases of ischemic bowel disease were analysed to determine the frequency and significance of fibrin thrombi in this condition. Fibrin thrombi were present in all 10 patients with occlusive ischemic bowel disease and in 7 of the 10 patients with nonocclusive ischemic bowel disease. In addition, fibrin thrombi were noted in a wide variety of specific and nonspecific inflammatory bowel diseases and in acute appendicitis. We conclude that fibrin thrombi are a nonspecific feature of tissue necrosis and that their mere presence in the bowel should not be regarded as an expression of disseminated intravascular coagulation.

Topics: Appendicitis; Colitis, Ulcerative; Crohn Disease; Fibrin; Humans; Intestinal Diseases; Intestinal Obstruction; Intestines; Ischemia; Necrosis; Thrombosis

Topics: Acute Kidney Injury; Animals; Blood Vessels; Brain; Coronary Vessels; Edema; Fibrin; Folic Acid; Kidney; Kidney Tubules; Liver; Male; Mesentery; Muscle, Smooth; Necrosis; Pancreas; Rats; Time Factors

The significance and frequency of fibrin thrombi (FT), the pathological hallmark of disseminated intravascular coagulation (DIC), in ischemic intestine were analyzed in a retrospective study of the infarcted bowel of patients with occlusive mesenteric ischemia (OMI) and nonocclusive mesenteric ischemia (NOMI). Representative intestinal sections were studied from 10 patients with NOMI of the small and/or large bowel and 12 patients, with OMI of varied etiology. Three patients with inflammatory bowel disease and 1 patient with DIC and bowel necrosis were also studied. Routine hematoxylin and eosin stains for fibrin were prepared for each specimen. The number of FT was quantitated. FT were identified in each of the 10 cases of NOMI; however in only 2 were they prominent. FT were identified in 6 of the 12 cases of OMI and in 4 of these 6 they were a prominent feature. Rare FT were present in the cases of inflammatory bowel disease and did not correlate with the inflammatory process. No FT were present in the intestinal sections of the DIC case. FT are a nonspecific feature of necrosis and can be identified in both occlusive and nonocclusive ischemic bowel disease. Their presence in the intestine of NOMI therefore cannot be used to implicate DIC as the primary cause of this entity.

Topics: Blood Platelets; Disseminated Intravascular Coagulation; Enteritis; Fibrin; Humans; Infarction; Intestinal Diseases; Intestines; Ischemia; Mesenteric Vascular Occlusion; Mesentery; Necrosis; Retrospective Studies; Thrombosis

Two patients who developed reversible renal failure during intermittent rifampicin therapy are described. Both had febrile reactions to rifampicin. The first was also found to have uraemia associated with swelling of the glomerular endothelial cells. The second developed tubular necrosis unassociated with haemolysis or shock. The pathogenesis of the renal lesion in these two patients, as revealed by light microscopy, immunofluorescence studies and electron microscopy, is discussed.

Topics: Acute Kidney Injury; Adult; Antibodies; Endothelium; Ethambutol; Fever; Fibrin; Humans; Immune Complex Diseases; Ischemia; Kidney Glomerulus; Kidney Tubules; Male; Necrosis; Rifampin; Tuberculosis, Pulmonary; Uremia

Retinal changes in accelerated hypertension were studied in seventeen monkeys with experimental hypertension by means of ophthalmoscopy and colour and flourescence photography during life, and by injection and digest preparations and light and electron microscopy after the animals had been killed. Cotton-wool spots developed in all but three monkeys. The arteries became tortuous and dilated and the light reflex decreased in those animals that became hypertensive. The earliest abnormality was a development of many points of fluorescein leakage on terminal arterioles or small arteries. Such leaking points were always present in relation to cotton-wool spots but were not confined to such areas. Focal narrowing of arteries was not observed but arteriolar occlusion and retrograde filling of the distal segment was present in three animals. Superficial linear haemorrhages were noted in five animals. Light microscopy revealed cotton-wool spots which were identical to those observed in man with a collection of swollen axons containing densely staining pseudonuclei. Study of the arterioles by electron microscopy showed findings ranging from normality to extensive necrosis. Many precapillary arteries were constricted and some were virtually occluded. Degenerative changes were present in smooth muscle cells in the wall of many of the constricted arterioles. Many arteries also showed insudation into their wall of plasma which had seeped into the muscular coat displacing and sometimes entirely replacing the smooth muscle cells. Except for arterioles with advanced necrosis, there was no indication of how plasma insudation occurred. Two arterioles with extensive necrosis showed a break within the endothelial cell cytoplasm through which penetration of plasma proteins had probably occurred. The extravascular tissues showed collections of amorphous material, sone of it with the typical banded configuration of fibrin. The sequence of events proposed to explain these features is as follows: (1) The arterioles constrict as the pressure rises, most likely as a result of vascular autoregulation. This may head to occlusion of the precapillary arterioles and is associated with necrosis of vascular smooth muscle. (2) Dilatation then occurs with insudation of plasma into the unsupported wall through a damaged endothelium. This stage probably corresponds to the autoregulatory break-point and is evidenced clinically by focal leakage of fluorescein. (3) Progressive plasma insudation

Topics: Animals; Arterial Occlusive Diseases; Basement Membrane; Blood Flow Velocity; Blood Pressure; Capillaries; Dilatation; Fibrin; Fluorescein Angiography; Haplorhini; Hypertension, Malignant; Muscle, Smooth; Necrosis; Ophthalmoscopy; Reflex, Pupillary; Retina; Retinal Artery; Retinal Diseases; Urea

Chronic pneumonia experimentally produced in 14 pigs with African swine fever (ASF) virus was studied by immunofluorescene (IF) and histopathologic techniques. Frozen sections prepared from pulmonary tissues of the infected pigs were stained with fluorescein-conjugated antiserums against ASF viral antigen, porcine immunoglobulin G (IgG), procine complement (C), and porcine fibrinogen. The viral antigen(s) was mainly seen in macrophages and cell debris in alveolar walls and lumens. This finding indicates that the virus replicated in the cytoplasm of alveolar macrophages that subsequently degenerated and released the viral antigen. Diffuse immunoglobulin (Ig) deposition was found in necrotic cells and debris. Immunoglobulin also was seen bound to intracytoplasmic inclusion bodies in some degenerating alveolar macrophages. This finding indicates that antibody against ASF viral antigen(s) excluded from blood circulation or produced by local immunocytes (or both) reacted with viral antigen at intramacrophage and extramacrophage levels and resulted in the formation of insoluble antigen-antibody (Ag-Ab) complexes. The participation of C in the immune complex was evident in the early stage of the pneumonia, but was less evident in the subsequent extensive, progressive necrotic processes. Fibrin deposits were visible only in the early necrotic area of alveolar walls and lumens. Possible mechanisms inducing extensive necrosis are discussed.

Topics: African Swine Fever; Animals; Antigen-Antibody Complex; Antigens, Viral; Complement System Proteins; DNA Viruses; Fibrin; Fibrinogen; Fluorescent Antibody Technique; Immune Sera; Immunoglobulin G; Lung; Macrophages; Necrosis; Pneumonia, Viral; Pulmonary Alveoli; Rabbits; Swine; Swine Diseases

Topics: Anemia, Hemolytic; Breast Diseases; Disseminated Intravascular Coagulation; Female; Fibrin; Gangrene; Humans; Middle Aged; Necrosis; Thrombophlebitis; Warfarin

The effects of intravenously administered endotoxin on the hepatic and systemic circulation as well as on the coagulation system were evaluated in normal rats (n = 26), in rats with experimental portal hypertension (n = 15), and in rats with portacaval anastomosis (n = 22). Endotoxin (1-5 mg/kg) in the normal rat leads to a prompt increase of transaminase activity and to a hyperdynamic circulation with a consequent increase in the total hepatic blood flow. In a later phase (6 h postoperatively) the hepatic artery dilated with a consequent hepatic arterial hyperperfusion. The coagulation system was affected with signs of consumption coagulopathy. In the rats with portal hypertension and portacaval collaterals as well as in those with portacaval anastomosis, the endotoxin injection resulted in acute liver necrosis within 12 to 15 hours. The hepatic artery became overdilated with a cardiac output fraction of 25% (normal 5-5%). Blood extravasates and thrombi, rich in fibrin, were detected in the liver. It is suggested that this exaggeration of the endotoxin effect was due to an impaired clearance function of the reticuloendothelial system, probably as consequence of portacaval collateral circulation. It is concluded that endotoxins (1) damage the liver even in a normal organism; (2) are potent to induce acute liver necrosis, if the reticuloendothelial system is altered; (3) have to be taken into consideration as contribution to the pathogenesis of acute as well as chronic liver diseases.

Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Bilirubin; Blood Coagulation Factors; Blood Glucose; Blood Volume; Cardiac Output; Collateral Circulation; Endotoxins; Erythrocyte Aggregation; Fibrin; Fibrinogen; Hypertension, Portal; Liver; Liver Circulation; Liver Diseases; Necrosis; Phagocytosis; Portacaval Shunt, Surgical; Rats; Regional Blood Flow; Time Factors

Lesions are described in the vocal cords of an unselected group of 91 infants dying as "cot deaths", 11 stillbirths and 107 infants and children dying from conventional diseases. The lesions have been classified into six types. After allowances for the effects of intubation, the same incidence and type of change was present in all but the stillbirths. This argues against them being a specific pathogenic mechanism confined to the cot death situation. The aetiology and pathogenesis are unexplained but indicate the existence of an unsuspected laryngeal disorder that merits further study in mechanism leading to child death.

Topics: Autopsy; Basement Membrane; Female; Fetal Death; Fibrin; Humans; Infant; Infant, Newborn; Intubation, Intratracheal; Laryngeal Diseases; Necrosis; Pregnancy; Sudden Infant Death; Ulcer; Vocal Cords

Topics: Abortion, Habitual; Abortion, Threatened; Animals; Basement Membrane; Colloids; Female; Fetal Death; Fetal Diseases; Fibrin; Glycosaminoglycans; Humans; Infant, Newborn; Infant, Premature; Iron; Mice; Necrosis; Placenta; Placenta Diseases; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Staining and Labeling; Trophoblasts

Administration of 0.5 mg bleomycin to mice twice weekly for 4 weeks induced pulmonary fibrosis. The initial site of injury was the intima of pulmonary arteries and veins where endothelial cells became edematous and were separated from the underlying basement membrane by large blebs. These lesions occurred after 2 weeks and were associated with infiltration of perivascular spaces by lymphocytes and plasma cells. Capillary endothelial blebbing and interstitial edema were observed after 4 weeks, when multifocal necrosis of type 1 alveolar epithelial cells was accompanied by fibrinous exudation into the alveoli. The process of repair was characterized by proliferation and metaplasia of type 2 epithelial cells, fibroblastic organization of alveolar fibrin and fibrosis of the interstitium within 8 to 12 weeks. The consistent induction of changes similar to those of diffuse pulmonary fibrosis or fibrosing alveolitis in man suggests that bleomycin-induced injury may provide a suitable model for the investigation of this ill-defined group of diseases.

Topics: Animals; Bleomycin; Capillaries; Disease Models, Animal; Endothelium; Epithelium; Exudates and Transudates; Fibrin; Fibroblasts; Lung; Lymphocytes; Metaplasia; Mice; Microscopy, Electron; Necrosis; Plasma Cells; Pulmonary Alveoli; Pulmonary Artery; Pulmonary Edema; Pulmonary Fibrosis; Pulmonary Veins

Topics: Animals; Basophils; Cartilage; Cell Nucleus; Collagen; Connective Tissue Cells; Ear, External; Eosinophils; Fibrin; Graft Rejection; Haplorhini; Necrosis; Surgery, Plastic; Transplantation, Autologous; Transplantation, Homologous; Wound Healing

Topics: Acute Kidney Injury; Biopsy; Cell Migration Inhibition; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Immune Complex Diseases; Male; Necrosis; Peritoneal Dialysis; Proteinuria; Remission, Spontaneous; Streptococcal Infections

Topics: Adolescent; Adult; Aged; Candidiasis; Child; Child, Preschool; Deglutition Disorders; Epithelial Cells; Esophagitis; Female; Fibrin; Heart; Herpes Simplex; Humans; Lung; Male; Middle Aged; Necrosis; Pneumonia; Respiratory Tract Infections; Simplexvirus; Trachea

Topics: Animals; Capillary Permeability; Clone Cells; Education, Medical, Graduate; Epithelial Cells; Epithelium; Fibrin; Humans; Hypoxia; Intestinal Mucosa; Mice; Necrosis; Neoplasms; Radiation Dosage; Radiation Effects; Radiation Injuries, Experimental; Radiobiology; Radiology; Radiotherapy; Rats; Research; Serum Albumin, Radio-Iodinated; United Kingdom

Rats were inoculated with viable Salmonella dublin organisms, or a crude S dublin endotoxin, at the fourteenth and nineteenth days of pregnancy. They were killed at intervals up to 96 hours after inoculation, and the pathogenesis of the lesions was compared. At each stage of pregnancy the initial lesions produced by live bacteria and crude endotoxin showed important similarities, confirming the significance of endotoxin in the pathogenesis of placental damage. There were differences in the later stages of the pathogenic process. Comparisons of the process of placental damage at the two stages of pregnancy have suggested that the same mechanism acts throughout the last third of pregnancy and that thrombosis and disseminated intravascular coagulation are not an important part of the mechanism of placental damage.

Topics: Animals; Disseminated Intravascular Coagulation; Endotoxins; Female; Fetal Death; Fibrin; Granulation Tissue; Hemorrhage; Necrosis; Neutrophils; Placenta; Placenta Diseases; Pregnancy; Pregnancy Complications, Infectious; Rats; Salmonella Infections, Animal; Sodium Chloride; Thrombosis; Time Factors; Toxemia; Uterus

Three cases with intracranial lesions developed evidence of disseminated intravascular coagulation which was confirmed at necropsy. The factors engendering this state, including release of potent thromboplastin from neural tissue are discussed and the danger of this intermediary mechanism of disease increasing the mortality of intracranial disease is demonstrated. Careful haematological investigation of all patients with intracranial disease is therefore advised, especially if they manifest evidence of a bleeding tendency.

Topics: Adult; Blood Cell Count; Blood Platelets; Brain Abscess; Brain Injuries; Cerebral Cortex; Cerebral Hemorrhage; Child; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Hemoglobinometry; Humans; Kidney; Male; Necrosis; Prothrombin Time; Thrombin

Topics: Adolescent; Adult; Anemia, Sickle Cell; Arthritis; Bone and Bones; Child; Child, Preschool; Erythrocytes, Abnormal; Female; Fibrin; Hemoglobin C Disease; Humans; Infarction; Joint Diseases; Male; Middle Aged; Mucins; Necrosis; Osteoporosis; Radiography; Sclerosis; Synovial Fluid; Synovial Membrane; Thalassemia; Uric Acid

Topics: Aged; Arthroplasty; Elbow; Elbow Joint; Female; Fibrin; Follow-Up Studies; Hip; Hip Joint; Histocytochemistry; Humans; Joint Prosthesis; Knee; Knee Joint; Male; Microscopy, Electron, Scanning; Middle Aged; Necrosis; Osteoarthritis; Postoperative Complications; Surgical Wound Infection; Synovial Membrane; Time Factors; Wound Healing

Topics: Age Factors; Amino Acids; Animals; Animals, Newborn; Aspartic Acid; Caseins; Dose-Response Relationship, Drug; Fibrin; Glutamates; Hypothalamus; Mice; Necrosis; Nervous System Diseases; Neurons; Protein Hydrolysates; Quaternary Ammonium Compounds

Topics: Aged; Basement Membrane; Endothelium; Female; Fibrin; Fluorescent Antibody Technique; Humans; Joint Diseases; Male; Microscopy, Electron; Middle Aged; Necrosis; Rheumatoid Factor; Scleroderma, Systemic; Staining and Labeling; Synovial Fluid; Synovial Membrane; Viscosity

Topics: Animals; Cell Aggregation; Fibrin; Gastric Mucosa; Granulation Tissue; Guinea Pigs; Histamine; Leukocytes; Male; Necrosis; Periodic Acid; Promethazine; Regeneration; Staining and Labeling; Stomach Ulcer; Time Factors

Topics: Female; Fibrin; Humans; Microscopy, Fluorescence; Necrosis; Placenta; Placenta Diseases; Pregnancy

Topics: Animals; Biopsy; Bronchi; Cilia; Dogs; Epithelial Cells; Exudates and Transudates; Fibrin; Graft Rejection; Hemorrhage; Lung; Lung Transplantation; Methods; Microscopy, Electron; Microscopy, Electron, Scanning; Necrosis; Pulmonary Alveoli; Pulmonary Edema; Replantation; Time Factors; Transplantation, Homologous

Topics: Adult; Autopsy; Basement Membrane; Biopsy; Biopsy, Needle; Epithelium; Female; Fibrin; Graft Rejection; Humans; Ischemia; Kidney; Kidney Cortex; Kidney Diseases; Kidney Glomerulus; Kidney Transplantation; Male; Microscopy, Electron; Necrosis; Thrombosis; Transplantation, Homologous

Topics: Animals; Capillaries; Epithelium; Female; Fibrin; Lipidoses; Lung; Lymphatic System; Macrophages; Male; Necrosis; Phagocytosis; Pneumonia; Pulmonary Alveoli; Pulmonary Edema; Salmonella; Salmonella Infections; Salmonella Infections, Animal; Swine; Time Factors; Toxins, Biological

Topics: Arterial Occlusive Diseases; Erythrocytes; Female; Fibrin; Humans; Infarction; Leukocytes; Necrosis; Placenta; Pregnancy; Thrombosis

Topics: Animals; Blood Cell Count; Blood Coagulation; Blood Coagulation Tests; Blood Platelets; Endothelium; Female; Fibrin; Fibrinogen; Hemorrhage; Injections, Intradermal; Microscopy, Electron; Necrosis; Prothrombin Time; Rabbits; Spider Bites; Spiders; Thrombosis; Time Factors; Venoms

Topics: Autopsy; Basal Ganglia; Brain; Disseminated Intravascular Coagulation; Female; Fetal Diseases; Fibrin; Humans; Hydrocephalus; Infant, Newborn; Ischemia; Male; Necrosis; Placenta; Placenta Diseases; Plasma Cells; Pregnancy; Thrombosis; Virus Diseases

Topics: Animals; Arthritis; Disease Models, Animal; Female; Fibrin; Formaldehyde; Histiocytes; Inflammation; Injections, Intra-Articular; Knee; Leukocytes; Lymphocytes; Necrosis; Plasma Cells; Rabbits; Serum Albumin, Bovine

Topics: Basement Membrane; Female; Fibrin; Humans; Necrosis; Placenta; Pregnancy

Topics: Acute Disease; Adult; Alanine Transaminase; Blood Coagulation Tests; Factor IX; Factor V; Factor VII; Factor VIII; Factor X; Female; Fibrin; Fibrinogen; Hepatic Encephalopathy; Hepatitis A; Humans; Middle Aged; Necrosis; Plasmapheresis; Prothrombin; Time Factors; Vitamin K

A patient with viral hepatitis in the third trimester of pregnancy is described. She developed acute hepatic failure in the postpartum period which was associated with evidence of intravascular coagulation. Following therapy with heparin and fresh-frozen plasma, the patient made a dramatic recovery. Hepatitis developed during the puerperium may predispose to pathological intravascular coagulation and hepatocellular necrosis may thereby be perpetuated.

Topics: Acenocoumarol; Acute Disease; Adult; Alanine Transaminase; Alkaline Phosphatase; Bilirubin; Blood Platelets; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Heparin; Hepatitis A; Humans; Necrosis; Plasma; Postpartum Period; Pregnancy; Pregnancy Complications, Infectious; Time Factors

Topics: Adult; Aged; Animals; Anticoagulants; Arterial Occlusive Diseases; Blood Flow Velocity; Blood Viscosity; Enzyme Therapy; Female; Fibrin; Foot; Hemolysin Proteins; Humans; Injections, Intravenous; Leg; Male; Middle Aged; Necrosis; Pain; Regional Blood Flow; Snakes; Venoms

Topics: Animals; Arteries; Benzopyrans; Fibrin; Hypoxia; Mesenteric Arteries; Microscopy, Electron; Muscle, Smooth; Necrosis; Phosphotungstic Acid; Rats; Staining and Labeling

Topics: Animals; Biopsy; Fibrin; Fibrinolysis; Graft vs Host Reaction; Kidney; Kidney Transplantation; Methods; Necrosis; Plasminogen; Rabbits; Thrombosis; Time Factors; Transplantation, Autologous; Transplantation, Homologous

Topics: Bacteria; Cell Membrane; Cell Nucleus; Child; Eosinophils; Erythrocytes; Extracellular Space; Fibrin; Golgi Apparatus; Humans; Lymph Nodes; Lymphadenitis; Lymphocytes; Macrophages; Male; Microscopy; Microscopy, Electron; Mitochondria; Monocytes; Necrosis; Phagocytosis; Typhoid Fever

Topics: Cicatrix; Epithelial Cells; Fibrin; Gastric Juice; Gastric Mucosa; Granulation Tissue; Humans; Necrosis; Peptic Ulcer Perforation; Stomach Ulcer

Topics: Animals; Basement Membrane; Bronchi; Cell Differentiation; Collagen; Connective Tissue Cells; Elastic Tissue; Epithelium; Fibrin; Fibroblasts; Histocytochemistry; Lung; Macrophages; Microscopy, Electron; Mitosis; Muscle, Smooth; Necrosis; Pseudorabies; Swine; Swine Diseases

Topics: Animals; Capillaries; Cell Membrane Permeability; Cytoplasm; Fibrin; Hypoxia; Mesenteric Arteries; Microscopy, Electron; Muscle, Smooth; Necrosis; Oxygen Consumption; Rats

Topics: Arthritis, Rheumatoid; Cell Differentiation; Connective Tissue; Fibrin; Fibroblasts; Humans; Necrosis; Synovial Membrane

Topics: Animals; Dog Diseases; Dogs; Fibrin; Intervertebral Disc Displacement; Ischemia; Necrosis; Spinal Cord; Syndrome

Four water-soluble carcinogens were injected at the same site subcutaneously into rats, mice or guinea-pigs, twice weekly for 5-8 weeks in order to study the evolution of the early tissue reaction. MNU was injected into rats as 0·1 ml. of 0·5% solution, and into mice as 0·1 ml. of 0·05% solution. NQO was administered to rats (0·1 or 0·2 ml. of 0·25 or 0·1%) mice (0·1 of 0·05%) and guinea-pigs (0·5 of 0·1%). Propane sultone and BEI were administered to rats only, the former as 0·1 ml. of 3% and the latter as 0·5 ml. of 2·0% solution.The principal features of the tissue reaction produced by each of the four compounds in rats were similar and consisted of destruction of subcutaneous tissue, deposition of fibrin and "fibrinoid", an abnormal pattern of fibroblastic proliferation with cytomegaly of some fibroblasts and deposition of mucopolysaccharide but little collagen formation. Moreover, the appearance of fibroblastic proliferation was delayed from the normal 2-5 days to 14-16 days.These features are consistent with the known early effects of carcinogens on proliferating target tissues, and differ considerably from those found in the early reactive lesions to repeated injection of solutions of substances possessing physical properties such as surface activity or hypertonicity, or which precipitate at the injection site.

Topics: Adipose Tissue; Animals; Azirines; Butyrates; Carcinogens; Cell Division; Collagen; Connective Tissue; Cyclic N-Oxides; Female; Fibrin; Fibroblasts; Glycosaminoglycans; Guinea Pigs; Injections, Subcutaneous; Male; Mice; Microscopy, Electron; Muscles; Naphthols; Necrosis; Nitroso Compounds; Quinolines; Rats; Skin; Sulfonic Acids; Urea

Topics: Animals; Basophils; Cell Membrane; Desmosomes; Dogs; Endoplasmic Reticulum; Fibrin; Inclusion Bodies; Lipids; Liver; Liver Transplantation; Microscopy; Microscopy, Electron; Mitochondria, Liver; Necrosis; Phagocytosis; Ribosomes; Time Factors; Transplantation Immunology; Transplantation, Homologous

Topics: Animals; Bone Marrow; Chemical and Drug Induced Liver Injury; Feces; Femur; Fibrin; Hemorrhage; Indium; Ions; Kidney; Kidney Tubules; Liver; Lung; Male; Mercury; Mice; Muscles; Necrosis; Oxides; Phagocytosis; Protein Binding; Spleen; Thrombocytopenia; Thrombosis; Water

Topics: Autopsy; Blood Pressure; Body Temperature; Delivery, Obstetric; Extraembryonic Membranes; Female; Fetal Death; Fibrin; Gestational Age; Humans; Infant, Newborn; Infant, Newborn, Diseases; Medical History Taking; Necrosis; Pregnancy; Prenatal Care; Time Factors

Topics: Arthritis, Rheumatoid; Chronic Disease; Fibrin; Humans; Inflammation; Microscopy, Electron; Necrosis; Synovial Membrane; Synovitis

Topics: Adolescent; Adult; Anemia, Hemolytic; Blood Coagulation Disorders; Blood Pressure; Child, Preschool; Desoxycorticosterone; Erythrocytes; Female; Fibrin; Glomerulonephritis; Humans; Hypertension, Malignant; Kidney Diseases; Male; Middle Aged; Necrosis; Nephrectomy; Urea; Vascular Diseases

Topics: Animals; Arteries; Blood Circulation; Capillary Permeability; Elastic Tissue; Fibrin; Humans; Membranes; Microscopy, Electron; Muscle, Smooth; Necrosis; Staining and Labeling; Vascular Diseases

Topics: Blood Vessels; Diphtheria; Fibrin; Granulomatosis with Polyangiitis; Humans; Hypertension, Malignant; Lupus Erythematosus, Systemic; Necrosis; Polyarteritis Nodosa; Pyelonephritis; Rheumatic Fever; Sepsis; Splenic Artery; Tuberculosis, Meningeal; Vascular Diseases

Topics: Adult; Autopsy; Biopsy; Connective Tissue; Elastic Tissue; Eosinophils; Female; Fibrin; Histocytochemistry; Humans; Inflammation; Lupus Erythematosus, Discoid; Lupus Erythematosus, Systemic; Microscopy; Microscopy, Electron; Middle Aged; Necrosis

Topics: Abortion, Septic; Adolescent; Adult; Anticoagulants; Antithrombins; Blood; Blood Coagulation Disorders; Blood Coagulation Factors; Child; Disseminated Intravascular Coagulation; Encephalitis; Encephalitis Viruses; Female; Fibrin; Fibrinogen; Fibrinolysis; Hemorrhagic Disorders; Humans; Liver; Male; Necrosis; Pituitary Gland; Pregnancy; Prostatic Neoplasms; Prothrombin; Sepsis; Shock, Septic; Spleen; Streptokinase

Topics: Arteriosclerosis; Arteriosclerosis Obliterans; Blood Vessels; Collagen; Connective Tissue; Diabetic Angiopathies; Elastic Tissue; Embolism; Endarteritis; Fibrin; Humans; Hyalin; Ischemia; Necrosis; Vasa Vasorum

Topics: Adolescent; Adult; Aged; Female; Fibrin; Fibroblasts; Glycosaminoglycans; Histocytochemistry; Humans; Male; Middle Aged; Necrosis; Rheumatoid Nodule

Topics: Aged; Agglutination; Animals; Blood Coagulation Disorders; Blood Platelets; Dogs; Female; Fibrin; Fibrinogen; Haplorhini; Humans; Middle Aged; Necrosis; Shock

Topics: Animals; Choroid; Cryosurgery; Epithelium; Fibrin; Macrophages; Melanins; Microscopy, Electron; Necrosis; Phagocytosis; Photoreceptor Cells; Rabbits; Regeneration; Retina; Retinal Pigments; Tissue Adhesions

Topics: Arthritis, Rheumatoid; Female; Fibrin; Histocytochemistry; Humans; Male; Necrosis; Placenta; Rheumatoid Nodule; Stomach Ulcer; Synovial Membrane

Topics: Animals; Aorta; Arteries; Female; Fibrin; Hypertension; Macrophages; Male; Necrosis; Rats

Topics: Arteries; Arthritis, Rheumatoid; Chronic Disease; Fibrin; Fibroblasts; Humans; Inflammation; Myocardium; Necrosis; Pericardium; Serous Membrane; Spleen; Tendons

Topics: Adolescent; Adult; Drug Hypersensitivity; Female; Fibrin; Histocytochemistry; Humans; Male; Middle Aged; Necrosis; Polysaccharides; Skin; Thrombosis; Vascular Diseases

Topics: Female; Fibrin; Humans; Infarction; Inflammation; Necrosis; Obstetric Labor, Premature; Placenta; Placentation; Pregnancy

Topics: Aged; Anuria; Cystitis; Diverticulum; Duodenal Ulcer; Female; Fibrin; Hernia, Inguinal; Humans; Ileum; Laparotomy; Male; Necrosis; Peritonitis; Rupture, Spontaneous; Tuberculosis, Urogenital; Urinary Bladder Calculi; Urinary Bladder Diseases; Urinary Bladder Neoplasms; Urination Disorders; Urography

Topics: Animals; Endotoxins; Eosinophils; Female; Fibrin; Injections, Intravenous; Lymphocytes; Macrophages; Microscopy, Electron; Necrosis; Pulmonary Artery; Rabbits; Shwartzman Phenomenon; Thrombosis; Trypan Blue

Topics: Aminocaproates; Animals; Blood Coagulation Tests; Chlorides; Endotoxins; Fibrin; Fibrinolysis; Heparin Antagonists; Kidney; Mercury; Necrosis; Protamines; Rabbits; Shwartzman Phenomenon

Topics: Cesarean Section; Extraembryonic Membranes; Female; Fibrin; Humans; Hypertension; Labor, Induced; Necrosis; Placenta; Pregnancy; Pregnancy Complications, Cardiovascular; Trophoblasts

Topics: Animals; Cytoplasm; Extracellular Space; Fibrin; Microscopy, Electron; Necrosis; Plasma; Rats; Spinal Cord; Wounds and Injuries

Topics: Animals; Blood Vessels; Dogs; Fibrin; Hydrochloric Acid; Hypertension; Necrosis; Norepinephrine; Rabbits; Vascular Diseases

Topics: Animals; Aorta; Aortic Diseases; Fibrin; Histological Techniques; Mesenteric Arteries; Microscopy, Electron; Necrosis; Rats

Topics: Brain Diseases; Brain Edema; Fibrin; Kidney Cortex Necrosis; Kidney Diseases; Kidney Glomerulus; Myocardial Infarction; Necrosis; Pathology; Pulmonary Embolism; Shwartzman Phenomenon; Thrombosis

Topics: Arterial Pressure; Arteries; Arteriosclerosis; Carotid Arteries; Fibrin; Hypertension; Necrosis; Pathology; Rats; Renal Artery; Research

In the presence of reticuloendothelial blockade, the intravenous injection of a protein antigen into specifically immunized rabbits or the infusion of soluble immune complexes into normal animals has been shown to result in the production of bilateral renal cortical necrosis. The similarity in the pathogenesis of this lesion and that seen in the classical generalized Shwartzman reaction produced by bacterial endotoxins is indicated by (a) the failure of both lesions to develop in animals pretreated with large doses of heparin, (b) by the finding of "heparin-precipitable fibrinogen" in the circulation, and (c) by the presence of massive fibrin deposits within the glomerular capillaries. These findings indicate that antigen-antibody reactions in vivo are capable of activating the blood coagulation system and that the mode of action of bacterial endotoxins may have an immunological basis.

Topics: Animals; Antigen-Antibody Complex; Antigen-Antibody Reactions; Capillaries; Endotoxins; Fibrin; Fibrinogen; Kidney Cortex Necrosis; Kidney Diseases; Kidney Glomerulus; Necrosis; Rabbits; Shwartzman Phenomenon

Topics: Aminocaproates; Aminocaproic Acid; Animals; Anticoagulants; Electrons; Fibrin; Kidney Diseases; Kidney Glomerulus; Necrosis; Nephrosclerosis; Pathology; Rabbits; Research; Thrombin; Thromboplastin; Thrombosis

Topics: Arteries; Arterioles; Fibrin; Humans; Lupus Erythematosus, Systemic; Necrosis; Polyarteritis Nodosa

Topics: Fibrin; Hypersensitivity; Immune System Diseases; Kidney Cortex Necrosis; Kidney Diseases; Muscle, Smooth; Necrosis; Shwartzman Phenomenon