fibrin and Prostatic-Neoplasms

Defibrination is a fairly common clinical entity seen in a wide variety of clinical disorders. With an awareness of the likely clinical settings, a high degree of suspicion, and widely available sensitive laboratory tests, the diagnosis is ordinarily easily made. The best therapy is usually that which is directed at the underlying disease rather than at the defibrination syndrome itself. In certain symptomatic cases, heparin and/or replacement therapy is indicated, especially if the underlying disorder cannot be immediately successfully treated. On occasion, antifibrinolytic therapy will be useful, always with due regard to the danger of renal cortical necrosis. Depending on the clinical setting, it may be advisable to give heparin with the antifibrinolytic therapy to minimize that danger.

Topics: Adult; Aged; Antifibrinolytic Agents; Blood Cell Count; Blood Coagulation Factors; Disseminated Intravascular Coagulation; Female; Fetal Death; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinolysis; Heparin; Humans; Male; Postoperative Complications; Pregnancy; Prostatic Neoplasms; Sepsis; Syndrome

Topics: Blood Coagulation; Bone Marrow; Chronic Disease; Disseminated Intravascular Coagulation; Fibrin; Fibrinogen; Humans; Liver; Lung Neoplasms; Male; Prostatic Neoplasms; Surgical Procedures, Operative

Topics: Blood Transfusion; Enzyme Inhibitors; Female; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Hemostatics; Humans; Leukemia; Liver Cirrhosis; Male; Pathology; Physiology; Polycythemia Vera; Pregnancy; Pregnancy Complications; Pregnancy Complications, Hematologic; Prostatectomy; Prostatic Neoplasms; Prothrombin; Thrombin; Thromboplastin

Increased risk of thromboembolic events is associated with prostate cancer, specifically linked to activation of tissue factor. Vitamin D has potential anticoagulant effects by the downregulation of tissue factor expression.. To evaluate the effects on clot formation, the morphological and viscoelastic profiles of prostate cancer patients, before and after ex vivo supplementation of Vitamin D was studied.. Participants were recruited into a metastatic, non-metastatic and reference group. Whole blood samples were treated ex vivo with a dose of 0.5μg/kg Calcitriol. Clot kinetics were assessed using Thromboelastography®. Morphology of the blood components were studied using scanning electron microscopy (SEM).. Results from the Thromboelastography® and SEM indicated no major differences between the non-metastatic group before and after treatment compared to the reference group. The Thromboelastography® showed that the metastatic group had an increased viscoelastic profile relating to a hypercoagulable state. Visible changes with regards to platelet activation and fibrin morphology were demonstrated with SEM analysis of the metastatic group. The viscoelastic and morphological properties for the non-metastatic group after treatment improved to be comparable to the reference group.. Vitamin D supplementation may lead to a more favorable viscoelastic profile, with less dangerous clots forming.

Topics: Dietary Supplements; Fibrin; Humans; Male; Prostatic Neoplasms; Thrombelastography; Thromboplastin; Thrombosis; Vitamin D

DNA 5-hydroxymethylcytosine (5hmC) is produced by dynamic 5mC oxidation process contributing to tissue specification, and loss of 5hmC has been reported in multiple cancers including genitourinary cancers. However, 5hmC is also cell-type specific, and its variability may exist between differentiated tumor cells and cancer stem cells. Thus, cancer-associated changes in 5hmC may be contributed by distinct sets of tumor cells within the tumor tissues.. Here, we applied a sensitive immunoprecipitation-based method (hMeDIP-seq) to analyze 5hmC changes during genitourinary carcinogenesis (including prostate, urothelial and kidney). We confirmed the tissue-specific distribution of 5hmC in genitourinary tissues and identified regional gain and global loss of 5hmC coexisting in genitourinary cancers. The genes with gain of 5hmC during tumorigenesis were functionally enriched in regulating stemness and hypoxia, whereas were associated with poor clinical prognosis irrespective of their differences in tumor type. We identified that gain of 5hmC occurred in soft fibrin gel-induced 3D tumor spheres with a tumor-repopulating phenotype in two prostate cancer cell lines, 22RV1 and PC3, compared with conventional two-dimensional (2D) rigid dishes. Then, we defined a malignant signature derived from the differentially hydroxymethylated regions affected genes of cancer stem-like cells, which could predict a worse clinical outcome and identified phenotypically malignant populations of cells from prostate cancer tumors. Notably, an oxidation-resistant vitamin C derivative, ascorbyl phosphate magnesium, restored 5hmC and killed the cancer stem cell-like cells leading to apoptosis in prostate cancer cell lines.. Collectively, our study dissects the regional gain of 5hmC in maintaining cancer stem-like cells and related to poor prognosis, which provides proof of concept for an epigenetic differentiation therapy with vitamin C by 5hmC reprogramming.

Topics: 5-Methylcytosine; Ascorbic Acid; Carcinogenesis; DNA; DNA Methylation; Fibrin; Humans; Magnesium; Male; Phosphates; Prostatic Neoplasms; Urogenital Neoplasms

The aim is to discuss the contribution of the DR-70 for the patients with high PSA level and which cutofflevel of DR-70 must be consideredthe biopsy decision. 93 patients with high prostate specific antigen level were enrolled into the study. Before the prostate biopsy, total PSA (tPSA), free PSA (fPSA), free/total PSA rate (f/tPSA), PSA density (PSAD) and DR-70 levels were recorded. The patients were divided into two groups according to the pathological outcome of benign (G1) or malignant (G2). G1 and G2 were compared with Mann-Whitney U test, Spearman's rho and ROC curve for analysis. The significance level is taken as .05 for all tests. The median age of patients in G1 and G2 was 62.52 and 68.22 years, respectively. The mean PV in G1 and G2 were 52.16 and 39.6 mL, respectively. The mean tPSA, PSAD and DR-70 levels in G1 and G2 were found as 7.19 and 18.74 ng/mL, 0.14 and 0.48 ng/mL/cc and 0.44 and 0.5 µg/mL, respectively. The mean age of the patients in G2 was statistically significantly higher than G1 (p=.001).The mean PV of the patients in G2 was statistically significantly lower than G1 (p=.001).The mean PSAD of the patients in G2 was statistically significantly higher than G1 (p=.001). There was no statistically significant difference on DR-70 levelsbetween G1 and G2 (p=.38). In Spearman's rhocorrelationanalysis, there was nostatistically significant relationships between DR-70 levels and pathology results in G2 (p=.24). ROC curve of tPSA, fPSA, f/tPSA, PSAD and DR-70 levelswere evaluated. ROC curve of PSAD shows a fair discriminant power with AUC = 0.71 (95% CI: 0.607-0.828) for differentiation between PCa and benign tissue in prostate biopsy with moderate specificity and high sensitivity (62.5% and 75.7%, resp., cut-off level: 0.1377 ng/mL). Contrary to literature and guidelines, cutoff level of PSAD as 0.13ng/mL/cc should be kept in mind and accordingly, a biopsy decision should be made. We think that DR-70 is no needed for additional evaluation before prostate biopsy.

Topics: Aged; Biomarkers, Tumor; Biopsy; Fibrin; Humans; Immunoassay; Male; Middle Aged; Predictive Value of Tests; Prostate-Specific Antigen; Prostatic Neoplasms; ROC Curve; Sensitivity and Specificity

Prostate cancer (PCa) is the most widespread tumor affecting males in Western countries. We propose a novel MRI molecular tetrameric probe based on the heptadentate gadolinium (Gd)-AAZTA (6-amino-6-methylperhydro-1,4-diazepinetetraacetic acid) that is able to in vivo detect PCa through the recognition of the fibrin-fibronectin (FB-FN) complex.. The peptide CREKA (Cys-Arg-Glu-Lys-Ala), targeting the FB-FN complex in the reactive stroma of the tumor, was synthesized by solid phase peptide synthesis (SPPS) and conjugated to the tetramer dL-(Gd-AAZTA). CREKA-dL-(Gd-AAZTA)

Topics: Acetates; Adenocarcinoma; Animals; Azepines; Biomarkers, Tumor; Cell Line, Tumor; Contrast Media; Fibrin; Fibronectins; Gadolinium; Humans; Magnetic Resonance Imaging; Male; Mice; Mice, Nude; Neoplasm Transplantation; Peptides; Prostatic Neoplasms; Protein Binding; Spectrometry, Mass, Electrospray Ionization

Cancer is a leading cause of thrombosis. We identify a new procoagulant mechanism that contributes to thromboembolism in prostate cancer and allows for safe anticoagulation therapy development. Prostate cancer-mediated procoagulant activity was reduced in plasma in the absence of factor XII or its substrate of the intrinsic coagulation pathway factor XI. Prostate cancer cells and secreted prostasomes expose long chain polyphosphate on their surface that colocalized with active factor XII and initiated coagulation in a factor XII-dependent manner. Polyphosphate content correlated with the procoagulant activity of prostasomes. Inherited deficiency in factor XI or XII or high-molecular-weight kininogen, but not plasma kallikrein, protected mice from prostasome-induced lethal pulmonary embolism. Targeting polyphosphate or factor XII conferred resistance to prostate cancer-driven thrombosis in mice, without increasing bleeding. Inhibition of factor XII with recombinant 3F7 antibody reduced the increased prostasome-mediated procoagulant activity in patient plasma. The data illustrate a critical role for polyphosphate/factor XII-triggered coagulation in prostate cancer-associated thrombosis with implications for anticoagulation without therapy-associated bleeding in malignancies.

Topics: Animals; Antibodies, Monoclonal, Humanized; Cell Line, Tumor; Factor XII; Factor XIIa; Fibrin; Humans; Male; Mice; Polyphosphates; Prostatic Neoplasms; Pulmonary Embolism; Secretory Vesicles; Thrombin; Thrombosis

To study the effectiveness of a peptide targeted nanoglobular Gd-DOTA complexes for MR molecular imaging of prostate cancer in a mouse orthotopic PC-3 prostate cancer model.. A CLT1 (CGLIIQKNEC) peptide-targeted generation 2 nanoglobular Gd-DOTA monoamide conjugate [CLT1-G2-(Gd-DOTA)] was used for imaging fibrin-fibronectin complexes in prostate tumor using a non-specific peptide KAREC modified conjugate, KAREC-G2-(Gd-DOTA) as a control. Cy5 conjugates of CLT1 and KAREC were synthesized for binding studies. Orthotopic PC-3 prostate tumors were established in the prostate of athymic male nude mice. MRI study was performed on a Bruker 7T small animal MRI system.. CLT1 peptide showed specific binding in the prostate tumor with no binding in normal tissues. The control peptide had little binding in normal and tumor tissues. CLT1-G2-(Gd-DOTA) resulted in stronger contrast enhancement in tumor tissue than KAREC-G2-(Gd-DOTA). CLT1-G2-(Gd-DOTA) generated ~100% increase in contrast-to-noise ratio (CNR) in the tumor compared to precontrast CNR at 1 min post-injection, while KAREC-G2-(Gd-DOTA) resulted in 8% increase.. CLT1-G2-(Gd-DOTA) is a promising molecular MRI contrast agent for fibrin-fibronectin complexes in tumor stroma. It has potential for diagnosis and assessing prognosis of malignant tumors with MRI.

Topics: Animals; Carbocyanines; Cell Line, Tumor; Contrast Media; Disease Models, Animal; Fibrin; Fibronectins; Fluorescent Dyes; Heterocyclic Compounds; Humans; Magnetic Resonance Imaging; Male; Mice; Mice, Nude; Molecular Imaging; Nanoparticles; Organometallic Compounds; Peptides, Cyclic; Prostatic Neoplasms; Transplantation, Heterologous

The purpose of this study was to assess the therapeutic and toxicological effects of cesium chloride (CsCl) administration in mice bearing prostate cancer tumors.. Three CsCl dose titration studies were completed in tumor-bearing and non-tumor-bearing athymic nude mice. All mice were administered either vehicle (controls), 150, 300, 600, 800, 1,000, or 1,200 mg/kg of CsCl once daily by oral gavage for 30 consecutive days. Body mass was measured daily, food and water consumption were measured every 2 days, and tumor volume was measured twice weekly. Histopathological analysis was conducted on tissues collected from each of the studies. Serum AST/ALT and creatinine were also measured.. Administration of 800-1,200 mg/kg CsCl reduced PC-3 tumor growth but had no effect on LNCaP tumors. Administration of 800-1,200 mg/kg CsCl also resulted in increased water consumption, bladder crystal development, and higher prevalence of cardiac fibrin clots. An observed loss in body mass was dependent on the xenograft type and concentration of CsCl administered. CsCl did not affect serum AST/ALT and creatinine levels.. CsCl may have a therapeutic effect against prostate cancer, but one cannot overlook the acute toxicities also described.

Topics: Administration, Oral; Animals; Antineoplastic Agents; Body Weight; Cell Line, Tumor; Cesium; Chlorides; Crystallization; Disease Models, Animal; Dose-Response Relationship, Drug; Fibrin; Heart; Liver; Liver Function Tests; Male; Mice; Mice, Nude; Prostate-Specific Antigen; Prostatic Neoplasms; Random Allocation; Thirst; Thrombosis; Urinary Bladder; Xenograft Model Antitumor Assays

The features of radiation or chemotherapy cystitis mimicking invasive urothelial cancer are not widely known.. A search of the consultation files from our institution between January 1996 and September 2003 identified 20 patients with bladder biopsies showing cystitis mimicking invasive urothelial cancer.. The mean age at diagnosis was 69 years (range, 40-85 years); 80% were males. Complete history was not available in 1 patient. Seventeen patients had a history of pelvic irradiation (15 prostate cancer and 2 endometrial cancer). Two patients had systemic chemotherapy (1 metastatic colon cancer and 1 mixed connective tissue disease). All patients presented with hematuria. The mean time from radiation and/or chemotherapy to presentation was 27 months (range, 0-84 months). All cases showed epithelial proliferation that mimicked invasive cancer within the lamina propria, with marked proliferation seen in 45% of cases. Mild to moderate nuclear pleomorphism was seen in all cases. A characteristic feature was the presence of pseudoinvasive urothelial nests wrapping around the vessels associated with fibrin deposition. Most cases did not show any mitoses (75%). Ulceration was seen in 39% of cases. All cases showed some degree of hemorrhage, fibrin deposition and fibrin thrombi, fibrosis, and acute and chronic inflammation, with hemosiderin identified in 60% of cases. Edema and vascular congestion were common features (95% and 80%, respectively). Thickened vessels and vascular changes associated with radiation injury were identified in 75% of cases. Seventeen patients were followed for a mean of 9 months (range, 0.25-37 months), and none developed bladder cancer.. Radiation or chemotherapy cystitis can show epithelial proliferations that may be confused with invasive urothelial carcinomas. Other findings characteristic of radiation or chemotherapy cystitis, such as hemorrhage, fibrin, and vascular changes, are often seen in association with the epithelial proliferations and are helpful in distinguishing it from invasive cancer. Pathologists must be aware that these changes may be seen with a remote radiation or chemotherapy history, where this information may not be provided or known at the time of the biopsy evaluation.

Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Colonic Neoplasms; Cystitis; Diagnosis, Differential; Endometrial Neoplasms; Epithelium; Female; Fibrin; Follow-Up Studies; Hemorrhage; Histocytochemistry; Humans; Male; Middle Aged; Mixed Connective Tissue Disease; Prostatic Neoplasms; Radiation Injuries; Radiotherapy; Thrombosis; Time Factors; Urinary Bladder; Urinary Bladder Neoplasms

To explore mechanisms of coagulation activation in adenocarcinoma of the prostate, the occurrence and distribution of components of coagulation and fibrinolysis pathways in situ were studied by means of immunohistochemical techniques applied to frozen sections of fresh malignant and benign hyperplastic prostatic tissue obtained at transurethral resection. Fibrinogen was distributed throughout the perivascular and tumor connective tissue in both malignant and benign disease but was not present in adjacent areas of normal prostate. Antibodies specific for fibrin and D-dimer crosslink sites stained vascular endothelium focally in both malignant and benign tissues. Both neoplastic cells and benign hyperplastic glandular epithelial cells stained weakly and in a patchy distribution for tissue factor and focally for low-molecular-weight urokinase-type plasminogen activator. Focal staining of vascular endothelium was also observed for tissue plasminogen activator and plasmin-antiplasmin complex neoantigen. By contrast, no tissue staining was observed for factor VII, factor X, factor XIII "a" subunit, high-molecular-weight urokinase-type plasminogen activator, plasminogen activator inhibitors 1 to 3, protein C, and protein S. Thus, the similarity in findings between benign hyperplastic and neoplastic prostate tissue, the lack of either an intact tumor cell-associated coagulation pathway or fibrin formation, and the presence of fibrin on vascular endothelium are consistent with the concept that coagulation activation in prostatic cancer may not be due to a direct effect of the tumor cells on the clotting mechanism. Rather, such activation may be induced by a soluble tumor product that activates procoagulant activity on certain host (for example, vascular endothelial) cells. These findings, together with the lack of effect of warfarin anticoagulation on the clinical course of patients with prostatic cancer, contrast with findings in certain other tumor types and suggest that coagulation activation may not contribute to progression of adenocarcinoma of the prostate.

Topics: Antibodies, Monoclonal; Endothelium, Vascular; Fibrin; Fibrinogen; Humans; Male; Molecular Weight; Plasminogen Activators; Prostatic Hyperplasia; Prostatic Neoplasms; Survival Rate; Thromboplastin; Warfarin

The isolation and partial characterization of a novel anticoagulant from the plasma of a patient with metastatic prostate cancer is described. The patient had a prolonged activated partial thromboplastic time, prothrombin time and thrombin time which did not correct by mixing with normal plasma. The reptilase time was normal and the prolonged thrombin time was corrected with protamine sulfate suggesting a heparin-like anticoagulant. A glycosaminoglycan anticoagulant (GAC) was isolated from the patient's plasma. The inhibitory activity of the GAC was destroyed by treatment with chondroitinase ABC. The GAC migrated on agarose gel electrophoresis between keratin sulfate and heparan sulfate. Purified GAC possessed only 2% (W/W) of the antithrombin III cofactor activity of porcine heparin. In assays using purified fibrinogen, the GAC was shown to directly inhibit fibrinogen proteolysis by thrombin. It is concluded that this glycosaminoglycan anticoagulant directly inhibits thrombin clotting of fibrinogen and is a new mechanism for abnormal hemostatic assays in cancer.

Topics: Aged; Aged, 80 and over; Antithrombin III; Blood Coagulation Tests; Catalysis; Fibrin; Glycosaminoglycans; Hemostasis; Humans; Male; Prostatic Neoplasms; Thrombin

Zymographic analysis of the supernates from confluent cultures of a rat prostate adenocarcinoma cell line, PA-III, revealed the existence of two molecular forms of specific plasminogen activators, one of molecular weight of approximately 80 000 and another of approximate molecular weight of 45 000, in sodium dodecyl sulfate. The low molecular weight form has been purified 364-fold in 66% yield from the culture medium by a combination of gel filtration on Sephacryl S-200 and affinity chromatography on Sepharose 4B-benzamidine. The purified material possessed a specific activity of 192 000 urokinase CTA units mg-1. This enzyme displayed activity toward human Glu1-plasminogen, characterized by a Km of 1.7 +/- 0.2 microM and a Vmax of 0.53 +/- 0.1 pmol of plasmin min-1 unit-1. A synthetic chromogenic substrate, H-D-Ile-Pro-Arg-p-nitroanilide (S-2288), was found for the activator. The enzyme possessed a Km of 0.33 mM and a kcat of 55 s-1 for S-2288. The activator was found to be a serine protease, inhibited by diisopropyl fluorophosphate (iPr2PF). At a concentration of 1 mM iPr2PF, and 30 nM enzyme, the half-time of this inhibition was 3.8 min. The 45 000 molecular weight enzyme was found to be inhibited by rabbit antibodies to human urokinase, thus characterizing the activator as a member of the urokinase class. The 80 000 molecular weight enzyme was not neutralized by anti-human urokinase but was neutralized by rabbit anti-human melanoma activator, likely allowing it to be classified as the tissue activator type.

Topics: Adenocarcinoma; Animals; Cell Line; Electrophoresis, Polyacrylamide Gel; Fibrin; Kinetics; Male; Molecular Weight; Plasminogen; Plasminogen Activators; Prostatic Neoplasms; Protein Binding; Rats; Urokinase-Type Plasminogen Activator

The plasminogen activator content of the extracts of excise prostate cancers (25 specimens) was determined with an azocasein assay and found to be on the average 1.7 times higher than that of extracts of excised prostate benign hyperplasias (29 specimens). Both groups contained the same average percentage of human urokinase type activator (approximately 45%) as determined by the inhibition of activity when anti-human urokinase antibody was included in the assay system. The two types of activators were partially purified and found to have distinctly different properties. The most striking difference was the large augmentation of activity o the non-urokinase enzyme in fibrinolysis. The implications of an enhanced fibrinolysis relative to azocaseinolysis (or other) is discussed, particularly with respect to its importance in the quantitation and characterization of activators by different investigators. Highly purified urokinase-like activator was found to be similar to commercial urokinase preparation with respect to molecular weight, isoelectric point, inhibition by the antibody, and inhibition by placenta inhibitor.

Topics: Fibrin; Humans; Hyperplasia; Male; Plasminogen Activators; Prostate; Prostatic Hyperplasia; Prostatic Neoplasms; Urokinase-Type Plasminogen Activator

Testing for soluble fibrin complexes was performed using a sensitive and reliable haemagglutination assay, with red cells sensitized by fibrin monomers. The principle is based on the fact that the monomers linked to red cells and induce their agglutination. This test, used in clinical trials, has revealed the presence of soluble complexes in every confirmed case of acute DIC, but also in Chronic DIC where diagnosis is difficult to establish (negative ethanol gelation test, normal or sub-normal levels of fibrin breakdown products). In Cirrhosis of the liver, the test gives positive results in a non negligible number of cases. Several hypotheses are made to explain why in certain confirmed cases of DIC, low fibrin breakdown products levels are found.

Topics: Aged; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Hemagglutination Tests; Humans; Liver Cirrhosis; Male; Prostatic Neoplasms; Solubility; Surgical Procedures, Operative; Thromboembolism

Topics: Alpha-Globulins; Antifibrinolytic Agents; Blood Coagulation; Blood Coagulation Factors; Depression, Chemical; Estrogens; Fibrin; Fibrinogen; Fibrinolysis; Humans; Macroglobulins; Male; Plasminogen; Prostatic Neoplasms; Time Factors; Veins

Topics: Adult; Aged; Antigens; Blood Coagulation; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Humans; Immunodiffusion; Immunoelectrophoresis; Leukemia, Myeloid; Male; Middle Aged; Plasma; Prostatic Neoplasms; Thrombin

Topics: Aged; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Dysgerminoma; Female; Fibrin; Humans; Male; Middle Aged; Neoplasm Metastasis; Pancreatic Neoplasms; Prostatic Neoplasms; Stomach Neoplasms; Testicular Neoplasms; Thrombophlebitis

Discrimination between the physiological cleavage fragments of fibrinogen and fibrin offers an approach to differentiation between fibrinogenolytic processes and fibrinolysis after coagulation. By use of the cleavage-associated neoantigen of fibrinogen (fg-D(neo)) as a molecular marker, characteristic differences between the D regions of fibrinogen derivatives and fibrin derivatives can be demonstrated. The expression of fg-D(neo) by X, Y, D:E complex, and D-fragments of fibrinogen or fibrin is shown to be quantitative and unitary. Characteristic differences between fg-D(neo) sites present on fibrinogen cleavage fragments, as contrasted to fibrin cleavage fragments, are indicated by different competitive inhibition slopes, and appear to reflect differential binding affinity of selected anti-fg-D(neo) antibodies for the specific molecular site. There is a linear relationship between the slope of quantitative competitive inhibition and the relative molar ratio of fibrinogen and fibrin derivatives. Identical immunochemical expressions are observed in vitro and in vivo, and support the thesis that cleavage in vivo is produced by plasmin. The differential immunochemical features of fg-D(neo) expression may be the result of stable conformational and/or subtle structural differences between the D region of fibrinogen and fibrin cleavage fragments and suggest that precise changes in the D region are associated with the fibrin transition. These molecular features not only provide additional insight into the molecular immunology and structure of fibrinogen, but also appear to offer a new molecular approach to discrimination between fibrinogenolytic mechanisms as contrasted to fibrinolysis secondary to coagulation.

Topics: Abruptio Placentae; Acute Kidney Injury; Adenocarcinoma; Binding Sites, Antibody; Binding, Competitive; Blood Coagulation Disorders; Epitopes; Female; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Humans; Immune Sera; Iodine Isotopes; Male; Melanoma; Meningococcal Infections; Peritonitis; Pregnancy; Prostatic Neoplasms; Radioimmunoassay; Structure-Activity Relationship

Topics: Aged; Blood Coagulation Tests; Blood Platelet Disorders; Chronic Disease; Disseminated Intravascular Coagulation; Fibrin; Gastrointestinal Hemorrhage; Heparin; Humans; Male; Middle Aged; Neoplasm Metastasis; Prostatic Neoplasms; Prothrombin Time; Thromboplastin

Topics: Aminocaproates; Blood Coagulation; Breast Neoplasms; Colonic Neoplasms; Female; Fibrin; Fibrinogen; Fibrinolysis; Gastrointestinal Neoplasms; Humans; Immunoelectrophoresis; Intestinal Neoplasms; Kidney Neoplasms; Lung Neoplasms; Lymphatic Metastasis; Male; Neoplasm Metastasis; Neoplasm Recurrence, Local; Pancreatic Neoplasms; Prostatic Neoplasms; Rectal Neoplasms; Thrombin; Urinary Bladder Neoplasms; Urogenital Neoplasms

Topics: Aged; Amputation, Surgical; Blood Coagulation; Blood Coagulation Tests; Child; Dilatation; Disseminated Intravascular Coagulation; Fibrin; Genital Diseases, Male; Humans; Male; Methods; Penile Diseases; Postoperative Complications; Prostatectomy; Prostatic Hyperplasia; Prostatic Neoplasms; Testicular Diseases; Urethral Diseases; Urethral Stricture; Urologic Diseases

Topics: Adult; Aged; Biguanides; Clofibrate; Coronary Disease; Ethylestrenol; Female; Fibrin; Fibrinogen; Fibrinolysis; Hemagglutination Inhibition Tests; Hemostasis; Humans; Immunoassay; Immunodiffusion; Immunoelectrophoresis; Liver Cirrhosis; Male; Metformin; Middle Aged; Neoplasm Metastasis; Nicotinic Acids; Physical Exertion; Plasminogen; Prostatic Neoplasms; Stimulation, Chemical; Time Factors; Tolazamide

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: Aminocaproates; Aminocaproic Acid; Antifibrinolytic Agents; Aprotinin; Drug Therapy; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Humans; Male; Prostatectomy; Prostatic Hyperplasia; Prostatic Neoplasms; Surgical Procedures, Operative; Trypsin Inhibitors; Urologic Diseases

Topics: Aminocaproates; Aminocaproic Acid; Amniotic Fluid; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Transfusion; Embolism; Embolism, Amniotic Fluid; Female; Fibrin; Fibrinolysin; Fibrinolysis; Gastrointestinal Hemorrhage; Hemorrhage; Humans; Male; Physiology; Plasminogen; Pregnancy; Prostatic Neoplasms

Topics: Carcinoma; Fibrin; Fibrinolysis; Humans; Male; Prostatic Neoplasms

Topics: Fibrin; Fibrinolysis; Humans; Male; Prostatic Neoplasms; Syndrome

Topics: Factor V; Fibrin; Fibrinolysis; Humans; Male; Prostatic Neoplasms; Vitamin B 12

Topics: Fibrin; Fibrinolysis; Hemorrhage; Humans; Male; Neoplasms; Prostatic Neoplasms; Syndrome

Topics: Fibrin; Fibrinolysis; Hemorrhagic Disorders; Humans; Male; Neoplasms; Prostatic Neoplasms