glycogen and Hyperplasia

Cowden's disease is a rare autosomal dominant condition characterized by multiple hamartomas of ectodermal, endodermal, and mesodermal origin affecting many organ systems. Gastrointestinal manifestation includes the formation of multiple polyps of various benign histopathological types throughout the alimentary tract. Recent literature suggests that the frequency of gastrointestinal involvement is approximately 70-85%. The diagnosis of Cowden's disease, however, relies mainly on subtle dermatologic findings, which may not be obvious to the gastroenterologist. We describe a patient with Cowden's disease and review the English literature on the topic of gastrointestinal polyposis and Cowden's disease. These studies suggest that gastrointestinal polyposis is commonly found in this disease, and that diffuse esophageal glycogenic acanthosis is a characteristic feature of Cowden's disease. We propose that the finding of extensive glycogenic acanthosis in the presence of other benign gastrointestinal polyposis should be considered pathognomonic for the diagnosis of Cowden's disease.

Topics: Colonic Polyps; Duodenal Neoplasms; Esophageal Diseases; Esophagoscopy; Ganglioneuroma; Glycogen; Hamartoma Syndrome, Multiple; Humans; Hyperplasia; Intestinal Polyps; Jejunal Neoplasms; Lipoma; Male; Middle Aged

Topics: Adenoma; Ascorbic Acid; Carcinoma; Cytodiagnosis; Glycogen; Glycosaminoglycans; Goiter, Nodular; Histocytochemistry; Humans; Hyperplasia; Karyometry; Precancerous Conditions; Thyroid Gland; Thyroid Neoplasms; Thyroiditis, Autoimmune

Topics: Animals; Calcium; Cats; Cattle; Dogs; Epithelial Cells; Extracellular Space; Glycogen; Golgi Apparatus; Hypercalcemia; Hyperplasia; Hypocalcemia; Microscopy, Electron; Microscopy, Electron, Scanning; Organoids; Parathyroid Glands; Parathyroid Hormone

Topics: Acid Phosphatase; Adenocarcinoma; Alkaline Phosphatase; Aminopeptidases; Bone Neoplasms; Breast Neoplasms; Cervix Uteri; Clinical Enzyme Tests; Diagnosis, Differential; Esterases; Female; Glucosephosphate Dehydrogenase; Glycogen; Glycosaminoglycans; Histocytochemistry; Humans; Hyperplasia; Microscopy, Fluorescence; Neoplasms; Nucleic Acids; Sex Chromatin; Uterine Cervical Neoplasms

Topics: Adenofibroma; Adenoma, Pleomorphic; Alkaline Phosphatase; Atrophy; Basement Membrane; Breast; Breast Diseases; Breast Neoplasms; Carcinoma; Carcinoma, Adenoid Cystic; Carcinosarcoma; Endocrine Glands; Epithelial Cells; Epithelium; Female; Glycogen; Humans; Hyperplasia; Lipids; Male; Middle Aged; Muscle, Smooth; Myoepithelioma; Myofibrils; Pigments, Biological; Salivary Gland Neoplasms; Sarcoma; Sweat Glands; Water

Topics: Adrenal Glands; Animals; Carbon Isotopes; Corticosterone; Culture Techniques; Desoxycorticosterone; Female; Fetus; Glucose; Glycogen; Humans; Hydrocortisone; Hydroxyprogesterones; Hydroxysteroid Dehydrogenases; Hyperplasia; Isomerases; Lactates; Mice; Pregnancy; Pregnenolone; Progesterone; Steroids; Tritium

A prospective case-control study was conducted to evaluate glycogen deposition within the detrusor and its correlation with the urodynamic findings in patients with bladder outlet obstruction (BOO) due to benign prostate hyperplasia (BPH).. Data from 50 patients with BPH (Study Group) and 20 controls (Control Group) were analyzed. BOO was confirmed by pressure-flow studies. The main outcome was glycogen deposition within the bladder wall. Bladder tissue biopsies were obtained from all patients, and histological assessment of the detrusor glycogen content was performed using Periodate Acid Schiff's (PAS) stain. The obtained glycogen score ranged from 0 (no staining of glycogen granules) to 3 (staining of glycogen granules within the detrusor adjacent to the urothelium).. Fifty patients and 20 controls were included. Increased glycogen deposition was observed in 37 (74%) and 2 (10%) patients in the Study and Control Group, respectively (p < 0.01, OR 25.6, 95% CI 5.2-125.8). In the subgroup analysis, no statistically significant difference was found between glycogen deposition score and IPSS, maximum detrusor pressure at maximum flow (PdetQmax) and duration of LUTS. In multivariate logistic regression, history of retention was the only variable which could predict high glycogen deposition (p = 0.019).. Our results demonstrate increased detrusor glycogen deposition in patients with BOO due to BPH, but the amount of deposition did not seem to correlate with symptom severity and duration or urodynamic findings.

Topics: Case-Control Studies; Glycogen; Humans; Hyperplasia; Male; Muscles; Prostate; Prostatic Hyperplasia; Urinary Bladder Neck Obstruction; Urodynamics

A functional placenta develops through a delicate interplay of its vascular and trophoblast compartments. We have identified a previously unknown expression domain for the endothelial-specific microRNA miR-126 in trophoblasts of murine and human placentas. Here, we determine the role of miR-126 in placental development using a mouse model with a targeted deletion of miR-126. In addition to vascular defects observed only in the embryo, loss of miR-126 function in the placenta leads to junctional zone hyperplasia at E15.5 at the expense of the labyrinth, reduced placental volume for nutrient exchange and intra-uterine growth restriction of the embryos. Junctional zone hyperplasia results from increased numbers of proliferating glycogen trophoblast (GlyT) progenitors at E13.5 that give rise to an expanded glycogen trophoblast population at E15.5. Transcriptomic profile of miR-126

Topics: Animals; Cell Proliferation; DNA Methylation; Embryo, Mammalian; Endothelial Cells; Female; Fetal Growth Retardation; Gene Expression Regulation, Developmental; Genomic Imprinting; Glycogen; Humans; Hyperplasia; Mice, Inbred C57BL; MicroRNAs; Placenta; Pregnancy; Transcriptome; Trophoblasts

Aflatoxin B1 (AFB1) and the hepatitis B virus X antigen (HBx) are linked to the formation of liver diseases and hepatocellular carcinoma (HCC). The aim of this study was to investigate the synergistic effects between HBx and AFB1 in causing liver disorders using a transgenic zebrafish animal model. Histopathology, Periodic acid-Schiff (PAS) staining, Sirius red staining, TdT-mediated dUTP Nick End Labeling (TUNEL) assay, immunohistochemistry, and quantitative reverse transcriptase-polymerase chain reaction (Q-RT-PCR) were used to examine the livers of the HBx transgenic fish injected with AFB1. We found that HBx and AFB1 synergistically promoted steatosis as indicated by histopathological examinations and the increased expression of lipogenic factors, enzymes, and genes related to lipid metabolism. Moreover, treatment of AFB1 in HBx transgenic fish accelerated the development of liver hyperplasia and enhanced the expression of cell cycle related genes. PCNA was co-localized with active caspase 3 protein expression in HBx zebrafish liver samples and human HBV positive HCC samples by double fluorescence immunostaining. Finally, we found that in human patients with liver disease, significant glycogen accumulated in the inflammation, cirrhosis stage, and all cases of hepatocellular and cholangiocellular carcinoma showed a moderate cytoplasmic accumulation of glycogen. Our data demonstrated a synergistic effect of AFB1 and HBx on the regulation of lipid metabolism related genes and cell cycle/division-related genes which might contribute to enhanced steatosis and hyperplasia at 5.75months.

Topics: Aflatoxin B1; Animals; Animals, Genetically Modified; Carcinoma, Hepatocellular; Caspase 3; Cell Cycle Proteins; Fatty Liver; Gene Expression; Glycogen; Hepatitis B; Humans; Hyperplasia; Immunohistochemistry; Injections, Intraperitoneal; Lipid Metabolism; Liver; Polymerase Chain Reaction; Proliferating Cell Nuclear Antigen; Trans-Activators; Viral Regulatory and Accessory Proteins; Zebrafish

Is there a molecular link between Wnt signaling in fallopian tube inflammation and ectopic tubal implantation?. Enhanced beta-catenin expression, reduced E-cadherin expression and glycogen accumulation in the tubal epithelia and hyperplasia in tubal arteries were found in ectopic tubal pregnancy, consistent with the effects induced by Wnt signaling and inflammation.. Chronic inflammation caused by infection can alter gene expression in the fallopian tube cells possibly leading to the development of ectopic pregnancy. Knockout mouse models have shown a relationship between Wnt/beta-catenin signaling and predisposition to tubal ectopic pregnancy.. Women with ectopic tubal pregnancy (n = 18) were included in the case group, while women with chronic salpingitis (n = 13) and non-pregnant women undergoing sterilization procedures or salpingectomy for benign uterine disease (n = 10) were set as the controls. This study was performed between January 2012 and November 2012.. The ampullary segments of fallopian tubes were collected from patients. Tissues of tubal pregnancy were separated into implantation sites and non-implantation sites. Beta-catenin and E-cadherin expression were determined using immunohistological and immunofluorescence staining. Glycogen production was measured with periodic acid Schiff by staining. The diameter and wall thickness of tubal arteries were evaluated by histological analysis method.. Immunohistological staining revealed that beta-catenin protein expression was 100% positive in the ectopic pregnant and inflamed tubal tissues, and the staining intensity was significantly higher than in non-pregnant tubal tissues. In contrast, E-cadherin expression was reduced in ectopic pregnant fallopian tubes, possibly as a consequence of increased Wnt signaling. Moreover, glycogen accumulated in the tubal cells, and hyperplasia was observed in the tubal arteries with ectopic pregnancy, which is consistent with the effects induced by Wnt signaling and inflammation. All these changes could create the permissive environment that promotes embryos to ectopically implant into the fallopian tube.. This finding requires a further confirmation about what activates Wnt signaling in ectopic tubal pregnancies. Also, it is generally recognized that Chlamydia infection is associated with ectopic pregnancy, and disturbs tubal epithelia via the Wnt signaling. However, the infection type in the samples used was salpingitis.. A better understanding of the underlying mechanisms leading to ectopic pregnancies may contribute to our knowledge of the pathogenesis of tubal disorders and infertility and to the prevention of tubal ectopic pregnancy.

Topics: Adult; Antigens, CD; Arteries; beta Catenin; Cadherins; Case-Control Studies; Disease Susceptibility; Down-Regulation; Fallopian Tube Diseases; Fallopian Tubes; Female; Glycogen; Humans; Hyperplasia; Models, Biological; Mucous Membrane; Neovascularization, Pathologic; Pregnancy; Pregnancy, Tubal; Up-Regulation; Wnt Signaling Pathway

Hepatocarcinogenesis is a multistep process that starts from fatty liver and transitions to fibrosis and, finally, into cancer. Many etiological factors, including hepatitis B virus X antigen (HBx) and p53 mutations, have been implicated in hepatocarcinogenesis. However, potential synergistic effects between these two factors and the underlying mechanisms by which they promote hepatocarcinogenesis are still unclear. In this report, we show that the synergistic action of HBx and p53 mutation triggers progressive hepatocellular carcinoma (HCC) formation via src activation in zebrafish. Liver-specific expression of HBx in wild-type zebrafish caused steatosis, fibrosis and glycogen accumulation. However, the induction of tumorigenesis by HBx was only observed in p53 mutant fish and occurred in association with the up-regulation and activation of the src tyrosine kinase pathway. Furthermore, the overexpression of src in p53 mutant zebrafish also caused hyperplasia, HCC, and sarcomatoid HCC, which were accompanied by increased levels of the signaling proteins p-erk, p-akt, myc, jnk1 and vegf. Increased expression levels of lipogenic factors and the genes involved in lipid metabolism and glycogen storage were detected during the early stages of hepatocarcinogenesis in the HBx and src transgenic zebrafish. The up-regulation of genes involved in cell cycle regulation, tumor progression and other molecular hallmarks of human liver cancer were found at later stages in both HBx and src transgenic, p53 mutant zebrafish. Together, our study demonstrates that HBx and src overexpression induced hepatocarcinogenesis in p53 mutant zebrafish. This phenomenon mimics human HCC formation and provides potential in vivo platforms for drug screening for therapies for human liver cancer.

Topics: Animals; Animals, Genetically Modified; Apoptosis; Biomarkers, Tumor; Carcinogenesis; Carcinoma, Hepatocellular; Cell Cycle; CSK Tyrosine-Protein Kinase; Enzyme Activation; Fibrosis; Gene Expression; Glycogen; Humans; Hyperplasia; Lipogenesis; Liver; Liver Neoplasms; Mutation; Neoplasm Metastasis; Organ Specificity; Proliferating Cell Nuclear Antigen; Recombinant Fusion Proteins; Signal Transduction; src-Family Kinases; Trans-Activators; Tumor Suppressor Protein p53; Viral Regulatory and Accessory Proteins; Zebrafish

Indications for liver biopsy in children are often specific to this age group, especially in young children for the diagnosis of cholestasis. Since liver biopsies are quite unfrequent in the children population and concern rare but various diseases, it is recommended to entrust the analysis to a specialized liver pathologist, in a laboratory where cryoconservation, specific immuno-stainings, enzymatic studies, and electron microscopy can be performed. Histology is complementary to other methods for the diagnosis, and is valuable for the evaluation of the prognosis, especially the staging of fibrosis and the grading of inflammatory diseases. In cases of co-morbidity or difficult differential diagnosis, histology can also be of great value. For metabolic disorders, the liver tissue can also be used for enzyme detection or evaluation of iron or copper overload. Biopsy is also a key element in the management after liver transplantation. The microscopic images shown here are representative of the most frequent liver diseases in childhood and illustrate the data outlined during the conference.

Topics: Biliary Tract; Biliary Tract Diseases; Biopsy; Child; Glycogen; Hamartoma; Hepatoblastoma; Hepatocytes; Humans; Hyperplasia; Liver; Liver Diseases; Metabolism, Inborn Errors

Glycogenic acanthosis is described as benign thickening of the esophageal squamous epithelium of unknown etiology. Although its etiology is unknown, it has been reported that glycogenic acanthosis may be related to gastroesophageal reflux and hiatal hernia. The aim of the present study was to review the patients who were diagnosed with glycogenic acanthosis on upper gastrointestinal endoscopy and to determine whether there is any association between glycogenic acanthosis and gastroesophageal reflux and hiatal hernia.. A total of 504 patients who underwent upper gastrointestinal endoscopy for evaluation of non-ulcer dyspepsia were reviewed retrospectively.. Glycogenic acanthosis was detected in 143 (28.3%) of those 504 patients. Of the 143 patients, 82 (57.3%) were male and 61 (42.7%) were female. Patients with glycogenic acanthosis were aged 20-83 years. Gastroesophageal reflux was detected in 50 (34.9%) cases with glycogenic acanthosis, while hiatal hernia was detected in 30 (20.9%) cases. Gastroesophageal reflux was detected in 102 (28.2%) control subjects, while hiatal hernia was detected in 50 (13.8%). Hiatal hernia was significantly higher in glycogenic acanthosis patients than in controls subjects (p<0.05). Glycogenic acanthosis patients had higher gastroesophageal reflux than seen in controls subjects, but the difference between groups was not statistically significant (p>0.05).. Our results suggest that glycogenic acanthosis is primarily an age-related disease. We demonstrated that glycogenic acanthosis may be associated with gastroesophageal reflux and hiatal hernia. Further studies are necessary to confirm these findings.

Topics: Adult; Age Factors; Aged; Aged, 80 and over; Case-Control Studies; Endoscopy, Gastrointestinal; Esophageal Diseases; Female; Gastroesophageal Reflux; Glycogen; Hernia, Hiatal; Humans; Hyperplasia; Male; Middle Aged; Retrospective Studies; Young Adult

A case of multifocal nodular oncocytic hyperplasia (MNOH) of the bilateral parotid gland is presented. An 80-year-old woman was admitted to hospital because of painless swellings in bilateral parotid regions. Histologically, the nodular lesion had incomplete capsules and engulfed the surrounding parotid gland at the periphery. The lesions were mostly composed of clear cells, while the peripheries of the lesions had typical oncocytic cells with abundant fine granules. The histological existence of the clear cell component in the lesions led to misdiagnoses of other clear cell neoplasms. However, this case had multiple nodules in bilateral glands. No evidence of malignant histological findings was found. Moreover, the clear cells, as well as the oncocytic cells, were demonstrated to have mitochondria and glycogen in their cytoplasm using special staining. Based on these findings, the diagnosis of this case was MNOH in the parotid gland. We also discuss the differential diagnosis for clear cell lesions.

Topics: Adenoma, Oxyphilic; Aged, 80 and over; Diagnosis, Differential; Female; Glycogen; Humans; Hyperplasia; Mitochondria; Oxyphil Cells; Parotid Diseases; Parotid Gland; Parotid Neoplasms; Treatment Outcome

A dual-tracer approach (dietary 14C-palmitate and intraperitoneal 3H-H2O) was used to assess the trafficking of dietary fat and net retention of carbon in triglyceride depots during the first 24 h of weight regain. Obesity-prone male Wistar rats were allowed to mature under obesogenic conditions for 16 wk. One group was switched to ad libitum feeding of a low-fat diet for 10 wk (Obese group). The remaining rats were switched to an energy-restricted, low-fat diet for 10 wk that reduced body weight by 14% and were then assessed in energy balance (Reduced group), with free access to the low-fat diet (Relapse-Day1 group), or with a provision that induced a minor imbalance (+10 kcal) equivalent to that observed in obese rats (Gap-Matched group). Fat oxidation remained at a high, steady rate throughout the day in Obese rats, but was suppressed in Reduced, Gap-Matched, and Relapse-Day1 rats though 9, 18, and 24 h, respectively. The same caloric excess in Obese and Gap-Matched rats led to less fat oxidation over the day and greater trafficking of dietary fat to visceral depots in the latter. In addition to trafficking nutrients to storage, Relapse-Day1 rats had more small, presumably new, adipocytes at the end of 24 h. Dietary fat oxidation at 24 h was related to the phosphorylation of skeletal muscle acetyl-CoA carboxylase and fatty acid availability. These observations provide evidence of adaptations in the oxidation and trafficking of dietary fat that extend beyond the energy imbalance, which facilitate rapid, efficient regain during the relapse to obesity.

Topics: Acetyl-CoA Carboxylase; Adaptation, Physiological; Adipocytes; Animals; Body Composition; Cell Proliferation; Diet, Fat-Restricted; Dietary Fats; Disease Models, Animal; Down-Regulation; Energy Intake; Energy Metabolism; Fatty Acids; Glycogen; Hyperplasia; Intra-Abdominal Fat; Male; Muscle, Skeletal; Obesity; Oxidation-Reduction; Phosphorylation; Rats; Rats, Wistar; Recurrence; Time Factors; Triglycerides; Weight Gain; Weight Loss

Prolonged copper deprivation in rats followed by refeeding with a normal diet has previously been used to induce the appearance of hepatocyte-like cells in the pancreas, but the effects on islet size and morphology have not been determined.. In the present study we investigated the distribution of pancreatic alpha- and beta-cells and of hepatocytes in adult rats fed a copper-deficient diet followed by refeeding with a normal diet. Immunohistochemical staining for insulin and glucagon showed that the islets of the copper-deficient group were up to 2.4 times larger in mass compared with controls. The islets were disorganized, with alpha-cells found in multiple layers at the periphery of the islet and sometimes deep in the core. Isolated alpha- and beta-cells were also found in increased numbers in the ductular system. Copper deprivation caused almost complete ablation of the acinar cells, and refeeding induced adipogenesis, acinar regeneration and hepatocyte-like cells. Ductular proliferation and nerve hyperplasia were also present. The hepatocytes tended to be associated with islets or with ducts, rather than with residual pancreatic exocrine tissue.. These data show that copper deficiency in rats, as well as inducing the appearance of hepatocytes, is capable of causing islet hyperplasia.

Topics: Animals; Copper; Glucagon; Glycogen; Hepatocytes; Hyperplasia; Insulin; Islets of Langerhans; Liver; Male; Metaplasia; Rats; Rats, Wistar

Topics: Biopsy; Diagnosis, Differential; Esophageal Diseases; Esophagoscopy; Female; Glycogen; Humans; Hyperplasia; Middle Aged; Mucous Membrane; Vocal Cords

A 62-yr-old man was referred for management of GI polyposis. Large bowel polyps were initially diagnosed >25 yr ago, and the patient had undergone multiple colonoscopies and polypectomies. Personal and family history were notable for thyroid goiter and hypothyroidism. Physical examination was notable for lingular papillomatosis. No cutaneous lesions were seen. Upper endoscopy revealed esophageal glycogen acanthosis. There were multiple polyps throughout the stomach and the small and large intestines. Histology of these polyps showed multiple cell types including juvenile polyps, inflammatory polyps with fibromuscular proliferation and lamina propria ganglion cells, and focal adenomatous change. A clinical diagnosis of Cowden syndrome was made. Mutation analysis revealed a variant in exon 8 of the PTEN gene. Direct sequencing revealed a germline heterozygous C.892-895InsA, which is predicted to result in a truncated PTEN protein. Cowden syndrome is an underdiagnosed, underrecognized, autosomal dominant, inherited syndrome. For the gastroenterologist, esophageal acanthosis and multiple hamartomatous polyps should suggest the diagnosis. Sensitive molecular diagnostic tests looking for mutations in the appropriate genes are clinically available. Together with genetic counseling, molecular diagnostic testing will allow more accurate risk assessment and surveillance for cancer for both the patient and family members.

Topics: Endoscopy; Esophageal Diseases; Esophagus; Gastrointestinal Neoplasms; Germ-Line Mutation; Glycogen; Hamartoma Syndrome, Multiple; Humans; Hyperplasia; Male; Middle Aged; Mucous Membrane; Pedigree; Phosphoric Monoester Hydrolases; Polyps; PTEN Phosphohydrolase; Skin Diseases; Tumor Suppressor Proteins

We investigated the impact of GLUT2 gene inactivation on the regulation of hepatic glucose metabolism during the fed to fast transition. In control and GLUT2-null mice, fasting was accompanied by a approximately 10-fold increase in plasma glucagon to insulin ratio, a similar activation of liver glycogen phosphorylase and inhibition of glycogen synthase and the same elevation in phosphoenolpyruvate carboxykinase and glucose-6-phosphatase mRNAs. In GLUT2-null mice, mobilization of glycogen stores was, however, strongly impaired. This was correlated with glucose-6-phosphate (G6P) levels, which remained at the fed values, indicating an important allosteric stimulation of glycogen synthase by G6P. These G6P levels were also accompanied by a paradoxical elevation of the mRNAs for L-pyruvate kinase. Re-expression of GLUT2 in liver corrected the abnormal regulation of glycogen and L-pyruvate kinase gene expression. Interestingly, GLUT2-null livers were hyperplasic, as revealed by a 40% increase in liver mass and 30% increase in liver DNA content. Together, these data indicate that in the absence of GLUT2, the G6P levels cannot decrease during a fasting period. This may be due to neosynthesized glucose entering the cytosol, being unable to diffuse into the extracellular space, and being phosphorylated back to G6P. Because hepatic glucose production is nevertheless quantitatively normal, glucose produced in the endoplasmic reticulum may also be exported out of the cell through an alternative, membrane traffic-based pathway, as previously reported (Guillam, M.-T., Burcelin, R., and Thorens, B. (1998) Proc. Natl. Acad. Sci. U. S. A. 95, 12317-12321). Therefore, in fasting, GLUT2 is not required for quantitative normal glucose output but is necessary to equilibrate cytosolic glucose with the extracellular space. In the absence of this equilibration, the control of hepatic glucose metabolism by G6P is dominant over that by plasma hormone concentrations.

Topics: Animals; Cell Membrane; Gene Expression Regulation; Gluconeogenesis; Glucose; Glucose Transporter Type 2; Glucose-6-Phosphate; Glycogen; Glycolysis; Hyperplasia; Liver; Mice; Monosaccharide Transport Proteins

A 33-year-old Japanese woman presented with a black papule on a pigmented lesion which had been on her right thigh since her early childhood. A hematoxylin-eosin-stained section revealed a sharply demarcated, acanthotic epidermis composed of enlarged clear cells, which stained positively for epithelial membrane antigen and negatively for carcinoembryonic antigen. With antikeratin antibodies, the tumor cells stained for AE1 and AE3, but did not stain for CAM5.2. They contained abundant glycogen. Histologically, we diagnosed the case as a clear cell acanthoma which developed in the pre-existing epidermal nevus. This is the second such case in the literature.

Topics: Adult; Female; Glycogen; Humans; Hyperplasia; Keratins; Mucin-1; Nevus, Pigmented; Skin Neoplasms

To confirm the eccrine acrosyringeal differentiation of eccrine syringofibroadenoma (ESFA) and to elucidate the histogenesis of its angiofibrotic stroma, a case of ESFA from a 45-year-old man was examined by light and electron microscopy. Histologically, the parenchyma featured anastomosing, slender epithelial cords containing small cuboidal cells and occasional duct-like structures. The stroma had increased numbers of mast cells, increased capillaries with swollen endothelial cells, and prominent fibrosis. Ultrastructurally, the following findings were characteristic of ESFA: a) abundant glycogen particles in epithelial cells, b) numerous intracytoplasmic and extracellular spaces lined with microvilli, c) intraepithelial duct formation, consisting of microvilli, vesicles, rod-shaped dense bodies, multivesicular dense bodies, and peripheral network of tonofilaments, and d) large numbers of mast cells, closely associated with fibroblasts, surrounding increased numbers of capillaries containing swollen endothelial cells. These ultrastructural features support the acrosyringeal differentiation of ESFA. We hypothesize that mast cell hyperplasia and degranulation may play an important role in the formation of the angiofibrotic stroma.

Topics: Adenofibroma; Adenoma, Sweat Gland; Cell Transformation, Neoplastic; Epithelium; Fibroblasts; Glycogen; Humans; Hyperplasia; Male; Mast Cells; Microscopy, Electron; Microvilli; Middle Aged; Sweat Gland Neoplasms

Topics: Colon; Colonic Neoplasms; Esophagus; Female; Ganglioneuroma; Glycogen; Hamartoma; Humans; Hyperplasia; Middle Aged; Neoplasms, Multiple Primary; Syndrome

Diagnostic features of glycogenic acanthosis of the esophagus on air-contrast radiography, endoscopy, and histopathologic studies in 10 selected cases are presented. Glycogenic acanthosis of the esophagus is a common benign entity, characterized by multifocal plaques of hyperplastic squamous epithelium with abundant intracellular glycogen deposits. At esophagoscopy or on autopsy specimens these lesions appear as slightly raised grey-white plaques which are usually 2-10 mm in diameter and may be confluent. They cause a finely nodular or cobblestone mucosal pattern demonstrable on double-contrast views of the well-distended esophagus. The findings are not associated with mucosal ulcerations, luminal narrowing, or mobility disturbance, although some patients may have coexistent hiatal hernia and gastroesophageal reflux.

Topics: Aged; Esophageal Diseases; Esophagoscopy; Female; Glycogen; Humans; Hyperplasia; Male; Middle Aged; Radiography

A nodular appearance of the esophageal mucosa was observed in 28.3% of 300 consecutive double-contrast esophagrams. This most commonly appeared as numerous uniformly sized, usually less than 3 mm, subtle, round elevations involving the entire esophageal surface. When carefully performed, endoscopy will almost always confirm these findings. Endoscopic biopsies performed in 10 patients demonstrated the nodules to represent glycogenic acanthosis--a combination of cellular hyperplasia and increased cellular glycogen. The radiographic appearance of these nodules, while usually characteristic, may vary and they may simulate pathologic processes, particularly moniliasis. Distinction can usually be made by clinical and radiologic criteria. Although the etiology is unknown, this seems to be of no clinical significance.

Topics: Adult; Aged; Biopsy; Diagnosis, Differential; Esophageal Diseases; Esophagoscopy; Esophagus; Female; Glycogen; Humans; Hyperplasia; Male; Middle Aged; Radiography

During 160 consecutive fiberoptic endoscopic examinations, glycogenic acanthosis was diagnosed in 24 patients. The endoscopic diagnosis was confirmed histologically in the first 14 patients from whom biopsies were obtained. No correlation with any other disease affecting the gastrointestinal tract was found including reflux esophagitis. This common benign condition must be differentiated from lesions of similar appearance and more important prognostic significance.

Topics: Biopsy; Esophageal Diseases; Esophagitis, Peptic; Esophagoscopy; Esophagus; Female; Fiber Optic Technology; Glycogen; Humans; Hyperplasia; Male; Prognosis

Sequential changes in skin metabolism have been studied in a model system of epidermal hyperplasia and hyperkeratinization induced by the application of n-hexadecane to shaved rat skin. The epidermal accumulation of glycogen typical of the hyperplastic response has been correlated with an increase in glycogenesis and a decrease in glycogenolysis. DNA synthesis was increased by 6 h after the start of hexadecane treatment and reached a maximum after one day. The concentration of skin cyclic AMP fell immediately after hexadecane application and subsequently rose to give a prolonged increase. Use of the combined topical application of hexadecane and the anti-inflammatory drugs triamcinolone acetonide, hydrocortisone and indomethacin showed that the hexadecane-induced changes in DNA synthesis and glycogen metabolism were linked to the initial fall in cyclic AMP concentration. The significance of the biphasic change in cyclic AMP levels is discussed as a possible system of control for the development and maintenance of hyperplasia.

Topics: Administration, Topical; Alkanes; Animals; Anti-Inflammatory Agents; Cyclic AMP; DNA; Epidermis; Glycogen; Glycogen Synthase; Hydrocortisone; Hyperplasia; In Vitro Techniques; Indomethacin; Male; Rats; Skin; Triamcinolone Acetonide

The authors explored a group of patients suffering from rheumatic pelvispondylitis from the point of view of muscular lesions: clinical muscular examination, anatomo-pathological investigation of the muscle (optical microscopy, histochemistry), electromyographic investigation, and determination of certain serum and muscle enzymes. Some muscular anomalies were observed, which were predominant in the muscles of the lumbar grooves, although there were some lesions of the quadriceps muscle, with a myogenous appearance, but without inflammation. The clearest anomalies were neurogenic and were present particularly in the muscles of the lumbar grooves.

Topics: Adult; Electromyography; Glycogen; Histocytochemistry; Humans; Hyperplasia; Leg; Male; Middle Aged; Motor Activity; Muscles; Muscular Diseases; Neural Conduction; Neurologic Manifestations; Neuromuscular Diseases; Reflex, Monosynaptic; Spine; Spondylitis, Ankylosing

Topics: Adenoma, Bile Duct; Animals; Autoradiography; Carcinoma, Hepatocellular; Cell Division; Cell Nucleus; Cell Transformation, Neoplastic; Fetal Proteins; Glycogen; Hyperplasia; Immunoelectrophoresis; Liver Neoplasms; Neoplasm Metastasis; Neoplasms, Experimental; p-Dimethylaminoazobenzene; Rats; Thymidine; Tritium

Topics: Animals; Carcinoma, Hepatocellular; Chemical and Drug Induced Liver Injury; Endoplasmic Reticulum; Glycogen; Hyperplasia; Liver; Liver Cirrhosis; Liver Neoplasms; Male; Microscopy, Electron; Rats; Ribosomes; Thioacetamide; Time Factors; Water

Topics: Adult; Aged; Alkaline Phosphatase; Carbohydrate Metabolism; Cell Membrane Permeability; Cell Nucleus; Cell Wall; Endometrium; Energy Metabolism; Estradiol; Female; Glucose-6-Phosphatase; Glycogen; Glycogen Synthase; Glycosaminoglycans; Histocytochemistry; Humans; Hyperplasia; Menopause; Microscopy, Electron; Middle Aged; Organ Culture Techniques; Ovulation; Progesterone; Uterine Hemorrhage; Uterine Neoplasms

Topics: Animals; Cartilage, Articular; Cytoplasmic Granules; Dietary Fats; Endoplasmic Reticulum; Fats, Unsaturated; Femur Head; Glycogen; Golgi Apparatus; Hyperplasia; Hypertrophy; Lysosomes; Male; Mice; Mice, Inbred C57BL; Microscopy, Electron; Microscopy, Phase-Contrast; Mitochondria; Oils; Pinocytosis; Time Factors; Zea mays

Topics: Cell Nucleus; Cytoplasm; Endoplasmic Reticulum; Female; Glycogen; Humans; Hyperparathyroidism; Hyperplasia; Infant, Newborn; Infant, Newborn, Diseases; Microscopy, Electron; Parathyroid Glands

Topics: Aged; Alcoholism; Autopsy; Biopsy; Diagnosis, Differential; Endoscopy; Epithelium; Esophageal Diseases; Esophagitis; Esophagoscopy; Esophagus; Gastroesophageal Reflux; Glycogen; Humans; Hyperplasia; Intestinal Mucosa; Leukoplakia; Male; Middle Aged; Periodic Acid; Smoking; Staining and Labeling

Topics: Animals; Calcitonin; Calcium; Cholecalciferol; Chromatin; Cytoplasm; Dogs; Endoplasmic Reticulum; Epithelial Cells; Female; Glycogen; Histocytochemistry; Hypercalcemia; Hyperplasia; Hypertrophy; Male; Microscopy, Electron; Parathyroid Glands; Thyroid Gland

Topics: Animals; Brain Stem; Cats; Cerebral Cortex; Glycogen; Hyperplasia; Inferior Colliculi; Microscopy, Electron; Myelin Sheath; Nerve Degeneration; Neural Pathways; Neurofibrils; Synapses; Synaptic Vesicles; Time Factors

Topics: Arteries; Biopsy; Chromatin; Endometrium; Endoplasmic Reticulum; Female; Fibrin; Glycogen; Golgi Apparatus; Humans; Hyperplasia; Microscopy, Electron; Mitochondria; Placenta; Pregnancy; Ribosomes; Trophoblasts

Topics: Endometrium; Female; Follow-Up Studies; Glycogen; Humans; Hyperplasia; Intrauterine Devices; Menstruation; Time Factors

Topics: Animals; Bronchi; Carnivora; Collagen; Cytoplasmic Granules; Desmosomes; Elastic Tissue; Endoplasmic Reticulum; Epithelium; Female; Glycogen; Golgi Apparatus; Histiocytes; Hyperplasia; Lipids; Lung; Lung Diseases; Male; Microscopy, Electron; Pneumonia, Lipid; Pulmonary Alveoli; Ribosomes; Staining and Labeling; Surface-Active Agents

Topics: Administration, Oral; Adrenal Cortex Hormones; Aminoglutethimide; Animals; Chemical and Drug Induced Liver Injury; Endoplasmic Reticulum; Female; Glycogen; Hyperplasia; Liver; Male; Microscopy, Electron; Microsomes, Liver; Rats

Topics: Adenoma; Adolescent; Adult; Autopsy; Biological Evolution; Biopsy; Cell Membrane; Cell Nucleus; Cilia; Cytoplasmic Granules; Endoplasmic Reticulum; Female; Glycogen; Golgi Apparatus; Humans; Hyperparathyroidism, Secondary; Hyperplasia; Inclusion Bodies; Lipids; Lysosomes; Male; Microscopy, Electron; Middle Aged; Mitochondria; Organoids; Parathyroid Glands; Parathyroid Neoplasms; Ribosomes

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Carcinogens; Carcinoma, Hepatocellular; Fluorenes; Glucose-6-Phosphatase; Glucuronidase; Glycogen; Histocytochemistry; Hyperplasia; L-Lactate Dehydrogenase; Liver Diseases; Liver Neoplasms; Male; Neoplasms, Experimental; Phosphorylase Kinase; Rats; Succinate Dehydrogenase

Topics: Age Factors; Animals; Body Weight; Chickens; Depression, Chemical; DNA; Drug Antagonism; Electrophoresis; Estradiol; Estrogen Antagonists; Female; Glucose; Glycogen; Hyperplasia; Hypertrophy; Lipid Metabolism; Ovalbumin; Oviducts; Progesterone; Proteins; RNA; Time Factors

Topics: Adolescent; Cardiomegaly; Cardiomyopathies; Diagnosis, Differential; Electrocardiography; Fluorescent Antibody Technique; Glycogen; Humans; Hyperplasia; Male; Microscopy, Electron; Muscle Proteins; Myocardium; Myofibrils; Sarcolemma

Topics: Adenofibroma; Breast Diseases; Breast Neoplasms; Cytodiagnosis; DNA; DNA, Neoplasm; Female; Glycogen; Glycosaminoglycans; Histocytochemistry; Humans; Hyperplasia; Lipid Metabolism; Microscopy, Fluorescence; RNA; RNA, Neoplasm

Topics: Basement Membrane; Blood-Brain Barrier; Brain Neoplasms; Capillaries; Cell Membrane Permeability; Collagen; Cytoplasm; Densitometry; Extracellular Space; Glycogen; Humans; Hyperplasia; Mitochondria; Neoplasm Proteins; Neuroglia

Topics: Animals; Body Weight; Cresols; Diet; Fats; Food Additives; Glycogen; Growth; Hepatomegaly; Hyperplasia; Hypertrophy; Liver; Male; Nitrogen; Nucleic Acids; Organ Size; Proteins; Rats; Water

Topics: Aged; Autopsy; Carcinoma, Squamous Cell; Epithelium; Esophageal Diseases; Esophageal Neoplasms; Esophagus; Female; Glycogen; Humans; Hyperplasia; Hypertrophy; Leukoplakia; Male; Middle Aged; Precancerous Conditions

Topics: Adult; Cervix Uteri; Female; Glycogen; Histocytochemistry; Humans; Hyperplasia; Uterine Cervical Dysplasia; Uterine Cervical Neoplasms

Topics: Epithelium; Glycogen; Glycosaminoglycans; Histocytochemistry; Humans; Hyperplasia; Mast Cells; Mouth Diseases; Palate; Precancerous Conditions; Staining and Labeling

Topics: Animals; Carcinogens; Ethionine; Fluorenes; Glucose-6-Phosphatase; Glucosyltransferases; Glycogen; Hyperplasia; Liver; Liver Glycogen; Liver Neoplasms; Male; Neoplasms, Experimental; Nucleic Acids; Proteins; Rats

Topics: Adenofibroma; Breast Diseases; Breast Neoplasms; Carcinoma; Carcinoma, Intraductal, Noninfiltrating; Cysts; Diagnosis, Differential; Female; Glucosyltransferases; Glycogen; Histocytochemistry; Humans; Hyperplasia; Methods; Polysaccharides

Topics: Animals; Cytoplasmic Granules; Diabetes Mellitus; Glycogen; Hyperplasia; Islets of Langerhans; Mice; Microscopy, Electron; Polymorphism, Genetic; Species Specificity

Topics: Adenoma; Adult; Endoplasmic Reticulum; Female; Glycogen; Golgi Apparatus; Humans; Hyperplasia; Microscopy, Electron; Middle Aged; Mitochondria; Parathyroid Diseases; Parathyroid Glands; Parathyroid Neoplasms

Topics: Glucosidases; Glycogen; Glycogen Storage Disease; Humans; Hyperplasia; Hypertrophy; Infant; Liver Diseases; Metabolic Diseases; Metabolism; Muscular Diseases

Topics: Abortion, Habitual; Acid Phosphatase; Alkaline Phosphatase; DNA; Endometriosis; Endometrium; Female; Glycogen; Histocytochemistry; Humans; Hyperplasia; Menopause; Pregnancy; Proteins; RNA

Topics: Carbohydrate Metabolism; Glycogen; Hyperplasia; Hypertrophy; Neoplasms; Palate

Topics: Adrenal Glands; Blood; Blood Chemical Analysis; Body Weight; Brain; Brain Chemistry; Carbohydrate Metabolism; Chemical Phenomena; Chemistry; Chlorides; Cold Temperature; Electroshock; Glucose; Glycogen; Hyperglycemia; Hyperplasia; Hypertrophy; Liver; Muscles; Neurochemistry; Physiology; Potassium; Rats; Research; Seizures; Sodium; Thymus Gland; Water

Topics: Adenocarcinoma; Disease; Endometrium; Female; Glycogen; Humans; Hyperplasia; Uterine Neoplasms