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Biomedical subjects

F S Gorelick

Publications and source records attributed to F S Gorelick.

61 records · Page 4Linked to original sources
PubMed1982

Regional differences in lectin binding to colonic epithelium by fluorescent and electron microscopy.

The distribution of glycosubstances in colonic epithelium using lectins that were rhodaminated for fluorescent microscopy or coupled to colloidal gold for electron microscopy has been studied. Findings, based on lectin binding patterns, indicate that the right, transverse, and left colon of the guinea pig differ in their content of glycoconjugates within goblet cells and along the brush border. Local variations of labeling were also observed within goblet cells between the upper and lower portions of crypts. Throughout the colon, corresponding to a region of supranuclear fluorescence, Ricin II-colloidal gold labeled the Golgi complex of both enterocytes and goblet cells. Ricin II-colloidal gold also labeled small (congruent to 800 A) vesicles in the apical portion of enterocytes in all colonic segments. Microvilli were labeled by Ricin II-colloidal gold in the right and transverse colon, a finding that correlated with the observed adhesion of bacteria in those segments.

Animals↗
PubMed1981

Ultrasonography of alcoholic liver disease with histological correlation.

In alcoholic liver disease (fatty infiltration, alcoholic cirrhosis), the liver is diffusely abnormal on ultrasound. Changes in size, dilatation of the hepatic veins, and ascites may also occur. The authors conducted a histological correlation of these abnormalities in 22 alcoholic patients and 16 controls, grading the changes on a scale of 0 to 4+ for fat, fibrosis, and necrosis and noting tumor whenever present. Ultrasound detected abnormality in 21 cases (sensitivity = 95%) and correctly identified 15 controls (specificity = 94%). Of the 5 tumors seen, 4 hepatomas were detected and biopsied and 1 metastatic squamous-cell carcinoma was missed. Applications of commercially available A-scan module are considered and its limitations discussed. With the exception of minimal change (1+ fat or fibrosis), ultrasound detected many of the pathological changes seen in alcoholic liver disease.

Adult↗
PubMed1981

Is gastroduodenitis part of the spectrum of peptic ulcer disease?

Gastroduodenitis should be included with duodenal ulcer and gastric ulcer in the spectrum of clinical disorders that have different pathogenetic mechanisms but a similar clinical picture. Published results of a clinical, endoscopic, radiologic, and histologic study of 100 patients presenting with gastrointestinal symptoms revealed that 61% had classic and 39% had atypical manifestations of peptic ulcer disease. We could not clinically distinguish the 24 patients with ulcer crater (40% of the classic group) from the 25 patients with acute gastroduodenitis without crater (41% of the classic group). Preliminary data of a prospective study compared the treatment responses of 19 patients with gastroduodenitis and 39 patients with peptic ulcer disease. These patients were diagnosed endoscopically and restudied after treatment with a bland diet and antacids seven times per day for 8 weeks. The responses to therapy in gastroduodenitis and peptic ulcer were as follows: endoscopically, 63 and 80%, respectively; histologically, 74 and 65%, respectively; symptomatically, 47 and 65%, respectively. Preliminary data on the duodenal epithelial thymidine uptake revealed an increased proliferative index in duodenitis patients but not in patients with peptic ulcer or control subjects.

Adult↗
PubMedDate not supplied

Intracellular proteolysis of pancreatic zymogens.

Activation of pancreatic digestive zymogens within the pancreatic acinar cell may be an early event in the development of pancreatitis. To detect such activation, an immunoblot assay has been developed that measures the relative amounts of inactive zymogens and their respective active enzyme forms. Using this assay, high doses of cholecystokinin or carbachol were found to stimulate the intracellular conversion of at least three zymogens (procarboxypeptidase A1, procarboxypeptidase B, and chymotrypsinogen 2) to their active forms. Thus, this conversion may be a generalized phenomenon of pancreatic zymogens. The conversion is detected within ten minutes of treatment and is not associated with changes in acinar cell morphology; it has been predicted that the lysosomal thiol protease, cathepsin B, may initiate this conversion. Small amounts of cathepsin B are found in the secretory pathway, and cathepsin B can activate trypsinogen in vitro; however, exposure of acini to a thiol protease inhibitor (E64) did not block this conversion. Conversion was inhibited by the serine protease inhibitor, benzamidine, and by raising the intracellular pH, using chloroquine or monensin. This limited proteolytic conversion appears to require a low pH compartment and a serine protease activity. After long periods of treatment (60 minutes), the amounts of the active enzyme forms began to decrease; this observation suggested that the active enzyme forms were being degraded. Treatment of acini with E64 reduced this late decrease in active enzyme forms, suggesting that thiol proteases, including lysosomal hydrolases, may be involved in the degradation of the active enzyme forms. These findings indicate that pathways for zymogen activation as well as degradation of active enzyme forms are present within the pancreatic acinar cell.

Animals↗
PubMedDate not supplied

Diabetes mellitus and the exocrine pancreas.

Diabetes and carbohydrate intolerance can occur in pancreatitis. Although one-half of patients with acute pancreatitis will have some evidence of glucose intolerance during their acute illness, few will require insulin administration on either a short- or long-term basis. The diabetes seen in acute pancreatitis is likely due to a combination of factors, including alerted insulin secretion, increased glucagon release, and decreased glucose utilization by the liver and peripheral tissue. Chronic pancreatitis is often associated with diabetes mellitus, with the incidence as high as 70 percent when pancreatic calcification is present. These patients tend to be very sensitive to the effects of insulin and hypoglycemia. This is probably secondary to concurrent hepatic disease, malnutrition, and a relative decrease in glucagon reserves. The diabetes seen in chronic pancreatitis is associated with decreased insulin production. Finally, although the endocrine pancreas may influence the exocrine gland through a portal system, primary diabetes mellitus probably does not result in clinically significant alterations in pancreatic exocrine function.

Blood Glucose↗