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Biomedical subjects

E Goldin

Publications and source records attributed to E Goldin.

At least 55 records · Page 3Linked to original sources
PubMed1997

Anemia worsens hyperdynamic circulation of patients with cirrhosis and portal hypertension.

This retrospective cohort study was aimed at investigating the effects of anemia on the hemodynamic disturbances associated with portal hypertension. In all, 202 consecutive nontreated portal-hypertensive patients referred for evaluation to our Hepatic Hemodynamic Laboratory were included. Compared to the nonanemic patients, anemic cirrhotic patients had an increased cardiac output (7.9 +/- 1.9 vs 7.1 +/- 2 liters/min, P < 0.01), and a decreased mean arterial blood pressure (82 +/- 11 vs 94 +/- 13 mm Hg, P < 0.0001) and systemic vascular resistance (838 +/- 235 vs 1102 +/- 356 dyn/sec/cm5, P < 0.0001). Similar results were obtained when Child A or Child B-C patients were analyzed separately. Multivariate logistic regression disclosed that hemoglobin concentration, in addition to age, sex azygos blood flow, and albumin concentration, was an independent factor influencing the degree of systemic vasodilation in cirrhotic portal-hypertensive patients. This study discloses that anemia worsens the hyperdynamic circulation associated with portal hypertension. Since hemoglobin concentration may change with time, this parameter should be taken into account when evaluating hemodynamics in portal-hypertensive patients.

Aldosterone↗
PubMed1997

Gastric mucosal damage in experimental diabetes in rats: role of endogenous glutathione.

BACKGROUND & AIMS: Spontaneous gastric damage occurs in diabetic rats, but the mechanism is unknown. The aim of this study was to assess the role of glutathione metabolism and gastric mucosal blood flow (GMBF) in the development of such spontaneous gastric damage. METHODS: Mucosal damage, GMBF, glutathione metabolism, and lipid peroxidation were measured in the stomach of diabetic and control rats. RESULTS: Spontaneous gastric damage occurred in fasted diabetic rats 4 weeks after streptozotocin administration or pancreatectomy. This was accompanied by a 50% decrement in mucosal content of glutathione; 48 hours after streptozotocin, the decrement of glutathione was only of 25% and no gastric damage was observed. Fed diabetic rats (4 weeks after streptozotocin) had normal glutathione levels and no damage; however, a 30% glutathione depletion achieved by buthionine-sulfoximine administration promoted significant damage. Gastric glutathione synthetic rate, levels of adenosine triphosphate, oxidized glutathione, and malonyldialdehyde were similar in all groups, whereas cysteine concentration was reduced in fasted diabetic animals. Exogenous cysteine attenuated the gastric damage. GMBF was not influenced by diabetes. CONCLUSIONS: Spontaneous gastric damage in fasted diabetic rats seems to be related to glutathione depletion as a result of limited availability of cysteine and not to increased glutathione oxidation. GMBF changes are not involved.

Animals↗
PubMed1997

Crohn's disease in late adolescence: acute onset or long-standing disease?

We studied retrospectively a group of 53 patients with Crohn's disease, diagnosed between 18 and 21 years of age. They had all undergone a thorough medical evaluation at age 17 before military service. They thus served as a unique group in whom the natural course of the disease, duration of signs and symptoms before diagnosis, and delay in diagnosis could be assessed. Other than a more frequently elicited history of nonspecific mild recurrent abdominal pain in childhood in the patient group, medical history, physical growth, sexual development, and laboratory parameters of inflammation did not differ in the patient group and the healthy control group. Crohn's disease in this group of young adults is likely one of acute onset and did not begin as an exacerbation of a more subtle and prolonged process.

Acute Disease↗
PubMed1997

Hepatobiliary graft-versus-host disease manifested by common and hepatic biliary duct obstruction.

BACKGROUND: A 26-year-old patient presented with ascending cholangitis 8 months after allogeneic bone marrow transplantation for immunoblastic lymphoma. METHODS AND RESULTS: Endoscopic retrograde cholangiopancreatography showed common and hepatic biliary duct obstruction that was attibuted to chronic graft-versus-host disease. CONCLUSION: This case indicates that hepatobiliary disease related to chronic graft-versus-host disease may involve major bile ducts causing obstruction.

Adult↗
PubMed1996

Increased blood hemoglobin attenuates splanchnic vasodilation in portal-hypertensive rats by nitric oxide inactivation.

BACKGROUND & AIMS: Nitric oxide, which is quenched by hemoglobin, has been implicated in the pathogenesis of portal hypertension. The aim of this study was to investigate the effects of increasing blood hemoglobin concentration by erythropoietin treatment on the gastrointestinal vasodilation associated with portal hypertension. METHODS: Portal-hypertensive and sham-operated rats treated with erythropoietin were studied 2 weeks after surgery. Hemodynamic and rheological parameters were measured in baseline conditions and after N(G)-nitro-L-arginine methyl ester (L-NAME) or sodium nitroprusside treatment. RESULTS: In portal-hypertensive rats, erythropoietin attenuated the increase in gastric mucosal and superior mesenteric artery blood flows and the decrease in arterial blood pressure and splanchnic vascular resistances. Those parameters were not affected by erythropoietin in sham-operated rats. A direct vascular effect of erythropoietin was ruled out by the lack of changes in blood pressure or mesenteric blood flow after intravenous erythropoietin administration and by a similar in vitro relaxation to acetylcholine in mesenteric artery rings. In portal-hypertensive rats, erythropoietin blunted the blood pressure response to sodium nitroprusside and attenuated the gastric and mesenteric blood flow response to L-NAME. CONCLUSIONS: Gastrointestinal vasodilation associated with portal hypertension can be attenuated by increasing blood hemoglobin concentration. Inactivation of overproduced NO by hemoglobin may account for this effect.

Animals↗
PubMed1996

Role of prostaglandins and nitric oxide in gastrointestinal hyperemia of diabetic rats.

The aim of the study was to characterize the gastric and mesenteric vascular changes induced by diabetes and the implication of endothelial [nitric oxide (NO) and prostaglandins] and humoral (glucagon) factors in such changes. Diabetes was induced in rats by a single streptozotocin injection. Four weeks later, gastric mucosa, left gastric artery, and superior mesenteric artery blood flows were measured using hydrogen gas clearance and perivascular ultrasonic flowmeter techniques, respectively, in anesthetized and fasted diabetic and control rats. Blood pressure, hematocrit, blood volume, and blood viscosity were also measured. Left gastric (41 +/- 6 vs. 25 +/- 4 ml.min-1.100 g-1) and superior mesenteric artery blood flows (83 +/- 8 vs. 65 +/- 4 ml.min-1.100 g-1) were significantly higher in diabetic than in control rats. The increased blood flow in the left gastric artery was distributed to a hypertrophic mucosa in diabetic rats; therefore, the blood flow per 100 g tissue in the gastric mucosa was not significantly different in diabetic compared with control rats. Pretreatment with indomethacin reduced both increase gastric and mesenteric flows of the diabetic rats to the same levels as in control rats. NG-nitro-L-arginine methyl ester decreased gastric blood flow in a dose-dependent manner and to a similar extent in diabetic and control rats. In contrast, an increased sensitivity to the higher doses of the NO inhibitor was observed in the mesenteric vascular bed of diabetic rats. Glucagon reduction achieved by somatostatin infusion did not influence either gastric or mesenteric blood flow in diabetic rats. In summary, the present study revealed an increase in gastric and mesenteric arterial blood flows in streptozotocin-induced diabetic rats. The gastrointestinal hyperemia seems to be due, at least in part, to the increased demand of a hypertrophic mucosa and is mediated primarily by endogenous prostaglandins. Increased vascular sensitivity to NO may also contribute to the mesenteric vasodilation.

Animals↗
PubMed1996

Reduced glutamine content in colonic polyps.

BACKGROUND: Glutamine is the most abundant amino acid in the body. It has a key role in nitrogen metabolism and is a major source of energy for the enterocyte and many other cells. Glutamine is also essential for tumor growth, and marked changes in organ glutamine metabolism are characteristic in cancer patients. METHODS: We have investigated the catabolism of glutamine in a classic premalignant condition: the colonic adenomatous polyp. The content of glutamine and activity of two catabolic enzymes, glutamine transferase and phosphate-dependent glutaminase, were studied in normal colon and in polyp mucosa. RESULTS: Free glutamine content and activity of glutaminase were significantly lower in polyps than in their adjacent mucosa. Glutamine transferase activity was significantly lower in polyp mucosa than in normal colon controls. CONCLUSIONS: Adenomatous polyps might behave as a glutamine trap, channeling glutamine to protein and nucleic acid synthesis. These changes in glutamine catabolism could play a role in colonic neoplasia pathogenesis.

Acyltransferases↗
PubMed1996

Esophageal malignancy after liver transplantation in a patient with Barrett's esophagus.

Patients undergoing liver transplantation are predisposed to develop extrahepatic malignancies. It is also known that patients with predisposed conditions, such as Barrett's esophagus, have higher rates of esophageal carcinoma. We present here a patient who underwent liver transplantation, had Barrett's esophagus, and developed esophageal malignancy a short time after transplantation. Liver transplantation may be associated with acceleration of the precancerous condition and the development of malignancies.

Adenocarcinoma↗
PubMed1995

[Endoscopic retrograde cholangiopancreatography in diagnosis of biliary atresia].

The differential diagnosis between neonatal hepatitis and biliary atresia in the newborn is difficult and has therapeutic implications. Despite important advances in diagnostic tools, 10-20% of newborns with jaundice remain without definitive diagnosis. In recent years ERCP has played a decisive role in achieving definitive anatomic diagnosis, thus avoiding unnecessary exploratory laparotomy. We present our experience with ERCP using a pediatric duodenoscope in 18 newborns with inconclusive diagnoses of neonatal cholestasis.

Biliary Atresia↗
PubMed1995

Plasma and tumor prolactin in colorectal cancer patients.

Fifteen consecutive patients with recently diagnosed colorectal cancer were studied for plasma and tumor tissue prolactin content. In eight patients (four men and four postmenopausal females), preoperative high plasmatic prolactin was found (mean 1553 nmol; range 516-3677 nmol). In three of them, prolactin was also present in the tumor cells. All plasma prolactin levels returned to normal after tumor resection and remained so during a three-month follow-up. The tumor stage by Duke distribution was similar for both high and normal plasmatic prolactin patients. The role of prolactin in the pathogenesis of colorectal cancer, and as a marker of the tumor, remains to be established. This is the first time that prolactin has been detected in human colon cancer.

Aged↗
PubMed1995

Cultured skin fibroblasts derived from patients with mucolipidosis 4 are auto-fluorescent.

Mucolipidosis 4 (ML4) is an autosomal recessive disorder with both lipid and mucopolysaccharide storage. The disease is characterized by severe visual impairment and psychomotor retardation. In our effort to find a phenotypic marker for ML4 fibroblasts, living cells were stained with fluorescent compounds. The staining pattern in cells was complicated by autofluorescence. A careful study revealed that auto-fluorescence by itself was a sufficient marker for viable ML4 fibroblasts. ML4 cells in cultures obtained from four unrelated patients contain auto-fluorescent material. Auto-fluorescence was noted over a wide range of excitation wavelengths from approximately 365 to approximately 546 nm. The most intense fluorescence was observed in the lower wave-length range. Cultured fibroblasts from normal individuals or obligate ML4 heterozygotes did not fluoresce under adequately controlled culture conditions. High passage number of inadequate feeding caused a small proportion of fibroblasts obtained from normal individuals to auto-fluoresce. The auto-fluorescent material co-localized with phase-dense inclusion bodies, shown to be lysosomes by staining with LAMP-ab. These findings imply that fluorescence may relate to the specific compound(s) stored in the lysosomes. In a comparative study, neuronal ceroid lipofuscinosis fibroblasts were also fluorescent. Fibroblasts from other diseases such as Gaucher disease and glycogenosis type 2 did not show any fluorescence. These findings are currently used in our functional cloning strategy for determining the gene involved in ML4.

Biomarkers↗
PubMed1994

The effect of ethanol on the expression of HLA class I genes in human colon adenocarcinoma cell lines.

The loss of HLA antigens by neoplastic cells may allow tumors to escape immune surveillance. We observed reduced expression of HLA antigens during human colon carcinogenesis. Since ethanol, which is associated with human colonic carcinogenesis, modulates the expression of HLA genes, we examined whether it affects the expression of HLA class I genes in human colon adenocarcinoma cell lines. Ethanol (1.7 x 10(-10) M to 1.7 x 10(-1) M), had no effect on the expression of HLA class I antigens on these colonocytes, the corresponding mRNA levels, or the expression of HLA constructs. Our findings do not support the hypothesis that ethanol may modulate the expression of HLA class I genes in human colon cancer cells.

Adenocarcinoma↗
PubMed1994

Mucolipidosis IV fibroblasts synthesize normal amounts of hyaluronic acid.

Mucolipidosis IV (ML IV) (McKusick 252650) is an autosomal recessive metabolic disorder that displays signs of both lipid and mucopolysaccharide (glycosaminoglycan) storage. It has been reported that fibroblasts from ML IV patients exhibit abnormally high synthesis of hyaluronic acid in culture. In our search for a biochemical marker that will enable positive identification of ML IV, we studied glycosaminoglycan synthesis in fibroblast cultures from patients with this disease. ML IV and normal control fibroblasts were incubated with [3H]glucosamine and [35S]sulphate. Labelled glycosaminoglycans were extracted from the cell layer and medium. Chondroitin sulphate and hyaluronic acid were determined by analysis of disaccharides after digestion with chondroitinase ABC. Synthesis of neither of these two glycosaminoglycans differed significantly between control and ML IV fibroblasts. Synthesis of hyaluronic acid was nearly linear for 24 h, with mean calculated values of 11.7 +/- 1.4 and 14.4 +/- 1.6 pg/cell per 24 h in control and ML IV cultures respectively. The variability within the two groups is attributed primarily to population variability and possibly to culture density. These experiments exclude the possibility that a general metabolic defect in hyaluronic acid synthesis is responsible for the ML IV phenotype, nor can such a defect be used as a diagnostic tool for the disease.

Adult↗