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Biomedical subjects

R Zandomeneghi

Publications and source records attributed to R Zandomeneghi.

At least 19 recordsLinked to original sources
PubMed1993

Primary systemic amyloidosis with giant hepatomegaly and portal hypertension: a case report and a review of the literature.

Amyloidosis is a manifestation of a group of diseases resulting from the variable infiltration of multiple organs by a fibrillar protein called amyloid. Hepatic involvement in amyloidosis is common both in the primary and in the secondary forms, whereas clinically-dominant liver amyloidosis is relatively rare. The authors describe a case of primary systemic amyloidosis with giant hepatomegaly, portal hypertension and renal insufficiency; the patient did not develop jaundice, ascites or gastrointestinal bleeding but died 6 months later, death being due to cerebral haemorrhage.

Adult↗
PubMed1992

Effect of aspirin and indomethacin on epidermal growth factor secretion in duodenal tissue fragments cultivated in vitro.

The aim of the present study was to determine the effect of aspirin and indomethacin on epidermal growth factor (EGF) secretion in duodenal tissue fragments cultivated in vitro. The fragments were obtained from healthy subjects by gastroscopy, cultured in McCoy's medium and gassed with 95% O2 and 5% CO2 at 37 degrees C. After an incubation of 30 min, the culture medium was decanted, and the quantity of hormone determined by radioimmunoassay. The mean EGF level detected in the medium was 10.94 ng/mg protein tissue. The addition of aspirin (final concentration 10(-7) M) to the medium reduced mean EGF levels to 7.5 ng/mg (p less than 0.05), whereas aspirin 10(-8) M did not produce such a modification. The addition of indomethacin (final concentration 10(-8) M) decreased mean EGF levels to 5.37 ng/mg (p less than 0.001). In all experimental conditions, the addition of anti-somatostatin (SRIF) antibodies determined a remarkable increase in EGF (p less than 0.01). The results of this study show aspirin and indomethacin to be direct, not SRIF-mediated inhibitors of EGF release.

Adult↗
PubMed1991

The role of epidermal growth factor in the pathogenesis of peptic ulcer disease.

Duodenal biopsies obtained from seven normal subjects and six ulcerous patients were cultured in vitro for 30 min at 37 degrees C under various experimental conditions. Epidermal growth factor (EGF) and somatostatin released in the culture medium were determined by radioimmunoassay. Under basal conditions, EGF and somatostatin levels were significantly higher in normal subjects (11.49 +/- 3.07 ng/mg protein and 3.06 +/- 0.8 ng/mg protein, respectively) than in ulcerous patients (6.9 +/- 1.98 ng/mg protein and 1.75 +/- 1.23 ng/mg protein, respectively). However, when antibodies to somatostatin and vasoactive intestinal polypeptide (VIP) were added together to the culture media, in ulcerous patients, EGF levels also were lower as absolute values, but were higher as a percentage of variation than controls (p less than 0.05). The fall of EGF secretion from tissue cultures of ulcerous patients could be the consequence of endocrine cellular loss or damage, rather than the cause of ulceration. Moreover, the EGF-producing cells around the lesion in ulcerous patients seems to be hyperactive, and this hyperfunction of EGF-producing cells might contribute to the in vivo repair of tissue damage.

Adult↗
PubMed1990

Role of vasoactive intestinal polypeptide (VIP) and endogenous somatostatin on the secretion of epidermal growth factor (EGF): studies on duodenal tissue cultures.

Epidermal Growth Factor (EGF)-containing cells have been found in Brunner's glands in the same area where several regulatory peptides are released. The present study was aimed at testing the release and the regulation of EGF secretion from cultured duodenal biopsies obtained from healthy individuals by gastroscopy. The effects and the interaction of VIP and somatostatin on the hormone release were studied. Duodenal biopsies were cultured at 37 degrees C in Mc Coy's buffer, gassed with 95% O2 and 5% CO2. After 30 min, the culture medium was decanted for the measurement of the hormones by RIA. To measure the protein content, the tissue was then homogenized; EGF detected in the culture was 11.5 ng/mg protein. The addition of VIP in the medium increased EGF mean levels to 21.6 ng/mg protein (P less than 0.01). The biopsies thus obtained were cultured with anti-somatostatin antibodies to evaluate the influence of endogenous somatostatin on EGF secretion. The inclusion of anti-somatostatin antibodies increased the EGF levels to 41.2 ng/mg protein (P less than 0.01). The combined addition of anti-somatostatin antibodies and VIP in the culture caused a mean EGF increase significantly higher than the values obtained separately by VIP and somatostatin (P less than 0.01). In conclusion, we can suggest a triangular interaction model of EGF release, where the somatostatin seems to be the negative monitor of over-secreted VIP and EGF from the gut.

Adult↗
PubMed1989

Effects of long-term glibenclamide administration on gastrointestinal and pancreatic hormones in normal fasting rats.

We previously reported that sulfonylurea treatment reduces insulin (IRI), glucagon (IRG) and somatostatin (SRIF) release following metabolic stimuli from the isolated perfused pancreas of normal rats and that a reduction in IRI, IRG and SRIF pancreatic content was also observed. The present work was undertaken to investigate the effects of long-term glibenclamide treatment on the gastrointestinal content of gut hormones in normal rats. Moreover, the effects of sulfonylurea treatment on IRI, IRG, and SRIF pancreatic content were also analyzed and compared to the peripheral hormone plasma levels. Two groups of male Sprague-Dawley rats received glibenclamide (1 mg/kg/day per os; n = 14) or placebo (distilled water; n = 10) for 5 months, respectively. Tissue contents of IRI, IRG and SRIF in acid-ethanol extracts of pancreas and of gastric inhibitory peptide (GIP), vasoactive intestinal polypeptide (VIP), entero-glucagon (gut-GLI) and SRIF in acid-ethanol extracts of intestine were determined. Blood glucose and plasma pancreatic hormone levels were also measured. Glibenclamide treatment lowered the levels of IRI, IRG and SRIF in the pancreatic tissue; in the same way gut-GLI, SRIF and VIP intestinal concentrations were significantly reduced, whereas no significant inhibition was detected in intestinal GIP content. Blood glucose levels and IRI and SRIF plasma concentrations were similar in the two groups. IRG plasma levels were reduced in the sulfonylurea group. These findings might suggest that sulfonylurea suppresses hormone biosynthesis in a non-specific manner.

Administration, Oral↗
PubMed1988

Effects of heroin addiction on the responses of glucose, C-peptide and insulin to a standard meal.

1. The aim of the study was to examine the responses of plasma glucose, C-peptide immunoreactivity (CPR) and total immunoreactive insulin (IRI) to a standard meal in heroin addicts, since the presence of immunoreactive beta-endorphin has been demonstrated in human endocrine pancreas. 2. Ten heroin addicts and 10 control subjects participated in the study. The addicts had been taking heroin (from 0.5 to 2 g/day) for at least 2 months and they had no detectable diseases. 3. After a 12 h fast, each subject received a standard meal; blood samples were taken at -15, 0, 15, 30, 60 and 120 min to determine glucose, CPR and IRI. Calculation of the CPR/IRI molar ratio was used as a semiquantitative estimation of the hepatic extraction of insulin. 4. No difference in plasma glucose was observed between the groups. Addicts had lower CPR than normals at 15, 30 and 120 min (P less than 0.01). On the contrary, IRI was higher in addicts than in normals (P less than 0.05 at -15 and 0 min, P less than 0.01 at 15, 30 and 60 min), except at 120 min. The CPR/IRI molar ratio was lower in addicts (P less than 0.01). 5. Heroin addiction seems to produce a beta-cell failure and contemporaneously a state of hyperinsulinaemia; blood glucose remains in the normal range. 6. We conclude that chronic heroin addiction may produce a change in the rate of hepatic extraction of insulin.

Adult↗
PubMed1986

[Bile acids in chronic hepatopathies].

The clinical value of measuring biliary acids in various chronic liver disease was investigated. The sample examined included 17 healthy subjects, 16 patients with active chronic hepatitis, 15 with cirrhosis of the liver and 14 with cholestatic cirrhosis. The following parameters were considered in each patient: blood bilirubin, gamma GT, alkaline phosphatase, cholinesterase, blood cholesterol, Quick time. The total pool of biliary acids was assayed by the enzymatic method on samples taken in the morning before breakfast and two hours after intake of 600 mg ursodeoxycholic acid. Total biliary increased with the progression of the pathological condition. Unlike all other indicators biliary acid assays after oral loading with ursodeoxycholic acid makes it possible to distinguish between subjects with active chronic hepatitis and those with cirrhosis of the liver.

Adult↗
PubMed1985

Human pancreatic polypeptide and somatostatin in chronic renal failure.

Human pancreatic polypeptide is the only hormone so far reported which clearly suppresses somatostatin release, suggesting that this peptide may have a role in controlling somatostatin secretion from the gut and pancreas. In this study endogenous high circulating human pancreatic polypeptide concentrations in patients with chronic renal failure do not decrease somatostatin circulating levels. The reduced clearance rate of somatostatin in chronic renal failure may partially account for the normal circulating levels of somatostatin observed in our patients with respect to controls. Renal insufficiency may, itself, induce an increase in some gastrointestinal peptides capable of stimulating somatostatin secretion.

Humans↗