[Systemic non-typhoid salmonelloses].
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Adult↗
Biomedical subjects
S Willemer
Publications and source records attributed to S Willemer.
Influence of experimental hyperthyroidism on blood and myocardial serotonin in rats.
Recent reports suggest a role for serotonin in the pathogenesis of primary hypertension and left ventricular (LV) hypertrophy. In this study, we have induced LV hypertrophy by oral feeding of thyroxine at increasing dosages (150-450 micrograms/kg b.wt.) over a 5-week period. The effects of hyperthyroidism on cardiovascular parameters, blood and myocardial serotonin concentrations were assessed. Water-fed rats and formerly hyperthyroid recovered animals served as controls. Thyroxine caused a significant LV hypertrophy: hyperthyroid rats 2.19 +/- 0.16*; controls 1.65 +/- 0.13 g/kg b.wt. (mean +/- SD; *P less than 0.05). An almost complete regression of LV hypertrophy occurred in the recovery group (1.66 +/- 0.20 g/kg b.wt.) 3 weeks after cessation of thyroid hormone application. Thyroxine-treated animals showed a significant increase of serotonin blood levels (thyroxine rats: 2108 +/- 781*, recovery: 1132 +/- 726, controls: 705 +/- 480 ng/ml; *P less than 0.05). The concentrations of serotonin in left ventricular myocardium were increased after thyroid hormone application, whereas the highest levels were found in the recovery group (thyroxine rats: 139.1 +/- 30.4, recovery: 167.2 +/- 43.1, controls: 68.9 +/- 27.9 mg/ml homogenate). Serotonin-containing cells in the left ventricular myocardium were stained immunohistochemically. They were localized perivascularly and were assumed to represent tissue mast cells. In experimental hyperthyroidism the serotonin levels in blood and heart are increased possibly indicating an interaction of both hormones in thyroxine-induced cardiomyopathy.
Administration, Oral↗
Influence of chronic drug-induced achlorhydria by substituted benzimidazoles on the endocrine stomach in rats.
The release of gastric somatostatinlike immunoreactivity and gastrin was studied in rats with chronic achlorhydria induced by the substituted benzimidazole BY 308. In vitro, stimulation of gastrin release by acetylcholine was slightly enhanced after 1 day of treatment but no further effects were observed compared to placebo controls. Four weeks of treatment evoked marked gastrin hypersecretion, which was atropine-resistant. Stimulation of gastrin release was inversely correlated to enhancement of basal gastrin levels. Chronic achlorhydria distinctly reduced somatostatin responses to isoproterenol, whereas potent stimulation was observed in controls. Treatment with BY 308 for 1 wk was associated with fully developed gastrin hypersecretion but isoproterenol-stimulated somatostatin release was still unaffected. Hypergastrinemia accompanied by increased antral gastrin and reduced antral and fundic somatostatin concentrations was also found in vivo after 4 wk of treatment with BY 308. It is concluded that chronic achlorhydria not only enhances storage and secretion of gastrin but also diminishes the secretion and tissue stores of somatostatin; adaptive changes of the somatostatin cell occur, however, with a much longer delay.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Tubular complexes in cerulein- and oleic acid-induced pancreatitis in rats: glycoconjugate pattern, immunocytochemical, and ultrastructural findings.
Ductlike tubular complexes in cerulein-induced pancreatitis and oleic acid-induced pancreatic insufficiency were studied to analyze further their origin and development. Immunocytochemistry for pancreatic enzymes, lectin-binding studies, and ultrastructural investigations were combined with autoradiographic quantitation of labeling indices of ductlike cells in tubular complexes. In one group of rats, pancreatitis was induced by infusion of cerulein (10 micrograms kg-1 h-1). In a second group, pancreatic insufficiency was induced by intraductal injection of oleic acid (50 microliters). The investigations were carried out at distinct intervals following induction of pancreatic injury. In both groups of animals, after 3 days, a significant widening of acinar lumina was paralleled by a decreasing height of acinar cells, which showed pronounced retrogressive changes. At this time, acinar cells bound all of the lectins used and retained their immunoreactivity for amylase, trypsinogen, chymotrypsinogen, and lipase. At further intervals, acinar structures formed typical ductlike complexes, with a progressive loss of immunoreactivity for pancreatic enzymes and a reduced lectin-binding for L-fucose and N-acetylgalactosamine. Autoradiographic quantitation demonstrated no significant labeling of acinar cells undergoing tubular dedifferentiation. In both models, tubular complexes were removed by macrophages. It is concluded that lining cells in tubular complexes represent degenerating acinar cells that have no regenerative potency and have lost their secretory and membrane characteristics.
Animals↗
Increased visualization of antral gastrin-producing G-cells after acute stimulation of gastrin release in the rat.
The effect of acute stimulation of gastrin release on the number of antral gastrin-producing G-cells stained by conventional immunohistology was investigated in two experimental models. The substituted benzimidazole derivate BY 308 was administered at a dosage that induces complete achlorhydria and thereby led to marked hypergastrinaemia. Two hours after drug administration, antral G-cell density was increased by 14% and 35% in 12-h and 48-h fasted rats, respectively. Both serum gastrin levels and G-cell density further increased after 3 and 8 days' treatment with BY 308 whereas the somatostatin (D)-cell count did not change prior to 8 days' administration. In the isolated, vascularly perfused rat stomach, acetylcholine was perfused for 36 min; this regimen increased gastrin release four-fold and enhanced the G-cell count by 24% whereas 8 min acetylcholine perfusion did not alter G-cell density significantly but stimulated gastrin output. The results of this study suggest that acute changes in the secretory activity of the gastrin cell are accompanied by an alteration of the staining characteristics thus indicating that an increase in the antral G-cell count does not solely depend upon formation of new cells.
Acetylcholine↗
[Endocrine pancreas tumor as a cause of exocrine pancreas insufficiency: problems of immunologic tumor diagnosis and classification].
The case of a 32-year old man with exocrine pancreatic insufficiency and progressive weight loss is reported. Ultrasound examination of the abdomen revealed a huge tumor of the pancreatic head. Smears obtained by a percutaneous fine-needle biopsy showed characteristics of a neuroendocrine tumor. Serum hormone levels and immunocytochemistry presented no evidence for a hormonal activity of the tumor. The exocrine pancreatic insufficiency was explained by an obstruction of the pancreatic duct system. In the present case report the problems of diagnostic approaches to endocrine pancreatic tumors are discussed.
Adenoma, Islet Cell↗
Pancreatic lesions and hormonal profile of pancreatic tumors in multiple endocrine neoplasia type I. An immunocytochemical study of nine patients.
Pancreatic specimens of nine patients suffering from multiple endocrine neoplasia type I (MEN I) were investigated with regard to tumor frequency and growth pattern, islet hyperplasia and endocrine cell neoformation, immunocytochemical hormone profile of the tumors, and correlation to clinical symptoms. The majority of the 201 tumors were microadenomas (diameter less than 0.5 cm), which frequently displayed a trabecular growth pattern. Microadenomatosis was considered the most distinct feature of the MEN I pancreas. Additional larger tumors (diameter greater than 1.0 cm) were found in five patients. Whereas islet hyperplasia appears not to belong to the spectrum of the pancreatic lesions in MEN I, nesidioblastosis was occasionally observed. Immunocytochemical screening revealed that among hormone-positive tumors (approximately 80% of the tumors), pancreatic polypeptide tumors (PPomas), glucagonomas, and insulinomas were the most frequent. The high incidence of PPomas in these pancreases probably accounts for the elevated serum PP levels found in many MEN I patients. Somatostatinomas, gastrinomas, vasoactive intestinal polypeptide tumors (VIPomas), and neurotensinomas were rare. Clinically overt hyperinsulinism, observed in two patients and associated with a large insulinoma, was cured by tumor resection. Eight of nine patients presented a Zollinger-Ellison's syndrome (ZES), but only in two patients were gastrin-producing tumors found. The source of gastrin in MEN I patients with a ZES, in whom no gastrinoma could be detected, remains unclear.
Adult↗
Human acute pancreatitis: its pathogenesis in the light of immunocytochemical and ultrastructural findings in acinar cells.
Human acute pancreatitis results from an autodigestive process frequently associated with alcohol abuse, gall stone disease and shock. Peripancreatic fat necrosis was identified as one of the earliest visible lesions, whereas acinar cell necrosis and haemorrhage were regarded as secondary changes. To examine the alterations in acinar cells in more detail, their enzyme content and fine structural features were studied immunocytochemically using antisera against alpha-amylase, lipase, trypsin, chymotrypsin and pancreatic stone protein, and electronmicroscopically in pancreatic tissues from patients with severe acute pancreatitis. Peripheral acinar cells in the immediate vicinity of fat necrosis were found to be heavily degranulated, while acinar cells at some distance of necrosis fully retained their enzyme content. Other frequent changes of the acinar cells included cuboidal transformation, loss of microvilli, increased occurrence of autophagosomes, and formation of enlarged acinar lumina. As there was no apparent cell membrane leakage or rupture of duct lumina, it is concluded that the acinar cells adjacent to fat necrosis release their granules by undirected basolateral extrusion. The findings thus suggest that one of the basic defects in acute pancreatitis is the uncontrolled release of enzymes from peripheral acinar cells into the interstitial space which, in turn, presumably by the action of lipase, leads to autodigestive fat necrosis.
Acute Disease↗
[Invasive forms of non-typhoid salmonelloses].
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Abscess↗
[Age-related changes in glycosaminoglycans in the cell nuclei of the rat liver--biochemical and histochemical pilot studies].
Cell nuclei of the livers of 12 male Wistar rats aged 24 months, and 16 male Wistar rats aged 4 months were isolated. 0.4 microCi [3H]-glucosamine/kg body weight were administered intraperitoneally. The livers of four animals were used for each biochemical analysis. The tissue was degraded by proteolysis, the glycosaminoglycans (GAGs) were isolated and the GAG types were determined by enzyme digestion, nitrite degradation and radiometry. The amount of GAGs was photometrically determined in single samples of pooled material of each of the two age groups. In paraffin sections (from other male Wistar rats of a different age), the influence of enzymes on specific GAG staining was observed. Most of the radioactivity was found in heparan sulfate (HS) and a lower content in chondroitin sulfates (CSs). In HS the incorporation increased with increasing age. The amount of HS showed no age-related differences. The results indicate an age-related activation of the HS metabolism. The GAG pattern and the age-related changes of the GAG types in total tissue (earlier results) are different from those in the nuclei. By histochemical methods, we observed a small but distinct effect of heparitinase in the cell nuclei.
Aging↗
[Age dependence of the early reaction in glycosaminoglycan metabolism of the rat liver on damage following a single dose of thioacetamide].
Wistar rats aged 7 or 22 months resp. were treated with 50 mg/kg of thioacetamide (TAA) i.p. The TAA-treated animals as well as control groups of the same ages and containing the same number of animals were injected i.p. with 3H-glucosamine (0.2 microCi/g body weight) 2 hours before sacrifice. Previously to sacrifice, the livers had been perfused in narcosis with NaCl (0.9%). Following degradation of the tissue by pronase, specimen of the substances precipitable by ethanol were digested with chondroitinases, streptomyces-hyaluronidase, keratanase, and nitrite. The quantities of substances were estimated photometrically using Alcian blue; radiometry was performed following precipitation with cetylpyridiniumchloride. In aging animals the amount of dermatan-sulphate (DS) and of the total acidic glycosaminoglycans (a.GAG) is increased as compared to the younger animals, although there ist no age related difference in the incorporation of glucosamine. The incorporation per microgram a.GAG (spec. act.) is decreased. Following TAA the amount of DS is increased in both age groups, whereas the total amount of GAG is increased only in the younger animals. The incorporation per mg dry weight is also increased in all GAG types of both age groups which is also the case with the spec. act. (with the exception of HS in the younger animals). The increase of the incorporation per mg dry weight in DS is significantly lower in the older TAA-animals as compared to the younger ones. HS shows the same tendency, but there is no significance. The age related increase of hydroxyproline parallels that of DS.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetamides↗