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Biomedical subjects

M Ziegler

Publications and source records attributed to M Ziegler.

At least 361 records · Page 20Linked to original sources
PubMed1981

Insulin immunohistochemistry of rodent CNS: apparent species differences but good correlation with radioimmunological data.

Using an indirect immunofluorescence technique the distribution of insulin was mapped in brains of Wistar strain rats and mice. Insulin immunoreactivity was found to be widely distributed throughout mouse CNS, whereas in rat brain a restriction of immunoreactive material to cerebral blood vessels and ependymal cells and/or tanycytes of the brain ventricles was observed. In radioimmunological studies the amount of insulin (IRI) was estimated for different brain areas (cerebral cortex, brain stem, cerebellum, hippocampus, thalamus and hypothalamus). In the case of Wistar rats very low levels of IRI were found. On the contrary, the same regions in mouse brain contained considerably greater amounts of IRI. The comparison between histochemical and biochemical data revealed a good correlation. It is concluded that part of the insulin measured by radioimmunoassay is associated with neuronal structures.

Animals↗
PubMed1981

Use of military antishock trouser in a child.

Angiographic localization and embolization has emerged as the preferred mode of therapy for arterial bleeding associated with pelvic fractures but is not always definitive. Our experience demonstrates the use of an external counter pressure device (MAST) as an essential part of the pediatric surgeon's armamentarium and suggests the need for concurrent venography during angiographic localization of pelvic bleeding sites.

Child↗
PubMed1981

Poor evidence for insulin/insulin-like immunoreactivity in the CNS of lower vertebrates.

The localization of insulin/insulin-like immunoreactivity was studied in the brain and the pancreas of an amphibian (clawed frog [Xenopus laevis Daudin]) and in the CNS of two teleost fishes (bream [Abramis brama L.] and rudd [Scardinius erythrophthalmus L.] using the indirect immunofluorescence technique. With exception of cerebellar Purkinje cells no neuronal elements were found to contain insulin-like material. The frog pancreas was characterized by a strong immunofluorescence in cells producing the polypeptide.

Animals↗
PubMed1981

Immunoreactive glucagon in neurons of various parts of the human brain. Demonstration by immunofluorescence technique.

The presence of glucagon-like immunoreactivity in nerve cells of different parts of the human brain was demonstrated by the indirect immunofluorescence technique. A bright fluorescent reaction was observed in the pyramidal cells of lamina V of the Neocortex. Less prominent concentrations of the glucagon-like material were detected in a few pyramidal cells of the Hippo-campus and in some neurons of the Presubiculum and Subiculum. Within the Corpus amygdaloideum, only a few magnocellular neurons showed a positive reaction. The Hypothalamus was evidenced by a moderate, but widely distributed, reaction in magnocellular and medium-sized nerve cells in different nuclei (especially Nuc. ventromedialis and Nuc. arcuatus). A strong immunofluorescence was localized to some neurocytes in the Nuc. amibigus, and Nuc. n. hypoglassi. The Purkinje cells of the cerebellar cortex were free from immunoreactive material, but fluorescence occurred in some very small nerve cells of the Cerebellum (probably granular cells). A dependence of the strength of immunofluorescence of the time delay between autopsy and death is shown.

Amygdala↗
PubMed1981

Biosynthesis of somatostatin in pancreatic islets of Wistar rats and its regulation by glucose.

Pancreatic islets of Wistar rats incorporate L-[3H]-phenylalanine into proteins which react after gentle trypsination with a specific somatostatin antiserum. These somatostatin-like peptides were separated by gel chromatography and found to be a 3.5 kilodalton peptide, a peptide co-eluating with somatostatin (1.7 kd) and a low molecular weight peptide (1.0 kd). The biosynthesis of somatostatin may be regulated by glucose. The highest incorporation rate was measured in islets isolated from fasted rats and incubated in low glucose concentration.

Animals↗
PubMed1981

[Immunohistochemical evidence of some peptidohormones in the central nervous system of normoglycemic and hyperglycemic rodents (author's transl)].

The content and the distribution of insulin, glucagon and somatostatin were studied in normoglycemic and hyperglycemic rodents by immunohistochemical techniques. A manifest Diabetes mellitus caused a striking decrease in somatostatin immunofluorescence. The insulin content suffered in a less pronounced manner. Data obtained with glucagon did not permit to draw unequivocal conclusions. In general, our findings speak about certain regulatory influence of the brain on glucose homeostasis.

Animals↗
PubMed1981

Reversal of diabetes by isogeneic transplantation of cultured pancreatic islets.

Pancreatic islets were isolated by collagenase digestion from female Wistar rats and cultured at 20 mmol/l glucose. The enhancement of Mg++ concentration from 0.8 mmol/l up to 5.3 mmol/l had a protecting effect on the glucose-induced insulin release in the subsequent short-time incubation and prevented the age-depending decrease of B-cell function. About 1,000 cultured islets injected into portal vein normalized the plasma glucose of streptozotocin-diabetic rats. The plasma glucose patterns during the glucose load were nearly identical to healthy controls. These findings suggest that the cultured islets maintain the ability to secrete insulin in response to glucose in vitro as well as in vitro and that such islets can reverse an experimentally induced diabetes.

Animals↗
PubMed1981

Hyperalimentation-induced cholestasis. Increased incidence and severity in premature infants.

Two hundren sixty-seven neonates who received parenteral nutrition were monitored for signs of liver dysfunction. Cholestatic jaundice occurred in we infants, with a higher incidence in the more immature infants. There was an inverse correlation between severity of jaundice and the degree of prematurity. Infants with cholestasis remained without gastrointestinal feedings and received parenteral nutrition for periods of time significantly higher than infants without cholestasis. The incidence of this complication did not seem to correlate with the amount of protein infusate (amino acid solution). A higher incidence of sepsis was noted in infants who were affected by cholestasis. Close monitoring for signs of liver dysfunction in all neonates receiving parenteral nutrition is strongly recommended.

Bilirubin↗
PubMed1981

Pancreatic glucagon response to glucose in obesity with normal and impaired carbohydrate tolerance.

Pancreatic glucagon (IRG) and insulin (IRI) secretion patterns were studied in obese subjects with normal (n = 7), borderline (n = 5) and pathological carbohydrate tolerance (n = 11), as well as in 19 non-obese healthy controls without a family history of diabetes, by means of a 2-h glucose infusion (12 mg/kg/min), primed by an initial injection of 0.33 g/kg glucose. With regard to the insulin secretion all obese groups were characterized by a significant hyperinsulinaemia during the late secretion phase, whereas the early insulin response ( delta IRI-area 0-5 min) was significantly reduced in obesity with pathological carbohydrate tolerance. There was no significant differences in fasting IRG levels among controls (29.7 +/- 6.1 pmol/l) and pathological glucose tolerance (31.2 +/- 4.6 pmol/l). In addition, absolute IRG levels and the IRG concentration pattern during glucose infusion were comparable in all groups confirming no alpha-cell resistance to glucose suppression in obesity, irrespective of normal or impaired carbohydrate tolerance. The molar IRI-IRG ratio was significantly increased during glucose infusion in all obese groups reflecting a relative anabolic state. There were no correlations between IRG secretion and relative body weight, glucose tolerance or insulin response to glucose.

Adult↗
PubMed1981

Secretion and biosynthesis of (pro)insulin by pancreatic islets isolated from fetuses of normal and diabetic women.

Insulin secretion, biosynthesis and content of isolated pancreatic islets prepared for fetuses of nondiabetic or insulin-dependent diabetic women were investigated in vitro. Glucose failed to stimulate the hormone release during an incubation period of 60 min in islets of fetuses from non-diabetic women. Prolongation of the glucose exposure or the addition of theophylline resulted in a significantly enhanced insulin release. The islets isolated from fetuses of insulin-dependent mothers are glucose-sensitive with respect to hormone release and biosynthesis. The results demonstrated that the human fetal B-cell is glucose-sensitive after glucose exposure. The differences between the islets of fetuses of nondiabetic and diabetic women are discussed as a response to the fetal plasma glucose levels.

Diabetes Mellitus↗
PubMed1981

[Urological diseases causing renal hypertension (author's transl)].

Based on experimental and clinical findings the publication demonstrates the pathogenesis of renal hypertension. The diagnostic and prognostic value of split renal function test and a split estimation of plasma renin activity is pointed out for the surgical management of renal hypertension. New urosurgical methods for the correction of renovascular diseases are described.

Humans↗
PubMed1981

Changes of early insulin responses to glucose in obese subjects with normal and impaired carbohydrate tolerance.

We have studied changes in the sensitivity of the early insulin response to glucose by means of an intravenous pulse-stimulation of 1.0 g, 2.5 g and 5.0 glucose at intervals of 30 min in 24 non-obese healthy controls without a family history of diabetes and in obese subjects with normal (n = 7) and pathological carbohydrate tolerance (n = 23). All subjects were characterized regarding carbohydrate tolerance (CHT) by using a 2 h-glucose infusion test (GIT; 12 mg/kg/min), primed by an initial injection of 0.33 g/kg glucose. Compared with controls the early insulin response (delta IRI-area 0-5 min) during GIT was slightly increased in obesity with normal CHT and it was significantly reduced in obesity with pathological CHT. With regard to the late insulin response phase (delta IRI-area 30-120 min) both obese groups were characterized by a significant hyperinsulinemia. During staircase glucose stimulation a dose-dependent significant increase of the maximal IRI-response was observed in controls whereas this strong relationship was lacking in the two obese groups. The dose-response curve in obesity with normal CHT was displaced toward the left of the control curve whereas a right shift was found in obesity with pathological CHT. There was a significant correlation between early insulin response during GIT and maximal insulin response revealed by staircase glucose stimulation in obese subjects with pathological CHT. No close relationship of this type could be detected in the other groups so far studied. Our findings suggest an increased sensitivity of the beta-cells to glucose in the hyperinsulinemia stages of obesity with normal CHT. In contrast to this, a reduced sensitivity of the early insulin response to glucose is suggested in obesity with pathological CHT. A staircase glucose stimulation seems to be a useful tool in studying the early insulin response to glucose.

Blood Glucose↗