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Biomedical subjects

G Richter

Publications and source records attributed to G Richter.

At least 163 records · Page 9Linked to original sources
PubMed1990

Dexamethasone pretreatment of rat insulinoma cells decreases binding of glucagon-like peptide-1(7-36)amide.

The effect of dexamethasone on binding of glucagon-like peptide-1(7-36)amide (GLP-1(7-36)amide) to rat insulinoma-derived cells (RINm5F) was investigated. Preincubation of RINm5F cells with dexamethasone (100 nmol/l) for 24 h resulted in a decrease of GLP-1(7-36)amide binding to 55.0 +/- 8.16% (mean +/- S.E.M.), incubation for 48 h to 39.1 +/- 1.76%, and for 72 h to 15.5 +/- 4.35% of maximal binding. The GLP-1(7-36)amide-induced stimulation of cyclic AMP (cAMP) production was significantly decreased to 61.03 +/- 7.4% of maximum production in cells pretreated with dexamethasone (100 nmol/l) for 48 h. The decreased binding was due to a reduction of the receptor number while the receptor affinity remained unchanged. These inhibitory effects on binding and cAMP formation induced by dexamethasone were completely abolished when the antiglucocorticoid RU 38486 (100 nmol/l) was added during preincubation with dexamethasone. RU 38486 alone had no effects. Our data suggest that the biological action of GLP-1(7-36)amide at the B-cell may be modified by glucocorticoids.

Animals↗
PubMed1990

[Enteral feeding in oncology].

Nutrition therapy is accepted to represent an important part of therapeutic strategy in cancer patients. In correlation to general clinical state, nutritional condition and anti-cancer therapy, nutrition has to be planned according to a stepwise concept. Under certain circumstances, enteral tube feeding is indicated. This procedure is affected by tumor lesions, digestion, resorption and tumor related metabolic disorders, and side effects of particulate anti-cancer therapy. In tumor patients, elemental (chemically defined) diets are predominant. Polymeric diets, however, occasionally represent another possible nutritional tool.

Cachexia↗
PubMed1990

[The lymphocyte transformation test in sarcoidosis].

A suppressive effect of the sarcoidosis serum on the mitogenic stimulation of lymphocytes could be confirmed statistically (p less than 1%). But there remained a lot of deviating results in distinct individual cases which could not be explained by subdividing the material in regard to different clinical points of view. The practical utility of the LTT as a diagnostic tool in sarcoidosis is therefore very limited. The partly missing suppression or even a stimulation compared to the culture with pooled AB-sera can be interpreted by the interesting phenomenon of a concentration dependent counter-current action of the sarcoidosis serum: On suboptimal PHA-dosage undiluted serum caused a significant reduction of the transformation rate of donor lymphocytes, 1:10 diluted serum was inefficient and in a 1:100 concentration it induced a stimulation (p less than 5%).

Adult↗
PubMed1990

Allergologic aspects of skin-cleansing products.

A review of the international literature and our patch test-results in 4637 patients with contact dermatitis and in 140 persons with a proven formaldehyde-allergy revealed: Skin-cleansing products may contain a lot of ingredients which are known as allergens in single cases or-more accidentally - in limited epidemic outbreaks of contact dermatitis, but compared with the enormous amount of their worldwide application the incidence of allergic side-effects is low. They are much more important (in 14% of our patients with contact dermatitis) as an irritant co-factor for sensitization due to other allergens.

Dermatitis, Contact↗
PubMed1990

[Hemodynamic consequences of portal decompression: which is the optimal shunt?].

Increased sinusoidal resistance in cirrhosis results in a decrease of the portal and a compensatory increase of the arterial blood supply to the liver. With increasing vascular resistance and development of extrahepatic collaterals stagnation and even reversion of the portal blood flow may occur. In the latter condition, the arterial blood leaves the liver through two routes: 1) through the sinusoids and the hepatic veins, and 2) through the portal vein. Experimental and clinical studies revealed that the arterio-portal pathway is metabolically inferior to the regular arterio-hepatic-venous pathway. This suggests a decrease in liver function with an increased incidence of hepatic encephalopathy (HE) in patients with reversed portal blood flow. Based on these findings, surgical shunts may be classified according to their effect on the arterial liver perfusion. The end-to-side shunt and the distal splenorenal shunt (DSRS) do not cause diversion of the arterial liver perfusion. In contrast, side-to-side shunts, with the portal vein available as an outflow tract, consistently lead to diversion of the arterial blood supply resulting in reversed portal blood flow. Thus, side-to-side shunts are supposed to have an increased incidence of HE due to decreased liver function. This hypothesis is supported by 7 controlled and randomized studies which reveal comparable results of end-to-side shunts and DSRS but significant disadvantages of side-to-side shunts compared to DSRS.

Hemodynamics↗
PubMed1989

Analysis of restriction fragment length polymorphism in lymphokine genes of normal and autoimmune mice.

Analysis of RFLP has been employed in lymphokine genes of autoimmune and normal mice. No polymorphism could be detected in the loci containing IL-2, IL-2 receptor, IL-5, and IFN-gamma in NZB, NZW, BxSB, and MRL/lpr mice when compared with normal mice. Allelic forms were identified in the IL-1 alpha gene of BALB/c and in the IL-4 gene of NZW. The frequency of the Bam HI RFLP in the TNF-alpha gene of NZW which has been proposed to be associated with the development of autoimmune disease in (NZB x NZW)F1 mice has been analyzed in a number of different inbred strains and in wild mice. Since the same allele is inherited in most autoimmune, healthy laboratory and wild mice the TNF-alpha gene does not seem to be one of the causal agents that contributes to the development of autoimmunity in (NZB x NZW)F1 mice.

Animals↗
PubMed1989

Internalization of glucagon-like peptide-1(7-36)amide in rat insulinoma cells.

Glucagon-like peptide-1(7-36)amide [GLP-1(7-36)amide] is supposed to be an important physiologic incretin. Recently, high affinity receptors for GLP-1(7-36)amide have been demonstrated on rat insulinoma-derived RINm5F cells. The present study examined the internalization and degradation of the GLP-1-receptor complex. Internalization of the peptide was time- and temperature-dependent. At 37 degrees C binding and internalization was rapid. At 60 min 35% of 125I-labeled GLP-1(7-36)amide was internalized. Incubation in the presence of increasing concentrations of non-labeled GLP-1(7-36)amide resulted in a decrease of internalization of 125I-labeled peptide indicating that this process is saturable. Incubation in the presence of 0.2 mM chloroquine, an inhibitor of intracellular hormone degradation, resulted in intracellular accumulation of 125I-GLP-1(7-36)amide. HPLC-supported analysis of cell content after internalization of 125I-GLP-1(7-36)amide during a 60-min incubation period at 37 degrees C revealed an elution profile showing two maxima of radioactivity: one represented intact labeled GLP-1(7-36)amide, the other an intracellular degradation product of the peptide. Chloroquine caused a 5-fold increase of the peak representing intact 125I-GLP-1(7-36)amide thus demonstrating inhibition of degradation of labelled peptide. Furthermore, a 4-fold increase of the other peak occurred possibly mirroring a delay of release of degradation products by chloroquine. It was excluded that chloroquine is able to interfere with GLP-1(7-36)amide-binding to its receptor.

Adenoma, Islet Cell↗
PubMed1989

Release of tryptophan and serotonin into the portal vein of the isolated perfused rat small intestine.

To investigate the release of serotonin from intestinal enterochromaffin cells, we used an in vitro technique which allows studies excluding overlapping influences from outside the gut. The entire small intestine of rats fed a standard or tryptophan-enriched (3% of total) diet was totally isolated by ligatures with the exception of the superior mesenteric artery and portal vein that supply and drain the intestine. Simultaneously to the vascular perfusion (Krebs-Ringer bicarbonate buffer, 0.4% human albumin, 5 mM glucose, 0.6 mM glutamine) the gut lumen was infused (buffer or 0.1 N HCL). Acidification of the gut lumen resulted in an increment of venously released tryptophan and serotonin. After feeding tryptophan-enriched food the release of tryptophan was increased. However, the total amount of released serotonin after tryptophan diet did not differ as compared to that after standard diet. Addition of a monoamino-oxidase inhibitor (pargyline) to the arterial perfusate enhanced the released amount of serotonin 3-fold in the portal venous effluent (at a concentration of 1 mM but not 0.1 mM). Recovery studies done by arterial infusions of serotonin (1 microM, 10 microM) and evaluation of the amounts venously released revealed a high loss of infused serotonin (40%-70%). Our data suggest gut-born serotonin to more likely play a paracrine role than a role as a classical hormone.

Animals↗
PubMed1989

Production of insulin-like growth factor binding proteins by small-cell lung cancer cell lines.

Conditioned serum-free media (CM) from small-cell lung cancer (SCLC) cell lines were examined for the presence of insulin-like growth-factor-binding proteins (IGF-BP). 6/9 SCLC cell lines secreted binding proteins with high affinity for IGFs. When [125I]IGF-I or [125I]IGF-II was incubated with the CMs, complexes of tracer with proteins could be demonstrated by gel filtration, by precipitation with polyethylenglycol, and after adsorption of unbound tracer with activated charcoal. Analysis of binding data according to the method of Scatchard resulted in linear plots for IGF-I and IGF-II. The dissociation constants were determined to be 0.106 nM for IGF-I and 0.209 nM for IGF-II binding. Cross-linking of [125I]IGF-I or [125I]IGF-II to the CMs followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) under nonreducing conditions revealed the presence of IGF-BPs with molecular masses in the range 24-32 kDa. The binding was competitively inhibited by addition of cold IGF-I and IGF-II but not by insulin. Northern blot hybridization with an IGF-BP cDNA probe encoding a low-molecular-weight IGF-BP from a human placenta cDNA library and Western blot analysis with a corresponding polyclonal antibody showed no expression of this gene. These data demonstrate that SCLC cell lines release IGF-BPs in culture supernatants, which differ from IGF-BPs detected in liver and placenta. These IGF-BPs might be important mediators in the autocrine/paracrine growth regulation of IGFs in SCLC.

Carcinoma, Small Cell↗
PubMed1989

Structure and evolution of mouse interleukin 6 gene.

Restriction fragment length polymorphism in the interleukin 6 gene of murine rodents extending phylogenetically from Mus musculus domesticus to the rat has been analyzed. Most species exhibit distinct restriction site patterns. In contrast, limited polymorphism was found in the tumor necrosis factor alpha gene indicating different selective pressure acting on both genes. The gene encoding interleukin 6 was isolated from a genomic library and the exon/intron organization was determined by restriction analysis and limited DNA sequence analysis. It consists of five exons which distribute over about seven kilobases, thus resembling in structure and organization the human counterpart. Furthermore, no restriction fragment length polymorphisms in the interleukin 6 gene of autoimmune strains NZB, NZW, MRL-lpr/lpr and BxSB could be detected for either EcoRI, BamHI or HindIII.

Animals↗
PubMed1989

[The vitamin A supply of laying hens including during rearing. 1. Testing of mixed feed with a varied vitamin A supplementation in chicks and young hens].

In seven experiments with 46,310 young animals from hatching to the 21st week the vitamin A supplement varied between 0 and 10,000 IU per kg mixed feed. Feed intake was significantly diminished in three out of seven experiments when chicken feed was given without vitamin A supplement. In the young chicken period 1,500 IU vitamin A supplement were sufficient for optimal body weight development, in the young hen period native carotene was sufficient. The variation of the body weight of the individual animals on the 126th day did not show any connection with vitamin A supply. The carotene content of the rations was sufficient to prevent deficiency symptoms. The livers and yolk sacs of one-day-old chickens on average contained 114 and 56 IU vitamin A/g substance when the parents had received mixed feed with 15,000 IU vitamin A/kg. There is a positive relation between the vitamin A supply of the young chickens and hens and the vitamin A content of the liver.

Animal Feed↗
PubMed1989

[The use of mixed feed with reduced content of vitamin A, E and nicotinic acid in the fattening of cairinas].

In three fattening experiments with 1344 male cairinas (Cairina moschata domestica L.) from hatching to the 77th day vitamin A supplement was reduced to 2500 IU/kg feed from hatching to the 21st day and to 1250 IU/kg feed from the 22nd to the 77th day. There was no supplementation of the feed with vitamin E or nicotinic acid. The reduction and elimination of the vitamin supplements on average did not have significant effects on fattening performance, feed intake, body weight, feed conversion and losses of animals in the starter and fattening periods. In the fattening period there was a tendency towards a higher intake and expenditure of feed in two experiments. Presumably the supplementation of 1250 IU/kg mixed feed is not always sufficient for an optimal fattening performance. In three production experiments with 33,850 cairinas no disadvantageous influence on fattening performance could be ascertained after a supplementation of 4,000 IU in the starter feed and 2,000 IU vitamin A in the fattening feed.

Animal Feed↗
PubMed1989

Interaction of glucagon-like peptide-1(7-36)amide and somatostatin-14 in RINm5F cells and in the perfused rat pancreas.

Glucagon-like peptide-1(7-36)amide [GLP-1(7-36)amide], a new important incretin candidate, binds to specific high-affinity receptors on rat insulinoma-derived beta-cells (RINm5F). In the present study, the effect of somatostatin-14 on the GLP-1(7-36)amide-induced insulin release and cAMP generation in this cell line was investigated. Somatostatin did not decrease basal insulin release of RINm5F cells. The GLP-1(7-36)amide-induced insulin release was decreased concentration dependently by somatostatin. Somatostatin, 1 microM reduced the maximally GLP-1(7-36)amide-stimulated (0.1 microM) insulin release to basal insulin levels. The GLP-1(7-36)amide-induced cAMP production was significantly decreased by somatostatin in a concentration-dependent manner. The GLP-1(7-36)amide concentration causing half-maximal cAMP production was 2.98 +/- 1.56 nM. Somatostatin left the EC50 unaltered but decreased the maximal GLP-1(7-36)amide effect for 32% in the presence of 1 nM somatostatin and for 50% at 1 microM. In additional experiments, the interaction of both hormones was evaluated in the perfused pancreas as a nontumor model. Somatostatin (1 nM, 1 microM) inhibited the glucose-induced (6.7 mM) and GLP-1(7-36)amide-potentiated (0.05, 0.5, and 5 nM) insulin release dose dependently. The biphasic pattern of insulin release remained preserved. The GLP-1(7-36)amide-induced insulin release is potently inhibited by somatostatin-14. This effect was demonstrated in different model systems for beta-cell function studies. The present data allow the conclusion that the somatostatin action upon GLP-1(7-36)amide effects is at least partly related to regulation of intracellular cyclic nucleotides.

Adenoma, Islet Cell↗
PubMed1989

Social relationships reflected by depressive inpatients.

In a study of 100 inpatients suffering from depressive symptoms, the influence of cognitive characteristics (negative automatic thoughts and dysfunctional attitudes) and of the severity of depression on the emotional reflections of social relationships were investigated at admission, discharge and 3 months follow-up. The reflections of strained relation and rejection in the family or partnership were significantly determined by negative cognitive patterns and severity of depression. The prognostic aspects of the assessed psychological characteristics and the psychotherapeutic implications of the results are discussed.

Adolescent↗
PubMed1989

Signal transmission after GLP-1(7-36)amide binding in RINm5F cells.

Glucagon-like peptide-1(7-36)amide [GLP-1(7-36)amide], probably representing an important incretin, binds to receptors on RINm5F cells resulting in an adenosine 3',5'-cyclic monophosphate increase. Guanine nucleotides (GTP, GTP-gamma-S, GDP-beta-S) decreased the binding of GLP-1(7-36)amide to receptors on RINm5F cell membranes. Further analysis revealed that GTP (10(-4) M) decreased the receptor affinity with an increase of the Kd from 2.5 +/- 0.99 x 10(-10) M to 9.43 +/- 2.16 x 10(-10) M. In cross-linking experiments the amount of labeled peptide linked to receptors was reduced in the presence of GTP (10(-4) M). Further studies investigated the involvement of membrane depolarization or changes in the cytosolic free calcium level in the intracellular signaling of GLP-1(7-36)amide-induced insulin secretion. In contrast to fuel and nonfuel secretagogues, GLP-1(7-36)amide did not cause a depolarization of the membrane potential. This was unaffected by various glucose concentrations (0-20 mM) or by previous cell depolarization by D-glyceraldehyde. Similarly, the cytosolic calcium concentration remained unchanged after addition of GLP-1(7-36)amide (10(-12)-10(-8) M). The effect of guanine nucleotides on binding of GLP-1(7-36)amide indicates that the action of the peptide is mediated by the adenylate cyclase system. GLP-1(7-36)amide binding neither changed the membrane potential nor altered the intracellular calcium concentration, making an involvement of the inositol 1,4,5-trisphosphate pathway or an activation of protein kinase C in the postreceptor signaling after GLP-1(7-36)amide binding unlikely.

Adenoma, Islet Cell↗