863 research outputs found
Dr. Louis Zucker, Alan Cline, Bernard Axelrad, Anatole Zucker, Rabbi Gordon, Nell Grossman, Miriam Rose, Helen Zinik, Eloise Bamberger, Nadine Rosenblum, Evelyn White, Dionne Drucker, Lynn Cohne
Black and white photograph of Dr. Louis Zucker, Alan Cline, Bernard Axelrad, Anatole Zucker, Rabbi Gordon, Nell Grossman, Miriam Rose, Helen Zinik, Eloise Bamberger, Nadine Rosenblum, Evelyn White, Dionne Drucker, and Lynn Cohne
Gastrin release in obese Zucker rats
In this study, gastrin release in the obese Zucker rat was investigated by in vivo and in vitro experiments. Obese rats exhibited normal plasma gastrin levels at 3 weeks (preobese), were moderately hypergastrinemic at 3 months and severely hypergastrinemic at 5 months, compared to lean littermates. Following oral peptone, plasma gastrin levels doubled in both lean and obese rats. Basal and vagally stimulated gastrin release from perfused stomachs was greater in obese compared to lean rats and atropine had no effect on basal gastrin release in either group. Basal somatostatin release from the perfused stomach was found not to differ in both groups of animals. Morphological studies revealed an increase in the number of gastrin-containing G-cells in adult obese rats compared to lean littermates, but not in 3-week-old pups compared to lean littermates, indicating a strong correlation between cell number and plasma gastrin levels. These data indicate that the obese Zucker rat exhibits fasting hypergastrinemia in vivo, a condition which appears after weaning and increases in severity with age. Gastrin hypersecretion persists from the vascularly perfused stomach preparation. The basal hypergastrinemia of the obese Zucker rat is independent of a hyperactive postganglionic cholinergic drive but is associated with and probably causally related to an increase in antral G-cell numbers.LR: 20061115; PUBM: Print; JID: 8100479; 0 (Gastrins); 51-55-8 (Atropine); 51110-01-1 (Somatostatin); ppublishSource type: Electronic(1
Salzinduzierte kardiale Umbauvorgänge beim metabolischen Syndrom - Einfluss einer Therapie mit Eplerenon
Hintergrund: Als Tiermodell des metabolischen Syndroms entwickeln Zucker Diabetic Fatty (ZDF)- Ratten spontan einen hyporeninämischen Hyperaldosteronismus und einen Diabetes mellitus Typ 2. Erhöhte systemische Aldosteronspiegel induzieren rezeptorvermittelte kardiale Umbauvorgänge (cardiac remodelling) und Fibrosierung. In der vorliegenden Studie untersuchten wir, ob im Tiermodell der systolische Blutdruck unter Hochsalzdiät ansteigt, und welchen Einfluss die Salzbelastung auf kardiale Umbauvorgänge hat. Zusätzlich untersuchten wir, ob die kardialen Endorganschäden durch eine Behandlung mit dem Aldosteron-Rezeptor-Antagonisten Eplerenon positiv beeinflussbar sind.
Methoden: Nach Einsetzen eines manifesten Diabetes mellitus Typ2 wurden ZDF-Ratten mit einer Normalsalz- (0,28%) oder Hochsalzdiät (5,5%) ernährt. Die Tiere der Hochsalzgruppe erhielten Eplerenon (100mg/kg/d) (ZDF+S+E), Hydralazin (25mg/kg/d) (ZDF+S+H) oder keine medikamentöse Behandlung (ZDF+S), die Tiere der Normalsalzgruppe Eplerenon (ZDF+E) oder keine medikamentöse Behandlung (ZDF). Als Kontrolle wurden normoglykämische Zucker Lean Ratten, in zwei Gruppen randomisiert: Hochsalz- (ZDL+S) oder Normalsalzdiät (ZDL). Der systolische Blutdruck wurde mit der Tailcuff-Methode gemessen. Die kardiale Hypertrophie wurde durch Bestimmung der echokardiographischen Septumdicke, des linksventrikulären Herzgewichts, sowie durch histologische Untersuchungen des linksventrikulären Fibrosegrades und des Kardiomyozytendurchmessers quantifiziert. Zusätzlich ermittelten wir die Konzentration der natriuretischen Peptide ANP und BNP im linken Ventrikel sowie deren Genexpression auf mRNA-Ebene.
Ergebnisse: Sowohl ZDL- als auch ZDF-Ratten zeigten einen signifikanten Anstieg des systolischen Blutdrucks unter Hochsalzdiät. Der Anstieg bei ZDF-Ratten war deutlich ausgeprägter als bei ZDL-Tieren. Eplerenon und Hydralazin konnten den Blutdruckanstieg in gleichem Maße verhindern. Eine Hochsalzdiät führte bei ZDF-Ratten, nicht aber bei ZDL-Ratten, zu einer signifikanten linksventrikulären Hypertrophie. Diese Veränderungen konnten durch eine Therapie mit Eplerenon tendenziell (keine Signifikanz) besser beeinflusst werden als unter einer Behandlung mit Hydralazin. ZDF Ratten entwickelten unter Hochsalzdiät eine linksventrikuläre Fibrosierung und Kardiomyozytenhypertrophie. Beides konnte durch eine medikamentöse Therapie mit Eplerenon oder Hydralazin nur geringfügig verbessert werden. Die ANP- und BNP-Proteinkonzentrationen waren bei diabetischen Tieren höher als bei nichtdiabetischen und konnten durch medikamentöse Behandlung nicht beeinflusst werden.
Fazit: Bei gleichzeitigem Vorliegen von Hyperaldosteronismus und nutritiver Salzbelastung entwickeln ZDF-Ratten einen überproportionalen Anstieg des systolischen Blutdrucks und eine kardiale Hypertrophie. Eplerenon und Hydralazin können den Blutdruckanstieg in gleichem Ausmaß verhindern. Eine Therapie mit Eplerenon kann salzinduzierte linksventrikuläre Veränderungen besser (positiv) beeinflussen als Hydralazin. Dabei könnte Eplerenon möglicherweise eine, durch die direkte Blockade kardialer Aldosteronrezeptoren vermittelte (über die bloße systemische Blutdrucksenkung hinausgehende) günstige Wirkung auf die kardiale Endorganschädigung haben
Movement of Star Scientists and Engineers and High-Tech Firm Entry
This paper analyzes the effects of top nanoscale scientists on industry entry in the comparative context of 5 major areas of science and technology, extending the concept of star scientist to all areas of science and technology. The results for nanotechnology are replicated using the comprehensive list of firms from NanoBank.org that provide an alternative industry entry measure not available for other high-tech fields. We follow careers 1981-2004 for 5,401 stars as identified in ISIHighlyCited.comSM, using their publication history to locate them each year. The number of stars in a U.S. region or in one of the top-25 science and technology countries generally has a consistently significant and quantitatively large positive effect on the probability of firm entry in the same area of science and technology. Other measures of academic knowledge stocks have weaker and less consistent effects. Thus the stars themselves rather than their potentially disembodied discoveries play a key role in the formation or transformation of high-tech industries. We identify separate economic geography effects in poisson regressions for the 179 BEA-defined U.S. regions, but not for the 25 countries analysis. Stars become more concentrated over time, moving from areas with relatively few peers to those with many in their discipline. A counter-flow operating on the U.S. versus the other 24 countries is the tendency of foreign-born American stars to return to their homeland when it develops sufficient strength in their area of science and technology. In contrast high impact articles and university articles and patents all tend to diffuse, becoming more equally distributed over time.
Gastric inhibitory polypeptide (GIP) and insulin release in the obese Zucker rat
The involvement of the gut hormone GIP (gastric inhibitory polypeptide, glucose-dependent insulinotropic polypeptide) in the hyperinsulinemia of the adult obese Zucker rat was investigated. Glucose, insulin, and GIP responses to oral glucose were compared in lean and obese rats. The sensitivity of the isolated, perfused pancreas to glucose and GIP was studied in basal and hyperglycemic conditions in lean and obese rats. Immunocytochemical studies of the gut and pancreas were also carried out. The glucose and GIP responses to oral glucose were similar in lean and obese rats, but obese animals were hyperinsulinemic compared with lean controls under fasting conditions and after oral glucose. The isolated, perfused pancreas of obese Zucker rats had an elevated insulin response to 300 mg/dl glucose. GIP increased the insulin response to 300 mg/dl glucose threefold in both lean and obese rats. At basal glucose levels (80 mg/dl), GIP augmented insulin release in obese but not in lean rats. Immunocytochemical studies demonstrated the presence of enlarged islets in obese rats due to an increase in the B-cell mass. A-, D-, and PP-cells appeared normal. Obese and lean rats had similar numbers of GIP-containing cells in the gut. This study suggests that GIP may contribute to the fasting hyperinsulinemia characteristic of adult obese Zucker rats. GIP infusion to achieve levels equivalent to those seen in the basal state are capable of stimulating insulin release in the absence of hyperglycemia in the obese rat, which suggests an impairment of the regulatory mechanisms controlling the glucose-dependent insulinotropic action of GIP in these animals.LR: 20061115; PUBM: Print; JID: 0372763; 0 (Gastrointestinal Hormones); 11061-68-0 (Insulin); 59392-49-3 (Gastric Inhibitory Polypeptide); ppublishSource type: Electronic(1
sj-docx-1-jbr-10.1177_07487304221128652 – Supplemental material for Modified Wavelet Analyses Permit Quantification of Dynamic Interactions Between Ultradian and Circadian Rhythms
Supplemental material, sj-docx-1-jbr-10.1177_07487304221128652 for Modified Wavelet Analyses Permit Quantification of Dynamic Interactions Between Ultradian and Circadian Rhythms by Jonathan P. Riggle, Leslie M. Kay, Kenneth G. Onishi, David T. Falk, Benjamin L. Smarr, Irving Zucker and Brian J. Prendergast in Journal of Biological Rhythms</p
sj-docx-2-jbr-10.1177_07487304221128652 – Supplemental material for Modified Wavelet Analyses Permit Quantification of Dynamic Interactions Between Ultradian and Circadian Rhythms
Supplemental material, sj-docx-2-jbr-10.1177_07487304221128652 for Modified Wavelet Analyses Permit Quantification of Dynamic Interactions Between Ultradian and Circadian Rhythms by Jonathan P. Riggle, Leslie M. Kay, Kenneth G. Onishi, David T. Falk, Benjamin L. Smarr, Irving Zucker and Brian J. Prendergast in Journal of Biological Rhythms</p
Cut-elimination, substitution and normalisation
Date of Acceptance: 01/2015We present a proof (of the main parts of which there is a formal version, checked with the Isabelle proof assistant) that, for a G3-style calculus covering all of intuitionistic zero-order logic, with an associated term calculus, and with a particular strongly normalising and confluent system of cut-reduction rules, every reduction step has, as its natural deduction translation, a sequence of zero or more reduction steps (detour reductions, permutation reductions or simplifications). This complements and (we believe) clarifies earlier work by (e.g.) Zucker and Pottinger on a question raised in 1971 by Kreisel.Peer reviewe
Glucokinase activity in isolated islets from obese fa/fa Zucker rats
Glucokinase (EC 2.7.1.2) activity of B-cells was measured in extracted pancreatic islets isolated from lean and obese fa/fa Zucker rats and maintained in primary culture overnight. Formation of [14C]glucose phosphoric esters from D-[U-14C]glucose was measured in the presence of unlabelled glucose from 0.05 to 0.50 mM for hexokinase (EC 2.7.1.1) activity, and 8.0-16.0 mM unlabelled glucose for glucokinase activity. Eadie-Hofstee analysis revealed that hexokinase kinetic parameters (Vmax and Km) for [14C]glucose phosphoric ester formation were similar in lean- and fa/fa-rat islets. For glucokinase, there was no difference in Vmax. between phenotypes. A non-significant tendency to increased sensitivity to glucose was noted in the fa/fa-rat islets (P = 0.13). In lean-rat islets, the glucokinase inhibitor mannoheptulose (3 mM) decreased Vmax. by 80% and increased the apparent Km from 3.3 +/- 0.7 mM to 12.2 +/- 2.0 mM (P < 0.05). There was no difference in Km or Vmax. in mannoheptulose-treated versus control islets from fa/fa rats. This lack of effect was consistent with reported effects of mannoheptulose on insulin secretion from fa/fa-rat islets [Chan, MacPhail and Mitton (1993) Can. J. Physiol. Pharmacol. 71, 34-39]. The data from glucose and mannoheptulose experiments support the hypothesis that glucokinase function is altered in fa/fa Zucker rats and may contribute to fasting hyperinsulinaemia in vivo in these animals.LR: 20061115; PUBM: Print; JID: 2984726R; 11061-68-0 (Insulin); 654-29-5 (Mannoheptulose); EC 2.7.1.1 (Hexokinase); EC 2.7.1.2 (Glucokinase); ppublishSource type: Electronic(1
Ultrastructural and secretory heterogeneity of fa/fa (Zucker) rat islets
Many previous studies of obese rodents documented biochemical changes in pancreatic islets that contribute to hyperinsulinemia in vivo. Those studies used heterogeneous populations of islets, although the size of islets from obese rats ranges from 500 microm. Here, functional and morphological changes in size-sorted ( 250 microm diameter) islets from obese Zucker (fa/fa) rats were correlated. Ultrastructural examination revealed that > 250 microm cultured islets had an increased number of immature secretory granules in the beta cells. The number of degranulated beta cells in > 250 and 250 microm, 250 microm islets compared with small islets. Studies of individual beta cells by reverse hemolytic plaque assay revealed 3-fold more cells from > 250 microm islets were stimulated by 1.4 mmol.l(-1) glucose than cells from < 125 microm islets. We conclude that functional defects in mixed size populations of islets from fa/fa rats are mainly due to alterations in the large islets, whereas smaller islets have relatively normal function. Exposure to high glucose exacerbates morphological and functional differences of large islets, which could have important implications in the transition to noninsulin-dependent diabetes when beta cell insulin production is unable to compensate for hyperglycemia.LR: 20061115; PUBM: Print; JID: 7500844; 11061-68-0 (Insulin); 50-99-7 (Glucose); 654-29-5 (Mannoheptulose); 7782-44-7 (Oxygen); ppublishSource type: Electronic(1
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