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UCL University College London Eprints (343,428 recursos)
UCL Eprints collects the work of UCL researchers and makes it freely available over the web, helping the worldwide scholarly community to discover UCL research. Institutional repositories like UCL Eprints complement the traditional academic publishing and scholarly communications processes. They raise the visibility of research and help to maximise its impact. UCL researchers are encouraged to deposit a copy of each journal article, conference paper, working paper, and any other research output, in the UCL Eprints at the earliest opportunity, ensuring that their research reaches as wide an audience as possible.

Mostrando recursos 161 - 180 de 343,367

161. Oblique water entry of a wedge into waves with gravity effect - Sun, SY; Sun, SL; Wu, GX

162. Management of respiratory diseases - Enright, S; Schreuder, FM

163. Characteristics of the flank magnetopause: Cluster observations - Haaland, S; Reistad, J; Tenfjord, P; Gjerloev, J; Maes, L; DeKeyser, J; Maggiolo, R; Anekallu, C; Dorville, N

164. Evolution and spontaneous regression of photoreceptor disruption secondary to posterior vitreous detachment: optical coherence tomography features. - Benson, SE; Sagoo, MS; Charteris, DG

165. Increasing uncoupling protein-2 in pancreatic beta cells does not alter glucose-induced insulin secretion but decreases production of reactive oxygen species. - Produit-Zengaffinen, N; Davis-Lameloise, N; Perreten, H; Bécard, D; Gjinovci, A; Keller, PA; Wollheim, CB; Herrera, P; Muzzin, P; Assimacopoulos-Jeannet, F
Levels of uncoupling protein-2 (UCP2) are regulated in the pancreatic beta cells and an increase in the protein level has been associated with mitochondrial uncoupling and alteration in glucose-stimulated insulin secretion. However, it is not clear whether an increase in uncoupling protein-2 per se induces mitochondrial uncoupling and affects ATP generation and insulin secretion.

166. Characterization of two distinct liver progenitor cell subpopulations of hematopoietic and hepatic origins. - Corcelle, V; Stieger, B; Gjinovci, A; Wollheim, CB; Gauthier, BR
Despite extensive studies, the hematopoietic versus hepatic origin of liver progenitor oval cells remains controversial. The aim of this study was to determine the origin of such cells after liver injury and to establish an oval cell line. Rat liver injury was induced by subcutaneous insertion of 2-AAF pellets for 7 days with subsequent injection of CCl(4). Livers were removed 9 to 13 days post-CCl(4) treatment. Immunohistochemistry was performed using anti-c-kit, OV6, Thy1, CK19, AFP, vWF and Rab3b. Isolated non-parenchymal cells were grown on mouse embryonic fibroblast, and their gene expression profile was characterized by RT-PCR. We identified a subpopulation...

167. Beta-cell-targeted expression of a dominant-negative hepatocyte nuclear factor-1 alpha induces a maturity-onset diabetes of the young (MODY)3-like phenotype in transgenic mice. - Hagenfeldt-Johansson, KA; Herrera, PL; Wang, H; Gjinovci, A; Ishihara, H; Wollheim, CB
Mutations in the transcription factor hepatocyte nuclear factor-1 alpha (HNF-1 alpha) cause maturity-onset diabetes of the young 3, a severe form of diabetes characterized by pancreatic beta-cell dysfunction. We have used targeted expression of a dominant-negative mutant of HNF-1 alpha to specifically suppress HNF-1 alpha function in beta-cells of transgenic mice. We show that males expressing the mutant protein became overtly diabetic within 6 wk of age, whereas females displayed glucose intolerance. Transgenic males exhibited impaired glucose-stimulated insulin secretion, detected both in vivo and in the perfused pancreas. Pancreatic insulin content was markedly decreased in diabetic animals, whereas the glucagon...

168. Activation of protein kinase B/cAkt in hepatocytes is sufficient for the induction of expression of the gene encoding glucokinase. - Iynedjian, PB; Roth, RA; Fleischmann, M; Gjinovci, A
Inhibitors of signalling pathways were used to dissect the mechanism of insulin action on expression of the gene encoding glucokinase in cultured rat hepatocytes. Wortmannin and LY 294002 completely prevented the insulin-induced increase in glucokinase mRNA seen in unhibited cells, indicating that the phosphoinositide 3-kinase module has a key role. A ligand inducible protein kinase B (PKB, also termed cAkt) fusion protein was expressed by using adenoviral transduction of hepatocytes in primary culture. The PKB activity of this protein was shown to be activated in transduced hepatocytes within 30 min of the addition of 4-hydroxytamoxifen and to stay high for...

169. Junctional communication of pancreatic beta cells contributes to the control of insulin secretion and glucose tolerance. - Charollais, A; Gjinovci, A; Huarte, J; Bauquis, J; Nadal, A; Martín, F; Andreu, E; Sánchez-Andrés, JV; Calabrese, A; Bosco, D; Soria, B; Wollheim, CB; Herrera, PL; Meda, P
Proper insulin secretion requires the coordinated functioning of the numerous beta cells that form pancreatic islets. This coordination depends on a network of communication mechanisms whereby beta cells interact with extracellular signals and adjacent cells via connexin channels. To assess whether connexin-dependent communication plays a role in vivo, we have developed transgenic mice in which connexin 32 (Cx32), one of the vertebrate connexins found in the pancreas, is expressed in beta cells. We show that the altered beta-cell coupling that results from this expression causes reduced insulin secretion in response to physiologically relevant concentrations of glucose and abnormal tolerance to...

170. Liver-specific enhancer of the glucokinase gene. - Iynedjian, PB; Marie, S; Wang, H; Gjinovci, A; Nazaryan, K
Glucokinase gene regions that are important for liver specific expression of the enzyme have been functionally identified using transient transfection of rat hepatocytes. Maximal luciferase activity was elicited by a reporter plasmid with 3.4 kilobase pairs of genomic DNA flanking the liver glucokinase promoter. Deletion of a gene fragment between -1000 and -600 with respect to the start of transcription resulted in a 60% decrease in luciferase activity. Further reduction, close to background level, occurred upon deletion of a 90-base pair sequence between -123 and -34. Reporter plasmids with the liver glucokinase promoter and any length of flanking sequence were...

171. Short-term insulin-induced glycogen formation in primary hepatocytes as a screening bioassay for insulin action. - Vu, L; Pralong, WF; Cerini, F; Gjinovci, A; Stöcklin, R; Rose, K; Offord, RE; Kippen, AD
We describe a novel bioassay to measure specific insulin-like activity in primary cultures of rat hepatocytes by determination of [3H]glycogen from d-[6-3H]glucose. The dose-response curve of insulin in this assay exhibited an EC50 of 0.42 (+/-0.04) nM, which is comparable to the dissociation constant of insulin from its receptor in hepatocytes. We used this assay to examine possible residual insulin-like activity of the four major fragments formed upon insulin degradation by insulin protease. Fragments A1-13B1-9, A1-14B1-9,and A14-21B14-30 showed no measurable activity. Although preparations of fragment A14-21B10-30 displayed dose-dependent agonist activity with an EC50 of 380 (+/-40) nM, we conclude that...

172. Glucokinase and cytosolic phosphoenolpyruvate carboxykinase (GTP) in the human liver. Regulation of gene expression in cultured hepatocytes. - Iynedjian, PB; Marie, S; Gjinovci, A; Genin, B; Deng, SP; Buhler, L; Morel, P; Mentha, G
Glucokinase and phosphoenolpyruvate carboxykinase are key enzymes of glucose metabolism in the rat liver. The former is considered to be instrumental in regulating glucose hepatic release/uptake according to the glycaemia level, and cytosolic phosphoenolpyruvate carboxykinase is a major flux-generating enzyme for gluconeogenesis. The level of expression of both enzymes and the regulation of their mRNAs in the human liver cell were investigated. Surgical biopsies of liver from patients undergoing partial hepatectomies and parenchymal hepatocytes derived from the biopsies were used to assay glucokinase, hexokinase and phosphoenolpyruvate carboxykinase activities. Hepatocytes were placed in culture and the actions of insulin, glucagon and...

173. In vivo phosphorylation of the Na,K-ATPase alpha subunit in sciatic nerves of control and diabetic rats: effects of protein kinase modulators. - Borghini, I; Geering, K; Gjinovci, A; Wollheim, CB; Pralong, WF
The phosphorylation state of the Na,K-ATPase alpha subunit has been examined in 32P-labeled sciatic nerves of control and streptozotocin-treated diabetic rats. Intact nerves were challenged with protein kinase (PK) modulators and alpha-subunit 32P labeling was analyzed after immunoprecipitation. In control nerves, the PKC activator phorbol 12-myristate 13-acetate (PMA) had little effect on alpha-subunit 32P labeling. In contrast, staurosporine, a PKC inhibitor, and extracellular calcium omission decreased it. In Ca(2+)-free conditions, PMA restored the labeling to basal levels. The cAMP-raising agent forskolin reduced the 32P labeling of the alpha subunit. The results suggest that nerve Na,K-ATPase is tonically phosphorylated by PKC...

174. Alpha, beta I, beta II, delta, and epsilon protein kinase C isoforms and compound activity in the sciatic nerve of normal and diabetic rats. - Borghini, I; Ania-Lahuerta, A; Regazzi, R; Ferrari, G; Gjinovci, A; Wollheim, CB; Pralong, WF
Defective protein kinase C (PKC) has been implicated in impaired Na+,K(+)-ATPase activity in the sciatic nerve of streptozotocin-induced diabetic rats. In the present study, alpha, beta I, beta II, gamma, delta, and epsilon isoform-specific antibodies were used in parallel to the measurement of compound PKC activity for the characterization of PKC distribution and isoform expression in sciatic nerves of normal and diabetic rats. To distinguish isoform expression between the axonal and glial compartments, PKC isoforms were evaluated in nerves subjected to Wallerian degeneration and in a pure primary Schwann cell culture. alpha, beta I, beta II, delta, and epsilon but...

175. Glucagon-like peptide-I-(7-37) suppresses hyperglycemia in rats. - Hendrick, GK; Gjinovci, A; Baxter, LA; Mojsov, S; Wollheim, CB; Habener, JF; Weir, GC
Glucagon-like peptide-(GLP) I-(7-37) is an endogenous hormone that has recently been demonstrated to be a potent insulin secretagogue. In these studies, GLP was administered during oral and intravenous (IV) glucose tolerance tests (OGTT and IVGTT, respectively) to determine whether this peptide could enhance postprandial insulin levels and thus reduce glycemic excursions. Surprisingly, during OGTT, GLP administration did not augment insulin secretion; however, GLP administration resulted in significantly lower glycemic excursions. In fasted rats, glycemic excursions were significantly reduced 10 and 20 minutes after receiving GLP (P < .001). Fed rats that received GLP had virtually no initial increase in plasma...

176. Cyclic adenosine monophosphate prevents the glucocorticoid-mediated inhibition of insulin gene expression in rodent islet cells. - Philippe, J; Giordano, E; Gjinovci, A; Meda, P
Dexamethasone negatively regulates insulin gene expression in HIT-15 cells. In vivo, however, an excess of glucocorticoids results in an increase in insulin biosynthesis and peripheral hyperinsulinemia. To resolve this contradiction, we have studied the effects of dexamethasone in primary rat islet cells. We show here that dexamethasone decreases insulin mRNA levels in single islet cells, as in HIT-15 cells, but does not affect these levels in reaggregated islet cells and increases them in intact islets of Langerhans. Because cAMP is an important regulator of insulin gene expression and intracellular cAMP content may be decreased in single beta cells, we investigated...

177. Unimpaired effect of insulin on glucokinase gene expression in hepatocytes challenged with amylin. - Nouspikel, T; Gjinovci, A; Li, S; Iynedjian, PB
Amylin appears to interfere with the action of insulin in muscle and possibly in liver. We have attempted to detect a direct antagonism between amylin and insulin in cultured rat hepatocytes. The stimulation of glucokinase gene expression was used as a marker of insulin action. Amylin proved ineffective in suppressing subsequent accumulation of glucokinase mRNA in response to maximal or submaximal doses of insulin. When applied to cells already induced by prior incubation with insulin alone, amylin failed to reverse induction, in contrast to the effectiveness of glucagon under the same conditions. Thus, amylin is not a physiological antagonist of...

178. Inverse relationship between glucose metabolism and glucose-induced insulin secretion in rat insulinoma cells. - Trautmann, ME; Blondel, B; Gjinovci, A; Wollheim, CB
Slowly growing X-ray-induced rat insulinomas and derived cell lines have been used as a model system for glucose-induced insulin release. During perfusions of tumors transplanted under the kidney capsule, the carbohydrates glucose and D-glyceraldehyde increased insulin secretion. These stimuli and the amino acids leucine and alanine also provoked insulin release in freshly isolated tumor cells. Under these conditions, glucose utilization had a Km of 4.6 mM and maximal velocity of 0.9 nmol/min/10(6) cells. A continuous cell line was established from such a preparation. In culture, glucose-induced insulin secretion was no longer detectable while responses to D-glyceraldehyde and amino acids were...

179. Stimulation by insulin of glucokinase gene transcription in liver of diabetic rats. - Iynedjian, PB; Gjinovci, A; Renold, AE
The purpose of this work was to investigate the molecular mechanism responsible for the induction of hepatic glucokinase in diabetic rats acutely treated with insulin. Experimental diabetes was provoked by injection of streptozotocin 8-10 days before the experiments. Regular insulin was given by three intraperitoneal injections at 8-h intervals, and the time course of glucokinase induction was followed over a time period of 24 h. The amount of glucokinase in liver was estimated by Western blotting of total cytosol protein with affinity-purified antibodies, as well as by conventional enzyme activity assay. Both measurements showed that glucokinase was reduced by more...

180. Direct stimulation of enzyme secretion from rat exocrine pancreas by neurotensin and its naturally occurring fragments. - Trimble, ER; Shaw, C; Bruzzone, R; Gjinovci, A; Buchanan, KD
Neurotensin stimulates amylase release from dispersed pancreatic acini at concentrations as low as 10(-15) M. The naturally occurring fragments of neurotensin (NT), NT 1-8 and NT 1-11, also stimulate amylase secretion at concentrations that occur in peripheral plasma (10(-11) M). The analogue D-Phe11 neurotensin was as potent as neurotensin itself with respect to stimulation of amylase secretion. Basal plasma neurotensin levels were approximately 10 pmol/L, a concentration that stimulates the exocrine pancreas in vitro. Increases in plasma neurotensin levels induced by infusion of neurotensin caused greater increases in secretion of pancreatic amylase than did similar changes of neurotensin concentration in...

 

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