Biomedical subjects
Publications and source records attributed to N Trivedi.
We study the Hubbard model with parameters relevant to cuprates using variational Monte Carlo for projected d-wave states. For doping 0 0. The Drude weight D(low) and superfluid density are consistent with experiment and D(low) approximately Z.
The understanding of the interplay of electron correlations and randomness in solids is enhanced by demonstrating that particle-hole ( p-h) symmetry plays a crucial role in determining the effects of disorder on the transport and thermodynamic properties of the half-filled Hubbard Hamiltonian. We show that the low-temperature conductivity decreases with increasing disorder when p-h symmetry is preserved, and shows the opposite behavior, i.e., conductivity increases with increasing disorder, when p-h symmetry is broken. The Mott insulating gap is insensitive to weak disorder when there is p-h symmetry, whereas in its absence the gap diminishes with increasing disorder.
Glucose-induced insulin secretion from hyperglycemic 90% pancreatectomized rats is markedly impaired, possibly because of loss of beta cell differentiation. Association of these changes with beta cell hypertrophy, increased mRNA levels of the transcription factor c-Myc, and their complete normalization by phlorizin treatment suggested a link between chronic hyperglycemia, increased c-Myc expression, and altered beta cell function. In this study, we tested the effect of hyperglycemia on rat pancreatic islet c-Myc expression both in vivo and in vitro. Elevation of plasma glucose for 1-4 days (glucose infusion/clamp) was followed by parallel increases in islet mRNA levels (relative to TATA-binding protein) of c-Myc and two of its target genes, ornithine decarboxylase and lactate dehydrogenase A. Similar changes were observed in vitro upon stimulation of cultured islets or purified beta cells with 20 and 30 mmol.liter(-1) glucose for 18 h. These effects of high glucose were reproduced by high potassium-induced depolarization or dibutyryl-cAMP and were inhibited by agents decreasing cytosolic Ca(2+) or cAMP concentrations. In conclusion, the expression of the early response gene c-Myc in rat pancreatic beta cells is stimulated by high glucose in a Ca(2+)-dependent manner and by cAMP. c-Myc could therefore participate to the regulation of beta cell growth, apoptosis, and differentiation under physiological or pathophysiological conditions.
Using path integral Monte Carlo we simulate a 3D system of up to 1000 magnetic flux lines by mapping it onto interacting bosons in (2+1)D. With increasing temperatures we find first order melting from an ordered solid to an entangled liquid signaled by a finite entropy jump and sharp discontinuities of the defect density and the structure factor S(G). For a particular density of strong columnar pins the crystal is transformed into a Bose glass phase with patches of crystalline order disrupted by the trapped vortices at the pinning sites but with no overall positional or orientational order. This glassy phase melts into a defected entangled liquid through a continuous transition.
BACKGROUND: Encapsulation of islets has been widely investigated as a treatment for diabetes. The characteristics and dynamics of insulin secretion by encapsulated islets in response to glucose and other secretagogues are not well understood. METHODS: In our study, macroencapsulated syngeneic islets at 3-4 wk after transplantation were studied for insulin release in response to i.v. glucose (hyperglycemic clamps at 250 or 350 mg/dl plasma glucose), arginine (i.v. bolus, 100 mg/kg), glucagon-like peptide-1 (i.v. infusion for 20 min, 2.2 pmol/kg/min), and meal challenge. Syngeneic islets (6000 islets) were encapsulated in alginate macrobeads (2-3 mm diameter) with or without poly-L-lysine coating and transplanted into the peritoneal cavity of STZ-diabetic Lewis rats. Normal (nontransplanted) and diabetic Lewis rats transplanted with "naked" islets under the kidney capsule served as controls. RESULTS: Animals transplanted with macrobeads displayed subnormal insulin responses to glucose, arginine, and glucagon-like peptide-1 despite achieving normoglycemia faster than animals with renal subcapsular islet transplants. Plasma insulin responses to meal challenges were blunted in animals with macrobeads resulting in increased plasma glucose excursions. CONCLUSIONS: We conclude that, after transplantation into diabetic Lewis rats, macroencapsulated islets have significantly impaired insulin secretion despite achieving normal fed glycemic levels.
Brush border membrane vesicles (BBMVs) were prepared from the 2nd instar larvae of Helicoverpa armigera. Binding of the activated Cry1Ac of Bacillus thuringiensis (Bt) toxin was shown by immunoblot. A 120-kDa protein was identified as a receptor for the Cry1Ac type delta-endotoxin. The aminopeptidase-N activity of BBMVs was measured as the hydrolysis of L-leucine p-nitroanilide. The specific activity was 35 units/mg protein. The BBMV preparation also showed low level of alkaline phosphatase activity. Zn++ chelating agents 2,2'-dipyridyl and 1,10-phenanthroline inhibited aminopeptidase activity at 10 mM concentration, indicating the presence of zinc-dependent aminopeptidase in the brush border of H. armigera. The aminopeptidase activity was increased with increasing concentration of delta-endotoxin. The purified 120-kDa binding protein was N-terminally sequenced. The first 10-amino-acid sequence showed 60-77% similarity with human cysteine-rich secretory protein-1 precursor, inhibin alpha chain precursor. Salmonella flagellar hook protein and yeast carboxypeptidase S.
Although type 2 diabetes mellitus is associated with insulin resistance, many individuals compensate by increasing insulin secretion. Putative mechanisms underlying this compensation were assessed in the present study by use of 4-day glucose (GLC; 35% Glc, 2 ml/h) and lipid (LIH; 10% Intralipid + 20 U/ml heparin; 2 ml/h) infusions to rats. Within 2 days of beginning the infusion of either lipid or glucose, plasma glucose profiles were normalized (relative to saline-infused control rats; SAL; 0.45% 2 ml/h). During glucose infusion, plasma glucose was maintained in the normal range by an approximately twofold increase in plasma insulin and an approximately 80% increase in beta-cell mass. During LIH infusion, glucose profiles were also maintained in the normal range. Plasma insulin responses during feeding were doubled, and beta-cell mass increased 54%. For both groups, the increase in beta-cell mass was associated with increased beta-cell proliferation (98% increase during GLC and 125% increase during LIH). At the end of the 4-day infusions, no significant changes were observed in islet-specific gene transcription (i.e., the expression of islet hormone genes, glucose metabolism genes, and insulin transcription factors were unaffected). Two days after termination of the infusions, the glucose-stimulated plasma insulin response was increased approximately 67% in glucose-infused animals. No sustained effect on insulin secretory capacity was observed in the LIH animals. The increase in plasma insulin response after glucose infusion was achieved in the absence of any change in insulin clearance. We conclude that, in rats, an increase in insulin demand after an increase in glucose appearance or free fatty acid leads to an increase in beta-cell mass, mediated in part by an increase in beta-cell proliferation, and that these compensatory changes lead to increased insulin secretion, normal plasma glucose levels, and the maintenance of normal islet gene expression.
A 20-fold increase in beta-cell mass has been found after transplantation of porcine neonatal pancreatic cell clusters (NPCCs). Here the mechanisms leading to this increased beta-cell mass were studied. NPCCs (4000 islet equivalents) generated after 8 days culture of digested neonatal pig pancreas were transplanted beneath the renal capsule of streptozotocin (STZ) diabetic and normoglycemic nude mice. Grafts were removed at 10 days, 6 weeks, and 20 weeks after transplantation for immunostaining and insulin content. Proliferation of beta-cells and duct cells was assessed morphometrically using double immunostaining for Ki-67 with insulin or cytokeratin 7 (CK7). Graft maturation was assessed with double immunostaining of CK7 and insulin. Apoptosis was determined using propidium iodide staining. beta-cell proliferation in NPCCs was higher after 8 days of culture compared with that found in neonatal pig pancreas. After transplantation, beta-cell proliferation remained high at 10 days, decreased somewhat at 6 weeks, and was much lower 20 weeks after transplantation. Diabetic recipients not cured at 6 weeks after transplantation had significantly higher beta-cell proliferation compared with those cured and to normoglycemic recipients. The size of individual beta-cells, as determined by cross-sectional area, increased as the grafts matured. Graft insulin content was 20-fold increased at 20 weeks after transplantation compared with 8 days cultured NPCCS: The proliferation index of duct cells was significantly higher in neonatal pig pancreas than in 8 days cultured NPCCs and in 10-day-old grafts. The incidence of apoptosis in duct cells appeared to be low. About 20% of duct cells 10 days post transplantation showed costaining for CK7 and insulin, a marker of protodifferentiation. In conclusion, the increase in beta-cell mass after transplantation of NPCCs is due to both proliferation of differentiated beta-cells and differentiation of duct cells into beta-cells.
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The abnormal insulin secretion found in human diabetics and animal models of diabetes has been attributed to the deleterious effects of chronic hyperglycemia and/or elevated circulating levels of nonesterified fatty acids (NEFAs). In this study, abnormal glucose-induced insulin secretion (GIIS) was generated by a 48-hour infusion of glucose and assessed by the isolated perfused pancreas technique. In these hyperglycemic animals, abnormal GIIS is accompanied by a decrease in plasma NEFAs, while plasma and, more importantly, islet triglycerides remain at levels comparable to those in the controls. It is concluded that the abnormal insulin secretion in this glucose infusion model was likely caused by 48 hours of hyperglycemia and not by changes in circulating or islet lipids.
We report a case of disseminated histoplasmosis in a 60-year-old non-immunocompromised patient who presented to us with fever and hepatosplenomegaly. Sonographic & CT examination of the abdomen showed bilateral adrenal masses. Cytological examination of the aspirated material from the mass showed yeast forms of H. capsulatum.
Activation of T cells requires both TCR-specific ligation by direct contact with peptide Ag-MHC complexes and coligation of the B7 family of ligands through CD28/CTLA-4 on the T cell surface. We recently reported that coadministration of CD86 cDNA along with DNA encoding HIV-1 Ags i.m. dramatically increased Ag-specific CTL responses. We investigated whether the bone marrow-derived professional APCs or muscle cells were responsible for the enhancement of CTL responses following CD86 coadministration. Accordingly, we analyzed CTL induction in bone marrow chimeras. These chimeras are capable of generating functional viral-specific CTLs against vaccinia virus and therefore represent a useful model system to study APC/T cell function in vivo. In vaccinated chimeras, we observed that only CD86 + Ag + MHC class I results in 1) detectable CTLs following in vitro restimulation, 2) detectable direct CTLs, 3) enhanced IFN-gamma production in an Ag-specific manner, and 4) dramatic tissue invasion of T cells. These results support that CD86 plays a central role in CTL induction in vivo, enabling non-bone marrow-derived cells to prime CTLs, a property previously associated solely with bone marrow-derived APCs.
Synthesis of 5R-Acetamido-4S-amino-4H-pyran-6R-O-( -ethyl)propyl and 6R-(1-oxo-2-ethyl)butyl 2-carboxylic acids (4 and 5) and their evaluation as inhibitors of influenza virus sialidase is described. Both compounds showed good inhibitory activity with marked selectivity for influenza A sialidase.
A novel synthesis of the bicyclo [2.2.2] octane ring system has been achieved utilising a tandem Henry cyclisation as the key stage. This chemistry has been employed in the synthesis of a potential inhibitor of influenza virus sialidase.
A case of solid papillary epithelial neoplasm (PSEN) of pancreas in a young woman is reported in which the nature of tumour was recognised pre-operatively by ultrasound guided Fine needle aspiration. The pre-operative cytologic diagnosis enabled prompt and appropriate surgical treatment. FNAC revealed large cell clumps in the aspirate showing branching papillary appearance in which multiple layers of tumour cells surrounded central vascular stalks. The above was confirmed on histopathological examination of the excised tumour tissue.
BACKGROUND: Macroencapsulation is a strategy to protect transplanted islets from rejection and autoimmune attack. This study addresses questions about the survival and function of macroencapsulated syngeneic islets. METHODS: Planar immunobarrier membrane diffusion devices were used for syngeneic islet transplantation. After being mixed with a 1% alginate solution, a total of 250, 500, 750 or 1000 islets were loaded into the devices, which were implanted into the epididymal fat pad(s) of streptozocin diabetic mice. RESULTS: The success rate for restoration of normoglycemia at week 4 was highest for the recipients receiving two devices, each with 500 islets. Loading 750 or 1000 islets provided no improvement over loading 500 islets in a single device. Devices containing 250 islets were rarely successful. There was a striking tendency of transplants to either bring glucose levels into the near normal range or to fail with marked hyperglycemia. After an overnight fast at 1 and 4 weeks, but not at 12 weeks, hypoglycemia was found. The insulin content of devices from animals with normalized glucose values was higher than the insulin content in failed devices. Islet volume was maintained for 12 weeks, and fibrosis did not increase. CONCLUSIONS: A relatively small mass of macroencapsulated islet tissue can survive and function well enough to normalize glucose levels for at least 12 weeks. Maintenance of glucose levels in the near-normal range seems to have a beneficial influence on graft success. The finding of fasting hypoglycemia raises important clinical questions about islet dysfunction. Important limitations in the requirements for islet packing density in macroencapsulation have been defined. New approaches for improving islet packing density must be developed to make diffusion-dependent macroencapsulation more practical.
Participants were recruited either for a study of sexual attitudes and behavior or for a study of attitudes and behavior without mention of sexuality. Both groups answered questions about their sexual behavior and completed the Self-Monitoring Scale, the Balanced F Scale, and the Social Responsibility Scale. No differences were found as a function of recruitment technique in the mean reports of subjects' sexual behavior, but substantial differences were found in some of the relationships between these personality variables and sexual behavior reports as a function of recruitment technique; the correlation between the balanced F Scale score and masturbation frequency for females was +0.61 for those recruited for a study of sexual behavior and -0.61 for those recruited for a study of general attitudes and behavior. In both groups, larger correlations were found between female sexual behavior and personality than between male sexual behavior and personality. In all groups, the Self-Monitoring Scale was significantly correlated with masturbation frequency. The results are discussed in terms of self-selection bias and self-presentation bias, both of which may affect research on sexuality.
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