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Academic literature on the topic 'GSIBs'

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Published: 8 May 2023

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Journal articles on the topic "GSIBs"

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Ozili, Peterson K. "Non-performing loans in European systemic and non-systemic banks." Journal of Financial Economic Policy 12, no. 3 (September 30, 2019): 409–24. http://dx.doi.org/10.1108/jfep-02-2019-0033.

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Purpose The distinction between systemic banks (GSIBs) and non-systemic banks (non-GSIBs) is driven by policy reasons. This study aims to examine the behaviour of non-performing loans in European GSIBs and non-GSIBs from 2004 to 2013. Design/methodology/approach The author uses regression methodology to analyse the association between non-performing loans (NPLs) and the state of the economy. Findings The author finds that more profitable banks witness higher NPLs regardless of them being systemic or non-systemic. Secondly, GSIBs have fewer NPLs during economic booms and during periods of increased lending, while non-GSIBs experience higher NPLs during periods of increased lending. The author also observes that European non-GSIBs that exceed regulatory capital requirement also experience higher NPLs. In the post-crisis period, there is a significant and negative relationship between NPLs and the economic cycle for GSIBs in the post-financial crisis period and a significant and positive relationship between NPLs, loan supply and bank profitability for GSIBs in the post-financial crisis period; on the other hand, there is a significant and negative relationship between NPLs and regulatory capital ratios for non-GSIBs in the post-financial crisis period and a significant and positive relationship between NPLs and bank profitability for non-GSIBs in the post-financial crisis period. The findings have implications. Originality/value To the best of the author’s knowledge, the literature on the determinants of NPL has not empirically examined the behaviour of NPLs in European GSIBs and non-GSIBs. This paper examines this issue to provide insights to help policymakers and academics understand the peculiarities of NPLs in Europe.
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Prefontaine, Jacques. "Implications Of Basel III For Capital, Liquidity, Profitability, And Solvency Of Global Systematically Important Banks." Journal of Applied Business Research (JABR) 29, no. 1 (December 27, 2012): 157. http://dx.doi.org/10.19030/jabr.v29i1.7563.

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The objective of this paper is to study the profitability and solvency implications of the proposed Basel III capital and liquidity requirements in the global banking context. The intent is to improve our understanding on how the Basel III capital and liquidity requirements impact upon the functioning of global systematically important banks (GSIBs), and how this knowledge could prove to be useful in answering questions of policy relevance like financial stability in economics. A longer-term perspective is taken in order to link capital and liquidity requirements with the notion of systemic risk within the evolution of the international financial and monetary system. Of special interest is the interaction between macroeconomic policy - including monetary, exchange rate and combined micro-macro-prudential policy within the setting of present-day Basel III regulatory and supervisory reforms. More specifically, the paper addresses two related issues: first, it studies and presents several financial indicators that GSIBs disclose; second, it examines how these same indicators could be related to GSIBs profitability and solvency.
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Beltran, Daniel O., Hannah Bensen, Amy Kvien, Erin McDevitt, Monica V. Sanz, and Pinar Uysal. "What are Large Global Banks Doing About Climate Change?" International Finance Discussion Paper, no. 1368 (January 2023): 1–28. http://dx.doi.org/10.17016/ifdp.2023.1368.

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We review the "climate action plans" of Global Systemically Important Banks (GSIBs) and the progress they are making toward achieving them. G-SIBs have identified the drivers of climate risk and their transmission channels to credit and other risks. Additionally, some have started to measure and model these risks. While most GSIBs have committed to fully offsetting their emissions by mid-century, they are only beginning to measure financed emissions resulting from their loans and investments, which comprise the vast majority of their emissions. G-SIBs have also committed to increase green finance and have started to do so. All told, despite some progress by large global banks to address climate change considerations, much work lies ahead to properly measure and disclose climate-related risks, and to better align financing activities with their net-zero targets.
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Vasilakopoulos, Konstantinos, Christos Tzovas, and Apostolos Ballas. "Banks’ risk and the impact of audit quality on income smoothing." Journal of Accounting and Management Information Systems 20, no. 3 (September 1, 2021): 425–53. http://dx.doi.org/10.24818/jamis.2021.03003.

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Research question: This paper investigates the impact that specific audit quality dimensions have upon European Union Banks’ income smoothing behavior. Motivation: Although previous studies have investigated the characteristics of audit quality, little is known about the audit quality in the banking sector. Excessive risk taking and business complexity may further impair auditors’ work and an audit’s outcome may be conditioned upon banks’ risk. Idea: We examine whether auditors’ independence influences bank managers’ decision to smooth income and whether this attribute depends on bank risk and systemic importance. We investigate the association between auditors’ industry specialization and auditors’ tenure with the level of Loan Loss Provisions Data: We use a sample of 133 banks from 26 European Union countries for the period 2006-2013. Tools: Similar to previous research, we use ordinary least squares analysis to test the results. Findings: Empirical findings provide evidence that the auditors’ industry expertise limits management’s discretion of high-risk banks to a greater extent relative to low risk banks. In contrast, our results imply that banks that retain the same auditor for a consecutive fiscal year are more likely to engage in income smoothing through LLPs. Furthermore, our study examines whether audit quality dimensions have different outcomes on income smoothing decisions between globally systemically important banks (GSIBs) and the rest of banks. Our results provide evidence that the impact of industry specialization and auditor tenure on EU banks accounting policy decisions differs between GSIBs and non-GSIBs. Contribution: Our analysis contributes in the existing body of research by focusing on the impact of audit quality on managements’ accounting discretion and the influence of banks’ special attributes on the audit process.
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Tok, Evren, and Abdurahman Jemal Yesuf. "Embedding Value-Based Principles in the Culture of Islamic Banks to Enhance Their Sustainability, Resilience, and Social Impact." Sustainability 14, no. 2 (January 14, 2022): 916. http://dx.doi.org/10.3390/su14020916.

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Value-based banks strive to build a self-sustaining banking model with inclusive and transparent governance that is sustainable and resilient to external disturbances. Initiatives for value-based intermediation in Islamic finance started in Malaysia. The growth in VBIBs is accompanied by claims about its relative resilience to crisis and efficiency compared to VBBs and conventional banks. However, little empirical evidence is available to support such claims. This study aims to analyze the resilience and efficiency of VBIBs compared to the VBBs and GSIBs. It highlights the role of value-based strategy in developing a sound and resilient Islamic banking system to overcome future crises and further strengthen the impacts of Islamic banks. The study used quantitative and content analysis research methods, with data collected from the annual reports of 10 VBIBs from 2017 to 2020. The empirical results show that VBIBs have better risk-adjusted capital levels and asset quality, enabling them to be more resilient during crises. They provide more satisfactory returns compared to the VBBs and GSIBs. However, VBBs have a better asset structure and growth rate, which contributes to the real economy. The overall findings suggest that adopting value-based strategies in Islamic banking improve banks’ sustainability, resilience, and social impacts by concentrating resources on value-based activities that provide economic resiliency and enhance inclusive and sustainable economic growth. The study fills gaps in the current Islamic finance literature concerning empirical studies on value-based Islamic banking. It also helps practitioners to understand the relative efficiency, resilience, and social impact of VBIBs.
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Tabor, Dale R., Cynthia H. Larry, and Richard F. Jacobs. "Differential Induction of Macrophage GSIB4 -Binding Activity." Journal of Leukocyte Biology 45, no. 5 (May 1989): 452–57. http://dx.doi.org/10.1002/jlb.45.5.452.

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Wang, Zhongshan, Xiaokun Xia, Meixian Zhang, Jiawei Fang, Yanqiang Li, and Meng Zhang. "Purification and Characterization of Glutathione Binding Protein GsiB from Escherichia coli." BioMed Research International 2018 (November 1, 2018): 1–7. http://dx.doi.org/10.1155/2018/3429569.

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Objectives. To purify and characterize the glutathione binding protein GsiB of glutathione importer (GSI) in Escherichia coli (E. coli). Results. The coding sequence of GsiB was cloned from E. coli MG1655 and expressed in BL21(DE3). GsiB protein was expressed and purified to homogeneity using Ni-affinity and gel filtration chromatography. SDS-PAGE of purified GsiB showed a single protein band of molecular mass 56 kDa, while native gel showed two bands around 56 kDa and 110 kDa. Gene knockout showed that GsiB was essential for GSI mediated glutathione import. Interactions of GsiA, B, C, and D were determined using bacterial two-hybrid method. Without glutathione, GsiB showed no direct interaction with the other three proteins. However, GsiB could interact with GsiC and GsiD when using glutathione as sole sulfur source. Conclusions. GsiB functions in E. coli was characterized which could help elucidate the glutathione import mechanism in gram-negative bacteria.
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Wilson, Bridget S., Xiangbing Meng, Tomas Mazel, Cheryl L. Willman, Susan Atlas, Richard Harvey, I.-Ming Chen, Stephen P. Hunger, Janet M. Oliver, and Stuart S. Winter. "Select γ-Secretase Inhibitors Induce Apoptosis in Pre-B ALL Cells and Disrupt the Balance Between Constitutive Notch Signaling and Repression." Blood 112, no. 11 (November 16, 2008): 1917. http://dx.doi.org/10.1182/blood.v112.11.1917.1917.

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Abstract Several γ secretase inhibitors (GSIs) were tested for the ability to induce apoptosis in precursor B acute lymphoblastic leukemia (pre-B ALL) cells. Of five GSI’s tested, treatment with two compounds resulted in effective killing of both pre-B lymphoblasts and cells from multiple pre-B ALL lines. Since Notch receptors represent an important group of γ secretase targets, we evaluated expression and activation status of Notch receptors in CD19+ lymphoblasts from pediatric pre-B ALL patients, as well as cultured pre-B ALL cells. We found that, unlike T-ALL where activating mutations are common, pre-B ALL cells appear to drive constitutive Notch signaling through autocrine signals. Blasts from 11 patients expressed 3 Notch receptors and multiple Notch counter-ligands. Expression of Notch pathway genes was also confirmed by microarray analysis of genes expressed in 207 children with high risk B precursor ALL. GSI treatment of pre-B ALL cells led to dephosphorylation of AKT and Foxo3, Bim expression and caspase activation. GSI treatment also blocked cleavage of Notch 1 and 2 to their active forms and inhibited expression of Notch targets, Hey2 and Myc. In contrast, increased expression of Hes1 and Hey1 was correlated with GSI-induced loss of the co-repressor, SMRT. GSI treatment appears to induce precursor B cell death by disrupting the balance between constitutive Notch signaling and repression.
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Weksler-Zangen, Sarah, Genya Aharon-Hananel, Carmit Mantzur, Tzemach Aouizerat, Ewa Gurgul-Convey, Itamar Raz, and Ann Saada. "IL-1β hampers glucose-stimulated insulin secretion in Cohen diabetic rat islets through mitochondrial cytochrome c oxidase inhibition by nitric oxide." American Journal of Physiology-Endocrinology and Metabolism 306, no. 6 (March 15, 2014): E648—E657. http://dx.doi.org/10.1152/ajpendo.00451.2013.

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A high-sucrose, low-copper-diet (HSD) induces inhibition of glucose-sensitive rats (CDs) but not Cohen diabetes-resistant rats (CDr). Copper-supplemented HSD increased activity of the copper-dependent mitochondrial respiratory chain enzyme cytochrome c oxidase (COX) and reversed hyperglycemia. This study examined the mechanism by which interleukin-1β modulates GSIS and the role of COX in this process. We measured COX activity, ATP content, GSIS, iNOS expression, and nitrite production with and without IL-1β, Nω-nitro-l-arginine, copper, or potassium cyanide in isolated islets of CDs and CDr fed different diets. We found reduced COX activity, ATP content, and GSIS in isolated islets of CDs rats fed a regular diet. These were severely reduced following HSD and were restored to regular diet levels on copper-supplemented HSD ( P < 0.01 vs. CDr islets). Potassium cyanide chemically reduced COX activity, decreasing GSIS and thus reinforcing the link between islet COX activity and GSIS. Interleukin-1β (2.5 U/ml) reduced GSIS and COX activity in CDs islets. Exposure to 10 U/ml interleukin-1β decreased GSIS and COX activity in both CDs and CDr islets, inducing a similar nitrite production. Nevertheless, the effect on GSIS was more marked in CDs islets. A significant iNOS expression was detected in CDs on the HSD diet, which was reduced by copper supplementation. Nω-nitro-l-arginine and copper prevented the deleterious effect of interleukin-1β on COX activity and GSIS. We conclude that reduced islet COX activity renders vulnerability to GSIS inhibition on low-copper HSD through two interrelated pathways: 1) by further reducing the activity of COX that is essential for β-cell ATP-production and insulin secretion and 2) by inducing the expression of iNOS and nitric oxide-mediated COX inhibition. We suggest that islet COX activity must be maintained above a critical threshold to sustain adequate GSIS with exposure to low-copper HSD.
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Kristinsson, Hjalti, David M. Smith, Peter Bergsten, and Ernest Sargsyan. "FFAR1 Is Involved in Both the Acute and Chronic Effects of Palmitate on Insulin Secretion." Endocrinology 154, no. 11 (November 1, 2013): 4078–88. http://dx.doi.org/10.1210/en.2013-1352.

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Free fatty acids (FFAs) have pleiotropic effects on the pancreatic β-cell. Although acute exposure to FFAs stimulates glucose-stimulated insulin secretion (GSIS), prolonged exposure impairs GSIS and causes apoptosis. FFAs exert their effects both via intracellular metabolism and interaction with the FFA receptor 1 (FFAR1/GPR40). Here we studied the role of FFAR1 in acute and long-term effects of palmitate on GSIS and insulin content in isolated human islets by using the FFAR1 agonist TAK-875 and the antagonist ANT203. Acute palmitate exposure potentiated GSIS approximately 3-fold, whereas addition of the antagonist decreased this potentiation to approximately 2-fold. In the absence of palmitate, the agonist caused a 40% increase in GSIS. Treatment with palmitate for 7 days decreased GSIS to 70% and insulin content to 25% of control level. These negative effects of long-term exposure to palmitate were ameliorated by FFAR1 inhibition and further aggravated by additional stimulation of the receptor. In the absence of extracellularly applied palmitate, long-term treatment with the agonist caused a modest increase in GSIS. The protective effect of FFAR1 inhibition was verified by using FFAR1-deficient MIN6 cells. Improved β-cell function by the antagonist was paralleled by the decreased apoptosis and lowered oxidation of palmitate, which may represent the potential mechanisms of protection. We conclude that FFAR1 in the pancreatic β-cell plays a substantial role not only in acute potentiation of GSIS by palmitate but also in the negative long-term effects of palmitate on GSIS and insulin content.
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Dissertations / Theses on the topic "GSIBs"

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Law, Wai-jun. "A validation study of the geriatric suicide ideation scale (GSIS) of Hong Kong for Chinese older adults." Click to view the E-thesis via HKUTO, 2003. http://sunzi.lib.hku.hk/hkuto/record/B43895268.

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Law, Wai-jun, and 羅偉真. "A validation study of the geriatric suicide ideation scale (GSIS) of Hong Kong for Chinese older adults." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B43895268.

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Lattuada, Roberto. "A triangulation based approach to three dimensional geoscientific modelling." Thesis, Birkbeck (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312757.

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Karandrea, Shpetim. "Identifying New Treatment Options and Risk Factors for Type 2 Diabetes: The Potential Role of Thymoquinone and Persistent Organic Pollutants." Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/7042.

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Type 2 Diabetes Mellitus (T2DM) is a metabolic disorder characterized by chronic hyperglycemia, which develops as a consequence of peripheral insulin resistance and defective insulin secretion from pancreatic β-cells. A high calorie diet coupled with physical inactivity are known risk factors for the development of T2DM; however, these alone fail to account for the rapid rise of the disease. Recent attention has turned to the role of environmental pollutants in the development of metabolic diseases. PBDEs (polybrominated diphenyl ethers) are environmental pollutants that have been linked to the development of type 2 diabetes (T2D), however, the precise mechanisms are not clear. In particular, their direct effect on insulin secretion is unknown. In this study, we show that two PBDE congeners, BDE-47 and BDE-85, potentiate glucose-stimulated insulin secretion (GSIS) in INS-1 832/13 cells. This effect of BDE-47 and BDE-85 on GSIS was dependent on thyroid receptor (TR). Both BDE-47 and BDE-85 (10 μM) activated Akt during an acute exposure. The activation of Akt by BDE-47 and BDE-85 plays a role in their potentiation of GSIS, as pharmacological inhibition of PI3K, an upstream activator of Akt, significantly lowers GSIS compared to compounds alone. This study suggests that BDE-47 and BDE-85 directly act on pancreatic β-cells to stimulate GSIS, and that this effect is mediated by the thyroid receptor (TR) and Akt activation. This can cause the β-cells to oversecrete insulin, potentially leading to hyperinsulinemia, insulin resistance, and high blood glucose. In contrast to the potential diabetogenic effects of POPs, there are several naturally-derived compounds which accomplish just the opposite, exerting sensitizing effect on the peripheral tissues and sparing effect on β-cells. TQ, a natural occurring quinone and the main bioactive component of plant Nigella sativa, undergoes intracellular redox cycling and re-oxidizes NADH to NAD+. TQ administration (20 mg/kg/bw/day) to the Diet-Induced Obesity (DIO) mice reduced their diabetic phenotype by decreasing fasting blood glucose and fasting insulin levels, and improved glucose tolerance and insulin sensitivity as evaluated by oral glucose and insulin tolerance tests (OGTT and ITT). Furthermore, TQ decreased serum cholesterol levels and liver triglycerides, increased protein expression of phosphorylated Akt, decreased serum levels of inflammatory markers resistin and MCP-1, and decreased the NADH/NAD+ ratio. These changes were paralleled by an increase in phosphorylated SIRT-1 and AMPKα in liver and phosphorylated SIRT-1 in skeletal muscle. TQ also increased insulin sensitivity in insulin-resistant HepG2 cells via a SIRT-1-dependent mechanism These findings are consistent with the TQ-dependent re-oxidation of NADH to NAD+, which stimulates glucose and fatty acid oxidation and activation of SIRT-1-dependent pathways. Taken together, these results demonstrate that TQ ameliorates the diabetic phenotype in the DIO mouse model of type 2 diabetes.
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Burchfield, James Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "The role of PKCε in pancreatic β-Cell secretory function and its contribution to the development of lipid induced secretory defects." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2008. http://handle.unsw.edu.au/1959.4/41539.

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Type 2 diabetes accounts for 85-90% of all people with diabetes and is currently estimated to affect more than 180 million people worldwide, a figure estimated to double by the year 2030. Thus understanding the basic biology of glucose homeostasis and how it is altered during disease progression is crucial to the development of safe and effective treatment regimes. The link between high dietary fat and the development of type Il diabetes is well established. Chronic treatment of pancreatic islets with the lipid palmitate induces defects in glucose stimulated insulin secretion (GSIS) akin to those seen in the development of type Il diabetes. Previous studies from our group have identified the lipid-activated kinase protein kinase C epsilon (PKCε) as a potential mediator of some of these effects. Deletion of PKCε in mice results in complete protection from high-fat diet induced glucose intolerance. This protection is associated with enhanced circulating insulin suggesting that PKCε may be involved in the regulation of insulin release from the pancreatic β-Cell. The data presented here suggests that PKCs plays an important role in the regulation of insulin secretion under both physiological and pathophysiological conditions. We demonstrate that PKCε can be activated by chronic lipid treatment and acute cholinergic stimulation. Under these conditions insulin secretion is enhanced by PKCε deletion or inhibition suggesting that PKCε is a negative regulator of insulin secretion. Mechanistically the PKCs mediated inhibition of insulin release by acute or chronic PKCε activation appears to be distinct. The effect of PKCε induced by palmitate pre-treatment appears to be distal to calcium influx. The pool of pre-docked vesicles is enhanced in palmitate pre-treated β-cells lacking PKCε suggesting that PKCε may be involved in the regulation of vesicle dynamics. In contrast, calcium dynamics induced by cholinergic stimulation are altered by PKCε deletion, suggesting an effect on either the calcium channels themselves or on the upstream signalling. Given the ability of PKCε to inhibit insulin secretion, inhibition of PKCε in the β-cells of people suffering from insulin resistance and (or) type II diabetes represents a novel target for the treatment of type II diabetes.
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Goulley, Joan. "Role of BMP signaling and ASNA1 in β-cells." Doctoral thesis, Umeå universitet, Umeå centrum för molekylär medicin (UCMM), 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1810.

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Patients with type II diabetes present alterations in glucose homeostasis due to insufficient amount of insulin (β-cell dysfunction) and inability to properly use the insulin that is secreted (insulin resistance). Combined genetical and environmental factors are believed to be responsible for these dysfunctions and the resulting impairment in glucose homeostasis. The pancreatic gland is composed of exocrine and endocrine tissues. The endocrine part of the organ couples glucose sensing to insulin release. Within this endocrine gland, also known as islets of Langerhans, the insulin secreting β-cell is the main player and therefore highly important for proper glucose metabolism. In this thesis, mice were developed in order to assess the role of BMP signaling molecule and Arsenite induced ATPase-1 (Asna1) for pancreas development and β-cell function. The mature β-cell responds to elevated glucose levels by secreting insulin in a tightly controlled manner. This physiological response of the β-cell to elevated blood glucose levels is critical for maintenance of normoglycaemia and impaired Glucose stimulated insulin secretion (GSIS) is a prominent feature of overt type 2 diabetes. Thus, the identification of signals and pathways that ensure and stimulate GSIS in β-cells is of great clinical interest. Here we show (Paper I) that BMPRIA and its high affinity ligand BMP4 are expressed in fetal and adult islets. We also provide evidence that BMPRIA signaling in adult β-cell is required for GSIS, and that both transgenic expression of Bmp4 in β-cells or systemic administration of BMP4 protein to mice enhances GSIS. Thus, BMP4-BMPRIA signaling in β-cells positively regulates the genetic machinery that ensures GSIS. Arsenite induced ATPase (Asna1), the homologue of the bacterial ArsA ATPase, is expressed in insulin producing cells of both mammals and the nematode Caenorhabditis elegans (C.elegans). Asna1 has been proposed to act as an evolutionary conserved regulator of insulin/insulin like factor signaling. In C.elegans, asna-1 has been shown to regulate growth in a non-cell autonomous and IGF-receptor dependent manner. Here we show that transgenic expression of ASNA1 in β-cells of mice leads to enhanced Aktactivity and β-cell hyperplasia (manuscript). ASNA1 transgenic mice develop, however, diabetes due to impaired insulin secretion. The expression of genes involved in secretion stimulus coupling and insulin exocytosis is perturbed in islets of these mice. These data suggest that activation of ASNA1, here mimicked by enhanced expression, positively influences β-cell mass but negatively affects insulin secretion.
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Papadopoulou, Stella. "FGFs and Wnts in pancreatic growth and β-cell function." Doctoral thesis, Umeå universitet, Umeå centrum för molekylär medicin (UCMM), 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-528.

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Mesenchymal-epithelial interactions are pivotal for proper pancreatic growth and development. The pancreatic progenitor cells present in the early pancreatic anlagen proliferate and eventually give rise to all pancreatic cell types. The Fibroblast Growth Factor 2b (FGFR2b) high-affinity ligand Fibroblast Growth Factor 10 (FGF10) has been linked to pancreatic epithelial cell proliferation and we have previously shown that Notch signalling controls pancreatic cell differentiation via lateral inhibition. By overexpressing FGF10 under the control of the Ipf1/Pdx1 promoter in mice, we have shown that persistent FGF10 activation in the embryonic pancreas of transgenic mice perturbs pancreatic epithelial cell proliferation and also inhibits pancreatic cell differentiation by maintaining Notch activation. In the Ipf1/Fgf10 transgenic mice, the pancreatic epithelial cells are ‘locked’ in an undifferentiated progenitor-like state with sustained proliferative capacity. Collectively, our data suggest a key role for FGFR2b/FGF10 signalling in the regulation of pancreatic growth and differentiation and that FGFR2b/FGF10 signalling interact with the Notch signalling pathway. Glucose homeostasis in mammals is critically dependent on co-ordinated glucose uptake, oxidative metabolism and insulin secretion in β-cells. Although, several key genes controlling various aspects of glucose sensing, glucose metabolism, insulin expression and secretion have been identified, we know relatively little about the molecular mechanisms that induce and maintain the expression of genes required for glucose-stimulated insulin secretion (GSIS) in β-cells. Attenuation of FGFR1c signalling leads to diabetes in mice. Overexpression of FGF2, a high-affinity FGFR1c ligand, under the control of the Ipf1/Pdx1 promoter also leads to diabetes in mice. The Ipf1/Fgf2 mice present with normal endocrine and exocrine differentiation but display impaired glucose-stimulated insulin secretion (GSIS), perturbed expression of genes required for glucose sensing uptake together with oxidative metabolism and increased expression of the FGF-signalling inhibitors Spry-2 and Pyst1/MKP3 in β-cells. Thus, stringent control of FGF signalling activation appears crucial for the maintenance of the regulatory circuit that ensures proper GSIS in pancreatic β-cells and hence normoglycaemia. The Wnt family of ligands via their receptors Frizzled (Frz) have been shown to mediate mesenchymal-epithelial interactions and cell proliferation in a variety of different systems. Expression of a plethora of Wnt ligands and Frz receptors has been previously reported in the pancreas and mice missexpressing Wnt1 and Wnt5a under the Ipf1/Pdx1 promoter display severely perturbed development. Here, we show the temporal and spatial expression of Wnt4, Wnt7b and Frz3 at different stages of pancreas development. To elucidate the role of Wnt signalling in the pancreas, we overexpressed a dominant negative form of mouse Frz8 under the Ipf1/Pdx1 promoter in mice. The Ipf1/Frz8CRD mice display severe pancreatic hypoplasia demonstrating that attenuation of Wnt signalling in the pancreas leads to perturbed pancreatic growth. Nevertheless, the transgenic mice present with normal endocrine and exocrine differentiation and remain normoglycaemic. The maintenance of normoglycaemia in these mice appears to be the consequence of a relative increase in endocrine cell number per pancreatic area combined with enhanced insulin biosynthesis and insulin secretion. Collectively our data provide evidence that Wnt signalling is required pancreatic growth but not adult β-cell function.
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Qiu, Yuhan. "The effect of a putative acyl-CoA synthetase 5 inhibitor on lipid accumulation and insulin release from clonal pancreatic beta-cell." Thesis, 2019. https://hdl.handle.net/2144/36632.

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It is estimated by the World Health Organization (WHO) that 422 million people had diabetes worldwide in 2014, including 30.3 million people in the US. The cost of treating the disease is has tripled from 2003-2013 due to the increased number of patients. One of the genes strongly associated with type 2 diabetes (T2D) is the transcription factor 7 like 2 (TCF7L2). A single nucleotide polymorphism (SNP) of the TCF7L2 results in increased expression of long chain acyl-CoA synthetase 5 (ACSL5) while deletion of this part of the TCF7L2 gene reduces ACSL5 mRNA level. The regulation of ACSL5 gene expression by the high risk TCF7L2 allele highlights the importance of investigating the role of ACSL5 in T2D. ACSL5 is one of a family of enzymes that activates FA to its CoA ester and is required for FA metabolism within cells. Mice lacking this protein have reduced fat mass and are more insulin sensitive. Chronic exposure of clonal pancreatic ß-cells to excess nutrients has been shown to result in increased intrinsic lipid droplets, reduced insulin content, a left-shift in glucose dose-dependent insulin secretion curve characterized by basal insulin hypersecretion (IH) and blunted glucose stimulated insulin secretion (GSIS). We tested the hypothesis that the use of a putative ACSL5 inhibitor (Adipo C) can reduce accumulated lipid droplets, rescue insulin content and reverse the left-shift in glucose dose-dependent insulin secretion curve. INS-1 (823/13) cells were cultured in either 4 mM or 11 mM glucose media representing physiological and excess nutrients environment. Adipo C (10-25 µM) was added to cells to both acutely (2 hrs) and chronically (72 hrs) inhibit ACSL5 activity. Thin layer chromatography with C11 Bodipy fatty acid (BFA) was used to detect acute fatty acid incorporation into neutral lipids. Nile red was used to visualize intrinsic lipid droplets inside cells. Intracellular Ca2+ activity was detected using fura 2. Insulin assay was measured by HTRF. Acute fatty acid incorporation and lipid accumulation were reduced in cells exposed to Adipo C. An Adipo C concentration dependent right shift of glucose dose-dependent insulin release and increased insulin content were observed. 11 mM glucose cells cultured in 25 µM Adipo C showed decreased intracellular Ca2+ activity at 3 mM glucose and increased Ca2+ activity at 12 mM glucose, which are characteristic of cells cultured in 4 mM glucose having reduced lipid stores. These results all indicate possible protective effects on -cells exposed to excess nutrients. Islets of T2D patients who have a physiologically elevated blood glucose level are exposed to a similar excess nutrient environment. Therefore, the results illustrated here warrant further research on Adipo C compound to explore its therapeutic potential on T2D.
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Books on the topic "GSIBs"

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Information, Global Securities, ed. GSI's primer to SEC research. Washington, DC: Global Securities Information, 2002.

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Brown, Phillip L. GSI's primer to SEC research. 2nd ed. New York, NY: Practising Law Institute, 2004.

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Philippines. Government Service Insurance System. GSIS Museo ng Sining collection. Pasay City: Government Service Insurance System, 2007.

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Dalisay, Jose Y. Decade of reform, decade of innovation: The GSIS under PGM Winston F. Garcia, 2001-2010. Pasay City: Government Service Insurance System, 2010.

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Y, Dalisay Jose. Decade of reform, decade of innovation: The GSIS under PGM Winston F. Garcia, 2001-2010. Edited by Philippines. Government Service Insurance System. Pasay City: Government Service Insurance System, 2010.

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Report on the Conference Workshop on the Launching of the OMB-Junior Graftwatch, February 18, 1993, 8 : 00 A.M.-5: 00 P.M., GSIS Social Hall, Arroceros St., Manila. Manila: Office of the Ombudsman, Community Relations and Operations Division, Community Coordination Bureau, Public Assistance and Corruption Prevention Office, 1993.

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Bod Rgya rtsom rig gsib bsdur gyi dpyad brjod. Mi rigs dpe skrun khan, 2001.

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Book chapters on the topic "GSIBs"

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Yosibash, Zohar. "Computing Generalized Stress Intensity Factors (GSIFs)." In Interdisciplinary Applied Mathematics, 133–56. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-1508-4_6.

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Sharma, Paul. "GSIIs and the Framework for Macroprudential Supervision: Strengthening GSIIs and Reducing the Systemic Risks They Pose." In Macroprudential Supervision in Insurance, 233–49. London: Palgrave Macmillan UK, 2014. http://dx.doi.org/10.1057/9781137439109_12.

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Huang, Yan. "GSiB: PSE Infrastructure for Dynamic Service-Oriented Grid Applications." In Lecture Notes in Computer Science, 430–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/3-540-44864-0_45.

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Ježek, Petr, Blanka Holendová, Martin Jabůrek, Jan Tauber, Andrea Dlasková, and Lydie Plecitá-Hlavatá. "Redox Signaling is Essential for Insulin Secretion." In Type 2 Diabetes [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.94312.

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In this review, we place redox signaling in pancreatic β-cells to the context with signaling pathways leading to insulin secretion, acting for example upon the action of incretins (GLP-1, GIP) and the metabotropic receptor GPR40. Besides a brief description of ion channel participation in depolarization/repolarization of the plasma membrane, we emphasize a prominent role of the elevated glucose level in pancreatic β-cells during glucose-stimulated insulin secretion (GSIS). We focus on our recent findings, which revealed that for GSIS, not only elevated ATP synthesis is required, but also fundamental redox signaling originating from the NADPH oxidase 4- (NOX4-) mediated H2O2 production. We hypothesized that the closing of the ATP-sensitive K+ channel (KATP) is only possible when both ATP plus H2O2 are elevated in INS-1E cells. KATP alone or with synergic channels provides an element of logical sum, integrating both metabolic plus redox homeostasis. This is also valid for other secretagogues, such as branched chain ketoacids (BCKAs); and partly for fatty acids (FAs). Branched chain aminoacids, leucine, valine and isoleucine, after being converted to BCKAs are metabolized by a series of reactions resembling β-oxidation of FAs. This increases superoxide formation in mitochondria, including its portion elevated due to the function of electron transfer flavoprotein ubiquinone oxidoreductase (ETF:QOR). After superoxide conversion to H2O2 the oxidation of BCKAs provides the mitochondrial redox signaling extending up to the plasma membrane to induce its depolarization together with the elevated ATP. In contrast, experimental FA-stimulated insulin secretion in the presence of non-stimulating glucose concentrations is predominantly mediated by GPR40, for which intramitochondrial redox signaling activates phospholipase iPLA2γ, cleaving free FAs from mitochondrial membranes, which diffuse to the plasma membrane and largely amplify the GPR40 response. These events are concomitant to the insulin release due to the metabolic component. Hypothetically, redox signaling may proceed by simple H2O2 diffusion or via an SH-relay enabled by peroxiredoxins to target proteins. However, these aspects have yet to be elucidated.
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"GSIS: Group Signature and ID-based Signature-Based Secure and Privacy-Preserving Protocol." In Vehicular Ad Hoc Network Security and Privacy, 21–49. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781119082163.ch2.

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Conference papers on the topic "GSIBs"

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Yosibash, Zohar, and Barna A. Szabó. "Failure Analysis of Composite Materials and Multi Material Interfaces." In ASME 1995 Design Engineering Technical Conferences collocated with the ASME 1995 15th International Computers in Engineering Conference and the ASME 1995 9th Annual Engineering Database Symposium. American Society of Mechanical Engineers, 1995. http://dx.doi.org/10.1115/detc1995-0145.

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Abstract Composite materials and multi-material interface problem usually have one or more singular points. In the neighborhood of these points the solution of two-dimensional linear elastostatic problems is characterized by a series of eigenpairs and their coefficients, called the generalized stress intensity factors (GSIFs). Accurate and reliable computation of the eigenpairs and the GSIFs is important because failure theories directly or indirectly involve these quantities. New efficient and accurate methods for numerical computation of the eigenpairs and the GSIFs, based on the p-version of the finite element method, are presented and demonstrated. Examples, representing two different kinds of singular points demonstrate that the method works well and produces results of high accuracy. Importantly, the method is applicable to anisotropic materials, multi-material interfaces, and cases where the singularities are characterized by complex eigenpairs.
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Goldberg, Mitchell D. "Global space-based inter-calibration system (GSICS)." In Optical Engineering + Applications, edited by Mitchell D. Goldberg, Hal J. Bloom, Allen H. Huang, and Philip E. Ardanuy. SPIE, 2007. http://dx.doi.org/10.1117/12.735246.

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Koerner, G. R. "Update on GSI's Geotextile Highway Separation Study." In Geo-Frontiers Congress 2005. Reston, VA: American Society of Civil Engineers, 2008. http://dx.doi.org/10.1061/40782(161)14.

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Zhang, Peng, Kenneth Holmlund, Mitch Goldberg, and Jerome Lafeuille. "The Global Space-based Inter-Calibration System (GSICS)." In IGARSS 2016 - 2016 IEEE International Geoscience and Remote Sensing Symposium. IEEE, 2016. http://dx.doi.org/10.1109/igarss.2016.7730440.

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Wu, Xiangqian, Tim Hewison, and Yoshihiko Tahara. "GSICS GEO-LEO intercalibration: baseline algorithm and early results." In SPIE Optical Engineering + Applications, edited by Mitchell D. Goldberg and Hal J. Bloom. SPIE, 2009. http://dx.doi.org/10.1117/12.825460.

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Liu, Yunmei, Kihyun Pyo, Christopher Cunningham, Thomas Chase, and David Kaber. "Driver Situation Awareness and Cognitive Workload Effects of Novel Interchange Configurations and Associated Signage." In 13th International Conference on Applied Human Factors and Ergonomics (AHFE 2022). AHFE International, 2022. http://dx.doi.org/10.54941/ahfe1002459.

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In recent years, there has been a push towards use of grade-separated interchange (GSI) design to increase the overall capacity of intersections. The primary recommendation has been to resolve physical intersection constraints, including signalized left turns (in the U.S.). However, few, if any, investigations have made comparisons of driver situation awareness (SA) and cognitive workload in navigating novel grade-separated configurations and how to effectively implement associated signage to promote driver and traffic safety at different types of interchanges. To address this research gap, this study designed and conducted a driving simulation experiment to compare driver SA and cognitive workload in negotiating standard GSIs vs. novel GSI conditions, including contra-flow and quadrant configurations. All GSIs accommodated cross-traffic flows (north, south, east, and west) with four-lane roadways running in each direction through urban environments. The experiment also manipulated driver exposure to lane assignment (LA) signs (present and absent) and decision point (DP) signs with either overhead or right-side mount configurations. Forty-eight (48) licensed drivers participated in the experiment with each driver experiencing each GSI configuration in two trials for a total of six experiment trials for each participant (total of 288 trials). Participants in the experiment were divided into two groups according to age, including young (18-24 yrs.) and middle-aged (25-64 yrs.). The participants were also assigned to unique combinations of LA and DP signs (LA present + DP overhead; LA present + DP right-side mounted; LA absent + DP overhead; LA absent + DP right-side mounted), which remained consistent across GSI configurations for each driver. A high-fidelity and full-motion driving simulator was used in this study. During each trial, a driver was required to maintain posted speed limits and to achieve a pre-identified destination (“Garden St. North), as posted on the LA and DP signs. At specific stopping points in each test trial, driver SA was assessed using the Situation Awareness Global Assessment Technique (SAGAT). The simulation scenario was frozen and drivers were posed with multiple queries addressing perception, comprehension, and projection of roadway conditions, vehicle and traffic states, and routes. Qualtrics survey software was used to present questions in an electronic format (using driver mobile devices) with all being randomly selected from a large pool of questions on the driving environment. Driver responses to queries were graded based on recordings of ground-truth simulator settings. That SAGAT output as a percentage of correct responses to all queries delivered at a simulation freeze with range [0,1]. Driver cognitive workload was assessed using the NASA Task Load index. The purpose of using this index was to determine the cognitive load imposed on drivers by the signage conditions in negotiating the various types of GSIs. At the beginning of the experiment, participants ranked the importance of six workload demand components, including mental, physical, temporal, performance, effort, and frustration for the driving task. At the end of each test trial, participants rated their perceived mental workload, according to the various demand components on a 100-point scale. The NASA TLX was calculated as the rank-weighted sum of the demand ratings scaled from 0 to 100 points. The results revealed driver SA and workload to significantly differ among GSIs. The standard and contra-flow GSIs were not different in driver SA but both were superior to the quadrant configuration. There were no significant differences in SA detected for the use (LA) and placement (DP) of signs. Regarding cognitive workload, results corresponded with SA findings, indicating the standard and contra-flow GSIs produced lower cognitive demands for drivers than the quadrant configuration. However, there were no significant differences in cognitive workload detected between the use and placement of signs. No interactions were detected among the GSI configurations and use and placement of signs for both SA and cognitive workload. In addition, correlation analyses were also applied to the SA and workload responses. Results indicated that SA and workload were complimentary in the context of the present experiment and they represent unique methods for assessing human behavior/performance in driving research.On the basis of these results, it was concluded that novel GSI designs influence driver SA and workload responses compared with standard interchanges; however, the presence of LA signs and positioning of DP signs does not appear to positively influence these responses. There is a need for additional empirical driving research to determine what aspects of GSI geometry and other traffic control devices may serve to promote comparable levels of driver SA and workload for new designs as compared to standard interchanges.
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Wu, Xiangqian, and Mitch Goldberg. "Global space-based inter-calibration system (GSICS): a status report." In Optical Engineering + Applications, edited by Mitchell D. Goldberg, Hal J. Bloom, Allen H. Huang, and Philip E. Ardanuy. SPIE, 2007. http://dx.doi.org/10.1117/12.734127.

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Yu, Fangfang, Xiangqian Wu, Yaping Li, Gordana Rancic, Likun Wang, M. K. Rama Varma Raja, Sueng-hee Sohng, Fuzhong Weng, and Mitchell Goldberg. "GSICS GEO-LEO inter-calibration: operation status at NOAA/NESDIS." In SPIE Optical Engineering + Applications, edited by Mitchell D. Goldberg and Hal J. Bloom. SPIE, 2009. http://dx.doi.org/10.1117/12.826146.

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Xiangqian, W., Fangfang Yu, Vladimir Kondratovich, Boryana Efremova, Xi Shao, Robert Iacovazzi, and Changyong Cao. "Evaluation of GOES-16 ABI on-orbit performance using GSICS." In 2017 IEEE International Geoscience and Remote Sensing Symposium (IGARSS). IEEE, 2017. http://dx.doi.org/10.1109/igarss.2017.8126956.

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Zhang, Yong, Xiuqing Hu, and Zhiguo Rong. "Onboard blackbody calibration models of FY-2D SVISSR based on GSICS." In SPIE Asia Pacific Remote Sensing, edited by Xiaoxiong Xiong and Haruhisa Shimoda. SPIE, 2014. http://dx.doi.org/10.1117/12.2068727.

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Reports on the topic "GSIBs"

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Boesch, H., H. Brindley, F. Carminati, N. Fox, D. Helder, T. Hewison, D. Houtz, et al. SI-traceable space-based climate observation system: a CEOS and GSICS Workshop. National Physical Laboratory, UK, 9-11 Sept 2019. National Physical Laboratory, January 2022. http://dx.doi.org/10.47120/npl.9319.

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