Relevant bibliographies by topics / Pancreatic beta-cell

Academic literature on the topic 'Pancreatic beta-cell'

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Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Pancreatic beta-cell"

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Rastogi, D. P., A. C. Saxena, and Sunil Kumar. "Pancreatic beta-cell regeneration." British Homeopathic Journal 77, no. 03 (July 1988): 147–51. http://dx.doi.org/10.1016/s0007-0785(88)80071-1.

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Abstract Cephalendra, indica ∅ (41% v/v alcoholic extract of the wild variety of Cephalendra indica Naud.), on regular administration in doses ranging from 25 μml to 75 μml/100 g of body weight (gbw) by the oral or intraperitoneal (ip) route produced a significant fall in blood sugar level in alloxan-induced diabetic rats. Biochemical studies showed stabilization of blood sugar level in 70% of cases of fourteen to twenty days after withdrawal of the drug. Histopathological studies revealed regeneration of pancreatic β cells. The hypothesis is that the drug acts through the hypothalamo-hypophysial-pancreatic axis, producing selective regeneration of β cells. The drug may indirectly release inhibitory factors from hypothalamic neurons, inhibiting the secretion of growth hormone and triggering insulin secretion from β cells. The therapeutic action of the drug on pancreatic β cells and lack of acute and subacute toxicity may open up new prospects in the treatment of diabetes mellitus.
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Thermos, K., M. D. Meglasson, J. Nelson, K. M. Lounsbury, and T. Reisine. "Pancreatic beta-cell somatostatin receptors." American Journal of Physiology-Endocrinology and Metabolism 259, no. 2 (August 1, 1990): E216—E224. http://dx.doi.org/10.1152/ajpendo.1990.259.2.e216.

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The characteristics of somatostatin (SRIF) receptors in rat pancreatic beta-cells were investigated using rat islets and the beta-cell line HIT-T15 (HIT). The biochemical properties of the SRIF receptors were examined with 125I-labeled des-Ala-1,Gly-2-desamino-Cys-3-[Tyr-11]- dicarba3,14-somatostatin (CGP 23996). 125I-CGP 23996 bound to SRIF receptors in HIT cells with high affinity and in a saturable manner. The binding of 125I-CGP 23996 to SRIF receptors was blocked by SRIF analogues with a rank order of potency of somatostatin 28 (SRIF-28) greater than D-Trp-8-somatostatin greater than somatostatin 14 (SRIF-14). To investigate the physical properties of the HIT cell SRIF receptor, the receptor was covalently labeled with 125I-CGP 23996 using photo-cross-linking techniques. 125I-CGP 23996 specifically labeled a protein of 55 kDa in HIT cell membranes. The size of the SRIF receptor in HIT cells is similar to the size of the SRIF receptor labeled with 125I-CGP 23996 in membranes of freshly isolated islets, suggesting that the physical properties of SRIF receptors in HIT cells and rat islet cells are similar. The binding studies suggest that beta-cells predominantly express a SRIF-28-preferring receptor. In freshly isolated islets, glucose- and arginine-stimulated insulin release was effectively blocked by SRIF-28 but not by SRIF-14. SRIF-14 did inhibit arginine-stimulated glucagon secretion from freshly isolated islets. The dissociation of the inhibitory effects of SRIF-28 and SRIF-14 on insulin and glucagon release from freshly isolated islets suggests that the two peptides act through different receptors in islets to regulate hormone secretion.
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Grossman, E., J. Tao, D. Lee, and A. Chong. "QUANTIFYING PANCREATIC BETA-CELL REGENERATION." Transplantation 86, Supplement (July 2008): 143. http://dx.doi.org/10.1097/01.tp.0000332375.84668.26.

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Grossman, Eric J., Jing Tao, David D. Lee, and Anita S. Chong. "Quantifying pancreatic beta-cell regeneration." Journal of the American College of Surgeons 207, no. 3 (September 2008): S106—S107. http://dx.doi.org/10.1016/j.jamcollsurg.2008.06.272.

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Bigam, David L., and A. M. James Shapiro. "Pancreatic transplantation: Beta cell replacement." Current Treatment Options in Gastroenterology 7, no. 5 (October 2004): 329–41. http://dx.doi.org/10.1007/s11938-004-0046-9.

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Russ, Holger A., Limor Landsman, Christopher L. Moss, Roger Higdon, Renee L. Greer, Kelly Kaihara, Randy Salamon, Eugene Kolker, and Matthias Hebrok. "Dynamic Proteomic Analysis of Pancreatic Mesenchyme Reveals Novel Factors That Enhance Human Embryonic Stem Cell to Pancreatic Cell Differentiation." Stem Cells International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/6183562.

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Current approaches in human embryonic stem cell (hESC) to pancreatic beta cell differentiation have largely been based on knowledge gained from developmental studies of the epithelial pancreas, while the potential roles of other supporting tissue compartments have not been fully explored. One such tissue is the pancreatic mesenchyme that supports epithelial organogenesis throughout embryogenesis. We hypothesized that detailed characterization of the pancreatic mesenchyme might result in the identification of novel factors not used in current differentiation protocols. Supplementing existing hESC differentiation conditions with such factors might create a more comprehensive simulation of normal development in cell culture. To validate our hypothesis, we took advantage of a novel transgenic mouse model to isolate the pancreatic mesenchyme at distinct embryonic and postnatal stages for subsequent proteomic analysis. Refined sample preparation and analysis conditions across four embryonic and prenatal time points resulted in the identification of 21,498 peptides with high-confidence mapping to 1,502 proteins. Expression analysis of pancreata confirmed the presence of three potentially important factors in cell differentiation: Galectin-1 (LGALS1), Neuroplastin (NPTN), and the Lamininα-2 subunit (LAMA2). Two of the three factors (LGALS1 and LAMA2) increased expression of pancreatic progenitor transcript levels in a published hESC to beta cell differentiation protocol. In addition, LAMA2 partially blocks cell culture induced beta cell dedifferentiation. Summarily, we provide evidence that proteomic analysis of supporting tissues such as the pancreatic mesenchyme allows for the identification of potentially important factors guiding hESC to pancreas differentiation.
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Laughlin, Maren. "Why Image the Pancreatic Beta Cell?" Current Medicinal Chemistry-Immunology, Endocrine & Metabolic Agents 4, no. 4 (December 1, 2004): 251–52. http://dx.doi.org/10.2174/1568013043357482.

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Smith, W. G. J., I. Hanning, D. G. Johnston, and C. B. Brown. "Pancreatic Beta-cell Function in CAPD." Nephrology Dialysis Transplantation 3, no. 4 (1988): 448–52. http://dx.doi.org/10.1093/oxfordjournals.ndt.a091696.

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Diedisheim, Marc, Masaya Oshima, Olivier Albagli, Charlotte Wennberg Huldt, Ingela Ahlstedt, Maryam Clausen, Suraj Menon, et al. "Modeling human pancreatic beta cell dedifferentiation." Molecular Metabolism 10 (April 2018): 74–86. http://dx.doi.org/10.1016/j.molmet.2018.02.002.

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Poitout, Vincent, Julie Amyot, Meriem Semache, Bader Zarrouki, Derek Hagman, and Ghislaine Fontés. "Glucolipotoxicity of the pancreatic beta cell." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1801, no. 3 (March 2010): 289–98. http://dx.doi.org/10.1016/j.bbalip.2009.08.006.

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Dissertations / Theses on the topic "Pancreatic beta-cell"

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Barlow, Jonathan. "Mitochondrial involvement in pancreatic beta cell glucolipotoxicity." Thesis, University of Plymouth, 2015. http://hdl.handle.net/10026.1/3314.

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High circulating glucose and non-esterified free fatty acid (NEFA) levels can cause pancreatic β-cell failure. The molecular mechanisms of this β-cell glucolipotoxicity are yet to be established conclusively. In this thesis by exploring mitochondrial energy metabolism in INS-1E insulinoma cells and isolated pancreatic islets, a role of mitochondria in pancreatic β-cell glucolipotoxicity is uncovered. It is reported that prolonged palmitate exposure at high glucose attenuates glucose-stimulated mitochondrial respiration which is coupled to ADP phosphorylation. These mitochondrial defects coincide with an increased level of mitochondrial reactive oxygen species (ROS), impaired glucose-stimulated insulin secretion (GSIS) and decreased cell viability. Palmitoleate, on the other hand, does not affect mitochondrial ROS levels or cell viability and protects against the adverse effects of palmitate on these phenotypes. Interestingly, palmitoleate does not significantly protect against mitochondrial respiratory or insulin secretion defects and in pancreatic islets tends to limit these functions on its own. Furthermore, strong evidence suggests that glucolipotoxic-induced ROS are of a mitochondrial origin and these ROS are somehow linked with NEFA-induced loss in cell viability. To explore the mechanism of glucolipotxic-induced mitochondrial ROS and associated cell loss, uncoupling protein-2 (UCP2) protein levels and activity were probed in NEFA exposed INS-1E cells. It is concluded that UCP2 neither mediates palmitate-induced mitochondrial ROS production and the related cell loss, nor protects against these deleterious effects. Instead, UCP2 dampens palmitoleate protection against palmitate toxicity. Collectively, these data shed important new light on the area of glucolipotoxicity in pancreatic β-cells and provide novel insights into the pathogenesis of Type 2 diabetes.
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Cui, Ju, and 崔菊. "Kinesin-1 in pancreatic beta cell and renal epithelial cell." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hdl.handle.net/10722/197835.

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Hanna, Katie. "Novel mechanisms of glucolipotoxic pancreatic beta cell death." Thesis, Nottingham Trent University, 2018. http://irep.ntu.ac.uk/id/eprint/35356/.

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Glucolipotoxicity (GLT) is the term given to the combined and damaging effect of increased glucose and fatty acid levels on pancreatic beta cells (β-cells) (Poitout et al, 2010). There is mounting evidence that glucolipotoxicity is the cause of the decline in β-cell function found in type 2 diabetes (T2D). T2D is a chronic metabolic disorder characterised by sustained elevated blood glucose and free fatty acids, with a continuously increasing prevalence (Olokoba et al, 2012). It is estimated 415 million people currently are living with diabetes and 193 million are undiagnosed, of those 90% are T2D cases. (chatterjee et al, 2017). There are multiple aims in this thesis including the identification of GLT-induced inflammatory pathways of the pancreatic β-cell resulting from NF-κB activation. To identify novel transcription factors associated with GLT-induced reduction in insulin secretion and insulin gene expression and whether their expression is associated with the presence CD40. To observe whether the addition of carnosine to cultured cells can prevent/reverse the up-regulation in GLT-induced factors which potentially result in β-cell damage. Finally, to observed whether GLT can induce histone modifications resulting from disruption in the TCA cycle. To mimic GLT conditions INS-1 rat pancreatic β-cells were cultured in media supplemented with 28mM glucose, 200µM palmitic acid and 200µM oleic acid. The results showed following 5-day incubation ±GLT, there was an increase in TNF receptor CD40 and a CD40-dependent increase in NF-κB. Further to this exposure of INS-1 cells to GLT conditions resulted in a 3.7-fold increase in iNOS mRNA and increased 4-HNE and 3-NT adduct formation (43.4% and 33% respectively) indicating potential GLT-induced β-cell damage. The addition of 10mM carnosine was able to prevent/reverse the up-regulation of GLT-induced NF-κB activity, iNOS protein expression and 4-HNE and 3-NT adduction, identifying it as a potential therapeutic strategy for T2D. GLT-induced up-regulation of CD40 is also shown to be involved in the modulation of various genes, including insulin. siRNA down-regulation of CD40 resulted in increased insulin gene expression via modulation of ID4. Independent of CD40, a protein usually associated with MODY is observed. GLT results in 33.3% down-regulation of HNF4α, which has a knock-on effect on Rab protein expression resulting in down-regulation of insulin secretion. There by indicating that HNF4α is important in normal insulin secretion. This research found that GLT can result in acetylation of histones H3 and H4, subsequent to TCA cycle dysregulation and disruption to fatty acid synthesis and cholesterol biosynthesis pathways, indicating that GLT can affect gene transcription.
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Hill, Jennifer. "Bacterial Regulation of Host Pancreatic Beta Cell Development." Thesis, University of Oregon, 2018. http://hdl.handle.net/1794/23140.

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Diabetes is a metabolic disease characterized by the loss of functional pancreatic beta cells. The incidence of diabetes has risen rapidly in recent decades, which has been attributed at least partially to alterations in host-associated microbial communities, or microbiota. It is hypothesized that the loss of important microbial functions from the microbiota of affected host populations plays a role in the mechanism of disease onset. Because the immune system also plays a causative role in diabetes progression, and it is well documented that immune cell development and function are regulated by the microbiota, most diabetes microbiota research has focused on the immune system. However, microbial regulation is also required for the development of many other important tissues, including stimulating differentiation and proliferation. We therefore explored the possibility that the microbiota plays a role in host beta cell development. Using the larval zebrafish as a model, we discovered that sterile or germ free (GF) larvae have a depleted beta cell mass compared to their siblings raised in the presence of bacteria and other microbes. This dissertation describes the discovery and characterization of a rare and novel bacterial gene, whose protein product is sufficient to rescue this beta cell developmental defect in the GF larvae. Importantly, these findings suggest a possible role for the microbiota in preventing or prolonging the eventual onset of diabetes through induction of robust beta cell development. Furthermore, the loss of rare bacterial products such as the one described herein could help to explain why low diversity microbial communities are correlated with diabetes.
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Westermark, Pål. "Models of the metabolism of the pancreatic beta-cell." Doctoral thesis, KTH, Numerical Analysis and Computer Science, NADA, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-408.

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The pancreatic β-cell secretes insulin in response to a raised blood glucose level. Deficiencies in this control system are an important part of the etiology of diabetes. The biochemical basis of glucose-stimulated insulin secretion is incompletely understood, and a more complete understanding is an important component in the quest for better therapies against diabetes.

In this thesis, mathematical modeling has been employed in order to increase our understanding of the biochemical principles that underlie glucosestimulated insulin secretion of the pancreatic β-cell. The modeling efforts include the glycolysis in theβ-cell with particular emphasis on glycolytic oscillations. The latter have earlier been hypothesized to be the cause of normal pulsatile insulin secretion. This model puts this hypothesis into quantitative form and predicts that the enzymes glucokinase and aldolase play important roles in setting the glucose concentration threshold governing oscillations. Also presented is a model of the mitochondrial metabolism in the β-cell, and of the mitochondrial shuttles that connect the mitochondrial metabolism to the glycolysis. This model gives sound explanations to what was earlier thought to be paradoxical behavior of the mitochondrial shuttles during certain conditions. Moreover, it predicts a strong signal from glucose towards cytosolic NADPH formation, a putative stimulant of insulin secretion. The model also identifies problems with earlier interpretations of experimental results regarding the β- cell mitochondrial metabolism. As an aside, an earlier proposed conceptual model of the generation of oscillations in the TCA cycle is critically analyzed.

Further, metabolic control analysis has been employed in order to obtain mathematical expressions that describe the control by pyruvate dehydrogenase and fatty acid oxidation over different aspects of the mitochondrial metabolism and the mitochondrial shuttles. The theories developed explain recently observed behavior of these systems and provide readily testable predictions.

The methodological aspects of the work presented in the thesis include the development of a new generic enzyme rate equation, the generalized reversible Hill equation, as well as a reversible version of the classical general modifier mechanism of enzyme action.

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Pinnick, Katherine Elizabeth. "Pancreatic fat accumulation and effects on beta cell function." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492051.

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Type 2 Diabetes Mellitus (T2DM) is characterised by impaired pancreatic 13-cell function resulting in inadequate insulin secretion. The mechanisms involved in 13-cell dysfunction are largely unknown. Elevated fasting plasma non-esterified fatty acid (NEFA) concentrations have been identified as a risk factor for the development of T2DM. The work in this thesis investigates functional effects of NEFA on the 13-cell. Prolonged exposure to elevated NEFA has previously been associated with impaired insulin secretion, reduced insulin content and altered gene expression and lipid metabolism in the 13-cell. Determining the reversibility of these defects may lead to a greater understanding of the underlying mechanisms. Increased pancreatic fat content is positively associated with body mass index in humans and this may expose the 13-cell to high NEFA concentrations. However, the in vivo concentration and composition of NEFA in the pancreas is not known. An in vitro model of 13-cell 'recovery' from the deleterious effects of fatty acids is presented. The longterm culture (>48h) of mouse islets and INS-1 cells with NEFA (0.5mM) impaired glucose and tolbutamide-stimulated insulin secretion, but this was partially reversed by culture for 24h in the absence of exogenous fatty acids. Culture with oleic acid led to the accumulation of triacylglycerol (TAG) in cytosolic lipid droplets. The protein ADFP was found in close association with these droplets. In contrast, culture with palmitic acid produced large cytoplasmic 'splits'. The removal of exogenous fatty acids from the culture media led to a visible reduction in these morphological features. Extraction of the cellular lipids confirmed an increase in the TAG content following culture with NEFA and demonstrated the incorporation of the experimental fatty acid into the TAG and phospholipid (PL) fractions. Following removal of the fatty acids for 24h, TAG content was reduced and NEFA-induced changes in TAG and PL fatty acid composition were partially reversed. A reduction in TAG content in 'recovering' cells indicated the presence of active Iipases. Culture with NEFA increased lipolysis as shown by the measurement of glycerol in the culture media, but this was reduced in 'recovering' cells. Lipase inhibitors inhibited glycerol release but failed to inhibit a reduction in TAG content, and did not confirm a role for Iipases in the recovery of stimulated insulin secretion. Exposure of INS-1 cells to NEFA increased their oxidative capacity for fatty acids and this remained elevated in 'recovering' cells. Treatment with the CPT-1 inhibitor, etomoxir (10I-lM), impaired the fatty acid oxidative capacity of the 13-cell but did not affect the recovery of insulin secretion. A number of genes were upregulated following prolonged culture with NEFA, these included insulin I and II, CPT-1 and UCP2. These genes all displayed reduced expression in cells cultured further in the absence of exogenous fatty acids. The content and composition of fat in tissues from mice was investigated. The TAG composition reflected the major fatty acids found in the diet, with elevated proportions of palmitic and palmitoleic acid indicating the contribution of de novo lipogenesis and desaturase activity to this fatty acid pool. Pancreatic PL were highly unsaturated compared to liver PL, with arachidonic acid accounting for -25% of the PL fatty acids. In mice fed a high-fat (40%) diet (HFD) which was compositionally matched to a control (5%) diet, a 20-fold increase in pancreatic fat was found by 15 weeks. Adipocytes, which were positively labeled for perilipin were observed in the exocrine tissue of the pancreas in HFD mice and lipid droplets labeled for ADFP were identified in the cytoplasm of exocrine cells. By 15 weeks, the fatty acid composition of the TAG, PL and NEFA fractions showed significant differences between HFD and control mice. Perilipin-positive adipocytes were also identified in human pancreas samples and the percentage adipocyte area in histological sections positively correlated (r=0.64) to total pancreatic TAG content. In conclusion, the in vitro findings show the deleterious effects of fatty acids are not permanent. However, increased fat accumulation in the pancreas, as seen in obesity, could expose the 13-cell to elevated NEFA concentrations which, over many years, may lead to irreversible 13-cell failure.
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Yang, Yu Hsuan Carol. "Identification and characterization of pancreatic beta-cell survival factors." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/46424.

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Hughes, Jonathan Martyn. "Streptozotocin and sugar transport in pancreatic beta cell lines." Thesis, University of Bath, 1993. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386772.

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Duffy, Joan. "Effects of insulin sensitising agents on pancreatic beta cell function." Thesis, University of Ulster, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399052.

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Halvorsen, Tanya L. "Growth regulation and differentiation in the human pancreatic beta cell /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3000408.

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Books on the topic "Pancreatic beta-cell"

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Illani, Atwater, Rojas Eduardo 1936-, and Soria Bernat, eds. Biophysics of the pancreatic [beta]-cell. New York: Plenum Press, 1986.

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Illani, Atwater, Rojas Eduardo, and Soria Bernat, eds. Biophysics of the pancreatic (beta)-cell. New York: Plenum Press, 1987.

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Seino, Susumu, and Graeme I. Bell, eds. Pancreatic Beta Cell in Health and Disease. Tokyo: Springer Japan, 2008. http://dx.doi.org/10.1007/978-4-431-75452-7.

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Susumu, Seino, and Bell Graeme, eds. Pancreatic beta cell in health and disease. [Tokyo]: Springer, 2008.

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Susumu, Seino, and Bell Graeme, eds. Pancreatic beta cell in health and disease. [Tokyo]: Springer, 2008.

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Duffy, Joan. Effects of insulin sensitising agents on pancreatic beta cell function. [S.l: The Author], 2003.

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Douglas, Hanahan, McDevitt Hugh O, and Cahill George F. 1927-, eds. Perspectives on the molecular biology and immunology of the pancreatic [beta] cell. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 1989.

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Caraher, Emma M. Studies on complement activation in IDDM patient sera and possible mechanisms of pancreatic [beta]-cell dysfunction and death. Dublin: University College Dublin, 1997.

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patterson, Steven. Homocysteine and the effects of other amino thiols on pancreatic beta cell function and insulin. [S.l: The Author], 2003.

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Picton, Sally Frances. Acute and long-term effects of nutrients, nutrient esters. drugs and cytotoxins on pancreatic beta cell function and integrity. [S.l: The Author], 2003.

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Book chapters on the topic "Pancreatic beta-cell"

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Lacy, Paul E. "Pancreatic Beta Cell." In Ciba Foundation Symposium - Aetiology of Diabetes Mellitus and its Complications (Colloquia on Endocrinology, Vol. 15), 75–88. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719350.ch5.

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Velasco, Myrian, Carlos Larqué, Carlos Manlio Díaz-García, Carmen Sanchez-Soto, and Marcia Hiriart. "Rat Pancreatic Beta-Cell Culture." In Neurotrophic Factors, 261–73. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7571-6_20.

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Hawthorne, Wayne John. "Beta Cell Therapies for Type 1 Diabetes." In Pancreatic Islet Biology, 285–322. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45307-1_12.

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Takasawa, Shin, Asako Itaya-Hironaka, Akiyo Yamauchi, Hiroyo Ota, Maiko Takeda, Sumiyo Sakuramoto-Tsuchida, Takanori Fujimura, and Hiroki Tsujinaka. "Regulators of Beta-Cell Death and Regeneration." In Pancreatic Islet Biology, 125–58. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45307-1_6.

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Collier, J. Jason, and Susan J. Burke. "Pancreatic Islet Beta-Cell Replacement Strategies." In Cell Engineering and Regeneration, 193–214. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-08831-0_3.

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Collier, J. Jason, and Susan J. Burke. "Pancreatic Islet Beta-Cell Replacement Strategies." In Cell Engineering and Regeneration, 1–23. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-37076-7_3-1.

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Fiaschi-Taesch, Nathalie, George Harb, Esra Karsiloglu, Karen K. Takane, and Andrew F. Stewart. "Cell Cycle Regulation in Human Pancreatic Beta Cells." In Stem Cell Therapy for Diabetes, 85–103. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-366-4_3.

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Téllez, Noèlia, and Eduard Montanya. "Determining Beta Cell Mass, Apoptosis, Proliferation, and Individual Beta Cell Size in Pancreatic Sections." In Methods in Molecular Biology, 313–37. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0385-7_21.

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Montanya, Eduard, and Noèlia Téllez. "Pancreatic Remodeling: Beta-Cell Apoptosis, Proliferation and Neogenesis, and the Measurement of Beta-Cell Mass and of Individual Beta-Cell Size." In Methods in Molecular Biology, 137–58. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-448-3_11.

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Ackeifi, Courtney A., Ethan A. Swartz, and Peng Wang. "Cell-Based Methods to Identify Inducers of Human Pancreatic Beta-Cell Proliferation." In Methods in Molecular Biology, 87–100. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7847-2_7.

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Conference papers on the topic "Pancreatic beta-cell"

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Müller, N., C. Wessel, K. Grieß, C. Polanski, and BF Belgardt. "The Tp53 network regulates pancreatic beta cell survival." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641770.

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Lorza-Gil, E., F. Gerst, M. Beilmann, HU Häring, and S. Ullrich. "Improved beta-cell function of human pancreatic microislets." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641824.

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Kluth, O., H. Aga, P. Gottmann, M. Stadion, S. Scherneck, U. Krus, C. Ling, JG Gerdes, and A. Schürmann. "The role of cilia genes in pancreatic beta-cell proliferation." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641775.

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Grieß, K., C. Polanski, D. Markgraf, E. Lammert, M. Roden, H. Stark, J. Brüning, and BF Belgardt. "The role of ceramide synthases in pancreatic beta cell demise." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641776.

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Vinchhi, Bakul, Christophe Boss, Aurelie Hermant, Nicolas Bouche, Umberto de Marchi, and Catherine Dehollain. "Optical pancreatic beta cell based biosensor, applications and glucose monitoring." In 2019 IEEE SENSORS. IEEE, 2019. http://dx.doi.org/10.1109/sensors43011.2019.8956793.

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Deep, Harkanwal, Pantelis Georgiou, and Christofer Toumazou. "A silicon pancreatic beta cell based on the phantom bursting model." In 2011 IEEE Biomedical Circuits and Systems Conference (BioCAS). IEEE, 2011. http://dx.doi.org/10.1109/biocas.2011.6107780.

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Sliker, Bailee, Cassie Liu, Brittany Poelaert, Benjamin Goetz, and Joyce C. Solheim. "Abstract B028: Beta 2-microglobulin promotes human pancreatic cancer cell migration." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-b028.

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Vinchhi, Bakul, Ninad Agashe, Christophe Boss, Aurelie Hermant, Nicolas Bouche, Umberto de Marchi, and Catherine Dehollain. "Pancreatic beta cell based optical biosensor and system for continuous glucose monitoring." In 2019 IEEE Biomedical Circuits and Systems Conference (BioCAS). IEEE, 2019. http://dx.doi.org/10.1109/biocas.2019.8919186.

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McVerry, Bryan J., Yoshio Watanabe, J. Crout, Euhan J. Lee, Baobo Zou, K. L. Skalka, Lia C. Romano, Adolfo Garcia-Ocana, Laura C. Alonso, and Christopher P. O'Donnell. "Endotoxemia Impairs Compensatory Pancreatic Beta Cell Secretory Function In Mildly Hyperglycemic Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4692.

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Simmons, D. J., M. Krukowski, L. X. Bi, and E. Mainous. "Positively and Negatively-Charged Ion Exchange Resins: Disparate Effects on Hard Tissue Repair." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0310.

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Abstract:
Abstract Bioelectrical investigations have long shown that surfaces of bone formation and resorption are negatively and positively charged respectively. We also know that in a number of experimental situations [1], implants of negatively-charged ion exchange resin (NCR= Sephadex, CM)are osteotropic, and that implants of positively-charged resin (PCR= Sephadex DEAE) strongly inhibit bone formation [2]. While the cellular mechanism of action for NCR is thought to involve the local production of transforming growth factor beta [3], the mechanics of PCR action is an unknown. Our laboratory has shown that PCR stunts the in vitro growth of medullary osteoprogenitor cells, normal and transformed osteoblasts, and a number of tumor cell lines [4], PCR was also able to strongly inhibit hamster pancreatic cell engraftment and the growth of established pancreatic cell tumors.
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Reports on the topic "Pancreatic beta-cell"

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Pernarowski, M., J. Kevorkian, and R. Miura. The Sherman-Rinzel-Keizer model for bursting electrical activity in the pancreatic. beta. -cell. Office of Scientific and Technical Information (OSTI), March 1990. http://dx.doi.org/10.2172/7165555.

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