Gotowe bibliografie tematyczne / Pancreatic beta-cell

Spis treści

  1. Artykuły w czasopismach
  2. Rozprawy doktorskie
  3. Książki
  4. Części książek
  5. Streszczenia konferencji
  6. Raporty organizacyjne

Gotowa bibliografia na temat „Pancreatic beta-cell”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 25 lipca 2025

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Artykuły w czasopismach na temat "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 (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-hypophys
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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 (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 soma
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Grossman, E., J. Tao, D. Lee, and A. Chong. "QUANTIFYING PANCREATIC BETA-CELL REGENERATION." Transplantation 86, Supplement (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 (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 (2004): 329–41. http://dx.doi.org/10.1007/s11938-004-0046-9.

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Bartolomé, Alberto. "The Pancreatic Beta Cell: Editorial." Biomolecules 13, no. 3 (2023): 495. http://dx.doi.org/10.3390/biom13030495.

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Russ, Holger A., Limor Landsman, Christopher L. Moss, et al. "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 hE
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Tambuwal, Umar M., Sabir A. Ahmad, Sada K. Bello, et al. "Comparing the Effect of Exercise and Metformin on Pancreatic Beta Cell Function in Nigerians with Prediabetes: A Randomized Controlled Trial." East African Scholars Journal of Medical Sciences 8, no. 04 (2025): 114–21. https://doi.org/10.36349/easms.2025.v08i04.001.

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Prediabetes is an important risk factor for the development of type 2 diabetes and is common in Nigeria. Effective intervention can reverse the underlying pathogenesis of pancreatic beta-cell dysfunction in prediabetes. Several studies have reported the prevalence of prediabetes across Nigeria, but lack information on the effect of intervention or natural outcome on pancreatic beta-cell function among Nigerians with prediabetes. The objective of this study was to determine and compare the effect of moderate exercise and metformin on pancreatic beta-cell function among participants with prediab
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Bouwens, Luc, and Ilse Rooman. "Regulation of Pancreatic Beta-Cell Mass." Physiological Reviews 85, no. 4 (2005): 1255–70. http://dx.doi.org/10.1152/physrev.00025.2004.

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Beta-cell mass regulation represents a critical issue for understanding diabetes, a disease characterized by a near-absolute (type 1) or relative (type 2) deficiency in the number of pancreatic beta cells. The number of islet beta cells present at birth is mainly generated by the proliferation and differentiation of pancreatic progenitor cells, a process called neogenesis. Shortly after birth, beta-cell neogenesis stops and a small proportion of cycling beta cells can still expand the cell number to compensate for increased insulin demands, albeit at a slow rate. The low capacity for self-repl
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Laughlin, Maren. "Why Image the Pancreatic Beta Cell?" Current Medicinal Chemistry-Immunology, Endocrine & Metabolic Agents 4, no. 4 (2004): 251–52. http://dx.doi.org/10.2174/1568013043357482.

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Rozprawy doktorskie na temat "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 coinci
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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
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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 b
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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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<p>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.</p><p>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 effo
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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 1
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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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Książki na temat "Pancreatic beta-cell"

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Brennand, Kristen Jennifer. Beta cell replication and differentiation. Harvard University, 2007.

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

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

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Seino, Susumu, and Graeme I. Bell, eds. Pancreatic Beta Cell in Health and Disease. 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. Springer, 2008.

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

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Lund, Per-Eric. Ca2+ signalling in the pancreatic [beta]-cell. Acta Universitatis Upsaliensis, 1994.

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

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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. University College Dublin, 1997.

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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 Laboratory, 1989.

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Części książek na temat "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). 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. 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. 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, et al. "Regulators of Beta-Cell Death and Regeneration." In Pancreatic Islet Biology. 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. 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. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-37076-7_3-1.

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Shetty, Roshni, Radhika Singh-Agarwal, Stefan Meier, Christian Goetz, and Andrew G. Edwards. "Reconstruction of a Pancreatic Beta Cell Network From Heterogeneous Functional Measurements." In Computational Physiology. Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-53145-3_5.

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AbstractIntercellular heterogeneity is fundamental to most biological tissues. For some cell types, heterogeneity is thought to be responsible for distinct cellular phenotypes and functional roles. In the pancreatic islet, subsets of phenotypically distinct beta cells (hub and leader cells) are thought to coordinate electrical activity of the beta cell network. This hypothesis has been addressed by experimental and computational approaches, but none have attempted to reconstruct functional specialization directly from measured heterogeneity. To evaluate if electrophysiologic heterogeneity alon
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Ragbetli, Murat Cetin, and Aysenur Kaya. "Histopathological Changes in Diabetic Pancreas." In Current Multidisciplinary Approach to Diabetes Mellitus Occurrence Mechanism. Nobel Tip Kitabevleri, 2023. http://dx.doi.org/10.69860/nobel.9786053359104.3.

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Histopathological changes in the diabetic pancreas are characterized by several key alterations that impact its structure and function. In type 1 diabetes mellitus (T1DM), autoimmune destruction of insulin-producing beta cells within the pancreatic islets results in their selective loss, termed insulitis. This process involves infiltration of immune cells such as T lymphocytes and macrophages into the islets, leading to progressive beta cell destruction and ultimately insulin deficiency. In contrast, type 2 diabetes mellitus (T2DM) is associated with insulin resistance and eventual beta cell d
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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. 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. Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0385-7_21.

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Streszczenia konferencji na temat "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, et al. "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, et al. "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, et al. "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, et al. "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 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 sho
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Raporty organizacyjne na temat "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), 1990. http://dx.doi.org/10.2172/7165555.

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Jiang, Yingling, Yan Hu, Yanying Guo, and Chen Lihua Chen. Stem Cell-derived Exosome Can Preserve Pancreatic Beta Cell Function：a systematic review and meta-analysis of preclinical studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2024. http://dx.doi.org/10.37766/inplasy2024.11.0005.

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