Relevant bibliographies by topics / Langerhans islet

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Academic literature on the topic 'Langerhans islet'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Langerhans islet"

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Miralles, Francisco, Tadej Battelino, Paul Czernichow, and Raphael Scharfmann. "TGF-β Plays a Key Role in Morphogenesis of the Pancreatic Islets of Langerhans by Controlling the Activity of the Matrix Metalloproteinase MMP-2." Journal of Cell Biology 143, no. 3 (November 2, 1998): 827–36. http://dx.doi.org/10.1083/jcb.143.3.827.

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Islets of Langerhans are microorgans scattered throughout the pancreas, and are responsible for synthesizing and secreting pancreatic hormones. While progress has recently been made concerning cell differentiation of the islets of Langerhans, the mechanism controlling islet morphogenesis is not known. It is thought that these islets are formed by mature cell association, first differentiating in the primitive pancreatic epithelium, then migrating in the extracellular matrix, and finally associating into islets of Langerhans. This mechanism suggests that the extracellular matrix has to be degraded for proper islet morphogenesis. We demonstrated in the present study that during rat pancreatic development, matrix metalloproteinase 2 (MMP-2) is activated in vivo between E17 and E19 when islet morphogenesis occurs. We next demonstrated that when E12.5 pancreatic epithelia develop in vitro, MMP-2 is activated in an in vitro model that recapitulates endocrine pancreas development (Miralles, F., P. Czernichow, and R. Scharfmann. 1998. Development. 125: 1017–1024). On the other hand, islet morphogenesis was impaired when MMP-2 activity was inhibited. We next demonstrated that exogenous TGF-β1 positively controls both islet morphogenesis and MMP-2 activity. Finally, we demonstrated that both islet morphogenesis and MMP-2 activation were abolished in the presence of a pan-specific TGF-β neutralizing antibody. Taken together, these observations demonstrate that in vitro, TGF-β is a key activator of pancreatic MMP-2, and that MMP-2 activity is necessary for islet morphogenesis.
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Da Silva Xavier, Gabriela. "The Cells of the Islets of Langerhans." Journal of Clinical Medicine 7, no. 3 (March 12, 2018): 54. http://dx.doi.org/10.3390/jcm7030054.

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Islets of Langerhans are islands of endocrine cells scattered throughout the pancreas. A number of new studies have pointed to the potential for conversion of non-β islet cells in to insulin-producing β-cells to replenish β-cell mass as a means to treat diabetes. Understanding normal islet cell mass and function is important to help advance such treatment modalities: what should be the target islet/β-cell mass, does islet architecture matter to energy homeostasis, and what may happen if we lose a particular population of islet cells in favour of β-cells? These are all questions to which we will need answers for islet replacement therapy by transdifferentiation of non-β islet cells to be a reality in humans. We know a fair amount about the biology of β-cells but not quite as much about the other islet cell types. Until recently, we have not had a good grasp of islet mass and distribution in the human pancreas. In this review, we will look at current data on islet cells, focussing more on non-β cells, and on human pancreatic islet mass and distribution.
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Bucher, Mathe, Bosco, Andres, Bühler, Morel, and Berney. "Islet of Langerhans Transplantation for the Treatment of Type 1 Diabetes." Swiss Surgery 9, no. 5 (October 1, 2003): 242–46. http://dx.doi.org/10.1024/1023-9332.9.5.242.

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Islet of Langerhans transplantation is gaining recognition as a therapy for type 1 diabetes. The procedure involves enzymatic digestion of the pancreatic tissue, purification of the islets from the exocrine tissue, infusion of the islets into the portal vein and implantation in the liver. Until 1999, an overall rate of insulin independence of 14% at one year was reported in the International Islet Transplant Registry. The results of the "Edmonton protocol" since 2000 were a breakthrough in the field, with reports of 80% insulin independence at 1-year after solitary islet transplantation in non uremic patients with brittle type 1 diabetes. A rapamycin-based, steroid-free, islet-sparing immunosuppressive regimen was designed and the problem of the insufficient islet mass was tackled by sequential infusions of islets isolated from at least two pancreata. The University of Geneva has been involved in clinical islet transplantation since 1992, and has performed 51 allogeneic and 17 autologous. Twenty-one patients have been transplanted in Geneva since 2002. They were five solitary islet transplants, 14 islet after kidney transplants and two simultaneous islet-kidney (SIK) recipients. Insulin independence was achieved in 67%.
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Goess, Ruediger, Ayse Mutgan, Umut Çalışan, Yusuf Erdoğan, Lei Ren, Carsten Jäger, Okan Safak, et al. "Patterns and Relevance of Langerhans Islet Invasion in Pancreatic Cancer." Cancers 13, no. 2 (January 11, 2021): 249. http://dx.doi.org/10.3390/cancers13020249.

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Background: Pancreatic cancer‐associated diabetes mellitus (PC‐DM) is present in most patients with pancreatic cancer, but its pathogenesis remains poorly understood. Therefore, we aimed to characterize tumor infiltration in Langerhans islets in pancreatic cancer and determine its clinical relevance. Methods: Langerhans islet invasion was systematically analyzed in 68 patients with pancreatic ductal adenocarcinoma (PDAC) using histopathological examination and 3D in vitro migration assays were performed to assess chemoattraction of pancreatic cancer cells to islet cells. Results: Langerhans islet invasion was present in all patients. We found four different patterns of islet invasion: (Type I) peri‐insular invasion with tumor cells directly touching the boundary, but not penetrating the islet; (Type II) endo‐insular invasion with tumor cells inside the round islet; (Type III) distorted islet structure with complete loss of the round islet morphology; and (Type IV) adjacent cancer and islet cells with solitary islet cells encountered adjacent to cancer cells. Pancreatic cancer cells did not exhibit any chemoattraction to islet cells in 3D assays in vitro. Further, there was no clinical correlation of islet invasion using the novel Islet Invasion Severity Score (IISS), which includes all invasion patterns with the occurrence of diabetes mellitus. However, Type IV islet invasion was related to worsened overall survival in our cohort. Conclusions: We systematically analyzed, for the first time, islet invasion in human pancreatic cancer. Four different main patterns of islet invasion were identified. Diabetes mellitus was not related to islet invasion. However, more research on this prevailing feature of pancreatic cancer is needed to better understand underlying principles.
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Goess, Ruediger, Ayse Ceren Mutgan, Umut Çalışan, Yusuf Ceyhun Erdoğan, Lei Ren, Carsten Jäger, Okan Safak, et al. "Patterns and Relevance of Langerhans Islet Invasion in Pancreatic Cancer." Cancers 13, no. 2 (January 11, 2021): 249. http://dx.doi.org/10.3390/cancers13020249.

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Background: Pancreatic cancer‐associated diabetes mellitus (PC‐DM) is present in most patients with pancreatic cancer, but its pathogenesis remains poorly understood. Therefore, we aimed to characterize tumor infiltration in Langerhans islets in pancreatic cancer and determine its clinical relevance. Methods: Langerhans islet invasion was systematically analyzed in 68 patientswith pancreatic ductal adenocarcinoma (PDAC) using histopathological examination and 3D in vitro migration assays were performed to assess chemoattraction of pancreatic cancer cells to isletcells. Results: Langerhans islet invasion was present in all patients. We found four different patterns of islet invasion: (Type I) peri‐insular invasion with tumor cells directly touching the boundary, but not penetrating the islet; (Type II) endo‐insular invasion with tumor cells inside the round islet; (Type III) distorted islet structure with complete loss of the round islet morphology; and (Type IV)adjacent cancer and islet cells with solitary islet cells encountered adjacent to cancer cells. Pancreatic cancer cells did not exhibit any chemoattraction to islet cells in 3D assays in vitro. Further, there was no clinical correlation of islet invasion using the novel Islet Invasion Severity Score (IISS), which includes all invasion patterns with the occurrence of diabetes mellitus. However, Type IV islet invasion was related to worsened overall survival in our cohort. Conclusions: We systematically analyzed, for the first time, islet invasion in human pancreatic cancer. Four different main patterns of islet invasion were identified. Diabetes mellitus was not related to islet invasion. However, moreresearch on this prevailing feature of pancreatic cancer is needed to better understand underlying principles.
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Crowther, N. J., C. F. Gotfredsen, A. J. Moody, and I. C. Green. "Immunological and insulin secretory studies on isolated porcine islets of Langerhans." Journal of Endocrinology 126, no. 1 (July 1990): 43–49. http://dx.doi.org/10.1677/joe.0.1260043.

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ABSTRACT Since porcine islets are considered a likely tissue source for islet transplantation we have studied the insulin secretory responses to stimuli and some of the cell surface antigen characteristics of porcine islet cells. In a static incubation system, the threshold level of glucose required for the stimulation of insulin secretion from freshly isolated porcine islets was found to be between 2·8 and 4·2 mmol glucose/l. Arginine (5 mmol/l) and 3-isobutyl-1-methylxanthine (1 mmol/l) potentiated insulin release induced by 8·3 mmol glucose/l. Leucine (5 mmol/l) initiated release in the presence of 2 mmol glucose/l. Neither β-hydroxybutyrate (10 mmol/l) nor octanoate (5 mmol/l) potentiated insulin release induced by 8·3 mmol glucose/l, but β-hydroxybutyrate initiated release in the presence of 2 mmol glucose/l while octanoate did not. A 125I-labelled protein A binding assay and an enzyme-linked immunosorbent assay system were used to detect antibody binding to islet and non-islet cells. Monoclonal antibodies raised against intact rat islets were shown to bind to both porcine and rat islet cells but not to rat hepatoma tissue culture cells or rat insulinoma cells. The serum from recently diagnosed type I diabetics was shown to bind to rat islet cells in a 125I-labelled protein A binding assay, while serum from control subjects showed little, if any, binding. Porcine islet cells were unable to distinguish between the sera of recently diagnosed type I diabetics and controls in a similar assay. In conclusion, porcine islets respond to many of the major insulin secretagogues to which human islets are sensitive. However, they have a lower secretory response to these compounds compared with that reported for human islets. Monoclonal antibody and human sera binding studies show that rat and porcine islets share some cell surface antigens but it remains to be seen whether the inability of porcine islets to discriminate between diabetic and non-diabetic sera is an advantage for transplantation, indicating less likelihood of an islet-specific autoimmune-like humoral attack. Journal of Endocrinology (1990) 126, 43–4
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Van Der Burg, Michael P. M., Onno R. Guicherit, Marijke Frölich, Frans A. Prins, Jan Anthonie Bruijn, and Hein G. Gooszen. "Cell Preservation in University of Wisconsin Solution during Isolation of Canine Islets of Langerhans." Cell Transplantation 3, no. 4 (July 1994): 315–24. http://dx.doi.org/10.1177/096368979400300408.

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Allogeneic islet transplantation in Type I diabetic patients is considerably hampered by the variable outcome of islet isolation and purification. After collagenase digestion of the pancreas, islet isolation is traditionally performed under hypothermic conditions in physiological solutions such as Hanks and RPMI. The University of Wisconsin solution (UWS) has been shown superior for hypothermic preservation of the pancreas. We, therefore, compared the UWS and RPMI for canine islet isolation and subsequent purification in either a conventional hyperosmotic density gradient of dextran in Hanks, or a novel normosmotic density gradient of Percoll in UWS. The isolation solution did not affect islet yield before purification (51% of the native islet mass). Loss of amylase (30%) and swelling of the acinar cells were observed in RPMI. In contrast, no loss of amylase and slight shrinkage of the acinar cells were observed in the UWS. Cell swelling affected the density separation and viability of the cells. Dextran density separation resulted in a 15% purity and 41% recovery of the islets isolated in RPMI, as compared to a 93% purity and 52% recovery of islets isolated in UWS. Percoll density separation improved the purity (99%) and recovery (74%) of islets isolated in UWS. Islets isolated in UWS demonstrated a superior basal and glucose stimulated insulin release during perifusion. Electron microscopy demonstrated a well-preserved islet ultrastructure after isolation in both solutions — except for slightly swollen mitochondria after isolation in RPMI. Autotransplantation of islets in pancreatectomised dogs was successful both after isolation in UWS and RPMI. We conclude that prevention of cell swelling during isolation and purification in the UWS resulted in an improved yield of viable and consistent virtually pure islets. Prevention of cell swelling during islet isolation should facilitate the analysis and control of other factors affecting outcome in man.
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Samejima, Tadashi, Kenji Yamaguchi, Hiroo Iwata, Noriyuki Morikawa, and Yoshito Ikada. "Gelatin Density Gradient for Isolation of Islets of Langerhans." Cell Transplantation 7, no. 1 (January 1998): 37–45. http://dx.doi.org/10.1177/096368979800700106.

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Isolation of islets of Langerhans (islets) has been performed by means of collagenase digestion of the pancreatic tissue combined with density gradient separation of islets from unwanted exocrine tissues. An enormous number of islets are necessary for clinical islet transplantation. The density gradient used for isolation of a large number of islets should satisfy several requirements in addition to those for the conventional density gradients, such as high viscosity for creating fine interfaces with a large area, easy sterilization, and low cost. This study is concerned with the development of a new density gradient made of low-molecular-weight gelatin. We isolated islets from the hamster pancreatic tissue using the gelatin density gradients. The yield and purity of islet and its insulin release function were compared with those of islets isolated using Ficoll and Ficoll-Conray density gradients that have been conventionally used. The new gelatin density gradient can separate islets from the unwanted exocrine tissue as effectively as the Ficoll density gradient and more effectively than the Ficoll-Conray density gradients. The islets collected using the gelatin gradient retain ability of insulin release increase in response to glucose stimulation, similar to those isolated by the Ficoll-Conray gradient and more than those collected by the Ficoll gradient. In addition, the gelatin effectively inhibited enzyme activities, that is, collagenase and proteolytic enzymes released from the exocrine tissue, and thus it can inhibit overdigestion of islets during their density gradient isolation. The gelatin gradient satisfies most of the additional requirements for islet isolation from the pancreatic tissue of large animals mentioned above. Although several factors, such as molecular weight of gelatin, osmolality of the gradient, and centrifugal conditions, still remain to be optimized, our results suggest that the gelatin gradient has potentiality to isolate islets from the pancreatic tissue of a large animal.
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Westermark, Gunilla T., and Per Westermark. "Transthyretin and Amyloid in the Islets of Langerhans in Type-2 Diabetes." Experimental Diabetes Research 2008 (2008): 1–7. http://dx.doi.org/10.1155/2008/429274.

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Transthyretin (TTR) is a major amyloid fibril protein in certain systemic forms of amyloidosis. It is a plasma protein, mainly synthesized by the liver but expression occurs also at certain minor locations, including the endocrine cells in the islets of Langerhans. With the use of immunohistochemistry and in situ hybridization, we have studied the distribution of transthyretin-containing cells in islets of Langerhans in type-2 diabetic and nondiabetic individuals. TTR expression was particularly seen in alpha (glucagon) cells. Islets from type-2 diabetic patients had proportionally more transthyretin-reactive islet cells, including beta cells. A weak transthyretin immunoreaction in IAPP-derived amyloid occurred in some specimens. In seeding experiments in vitro, we found that TTR fibrils did not seed IAPP while IAPP fibrils seeded TTR. It is suggested that islet expression of transthyretin may be altered in type-2 diabetes.
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Hurst, R. D., S. L. F. Chan, and N. G. Morgan. "Effects of benextramine on the adrenergic inhibition of insulin secretion in isolated rat pancreatic islets." Journal of Molecular Endocrinology 2, no. 2 (March 1989): 99–105. http://dx.doi.org/10.1677/jme.0.0020099.

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ABSTRACT Insulin secretion from isolated rat islets of Langerhans in the presence of 4 mm glucose averaged 2·26 ± 0·20 (s.e.m.) ng/islet per 90 min and was significantly (P<0·001; n=30) increased to 3·28 ± 0·21 ng/islet per 90 min by the covalent α-adrenoceptor antagonist benextramine (10 μm). Glucose (20 mm) also increased the secretion rate (to 6·24 ± 6·0 ng/islet per 90 min) but, under these conditions, the response was not further enhanced by benextramine. Clonidine and noradrenaline (1 nm–10 μm) each caused dose-dependent inhibition of glucose-induced insulin secretion which was maximal at 1 μm. Benextramine, when added simultaneously with the agonist, relieved, in a dosedependent manner, the inhibition of secretion induced by either clonidine or noradrenaline with similar sensitivity. Even after a 30-min preincubation with benextramine the antagonist failed to differentiate between noradrenaline, adrenaline and clonidine with respect to inhibition of insulin secretion. In contrast to its effects on adrenergic responses, short-term treatment with benextramine did not significantly affect muscarinic—cholinergic receptor-mediated 45Ca2+ efflux from rat islets of Langerhans perifused in Ca2+-depleted medium. These data suggest that benextramine does not differentiate between clonidine and noradrenaline in rat islets of Langerhans but that it does show preference for α-adrenoceptors in this tissue.
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Dissertations / Theses on the topic "Langerhans islet"

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Ar'Rajab, Aamer. "Islet transplantation in the treatment of diabetes number of islets, functional regulation and metabolic control /." Lund : Dept. of Surgery, Lund University, 1991. http://catalog.hathitrust.org/api/volumes/oclc/38187937.html.

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Nyqvist, Daniel. "In vivo imaging of islet cells and islet revascularization /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-116-6/.

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Alves, Figueiredo Hugo Jorge. "Improving islet-graft revascularization." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/586309.

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El trasplante de islotes ha sido reconocido como una prometedora opción de tratamiento de la diabetes tipo 1 (DT1) tras la introducción del protocolo de Edmonton, el cual enfatiza el requerimiento de un adecuado número de islotes donantes así como el uso de regímenes de inmunosupresores libres de esteroides. Además es un procedimiento quirúrgico menos invasivo y que conlleva menos complicaciones comparado con el trasplante de páncreas. A pesar de los importantes avances establecidos por el protocolo de Edmonton, el uso clínico del trasplante de islotes para el tratamiento de pacientes DT1 continúa siendo limitado, debido en gran parte a los retos post-trasplante. Tras el trasplante, los islotes son separados de su red vascular nativa, por lo que la funcionalidad y supervivencia del injerto dependerá del restablecimiento de nuevos vasos en el injerto para derivar el flujo sanguíneo al sistema vascular del huésped. Sin embargo, los estudios han demostrado que el grado de revascularización de los islotes trasplantados es considerablemente menor que el de la microvasculatura nativa de los islotes pancreáticos, incluso a los 9 meses del injerto . Ésta retrasada y insuficiente revascularización priva los nuevos islotes injertados de oxígeno y nutrientes, pudiendo provocar su muerte celular y el fallo temprano del injerto. En el estudio realizado, identificamos, por primera vez, la proteína tirosina fosfatasa 1B (PTP-1B) como una diana terapéutica, capaz de mejorar la revascularización de los injerto pancreáticos sin comprometer la masa ß-celular del injerto y la principal mediadora de la acción del tratamiento del tungstato sódico en la revascularización de islotes. Además hemos identificado el mecanismo por lo cual la PTP-1B induce la revascularización. Nuestros datos apuntan que en la ausencia de PTP-1B, los islotes pancreáticos expresan y secretan el factor de crecimiento del endotelio vascular A (VEGFA), una citoquina pro-angiogénica, mediante la activación de la PGC1 alpha y ERR-alpha de forma independiente de hipoxia. Finalmente hemos comprobado que éste mecanismo de inducción de VEGFA se conserva en islotes humanos. De ésta forma concluimos que PTP-1B es una diana prometedora en el desarrollo de nuevas terapias para la mejora de la revascularización de injertos de islotes.
Islet transplantation is considered a potentially curative treatment for type 1 diabetes, Despite the key important advances achieved by the establishment of the Edmonton protocol, islet transplantation remains clinically limited due to several challenges, which lead to massive islet loss or failure of the grafts. Therefore searching for new targets to facilitate islet revascularization may lead to improved future results in cell transplantation.Islets native architecture is characterized by a dense vessel network that, delivers oxygen, hormones, glucose, and nutrients to islet’s cells allowing them to function correctly. After transplantation, the survival and function of islet grafts must depend on the reestablishment of new vessels within the grafts to derive blood flow from the host vascular system. This vascular network is severed when islets are isolated for transplantation, and even though islets freely revascularize, they do not reach the levels of vascularization present in endogenous pancreatic islets, which results in the impairment of grafts function and survival. Altogether, the lack of a proper vascular network account as the primary responsible for early graft loss. Although the molecular mechanisms underlying islet revascularization remain elusive, a number of factors have been implicated, such as the vascular endothelial growth factor A (VEGFA), a key angiogenic molecule that acts to stimulate new vessel formation. VEGFA expression in transplanted islets is significantly impaired, which is further pronounced in prevailing hyperglycemia, and coincides with delayed and insufficient islet revascularization in diabetic mice In this thesis we identify for the first time, tyrosine phosphatase PTP-1B as a target for improving graft revascularization. We targeted PTP-1B, either by its inhibition, following a sodium tungstate treatment after transplantation, or by transplanting islets lacking PTP-1B, using a genetic model of PTP-1B knock-out, or following genetic silencing, using siRNA and shRNA Lentivirus particles. Following transplantation into the anterior chamber of the eye in diabetic mice, islet-grafts showed increased revascularization by inducing the expression of VEGF-A by ß-cells in the graft. This improved revascularization was followed by an improvement of islet-graft survival and function, as transplanted mice recovered normoglycemia and glucose tolerance. Furthermore, we demonstrated that PTP-1B induces VEGF-A expression and secretion in islets by upregulating HIF1A-independent PGC1α/ERRα signaling. Finally, we demonstrated that this regulatory mechanism is conserved in human islets. Together, these findings unravel the potential role of PTP-1B as a target for improving islet transplantation outcomes.
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Blais, Debbie Lin Marie. "Becoming an islet cell allotransplant recipient." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq21258.pdf.

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Johansson, Ulrika. "Formation of Composite Islet Grafts A novel strategy to promote islet survival and revascularization /." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-102788.

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Coffey, Lane Claire Katherine. "Immune Cells, Inflammatory Molecules, and CD40 in Nonhuman Primate Islets of Langerhans." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/430.

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Type 1 Diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing beta cells in the pancreas. Amelioration of T1D and the prevention of its detrimental complications are possible through islet transplantation, wherein hormone-producing clusters of cells, islets of Langerhans (islets), are separated from the pancreas and transplanted into a diabetic patient. However, alterations due to the effects of organ recovery, cold ischemia time (CIT), and islet isolation may increase the inflammatory and immunogenic properties of these islets, thereby predisposing them to functional impairment and rejection in a transplant. Understanding the inflammatory properties of islets will allow for the development of strategies that decrease early islet loss and effectively enhance engraftment and long-term function. Therefore, the aims of this study were to 1) identify and characterize populations of antigen presenting cells (APC) and other immune cells in nonhuman primate (NHP) islets in situ and after isolation; and 2) characterize the expression and functional role of CD40 and the IFN alpha receptor in NHP islets, including their effects on islet immunogenicity. A surprising result of these studies was that half of the APC present in isolated NHP islets were B lymphocytes. We observed that the number of islet-resident immune cells increased with islet size, and described the localization pattern of these cells within islets. We characterized CD40 expression in NHP islets, demonstrating that multiple CD40 isoforms are expressed, and made the novel finding that functional CD40 is expressed on the somatostatin-producing δ cells. When CD40 was stimulated with its ligand, it induced downstream signaling changes, increased proinflammatory cytokine release, and increased islet immunogenicity. Based on our results, we have hypothesized a model of CD40 signaling in islet δ cells. Microarray analysis revealed expression changes in many inflammatory molecules integral to inflammation, the immune response, and apoptosis in islets that had endured increased CIT, demonstrating the unfavorable conditions created within islets following organ recovery, CIT, and islet isolation. Furthermore, we demonstrated that the IFN alpha receptor is present on isolated NHP islets, and that stimulation with IFN alpha leads to increased proinflammatory cytokine release, surface receptor upregulation, and a decrease in immunogenicity. In summary, in NHP islets we have defined the type and quantity of immune cells, the inflammatory molecules expressed, including CD40 and the IFN alpha receptor, and their downstream functional roles in an immune response.
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Cabric, Sanja. "Pancreatic Islet Transplantation : Modifications of Islet Properties to Improve Graft Survival." Doctoral thesis, Uppsala University, Department of Oncology, Radiology and Clinical Immunology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8333.

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During the past decade clinical islet transplantation has become a viable strategy for curing type 1 diabetes. The limited supply of organs, together with the requirement for islets from multiple donors to achieve insulin independence, has greatly limited the application of this approach.

The islets are infused into the liver via the portal vein, and once exposed to the blood, the grafted tissue has been shown to be damaged by the instant blood-mediated inflammatory reaction (IBMIR), which is characterized by coagulation and complement activation as well as leukocyte infiltration into the islets. Islet revascularization is a subsequent critical step for the long-term function of the transplanted graft, which may partially be impeded by the IBMIR.

In this thesis, we have explored novel strategies for circumventing the effects of the IBMIR and facilitating islet revascularization.

Systemic inhibitors of the IBMIR are typically associated with an increased risk of bleeding. We therefore evaluated alternative strategies for modulating the islets prior to transplantation. We demonstrated, using an adenoviral vector, that a high level of expression and secretion of the anticoagulant hirudin could be induced in human islets. An alternative approach to limiting the IBMIR was developed in which anticoagulant macromolecular heparin complexes were conjugated to the islet surface. This technique proved effective in limiting the IBMIR in both an in vitro blood loop model and an allogeneic porcine model of islet transplantation. An increased adhesion of endothelial cells to the heparin-coated islet surface was demonstrated, as was the capacity of the heparin conjugate to bind the angiogenic factors VEGF and FGF; these results have important implications for the revascularization process.

The outcome of the work in this thesis suggests that modulation of the islet surface is an attractive alternative to systemic therapy as a strategy for preventing the IBMIR. Moreover, the same techniques can be employed to induce revascularization and improve the engraftment of the transplanted islets. Ultimately, improved islet viability and engraftment will make islet transplantation a more effective procedure and increase the number of patients whose diabetes can be cured.

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Ma, Zhi. "Islet amyloid polypeptide (IAPP) : mechanisms of amyloidogenesis in the pancreatic islets and potential roles in diabetes mellitus /." Linköping : Univ, 2001. http://www.bibl.liu.se/liupubl/disp/disp2001/med655s.pdf.

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Sörenby, Anne. "Strategies to improve macroencapsulated islet graft survival /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-304-7/.

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Skog, Oskar. "Effects of Enterovirus Infection on Innate Immunity and Beta Cell Function in Human Islets of Langerhans." Doctoral thesis, Uppsala universitet, Klinisk immunologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-172586.

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This thesis focuses on enteroviral effects on human pancreatic islets. Most knowledge of viral effects on host cells relies on studies of immortalized cell lines or animal models. The islets represent a fundamentally different and less well studied cellular host. Also, enterovirus has been implicated in the etiology of type 1 diabetes (T1D). We show that when enterovirus replicates in human islets it activates innate immunity genes and induces secretion of the chemokines MCP-1 and IP-10. An important difference in activation of innate immunity by replicating EV and synthetic dsRNA is suggested, since the chemokine secretion induced by EV infection but not by dsRNA is reduced by female sex hormone. We also demonstrate a direct antiviral effect of nicotinamide, and even though this substance failed to prevent T1D in a large-scale study, this finding could have implications for the treatment/prevention of virus- and/or immune-mediated disease. We also had access to human pancreata from two organ donors with recent onset T1D and several donors with T1D-related autoantibodies, which gave us the opportunity to study ongoing pathogenic processes at and before the onset of T1D. Despite this, we could neither confirm nor reject the hypothesis that EV is involved in T1D development. Several observations, such as ultrastructural remodeling of the beta cell, activation of innate immunity, and immunopositivity to EV capsid protein 1, supported an ongoing virus infection, but direct evidence is still lacking. An interesting finding in the donors with recent onset T1D was that the islets were positively stained for insulin, but did not secrete insulin in response to glucose-stimulation. A similar effect was observed in EV-infected islets in vitro; EV destroyed islet function and insulin gene expression, but the islets still stained positive for insulin. This may be indicative of that a functional block in addition to beta cell destruction is involved in T1D pathogenesis. In conclusion, these studies of EV in isolated human islets in vitro support that this virus can cause T1D in vivo, but future studies will have to show if and how frequently this happens.
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Books on the topic "Langerhans islet"

1

Parker, James N., and Philip M. Parker. The official patient's sourcebook on islet cell carcinoma. Edited by Icon Group International Inc and NetLibrary Inc. San Diego, Calif: Icon Health Publications, 2002.

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Pancreas, islet and stem cell transplantation for diabetes. 2nd ed. Oxford: Oxford University Press, USA, 2010.

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Kulkarni, Rohit N. Islet cell growth factors. Austin, Tex: Landes Bioscience, 2011.

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The Pancreatic Islet Cell Transplantation Act of 2004: Report (to accompany S. 518). [Washington, D.C: U.S. G.P.O., 2004.

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Kibenge, Molly J. Twinomwe. The relationship between the hypothalamo-pituitary-adrenal axis and the development and persistence of pancreatic islet defects in obese zucker (fa/fa) rats. Charlottetown: University of Prince Edward Island, 1994.

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United States. Congress. House. Committee on Energy and Commerce. Pancreatic Islet Cell Transplantation Act of 2004: Report (to accompany H.R. 3858) (including cost estimate of the Congressional Budget Office). [Washington, D.C: U.S. G.P.O., 2004.

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United States. Congress. House. Committee on Energy and Commerce. Pancreatic Islet Cell Transplantation Act of 2004: Report (to accompany H.R. 3858) (including cost estimate of the Congressional Budget Office). [Washington, D.C: U.S. G.P.O., 2004.

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United States. Congress. House. Committee on Energy and Commerce. Pancreatic Islet Cell Transplantation Act of 2004: Report (to accompany H.R. 3858) (including cost estimate of the Congressional Budget Office). [Washington, D.C: U.S. G.P.O., 2004.

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service), SpringerLink (Online, ed. The Islets of Langerhans. Dordrecht: Springer Science+Business Media B.V., 2010.

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Islam, Md Shahidul, ed. The Islets of Langerhans. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3271-3.

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Book chapters on the topic "Langerhans islet"

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De Bartolo, Loredana, and Antonietta Messina. "Langerhans Islet." In Encyclopedia of Membranes, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-40872-4_713-1.

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De Bartolo, Loredana, and Antonietta Messina. "Langerhans Islet." In Encyclopedia of Membranes, 1087–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-44324-8_713.

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Lakey, Jonathan R. T., Lourdes Robles, Morgan Lamb, Rahul Krishnan, Michael Alexander, Elliot Botvinick, and Clarence E. Foster. "Islet Encapsulation." In Islets of Langerhans, 1297–309. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-6686-0_29.

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La Rosa, Stefano. "Islet of Langerhans." In Encyclopedia of Pathology, 1–4. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-28845-1_5191-1.

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Balamurugan, A. N., Gopalakrishnan Loganathan, Amber Lockridge, Sajjad M. Soltani, Joshua J. Wilhelm, Gregory J. Beilman, Bernhard J. Hering, and David E. R. Sutherland. "Islet Isolation from Pancreatitis Pancreas for Islet Autotransplantation." In Islets of Langerhans, 1199–227. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-6686-0_48.

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Hermann, Martin, Raimund Margreiter, and Paul Hengster. "Human Islet Autotransplantation." In Islets of Langerhans, 1229–43. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-6686-0_21.

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Marzorati, Simona, and Miriam Ramirez-Dominguez. "Mouse Islet Isolation." In Islets of Langerhans, 83–107. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-6686-0_33.

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Lakey, Jonathan R. T., Lourdes Robles, Morgan Lamb, Michael Alexander, Elliot Botvinick, and Clarence E. Foster. "Islet Encapsulation." In Islets of Langerhans, 2. ed., 1–13. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6884-0_29-2.

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Lakey, Jonathan R. T., Lourdes Robles, Morgan Lamb, Rahul Krishnan, Michael Alexander, Elliot Botvinick, and Clarence E. Foster. "Islet Encapsulation." In Islets of Langerhans, 2. ed., 1–12. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-6884-0_29-3.

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Drews, Gisela, Peter Krippeit-Drews, and Martina Düfer. "Electrophysiology of Islet Cells." In Islets of Langerhans, 249–303. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-6686-0_5.

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Conference papers on the topic "Langerhans islet"

1

Mendoza-Elias, Joshua E., José Oberholzer, and Yong Wang. "Microfluidics for Live-Cell Imaging Pancreatic Islets of Langerhans for Human Transplant." In ASME 2014 4th Joint US-European Fluids Engineering Division Summer Meeting collocated with the ASME 2014 12th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/fedsm2014-21159.

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Since the introduction of the Edmonton Protocol in 2000, islet transplantation has been emerging as promising therapy for Type I diabetes mellitus (T1DM) and currently is the only therapy that can achieve glycemic control without the need for exogenous insulin. Transplanting islet cells has several advantages over transplanting a whole pancreas in that it involves only a minor surgical procedure with low morbidity and mortality, and at a significantly lower cost. However, an obstacle to realizing this goal is a lack of an islet potency index as required by the U.S. Food and Drug Administration (FDA) biologics licensing, as well as a more complete understanding of the physiological mechanisms governing islet and β-cell physiology. Recently, the University of Illinois at Chicago (UIC) has developed a microfluidic platform that can mimic in vivo islet microenvironments through precise and dynamic control of perifusing culture media and oxygen culture levels; all while measuring functionally relevant factors including intracellular calcium levels, mitochondrial potentials, and insulin secretion. By developing an understanding of the physiology and pathophysiology of islets we can more effectively develop strategies that reduce metabolic stress and promote optimization in order to achieve improved success of islet transplantation and open new clinical avenues. The presentation begins by introducing key issues in the field of pancreatic islet transplantation as a clinical therapy for T1DM. This is followed by brief review various technologies that have been developed to study islet cells. The presentation then describes the design, application, and evolution of UIC’s microfluidic-based multimodal islet perifusion and live-cell imaging system for the study of pancreatic islet and β-cell physiology. The article then concludes presenting initial findings from studies seeking to develop an islet potency test.
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Banks, Dylan, Christina Morris, Joan Omeru, Wang Wei, Pantelis Georgiou, and Christofer Toumazou. "A CMOS pancreatic islet of Langerhans for automatic glycemic regulation." In 2011 IEEE Biomedical Circuits and Systems Conference (BioCAS). IEEE, 2011. http://dx.doi.org/10.1109/biocas.2011.6107777.

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Berggren, Per-Olof. "The islet of Langerhans is a master regulator of glucose homeostasis." In 2010 IEEE Photonics Society Winter Topicals Meeting Series (WTM 2010). IEEE, 2010. http://dx.doi.org/10.1109/photwtm.2010.5421943.

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Jansen, T., M. Buitinga, M. Boss, E. de Koning, M. Engelse, M. Nijhoff, O. Korsgren, O. Eriksson, M. Brom, and M. Gotthardt. "Assessment of intrahepatic islet of Langerhans transplantation with dynamic Ga-68-NODAGA-exendin PET imaging." In NuklearMedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1683646.

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Švihlík, Jan, Jan Kybic, and David Habart. "Automated separation of merged Langerhans islets." In SPIE Medical Imaging, edited by Martin A. Styner and Elsa D. Angelini. SPIE, 2016. http://dx.doi.org/10.1117/12.2216798.

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Švihlík, Jan, Jan Kybic, David Habart, Zuzana Berková, Peter Girman, Jan Kříž, and Klára Zacharovová. "Classification of microscopy images of Langerhans islets." In SPIE Medical Imaging, edited by Sebastien Ourselin and Martin A. Styner. SPIE, 2014. http://dx.doi.org/10.1117/12.2043621.

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South, Jack C. M., and William J. Gullick. "Abstract C48: The role of the neuregulins and their receptors in the islets of Langerhans." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-c48.

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Schönecker, S., KH Boven, and U. Kraushaar. "Beta-Screen: Non-invasive and easy to use MEA-based parallelized screening system for intact islets of Langerhans." In Late breaking Abstracts – Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1657802.

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Nieto-Chaupis, Huber. "Frequency-Based Releasing of Insulin in the Langerhans Islets To Counteract the Beginning of the Type-2 Diabetes in Pre-diabetes Patients." In 2019 IEEE 9th Annual Computing and Communication Workshop and Conference (CCWC). IEEE, 2019. http://dx.doi.org/10.1109/ccwc.2019.8666461.

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Husen, Saikhu Akhmad, Salamun, Arif Nur Muhammad Ansori, Raden Joko Kuncoroningrat Susilo, Suhailah Hayaza, and Dwi Winarni. "The Effect of Alpha-mangostin in Glucose Level, Cholesterol Level, and Diameter of the Islets of Langerhans of STZ-induced Diabetic Mice." In 2nd International Conference Postgraduate School. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0007547005610566.

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