Relevant bibliographies by topics / Islands of Langerhans – Transplantation

Academic literature on the topic 'Islands of Langerhans – Transplantation'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Islands of Langerhans – Transplantation"

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Sassa, Mariko, Yasuhiro Iwanaga, and Yuichiro Yamada. "3. Transplantation of Island of Langerhans and Regenerative Therapy." Nihon Naika Gakkai Zasshi 98, no. 4 (2009): 817–23. http://dx.doi.org/10.2169/naika.98.817.

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Voltarelli, Julio C., Carlos E. B. Couri, Maria-Carolina B. Oliveira, Ana-Beatriz P. L. Stracieri, Daniela A. Moraes, Dannielle F. Godoi, Marina A. Coutinho, et al. "Autologous Hematopoietic Stem Cell Transplantation for Type I Diabetes Mellitus." Blood 104, no. 11 (November 16, 2004): 5224. http://dx.doi.org/10.1182/blood.v104.11.5224.5224.

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Abstract Insulin-dependent type I diabetes mellitus (IDDM) is caused by autoimmune destruction of pancreatic β-islet cells mediated by inflammatory T cells. The pathogenic process evolves gradually for several years and becomes symptomatic when most Langerhans islands are destroyed. Antibodies against β-cell antigens (like anti-glutamic acid decarboxylase, GAD) are markers of the autoimmune reaction and levels of proinsulin C-peptide correlate with endogenous insulin secretion. Several immunosuppressive regimens have demonstrated clinical and laboratorial benefit in early onset IDDM, presumably sparing islets reserve, but most responses were transient and long term toxicity limited their continuous use. In view of durable remissions observed in various autoimmune diseases treated with high-dose immunosuppression and autologous hematopoietic stem cell transplantation (AHSCT), we started in December/03 a phase I/II trial of AHSCT in early-onset IDDM. Patients from 12–35 years old with <6 weeks from diagnosis have their peripheral blood stem cells mobilized with 2 g/m2 cyclophosphamide and 10 mcg/kg G-CSF, cryopreserved and reinfused (>2 million/kg) after conditioning with 200 mg/kg cyclophosphamide and 4,5 mg/kg rabbit antithymocyte globulin- ATG (Thymoglobuline, SangStat). End points of the study are insulin needs (U/kg/d), glycosilated hemoglobin levels, anti-GAD titers and C-peptide levels. Four patients have been transplanted and the insulin usage of the first three patients is shown in the Figure. The first patient received high dose of steroids to prevent ATG hypersensitivity and showed increasing needs of insulin after mobilization. The other two patients received minimal (#2) or no (#3) steroid dose during conditioning and showed decreasing needs of insulin after mobilization (Figure). Patient #2 presented bilateral pneumonia while pancytopenic, recovered after treatment with antibiotics and Amphotericin-B but did not require insulin therapy. A fourth patient has just been discharged from the BMT Unit. Immunologic studies in the three patients with longer follow-up showed a progressive shift from Th1 to Th2 cytokine profile after transplantation which could provide a mechanism for the modulation of the autoimmune process by high dose immunosuppression and autologous HSC. In conclusion, the preliminary results are encouraging but must be validated with a larger number of patients (12 planned in this phase) and a longer followup (5 years). Figure Figure
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Kovpak, V. V. "Вплив трансплантації культур клітин на перебіг експериментального цукрового діабету у тварин." Scientific Messenger of LNU of Veterinary Medicine and Biotechnologies 19, no. 78 (April 7, 2017): 41–47. http://dx.doi.org/10.15421/nvlvet7809.

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As we know from the literature data, type 1 diabetes mellitus occurs due to the loss of β-cells of island of Langerhans, manufacturing insulin, by the organism, which causes its deficiency. The treatment of this type of diabetes, even at early stages, lies in the substitution therapy together with a careful control of blood glucose which may last for life. It is for this reason that the cellular technologies as an alternative method of treatment of this pathology are growing more and more relevant.Objective of the study: to study the impact of allogenic transplantation of the cultures of bone marrow, lipid tissue and pancreas cells on the course of experimentally generated diabetes mellitus in animals.Task: 1. To obtain the cultures of bone marrow, lipid tissue and pancreas cells in rats. 2. To compare the impact of allogenic transplantation of the cultures of bone marrow, lipid tissue and pancreas cells in the course of experimentally generated diabetes mellitus in rats. 3. To study the impact of pancreas cells culture on the course of experimental diabetes mellitus in cats.The studies were conducted using clinically healthy animals (30 males of white non-pedigree rats with body weight of 200–250 g, aged 4–5 months; 9 white non-pedigree junior rats aged 12 days; 4 mongrel cats aged 15–17 months) and missed fetuses of cats remained after obstetric aid.Alloxan diabetes was generated by means of single subcutaneous injection of alloxane monohydrate in the dose of 150 mg/kg in the form of 5% solution on citrate buffer (pH 4.5) after preliminary 24-hour absolute diet with free access to water.The cultures of bone marrow and pancreas cells were obtained from the bone marrow of tubular bones and pancreas of puppies aged 12 days correspondingly, lipid tissue – from rats aged 4–5 months. The culture of cats’ pancreas cells was obtained from the pancreas of cat fetuses. Cell culture process was carried out according the standard method in CO2- incubator. Glucose level in blood serum was determined by means of electrochemical analysis.The results of the study. The authors studied the impact of allogenic transplantation cells culture of bone marrow, lipid tissue and pancreas on the course of experimentally generated diabetes mellitus in rats. The study revealed the decrease of glucose level in the blood of the animals under investigation at cell material transplantation. The most efficient culture for experimental diabetes mellitus therapy is the culture of pancreas cells which has become the cause of its further study in cats.During allogenic transplantation cells culture of pancreas in cats the authors observed abrupt decrease of glucose level in the blood of the animals under investigation immediately after cell transplantation with the further approximation to the initial state.The experimental models presented the positive effect of cell culture transplantation providing the grounds for the further implementation of this diabetes mellitus therapy method in the clinical practice.
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Nakagawara, Gizo. "Transplantation of islets of Langerhans." Journal of Hepato-Biliary-Pancreatic Surgery 1, no. 5 (October 1994): 542–45. http://dx.doi.org/10.1007/bf01211917.

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Penfornis, Alfred. "Langerhans islet preparation in cell transplantation." Transfusion Science 18, no. 2 (June 1997): 235–41. http://dx.doi.org/10.1016/s0955-3886(97)00016-7.

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6

Barakat, Hassan, Khaled Al-Roug, Raya Algonaiman, Sami A. Althwab, Hani A. Alfheeaid, Raghad M. Alhomaid, Mona S. Almujaydil, Taqwa Bushnaq, and Tarek A. Ebeid. "Biological Assessment of Stevioside and Sucralose as Sucrose Substitutes for Diabetics on STZ-Induced Diabetes in Rats." Molecules 28, no. 3 (January 17, 2023): 940. http://dx.doi.org/10.3390/molecules28030940.

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Numerous food organizations have identified excessive calorie consumption and accompanying ailments as significant health risks associated with high sugar consumption. Administering stevioside (ST), sucralose (SU), and the two synergically (SU+ST) affected normal rats’ weight gain. In the current study, SU showed the highest undesired effect. Indeed, administering the three treatments to diabetic rats (DR) did not improve the rats’ weight gain. Although, insulin injection synergically with the treatments improved the weight gain, as recorded after three weeks. The best-improving rate was observed in the ST group. After the administration of ST and ST+SU to the DR, the blood glucose level (GL) was positively affected, with SU having no effects on reducing the GL. A considerable reduction in serum insulin (SIL) was noted in the DR+SU group. On the contrary, ST did not negatively affect the SIL, rather an improvement was recorded. In addition, giving SU did not significantly affect the ALT level in the DR or normal rats (NR). A significant improvement in total bilirubin (TBILI) was observed when insulin was injected with ST or SU in DR groups. Further, triglycerides (TG) after administering ST, SU, or ST+SU to NR had no significant difference compared to the control group (NR). Although, the three treatments markedly but not significantly lowered TG in the DR. For total cholesterol (CHO), both DR and NR had no significant effect after the three treatments. No histopathological alterations were recorded in the NR group. Diffuse and severe atrophy of the islands of Langerhans due to depletion of their cells and mild papillary hyperplasia of the pancreatic ducts were represented by a slightly folded ductal basement membrane and newly formed ductules in STZ-DR. Simultaneous atrophy and absence of the cells of islands of Langerhans besides ductal hyperplasia were evident in DR+SU. Hyperplastic ductal epithelium and atrophic Langerhans cells were seen in DR+SU+In. Degeneration and mild atrophy were observed in the islands of Langerhans structures. There was essentially no noticeable change after utilizing ST. A slight shrinkage of the Langerhans’ islets was detected in DR+ST. In DR+ST+In, no histopathological alterations in the islands of Langerhans were recorded. Congestion in the stromal blood vessels associated with degenerative and necrotic changes in the cells of the islands of Langerhans in DR+SU+ST was observed. In NR+SU, congestion of the blood vessels associated with mild atrophy in the islands of Langerhans and dilatation in stromal blood vessels was noticed. In conclusion, ST is safe, and SU should be taken cautiously, such as mixing with ST and/or taken at a very low concentration to avoid its drastic effect on the human body.
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7

Triponez, F., J. Oberholzer, J. Lou, and P. Morel. "La transplantation d'îlots de Langerhans: quo vadis." Chirurgie 124, no. 1 (February 1999): 5–12. http://dx.doi.org/10.1016/s0001-4001(99)80036-1.

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PENFORNIS, A. "Langerhans islet preparation in cell transplantation*1." Transfusion Science 18, no. 2 (June 1997): 235–41. http://dx.doi.org/10.1016/s0955-3886(97)90050-3.

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Zandi, Parissa, Yves Panis, Dominique Debray, Olivier Bernard, and Didier Houssin. "Pediatric liver transplantation for langerhans' cell histiocytosis." Hepatology 21, no. 1 (January 1995): 129–33. http://dx.doi.org/10.1002/hep.1840210122.

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DAVIS, D. J., M. A. MACAULAY, A. S. MACDONALD, and B. L. ESTABROOKS. "ISLETS OF LANGERHANS IN DOG PANCREAS." Transplantation 45, no. 6 (June 1988): 1099–103. http://dx.doi.org/10.1097/00007890-198806000-00020.

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Dissertations / Theses on the topic "Islands of Langerhans – Transplantation"

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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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Teague, Warwick J. "Mesenchyme-to-epithelial transition in pancreatic organogenesis." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670115.

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Wong, Jeffrey K. W. "Chemokines and chemokine receptors in islet xenograft rejection." Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/28055.

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This project investigates the role of chemokine and chemokine receptors in a model of CD4 T cell dependent cellular xenograft rejection, specifically the transplantation of fetal pig pancreas tissue to the renal subcapsular space of mice. Chemokines and chemokine receptor gene expression was assessed by cDNA arrays, and confirmed by multi-probe ribonuclease protection assay. Immunostaining for a selected chemokine, RANTES was performed to demonstrate upregulation at the protein level. These methods were applied to several different models to dissect the role Chemokines and their receptors in this process. Comparisons were made with: an allografi model, a model where indefinite xenograft survival could be achieved by short term costimulatory blockade with CTLA4-Fc and MR1, and an immunodeficient mouse recipient (RAG—1 KO, lacks B and T cells) that was reconstituted with either unfractionated leucocytes or purified CD4 T cells. The main findings were: 1. Allograft rejection and cellular xenografi rejection are THl type CD4 T cell dependent processes as shown by the common T cell chemokine genes (Ltn, IP-lO, and Mig) expressed in both models; however macrophages are the main effector cell in cellular xenografi rejection as evidenced by the selective upregulation of MCP-l and its receptor CCR2, as well as other macrophage markers 2. Of the Chemokines / receptors upregulated in this model of cellular xenograft rejection (Ltn, IP-lO, MCP-l, RANTES, MIP-lB, eotaxin) only MCP-l and IP-lO are CD4 T cell dependent, while Ltn expression is dependent upon a non-CD4 T cell leucocyte subset. 3. CTLA4-Fc and MR1 therapy resulted in indefinite fetal porcine islet survival and function in diabetic immune competent wild type C57BL/6 mice. This treatment suppresses the early upregulation of chemokines and chemokine receptors seen in untreated animals, and this corresponds with a significant reduction CD4 T cell and macrophage grafi infiltration at these time points, consistent with a role for select chemokine / receptors in the mechanism by which this therapy leads to indefinite graft survival. 4. In addition we studied the functioning of fetal porcine islet tissue in diabetic mice and found they developed and controlled glucose metabolism in a piglike manner, and different to normal mice, and thus conclude the development and function of fetal tissue in cross species transplantation is dependent upon the origins of the progenitor cells and not the xenogeneic environment i.e. nature not nurture (in this case anyway). We conclude that select chemokines and their receptors are important factors in the recruitment of effector cells mediating graft rejection in this model of cellular xenograft rejection and these chemokine pathways and networks may represent potential future therapeutic targets.
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Wang, Xiao Yang. "Approaches to induce islet allograft tolerance by liver allografting and to improve fetal pig islet function by gut hormones." Thesis, The University of Sydney, 1999. https://hdl.handle.net/2123/27740.

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This thesis examined (1) the effect of liver transplantation on tolerance induction to islet allografts; (2) the effects of gut hormones (CCK, GLP-1) on fetal pig islets. Liver allografts in tolerant strain combinations are unique in their ability to induce tolerance to other organ and skin grafts from the same donor strain in the absence of immunosuppression. Whether liver transplantation has the same effect on islet allografts is unknown. Studies in this thesis demonstrate that the protective effect of liver transplantation on islet allografts varies with the time of liver grafting. Islet allografts in the PVG —> DA combination were rapidly rejected. Rejection was delayed, but not prevented, when islets were transplanted simultaneously with the liver. Liver transplantation protected subsequently transplanted islet allografts from rejection and reversed ongoing rejection in previously placed islet grafts, in both cases leading to the tolerance of the islet allografts. There was a progressive increase of cell infiltration from day 2 to day 7 in both rejecting and tolerant islet allografts. The intensity of infiltration did not relate to the outcome of grafts. Islet rejection was characterised by an early dominance of monocytes/macrophages and CD25+ T cells in the infiltrate, a high incidence of apoptotic B cells in grafts, and a sensitised status in the MLR. Tolerance of islet allografts was associated with increased numbers of dendritic cells in the graft infiltrates, upregulation of FasL and prominent apoptosis of alloreactive leukocytes in the spleen and islet grafts, as well as donor-specific suppression in long—term survivors. It is suggested that islet allograft tolerance induced by liver transplantation is the result of an active immune regulation process which involves the deletion of donor-specific alloreactive lymphocytes by apoptosis. Transplantation of fetal pig pancreatic islets is capable of reversing diabetes in rodents, but several months are required to achieve this. During this time fetal [3 cells proliferate, differentiate and mature in their ability to secrete insulin when challenged with glucose. The study in Chapter 6 showed that CCK, GLP-l can induce the maturation and differentiation of fetal pig [5 cells during culture of fetal pig islet cell clusters (lCCs) in vitro. Two months after the ICCs were transplanted beneath kidney capsule of SCID mice, perfusion of the graft showed that ICCs previously exposed to CCK, GLP-1 for 4 days secreted insulin in response to glucose, whereas the control grafts remained glucose unresponsive. It is suggested that exposure of fetal pig lCCs to CCK, GLP-1 is likely to be advantageous in enhancing their ability to normalise blood levels when transplanted into diabetic recipients.
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Wilson, John Tanner. "Biomolecular strategies for cell surface engineering." Diss., Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/33846.

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Islet transplantation has emerged as a promising cell-based therapy for the treatment of diabetes, but its clinical efficacy remains limited by deleterious host responses that underlie islet destruction. In this dissertation, we describe the assembly of cell surface-supported thin films that confer molecular-level control over the composition and biophysicochemical properties of the islet surface with implications for improving islet engraftment. Specifically, the process of layer-by-layer (LbL) polymer self assembly was employed to generate nanothin films of diverse architecture with tunable properties directly on the extracellular surface of individual islets. Importantly, these studies are the first to report in vivo survival and function of nanoencapsulated cells, and have helped establish a conceptual framework for translating the diverse applications of LbL films to cellular interfaces. Additionally, through proper design of film constituents, coatings displaying ligands and bioorthogonally reactive handles may be generated, providing a modular strategy for incorporating exogenously derived regulators of host responses alongside native constituents of the islet surface. Towards this end, a strategy was developed to tether thrombomodulin to the islet surface in a site-specific manner, thereby facilitating local generation of the powerful anti-inflammatory agent, activated protein C. Collectively, this work offers novel biomolecular strategies for cell surface engineering with broad biomedical and biotechnological applications in cell-based therapeutics and beyond.
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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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Phelps, Edward Allen. "Bio-functionalized peg-maleimide hydrogel for vascularization of transplanted pancreatic islets." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/45899.

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Type 1 diabetes affects one in every 400-600 children and adolescents in the US. Standard therapy with exogenous insulin is burdensome, associated with a significant risk of dangerous hypoglycemia, and only partially efficacious in preventing the long term complications of diabetes. Pancreatic islet transplantation has emerged as a promising therapy for type 1 diabetes. However, this cell-based therapy is significantly limited by inadequate islet supply (more than one donor pancreas is needed per recipient), instant blood-mediated inflammatory reaction, and loss of islet viability/function during isolation and following implantation. In particular, inadequate revascularization of transplanted islets results in reduced islet viability, function, and engraftment. Delivery of pro-vascularization factors has been shown to improve vascularization and islet function, but these strategies are hindered by insufficient and/or complex release pharmacokinetics and inadequate delivery matrices as well as technical and safety considerations. We hypothesized that controlled presentation of angiogenic cues within a bioartificial matrix could enhance the vascularization, viability, and function of transplanted islets. The primary objective of this dissertation was to enhance allogenic islet engraftment, survival and function by utilizing synthetic hydrogels as engineered delivery matrices. Polyethylene glycol (PEG)-maleimide hydrogels presenting cell adhesive motifs and vascular endothelial growth factor (VEGF) were designed to support islet activities and promote vascularization in vivo. We analyzed the material properties and cyto-compatibility of these engineered materials, islet engraftment in a transplantation model, and glycemic control in diabetic subjects. The rationale for this project is to establish novel biomaterial strategies for islet delivery that support islet viability and function via the induction of local vascularization.
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Clayton, Heather Anne. "The encapsulation and transplantation of islets of Langerhans." Thesis, University of Leicester, 1992. http://hdl.handle.net/2381/34306.

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Although several clinical human islet transplants have been performed, allograft rejection has been a major problem. Encapsulation in sodium alginate/poly-l-lysine has been proposed as a method to protect the islets from rejection and autoimmune destruction. The aims of this project were to determine optimum capsule composition and to assess encapsulated islet function following transplantation using the spontaneously diabetic BioBreeding (BB/d) rat as a model of autoimmune insulin-dependent diabetes. The membrane integrity of islets, determined by microfluorometry, was not adversely affected by encapsulation. During perifusion, the stimulation increase of encapsulated islets was decreased relative to controls, but the stimulation index and response time were unaffected. Capsule composition did not affect these results. The biocompatibility of the capsules was related to their composition. The presence of an outer layer of alginate, and the preparation of alginate used, reduced the severity of pericapsular fibrosis. Capsules implanted in the peritoneal cavity provoked a more severe response than those placed in the renal subcapsular space. BB/d rats displayed a marked response to the capsules. Transplantation experiments demonstrated that 3000 non-encapsulated or 5000 encapsulated islets were the minimum number required to reverse streptozotocin-induced diabetes when transplanted into the peritoneal cavity. An intense pericapsular fibrosis led to failure of the encapsulated grafts. Further transplants into the BB/d rat were postponed to allow the cause of fibrosis to be investigated. The alginate was found to be contaminated with protein and this was removed by dialysis. In vitro experiments with the dialysed alginate demonstrated that treatment of the alginate did not affect the viability of encapsulated islets. Biocompatibility studies showed that capsules coated with dialysed alginate remained free from pericapsular fibrosis, even in the BB/d rat, when tested over the time interval which had resulted in the development of severe fibrosis of capsules coated with untreated alginate.
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Koulmanda, Maria. "Transplantation of organ cultured foetal islets of Langerhans in mice." Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/29492.

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Foetal islets are functionally immature but retain their capacity for proliferation if harvested and cultured in an appropriate manner. Graft function was shown to depend largely on the gestational age and conditions of organ culture prior to transplantation. The required period of organ culture for optimal graft function was investigated for foetal mouse pancreas of different gestational ages. The growth of the graft in situ also depended on the diabetic state of the host, and chronic hyperglycaemia appeared to impair graft function. Subsequent studies using NOD recipient mice as a model for IDDM showed that recurrent autoimmune disease was seen in foetal islet isografts but rapid rejection of allografts and foetal pig xenografts also occurred. The striking differences seen between the allo-, and xenograft response was the presence of many eosinophils that dominated the infiltrate at the xenograft site. However, HAR was not a problem in this discordant xenograft and Gal(1-3)Gal expression, the major epitope for xenoreactive Ab, was not present on differentiated cells but was detectable on ductal cells. A brief treatment with a specific anti-CD4 MAb (GK1.5) had a profound effect in the survival of xenografts in NOD mice. There were consistent differences in xenograft survival and in the number of circulating T and B cells in other strains of mice, e.g. CBA, BALB/c, C57BL/6 compared to NOD mice. Prolongation of xenograft survival for up to 12 weeks was achieved with the use of peri-transplant and weekly treatment with anti-CD4 or anti-CD3 MAbs especially when the graft has been "immunomodulated" by using 90% O2 in organ culture. Using this protocol foetal pig xenografts maturing under the kidney capsule of spontaneously diabetic NOD mice reversed hyperglycaemia and appeared also to secrete growth factor(s) that induced regeneration of cells in the host pancreas.
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Rafael, Ehab. "Cell transplantation and immunoisolation : studies on a macroencapsulation device /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3883-0/.

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Books on the topic "Islands of Langerhans – Transplantation"

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G, Gruessner Rainer W., and Sutherland David E. R, eds. Transplantation of the pancreas. New York: Springer, 2004.

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

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Transplantationsversuche mit isolierten Langerhansschen Inseln in der Behandlung des Diabetes mellitus (Typ I). Stuttgart: F. Steiner, 1998.

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Vladimír, Bartoš. Diabetes mellitus a transplantace pankreatu. Praha: Academia, 1990.

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M, Peterson C., Jovanovic-Peterson Lois, and Formby Bent, eds. Fetal islet transplantation: Implications for diabetes. New York: Springer-Verlag, 1988.

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Bernat, Soria, and International Meeting of the Pancreatic Islet Study Group (1st : 1994 : Alicante, Spain), eds. Physiology and pathophysiology of the islets of Langerhans. New York: Plenum Press, 1997.

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Angeles de Dios de Martina. Mario Chapo Bortagaray: Un visionario de la medicina. Resistencia, Chaco, Argentina: Librería de la Paz, 2006.

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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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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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Book chapters on the topic "Islands of Langerhans – Transplantation"

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Cravedi, Paolo, Piero Ruggenenti, and Giuseppe Remuzzi. "Successes and Disappointments with Clinical Islet Transplantation." In Islets of Langerhans, 1245–74. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-6686-0_23.

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Wolff, Günther. "Paul Langerhans — of Islets and Islands." In Diabetes Its Medical and Cultural History, 336–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-48364-6_23.

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Cravedi, Paolo, Piero Ruggenenti, and Giuseppe Remuzzi. "Successes and Disappointments with Clinical Islet Transplantation." In Islets of Langerhans, 2. ed., 1–27. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6884-0_23-1.

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Al-Abdullah, I. H., M. S. A. Kumar, M. S. Al-Adnani, and G. M. Abouna. "Does pretreatment of islets of Langerhans with deoxyguanosine improve allograft survival without immunosuppression?" In Organ Transplantation 1990, 409–14. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3386-9_54.

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Federlin, K., B. J. Hering, and R. G. Bretzel. "Transplantation of Isolated Islets of Langerhans as Treatment of Diabetes Mellitus." In Cellular Therapy, 87–109. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-03509-2_6.

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Philipp, Wolfgang, and Lilly Speicher. "Langerhans Cells in the Recipient Cornea as Prognostic Indicator in Corneal Transplantation." In Advances in Corneal Research, 173–79. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5389-2_17.

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Cohrs, Christian M., Chunguang Chen, and Stephan Speier. "Transplantation of Islets of Langerhans into the Anterior Chamber of the Eye for Longitudinal In Vivo Imaging." In Methods in Molecular Biology, 149–57. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0385-7_11.

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"Pulmonary Langerhans Cell Histiocytosis and Lymphangioleiomyomatosis." In Lung and Heart-Lung Transplantation, 247–74. CRC Press, 2006. http://dx.doi.org/10.3109/9781420019285-12.

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Bourke, S. J. "Pulmonary Langerhans’ cell histiocytosis." In Oxford Textbook of Medicine, edited by Pallav L. Shah, 4256–57. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0425.

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Abstract:
Pulmonary Langerhans’ cell histiocytosis is characterized by a reactive monoclonal proliferation of activated histiocytes in the distal bronchioles, resulting in inflammatory nodules, cyst formation, and fibrosis. Langerhans’ cells are a particular type of histiocyte derived from dendritic cells in the bone marrow. They normally migrate in the blood to the squamous epithelium of the skin, lungs, gastrointestinal, and female genital tract, where they are involved in antigen presentation to T cells. It presents with cough, breathlessness, and (sometimes) systemic symptoms. Chest radiography and CT typically show nodules which then cavitate and may rupture, causing pneumothorax. Corticosteroids and/or cytotoxic drugs are of some benefit, and lung transplantation is an option for progressive disease.
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Srinivasan, Parthi. "Treatment of diabetes (Type I) through transplantation." In Oxford Textbook of Endocrinology and Diabetes, 2015–18. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.1597.

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Type 1 diabetes mellitus (T1DM) is an autoimmune disease associated with selected genetic HLA alleles, which results in the permanent destruction of beta cells of the pancreatic islets of Langerhans, with subsequent insulinopenia and hyperglycaemia (1). Meta-analysis indicates that high birth weight and increased early weight gain may be risk factors for type 1 diabetes (2). The clinical state leads to significant increase in premature mortality and morbidity, including through accelerated atherosclerosis, cardiac autonomic neuropathy, and possibly intrinsic cardiomyopathy (3). Intensive exogenous insulin therapy can be effective in preventing the progression of such morbidity, but carries with it a three- to six- fold increase in risk of life threatening hypoglycaemia (see Chapter 13.4.8). Clinicians seeking an alternative therapy or even potential cure of T1DM through replacement of the destroyed pancreatic beta cells conducted the first whole organ pancreas transplant (PT) in Minneapolis in 1966. Although now accepted as effective treatment for T1DM, PT involves major surgery, with its attendant complications. Recognition of this led, in the early nineties, to trials of islet allograft transplantation (IT), as this limits the transplant procedure to the islets. Representing only 2% of the whole organ, they are the only part of it that is abnormal in T1DM. Shapiro’s report in 2000 of consistent insulin independence without major surgery led to a worldwide increase in clinical IT (4). We herein discuss the two options in brief, pose our opinions and conclude with some thought to a few future novel therapies for the disease.
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Conference papers on the topic "Islands of Langerhans – Transplantation"

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Wajda, N. A., Z. Zhu, R. Jandarov, and N. Gupta. "Clinical Outcomes and Survival Following Lung Transplantation in Patients with Pulmonary Langerhans Cell Histiocytosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4732.

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Kenchadze, George. "Large Mammalian Model for Extrahepatic Langerhans Transplantation for the Treatment of Type 1 Diabetes." In 2nd International Conference on Advanced Research in Applied Science and Engineering. GLOBALKS, 2020. http://dx.doi.org/10.33422/2nd.rase.2020.03.100.

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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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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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