Relevant bibliographies by topics / Human pancreatic islet

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Academic literature on the topic 'Human pancreatic islet'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "Human pancreatic islet"

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Santangelo, Carmela, Angela Scipioni, Lorella Marselli, Piero Marchetti, and Francesco Dotta. "Suppressor of cytokine signaling gene expression in human pancreatic islets: modulation by cytokines." European Journal of Endocrinology 152, no. 3 (March 2005): 485–89. http://dx.doi.org/10.1530/eje.1.01856.

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Objective: Suppressor of cytokine signaling (SOCS) proteins negatively regulate signal transduction of several cytokines. Since cytokines participate in the pancreatic islet damage in type 1 diabetes, the aim of our study was to investigate the expression of SOCS-1, -2 and -3 in isolated human islets, in basal conditions and after exposure, in vitro, to a combination of interferon (IFN)-γ, interleukin (IL)-1β and tumor necrosis factor (TNF)-α cytokines and in control and in type 1 diabetic human pancreata, to establish (i) whether SOCS molecules are constitutively expressed in human pancreatic islets and (ii) whether their expression can be modulated in vitro by proinflammatory cytokines or ex vivo by an islet inflammatory process. Methods: Gene expression of SOCS-1, -2 and -3 was evaluated by RT-PCR in untreated and cytokine-treated isolated human pancreatic islets and their protein expression by immunohistochemistry in control and in type 1 diabetic human pancreata paraffin-embedded sections. Results: We found that SOCS-1, -2 and -3 mRNA is constitutively, although weakly, expressed in human pancreatic islets, similar to the expression observed in control pancreata by immunohistochemistry. SOCS-1, -2 and -3 mRNA expression was strongly increased in human islets after exposure, in vitro, to IFN-γ, IL-1β and TNF-α. Accordingly, an intense and islet-specific immunohistochemical staining for all three SOCS was detected in pancreata from type 1 diabetic patients. Conclusion: SOCS-1, -2 and -3 genes are constitutively expressed in human pancreatic islets; their expression increases after exposure to proinflammatory cytokines and during an autoimmune inflammatory process, raising the possibility that these molecules act as key regulators of cytokine signaling in pancreatic islets.
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Omori, Keiko, Eiji Kobayashi, Hirotake Komatsu, Jeffrey Rawson, Garima Agrawal, Mounika Parimi, Alina R. Oancea, et al. "Involvement of a proapoptotic gene (BBC3) in islet injury mediated by cold preservation and rewarming." American Journal of Physiology-Endocrinology and Metabolism 310, no. 11 (June 1, 2016): E1016—E1026. http://dx.doi.org/10.1152/ajpendo.00441.2015.

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Long-term pancreatic cold ischemia contributes to decreased islet number and viability after isolation and culture, leading to poor islet transplantation outcome in patients with type 1 diabetes. In this study, we examined mechanisms of pancreatic cold preservation and rewarming-induced injury by interrogating the proapoptotic gene BBC3/Bbc3, also known as Puma (p53 upregulated modulator of apoptosis), using three experimental models: 1) bioluminescence imaging of isolated luciferase-transgenic (“Firefly”) Lewis rat islets, 2) cold preservation of en bloc-harvested pancreata from Bbc3-knockout (KO) mice, and 3) cold preservation and rewarming of human pancreata and isolated islets. Cold preservation-mediated islet injury occurred during rewarming in “Firefly” islets. Silencing Bbc3 by transfecting Bbc3 siRNA into islets in vitro prior to cold preservation improved postpreservation mitochondrial viability. Cold preservation resulted in decreased postisolation islet yield in both wild-type and Bbc3 KO pancreata. However, after culture, the islet viability was significantly higher in Bbc3-KO islets, suggesting that different mechanisms are involved in islet damage/loss during isolation and culture. Furthermore, Bbc3-KO islets from cold-preserved pancreata showed reduced HMGB1 (high-mobility group box 1 protein) expression and decreased levels of 4-hydroxynonenal (4-HNE) protein adducts, which was indicative of reduced oxidative stress. During human islet isolation, BBC3 protein was upregulated in digested tissue from cold-preserved pancreata. Hypoxia in cold preservation increased BBC3 mRNA and protein in isolated human islets after rewarming in culture and reduced islet viability. These results demonstrated the involvement of BBC3/Bbc3 in cold preservation/rewarming-mediated islet injury, possibly through modulating HMGB1- and oxidative stress-mediated injury to islets.
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Norman, Daniel, Carl Johan Drott, Per-Ola Carlsson, and Daniel Espes. "Irisin—A Pancreatic Islet Hormone." Biomedicines 10, no. 2 (January 25, 2022): 258. http://dx.doi.org/10.3390/biomedicines10020258.

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Irisin is a myokine involved in glucose homeostasis. It is primarily expressed in skeletal muscle, but also in the pancreas. This study aimed to elucidate its presence and role in the islets of Langerhans—i.e., its effect on insulin and glucagon secretion as well as on blood flow in the pancreas. The precursor of irisin, fibronectin type III domain-containing protein 5 (FNDC5), was identified in rat and human islets by both qPCR and immunohistochemistry. Both α- and β-cells stained positive for FNDC5. In human islets, we found that irisin was secreted in a glucose-dependent manner. Neither irisin nor an irisin-neutralizing antibody affected insulin or glucagon secretion from human or rat islets in vitro. The insulin and glucagon content in islets was not altered by irisin. The intravenous infusion of irisin in Sprague Dawley rats resulted in nearly 50% reduction in islet blood flow compared to the control. We conclude that irisin is an islet hormone that has a novel role in pancreatic islet physiology, exerting local vascular effects by diminishing islet blood flow without affecting insulin secretion per se.
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Chadwick, D. R., G. S. M. Robertson, P. Toomey, H. Contractor, S. Rose, R. F. L. James, P. R. F. Bell, and N. J. M. London. "Pancreatic Islet Purification Using Bovine Serum Albumin: The Importance of Density Gradient Temperature and Osmolality." Cell Transplantation 2, no. 4 (July 1993): 355–61. http://dx.doi.org/10.1177/096368979300200419.

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Euro-Ficoll and bovine serum albumin (BSA) are two of the most commonly used density gradient media for the purification of pancreatic islets. Euro-Ficoll is based upon Euro-Collins, a cold storage medium, and must, therefore, be used at 4°C. The ionic composition of BSA, however, is likely to contribute to hypothermic cellular swelling, and this may influence the efficiency of islet purification using this medium at 4°C. Experience in this laboratory also suggested that batch-to-batch variation in islet purity using BSA was related to differences in BSA osmolality. The aim of this study was to assess the effect of gradient medium temperature and osmolality on the purification of human and porcine islets using BSA. Pancreata were collagenase-digested, and islets were purified on continuous linear density gradients of BSA. The distribution of insulin and amylase in each gradient was assayed, and used to calculate the median density of islets and exocrine tissue, and the efficiency of islet purification (%amylase contamination at a fixed insulin yield), using: 1) gradient osmolalities of 300, 400, and 500 mOsm/kg H2O (seven porcine pancreata), and 2) gradients at 4°C and at 22°C (eight human and seven porcine pancreata). Increase in density gradient osmolality produced increases in porcine exocrine tissue density which exceeded changes in islet density, resulting in improved islet purity, maximal at a BSA osmolality of 400 mOsm/kg H2O. For human pancreata there was no significant change in pancreatic tissue densities nor islet purity with temperature. For porcine pancreata the densities of exocrine tissue and islets were lower at 4°C than at 22°C. This reduction in density with temperature was greater for exocrine tissue, resulting in lesser islet purity at 4°C compared to 22°C (p = 0.036). In conclusion, islet purification using BSA is influenced by density gradient temperature and osmolality. For porcine pancreata, a temperature of 22°C, and an osmolality of 400 mOsm/kg H2O are optimal.
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Graves, Leo, Mine Aksular, Riyadh Alakeely, Daniel Ruiz Buck, Adam Chambers, Fernanda Murguia-Meca, Juan-Jose Plata-Muñoz, et al. "Improved Baculovirus Vectors for Transduction and Gene Expression in Human Pancreatic Islet Cells." Viruses 10, no. 10 (October 20, 2018): 574. http://dx.doi.org/10.3390/v10100574.

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Pancreatic islet transplantation is a promising treatment for type 1 diabetes mellitus offering improved glycaemic control by restoring insulin production. Improved human pancreatic islet isolation has led to higher islet transplantation success. However, as many as 50% of islets are lost after transplantation due to immune responses and cellular injury, gene therapy presents a novel strategy to protect pancreatic islets for improved survival post-transplantation. To date, most of the vectors used in clinical trials and gene therapy studies have been derived from mammalian viruses such as adeno-associated or retrovirus. However, baculovirus BacMam vectors provide an attractive and safe alternative. Here, a novel BacMam was constructed containing a frameshift mutation within fp25, which results in virus stocks with higher infectious titres. This improved in vitro transduction when compared to control BacMams. Additionally, incorporating a truncated vesicular stomatitis virus G protein increased transduction efficacy and production of EGFP and BCL2 in human kidney (HK-2) and pancreatic islet β cells (EndoC βH3). Lastly, we have shown that our optimized BacMam vector can deliver and express egfp in intact pancreatic islet cells from human cadaveric donors. These results confirm that BacMam vectors are a viable choice for providing delivery of transgenes to pancreatic islet cells.
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Brissova, Marcela, Michael J. Fowler, Wendell E. Nicholson, Anita Chu, Boaz Hirshberg, David M. Harlan, and Alvin C. Powers. "Assessment of Human Pancreatic Islet Architecture and Composition by Laser Scanning Confocal Microscopy." Journal of Histochemistry & Cytochemistry 53, no. 9 (May 27, 2005): 1087–97. http://dx.doi.org/10.1369/jhc.5c6684.2005.

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The recent success of pancreatic islet transplantation has generated considerable enthusiasm. To better understand the quality and characteristics of human islets used for transplantation, we performed detailed analysis of islet architecture and composition using confocal laser scanning microscopy. Human islets from six separate isolations provided by three different islet isolation centers were compared with isolated mouse and non-human primate islets. As expected from histological sections of murine pancreas, in isolated murine islets α and δ cells resided at the periphery of the β-cell core. However, human islets were markedly different in that α, β, and δ cells were dispersed throughout the islet. This pattern of cell distribution was present in all human islet preparations and islets of various sizes and was also seen in histological sections of human pancreas. The architecture of isolated non-human primate islets was very similar to that of human islets. Using an image analysis program, we calculated the volume of α, β, and δ cells. In contrast to murine islets, we found that populations of islet cell types varied considerably in human islets. The results indicate that human islets not only are quite heterogeneous in terms of cell composition but also have a substantially different architecture from widely studied murine islets.
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Liggins, C., D. J. Orlicky, L. A. Bloomquist, and Roberto Gianani. "Developmentally Regulated Expression of Survivin in Human Pancreatic Islets." Pediatric and Developmental Pathology 6, no. 5 (September 2003): 392–97. http://dx.doi.org/10.1007/s10024-003-2014-0.

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Islet cell apoptosis plays a role in both normal development of the endocrine pancreas and in the pathogenesis of Type I and Type II diabetes. The molecular mechanisms regulating islet cell death and survival in both normal and pathological situations are still not completely elucidated. The inhibitor of apoptosis protein (IAP) Survivin has an anti-apoptotic function mediated by several mechanisms; these include inhibiting caspase 3 and caspase 7. Survivin expression has been reported in human fetal islets and it may play a role in pancreatic remodeling and islet homeostasis. However, there are no data concerning either its expression in neonate or adult islets or its expression in any specific subtype of islet cells. We identified Survivin expression by immunohistochemistry in alpha cells and beta islet cells of 5/5 fetal pancreases. In contrast, fetal delta cells failed to demonstrate any detectable level of Survivin expression. Survivin expression was subsequently lost in the beta cells but not the alpha cells of 5/5 newborns and 5/5 adult subjects. Neonatal and adult delta cells maintained the lack of Survivin expression seen in fetal islets. These data show that different subtypes of islet cells differ in their pattern of Survivin expression. Furthermore, expression of Survivin in the beta cells is developmentally regulated.
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Forbes, Shareen, Andrew R. Bond, Kayleigh L. Thirlwell, Paul Burgoyne, Kay Samuel, June Noble, Gary Borthwick, et al. "Human umbilical cord perivascular cells improve human pancreatic islet transplant function by increasing vascularization." Science Translational Medicine 12, no. 526 (January 15, 2020): eaan5907. http://dx.doi.org/10.1126/scitranslmed.aan5907.

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Islet transplantation is an efficacious therapy for type 1 diabetes; however, islets from multiple donor pancreata are required, and a gradual attrition in transplant function is seen. Here, we manufactured human umbilical cord perivascular mesenchymal stromal cells (HUCPVCs) to Good Manufacturing Practice (GMP) standards. HUCPVCs showed a stable phenotype while undergoing rapid ex vivo expansion at passage 2 (p2) to passage 4 (p4) and produced proregenerative factors, strongly suppressing T cell responses in the resting state and in response to inflammation. Transplanting an islet equivalent (IEQ):HUCPVC ratio of 1:30 under the kidney capsule in diabetic NSG mice demonstrated the fastest return to normoglycemia by 3 days after transplant: Superior glycemic control was seen at both early (2.7 weeks) and later stages (7, 12, and 16 weeks) versus ratios of 1:0, 1:10, and 1:50, respectively. Syngeneic islet transplantation in immunocompetent mice using the clinically relevant hepatic portal route with a marginal islet mass showed that mice transplanted with an IEQ:HUCPVC ratio of 1:150 had superior glycemic control versus ratios of 1:0, 1:90, and 1:210 up to 6 weeks after transplant. Immunodeficient mice transplanted with human islets (IEQ:HUCPVC ratio of 1:150) exhibited better glycemic control for 7 weeks after transplant versus islet transplant alone, and islets transplanted via the hepatic portal vein in an allogeneic mouse model using a curative islet mass demonstrated delayed rejection of islets when cotransplanted with HUCPVCs (IEQ:HUCPVC ratio of 1:150). The immunosuppressive and proregenerative properties of HUCPVCs demonstrated long-term positive effects on graft function in vivo, indicating that they may improve long-term human islet allotransplantation outcomes.
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Barbieux, Charlotte, Géraldine Parnaud, Vanessa Lavallard, Estelle Brioudes, Jérémy Meyer, Mohamed Alibashe Ahmed, Ekaterine Berishvili, Thierry Berney, and Domenico Bosco. "Asymmetrical distribution of δ and PP cells in human pancreatic islets." Journal of Endocrinology 229, no. 2 (May 2016): 123–32. http://dx.doi.org/10.1530/joe-15-0542.

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The aim of this study was to evaluate the location of PP and δ cells in relation to the vascularization within human pancreatic islets. To this end, pancreas sections were analysed by immunofluorescence using antibodies against endocrine islet and endothelial cells. Staining in different islet areas corresponding to islet cells adjacent or not to peripheral or central vascular channels was quantified by computerized morphometry. As results, α, PP and δ cells were preferentially found adjacent to vessels. In contrast to α cells, which were evenly distributed between islet periphery and intraislet vascular channels, PP and δ cells had asymmetric and opposite distributions: PP staining was higher and somatostatin staining was lower in the islet periphery than in the area around intraislet vascular channels. Additionally, frequencies of PP and δ cells were negatively correlated in the islets. No difference was observed between islets from the head and the tail of the pancreas, and from type 2 diabetic and non-diabetic donors. In conclusion, the distribution of δ cells differs from that of PP cells in human islets, suggesting that vessels at the periphery and at the centre of islets drain different hormonal cocktails.
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Ohsawa, Haruhiko, Azuma Kanatsuka, Yoshiharu Tokuyama, Takahide Yamaguchi, Hideichi Makino, Sho Yoshida, Hiroshi Horie, Atsuo Mikata, and Yoshibumi Kohen. "Amyloid protein in somatostatinoma differs from human islet amyloid polypeptide." Acta Endocrinologica 124, no. 1 (January 1991): 45–53. http://dx.doi.org/10.1530/acta.0.1240045.

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Abstract. Amyloid deposits in somatostatinomas are rare observations. To examine the characteristics of this amyloid, we compared amyloid deposits in a somatostatinoma to those found in pancreatic tissue in patients with Type II diabetes mellitus and in insulinomas, using immunohistochemical techniques and specific antibodies to islet amyloid polypeptide or other pancreatic hormones, as well as electron-microscopy. Antibodies to islet amyloid polypeptide regions 8-17 or 25-37 were confirmed to be specific. Amyloid deposits in patients with Type II diabetes mellitus and in insulinomas, but not those in the somatostatinoma strongly reacted with these antibodies, or to an antibody to amyloid P component. Amyloid deposits in the somatostatinoma were not reactive with antibodies to somatostatin or to other pancreatic hormones. Electron-microscopic examinations revealed that amyloid fibrils in the somatostatinoma were thinner and more randomly distributed than were those in islets from patients with Type II diabetes mellitus. As amyloid in somatostatinomas is unlike that consisting of islet amyloid polypeptide or other mature pancreatic hormones, it may be a novel type of local amyloid in pancreatic islets.
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Dissertations / Theses on the topic "Human pancreatic islet"

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Jackson, Andrew M. Naziruddin Bashoo. "Analysis of inflammatory changes in human pancreatic islet cells." Waco, Tex. : Baylor University, 2009. http://hdl.handle.net/2104/5344.

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Walker, Jonathan Neil. "The influence of donor body mass index on human pancreatic islet function, structure and islet transplant outcome." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:43101adf-d93a-42fc-b435-2b2ce5a13c2b.

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Background: Pancreatic islet transplantation for type-1 diabetes has resulted in considerable success over the past decade. However, the worldwide shortage of pancreatic donors remains a major challenge. In an attempt to expand the donor pool, pancreases from obese organs donors (>30 kg/m²) are now routinely offered to islet transplantation in the UK. In addition, it has been suggested that pancreases from donors with early type-2 diabetes mellitus may also be suitable. However, for both these donor groups, although high islet yields (IEQ) may be obtained, it is unclear whether these islets function optimally. An additional approach to the donor shortage is to minimise the number of donors required per islet recipient. One strategy to achieve this is to use different pharmacological agents to enhance post-transplant islet function. Aims: The aims of this thesis were fourfold; 1) To determine whether islets isolated from high BMI donors function normally in vitro and in vivo; 2) To establish why islet yields are higher from obese donors; 3) To determine whether islets from donors with type-2 diabetes are suitable for islet transplantation; 4) To investigate whether glucagon-like peptide 1 receptor agonist therapy improves post-transplant islet graft function. Results: Stimulated insulin and glucagon secretion, and markers of mitochondrial function (intra-islet ATP content and mitochondrial copy number) were compared in islets isolated from obese (BMI>30kg/m²; n= 27) and non-obese (BMI<28kg/m²; n=25) donors. No differences in secretory function or intra-islet ATP were observed between the two groups. Pancreatic lipid and intra-islet triglyceride concentrations were higher in the obese group. In vivo clinical outcomes of patients transplanted in Oxford and a larger cohort (n=35) in Edmonton, Canada with islets from obese or non-obese donors showed no differences in post-transplant outcomes. Improved islet yields were shown to be a result of improved islet recovery of larger islets, in obese donors. Abnormal insulin and glucagon secretory responses were observed in islets from type-2 diabetic subjects (n=6) and islet amyloid content was significantly higher in diabetes. The glucagon-like peptide 1 receptor agonist, exenatide, administered for 20 weeks, significantly improved graft function in patients whom islet function was impaired. Conclusion: The high lipid environment of islets isolated from donors with high BMI appears not to be deleterious to their function either in vitro or when transplanted, supporting the use of islets from high BMI donors for clinical islet transplantation. However, islet dysfunction and pathological changes indicate that islets from type-2 diabetic donors are unsuitable. Therapeutic options such as exenatide, improve transplanted islet viability and function, and could have a significant role in the future of beta-cell replacement therapy for type-1 diabetes.
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Bakshi, Vishwas J. "Automated Human Pancreatic Islet Isolation System for Islet Transplantation in Patients with Type-i Insulin Dependent Diabetes Mellitus." University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1078278715.

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Bakshi, Vishwas. "Automated human pancreatic islet isolation system for islet transplanttion in patients with Type-I insulin dependent Diabetes Mellitus." Cincinnati, Ohio : University of Cincinnati, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1078278715.

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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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Elshebani, Asma Basheir. "Studies of the Effect of Enterovirus Infection on Pancreatic Islet Cells." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7208.

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Mokhtari, Dariush. "MEKK-1 and NF-κB Signaling in Pancreatic Islet Cell Death." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8896.

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Type 1 diabetes is an autoimmune disease resulting in the selective destruction of the insulin producing β-cells in the pancreas. Pro-inflammatory cytokines and the free radical nitric oxide (NO) have been implicated in mediating the destruction of β-cells, possibly through activation of the mitogen activated protein kinases (MAPKs) JNK, ERK and p38. In addition to MAPKs, cytokine signaling also results in activation of the transcription factor nuclear factor-kappaB (NF-κB). The upstream signaling events leading to MAPK and NF-κB activation in β-cells are not well known. The work presented in this thesis therefore aims at characterizing the regulation of MAPKs and NF-κB in human islets, with emphasis on the role of the MAPK activator MAP/ERK kinase kinase-1 (MEKK-1) in islet cell death. It was found that MEKK-1 was phosphorylated in response to the nitric oxide donor DETA/NONOate (DETA/NO), the β-cell toxin streptozotocin (STZ) and pro-inflammatory cytokines and that MEKK-1 downstream signaling in response to the same treatments involved activation of JNK but not ERK and p38. MEKK-1 was also found to be essential for cytokine-induced NF-κB activation. MEKK-1 downregulation protected human islet cells from DETA/NO-, STZ, and cytokine-induced cell death. Furthermore, overexpression of the NF-κB subunit c-Rel protected human islet cells from STZ and hydrogen peroxide-induced cell death indicating that NF-κB activity protects against cell death in human islets. In summary, these results support an essential role for MEKK-1 in the activation of JNK and NF-κB, with important consequences for human islet cell death and that strategies preventing human islets death by inhibition of the JNK pathway instead of NF-κB might be suitable.
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Scott, Ryan 1981. "Investigating the natural history of human islet-derived duct-like structures transplanted subcutaneously into nude mice." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112362.

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Islet plasticity has proven to be an important platform for the engineering of alternative islet tissue for transplantation. In vitro studies have shown the ability of islets to transdifferentiate into duct-like epithelial structures (DLS) thought to possess progenitor cells capable of replenishing damaged tissue within the pancreas. The aim of this study was to investigate the natural history of human derived duct-like epithelial structures transplanted into nude mice.
Human islet derived duct-like structures from three cadaver pancreases were subcutaneously transplanted into 6-8 week old male HSD athymic nude-Foxn1 mice. Six mice were sacrificed at day 3, 7, 14 and 21 from each time period. DLS were also placed in matrigel for in-vitro control samples. DLS were processed for immunohistochemistry for endocrine markers, epithelial markers, cell death and proliferation markers, islet maturation markers and angiogenic factors.
Our results show that as DLS are transplanted, there is an increase in cell death and proliferation. This increase in cell death and proliferation causes an increase in PDX-1 expression as well as VEGF, an angiogenic factor. But over time, transplanted DLS do not show an increase in cell death and show a small decrease in cell proliferation from pre-transplanted DLS. At day 3 of engraftment, DLS show a significant expression of PDX-1. We see a small increase in endocrine tissue after 3 days of transplantation, then an increase in endocrine cell death, which returns the percentage of endocrine cells back to pre-transplantation levels at day 21. DLS were shown to express VEGF, and once transplanted into an initial hypoxic environment there is a substantial increase in expression, followed by a recruitment of microvessels. Although there is a dynamic change in expression of cell markers throughout engraftment, there is no significant change in DLS size, nuclei per DLS or cell morphology over time.
DLS have been shown to survive subcutaneous transplantation and possess an initial increase in cell proliferation leading to increases in PDX-1 and VEGF expression. Transplanted DLS have shown to possess significant angiogenic properties with the recruitment of microvessels into subcutaneous DLS grafts. Subcutaneous DLS transplantation could be used in combination with islet transplantation to alleviate current problems with islet transplantation such as islet cell death and insufficient blood supply.
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Odori, Shinji. "GPR119 expression in normal human tissues and islet cell tumors: evidence for its islet-gastrointestinal distribution, expression in pancreatic beta and alpha cells, and involvement in islet function." Kyoto University, 2013. http://hdl.handle.net/2433/174786.

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Moran, Castany Ignasi. "Discovery of novel genes and genetic regulatory mechanisms through integrative genomic, epigenetic and transcriptional analysis in human pancreatic islet cells." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/54917.

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Diabetes mellitus is a metabolic disorder characterized by a rise in blood sugar levels, estimated to currently affect more than 300 million people worldwide. Even though pancreatic islet β-cells play a central role in all major forms of the disease, their transcriptome is still not fully characterised. Furthermore, type 2 diabetes susceptibility is known to be affected by non-coding genomic variation, but the impact of these variants on gene regulation and their disease implications remain to be elucidated. In the first part of this project, I integrated the analysis of RNA sequencing datasets with maps of epigenomic features, resulting in the identification of 1,128 long non-coding RNA (lncRNA) genes in human pancreatic islets. Islet lncRNAs were enriched for tissue-specific expression, and a subset were shown to be regulated during endocrine differentiation or in response to changes in glucose. Furthermore, lncRNA orthologs in mouse islets were identified, which displayed similar regulatory properties to their human counterparts. Taken together, these analyses led to the identification of a novel class of genes active in human and mouse pancreatic islets, opening new avenues for the study of diabetes development and therapeutic strategies. In the second part of this project, I analysed the RNA-seq datasets and genotypes of 27 human islet samples, and developed a methodology to study the effect of non-coding genomic variation on gene regulation. This revealed hundreds of genes under allele-specific expression, consistently across many independent individuals. Some of these genes performed known roles in human islets, or resided within GWAS loci for type 2 diabetes and related traits. These findings could be used to identify functional cis-regulatory genetic variants impacting the human islet transcriptome, some of which could lead to the development of diabetes. Collectively, these projects uncovered novel components of the human islet transcriptome, and provided new methodologies to study the effects of genomic regulatory variation on gene transcription.
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Books on the topic "Human pancreatic islet"

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Tyrberg, Bjorn. Neogenesis and Alloxan Toxicity in Pancreatic Islets, With Special Reference to the Transplanted Human B-Cell. Uppsala Universitet, 1999.

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Book chapters on the topic "Human pancreatic islet"

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Wong, Wilson, Anandwardhan A. Hardikar, and Mugdha V. Joglekar. "Generation of Human Islet Progenitor Cells via Epithelial-to-Mesenchymal Transition." In Pancreatic Islet Biology, 217–40. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45307-1_9.

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Formby, Bent, Liberty Walker, and Charles M. Peterson. "Studies of Human Fetal Pancreatic Islets in Vitro." In Fetal Islet Transplantation, 55–66. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3766-2_4.

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Peterson, Charles M., Lois Jovanovic-Peterson, Bent Formby, and Lee Ducat. "Perspectives on Use of Human Fetal Pancreatic Tissue in the Field of Research on Diabetes Mellitus: An Introduction." In Fetal Islet Transplantation, 1–7. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3766-2_1.

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Zibolka, Juliane, Ina Bähr, Elmar Peschke, Eckhard Mühlbauer, and Ivonne Bazwinsky-Wutschke. "Human and Rodent Cell Lines as Models of Functional Melatonin-Responsive Pancreatic Islet Cells." In Melatonin, 329–52. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2593-4_35.

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Ruiz-Santiago, Sergio, José Rafael Godínez-Fernández, and Gerardo Jorge Félix-Martínez. "Simulating the Loss of $$\beta $$-cell Mass in a Human Pancreatic Islet: Structural and Functional Implications." In IFMBE Proceedings, 204–11. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-18256-3_22.

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Bloothooft, Meye, Joseph G. Shuttleworth, Gabriel Neiman, Ishan Goswami, and Andrew G. Edwards. "Recapitulating Functional Heterogeneity in Electrophysiologically Active Tissues." In Computational Physiology, 45–64. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-25374-4_4.

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AbstractInter-cellular heterogeneity is central to the dynamic range and robustness of function in many tissues, particularly electrically excitable tissues. In pancreatic islet &#x1D6FD;-cells, inter-cellular heterogeneity underlies the range of insulin response to glucose. In human-induced-pluripotent stem cell-derived cardiomyocytes (hiPSCCMs), inter-cellular heterogeneity presents a key challenge for drug screening applications. In this study, we assess the ability to reconstruct inter-cellular heterogeneity in silico by applying a &#x201C;population of models&#x201D; (PoMs) framework, i.e. collections of computational cells created via Monte Carlo variation of model parameters. We define parameter variation based on experimentally observed heterogeneity in properties such as ion current conductances and enzymatic affinities. We then assess the accuracy of those reconstructions, based on the degree to which variation in PoM outputs (e.g. action potential duration) matches experimentally observed variation. We report that this &#x201C;ground-up&#x201D; approach underestimates functional heterogeneity in the hiPSC-CM population, but overestimates it in adult human cardiomyocytes. In contrast, the &#x1D6FD;-cell PoM captures three distinct and physiologically relevant subclasses of &#x1D6FD;-cell function. In the future, we expect PoM approaches like these willpermit incorporation of realistic cellular heterogeneity in detailed models of intact tissues, and thereby aid development of sophisticated tissue-engineered platforms for therapeutics.
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Smura, Teemu, and Merja Roivainen. "Enterovirus Infection of Cultured Human Pancreatic Islets." In Diabetes and Viruses, 299–312. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4051-2_28.

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Wei, Lingling. "Isolation and Purification of Human Pancreatic Islets." In Methods in Molecular Biology, 219–32. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2807-2_16.

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Novials, A., R. Gasa, J. Fernandez-Alvarez, and R. Gomis. "IAPP and Insulin Regulation in Human Pancreatic Islets." In Advances in Experimental Medicine and Biology, 363–69. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1819-2_48.

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Halberstadt, Craig, Deana Williams, and Paul Gores. "Isolation of Human Cadaveric Pancreatic Islets for Clinical Transplantation." In Methods in Molecular Biology, 227–59. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-363-3_20.

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Conference papers on the topic "Human pancreatic islet"

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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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Holfinger, Steven, Rashmeet Reen, William Ackerman, Douglas Kniss, and Keith J. Gooch. "PANC-1 Migration and Cluster Formation is Regulated by Short Range Mechanical Forces." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53593.

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Islet cell transplantation has already shown improved control of glucose levels and the potential to achieve insulin independence in type 1 diabetes mellitus, however there is a shortage of organ donors needed to match patient needs [1–2]. In the search for alternative sources of islets, many cell types have shown signs of β-cell differentiation by secreting c-peptide, insulin, and glucagon [3–5]. When maintained in serum-free medium, human epithelial-like pancreatic adenocarcinoma (PANC-1) cells and human-islet derived precursor cells (hIPCs) can go through a morphological transition and cluster [6]. These islet-like cell aggregates subsequently express glucagon, somatostatin, and insulin, indicating that clustering may play an important role in differentiation towards β-cells [7].
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Porter, J. M., L. Guerassimoff, F. R. Castiello, and Maryam Tabrizian. "Synthesis and Screening of Novel Peptides on Human Pancreatic Islets for Type 1 Diabetes Therapies*." In 2020 42nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) in conjunction with the 43rd Annual Conference of the Canadian Medical and Biological Engineering Society. IEEE, 2020. http://dx.doi.org/10.1109/embc44109.2020.9175493.

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