Relevant bibliographies by topics / Β-cell replacement

Academic literature on the topic 'Β-cell replacement'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Β-cell replacement"

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Castro-Gutierrez, Roberto, Aaron W. Michels, and Holger A. Russ. "β Cell replacement." Current Opinion in Endocrinology & Diabetes and Obesity 25, no. 4 (August 2018): 251–57. http://dx.doi.org/10.1097/med.0000000000000418.

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Schuetz, Christian, Takayuki Anazawa, Sarah E. Cross, Leticia Labriola, Raphael P. H. Meier, Robert R. Redfield, Hanne Scholz, Peter G. Stock, and Nathan W. Zammit. "β Cell Replacement Therapy." Transplantation 102, no. 2 (February 2018): 215–29. http://dx.doi.org/10.1097/tp.0000000000001937.

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Dirice, Ercument. "β-cell Heterogeneity: The Key to β-cell Replacement Therapy." Pancreas - Open Journal 2, no. 1 (November 8, 2018): e10-e11. http://dx.doi.org/10.17140/poj-2-e009.

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Fellous, Tariq G., Naomi J. Guppy, Mairi Brittan, and Malcolm R. Alison. "Cellular pathways to β-cell replacement." Diabetes/Metabolism Research and Reviews 23, no. 2 (2007): 87–99. http://dx.doi.org/10.1002/dmrr.692.

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Muschter, N., A. Richter, H. Ahrens, G. Gosheger, M. Fehr, J. Bullerdiek, and G. Hauschild. "Cartilage replacement in dogs." Veterinary and Comparative Orthopaedics and Traumatology 22, no. 03 (2009): 216–21. http://dx.doi.org/10.3415/vcot08-02-0021.

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SummaryThe objective of this study was to examine the behaviour of canine chondrocytes following colonisation of a β-tricalcium phosphate (β-TCP, Cerasorb®, Curasan) matrix. In total, five of these cylinders were inoculated with 1.5 ml of cell suspension and subsequently incubated for about one week. In the second part of the experiment, another five Cerasorb® cylinders were each studded with two cartilage chips of variable size and then incubated for about one week. The series of experiments were analyzed using cell staining and imaging techniques that included scanning electron microscopy. Cell migration onto the matrix was proven for both colonization methods. It was observed that colonising the cylinders by pipetting cell suspension on them produced far better results, with respect to both growth rate and spreading of the cells, than did colonisation by studding with cartilage chips. A homogenous, surface-covering colonisation with predominantly living cells was demonstrated by scanning electron microscopy in the chondrocyte morphology. In comparison to cell-culture controls, there was a clearly better colonisation, with cells attached to both the material's primary grains and its micropores. The ceramic studied is well accepted by canine chondrocytes, and appears to be fundamentally well-suited as a matrix for bio-artificial bone-cartilage replacement. Additional qualitative analyses and a series of experiments aiming to accelerate cell proliferation are planned for subsequent studies.
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Salinno, Cota, Bastidas-Ponce, Tarquis-Medina, Lickert, and Bakhti. "β-Cell Maturation and Identity in Health and Disease." International Journal of Molecular Sciences 20, no. 21 (October 30, 2019): 5417. http://dx.doi.org/10.3390/ijms20215417.

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The exponential increase of patients with diabetes mellitus urges for novel therapeutic strategies to reduce the socioeconomic burden of this disease. The loss or dysfunction of insulin-producing β-cells, in patients with type 1 and type 2 diabetes respectively, put these cells at the center of the disease initiation and progression. Therefore, major efforts have been taken to restore the β-cell mass by cell-replacement or regeneration approaches. Implementing novel therapies requires deciphering the developmental mechanisms that generate β-cells and determine the acquisition of their physiological phenotype. In this review, we summarize the current understanding of the mechanisms that coordinate the postnatal maturation of β-cells and define their functional identity. Furthermore, we discuss different routes by which β-cells lose their features and functionality in type 1 and 2 diabetic conditions. We then focus on potential mechanisms to restore the functionality of those β-cell populations that have lost their functional phenotype. Finally, we discuss the recent progress and remaining challenges facing the generation of functional mature β-cells from stem cells for cell-replacement therapy for diabetes treatment.
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Calafiore, Riccardo, Pia Montanucci, and Giuseppe Basta. "Stem cells for pancreatic β-cell replacement in diabetes mellitus." Current Opinion in Organ Transplantation 19, no. 2 (April 2014): 162–68. http://dx.doi.org/10.1097/mot.0000000000000055.

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OBERHOLZER, JOSÉ, CHRISTIAN TOSO, FRÉDÉRIC RIS, PASCAL BUCHER, FRÉDÉRIC TRIPONEZ, ALP DEMIRAG, JINNING LOU, and PHILIPPE MOREL. "β Cell Replacement for the Treatment of Diabetes." Annals of the New York Academy of Sciences 944, no. 1 (January 25, 2006): 373–87. http://dx.doi.org/10.1111/j.1749-6632.2001.tb03849.x.

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Choi, Soo Bong, Jin Sun Jang, and Sunmin Park. "Estrogen and Exercise May Enhance β-Cell Function and Mass via Insulin Receptor Substrate 2 Induction in Ovariectomized Diabetic Rats." Endocrinology 146, no. 11 (November 1, 2005): 4786–94. http://dx.doi.org/10.1210/en.2004-1653.

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The prevalence and progression of type 2 diabetes have increased remarkably in postmenopausal women. Although estrogen replacement and exercise have been studied for their effect in modulating insulin sensitivity in the case of insufficient estrogen states, their effects on β-cell function and mass have not been studied. Ovariectomized (OVX) female rats with 90% pancreatectomy were given a 30% fat diet for 8 wk with a corresponding administration of 17β-estradiol (30 μg/kg body weight) and/or regular exercise. Amelioration of insulin resistance by estrogen replacement or exercise was closely related to body weight reduction. Insulin secretion in first and second phases was lower in OVX during hyperglycemic clamp, which was improved by estrogen replacement and exercise but not by weight reduction induced by restricted diets. Both estrogen replacement and exercise overcame reduced pancreatic β-cell mass in OVX rats via increased proliferation and decreased apoptosis of β-cells, but they did not exhibit an additive effect. However, restricted diets did not stimulate β-cell proliferation. Increased β-cell proliferation was associated with the induction of insulin receptor substrate-2 and pancreatic homeodomain protein-1 via the activation of the cAMP response element binding protein. Estrogen replacement and exercise shared a common pathway, which led to the improvement of β-cell function and mass, via cAMP response element binding protein activation, explaining the lack of an additive effect with combined treatments. In conclusion, decreased β-cell mass leading to impaired insulin secretion triggers glucose dysregulation in estrogen insufficiency, regardless of body fat. Regular moderate exercise eliminates the risk factors of contracting diabetes in the postmenopausal state.
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Tan, Gemma, Andrew G. Elefanty, and Edouard G. Stanley. "β-cell regeneration and differentiation: how close are we to the ‘holy grail’?" Journal of Molecular Endocrinology 53, no. 3 (December 2014): R119—R129. http://dx.doi.org/10.1530/jme-14-0188.

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Diabetes can be managed by careful monitoring of blood glucose and timely delivery of exogenous insulin. However, even with fastidious compliance, people with diabetes can suffer from numerous complications including atherosclerosis, retinopathy, neuropathy, and kidney disease. This is because delivery of exogenous insulin coupled with glucose monitoring cannot provide the fine level of glucose control normally provided by endogenous β-cells in the context of intact islets. Moreover, a subset of people with diabetes lack awareness of hypoglycemic events; a status that can have grave consequences. Therefore, much effort has been focused on replacing lost or dysfunctional β-cells with cells derived from other sources. The advent of stem cell biology and cellular reprogramming strategies have provided impetus to this work and raised hopes that a β-cell replacement therapy is on the horizon. In this review, we look at two components that will be required for successful β-cell replacement therapy: a reliable and safe source of β-cells and a mechanism by which such cells can be delivered and protected from host immune destruction. Particular attention is paid to insulin-producing cells derived from pluripotent stem cells because this platform addresses the issue of scale, one of the more significant hurdles associated with potential cell-based therapies. We also review methods for encapsulating transplanted cells, a technique that allows grafts to evade immune attack and survive for a long term in the absence of ongoing immunosuppression. In surveying the literature, we conclude that there are still several substantial hurdles that need to be cleared before a stem cell-based β-cell replacement therapy for diabetes becomes a reality.
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Book chapters on the topic "Β-cell replacement"

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Hayek, Alberto, Gillian M. Beattie, and Fred Levine. "Gene Therapeutic Approaches for β-Cell Replacement." In Molecular Basis of Pancreas Development and Function, 373–400. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1669-9_23.

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Sarkar Dey, Subhanwita, Noriko Yoshida, and Kouichi Hasegawa. "Overview of Pancreatic Replacement of β-Cells from Various Cell Sources." In Stem Cell Therapy for Organ Failure, 181–93. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2110-4_14.

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de Vries, Rick, Adam Stell, Sami Mohammed, Carolin Hermanns, Adela Helvia Martinez, Marlon Jetten, and Aart van Apeldoorn. "Bioengineering, biomaterials, and β-cell replacement therapy." In Transplantation, Bioengineering, and Regeneration of the Endocrine Pancreas, 461–86. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-814831-0.00033-6.

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Elliyanti, Aisyah. "Radioiodine for Graves’ Disease Therapy." In Graves' Disease [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96949.

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Radioiodine-131 (RAI) is an isotope of the chemical element iodine and is commonly used for hyperthyroidism, including Graves’ disease. It is given orally, and its concentration in the thyroid gland. The RAI transport involves a natrium iodide symporter (NIS) role that brings two cations sodium (Na+) and one anion of iodide (I-) across the membrane. The process is facilitated by the enzyme Na+/K+ ATPase. RAI is a beta (β) and gamma (γ) particles emitter. β particle is used for therapy and γ particle for imaging (theranostic). β particle inhibits cell growth by inducing cell death through apoptosis or necrosis of some of the sufficient thyroid cells. The aim of RAI therapy in Graves’ disease is to control hyperthyroidism and render the patient hypothyroidism. It is easier to manage patients with hypothyroidism with levothyroxine and fewer complications. This review will focus on RAI’s therapeutic approach in Graves’ disease, including patient preparation, selecting activity dose, adverse events, contraindication, controversies issues such as malignancy and fertility, the follow-up to ensuring the patient remains euthyroid or need a replacement therapy if they become hypothyroidism. RAI therapy is safe as definitive therapy and cost-effective for Graves’ disease therapy.
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Conference papers on the topic "Β-cell replacement"

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Kim, Minwook, Isaac E. Erickson, Jason A. Burdick, George R. Dodge, and Robert L. Mauck. "Differential Chondrogenic Potential of Human and Bovine Mesenchymal Stem Cells in Agarose and Photocrosslinked Hyaluronic Acid Hydrogels." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19461.

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Articular cartilage has a limited regenerative capacity, and there exist no methodologies to restore structure and function after damage or degeneration. This has focused intense work on cell-based therapies for cartilage repair, with considerable literature demonstrating that chondrocytes in vitro and in vivo can generate cartilage-like tissue replacements. However, use of primary cells is limited by the amount and quality of autologous donor cells and tissue. Multipotential mesenchymal stem cells (MSCs) derived from bone marrow offer an alternative cell source for cartilage tissue engineering. MSCs are easily accessible and expandable in culture, and differentiate towards a chondrocyte-like phenotype with exposure to TGF-β [1]. For example, we have shown that bovine MSCs undergo chondrogenic differentiation and mechanical maturation in agarose, self-assembling peptide, and photocrosslinkable hyaluronic acid (HA) hydrogels [2]. HA hydrogels are particularly advantageous as they are biologically relevant and easily modified to generate a range of hydrogel properties [3]. Indeed, bovine MSCs show a strong dependence of functional outcomes on the macromer density of the HA gel [4]. To further the clinical application of this material, the purpose of this study was to investigate functional chondrogenesis of human MSCs in HA compared to agarose hydrogels. To carry out this study, juvenile bovine and human MSCs were encapsulated and cultured in vitro in HA and agarose hydrogels, and cell viability, biochemical, biomechanical, and histological properties were evaluated over 4 weeks of culture.
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Huang, Alice H., Brendon M. Baker, Gerard A. Ateshian, and Robert L. Mauck. "Sliding Contact Loading Improves the Tensile Properties of MSC-Based Engineered Cartilage." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19292.

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Articular cartilage is a load-bearing surface whose mechanical function arises from its unique properties. The structural and mechanical properties of mature cartilage are inhomogeneous through the depth and anisotropic. Tissue maturation is directed by mechanical forces; loading induces remodeling of the immature matrix, leading to increases in compressive and tensile properties and the development of tissue anisotropy [1, 2]. Limitations in cartilage repair strategies have engendered numerous efforts to engineer functional replacements. As mesenchymal stem cells (MSCs) undergo chondrogenesis in 3D culture, this cell type has been increasingly utilized in these efforts [3]. Despite their initial promise however, generating MSC-based constructs with the mechanical complexity and integrity of cartilage remains a challenge; the properties of MSC-seeded hydrogels are consistently lower than those of the native tissue [4, 5]. As mechanical stimulation is critical to cartilage development and maturation, bioreactor systems that simulate the native mechanical environment of cartilage may bridge these functional disparities. Indeed, dynamic axial compression enhances the compressive properties of both chondrocyte- and MSC-based engineered cartilage, though collagen content remains low [6, 7]. While promising, these studies were not designed to generate either depth-dependence or constructs with improved tensile properties. We therefore developed a new sliding contact bioreactor system that can better recapitulate the mechanical stimuli arising from joint motion (two contacting cartilage layers). In previous experiments using this system, we demonstrated improved expression of chondrogenic genes with short-term sliding contact of MSC-seeded agarose; these changes in gene expression were dependent on both axial strain and TGF-β supplementation [8]. Furthermore, FEM analysis of sliding contact showed that tensile strains (parallel to the sliding direction) and fluid efflux/influx were depth-dependent and highest in the region closest to the construct surface [8]. In the current study, we applied long-term sliding contact to MSC-seeded agarose constructs using the optimized parameters previously determined. We hypothesized that sliding contact would improve tensile properties and direct depth-dependent matrix remodeling.
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Campos, M., L. Santos, J. Lobato, C. Melo, and B. Justica. "HTLV III/LAV ANTIBODY STATUS, AND IMMUNOLOGICAL ABNORMALITIES IN A HEMOPHILIC POPULATION FROM PORTUGAL Campos." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644143.

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An immunological study in a population of 46 hemophiliacs (A and B)under replacement therapy mainly with cryo, plasma and eventually withccmercial concentrates was carried out to detect changes related to HTLV III infection and those due totreatment. We followed the patients during 85-87 and we evaluate the abnormalities over a period of 2 years . Methods. Ig's (nephelometry): total lymphocytes, T3, T4, T8 subsets and B cells (IF microcopy):delayed hypersensivity skin tests (DHST) ,7 antigens: serology for HTLV III (ELISA and WB) (β 2 microglobulin (ELISA) Results. In 85,10 patients had anti HTLV III(28%) and all these received concentrates.9 out 46 had never been treated with concentrates and all were negative for HTLV III . Most of the HTLV III +ve patients showed lymphopenia, low T4 and total B cells, anergy or depressed DHST,increase Ig levels, mainly IgG and IgM. Among the HILV -ve patients there were no significant diferences between tose treated withconcentrates and most showed only an increased Ig's levels (IgG and IgM During 85 and 86 all the patients were treated with plasma, cryo and heat-treated concentrates. In the end of 86 none of the seronegative showed seroconversion. Among the 10 seropositives in 85,1 died (AIDS) ,1 is in ARC and 8 are ssymptomatic . All theseroposi tive patients shows high levels of β2 microglobulin.Conclusions . The low incidence of seropositivity for HTLV III,is probably due to the scarce use of comercial concentrates before 85. The absence of seroconversion despite the use of heat-treated concentrates is probably due to the safe of the product s. We must emphazise the absence of clinical symptoms in 8 seropositive patientsduring two years. There is a positive correlation between the level of (β2 microgldbulin and the seropositivity. Theimmunological profile observed is related more to the parenteraladministration of blood products thanto the specific composition and/or method of preparation of the therapeutic products. The serological profile from the HTLV III +ve patients isprobably a result of the administration in the past of comercial concentrates virus infected.
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