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1 ibraries, each from an individual pancreatic islet cell.
2  exit the cell cycle, and differentiate into islet cells.
3 or RNA sequencing of single mouse pancreatic islet cells.
4 demonstrate an acinar cell defect but normal islet cells.
5 ted insulin secretion (GSIS) and survival of islet cells.
6 of live-cell phenotypes in single developing islet cells.
7 , cardiomyocytes, and insulin-producing beta islet cells.
8 structs transduced in MIN6 cells and primary islet cells.
9 ing pancreas development as well as in adult islet cells.
10 m stage cells (CXCR4+ cells), and pancreatic islet cells.
11 ents IGF-1-induced survival of primary mouse islet cells.
12 lored whether Hes3 also regulates pancreatic islet cells.
13 distinct spatial-temporal patterns in rodent islet cells.
14 transcription factor in developing and adult islet cells.
15 primary C57BL/6J mouse and nondiabetic human islet cells.
16 OD mice that express an NKG2D ligand in beta-islet cells.
17  and human pancreas and sorted primary human islet cells.
18 r without (n = 8) intraabdominally engrafted islet cells.
19 omers in pancreatic rat insulinoma and human islet cells.
20 ility of (18)F-fallypride as a PET agent for islet cells.
21 entiation into exocrine acinar and endocrine islet cells.
22 ruction of insulin-producing pancreatic beta-islet cells.
23 ic predispositions affecting both immune and islet cells.
24 f NF-kappaB transcription factor and control islet cells.
25  without various indirect effects from other islet cells.
26 aimed to assess these findings in East-Asian islet-cells.
27 tein-coupled receptors that are expressed by islets cells.
28 ferentiated hESCs as compared with CXCR4+ or islets cells.
29  secretion by increasing oxidative stress in islets cells.
30  mutations, including significant pancreatic islet cell adaptation in obesity-associated tumors.
31     Experiments were carried out with single islet cells adherent to chimeric proteins made of functi
32 n beta-cell reconstitution from heterologous islet cells after near-total beta-cell loss in mice.
33 vide islet cells with glutamate, (b) protect islet cells against high extracellular glutamate concent
34 n insulin-producing beta-cells in a model of islet cell aggregate formation.
35 nhbb or addition of activin B stimulates rat islet cell and beta-cell proliferation, and the activin
36 ates Pdx-1-stimulated proliferation of total islet cells and beta cells.
37 the cell cycle during the differentiation of islet cells and demonstrate that the subsequent down-reg
38 uppressed NF-kappaB activation in both human islet cells and immune cells.
39 SAs bound to allogeneic targets expressed by islet cells and induced their destruction in vitro; howe
40 of the complex network of cross talk between islet cells and its effects on beta-cell function.
41 activation of this pathway is detrimental to islet cells and likely promotes damaging autoimmunity an
42           (18)F-fallypride bound to isolated islet cells and pancreatic sections with an endocrine or
43 and contain time-series expressions in human islet cells and rat INS-1E cells.
44 e dually linked in both their secretion from islet cells and their action in the liver.
45 ODY genes in the development of pancreas and islet cells and to evaluate their significance in regula
46  a reciprocal interaction between pancreatic islet cells and vascular endothelial cells (EC) in which
47 ed with an augmented number of proliferative islet cells and with resistance to streptozotocin-induce
48 eart, lung, liver, pancreas, intestinal, and islet cells), and (c) the application of antibody testin
49 ing, (ii) single-cell genomics of pancreatic islet cells, and (iii) metaanalysis of lung adenocarcino
50 ased GLT-induced cytosolic calcium influx in islet cells, and all measured beta-cell-protective effec
51 elopmental programs that generate functional islet cells, and that are relevant to human pancreatic d
52 ssion of TRB3 84R in mouse beta cells, human islet cells, and the murine beta cell line MIN6 revealed
53 t focus on the differentiation of pancreatic islet cells, and their applications in regenerative medi
54 iabetes-associated autoantibodies, including islet cell antibodies (ICAs), reflect adaptive immunity,
55  were analyzed using radiobinding assays and islet cell antibodies with immunofluorescence during a m
56 atter was defined as repeated positivity for islet-cell antibodies plus for at least 1 of 3 other dia
57              CD8(+) T-cell responses against islet cell antigens, thought to play a central role in d
58                           GABA reduced human islet cell apoptosis in culture, such that the yield of
59                          TCDC did not change islet cell apoptosis.
60 he protective mechanism in berberine against islet cell apoptosis.
61 etical risk of tumor cell dissemination when islet cells are transplanted into the portal vein.
62 ncreatic ductal epithelial cells (PDECs) and islet cells as causative in CF.
63 ttachment and growth of primary human or rat islet cells as monolayers on glass surfaces.
64                   Adhesion tests showed that islet cells attached to N-cad/Fc and E-cad/Fc acquired,
65 e 3 years from 22 case children in whom anti-islet cell autoantibodies developed, and 22 matched cont
66 0.5 and 2 years in the children in whom anti-islet cell autoantibodies developed.
67 ssociated antigen-2 antibodies (IA-2As), and islet cell autoantibodies were measured at time of diagn
68  these autoantibodies did not correlate with islet cell autoantibodies.
69 and 22 matched control children who remained islet cell autoantibody-negative in follow-up.
70                  No differences between anti-islet cell autoantibody-positive and -negative children
71                              Type 1 diabetes islet cell autoantigen 512 (ICA512/IA-2) is a tyrosine p
72                                       ICA69 (islet cell autoantigen 69 kDa) is a protein implicated i
73                             Although several islet cell autoantigens are known, the breadth and spect
74 erogeneity in autoantibody responses against islet cell autoantigens including two polymorphic varian
75 f the microbiome in the pathogenesis of anti-islet cell autoimmunity and type 1 diabetes.
76  the gut microbiome in children in whom anti-islet cell autoimmunity developed.
77                             Evidence of anti-islet cell autoimmunity in type 1 diabetes appears in th
78 ted in T2D subjects, implying a role for the islet cell-autonomous clocks in T2D progression.
79 e conclude that hypoglycemia in SCHAD-CHI is islet cell-autonomous.
80                     Total pancreatectomy and islet cell autotransplantation (TPIAT) has been increasi
81 y plays a critical role in the regulation of islet cell biology.
82 ival of both MIN6 beta-cells and dissociated islet cells, both at a very low cell-packing density (<
83 anc) mice also had some minor alterations in islet cells, but beta-cell development was not affected.
84                                 In dispersed islet cells, but not in intact islets or in vivo, pro-pr
85 tes (GG) were coencapsulated with pancreatic islet cells by using protamine sulfate as a clinical-gra
86               To investigate whether primary islet cells can produce EXOs, we isolated cells from the
87  differentiation and development, as well as islet cell carcinogenesis.
88 ry neoplasm generated is a highly metastatic islet cell carcinoma of the pancreas.
89    Nor1 overexpression in both INS and human islet cells caused apoptosis, whereas siRNA-mediated Nor
90 progression, driving the destruction of beta-islet cells, causing hyperglycemia and ultimately death.
91 duced dominant tolerance to porcine neonatal islet cell cluster (NICC) xenografts in mice.
92 perturbed endocrine cell differentiation and islet cell clustering in VEGF-A overexpressing embryos.
93                                     Neonatal islet cell clusters (ICCs) from INSLEA29Y transgenic (LE
94            While alpha and beta cells formed islet cell clusters in control embryos at E16.5, the inc
95 nd (3) diabetic patients receiving fetal pig islet cell clusters xenograft together with a kidney all
96         To test this hypothesis, we examined islet cell composition in a streptozotocin (STZ)-induced
97 eration and insulin secretion of dissociated islet cells, contributing to the reduced beta-cell mass
98 n important regulator of gene expression and islet cell coordination.
99  cell type exhibits hallmarks of its primary islet cell counterpart including cell-specific expressio
100  ADK-Is is cell type-selective: treatment of islet cell cultures with ADK-Is increases replication of
101 ltiple factors including islet availability, islet cell damage caused by collagenase during isolation
102 erleukin-1beta- and interferon-gamma-induced islet cell death in vitro.
103 Diabetes, but the link of hIAPP structure to islet cell death remains elusive.
104 ic overgrowth often causes microencapsulated islet-cell death and graft failure.
105                          Flow-sorted ALDH(+) islet cells demonstrate impaired glucose-induced insulin
106  differentiation and islet development while islet cell-derived angiogenic factors promote EC recruit
107 nifested as a pancreatic insulitis with beta-islet cell destruction and systemic glucose intolerance.
108                                  Nrp2 mutant islet cells developed in proper numbers, but had defects
109 red novel functions of NEUROD1 during murine islet cell development and during the differentiation of
110 r signals identified factors that stimulated islet cell development.
111 lls (EC) in which EC-derived signals promote islet cell differentiation and islet development while i
112 in-1 (Ang1), or angiopoietin-2 (Ang2) during islet cell differentiation and islet development.
113   Although the molecular pathways underlying islet cell differentiation are beginning to be resolved,
114 transcription factors that are essential for islet cell differentiation have been well characterized;
115 scription factor neurogenin3 (Ngn3) triggers islet cell differentiation in the developing pancreas.
116 o parse out the spatiotemporal regulation of islet cell differentiation, we used a Neurog3-Cre allele
117                   Thus, mammalian pancreatic islet cells display cell-type-specific epigenomic plasti
118 tion are exerting their disease risk through islet-cell dysfunction.
119 ofound dose-dependent deleterious effects on islet cell engraftment.
120 ion in sites that might be more favorable to islet cell engraftment.
121 ll-molecule cargoes in beta-cells over other islet cells ex vivo or other cell-types in an organismal
122                                 Importantly, islet cells exhibit plasticity in altering their endocri
123                                We found that islet cells expressed the genes encoding all of the prod
124                            Here we show that islet cells expressing insulin, glucagon, or somatostati
125 tory program to correctly specify pancreatic islet cell fates.
126 ucose-regulated hormone secretion, and human islet cells follow a similar pattern.
127 promote growth, function, and engraftment of islet cells following transplantation.
128 uction was assessed by acute knockdown using islet cells from Atf6alpha (flox/flox) mice transduced w
129   Experiments were performed with islets and islet cells from C57BL/6N wild-type and FXR-knockout (KO
130 glycemia in diabetic mice and protects human islet cells from cell death.
131 eptozotocin (STZ)-treated primary pancreatic islet cells from ICR mice to unravel the protective mech
132 ential to pancreatic morphogenesis and adult islet cell function and maintenance.
133 cretion resulting from changes in pancreatic islet cell function and/or mass.
134 study indicated that, from the standpoint of islet cell function, linagliptin would be more effective
135 ors associated with pancreas development and islet cell function, we analyzed how an endogenous delet
136 that LD enrichment could be impactful to T2D islet cell function.
137 omoters and enhancers to repress alternative islet cell genes including ghrelin, glucagon, and somato
138 nd in silico replications of mouse and human islet cell genes were performed.
139 type 1 diabetic recipients of an intraportal islet-cell graft under maintenance immunosuppression (IS
140 ressants in 35 type 1 diabetic recipients of islet cell grafts prepared from a median of 6 donors (ra
141 ty type 1 diabetes recipients of intraportal islet cell grafts under antithymocyte globulin induction
142          Allosensitization to cultured human islet cell grafts was low when assessed by CDC assay but
143 2 diabetes and contributes to the failure of islet cell grafts.
144  The formation of hIAPP amyloid plaques near islet cells has been linked to the death of insulin-secr
145 sis and proliferation, but during adulthood, islet cells have a very slow turnover.
146            TSPAN-7 is enriched in pancreatic islet cells; however, the function of islet TSPAN-7 has
147 as and four additional positive lesions (two islet-cell hyperplasia and two uncharacterised lesions)
148                           One true negative (islet-cell hyperplasia) and one false negative (malignan
149 he genetic and molecular factors controlling islet cell identity and function.
150                                   Changes to islet cell identity in response to type 2 diabetes (T2D)
151 oliferating betaTC-6 cells, but not in human islet cells; (ii) down-regulation of ZBED6 in betaTC-6 c
152 id bilayers, but appear to have no effect on islet cells in culture.
153 ptide-lipid interactions with its effects on islet cells in culture.
154 venly distributed in postjuvenile acinar and islet cells in donors without diabetes, LDs were enriche
155 TF6 pathways are simultaneously activated in islet cells in response to acute stress and that ATF6alp
156 B-dependent fashion) and translated by human islet cells in response to in vitro inflammatory stimuli
157 ed destruction of the insulin-producing beta-islet cells in the pancreas.
158 IL15/IL-15Ralpha expression was increased in islet cells in the prediabetic stage, and inhibition of
159 eptor (D(2)/D(3)R)-based PET method to study islet cells in the rat pancreas and in islet cell transp
160 s surrogate beta-cells and human HLA-A*24(+) islet cells in vitro.
161 e long-term insulin secretion by xenografted islet cells in vivo, and represent a novel contrast agen
162 t on the NOD background despite an increased islet cell infiltrate with markedly increased numbers of
163 n the face of hypercytokinemia and potential islet cell injury.
164 sults from a limited understanding of immune-islet cell interactions within the pancreas and relevant
165              A landscape with multiple intra-islet cell interconversion events is emerging, offering
166 rable leakage of the contrast agent into the islet cell interstitium.
167 et amyloid polypeptide (hIAPP) in pancreatic islet cells is implicated in the pathogenesis of type II
168 et, that insulin secretion, intrinsic to the islet cells, is a key mechanism underlying the associati
169 ssion of miR-29a/b/c in MIN6 and dissociated islet cells led to impairment in glucose-induced insulin
170 lets at population, single islet, and single islet cell levels.
171                  Snord116 may play a role in islet cell lineage specification.
172 TC1 (alphaTC1) and Beta-TC-6 (betaTC6) mouse islet cell lines are cellular models of islet (dys)funct
173 ucose and lipid impair beta cell function in islet cell lines, cultured rodent and human islets, and
174 ar to be significant differences in pancreas islet cell lipid handling between species, and the human
175           A noninvasive method that measures islet cell loss and also tracks the fate of transplanted
176 entify how acinar cell proteases cause human islet cell loss before and after transplantation of impu
177                                              Islet cell loss in the pancreas results in diabetes.
178 ent with DXM improved islet insulin content, islet cell mass and blood glucose control.
179 reatic progenitors had significantly reduced islet cell mass at birth, caused by decreased endocrine
180  insulin sensitivity and restored pancreatic islet cell mass, neuronal innervation and microbiome com
181  of A1AT to impure islet cultures maintained islet cell mass, restored insulin levels, and preserved
182 m a more rigid structure, often encasing the islet cell mass.
183 ted the hypothesis that enriching pancreatic islet cell membranes with EPA, thereby reducing arachido
184 roach using objective assessments focused on islet cell mitochondrial integrity and in vitro function
185                     When mimicked in newborn islet cells, modifications in the level of specific micr
186                                          The islet cell monolayer cultures on glass stably maintain d
187 initial bursting discharge, Ih currents, and islet cell morphology.
188 ntal differences, five studies of pancreatic islet cells, mouse embryogenesis datasets and the integr
189 tion of glucagon secretion where neighboring islet cells negatively regulate glucagon secretion throu
190 ssion of miR-26a in mice increases postnatal islet cell number in vivo and endocrine/acinar colonies
191                                     However, islet cell number is maintained and insulin secretion is
192 ted from loss of islet cell size rather than islet cell number.
193 tes to the alteration of beta-cell identity, islet cell numbers and morphology, and gene expression b
194  this pathogenic process was active in human islet cells obtained from donors with type 2 diabetes; t
195 ly transcript 1epsilon (RAE1epsilon) in beta-islet cells of the pancreas, we found that RAE1 expressi
196 nolayers of adherent and well-spread primary islet cells on glass coverslips is required for detailed
197       Expression of hIAPP in purified monkey islet cells or a murine beta cell line resulted in pro-h
198 ely 40-microm) pseudoislets using all of the islet cells or only some of the cell types, which allowe
199 e treated with alloxan to destroy pancreatic islet cells, or mock-treated with vehicle, and maintaine
200                                We found that islet cell organization, beta-cell mass, and beta-cell f
201    They suggested a secretin-like hormone of islet cell origin explains WDS and achlorhydria.
202 ), 67 SNPs for type 2 diabetes in pancreatic islet cells (P = 0.003) and the liver (P = 0.003), and 1
203 direct effects of autonomic nervous input on islet cell physiology cannot be studied in the pancreas.
204 down-regulation of Neurog3 allows the mature islet cell population to expand.
205 ted the hypothesis that HLA-A24 molecules on islet cells present preproinsulin (PPI) peptide epitopes
206                                        Human islet cells process and present PPI(3-11), rendering the
207 ells expressed Sema3a, while central nascent islet cells produced the semaphorin receptor neuropilin
208  in the field require the standardization of islet cell product isolation processes, and this work ai
209 ghted the presence of a heterogeneity in the islet cell product process and product release criteria.
210                  Organ growth and pancreatic islet cell proliferation and mass were examined in sheep
211 slets, Inhbb overexpression stimulates total islet cell proliferation and potentiates Pdx-1-stimulate
212 eported that Pdx-1 overexpression stimulates islet cell proliferation, but the mechanism remains uncl
213 s sufficient to stimulate both rat and human islet cell proliferation.
214                                   Pancreatic islet cells provide the major source of counteractive en
215                   Assays for assessing human islet cell quality, which provide results before transpl
216 ve broader implications on the regulation of islet cell ratios and their ability to effectively respo
217                        When cultured, murine islet cells reassociate to form pseudoislets, which reco
218 enes, including those involved in regulating islet cell recovery and proliferation, and identify addi
219 th coincident enhancement of nuclear Nrf2 in islet cells, reduced beta-cell oxidative stress, and pre
220                                              Islet cell replacement can effectively treat diabetes bu
221 f disease would require strategies combining islet cell replacement with immunotherapy that are curre
222 ent strategy to examine age-associated human islet cell replication competence and reveal mechanisms
223    Furthermore, a GABAA-R PAM promoted human islet cell replication in vitro.
224  of the embryonic endocrine pancreas and the islet cell replication that occurs in an adult animal.
225 ls of exogenous GABA further increased human islet cell replication.
226 arkably, miR-375 normalization in LP-derived islet cells restores beta-cell proliferation and insulin
227  Loss of YIPF5 function in stem cell-derived islet cells resulted in proinsulin retention in the ER,
228                                    Dispersed islet cells secrete aberrant levels of glucagon and insu
229                                        Acute islet cell secretory responses were determined under fas
230  regulation, and revealed that pig and human islet cells share characteristic features that are not o
231 origins in different germ layers, pancreatic islet cells share many common developmental features wit
232  PDECs directly reduced insulin secretion in islet cells significantly.
233 ithin the islet, which resulted from loss of islet cell size rather than islet cell number.
234      Guided by an observation that dispersed islet cells spread and adhere well on glass surfaces in
235 a distinguishing transcription factor within islet cell subtype specification.
236 human gene expression and epigenomic data in islet cell subtypes constitutes a truly valuable resourc
237 ed cell types (for example, other pancreatic islet cells such as alpha-cells, or other cells derived
238                          GABA improved human islet cell survival and had suppressive effects on human
239 elin promotes pancreatic beta-cell and human islet cell survival and prevents diabetes in streptozoto
240  fluorescence-enhanced (NIR-FE) detection of islet cell-targeting autoantibodies.
241 ecific NIR FI in the nuclei and cytoplasm of islets cells than in non-treated control mice and this f
242 tecture between alphaTC1/betaTC6 and primary islet cells that can be leveraged in functional (epi)gen
243 lity to sophisticated analyses of pancreatic islet cells that reveal new biological insights, as demo
244 ial signaling axis that instructs developing islet cells to disperse throughout the pancreas.
245 e performed timed exposures of primary mouse islet cells to ER stressors and measured the early trans
246 d for delivery of donor syngeneic pancreatic islet cells to reverse hyperglycemia in murine streptozo
247 ed pseudoislets reconstituted from dispersed islet cells to study alpha-cells with and without variou
248 resentation of insulin epitopes by dispersed islet cells to T cells was impaired, and (iii) the devel
249 h repeated positivity for antibodies against islet cells) together with positivity for at least one o
250 their consequences for the quality of single-islet cell transcriptome data.
251 tment option for type 1 diabetes, pancreatic islet cell transformation has been hindered by immune sy
252 ification could potentially lead to improved islet cell transplant outcomes.
253                 The use of tacrolimus in our islet-cell transplant protocol caused an initial 20% red
254                               The promise of islet cell transplantation cannot be fully realized in t
255                                              Islet cell transplantation has limited effectiveness bec
256  analysis plans for future pivotal trials of islet cell transplantation in type 1 diabetes.
257 nts with type 1 diabetes of longer duration, islet cell transplantation may be more effective than me
258  vs placebo (RR 0.60; 95% CI 0.41-0.86), and islet cell transplantation vs medical therapy (RR 0.25;
259 -2 diabetes, and also reduces the success of islet cell transplantation.
260 oon retrograde transvenous obliteration, and islet cell transplantation.
261 red a risk factor for liver, intestinal, and islet cell transplantation.
262 e loss of functional islets after allogeneic islet cell transplantation.
263 ed its efficacy in a rhesus macaque model of islet cell transplantation.
264 study islet cells in the rat pancreas and in islet cell transplantation.
265 ing of allograft injury in humans undergoing islet cell transplantation.
266  CXCR4-CXL12 axis, to promote engraftment of islet cell transplantation.
267 ed inflammatory loss of graft function after islet cell transplantation.
268 so show that for encapsulated rat pancreatic islet cells transplanted into streptozotocin-treated dia
269 2 diabetes and contributes to the failure of islet cell transplants, however the mechanisms of IAPP-i
270  amyloid formation in type 2 diabetes and in islet cell transplants.
271 ng somatic gene transfer in a mouse model of islet cell tumorigenesis, we demonstrate that RHAMM isof
272  neuroendocrine tumors (pNET), also known as islet cell tumors, exhibit a wide range of biologic beha
273  is essential for pancreatic development and islet cell type differentiation.
274 othesis is based on the assumption that each islet cell type has a specific pattern of miRNA expressi
275 standing of the molecular components of each islet cell type that govern islet (dys)function, particu
276                                      A fifth islet cell type, the ghrelin-producing epsilon cells, is
277 ing Myt1 as a marker but not determinant for islet-cell-type specification.
278 e intra-islet interactions between different islet cell types functions not only to reduce the superf
279 of this homologue reduced the numbers of all islet cell types including the insulin-producing beta-ce
280 c basis for the observed plastic identity of islet cell types, and have implications for beta-cell re
281 ene in mice leads to loss of most pancreatic islet cell types, the functional consequences of Pax6 lo
282 ights into genes and pathways characterizing islet cell types.
283 n were detected in macrophages but not other islet cell types.
284 ical to ensure there is a correct balance of islet cell types.
285 pressing progenitors give rise to four major islet cell types: alpha, beta, delta, and gamma; when an
286 odeficiency mice received transplanted human islet cells under the kidney capsule and adoptively tran
287 system for longitudinal examination of human islet cells undergoing developmental/metabolic/pharmacog
288                   Diminishment of functional islet cells' VTCN1 is caused by the active proteolysis b
289  whether cadherin-mediated adhesion of human islet cells was affected by insulin secretagogues and ex
290      We observed that cadherin expression in islet cells was not affected by insulin secretagogues.
291 human leukocyte antigen (HLA) class I on the islet cells, we examined its expression in subjects with
292  The viability and glucose responsiveness of islet cells were assessed in vitro, and in vivo insulin
293 validate the approach, single rat pancreatic islet cells were rapidly analyzed with optically guided
294                 Although yields of recovered islet cells were relatively low, the ratios of bulk-sort
295                                          Rat islet cells were transplanted into the spleen and visual
296                                          448 islet-cells were captured from three East-Asian non-diab
297 Slc1a2) has been hypothesized to (a) provide islet cells with glutamate, (b) protect islet cells agai
298 ed 622 cells, allowing identification of 341 islet cells with high-quality gene expression profiles.
299  normal human juvenile pancreatic acinar and islet cells, with numbers subsequently increasing throug
300 in cytokine-treated and virus-infected human islet cells, with up-regulation of gene networks involve

 
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