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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.
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
35 nhbb or addition of activin B stimulates rat islet cell and beta-cell proliferation, and the activin
37 the cell cycle during the differentiation of islet cells and demonstrate that the subsequent down-reg
39 SAs bound to allogeneic targets expressed by islet cells and induced their destruction in vitro; howe
41 activation of this pathway is detrimental to islet cells and likely promotes damaging autoimmunity an
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
65 e 3 years from 22 case children in whom anti-islet cell autoantibodies developed, and 22 matched cont
67 ssociated antigen-2 antibodies (IA-2As), and islet cell autoantibodies were measured at time of diagn
74 erogeneity in autoantibody responses against islet cell autoantigens including two polymorphic varian
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.
85 tes (GG) were coencapsulated with pancreatic islet cells by using protamine sulfate as a clinical-gra
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.
92 perturbed endocrine cell differentiation and islet cell clustering in VEGF-A overexpressing embryos.
95 nd (3) diabetic patients receiving fetal pig islet cell clusters xenograft together with a kidney all
97 eration and insulin secretion of dissociated islet cells, contributing to the reduced beta-cell mass
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
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.
109 red novel functions of NEUROD1 during murine islet cell development and during the differentiation of
111 lls (EC) in which EC-derived signals promote islet cell differentiation and islet development while i
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
121 ll-molecule cargoes in beta-cells over other islet cells ex vivo or other cell-types in an organismal
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
131 eptozotocin (STZ)-treated primary pancreatic islet cells from ICR mice to unravel the protective mech
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
137 omoters and enhancers to repress alternative islet cell genes including ghrelin, glucagon, and somato
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
144 The formation of hIAPP amyloid plaques near islet cells has been linked to the death of insulin-secr
147 as and four additional positive lesions (two islet-cell hyperplasia and two uncharacterised lesions)
151 oliferating betaTC-6 cells, but not in human islet cells; (ii) down-regulation of ZBED6 in betaTC-6 c
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
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
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
164 sults from a limited understanding of immune-islet cell interactions within the pancreas and relevant
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
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
176 entify how acinar cell proteases cause human islet cell loss before and after transplantation of impu
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
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
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
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
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
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.
205 ted the hypothesis that HLA-A24 molecules on islet cells present preproinsulin (PPI) peptide epitopes
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.
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
216 ve broader implications on the regulation of islet cell ratios and their ability to effectively respo
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
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
224 of the embryonic endocrine pancreas and the islet cell replication that occurs in an adult animal.
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,
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
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
239 elin promotes pancreatic beta-cell and human islet cell survival and prevents diabetes in streptozoto
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
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
251 tment option for type 1 diabetes, pancreatic islet cell transformation has been hindered by immune sy
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;
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
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
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
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
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
289 whether cadherin-mediated adhesion of human islet cells was affected by insulin secretagogues and ex
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
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