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1 stine, 40 kidney, 20 livers, 24 lungs, and 7 pancreata).
2 ing of embryonic day (e) 13.5 and 15.5 mouse pancreata.
3 al neoplasias and PDAs compared with healthy pancreata.
4 yses of the IkappaBalpha- and RelA-deficient pancreata.
5 neutrophil recruitment compared with normal pancreata.
6 antities of insulin were present in most T1D pancreata.
7 alpha-cells in Gcgr(-/-) and Gcgr(Hep)(-/-) pancreata.
8 istologic examination of salivary glands and pancreata.
9 is is induced in postpartum FoxM1(Deltapanc) pancreata.
10 tained primary cilia in both human and mouse pancreata.
11 ding outpouches of ducts in murine and human pancreata.
12 the native insulin B:9-23 sequence in their pancreata.
13 +/- 3.0%) and obese diabetic (18.5 +/- 3.6%) pancreata.
14 tion of PGC-GdDTPA-F in diabetic and control pancreata.
15 P < 0.01) in obese diabetic (0.49 +/- 0.17%) pancreata.
16 rine embryonic stem cells to early endocrine pancreata.
17 n secretion compared to islets from SCS only pancreata.
18 man islets were obtained from research-grade pancreata.
19 ic islets of Langerhans of adult human donor pancreata.
20 et, very few beta-cells persist within their pancreata.
21 ation is an insufficient supply of cadaveric pancreata.
22 fected pancreata but not in CVB3/GA-infected pancreata.
23 ext, we analyzed the oxidative stress in the pancreata.
24 target, was also activated in the Ucp2(-/-) pancreata.
25 glucagon was similar to that from wild-type pancreata.
26 mes of VXM after transplantation of imported pancreata.
27 let development in Neurog3-null mutant mouse pancreata.
30 atic Organ Donors With Diabetes (nPOD) human pancreata across a wide range of ages and T1D disease du
32 d on studies of human, mouse, and guinea pig pancreata, alcohol disrupts expression and localization
33 long-term high fat diet (HFD), M4K4 iKO mice pancreata also displayed reduced beta cell mass, fewer p
34 revealed mosaic MANF expression in postnatal pancreata and a significant correlation between the numb
37 acceptance criteria for deceased donor organ pancreata and critical raw materials, PHPI product speci
39 ation with infusions from two to three donor pancreata and Edmonton immunosuppression consistently ac
41 ple experimental systems, including perfused pancreata and isolated islets of rodent or human origin.
45 ssfully and consistently produced from human pancreata and maintain their innate molecular and spatia
49 proves contrast between healthy and diabetic pancreata and provides a potential avenue for achieving
51 om three independent hPSC lines, human fetal pancreata, and adult human islets points to two major co
52 s on patient safety and care, prudent use of pancreata, and consolidates PII expertise and experience
53 As were cloned and sequenced from developing pancreata, and expression of a subset of these genes was
54 pproaches, organotypic cultures of embryonic pancreata, and genomics, we found that sphingosine-1-pho
55 as greatly accelerated in Mist1KO/KrasG12D/+ pancreata, and in vitro assays revealed that Mist1KO aci
56 ot used are smaller than numbers of kidneys, pancreata, and livers because intestines, hearts, and lu
57 -fixed paraffin-embedded surgically resected pancreata, and were analyzed by methylation-specific pol
58 crine congenital defects of Prox1(DeltaPanc) pancreata appeared to initiate a gradual process of dete
60 ween 3.5 and 6.2 in otherwise transplantable pancreata are not associated with different short-term o
61 ese data also suggest that many good quality pancreata are not procured, emphasizing the need for imp
62 After donor cross-clamp in Houston, donor pancreata arrived at DRI and the isolation process began
63 ing was performed on wild-type and MafB(-/-) pancreata at embryonic day 18.5, with candidates evaluat
66 extend the acceptable preservation period of pancreata before islet isolation and increase islet yiel
70 cells are specified normally in Hox6 mutant pancreata, but fail to mature into hormone-producing cel
71 , and delta-cells from human fetal and adult pancreata by intracellular staining for the cell-specifi
73 etion or heterozygous loss of Bap1 in murine pancreata causes genomic instability, tissue damage, and
78 le Gata4/Gata6 mutant mice failed to develop pancreata, died shortly after birth, and displayed hyper
79 histologically similar to WT, whereas K8/K18 pancreata displayed age-enhanced vacuolization and atrop
81 ss was normal in postpartum FoxM1(Deltapanc) pancreata due to a combination of increased beta-cell si
82 ir and resuscitate warm ischemically injured pancreata during preservation, improve pancreas graft su
84 F-alpha, MIP-1alpha, IL-12, and IFN-gamma in pancreata, endotoxin, or anti-CD3-stimulated splenic cel
90 gram (HPAP) to procure human type 1 diabetes pancreata for an extensive array of tissue-based, cellul
96 ive (AMY(+)) acinar cells were detectable in pancreata from all study groups, tissues from individual
100 lipase, and/or trypsinogen in 78 organ donor pancreata from birth through adulthood in control subjec
103 es, and the histopathological examination of pancreata from diabetic organ donors with the goal of pr
104 A substantial nationwide underutilization of pancreata from donor procurements is demonstrated in the
105 adopted a new allocation algorithm in which pancreata from donors >30 kg/m or >50 years of age are,
111 xpression of hepatic markers was examined in pancreata from mice genetically modified to secrete elev
114 onist enhanced insulin secretion in perfused pancreata from neonatal streptozotocin-induced diabetic
127 recise tissue distribution of CD8 T cells in pancreata from T1D, T2D, autoantibody-positive, and heal
129 in or sodium taurocholate than control mice; pancreata from the Bcl3(-/-) mice with AP had greater nu
135 ntitative RT-PCR showed that the Pax6(PE/PE) pancreata had a significant decrease in Pax6, glucagon,
139 lpha-specific gene expression, and Grg3(+/-) pancreata have more alpha-cells and more polyhormonal ce
142 RNA sequencing of islets from persufflated pancreata identified reduced inflammatory and greater me
143 elded significantly more islets than control pancreata (IEQ/g: 2134+/-297 vs. 1477+/-145 IEQ/g or 65,
147 e disposition and outcomes of deceased donor pancreata in the United States between January 1, 2000 a
149 , insulin-producing cell lines, and perfused pancreata indicated xenin-25 does not enhance GIP-mediat
150 ed with NKX6-1 and PTF1A in human developing pancreata, indicating that it marks the multipotent panc
151 ic ghrelin-producing cells are maintained in pancreata lacking the essential endocrine lineage regula
152 ficiency in both the PKC78(f/+) and c78(f/+) pancreata leads to reduction of epidermal growth factor
153 proach are an inadequate supply of cadaveric pancreata, lifelong immunosuppression, and chronic graft
155 dichotomy raises the hypothesis that K8-null pancreata may undergo compensatory cytoprotective gene e
156 measured via immunohistochemical analysis of pancreata measuring loss of acini, fibrosis, inflammatio
158 ived cells were observed in the nonendocrine pancreata, no pancreatic beta-cells were identified that
162 we observed no abnormal pathology within the pancreata of 23 Pdx1-Cre;Smad4(lox/lox) animals that wer
166 f the CCR2-ligand (CCL2) was observed in the pancreata of cadaveric donors, suggesting that beta-cell
168 y qRT-PCR using RNA derived from spleens and pancreata of cured mice validated the suppression of mos
170 greater accumulation of PGC-GdDTPA-F in the pancreata of diabetic animals compared with controls.
173 rx(+) cells was significantly reduced in the pancreata of embryos deficient for the Islet-1 (Isl-1) t
177 i, we electroporated oncogenic plasmids into pancreata of LSL-KrasG12D x p53fl/fl mice; mutant Kras w
181 verse relaxation time (T2) shortening in the pancreata of mice injected with the MN-Ex10-Cy5.5 probe
182 n of an activated form of KRAS (KrasG12D) in pancreata of mice is sufficient to induce formation of p
184 plex II(+)CD11c(+) DCs increased 100-fold in pancreata of mice with acute pancreatitis to account for
187 contrast-induced activation of NF-kappaB in pancreata of mice, this was observed by live imaging of
190 imulated insulin secretion from the perfused pancreata of MKR mice and reduced the beta-cell mass.
192 leakage, as an indicator of inflammation, in pancreata of mouse models of type 1 diabetes ex vivo or
193 educed immune infiltration and activation in pancreata of NOD mice as well as humanized NOD Scid IL2
196 4 and IL-10 were significantly higher in the pancreata of OGG-1(-/-) mice as compared with the levels
203 e mainly found in pancreatic lymph nodes and pancreata of recipients, indicating that the transferred
205 entage of polyhormonal cells in the neonatal pancreata of Snord116p-/m+ mice, due primarily to an inc
207 ed PDX1 rescues the Pdx1-null phenotype; the pancreata of these mice develop and function normally.
209 c periductal lymphocytic infiltration in the pancreata of transgenic mice, predominantly CD4+ T lymph
210 as IFN-gamma production was increased in the pancreata of treated animals, insulin expression was str
212 c patients directly, we isolated islets from pancreata of type 2 diabetic cadaveric donors (n = 14) a
213 esions and more foci of invasive cancer than pancreata of unexposed mice (controls); radiation reduce
215 ransgenic mice compared with normal, control pancreata of WT mice (mean intensity, 0.25 lau +/- 0.25)
216 - and beta-cell subsets from fetal and adult pancreata offers clear implications for strategies that
217 ed at any of the 15 CpG islands in 15 normal pancreata or in an immortalized normal pancreatic duct e
218 number of islets of Langerhans (two to four pancreata per recipient) into patients with type I diabe
221 lls detected in heterozygous and hypomorphic pancreata, possibly those that express low levels of Neu
225 All pancreatic islets were isolated from pancreata procured in Houston and subsequently transport
227 btypes, and beta-cell and alpha-cell mass in pancreata recovered from organ donors with type 1 diabet
229 cent analyses of transgenic rodent and human pancreata reveal a number of novel heterogeneity markers
230 Histologic analyses of RARdn-expressing pancreata revealed a decrease in beta-cell mass and insu
232 peri-islet cell accumulations in RIPLT alpha pancreata: separation into T and B cell areas was more d
235 observations, immunohistological analysis of pancreata showed that CD105(+) cells are restricted to t
237 techniques for isolating islets require that pancreata stored with University of Wisconsin solution (
238 negative constructs and isolated human fetal pancreata suggest that c-Src is at least partially respo
239 /progenitor cells, prepared from human adult pancreata survive engraftment and produce tissue chimeri
243 y distinct from normal ducts; even in normal pancreata they display PanIN and metaplastic features, s
244 t isolation and reduce the need for multiple pancreata to achieve insulin independence in the recipie
245 ith placental defects, so we explanted E12.5 pancreata to allow endocrine differentiation to occur in
246 or influencing islet function is exposure of pancreata to cold ischemia during unavoidable windows of
247 ison with UW organ preservation, exposure of pancreata to the TLM result in greater islet yields and
249 ignaling was inhibited in cultured embryonic pancreata using morpholine-ring antisense against GIP li
252 al recovered islet mass from type 2 diabetic pancreata was significantly less than that from nondiabe
253 tablish the functional role of PERK in adult pancreata, we generated mice harboring a conditional PER
254 s of thousands of cells in human organ donor pancreata, we show that quantitative graph characteristi
259 Morphological defects in Gata4/Gata6 mutant pancreata were apparent during embryonic development, an
270 or resveratrol (HFS+Resv) for 24 months, and pancreata were examined before overt dysglycemia occurre
279 composed of rat-derived cells, the resulting pancreata were of mouse size, rendering them insufficien
281 tween January 16, 2002 and June 30, 2003, 39 pancreata were procured and processed for PIT at a dista
286 ntly prepared from these mouse-rat chimaeric pancreata were transplanted into mice with streptozotoci
291 insulin-positive cells found in Nkx6.1(-/-) pancreata, which lack the majority of second-phase beta
292 This damage may be prevented by treating pancreata with a p38MAPK inhibitor (p38IH) before cold p
293 raft loss was significantly more frequent in pancreata with arterial damage (p = 0.04) and in those w
294 underwent single-pass perfusion of isolated pancreata with low and high glucose concentration (n = 4
296 t NKG2D and its ligands are present in human pancreata, with expression of NKG2D and its ligands incr
297 -16 mice developed dedifferentiated exocrine pancreata within 2 months of age and became malnourished