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1  injury and improved survival independent of pancreatic injury.
2 enhance pancreatic recovery and disorders of pancreatic injury.
3 stic ductal lesions by oncogenic Kras and/or pancreatic injury.
4 alcium signaling very early in the course of pancreatic injury.
5 e course, and downstream consequences during pancreatic injury.
6 ss to intra-acinar trypsinogen activation in pancreatic injury.
7 gically activated trypsin protecting against pancreatic injury.
8 ogen activation and inflammatory pathways in pancreatic injury.
9 tatus of duct cells as important entities in pancreatic injury.
10 iate downstream cellular events resulting in pancreatic injury.
11 es in our understanding of the mechanisms of pancreatic injury.
12  reduced only transiently (49-77 days) after pancreatic injury.
13 pancreatitis, whereas other drugs may reduce pancreatic injury.
14 ociated with predisposition to liver but not pancreatic injury.
15 oth of which were in control animals without pancreatic injury.
16 ich link ethanol abuse to the development of pancreatic injury.
17  a new model for studying alcohol-associated pancreatic injury.
18 ar-to-ductal metaplasia (ADM) in response to pancreatic injury.
19 neutrophils which harness NETs and alleviate pancreatic injury.
20  mesenteric injuries, and two (29%) of seven pancreatic injuries.
21 nitor kinase 1 (HPK1) was upregulated during pancreatic injury and ADM.
22 hts into the documented link between chronic pancreatic injury and an increased risk for pancreatic c
23 ignificantly correlated with severity of the pancreatic injury and animal survival; reg I/PSP levels
24  cells are recruited to the site of moderate pancreatic injury and contribute to beta-cell regenerati
25 enerative disorders and cancers is marred by pancreatic injury and diabetic syndrome observed in PERK
26 ate beta-cell replication in mouse models of pancreatic injury and disease.
27 Reg III/PAP levels are a sensitive marker of pancreatic injury and early in the disease may be a usef
28 tivation of trypsinogen activation can cause pancreatic injury and has been associated with chronic p
29 creases glucagon levels, thereby alleviating pancreatic injury and insulin resistance.
30 2 is up-regulated following cerulein-induced pancreatic injury and is required for tissue repair by p
31  is necessary for the maximal propagation of pancreatic injury and its associated inflammation.
32           Acute pancreatitis begins as acute pancreatic injury and may generate a systemic inflammato
33 cal role in the regulation of progression of pancreatic injury and mediation of pancreatitis-associat
34 n domain receptor 1 in tissue homeostasis in pancreatic injury and pancreatic ductal adenocarcinoma p
35 nowledge, that VPA shifts the balance toward pancreatic injury and pancreatitis through HDAC inhibiti
36 ular traps (NETs) formation that exacerbates pancreatic injury and systemic inflammation.
37 tibodies against ICAM-1 decreased both local pancreatic injury and systemic lung injury compared with
38 on accelerated PanIN formation and increased pancreatic injury and the number of high-grade lesions a
39 njury and dysfunction), lipase (indicator of pancreatic injury), and creatine kinase (an indicator of
40 hepatocellular injury), lipase (indicator of pancreatic injury), and creatine kinase (indicator of ne
41 te renal dysfunction, hepatocellular injury, pancreatic injury, and increased plasma concentrations o
42  epigenetic state emerges within 48 hours of pancreatic injury, and involves an 'acinar-to-neoplasia'
43  calcineurin inhibitor-associated kidney and pancreatic injury, and retrospective studies of SGLT2i i
44 contributes to the initiation of CCK-induced pancreatic injury, and that blockade of this secretory p
45 eview will first discuss factors influencing pancreatic injury, and then conclude with studies detail
46  we investigated SP-D functions in the acute pancreatic injury (API) with C57BL/6 Wild-type (WT) and
47 the mechanisms leading to alcohol-associated pancreatic injury are unclear.
48 e pancreas and their potential modulation of pancreatic injury are unknown.
49 ghlight molecular and cellular mechanisms of pancreatic injury arising from acute and chronic pancrea
50   However, the mice did not have evidence of pancreatic injury at baseline, other than an elevated se
51 plays an important role in the regulation of pancreatic injury but not pancreatic edema or increased
52 acinar trypsinogen activation leads to early pancreatic injury, but the inflammatory response of acut
53                       In the adult pancreas, pancreatic injury by partial duct ligation (PDL) has bee
54                 In mice with pancreatitis or pancreatic injury, elimination of Numb causes dedifferen
55 y was analyzed to determine the frequency of pancreatic injuries, identify factors associated with da
56 lthough trypsin-mediated cell death leads to pancreatic injury in early stages of pancreatitis, multi
57 d that a low dose Cae (5 ug/kg) could induce pancreatic injury in HTG mice while there was no obvious
58  Gut microbiota dysbiosis is associated with pancreatic injury in HTGP and the mechanism remains uncl
59 on reduced the severity of caerulein-induced pancreatic injury in mice on a low-phosphate diet under
60 ctivation, necrosis, and other parameters of pancreatic injury in mice with L-arginine AP.
61 y, while L-arginine induced extremely severe pancreatic injury including necrosis and neutrophil infi
62               Further, IMT treatment reduced pancreatic injury, inflammation, extracellular matrix de
63 ted by bile acid exposure, bile acid-induced pancreatic injury is dependent on calcineurin activation
64    Individual laboratory indexes (markers of pancreatic injury, markers of inflammatory response), wh
65 ry pancreatitis and indicate that persistent pancreatic injury might be causally linked to chronic pa
66              We also extended our studies to pancreatic injury models (partial pancreatectomy and str
67 models of pancreatitis, but it did not alter pancreatic injury/necrosis in either model.
68                                  Parenchymal pancreatic injuries not involving the ductal system rare
69 inar-to-ductal metaplasia (ADM) results from pancreatic injury or KRAS activation, and is an early st
70 systemic inflammatory response and extensive pancreatic injury seen in acute pancreatitis.
71                  This report summarizes this pancreatic injury, the role of cytokines in the pathogen
72 ally activated in CP and is induced early in pancreatic injury through pathologic calcium signaling i
73  causes multiple-organ dysfunction including pancreatic injury, thus resulting in high mortality.
74 Es in plasma and pancreas were measured, and pancreatic injury was assessed during a 48-hour period f
75 de TAP were measured in lymph and blood, and pancreatic injury was determined.
76            All mice developed severe AP, and pancreatic injury was equally severe in both treated and
77                  In an experimental model of pancreatic injury, we found that VPA delayed recovery of
78               Rather, PDL stimulates massive pancreatic injury, which alters pancreatic composition a
79  that hypertriglyceridemic mice exhibit mild pancreatic injury with elevated intra-acinar nonendoplas
80 sed pancreatic SP-D levels and caused severe pancreatic injury with higher serum amylase 24 h after C
81 P levels in both lymph and blood and reduced pancreatic injury, with no significant differences betwe