ライフサイエンスコーパス: pancreatic injury

1 stic ductal lesions by oncogenic Kras and/or pancreatic injury.

2 alcium signaling very early in the course of pancreatic injury.

3 e course, and downstream consequences during pancreatic injury.

4 ss to intra-acinar trypsinogen activation in pancreatic injury.

5 ogen activation and inflammatory pathways in pancreatic injury.

6 tatus of duct cells as important entities in pancreatic injury.

7 iate downstream cellular events resulting in pancreatic injury.

8 reduced only transiently (49-77 days) after pancreatic injury.

9 pancreatitis, whereas other drugs may reduce pancreatic injury.

10 ociated with predisposition to liver but not pancreatic injury.

11 oth of which were in control animals without pancreatic injury.

12 ich link ethanol abuse to the development of pancreatic injury.

13 enhance pancreatic recovery and disorders of pancreatic injury.

14 mesenteric injuries, and two (29%) of seven pancreatic injuries.

15 hts into the documented link between chronic pancreatic injury and an increased risk for pancreatic c

16 ignificantly correlated with severity of the pancreatic injury and animal survival; reg I/PSP levels

17 cells are recruited to the site of moderate pancreatic injury and contribute to beta-cell regenerati

18 enerative disorders and cancers is marred by pancreatic injury and diabetic syndrome observed in PERK

19 Reg III/PAP levels are a sensitive marker of pancreatic injury and early in the disease may be a usef

20 tivation of trypsinogen activation can cause pancreatic injury and has been associated with chronic p

21 2 is up-regulated following cerulein-induced pancreatic injury and is required for tissue repair by p

22 is necessary for the maximal propagation of pancreatic injury and its associated inflammation.

23 Acute pancreatitis begins as acute pancreatic injury and may generate a systemic inflammato

24 cal role in the regulation of progression of pancreatic injury and mediation of pancreatitis-associat

25 nowledge, that VPA shifts the balance toward pancreatic injury and pancreatitis through HDAC inhibiti

26 tibodies against ICAM-1 decreased both local pancreatic injury and systemic lung injury compared with

27 on accelerated PanIN formation and increased pancreatic injury and the number of high-grade lesions a

28 njury and dysfunction), lipase (indicator of pancreatic injury), and creatine kinase (an indicator of

29 hepatocellular injury), lipase (indicator of pancreatic injury), and creatine kinase (indicator of ne

30 te renal dysfunction, hepatocellular injury, pancreatic injury, and increased plasma concentrations o

31 contributes to the initiation of CCK-induced pancreatic injury, and that blockade of this secretory p

32 eview will first discuss factors influencing pancreatic injury, and then conclude with studies detail

33 we investigated SP-D functions in the acute pancreatic injury (API) with C57BL/6 Wild-type (WT) and

34 the mechanisms leading to alcohol-associated pancreatic injury are unclear.

35 e pancreas and their potential modulation of pancreatic injury are unknown.

36 ghlight molecular and cellular mechanisms of pancreatic injury arising from acute and chronic pancrea

37 However, the mice did not have evidence of pancreatic injury at baseline, other than an elevated se

38 plays an important role in the regulation of pancreatic injury but not pancreatic edema or increased

39 acinar trypsinogen activation leads to early pancreatic injury, but the inflammatory response of acut

40 In the adult pancreas, pancreatic injury by partial duct ligation (PDL) has bee

41 In mice with pancreatitis or pancreatic injury, elimination of Numb causes dedifferen

42 y was analyzed to determine the frequency of pancreatic injuries, identify factors associated with da

43 d that a low dose Cae (5 ug/kg) could induce pancreatic injury in HTG mice while there was no obvious

44 ctivation, necrosis, and other parameters of pancreatic injury in mice with L-arginine AP.

45 y, while L-arginine induced extremely severe pancreatic injury including necrosis and neutrophil infi

46 ted by bile acid exposure, bile acid-induced pancreatic injury is dependent on calcineurin activation

47 Individual laboratory indexes (markers of pancreatic injury, markers of inflammatory response), wh

48 ry pancreatitis and indicate that persistent pancreatic injury might be causally linked to chronic pa

49 We also extended our studies to pancreatic injury models (partial pancreatectomy and str

50 models of pancreatitis, but it did not alter pancreatic injury/necrosis in either model.

51 Parenchymal pancreatic injuries not involving the ductal system rare

52 inar-to-ductal metaplasia (ADM) results from pancreatic injury or KRAS activation, and is an early st

53 This report summarizes this pancreatic injury, the role of cytokines in the pathogen

54 ally activated in CP and is induced early in pancreatic injury through pathologic calcium signaling i

55 causes multiple-organ dysfunction including pancreatic injury, thus resulting in high mortality.

56 Es in plasma and pancreas were measured, and pancreatic injury was assessed during a 48-hour period f

57 de TAP were measured in lymph and blood, and pancreatic injury was determined.

58 All mice developed severe AP, and pancreatic injury was equally severe in both treated and

59 In an experimental model of pancreatic injury, we found that VPA delayed recovery of

60 Rather, PDL stimulates massive pancreatic injury, which alters pancreatic composition a

61 sed pancreatic SP-D levels and caused severe pancreatic injury with higher serum amylase 24 h after C

62 P levels in both lymph and blood and reduced pancreatic injury, with no significant differences betwe