ライフサイエンスコーパス: acute pancreatitis

1 s a novel target of CVB3 during CVB3-induced acute pancreatitis.

2 mplicate in the pathogenesis of CVB3-induced acute pancreatitis.

3 and urine has been used in the diagnosis of acute pancreatitis.

4 ge-associated susceptibility of CVB3-induced acute pancreatitis.

5 predict the development of organ failure in acute pancreatitis.

6 icting the development of the severe form of acute pancreatitis.

7 live bacteria is alone sufficient to induce acute pancreatitis.

8 ecretion coupling and the pathophysiology of acute pancreatitis.

9 ctivin may be a therapeutic target in severe acute pancreatitis.

10 inflammation and plays an important role in acute pancreatitis.

11 been emphatically reinforced in the onset of acute pancreatitis.

12 betes was admitted with epigastric pain from acute pancreatitis.

13 to the emergency department in patients with acute pancreatitis.

14 and fatty acids, which is a major trigger of acute pancreatitis.

15 We examined the direct effects of ethanol on acute pancreatitis.

16 are needed to better predict the severity of acute pancreatitis.

17 during the early onset of mild, subclinical, acute pancreatitis.

18 in in vivo models of acute liver injury and acute pancreatitis.

19 nar cells to generate pancreatic fibrosis in acute pancreatitis.

20 The major reason for enrollment was acute pancreatitis.

21 ivation, an initiating step in the course of acute pancreatitis.

22 nificant among cases of both severe and mild acute pancreatitis.

23 measured in plasma from human patients with acute pancreatitis.

24 pancreatitis, even if there is no history of acute pancreatitis.

25 ate a paradigm shift in our understanding of acute pancreatitis.

26 alyzed factors associated with recurrence of acute pancreatitis.

27 cy in predicting persistent organ failure in acute pancreatitis.

28 h SOM for patients with idiopathic recurrent acute pancreatitis.

29 ciate with increased hospital admissions for acute pancreatitis.

30 ifying patients at higher risk for recurrent acute pancreatitis.

31 are currently active in clinical research on acute pancreatitis.

32 similar effects in preventing recurrence of acute pancreatitis.

33 vestigated the roles of DC in development of acute pancreatitis.

34 and NLRP3 were required for inflammation in acute pancreatitis.

35 uired for the development of inflammation in acute pancreatitis.

36 ative contributions of these pathways during acute pancreatitis.

37 vide a new therapeutic strategy for treating acute pancreatitis.

38 ivation, has previously been shown to induce acute pancreatitis.

39 beneficial in the prevention or treatment of acute pancreatitis.

40 g time, was shown to be sufficient to induce acute pancreatitis.

41 n in taurolithocholic acid 3-sulfate-induced acute pancreatitis.

42 iews recent advances in our understanding of acute pancreatitis.

43 on by blocking acinar regeneration following acute pancreatitis.

44 and behavioral outcomes in a mouse model of acute pancreatitis.

45 c acinar development, is activated following acute pancreatitis.

46 rence between sexes for pancreatic cancer or acute pancreatitis.

47 in PSCs and this may be helpful in treating acute pancreatitis.

48 lar mechanism of CB2R-mediated protection in acute pancreatitis.

49 both early and late proinflammatory genes in acute pancreatitis.

50 e lineage-specific regeneration after severe acute pancreatitis.

51 ential risk of severe complications, such as acute pancreatitis.

52 acinar cell pathogenesis in animal models of acute pancreatitis.

53 deficiency on cerulein- and arginine-induced acute pancreatitis.

54 gainst PAC necrosis evoked by agents causing acute pancreatitis.

55 atic PTP1B in cerulein- and arginine-induced acute pancreatitis.

56 regeneration after the induction of a severe acute pancreatitis.

57 [84%]) reported prior recurrent episodes of acute pancreatitis.

58 ischemia with the possibility of developing acute pancreatitis.

59 plays a critical role in the development of acute pancreatitis.

60 se A2 and play a role in the pathogenesis of acute pancreatitis.

61 with decreased risk of non-gallstone-related acute pancreatitis.

62 ctal cells and pancreatic regeneration after acute pancreatitis.

63 parately, with risk of non-gallstone-related acute pancreatitis.

64 al inhibition may be of therapeutic value in acute pancreatitis.

65 pancreatitis were similar in the two groups (acute pancreatitis, 0.3% in the saxagliptin group and 0.

66 BES and 47.2% who received DES had recurrent acute pancreatitis (95% confidence interval, -22.3 to 24

67 who received the sham surgery had recurrent acute pancreatitis (95% confidence interval, -49.5 to 17

68 sis in two dissimilar experimental models of acute pancreatitis (a secretagogue-induced model and a m

69 miR-21 is overexpressed in a murine model of acute pancreatitis, a pathologic condition involving RIP

70 pancreatitis is the most common etiology of acute pancreatitis, accounting for 30-60% of cases.

71 During acute pancreatitis, adipose tissue release FA-Cl, which

72 85), and mild acute pancreatitis; adjusted OR 0 .

73 e have been implicated in the progression of acute pancreatitis, although their precise role remains

74 or gallstone aetiology but not for alcoholic acute pancreatitis, although these increases in mortalit

75 Acute pancreatitis, an inflammatory disorder of the panc

76 The study included 221 patients treated for acute pancreatitis and 345 healthy subjects as a control

77 Among 6,161 cases of acute pancreatitis and 61,637 controls, current use of a

78 given after injury, reduced the severity of acute pancreatitis and acute liver injury.

79 Acute pancreatitis and chronic pancreatitis are complex

80 e cells are important in the pathogenesis of acute pancreatitis and determine disease severity.

81 Endoprotease activation is a key step in acute pancreatitis and early inhibition of these enzymes

82 y, causing all treated animals to succumb to acute pancreatitis and hyperglycemic coma.

83 consecutive adults with abdominal surgery or acute pancreatitis and ICU stay 72 hours or longer were

84 presents with upper abdominal pain, signs of acute pancreatitis and massive gastrointestinal bleeding

85 acinar-ductal metaplasia (ADM) occurs during acute pancreatitis and might be viewed as a prelude to p

86 quired for pancreatic viability in mice with acute pancreatitis and might protect organs against cell

87 he experienced a 10-day hospitalization for acute pancreatitis and neutropenia.

88 rs had limited impact on mortality following acute pancreatitis and no significant impact when adjust

89 ive complications, one case of postoperative acute pancreatitis and one case of postoperative bleedin

90 ith autoimmune inflammatory diseases such as acute pancreatitis and Sjogren syndrome.

91 be developed for treatment of patients with acute pancreatitis and Sjogren syndrome.

92 al secretion in protecting the pancreas from acute pancreatitis and strongly suggest that improved du

93 However, the role of POSTN in acute pancreatitis and subsequent regeneration processes

94 ic sphincterotomy in patients with recurrent acute pancreatitis and the prognostic significance of pa

95 : Smoking increases the risk of nongallstone acute pancreatitis and the progression of acute pancreat

96 quency of genetic mutations in patients with acute pancreatitis and to investigate their relationship

97 % CI 0.85-1.58) per 100 000 person-years for acute pancreatitis, and 9.62 cases (95% CI 7.86-11.78) p

98 al trials, included adults hospitalized with acute pancreatitis, and compared early versus delayed fe

99 Gallstones are the most common cause of acute pancreatitis, and early cholecystectomy eliminates

100 nts lung and kidney damage in a rat model of acute pancreatitis, and is progressing into preclinical

101 the incidences of both pancreatic cancer and acute pancreatitis, and mortality from pancreatic cancer

102 hosis, hepatocellular carcinoma, gallstones, acute pancreatitis, and pancreatic cancer.

103 rs might be associated with a lesser risk of acute pancreatitis, and that the protective association

104 , the role of trypsin in acute and recurrent acute pancreatitis, and the discovery of a pancreatitis

105 Early detection of infection in acute pancreatitis (AP) affects the choice of treatment

106 Acute pancreatitis (AP) and chronic pancreatitis (CP) sh

107 Acute pancreatitis (AP) and chronic pancreatitis (CP) tr

108 Although ethanol causes acute pancreatitis (AP) and lipolytic fatty acid (FA) ge

109 e trypsinogen activation and inflammation in acute pancreatitis (AP) are unclear.

110 In acute pancreatitis (AP) bacterial translocation is consi

111 was induced in mice by repeated episodes of acute pancreatitis (AP) based on caerulein hyperstimulat

112 ype of immune response during development of acute pancreatitis (AP) determines disease severity.

113 ensin system (RAS) and vitamin D system with acute pancreatitis (AP) development and severity.

114 rypsinogen activation in the pathogenesis of acute pancreatitis (AP) has not been clearly established

115 Acute pancreatitis (AP) is a common acute abdominal dise

116 Acute pancreatitis (AP) is a common and devastating gast

117 Acute pancreatitis (AP) is a common and devastating infl

118 Acute pancreatitis (AP) is a painful inflammatory disord

119 Acute pancreatitis (AP) is an inflammatory disease in wh

120 Acute pancreatitis (AP) is an inflammatory disease, and

121 racterising the effects of caerulein-induced acute pancreatitis (AP) on the vagal neurocircuitry modu

122 Experimental studies in acute pancreatitis (AP) suggest a strong association of

123 In acute pancreatitis (AP) tumor necrosis factor-alpha medi

124 Acute pancreatitis (AP) was induced in C57BL/6 (control)

125 es mitochondrial dysfunction and necrosis in acute pancreatitis (AP), a condition without specific dr

126 utrophils are involved in the development of acute pancreatitis (AP), but it is not clear how neutrop

127 fine a therapeutic program for mild-moderate acute pancreatitis (AP), often recurrent, which at the e

128 Unlike acute pancreatitis (AP), we find that alternatively acti

129 exclusion of common etiological reasons for acute pancreatitis (AP), whereafter the patients were ra

130 a novel role for KMO in the pathogenesis of acute pancreatitis (AP).

131 erapeutic role for CO and CO-primed cells in acute pancreatitis (AP).

132 Obese patients have worse outcomes during acute pancreatitis (AP).

133 current evidence about fluid therapy (FT) in acute pancreatitis (AP).

134 kappaB1p50 and RelA) is activated rapidly in acute pancreatitis (AP).

135 cidence together with the clinical course of acute pancreatitis (AP).

136 signaling pathways that initiate and promote acute pancreatitis (AP).

137 in prediction of the severity and outcome of acute pancreatitis (AP).

138 ple organ dysfunction (MODS) in experimental acute pancreatitis (AP).

139 tory response, local injury, and outcomes of acute pancreatitis (AP).

140 The cellular mediators of acute pancreatitis are incompletely understood.

141 Epidemiologic data on the role of diet in acute pancreatitis are sparse.

142 multifactorial, whereas recurrent attacks of acute pancreatitis are thought to precede the developmen

143 enes in initiation and development of severe acute pancreatitis as a model of acute inflammation.

144 sociation with risk of non-gallstone-related acute pancreatitis as that observed for total fish consu

145 Here, we used a mouse model of acute pancreatitis-associated (AP-associated) ALI to det

146 rate of infection or death in patients with acute pancreatitis at high risk for complications.

147 Later, he was found to have acute pancreatitis, biliary obstruction, gastric outlet

148 chronic alcohol consumers develop recurrent acute pancreatitis but very heavy drinking associates wi

149 may play a role in the autodigestive disease acute pancreatitis, but little is known about its pancre

150 risk are those with septic shock and severe acute pancreatitis, but the adverse effects of IAH may a

151 d with a TLR9 antagonist before induction of acute pancreatitis by caerulein or retrograde bile duct

152 We induced acute pancreatitis by repeated caerulein injections and

153 To estimate relative risk of acute pancreatitis, by degree of severity, among users o

154 Alcohol-related acute pancreatitis can be mediated by a combination of a

155 Recurrent acute pancreatitis can progress to chronic pancreatitis,

156 Our ability to predict the severity of acute pancreatitis cannot be expected to improve unless

157 s are involved in important diseases such as acute pancreatitis, chronic inflammatory lung diseases,

158 of the worldwide incidence and mortality of acute pancreatitis, chronic pancreatitis, pancreatic cys

159 blockers was followed by a decreased risk of acute pancreatitis, compared to non-users, adjusted OR 0

160 uid status during the early course of severe acute pancreatitis, compared with a treatment strategy o

161 As rates of hospitalization for acute pancreatitis continue to increase, so does demand

162 The recurrence of unexplained acute pancreatitis could be treated with empirical chole

163 view approaches to best manage patients with acute pancreatitis, covering diagnosis, risk and prognos

164 REPORT: A 44-year-old man with a history of acute pancreatitis developed a pseudoaneurysm of the pan

165 tic injury, but the inflammatory response of acute pancreatitis develops independently, driven by ear

166 were highly susceptible to cerulein-induced acute pancreatitis, displaying an enhanced level of dama

167 suggest that early feeding in patients with acute pancreatitis does not seem to increase adverse eve

168 and glucagon, and adults slowly recover from acute pancreatitis due to a 2-fold impairment in Sox9 up

169 rtality for patients admitted with alcoholic acute pancreatitis during August to October, in August 2

170 The odds of recurrent acute pancreatitis during follow-up evaluation were sign

171 e primary outcome was incidence of recurrent acute pancreatitis during the follow-up period (minimum,

172 were diagnosed with at least one episode of acute pancreatitis during therapy.

173 We suggest that multiple, subclinical, acute pancreatitis episodes can accumulate in fibrosis d

174 p.N34S in SPINK1 may predispose patients to acute pancreatitis, especially in those abusing alcohol,

175 logical prevention or specific treatment for acute pancreatitis exists.

176 nd CB(-/-) mice by twice-weekly induction of acute pancreatitis for 10 weeks; acute pancreatitis was

177 tivation, observed within acini early during acute pancreatitis for a long time, was shown to be suff

178 potentially fatal disease of the pancreas is acute pancreatitis, for which there is no treatment.

179 mice given injections of cerulein, to induce acute pancreatitis, had higher levels of NF-kappaB activ

180 sponses during the early stages of alcoholic acute pancreatitis has not been evaluated.

181 ults from cytokine-based clinical trials for acute pancreatitis have been disappointing, so strategie

182 icle, recent advances in the pathogenesis of acute pancreatitis have been reviewed.

183 ported with AMG145 (coronary artery disease, acute pancreatitis, hip fracture, syncope).

184 The morbidity rate of hypertriglyceridemic acute pancreatitis (HTG-AP) increased rapidly over the l

185 can prevent recurrent attacks of idiopathic acute pancreatitis (IAP).

186 Biliary pancreatitis is the leading cause of acute pancreatitis in both children and adults.

187 ies pertinent to classifying the severity of acute pancreatitis in clinical practice and research.

188 erent clinical presentation in patients with acute pancreatitis in ICU, with better discriminatory po

189 ption of the Golgi ribbon and development of acute pancreatitis in mice.

190 B activation correlates with the severity of acute pancreatitis in mice.

191 cts against caerulein- or L-arginine-induced acute pancreatitis in mice.

192 d ductal function, increased the severity of acute pancreatitis in the two mouse models tested.

193 shown to occur in the auto-digestive disease acute pancreatitis in vivo, consistently elicited substa

194 ty and primary care data for 10 589 cases of acute pancreatitis in Wales, UK (population 3.0 million)

195 One patient (0.7%) developed acute pancreatitis (in the basal-bolus group).

196 As incidence (and admission rates) of acute pancreatitis increase, so does the demand for effe

197 Injection of ethanol + POA produced acute pancreatitis indicated by significant increases in

198 The severity of acute pancreatitis induced by combination of ethanol and

199 severity in two established murine models of acute pancreatitis induced by either cerulein or IL-12 +

200 suscitation was started 2 hours after severe acute pancreatitis induction and continued for 6 hours a

201 stroke volume index assessed prior to severe acute pancreatitis induction as therapeutic hemodynamic

202 vasodilation before and 6 hours after severe acute pancreatitis induction, revealed less impairment i

203 refore, we investigate the role of miR-21 in acute pancreatitis injury and necroptosis.

204 l course and severity of disease, (b) divide acute pancreatitis into interstitial edematous pancreati

205 Acute pancreatitis is a complex disorder involving both

206 Acute pancreatitis is a human disease in which the pancr

207 Acute pancreatitis is a painful, life-threatening disord

208 Acute pancreatitis is a potentially lethal disease, with

209 Acute pancreatitis is a serious and sometimes fatal infl

210 Acute pancreatitis is a serious and sometimes fatal infl

211 Acute Pancreatitis is a substantial health care challeng

212 Although the susceptibility of CVB3-induced acute pancreatitis is age-dependent, the underlying mech

213 nd need for new markers in stratification of acute pancreatitis is also uncertain.

214 Acute pancreatitis is among the most common and costly r

215 ratory distress syndrome (ARDS) secondary to acute pancreatitis is associated with a poor prognosis.

216 Acute pancreatitis is associated with alcohol abuse, gal

217 Acute pancreatitis is characterized by early activation

218 Knowledge of the molecular mechanisms of acute pancreatitis is largely based on studies using rod

219 Acute pancreatitis is one of the common causes of aspara

220 Acute pancreatitis is one of the most frequent gastroint

221 uch scientific scrutiny, the pathogenesis of acute pancreatitis is still not well understood.

222 Acute pancreatitis is the leading cause of hospitalizati

223 Acute pancreatitis is the most common complication of di

224 Acute pancreatitis is the most common major complication

225 Globally, acute pancreatitis is the most common pancreatic disease

226 Also, the connection with severity of acute pancreatitis is unknown.

227 n and pain-associated behavior in a model of acute pancreatitis - known to also rely on TRPV4 and TRP

228 Patients with recurrent acute pancreatitis likely have chronic pancreatitis, do

229 e is known about whether mortality following acute pancreatitis may be influenced by the following fi

230 udy was to establish how mortality following acute pancreatitis may be influenced by these five facto

231 tween the detected mutations and severity of acute pancreatitis: mild acute pancreatitis, mutation of

232 r for gallstone aetiology, but for alcoholic acute pancreatitis, mortality was increased significantl

233 ently it has been identified as a target for acute pancreatitis multiple organ dysfunction syndrome (

234 (2.8%) and CTRC in 2 (1.4%) patients; severe acute pancreatitis, mutation of CFTR and CTRC in 1 (2.6%

235 ons and severity of acute pancreatitis: mild acute pancreatitis, mutation of CFTR in 4 (2.8%) and CTR

236 One hundred sixty-one patients with acute pancreatitis, of which 107 were subclassified acco

237 Patients with nongallstone-related acute pancreatitis or chronic pancreatitis of any cause

238 blood levels of MIR122 and EPO in mice with acute pancreatitis or steatohepatitis, and also in patie

239 t decreased risk associated with both severe acute pancreatitis, (OR 0 .

240 des more reliable information for predicting acute pancreatitis outcomes than do the current scoring

241 tals when compared with small hospitals, for acute pancreatitis overall and for gallstone aetiology b

242 , in August 2004, and in large hospitals for acute pancreatitis overall and for gallstone aetiology,

243 nt variation according to calendar month for acute pancreatitis overall or for gallstone aetiology, b

244 ficant between-group differences in rates of acute pancreatitis (P=0.07) or pancreatic cancer (P=0.32

245 cute coronary syndrome, and the incidence of acute pancreatitis, pancreatic cancer, medullary thyroid

246 idate as a clinical marker to identify those acute pancreatitis patients with severe disease who woul

247 secreted inflammatory mediators elevated in acute pancreatitis patients, including IL-6, tumor necro

248 We review how to manage patients with acute pancreatitis, paying attention to diagnosis, diffe

249 Acute pancreatitis, recurrent acute pancreatitis (RAP) and chronic pancreatitis are in

250 The role of genetics in acute pancreatitis, RAP and progression to chronic pancr

251 ics and the dual role of oxidative stress in acute pancreatitis, recognition of endoplasmic reticulum

252 Acute pancreatitis, recurrent acute pancreatitis (RAP) a

253 gement of patients with idiopathic recurrent acute pancreatitis requires clarification.

254 Induced acute pancreatitis results in a substantial release not

255 fat necrosis has been associated with severe acute pancreatitis (SAP) for over 100 years; however, it

256 Initial management of severe acute pancreatitis (SAP) is conservative.

257 , ALI is also a major complication in severe acute pancreatitis (SAP).

258 l volume and outcome in patients with severe acute pancreatitis (SAP).

259 otein (a), and its role in the management of acute pancreatitis secondary to severe hypertriglycerida

260 stroke volume index assessed prior to severe acute pancreatitis served as primary hemodynamic goal.

261 The Atlanta definitions of acute pancreatitis severity are ingrained in the lexicon

262 ent of a new international classification of acute pancreatitis severity was sent to all surgeons, ga

263 In severe acute pancreatitis, the administration of fluids in the

264 tal luminal lactate predicts the severity of acute pancreatitis, the length of hospital stay, the nee

265 Within the first 6 hours of severe acute pancreatitis, the study group received a total of

266 red a distinct immune phenotype in mice with acute pancreatitis; they expressed higher levels of majo

267 ort studies (35 on pancreatic cancer, ten on acute pancreatitis, three on chronic pancreatitis, and n

268 increased 100-fold in pancreata of mice with acute pancreatitis to account for nearly 15% of intrapan

269 ne acute pancreatitis and the progression of acute pancreatitis to chronic pancreatitis.

270 g tube is often used in patients with severe acute pancreatitis to prevent gut-derived infections, bu

271 ecutive patients admitted to hospital due to acute pancreatitis to test the hypothesis that a single

272 has modified the Atlanta classification for acute pancreatitis to update the terminology and provide

273 atient with DKA-induced hypertriglyceridemic acute pancreatitis treated successfully with plasmaphare

274 pecific role of the duct in the induction of acute pancreatitis using well-established disease models

275 cted in 6.3%, 2.3% and 1.8% of patients with acute pancreatitis versus 3.2%, 3.8% and 1.2% of volunte

276 t autophagy might play a deleterious role in acute pancreatitis via intra-acinar activation of digest

277 ore conclude that bradykinin plays a role in acute pancreatitis via specific actions on PSCs.

278 The optimal threshold for predicting severe acute pancreatitis was 100 mL.

279 Acute pancreatitis was induced by administration of lipo

280 Acute pancreatitis was induced by caerulein stimulation

281 nduction of acute pancreatitis for 10 weeks; acute pancreatitis was induced by hourly intraperitoneal

282 Acute pancreatitis was induced by injection of cerulein

283 Acute pancreatitis was induced in Bmi1(-/-) mice with ce

284 Acute pancreatitis was induced in CD11c.DTR mice using c

285 Acute pancreatitis was induced in rats by intraductal in

286 Acute pancreatitis was the most common reason for hospit

287 hort of unselected consecutive patients with acute pancreatitis we observed a tendency of increased r

288 To test the role of ER homeostasis in acute pancreatitis, we manipulated GRP78 levels, a major

289 Furthermore, in a model of acute pancreatitis, we observed substantive luminal acid

290 and cases of incident non-gallstone-related acute pancreatitis were identified by linkage to the Swe

291 First-time cases with acute pancreatitis were identified in the National Patie

292 in women) of incident non-gallstone-related acute pancreatitis were identified.

293 mage but not in the inflammatory response of acute pancreatitis, which was shown to be induced by NFk

294 S: It is important to identify patients with acute pancreatitis who are at risk for developing persis

295 We enrolled patients with acute pancreatitis who were at high risk for complicatio

296 t retrospective study included patients with acute pancreatitis who were examined with computed tomog

297 (ARP) is defined as more than two attacks of acute pancreatitis with complete or almost complete reso

298 To replicate human acute pancreatitis with hamsters, we comparatively studi

299 ly life-threatening vascular complication of acute pancreatitis, with a mortality rate of 20-43% in u

300 r cells are an early and critical feature in acute pancreatitis, yet it is unclear how these signals