ライフサイエンスコーパス: acute pancreatitis

1 r several pathological conditions, including acute pancreatitis.

2 rence between sexes for pancreatic cancer or acute pancreatitis.

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

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

5 both early and late proinflammatory genes in acute pancreatitis.

6 e lineage-specific regeneration after severe acute pancreatitis.

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

8 acinar cell pathogenesis in animal models of acute pancreatitis.

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

10 gainst PAC necrosis evoked by agents causing acute pancreatitis.

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

12 regeneration after the induction of a severe acute pancreatitis.

13 [84%]) reported prior recurrent episodes of acute pancreatitis.

14 m samples from patients with mild and severe acute pancreatitis.

15 ischemia with the possibility of developing acute pancreatitis.

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

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

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

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

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

21 which caused organ failure in the absence of acute pancreatitis.

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

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

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

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

26 cally occurs 3 to 5 weeks after the onset of acute pancreatitis.

27 predict the development of organ failure in acute pancreatitis.

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

29 live bacteria is alone sufficient to induce acute pancreatitis.

30 ecretion coupling and the pathophysiology of acute pancreatitis.

31 es, and in vivo efficacy in a mouse model of acute pancreatitis.

32 inflammation and plays an important role in acute pancreatitis.

33 been emphatically reinforced in the onset of acute pancreatitis.

34 betes was admitted with epigastric pain from acute pancreatitis.

35 to the emergency department in patients with acute pancreatitis.

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

37 ed 21 cases of hepatotoxicity and 3 cases of acute pancreatitis.

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

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

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

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

42 nar cells to generate pancreatic fibrosis in acute pancreatitis.

43 The major reason for enrollment was acute pancreatitis.

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

45 measured in plasma from human patients with acute pancreatitis.

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

47 vs 5 (0.1%) events of adjudication-confirmed acute pancreatitis.

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

49 alyzed factors associated with recurrence of acute pancreatitis.

50 s showed elevated diastase levels indicating acute pancreatitis.

51 hibit increased severity of cerulein-induced acute pancreatitis.

52 and miR-216b KOs following caerulein-induced acute pancreatitis.

53 onse and extensive pancreatic injury seen in acute pancreatitis.

54 mmatory responses of these cell types during acute pancreatitis.

55 the most important determinant of outcome in acute pancreatitis.

56 glimepiride group with adjudicated-confirmed acute pancreatitis.

57 on outcome, and therapy of organ failure in acute pancreatitis.

58 F carrier status who suffered from recurrent acute pancreatitis.

59 potently protective against cerulein-induced acute pancreatitis.

60 nt from a cohort of patients presenting with acute pancreatitis.

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

62 ctal cells and pancreatic regeneration after acute pancreatitis.

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

64 44/220), cholelithiasis (14.5%, 32/220) and acute pancreatitis (0.6%, 4/602), respectively.

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 Acute pancreatitis, a common cause of hospitalization in

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

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

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

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

72 In addition, the PAK patient developed acute pancreatitis after CAR-T therapy.

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 he pattern of visceral adipose injury during acute pancreatitis and acute diverticulitis to determine

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

80 lacebo group (0.87%); this patient developed acute pancreatitis and bacteremia after the procedure.

81 is seen in approximately 20% of all cases of acute pancreatitis and defines "severe acute pancreatiti

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

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

84 creases the severity of secretagogue-induced acute pancreatitis and has no effect on chronic pancreat

85 nses in ex vivo and in vivo rodent models of acute pancreatitis and human pancreatic acini.

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

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

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

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

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

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

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

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

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

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

96 ficantly between patients with initial-stage acute pancreatitis and those without imaging or laborato

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

98 % CI 0.85-1.58) per 100 000 person-years for acute pancreatitis, and 9.62 cases (95% CI 7.86-11.78) p

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

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

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

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

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

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

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 the different classifications of severity in acute pancreatitis (AP) and to investigate which charact

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

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

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

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

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

115 Acute pancreatitis (AP) is a painful inflammatory disord

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

117 Acute Pancreatitis (AP) is sudden onset pancreas inflamm

118 Acute pancreatitis (AP) of different etiologies is assoc

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

120 , autosomal-dominant disorder with recurrent acute pancreatitis (AP) progressing to chronic pancreati

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

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

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

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

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

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

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

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

129 fat or circulating triglycerides may worsen acute pancreatitis (AP)-associated local and systemic in

130 EH) reduces inflammatory diseases, including acute pancreatitis (AP).

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

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

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

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

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

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

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

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

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

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

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 Acute pancreatitis-associated adipose tissue had ongoing

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

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

149 re typically develops early in the course of acute pancreatitis, but also may develop later due to in

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

151 We induced severe acute pancreatitis by partial duct ligation with caerule

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

157 urgery (11% vs 5%; P = .43), or in recurrent acute pancreatitis, chronic pancreatitis, Izbicki pain s

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 incidence of acute pancreatitis continues to rise, inducing substanti

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

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

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

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

167 T-cell activation and severity of acute pancreatitis did not differ significantly between

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

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

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

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

172 Early oral refeeding in mild acute pancreatitis (EORVsUOR).

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

174 by such clinical features as abdominal pain, acute pancreatitis, eruptive xanthomas, and lipemia reti

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

176 ays following initiation of azathioprine, 40 acute pancreatitis events occurred (incidence rate 49.1

177 logical prevention or specific treatment for acute pancreatitis exists.

178 manifestations ranging from abdominal pain, acute pancreatitis, exocrine and/or endocrine dysfunctio

179 effects of CM4620 in preventing or reducing acute pancreatitis features and severity.

180 obstruction; biliary obstruction; recurrent acute pancreatitis; fistulas; or persistent systemic inf

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

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

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

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

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

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

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

188 en use of azathioprine and increased risk of acute pancreatitis in adult inflammatory bowel disease.

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

190 azathioprine is associated with the risk of acute pancreatitis in children with inflammatory bowel d

191 ine was associated with an increased risk of acute pancreatitis in children with inflammatory bowel d

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

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

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

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

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

197 plexes, attenuates acinar cell pathology and acute pancreatitis in mouse experimental models.

198 nistration of CM4620 reduces the severity of acute pancreatitis in the rat, a hitherto untested speci

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

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

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

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

203 use was associated with an increased risk of acute pancreatitis (incidence rate ratio 5.82 [95% CI 2.

204 Key features of acute pancreatitis include excess cellular Ca(2+) entry

205 urst and inflammatory gene expression during acute pancreatitis, including in immune cells which may

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

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

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

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

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

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

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

213 r injury without affecting NEFA signaling or acute pancreatitis induction.

214 ssors (environmental and genetic) that cause acute pancreatitis initially cause injury to organelles

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

216 Acute pancreatitis is a complex disorder involving both

217 Acute pancreatitis is a human disease in which the pancr

218 Acute pancreatitis is a potentially lethal disease, with

219 Acute pancreatitis is a serious and sometimes fatal infl

220 Acute Pancreatitis is a substantial health care challeng

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

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

223 Acute pancreatitis is among the most common and costly r

224 Acute pancreatitis is an inflammatory disorder of the ex

225 Acute pancreatitis is associated with alcohol abuse, gal

226 Acute pancreatitis is characterized by premature intrace

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

228 Acute pancreatitis is one of the common causes of aspara

229 Acute pancreatitis is one of the most frequent gastroint

230 Acute pancreatitis is the leading cause of hospitalizati

231 Acute pancreatitis is the most common complication of di

232 Acute pancreatitis is the most common major complication

233 Globally, acute pancreatitis is the most common pancreatic disease

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

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

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

237 Acute pancreatitis may be associated with both local and

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

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

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

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

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

243 (2.8%) and CTRC in 2 (1.4%) patients; severe acute pancreatitis, mutation of CFTR and CTRC in 1 (2.6%

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

245 The risk of acute pancreatitis needs to be considered when deciding

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

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

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

249 es of acute pancreatitis and defines "severe acute pancreatitis." Organ failure typically develops ea

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

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

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

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

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

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

256 ammatory signalling as central mechanisms in acute pancreatitis pathobiology.

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

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

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

260 Incident acute pancreatitis (physician-assigned diagnosis with IC

261 male with past medical history of recurrent acute pancreatitis presented for evaluation following a

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

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

264 Acute pancreatitis, recurrent acute pancreatitis (RAP) a

265 Induced acute pancreatitis results in a substantial release not

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

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

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

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

270 Acute pancreatitis severity scores have limited proficie

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

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

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

274 ons for correction of organelle functions in acute pancreatitis to create a discussion for clinical t

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

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

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

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

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

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

281 Acute pancreatitis was induced by administration of lipo

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

283 Acute pancreatitis was induced in rats by intraductal in

284 ase activation, severity of cerulein-induced acute pancreatitis was similar in Ctrl-KO and C57BL/6N m

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

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

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

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

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

290 x of suspicion such as recurrent episodes of acute pancreatitis when imaging is normal or equivocal.

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

292 s in the context of a patient with recurrent acute pancreatitis who chooses to delay surgery until af

293 ion of contrast material in 27 patients with acute pancreatitis who underwent the examination 48 to 7

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

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

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

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

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

299 ses the practical considerations in managing acute pancreatitis within the first 72 hours after the p

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