ライフサイエンスコーパス: pancreatitis

1 ily history of pancreatic cancer and chronic pancreatitis).

2 of normal (ULN), and imaging compatible with pancreatitis.

3 treatment, including asparaginase-associated pancreatitis.

4 ad cancer and 91 (11%) had benign conditions/pancreatitis.

5 lp screen for potential treatments for human pancreatitis.

6 patients with cancer differs from those with pancreatitis.

7 ias) enrolled patients with mild to moderate pancreatitis.

8 rosclerosing inflammatory variant of chronic pancreatitis.

9 between sexes for pancreatic cancer or acute pancreatitis.

10 parenchymal necrosis, indicating necrotizing pancreatitis.

11 tified in patients with pancreatic cancer or pancreatitis.

12 kedly increased risk of asparaginase-induced pancreatitis.

13 ay an anti-inflammatory role in experimental pancreatitis.

14 rainage for (suspected) infected necrotizing pancreatitis.

15 methionine, is known to induce steatosis and pancreatitis.

16 Cs and this may be helpful in treating acute pancreatitis.

17 on was observed following chemically induced pancreatitis.

18 ng loss, orchitis, oophoritis, mastitis, and pancreatitis.

19 tory responses, but has not been assessed in pancreatitis.

20 dney dysfunction and clinical posttransplant pancreatitis.

21 ng ERCP, including those at average risk for pancreatitis.

22 ssion were analyzed after chemically induced pancreatitis.

23 chanism of CB2R-mediated protection in acute pancreatitis.

24 ion reduces disease severity in experimental pancreatitis.

25 persistent ADM after acute caerulein-induced pancreatitis.

26 - FBSD") and with idiopathic acute recurrent pancreatitis.

27 of common bile duct (CBD) stone removal and pancreatitis.

28 ectal indomethacin did not prevent post-ERCP pancreatitis.

29 arly and late proinflammatory genes in acute pancreatitis.

30 age-specific regeneration after severe acute pancreatitis.

31 risk of severe complications, such as acute pancreatitis.

32 ells and pancreatic regeneration after acute pancreatitis.

33 es from hypertension to stroke, diabetes and pancreatitis.

34 ied at least one of these variants developed pancreatitis.

35 ecrease in the absolute rate and severity of pancreatitis.

36 uch as acinar-to-beta-cell reprogramming and pancreatitis.

37 ation generally refers to calcifying chronic pancreatitis.

38 sociation of PRSS2 mutations with hereditary pancreatitis.

39 of catheter drainage in infected necrotizing pancreatitis.

40 cell pathogenesis in animal models of acute pancreatitis.

41 only high-risk patients to prevent post-ERCP pancreatitis.

42 y outcome was overall ocurrence of post-ERCP pancreatitis.

43 have important implications in acute biliary pancreatitis.

44 f overall complications, including post-ERCP pancreatitis.

45 ency on cerulein- and arginine-induced acute pancreatitis.

46 2-0.47) per 100 000 person-years for chronic pancreatitis.

47 PAC necrosis evoked by agents causing acute pancreatitis.

48 apoptosis but not necrosis in two models of pancreatitis.

49 he major risk factors for chronic calcifying pancreatitis.

50 nt among cases of both severe and mild acute pancreatitis.

51 may be a therapeutic target in severe acute pancreatitis.

52 lly expressed genes during the initiation of pancreatitis.

53 ias) included patients with predicted severe pancreatitis.

54 g the optimal surgical treatment for chronic pancreatitis.

55 tion of activin conveys survival benefits in pancreatitis.

56 ets for treating or reducing the severity of pancreatitis.

57 is, accelerates the development of alcoholic pancreatitis.

58 ch is especially dangerous for patients with pancreatitis.

59 e exposure developed asparaginase-associated pancreatitis.

60 tomy specimens from 20 patients with chronic pancreatitis, 13 with low-grade side-branch IPMNs, and 1

61 surgical samples (24 PDAC, 7 IPMN, 6 chronic pancreatitis, 15 C), and set 2-95 endoscopic ultrasound-

62 s developed a second asparaginase-associated pancreatitis, 22 (52%) of 43 being severe.

63 r after diagnosis of asparaginase-associated pancreatitis, 31 (11%) of 275 patients still needed insu

64 Of 465 patients with asparaginase-associated pancreatitis, 33 (8%) of 424 with available data needed

65 ATF3 maintain a mature cell phenotype during pancreatitis, a finding supported by maintenance of junc

66 ith ATP synthase mediates L-arginine-induced pancreatitis, a model of severe AP the pathogenesis of w

67 ng 59 after a severe asparaginase-associated pancreatitis (abdominal pain or pancreatic enzymes at le

68 IMS: Smoking, an independent risk factor for pancreatitis, accelerates the development of alcoholic p

69 ecifically, caerulein induced mild edematous pancreatitis accompanied by minimal lung injury, while L

70 ch established risk factors, such as chronic pancreatitis, acinar cell damage, and/or defective autop

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

72 Other than pancreatitis, adverse events occurred in 41 (3%; two sev

73 ctal indometacin decreases the occurrence of pancreatitis after endoscopic retrograde cholangiopancre

74 Rectal indomethacin reduces the risk of pancreatitis after endoscopic retrograde cholangiopancre

75 Autoimmune pancreatitis (AIP) is a rare and underdiagnosed fibroscl

76 Among 6,161 cases of acute pancreatitis and 61,637 controls, current use of angiote

77 There were two minor AEs-subclinical pancreatitis and a mucosal ulcer that had healed by the

78 everity of the first asparaginase-associated pancreatitis and a second asparaginase-associated pancre

79 PDA is associated with chronic pancreatitis and acinar cell dedifferentiation.

80 cardiovascular diseases, Alzheimer disease, pancreatitis and diabetes.

81 AK4 in pancreatic disease models such as for pancreatitis and different pancreatic cancer forms.

82 ic FAEE concentrations in alcoholics without pancreatitis and high FA concentrations in pancreatic ne

83 creatic regeneration after caerulein-induced pancreatitis and in Kras(G12D)-driven PDAC development.

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

85 in the early, acinar cell-dependent phase of pancreatitis and much greater in the later, inflammatory

86 y is directly relevant to the pathologies of pancreatitis and pancreatic adenocarcinoma.

87 Yet the signaling events involved in chronic pancreatitis and pancreatic cancer progression and metas

88 will finally make the difference in treating pancreatitis and pancreatic cancer successfully.

89 n this study, we show that, in human chronic pancreatitis and pancreatic cancer tissues, Cad-11 expre

90 have been implicated in the pathogenesis of pancreatitis and pancreatic cancer, and PARP inhibition

91 te cells, has important functions in chronic pancreatitis and pancreatic cancer.

92 iescent, only to become activated in chronic pancreatitis and pancreatic cancer.

93 ed in the pancreas, such as type 1 diabetes, pancreatitis and pancreatic cancer.

94 nce of type 3c diabetes secondary to chronic pancreatitis and pancreatic ductal adenocarcinoma, and h

95 y of life and restrict treatment options for pancreatitis and PDA.

96 njury and may provide a link between chronic pancreatitis and PDAC.

97 ing complications of asparaginase-associated pancreatitis and risk of re-exposing patients who suffer

98 However, the role of POSTN in acute pancreatitis and subsequent regeneration processes has n

99 al growth, pregnancy, and in mouse models of pancreatitis and type 1 diabetes (T1D).

100 polymorphisms were associated (P < .05) with pancreatitis, and 13 of 24 patients who carried at least

101 .85-1.58) per 100 000 person-years for acute pancreatitis, and 9.62 cases (95% CI 7.86-11.78) per 100

102 x1b, are involved in pancreatic development, pancreatitis, and carcinogenesis, although the biologica

103 als, included adults hospitalized with acute pancreatitis, and compared early versus delayed feeding

104 ng and kidney damage in a rat model of acute pancreatitis, and is progressing into preclinical develo

105 pulmonary disease, acquired rhinosinusitis, pancreatitis, and lethal secretory diarrhea (e.g. choler

106 cidences of both pancreatic cancer and acute pancreatitis, and mortality from pancreatic cancer, were

107 ten on acute pancreatitis, three on chronic pancreatitis, and none on pancreatic cysts) were identif

108 hepatocellular carcinoma, gallstones, acute pancreatitis, and pancreatic cancer.

109 tribution and activation during experimental pancreatitis, and regulates disease severity by potently

110 ht be associated with a lesser risk of acute pancreatitis, and that the protective association was si

111 Although ethanol causes acute pancreatitis (AP) and lipolytic fatty acid (FA) generati

112 Acute pancreatitis (AP) is a common acute abdominal disease, 1

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

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

115 Acute pancreatitis (AP) is a painful inflammatory disorder of

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

117 Acute pancreatitis (AP) was induced in C57BL/6 (control) and B

118 ochondrial dysfunction and necrosis in acute pancreatitis (AP), a condition without specific drug tre

119 diction of the severity and outcome of acute pancreatitis (AP).

120 gan dysfunction (MODS) in experimental acute pancreatitis (AP).

121 el role for KMO in the pathogenesis of acute pancreatitis (AP).

122 e together with the clinical course of acute pancreatitis (AP).

123 ing pathways that initiate and promote acute pancreatitis (AP).

124 st 30% of patients with infected necrotizing pancreatitis are successfully treated with catheter drai

125 actorial, whereas recurrent attacks of acute pancreatitis are thought to precede the development of C

126 Pediatric acute recurrent pancreatitis (ARP) and chronic pancreatitis (CP) are poo

127 Acute recurrent pancreatitis (ARP) is defined as more than two attacks o

128 emia, osteonecrosis, asparaginase-associated pancreatitis, arterial hypertension, posterior reversibl

129 n initiation and development of severe acute pancreatitis as a model of acute inflammation.

130 usion criteria were neoadjuvant treatment or pancreatitis as only diagnosis.

131 ased on clinical symptoms, bilirubin, ulcer, pancreatitis, ascites, or radioembolization-induced live

132 models are ideally suited for the studies of pancreatitis associated with altered metabolism in human

133 rine models of AP and significantly improved pancreatitis-associated acute lung injury.

134 nd regenerating islet-derived protein 3 beta/pancreatitis-associated protein were observed after surg

135 or, regenerating islet-derived protein 3beta/pancreatitis-associated protein, amylase, lipase, glucos

136 een 1997 and 2013, patients with necrotizing pancreatitis at the Liverpool Pancreas Center were revie

137 complete resolution of symptoms and signs of pancreatitis between episodes.

138 was no significance difference in post-ERCP pancreatitis between EST and EPBD.

139 INK1) gene are associated with human chronic pancreatitis, but the underlying mechanisms remain unkno

140 Mutations in PRSS1 cause hereditary pancreatitis by altering cleavage of regulatory nick sit

141 We induced acute pancreatitis by repeated caerulein injections and isolat

142 Induction of acinar pancreatitis by supramaximal cholecystokinin (CCK-8) sti

143 To estimate relative risk of acute pancreatitis, by degree of severity, among users of angi

144 Acute biliary pancreatitis, caused by bile reflux into the pancreas, i

145 ical responses and organellar disorders with pancreatitis-causing treatments as observed in rodent ac

146 e worldwide incidence and mortality of acute pancreatitis, chronic pancreatitis, pancreatic cysts, an

147 rs was followed by a decreased risk of acute pancreatitis, compared to non-users, adjusted OR 0 .

148 However, experimental pancreatitis converts Kras mutant Dclk1+ cells into pote

149 Immunohistochemical analysis of chronic pancreatitis (CP) and peritumoral areas in PDAC tissues

150 ute recurrent pancreatitis (ARP) and chronic pancreatitis (CP) are poorly understood.

151 Pain management of patients with chronic pancreatitis (CP) can be challenging.

152 Patients with chronic pancreatitis (CP) frequently have genetic risk factors f

153 Chronic pancreatitis (CP) is a fibro-inflammatory disease leadin

154 Chronic pancreatitis (CP) is a progressive inflammatory disease

155 iocarcinoma, n = 5) or nonmalignant (chronic pancreatitis [CP], n = 15) origin.

156 rospective study of 91 patients with chronic pancreatitis; data were collected from patients seen at

157 Chronic pancreatitis describes a wide spectrum of fibro-inflamma

158 bjective monitoring of patients with chronic pancreatitis, determining risk for readmission to hospit

159 Many patients with chronic pancreatitis develop diabetes (chronic pancreatitis-rela

160 T: A 44-year-old man with a history of acute pancreatitis developed a pseudoaneurysm of the pancreati

161 Pancreatitis developed in 5 (2 in the 75-mg group and 3

162 g had two versus one asparaginase-associated pancreatitis did not differ (three [7%] of 42 vs 28 [12%

163 eatitis and a second asparaginase-associated pancreatitis did not involve an increased risk of compli

164 ine and serum samples for early diagnosis of Pancreatitis disease.

165 st that early feeding in patients with acute pancreatitis does not seem to increase adverse events an

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

167 Among patients with mild to moderate pancreatitis, early feeding was associated with reduced

168 l prevention or specific treatment for acute pancreatitis exists.

169 gnosis, and management of chronic calcifying pancreatitis, focusing on pain management, the role of e

170 reoperations (for reasons other than chronic pancreatitis), gastrointestinal problems, and other surg

171 Tissues from patients with pancreatitis had markers of mitochondrial damage and imp

172 boxypeptidase A2, was highly associated with pancreatitis (hazard ratio, 587; 95% CI, 66.8 to 5166; P

173 morbidity rate of hypertriglyceridemic acute pancreatitis (HTG-AP) increased rapidly over the last de

174 The symptoms of pancreatitis improved over a few days, and the laborator

175 lications included bleeding in 3.4 % (2/58), pancreatitis in 8.6 % (5/58) and biliary tract infection

176 te smoke promotes cell death and features of pancreatitis in EtOH-sensitized acinar cells by suppress

177 anti-inflammatory drug, is given to prevent pancreatitis in high-risk patients undergoing endoscopic

178 ted CTSB but not trypsinogen in vitro During pancreatitis in pancreas-specific CTSD(f/f)/p48(Cre/+) a

179 n ancestry were independent risk factors for pancreatitis in patients with acute lymphoblastic leukem

180 e course of taurocholate-induced necrotizing pancreatitis in rats and in vitro in rat pancreatic AR42

181 into the pancreatic duct induced necrotizing pancreatitis in the head of pancreas and lighter inflamm

182 Only one serious adverse event (pancreatitis in the study group) was deemed as possibly

183 to occur in the auto-digestive disease acute pancreatitis in vivo, consistently elicited substantial

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

185 Risk factors associated with pancreatitis included genetically defined Native America

186 by common variants modestly associated with pancreatitis included purine metabolism and cytoskeleton

187 Pancreatitis increases formation of PanINs in mice that

188 The severity of acute pancreatitis induced by combination of ethanol and fatty

189 ty in two established murine models of acute pancreatitis induced by either cerulein or IL-12 + IL-18

190 f pathological injury is consistent with the pancreatitis induced in mice and rat using the same meth

191 Animal studies suggest that pancreatitis-induced acinar-to-ductal metaplasia (ADM) i

192 sues of mice resulted in increased levels of pancreatitis-induced ADM.

193 on of Slug with Kras also attenuated chronic pancreatitis-induced changes in ADM development and fibr

194 Pancreatitis is a common disorder with significant morbi

195 Acute pancreatitis is a complex disorder involving both premat

196 Pancreatitis is a debilitating disease of the exocrine p

197 Acute pancreatitis is a potentially lethal disease, with a ris

198 Chronic pancreatitis is a prominent risk factor for the developm

199 Acute Pancreatitis is a substantial health care challenge with

200 Acute biliary pancreatitis is a sudden and severe condition initiated

201 d for new markers in stratification of acute pancreatitis is also uncertain.

202 Acute pancreatitis is among the most common and costly reasons

203 owledge of the molecular mechanisms of acute pancreatitis is largely based on studies using rodents.

204 Acute pancreatitis is one of the common causes of asparaginase

205 Globally, acute pancreatitis is the most common pancreatic disease whils

206 Pancreatitis is the most important risk factor for pancr

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

208 ROUND & AIMS: The clinical course of chronic pancreatitis is unpredictable.

209 pain-associated behavior in a model of acute pancreatitis - known to also rely on TRPV4 and TRPA1.

210 Among patients with severe pancreatitis, limited evidence revealed no statistically

211 ing anterograde endosomal trafficking during pancreatitis maintains VAMP8-dependent secretion, thereb

212 Together, our data suggest that chronic pancreatitis may trigger TGFbeta1-mediated beta-cell EMT

213 ents and, for patients with mild to moderate pancreatitis, may reduce length of hospital stay.

214 s the roles of autophagy and inflammation in pancreatitis, mechanisms of deregulation, and connection

215 Parameters of pancreatitis, mitochondrial function, autophagy, ER stre

216 choledocholithiasis, cholangitis, or biliary pancreatitis), mortality, and cost by CCY cohort.

217 it has been identified as a target for acute pancreatitis multiple organ dysfunction syndrome (AP-MOD

218 with supraphysiologic CCK-8 levels to mimic pancreatitis, Munc18c-depleted (Munc18c(+/-)) mouse acin

219 rthotopic liver transplant (n = 73), chronic pancreatitis (n = 35), or postoperative injury (n = 4),

220 able to genetic mutation (n = 9), idiopathic pancreatitis (n = 6), idiopathic pancreatitis with pancr

221 three or more patients given ponatinib were pancreatitis (n=5), atrial fibrillation (n=3), and throm

222 exocytosis in part explained the less severe pancreatitis observed in Munc18c(+/-) mice after hyperst

223 Post-ERCP pancreatitis occurred in 18 (6%) of 305 high-risk patien

224 alyzed pancreatic tissues from patients with pancreatitis or PDAC by immunohistochemistry.

225 saccharide (LPS, 3 mg/kg per week) to induce pancreatitis or saline (control).

226 levels of MIR122 and EPO in mice with acute pancreatitis or steatohepatitis, and also in patients wi

227 tly in healthy children, or in patients with pancreatitis or T1D.

228 eased risk associated with both severe acute pancreatitis, (OR 0 .

229 patients with suspected hypertriglyceridemic pancreatitis; or diagnosing hypertriglyceridemia in pati

230 nts who did versus those who did not develop pancreatitis (P = .001).

231 oronary syndrome, and the incidence of acute pancreatitis, pancreatic cancer, medullary thyroid carci

232 fferences were seen in severe hypoglycaemia, pancreatitis, pancreatic cancer, or medullary thyroid ca

233 and mortality of acute pancreatitis, chronic pancreatitis, pancreatic cysts, and pancreatic cancer in

234 ified causes of type 3c diabetes are chronic pancreatitis, pancreatic ductal adenocarcinoma, haemochr

235 Chronic pancreatitis, pancreatic intra-epithelial neoplasia, and

236 Expression of TIMP1 is increased in chronic pancreatitis, pancreatic intra-epithelial neoplasia, and

237 amples from patients in Germany with chronic pancreatitis, pancreatic intra-epithelial neoplasia, or

238 ured from a retrospective clinical cohort of pancreatitis patients and high activin levels in patient

239 as a clinical marker to identify those acute pancreatitis patients with severe disease who would bene

240 ted inflammatory mediators elevated in acute pancreatitis patients, including IL-6, tumor necrosis fa

241 U/L) in different urine and serum samples of pancreatitis patients.

242 of rectal indomethacin to prevent post-ERCP pancreatitis (PEP) in a variety of patients.

243 ary outcome was the development of post-ERCP pancreatitis (PEP), defined by new upper-abdominal pain,

244 c inflammatory diseases, such as colitis and pancreatitis, predispose to gastrointestinal (GI) adenoc

245 Pancreatitis predisposes to PDAC because it induces a pr

246 ation were used to develop a 3-stage chronic pancreatitis prognosis score (COPPS).

247 reduced the extent of PAC necrosis evoked by pancreatitis-promoting agents and we therefore conclude

248 Percutaneous coagulation of a post-pancreatitis pseudoaneurysm is a relatively easy and saf

249 The corresponding pancreatitis rates were 3.4, 7.0 and 6.8% and the postop

250 ronic pancreatitis develop diabetes (chronic pancreatitis-related diabetes [CPRD]) through an undeter

251 At least 1 gene mutation in pancreatitis-related genes was found in 48% of patients

252 Pancreatitis remains a diagnostic challenge in patients

253 Within 8 years of asparaginase-associated pancreatitis, risk of abdominal symptoms dropped from 8%

254 ic tissues, 63 PDAC sections, and 49 chronic pancreatitis samples).

255 Although there was no difference in pancreatitis severity in the acute inflammatory phase, t

256 r mechanisms in humans, we performed ex vivo pancreatitis studies in human acini isolated from cadave

257 tations in PRSS2 are not found in hereditary pancreatitis suggesting that activation of this isoform

258 is required to reduce injury associated with pancreatitis, the factors that promote this repression a

259 romoter methylation in both PDAC and chronic pancreatitis, the latter of which is a major risk factor

260 ACs against damage caused by agents inducing pancreatitis, therefore also inhibit Ca(2+) signal gener

261 udies (35 on pancreatic cancer, ten on acute pancreatitis, three on chronic pancreatitis, and none on

262 rane of activated PSCs isolated from chronic pancreatitis tissues and in pancreatic cancer cells meta

263 Human pancreatitis tissues were analyzed by immunofluorescence

264 posing patients with asparaginase-associated pancreatitis to asparaginase, 18 acute lymphoblastic leu

265 ffered an episode of asparaginase-associated pancreatitis to asparaginase.

266 nhibition of VAMP8-mediated secretion during pancreatitis triggers intracellular trypsin accumulation

267 In summary, CTSB in pancreatitis undergoes activation in a secretory, vesicu

268 nclude that bradykinin plays a role in acute pancreatitis via specific actions on PSCs.

269 ders (hepatitis, brain and cardiac ischemia, pancreatitis, viral infection and inflammatory diseases)

270 Post-ERCP pancreatitis was also less frequent in average-risk pati

271 Asparaginase-associated pancreatitis was defined by at least two criteria: abdom

272 The severity of pancreatitis was evaluated by serum amylase activity, pa

273 Pancreatitis was induced in C57BL/6J mice (control) and

274 Pancreatitis was induced in mice by administration of ce

275 Chronic pancreatitis was induced with cerulein in C57BL/6 mice,

276 The incidence of pancreatitis was nonsignificantly lower in the liragluti

277 Risk of a second asparaginase-associated pancreatitis was not associated with any baseline patien

278 the risk of a second asparaginase-associated pancreatitis was not associated with severity of the fir

279 For instance, in preclinical mouse models, pancreatitis was significantly attenuated after genetic

280 ific regions, while the incidence of chronic pancreatitis was significantly higher in the European re

281 The incidence of chronic pancreatitis was twice as high in men as in women, altho

282 prominent macrophage infiltration in chronic pancreatitis, we hypothesized that (125)I-iodo-DPA-713,

283 Furthermore, in a model of acute pancreatitis, we observed substantive luminal acidificat

284 inical risk factors for asparaginase-induced pancreatitis, we studied a cohort of 5,185 children and

285 Patients with cholangitis or pancreatitis were excluded.

286 Early kidney dysfunction and clinical pancreatitis were higher in the control group than in ei

287 First-time cases with acute pancreatitis were identified in the National Patient Reg

288 in quality of life after surgery for chronic pancreatitis were seen between the interventions.

289 , such as diabetes mellitus (DM) and chronic pancreatitis, were compared.

290 veloped after an episode of acute on chronic pancreatitis which was treated by direct percutaneous pu

291 and readmission in adults hospitalized with pancreatitis who received early versus delayed feeding.

292 Patients with chronic pancreatitis who were planned for elective surgical trea

293 is defined as more than two attacks of acute pancreatitis with complete or almost complete resolution

294 To replicate human acute pancreatitis with hamsters, we comparatively studied the

295 idiopathic pancreatitis (n = 6), idiopathic pancreatitis with pancreas divisum (n = 3), and alcohol

296 e-threatening vascular complication of acute pancreatitis, with a mortality rate of 20-43% in untreat

297 se genes was observed only upon induction of pancreatitis, with pathways involved in inflammation, ac

298 long-term outcomes of patients with chronic pancreatitis within 24 months after surgery.

299 reduced the overall occurrence of post-ERCP pancreatitis without increasing risk of bleeding.

300 Use of the term chronic pancreatitis without qualification generally refers to c