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1 risk factor, such as reflux esophagitis and gallstones.
2 a neoplasm in the group of patients without gallstones.
3 bile cholesterol and, thus, the formation of gallstones.
4 al inhibitor of initial biofilm formation on gallstones.
5 These cancers are associated with gallstones.
6 believed to be intermediates in formation of gallstones.
7 associated with the presence of cholesterol gallstones.
8 s frequently associated with the presence of gallstones.
9 iliary cholesterol secretion and cholesterol gallstones.
10 thogenic diet, all of the LIRKO mice develop gallstones.
11 equired for biofilm formation on cholesterol gallstones.
12 ol crystallization in biles of patients with gallstones.
13 tabolism and the pathogenesis of cholesterol gallstones.
14 as been demonstrated to be a risk factor for gallstones.
15 hanisms of previously noted risk factors for gallstones.
16 utput compared to WT mice, they still formed gallstones.
17 abdominal ultrasound examinations to detect gallstones.
18 It is also a core protein of cholesterol gallstones.
19 risks of hepatitis (21 [0.5%] vs 18 [0.4%]), gallstones (106 [2.3%] vs 106 [2.3%]), or cancer (438 [9
21 ice developed significantly more cholesterol gallstones (27%-80% prevalence) than Rag mice ( approxim
24 isease, cirrhosis, hepatocellular carcinoma, gallstones, acute pancreatitis, and pancreatic cancer.
25 tals, for acute pancreatitis overall and for gallstone aetiology but not for alcoholic acute pancreat
26 month for acute pancreatitis overall or for gallstone aetiology, but for alcoholic acute pancreatiti
27 itals for acute pancreatitis overall and for gallstone aetiology, the study factors had limited impac
29 A and yihV-yihW) is a crucial determinant in gallstone and cholesterol biofilms but that expression o
30 rticipants (591 of 5928); of these, 6.8% had gallstones and 3.2% had cholecystectomy at baseline.
32 e long-term occurrence of clinical events of gallstones and associations between ultrasound observati
34 nce inflammatory responses may predispose to gallstones and biliary tract cancer, suggesting the need
35 f chronic inflammation in the development of gallstones and biliary tract cancer, we examined the ris
41 ated that salmonellae form biofilms on human gallstones and cholesterol-coated surfaces in vitro and
42 onellae form bile-mediated biofilms on human gallstones and cholesterol-coated surfaces in vitro.
43 atients might have higher risk in developing gallstones and conducted a population-based study to exa
44 bladder motility and cholesterol absorption, gallstones and expression of the mucin genes in gallblad
47 search has focused on the pathophysiology of gallstones and on clarifying the underlying mechanisms o
48 absorption inhibitor ezetimibe could prevent gallstones and promote gallstone dissolution in mice and
50 pite the well-documented association between gallstones and the metabolic syndrome, the mechanistic l
60 sporter, Abcg5/g8, is Lith9 in mice, and two gallstone-associated variants in ABCG5/G8 have been iden
61 fR mutant formed extensive biofilms on mouse gallstones at 7 and 21 days postinfection; DeltafimAICDH
62 as scanned with (n = 86) or without (n = 85) gallstones at CT by using 80, 100, 120, and 140 kVp.
63 tant for attachment to and/or persistence on gallstones at later points of chronic infection, whereas
65 These findings offer direct evidence that gallstone biofilms occur in humans and mice, which facil
67 t with ezetimibe promoted the dissolution of gallstones by forming an abundance of unsaturated micell
68 ategy for preventing or treating cholesterol gallstones by inhibiting intestinal cholesterol absorpti
70 ABCG5/8 and NPC1L1 expression was similar in gallstone carriers and controls regardless of p.D19H pre
71 cholesterol absorption but not synthesis in gallstone carriers was diminished by about 21% based on
72 ls 28%, P = 0.0347 and wild type controls to gallstone carriers with 19H allele 37%, P = 0.0030).
74 ithogenesis, we investigated the biliary and gallstone characteristics in male wild-type (WT), ABCG5(
75 s, American Society of Anesthesiology score, gallstone characteristics, local inflammation, blood los
76 ous adverse event in the intervention group (gallstones) could be attributable to rapid and excessive
80 sk of coronary artery disease, hypertension, gallstones, diabetes, cancer, metabolic syndrome, and vi
81 astrointestinal cancers were associated with gallstone disease (11.2% of patients with gallstone dise
83 t-side colon cancer was also associated with gallstone disease (2.57% of patients with gallstone dise
87 cally different populations of patients with gallstone disease (GSD) and stone-free controls to ident
92 er UDCA reduces the incidence of symptomatic gallstone disease after Roux-en-Y gastric bypass or slee
96 y lipid secretion plays an important role in gallstone disease and reverse cholesterol transport (RCT
98 cipants biennially reported their history of gallstone disease and whether they had undergone cholecy
100 andomized controlled trials with symptomatic gallstone disease as primary endpoint have not been cond
101 he identification of susceptibility loci for gallstone disease by use of animal models suggest geneti
103 Breast cancer had a weak association with gallstone disease depending on other factors (10.6% of p
105 ence interval: 2.39 to 3.39) for symptomatic gallstone disease for individuals with a genotype score
106 potential risk factors, the relative risk of gallstone disease for men in the highest quintile was 1.
110 es of heme and non-heme iron and the risk of gallstone disease in a cohort of 44 758 US men from 1986
111 umption of saturated fatty acids and risk of gallstone disease in a cohort of 44,524 US men from 1986
122 y), fibrosis/cirrhosis (HR 5.11; 3.29-7.96), gallstone disease or cholangitis (HR 2.72; 2.55-2.91, an
123 nd rs4245791 were associated positively with gallstone disease risk, whereas the association for the
125 th gallstone disease (2.57% of patients with gallstone disease vs 0.96% without; hazard ratio, 2.04;
126 th gallstone disease (11.2% of patients with gallstone disease vs 6.64% without; hazard ratio, 1.50;
127 ing on other factors (10.6% of patients with gallstone disease vs 7.41% without; hazard ratio, 1.44;
128 y adjusted hazard ratio (HR) for symptomatic gallstone disease was 2.84 (95% confidence interval [CI]
134 1,140 consecutive patients with symptomatic gallstone disease were recruited during 2008-2010 at Kuo
135 ctiveness of three diagnostic strategies for gallstone disease with possible choledocholithiasis: non
137 er ABCG8 as a locus associated with risk for gallstone disease, but findings have not been reported f
138 smooth muscle (GBSM) function that occurs in gallstone disease, but their mechanism of action is unkn
139 t abdominal ultrasound examination to detect gallstone disease, but were not informed of their gallst
140 mated causal odds ratio (OR) for symptomatic gallstone disease, by instrumental variable analysis for
141 y index, race, admission acuity, complicated gallstone disease, hospital teaching status, and open ve
142 low-up, we documented 2350 incident cases of gallstone disease, of which 1387 cases required cholecys
143 his locus to a more diverse ethnic group for gallstone disease, susceptibility to biliary cancer, and
144 pplications in cholestatic liver disease and gallstone disease, two serious health concerns for human
145 yperhomocysteinemia can occur in cholesterol gallstone disease, we hypothesized that this may result
147 evated BMI and increased risk of symptomatic gallstone disease, which is most pronounced in women.
163 sition, such as that observed in cholesterol gallstone disease.Due to the challenges in directly stud
164 CG8 has been identified as a risk factor for gallstone disease; this variant has been associated with
166 etimibe could prevent gallstones and promote gallstone dissolution in mice and reduce biliary cholest
167 ocumented 2468 incident cases of symptomatic gallstones during 597 699 person-years of follow-up.
169 e evidence that Helicobacter species promote gallstone formation and hepatobiliary tumors in laborato
171 are markedly predisposed toward cholesterol gallstone formation due to at least two distinct mechani
173 e severity of and shortened the interval for gallstone formation in PKCbeta(-/-) mice and was associa
177 2A(-/-) mice fed a lithogenic diet had rapid gallstone formation, an increased cholesterol saturation
179 ersecretion as the mechanism for cholesterol gallstone formation, thereby drawing a link between "pos
180 stinal cholesterol absorption contributes to gallstone formation, we explored whether the potent chol
181 derived cholesterol from plasma to bile, and gallstone formation, which works independently of the AB
191 as significant biofilms were not detected on gallstones from Escherichia coli infected gallbladders.
192 nd bacterial biofilms could be visualized on gallstones from these carriers whereas significant biofi
200 t Sample from 2004 to 2009 was performed for gallstone ileus cases treated surgically by enterotomy w
203 from 2004 to 2009, 3268 (0.095%) were due to gallstone ileus-an incidence lower than previously repor
205 respectively; P = .02) and the presence of a gallstone in the gallbladder infundibulum (78% and 22% f
206 s acute cholecystitis) and the presence of a gallstone in the gallbladder infundibulum are associated
207 , the Cox regression analysis of the risk of gallstone in the osteoporosis and comparison cohorts yie
208 ium double mutant formed a mature biofilm on gallstones in a test tube assay and in a new, gallstone-
210 eeks, 90% Apobec-1(-/-) mice developed solid gallstones in comparison with 16% wild type controls.
212 te is highly associated with the presence of gallstones in the gallbladder of infected carriers upon
213 form biofilms on the surfaces of cholesterol gallstones in the gallbladders of mice and human carrier
215 describe an unusual case of infected spilled gallstones in the right sub-phrenic space, prospectively
216 mechanism causing an increased incidence of gallstones in these patients have as yet not been identi
218 increased biliary cholesterol secretion and gallstones in WT, but not ABCG5(-/-)/G8(-/-) or ABCG8 (-
220 allstones in a test tube assay and in a new, gallstone-independent assay using cholesterol-coated Epp
223 astatin for the resolution and prevention of gallstones is promising, but larger studies are needed.
225 epatocellular damage, TG2(-/-) mice had more gallstones, jaundice, and ductal proliferation than wild
226 n mice identified a susceptibility locus for gallstones (Lith6) spanning the Apobec-1 locus, the stru
229 liver function values in serum (n = 28) and gallstones (n = 46) of consecutively cholecystectomized
230 -year follow-up period, 114 and 311 cases of gallstone occurred in the osteoporosis and comparison co
231 as found to be significantly associated with gallstones (odds ratio [OR] = 2.9, P = 0.0220, 95% confi
233 dary endpoints consist of the development of gallstones on ultrasound at 24 months, number of cholecy
234 is study was to determine if screen-detected gallstones or cholecystectomy are associated with occurr
236 iopancreatography (ERCP) in 59 patients with gallstone, other benign disease, tumour, and primary scl
239 consensus among surgeons that patients with gallstone pancreatitis should undergo cholecystectomy to
240 ents in the treatment of patients with acute gallstone pancreatitis with regards to the timing of ERC
241 oscopic management of choledocholithiasis in gallstone pancreatitis, a newer approach in the endoscop
243 formed within 48 hours of admission for mild gallstone pancreatitis, regardless of resolution of abdo
244 ble for the onset of clinical biliary (i.e., gallstone) pancreatitis and creates highly reproducible
245 likely to be crucial factors in cholesterol gallstone pathogenesis, rather then merely the result of
246 l absorption as well as de novo synthesis in gallstone patients stratified according to 19H risk alle
251 tumour plus PSC group was also lower than in gallstone plus other benign disease group (p < 0.05).
253 formation of undesirable assemblies such as gallstone precursors, and how they can stabilize free-fl
254 tically significant increases in cholesterol gallstone prevalence compared with uninfected mice (81%
255 layed biliary lipid secretion rates and high gallstone prevalence rates similar to WT mice without an
256 ve provided insight into the pathogenesis of gallstones, primary biliary cirrhosis, and primary scler
257 ent views of the pathogenesis of cholesterol gallstones, promote further research on the pathways inv
258 ile-induced biofilm formation on cholesterol gallstones promotes gallbladder colonization and mainten
261 imilarly shaped association with risk of non-gallstone-related acute pancreatitis as that observed fo
262 naire at baseline, and cases of incident non-gallstone-related acute pancreatitis were identified by
263 men and 111 cases in women) of incident non-gallstone-related acute pancreatitis were identified.
266 atients with their 2-year risk of developing gallstone-related complications, allowing patients and p
267 ity Hospital, Geneva, Switzerland, for acute gallstone-related conditions with an intermediate risk o
268 s of care and modeled their risk of emergent gallstone-related hospitalization or cholecystectomy at
272 (e.g., between plasma campesterol levels and gallstones risk; and between immunoglobulin A and juveni
273 experiments using Nramp1(+/+) mice harboring gallstones showed that only the DeltaycfR mutant formed
274 r 2, P < .05 for each reader), regardless of gallstone size (<1.0 cm vs > or =1.0 cm in diameter, P <
279 study population comprised 664 subjects with gallstones; subjects were not informed of their gallston
280 nfection; DeltafimAICDHF was not observed on gallstone surfaces after the 7-day-postinfection time po
281 we hypothesize that bile-induced biofilms on gallstone surfaces promote gallbladder colonization and
282 analyzed data from the Swedish Registry for Gallstone Surgery and Endoscopic Retrograde Cholangiopan
283 also registered in the Swedish registry for gallstone surgery and ERCP (GallRiks) and correlations b
285 is a validated national quality registry for gallstone surgery and ERCP, serving as a base for audit
286 s observation prompted us to compare dietary gallstone susceptibility in Apobec-1(-/-) mice and conge
289 became elevated during cholelithogenesis in gallstone-susceptible C57L, C57BL/6, and SWR mice but no
291 fed a lithogenic diet developed cholesterol gallstones that supported biofilm formation during persi
292 However, we hypothesize that in addition to gallstones, the gallbladder epithelium aids in the estab
293 for association with gallbladder disease or gallstones, top bilirubin SNPs in UGT1A1 and SLCO1B1 wer
296 ne system in the pathogenesis of cholesterol gallstones was not considered a valid topic of research
297 ty markers in circulation, a 58% increase in gallstone weight, a 40% increase in hepatic cholesterol
298 tone patients vs overweight subjects without gallstones were examined before (day 0) and at 30 days a
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