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1 ranslational nonhuman primate model of heavy alcohol consumption.
2 of the DMS, which concurrently contribute to alcohol consumption.
3  "high-risk drinking levels" to reduce their alcohol consumption.
4 evel, physical activity, smoking status, and alcohol consumption.
5  therapeutic strategy for reducing excessive alcohol consumption.
6  patterns of expression that correlated with alcohol consumption.
7 res, drinking in the dark and scheduled high alcohol consumption.
8 acologically modifying such responses alters alcohol consumption.
9 ome whereas ALD is associated with excessive alcohol consumption.
10 ue-specific MAOA expression and the level of alcohol consumption.
11 N4B was significantly correlated to lifetime alcohol consumption.
12  Canada, and Australia, reported no or light alcohol consumption.
13 e in adult rats with a history of adolescent alcohol consumption.
14  drinking and in mice after binge or chronic alcohol consumption.
15 and lifestyle factors, including smoking and alcohol consumption.
16 R but not D2R activity in the DMS attenuates alcohol consumption.
17 erse BXD strains of mice predicted voluntary alcohol consumption.
18 e modal e-intervention was brief feedback on alcohol consumption.
19 , and related processes, underlying lifetime alcohol consumption.
20  drive the development of pathological heavy alcohol consumption.
21 NN3 as a mediator of voluntary and excessive alcohol consumption.
22  baseline demographics or levels/patterns of alcohol consumption.
23  and exhibit acetaldehyde accumulation after alcohol consumption.
24 ity, education, marital status, smoking, and alcohol consumption.
25 trasound criteria for fatty liver and absent alcohol consumption.
26 er liver function, which is a marker of high alcohol consumption.
27 ed negative binomial regression analysis for alcohol consumption.
28 rugs with the greatest potential to decrease alcohol consumption.
29 lopment of PKCepsilon inhibitors that reduce alcohol consumption.
30 re studies investigating the neurobiology of alcohol consumption.
31 loci in KLB, a gene recently associated with alcohol consumption.
32 (sCD163) are associated with the quantity of alcohol consumption.
33  to average BMI (2.0%, 1.4-2.7), whereas low alcohol consumption (0.01-2.5 g per day) and high BMI ha
34 ac causes (3.17, 2.68-3.75; 9.1%, 8.0-10.2), alcohol consumption (2.09, 1.64-2.67 for high or heavy e
35 king; 30.3% (95% CI: 23.3-37.4%) for current alcohol consumption; 24.4% (95% CI: 14.7-30.2%) for over
36 myocardial infarction, thyrotoxicosis, acute alcohol consumption, acute pericardial disease, pulmonar
37 women) that 1) provides robust evidence that alcohol consumption adversely affects several cardiovasc
38 cohol relapse was defined as any evidence of alcohol consumption after transplant, which was assessed
39                                              Alcohol consumption, age, axial length/corneal curvature
40                              To determine if alcohol consumption alters cortical encoding of rewards
41 -DOT, having cirrhosis and receiving 9H-SAT, alcohol consumption among men, and use of concomitant me
42 hol drinker in all groups, but prevalence of alcohol consumption amongst females was very low.
43 ng adults and is a risk factor for excessive alcohol consumption and alcohol dependence.
44 his study replicates the association between alcohol consumption and alcohol metabolizing genes and K
45                                       Excess alcohol consumption and alcohol use disorders (AUDs) are
46  IV-VI, in vivo, significantly reduced their alcohol consumption and blood alcohol concentrations ach
47 sphatidylcholines were associated with lower alcohol consumption and BMI and with a healthier diet.
48  and environmental factors, such as smoking, alcohol consumption and body mass index.
49          To evaluate the association between alcohol consumption and breast cancer risk in younger wo
50 olate intake, a positive association between alcohol consumption and breast cancer was found among wo
51        Among females, no association between alcohol consumption and clinical AL progression was obse
52           Studies on the association between alcohol consumption and colorectal cancer (CRC) prognosi
53 inhibitor RG108 prevented both escalation of alcohol consumption and dependence-induced downregulatio
54 cular basis for impaired immunity with heavy alcohol consumption and enhanced immune response with mo
55                                              Alcohol consumption and folate intake were measured by f
56 n, there was a U-shaped relationship between alcohol consumption and HF incidence, with a nadir at li
57 ic asthma, rhinitis, and eczema) and between alcohol consumption and IgE levels and allergic disease.
58 lored potential causal relationships between alcohol consumption and IgE levels and allergic disease.
59 hd2 is a conserved resilience factor against alcohol consumption and its escalation, working through
60 nce for an epigenetic marker associated with alcohol consumption and its underlying neurobehavioral p
61            Although the relationship between alcohol consumption and liver disease is well establishe
62 r data suggest that the relationship between alcohol consumption and lung carcinoma differs by histol
63 pectively evaluated the relationship between alcohol consumption and lung carcinoma in 492,902 person
64 in both primary and secondary care to detect alcohol consumption and misuse among people diagnosed wi
65 ffer by socioeconomic status, accounting for alcohol consumption and other health-related factors.
66                            The potential for alcohol consumption and other risk factors (including sm
67 m AF and had completed a questionnaire about alcohol consumption and other risk factors for chronic d
68         We investigated associations between alcohol consumption and outcomes in a prospective cohort
69 on, associations between lifetime and recent alcohol consumption and overall, CRC-specific, recurrenc
70 d that mTORC1 is necessary for the sustained alcohol consumption and preference across the initial dr
71 g the first alcohol drinking session reduced alcohol consumption and preference of a subsequent drink
72 he dorsal striatum or DMS of rats, increased alcohol consumption and preference, with no similar effe
73 ng, and diminished ALDH1a1 leads to enhanced alcohol consumption and preference.
74  anti-FGF2 neutralizing antibody, suppressed alcohol consumption and preference.
75                         Associations between alcohol consumption and prognosis varied according to pr
76 served, only one was modulated by adolescent alcohol consumption and showed strongest modulation afte
77 conomic status (SES), body mass index (BMI), alcohol consumption and smoking status that reach the si
78 ol tolerance is a key step toward escalating alcohol consumption and subsequent dependence.
79 evidence that blood MAOA expression predicts alcohol consumption and that heavy alcohol use is linked
80 sought to explore the influence of stroke on alcohol consumption and to uncover the underlying nigros
81                           Repeated cycles of alcohol consumption and withdrawal in mice strengthened
82 asal amygdala to CeA projections showed that alcohol consumption and withdrawal were associated with
83 egression, genetic overlap was found between alcohol consumption and years of schooling (rG=0.18, s.e
84 ine associations between lifestyle (smoking, alcohol consumption, and activity levels) and deficienci
85 nd was further stratified by smoking status, alcohol consumption, and body mass index (BMI).
86 ng SSc status, age, sex, education, smoking, alcohol consumption, and body mass index, only SSc statu
87 sted for age, race, educational level, daily alcohol consumption, and cohort.
88  and 95% CIs, adjusting for smoking history, alcohol consumption, and detection of HPV-16 for beta- a
89 , including breast-feeding, tobacco smoking, alcohol consumption, and exposure to domesticated furry
90 , weight change since age 21 years, smoking, alcohol consumption, and family histories of myocardial
91 ate hypothetical effects of habits (smoking, alcohol consumption, and fat and carbohydrates consumpti
92 he emergency department because of excessive alcohol consumption, and healthy volunteers.
93 when adjusted for current cigarette smoking, alcohol consumption, and illicit drug use.
94  socio-demographic characteristics, smoking, alcohol consumption, and physical activity was assessed
95 nd handgrip strength), behavioural (smoking, alcohol consumption, and physical activity), socioeconom
96  morbidity and mortality, and tobacco usage, alcohol consumption, and poor oral hygiene are establish
97 fter adjusting for waist, physical activity, alcohol consumption, and smoking (P < 0.0007).
98 enarche, age at first birth, family history, alcohol consumption, and smoking status, which suggests
99                                         BMI, alcohol consumption, and smoking were associated with li
100 nd social activity, physical activity, diet, alcohol consumption, and smoking-and cognition, adjustin
101                                      Chronic alcohol consumption appears to perturb the coordinated m
102 erations following the first experience with alcohol consumption are not fully understood.
103 eta signaling dramatically reduced excessive alcohol consumption, as did selective inhibition of D1-M
104 e-inter ventions produce small reductions in alcohol consumption at 6 months, but there is little evi
105 birth for higher paternal, but not maternal, alcohol consumption before pregnancy, and similar but we
106  this increased harm reflects differences in alcohol consumption between these socioeconomic groups,
107 ons > 80 mg/dl) suppressed, whereas moderate alcohol consumption (blood ethanol concentrations < 50 m
108 ctors assessed at baseline included smoking, alcohol consumption, body mass index, and serum levels o
109 tatus, diabetes mellitus, educational level, alcohol consumption, body mass index, physical activity,
110 , education, hypertension duration, smoking, alcohol consumption, body mass index, sedentary behavior
111  biologically proximal environmental factors alcohol consumption, body mass index, smoking and matern
112 ve role of accumbal indirect pathway D2Rs in alcohol consumption but emphasize their importance in pr
113 LDH2 and ADH1B, are strongly associated with alcohol consumption but have limited impact in European
114  infection should be counseled against heavy alcohol consumption, but complete abstinence may not be
115 ely higher cardiovascular risk following any alcohol consumption, but, by 24 hours, only heavy alcoho
116                                      Indeed, alcohol consumption can disrupt the intestinal epithelia
117                          KEY POINTS: Chronic alcohol consumption causes a spectrum of liver diseases,
118                                  Obesity and alcohol consumption contribute to steatohepatitis, which
119 -44 years in Nurses' Health Study II who had alcohol consumption data in 1991.
120                   Our data show that chronic alcohol consumption decreases BAT mass, with a resultant
121 in alcohol use has revealed a trend in which alcohol consumption decreases or ceases immediately foll
122 l and bacterial infections, whereas moderate alcohol consumption decreases the incidence of colds and
123 ponse was defined as complete abstinence (no alcohol consumption during 3 months of acamprosate treat
124 , and naturalistic measures revealed reduced alcohol consumption during the 1-week treatment phase an
125  independent phenotypes reflecting subjects' alcohol consumption during the past year, based on self-
126 atment) while nonresponse was defined as any alcohol consumption during this period.
127 her adjustment for body mass index, smoking, alcohol consumption, education, and urinary sodium and m
128 le model, we adjusted for age, sex, smoking, alcohol consumption, education, diet, and other physical
129 agnosis of AH, defined as a history of heavy alcohol consumption, elevated AST and/or ALT (<300 U/L),
130   For systolic blood pressure, self-reported alcohol consumption emerged as our top finding (a 0.04 i
131 ls from advantaged areas for given levels of alcohol consumption, even after accounting for different
132 ndings corroborate our hypothesis that heavy alcohol consumption facilitates use of alternative energ
133 ass index, history of diabetes mellitus, and alcohol consumption from questionnaires to identify unde
134  reported to be associated with variation in alcohol consumption, genetic factors are estimated to ex
135 responding to 10,413 patient-months at risk, alcohol consumption (&gt;/=30 g/day) was associated with mo
136  was conducted to estimate its relation with alcohol consumption habits separately in both sets.
137                                      Current alcohol consumption had differing associations by clinic
138                                              Alcohol consumption has been associated with an increase
139                                     However, alcohol consumption has been associated with both benefi
140                                              Alcohol consumption has been linked to over 200 diseases
141                             Compared with no alcohol consumption, heavy alcohol intake is associated
142 istic regression that accounted for smoking, alcohol consumption, hepatitis infection, and other esta
143 factor profile to the lowest weight gain, no alcohol consumption, high physical activity level, breas
144 sive disorder, anxiety disorder, smoking and alcohol consumption, illicit substance use, ever having
145    Here, we test the hypothesis that chronic alcohol consumption impairs retinoic acid signaling in b
146 de association study (GWAS) of self-reported alcohol consumption in 112 117 individuals in the UK Bio
147            Voluntary prolonged and excessive alcohol consumption in a 2-bottle choice procedure incre
148 -evoked plasticity in the DMS contributes to alcohol consumption in a cell type-specific manner.
149 nslocation within both regions reduced binge alcohol consumption in a manner requiring intact group 1
150 ated brain region, were sufficient to reduce alcohol consumption in dependent animals.
151 the hypothesis that TLR4 regulates excessive alcohol consumption in different species and different m
152 ting this projection is sufficient to reduce alcohol consumption in HAD mice.
153 armacotherapy for tobacco addiction, reduces alcohol consumption in humans and rodents.
154 ecule inhibitors of PKCepsilon should reduce alcohol consumption in humans.
155  twins, supporting a possible causal role of alcohol consumption in lowering CAD death risk.
156                                     Moderate alcohol consumption in patients with nonalcoholic fatty
157 iously demonstrated that moderate adolescent alcohol consumption in rats promotes suboptimal decision
158 xclude former drinkers, who may have changed alcohol consumption in response to diagnosis.
159 eceptors partially reversed the reduction in alcohol consumption in RGS6(-/-) animals.
160 for blood pressure, waist circumference, and alcohol consumption in the Chinese context.
161 ed a genome-wide association study (GWAS) of alcohol consumption in the large Genetic Epidemiology Re
162 st target liver injury in the short term and alcohol consumption in the long term; thus, health agenc
163                                              Alcohol consumption in western pregnant women is not unc
164 od pressure, physical activity, smoking, and alcohol consumption) in late adolescence using a cross-c
165                                              Alcohol consumption increased the risk of clinical AL pr
166                  Importantly, we report that alcohol consumption increases the complexity of dendriti
167           Together, our results suggest that alcohol consumption increases the expression of Fgf2 in
168               Here, we report that excessive alcohol consumption increases the translation of downstr
169 les of systemic administration of alcohol or alcohol consumption induces a long-lasting increase in A
170                                              Alcohol consumption is a complex trait determined by bot
171                                    Excessive alcohol consumption is a known risk factor for stroke, b
172  commonly abused drug worldwide, and chronic alcohol consumption is a major etiological factor in the
173                                      Chronic alcohol consumption is accompanied by intestinal dysbios
174                                      Chronic alcohol consumption is accompanied by intestinal dysbios
175           The mechanism by which the rate of alcohol consumption is altered following surgery has bee
176                                         High alcohol consumption is associated observationally and ge
177          Recent studies also have shown that alcohol consumption is associated with alterations in th
178                                    Excessive alcohol consumption is associated with cardiomyopathy, b
179           We tested the hypothesis that high alcohol consumption is associated with high IgE levels a
180                                         High alcohol consumption is associated with high IgE levels i
181                                              Alcohol consumption is associated with increased risk of
182                                 Higher usual alcohol consumption is associated with lower CAD mortali
183                      We investigated whether alcohol consumption is associated with risk of cutaneous
184                            Moderate, regular alcohol consumption is generally associated with a lower
185  disease associated with different levels of alcohol consumption is higher for patients infected with
186                                Evidence that alcohol consumption is inversely associated with long-te
187                                     Although alcohol consumption is linked to increased aggression, i
188                                              Alcohol consumption is proposed to be the third most imp
189    Increasing evidence suggest that low-dose alcohol consumption (LAC) reduces the incidence and impr
190  and sCD163 were higher among ED with recent alcohol consumption (last drink <10 days before enrollme
191        BACKGROUND & AIMS: Chronic, excessive alcohol consumption leads to alcoholic liver disease (AL
192 observational studies; however, whether high alcohol consumption leads to high IgE levels and allergi
193 ts was negatively correlated with subsequent alcohol consumption level.
194           This loop leads to facilitation of alcohol consumption, marking FGF2 as a potential new the
195 al activity, fast-food consumption, smoking, alcohol consumption, marriage, and childbearing (women)
196            Further, the results suggest that alcohol consumption may activate endothelial EVs towards
197 er 60 years old, adenomatous polyp and heavy alcohol consumption may affect the risk of development o
198                                              Alcohol consumption may be a modifiable lifestyle factor
199    Low dosages (</=1.37 g of alcohol/day) of alcohol consumption may be beneficial to prevent periodo
200  Observational studies suggest that moderate alcohol consumption may be protective for cardiovascular
201 'Adaptive' responses of the liver to chronic alcohol consumption may underlie the development of cell
202 eful diagnostic test to detect current heavy alcohol consumption.Molecular Psychiatry advance online
203           Further dissection of genes within alcohol consumption networks revealed the potential inte
204  unacceptable harmful consequences of excess alcohol consumption, obesity, and viral hepatitis.
205 cant SNP-based heritability of self-reported alcohol consumption of 13% (se=0.01).
206 he wearable sensor has the ability to detect alcohol consumption of up to 11 standard drinks in the U
207 f this study is to investigate the impact of alcohol consumption on clinical attachment loss (AL) pro
208  of this study is to determine the effect of alcohol consumption on the levels of subgingival periodo
209 d to encourage those who cannot reduce their alcohol consumption on their own, despite substantial ha
210            Exosomes isolated from sera after alcohol consumption or from in vitro ethanol-treated hep
211 se or diabetics or pediatric) and no data on alcohol consumption or other liver diseases.
212 OR, 2.18; 95% CI, 1.26 to 3.78) and moderate alcohol consumption (OR, 2.09; 95% CI, 1.14 to 3.83) amo
213 ed harmful either to individuals (e.g., high alcohol consumption) or the collective (e.g., high energ
214 erence, body mass index, smoking status, and alcohol consumption over a 17-year period both before an
215                                Data on usual alcohol consumption over the past year were collected.
216 en the FTO variant and each of: frequency of alcohol consumption (P=3.0 x 10(-4)); deviations from me
217         Adjustment for age, sex, heart rate, alcohol consumption, pack-years of smoking, all componen
218 social integration, depressive symptoms, and alcohol consumption partially mediated the association a
219 um as an important neuroanatomical region in alcohol consumption phenotype and as a target for pharma
220 ce for a causative role of the cerebellum in alcohol consumption phenotype is lacking.
221 erebellar response to alcohol contributes to alcohol consumption phenotype, and targeting the cerebel
222 r responses to alcohol vary as a function of alcohol consumption phenotype, representing a potential
223 sly reported SNP rs1229984 in ADH1B and both alcohol consumption phenotypes (OR=0.79, P=2.47 x 10(-20
224                        We assessed these two alcohol consumption phenotypes in each race/ethnicity gr
225 ndex, socioeconomic position, diet, smoking, alcohol consumption, physical activity level, and C-reac
226  analyses: weight change since age 18 years, alcohol consumption, physical activity level, breastfeed
227 GRSs on lipid levels were modulated by diet, alcohol consumption, physical activity, and smoking or t
228  body mass index, education, smoking status, alcohol consumption, physical activity, family history o
229             We show that moderate adolescent alcohol consumption potentiates stimulus-evoked phasic d
230 Together, our results suggest that excessive alcohol consumption produces a change in BDNF signaling
231                  Specifically, we found that alcohol consumption produces a long-lasting enhancement
232 drome, the first three questions focusing on alcohol consumption provide information that is comparab
233 .21; P < .001), smoking (r = 0.10; P < .02), alcohol consumption (r = 0.11; P = .01), cardiovascular
234 - 11%, p = 0.005) and in proportion to daily alcohol consumption (r = 0.36, p = 0.01) but found that
235 18; p<0.0001) and positively correlated with alcohol consumption (r=0.12; p<0.0001).
236                       Overall, chronic heavy alcohol consumption reduced the expression of immune gen
237                 Recommendations for moderate alcohol consumption remain controversial, particularly i
238 ogical mechanism underpinning its effects on alcohol consumption remains to be determined.
239       We assessed the relation between acute alcohol consumption, reproductive hormones, and markers
240                                          The alcohol consumption revealed in this study is similar to
241 lyps (RR, 2.18; 95% CI, 1.18-4.61) and heavy alcohol consumption (RR, 1.82; 95% CI, 1.04-3.08) were i
242 ic variant in the ALDH2 gene associated with alcohol consumption, rs671, we performed a Mendelian ran
243 predict rate of binging during an individual alcohol consumption session.
244  studied extensively-they include pattern of alcohol consumption, sex, environmental factors (such as
245  to families, and the documented increase in alcohol consumption since removal of the above-inflation
246 r putative confounders (total energy intake, alcohol consumption, smoking status, and physical activi
247 D13 rs623908, CETP rs820299, LIPA rs1412444, alcohol consumption, smoking status, or physical activit
248 ent employment), and behavioral (eg, regular alcohol consumption, smoking) domains.
249 ss index, healthy diet, sedentary lifestyle, alcohol consumption, smoking, and urinary sodium excreti
250 festyle risk factors (body mass index [BMI], alcohol consumption, smoking, diet, and exercise).
251 pocampal volume was associated with previous alcohol consumption (standardized estimate, -0.04; P = .
252 ted to explain about half of the variance in alcohol consumption, suggesting that additional loci rem
253  in the DMS, and that striatal FGF2 promotes alcohol consumption, suggesting that FGF2 in the DMS is
254 justed HRs for a twin with 10-g higher daily alcohol consumption than his co-twin were 0.90 (95% CI:
255 th in vivo genetic perturbations and chronic alcohol consumption that cause myopathy.
256         Unlike behaviors such as smoking and alcohol consumption, the effect of GWG throughout pregna
257 cular effects of habitual moderate and heavy alcohol consumption, the immediate risks following alcoh
258 icking glutamatergic strengthening, promoted alcohol consumption; the same effect was induced by D2-M
259 a wearable biochemical sensor for monitoring alcohol consumption through the detection and quantifica
260  but suppressing activity with hM4Di reduced alcohol consumption to a similar extent as lesioning wit
261  153) of the control group had reduced their alcohol consumption to sex-specific National Institute o
262 this study is similar to that of the general alcohol consumption tradition in Finland.
263 plicating AUTS2, SGOL1 and SERPINC1 genes in alcohol consumption traits in non-Hispanic whites.
264  obtained baseline demographics and data for alcohol consumption (units per week and binge drinking)
265                In contrast, chronic moderate alcohol consumption upregulated the expression of genes
266  adjusted for possible confounders (maternal alcohol consumption, use of folic acid supplements, age,
267 erebral ischemic small-vessel disease, heavy alcohol consumption (vs light to moderate consumption; r
268 tic correlation (rG) between male and female alcohol consumption was 0.90 (s.e.=0.09, P-value=7.16 x
269                                              Alcohol consumption was assessed at baseline by asking p
270  associated with a higher risk, and moderate alcohol consumption was associated with a lower risk of
271                   Compared with nondrinking, alcohol consumption was associated with a modest nonline
272 w-risk dietary choice together with moderate alcohol consumption was associated with a relative risk
273                                     Moderate alcohol consumption was associated with an immediately h
274                                         High alcohol consumption was associated with high IgE levels
275                                  In general, alcohol consumption was associated with higher levels of
276  in this population of younger women, higher alcohol consumption was associated with increased risk o
277                                              Alcohol consumption was not associated with breast cance
278                                              Alcohol consumption was not associated with breast cance
279                                              Alcohol consumption was not associated with total mortal
280                      A negative influence of alcohol consumption was observed on clinical and microbi
281                         We evaluated whether alcohol consumption was prospectively associated with CA
282 ndividuals at risk for liver fibrosis due to alcohol consumption, we found elastography to be an exce
283 n and enhanced immune response with moderate alcohol consumption, we performed a transcriptome analys
284                           Four categories of alcohol consumption were defined: 1) non-drinker; 2) </=
285 late MSN activity, and their consequences on alcohol consumption were measured.
286 ctivity, healthy diet, and light-to-moderate alcohol consumption were positively associated with cogn
287                                     Data and alcohol consumption were prospectively recorded in 398 p
288 adenomatous polyp, current smoking and heavy alcohol consumption were significantly associated with d
289 alth behaviors (diet, physical activity, and alcohol consumption) were associated with lower mortalit
290 in cognitive abilities associated with heavy alcohol consumption, whereas increased cerebellar connec
291 FGF2 into the dorsomedial striatum increases alcohol consumption, whereas inhibiting the endogenous F
292 seeking/low anxiety associated with enhanced alcohol consumption, which may be related to cortex func
293 for biological networks related to excessive alcohol consumption, which may prove fundamentally impor
294                                              Alcohol consumption (WHO drinking risk levels) and alcoh
295     Our results suggest that associations of alcohol consumption with blood pressure and HDL-choleste
296             We previously associated chronic alcohol consumption with lower intestinal levels of the
297 sociations of lifetime and 1-y prediagnostic alcohol consumption with relevant prognostic outcomes we
298 ex (weight (kg)/height (m)(2)), smoking, and alcohol consumption with risk of fatal prostate cancer i
299 indings implicating the KLB and GCKR loci in alcohol consumption, with strongest associations observe
300  childbirth, and that risk did not differ by alcohol consumption (yes vs. no) or racial/ethnic group.

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