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1 se, chronic lung disease, diabetes mellitus, alcoholism).
2 me 4q has been linked to alcohol dependence (alcoholism).
3 ues may thus be an inherited risk factor for alcoholism.
4 everal neuropsychiatric disorders, including alcoholism.
5 in the human brain and how it is affected in alcoholism.
6 relief and its role in determining risk for alcoholism.
7 in subjects with a greater genetic risk for alcoholism.
8 to important interactions between stress and alcoholism.
9 ation of the NPSR as a therapeutic target in alcoholism.
10 ld be further evaluated for the treatment of alcoholism.
11 thanol is inversely correlated with risk for alcoholism.
12 may be a critical step in the progression of alcoholism.
13 logy of many psychiatric disorders including alcoholism.
14 pression, anxiety disorders, drug abuse, and alcoholism.
15 receptor as a useful therapeutic target for alcoholism.
16 t stimuli all can affect individual risk for alcoholism.
17 ial response to pharmacological treatment of alcoholism.
18 2) have been shown to play a central role in alcoholism.
19 unique therapeutic effects in narcolepsy and alcoholism.
20 n the Collaborative Study on the Genetics of Alcoholism.
21 pothesis generation and follow-up studies of alcoholism.
22 ect individuals' vulnerability to developing alcoholism.
23 pharmacological target for the treatment of alcoholism.
24 ve a suitable target for reducing relapse in alcoholism.
25 erience are formed during the development of alcoholism.
26 matter atrophy in poor clinical outcomes in alcoholism.
27 mber of neuropsychiatric diseases, including alcoholism.
28 on of the use of EEG as an endophenotype for alcoholism.
29 e behavior and pharmacological therapies for alcoholism.
30 could play an important role in the risk for alcoholism.
31 tructured Assessment for Drug Dependence and Alcoholism.
32 ol consumption in a preclinical rat model of alcoholism.
33 ch may play a key role in the development of alcoholism.
34 ed an analysis of genomic studies related to alcoholism.
35 m the Collaborative Study on the Genetics of Alcoholism.
36 play an important role in the development of alcoholism.
37 as hence become a possible strategy to treat alcoholism.
38 pression, is associated with higher risk for alcoholism.
39 new target for therapeutic intervention for alcoholism.
40 s well as represent a therapeutic target for alcoholism.
41 being tested clinically for the treatment of alcoholism.
42 otects nearly all carriers of this gene from alcoholism.
43 ents a potential medication for treatment of alcoholism.
44 ants further investigation as a treatment in alcoholism.
45 s a clear need for new therapeutics to treat alcoholism.
46 mi-Structured Assessment for the Genetics of Alcoholism.
47 derlie some of the behaviors associated with alcoholism.
48 odeling, caused by histone modifications, in alcoholism.
49 o our understanding of the neural control of alcoholism.
50 a potential target for clinical treatment of alcoholism.
51 us, NFKB1 is an excellent candidate gene for alcoholism.
52 association of NFKB1, located at 4q24, with alcoholism.
53 se donors' hearts regardless of a history of alcoholism.
54 levels of D(2) receptors may protect against alcoholism.
55 likely to be complicated by panic attacks or alcoholism.
56 dehydrogenase (ADH) genes, affected risk for alcoholism.
57 the study of complex human disorders such as alcoholism.
58 ndividuals are either alcoholics or prone to alcoholism.
59 increased in those at high familial risk for alcoholism.
60 actures), high body mass index, smoking, and alcoholism.
61 mi-Structured Assessment for the Genetics of Alcoholism.
62 ia opioid receptors, and is also involved in alcoholism.
63 sferases as potential therapeutic targets in alcoholism.
64 a mifepristone as a therapeutic strategy for alcoholism.
65 armacotherapeutic target in the treatment of alcoholism.
66 nts associated with early onset drinking and alcoholism.
67 dolescents and young adults at high risk for alcoholism.
68 dentify novel pharmacologic targets to treat alcoholism.
69 eased dopamine transmission in the cortex in alcoholism.
70 ence, with implications for vulnerability to alcoholism.
71 are impaired in addictive disorders such as alcoholism.
72 investigated as a promising target to treat alcoholism.
73 executive function, relapse, and outcome in alcoholism.
74 st to mitigate the pulmonary consequences of alcoholism.
75 used for several decades in the treatment of alcoholism.
76 e may represent an important risk factor for alcoholism.
77 ediated epigenetic mechanisms in anxiety and alcoholism.
79 proportion of alcoholic etiology and active alcoholism (37% versus 10%), higher platelet count, and
80 e affected individuals with earlier onset of alcoholism (55% of the sample with onset < or =21 years)
81 ailure, 30% for self-reported alcohol use or alcoholism, 6% for body mass index, and 20% for unemploy
82 US National Institute on Alcohol Abuse and Alcoholism (AA012388, AA017168, AA005965, AA013521-INIA)
83 the type of ACLF precipitating event (active alcoholism/acute alcoholic hepatitis, bacterial infectio
85 nt and combined effects of HIV infection and alcoholism along with other factors (acquired immune def
94 tudies have suggested an association between alcoholism and DNA methylation, a mechanism that can med
98 lone (n = 87), HIV infection alone (n = 42), alcoholism and HIV infection comorbidity (n = 52) and no
99 or early diagnosis and improved prognosis of alcoholism and identify future pharmacological targets f
102 preliminary work on the pharmacogenetics of alcoholism and its treatment has been promising, the ass
103 A link between highly stigmatized views of alcoholism and lack of services suggests that stigma red
104 talloid volumes, more often had a history of alcoholism and liver disease, and had greater ventilator
105 n plays a role in jeopardizing recovery from alcoholism and may serve as a neural marker to identify
108 lop novel pharmacological therapies to treat alcoholism and other addiction-related and compulsive be
109 a stress-related neuropeptide implicated in alcoholism and other addictions, further amplifies the P
112 ce variation in this gene is associated with alcoholism and Parkinson's disease, among other disorder
115 ously been associated to a decreased risk of alcoholism and shown to be under selection in East Asian
117 gic state contributes to the pathogenesis of alcoholism and that acamprosate may exert its actions by
118 o further characterize genetic influences in alcoholism and the effects of alcohol consumption on pre
122 ffect of naltrexone as a pharmacotherapy for alcoholism, and a recent study has suggested that the ef
123 es, inflammatory bowel disease, hepatitis B, alcoholism, and alcoholic liver disease did not reduce t
126 with positive family history, early onset of alcoholism, and maximum number of drinks in adults as we
129 the National Institute on Alcohol Abuse and Alcoholism, and the National Institute on Drug Abuse.
131 occurrence, by age 50, of major depression, alcoholism, and use of mood-altering drugs (tranquilizer
137 that therapeutic responses to naltrexone in alcoholism are moderated by variation at the mu-opioid r
138 individual differences in alcohol abuse and alcoholism, as well as represent a therapeutic target fo
139 , the Collaborative Study on the Genetics of Alcoholism (ascertained for alcohol use disorder; n = 64
140 hat subtle white matter fiber degradation in alcoholism attenuated the normal pattern of hemispheric
141 hol (National Institute on Alcohol Abuse and Alcoholism binge model) or chow diets along with water c
142 rative disorder, personality traits, type II alcoholism, borderline personality disorders, aggressive
143 Asian populations and reduces their risk for alcoholism, but because of very low allele frequencies t
144 riety of neuropsychiatric diseases including alcoholism, but development of NMDAR antagonists for the
145 Acamprosate is approved for the treatment of alcoholism, but its mechanism of action remains unclear.
146 luntary alcohol consumption is a hallmark of alcoholism, but its neural substrates remain unknown.
147 rawal is included in diagnostic criteria for alcoholism, but the contribution of acute withdrawal rel
148 vels of D(2) receptors could protect against alcoholism by regulating circuits involved in inhibiting
149 herapeutic value of the DOR for treatment of alcoholism by showing that its relevant synaptic action
150 bjects (n = 57) as well as in a rat model of alcoholism by state-of-the-art (1)H-magnetic magnetic re
152 ompromise of microstructural connectivity in alcoholism can influence modulation of functional connec
154 of control over drinking is a key deficit in alcoholism causally associated with malfunction of the m
155 To determine if ethanol consumption and alcoholism cause global DNA methylation disturbances, we
156 d the Collaborative Study on the Genetics of Alcoholism (COGA), we identified a subnetwork of 39 gene
157 m the Collaborative Study on the Genetics of Alcoholism (COGA), we performed a genome-wide associatio
158 : the Collaborative Study on the Genetics of Alcoholism (COGA); the Study of Addiction, Genetics, and
160 iseases such as obesity, mood disorders, and alcoholism could be better resolved by the use of small-
162 In 2001-2002, women with a family history of alcoholism (defined as having a biological parent or sib
163 pse risk.SIGNIFICANCE STATEMENT Persons with alcoholism demonstrate increased motor impulsivity durin
164 from humans for the glutamate hypothesis of alcoholism, demonstrate the comparability of human and a
165 chiatric disorders, such as addiction and/or alcoholism, depression, anxiety, epilepsy and schizophre
166 neurobehavioral disorders including anxiety, alcoholism, depression, autism, and obsessive-compulsive
167 hy associated with vincristine chemotherapy, alcoholism, diabetes, and human immunodeficiency virus/a
168 trics which are normally impacted in chronic alcoholism (e.g., reaction time and threshold detection)
169 n immunodeficiency virus (HIV) infection and alcoholism each carries liability for disruption of brai
173 (the Collaborative Study on the Genetics of Alcoholism) genome-wide association study (GWAS) data se
174 endency for various behavioral components of alcoholism have been identified; recent applications of
175 ndividuals family-history positive (FHP) for alcoholism have increased risk for the disorder, which m
177 ce status significantly correlated with age, alcoholism, hypoalbuminemia, hyperbilirubinemia, renal i
178 the National Institute on Alcohol Abuse and Alcoholism in a large representative sample of US adults
179 DH genes and analyzed their association with alcoholism in a set of families with multiple alcoholic
180 type consisting of compulsivity, anxiety and alcoholism in addition to the characteristic motor pheno
181 effects of this allele on the development of alcoholism in adolescents and young adults, and demonstr
184 the National Institute on Alcohol Abuse and Alcoholism in collaboration with the Office of Dietary S
186 l relevance to adolescent binge drinking and alcoholism in humans to test whether alcohol damages mye
187 1, and gamma1 subunits genetically linked to alcoholism in humans, our findings indicate that these n
190 rphism has been convincingly associated with alcoholism in numerous studies of several populations in
193 mal atRA shares pathological conditions with alcoholism, inhibition of retinol (vitamin A) activation
194 hat disulfiram, a drug used to treat chronic alcoholism, inhibits G. lamblia CK and kills G. lamblia
195 f the Integrative Neuroscience Initiative on Alcoholism (INIA-Neuroimmune) consortium participated in
196 f the Integrative Neuroscience Initiative on Alcoholism (INIA-Neuroimmune) consortium tested the hypo
215 est, given the fact that early-onset type II alcoholism is more common among men and that, among addi
224 drug abuse pharmacotherapies, especially for alcoholism, little is known about the role of this syste
225 ol use disorder, including family history of alcoholism, male sex, impulsivity, and low level of resp
226 ave shown that the effects of naltrexone for alcoholism may be moderated by the Asn40Asp single-nucle
229 ath with significantly raised mortality were alcoholism, motor vehicle accidents with pedestrians, mo
231 60% diminished in subjects with a history of alcoholism (n = 6) as compared to subjects without a his
232 the association between alcohol dependence (alcoholism not in remission and/or alcohol withdrawal) a
233 g obsessive-compulsive disorder, autism, and alcoholism, occur more frequently in ALS kindreds than i
235 m the Collaborative Study of the Genetics of Alcoholism on alcohol dependence in a sample of moderate
236 this research is to determine the effects of alcoholism on zinc bioavailability and alveolar macropha
237 inor allele of rs1439047 on NTRK2 delays the alcoholism onset age, but the additive minor allele of r
238 nor allele of rs63319 on ALDH1A1 advance the alcoholism onset age; and the dominant minor allele of r
240 ological parent or sibling with a history of alcoholism or alcohol problems) had 49% higher odds of o
241 symptoms of nausea and diarrhea, history of alcoholism or chronic lung disease, and abnormal laborat
242 y gastrointestinal symptoms and a history of alcoholism or chronic lung disease, may be useful in gui
243 hippocampus in PTSD is unrelated to comorbid alcoholism or to chronicity, this study estimated hippoc
244 CI: 2.2, 14.5), self-reported alcohol use or alcoholism (OR = 2.9, 95% CI: 1.5, 5.4), body mass index
246 hizophrenia, psychosis, suicide, depression, alcoholism, or autism (relative risk [RR], 1.50; 95% CI,
247 ntially traumatic lifetime noncombat events, alcoholism, or the presence of a comorbid affective or a
248 Identification of genes predisposing to alcoholism, or to alcohol-related behaviors in animal mo
249 e that a gene(s) on chromosome 9p influences alcoholism, our results can facilitate human research on
250 ere the Child-Pugh score (p = 0.003), active alcoholism (p = 0.035), and no antibiotic prophylaxis (p
251 tions in NFKB1 appear to affect the risk for alcoholism, particularly contributing to an earlier onse
252 genes may contribute to the vulnerability to alcoholism, particularly in the context of environmental
253 Food and Drug Administration (FDA)-approved alcoholism pharmacotherapy, naltrexone, relative to plac
255 ry artery disease, congestive heart failure, alcoholism, proteinuria, reduced kidney function, and hy
256 unction in patients with a family history of alcoholism, raising the possibility that alcohol effects
257 ntrations and reported no history of stroke, alcoholism, recent anemia therapy, or diseases of the li
259 iation (after Bonferroni correction) with an alcoholism-related phenotype for four different single-n
262 miologic support for a link between familial alcoholism risk and obesity in women and possibly in men
263 We did an extended longitudinal study of alcoholism's trajectory of effect on selective fibre bun
265 mmon, complex psychiatric diseases including alcoholism, schizophrenia, and anxiety disorders, althou
266 the National Institute on Alcohol Abuse and Alcoholism showed that liver cirrhosis was the 12th lead
270 n expression such as psychological distress, alcoholism, substance use, and delirium allow clinicians
271 n the Collaborative Study on the Genetics of Alcoholism, suggest that it is involved in a general ext
272 e, an FDA-approved drug for the treatment of alcoholism, suggesting that their increased glutamatergi
273 sk-free model to simultaneously characterize alcoholism susceptibility and onset age in 65 independen
274 minor allele of rs2134655 on DRD3 increases alcoholism susceptibility; the dominant minor allele of
276 Immunosuppression is a major complication of alcoholism that contributes to increased rates of opport
278 conveys a well-confirmed protection against alcoholism, that modern phenotypic manifestation does no
279 rmine whether this allele is associated with alcoholism, the authors conducted a Human Genome Epidemi
280 ession, antisocial personality disorder, and alcoholism, the authors could identify the original crit
281 idence of association of this insertion with alcoholism; the longer allele (with the indel), which ha
282 m the Collaborative Study on the Genetics of Alcoholism to identify novel genes affecting risk for al
284 te that MT-7716 is a promising candidate for alcoholism treatment remaining effective with chronic ad
285 GABAB) receptor undergoes splicing and is an alcoholism treatment target, but there is little informa
286 support a personalized medicine approach to alcoholism treatment that takes into account OPRM1 genot
289 anagement and remained after controlling for alcoholism typology and baseline demographic differences
290 mean age 25, with a varied family history of alcoholism underwent two [(11)C]RAC PET scans: one while
292 s tested whether perceived stigmatization of alcoholism was associated with a lower likelihood of rec
294 within that region that are associated with alcoholism, we have tested the association of NFKB1, loc
295 op 14 Collaborative Study of the Genetics of Alcoholism, where the MQLS detects genomewide significan
296 were only significant in the two groups with alcoholism, which exhibited 0.65-1.2 SD abnormalities in
299 osal regions were differentially affected by alcoholism, with the genu more affected than the spleniu
300 , the Collaborative Study of the Genetics of Alcoholism, yielded replication for DKK2 but not EGF.
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