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1 o neuronal hyperexcitability observed during alcohol withdrawal.
2 especially for individuals with histories of alcohol withdrawal.
3 ounted for 68% of the genetic variability in alcohol withdrawal.
4 line) were sensitive to alcohol exposure and alcohol withdrawal.
5 alysis) in 96 sAUD patients hospitalized for alcohol withdrawal.
6 ations, 12 889 (56.3%) used an order set for alcohol withdrawal.
7 ed morbidity, including hospitalizations for alcohol withdrawal.
8 the negative affective state associated with alcohol withdrawal.
9 , probably in the context of intoxication or alcohol withdrawal.
10 ents regimens for patients hospitalized with alcohol withdrawal.
11 e GABA hyposensitivity of VTA neurons during alcohol withdrawal.
12 were absent in MrgprB2-deficient mice during alcohol withdrawal.
13 stress and anxiety symptoms during drug and alcohol withdrawal.
14 plays a role in the aversive consequences of alcohol withdrawal.
15 mood states like anxiety experienced during alcohol withdrawal.
16 ement of the nicotinic cholinergic system in alcohol withdrawal.
17 trial, intranasal oxytocin potently blocked alcohol withdrawal.
18 ce of the Fkbp5 gene enhances sensitivity to alcohol withdrawal.
19 ptor availability during acute and prolonged alcohol withdrawal.
20 e 4 with a large effect on predisposition to alcohol withdrawal.
21 subspecialty consultations, and anticipated alcohol withdrawal.
22 onfidence interval 0.01 to 0.09)), opioid or alcohol withdrawal (0.14 (0.01 to 0.27)), and admissions
23 idence interval 0.08 to 0.69)) and opioid or alcohol withdrawal (0.31 (0.014 to 0.58)), but no change
25 number of 22-kHz USVs observed during acute alcohol withdrawal and a KOR agonist (U50,488) resulted
26 of the negative affective state produced by alcohol withdrawal and abstinence, which is critical for
27 e medical ICU solely for treatment of severe alcohol withdrawal and b) to determine whether a strateg
28 es negative affective states induced by both alcohol withdrawal and conditioned stimuli as being prod
30 assess patterns of neuronal activity during alcohol withdrawal and following reaccess in a well-char
31 negative affect during acute and protracted alcohol withdrawal and following stress in adulthood.
32 rasonic vocalizations (USVs) associated with alcohol withdrawal and KOR activation in adult male wist
33 nce for beneficial effects of KD on managing alcohol withdrawal and on reducing alcohol drinking.
34 pport the role of ceftriaxone in alleviating alcohol withdrawal and open a novel pharmacologic avenue
37 zenil uptake correlated with the severity of alcohol withdrawal and the number of days since the last
38 (KOR) system mediates phenotypes related to alcohol withdrawal and withdrawal-like negative affectiv
39 pendence (alcoholism not in remission and/or alcohol withdrawal) and sepsis, septic shock, and hospit
40 e admitted by a surgical service, have acute alcohol withdrawal, and be managed with pressure-control
41 trations, by drugs used for the treatment of alcohol withdrawal, and by taurine, an ingredient of cer
42 e in the management of seizures secondary to alcohol withdrawal, and in those due to theophylline or
43 , as determined by M30 levels, occurs during alcohol withdrawal, and survival data point toward a nov
44 und to be increased, or not affected, during alcohol withdrawal, and to show no differences from CON
45 f AC differs from DCM and relies directly on alcohol withdrawal, as left ventricular ejection fractio
46 fore tested whether GDNF in the VTA reverses alcohol withdrawal-associated DA deficiency and/or posse
47 06) in heavy drinkers primarily admitted for alcohol withdrawal before and after alcohol detoxificati
48 narrowing are not reversed immediately after alcohol withdrawal but persist during early abstinence.
50 ble for 26% of the genetic variance in acute alcohol withdrawal convulsion liability to a >35 centimo
51 pression-like behavior in animals undergoing alcohol withdrawal, further advocating the RMTg as a pot
52 central nucleus of the amygdala (CeA) during alcohol withdrawal has been hypothesized to induce high
53 a medical ICU solely for treatment of severe alcohol withdrawal have a high incidence of requiring me
54 ntly increased glutamate levels during acute alcohol withdrawal in corresponding prefrontocortical re
57 ons, screening, assessment, and treatment of alcohol withdrawal in the general hospital population.
60 al.(1) identify a peripheral mechanism of an alcohol-withdrawal-induced headache-like condition, whic
63 or developing novel treatment approaches for alcohol-withdrawal-induced mood and anxiety disorders.
67 ribute to adverse affective disorders during alcohol withdrawal, likely through PKC-gamma/betaCaMKII-
69 the deficiency of RMTg NOP signaling during alcohol withdrawal mediates anxiety- and depression-like
71 m tremens, the most serious manifestation of alcohol withdrawal, occurs in approximately 5% of hospit
72 red either following short periods (24 h) of alcohol withdrawal, or 90 m following alcohol consumptio
73 or treating anxiety, epilepsy, muscle spasm, alcohol withdrawal, palliation, insomnia, and sedation a
77 f amygdala) and prevented the development of alcohol withdrawal-related anxiety in rats as measured b
80 interval-specific congenic lines, show that alcohol withdrawal severity is genetically correlated wi
81 reases in cell proliferation correlated with alcohol withdrawal severity, proliferation remained incr
85 that this effect was more pronounced during alcohol withdrawal, suggesting that AdipoR2 signaling ma
86 lyses indicated a significant interaction of alcohol withdrawal symptom score by treatment by full-do
87 ronic, heavy use increases the likelihood of alcohol withdrawal symptoms and associated secondary out
88 ntin has demonstrated efficacy in mitigating alcohol withdrawal symptoms and preventing relapse drink
90 These data support further evaluation of alcohol withdrawal symptoms as a prognostic indicator of
91 ol dependence (N=100) with varying levels of alcohol withdrawal symptoms assessed at treatment entry.
95 lly, to investigate the effect of MT-7716 on alcohol withdrawal symptoms, Wistar rats were withdrawn
100 ent of alcohol use disorder in patients with alcohol withdrawal symptoms: a randomized clinical trial
101 ption (r42 = -0.32, P < .05) and more severe alcohol-withdrawal symptoms (r38 = -0.35, P < .05).
103 al monotherapy is increasingly used to treat alcohol withdrawal syndrome (AWS) in hospitalized patien
110 ine occurrence, predictors, and prognosis of alcohol withdrawal syndrome and delirium tremens in pati
113 commonly used to treat complications such as alcohol withdrawal syndrome are often contraindicated by
115 ital length of stay, ICU length of stay, and alcohol withdrawal syndrome complications differed signi
118 factors, and screening tools associated with alcohol withdrawal syndrome in the ICU are reviewed.
122 rome complications differed significantly by alcohol withdrawal syndrome severity and were worse with
123 Mortality also significantly differed by alcohol withdrawal syndrome severity but was only greate
126 stigate non-y-aminobutyric acid pathways for alcohol withdrawal syndrome treatment; 2) harnessing ret
128 inical outcomes, pharmacologic treatment for alcohol withdrawal syndrome, and Clinical Institute With
129 s repeated alcohol use leading to tolerance, alcohol withdrawal syndrome, and physical and psychologi
130 ns, injury characteristics, risk factors for alcohol withdrawal syndrome, clinical outcomes, pharmaco
131 extremely complex, as manifestations such as alcohol withdrawal syndrome, craving and physical depend
132 , 68 adults with AUD, including a history of alcohol withdrawal syndrome, received 1,200 mg/day of ga
134 included pain, sedation, status asthmaticus, alcohol withdrawal syndrome, status epilepticus, and acu
135 ting critically ill patients including pain, alcohol withdrawal syndrome, status epilepticus, and acu
139 ize studies addressing the drug treatment of alcohol withdrawal syndromes in inpatient populations, w
140 al pharmacologic strategies for treatment of alcohol withdrawal syndromes in the critically ill.
141 pathophysiology, diagnosis, and treatment of alcohol withdrawal syndromes in the intensive care unit
142 h the diagnosis and treatment strategies for alcohol withdrawal syndromes in the intensive care unit.
143 ns in dopamine transporter (DAT) sites after alcohol withdrawal, the role of DAT in influencing eithe
144 tribute to neuronal hyperexcitability during alcohol withdrawal, these findings suggest an important
145 O) and wild-type (WT) mice were assessed for alcohol withdrawal using handling-induced convulsions (H
147 trexone-gabapentin group, while a history of alcohol withdrawal was associated with better response i
150 related to unhealthy alcohol consumption and alcohol withdrawal were invited to participate in a work
152 tral role for the LHb in hyperalgesia during alcohol withdrawal, which may be due in part to the supp
153 uroadaptations in GABAA receptor levels over alcohol withdrawal will provide critical insights for th
154 aptive changes in HPA axis regulation during alcohol withdrawal with concomitant effects on withdrawa
155 o identify, assess, risk-stratify, and treat alcohol withdrawal with evidence based interventions.
157 he observed increase in HDAC activity during alcohol withdrawal with the HDAC inhibitor, trichostatin
159 zation of trigeminal ganglia (TG) neurons in alcohol-withdrawal WT mice, but not in alcohol-withdrawa