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1 a-III excretion correlating with the rise in blood alcohol.
2 by ethanol (EtOH) at concentrations seen in blood alcohol after binge drinking, and diminished ALDH1
3 king that was associated with high levels of blood alcohol and a reduction in somatic symptoms of eth
4 ol doses; namely, a placebo dose [equivalent Blood Alcohol Concentration (BAC) = 0.00%], a low dose o
6 a significant difference in relation to the blood alcohol concentration (BAC) as a function of gende
7 effects of alcohol vary between limbs of the blood alcohol concentration (BAC) curve (i.e., whether B
12 ragastrically with the ethanol solution, the blood alcohol concentration (BAC) was found to peak late
14 wer body temperature (p = 0.045), and higher blood alcohol concentration (p = 0.012); vascular fillin
15 ge of 8.5 standard alcohol drinks (estimated blood alcohol concentration [eBAC]=0.115 g/dl) versus 3.
16 hat it is a criminal offense to drive with a blood alcohol concentration above the state's legal limi
17 ing as significant at doses as low as 0.026% blood alcohol concentration and increasing to moderate/l
18 nitoring chronic alcohol abstinence, whereas blood alcohol concentration and urinary EtG are the most
19 ect to demographic factors, injury type, and blood alcohol concentration and urine toxicology results
21 cle crashes was lower when laws specifying a blood alcohol concentration of 0.08 g/dl per se (laws st
22 usly administered 6% v/v ethanol to a target blood alcohol concentration of 0.08% or placebo between
23 tar rats exposed to alcohol vapor had a mean blood alcohol concentration of 176.2 mg/dl during the la
24 se decreased as both the child's age and the blood alcohol concentration of the child's driver increa
25 tion in the laboratory, the maximum achieved blood alcohol concentration was influenced in an allele-
27 ubation controls, (3) 3 g/kg/day of alcohol (blood alcohol concentration {BAC}=139.9 mg/dl), (4) 4 g/
28 dramine (50 mg), alcohol (approximately 0.1% blood alcohol concentration), or placebo, given at weekl
29 and peer norms) on alcohol expenditure, peak blood alcohol concentration, alcohol dependence, and acc
31 al aldehyde dehydrogenase, in part determine blood alcohol concentration, thereby contributing to the
33 ol concentrations equivalent to 0.05 to 0.08 blood-alcohol concentration-levels that would be mildly
35 binge alcohol drinking (intake resulting in blood alcohol concentrations (BACs) >/=80 mg% within a 2
38 t rodent models do not result in binge-level blood alcohol concentrations (BACs), and to better under
40 cant differences in vital signs or estimated blood alcohol concentrations between PT150 non-exposed a
41 quate to intoxicating through to supralethal blood alcohol concentrations in humans and provides an i
47 previous studies have focused on deficits at blood-alcohol concentrations (BACs) above about 0.04%.
50 ale (P < 0.0001), Black (P < 0.0001), have a blood alcohol content above 80 mg/dL (P < 0.0001), and s
52 At admission, 36.7% of e-scooter users had a blood alcohol content higher than the legal threshold (n
53 supported than opposed policies to lower the blood alcohol content limit for driving, prohibit alcoho
55 es (P<.001) during the ascending limb of the blood alcohol curve and remained significantly above bas
57 mal enhancement at 16 mM, close to the legal blood alcohol driving limit in most U.S. states (17.4 mM
58 to test the hypothesis that the presence of blood alcohol has a clinically significant impact on GCS
60 concentration six times lower than the legal blood-alcohol intoxication (driving) limit in most state
61 ng methamphetamine had a significantly lower blood alcohol level compared with the control group.
62 s a blood alcohol level of at least 0.05%; a blood alcohol level greater than 0; and a blood alcohol
64 ven at concentrations as low as 10 mm (legal blood alcohol level in the United States is below 0.08 g
65 as relevant and comparable to that seen at a blood alcohol level of 0.05%, the legal limit in many co
66 ary seatbelt laws, maximum speed limit laws, blood alcohol level of 0.08, and administrative license
67 ethanol in utero (average maternal and fetal blood alcohol level of 25 mg/dl) promotes premature tang
69 vel of at least 2.5 ng per milliliter plus a blood alcohol level of at least 0.05%; a blood alcohol l
74 ing; whereas, among those who had a negative blood-alcohol level and most likely were awake at the ti
77 rom the HS/Npt line) to achieve intoxicating blood alcohol levels (BALs) after binge-like drinking.
78 no significant differences between groups in blood alcohol levels (BALs), these results are not due t
79 gnificantly shorter sleeping time and higher blood alcohol levels after regaining reflex than adult r
80 olerance during adolescence and suggest that blood alcohol levels alone do not fully explain ethanol-
81 cts of intoxication, despite greater initial blood alcohol levels and ethanol hypothermia in the form
83 concentrations comparable with or less than blood alcohol levels associated with intoxication and at
87 of the distilled drinks promoted a spike in blood alcohol levels more quickly than ingestion of the
91 ere significantly correlated with changes in blood alcohol levels on both the ascending (P<.001) and
93 ding low inositol levels in response to high blood alcohol levels support a mechanism of reversible o
95 3 g/kg b.wt., i.p.) resulted in elevation of blood alcohol levels, ACTH and corticosterone in all gro
96 d the effects of four alcoholic beverages on blood alcohol levels, plasma insulin concentrations and
98 Chronic-binge ethanol feeding leads to high blood alcohol levels; thus, this simple model will be ve
100 me alone, and 69 (53%) of 130 adults who had blood alcohol measured were intoxicated (blood alcohol c
101 tine were currently drug dependent, 11.7% of blood alcohol-negative and 3.9% of drug-negative patient
103 I (Head Abbreviated Injury Score [AIS]), and blood alcohol testing status were known, were included.
104 e frequently monitored with random urine and blood alcohol tests; patients found positive were exclud