bluuebunny/crossref_metadata_2025 huggingface dataset:
Serum β‐Hexosaminidase in Young University Students
Authors: Nyström Mikael , Peräsalo Juhani , Salaspuro Mikko
Published: April 2006

In a sample of 203 first‐year university students, serum β‐hexosaminidase (β‐HEX) was studied as a possible marker of heavy drinking. There are no previous studies on β‐HEX in a young nonalcoholic population. All students were healthy and without regular medication except the use of p‐pills in 49 of the 123 female students. Alcohol consumption was measured on a frequency‐volume scale. Serum β‐HEX did not correlate with reported drinking, γ‐glutamyl transferase (GGT), mean corpuscular volume (MCV) nor alcohol problems. The mean β‐HEX of 26 teetotalers did not differ from that of the heaviest drinking group (n= 25). A new finding was a significant (p= 0.009) increase of serum β‐HEX in female students using oral contraceptives. We conclude that serum β‐HEX is a poor indicator of alcohol consumption in young university students and if elevated the use of p‐pills must be considered.
Urinary Markers of Chronic Excessive Ethanol Consumption
Authors: Tang Bing K.
Published: April 2006

A gas chromatographic mass spectrometric procedure is described for the measurement of free ethanol and conjugates of ethanol and acetaldehyde. It was demonstrated that conjugates of ethanol and acetaldehyde were present in urine of alcoholics. Urinary levels of free ethanol and the conjugates in abstaining alcoholics were higher than those of social drinkers. On the average, alcoholics excreted equal amounts of free ethanol and ethanol conjugates while controls eliminated three parts of ethanol conjugates to one part of free ethanol. After 14 days of abstinence, 16/23 (70%) of alcoholics had levels of free ethanol and acetaldehyde conjugates higher than the mean +2 sd of social drinkers for these substances. When the molar ratio of ethanol conjugates/free ethanol was considered, five more subjects who were alcoholics could be classified as being alcoholics. There was one false positive among 46 control subjects.
Aggressive and Nonaggressive Behavior as a Function of Alcohol Intoxication and Frustration in Women
Authors: Gustafson Roland
Published: April 2006

An experiment tested whether alcohol increases aggression in women in a situation in which both an aggressive and a nonaggressive response alternative of equal instrumentality and of equal variability are available. Subjects were assigned to one of three groups, namely, an alcohol, a placebo, or a control group. The alcohol dose was 1.0 ml of pure alcohol/kg body weight. After drinking their respective drink, subjects were instructed to supervise a bogus partner on a visual scan test over a series of trials. Each time this partner made a mistake, subjects could either give an uncomfortable electric shock (scale 1 to 10) or a comfortable vibration (scale 1 to 10) to the partner. Aggressive and nonaggressive behavior was measured as numbers, intensities, and durations of shocks or vibrations, respectively. Neither alcohol nor frustration differentiated the groups on aggressive or nonaggressive behavior. All groups were significantly more inclined to use the nonaggressive alternative irrespective of alcohol dose and level of frustration. In conclusion it was stated that women do not increase their aggression as a function of alcohol in a situation with more than one response alternative available. The need to incorporate gender differences as to aggressive effects of alcohol was stressed.
Male Physical Aggression as a Function of Alcohol Intoxication and Frustration: Experimental Results and Methodological Considerations
Authors: Gustafson Roland
Published: April 2006

Forty‐five undergraduate students were assigned to either an Alcohol, a Placebo, or a Control group. The alcohol dose was 0.80 g of 100% alcohol/kg body weight. Subjects were informed that they could win a sum of money depending on the performance of a partner. They then supervised the partner over a series of trials on a visual scan test and could influence the partner by either giving an uncomfortable electric shock (aggressive alternative) or a comfortable vibration (nonaggressive alternative) at each incorrect response from the partner. Both alternatives were said to be equally instrumental in reaching the goal of winning the money and both could be varied in intensity on a 10‐point scale and without limits in terms of duration. Aggression was measured as number of aggressive responses chosen, and in terms of intensity and duration. Nonaggression was measured in terms of intensity and duration. Intoxicated subjects did not increase their aggression but all groups chose significantly more nonaggressive responses and did so with higher intensity and duration. Frustration did not significantly affect these types of responding. Results are discussed in terms of methodological considerations and the importance of using realistic experimental paradigms is stressed. Also, theoretical implications are discussed.
Studies on Ethanol‐Brain Catalase Interaction: Evidence for Central Ethanol Oxidation
Authors: Aragon C. M. G. , Amit Z. , Stotland L. M.
Published: April 2006

The purpose of the present investigation was to further study the relationship between ethanol and brain catalase in vivo. Rats were pretreated intraperitoneally (ip) with varying doses of ethanol or saline min prior to administration of cyanamide (0.68 mmol/kg; ip), 4‐hydroxypyrazole (1 mmol/kg; ip) or saline. Rat tissues were perfused in situ under ether anaesthesia. Brain catalase activity was measured using the Clark electrode. Results confirmed inhibition of brain catalase activity by cyanamide and 4‐hydroxypyrazole, Ethanol protected catalase from cyanamide and 4‐hydroxypyrazole inactivation in a dose‐related manner. In a second study, homogenates from perfused brains were incubated in the presence of glucose and glucose oxidase with ethanol or saline and cyanamide or saline. Cyanamide was shown to inhibit the catalase activity in vitro in a dose‐related manner. Ethanol prevented this inhibition of catalase when added to the incubation medium prior to cyanamide. These data suggest a competition between ethanol and inhibitors for the H2O2‐catalase compound. They also confirm the presence and generation of H2O2 in the rat brain in vivo, and overall seem to support the notion that centrally formed acetaldehyde via brain catalase may be responsible for some of the psychopharmacological actions of ethanol.
Interactive Effects of Ethanol and Caffeine on Rat Fetal Hepatocyte Replication and EGF Receptor Expression
Authors: Henderson George I. , Baskin Gordon S. , Frosto Teri A. , Schenker Steven
Published: April 2006

This study reports on the interactive effects of ethanol and caffeine on growth of rat fetal hepatocytes. Exposure of cultured rat fetal hepatocytes (RFH) to ethanol in concentrations above 1 mg/ml, causes a blockade of EGF‐dependent cell replication along with an overexpression of surface EGF receptors (EGF‐R). However, RFHs exposed for 24 hours to ethanol at a concentration of 1 mg/ml alone had little effect on cell replication. Caffeine, when combined with this concentration of alcohol, progressively impaired RFH growth by up to 100%. Caffeine alone up to 10 μg/ml, on the other hand, caused a progressive increase in RFH replication associated with a 69% enhancement of DNA synthesis. Caffeine concentrations in excess of 50 μg/ml had no effect on replicative capacity. Concomitant caffeine exposure had no effect on the ethanol‐related increase in cell DNA content, yet it caused a further enhancement of the cell protein accrual induced by ethanol alone. Caffeine (10 μg/ml) alone had no effect on EGF‐R expression, while ethanol (2 mg/ml) increased it by almost 200%. Addition of caffeine to ethanol reduced this enhanced EGF binding by 45%. Scatchard analysis indicated that no treatment altered ligand affinity for the receptor, but that the alterations in binding caused by ethanol and the caffeine/ethanol combination reflected changes in binding capacity, in both low and high affinity components. It is concluded that (1) ethanol blocks EGF‐mediated replication accompanied by a reduction in DNA synthesis, (2) caffeine alone at low concentrations has the opposite effect and can actually potentiate the EGF‐mediated mitogenic response, (3) caffeine in combination with ethanol acts synergistically to reduce RFH replication. We suggest that the ethanol‐induced perturbation of the EGF‐R may be due to an altered cAMP kinase that plays a regulatory role in EGF‐R expression.
Typical Patterns and Cost of Alcoholism Treatment across a Variety of Populations and Providers
Authors: Holder Harold D. , Blose James O.
Published: April 2006

This paper presents data on the utilization of alcoholism treatment services in three populations of insurance enrollees: enrollees covered by the insurance plan of a large midwestern manufacturing firm, 1981–1987 (N= 1,425); enrollees of the California Health Insurance Plan of the Public Employees Retirement System, 1974–1976 (N= 766); U.S. government civilian employees enrolled with the Aetna Insurance Company, 1980–1983 (N= 1,697). The average age of the treated alcoholics in these three groups ranged from 37 to 51. Between two‐thirds and three‐quarters were male. Inpatient alcoholism treatment services were more frequently used than outpatient, with inpatient admissions averaging between 1.2 and 1.5 per person. For enrollees of the midwestern manufacturing firm, total alcoholism treatment costs averaged $4,665 per person (December 1985 dollars). The influence of insurance plan coverage and other factors on utilization patterns is discussed.
Effect of Chronic Ethanol Treatment and Selective Breeding for Sensitivity to Ethanol on Calcium Release Induced by Inositol Trisphosphate for Ethanol from Brain and Liver Microsomes
Authors: Daniell Laura C. , Harris R. Adron
Published: April 2006

Our previous work showed that ethanol increases the resting intracellular free calcium concentration (CA,) in synaptosomes and releases calcium from an inositol trisphosphate (IP3)‐insensitive calcium store of brain microsomes. In this report, we investigated the effects of chronic ethanol treatment and selective breeding for hypnotic sensitivity to ethanol on IP3 and ethanol‐stimulated calcium release from brain and liver microsomes. Chronic ethanol treatment did not alter IP3,‐stimulated calcium release from brain microsomes or ethanol‐stimulated calcium release from brain or liver microsomes. Chronic ethanol treatment increased the spontaneous release of calcium from brain but not liver microsomes. In microsomes isolated from cerebellum or cerebral cortex of long‐sleep (LS) and short‐sleep (SS) mice, ethanol and IP3 released calcium in a concentration dependent manner. The amount of calcium released by ethanol and IP3 was larger in microsomes isolated from cerebellum than microsomes from cerebral cortex. However, the amount of calcium released by ethanol and IP3 did not differ between the two lineseither brain area. These results do not support the idea that the hypnotic effects of ethanol are due to ethanol‐induced calcium release from a nonmitochondrial intracellular calcium store in brain tissue. The development of ethanol tolerance and dependence also does not appear to be associated with altered ability of ethanol to release calcium from non‐mitochondrial intracellular stores; however, effects of chronic ethanol exposure on spontaneous release of intracellular calcium could alter neuronal function in ethanol dependence.
Effect of Dihydrotestosterone on the Rate of Ethanol Elimination in Healthy Men
Authors: Vaubourdolle M. , Guechot J. , Chazouilleres O. , Poupon R. E. , Giboudeau J.
Published: April 2006

Testosterone (T) and, more potently, dihydrotestosterone (DHT), are in vitro inhibitors of hepatic alcohol dehydrogenase (ADH). An increase in the rate of ethanol disappearance (RED) in man has been observed after orchidectomy. We thus investigated the influence of DHT administration on RED in 10 healthy male volunteers. RED was estimated after an oral ethanol bolus (0.6 g/kg), before and after a 14‐day treatment with DHT (2 × 125 mg per day percutaneously; Andractim, Besins Iscovesco, France). A mean 11.5‐fold increase in DHT levels and a 2.0‐fold decrease in T values were observed after DHT administration, confirming the good compliance with treatment. RED was decreased after DHT (0.168 ± 0.043 vs. 0.137 ± 0.043 g/l/hr; mean ± SD; p < 0.01 using Wilcoxon's paired comparison test). These data are consistent with a DHT‐induced inhibition of hepatic ADH in vivo. This could have a beneficial effect by decreasing acetaldehyde production in alcoholic patients, in whom marked hypoandrogenism frequently occurs.
Acute Ethanol Intoxication Suppresses E. Coli Lipopolysaccharide Enhanced Glucose Utilization by Hepatic Nonparenchymal Cells
Authors: D'Souza Nympha B. , Bautista Abraham P. , Bagby Gregory J. , Lang Charles H. , Spitzer John J.
Published: April 2006

During infection or endotoxemia, the immune system is activated and its energy needs increase. Alcohol (ETOH) intoxication on the other hand suppresses the immune system and increases susceptibility to infection. Since the liver is the primary site both for metabolism of ETOH and detoxification of bacterial lipopolysaccharides (LPS), this investigation was directed at studying the effect of acute ETOH intoxication on the LPS‐induced enhancement of in vivo glucose utilization in different types of hepatic cells. Rats were given an intravenous (IV) injection of ETOH followed by a constant infusion for 7 hr to maintain blood alcohol levels at about 175 mg/dl. E. coli LPS was administered IV at 4 hr and in vivo glucose utilization by the different types of liver cells was estimated 3 hr later using the 14C‐2‐deoxyglucose technique. Hepatocytes (HP), Kupffer (KC), and endothelial cells (EC), as well as the sequestered polymorphonuclear leukocytes (PMN), were separated from the liver by collagenasepronase digestion followed by centrifugal elutriation and Ficoll‐Hypaque density gradient centrifugation. The number of PMN in the liver was increased several‐fold 3 hr after LPS administration. The presence of ETOH did not inhibit the LPS‐induced neutrophil migration into the liver. ETOH depressed the LPS‐induced increase in glucose uptake in both EC and KC by 50 to 80%, respectively. It also reduced the LPS‐induced increase of plasma tumor necrosis factor activity by 80%. ETOH alone did not produce any significant changes in the parameters studied. Since enhanced glucose metabolism of immunologically active cells is part of the host's immune response to LPS, ETOH by suppressing this normal response may contribute to the increased susceptibility of alcoholics to infection.
Responses to Cholinergic Agonists of Rats Selectively Bred for Differential Sensitivity to Ethanol
Authors: de Fiebre Christopher M. , Romm Elena , Collins Jeffery T. , Draski Laura J. , Deitrich Richard A. , Collins Allan C.
Published: April 2006

Alcoholics are almost invariably heavy users of tobacco. Both alcoholism and smoking appear to be influenced by genetic factors but it is not known whether the same or different genes regulate the abuse of ethanol and nicotine. Recent studies have demonstrated that the long‐sleep (LS) and short‐sleep (SS) mouse lines, which were selectively bred for differences in ethanol‐induced anesthesia (“sleep‐time”), also differ in several effects of nicotine and the muscarinic agonist, oxotremorine. In order to determine whether or not these differences are due to chance, the relative sensitivites of rat lines which were selectively bred for differences in ethanol‐induced sleep‐time were determined. The high alcohol sensitivity (HAS) rat line was more sensitive to the locomotor and body temperature depressant effects of nicotine than was the low alcohol sensitivity (LAS) rat line. The control line (CAS) was intermediate in sensitivity. The rat lines did not differ in sensitivity to oxotremorine's hypothermia‐producing effects. The numbers and affinities of two classes of brain nicotinic receptors were measured in eight brain regions. No differences among the rat lines were detected. These results suggest that ethanol elicits some of its depressant actions via an effect on brain nicotinic systems, but the differences in sensitivity to ethanol and nicotine are probably not due to differences in the number of brain nicotinic receptors. Perhaps this interaction explains the high correlation between alcoholism and smoking in humans.
Binding of Anti‐Acetaldehyde IgG Antibodies to Hepatocytes with an Acetaldehyde‐Phosphatidylethanolamine Adduct on Their Surface
Authors: Trudell J. R. , Ardies C. M. , Green C. E. , Allen K.
Published: April 2006

We have previously shown that antibodies raised against acetaldehyde adducts of protein cross‐react with an acetaldehyde adduct of dioleoylphosphatidylethanolamine, N‐ethyl‐dioleoylphosphatidylethanolamine, when the latter is incorporated into hexagonal phase phospholipid micelles. In the present study we demonstrate that these same IgG antibodies cross‐react with N‐ethyl‐dioleoylphosphatidylethanolamine when this adduct is incorporated into the surface of hepatocytes. Hapten‐specific IgG antibodies were purified from the sera of rabbits sensitized to an albumin‐acetaldehyde conjugate that had been reduced with sodium cyanoborohydride (N‐ethy‐RSA). The N‐ethyl‐RSA was coupled to an Affi‐Gel‐10 column to affinity purify the lgG. Liposomes containing N‐ethyl‐dioleoylphosphatidylethanolamine were fused with isolated hepatocytes, the affinity purified primary IgG antibodies were added, then fluoresceinconjugated second antibodies were added, and antibody binding to hepatocytes was measured by flow cytometry. The fluorescence of these hepatocytes was significantly greater (p < 0.01) than control hepatocytes prepared with (1) pre‐immune primary IgG antibodies with fluorescein‐conjugated second antibodies, (2) no primary antibody but with fluorescein‐conjugated second antibodies, and (3) no fluorescein‐conjugated second antibodies.
Does the Presence of a Measurable Blood Alcohol Level in a Potential Organ Donor Affect the Outcome of Liver Transplantation?
Authors: Hassanein Tarek I. , Gavaler Judith S. , Fishkin David , Gordon Robert , Starzl Thomas E. , Van Thiel David H.
Published: April 2006

The widespread application of hepatic transplantation has created a tremendous demand for donor organs. An assessment of donor parameters is thought to be important in selecting good donors; however, the criteria utilized have not been standardized. This study was performed to determine the effect of a measurable donor blood alcohol level on graft survival. Fifty‐two patients who underwent orthotopic liver transplantation at the University of Pittsburgh were included in the study. Twenty‐five patients received liver grafts from donors having a blood alcohol level between 0.04 and 0.4 g/I with a mean of 0.17 g/I. Twenty‐seven patients received a liver graft from a donor who had no measurable blood alcohol. There were no differences between these two groups of donors regarding the time of initial hospitalization until the time of donation. Graft failure within the first 30 days was 24% for those receiving an organ from an alcohol‐positive donor as compared with 22.2% in those receiving an organ from an alcohol negative donor. The recipient mortality rate was 16% and 11%, respectively. No relationships between the donor blood alcohol level and organ performance, frequency of primary graft nonfunction, or number of episodes of acute cellular rejection were evident. Based upon these data, the presence of a measurable blood alcohol level in a donor should not mitigate against organ donation.
Direct Measurement of Fast Axonal Organelle Transport in Chronic Ethanol‐Fed Rats
Authors: McLane Jerry A. , Atkinson Mark B. , McNulty John , Breuer Anthony C.
Published: April 2006

While indirect methods have been used, direct evaluation and measurement of the fast axonal transport system itself in chronic ethanolfed rats have not been carried out previously. We evaluated this system using analog and digital image enhancement of differential interference contrast optical images in real time to assess the effect of ethanol on fast intra‐axonal organelle traffic in rat sural nerve. A radiolabeling method for evaluating fast axonal transport was used in similar animals to compare the indirect and direct techniques. Also, the concentration of organelles (mitochondria, large and small clear vesicles, dense vesicles, and membranous whorls) in the annulospiral sensory nerve endings of muscle spindles from a foot muscle (flexor digitorum brevis) of these same animals was quantitated from electron micrographs. Rats were fed an ethanol‐containing liquid diet for one to five months. Three observations were made; (1) There was no statistically significant change in the mean organelle speed in the anterograde direction, but the mean organelle speed in the retrograde direction increased 11%, 9%, and 17% (statistically significant) at 3, 4, and 5 months of ethanol exposure, respectively. (2) Significant increases in organelle content of sensory nerve endings were seen at 2 and 3 months of intoxication. (3) Increases in organelle densities in terminals were transitory and returned to normal in the face of on‐going ethanol administration. We conclude: (1) There is no permanent impairment of fast axonal organelle transport in this model after 5 months of exposure. (2) Sensory endings on muscle spindles show transitory increases in organelle density. (3) Retrograde speed increases may be a partial compensatory mechanism to help restore normal terminal organelle density. Both the return of sensory organelle content to normal and the increase in the number of retrograde organelles moving at the higher transport rates suggest the activation of compensatory mechanisms in the neuron early in the course of sustained ethanol intoxication.
Effects of Indomethacin, Aspirin, and Acetaminophen on Ethanol Diuresis in Rats
Authors: Morato Gina Struffaldi , Lemos Tadeu , Morato Edelton Flavio
Published: April 2006

A number of studies have indicated that prostaglandin synthetase inhibitors (PGSI) can antagonize several effects of ethanol. This study examines the influence of intraperitoneal pretreatment with the PGSI indomethacin (5.0 or 10.0 mg/kg), aspirin (15.0 or 30.0 mg/ kg) and acetaminophen (15.0 or 30.0 mg/kg) on the diuretic effect produced by orally administered ethanol (4.0 g/kg) in female rats. Pretreatments with indomethacin and aspirin led to an antagonism of ethanol's diuretic effect. Nevertheless, acetaminophen failed to antagonize this effect. These results are in agreement with data from the literature on PGSI versus ethanol and suggest possible involvement of prostaglandins in the diuretic effect of ethanol.
Selective Breeding of Rats Differing in Sensitivity to the Effects of Acute Ethanol Administration
Authors: Draski Laura J. , Spuhler Karen P. , Erwin V. Gene , Baker Rodney C. , Deitrich Richard A.
Published: April 2006

Selective breeding of rats for sensitivity to the anesthetic effects of ethanol is being carried out with rats derived from the genetically heterogeneous N/Nih stock. Thirteen generations of within family selection have been achieved with replicate high (HAS), low (LAS) and control alcohol sensitive (CAS) lines. Significant separation between lines on sleep time and blood ethanol concentration (BEC) at awakening following ethanol administration has been achieved. In general, the results obtained so far replicate the findings with short (SS) and long (LS) sleep mice. One exception is that the high alcohol sensitivity rats (HAS) also appear more sensitive to pentobarbital relative to LAS rats. This finding is opposite to that which occurs with SS and LS mice where the low ethanol sensitive SS mice appear more sensitive to pentobarbital than the LS mice.
Ethanol Decreases Cytosolic‐Free Calcium Ions in Vascular Smooth Muscle Cells As Assessed by Digital Image Analysis
Authors: Zhang A. , Cheng T.P.O. , Altura B.M.
Published: April 2006

Effects of ethanol on intracellular‐free Ca2+ concentration in cultured rat aortic smooth muscle cells were examined by digital imaging fluorescence microscopy using the Ca2+ fluorescence indicator, fura‐2. Ethanol induced dose‐dependent decrements in cytosolic‐free Ca2+ concentration at 45 mM and 90 mM, which was consistent with previously reported observations of relaxation in intact rat aortic tissues. However, ethanol at high pharmacological concentrations (e.g., 450 mm) failed to induce any further inhibition in cytosolic‐free Ca2+ concentration. Our results suggest that the vasodilator effects of ethanol, observed on intact blood vessels, may result in part from an interference with the availability of Ca2+ for excitation‐contraction coupling in vascular smooth muscle cells.
Neuroendocrine Evidence for Reduced Dopamine Receptor Sensitivity in Alcoholism
Authors: Balldin Jan I. , Berggren Ulf C. , Lindstedt Göran
Published: April 2006

Postsynaptic dopamine (DA) receptor sensitivity was assessed during abstinence in 15 male patients with alcohol dependence. The DA receptor sensitivity was evaluated using growth hormone (GH) responses to the DA receptor agonist apomorphine (0.18–0.24 mg intravenously). The patients were cared for in an alcoholism treatment unit for the 2 months prior to the investigation. They were carefully controlled for sobriety during this period. Thirteen healthy men were used as controls. The maximum GH responses to apomorphine were significantly reduced in patients compared with those in the control group. The patients had a significantly higher proportion of blunted GH responses. The findings suggest reduced postsynaptic DA, possibly D2, receptor sensitivity in abstinent alcoholics. The question whether this abnormal DA receptor status is genetically determined or acquired after long‐term alcohol consumption remains to be addressed.
Carbohydrate‐Deficient Transferrin (CDT) in Serum as a Possible Indicator of Heavy Drinking in Young University Students
Authors: Nyström Mikael , Perasalo Juhani , Salaspuro Mikko
Published: April 2006

Carbohydrate‐deficient transferrin (CDT) in serum was studied as a possible marker of heavy drinking in a sample of 187 female and 102 male 1st year university students from Finland. CDT was measured by a new radioimmunoassay (Pharmacia CDT RIA). Alcohol consumption was measured on a quantity‐frequency scale.

For female students CDT was 18.2 ± 0.45 units/liter (mean ± SEM) and for male students 13.3 ± 0.48 units/liter. 9.6% of female students and 7.8% of male students had elevated CDT with a cutoff level of 26 units/liter for females and 20 units/liter for males. The correlation between CDT and reported alcohol consumption was 0.30 (p < 0.001) for females and 0.25 (p= 0.014) for males. Those reporting a consumption of at least 10 kg of pure ethanol per year were considered as heavy drinkers (3.7% of females and 22.5% of males). In female students the average CDT of heavy drinkers did not differ significantly from that of social drinkers but in teetotalers CDT was significantly (p < 0.03) lower than in female alcohol users. In male students the average CDT of heavy drinkers was higher than the average of social drinkers (p < 0.1) and significantly higher than the average of teetotalers (p < 0.001). In the detection of heavy drinking among male students elevated CDT had a specificity of 96.2% and a sensitivity of 21.7%. None of the seven heavy drinking female students had an elevated CDT.

As compared with the other laboratory markers of alcoholism (gamma glutamyltransferase, mean corpuscular volume, and highdensity lipoprotein cholesterol, and β‐hexosaminidase), which in this student population have been proven to be unspecific indicators of heaving drinking, CDT had a better correlation to reported drinking.
The Psychiatric Diagnosis of Alcoholism: Critique and Proposed Reformulation
Authors: Tarter Ralph E. , Moss Howard B. , Arria Amelia , Mezzich Ada C. , Vanyukov Michael M. , Mill John Stuart
Published: April 2006

A taxonomy of alcohol problem involvement is proposed which encompasses categorical and dimensional approaches to classification. It is argued that contemporary nosology such as that described in DSM or ICD cannot, in principle, yield discrete categories containing homogeneous membership. Nor does current classification and diagnosis yield sufficient specific information necessary for effective treatment. These limitations are not resolvable by additional empirical research; rather, as discussed herein, a new conceptual framework and focus are required. The proposed new taxonomy comprises the first step in developing a comprehensive and clinically useful method for characterizing the alcohol consuming population.
Alcohol and Social Influences: Yielding among Male Social Drinkers to Social Pressure
Authors: Gustafson Roland
Published: April 2006

Thirty men participated as paid volunteers in an experiment exploring whether alcohol intoxication makes a person more or less likely to yield to social pressure. Subjects were randomly assigned to either a Control, a Placebo, or an Alcohol group. The alcohol dose was 0.8 ml of 100% alcohol/kg body weight. Subjects first estimated the length of a line, then received feedback from either a male or a female reference group (social pressure), and finally made a second estimation. This procedure was repeated 30 times. The analysis indicated that the only effect of intoxication was to become more resistant in terms of number of yieldings to social pressure, provided the feedback came from a male reference group. Locus of control in terms of internality significantly predicted number of yieldings for the Alcohol group, although the analysis indicated no significant differences between groups as to mean locus of control scores.
Tumor Necrosis Factor in Alcohol Enhanced Endotoxin Liver Injury
Authors: Honchel Ronald , Ray Mukunda B. , Marsano Luis , Cohen Donald , Lee Eun , Shedlofsky Steven , McClain Craig J.
Published: April 2006

Endotoxin administration causes liver injury. Patients with alcoholic liver disease frequently have portal vein and systemic endotoxemia, and some investigators have suggested that endotoxin plays an etiologic role in alcoholic liver injury. Many of the metabolic effects of endotoxin are mediated by the cytokine tumor necrosis factor (TNF). It was the purpose of this study to determine whether TNF plays a role in ethanol‐enhanced endotoxin liver injury. Rats were fed either a diet in which 36% of the calories were from ethanol or an isocaloric control diet. After 6 weeks, groups of 10 rats were intravenously injected with either saline, 1 mg/kg endotoxin, or 30 μg/kg of a prostaglandin E1 (PGE1) analogue + 1 mg/kg endotoxin 24 hr prior to sacrifice. Ethanol/endotoxin‐treated rats had significantly higher liver enzyme levels (ALT 1064 ± 355 IU/liter, AST 2024 ± 515 IU/liter) compared with isocaloric/endotoxin controls (ALT 237 ± 54 IU/liter, AST 602 ± 80 IU/liter). Ethanol/endotoxin rats also had significantly higher peak serum TNF concentrations (992 ± 200 units/ml) compared with isocaloric/endotoxin controls (344 ± 96 units/ml). Pretreatment of ethanol/endotoxin rats with PGE1 caused significant attenuation of liver injury (ALT: 267 ± 64 IU/liter, AST 612 ± 77 IU/liter) and a diminished serum TNF response. In contrast to chronic ethanol administration, acute gavage with 2 mg/kg ethanol (30% w/v) followed by intravenous injection of 2 mg/ kg endotoxin produced significantly lower peak serum TNF concentrations (401 ± 76 units/ml) than gavage with distilled water (1152 ± 208 units/ml).

We conclude that chronic ethanol feeding enhances endotoxin‐stimulated peak serum TNF concentrations, endotoxin liver injury, and pretreatment with the TNF synthesis inhibitor PGE1 attenuates this liver injury. Furthermore, acute and chronic alcohol feeding appear to have opposite effects on endotoxin stimulated serum TNF levels.
Long‐Term Abstinent Alcoholics Have Normal Memory
Authors: Reed Robert J. , Grant Igor , Rourke Sean B.
Published: April 2006

It is generally believed that many non‐Korsakoff alcoholics have subtle defects in memory. To determine whether such defects vary as a function of length of abstinence (LOA), we performed extensive memory testing with (1) recently detoxified (n= 31; LOA‐29 days); (2) intermediate‐term abstinent (n= 28; LOA = 1.9 years); (3) long‐term abstinent (n= 32; LOA‐7.0 years) alcoholics; and (4) nonalcoholic controls (n= 37). All subjects were matched on age and education. Alcoholics were matched on years of alcoholic drinking. Memory measures were divided into the following domains: verbal learning, verbal recall, visual learning, visual recall, and paired associate learning. A series of MANOVAs were conducted that revealed a significant relationship between visual learning and length of abstinence, and a significant interaction between age and length of abstinence on visual recall. Long‐term abstinent subjects were not significantly different from controls on any test. We conclude that memory disturbance demonstrable among recently detoxified alcoholics in the early weeks of their abstinence is not evident in demographically matched long‐term abstinent alcoholics with similar drinking histories.
Interpersonal Problem‐Solving in Male and Female Alcoholics
Authors: Nixon Sara Jo , Tivis Rick , Parsons Oscar A.
Published: April 2006

This study compared the performance of alcoholics (18 male, 16 female) with community controls (15 male, 12 female) on the Adaptive Skills Battery (ASB), a test ofinterpersonalproblem‐solving. The ASB consists of 30 situations. Fifteen situations require subjects' typical responses and 15, their optimal responses. Male and female alcoholics were inferior to controls in their typical responses [F(1,57) = 45.22,p= 0.0001], but did not differ on the optimal responses (F< 1). Further analyses indicated that decreased feelings of self‐efficacy could not account for the alcoholic deficit. Females were superior to males in the optimal response condition [(F(1,56) = 9.90,p= 0.003]. No significant group × sex interactions were obtained. Performance on the ASB was not correlated with performance on traditional measures of problem‐solving. Post‐hoc correlational analyses revealed differential patterns between depression scores and performance for alcoholics and controls. These data suggest that (1) female and male alcoholics exhibit similar interpersonal problem solving deficits, (2) alcoholic self‐efficacy expectancies cannot account for the impairment, (3) the ASB appears to assess aspects of problem‐solving not typically examined, and (4) the role of depression in alcoholic performance deserves continued empirical evaluation.
The Associations of Alcohol Drinking and Drinking Cessation to Measures of the Immune System in Middle‐Aged Men
Authors: Mili Fatima , Flanders W. Dana , Boring John R. , Annest J. Lee , DeStefano Frank
Published: April 2006

To estimate the association between the immunologic responses of the cell‐mediated and humoral systems and alcohol drinking, we used data from the Vietnam Experience Study conducted by the Centers for Disease Control. That study, conducted from 1985 to 1986, was based on a random sample of 4462 male, Vietnam‐era, U.S. veterans. By using linear regression, we evaluated how (1) the number of alcoholic drinks the subjects consumed per month and (2) the drinking cessation of certain subjects were associated with their relative and absolute T, B, CD4, and CD8 lymphocyte counts and immunoglobulin A (IgA), IgM, and IgG levels. We used geometric means and percentage differences in geometric means of immune status to measure the associations and adjusted these values to account for the effect of covariates. The results indicated that measures of immune status differed among the drinking categories and that, generally, the differences changed after adjustment for covariates. These differences consisted, as alcohol consumption increased, of higher IgA and IgM levels, relative T and CD4 lymphocytes, and the ratio of CD4 to CD8 cells, and of lower IgG levels, relative B and CD8 lymphocytes, absolute lymphocyte, and lymphocyte subset counts after adjusting for other covariates. Among former drinkers, we found no clear‐cut pattern in measures of immunity for a few years after cessation and then found that values of former drinkers tended to return toward values of nondrinkers as they continued to abstain.
Ethanol Inhibits C6 Cell Growth: Fetal Alcohol Syndrome Model
Authors: Isenberg Keith , Zhou Xia , Moore Blake W.
Published: April 2006

Maternal consumption of ethanol produces a pattern of malformations, including nervous system abnormalities, in the developing fetus, a state called Fetal Alcohol Syndrome. We report the dose‐dependent inhibition by ethanol of the growth of a glioma derived cell line, C6 cells; the effects occur at ethanol concentrations commonly encountered in the blood during human intoxication. The effects occur with different morphological subtypes of the cell line and do not occur when the cells are exposed to iso‐osmolar concentrations of other chemicals. The results demonstrate that c6 cells are a model for the study of the effects of ethanol on nervous system cell growth.
Studies on a Wearable, Electronic, Transdermal Alcohol Sensor
Authors: Swift Robert M. , Martin Christopher S. , Swette Larry , LaConti Anthony , Kackley Nancy
Published: April 2006

The measurement of alcohol consumption over long time periods is important for monitoring treatment outcome and for research applications. Giner, Inc. has developed a wearable device that senses ethanol vapor at the surface of the skin, using an electrochemical cell that produces a continuous current signal proportional to ethanol concentration. A thermistor monitors continuous contact of the sensor with the skin, and a data‐acquisition/logic circuit stores days of data recorded at 2‐ to 5‐min intervals. Testing of this novel ethanol sensor/recorder was conducted on nonalcoholic human subjects consuming known quantities of ethanol and on intoxicated alcoholic subjects. The transdermal sensor signal closely follows the pattern of the blood alcohol concentration curve, although with a delay. This paper describes the concept of electrochemical ethanol measurement and presents some of the clinical data collected in support of the sensor/recorder development.
Predicting Alcohol Impairment: Perceived Intoxication Versus BAC
Authors: Nicholson Mary E. , Wang MinQi , Airhihenbuwa Collins O. , Mahoney Beverly S. , Maney Dolores W.
Published: April 2006

The purpose of this study was to report the relationship among perceived intoxication, performance impairment, and actual blood alcohol concentration (BAC) levels. Fifteen subjects, aged 21 to 40, completed both single‐ and double‐dose sessions of alcohol consumption. BACs, reaction and anticipation time, and perceived intoxication data were collected during both sessions. Analysis of data showed that perceived intoxication was significantly related to performance impairment, but the actual BAC was not.
Effects of Ethanol and Carbon Tetrachloride upon Vitamin A Status of Rats
Authors: Chapman K. , Prabhudesai M. , Erdman J. W.
Published: April 2006

The effects of ethanol and carbon tetrachloride (CCl4) upon tissue vitamin A, liver lipids, liver cytochrome P450 and hepatic morphology were investigated. It was anticipated that CCl4 treatment would have more severe effects upon vitamin A status because CCI4 provides greater hepatic injury than does ethanol. After a 2‐week standardization feeding period, young male rats were divided into four groups. For 5 weeks one group of rats (n = 17) received ethanol in liquid diets (30% of calories) while another (n = 8) was exposed to CCI4 inhalation twice a week along with phenobarbital in the diet. All groups received the National Regulatory Commission recommended level for vitamin A. Comparison of ethanol and its pair‐fed control group (n = 17) revealed: decreased hepatic vitamin A, no change in serum vitamin A, increased percentage of liver lipid, and cytochrome P450 with moderate fat accumulation in hepatocytes. Comparison of the CCI4 ‐phenobarbitol group with pair‐fed controls (n = 8) showed: increased serum vitamin A, decreased hepatic vitamin A, increased cytochrome P4501 marked hepatic fat accumulation, hepatic cell necrosis, and early cirrhosis. Thus, CCl4, (with phenobarbitol), which is a more potent hepatotoxin as evidenced by a more elevated cytochrome P450 and distorted liver morphology, not only reduced liver vitamin A, but also increased serum vitamin A. The extent of substrate and/or organ specificity remains to be elucidated.
Interaction between Ethanol and Calcium Channel Blockers in Humans
Authors: Perez‐Reyes Mario , White W. Reid , Hicks Robert E.
Published: April 2006

The purpose of this study was to test the hypothesis that pretreatment with Ca2+ channel blockers would antagonize the effects of ethanol intoxication in humans. The Ca2+ channel blockers verapamil and nifedipine were chosen because preclinical research has shown them to decrease certain behavioral effects of ethanol in animals. Sixteen healthy, male, paid volunteers, moderate users of ethanol, participated in the study (six in the verapamil and 10 in the nifedipine paradigms). Gelatin capsules containing verapamil (80 mg, 160 mg, or placebo) were administered orally 90 min before ethanol ingestion; whereas, gelatin capsules containing nifedipine (10 mg, 20 mg, or placebo) were administered 30 min before ethanol ingestion. Ethanol (0.85 g/kg or placebo) was administered over a 30‐min interval. Subjects were tested in a single‐blind, latin‐square, cross‐over design with each of the following six conditions: placebo ethanol‐placebo blocker, placebo ethanol‐low dose blocker, placebo ethanol‐high dose blocker, ethanol‐placebo blocker, ethanol‐low dose blocker, and ethanol‐high dose blocker. The variables measured in this study were subjective rating of ethanol intoxication, Addiction Research Center Inventory alcohol scale, heart rate, blood pressure, short‐term memory, accuracy and latency of response in the Simulator Evaluation of Drug Impairment task, and blood ethanol concentrations by breath analyzer. Results indicate that pretreatment with either verapamil or nifedipine failed to antagonize the inebriating effects of ethanol including its decremental effects on short‐term memory and psychomotor performance.
Protective Effect of Oral Acetylcysteine against the Hepatorenal Toxicity of Carbon Tetrachloride Potentiated by Ethyl Alcohol
Authors: Simko Vlado , Michael Shoukry , Katz Jeffrey , Oberstein Edwin , Popescu Andrea
Published: April 2006

Considering the well‐documented protection of acetylcysteine (AC) in hepatotoxicity related to acetaminophen, we studied the preventive potential of AC against mild hepatotoxicity of CCl4, potentiated with ethyl alcohol (ETH) and the role of tissue glutathione. Rats fed a liquid diet with 30% of energy from ETH, had intraperitoneal CCl4 administered in three injections, at 7‐day intervals. AC was ingested at the level for acetaminophen overdose. ETH markedly potentiated the injury induced by CCl4, as evidenced by higher values of serum alanine aminotransferase (ALT), urinary bile acids (BA), serum creatinine, histological score of liver cell necrosis, mortality and by lower body weights and lower liver glutathione, when compared with CCl4 alone. Protective effect of AC consisted of a lesser hepatocytic necrosis, better body weights and higher liver glutathione. We conclude, that AC favorably modifies liver damage induced by CCl4 and potentiated with ETH. There is a preventive role for AC in subjects who combine ETH overuse with exposure to hepatotoxic xenobiotics, whose toxicity is modified by tissue glutathione.
Ethanol Tolerance in a Genetically Insensitive Selected Mouse Line
Authors: Limm Margaret , Crabbe John C.
Published: April 2006

Mouse lines genetically susceptible (COLD) or resistant (HOT) to the acute hypothermic effects of ethanol were previously shown to differ in tolerance development: HOT mice did not develop tolerance, while COLD mice did. The present experiment increased the thermal load on HOT and COLD mice by administering ethanol chronically at an ambient temperature of 4°C. Under these conditions, initial hypothermic responses were as large as 10°C. Both HOT and COLD mouse lines developed significant tolerance by the third daily injection. Tolerance was dose‐dependent: significant tolerance was seen only at the higher doses. HOT and COLD mouse lines developed approximately equal degrees of tolerance. Results support the hypothesis of a role for functional demand in the development of tolerance.
Iron Uptake from Transferrin and Asialotransferrin by Hepatocytes from Chronically Alcohol‐Fed Rats
Authors: Potter Barry J. , McHugh Teresa A. , Beloqui Oscar
Published: April 2006

Chronic alcohol intake is often associated with alterations to iron homeostasis and an increase in the serum levels of carbohydrate‐deficient transferrin. As the liver is a major iron storage site and also synthesizes transferrin, the normal serum iron transport protein, the aim of this study was to test the hypothesis that these disturbances in iron homeostasis were caused by altered hepatocyte iron uptake from the abnormal transferrin. To achieve this, we have investigated iron uptake from both transferrin and asialotransferrin by hepatocytes from male Sprague‐Dawley rats fed the De Carli and Lieber alcohol diet. Iron uptake from transferrin by hepatocytes from alcoholic rats was less than 60% that of control values, and in the presence of 50 mM ethanol decreased still further to 35% of the uptake by the corresponding control cells. Iron uptake from rat asialotransferrin was reduced in both groups when compared to that observed from normal transferrin; 13% by control cells and 39% by hepatocytes from alcohol‐fed rats. Alcohol, however, had no further effect on asialotransferrin uptake by either hepatocytes from alcohol‐fed rats, or their pair‐fed controls. Transferrin binding to hepatocytes was also influenced by the alcohol diet. Although there was no difference in binding at 37°C, cells from alcohol‐fed rats bound 85% of this total at 4°C, compared to 44% by control hepatocytes. Similar values were also obtained for hepatocyte binding of asialotransferrin; alcohol feeding resulted in an increase in binding at 4°C to 73% from 58% with control cells. The presence of alcohol in the medium did not significantly affect any of these values. These studies suggest that chronic alcohol intake decreases liver iron uptake from transferrin. The siderosis seen in some alcoholics may not be caused by iron uptake from asialotransferrin since, at least in the rat, hepatocytic iron uptake from this molecule is decreased in all groups. The data presented here suggest that there is a defect in the membrane receptor recycling mechanism for transferrin, which occurs as a result of long‐term alcohol abuse.