bluuebunny/crossref_metadata_2025_split huggingface dataset:
Herpesvirus Infection of the Respiratory Tract in Patients with Alcoholic Hepatitis
Authors: Pol Stanislas , Durand François , Bernuau Jacques , Colin Jean‐François , Dubois Frédéric , Hautekeete Marc , Rouzioux Christine , Degott Claude , Rueff Bernard , Benharnou Jean‐Pierre 
Published: April 2006

Respiratory herpesvirus infections have rarely been described in alcoholics. We report four cases of severe respiratory herpesvirus infections in patients with alcoholic liver disease. Two were related to Herpes Simplex Virus and two to Cytomegalovirus. Both chronic alcoholism and severe liver disease induce immunosuppression, which might account for these unusual herpesvirus infections of the respiratory tract.These cases suggest that infections with herpesviruses should be considered in patients with alcoholic liver disease and pulmonary or tracheobronchial disease unresponsive to standard antibiotic therapy. Bronchoscopy, viral culture, and serological tests appear warranted, particularly given the existence of specific therapy.
Effect of Chronic Alcohol Feeding on Hepatic Iron Status and Ferritin Uptake by Rat Hepatocytes
Authors: Zhang H. , Loney L. A. , Potter B. J. 
Published: April 2006

Alcohol abuse is known to cause disturbances to iron homeostasis in man and is associated with elevated serum ferritin levels. We have previously shown that ethanol metabolism in the rat hepatocyte is associated with an immediate reduction in ferritin uptake by this cell. In this study we have examined the effect of pair‐feeding the Lieber‐DeCarli liquid alcohol diet on ferritin uptake by rat hepatocytes.Rat liver ferritin was radiolabeled with 59Fe in vivo and isolated by conventional techniques. Rats were pair‐fed the Lieber‐DeCarli liquid alcoholic diet for 4–6 weeks. Hepatocytes, isolated from their livers by collagenase perfusion, were incubated with [59Fe]ferritin in L‐15 medium at 37°C and 4° to measure ferritin uptake and binding. The in vitro effect of ethanol on these hepatocytes was also studied. Ferritin and iron parameters were measured in the sera and hepatocytes of these animals and a comparable group of normal chowfed rats.The rate of ferritin uptake by hepatocytes from alcohol‐fed rats was significantly faster than that of their pair‐fed controls (0.743 ± 0.061 vs. 0.540 ± 0.042 ng/min/106 cells, p < 0.05). However, the rats on Lieber‐DeCarli control diet exhibited a lower hepatocyte ferritin uptake rate than chow‐fed animals (79.3 ± 8.1% of the control values, p < 0.01). In vitro incubation of cells in 100 mm ethanol resulted in less inhibition of ferritin uptake by hepatocytes from alcoholic rats than from their pair‐fed controls (11 ± 7.1% inhibition vs. 43.6 ± 10.7% for controls, p < 0.05). Receptor‐mediated binding of ferritin to hepatocytes showed a 61% increase in saturable binding capacity for alcoholic rats (15,820 ± 4950 molecules/cell vs. 9798 ± 3622, p= 0.05). The presence of ethanol in the medium did not affect ferritin binding significantly.Although there was no significant difference in the serum iron values between all three groups, transferrin concentrations were markedly elevated in the alcohol‐fed rats, resulting in a much lower transferrin iron saturation than for the control animals. Because the corresponding serum values for the diet controls were intermediate between those for the alcohol‐fed rats and the chow‐fed animals, these findings may reflect dietary restriction by the liquid diet, which is exacerbated by the addition of alcohol.These findings suggest that there is increased iron uptake by the hepatocyte following chronic alcohol administration, which may be due to the increased ferritin receptors. This is supported by the observation that this alcohol treatment also causes a depletion of serum ferritin. However, the decreased iron content in the alcohol‐fed rats indicate that this may be due to a response to changes in iron homeostasis by the hepatocyte and/or redistribution in the body.
Ratings of Fetal Alcohol Syndrome Facial Features by Medical Providers and Biomedical Scientists
Authors: Abel Ernest L. , Martier Susan , Kruger Michael , Ager Joel , Sokol Robert J. 
Published: April 2006

Medical providers, (obstetricians, pediatricians) and biomedical research scientists engaged in fetal alcohol research for many years evaluated facial photographs of newborns previously diagnosed clinically as having or not having fetal alcohol syndrome (FAS). Medical providers and biomedical scientists did not differ significantly in their ratings. Children independently diagnosed as having FAS were distinguished from non‐FAS children by both groups. Providing raters with additional information about children (e.g., birth weight) did not alter judgements significantly.Raters were highly consistent in the ratings they assigned to children (r= 0.96). Accuracy was assessed using signal detection measures (e.g., likelihood ratio, d'). Based on these measures, the two occupational groups did not differ significantly, and rater accuracy was highly significant. Mean ratings were highly correlated with positive maternal Michigan Alcohol Screening Test scores (r= 0.84). These results suggest that the facial features associated with fetal alcohol exposure are readily identifiable, and this, in turn, implies that recognition problems need not be a major contributor to ascertainment of FAS.
Intravenous Flunitrazepam in the Treatment of Alcohol Withdrawal Delirium
Authors: Pycha Roger , Miller Carl , Barnas Christian , Hummer Martina , Stuppäck Christoph , Whitworth Alexandra , Fleischhacker W. Wolfgang 
Published: April 2006

Alcohol withdrawal delirium (AWD) requires treatment with an adequate sedative, anticonvulsant, and antipsychotic agent next to general intensive care measures, Optimal medication should have a rapid onset of action and the possibility of parenteral application. A specific antagonist should be available. Flunitrazepam is a benzodiazepine that fulfills all these criteria.Twenty five patients suffering from AWD (mean age 45 years) took part in an open trial and underwent treatment with infusions of flunitrazepam (concentration: 8 mg/250 ml NaCl; speed, 250 ml/hr). Psychopathological, vegetative, and vital parameters were assessed every hour.All patients survived. They were treated with a mean total dose (SD) of 83.9 (45.4) mg of flunitrazepam (1.3 mg/kg body weight), which induced sedation 13.2 (5.3) min after the initiation of intravenous treatment. The mean duration of AWD (85.1 ± 39.4 hr) corresponded to other studies, whereas the frequency of preexisting and concomitant diseases was higher (92%) in our patients. A patient who suffered from bronchitis and had a nasopharyngeal tamponade showed severe respiratory depression after having received 4 mg of flunitrazepam. This complication remitted immediately when 0.5 mg of flumazenil was given intravenously. No epileptic manifestation was observed during the treatment or after discontinuation of flunitrarepam. Vegetative and psychopathological symptoms (tremor, sweating, hallucinations, confusion, and restlessness) remitted rapidly.Our data suggest that intravenous flunitrazepam can be an efficacious and safe alternative to traditional treatment strategies of AWD.
Dose‐ and Age‐Dependent Effects of Prenatal Ethanol Exposure on Hippocampal Metabotropic‐Glutamate Receptor‐Stimulated Phosphoinositide Hydrolysis
Authors: Queen Susan A. , Sanchez Christian F. , Lopez Samantha R. , Paxton Linda L. , Savage Daniel D. 
Published: April 2006

Prenatal ethanol exposure reduces the density of the N‐methyl‐D‐aspartate (NMDA) receptor agonist binding sites and decreases the capacity to elicit long‐term potentiation (LTP) in hippocampal tormation of 45‐day‐old rat offspring. We hypothesized that prenatal ethanol exposure would reduce metabotropic‐glutamate receptor (mGluR)‐activated phosphoinositide hydrolysis also. Sprague‐Dawley rat dams were fed a liquid diet containing either 3.35% (v/v) ethanol or 5.0% ethanol throughout gestation. Control groups were pair‐fed either isocalorically matched 0% ethanol liquid diets or lab chow ad libitum. (1S,3R)‐1‐aminocyclopentane‐1,3‐dicarboxylic acid (trans‐ACPD) stimulated inositol‐1‐phosphate (IP1) accumulation via activation of the mGluR in offspring whose mothers consumed the 3.35% ethanol liquid diet was not different compared with the control groups. Furthermore, trans‐ACPD stimulated IP1 accumulation in 10 to 13‐day‐old offspring of the 5.0% ethanol diet group was not different compared with the control groups. However, trans‐ACPD stimulated IP1 accumulation was reduced significantly in 56‐ to 82‐day‐old offspring of dams fed the 5.0% ethanol liquid diet compared with the control groups. In contrast, bethanechol stimulated IP1 accumulation, mediated via activation of muscarinic cholinergic receptors, was not affected by maternal consumption of either ethanol liquid diet.These results suggest both dose‐ and age‐dependent effects of prenatal ethanol exposure on hippocampal responsiveness to trans‐ACPD‐activated phosphoinositide hydrolysis. Furthermore, the ability of the 3.35% ethanol diet to alter hippocampal NMDA receptors without altering the mGluR response suggests a differential sensitivity to the effects of ethanol exposure in utero among hippocampal glutamate receptor subtypes. Recent studies indicate that activation of mGluRs facilitates NMDA receptor‐dependent LTP. Thus, higher blood ethanol concentrations achieved by consumption of the 5.0% ethanol liquid diet adversely affects an additional glutamate receptor mechanism associated with LTP. This additional effect may lead to an even greater impact of prenatal ethanol exposure on LTP than occurs when NMDA receptor function alone is affected by maternal consumption of more moderate quantities of ethanol.
Synthesis of Ventricular Mitochondrial Proteins In Vivo: Effect of Acute Ethanol Toxicity
Authors: Siddiq Tahir , Salisbury Jonathan R. , Richardson Peter J. , Preedy Victor R. 
Published: April 2006

Most studies on the pathological responses of the heart to ethanol have been conducted in isolated systems. The objectives of this study were to determine (1) the synthesis rate of ventricular mitochondrial proteins in vivo and (2) whether the synthesis rates of these proteins are perturbed by acute ethanol exposure in vivo.Fractional rates of protein synthesis [defined as the percentage of tissue protein renewed each day; i.e., ks (%/day)] were determined in male Wistar rats by in vivo injection of a flooding dose of L‐[4‐3H] phenylalanine. Subsarcolemmal mitochondria were released by polytron treatment, and the isolation of interfibrillar mitochondria involved treatment of the cardiac homogenate with the proteolytic enzyme Nagarse.In the control rats mean ks values of 22.4%/day were observed for mixed cardiac proteins. The synthesis rates of subsarcolemmal and interfibrillar mitochondrial proteins were lower, i.e., 16.9%/day and 10.9%/day, respectively. Acute ethanol administration (75 mmol/kg body weight ip, 2.5 hr) depressed the fractional rate of protein synthesis in all cardiac fractions, including those pertaining to the mitochondria, as follows: mixed fraction—21%, p < 0.01; subsarcolemmal mitochondria—23%, p < 0.01; interfibrillar mitochondria—26%, p < 0.05; and nuclear fraction—20%, p < 0.05.In conclusion, the reduced synthesis rate of the mitochondrial proteins in response to acute ethanol exposure may in some way be partly connected with the depression in myocardial contractility and associated functional damage of mitochondrial metabolism.
Hypothalamic‐Pituitary‐Thyroid (HPT) Axis in Chronic Alcoholism. I. HPT Axis in Chronic Alcoholics During Withdrawal and After 3 Weeks of Abstinence
Authors: Baumgartner Andreas , Rommelspacher Hans , Otto Monika , Schmidt Lutz G. , Kürten Irene , Gräf Klaus‐Jürgen , Campos‐Barros Angel , Platz Werner 
Published: April 2006

Thyroxine (T4), free T4 (fT4), triiodothyronine (T3 free T3 (fT3), reverse T3 (rT3), thyrotropine (TSH), thyroxine binding globulin (TBG), and T3 uptake were measured in 14 chronic alcoholics during withdrawal and after 21 days of abstinence. Results were compared with those of 16 healthy volunteers. During withdrawal, the fT4 and fT3 concentrations were subnormal, whereas the respective protein‐bound fractions were normal. T4, T3, and TBG increased during the abstinence period, T3 and TBG being significantly higher than in normals at the second measuring time. T3 uptake values fell, but remained well within the normal range at both measuring times. During abstinence, the fT3 levels remained significantly lower than in healthy subjects. rT3 concentrations decreased, but not significantly. The TSH values were normal throughout.These results showed numerous abnormalities in the hypothal‐amic‐pituitary‐thyroid axis in alcoholics, the reasons for which are as yet unclear. The following possible interpretations are suggested: 1. The abnormally low serum fT3 and ff4 levels during withdrawal might reflect an increase in tissue uptake. 2. The increases in T4‐and partty those in T3‐during abstinence seem to reflect increased binding by TBG, the level of which rose markedly for reasons as yet unknown. 3. If increases in TBG during abstinence are taken into account, the decreases in rT3 concentrations may reach the level of statistical significance. These falls in rT3 concentrations may reflect an increase in rT3 metabolization (deiodination) in various tissues, including the CNS, leading to a reduction in serum rT3 bioavail‐ability. 4. Factors such as liver disease, protein caloric malnutrition, and “psychological stress” do not fully explain all these abnormalities. A direct effect of ethanol on intracellular thyroid hormone metabolism and/or function seems conceivable.
Mitochondrial Function Reflected by the Decarboxylation of [13C]Ketoisocaproate Is Impaired in Alcoholics
Authors: Witschi Anne , Mossi Sandro , Meyer Beat , Junker Edith , Lauterburg Bemhard H. 
Published: April 2006

Mitochondria of patients with alcoholic liver disease exhibit structural abnormalities, and mitochondria isolated from animals exposed to ethanol are functionally deficient when studied in vitro. To assess possible functional consequences of these ethanol‐associated alterations in vivo, we measured mitochondrial function in alcoholics noninvasively with a breath test.A mitochondrial function, the decarboxylation of ketoisocaproate (KICA), was assessed by measuring the exhalation of 13CO2 following the administration of 1 mg/kg 2‐keto[1‐13C]isocaproic acid, the decarboxylation of which occurs in mitochondria. The results of the KICA breath test in 12 alcoholic subjects were compared with the results in healthy controls and patients with nonalcoholic liver disease. The peak exhalation of 13CO2 and the fraction of the administered dose decarboxylated in 120 min were both significantly lower in alcoholics than in healthy controls and patients with nonalcoholic liver disease. In alcoholics, KICA decarboxylation was impaired in the presence of normal quantitative liver function tests such as the aminopyrine breath test and galactose elimination capacity, indicating that KICA decarboxylation does not simply reflect a decreased functional hepatic mass. The enrichment of circulating KICA with [13C]KICA was similar in alcoholics and controls, indicating that a decreased bioavailability or an increased dilution of labeled KICA cannot account for the decreased exhalation of 13CO2It is concluded that mitochondrial function as reflected by KICA decarboxylation is impaired in chronic alcoholics. The functional impairment is specific for ethanol abuse and not a reflection of decreased global hepatic function. KICA decarboxylation could thus be useful as a marker for excessive ethanol consumption.
Examination of the Tridimensional Personality Hypothesis of Alcoholism Using Empirically Multivariate Typology
Authors: Yoshino Aihide , Kato Motoichiro , Takeuchi Mika , Ono Yutaka , Kitamura Toshinori 
Published: April 2006

Cloninger (1987) has hypothesized a tridimensional personality theory for two types of alcoholism, type 1 and type 2, that exhibit oppodng clinical characteristics and personality traits. The Tridimensional Personality Questionnaire (TPQ) is designed to test this hypothesis on three independent dimensions—novelty seeking (NS), harm avoidance (HA), and reward dependence (RD)—to evaluate the personality trait. We examined the tridimensional personality hypothesis by comparing TPQ scores between two empirically derived multivariate types of alcoholism.The present study included 191 male subjects with alcoholism. A cluster analysis was conducted using clinical characteristics, and two empirical types, type A and type B, were identified. Type A similar to Cloninger's type 1 and type B is similar to type 2. The TPQ scores given to these two empirical types were compared. Scores on the NS and RD scales were in good agreement with the hypothesis, whereas the HA score was discordant with the hypothesis. HA is highly correlated with the depression scale score that is elevated in type B. We discussed the possibility that type B, which may be called a familial early‐onset alcoholism, is related to character spectrum disorder.
Differences in Recent Life Events between Alcoholic and Depressive Nonalcoholic Suicides
Authors: Heikkinen Martti E. , Aro Hillevi M. , Henriksson Markus M. , Isometsä Erkki T. , Sarna Seppo J. , Kuoppasalmi Kimmo I. , Lönnqvist Jouko K. 
Published: April 2006

The purpose of this study was to investigate the main differences in recent life events preceding suicide between alcoholic and depressive nonalcoholic suicide victims, how much these differences were sex‐ and age‐dependent, and how social support varied between these groups.Using the psychological autopsy method, retrospective best‐estimate diagnoses by DSM‐III‐R criteria were assigned to a randomized 16.4% sample (n= 229) of suicide victims drawn from a 1‐year total nationwide suicide population (n= 1,397) in Finland. Life events during the last 3 months (32 items) and social support (6 items) of 75 suicide victims with alcohol abuse/dependence diagnoses were compared with those of 69 nonalcoholic depressive victims.Among male suicides, the alcoholics had experienced more separations and family discord, financial trouble, and unemployment, whereas the depressives had experienced more somatic illness. Among females, adverse interpersonal events had been common in both alcoholic and depressive victims. Among the alcoholics, unlike the depressives, the number of adverse interpersonal life events had not diminished with increasing age. Living alone had been twice as common among the alcoholic suicides and, in these cases, recent separation, unemployment, and financial trouble were remarkably common, suggesting a concurrent stressor effect.Our results confirm and extend the earlier findings of excess interpersonal stressors among alcoholic suicides compared with depressive suicides. The findings suggest that multiple adverse life events and living alone need to be taken into account in clinical practice when assessing psychosocial stress and suicidal danger in alcoholism.
Women, Alcohol, and Red Cells
Authors: Seppä Kaija , Sillanaukee Pekka 
Published: April 2006

Alcohol abuse is known to increase erythrocyte mean cell volume mainly as a consequence of direct toxic effect on the developing red cell. The influence of alcohol on other red cell parameters is unclear. The objective of this cross‐sectional survey was to examine the consequences of different alcohol amounts on red cell parameters among women.We compared red cell parameters between female alcoholics, heavy drinkers, and controls. Controls (n= 138) and heavy drinkers (n= 65) consisted of consecutive 40‐ and 45‐year‐old women participating in the health screening, and alcoholics (n= 73) of consecutive women coming to a detoxification clinic.Alcoholics had significantly smaller erythrocyte counts (p < 0.01), and higher erythrocyte mean cell volume values (p < 0.001), reticulocyte counts (p < 0.01), and red cell distribution width values (p < 0.001) than controls. No difference between these groups was found, however, in hemoglobin distribution width value. The only red cell difference between controls and heavy drinkers was erythrocyte mean cell volume, which was significantly higher among heavy drinkers (p < 0.001). In alcoholics, red cell distribution width values were even more often increased (in 44%) than erythrocyte mean cell volume values (in 34%). This increase in red cell distribution width was not solely explained by iron deficiency or liver disease.Chronic alcohol abuse not only affects erythrocyte mean cell volume values, but also leads to anisocytosis seen in blood count as an increased red cell distribution width value.
Delayed Pro‐Opiomelanocortin Activation after Ethanol Intake in Man
Authors: Ekman Ann‐Charlotte , Vakkuri Olli , Vuolteenaho Olli , Leppäluoto Juhani 
Published: April 2006

To elucidate the effect of ethanol on the secretion of ACTH and β‐endorphin (BE) as the representatives of the pro‐opiomelanocortin (POMC) system, as well as cortisol as the hypophyseally regulated peripheral hormone, we measured concentrations of serum ethanol and plasma ACTH, BE, and cortisol at 1‐ to 4‐hr intervals for 12 hr after administration of 0.5 and 1.0 g ethanol/kg of body weight and placebo drinks between 1900–1945 hr to nine healthy volunteers according to a double‐blind, cross‐over design.Plasma ACTH, BE, and cortisol showed an expected diurnal rhythm with the highest levels at 0700 hr. Intake of ethanol had no statistically significant effects on plasma ACTH up to 0700 hr in the morning. The higher dose caused increased levels of BE at 0100 hr and both doses at 0200 hr. Plasma cortisol at 0400 hr was higher in subjects receiving 1.0 g ethanol/kg than in those receiving placebo (p < 0.05). Our present observation that plasma ACTH was unchanged after ethanol intake, but plasma BE was increased at 0100‐0200 hr may be due to the fact that our BE antiserum cross‐reacts with β‐lipotropin, which has a considerably longer half‐life than ACTH or BE, and also to the long sampling interval. Thus, the POMC system may have been stimulated after ethanol intake. The nocturnal rise of plasma cortisol levels at 0400 hr, 2‐3 hr after the peak in plasma BE, may be caused by the increased secretion of POMC. Because the ethanol dose of 1.0 g/kg body weight stimulated the POMC system but the 0.5 g/kg body weight did not, we conclude that higher ethanol doses induce increases in stress hormone secretion.