Alcoholism ; metabolism ; pathology ; Animals ; Humans ; Orexins ; metabolism

Disulfiram is the commonly prescribed drug for the treatment of alcohol dependence. It's major metabolite (diethyldithiocarbamate) is an inhibitor of dopamine-betahydroxylase, an enzyme that catalyzes the metabolism of dopamine to norepinephrine resulting in psychosis. We recommend that disulfiram should be used at the lowest effective dose, possibly 250 mg daily and caution should be taken while prescribing disulfiram for patients with personal and familial antecedents of psychosis.
Alcoholism ; Disulfiram* ; Dopamine ; Humans ; Metabolism ; Norepinephrine ; Psychotic Disorders*

We report the FDG PET findings in a patient with Marchiafava-Bignami disease (MBD) in whom there was diffusely reduced metabolism in the whole brain cortex and strongly decreased metabolism in the thalami. The use of FDG PET helps provide an understanding of the neurologic manifestations and prognosis of MBD.
Alcoholism ; Brain ; Humans ; Marchiafava-Bignami Disease* ; Metabolism ; Neurologic Manifestations ; Prognosis

Ethyl glucuronide is a specific metabolite of ethanol. There have been plenty of articles referring its pharmacokinetics, detection and application as a specific bio-marker of alcohol intake. This article reviews various analytical methods of EtG, relationship between EtG quantification and ethanol intake, and criteria for determining chronic alcohol abuse, and origin of ethanol found in the cadavers by EtG analysis. EtG has its potential application in forensic toxicology.
Alcoholism/metabolism* ; Forensic Toxicology/methods* ; Glucuronates/urine* ; Hair/chemistry* ; Humans

Alcoholism ; metabolism ; Animals ; Brain ; metabolism ; Chemokine CCL2 ; genetics ; metabolism ; Male ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, CCR2 ; genetics ; metabolism

Osteonecrosis has been found in association with non-traumatic pathological conditions such as alcoholism, sickle cell hemoglobinopathies, Gaucher's disease and decompression sickness. It is also a major compcation in surviving renal transplantation patients where it is generally believed to be a result of immunosupressive systemic corticosteroid administration. The precise etiology of osteonecrosis is still unknown, but many hypotheses have presented; interruption of the blood supply, direct cytotoxic effect, incresed intraosseous pressure and decreased venous return. Whatever the caused or the starting point, and whatever the pathologic process, blockage of the osseous microcirculation with intramedullary stasis appears to be the common denominator. In the present study, our purpose is to examine the microvascular structural changes and corresponding pathological changes of rabbit's femoral head by disturbance of lipid metabolism resulting from the administration of a large dose of the steroid. The results were as follows:1. In the study group (steroid-treated);there was a relatively increased empty lacuna within the rabbit's femoral head suchondral bone at 3 weeks in contrast with the control group. (control:10.72%, study:20.8%,P<0.01.). 2. Early definite marrow necrosis was found since 3 wekks, a marrow focal osteonecrosis since 5 weeks, and roentgenographically osteoporosis since 5 weeks in the study group. 3. In the histological study, the more degenerative vascular changes were found in the subchondral plate as weekly time was relapsed (H & E), and the subchondral vessels were filled with fat in most of the steroid-treated group (Oil-red 0). 4. In the microangiographic study, the chnges of vascular pattern of the subchondral area was found in the more steroid treated group. ie, it was shown to be dissimilar in size, irregulary spaced and not orderly arranged side by side in a line with disappearing focal vascular shadow.
Adult ; Alcoholism ; Bone Marrow ; Decompression Sickness ; Gaucher Disease ; Head ; Hemoglobinopathies ; Humans ; Kidney Transplantation ; Lipid Metabolism ; Microcirculation ; Necrosis ; Osteonecrosis ; Osteoporosis

Alcoholism ; metabolism ; Animals ; Cyclin-Dependent Kinase 5 ; metabolism ; Glucosides ; pharmacology ; Male ; Prefrontal Cortex ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stilbenes ; pharmacology

OBJECTIVES: To observe the changes of expression of α-synuclein （α-syn） and neuronal apoptosis in brain cortex of acute alcoholism rats and to explore the mechanism of the damage caused by ethanol to the neurons. METHODS: The model of acute alcoholism rat was established by 50% alcohol gavage. The α-syn and caspase-3 were detected by immunohistochemical staining and imaging analysis at 1 h, 3 h, 6 h and 12 h after acute alcoholism. The number of positive cell and mean of optical density were detected and the trend change was analyzed. The variance analysis and t-test were also performed. RESULTS: The number of α-syn positive cell and average optical density in brain cortex of acute alcoholism rat increased significantly and peaked at 6 hour with a following slight decrease at 12 h, but still higher than the groups at 1 h and 3 h. Within 12 hours after poisoning, the number of caspase-3 positive cell and average optical density in brain cortex of rats gradually increased. CONCLUSIONS The abnormal aggregation of α-syn caused by brain edema and hypoxia may participate the early stage of neuronal apoptosis in brain cortex after acute alcoholism.
Alcoholism/pathology* ; Animals ; Apoptosis ; Brain Edema/pathology* ; Caspase 3/metabolism* ; Cerebral Cortex/pathology* ; Ethanol ; Hypoxia/pathology* ; Neurons/pathology* ; Rats ; alpha-Synuclein/metabolism*

To define the molecular basis of ethanol dependence, changes in the phosphorylation of cAMP response element binding protein (CREB) in the nucleus accumbens of rats after acute and chronic ethanol administration were detected using immunohistochemistry. The results demonstrate that the expression of phospho-CREB (p-CREB) protein in the rat nucleus accumbens significantly increased after 15 min of acute ethanol exposure, reaching a peak at 30 min after ethanol administration. The increment remained after 1 or 6 h of ethanol exposure compared to the control rats. In contrast, chronic intake of ethanol solution obviously decreased the expression of p-CREB protein compared to the control rats. The decrement remained 24 h or 72 h after ethanol withdrawal, and returned to the control levels after 7 d of ethanol withdrawal. The results suggest that an acute ethanol administration led to an increase in the phosphorylation of CREB in the nucleus accumbens, but chronic ethanol administration produced a decrement, which is possibly one of the molecular mechanisms of alcohol dependence.
Alcoholism ; metabolism ; physiopathology ; Animals ; Cyclic AMP Response Element-Binding Protein ; chemistry ; metabolism ; Ethanol ; pharmacology ; Male ; Nucleus Accumbens ; metabolism ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Substance Withdrawal Syndrome ; metabolism ; physiopathology ; Substance-Related Disorders ; metabolism ; physiopathology

OBJECTIVE: To determine whether chronic alcoholism alters the expression levels of Vasoactive intestinal polypeptide (VIP) and its receptor (VIPR1) in the cochlea of chronic alcoholism rats. METHOD: We measured their expression levels in 30 SD rats, in which we created models of different degrees of chronic alcoholism. We investigated the presence of the mRNA of VIP in the cochlea of chronic alcoholism rats and controls by reverse transcription-polymerase chain reaction (RT-PCR) method. We investigated the presence of proteins of VIPR1 in poisoned rats and controls by western blot. We also evaluated the local distribution of VIP cells by immunohistochemistry. RESULT: We found that the levels of VIP and VIPR1 were downregulated in the chronic alcoholism groups compared to the controls group. The differences in some expression levels were significant different between chronic alcoholism rats and control rats. Moreover, at different degrees of alcohol poisoning in rats, the contents of VIP and VIPR1 differed. Decreased levels of VIP and VIPR1 were detected in the deep chronic alcoholism group compared to the group with low-degree poisoning (P < 0.05). In spiral ganglion cell plasm the expression of VIP and VIPR1 had no significant difference in three groups (P > 0.05). CONCLUSION These results suggest that VIP and VIPR1 play an important role in the auditory function in rats with chronic alcoholism. Chronic alcoholism may cause a peptide hormone secretion imbalance in the auditory system, eventually leading to hearing loss.
Alcoholism ; metabolism ; Animals ; Cochlea ; metabolism ; Disease Models, Animal ; Down-Regulation ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley ; Receptors, Vasoactive Intestinal Polypeptide, Type I ; metabolism ; Spiral Ganglion ; Vasoactive Intestinal Peptide ; metabolism