When men drink excessive amounts of alcohol over a prolonged period, they may develop neurological diseases, such as peripheral neuropathy, Wernicke encephalopathy, and alcohol-induced cerebellar degeneration. Trace elements in the brain can lead to the increased expression of receptors, enzymes for the synthesis and metabolism of the neurotransmitter, and proteins that modulate function, ets. It is possible that various neurological symptoms occur when trace elements in the brain are affected by excessive consumption of alcohol, even though the trace elements in the brain are maintained at a constant level. Drinking excessive levels of alcohol increases the level of zinc in the brain, while lower levels of zinc in blood are seen in men with signs of chronic excessive alcohol consumption, such as with alcoholic cirrhosis. It is speculated that increased free radicals by acute alcoholic intake, cause zinc to be increased in the brain in response to this phenomenon. Copper is closely related to neurological diseases, such as Wilson′s disease or Menkes disease, but there have been no reports regarding encephalopathy induced by changes in copper and its metabolites in the brain due to drinking. About 80% of manganese in the brain exists within the astrocytes, and is involved in glutamine metabolism. However, there have not been many reports concerning the relation between alcohol and manganese. Low levels of manganese in the blood are observed in chronic alcoholics and these patients exhibit delirium tremens, tetany, convulsions, athetosis and involuntary movement. The level of iron in the blood increases with chronic excessive alcohol drinking, but there have been no reports indicating that iron levels in the brain are modified by alcohol intake. Metal-lothionein (MT) contributes significantly to zinc and copper metabolism and functions as a protective protein, but MT in the brain is increased when the MT-I overexpressing transgenic mouse (MT-I*) is administered 4 g/kg of ethanol by a gastric tube. Acute ethanol administration can generate oxygen free radicals and cause oxidative stress in the brain. The mechanism of induction of MT in the brain after oral ethanol administration may be associated with oxidative stress caused by ethanol or its metabolites, and can be considered a protective mechanism against ethanol toxicity.
We report a case of a 53-year-old man with thymic carcinoid in multiple endocrine neoplasm-type I. He exhibited icterics while he was being treated for diabetes mellitus. Subtotal parathyroidectomy and autoimplantation was performed. Surgical treatment was not sufficient because of chronic pancreatitis. The gastrioma was inoperable and complicated by unresectable thymic carcinoid tumor. Thus, the patient was willing to undergo conservative therapy with irradiation and octreotide. The thymic carcinoid tumor responded well and the disease is stable at present, based on clinical and imaging findings.
A new program, analysis of single nucleotide polymorphism (SNP), started in the Basic Medical Experiment Course for 3rd grade students of Nihon University School of Medicine. After hearing lectures about SNP, polymerase chain reac-tion (PCR), and ethical rules regarding human samples, students extracted DNA from their own saliva and examined SNPs for aldehyde dehydrogenase 2 (ALDH2) and actinin 3 (ACTN3) genes with allele-specific amplification PCR and TaqMan SNP genotyping PCR, respectively. ALDH2 is involved in ethanol metabolism and its SNP is associated with ethanol tolerance. ACTN3 is an actin-binding protein in skeletal muscles and its SNP is differently associated with sprint and endurance athletes at the Olympic level. Students discussed their genotypes and the reported phenotypes with great interest. The application of a new molecular biology technique in medical science during a student experiment program could have great educational effects on medical students.