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.

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症例は 53 歳，男性．糖尿病にて他医フォロー中，黄疸出現し，当院紹介となる．精査にて副甲状腺腫，十二指腸ガストリノーマとの診断より，遺伝子解析を行ったところ多発性内分泌腺腫症 1 型の診断を得た．副甲状腺腫に対して副甲状腺全摘術 + 自家移植施行された．十二指腸ガストリノーマは十二指腸に広範囲に認められ，慢性膵炎合併のため，切除困難であり，胸腺カルチノイド腫瘍の合併が認められたため，胸腺カルチノイド腫瘍への放射線照射とオクトレオチドの皮下投与を行った．以上の治療にて縦隔腫瘍は著しく縮小し，17 ヶ月にわたって病状の進行を認めていない．

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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.

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骨盤部悪性骨・軟部腫瘍に対する手術療法を行うにあたって，骨盤の解剖学的所見，部位分類，および切除分類などを知る必要がある．骨盤部悪性骨腫瘍の切除は解剖学的にも複雑で，出血も予測できないこともあり，腫瘍を広範切除するには術者の腕にかかることが多い．患肢温存ができても再建はさらに困難で，下肢の安定性，死腔の処理，血管移植，また，術後神経障害，鼠径ヘルニア，感染などさまざまな問題がある．これらを解決するには腹部外科，心血管外科，形成外科，泌尿器科，婦人科，麻酔科などとの連携治療が重要である．

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昆虫など大部分の無脊椎動物は短命であるが，タラバガニやダイオウイカなどは獲得免疫系を有しないにも関らず，30 年を超える寿命がある．興味深いことに自然界で採集される無脊椎動物には悪性腫瘍の報告が殆ど見られず，有顎魚類以上で初めて悪性腫瘍がしばしば見られるようになる．子宮内で胎児・胎盤を育てる真胎生は大部分の哺乳類で見られるが，哺乳類特有のものではなく，他の脊椎動物門のみならず無脊椎動物にも見られることがある．特異免疫系は軟骨魚類のレベルで進化したシステムであるが，真胎生を行う脊椎動物は父親由来の抗原を有する胎児に対して免疫学的拒絶を来たす可能性があり，その制御が重要な課題となる．近年，胎児胎盤が母体の免疫学的拒絶を免れるシステムが明らかにされるに至った．興味深いことにその多くは悪性腫瘍が拒絶を免れるために使用するメカニズムと一致している．悪性腫瘍の立場からすると，新たな免疫回避機構を発明するよりは，胎児胎盤が母体の拒絶を免れるシステムを用いたほうが手っ取り早いということになる．この事実から，脊椎動物における悪性腫瘍の出現は胎児胎盤の生着を許すような抑制性免疫システムの進化に依存する，言い換えれば進化の上でのトレードオフになっているのではないかという仮説を導くことができる1)．

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