Genomic organization and promoter function of the mouse uncoupling protein 2 (UCP2) gene1The nucleotide sequences reported in this paper will appear in the DDBJ, and GenBank/EMBL Data Bank with accession number AB012159.1

AbstractWe cloned and characterized the mouse uncoupling protein 2 (UCP2) gene and its promoter region. The gene spans approximately 6.3 kb and contains eight exons and seven introns. Two short exons are located in the 5′ untranslated region, and each of the remaining exons encodes one of the transmembrane domains. 3′-RACE analysis showed that a polyadenylation signal 257 bp downstream from the stop codon was functional. Primer extension analysis indicated a single transcriptional start site 369 bp upstream from the translational start site. The promoter region lacks both TATA and CAAT boxes but is GC-rich. A construct containing 1250 bp of the promoter region showed significant activity in all 6 cell lines examined, and the region between −160 and −678 bp exhibited strong positive regulatory activity. These features of the UCP2 gene are different from those of the UCP1 gene and may contribute to its ubiquitous expression

Identification of nesfatin-1 as a satiety molecule in the hypothalamus

The brain hypothalamus contains certain secreted molecules that are important in regulating feeding behaviour. Here we show that nesfatin, corresponding to NEFA/nucleobindin2 (NUCB2), a secreted protein of unknown function, is expressed in the appetite-control hypothalamic nuclei in rats. Intracerebroventricular (i.c.v.) injection of NUCB2 reduces feeding. Rat cerebrospinal fluid contains nesfatin-1, an amino-terminal fragment derived from NUCB2, and its expression is decreased in the hypothalamic paraventricular nucleus under starved conditions. I.c.v. injection of nesfatin-1 decreases food intake in a dose-dependent manner, whereas injection of an antibody neutralizing nesfatin-1 stimulates appetite. In contrast, i.c.v. injection of other possible fragments processed from NUCB2 does not promote satiety, and conversion of NUCB2 to nesfatin-1 is necessary to induce feeding suppression. Chronic i.c.v. injection of nesfatin-1 reduces body weight, whereas rats gain body weight after chronic i.c.v. injection of antisense morpholino oligonucleotide against the gene encoding NUCB2. Nesfatin-1-induced anorexia occurs in Zucker rats with a leptin receptor mutation, and an anti-nesfatin-1 antibody does not block leptin-induced anorexia. In contrast, central injection of alpha-melanocyte-stimulating hormone elevates NUCB2 gene expression in the paraventricular nucleus, and satiety by nesfatin-1 is abolished by an antagonist of the melanocortin-3/4 receptor. We identify nesfatin-1 as a satiety molecule that is associated with melanocortin signalling in the hypothalamus

コウジョウセン クリーゼ 20レイ ノ チリョウ ト ヨゴ : コウジョウセン クリーゼ シンダン キジュン オ モチイタ ケントウ

日本甲状腺学会から甲状腺クリーゼの診断基準が2008 年に発表された.2004 年4 月から2009 年3月に当院で臨床的に甲状腺クリーゼと診断,治療した20 症例を,その診断基準にあてはめ,治療と予後等について解析した.基礎疾患は全例バセドウ病だった.誘因として服用不規則や中断が9 例,感染症6 例,糖尿病性ケトアシドーシス3 例,情動ストレス2 例,脳血管障害1 例,外傷1 例だった.診断基準で確定診断例が15例,疑い例が1 例,除外症例が4 例だった.症状では中枢神経症状が疑い・確定診断例では11 例,脈拍130/分以上は12 例認められたが,除外例では認められなかった.治療としてはチアマゾールが全症例に使用されていた.ヨードは13 例,b ブロッカーは17 例,ステロイドは12 例の症例で使用されており全例救命できた.服用不規則や中断,感染症が誘引となりやすく,症状では中枢神経症状・脈拍が特にクリーゼの診断には重要と考えられた.後遺症を残す重症例は6 例で全て新診断基準によって確定診断された症例であり,新診断基準は予後への有用性も期待できると考えられた.The Japan Thyroid Association established diagnosticcriteria for thyroid crisis in 2008. Using these criteria, weanalyzed 20 cases clinically diagnosed as thyroid crisis andtreated in our hospital from April 2004 to March 2009. Allpatients had Basedow\u27s disease at the basal disease. Thecauses were irregular compliance or interruption of treatment(9 cases), infection (6 cases), diabetic ketoacidosis (3cases), emotional stress( 2 cases), stroke( 1 case), and trauma(1 case). Fifteen cases were confirmed as thyroid crisis,1 case was suspected as thyroid crisis, and 4 cases were rejectedas thyroid crisis according to the diagnostic criteria.Central nervous symptoms were observed in 11 cases, andtachycardia (over 130 beats/min) in 12 cases in the definitiveand suspicious cases, although there were no centralnervous symptoms or tachycardia in the excluded cases.Thiamazole was administered to all patients. In addition, iodine(13 cases), b -blocker (17 cases), and corticosteroids(12 cases) were administered. All patients were recovered.Irregular internal use, stopping treatment, and infectionwere likely to induce thyroid crisis. In paticular, centralnervous symptoms and tachycardia were important factorsfor diagnosis. As 6 serious cases with aftereffect were diagnosedas definitive cases of thyroid crisis according to thenew criteria, these new criteria may be useful to predictthe prognosis

Severe Hypoglycemia Accompanied with Thyroid Crisis

We report a 32-year-old Japanese women with severe hypoglycemia accompanied with thyroid crisis. She complained of dyspnea, general fatigue, and leg edema. She was diagnosed with hyperthyroidism with congestive heart failure and liver dysfunction. Soon after admission, sudden cardiopulmonary arrest occurred. She was then transferred to the intensive care unit. Her serum glucose level was 7 mg/dl. Intravenous glucose, hydrocortisone, diuretics, and continuous hemodiafiltration (CHDF) saved her. We considered that hypoglycemia occurred due to heart failure and liver dysfunction due to thyroid crisis