Downsian Positions of Parties and Districts from the Numbers of Votes with Examples of Japanese Congressional Elections 1983 - 2004

This paper proposes, under assumptions of sincere voters with some additional conditions, to calculate the positions of parties and districts by “solving” a system of equations whose left hand sides are theoretical predictions and theright hand sides are the actual numbers of votes gained by the parties in the districts. The positions of parties and prefectures are calculated for the seats for the proportional representation in the Japanese congressional elections 1983 – 2004. The result reveals that the competition in these elections was not between the right and the left, but between the urban and the rural

A frameshift deletion mutation in the cardiac myosin-binding protein C gene associated with dilated phase of hypertrophic cardiomyopathy and dilated cardiomyopathy

SummaryObjectivesA few studies reported that some mutations in the cardiac myosin-binding protein C (MyBPC) gene were associated with dilated phase of hypertrophic cardiomyopathy (D-HCM) resembling dilated cardiomyopathy (DCM). We studied 5 unrelated cardiomyopathy probands caused by an identical mutation in the MyBPC gene. The results of clinical and genetic investigations in these patients are presented in this paper.MethodsWe analyzed MyBPC gene in DCM patients as well as patients with HCM.ResultsAn R945fs/105 mutation, 2-base deletion at nucleotides 18,535 and 18,536, was identified in 4 of the 176 HCM probands and in 1 of the 54 DCM probands. Genetic analysis in relatives of those probands revealed another one member with this mutation. A total of 6 subjects had R945fs/105 mutation. The mean age of these six patients at diagnosis was 61 years. At initial evaluation, three of them were diagnosed as having HCM with normal left ventricular (LV) systolic function. The other two patients already had D-HCM. The remaining one patient was diagnosed as having DCM because of reduced LV systolic function (ejection fraction=31%) without increased LV wall thickness. During follow-up (7.6 years), all three patients with impaired LV systolic function were admitted for treatment of heart failure and/or sustained ventricular tachycardia. Finally, one patient with the diagnosis of D-HCM died of heart failure.ConclusionsThe patients with this mutation may develop LV systolic dysfunction and suffer from cardiovascular events through mid-life and beyond

Do seabirds mated for life synchronize their migration timing and at-sea activity outside the breeding period? Tracking movement and behavior of Rhinoceros auklet pairs during the non-breeding and pre-laying periods

第6回極域科学シンポジウム[OB] 極域生物圏11月16日（月）　国立極地研究所１階交流アトリウ

Glyceraldehyde-3-phosphate Dehydrogenase Aggregates Accelerate Amyloid-β Amyloidogenesis in Alzheimer Disease

peer reviewedAlzheimer disease (AD) is a progressive neurodegenerative disorder characterized by loss of neurons and formation of pathological extracellular deposits induced by amyloid-β peptide (Aβ). Numerous studies have established Aβ amyloidogenesis as a hallmark of AD pathogenesis, particularly with respect to mitochondrial dysfunction. We have previously shown that glycolytic glyceraldehyde-3-phosphate dehydrogenase (GAPDH) forms amyloid-like aggregates upon exposure to oxidative stress and that these aggregates contribute to neuronal cell death. Here, we report that GAPDH aggregates accelerate Aβ amyloidogenesis and subsequent neuronal cell death both in vitro and in vivo. Co-incubation of Aβ40 with small amounts of GAPDH aggregates significantly enhanced Aβ40 amyloidogenesis, as assessed by in vitro thioflavin-T assays. Similarly, structural analyses using Congo red staining, circular dichroism, and atomic force microscopy revealed that GAPDH aggregates induced Aβ40 amyloidogenesis. In PC12 cells, GAPDH aggregates augmented Aβ40-induced cell death, concomitant with disruption of mitochondrial membrane potential. Furthermore, mice injected intracerebroventricularly with Aβ40 co-incubated with GAPDH aggregates exhibited Aβ40-induced pyramidal cell death and gliosis in the hippocampal CA3 region. These observations were accompanied by nuclear translocation of apoptosis-inducing factor and cytosolic release of cytochrome c from mitochondria. Finally, in the 3×Tg-AD mouse model of AD, GAPDH/Aβ co-aggregation and mitochondrial dysfunction were consistently detected in an age-dependent manner, and Aβ aggregate formation was attenuated by GAPDH siRNA treatment. Thus, this study suggests that GAPDH aggregates accelerate Aβ amyloidogenesis, subsequently leading to mitochondrial dysfunction and neuronal cell death in the pathogenesis of AD

世界を制作＝認識する : ブルーノ・ラトゥール×アルフレッド・ジェル

春日直樹編『現実批判の人類学――新世代のエスノグラフィへ』（2011年, 世界思想社）所収29

機械の時間 : テクノロジーにおける「新しさ」をめぐって

西井凉子編『時間の人類学――情動・自然・社会空間』（2011年, 世界思想社）所収22