超小型宇宙機に用いられる電子部品の放射線耐性に関する研究

University of Tokyo(東京大学

コウクウナイ ソウチ オ モチイタ ヘイソクガタ スイミンジ ムコキュウ ショウコウグン ノ イチショウレイ

We experienced a case of obstructive sleep apnea syndrome (OSAS) improved by treatment with an oral appliance. The patient was a 60-year-old female with OSAS. Using the polysomnography, we evaluated apnea by AHI (apnea hypopnea index) and the lowest oxygen saturation (SpO_2) ; before and after wearing an oral appliance. Using the cephalometrics radiogram, we evaluated the airway area magnification by comparing the airway area in each part of upper airway ; before and after wearing an oral appliance. Using 3 dimensional-computed tomography (3D-CT), we diagnosed the airway volume magnification by comparing the airway volume behind the soft palate and the tongue ; before and after wearing an oral appliance. The results were as follows ; 1. AHI was improved from 33.8 to 7.6 and the lowest SpO_2 was improved from 82% to 90%. 2. The airway area behind the soft palate and the tongue remarkably increased. 3. Wearing the oral appliance made the airway magnify up to 162%. The above results showed that wearing an oral appliance magnified space of airway, and the bad effect to circulatory organ was decreased by the improvement of apnea. So we recognized that oral appliance therapy was an effective treatment for OSAS

Heterogeneity of ubiquitin pathology in frontotemporal lobar degeneration: classification and relation to clinical phenotype

We have investigated the extent and pattern of immunostaining for ubiquitin protein (UBQ) in 60 patients with frontotemporal lobar degeneration (FTLD) with ubiquitin-positive, tau-negative inclusions (FTLD-U), 37 of whom were ascertained in Manchester UK and 23 in Newcastle-Upon-Tyne, UK. There were three distinct histological patterns according to the form and distribution of the UBQ pathology. Histological type 1 was present in 19 patients (32%) and characterised by the presence of a moderate number, or numerous, UBQ immunoreactive neurites and intraneuronal cytoplasmic inclusions within layer II of the frontal and temporal cerebral cortex, and cytoplasmic inclusions within granule cells of the dentate gyrus; neuronal intranuclear inclusions (NII) of a “cat’s eye” or “lentiform” appearance were present in 17 of these patients. In histological type 2 (16 patients, 27%), UBQ neurites were predominantly, or exclusively, present with few intraneuronal cytoplasmic inclusions within layer II of the cerebral cortex, while in histological type 3 (25 patients, 42%), UBQ intraneuronal cytoplasmic inclusions either within the cortical layer II or in the granule cells of the dentate gyrus, with few or no UBQ neurites, were seen. In neither of these latter two groups were NII present. The influence of histological type on clinical phenotype was highly significant with type 1 histology being associated clinically with cases of frontotemporal dementia (FTD) or progressive non-fluent aphasia (PNFA), type 2 histology with semantic dementia (SD), and type 3 histology with FTD, or FTD and motor neurone disease (MND)

Molecular Pathology of Lewy Body Diseases

Lewy body diseases are characterized by the presence of Lewy bodies, alpha-synuclein(AS)-positive inclusions in the brain. Since their main component is conformationally modified AS, aggregation of the latter is thought to be a key pathogenic event in these diseases. The analysis of inclusion body constituents gives additional information about pathways also involved in the pathology of synucleinopathies. Widespread mitochondrial dysfunction is very closely related to disease development. The impairment of protein degradation pathways, including both the ubiquitin-proteasome system and the autophagy-lysosome pathway also play an important role during the development of Lewy body diseases. Finally, differential expression changes of isoforms corresponding to genes primarily involved in Lewy body formation point to alternative splicing as another important mechanism in the development of Parkinson’s disease, as well as dementia with Lewy bodies. The present paper attempts to give an overview of recent molecular findings related to the pathogenesis of Lewy body diseases

Are tangles as toxic as they look?

Neurofibrillary tangles are intracellular accumulations of hyperphosphorylated and misfolded tau protein characteristic of Alzheimer's disease and other tauopathies. Classic cross-sectional studies of Alzheimer patient brains showed associations of tangle accumulation with neuronal loss, synapse loss, and dementia, which led to the supposition that tangles are toxic to neurons. More recent advances in imaging techniques and mouse models have allowed the direct exploration of the question of toxicity of aggregated versus soluble tau and have surprisingly challenged the view of tangles as toxic species in the brain. Here, we review these recent experiments on the nature of the toxicity of tau with particular emphasis on our experiments imaging tangles in the intact brain through a cranial window, which allows observation of tangle formation and longitudinal imaging of the fate of tangle-bearing neurons. Neurofibrillary tangles (NFT) were first described in 1906 by Alois Alzheimer based on Bielschowsky silver staining of the brain of his demented patient Auguste D (Alzheimer 1907; Goedert and Spillantini 2006). These intraneuronal aggregates have subsequently been found to be composed primarily of hyperphosphorylated tau protein and are definitive pathological lesions not only in Alzheimer's disease but also in a class of neurodegenerative tauopathies (Goedert et al. 1988; Spires-Jones et al. 2009). NFT pathology in Alzheimer's disease (AD) correlates closely with cognitive decline and synapse and neuronal loss (Braak and Braak 1997; Bretteville and Planel 2008; Congdon and Duff 2008; Mocanu et al. 2008b; Spires-Jones et al. 2009). As a result, NFT have long been considered indicative of impending neuronal cell death. More recent evidence, however, opposes this classical view. Here we review evidence addressing the question of whether NFT cause structural or functional neuronal damage

〈PAPERS and REPORTS〉KARAOKE SYSTEM AUTOMATICALLY MANIPULATING A SINGING VOICE

A karaoke system that manipulates a singing voice has been developed. It has two functions. One is “pitch correction mode,” which converts an out-of-tune vocal sound into one that is in tune. The other is “sub-melody singing generation mode,” which converts solo singing into a duet. Target pitch height for pitch conversion was obtained by adding several F0 fluctuations to a vocal melody written in a MIDI file. Because a speech analysis and synthesis method named TANDEM-STRAIGHT is used for converting the pitch height in this system, it will be easy to introduce a “voice-quality conversion mode” into the system.歌声を操作するカラオケシステムを開発した。このシステムは２つの機能を有する。一つは「ピッチ制御モード」であり、音高が外れた歌声を正しい音高の歌声に変換する。もう一つは「副旋律歌声生成モード」であり、単独歌唱を二重唱に変換するものである。ピッチ変換の際に目標となる音高は、MIDIファイルに記述されたボーカルメロディにF0摂動が付与されたものである。本システムではTANDEM-STRAIGHTと呼ばれる音声分析合成手法を使って音高を変換しているため、「声質変換モード」の導入も容易である