名寄市立大学における看護学生の情報スキルとeラーニングに関するニーズの調査

eラーニングシステムを本学に円滑に導入するための準備段階として,本研究では本学看護学生の情報通信機器に対するスキルおよびeラーニングに対するニーズを調査し,本学におけるeラーニングシステムの実現可能性について考察した。その結果,多くの学生がeラーニングでの学習を望んでおり,時間的・場所的制約の解消に加えて,情報量の多さやマルチメディア性に期待する声がアンケート調査より得られた。また,eラーニングを実施するにあたって,学生の情報スキル,インフラ整備ともに十分であると認められた。よって学生側のeラーニングに対するレディネスは整っており,本学へのeラーニングシステムの構築について早急な対応が望まれることが示唆された。This paper is intended as an investigation into the potential of e-learning in Nayoro City University. A survey revealed that many nursing students desired to study in an e-learning environment. Additionally, they expected e-learning curricula to provide a wider range of information through multimedia-based materials, and to resolve constraints of time and place. Furthermore, it was shown that students\u27 IT skills and the infrastructure situation are sufficient for the implementation of e-learning. Therefore, it was established that students are ready for e-learning, and the urgency of immediate action towards the construction of an e-learning system at Nayoro City University was demonstrated

Antipsychotic olanzapine-induced misfolding of proinsulin in the endoplasmic reticulum accounts for atypical development of diabetes

オランザピンの非典型的糖尿病誘発機構を解明 --体重増加以外にも注意が必要--. 京都大学プレスリリース. 2020-12-02.Second-generation antipsychotics are widely used to medicate patients with schizophrenia, but may cause metabolic side effects such as diabetes, which has been considered to result from obesity-associated insulin resistance. Olanzapine is particularly well known for this effect. However, clinical studies have suggested that olanzapine-induced hyperglycemia in certain patients cannot be explained by such a generalized mechanism. Here, we focused on the effects of olanzapine on insulin biosynthesis and secretion by mouse insulinoma MIN6 cells. Olanzapine reduced maturation of proinsulin, and thereby inhibited secretion of insulin; and specifically shifted the primary localization of proinsulin from insulin granules to the endoplasmic reticulum. This was due to olanzapine’s impairment of proper disulfide bond formation in proinsulin, although direct targets of olanzapine remain undetermined. Olanzapine-induced proinsulin misfolding and subsequent decrease also occurred at the mouse level. This mechanism of olanzapine-induced β-cell dysfunction should be considered, together with weight gain, when patients are administered olanzapine

ビョウインマエ シンパイ テイシ ニオケル キュウキュウ キュウメイシ ノ キカン ソウカン ニツイテ : ホンケン ノ ゲンジョウ ト コンゴ ノ カダイ

Activities of Japanese Paramedics have increased and advanced year by year. Especially, intubation for OHCPA（out of hospital cardiopulmonary arrest） is approved since July 2004, but it is necessary to finish the training in Fire-fighter’s school and intubation practice in hospitals. In Fire-fighter’s school, Paramedics attend lectures and simulation, and in hospital, intubation practice for patients. Medical-control is the system for keeping the qualities and verification of details in the scene of pre-hospital medical care. This report discusses the states and problems of paramedic intubation, practice in hospital, airway management, from the questionnaire survey

Transforming somatic mutations of mammalian target of rapamycin kinase in human cancer

Mammalian target of rapamycin (mTOR) is a serine-threonine kinase that acts downstream of the phosphatidylinositol 3-kinase signaling pathway and regulates a wide range of cellular functions including transcription, translation, proliferation, apoptosis, and autophagy. Whereas genetic alterations that result in mTOR activation are frequently present in human cancers, whether the mTOR gene itself becomes an oncogene through somatic mutation has remained unclear. We have now identified a somatic non-synonymous mutation of mTOR that results in a leucine-to-valine substitution at amino acid position 2209 in a specimen of large cell neuroendocrine carcinoma. The mTOR(L2209V) mutant manifested marked transforming potential in a focus formation assay with mouse 3T3 fibroblasts, and it induced the phosphorylation of p70 S6 kinase, S6 ribosomal protein, and eukaryotic translation initiation factor 4E-binding protein 1 in these cells. Examination of additional tumor specimens as well as public and in-house databases of cancer genome mutations identified another 28 independent non-synonymous mutations of mTOR in various cancer types, with 12 of these mutations also showing transforming ability. Most of these oncogenic mutations cluster at the interface between the kinase domain and the FAT (FRAP, ATM, TRRAP) domain in the 3-D structure of mTOR. Transforming mTOR mutants were also found to promote 3T3 cell survival, and their oncogenic activity was sensitive to rapamycin. Our data thus show that mTOR acquires transforming activity through genetic changes in cancer, and they suggest that such tumors may be candidates for molecularly targeted therapy with mTOR inhibitors