5 research outputs found
ショクジ セッシュ キジュン 2010ネンバン ニ ヨル カンリ エイヨウシ ヨウセイ カテイ ノ ジョシ ガクセイ ノ エイヨウ シンタイ カツドウ ヒョウカ
The purpose of this study was to assess the nutritional status of women university students in the third-grade of a registered dietitian training course, based on the Dietary Reference Intakes for Japanese(2010). We initially selected 46 students, and obtained valid responses from 41 students(89.1%). We performed body measurements, blood tests, a dietary weighing method for 3 days, and the measurement of physical activity by the accelerometer. In regard to the physique and blood test of the subjects, 24.4% were underweight, 4.9% were obese and 20.0% were anemic. The dietary weighing method showed that the rate of women who took vitamin C below the estimated average requirement was 90.0%, that of folic acid, iron and calcium were 41.0%, 83.0%, and 68.0% respectively. While the rate of salt intake greater than the dietary goal (7.5g/day)was 36.5%, the rate of fat energy ratio greater than the dietary goal(30%)was 31.7%. The average number of steps per day was 8,907 ± 2,293. These results showed that there was an overall insufficient intake of total energy, vitamins, and minerals, indicating that further nutritional management for the women students is required
Modeling the early phenotype at the neuromuscular junction of spinal muscular atrophy using patient-derived iPSCs.
Spinal muscular atrophy (SMA) is a neuromuscular disorder caused by mutations of the survival of motor neuron 1 (SMN1) gene. In the pathogenesis of SMA, pathological changes of the neuromuscular junction (NMJ) precede the motor neuronal loss. Therefore, it is critical to evaluate the NMJ formed by SMA patients' motor neurons (MNs), and to identify drugs that can restore the normal condition. We generated NMJ-like structures using MNs derived from SMA patient-specific induced pluripotent stem cells (iPSCs), and found that the clustering of the acetylcholine receptor (AChR) is significantly impaired. Valproic acid and antisense oligonucleotide treatment ameliorated the AChR clustering defects, leading to an increase in the level of full-length SMN transcripts. Thus, the current in vitro model of AChR clustering using SMA patient-derived iPSCs is useful to dissect the pathophysiological mechanisms underlying the development of SMA, and to evaluate the efficacy of new therapeutic approaches