Molecular-dynamics simulations of glass formation and crystallization in binary liquid metals: Cu-Ag and Cu-Ni

We used molecular dynamics (MD) to obtain an atomistic description of the melting, glass formation, and crystallization processes in metal alloys. These studies use the quantum Sutton-Chen many-body potentials for Cu, Ni, and Ag to examine the Cu4Ag6 and CuNi alloys. Using cooling rates in the range of 2×10^12 to 4×10^14 K/s, we find that CuNi and pure Cu always form a face-centered-cubic (fcc) crystal while Cu4Ag6 always forms a glass (with Tg decreasing as the quench rate increases). The crystal formers have radius ratios of 1.025 (CuNi) and 1.00 (Cu) while the glass former (CuAg) has a ratio of 1.13, confirming the role of size mismatch in biasing toward glass formation

Alterations in Maternal–Fetal Heart Rate Coupling Strength and Directions in Abnormal Fetuses

Because fetal gas exchange takes place via the maternal placenta, there has been growing interests in investigating the patterns and directions of maternal-fetal cardiac coupling to better understand the mechanisms of placental gas transfer. We recently reported the evidence of short-term maternal–fetal cardiac couplings in normal fetuses by using Normalized Short Time Partial Directed Coherence (NSTPDC) technique. Our results have shown weakening of coupling from fetal heart rate to maternal heart rate as the fetal development progresses while the influence from maternal to fetal heart rate coupling behaves oppositely as it shows increasing coupling strength that reaches its maximum at mid gestation. The aim of this study is to test if maternal-fetal coupling patterns change in various types of abnormal cases of pregnancies. We applied NSTPDC on simultaneously recorded fetal and maternal beat-by-beat heart rates collected from fetal and maternal ECG signals of 66 normal and 19 abnormal pregnancies. NSTPDC fetal-to-maternal coupling analyses revealed significant differences between the normal and abnormal cases (normal: normalized factor (NF) = −0.21 ± 0.85, fetus-to-mother coupling area (A_fBBI→ mBBI) = 0.44 ± 0.13, mother-to-fetus coupling area (A_mBBI→ fBBI) = 0.46 ± 0.12; abnormal: NF = −1.66 ± 0.77, A_fBBI→ mBBI = 0.08 ± 0.12, A_mBBI→ fBBI = 0.66 ± 0.24; p < 0.01). In conclusion, maternal-fetal cardiac coupling strength and direction and their associations with regulatory mechanisms (patterns) of developing autonomic nervous system function could be novel clinical markers of healthy prenatal development and its deviation. However, further research is required on larger samples of abnormal cases

Tone entropy analysis of foetal heart rate variability

Development of the foetal autonomic nervous system can be indirectly understood by looking at the changes in beat to beat variability in foetal heart rates. This study presents Tone-Entropy (T-E) analysis of foetal heart rate variability (HRV) at multiple lags (1–8) to understand the influence of gestational ages (early and late) on the development of the foetal autonomic nervous system (ANS). The analysis was based on foetal electrocardiograms (FECGs) of 46 healthy foetuses of 20–32 weeks (early group) and 22 foetuses of 35–41 weeks (late group). Tone represents sympatho-vagal balance and entropy the total autonomic activities. Results show that tone increases and entropy decreases at all lags for the late foetus group. On the other hand, tone decreases and entropy increases at lags 1–4 in the early foetus group. Increasing tone in late foetuses might represent significant maturation of sympathetic nervous systems because foetuses approaching to delivery period need increased sympathetic activity. T-E could be quantitative clinical index to determine the early foetuses from late ones on the basis of maturation of autonomic nervous system

動脈硬化における尿酸の関与

学位の種別: 課程博士審査委員会委員 : （主査）東京大学教授 秋下 雅弘, 東京大学教授 矢冨 裕, 東京大学教授 佐藤 伸一, 東京大学准教授 山内 敏正, 東京大学講師 槙田 紀子University of Tokyo(東京大学

Intrauterine Pressures Adjusted by Reichert's Membrane Are Crucial for Early Mouse Morphogenesis

Mammalian embryogenesis proceeds in utero with the support of nutrients and gases from maternal tissues. However, the contribution of the mechanical environment provided by the uterus to embryogenesis remains unaddressed. Notably, how intrauterine pressures are produced, accurately adjusted, and exerted on embryos are completely unknown. Here, we find that Reichert’s membrane, a specialized basement membrane that wraps around the implanted mouse embryo, plays a crucial role as a shock absorber to protect embryos from intrauterine pressures. Notably, intrauterine pressures are produced by uterine smooth muscle contractions, showing the highest and most frequent periodic peaks just after implantation. Mechanistically, such pressures are adjusted within the sealed space between the embryo and uterus created by Reichert’s membrane and are involved in egg-cylinder morphogenesis as an important biomechanical environment in utero. Thus, we propose the buffer space sealed by Reichert’s membrane cushions and disperses intrauterine pressures exerted on embryos for egg-cylinder morphogenesis

MicroRNA-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiac myocytes

GLUT4 shows decreased levels in failing human adult hearts. We speculated that GLUT4 expression in cardiac muscle may be fine-tuned by microRNAs. Forced expression of miR-133 decreased GLUT4 expression and reduced insulin-mediated glucose uptake in cardiomyocytes. A computational miRNA target prediction algorithm showed that KLF15 is one of the targets of miR-133. It was confirmed that over-expression of miR-133 reduced the protein level of KLF15, which reduced the level of the downstream target GLUT4. Cardiac myocytes infected with lenti-decoy, in which the 3′UTR with tandem sequences complementary to miR-133 was linked to the luciferase reporter gene, had decreased miR-133 levels and increased levels of GLUT4. The expression levels of KLF15 and GLUT4 were decreased at the left ventricular hypertrophy and congestive heart failure stage in a rat model. The present results indicated that miR-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiomyocytes