Electron transport in InGaO3(ZnO)m (m=integer) studied using single-crystalline thin films and transparent MISFETs

We have investigated the characteristics of transparent metal-insulator-semiconductor field-effect transistors (MISFETs) fabricated using InGaO₃(ZnO)_m (m=integer) single-crystalline thin films as n-channel layers and amorphous alumina as gate insulator films. The MISFETs exhibit good characteristics such as insensitivity to visible light illumination, off-current as low as ∼1 nA with a positive threshold voltage of ∼3 V and on/off current ratio of 10⁵. The field-effect mobility increased from ∼1 to ∼10 cm² (V s)⁻¹ as the m-value increased. Room temperature Hall mobility also increased. However, unexpectedly these values were lower than the field-effect mobility. It is explained by existence of shallow localized state in the homologous compounds.     

A scheme of picosecond pulse shaping using gain saturationcharacteristics of semiconductor laser amplifiers

To obtain high power, well shaped picosecond pulses from gain-switched semiconductor lasers, the use of dynamic gain saturation characteristics of semiconductor laser amplifiers was investigated theoretically and experimentally. A configuration of a reflected-wave amplifier (RWA) with single-side external coupling is introduced for pulse shaping, which is found to be suitable for enhancing dynamic gain saturation. By a combination of a distributed feedback laser oscillator at 1.3 μm in wavelength and a reflected-wave amplifier of 400 μm cavity length with asymmetric facet reflectivities of 0.01% and 30%, single-mode optical pulses with almost no tailing, full width at half maximum of 15 ps, and peak power exceeding 50 mW were obtained without pulse broadening, despite the considerable tail structure of the incident pulse     

Dissimilarity scaling and INDSCAL analysis in the study of flavour differences between normal pHu and DFD beef

Overall dissimilarity measurement of paired stimuli followed by Individual Differences Scaling (INDSCAL) analysis was used to study flavour perception in a set of beef extracts. The experiment was designed to determine whether pH contributed to flavour difference between beef of “normal” ultimate pH (pHu5.8) and “dark-cutting” (DFD) beef (pHu6.2). Assessors distinguished the flavour of “normal” pHu and DFD beef both by a combination of pH and titratable acidity, and a second dimension independent of pH. The chemicals added to adjust pH independently of the original muscle composition contributed a third flavour dimension. Substantial assessor variation was observed in the relative weight given to the three flavour dimensions, and this is discussed in relation to the task of judging overall dissimilarity.     

Responses of plasma norepinephrine and heart rate during exercise in patients after Fontan operation and patients with residual right ventricular outflow tract obstruction after definitive reconstruction

In a fetal autopsy series, we have explored the occurrence of renal tubular dysgenesis in twins. Renal tubular dysgenesis was found exclusively among those monozygotic twins with evidence of twin transfusion syndrome, particularly in those donor twins with oligohydramnios and growth restriction. We infer that hypotension in the donor twin of the twin transfusion syndrome pair is responsible for the failure of proximal convoluted tubule differentiation, and the disturbance of renal function is manifested as oligohydramnios prenatally, and either oliguria or tubular dysfunction postnatally.     

Regulation of Kv4.2 and Kv1.4 K+ channel expression by myocardial hypertrophic factors in cultured newborn rat ventricular cells

Postnatal development and myocardial hypertrophy are associated with alterations in cardiac voltage-gated K+ channels. To investigate mechanisms underlying this K+ channel remodeling, expression of Kv4.2 and Kv1.4 K+ channel alpha-subunits was examined in cultured newborn rat ventricular myocytes by Western blot analysis using polyclonal antibodies against each of the subunits. At day 5 of cell culture, Kv1.4 protein was expressed at higher level than Kv4.2; as the age of culture progressed, Kv1.4 was significantly diminished while Kv4.2 increased with time in culture and became the predominant K+ channel protein. Such K+ channel isoform switch from Kv1.4 to Kv4.2 resembles that of the development in vivo. A 72-h treatment with exogenous triiodothyronine (T3, 0.1 microM) to cultured neonatal myocytes enhanced the expression of Kv4.2 by 73% and decreased the Kv1.4 expression by 22%. The effects of T3 were associated with an increase in the protein-to-DNA ratio indicating myocyte hypertrophy. On the other hand, a 72-h treatment with cardiac non-myocyte cell (NMC)-conditioned growth medium (NCGM) or phenylephrine (20 microM) induced similar cell hypertrophy, but in sharp contrast to T3, both markedly suppressed the Kv4.2 channel protein level. In addition, the trophic and the Kv4.2-downregulating effects of NCGM could be mimicked by exogenous endothelin-1 (0.1 microM), a paracrine factor secreted from cardiac NMCs. Our observations for the first time suggest that cardiac Kv4.2 and Kv1.4 K+ channel alpha-subunits are differentially regulated by a variety of myocardial hypertrophic factors. That T3 accelerated the developmental K+ channel isoform switch from Kv1.4 to Kv4.2 in vitro indicates the critical importance of thyroid hormone in postnatal K+ channel remodeling. Cardiac NMCs and alpha-adrenoceptor activation may contribute to the reduced outward K+ channel density in hypertrophied cardiomyocytes.     

Protein modelling using a chimera reference protein derived from exons

Bovine pancreatic /S-trypsin (PDB ID-code: 1TPO) which is registeredin the Brookhaven Protein Data Bank (PDB) consists of four exons.The results of homology searches for each exon in the PDB showedthat homologous proteins were tonin (PDB ID-code: 1TON), ratmast cell protease (PDB ID-code: 3RP2_A), kaffikrein A (PDBID-code: 2PKA_B) and kallikrein A (2PKA_B) respectively. Thus,for the three-dimensional structure prediction of 1TPO, a chimeraprotein was constructed from the three proteins mentioned aboveand the 3-D structure prediction was performed using this chimerareference protein. The modelled structure of 1TPO was energeticallyoptimized by molecular mechanics and molecular dynamics simulationand was compared with its X-ray crystal structure registeredin the PDB. The root mean square deviations (r.m.s.d.) of mainchain atoms and the neighbouring active site (5 sphere fromHis57, AsplO2 and Serl95) between the modelled structure andthe X-ray structure were 1.66 and 0.94 respectively. Porcinepancreatic elastase (PDB ID-code: 3EST) which is registeredin the PDB was used as the reference protein and the modelledstructure from 3EST was also compared with the X-ray data. Ther.m.s.d. of main chain atoms and that of the active site were2.14 and 1.18 respectively. These results dearly support thepropriety of this method using the chimera reference protein.     

Preparation of multiple oxide BaTiO3 fibres by the sol-gel method

Multiple oxide BaTiO₃ gel fibres were prepared by the sol-gel method from Ba(OC₂H₅)₂-Ti(O-isoC₃H₇)₄-H₂O-C₂H₅OH-CH₃COOH and Ba(CH₃COO)₂-Ti(O-isoC₃H₇)₄-H₂O-CH₃COOH solutions. Relatively long gel fibres of 10cm length were obtained from both solutions in the limited composition region. The latter solution in particular showed a spinnability even when it contained no water. Therefore, the occurrence of spinnability of the solution was considered to be due to the formation of linear polymers composed of bridging acetate groups such as TiO-C(CH₃)-O-Ti rather than metalloxane bonding as Ti-O-Ti. Addition of water to the solutions seems to break the bridging acetate bonds and replace some of them by bridging oxygen bonds. The as-drawn gel fibres which were X-ray amorphous crystallized into BaTiO₃ ceramic fibres of 5mm average length upon heating above 600 ° C. However, the gel fibres drawn from the sols without water became powdery on heating because of the lack of Ti-O-Ti metalloxane bonds. The crystallization behaviour of the BaTiO₃ gel fibres is discussed based on the infrared spectroscopy, X-ray diffraction analysis and thermogravimetric-differential thermal analysis.     

The Attenuated Secretion of Hyaluronan by UVA-Exposed Human Fibroblasts Is Associated with Up- and Downregulation of HYBID and HAS2 Expression via Activated and Inactivated Signaling of the p38/ATF2 and JAK2/STAT3 Cascades

Little is known about the effects on hyaluronan (HA) metabolism of UVA radiation. This study demonstrates that the secretion of HA by human dermal fibroblasts (HDFs) is downregulated by UVA, accompanied by the down- and upregulation of mRNA and protein levels of the HA-synthesizing enzyme (HAS2) and the HA-degrading protein, HYaluronan Binding protein Involved in HA Depolymerization(HYBID), respectively. Signaling analysis revealed that the exposure distinctly elicits activation of the p38/MSK1/CREB/c-Fos/AP-1 axis, the JNK/c-Jun axis, and the p38/ATF-2 axis, but downregulates the phosphorylation of NF-kB and JAK/STAT3. A signal inhibition study demonstrated that the inhibition of p38 significantly abrogates the UVA-accentuated mRNA level of HYBID. Furthermore, the inhibition of STAT3 significantly downregulates the level of HAS2 mRNA in non-UVA exposed HDFs. Analysis using siRNAs demonstrated that transfection of ATF-2 siRNA but not c-Fos siRNA abrogates the increased protein level of HYBID in UVA-exposed HDFs. An inhibitor of protein tyrosine phosphatase but not of protein serine/threonine phosphatase restored the diminished phosphorylation level of STAT3 at Tyr 705, accompanied by a significant abolishing effect on the decreased mRNA expression level of HAS2. Silencing with a protein tyrosine phosphatase PTP-Meg2 siRNA revealed that it abrogates the decreased phosphorylation of STAT3 at Tyr 705 in UVA-exposed HDFs. These findings suggest that the UVA-induced decrease in HA secretion by HDFs is attributable to the down- and upregulation of HAS2 and HYBID expression, respectively, changes that are mainly ascribed to the inactivated signaling of the STAT3 axis due to the activated tyrosine protein phosphatase PTP-Meg2 and the activated signaling of the p38/ATF2 axis, respectively.