In-rich InGaN/GaN quantum wells grown by metal-organic chemical vapor deposition

Growth mechanism of In-rich InGaN/GaN quantum wells (QWs) was investigated. First, we examined the initial stage of InN growth on GaN template considering strain-relieving mechanisms such as defect generation, islanding, and alloy formation at 730 degrees C. It was found that, instead of formation of InN layer, defective In-rich InGaN layer with thickness fluctuations was formed to relieve large lattice mismatch over 10% between InN and GaN. By introducing growth interruption (GI) before GaN capping at the same temperature, however, atomically flat InGaN/GaN interfaces were observed, and the quality of In-rich InGaN layer was greatly improved. We found that decomposition and mass transport processes during GI in InGaN layer are responsible for this phenomenon. There exists severe decomposition in InGaN layer during GI, and a 1-nm-thick InGaN layer remained after GI due to stronger bond strength near the InGaN/GaN interface. It was observed that the mass transport processes actively occurred during GI in InGaN layer above 730 degrees C so that defect annihilation in InGaN layer was greatly enhanced. Finally, based on these experimental results, we propose the growth mechanism of In-rich InGaN/GaN QWs using GI.open9

Regulation of loop extrusion on the interphase genome

In the human cell nucleus, dynamically organized chromatin is the substrate for gene regulation, DNA replication, and repair. A central mechanism of DNA loop formation is an ATPase motor cohesin-mediated loop extrusion. The cohesin complexes load and unload onto the chromosome under the control of other regulators that physically interact and affect motor activity. Regulation of the dynamic loading cycle of cohesin influences not only the chromatin structure but also genome-associated human disorders and aging. This review focuses on the recently spotlighted genome organizing factors and the mechanism by which their dynamic interactions shape the genome architecture in interphase. © 2023 Informa UK Limited, trading as Taylor & Francis Group.FALS

Swedish amyloid precursor protein mutation increases phosphorylation of eIF2alpha in vitro and in vivo

Swedish double mutation (KM670/671NL) of amyloid precursor protein (Swe-APP), a prevailing cause of familial Alzheimer's disease (FAD), is known to increase in Abeta production both in vitro and in vivo, but its underlying molecular basis leading to Alzheimer's disease (AD) pathogenesis remains to be elucidated, especially for the early phase of disease. We have confirmed initially that the expression of Swe-APP mutant transgene reduced cell viability via ROS production but this effect was eliminated by an anti-oxidative agent, vitamin E. We also found that eukaryotic translation initiation factor-2alpha (eIF2alpha), which facilitates binding of initiator tRNA to ribosomes to set on protein synthesis, was phosphorylated in cultured cells expressing Swe-APP. This increase in phosphorylated eIF2alpha was also attenuated significantly by treatment with vitamin E. The finding that eIF2alpha became highly phosphorylated by increased production of Abeta was substantiated in brain tissues of both an AD animal model and AD patients. Although an increase in Abeta production would result in cell death eventually (in late-phase of the disease), the altered phosphorylation state of eIF2alpha evoked by Abeta may account for the decreased efficacy of mRNA translation and de novo protein synthesis required for synaptic plasticity, and may consequently be one of molecular causes for impairment of cognitive functions exhibited in the early phase of AD patients

Electroreflectance and photoluminescence study on InGaN alloys

Photoluminescence (PL) and electroreflectance (ER)measurements on In-rich In xGa 1-xN films grown by using metal-organic chemical vapor deposition at 640 ??C and 670 ??C were performed. Franz-Keldysh Oscillations (FKO's) were observed in the ER spectra. The analysis of the FKO's shows phase separation of InN for the In 0.8Ga 0.2N film, regardless of the growth temperature, whereas in the PL spectrum multiple peaks were resolved only in the sample grown at 640 ??C. This indicates that phase separation exists in this kind of In-rich InGaN alloy independent of the growth temperature. From a deconvolution of the FKO signal in the ER spectra, the bandgap energy of In-rich In xGa 1-xN could be estimated. The dependence of the bandgap energy of the In xGa 1-xN alloy on the In composition (x) was obtained from this information.open2

Compositional analysis of In-rich InGaN layers grown on GaN templates by metalorganic chemical vapor deposition

In-rich InGaN layers were successfully grown on GaN templates by metalorganic chemical vapor deposition. In incorporation in InGaN layer was enhanced by decreasing the growth temperature, and In-rich InGaN layer with In content higher than 70% was obtained below 670 ??C. Especially, double peaks from In-rich InGaN grown at 640 ??C appeared in X-ray diffraction pattern and photoluminescence (PL). The further investigation of strain status of InGaN layers by reciprocal space mapping (RSM) clarified that In-rich InGaN layers were fully relaxed and consisted of InGaN alloys of two different In contents of 82% and 97%, respectively. As a result, we confirmed that compositional inhomogeneity which is mainly reported in Ga-rich InGaN layer could exist in In-rich InGaN layer higher than 80%. We also investigated In incorporation behavior in InGaN at low temperature (640 ??C). In content in InGaN layer was found to be controlled by just changing input gas phase mole fraction (TMIn/(TMGa+TMIn)) at low growth temperature and a linear relationship was observed between In content in InGaN layers and gas phase mole fraction.close141

Minocycline attenuates neuronal cell death and improves cognitive impairment in Alzheimer's disease models

Minocycline is a semi-synthetic tetracycline antibiotic that effectively crosses the blood-brain barrier. Minocycline has been reported to have significant neuroprotective effects in models of cerebral ischemia, traumatic brain injury, amyotrophic lateral sclerosis, and Huntington's and Parkinson's diseases. In this study, we demonstrate that minocycline has neuroprotective effects in in vitro and in vivo Alzheimer's disease models. Minocycline was found to attenuate the increases in the phosphorylation of double-stranded RNA-dependent serine/threonine protein kinase, eukaryotic translation initiation factor-2 alpha and caspase 12 activation induced by amyloid beta peptide1-42 treatment in NGF-differentiated PC 12 cells. In addition, increases in the phosphorylation of eukaryotic translation initiation factor-2 alpha were attenuated by administration of minocycline in Tg2576 mice, which harbor mutated human APP695 gene including the Swedish double mutation and amyloid beta peptide(1-42)-infused rats. We found that minocycline administration attenuated deficits in learning and memory in amyloid beta peptide(1-42)-infused rats. Increased phosphorylated state of eukaryotic translation initiation factor-2 alpha is observed in Alzheimer's disease patients' brains and may result in impairment of cognitive functions in Alzheimer's disease patients by decreasing the efficacy of de novo protein synthesis required for synaptic plasticity. On the basis of these results, minocycline may prove to be a good candidate as an effective therapeutic agent for Alzheimer's disease