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Herein, the photoelectric properties of Ta‐doped β‐Ga2O3 are studied based on first‐principles density functional theory calculation. The effects of interstitial H and O vacancies on the properties of the system are also considered. The electronic structure, dielectric function, absorption spectrum, mobility, and conductivity of all the systems are studied and analyzed. The results show that Ta‐doped β‐Ga2O3 is an n‐type direct‐bandgap semiconductor. With the increase in Ta doping concentration, the dielectric constant, polarization ability, and charge binding ability of the system gradually increase, the bandgap gradually narrows, and the absorption spectra of systems redshift. The main absorption wavelengths of all systems are in the wavelength range of less than 300 nm. Therefore, Ta‐doped β‐Ga2O3 has an ultraviolet detection ability. The introduction of Ta is beneficial to improve the conductivity of the system. Interstitial H can improve the conductivity of the system. [ABSTRACT FROM AUTHOR]

Herein, the photoelectric properties of Ta‐doped β‐Ga2O3 are studied based on first‐principles density functional theory calculation. The effects of interstitial H and O vacancies on the properties of the system are also considered. The electronic structure, dielectric function, absorption spectrum, mobility, and conductivity of all the systems are studied and analyzed. The results show that Ta‐doped β‐Ga2O3 is an n‐type direct‐bandgap semiconductor. With the increase in Ta doping concentration, the dielectric constant, polarization ability, and charge binding ability of the system gradually increase, the bandgap gradually narrows, and the absorption spectra of systems redshift. The main absorption wavelengths of all systems are in the wavelength range of less than 300 nm. Therefore, Ta‐doped β‐Ga2O3 has an ultraviolet detection ability. The introduction of Ta is beneficial to improve the conductivity of the system. Interstitial H can improve the conductivity of the system. [ABSTRACT FROM AUTHOR]

Background: Megalencephalic leukoencephalopathy with subcortical cysts (MLC) is a rare, inherited disorder that causes epilepsy, intellectual disorders, and early onset macrocephaly. MLC1 has been identified as a main pathogenic gene. Methods: Clinical data such as magnetic resonance imaging (MRI), routine blood tests, and physical examinations were collected from proband. Trio whole‐exome sequencing (WES) of the family was performed, and all variants with a minor allele frequency (<0.01) in the exon and canonical splicing sites were selected for further pathogenic evaluation. Candidate variants were validated using Sanger sequencing. Results: Here, we report a new homozygous variant identified in two children from the same family in the MLC1 gene [NM_015166.4: c.838_843delinsATTTTA, (p.Ser280_Phe281delinsIleLeu)]. This variant is classified as variant of uncertain significance (VUS) according to the ACMG guidelines. Further experiments demonstrate that the newly identified variant causes a decrease of MLC1 protein levels when expressed in a heterologous expression system. Conclusion: Our case expands on this genetic variation and provides new evidence for the clinical diagnosis of MLC1‐related MLC. [ABSTRACT FROM AUTHOR]

Background: Gut dysmotility is common after ischemic stroke, but the mechanism underlying this response is unknown. Under homeostasis, gut motility is regulated by the neurons of the enteric nervous system that control contractile/relaxation activity of muscle cells in the gut wall. More recently, studies of gut inflammation revealed interactions of macrophages with enteric neurons are also involved in modulating gut motility. However, whether poststroke gut dysmotility is mediated by direct signaling to the enteric nervous system or indirectly via inflammatory macrophages is unknown., Methods and Results: We examined these hypotheses by using a clinically relevant permanent intraluminal midcerebral artery occlusion experimental model of stroke. At 24 hours after stroke, we performed in vivo and ex vivo gut motility assays, flow cytometry, immunofluorescence, and transcriptomic analysis. Stroke-induced gut dysmotility was associated with recruitment of muscularis macrophages into the gastrointestinal tract and redistribution of muscularis macrophages away from myenteric ganglia. The permanent intraluminal midcerebral artery occlusion model caused changes in gene expression in muscularis macrophages consistent with an altered phenotype. While the size of myenteric ganglia after stroke was not altered, myenteric neurons from post-permanent intraluminal midcerebral artery occlusion mice showed a reduction in neuronal nitric oxide synthase expression, and this response was associated with enhanced intestinal smooth muscle contraction ex vivo. Finally, chemical sympathectomy with 6-hydroxydopamine prevented the loss of myenteric neuronal nitric oxide synthase expression and stroke-induced slowed gut transit., Conclusions: Our findings demonstrate that activation of the sympathetic nervous system after stroke is associated with reduced neuronal nitric oxide synthase expression in myenteric neurons, resulting in impaired smooth muscle relaxation and dysregulation of gut transit.