A Reliable Low-Latency Multipath Routing Algorithm for Urban Rail Transit Ad Hoc Networks.

With the advancement of urban rail transit towards intelligence, the demand for urban rail transit communication has increased significantly, but the traditional urban rail transit vehicle-ground communication system has been unable to meet the future vehicle-ground communication requirements. To improve the performance of vehicle-ground communication, the paper proposes a reliable low-latency multipath routing (RLLMR) algorithm for urban rail transit ad hoc networks. First, RLLMR combines the characteristics of urban rail transit ad hoc networks and uses node location information to configure a proactive multipath to reduce route discovery delay. Second, the number of transmission paths is adaptively adjusted according to the quality of service (QoS) requirements for vehicle-ground communication, and then the optimal path is selected based on the link cost function to improve transmission quality. Third, in order to enhance the reliability of communication, a routing maintenance scheme has been added, and the static node-based local repair scheme is used in routing maintenance to reduce the maintenance cost and time. The simulation results show that compared with traditional AODV and AOMDV protocols, the proposed RLLMR algorithm has good performance in improving latency and is slightly inferior to the AOMDV protocol in improving reliability. However, overall, the throughput of the RLLMR algorithm is better than that of the AOMDV.

A deep intronic splice variant of the COL4A5 gene in a Chinese family with X-linked Alport syndrome.

Background: X-linked Alport syndrome (XLAS) is caused by pathogenic variants in COL4A5 and is characterized by progressive kidney disease, hearing loss, and ocular abnormalities.The aim of this study was to identify gene mutations in a Chinese family with XLAS, confirm a diagnosis, and provide an accurate genetic counseling. Methods: The proband was a 5-year-old male with microscopic hematuria and a family history of renal disease in 5 relatives.His relatives had microhematuria with or without proteinuria. His maternal uncle developed renal failure at the age of 35 years. He was evaluated by renal biopsy,whole-exome sequencing (WES) and whole-genome sequencing (WGS) for Alport syndrome. RT-PCR and cDNA Sanger sequencing were performed on RNA extracted from the skin of the proband. Then, a splicing reporter minigene assay was used to examine the effect of the variation on the splicing of the primary transcript in transfected cells. Results: Pathological examination of the kidney of the proband revealed diffuse thinning of the glomerular basement membrane, and immunofluorescence analysis indicated normal expression of the α5 chain in the basement membrane. No phenotype-associated candidate variant was detected in the proband via WES. A novel deep intronic COL4A5 variant (c.385-716G > A), which is segregated with disease in this family, was identified using WGS. In-vitro minigene assay and in-vivo RT-PCR analysis demonstrated that the variant could produce both normal and abnormal transcripts. The abnormal transcripts showed that the variant activated a cryptic splice site, introducing a 147 bp pseudoexon into the mRNA sequence and consequently generating a premature termination codon (p.G129Afs*38) and leading to frameshifting and truncation of the α5 (collagen IV) protein. Conclusion: This is the first report of the novel c.385-716G > A splicing mutation in the COL4A5 gene, which illustrates the importance of performing WGS to find additional mutations in WES-negative patients with highly suspected forms of genetic diseases. The same results obtained from the in-vitro and in-vivo splicing experiments confirm the consistency between the minigene assay and RT-PCR analysis. In addition, this study highlights the importance of functional analysis in diagnosis and genetic counseling in AS.

Protective effect of miconazole on rat myelin sheaths following premature infant cerebral white matter injury.

The aim of the present study was to investigate the protective effects of miconazole on myelin sheaths following cerebral white matter damage (WMD) in premature infant rats. Sprague Dawley rats (3-days-old) were randomly divided into four groups (n=30 each) as follows: Sham surgery group, WMD model group, 10 mg/kg/day treatment group and 40 mg/kg/day treatment group. A cerebral white matter lesion model was created by ligating the right common carotid artery for 80 min. Treatment groups were administered with 10 or 40 mg/kg miconazole at 4-8 days following birth (early treatment group) or 5-11 days following birth (late treatment group). Rats in the model group received the same concentration of dimethylsulfoxide. Myelin basic protein (MBP) immunohistochemical staining and western blotting were used to detect the expression of cerebral white matter-specific MBP, and changes in myelin structure were observed using transmission electron microscopy. No swelling or necrosis was observed in the corpus callosum of the sham group rats, whereas rats in the model group demonstrated edema, loose structure, fiber disorder, inflammatory gliocytes and selective white matter lesions. Following treatment with miconazole, MBP expression in the corpus callosum was significantly higher compared with the model group. Furthermore, in the model group, myelin sheaths in the corpus callosum were loose with small vacuoles, there was a marked decrease in thickness and structural damage was observed. Conversely, a marked improvement in myelination was observed in the treatment group. The results of the present study suggest that miconazole is able to promote formation of the myelin sheath to ameliorate premature cerebral white matter lesions caused by ischemia or hypoxia in rats.