Assessing spatiotemporal bikeability using multi-source geospatial big data:A case study of Xiamen, China

This study focuses on the development of a new framework for evaluating bikeability in urban environments with the aim of enhancing sustainable urban transportation planning. To close the research gap that previous studies have disregarded the dynamic environmental factors and trajectory data, we propose a framework that comprises four sub-indices: safety, comfort, accessibility, and vitality. Utilizing open-source data, advanced deep neural networks, and GIS spatial analysis, the framework eliminates subjective evaluations and is more efficient and comprehensive than prior methods. The experimental results on Xiamen, China, demonstrate the effectiveness of the framework in identifying areas for improvement and enhancing cycling mobility. The proposed framework provides a structured approach for evaluating bikeability in different geographical contexts, making reproducing bikeability indices easier and more comprehensive to policymakers, transportation planners, and environmental decision-makers.</p

Shen-Fu Injection Preconditioning Inhibits Myocardial Ischemia-Reperfusion Injury in Diabetic Rats: Activation of eNOS via the PI3K/Akt Pathway

The aim of this paper is to investigate whether Shen-fu injection (SFI), a traditional Chinese medicine, could attenuate myocardial ischemia-reperfusion (MI/R) injury in diabetes. Streptozotocin-induced diabetic rats were randomly assigned to the Sham, I/R, SFI preconditioning, and SFI plus wortmannin (a phosphatidylinositol 3-kinase inhibitor) groups. After the treatment, hearts were subjected to 30 min of coronary artery occlusion and 2 h reperfusion except the Sham group. Myocardial infarct size and cardiomyocytes apoptosis were increased significantly in MI/R group as compared with the Sham group. SFI preconditioning significantly decreased infarct size, apoptosis, caspase-3 protein expression, MDA level in myocardial tissues, and plasma level of CK and LDH but increased p-Akt, p-eNOS, bcl-2 protein expression, and SOD activity compared to I/R group. Moreover, SFI-induced cardioprotection was abolished by wortmannin. We conclude that SFI preconditioning protects diabetic hearts from I/R injury via PI3K/Akt-dependent pathway

Pathogenicity and functional analysis of CFAP410 mutations causing cone-rod dystrophy with macular staphyloma

BackgroundCone-rod dystrophy (CORD) caused by pathogenic variants in CFAP410 is a very rare disease. The mechanisms by which the variants caused the disease remained largely unknown. CFAP410 pathogenic variants were identified in a cone-rod dystrophy with macular staphyloma patient. We explored the pathogenicity and performed functional analysis of two compound heterozygous mutations.MethodsA 6-year-old boy complained decreased vision for 1 year, underwent ocular examinations together with systemic X-ray check. Blood sample was taken for targeted next generation sequencing (Tg-NGS). Pathogenicity of identified variants was determined by ACMG guideline. Mutated plasmids were constructed and transferred to HEK293T cells. Cell cycle, protein stability, and protein ubiquitination level was measured.ResultsThe best-corrected visual acuity of proband was 0.20 bilaterally. Fundus showed macular staphyloma and uneven granular pigment disorder in the periphery of the retina. SS-OCT showed thinning and atrophy of the outer retina, residual ellipsoid zone (EZ) in the fovea. Scotopic and photopic ERG responses severe reduced. Two heterozygous missense pathogenic variants, c.319 T &gt; C (p.Tyr107His) and c.347 C &gt; T (p.Pro116Leu) in exon 4 of the CFAP410, were found and were pathogenic by the ACMG guideline. In vitro, pathogenic variants affect cell cycle. Immunofluorescence and western blotting showed that the mutant proteins decreased expression levels protein stability. Meanwhile, co-IP data suggested that ubiquitination level was altered in cells transferred with the mutated plasmids.ConclusionCompound heterozygous pathogenic variants c.319 T &gt; C and c.347 C &gt; T in CFAP410 caused CORD with macular staphyloma. The pathogenic mechanisms may be associated with alternations of protein stability and degradation through the ubiquitin-proteasome pathway

Nitroglycerine-induced nitrate tolerance compromises propofol protection of the endothelial cells against TNF-α: the role of PKC-β2 and NADPH oxidase

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NLRP3 Inflammasome Activation-Mediated Pyroptosis Aggravates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats

The reactive oxygen species- (ROS-) induced nod-like receptor protein-3 (NLRP3) inflammasome triggers sterile inflammatory responses and pyroptosis, which is a proinflammatory form of programmed cell death initiated by the activation of inflammatory caspases. NLRP3 inflammasome activation plays an important role in myocardial ischemia/reperfusion (MI/R) injury. Our present study investigated whether diabetes aggravated MI/R injury through NLRP3 inflammasome-mediated pyroptosis. Type 1 diabetic rat model was established by intraperitoneal injection of streptozotocin (60 mg/kg). MI/R was induced by ligating the left anterior descending artery (LAD) for 30 minutes followed by 2 h reperfusion. H9C2 cardiomyocytes were exposed to high glucose (HG, 30 mM) conditions and hypoxia/reoxygenation (H/R) stimulation. The myocardial infarct size, CK-MB, and LDH release in the diabetic rats subjected to MI/R were significantly higher than those in the nondiabetic rats, accompanied with increased NLRP3 inflammasome activation and increased pyroptosis. Inhibition of inflammasome activation with BAY11-7082 significantly decreased the MI/R injury. In vitro studies showed similar effects, as BAY11-7082 or the ROS scavenger N-acetylcysteine, attenuated HG and H/R-induced H9C2 cell injury. In conclusion, hyperglycaemia-induced NLRP3 inflammasome activation may be a ROS-dependent process in pyroptotic cell death, and NLRP3 inflammasome-induced pyroptosis aggravates MI/R injury in diabetic rats

LncRNA HCP5 : A Potential Biomarker for Diagnosing Gastric Cancer

BackgroundIt has been reported that long non-coding RNAs (lncRNAs) can be regarded as a biomarker and had particular clinical significance for early screening and gastric cancer (GC) diagnosis. Therefore, this study aimed to investigate whether serum HCP5 could be a new diagnostic biomarker.MethodsFiltered out the HCP5 from the GEO database. The specificity of HCP5 was verified by real-time fluorescence quantitative PCR (qRT-PCR), and then the stability of HCP5 was verified by room temperature storage and repeated freeze-thaw experiments. Meanwhile, the accuracy of HCP5 was verified by agarose gel electrophoresis (AGE) and Sanger sequencing. Simultaneously, the expression level of serum HCP5 was detected by qRT-PCR in 98 patients with primary gastric cancer, 21 gastritis patients, 82 healthy donors, and multiple cancer types. Then, the methodology analysis was carried on. Moreover, receiver operating characteristic (ROC) was used to evaluate its diagnostic efficiency.ResultsqRT-PCR method had good repeatability and stability in detecting HCP5. The expression level of HCP5 in the serum of gastric cancer patients was remarkably higher than that of healthy controls, and it could distinguish gastritis patients from healthy donors. Besides, the expression of HCP5 was increased dramatically in MKN-45 and MGC-803. The FISH assay showed that HCP5 was mainly distributed in the cytoplasm of MKN-45 and BGC-823 cells. When HCP5 was combined with existing tumor markers, the diagnostic efficiency of HCP5 was the best, and the combined diagnosis of carcinoembryonic antigen (CEA), carbohydrate antigen199 (CA199), and HCP5 can significantly improve the diagnostic sensitivity. Besides, compared with the expression levels of thyroid cancer (THCA), colorectal cancer (CRC), and breast cancer (BRCA), serum HCP5 in gastric cancer was the most specific. Moreover, the high expression of serum HCP5 was related to differentiation, lymph node metastasis, and nerve invasion. The term of serum HCP5 after the operation was significantly lower than that of patients with primary gastric cancer.ConclusionSerum HCP5 can be used as a potential biomarker of non-invasive fluid biopsy, which had a unique value in the early diagnosis, development, and prognosis of gastric cancer

Learned Smartphone ISP on Mobile GPUs with Deep Learning, Mobile AI & AIM 2022 Challenge: Report

The role of mobile cameras increased dramatically over the past few years, leading to more and more research in automatic image quality enhancement and RAW photo processing. In this Mobile AI challenge, the target was to develop an efficient end-to-end AI-based image signal processing (ISP) pipeline replacing the standard mobile ISPs that can run on modern smartphone GPUs using TensorFlow Lite. The participants were provided with a large-scale Fujifilm UltraISP dataset consisting of thousands of paired photos captured with a normal mobile camera sensor and a professional 102MP medium-format FujiFilm GFX100 camera. The runtime of the resulting models was evaluated on the Snapdragon's 8 Gen 1 GPU that provides excellent acceleration results for the majority of common deep learning ops. The proposed solutions are compatible with all recent mobile GPUs, being able to process Full HD photos in less than 20-50 milliseconds while achieving high fidelity results. A detailed description of all models developed in this challenge is provided in this paper

Effects of N-Acetylcysteine on Nicotinamide Dinucleotide Phosphate Oxidase Activation and Antioxidant Status in Heart, Lung, Liver and Kidney in Streptozotocin-Induced Diabetic Rats

Purpose: Hyperglycemia increases reactive oxygen species (ROS) and the resulting oxidative stress plays a key role in the pathogenesis of diabetic complications. Nicotinamide dinucleotide phosphate (NADPH) oxidase is one of the major sources of ROS production in diabetes. We, therefore, examined the possibility that NADPH oxidase activation is increased in various tissues, and that the antioxidant N-acetylcysteine (NAC) may have tissue specifc effects on NADPH oxidase and tissue antioxidant status in diabetes. Materials and Methods: Control (C) and streptozotocin-induced diabetic (D) rats were treated either with NAC (1.5 g/kg/ day) orally or placebo for 4 weeks. The plasma, heart, lung, liver, kidney were harvested immediately and stored for biochemical or immunoblot analysis. Results: levels of free 15-F 2t-isoprostane were increased in plasma, heart, lung, liver and kidney tissues in diabetic rats, accompanied with significantly increased membrane translocation of the NADPH oxidase subunit p67phox in all tissues and increased expression of the membrane-bound subunit p22phox in heart, lung and kidney. The tissue antioxidant activity in lung, liver and kidney was decreased in diabetic rats, while it was increased in heart tissue. NAC reduced the expression of p22phox and p67phox, suppressed p67phox membrane translocation, and reduced free 15-F 2t-isoprostane levels in all tissues. NAC increased antioxidant activity in liver and lung, but did not signifcantly affect antioxidant activity in heart and kidney. Conclusion: The current study shows that NAC inhibits NADPH oxidase activation in diabetes and attenuates tissue oxidative damage in all organs, even though its effects on antioxidant activity are tissue specifc. © Yonsei University College of Medicine 2012.link_to_OA_fulltex