Impact of the COVID-19 pandemic on urban human mobility - A multiscale geospatial network analysis using New York bike-sharing data.

The COVID-19 pandemic breaking out at the end of 2019 has seriously impacted urban human mobility and poses great challenges for traffic management and urban planning. An understanding of this influence from multiple perspectives is urgently needed. In this study, we propose a multiscale geospatial network framework for the analysis of bike-sharing data, aiming to provide a new perspective for the exploration of the pandemic impact on urban human mobility. More specifically, we organize the bike-sharing data into a network representation, and divide the network into a three-scale structure, ranging from the whole bike system at the macroscale, to the network community at the mesoscale and then to the bicycle station at the microscale. The spatiotemporal analysis of bike-sharing data at each scale is combined with visualization methods for an intuitive understanding of the patterns. We select New York City, one of the most seriously influenced city by the pandemic, as the study area, and used Citi Bike bike-sharing data from January to April in 2019 and 2020 in this area for the investigation. The analysis results show that with the development of the pandemic, the riding flow and its spatiotemporal distribution pattern changed significantly, which had a series of effects on the use and management of bikes in the city. These findings may provide useful references during the pandemic for various stakeholders, e.g., citizens for their travel planning, bike-sharing companies for bicycle dispatching and bicycle disinfection management, and governments for traffic management.

Medium-chain acyl-coenzyme A dehydrogenase deficiency: Six cases in the Chinese population.

BACKGROUND: Medium-chain acyl-coenzyme A dehydrogenase deficiency (MCADD) is a rare autosomal recessive disorder that affects the degradation of medium-chain fatty acids. Few cases of MCADD have been documented to date in mainland China. METHODS: Medium-chain acyl-coenzyme A dehydrogenase deficiency was diagnosed in six patients (three girls and three boys) from six unrelated Chinese families at ages ranging from 10 days to 3 years old. The diagnosis was confirmed by the identification of a primary biomarker of serum octanoyl-carnitine (C8) and genetic pathogenic mutations. RESULTS: Only two patients were admitted because of vomiting, diarrhea, myasthenia, and coma; the other four patients were diagnosed via the newborn screening process. Six mutations were found in acyl-CoA dehydrogenase medium chain (ACADM). One mutation (c.727C>T) was novel and the others (c.158G>A, c.387+1delG, c.449_452del, c.1045C>T, and c.1085G>A) have been previously reported. CONCLUSIONS: Six Chinese cases of MCADD were identified. One novel mutation was found. c.449_452del and c.1085G>A were common mutations in this study.

Perfluorooctanoic acid and perfluorooctanesulfonic acid induce immunotoxicity through the NF-κB pathway in black-spotted frog (Rana nigromaculata).

Perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) are widely detected in the environment and wild animals, thus posing a threat to wildlife and public health; however, knowledge about their immunotoxicity and the underlying mechanism remains limited. In the present study, male black-spotted frogs (Rana nigromaculata) were exposed to environmentally relevant concentrations (0, 1, and 10 µg/L) of PFOA or PFOS for 21 days; subsequently, biochemical analysis, molecular docking, and gene expression determination were conducted. The results indicated that exposure to 10 µg/L PFOA decreased the serum levels of immunoglobulin A. PFOS exposure significantly increased the hepatic levels of interleukin-1ß, interleukin-6, tumor necrosis factor-α, interferon-γ, and nitric oxide; but PFOA significantly increased the levels of only tumor necrosis factor-α. Furthermore, PFOA and PFOS exposure significantly decreased the activity of inducible nitric oxide synthase and total nitric oxide synthase. IBRv2 analysis indicated that PFOA and PFOS had a similar effect on these immune indicators, but PFOS was more toxic than PFOA. Molecular docking revealed that PFOA and PFOS can bind to nuclear factor-κB (NF-κB) by forming stable hydrogen bonds. PFOA and PFOS exposure upregulated the gene expression of NF-κB and its downstream genes. Significant correlations between the expression of genes involved in the NF-κB pathway and immune-related indicators suggests that PFOA- and PFOS-induced immunotoxicity was associated with the activation of NF-κB. Our findings provide novel insights into the potential role of NF-κB in immunotoxicity induced by PFOA and PFOS in frogs.