Tied Infections: How Social Connectedness to Other COVID-19 Patients Influences Illness Severity.

Expanding on recent research on the transmission of COVID-19 via social networks, this article argues that exposure to familial and other close contacts who already have the disease may increase the severity of one's subsequent illness. We hypothesize that having family members or close contacts who were diagnosed with COVID-19 before one's own diagnosis exacerbates illness severity due to several potential mechanisms including changes in available social support access, increased stress and strain, and increased viral load due to the nature of one's exposure to the novel coronavirus. We analyze administrative data of all 417 patients who were diagnosed with COVID-19 in the Chinese city of Shenzhen between January 8 and February 25, 2020. Our analyses show that, when patients had family members or close ties diagnosed with COVID-19, they experienced more severe illness. We also find that patients with infected family members or close contacts did not have significantly extended total illness duration, due to their reduced time to diagnosis. The implications of both findings are discussed.

A dataset of storm surge reconstructions in the Western North Pacific using CNN.

The relatively short duration of available tide gauge records poses challenges for conducting comprehensive statistical analyses of storm surges in the Western North Pacific. To address this issue, we employ a convolutional neural network model to reconstruct the maximum daily storm surge at 160 tide gauges from 1900 to 2010 in the Western North Pacific. The reconstructed dataset serves multiple purposes. Firstly, it facilitates the identification of regions where notable changes in the storm surges have occurred in the past. Additionally, the dataset enables long-term analyses of the storm surge climate, offering insights into historical patterns and variations. Furthermore, it provides a solid foundation for conducting robust extreme value analyses. To ensure accessibility, the data are publicly available through a repository, allowing for easy access and utilization by the broader scientific community and the general public. Overall, our research contributes to the field of oceanography by providing a dataset that aids in understanding the historical storm surge dynamics in the Western North Pacific region.

Construction of lncRNA-miRNA-mRNA regulatory network in severe asthmatic bronchial epithelial cells: A bioinformatics study.

Asthma is a chronic respiratory disease caused by environment-host interactions. Bronchial epithelial cells (BECs) are the first line of defense against environmental toxins. However, the mechanisms underlying the role of BECs in severe asthma (SA) are not yet fully understood. Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) have been shown to play important roles in the regulation of gene expression in the pathogenesis of SA. In this study, bioinformatics was used for the first time to reveal the lncRNA-miRNA-mRNA regulatory network of BECs in SA. Five mRNA datasets of bronchial brushing samples from patients with SA and healthy controls (HC) were downloaded from the Gene Expression Omnibus (GEO) database. A combination of the Venn diagram and robust rank aggregation (RRA) method was used to identify core differentially expressed genes (DEGs). Protein-protein interaction (PPI) analysis of core DEGs was performed to screen hub genes. The miRDB, miRWalk, and ENCORI databases were used to predict the miRNA-mRNA relationships, and the ENCORI and starBase v2.0 databases were used to predict the upstream lncRNAs of the miRNA-mRNA relationships. Four core DEGs were identified: carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5), interleukin-1 receptor type 2 (IL1R2), trefoil factor 3 (TFF3), and vascular endothelial growth factor A (VEGFA). These 4 core DEGs indicated that SA was not significantly associated with sex. Enrichment analysis showed that the MAPK, Rap1, Ras, PI3K-Akt and Calcium signaling pathways may serve as the principal pathways of BECs in SA. A lncRNA-miRNA-mRNA regulatory network of the severe asthmatic bronchial epithelium was constructed. The top 10 competing endogenous RNAs (ceRNAs) were FGD5 antisense RNA 1 (FGD5-AS1), metastasis associated lung adenocarcinoma transcript 1 (MALAT1), X inactive specific transcript (XIST), HLA complex group 18 (HCG18), small nucleolar RNA host gene 16 (SNHG16), has-miR-20b-5p, has-miR-106a-5p, hsa-miR-106b-5p, has-miR-519d-3p and Fms related receptor tyrosine kinase 1 (FLT1). Our study revealed a potential mechanism for the lncRNA-miRNA-mRNA regulatory network in BECs in SA.

Research trends and hotspots of exosomes in respiratory diseases.

Currently, theoretical studies on exosomes in respiratory diseases have received much attention from many scholars and have made remarkable progress, which has inestimable value and potential in future clinical and scientific research. Unfortunately, no scholar has yet addressed this field's bibliometric analysis and summary. We aim to comprehensively and profoundly study and explore the present situation and highlights of exosome research at the stage of respiratory diseases and to provide meaningful insights for the future development of this field. The WOSCC literature was gathered for the study using bibliometrics, and the data were collected and analyzed using CiteSpace, VOSviewer, Microsoft Excel, and Endnote software. The publication language is "English," and the search strategy is TS = (exosome OR exosomes OR exosomal) AND TS = (respiratory OR lung). The search time is from the beginning of the WOS construction, and the deadline is July 11, 2022, at 22:00 hours. The literature types selected were dissertation, review paper, and online published paper. The analysis includes 2456 publications in 738 journals from 76 countries, 2716 institutions, and 14,568 authors. The field's annual publications have been rising, especially in recent years. China and the US lead research, and prominent universities, including Harvard Medical School, Shanghai Jiao Tong University, and Fudan University, are essential research institutes. Takahiro Ochiya, whose research focuses on exosomes and lung cancer, and Clotilde Théry, a pioneering exosome researcher, are the most cited authors in this field. The key terms include lung cancer, non-small cell lung cancer, mesenchymal stem cells, intercellular communication, exosomal miRNAs, and oncology. Cell biology, biochemistry & biotechnology, and oncology are related fields. The final summary of research hotspots is exosomes and lung cancer, mesenchymal stem cell-derived exosomes and lung inflammation, and miRNAs in exosomes as biomarkers for respiratory illnesses. The present research situation and relevant hotspots of the area were analyzed through bibliometric studies on exosomes in respiratory diseases. The research development in this field has a considerable upside, and the exosome's function in diagnosing, treating, monitoring, and prognosis of respiratory illnesses cannot be taken lightly. Moreover, we believe the research results will bring the gospel to many patients with clinical respiratory diseases shortly.

Serine hydroxymethyltransferase 2 knockdown induces apoptosis in ccRCC by causing lysosomal membrane permeabilization via metabolic reprogramming.

Serine hydroxymethyltransferase 2 (SHMT2) plays an important role in converting serine to glycine and supplying carbon to one-carbon metabolism to sustain cancer cell proliferation. However, the expression, function, and underlying mechanisms of SHMT2 in clear cell renal cell carcinoma (ccRCC) remain largely unknown. In this study, we demonstrated that SHMT2 was upregulated in ccRCC tissues compared with controls and associated with patient survival. SHMT2 knockdown inhibited proliferation, migration, and invasion in ccRCC cells. Overexpression of SHMT2 promoted tumor progression. Mechanistically, SHMT2 depletion disrupted one-carbon metabolism, increased reactive oxygen species (ROS) levels, and decreased ATP levels via metabolic reprogramming, which destroyed cell homeostasis. The SHMT2 knockdown-induced stress activated autophagy. A mass of autophagosomes fused with lysosomes, resulting in lysosomal membrane permeabilization (LMP) and leakage of lysosomal contents into the cytoplasm, which eventually led to apoptosis. Our work reveals that SHMT2 functions as an oncogenic gene to promote ccRCC progression. SHMT2 depletion induces apoptosis by causing LMP through excessive activation of the autophagy-lysosome pathway via metabolic reprogramming.

High-speed DNA-based rolling motors powered by RNase H.

DNA-based machines that walk by converting chemical energy into controlled motion could be of use in applications such as next-generation sensors, drug-delivery platforms and biological computing. Despite their exquisite programmability, DNA-based walkers are challenging to work with because of their low fidelity and slow rates (∼1 nm min(-1)). Here we report DNA-based machines that roll rather than walk, and consequently have a maximum speed and processivity that is three orders of magnitude greater than the maximum for conventional DNA motors. The motors are made from DNA-coated spherical particles that hybridize to a surface modified with complementary RNA; the motion is achieved through the addition of RNase H, which selectively hydrolyses the hybridized RNA. The spherical motors can move in a self-avoiding manner, and anisotropic particles, such as dimerized or rod-shaped particles, can travel linearly without a track or external force. We also show that the motors can be used to detect single nucleotide polymorphism by measuring particle displacement using a smartphone camera.