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Background Lupus nephritis (LN) is an autoimmune-related kidney disease with a poor prognosis, however the potential pathogenic mechanism remains unclear and there is a lack of precise biomarkers. Therefore, a thorough screening and identification of renal markers in LN are immensely beneficial to the research on its pathogenic mechanisms and treatment strategies. Methods We utilized bioinformatics to analyze the differentially expressed genes (DEGs) at the transcriptome level of three clusters: total renal, glomeruli, and renal tubulointerstitium in the GEO database to discover potential renal biomarkers of LN. We utilized NephroSeq datasets and measured mRNA and protein levels in the kidneys of MRL/lpr mice to confirm the expression of key DEGs. Results Seven significantly differential genes (EGR1, MME, PTPRC, RORC, MX1, ZBTB16, FKBP5) were revealed from the transcriptome database of GSE200306, which were mostly enriched in the pathway of the hematopoietic cell lineage and T cell differentiation respectively by KEGG and GO analysis. The seven hot differential genes were verified to have consistent change trends using three datasets from NephroSeq database. The receiver operating characteristic (ROC) curve indicated that five DEGs (PTPRC, MX1, EGR1, MME and RORC) exhibited a higher diagnostic ROC value in both the glomerulus and tubulointerstitium group. Validation of core genes using MRL/lpr mice showed that MME and PTPRC exhibit significantly differential mRNA and protein expression patterns in mouse kidneys like the datasets. Conclusions This study identified seven key renal biomarkers through bioinformatics analysis using the GEO and NephroSeq databases. It was identified that MME and PTPRC may have a high predictive value as renal biomarkers in the pathogenesis of LN, as confirmed by animal validation.

In mid-December 2019, a novel atypical pneumonia broke out in Wuhan, Hubei Province, China and was caused by a newly identified coronavirus, initially termed 2019 Novel Coronavirus and subsequently severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). As of 19 May 2020, a total of 4,731,458 individuals were reported as infected with SARS-CoV-2 among 213 countries, areas or territories with recorded cases, and the overall case-fatality rate was 6.6% (316,169 deaths among 4,731,458 recorded cases), according to the World Health Organization. Studies have shown that SARS-CoV-2 is notably similar to (severe acute respiratory syndrome coronavirus) SARS-CoV that emerged in 2002–2003 and Middle East respiratory syndrome coronavirus (MERS-CoV) that spread during 2012, and these viruses all contributed to global pandemics. The ability of SARS-CoV-2 to rapidly spread a pneumonia-like disease from Hubei Province, China, throughout the world has provoked widespread concern. The main symptoms of coronavirus disease 2019 (COVID-19) include fever, cough, myalgia, fatigue and lower respiratory signs. At present, nucleic acid tests are widely recommended as the optimal method for detecting SARS-CoV-2. However, obstacles remain, including the global shortage of testing kits and the presentation of false negatives. Experts suggest that almost everyone in China is susceptible to SARS-CoV-2 infection, and to date, there are no effective treatments. In light of the references published, this review demonstrates the biological features, spread, diagnosis and treatment of SARS-CoV-2 as a whole and aims to analyse the similarities and differences among SARS-CoV-2, SARS-CoV and MERS-CoV to provide new ideas and suggestions for prevention, diagnosis and clinical treatment.

Background Kawasaki disease (KD) is an acute febrile illness of early childhood. The exact etiology of the disease remains unknown. At present, research on KD is mostly limited to susceptibility genes, infections, and immunity. However, research on the correlation between gut microbiota and KD is rare. Methods Children with a diagnosis of acute KD and children undergoing physical examination during the same period were included. At the time of admission, the subjects’ peripheral venous blood and feces were collected. Faecal samples were analyzed for bacterial taxonomic content via high-throughput sequencing. The abundance, diversity, composition, and characteristic differences of the gut microbiota in KD and healthy children were compared by alpha diversity, beta diversity, linear discriminant analysis and LDA effect size analysis. Blood samples were used for routine blood examination, biochemical analysis, and immunoglobulin quantitative detection. Results Compared with the control group, the community richness and structure of gut microbiota in the KD group was significantly reduced (Chao1 richness estimator, mean 215.85 in KD vs. mean 725.76 in control, p < 0.01; Shannon diversity index, mean 3.32 in KD vs. mean 5.69 in control, p < 0.05). LEfSe analysis identified two strains of bacteria significantly associated with KD: Bacteroidetes and Dorea. Bacteroidetes were enriched in healthy children (mean 0.16 in KD vs. mean 0.34 in control, p < 0.05). Dorea was also enriched in healthy children but rarely existed in children with KD (mean 0.002 in KD vs. mean 0.016 in control, p < 0.05). Compared with the control, IgA and IgG in the KD group decreased (IgA, median 0.68 g/L in KD vs. median 1.06 g/L in control, p < 0.001; IgG, median 6.67 g/L in KD vs. median 9.71 g/L in control, p < 0.001), and IgE and IgM levels were not significantly changed. Conclusions Dysbiosis of gut microbiota occurs in children with acute KD and may be related to the etiology or pathogenesis of KD. It is worth noting that for the first time, we found that Dorea, a hydrogen-producing bacterium, was significantly reduced in children with acute KD. Overall, our results provide a theoretical basis for the prevention or diagnosis of KD based on intestinal microecology.

Background Beginning in December 2019, coronavirus disease 2019 (COVID-19) caused an outbreak of infectious pneumonia. The Chinese government introduced a series of grounding measures to prevent the spread of COVID-19. The living and working patterns of many scientific researchers also underwent significant changes during this period. Methods An opportunity sample (n = 251) was obtained in China using a questionnaire with 42 questions on scientific research progress and psychological stress during the COVID-19 epidemic. Results Of the 251 participants, 76.9% indicated that their research was affected by the COVID-19 outbreak, and participants who were affected by the outbreak had higher stress levels than those who were not affected. Participants who conducted COVID-19 research and indicated concern that they would fail to finish the research on time were more likely to indicate high levels of stress. Respondents indicated that extending deadlines (64.1%), receiving support from superiors for research (51.8%), and increasing benefits for researchers (51.0%) would likely relieve outbreak-related stress. Conclusion The COVID-19 outbreak had a major impact on the experiments of researchers in the life sciences, especially in basic and clinical medicine. It has also caused high levels of psychological stress in these populations. Measures should be taken to relieve psychological pressure on basic medical researchers and students who will soon complete their degrees (e.g., Master’s and PhD candidates in graduation years).