An outbreak of novel coronavirus pneumonia occurred worldwide since December 2019, which had been named COVID-19 subsequently. It is extremely transmissive that infection in pregnant women were unavoidable. The delivery process will produce large amount of contaminated media, leaving a challenge for medical personnel to ensure both the safety of the mother and infant and good self-protection. Only rare cases of pregnant women with COVID-19 are available for reference. Here, we report a 30-year-old woman had reverse transcription polymerase chain reaction-confirmed COVID-19 at 36 weeks 2 days of gestation. Significant low and high variability of fetal heart rate baseline and severe variable decelerations were repeated after admission. An emergency cesarean section at 37 weeks 1 day of gestation under combined spinal and epidural anesthesia was performed with strict protection for all personnel. Anesthesia and operation went uneventfully. None of the participants were infected. We can conclude that when confronted with cesarean section in parturient with COVID-19, careful planning and detailed preparation can improve the safety of the mother and infant and reduce the risk of infection for medical staff to help preventing and controlling the epidemic.

Activation of peroxisome proliferator‐activated receptor (PPAR)‐γ suppresses proliferation of rat pulmonary artery smooth muscle cells (PASMCs), and therefore ameliorates the development of pulmonary hypertension in animal models. However, the molecular mechanisms underlying this effect remain largely unknown. This study addressed this issue. The PPARγ agonist rosiglitazone dose‐dependently stimulated heme oxygenase (HO)‐1 expression in PASMCs, 5 μm rosiglitazone inducing a 12.1‐fold increase in the HO‐1 protein level. Cells pre‐exposed to rosiglitazone showed a dose‐dependent reduction in proliferation in response to serotonin; this was abolished by pretransfection of cells with sequence‐specific small interfering RNA against HO‐1. In addition, rosiglitazone stimulated p21WAF1 expression in PASMCs, a 2.34‐fold increase in the p21WAF1 protein level being achieved with 5 μm rosiglitazone; again, this effect was blocked by knockdown of HO‐1. Like loss of HO‐1, loss of p21WAF1 through siRNA transfection also reversed the inhibitory effect of rosiglitazone on PASMC proliferation triggered by serotonin. Taken together, our findings suggest that activation of PPARγ induces HO‐1 expression, and that this in turn stimulates p21WAF1 expression to suppress PASMC proliferation. Our study also indicates that rosiglitazone, a medicine widely used in the treatment of type 2 diabetes mellitus, has potential benefits for patients with pulmonary hypertension.

Lung adenocarcinoma (LUAD) is the most common histological subtype of non-small cell lung cancer, but novel biomarkers for early diagnosis are lacking. Extensive effort has been exerted to identify miRNA biomarkers in LUAD. Unfortunately, high inter-lab variability and small sample sizes have produced inconsistent conclusions in this field. To resolve the above-mentioned limitations, we performed a comprehensive analysis based on LUAD miRNome profiling studies using the robust rank aggregation (RRA) method. Moreover, miRNA-gene interaction network, pathway enrichment analysis and Kaplan-Meier survival curves were used to investigate the clinical values and biological functions of the identified miRNAs. A total of six common differentially expressed miRNAs (DEMs) were identified in LUAD. An independent cohort further confirmed that four miRNAs (miR-21-5p, miR-210-3p, miR-182-5p and miR-183-5p) were up-regulated and two miRNAs (miR-126-3p and miR-218-5p) were down-regulated in LUAD tissues. Pathway enrichment analysis also suggested that the above-listed six DEMs may affect LUAD progression via the estrogen signaling pathway. Survival analysis based on the TCGA dataset revealed the potential prognostic values of six DEMs in patients with LUAD (P-value<0.01). In conclusion, we identified a panel of six miRNAs from LUAD using miRNome profiling studies. Our results provide evidence for the use of these six DEMs as novel diagnostic and prognostic biomarkers for LUAD patients.

Background Circular RNAs (circRNAs) are a new type of extensive non-coding RNAs that regulate the activation and progression of different human diseases, including cancer. However, information on the underlying mechanisms and clinical significance of circRNAs in lung squamous cell carcinoma (LUSC) remains scant. Methods The expression profile of RNAs in 8 LUSC tissues, and 9 healthy lung tissues were assayed using RNA sequencing (RNA-seq) techniques. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to profile the expression of circPVT1 and its relationship with the prognosis of LUSC, i.e., survival analysis. Moreover, in vitro and in vivo experiments were performed to evaluate the impacts of circPVT1 on the growth of tumors. RNA pull-down tests, mass spectrometry, dual-luciferase reporter assessment, and RNA immune-precipitation tests were further conducted to interrogate the cross-talk between circPVT1, HuR, or miR-30d/e in LUSC. Results Our data showed that circPVT1 was upregulated in LUSC tissues, serum, and cell lines. LUSC patients with higher circPVT1 expression exhibited shorter survival rates. The in vivo and in vitro data revealed that circPVT1 promotes the proliferation of LUSC cells. Additionally, mechanistic analysis showed that HuR regulated circPVT1. On the other hand, circPVT1 acted as a competing endogenous RNA (ceRNA) of miR-30d and miR-30e in alleviating the suppressive influences of miR-30d and miR-30e on its target cyclin F (CCNF). Conclusion CircPVT1 promotes LUSC progression via HuR/circPVT1/miR-30d and miR-30e/CCNF cascade. Also, it acts as a novel diagnostic biomarker or treatment target of individuals diagnosed with LUSC.

Sirtuin 1 (SirT1) is involved in the pathogenesis of allergic asthma. This study aimed to investigate whether eX-527, a specific SirT1 inhibitor, exerted suppressive effects on allergic airway inflammation in mice submitted to ovalbumin (oVa) inhalation. in addition, this study assessed whether such a protective role was mediated by autophagy suppression though mammalian target of rapamycin (mTor) activation. Female c57Bl/6 mice were sensitized to oVa and eX-527 (10 mg/kg) was administered prior to oVa challenge. The study found that eX-527 reversed oVa-induced airway inflammation, and reduced OVA-induced increases in inflammatory cytokine expression, and total cell and eosinophil counts in bronchoalveolar lavage fluid. In addition, EX-527 enhanced mTor activation, thereby suppressing autophagy in allergic mice. To assess whether EX-527 inhibited airway inflammation in asthma through the mTor-mediated autophagy pathway, rapamycin was administered to mice treated with eX-527 after oVa sensitization. all effects induced by eX-527, including increased phosphorylated-mTor and decreased autophagy, were abrogated by rapamycin treatment. Taken together, the present findings indicated that EX-527 may inhibit allergic airway inflammation by suppressing autophagy, an effect mediated by mTor activation in allergic mice.