Xiumei Li

Background: The presence of biological particles in the air inside operating theatres has the potential to cause severe surgical site infections. Recently, laminar airflow systems have been regarded as a means to reducing surgical site infections using airborne microbes. Still, other publications have argued the benefits of laminar airflow systems, stating the likelihood of adverse effects. Therefore, we will conduct this systematic study to evaluate the applicational value of adopting laminar airflow systems in operating theatres to minimize surgical site infections. Methods: Reporting of this study adheres to the guidelines of Preferred Reporting Items for Systematic Review and Meta-analysis Protocols. The authors will perform a systematic search on MEDLINE, Web of Science, EMBASE, the China national knowledge infrastructure, and the Cochrane Library from their commencement until June 2021. The search will identify relevant randomized and non-randomized controlled trials that evaluates the applicational value of using laminar airflow ventilation in surgical theatres to minimize surgical site infections. There are no restrictions on language. Two authors will independently screen the identified studies, perform data extraction, and use an appropriate method to evaluate the bias risk in the included studies. Results: The work done in the present study will enhance the existing literature on the applicational value of laminar airflow ventilation in surgical theatre to reduce surgical site infections. Conclusion: The outcomes are a reference for healthcare practitioners and patients when making informed decisions regarding care during surgeries.

Esophageal cancer (EC) is the eighth most prevalent cancer and the sixth leading cause of cancer-related mortality worldwide. As an antiapoptotic and a proapoptotic protein, respectively, survivin and Bad play an important role in carcinogenesis of the most human cancers including EC. However, the regulatory relationships between them remain unclear. We sought to investigate the effects of survivin knockdown and overexpression on the expression of Bad gene, cell cycle progression, and apoptosis of esophageal carcinoma cell. The mRNA expression levels of survivin and Bad were determined in EC tissue samples. The knockdown and overexpression experiments were performed in ECA109 and KYSE450 cells via transfection with survivin overexpression and shRNA plasmids. A Bad overexpression experiment was conducted to confirm the biological effect on knockdown of survivin via modulating Bad expression. RT-qPCR and Western blot analysis were used to detect mRNA and protein expression, respectively. Cell cycle and apoptosis were analyzed by flow cytometry. The chromatin immunoprecipitation (ChIP) was conducted to determine the binding sites of survivin on the promoter of Bad gene. By analyzing the mRNA expression of survivin and Bad in 40 ESCC patient specimens, we found that the positive expression rate of survivin in tumor tissues (88%, 35/40) was remarkably high, compared with the distal nontumor tissues (48%, 19/40, < 0.01). On the other hand, the positive expression rate of Bad in tumor tissues (70%, 28/40) was remarkably low, compared with the distal nontumor tissues (95%, 38/40, < 0.01). Overexpression of survivin decreases Bad mRNA and protein expression and promotes transformation of cell cycle to S phase. Conversely, knockdown of survivin increases Bad mRNA and protein expression and induces cell cycle arrest and apoptosis. Bad overexpression inducing apoptosis of esophageal carcinoma cell shows the similar apoptotic effect with survivin knockdown. ChIP assays indicate that survivin directly binds to the Bad promoter region, diminishing the transcriptional activity of Bad. In conclusion, the result suggested that survivin regulates Bad gene expression by binding to its promoter and modulates cell cycle and apoptosis in esophageal carcinoma cell.

A follow-up study was performed with 169 women of childbearing age who underwent ultrasound-guided percutaneous microwave ablation (UPMWA) therapy for symptomatic uterine fibroids in the Chinese PLA General Hospital from June 2007 to December 2014. This study aimed to observe the incidence of unplanned pregnancies in these women after UPMWA treatment in order to evaluate its effect on natural conception. Ten unplanned pregnancies in nine women were occurred. Of the nine patients, six did not want the pregnancy and chose for induced abortion to end the pregnancy at an early stage. Three chose to continue with the pregnancy and gave birth to a healthy term infant delivered by cesarean section (of these three patients, two had been previously diagnosed as infertility). None of the patients had any serious obstetric complications. After UPMWA treatment for uterine fibroids, patients may conceive naturally, the impact of the procedure on fertility and pregnancy outcomes is worthy of further prospective study in larger sample.

Background: Essential hypertension (EH) is a complex disease as a consequence of interaction between environmental factors and genetic background, but the pathogenesis of EH remains elusive. The emerging tools of network medicine offer a platform to explore a complex disease at system level. In this study, we aimed to identify the key proteins and the biological regulatory pathways involving in EH and further to explore the molecular connectivities between these pathways by the topological analysis of the Protein-protein interaction (PPI) network. Result: The extended network including one giant network consisted of 535 nodes connected via 2572 edges and two separated small networks. 27 proteins with high BC and 28 proteins with large degree have been identified. NOS3 with highest BC and Closeness centrality located in the centre of the network. The backbone network derived from high BC proteins presents a clear and visual overview which shows all important regulatory pathways for blood pressure (BP) and the crosstalk between them. Finally, the robustness of NOS3 as central protein and accuracy of backbone were validated by 287 test networks. Conclusion: Our finding suggests that blood pressure variation is orchestrated by an integrated PPI network centered on NOS3.