Establishment of a Chinese critical care database from electronic healthcare records in a tertiary care medical center.

The medical specialty of critical care, or intensive care, provides emergency medical care to patients suffering from life-threatening complications and injuries. The medical specialty is featured by the generation of a huge amount of high-granularity data in routine practice. Currently, these data are well archived in the hospital information system for the primary purpose of routine clinical practice. However, data scientists have noticed that in-depth mining of such big data may provide insights into the pathophysiology of underlying diseases and healthcare practices. There have been several openly accessible critical care databases being established, which have generated hundreds of scientific outputs published in scientific journals. However, such work is still in its infancy in China. China is a large country with a huge patient population, contributing to the generation of large healthcare databases in hospitals. In this data descriptor article, we report the establishment of an openly accessible critical care database generated from the hospital information system.

Maternal serum zinc level is associated with risk of preeclampsia: A systematic review and meta-analysis.

Background: Preeclampsia (PE) is a multi-organ syndrome that onsets in the second half of pregnancy. It is the second leading cause of maternal death globally. The homeostasis of zinc (Zn) levels is important for feto-maternal health. Objective: We aimed to collect all studies available to synthesize the evidence regarding the association between maternal Zn levels and the risk of preeclampsia. Methods: A systematic review and meta-analysis was conducted via searching seven electronic databases [PubMed, Web of Science, Embase, African Journals Online (AJOL), ClinicalTrial.gov, and two Chinese databases: Wanfang and Chinese National Knowledge Infrastructure, CNKI]. Studies reporting maternal serum Zn levels in pregnant women with or without preeclampsia were included. Eligible studies were assessed through Newcastle-Ottawa Scale (NOS) and the meta-analysis was performed via RevMan and Stata. The random-effects method (REM) was used for the meta-analysis with 95% confidence interval (CI). The pooled result was assessed using standard mean difference (SMD). The heterogeneity test was carried out using I 2 statistics, and the publication bias was evaluated using Begg's and Egger's test. Meta-regression and sensitivity analysis was performed via Stata software. Results: A total of 51 studies were included in the final analysis. 6,947 participants from 23 countries were involved in our study. All studies went through the quality assessment. The pooled results showed that maternal serum Zn levels were lower in preeclamptic women than in healthy pregnant women (SMD: -1.00, 95% CI: -1.29, -0.70). Sub-group analysis revealed that geographical, economic context, and disease severity may further influence serum Zn levels and preeclampsia. Limitations: There are significant between-study heterogeneity and publication bias among included studies. Conclusions: A lower level of maternal Zn was associated with increased risks of preeclampsia. The associations were not entirely consistent across countries and regions worldwide. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=337069, Identifier: CRD42022337069.

Long Non-coding RNA SNHG12, a New Therapeutic Target, Regulates miR-199a-5p/Klotho to Promote the Growth and Metastasis of Intrahepatic Cholangiocarcinoma Cells.

Background: Small nucleolar RNA host gene 12 (SNHG12) is a newly identified long non-coding RNA (lncRNA) whose involvements have been explored in several cancers. Our study aimed to explore the functions of SNHG12 on intrahepatic cholangiocarcinoma (ICC) progression and its interaction with miR-199a-5p and Klotho. Methods: RT-PCR was performed to examine the expressions of SNHG12, miR-199a-5p and Klotho in ICC cells. Cell counting kit-8 (CCK-8), colony formation assays and transwell assays were applied to analyze the proliferation, migration and invasion of ICC cells. Luciferase assays, RIP assays and RNA pull-down assays were carried out to demonstrate the direct binding relationships among SNHG12, miR-199a-5p and Klotho. The xenograft nude models were applied to test the effects of SNHG12 on ICC tumor growth. Results: The expression of SNHG12 and Klotho was distinctly increased in ICC cells, while miR-199a-5p expressions were decreased. Functionally, the silence of SNHG12 inhibited the proliferation and metastasis of ICC cells, while miR-199a-5p overexpression exhibited an opposite result. Mechanistically, Knockdown of SNHG12 significantly suppressed the expressions of miR-199a-5p by sponging it, and then increased Klotho expression. The final in vivo experiments suggested that the silence of SNHG12 distinctly inhibited tumor growth. Conclusion: Our findings indicated that SNHG12 inhibited cell proliferation and metastasis process of ICC cells through modulating the miR-199a-5p/Klotho axis and it is expected to become a potential therapeutic target for ICC.

mir-155 regulates cardiac allograft rejection by targing the expression of suppressor of cytokine signaling-1 (DOCS1) in dendritic cells.

Previously, we observed that mir-155 is induced during dendritic cell (DC) differentiation. We now demon-strated convincing evidence indicating that mir-155 promotes DC maturation and regulates its capacity for antigen presentation and induction of alloreactive T cell activation. Interestingly, the induction of miR-155 expression in DCs is dependent on the TLR4/Myd88/NF-κB signaling. Our mechanistic studies further revealed that SOCS1 is a direct target for mir-155, and by binding to its 3'UTR, mir-155 is likely to affect SOCS1 translation. Suppression of mir-155 expression in DCs significantly attenuated LPS-induced DC maturation along with reduced capability to stimulate allogeneic T cell proliferation. As a result, administration of antagomiR-155 provided protection for cardiac allografts from rejection. Together, our data support that suppression of miR-155 in DCs could be a viable therapeutic strategy for prevention and treatment of allograft rejection in clinical setting of transplantation.