Objective:To investigate the effect of focal adhesion kinase related non kinase (FRNK) on the activation and migration of hepatic stellate cells (HSCs).Methods:Human liver tissue was divided into healthy control group and fibrosis group from March 2019 to September 2019 in Affiliated Hospital of Guizhou Medical University. C57BL/6 mice were divided into wild type (WT) and FRNK gene knockout type (FRNK -/-) groups. The liver fibrosis model was established with carbon tetrachloride (CCl 4). After that, FRNK gene overexpression (Ad-FRNK) was constructed with adenovirus vector. HE and Masson staining were used to evaluate the pathological changes and fiber deposition of liver tissue. Western blot was used to detect the expression of PY397-FAK and α-SMA protein. Mouse primary HSCs were extracted, and the effect of FRNK on HSCs migration was detected by wound healing, activation of Rac and Rho was detected by Western blot. Results:The expression of PY397-FAK protein in human liver tissue with hepatic fibrosis was significantly higher than that in healthy control group (0.88±0.09 vs. 0.73±0.09). FRNK was significantly lower than that in control group(0.68±0.09 vs. 0.79±0.11). After animal model was set up, the degree of liver fibrosis in FRNK -/-mice (153±13)% was more serious than that in WT (100%) group. The expression of PY397-FAK and α-SMA protein was significantly elevated (2.50±0.23 vs. 0.75±0.09, 1.46±0.20 vs. 0.92±0.10). After FRNK gene was re-expressed (100%), the degree of liver fibrosis was mainly reversed [(74±6)%], and the expression of PY397-FAK and α-SMA was accordingly decreased(0.68±0.11 vs. 1.12±0.19,0.68±0.10 vs. 0.85±0.06). In vitro, FRNK inhibited the migration of HSCs [WT∶FRNK -/-∶Ad-FRNK,(339±49)%∶(580±53)%∶(259±33)%] and the activation of Rac and Rho proteins (Rac: 0.54±0.07 vs. 0.91±0.10 vs. 0.77±0.12,Rho:0.45±0.05 vs. 0.64±0.06 vs. 0.53±0.07), all P<0.01. Conclusions:FRNK can inhibit the activation and migration of HSCs which contributed to liver fibrosis. The potential mechanism is related to down regulation of PY397-FAK and inhibition of Rac and Rho activation.

Objective To systematically evaluate the correlation between vitamin D deficiency in early pregnancy and the outcome of preterm birth.Method PubMed,Embase,the Cochrane Library,Web of Science,Ebsco,CBM,CNKI and Wanfang Data databases were searched to collect cohort studies and case-control studies on the correlation between vitamin D deficiency in early pregnancy and preterm birth outcomes,and the retrieval time was from the establishment of the database to June 2019.Two researchers independently reviewed the literature,extracted the data and evaluated the risk of bias in the included studies.RevMan 5.3 software was used for Meta analysis.Result A total of 6 cohort studies and 3 nested case-control studies were included.A total of 30 891 newborns were included,including 1 912 premature infants.3 Chinese articles and 6 English articles were reviewed including three studies from China,three from North America,two from Europe and one from Australia.The diagnostic criteria for vitamin D deficiency and preterm birth were similar in these studies.After adjusting for age,race and other confounding factors,Meta-analysis results showed that vitamin D deficiency in early pregnancy did not increase the risk of preterm birth (OR =1.04,95％ CI 0.90 ～ 1.20,P =0.63).Subgroup analysis were conducted according to the study type,measurement method and regional population,and the results were consistent with the overall results.No significant publication bias was found in the meta-analysis results.Conclusion Current evidence suggests that vitamin D deficiency in early pregnancy has no significant influence on preterm birth.