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.

Esophageal cancer is a unique malignant disease in China. A fundamental difference exists between the Chinese population and the western population on esophageal cancer in terms of epidemiology, histogenesis, and carcinogenic risk factors. Therefore, ap-plying the western academic achievements to Chinese is difficult. Thus, Chinese scientists have the responsibility to conquer esopha-geal cancer in China. This article reviews the progress of esophageal cancer focused on the molecular mechanism for interactions of ge-netic and environmental risk factors and human esophageal multistage carcinogenesis.

Objective To observe the expression of survivin and Aurora B in human pancreatic cancer BXPC3 cells after the treatment of sulindac and to explore the potential mechanism. Methods MTr assay was used to determine the effect of sulindac on the proliferation of the BXPC3 cells. RT-PCR was used to detect the expression of mRNA level of survivin and Aurora B, western blot was used to detect protein expression of survivin and Aurora B Thr-232. Cell cycle and apoptosis were detected by flow eytometry (FCM). Results The BXPC3 cells were inhibited by sulindac in a dose and time-dependent manner; the expression of mRNA of survivin and Aurora B were both significantly decreased from 1.5644 and 0.6554 to 0. 4372 and 0.1132 (P< 0.01), the expression of survivin protein and the phosphorylation of Aurora B Thr-232 were also decreased from 1.2735 and 0.4680 to 0.2126 and 0.2546 (P<0.01); the proportion of cells in the G0/G1 phase was increased from (56.65±1.93)% to (70.58±3.21)% (P<0.01). Conclusions Sulindac had inhibitory effects on the growth of BXPC3 cells, the possible mechanism was via decreasing the expression of survivin which depressed the activity of Aurora B, then the CPC was influenced. The most of the cells were blocked in the G0/G1 phase, and the cells' mitosis was inhibited.

Objective To investigate the effect of genistein on Notch-1, SHH and HHIP gene expression and on the cell cycle and proliferation of of BxPC3 cells. Methods Human pancreatic cancer cell line BxPC3 was cultured. The BxPC3 cells were treated with genistein and then the total RNA and protein were extracted. RT-PCR was used to detect the expression of Notch-1 mRNA, SHH mRNA and HHIP mRNA. Noteh-1 and SHH protein was determined by western blotting. MTT assay was used to detect proliferation of BxPC3 cells. The cell cycle of BxPC3 cells was measured by Propidium iodide (PI) and flow cytometry. Results The inhibiting rate was 67.17%±2.32% when BxPC3 cell lines were treated by 20μg/ml genistein for 48 hours. Notch-1 mRNA was down-regulated from 2.454±0.068 to 1.304±O.169 ; SHH mRNA was down-regulated from 0.959±0.023 to O.472±0.077 ; HHIP mRNA was up-regulated from 0.625±O.158 to 1.761±0.121. Notch-1 protein expression was down-regulated from 1.361±0.109 to 0.760±0.114; SHH protein expression was down-regulated from 0.265±0.018 to 0.129±0.013. (52.77±9.47)% cells were hindered in G2/M stage. Conclusions Genistein could down-regulate Notch-1 expression and inactivate Hedgehog signaling pathway and inhibit the proliferation of pancreatic cancer cells.

Objective To investigate the common risk factors of primary hepatocellular cancer (PHC) in Guizhou province . Methods The group case-control study was adopted .The main related-factors of primary PHC in Guizhou provincial population and the relation between drinking combined hepatitis B viral infection with the PHC occurrence were analyzed by the unconditional Logistic regression analysis and the stratification analysis .Results Drinking(OR=2 .948 ,95% CI 2 .096-4 .146 ,P=0 .000) ,eco-nomic status 5 years ago(OR=0 .386 ,95% CI 0 .279 -0 .534 ,P= 0 .000) ,family history of PHC(OR= 2 .402 ,95% CI 1 .372 -4 .206 ,P=0 .002) ,cigarette smoking (OR=3 .468 ,95% CI 2 .265 -5 .311 ,P=0 .000) ,chronic liver disease(OR= 1 .502 ,95% CI 1 .054-2 .141 ,P=0 .024) ,HBV infection(OR=31 .999 ,95% CI 19 .318 -53 .002 ,P=0 .000) and diabetes mellitus(OR=4 .750 , 95% CI 2 .761-8 .171 ,P=0 .000) ,the differences between the patients group and the control group had statistical significance ;the OR value of drinking combined with HBV infection was 96 .903(95% CI 35 .265-266 .275 ,P=0 .000) .Conclusion HBV infection is still the common risk factor of PHC in Guizhou provincial population .Drinking can increase the risk in the individuals infected with HBV .

Objective:To investigate the expression level of synaptophysin (Syn), tissue neuronal cell adhesion molecule 56 (CD56) and chromogranin A (CgA) in 92 primary esophageal small cell carcinoma (PESC) and to explore its repationship with clinicopathological features and clinical outcome. Methods:Immunohistochemical studies of CD56, CgA, and Syn were performed in 92 paraffin-embed-ded tissues with clinical-related information obtained from 500,000 esophageal and gastric cardia carcinoma databases established by Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital of Zhengzhou University in Henan, China. Binary logistic regression was used to analyze the correlations of CgA, Syn, and CD56 expression with clinicopathological features. Kaplan-Mei-er survival analysis and Cox proportional hazards regression models were performed for univariate and multivariate survival analyses. Log-rank test was used to compare the difference in survival rates. Results:The CgA-positive expression rate in PESC at lower segment of esophagus (72.2%) was higher than those at the middle and lower segments (41.1%, 10.0%) (P=0.001). The expression level of CD56, CgA, and Syn was not correlated with gender (P=0.262, 0.998, 0.931), age (P=0.250, 0.998, 0.703), tumor invasion (P=0.253, 0.997, 0.061), and lymph node metastasis (P=0.767, 0.998, 0.613). Univariate analysis showed no survival influence in patients with and without lymph node metastasis (P=0.563). Multivariate survival analysis showed that patients with PESC mixed squamous cell car-cinoma (HR=2.58;95%Cl, 1.11-5.98) and higher CgA protein expression (HR=1.87;95%Cl, 1.02-3.43) exhibited a longer survival time than those with pure PESC and without CgA expression. Conclusion:Tissue CgA level was associated with tumor location in PESC. His-tological type and tissue CgA expression were independent important prognostic factors, and lymph node metastasis exerted no influ-ence on survival in PESC.

Non-alcoholic fatty liver disease (NAFLD) is a common liver disease in clinical practice and has a complex pathogenesis. At present, the "two- or three-hit" theory is still widely acknowledged as the major pathogenesis of NAFLD. However, in recent years, the role of liver immunological inflammation in the development and progression of NAFLD has been taken more and more seriously. This article elaborates on the mechanism of liver immunological inflammation in the development and progression of NAFLD from the perspective of liver immunological inflammation.

Objective: To observe the effects of blueberry and nuclear expression of transcription factor-кb (NF-кb) p65 in an experimental rat model of liver fibrosis. Methods: Forty-five Sprague-Dawley rats were randomly divided into isotonic saline control group (A); model group (B); blueberry juice prevention group (C, 15 g/kg); dan-shao-hua-xian capsule prevention group (D, 1 g/kg); and blueberry juice + dan-shao-hua-xian capsule prevention group (E). Rat liver fibrosis model was established by covalent compound carbon tetrachloride (CCl₄). Each prevention group was given the corresponding dose of blueberry juice or (and) dan-shao-hua-xian capsule, and the rats were sacrificed after 8 weeks. The degree of liver fibrosis was evaluated by hematoxylin and eosin stain. A liver tissue of NF-κBp65 was detected by immunohistochemical method. The NF-κBp65 protein expression of liver tissue and transforming growth factor (TGF) β1 was detected by Western blot. Data of multiple groups were compared by one-way analysis of variance, and rank sum test. Results: Immunohistochemistry detected that TGFβ1 protein was mainly expressed in mesenchymal origin of hepatic stellate cells. The expression level of group A (3.75 ± 1.67) was low, while those of group B (9.00 ± 2.07), C (7.33 ± 1.00), D (6.00 ± 1.51), and E (3.5 ± 1.41) were high. However, the expression level of TGF-β1 protein in hepatic tissues of group B was significantly higher than that of group C, D and E [group E: 3.5 ± 1.41, F = 18.350, P < 0.05]. In addition, group D was higher than group E (P < 0.05). The expression of NF- kappa Bp65 protein was very complex, and the expression patterns in different groups were different (Statistical calculation of experimental data were based on expression of liver cells). Compared with group B (4.37 ± 2.13), the relative expression levels of NF-κBp65 protein in-group A (0.46 ± 0.25), group C (2.76 ± 1.01), group D (2.13 ± 1.51), group E (1.88 ± 0.99) were significantly decreased (F = 27.490, P < 0.05), and the expression trend was consistent with TGFβ1 protein. Western blot detected NF-κBp65 protein in liver tissues of rats. Compared with group A, levels in groups B, C, D and E were significantly increased (F = 96.983, P < 0.05), and groups C, D and E were significantly lower. The E group was significantly lower than the C group (F = 96.983, P < 0.05), and the degree of hepatic fibrosis was lower in each prevention group than in the B group (T = 24.1, P < 0.05). Conclusion Blueberries have preventive effect on CCl4-induced hepatic fibrosis in rats, and its preventive mechanism may inhibit the expression and activation of NF-κBp65 in hepatocytes, thereby reducing TGFβ1- mediated production or activation.

Objective:To observe the effect of nocturnal nutritional support on the improvement of nutritional status and liver function in patients with hepatitis B cirrhosis.Methods:A total of 60 patients with hepatitis B cirrhosis who were treated at the Affiliated Hospital of Guizhou Medical University from April 2011 to August 2018 were selected, and they were divided into nutritional intervention group and control group according to the random digital table method, with 30 cases in each group.The two groups were given basic medical treatment, and the nutritional intervention group was given basic treatment plus 30g of complex functional nutrients, once per night, for 12 weeks.The changes of liver function and nutritional status of the two groups were observed every 4 weeks, and the occurrence of complications was recorded.Results:Before intervention, the ALB, PA, TBIL, body mass index, triceps cutaneous fold thickness and grip strength had no statistically significant differences between the two groups(all P>0.05). After 12 weeks of intervention, the albumin [(32.61±1.78) g/L], pre-albumin [(116.65±11.92) g/L], total bilirubin [(36.6±5.86)μmol/L], body mass index [(22.23±2.92) kg/m 2], skinfold [(17.34±1.31) mm], the grip strength [(23.36±2.44)kg] in the intervention group were superior to the control group[(30.38±1.58)g/L, (101.22±7.76)g/L, (47.75±4.83)μmol/L, (21.07±2.11)kg/m 2, (16.07±1.40)mm, (20.01±2.70)kg], the differences were statistically significant between the two groups( t=4.946, 5.105, 5.881, 2.407, 2.272, 3.805, all P<0.05). The incidence of the complications in the intervention group was 10%(3/30), which in the control group was 33%(10/30), the difference was statistically significant between the two groups(χ 2=4.381, P=0.033). Conclusion:Providing nutritional support at night can improve the nutritional status of patients with hepatitis B cirrhosis, promote the repair of liver function, and reduce the incidence of complications.

Doxorubicin (Dox) is widely used to the treatment of cancer, however, it could cause damage to gastric mucosa. To investigate the protective effects and related mechanisms of coenzyme Q10 (CoQ10) and vitamin C (VC) on Dox-induced gastric mucosal injury, we presented the survey of the 4 groups of the rats with different conditions. The results showed Dox treatment significantly induced GES-1 apoptosis, but preconditioning in GES-1 cells with VC or CoQ10 significantly inhibited the Dox-induced decrease and other harm effects, including the expression and of IκKβ, IκBα, NF-κB/p65 and tumor necrosis factor (TNF-α) in GES-1 cells. Moreover, high-throughput sequencing results showed Dox treatment increased the number of harmful gut microbes, and CoQ10 and VC treatment inhibited this effect. CoQ10 and VC treatment inhibits Dox-induced gastric mucosal injury by inhibiting the activation of the IkKB/IκBα/NF-κB/p65/TNF-α pathway, promoting anti-inflammatory effects of gastric tissue and regulating the composition of the intestinal flora.