Although talus fractures are not common among foot and ankle injuries, their treatment is difficult because of their complications and poor prognosis. They can be treated conservatively or surgically, with a variety of treatment protocols. At present, the main strategy of surgical treatment is to use strong and effective fixation to restore anatomic structure of the talus and preserve blood supply to the talus as much as possible so that deformity can be avoided and early healing be facilitated. This paper reviews the difficulties and current situation, and summarizes principles and the latest progress in clinical treatment of talus fractures, hoping to provide useful references for the treatment.

Objective To investigate the role of malondialdehyde(MDA),superoxide dismutase(SOD),and interleukin-1β (IL-1β) played in the pathogenesis of acute gouty arthritis and the treatment efficacy of probucol.Methods Acute gouty arthritis model in rat was established with injection of monosodium urate monohydrate (MSU) into the ankle joint cavity,then the joint swelling index was observed periodically,and MDA,SOD,IL-1β,and white blood cell count in the synovial fluid were determined by 72 h.Results The joint swelling index gradually increased,reaching a peak by 11h,and this finding was most obvious in the model group.The joint swelling index in the group treated with high-dose of probucol was significantly lower than that in the model group by 48 h(P＜0.05).The joint swelling indices in the groups treated with moderate and high doses of probucol were lower than that in the model group by 72 h(P＜0.05).The values of MDA in the moderate and high-dose groups were (14.45±3.11) and (11.54 ±3.10) nmol/ml respectively,being significantly lower than that in the model group[(24.46±4.27) nmol/ml,P＜0.01].The amounts of SOD in the moderate and high-dose groups were (25.56±4.51) and (44.61±4.11)U/ml respectively,being higher than that in the model group[(13.32±2.02) U/ml,P＜0.01].The amount of IL-1β in the high-dose group was lower than that in the model group[(15.41 ± 3.12 vs 19.87±3.99)pg,P＜0.05].The white blood cell counts in the moderate and high-dose groups were (11.08±1.64)×l0~7/L and (7.43±1.52) x 10~7/L,being lower than that in the model group[(14.18±2.30)×10~7/L,P＜0.01].Conclusion The levels of MDA and IL-1β in the synovial fluid were raised,while SOD was significantly decreased in acute gouty arthritis.Moderate and high-doses of probucol can effectively control acute gouty arthritis attack.The efficacy of high-dose probucol was equal to that of colchicines.

Objective:To study the relationship between the expression of tumor markers and radical resection in patients with gastric cancer.Methods:The medical records of gastric cancer patients undergoing surgery in Department of Gastrointestinal Surgery, Puji District, Dongguan People′s Hospital Affiliated to Southern Medical University from June 2018 to December 2019 were retrospectively analyzed, and 136 patients were selected.Collected patient data, including general information, the expression levels of tumor markers carcinoembryonic antigen(CEA), carbohydrate antigen 19-9(CA19-9), carbohydrate antigen 72-4(CA72-4), and the surgical method used.The relationship between the expression of tumor markers and radical resection was observed.Results:There was no statistically significant difference in the radical resection rate of gastric cancer in different genders, ages, and locations of gastric cancer (all P>0.05). TNM classification (tumor node metastasis classification) stage III patients had a lower radical resection rate (63.3%(38/60)) than stage I (100%(27/27)) and II (100%(49/49)) (χ 2=58.166 and 81.208, P<0.001). The radical resection rate of CEA(+ ) patients (47.8%(44/92)) was lower than that of CEA(-) patients (90.9%(40/44))(χ 2=23.394, P<0.001). The radical resection rate of CA19-9(+ ) patients (47.7%(42/88)) was lower than that of CA19-9(-) patients(87.5%(42/48))(χ 2=20.804, P<0.001). The radical resection rate of CA72-4(+ ) patients (54.3%(51/94)) was lower than that of CA72-4(-) patients (78.6%(33/42)) (χ 2=7.268, P=0.007). The variables with P<0.1 in univariate analysis were included in the logistic regression model, including 4 variables including TNM stage, CEA, CA19-9, and CA72-4.The results showed that TNM staging ( OR=1.169, 95% CI=0.925-1.634, P=0.001), CEA ( OR=1.067, 95% CI=1.364-4.338, P=0.024), CA19-9( OR=3.012, 95% CI=1.679-6.317, P=0.007), and CA72-4 were independent risk factors for radical resection( OR=5.364, 95% CI=0.675-3.224, P=0.004). The number of positive expressions of tumor markers was negatively correlated with the radical resection rate ( r=-0.621, P<0.05). The expression levels of CEA, CA19-9, and CA72-4 in patients with radical resection were 75.36(3.76, 198.20)μg/L, 152.76(34.81, 241.09)kU/L, 126.60(4.01, 218.07)kU/L, respectively.The expression levels of CEA, CA19-9, and CA72-4 in the radically resected patient group were 173.65(120.78, 254.87) μg/L, 255.88(102.45, 395.11) kU/L, 201.71(79.15, 325.92)kU/L.The expression level of CEA, CA19-9, CA72-4 in the group with radical resection were lower than that in the group with no radical resection, and the difference was statistically significant (the Z values were 10.672, 8.945, 9.862, all P<0.001). ROC curve showed that AUC of CEA, CA19-9 and CA72-4 were 0.627, 0.714 and 0.768, respectively.The best cut-off value of CA72-4 was 87.62 kU/L, the sensitivity was 88.1% (74/84) and the specificity was 90.4% (47/52). Conclusion:The expression levels and number of tumor markers CEA, CA19-9, CA72-4 in patients with gastric cancer were correlated with the risk of radical resection.

AIM To explore possible action mechanism of antidepressants. METHODS Using flow cytometry, the cell proliferation was detected. The proliferation of hippocampal progenitor cells and level of brain derived neurotrophic factor (BDNF) were measured by immunohistochemistry. RESULTS Treatment with N methyl D aspartate (NMDA) 600 ?mol?L -1 for 3 d significantly decreased the percentage of S phase in PC12 cells, while in the presence of classical antidepressants, desipramine (DIM) or fluoxetine (FLU) 1, 5 ?mol?L -1 , the percentage of S phase increased. Furthermore, the proliferation of hippocampal progenitor cells, as well as the BDNF level in dentate gyrus (subgranular zone) significantly decreased in chronically stressed mice for 24 d, while chronic administration with DIM or FLU 10 mg?kg -1 (ip) normalized it. Meanwhile, the BDNF level in dentate gyrus also elevated after DIM or FLU treatments. CONCLUSION Up regulation of the hippocampal neurogenesis is the common action mechanism for antidepressants, which may be closely related to the elevation of BDNF level at the same time.

AIM:To investigate the influence of high-mobility group box 1 (HMGB1) on the proliferation of neural stem cells in peri-infarction cortex of focal cerebral ischemia/reperfusion model rats .METHODS: Male SD rats (n=48) were randomly divided into sham group , ischemia/reperfusion (I/R) group, RNA interference group and nega-tive interference group .The rat middle cerebral artery was blocked to establish focal cerebral I /R model ( ischemia for 1 h and reperfusion for 7 d).Lentivirus vector of HMGB1 shRNA was used to suppress the HMGB1 protein expression in the rat brain.The effect of RNA interference was evaluated by the methods of double-immunofluorescence labeling of HMGB 1/GFAP and Western blotting .The proliferation of neural stem cells in the peri-infarction cortex was assessed by double labe-ling of BrdU/nestin.RESULTS: The protein expression of HMGB1 in I/R group was much higher than those in sham group (P<0.05).RNA interference effectively inhibited the HMGB1 expression (P<0.05).Double labeled BrdU/nestin positive cells in I/R group were more than that in sham group (P<0.05).The double labeled BrdU/nestin positive cells were significantly decreased in RNA interference group (P<0.05).CONCLUSION:Focal cerebral ischemia/reperfusion injury promotes the proliferation of neural stem cells in peri-infarction cortex by increasing HMGB 1 protein level .

Objective To observe the effect of TanshinoneⅡA( TanⅡA) on endometriosis( EMS) rat model and study the possible mechanism. Methods EMS rat model was established by autologous endometrium transplantation. EMS rats were randomly divided into five groups: high-, medium-, low-dose TanⅡA group, mifepristone group and model control group( n=10), the other ten normal rats as normal control group.The rats in the model control group and normal control group were given 0.9% sodium chloride solution. The rats in the mifepristone group were given 25 mg . kg-1 . d-1 mifepristone. The rats in the high-, medium-, low-dose TanⅡA groups were given 30, 20 and 10 mg.kg-1.d-1 TanⅡA, respectively.Four weeks after the treatment, the volume of endometriotic implants in each rat was measured. Pathological changes of ectopic endometrium were observed under light microscope.Expression levels of Bcl-2, Bax and Caspase-9 in ectopic endomembrane of rats were determined by Western blotting. Results High and medium dose TanⅡA and mifepristone significantly reduced the volume of ectopic lesions(P<0.05).As compared with model control group, the inhibition rate of the ectopic lesions in low-, medium-, high-dose TanⅡA groups and mifepristone group was 17.81%, 57.78%, 58.88% and 64.12%, respectively.High and medium dose TanⅡA and mifepristone promoted atrophy of ectopic endometrium, inhibited the expression of Bcl-2 protein and promoted the expression of Bax and Caspase-9 in ectopic tissues( P<0.05) . Conclusion TanⅡA significantly decreases the size of ectopic lesions in rats, possibly through reducing the expression of Bcl-2 and increasing the expression of Bax and Caspase-9 to regulate cell apoptosis.

[ ABSTRACT] AIM:To investigate the effect of silencing cell division cycle 25a ( CDC25a) gene on the prolifera-tion of human hepatoma HepG2 cells.METHODS:CDC25a gene in human hepatoma HepG2 cells was silenced by RNA interference.Real-time PCR was applied to detect the expression of CDC25a, cyclin E and CDK2 at mRNA levels in the HepG2 cells.Western blotting was applied to detect the expression of CDC25a at protein level.In addition, MTT assay, Giemsa staining and flow cytometry were used to measure the proliferation of human hepatoma HepG2 cells.RESULTS:The expression of CDC25a at mRNA and protein levels in RNA silence group was lower than those in negative control group and normal control group (P<0.05).The mRNA expression of cyclin E and CDK2 in silence group was lower than that in negative control group and normal control group (P<0.05).The cell proliferation in silence group was lower than that in negative control group and normal control group ( P<0.05) .The results of flow cytometry revealed that the cells in silence group were blocked in G1 phase.CONCLUSION:Infection of LV-CDC25a-RNAi recombinant to the HepG2 cells effec-tively inhibits the CDC25a gene expression and the proliferation of human hepatoma cells, and arrests the cells in G1 phase, suggesting that CDC25a gene may be a key target for the treatment of liver cancer.

Objective:To explore the inhibition of microRNA (miRNA, miR)-5590-3p on the expression of transforming growth factor beta typeⅡreceptor (TGFBR2) gene and its effect on the invasion and proliferation of gastric cancer cell line HS-746T.Methods:The gastric cancer cell line was cultured in vitro. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to analyze the expression of miR-5590-3p in gastric cancer tissues and cell lines. The miR-NC and miR-5590-3p mimic were transfected into gastric cancer cell line HS-746T by lipofection, and named as miR-NC group and miR-5590-3p group, respectively. qRT-PCR was used to measure transfection effects. Transwell assay and cell counting kit-8 (CCK-8) assay were used to detect cell invasion and proliferation after transfection. The bioinformatics software predicts and the dual luciferase reporter gene system validates the target gene of miR-5590-3p. qRT-PCR and western blot were used to measure the expression of TGFBR2 and its downstream proteins in the transfected cells. Results:The expression of miR-5590-3p in gastric cancer tissues was significantly lower than that in adjacent tissues ( P<0.01). The expression of miR-5590-3p in gastric cancer cell lines was significantly lower than that in normal gastric mucosal epithelial cells ( P<0.05), and lowest in HS-746T cells ( P<0.01). After transfection, the expression of miR-5590-3p in miR-5590-3p group (11.76±0.21) was significantly higher than that in miR-NC group (1.06±0.21), with statistically significant difference ( P<0.01). The number of invasive cells in miR-NC group and miR-5590-3p group were (101.20±15.47) and (26.53±6.53), respectively, and the invasion ability of miR-5590-3p group was significantly decreased ( P<0.01). Compared with the miR-NC group, the cell proliferation ability of the miR-5590-3p group was significantly decreased ( P<0.05). Bioinformatics software showed that the target gene for miR-5590-3p is TGFBR2. The dual luciferase reporter gene system confirmed that miR-5590-3p can target the TGFBR2 gene ( P<0.01). Western blot results showed that compared with miR-NC group, the expression of TGFBR2 in HS-746T cells in miR-5590-3p group was significantly decreased ( P<0.01), the expression of ZEB-1 and ZEB-2, and the expression of CDK1 and cyclin B proteins were decreased as well. Conclusions:miR-5590-3p can inhibit the invasion and proliferation of gastric cancer cell HS-746T by targeting and regulating the expression of TGFBR2 gene.

Objective:To investigate the serum hepcidin level and risk factors associated with peripheral arterial disease (PAD) and foot ulcer in type 2 diabetic patients.Methods:From January 2019 to June 2019, 70 patients with type 2 diabetes in Department of Endocrinology of Xiangya Third Hospital were selected, including 21 newly diagnosed patients with type 2 diabetes (DM group), 23 patients with lower extremity vascular disease (PAD group) and 26 patients with foot ulcer (DF group). Serum hepcidin was determined by enzyme linked immunosorbent assay (ELISA). The serum levels of hepcidin in different groups were compared, and the correlation between diabetic lower extremity vascular disease and foot ulcer was analyzed.Results:⑴ The hemoglobin, albumin, triglycerides and total cholesterol were significantly lower in DF group compared with PAD and DM groups ( P<0.05), while the DF group patients were with higher white blood cell (WBC) count and high sensitivity C reactive protein (hs-CRP) than patients in PAD and DM groups ( P<0.05). DF group also showed significantly higher WBC, hs-CRP and neutrophil ratio level (NEUT%) than DM group ( P<0.05). The inflammatory indicators of WBC, hs-CRP and NEUT% showed no significant difference between DM group and PAD group ( P>0.05). ⑵ The levels of hepcidin in DF and PAD groups were higher than those in DM group, while that in DF group were higher than those in PAD group ( P<0.05); Hepcidin was positively correlated with systolic blood pressure, WBC count, NEUT% and ferritin ( P<0.05), and negatively correlated with hemoglobin, glycosylated hemoglobin, albumin and 25-hydroxyvitamin D ( P<0.05). ⑶ Binary multivariate logistic regression analysis showed that elevated hepcidin level was an independent risk factor for diabetic foot ulcer [ OR=1.755, 95% CI: 1.063-2.897, P=0.028]. Conclusions:The fluctuation of serum hepcidin level in diabetic patients is related to the stimulation of inflammation, the degree of anemia and the nutritional status, which means it might be an early indicator of inflammation in diabetic patients with peripheral arterial disease. Moreover, the increase of hepcidin is an independent risk factor for diabetic foot ulcers in our study.