Objective To determine whether focal adhesion kinase (FAK) signal pathway was involved in migration of hepatocarcinoma cells by inhibiting focal adhesion kinase (FAK) phosphorylation in HepG2 cells with focal adhesion related nonkinase (FRNK). Methods The recombinant of FRNK and pEGFP-C2, an endogenous inhibitor of FAK activation,was transfected into HepG2 cells. HepG2 migration was examined by transmembrane assay. FAK and phosphatinositol 3-kinase (PI3-K) phosphorylation were detected by immunoprecipitation method. Confocal scanning microscopy was used to verify nuclear translocation of nuclear factor-kappa B (NF-?B). Results The transfection of FRNK recombinant plasmid could inhibit HepG2 migration, FAK and PI3-K phosphorylation decreased by 50.2 percent and 39.5 percent respectively. Furthermore, NF-?B translocation was down-regulated from 3.495?0.227 to 1.182?0.106. Conclusion These results suggested FAK was a main signal pathway in mediating HepG2 migration. Over expression of FRNK might inhibit signal transduction of FAK via depression of the phosphorylation of PI3-K and NF-?b activation, resulting in the decrease in migration of hepatocarcinoma cell.

Objective To investigate the difference and significance of the glucocorticoid receptors of the peripheral leukocytes in patients with acute spinal cord injury or with chronic spinal cord compression. Methods Glucocorticoid receptors binding sites on the peripheral leukocytes in 20 patients with acute spinal cord injury and 21 patients with chronic spinal cord compression were measured by the radioligand binding assay. Results Glucocorticoid receptors binding sites on peripheral leukocytes from the patients with acute spinal cord injury is 2 517?857.8 per cell, the patients with chronic spinal cord compression is 4 225?1 271 per cell and outcome is 2 279?921 per cell in the patients with complete paralysis, 2 806?718 per cell in the incomplete paralysis patients. T test was used to evaluate the final outcome. Conclusion Glucocorticoid receptors binding sites on the peripheral leukocytes consist of two kinds: the high affinity binding sites and the low affinity binding sites. The high affinity glucocorticoid receptors binding sites on peripheral leukocytes in patients with acute spinal cord injury decrease and low affinity binding sites remain unchanged. Large doses of glucocorticoid combine the low affinity binding sites on peripheral leukocytes which inhibits the tendency of movement of leukocytes to the injured spinal cord; so inflammatory reaction produced by acute injury can be alleviated and thus the spinal cord was protected. There is no curative effect by using large doses of glucocorticoid to treat patients with chronic spinal cord compression.

Objective To test thyroid-stimulating hormone (TSH) suppress GLUT4 expression and translocation by stimulating TNF-α secretion in 3T3-L1 adipocytes via a cAMP-PKA pathway.Methods 3T3-L1 preadipocytes were induced to differentiate into adipocytes.The adipocytes were treated with bovine TSH,Forskolin,H89 and Rapamycin,respectively.The concentration of TNF-α in the cell culture medium was measured by ELISA.The level of GLUT4 mRNA in adipocytes was assessed by real time polymerase chain reaction.Protein levels of GLUT4 in total cell lysates and plasma membrane lysates were quantified by Western blotting.Results Incubating 3T3-L1 adipocytes with TSH markedly increased the concentration of TNF-α in medium in a time-and dosedependent manner (P ＜ 0.05); meanwhile,the levels of GLUT4 mRNA and total and plasma membrane GLUT4 protein were decreased in a dose-dependent manner (P＜0.05 or ＜0.01).H89 and rapamycin could block the above effects respectively (326.7±43.2 vs.341.9±12.0,P＞0.05).However,there was no statistical difference in the TNF-α levels between stimulation with 1 μmmol/L forskolin versus 0.04 μmmol/L bovine TSH (481.9± 28.4 vs.522.7± 36.2,P＞0.05).Conclusions TSH can down-regulate GLUT4 expression and translocation in 3T3-L1 adipocytes by stimulating TNF-α secretion through a cAMP-PKA pathway.

Objective To examine the expression of angiopoietin-like protein(ANGPTL)3 in kidneys from children with primary nephrotic syndrome. Methods Immunohistochemistry for ANGPTL3 was performed in kidney biopsies from patients with nephrotic syndrome or hematuria, including MCD (n=31), MN(n=6), FSGS (n=6), TBMN (n=10), IgA nephropathy (IgAN) with mesangial proliferation (n=16). Normal renal tissue of 2 cases with nephrectomy for tumor were used as control. According to the episode, four groups were divided ("12 months"). The expression was quantitatively examined with IMS color image analysis system, using positive index (PI) as sediment degree of ANGPTL3 in glomeruli or tubules. Immunofluorescence for ANGPTL3 co-labeling with WT1 and perlecan was applied to show the distribution of ANGPTL3. Results (1) The PI levels of ANGPTL3 in glomeruli of MCD(7.49?1.96) and MN (6.27?0.98) were significantly higher than those of TBMN (0.02?0.001), FSGS (3.14?0.49) or normal control(0.02?0.001) respectively (all P

Objective To study the incidence frequency of prothrombin G20210A (FⅡ G20210A)mutation in the patients with pulmonary thromboembolism(PTE)in northeast China,and to clarify the predictive value of FⅡG20210A mutation detection in PTE of the population in northeast China.Methods 60 PTE patients(PTE group) and 80 sex-matched healthy controls(control group)from the same geographic area were selected.All the patients were diagnosed by lung ventilation/perfusion scan and/or multi-slice CT pulmonary angiography(CTPA)as well as medical history.The genome DNA was extracted from the whole blood using alcohol.Polymerase chain reaction (PCR),restriction fragment length polymorphisms(RFLP)analysis with HindⅢ restriction enzyme and sepharose gel electrophoresis were used to identify the F Ⅱ G20210A mutation in PTE group and control group. Results After digested by HindⅢ restriction enzyme,only the fragments of 407 and 99 bp were found in PTE group.The frequency of FⅡ G20210A mutation was 0%,there was no statistical difference compared with contol group(P>0.05).There were no heterozygote and homozygote mutation of FⅡ G202210A gene in PTE group and control group.Conclusion The incidence of FⅡ G20210A mutation in the PTE patients in northeast China is very low,and the detection of FⅡ G20210A mutation may have no predictive value in PTE of the population in northeast China.

Objective To study the role of signal transducer and activator of transcription3 (Stat3) in alveolar type Ⅱ epithelial cells (AT-Ⅱ) treated with the serum from rat model of severe acute pancreatitis. Methods AT-Ⅱ cells of primary culture were treated with serum from rat model of severe acute pancreatitis (SAP group),or SAP serum+AG490 (JAK inhibitor),while the normal cell control was set. AT-Ⅱ cells after treatment were collected to determine activation of Stat3 by EMSA,Stat3 mRNA expression by RT-PCR,and surfactant protein C (SP-C) level in AT-Ⅱ cells by flow cytometry. Results Stat3 protein and mRNA levels were enhanced in SAP group (P

Objective:To assess the safety and efficacy of riboflavin/ultraviolet-A-induced accelerated epithelium-off corneal collagen cross-linking (CXL) for teenagers with keratoconus.Methods:In this case series study, 25 eyes of 18 patients with primary keratoconus who underwent riboflavin/ultraviolet-A-induced accelerated epithelium-off CXL in Zhengzhou Second People's Hospital from January 2017 to February 2018 were included, and the average age of patients was (14.4±1.3) years.The uncorrected visual acuity (UCVA), best corrected visual acuity (BCVA), spherical equivalent (SE), maximum keratometry reading (K max), thinnest corneal thickness (TCT), posterior corneal elevation (PCE) and endothelial cell density (ECD) were measured before and after CXL.The patients were followed up for one year.The complications and adverse reactions were recorded.The study adhered to the Declaration of Helsinki and was approved by an Ethics Committee of Zhengzhou Second People's Hospital (No.KY2017002). Written informed consent was obtained from each patient and their guardian prior to the surgery. Results:The mean UCVA (LogMAR) was 0.96±0.35 at baseline, which was significantly improved to 0.84±0.33 at 1 year postoperatively ( t=-5.765, P<0.01). The mean BCVA (LogMAR) was 0.45±0.22 preoperatively, which was significantly improved to 0.34±0.26 at 1 year postoperatively ( t=-4.843, P<0.01). The mean SE was (8.66±5.11)D at baseline, which was significantly higher than (8.07±5.21)D at 1 year postoperatively ( t=-3.253, P=0.003). The K max was reduced from (58.58±9.07)D preoperatively to (56.25±9.98)D at 1 year postoperatively, with significant difference between the two time points ( t=-4.357, P<0.01). The K max was reduced more than 1 D in 17 eyes (68%), was stable in 6 eyes(24%), and was increased more than 1 D in 2 eyes (8%). The TCT was reduced from (485.0±32.5)μm at baseline to (475.3±35.5)μm at 1 year postoperatively, with significant difference between the two time points ( t=-4.266, P<0.01). The differences of PCE and ECD between preoperative and postoperative 1 year were not statistically significant ( t=1.023, P=0.316; t=-1.424, P=0.167). There was one eye suffering peripheral sterile corneal infiltrate 2 days postoperatively, and favorable prognosis was achieved after the topical steroids application.No complication was encountered in other subjects. Conclusions:Riboflavin/ultraviolet-A-induced accelerated epithelium-off CXL is safe and effective in teenagers with keratoconus during the 1-year follow-up.The long-term effects need further observation.

Objective: To observe the influence of sot alol on the QT dispersion in patients with atrioventricular accessory pathways u nderwent radiofrequency catheter ablation (RFCA). Methods: Thirt y-six patients were divided into 2 groups by random. One was the drug group(18 cases) treated by RFCA， and sotalol 160 mg was orally administered and intracar diac electrophysiological study was performed every 30 min for 5 times. Th e other group(control group, 18 cases) only treated by RFCA.QTd,QTcd and QTLcd w ere measured before and after RFCA. Results: There was no signif icant difference with QT dispersion before and after RFCA in control group. When compared with before RFCA, QTd in patients administered sotalol was (30.9 ±14.3) ms vs (24.7±9.6) ms; QTcd(33.7±17.1) ms vs (25.2±10.1) ms; QT Lcd(30.8±14.1)ms vs (25.6±19.4) ms (P<0.05). Conclusion: Sotalol can slightly lower QT dispersion, which is beneficial for preventing malignant ventricular arrthythmia. It is safe in RFCA in pateints with accessory pathway.

Objective To observe the expressions of matrix metalloproteinase-9 mRNA and the change of cerebral edema after diffuse brain injury in rats and discuss their correlation.Methods Marmaruu's diffuse brain injury model of rat was made.Real-time quantitative RT-PCR,dry-wet meth- od,histological techniques and electron microscope were used to determine the expressions of MMP-9 containing water in brain tissue and inflammatory reaction and uhrastructural changes of blood capillary at different time phases after truama.Results The expressions of MMP-9 mRNA started to increase at 1 hour,peaked at 12 hours(P