Objective To observe the impact of different culture conditions on the growth of the endothelial progenitor cells(EPCs) from rat peripheral blood. Methods Mononuclear cells obtained from rat peripheral blood were isolated by using density gradient centrifugation. According to the culture medium added with vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and the dishes were precoated with fibronectin or not, the mononuclear cells were divided into different groups and cultured under different conditions in vitro to compare the differences of the growth conditions. The different growth conditions were recorded and the result was calculated by statistics software. At last, the cells were identified by immunohistochemistry and immunofluorescence. Results The mononuclear cells from rat peripheral blood grew in the manner of keeping close to the wall in vitro. The cells and cell colonies cultured for 7 days hinted:under the same culture conditions, precoating FN was beneficial to the adherent proliferation of EPCs (t=4.43, P＜0.05; t=3.70, P＜0.05). Excluding the impact of fibronectin, growth factors could promote mononuclear cells differentiation to EPCs, indicating that growth factors enhanced proliferation of EPCs (t =-13.22, P＜0.01; t =-10.96, P＜0.01). Immunohistochemistry and immunofluorescence showed that, at day 4, 7, 10 of cells cultured, CD34 and CD133 expressions were increased gradually [(35.7±4.2)%, (60.1±3.8)%, (81.8±6.4)%; (3.2±0.9)%, (18.4±7.3)%,(32±3.8)%, respectively]; at day 14, both were decreased [(32.1±5.4)%, (1.9±2.7)%]; but Flk-1was increased at day 4, 7,10, 14 [(31.2±3.5)%, (40.6±5.3)%, (71.2±8.4)%, (81.5±4.1)%].Conclusions Fibronectin is conducive to adhesion and proliferation of EPCs. VEGF and bFGF play an important role in the differentiation of EPCs. The success culture of EPCs in vitro will provide a sufficient number of seed cells for its application in vascular tissue engineering, and offer new ideas for peripheral blood stem cell transplantation for the treatment of various diseases.

Objective To investigate the clinical effect of fluticasone propionate combined with noninvasive positive pressure ventilation in the treatment of chronic obstructive pulmonary disease (COPD).Methods 88 cases of COPD patients from October 2014 to October 2016 in our hospital were selected and randomly divided into two groups of the control group observation group with 44 cases in each group.The control group was treated with conventional treatment, the observation group was treated with fluticasone propionate plus noninvasive positive pressure ventilation, and then the curative effect of the two groups was compared.Results The total effective rate of observation group was 100% higher than that of the control group 70.5%, the difference was statistically significant (P<0.05), after treatment, the observation group of FVC (2.50 +0.32) L, FEV1 (1.36 +0.20) L, FEV1%(51.23+4.32), PaO2(10.51+2.10) kPa, PaCO2(5.15 +1.19) kPa, compared with the control group, the difference was statistically significant (P<0.05), the observation group recurrence rate 4.5% was lower than the control group 13.6%, the difference was statistically significant (P <0.05).Conclusion COPD patients with fluticasone propionate combined noninvasive positive pressure ventilation, can effectively improve lung function, reduce disease recurrence rate, a significant effect.

AIM: To investigate the possible role of nuclear transcription factor kappa B (NF-?B), Bcl-2, Bax and caspase-3 in etodolac-induced apoptosis of liver tumor SMMC7721 cell line. METHODS: Cell apoptosis was determined by flow cytometry analysis with PI staining and DNA laddering. Expression of Bcl-2 and Bax protein was measured by Western blotting. Caspase-3 activity was evaluated by active caspase-3 apoptosis kit with flow cytometry. NF-?B activation was detected by ELISA-based TransAM~(TM) NF-?B p65/p50 kit. RESULTS: Etodolac, a selective COX-2 inhibitor, stimulated apoptosis in liver tumor SMMC7721 cell line significantly. Flow cytometry showed that the apoptotic rate was 16.3%?3.1%, 19.9%?3.6%, 22.9%?3.2%, 31.2%?3.3% with different concentrations of etodolac (0.25, 0.50, 1.0 or 2.0 mmol/L), while the apoptotic peak did not appear in the control group (0 mmol/L) (P

Objective To explore the relationship between bone mineral density(BMD) and body tat disrribution in the aged in Ningbo area of China. Methods The BMD of lumbar vertebra and total body bones as well as body composition were measured by dual-energy X-ray absorptiometry (DXA) in 61 aged males, and also in 63 aged females as control group. Results In the aged males, a negative correlation was found between BMD and age, while BMI, muscle, trunk fat were positively correlated with BMD. As for the aged female, age, BMI, muscle and fat were all positively correlated with BMD. Conclusions The correlation between body fat and BMD is closer in females than in males in the aged. There is a positive correlation between trunk fat and lumbar spine BMD, and it indicates that central obesity may have a protective effect on lumbar spine BMD.

Objective To observe the influence of inactive FRMD4A gene′s expression on the biological behavior of tongue cancer CAL-27cell. Methods FRMD4A-siRNA was transfered into CAL-27 cell by lipidosome, to the expression of FRMD4A-siRNA in CAL-27 cell after transfection was detect by qRT-PCR cell proliferation , was checked by CCK-8,the influence of inactive FRMD4A gene on cell cycle distribution of CAL-27 cell was assayed by flow cytometry. Results Compared with the control group, FRMD4A mRNA expression significantly reduced in FRMD4A-siRNA interfering group (94%) and the cell proliferation index decreased(P<0.05). The cell cycle arrested in G1 period (P<0.05). Conclusion FRMD4A-siRNA could effectively inhibit FRMD4A mRNA expression in tongue cancer CAL-27cell, impact the distribution of cell cycle, and reduce cell proliferation.

Objective To evaluate the effect of sevoflurane postconditioning on microRNA-133a (miR-133a) expression during myocardial ischemia-reperfusion (I/R) in mice.Methods Thirty adult male C57 mice,weighing 20-30 g,were randomized to 3 groups (n =10 each) using a random number table:control group (group C),I/R group,and sevoflurane postconditioning group (group SP).In I/R and SP groups,hearts from adult male C57 mice were exposed and subjected to 30 min of ischemia and 180 min of reperfusion in anesthetized mice according to the method described by Das et al.In group C,only thoracotomy was performed without ligation of the coronary artery.In group SP,2.4％ sevoflurane was inhaled for 5 min starting from the onset of reperfusion to perform sevoflurane postconditioning.At 180 min of reperfusion,blood samples from the femoral vein were collected for determination of serum lactic dehydrogenase (LDH) and creatine kinase (CK) activities using the colorimetric method.The mice were then sacrificed,and myocardial specimens were obtained for determination of myocardial infarct size,miR133a and caspase-9 mRNA expression (by real-time reverse transcriptase polymerase chain reaction),and caspase-9 expression (by Western blot).Results Compared with group C,the serum LDH and CK activities and myocardial infarct size were significantly increased in I/R and SP groups,the expression of miR-133a was significantly down-regulated,and the expression of caspase-9 protein and mRNA was significantly up-regulated in group I/R,and the expression of miR-133a and caspase-9 protein and mRNA was significantly up-regulated in group SP (P＜0.05).Compared with group I/R,the serum LDH and.CK activities and myocardial infarct size were significantly decreased,the expression of miR-133a was significantly up-regulated,and the expression of caspase-9 protein and mRNA was significantly downregulated in group SP (P＜0.05).Conclusion The mechanism by which sevoflurane postconditioning inhibits cell apoptosis during myocardial I/R is related to up-regulation of miR-133a expression in mice.

Objective The inhibitory effects of avastin on new blood vessels in nonproliferation diabetic retinopathy, age-related macular degeneration and neovascular glaucoma have been demonstrated. But only seldom report of avastin on corneal neovascularization(CNV) was seen. Present study was to evaluate the effect of topical bevacizumab (avastin) on experimental corneal neovascularization in mice. Methods Thirty eyes of 30 Balb/c mice were chemically cauterized by applying a 2 mm-diameter filter paper soaked 1 mol/L NaOH solution at the central cornea for 40 s. All animals were randomly assigned to five groups, including 1 mg/mL, 3 mg/mL and 5 mg/mL bevacizumab eye drops group respectively, 1 mg/mL dexamethasone sodium phosphate eye drops group (positive control) and normal saline solution group (negative control) . The drug was topically utilized twice per day. CNV was examined under the slim lamp on the 3rd, 7th and 14th day after alkali burn. Animals were killed on the 14th day after alkali burn. Area of CNV was calculated in terms of pixels on digital photographs. The use of animals followed the Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission. Results No significant difference was found in the grade of corneal injury among five groups (F = 0. 201, P = 0. 935). The area of neovascularization at the cornea surface was (37.11 ±3.17)% in 1 mg/mL bevacizumab group, (29.75 ±3.56)% in 3 mg/mL bevacizumab group, (18. 76 ± 2. 55) % in 5 mg/mL bevacizumab group, (20. 91 ± 2. 75) % in dexamethasone group and (41. 65 ±2. 11)% in normal saline group, showing a significant difference among groups(F = 71. 687, P =0. 000) with the further comparative decline in 5 mg/mL bevacizumab group compared with other groups (P ＜ 0. 01) . Conclusion The topical use of bevacizumab (avastin) inhibits alkali burn-induced CNV in mice.

Objective To evaluate the role of Janus kinase 2-signal transducer and activator of transcription 3 (JAK2-STAT3) signaling pathway in sevoflurane postconditioning-induced inhibition of mitochondrial permeability transition pore (mPTP) opening during myocardial ischemia-reperfusion (I/R)in rats.Methods Sixty pathogen-free healthy male Sprague-Dawley rats,weighing 250-300 g,were divided into 4 groups (n=15 each) using a random number table:I/R group,sevoflurane postconditioning group (group SP),AG-490 group (group AG) and sevoflurane postconditioning plus AG-490 group (group SP+AG).Myocardial I/R was induced by 30 min ligation of the left anterior descending branch of coronary artery followed by 120 min reperfusion.In group SP,2.8％ sevoflurane was inhaled for 15 min starting from 2 min before reperfusion.JAK2 inhibitor AG-490 3 mg/kg was intravenously injected at 10 min before reperfusion in group AG.In group SP+AG,AG-490 3 mg/kg was intravenously injected at 10 min before reperfusion,and 2.8％ sevoflurane was inhaled for 15 min starting from 2 min before reperfusion.At 15 min of reperfusion,5 rats were sacrificed and myocardial specimens were obtained for determination of the expression of JAK2,phosphorylated JAK2 (p-JAK2),STAT3 and phosphorylated STAT3 (p-STAT3)in myocardial tissues by Western blot.The ratios of p-JAK2 to JAK2 expression (p-JAK2/JAK2) and pSTAT3 to STAT3 expression (p-STAT3/STAT3) were calculated.Five rats were sacrificed at the end of reperfusion for measurement of myocardial infarct size.The left 5 rats were selected and sacrificed,myocardial specimens were obtained,and the opening of mPTP was detected by a calcein-cobalt quenching method.Results Compared with group I/R,the myocardial infarct size and mPTP opening were significantly decreased,and JAK2/p-JAK2 and STAT3/p-STAT3 were increased in group SP (P＜0.05),and no significant change was found in the parameters mentioned above in SP+AG and AG groups (P＞0.05).Compared with group SP,the myocardial infarct size was significantly enlarged,the extent of mnPTP opening was aggravated,and JAK2/p-JAK2 and STAT3/p-STAT3 were decreased in SP+AG and AG groups (P＜0.05).Conclusion The mechanism by which sevoflurane postconditioning inhibits the opening of mPTP during myocardial I/R is related to activation of JAK2-STAT3 signaling pathway in rats.

Objective To investigate the efficacy evaluation of early continuous renal replacement therapy (CRRT) for severe acute pancreatitis in intensive care unit (ICU).Methods Prospective study was performed for 84 patients with severe acute pancreatitis admitted to the Xinjiang Provincial People's Hospital from June 2015 to March 2017.Those patients were divided into two groups by computer random coding:42 cases treated with CRRT (observation group), and 42 cases received routine treatment (control group).Statistically analysis was carried out between two groups regarding curative effect, symptom improvement, ICU hospitalization time, and serum markers before and after treatment.Results The total ef fective rate was 92.86 ％ in the observation group, and 85.71％ in the control group, without significant difference between two groups (F =0.516, P =0.632).Patients with symptoms, vital signs stable time, gastrointestinal function recovery time, and hospitalization time of ICU were significantly lower in the observation group than the control group [(3.16 ± 1.28) days:(5.21 ± 1.45) days, t =3.518, P =0.017, (2.55 ± 1.36) days:(4.34 ± 1.51) days, t =2.519, P =0.034, (4.46 ± 1.28) days:(6.28 ± 1.51) days, t=2.685,P=0.028, (15.06±2.24)days:(19.34 ±3.28) days, t=6.983, P=0.009].There is no significant differences in amylase (AMS), interleukin (IL)-6, C-reaction protein (CRP), tumor necrosis factor (TNF)α, prothrombin time (PT) and fibrinogen (FIB) before treatment between two groups (P ＞ 0.05).The observation group were significantly lower than the control group in AMS, IL-6, CRP, TNF-α, PT, and FIB levels after treatment [(206.59 ± 19.51) U/L:(258.12 ± 22.43) U/L, t =11.234, P=0.001, (34.58 ±6.41)ng/L:(41.36 ± 8.52) ng/L, t =4.121,P =0.013, (88.24 ± 6.95) ng/L:(104.33 ±10.82) ng/L, t=8.109,P=0.002, (178.35 ±27.43)pg/ml:(249.28 ±34.33)pg/ml, t=7.384,P=0.007, (12.48±3.54)s:(14.56 ±4.62)s, t =6.473,P=0.011, (3.38±1.55)g/L:(4.57 ± 2.86)g/L, t =4.108, P =0.041].Two groups of patients after treatment were cured, and no serious complications occurred during hospitalization.Conclusions For patients with severe acute pancreatitis, the overall effective rate of CRRT in ICU was high, the clinical symptoms relieved quickly, the level of serum indicators improved effectively.

Objective To investigate the potential mechanism of circRNA SAMD8(circ-SAMD8)in development of pancreatic ductal adenocarcinoma(PDAC).Methods The expression profile of circRNAs in PDAC tissues was analyzed based on Microarray data(GSE79634).Quantita-tive real-time polymerase chain reaction(qRT-PCR)was used to verify the expression of circ-SAMD8(hsa_circ_0006148)in PDAC tissues and cells(CFPAC-1 and PANC-1).The target microRNA(miRNA)of circ-SAMD8 and its downstream mRNA were predicted by bioinformatics analysis,and identified by double luciferase reporter gene assay.The proliferation ability of PDAC cells was detec-ted by MTT assay and colony formation assay.The expression levels of anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax were detected by Western blot.The percentage of apoptotic cells was detected by flow cytometry.Results The expression levels of circ-SAMD8 in PDAC tissues and cells were significantly lower than those in paracancer tissues and normal cells(P＜0.05).Overexpression of circ-SAMD8 could effectively promote apoptosis of PDAC cells and inhibited proliferation of PDAC cells.Dual luciferase reporter gene experiments showed that miR-223-3p was a potential interacting mol-ecule of circ-SAMD8,and the downstream mRNA target of miR-223-3p was RHOB.The miR-223-3p was abnormally overexpressed in PDAC tissues and cells,accompanied by low RHOB expression.In PDAC cells transfected with miR-223-3p mimics or sh-circ-SAMD8,RHOB expression was significantly decreased,proliferation ability was enhanced,and apoptosis rate was decreased.Conclusion Circ-SAMD8 regulates the expression of RHOB downstream by sponging miR-223-3p,and effectively inhibits the occurrence and development of PDAC.