Objective To explore the feasibility and effectiveness of gradient elastic compression stockings in prevention of venous stasis in patients undergoing laparoscopic cholecystectomy(LC). Methods 160 LC patients were randomized into the experimental group(75 cases)and the control group (85 cases).Routine nursing care and treatment were performed in both groups,and gradient elastic compression stockings were used in the experimental group.Venous pressure was measured in four different periods (T1,T2,T3,T4). Results The venous pressure in T2,T3 and T4 in the experimental group was significantly lower than that in the control group. Conclusions Use of gradient elastic compression stockings is effective and feasible in preventing LC-induced venous stasis.

Objective To determine whether Morphine has the ability to enhance HIV-1 replication in MT2 and Macrophage in vitro and assess the influence of Naloxone on Morphine2s effect.Methods MT2 cells were randomly assigned into 4 groups: (1) Morphine treatment for MT2 group, (2) Morphine+Naloxone co-treatment for MT2 group, (3) Naloxone treatment for MT2 group and (4) MT2 Control;Macrophages were also randomly assigned into 4 groups: (5) Morphine treatment for Macrophage group, (6) Morphine+Naloxone co-treatment for Macrophage group, (7) Naloxone treatment for Macrophage group and (8) Macrophage Control. Group (2), (3), (6) and (7) were pre-treated with 10-8 mol/L Naloxone for 0.5 h, and then group (1) and (2) were treated with 10-12, 10-10 and 10-8 mol/L Morphine for 24 h;group (5) and (6) were disposed of 10-10 mol/L Morphine for 24 h.All 8 groups were added in HIV-1 viral strain with 50% tissue culture infective dose(TCID50).P24 antigen in MT2 cells culture supernatant at day 3, 4, 5 and 6, and in Macrophages culture supernatant at day 4, 6, 8, 10 and 12 after infection were determined with ELISA.Student2s t-test and ANOVA were used to compare the differential expression in different groups, and repeated measures ANOVA was used to compare the increasing or decreasing expression of p24 antigen in morphine treatment groups than that in the control group at different time points.Results On the 3rd day of infection with HIV-1 in MT2 cells, the expression of p24 antigen in 10-12, 10-10 and 10-8mol/L dose of group (1) were (4.44?.30), (5.59?.25) and (4.60?.24) ng/ml respectively, compared to control[(1.93?.05) ng/ml, t= 14.15, 24.74 and 19.14, all P<0.01].On the 4th day, 10-12, 10-10 and 10-8mol/L dose of group (1) resulted in a significant increase of p24 antigen expression [(24.30?.66), (31.73?.17) and (26.02?.37) ng/ml]in culture supernatants compared to control[(8.03?.09) ng/ml, t=10.59, 34.92 and 81.2, all P<0.01].On the 5th day, the expression of p24 antigen in 10-12, 10-10 and 10-8 mol/L dose of group (1) were (56.30?.26), (81.77?.49) and (63.66?.57) ng/ml respectively, compared to control [(15.30?.91) ng/ml, t= 45.83, 43.51 and 30.07, all P<0.01].On the 6th day, the expression of p24 antigen in 10-12, 10-10 and 10-8 mol/L dose of group (1) were (150.70?.97), (243.09?.93) and (173.72?.73) ng/ml respectively, compared to control [(41.01?.84) ng/ml, t= 21.09, 39.02 and 29.55, all P<0.01].The enhanced multiple of p24 antigen expression in three doses of morphine treatment group compared to control increased with HIV-1 infected MT2 cells time, trend analysis of repeated measurements showed statistically significant time effect (F=842.18, P<0.01). On the 4th day of infection with HIV-1 in Macrophage cells, the expression of p24 antigen in 10-12, 10-10 and 10-8 mol/L dose of group (5) were (0.68?.15), (0.87?.41) and (0.75?.09) ng/ml respectively, compared to control [(0.60?.01) ng/ml, t= 7.27, 11.06 and 3.02, all P<0.05]. On the 6th day, 10-12, 10-10 and 10-8 mol/L dose of group (5) resulted in a significant increase of p24 antigen expression[(1.64?.57) , (2.07?.12 ) and (1.75?.17) ng/ml]in culture supernatants compared to control [(1.16?.07) ng/ml, t=8.93, 11.3 and 5.45, all P<0.01].On the 8th day, the expression of p24 antigen in 10-12, 10-10 and 10-8 mol/L dose of group (5) were (6.31?.17), (8.81?.34) and (7.19?.11) ng/ml respectively, compared to control [(3.84?.45) ng/ml, t=8.83, 15.11 and 12.42, all P<0.01]. On the 10th day, the expression of p24 antigen in 10-12, 10-10 and 10-8 mol/L dose of Morphine treated group were (32.30?7.55), (50.74?7.55) and (39.74?.56) ng/ml respectively, compared to control [(17.55?.86) ng/ml, t= 13.65, 17.84 and 36.69, all P<0.01].The enhanced multiple of p24 antigen expression in three doses of group (5) compared to control increased with HIV-1 infected Macrophage cells time, trend analysis of repeated measurements showed statistically significant time effect (F=135.58, P<0.01).Conclusions Morphine has the ability to enhance HIV-1 replication in MT2 cell and Macrophage. This Morphine-mediated increase of p24 antigen expression can be blocked by Naloxone.

Objective To explore the effect and mechanism of microRNA (miR)-155-5p on myocardial pyroptosis in rats with myocardial ischemia-reperfusion injury (IRI). Methods Sixty SD rats were randomly divided into sham group, IRI group, agomir-NC group, miR-155-5p agomir group, antagomir-NC group, and miR-155-5p antagomir group, with 10 rats in each group. Echocardiography was used to measure the left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular ejection fraction (LVEF), and left ventricular fractional shortening (LVFS) of rats. Enzyme-linked immune absorbent assay (ELISA) was used to detect the levels of creatine kinase isoenzyme (CK-MB), lactate dehydrogenase (LDH), and cardiac troponin T (cTnT) in serum, as well as the levels of interleukin (IL)-1β, IL-6, IL-18, and tumor necrosis factor (TNF)-α in myocardial tissue of rats. Hematoxylin-eosin staining was used to observe pathological changes in rat myocardial tissue. Real-time fluorescent quantitative polymerase chain reaction was used to detect the expression levels of miR-155-5p and silent information regulator 1 (SIRT1) messenger RNA (mRNA) in myocardial tissue of rats. Dual-luciferase reporter gene assay was used to verify the targeting relationship between miR-155-5p and SIRT1. Western blot was used to detect the expression levels of SIRT1, NOD-like receptor protein 3 (NLRP3), cleaved cysteine aspartate specific proteinase-1 (Cleaved Caspase-1), and gasdermin D (GSDMD) proteins in myocardial tissue of rats. Results Compared with the sham group, the LVEDD and LVESD of rats in the IRI group were increased, LVEF and LVFS were decreased, serum levels of CK-MB, LDH, and cTnT were increased, IL-1β, IL-6, IL-18 and TNF-α levels in myocardial tissue were increased, myocardial tissue structure was severely damaged, myocardial fibers were disordered, relative expression of NLRP3, Cleaved Caspase-1, and GSDMD proteins were increased, and the relative expression of SIRT1 protein was decreased (all P<0.05/5). Compared with the IRI group, the rats in the miR-155-5p agomir group had increased LVEDD and LVESD, decreased LVEF and LVFS, increased serum levels of CK-MB, LDH, and cTnT, increased myocardial tissue levels of IL-1β, IL-6, IL-18, TNF-α, aggravated myocardial tissue lesions, increased relative expression of NLRP3, Cleaved Caspase-1, and GSDMD proteins, and decreased relative expression of SIRT1 protein, and the rats in the miR-155-5p antagomir group had decreased LVEDD and LVESD, increased LVEF and LVFS, decreased serum levels of CK-MB, LDH, and cTnT, decreased myocardial tissue levels of IL-1β, IL-6, IL-18, TNF-α, reduced myocardial tissue lesions, decreased relative expression of NLRP3, Cleaved Caspase-1, and GSDMD proteins, and increased relative expression of SIRT1 protein (all P<0.05/5). miR-155-5p was negatively correlated with the expression levels of SIRT1 in rat myocardial tissue, and SIRT1 was a target gene of miR-155-5p. Conclusions miR-155-5p may participate in the regulation of myocardial IRI in rats by targeting the downregulation of SIRT1 and promoting NLRP3-mediated myocardial pyroptosis.