Objective To study whether carvacrol can cause apoptosis in non-small cell lung cancer (NSCLC) cell line NCI-H1299, and explore its possible molecular mechanism. Methods NCI-H1299 cells were treated with different concentrations of carvacrol (20, 40, 60 and 80μmol/L) for 24 or 48 h. The viability of cells was evaluated by MTT assay, apoptosis was analyzed by flow cytometry (FCM) and the effect of carvacrol on metastasis of NCI-H 1299 was analyzed by Transwell assay. The expression level of caspase-9, MMP-9 and TIMP-1 were detected by quantitative realtime-PCR and Western blot assay. Results After treatment with carvacrol, the viability of NCI-H1299 cells was suppressed dramatically (P<0.05), without dose-dependent manner (P>0.05). After being incubated with carvacrol for 24 h, FCM analysis indicated that carvacrol effectively induced apoptosis in NCI-H1299 cells (P<0.05), without dose-dependent manner (P>0.05). The ability of invasion was decreased (40.67±3.63 vs. 76.00±5.78). Carvacrol inhibited the protein and mRNA expression levels of caspase-9, but increased the expression of MMP-9 and TIMP-1 (P<0.05). Conclusion Carvacrol can induce apoptosis of NCI-H1299 cells and inhibit their invasion, which may be associated with up-regulation of caspase-9 expression and down-regulation of MMP-9 expression.

Objective Investigate the changes of adhesion molecule on myocardium in patients during mitral valve replacement(MVR) operation on beating heart. Methods Patients were divided into two groups. There were 16 patients in control group (aorta crossclamped and middle hypothermic) and 14 patients in experimental group (aorta unclamped and moderate hypothermic). Samples of right atrial were obtained before CPB, 30 min after CPB. Immunohistochemistry were employed to dectect the expression of ICAM-1 and VCAM-1 on cardiac myocytes. Results Comparing with those before CPB, ICAM-1 and VCAM-1 on cardiac myocytes and myocardial vascular endothelial cells increase significantly in both groups(P

Objective To expose the effect and its potential mechanism of vinpocetine (Vinp) on the restenosis of dia?betic grafted veins. Methods Thirty-six Sprague-Dawley rats were randomized into saline control group and Vinp treat?ment group. The autologous jugular vein to carotid artery transplantation was performed in diabetic model rats. Normal sa?line or Vinp were intraperitoneally injected. The rats were sacrificed at 0, 2 or 4 weeks after surgery, then the grafted veins were harvested. The pathological sections were used to detect the effect of Vinp on intimal hyperplasia. The protein expres?sion of proliferating cell nuclear antigen (PCNA) was detected by immunohistochemical method, and which was described by cell proliferation index. The phosphorylation of NF-κB was detected by Western blot assay. Results The treatment of Vinp on intimal hyperplasia in vivo was significant at two weeks after surgery (17.06±5.10)μm versus control group (39.79±7.84μm, P<0.01), (30.94±5.18)μm versus (63.67±18.09)μm at four weeks after surgery (P<0.01). Vinp treatment effectively reduced the protein expression of PCNA [2 weeks:(21.07±1.38)%vs. (28.13±1.35)%,P<0.01;4 weeks:(31.73±1.38)%vs. (63.67 ± 18.09)%, P<0.01]. The treatment of Vinp inhibited phosphorylation of NF-κB at two weeks (1.08 ± 0.42 vs. 0.84 ± 0.12, P < 0.01). Conclusion Vinpocetine can effectively attenuate intimal hyperplasia in diabetic grafted veins, which might be related to its effect on inhibiting phosphorylation of NF-κB as well as inflammation.

ObjectiveTo study the impact of type 2 diabetes mellitus on endothelium of great saphenous vein in patients with coronary heart disease.MethodsPatients undergoing coronary artery bypass grafting were selected, 20 with type 2 diabetes mellitus (experimental group) and another 20 patients without (control group).The rings of great saphenous vein in I cm length were taken from those patients and then divided into 3 segments.The structure of endothelium was evaluated by the microscope and the changes of venous tone were measured in organ chamber at 37C with a constant supply of oxygen.Venous vasoconstriction was induced by phenylephrine (10-5 mol/L) and vasodilatation induced by nitroglycerin or acetylcholine (10-9 ～ 10-5 mol/L).ResultsMore damages of ultrastructure of the endothelium of saphenous vein were found in experimental group than in control group.There were no significant differences regarding the venous tone between the two groups (P ＞0.05) when vasoconstriction induced by phenylephrine and vasodilatation by nitroglycerin.However, the vasodilatation induced by acetylcholine was significantly decreased in experimental group than in control group (P ＜ 0.05).Conclusion Type 2 diabetes mellitus can aggravate the damage of endothelium of saphenous vein in patients with coronary artery disease.

Objective To observe the effect of smoking on the great saphenous vein tension. Methods The rings of great saphenous vein in 3mm long of selected from 31 patients with coronary artery bypass grafting were divided into three groups :smoking over 10 years( group A, n = 12 ), ex-smoking over 1 years ( group B, n =9 ) and non-smoking( group C, n =10). The changes of the tone were measured in organ chamber at 37℃ with a constant supply of oxygen when vasoconstriction induced by phenylephrine ( 10 -9 - 10 -5 mmol/L), and vasodilatation by acetylcholine ( 10 -9 - 10 -5 mmol/L) or nitroglycerin( 10 -9 - 10 -4 mmol/L)after the rings were precontracted by 10 -5 mmol/L phenylephrine. Results Vasoconstriction induced by phenylephrine and vasodilatation by nitroglycerin is no significant difference among three groups. Compared with group A, vasodilatation by acetylcholine was significantly increased in group B or C, while there is no significant difference between group B and C. Conclusion Smoking has a deleterious effect on the endothelial function of great saphenous vein, however, smoking cessation over 1 year may help to restore the endothelial function impaired by smoking.

Abstract: Objective To analyze the accuracy and feasibility of GeneXpert MTB/RIF (GeneXpert) detection in the detection of Mycobacterium tuberculosis and the characteristics of rifampicin-resistant rpoB gene mutations. Methods A total of 4 234 sputum samples from suspected tuberculosis patients diagnosed in Sanya tuberculosis designated hospitals from 2015 to 2021 were selected and subjected to sputum smear, solid culture, drug sensitivity test by solid proportion method and GeneXpert detection. Results The positive detection rates of sputum smear, solid culture and GeneXpert of 4 234 sputum samples were 29.24% (1 238/4 234), 32.17% (1 362/4 234) and 35.40% (1 499/4 234), respectively. The positive detection rate of GeneXpert was higher than that of sputum smear, and the difference was statistically significant (χ2=36.775, P<0.01). It was slightly higher than solid culture, and the difference was not statistically significant (χ2=9.908, P=0.02). Taking solid culture results as the gold standard, the sensitivity and specificity of GeneXpert for detecting MTB were 91.04% (1 240/1 362) and 90.98% (2 613/2 872), respectively. According to the proportional drug susceptibility test results as the gold standard, the sensitivity and specificity of GeneXpert in detecting rifampicin resistance were 96.96% (96/99) and 98.86% (1 128/1 141), respectively, with the consensus rate of 98.71%. The accuracy of rifampicin resistance in GeneXpert group without probe mutation was significantly lower than that in group with probe mutation. There was a statistical difference in probe mutation frequency between newly treated and retreated cases. The analysis of rpoB gene mutation frequency characteristics showed: Probe E (50.00%) > Probe A (22.12%) > Probe D (14.42%) > Probe B (6.73%) > combined probe (5.77%) > Probe C (0.96%). Conclusions GeneXpert detection can quickly and effectively diagnose rifampicin-resistant tuberculosis, which is helpful for early clinical diagnosis and treatment. In this region, the rpoB gene mutation probes of rifampicin-resistant tuberculosis mainly occurr in Probe E and Probe A, with the least mutations in Probe C.

Objective To study the effect of Pioglitazone(PIO) on intimal hyperplasia after vein graft and its potential mechanism.Methods 32 male Sprague-Dawley rats were randomly divieded into two groups,one admisnistrated with PIO(3 mg· kg-1 · d-1) and the other with saline.A week later,the right common carotid arteries were reconstructed using homolateral external jugular veins in rats.The drugs treatment was continued after surgery for 2 or 4 weeks until grafted veins were harvested.The neointima thickness was measured by Computer image analysis software.To observe the activation of ERK1/2 pathway,the western blot were performed.In vitro,human great saphenous vein smooth muscle cells were co-cultured with PIO,and cells proliferation was detected by the CCK-8 assay.The TUNEL staining was performed to determine apoptosis.Results PIO treatment significantly attenuated intimal thickening compared with the the control group both at second [(8.56 ± 1.64) μm vs (25.44 ± 0.89) μm,P ＜ 0.01] and fourth week [(10.51 ± 1.47) μm vs (35.69 ± 1.07) μm,P ＜ 0.01)] after veins graft.Also PIO inhibited the ERK1/2 activation in grafted veins.In vitro,PIO significantly reduced PDGF-induced cells proliferation and increased cells apoptosis.Conclusion PIO effectively improved intimal hyperplasia in grafted veins perhaps associated with its ability to suppress vascular smooth muscle cells proliferation and enhance cell apoptosis,and might be related to the down regulation of ERK1/2 activity.

Objective To study the effect of Perfadex and Wisconsin Unviersity solution on the function of pulmonary artery endothelium.Methods Small lobe pulmonary arteries were dissected from nine porcine lungs.The artery from each lung was cut into six rings in 2mm.Two of them were randomly incubated in Krebs,Perfadex or Wisconsin Unviersity solution (UW solution) at 4℃ for 4 hours.Endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation (percentage of-7.5 logM U46619 precontraction) induced by bradykinin or calcium ionophone A23187 in the present of indomethacin,L-NNA and oxyhemoglobin were measured at 37 ℃ in the organ chambers.Results Vasoconstriction induced by U46619 is no significant difference among three groups (P＞ 0.05).Compared with Krebs group,the relaxation induced by bradykinin or A23187 was significantly decreased in Perfadex group (P＜0.01),while there is no significant difference in UW group (P＞0.05).Conclusion Endothelium-derived hyperpolarizing factor (EDHF) plays an important role in endothelium-mediated relaxation of porcine pulmonary artery.EDHF-mediated relaxation is impaired when the lung preserved with Wisconsin Unviersity solution,wheras its function is not affected by Perfadex solution.

Objective To study the effect of nicorandil on the function of coronary artery endothelium during hypoxiareoxygenation.Methods Forty-five fresh porcine left anterior descending coronary artery rings in 2mm long were randomly divided into five groups.Control group ( n =9):incubation in Krebs-Henseleit (KH) at 37℃ for 90 minutes with a constant supply of oxygen ; Group A ( n =9):30-minute hypoxia ( PO2 ＜ 15 mm Hg) followed by 30 minutes reoxygenation in KH at 37℃ ; Group B ( n =9):60-minute hypoxia followed by 30 minutes reoxygenation in KH at 37 ℃ ; Group C ( n =9):60-minute hypoxia followed by 30 minutes reoxygenation in KH added nicorandil ( 0.2 μmol/L) at 37 ℃ ; Group D ( n =9 ):60-minute hypoxia followed by 30 minutes reoxygenation in KH added nicorandil (0.2 μmol/L) and 5-hydroxydecanoate ( 10μmol/L) at 37 ℃.The endothelium-derived hyperpolarizing factor (EDHF) -mediated relaxation ( U46619 precontraction) induced by bradykinin in the present of indomethacin (7 μmol/L),LNNA (300 μmol/L) and oxyhemoglobin (20 μmol/L)were measured in the organ chambers.Results Compared with control group,the relaxation was significantly decreased in group A,B and D ( P ＜ 0.001 ),while there is no significant difference in group C ( P ＞ 0.05 ).Compared with group A,the relaxation was significantly reduced in group B and D (P ＜0.001 ).Conclusion Hypoxia-reoxygenation impairs EDHF mediated relaxation in coronary artery with more injury during prolonged hypoxia.This function can be restored by preconditioning with nicorandil The mechanism is mainly related to the mitochondrial ATP-sensitive K + channels.

Objective : To investigate the factors affecting concurrent sarcopenia among patients with cardiovascular diseases, so as to provide insights into early identification and prevention of cardiovascular diseases complicated with sarcopenia. Methods: A total of 250 inpatients with cardiovascular diseases in the Sixth Division Hospital of Xinjiang Production and Construction Corps were recruited and divided into the sarcopenia and non-sarcopenia groups according to the diagnostic criteria of sarcopenia. Subjects' basic characteristics, body mass index, blood biochemical indicators and human body composition parameters were collected using questionnaire surveys, and factors affecting concurrent sarcopenia among patients with cardiovascular diseases using a multivariable logistic regression model. Results: Among the 250 patients with cardiovascular diseases, there were 149 males (59.60%) and 101 females (40.40%). The overall prevalence of sarcopenia was 8.40% among the study subjects. The mean age and body mass index were (75.19±9.74) and (20.77±2.19) kg/m2 in the sarcopenia group and (65.24±11.50) years and (25.85±2.87) kg/m2 in the non-sarcopenia group. Multivariable logistic regression analysis identified age (OR=1.115, 95%CI: 1.030-1.207) and body mass index (OR=0.582, 95%CI: 0.445-0.761) were as factors affecting concurrent sarcopenia among patients with cardiovascular diseases. Conclusion Advanced age and low body mass index may increase the risk of concurrent sarcopenia among patients with cardiovascular diseases.