Objective To investigate the change of plasma visfatin in patients with coronary heart disease and its clinical significance.Methods A total of 310 patients with coronary heart disease (ACS group:n =217; SAP group:n =93) and of 90 healthy subjects with a matched age and gender were included in this study.The plasma concentration of visfatin of each subject was measured using ELISA assay,and each patient underwent selective coronary angiography examination.A total of 85 cases of patients in CHD group underwent 64-slice CT coronary imaging to evaluate the main plaque within the coronary.Results The visfatin,LDL,BMI,blood glucose levels was significantly higher in CHD group[ ( 128.18 ± 13.86)ng/ml,(3.63 ± 1.48) mmol/L,( 26.18 ± 1.82) kg/m2,(7.25 ± 2.03 ) mmol/L] than in control group [ (75.96 ± 10.27 )ng/ml,(2.64 ± 0.53 ) mmol/L,( 23.51 ± 0.89 ) kg/m2,(5.11 ± 1.53 ) mmol/L,P ＜ 0.05 ],respectively.The visfatin level in the ACS group [ ( 145.57 ± 19.95 ) ng/ml ] was significantly higher than the SAP group [ (110.79 ±7.78)ng/ml,P ＜0.05].The visfatin concentration gradually increased with the aggravation of the complexity of coronary lesion types and severity of coronary lesions( P ＜ 0.05).The plasma visfatin concentrations in Soft plaque group and the fibrous plaque group were significantly higher than calcified plaque (P ＜ 0.05).HDL-C and Gensini score of coronary lesions were negatively correlated ( r =- 0.055,P ＜0.05) ; LDL-C,Glu,and visfatin was positively correlated with coronary lesions Gensini score ( r =0.464,0.279,0.531,P ＜ 0.05 ),respectively.Conclusions The plasma visfatin level in patients with Coronary heart disease increased and affected its lipid metabolism.It may be an important inflammatory factors promoting arterial atherosclerosis occurs and development,which has a certain value to the judgment of coronary lesions and plaque stability combined with 64-slice spiral CT examination.

Objective: To examine the effect of SiO2 exposure on the airway surface microenvironment and NIMA-related kinase 7 (NEK7)/nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome in rats. Methods: Twenty-four specific pathogen-free male rats of the SD strain were randomly divided into the control group and the model group, of 12 rats in each group. Rats in the model group were given SiO2 suspensions through disposable tracheal intubation perfusion to model silicosis in rats, while rats in the control group was perfused with the same amount of physiological saline. The pH value and glucose level were measured in the rat bronchoalveolar lavage fluid (BALF) 14 and 28 days after modeling. Lung tissues were stained with HE and Masson and the distribution of inflammatory cells and the deposition of pulmonary interstitial collagens were observed in lung tissues under a light microscope. The expression of transforming growth factor β1 (TGF-β1), collagen type Ⅰ(ColⅠ), collagen type Ⅲ (Col Ⅲ), interleukin-1β (IL-1β), NLRP3, N-terminal domain of Gasdermin D (GSDMD-NT), caspase-1, and NEK7 was quantified in lung specimens using immunohistochemistry. Results: Lower pH values were measured in rat BALF in the model group than in the control group 14 [(6.38±0.05) vs. (6.68±0.08), P<0.05] and 28 days after modeling [(6.63±0.14) vs. (6.86±0.05), P<0.05], while higher glucose levels were seen in the model group than in the control group 14 [(0.39±0.06) vs. (0.31±0.04) mg/dL, P<0.05] and 28 days after modeling [(0.39±0.08) vs. (0.31±0.06) mg/dL, P<0.05]. HE and Masson staining showed mild to moderate alveolitis and pulmonary fibrosis in rats 14 days post-exposure to SiO2, and showed moderate to severe alveolitis and pulmonary fibrosis 28 days post-exposure. Immunohistochemistry detected higher TGF-β1, ColⅠ, Col Ⅲ, IL-1β, NLRP3, GSDMD-NT, caspase-1 and NEK7 expression in rat lung tissues in the model group than in the control group (all P<0.05). Conclusions SiO2 exposure may cause changes in rat airway surface microenvironment, including BALF acidification and elevated glucose. Pyroptosis induced by activation of NEK7-associated NLRP3 inflammasome may be an important mechanism of pulmonary fibrosis caused by silicosis.

Objective To explore the association between plasma resistin levels and acute coronary syndrome. Methods Four hundred patients were divided into coronary heart disease (CHD) group（310）and control group（90）according to the coronary Angiography (CAG). And CHD group was divided into ACS subgroup（n＝217）and SAP subgroup（n＝93）according to the clinical information. 85 cases in CHD group were underwent 64-slice spiral computed tomography coronary artery imaging. The severity and extent of coronary lesions were analyzed by CAG and graded by means of Gensini coronary score system. Resistin level in plasma of all patients was determined by enzyme linked immunosorbent assay. Results Resistin levels in CHD group［(889.1±248.2)pg/ml］ were significant higher compared with the control group［(261.6±111.9)pg/ml］ (P＜0.05), and resistin levels in ACS subgroup［(1260.0±368.0)pg/ml］ were much higher than that in SAP subgroup［(518.3±128.4)pg/ml］ (P＜0.05). Conclusions The resistin levels of patients with acute coronary syndrome increased significantly and might be associated with the vulnerable plaque. Resistin levels and 64 slice spiral computed tomography coronary artery imaging can be used to detect the vulnerable plaque in CHD patients.

AIM:The purpose of the present study was to investigate the effect of interleukin-10(IL-10)on the proliferation and calcineurin(CaN)activity in cultured cardiac fibroblasts(CFs)induced by arginine vasopressin(AVP).METHODS:The CFs of left ventricle in neonatal Sprague-Dawley rats were isolated and cultured by trypsin digestion and selective plating technique.Then the proliferation rates of cells were determined by using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay(A490 value).Cell cycle distribution was determined with flowcytometry technique.The CaN activity was measured by ultra-violet spectrophotography.RESULTS:(1)MTT colorimetry showed that 10-7 mol/L AVP significantly increased A490 value of CFs in comparison with control group(P

Objective:To determine the relationship between serum resistin levels and carotid intima media(IMT)thickness in patients with essential hypertension. Methods:This study consisted of 272 patients with essential hypertension. The patients were divided into three groups according to their serum resistin levels. Group 1,n=91,serum resistin level 1.233-3.701 ng/ml;Group 2,n=91,serum resistin level 3.728-8.777 ng/ml;and Group 3,n=90,serum resistin level 8.809-28.658 ng/ml. Results:The carotid IMT and maximum carotid IMT of Group 3 were the highest in three groups.(P＜0.05).As shown in multivariate analysis for factors affecting carotid IMT,serum resistin level(β=0.220,t=5.793,P=0.000)was independently associated with the carotid IMT after controlling the age,blood glucose,uric acid,low-density lipoprotein cholesterol,systolic blood pressure and diastolic blood pressure. Serum resistin level(β=0.189,t=4.733,P=0.000)was independently associated with the maximum carotid IMT after controlling the age,blood glucose,body mass index,diastolic blood pressure,diabetes mellitus,high sensitivity C reactive protein,total cholesterol and triglyceride. Conclusion:Serum resistin was independently associated with the increased carotid IMT in essential hypertension patients.

Objective To investigate the relation between activator protein-1(AP-1)and coronary atheroselerotic changes and the potential role of AP-1 in the stabilization of atherosclerotic plaques in patients with coronary heart disease(CHD).Method 142 patients were included in this study and divided into CHD group(107)and control group(35)according to coronary angiography(CAG).The CHD group was further divided into a stable angina pectoris(SAP)group(32)and all acute coronary syndrome(ACS)group (75)according to the clinical manifestations.In addition,the CHD group was divided into A type group,B type group and C type group according to the standard of ACC/AHA coronary change in 1988.Meanwhile,the CHD group was further divided into light stenosis group,moderate stenosis group and severe stenosis group according to the degree of coronary lesion.The lysate of cells was obtained through lysis of the leucocyts from peripheral blood with cell lysis buffer.The amount of Phospho.c-Jun in lysate was measured with enzyme-linked immunosorbent assay(ELISA).The results were demonstrated with absorbance,which reflects the amount of AP-1.Results The main coronary changes in the SAP group were A type(68.7%)and the changes were mainly of light degree(53.1%);the main coronary changes in the ACS group were B type(52.0%)or C type(37.3%)and the changes were mainly of heavy degree(66.7%).The absorbance of Phospho-c-Jun in CHD group was significantly higher than that in the control subjects (1.43±0.33 vs 0.71±0.13,P＜0.001).The absorbance of Phospho-c-Jun in the ACS group was significantly higher than that in the SAP group(1.56±0.28 vs 1.14±0.25,P＜0.001).The absorbance of Phospho-c-Jun increased gradually from A type group to C type group(1.18±0.27 vs 1.42±0.26 vs 1.71±0.27,P＜0.001)and from light stenosis group to severe stenosis group(1.09±0.20 vs 1.37±0.26 ys 1.60±0.29,P＜0.001).Conclusion There is a significant relationship between AP-1 and coronary atherosclerotic changes.AP-1 may be a factor that can predict coronary arteriosclerotic progression and stability of the plaque.

Objective To investigate the relationship between the plasma adiponectin concentration and coronary arteriosclerosis change in patient with coronary heart disease(CHD).Method 142 patients were divided into CHD group and control group according to the Coronary Angiography(CAG).CHD group were further divided into stable angina pectoris(SAP)subgroup and acute coronary syndrome (ACS)subgroup according to the clinical property.According to the type of coronary change,CHD group wag divided into A type group, B type group and C type group,meanwhile according to the degree of coronary lesion,CHD group was divided into light stenosis group, moderate stenosis group and severe stenosis group.The plasma adiponectin concentration was measured by ELISA.Results The plasma adiponectin concentration in CHD group was significant lower than that in control group.The plasma adiponectin concentration in ACS subgroup was significant lower than that in SAP subgroup.The plasma adiponectin concentration decreased gradually from A type group to C type group and from light stenosis group to severe stenosis group(P＜0.001).Conclusions Adiponectin is a negative regulatory factor of coronary atherosclerosis,and Hypoadiponectin may be used to predict the change of coronary arteriosclerosis and the stability of plaque.

Endometrial cancer has been identified by The Cancer Genome Atlas program with four molecular subtypes by genome sequence analysis. Clinical trials to select suitable immunotherapeutic agents based on the different immune characteristics of each subtype have been conducted in several countries and have made important progress. The main clinical applications of immune checkpoint inhibitors include anti-programmed cell death protein-1/programmed death-ligand 1 antibodies and poly ADP-ribose polymerase inhibitors. Optimizing drug selection and drug combination based on the target characteristics of different immune checkpoint inhibitors may provide new opportunities for immunotherapy of endometrial cancer and bring new light to improve survival rates.

OBJECTIVETo investigate the effect of environmental risk factors on the development of stroke.

METHODSWith the use of cold-stimuli plus high-salt intake as environmental risk factors, a hypertension model with the complication of stroke was established in rats, then, a new technique, suppression subtractive hybridization (SSH), was used to identify the differential genes which specifically expressed in total cerebrum tissue of rat in each group. Comparison was made between control group and stroke group.

RESULTSBy the application of SSH, a total of 576 clones were generated in this study from two subtractive libraries, among them 456 clones were usable and were analyzed. Genes for cell/organs defense were down-regulated in stroke group and metabolism transcripts were shown to be up-regulated (P<0.01).

CONCLUSIONCell/organs defense genes may play important roles in the development of stroke. The above findings suggested that environmental risk factors could genetically alter individual sensitivity to stroke.

Animals ; Brain ; metabolism ; pathology ; Cell Division ; genetics ; Cold Temperature ; DNA, Complementary ; chemistry ; genetics ; Expressed Sequence Tags ; Gene Expression Regulation ; drug effects ; Immunity, Innate ; genetics ; Male ; RNA, Messenger ; drug effects ; genetics ; metabolism ; Rats ; Rats, Wistar ; Sequence Analysis, DNA ; Signal Transduction ; genetics ; Sodium Chloride, Dietary ; administration & dosage ; Stroke ; genetics

Silicotic nodules and pulmonary fibrosis are histopathological appearance in silicosis patients after long-term inhalation of crystalline silica particles, and are difficult to reverse and recover. Research on the pathogenesis and treatment strategies of silicosis has significantly lagged behind medical progress and clinical needs, resulting in the disease remaining a thorny clinical problem. Traditional Chinese medicine extracts or compound preparations have become a hot issue in exploring silicosis treatment strategies in recent years. This paper described the main pathological processes of pulmonary fibrosis caused by silicosis, followed by introducing its main pathogenesis mechanisms, including transforming growth factor-β1 (TGF-β1)/Smad signaling pathway, oxidative stress reaction, apoptosis, and autophagy. In addition, it briefly described the research progress, targets, and intervention effects of selected traditional Chinese medicine extracts, which provides a scientific basis for the theoretical and clinical research of traditional Chinese medicine extracts in inhibiting pulmonary fibrosis. To change the clinical status quo of silicosis fibrosis which is difficult to control and reverse, the paper proposed that we can further explore the pathogenesis and progression mechanisms of silicosis and drug treatment strategy, and focus on the transformation of basic research into clinical practice.