Chronic obstructive pulmonary disease(COPD) is a chronic inflammatory disease characterized by infiltration of T-lymphocytes,which plays a key role in the immune response of human.Exploration on the characters of immune response in the pathologic process related to COPD may be useful to explore the mechenism of immunity response in COPD patients,thus,contrubute to improve the knowledge of COPD and investigating new avenues of treatment.

Objective:To study the effect of erythromycin(EM) on cigarette smoke-induced histone deacetylase-3(HDAC3) protein expression in human macrophages in vitro .Methods:The Aqueous cigarette smoke extract ( CSE) was always prepared fresh on the day of the experiment .The U937 monocytic cells were differentiated into macrophages by using phorbol 12-myristate 13-acetate (PMA) according to standard procedures .The U937 differentiated cells were treated with either CSE (1%) or EM (1 μg/ml) pre-treatment, and HDAC inhibitor trichostatin A (TSA;100 ng/ml) for 24 h.HDAC activity was measured with a colorimetric assay kit and Western blot was used for HDAC3 and factor nuclear-kappaB (NF-κB) protein assays.The levels of tumor necrosis factor-α(TNF-α) release in the supernatant were determined by enzyme linked immunosorbent assay (ELISA).Results:CSE(1%) significantly de-creased HDAC activity and HDAC 3 protein levels at 24 h.Preincubation with EM (1μg/ml ) for 24 h significantly inhibit CSE (1%) induced decrease of HDAC3 protein expression.Furthermore, Preincubation with EM(1 μg/ml) for 24 h significantly inhibit NF-κB activity and TNF-αrelease in human macrophages .Conclusion:EM is able to restore HDAC3 levels decreased by cigarette smoke and inhibit NF-κB activity resulting in decreasing CSE-mediated TNF-αrelease, which has shown an important explanation that EM possess the anti-inflammatory effect induced by cigarette smoke .

This study designed an audio signal acquisition system to achieve real-time detection of R peak for heart rate variability (HRV) analysis, substituting ECG-specific data acquisition board with sound card. It is proved that the R peak with low frequency can be gathered by sound card. The comparison with PowerLab signal acquisition system has shown that the acquisition system of R peak could accurately detect the R peak. The R peak detected by sound card and PowerLab signal acquisition system completely overlap each other, while RR intervals has no difference. The HRV analysis was accurate and reliable with the RR interval from sound card. This low cost, high performance, strong compatibility and easy upgraded acquisition system of R peak compared with the traditional data acquisition board has the value of practical uses and might have broad applications in the future.
Algorithms ; Electrocardiography ; methods ; Heart Rate ; physiology ; Humans ; Monitoring, Physiologic ; instrumentation ; Signal Processing, Computer-Assisted ; instrumentation ; Sound

ObjectiveTo study the pathological characteristics of intra-acinar pulmonary artery inflammation and its correlation with smoking index and disease progression in smokers with normal lung function and smokers with chronic obstructive pulmonary disease (COPD).MethodsPatients requiting lung resection for peripheral lung cancer were divided into group A (nonsmokers with normal lung function,n = 10), group B (smokers with normal lung function, n = 13), and group C (smokers with stable COPD,n = 10).The lung tissue far away from rumor were resected to compare the pathological changes of intraacinar pulmonary arteries and infiltration level of inflammatory cell in pulmonary non-muscularized arteries (NMA), pulmonary partially muscularized arteries (PMA) and muscularized arteries (MA) among the three groups.The correlation analysis was made among infiltration level, smoking index, percentage of predicted value of forced expiratory volume in one second (FEV,％ Pred), six-minute-walk distance (6MWD) and BODE index.Results (1) Both group B and group C showed the intima and media thickness of MA was significantly higher, the lumen area of MA was narrower and the proportion of MA was higher, and collagenous fiber of MA adventitial proliferated and area increased in group C(P ＜0.05 or P ＜0.01).(2) In group B and group C, the percentage of the intra-acinar pulmonary arteries that contained leukocytes, T lymphocytes, CD8+ T lymphocytes and the number of these positive cells infiltrating the intraacinar pulmonary arteries were increased, especially an increased number of CD8+ T lymphocytes infiltrating in the arterial adventitia as compared with group A, moreover there were significant difference between group C and group B (P ＜ 0.05 or P ＜ 0.01).In group B and group C, the degree of these positive cellsinfiltrating NMA, PMA and MA presented a decreasing sequence (P ＜ 0.05 or P ＜ 0.01).Among the intima, media and adventitia of MA, the infiltration of these positive cells was the highest in the adventitia.Among group A, group B and group C, infiltration degree of CD4+ T lymphocyte, B lymphocyte, macrophage and neutrophil demonstrated no significant difference, also among NMA, PMA and MA (P ＞ 0.05).(3)The number of leukocytes, T lymphocytes, CD8+T lymphocytes infiltrating MA showed a positive correlation with the thickness of MA (r =0.563,0.627,0.589 ,P ＜0.01 ,respectively) and smoking index (r =0.551,0.665, 0.600, P ＜ 0.01, respectively), moreover the degree of these cells infiltrating MA demonstrated negative correlation with FEV1 ％ Pred (r = - 0.763, - 0.703, - 0.767, P ＜ 0.01, respectively).Also infiltrating degree of T lymphocytes and CD8+ T lymphocytes was positively correlated with BODE(r = 0.390,0.476,P ＜ 0.05, respectively). Furthermore the infiltrating degree of CD8+ T lymphocytes had negative correlation with 6MWD (r = - 0.356, P ＜ 0.05).Conclusions(1) Pulmonary arterial inflammation appears in smokers with normal lung function and smokers with COPD patients.It involves in all types of intra-acinar pulmonary arteries especially NMA and infiltrates whole layer of MA with a characteristic of CDs+T lymphocytes infiltrating in the adventitia of intra-acinar pulmonary arteries. (2)Pulmonary inflammation is closely correlated to cigarette smoking and clinical parameters such as BODE index, FEV1％pred and 6MWD.It is one of the key factors affecting the progression of COPD.

To investigate the herbal medicines which play a main role in Chinese herbal formula Jianpi Huoxue Decoction for improving intestinal permeability and protect alcohol-induced liver injury and intestine damage, and to explore the analysis method for the material base of pharmacological effects of the Chinese herbal compound.

OBJECTIVE: To study the mechanism of Qushi Huayu Decoction (QHD), a compound of traditional Chinese herbal medicine, in prevention and treatment of non-alcoholic steatohepatitis (NASH). METHODS: Thirty-five Wistar male rats were randomly divided into normal group, untreated group, QHD group and Ganle (diisopropylamine dichloroacetate) group. The rats except those in normal group were subcutaneously injected with carbon tetrachloride (CCl(4)) for 4 weeks (twice per week) and simultaneously fed with high-fat and low-protein diet for 2 weeks to induce NASH. Then, the rats were administrated with QHD, Ganle, or distilled water for 2 weeks, respectively. After harvest, alanine aminotransferase (ALT) activity and tumor necrosis factor-alpha (TNF-alpha) content in serum as well as triglyceride (TG) and free fatty acid (FFA) in liver tissue were evaluated, and relativity analysis among these parameters was performed. Cathepsin B (Ctsb), phospho-inhibitor kappa B (P-IkappaB), TNF-alpha protein expressions in liver tissue were assayed with western-blot. The expression and distribution of ctsb in liver tissue were observed with immunohistochemical method. RESULTS: The contents of TG, FFA and activity of ALT were significantly decreased in QHD group. While in the Ganle group, only the activity of ALT in serum was decreased significantly. Expressions of Ctsb, P-IkappaB and TNF-alpha proteins in liver tissues and serum TNF-alpha level were all enhanced in untreated group which, however, were significantly inhibited in the QHD group. And as expected, there were significant relativities among contents of TG in liver tissues and the content of FFA in liver tissue and activity of ALT in serum, content of TNF-alpha in serum and content of FFA in liver tissue and activity of ALT in serum. CONCLUSION: The inhibiting effects of QHD on fat deposition and inflammation in liver are related with its inhibition on the "FFA-Ctsb-TNF-alpha" pathway of lipo-toxicity.

Objective To understand the general self-efficacy level of patients with tuberculosis(TB patients) and its influencing factors, provide evidence for improving the general self-efficacy of TB patients.Methods All TB inpatients in a comprehensive pulmonary hospital were conducted face-to-face survey through a general questionnaire and general self-efficacy scale, self-efficacy level of TB patients and its influencing factors were analyzed.Results Mean scale of general self-efficacy of 402 TB patients was (20.4±4.2), of which only 14 cases(3.5%)showed a high level self-efficacy.163(40.5%), 225(56.0%), and 14(3.5%)patients were with low(10~),medium(20~), and high(30~) self-efficacy scale.The general self-efficacy level of TB patients was influenced by the course of disease(P<0.001), residence(P=0.012), whether or not attended the lecture on tuberculosis education(P=0.034), whether or not conducted physical exercise(P=0.053,stepwise multiple linear regression analysis: P=0.017), working status(P=0.027), No.of hospitalization due to TB(P=0.002), family economic situation(P=0.027), and education level(P=0.020).Conclusion TB patients' self-efficacy level is low, and the general self-efficacy level and its influencing factors should be assessed by health care workers during the follow-up for patients, individualized nursing intervention for improving the TB patients' self-efficacy level should be developed.

Objective To explore the influence of elevating the oxygen pressure on articular chondrocytes in vitro.Method A hydrogen peroxide induced human articular chondrocyte damage model was established.Then the articular chondrocyte viability was detected using the CCK-8 kit.Collagen Ⅱ(COL Ⅱ),The expression levels of aggrecan (ACAN),matrix metalloproteinase 13 (MMP13) and adisintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) were detected using the realtime PCR and Western blotting.Result The viability of articular chondrocytes improved at 12 h but decreased at 24 h after the stimulation of hydrogen peroxide.Twenty-four hours later,the average expression level of COL Ⅱ and ACAN decreased(P＜0.05),while that of MMP13 and ADAMTS5 elevated(P＞0.05).Conclusion Hydrogen peroxide induced elevation of the extracellular oxygen pressure can influence the synthesis and degradation of the articular chondrocyte extracellular matrix.

Objective To study the pathological characteristics of interleukin-16 (IL-16) and CXC chemokine receptor 3 (CXCR3) in pulmonary artery of smokers with normal lung function and smokers with chronic obstructive pulmonary disease (COPD). Methods We examined surgical specimens from three groups of subjects undergoing lung resection for localized pulmonary lesions: group NS(nonsmokers with normal lung function, n=10); group S (smokers with normal lung function, n=13); group COPD (smokers with stable COPD, n=10). The clinical datas including blood gas analysis, pulmonary function,BMI, smoking index, BODE index, six-minute-walk distance (6MWD), Medical Research Council dyspened scale (MRC), St. George Respiratory Questionnaire (SGRQ) were recorded in all subjects before the operation. We applied technique of hematoxylin-eosin staining to observe pathomorphological changes of the pulmonary arteries. The concentration of IL-16 in lung tissues were measured by ELISA. Muscularized arteries were examined with immunohistochemical methods to identify T-lymphocytes (CD_3), CD_4 T-lymphocytes, CD_8 T-lymphocytes, IL-16, CXCR3. The correlation of IL-16 and CXCR3 in muscnlarized arteries in smokers with stable COPD were analysed. Results (1) The group COPD showed the highest concentration of IL-16 in lung tissue (P <0. 01) . The concentration of IL-16 in group S was higher than group NS (P<0.05). (2) Both in group S and group COPD, the percentage of the muscularized arteries that contained CXCR3 and IL-16 were increased as compared with group NS (P < 0. 01). Moreover there were statistical significance have been observed between group COPD and group S(P < 0.01). (3) The intensity of IL-16 infiltrating the muscularized arteries in group COPD showed a positive correlation with CD_3~+ T-lymphocytes, CD_8~+ T-lymphocytes, CXCR3 (r=0.639,0. 803,0. 696; P < 0. 05 or P < 0. 01), smoking index, BODE index (r= 0.737,0. 704; P < 0. 05). There was inverse relationship between the content of IL-16 in the muscularized arteries in group COPD and forced expiratory volume in one second% predicted (FEV_1 % Pred) and 6MWD (r=-0.803,-0.787; P<0.01). We also found the intensity of CXCR3 infiltrating the muscularized arteries in group COPD showed a positive correlation with CD_3~+ T-lymphocytes,CD_8~+ T-lymphocytes(r=0.650,0.767; P<0.05), smoking index, BODE index (r=0.650,0.767; P< 0.05). There was inverse relationship between the content of CXCR3 in the muscularized arteries in group COPD and FEV_1 % Pred and 6MWD (r=-0.778,-0.774;P<0.01). Conclusions (1) Both in group S and group COPD, IL-16 and CXCR3 were mainly expressed in lymphocytes which were correlated with CD_8~+ T-lymphocytes infiltrating the muscularized arteries. There were some suggestion that IL-16 prohaly recruited CD_8~+ T-lymphocytes into muscularized arteries by enhancing the expression of CXCR3. (2) The intensity of IL-16 and CXCR3 were correlated with the index of clinical and pulmonary function that suggested pulmonary arterial inflammation might be one of the key factors associated with the progression of COPD, and inhibiting the pulmonary artery inflammation played an important role in prevention and cure of COPD.

Objective: To investigate the effects of Yiguanjian Decoction, a compound traditional Chinese herbal medicine, on collagen metabolism of hepatic tissues in rats with carbon tetrachloride (CCl(4))-induced liver fibrosis. Methods: Liver fibrosis was induced in rats by intraperitoneal injection of 50% CCl(4)-olive oil solution at a dose of 1 mL/kg body weight, twice per week for 9 consecutive weeks. Six rats were sacrificed for dynamic observation at the end of the 3rd and 6th week respectively, and the other rats were divided into 9-week untreated group and Yiguanjian Decoction group which was given Yiguanjian Decoction intragastrically in the subsequent 3-week modeling period. Another 6 rats were used as normal group. Rats in the normal group and 9-week untreated group were treated with distilled water. At the end of the 9th week, all rats were sacrificed, and their blood serum and liver tissue were collected for measuring hepatic histology and expressions of α-smooth muscle actin (α-SMA), tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2, matrix metalloproteinase (MMP)-13, MMP-14, collagen type I (Col I), and activities of MMP-2 and -9. Results: Compared with the normal group, collagen fiber deposition, expressions of α-SMA, Col I, TIMP-1, TIMP-2, MMP-13 and MMP-14 and activities of MMP-2 and -9 in the liver tissues gradually increased in the untreated group (P<0.05, P<0.01). These changes were significantly suppressed by Yiguanjian Decoction. Conclusion: Yiguanjian Decoction exerts inhibition on formation of CCl(4)-induced cirrhosis in rats. The therapeutic mechanism may be related to inhibiting hepatic stellate cell activation, collagen secretion, and promoting collagen fiber degradation.