Angiotensin-(1-7) decreases the expression of collagen I via TGF-ß1/Smad2/3 and subsequently inhibits fibroblast-myofibroblast transition.

Previous studies have shown that the RAS (renin-angiotensin system) might participate in airway remodelling in asthma. As a main component of the RAS, Ang-(1-7) [angiotensin-(1-7)] has been reported in few studies regarding its protective effect on asthma. However, the functional roles and relevant signalling pathways of Ang-(1-7) have not been well illustrated. In the present study, we analysed the effect of Ang-(1-7) on AngII (angiotensin II)-induced HLF (human lung fibroblast)-MF (myofibroblast) transition by detecting Col-I (collagen type I), TGF-ß1 (transforming growth factor-ß1) and α-SMA (α-smooth muscle actin) expression. We explored further the possible signalling pathways involved in HLF-MF transition. Our results showed that Ang-(1-7) could down-regulate the expression of Col-I, α-SMA and TGF-ß1/Smad2/3 (all P<0.05). A significant decrease was found in phosphorylation of PI3K (phosphoinositide 3-kinase), Akt, p38-MAPK (mitogen-activated protein kinase) and JNK (c-Jun N-terminal kinase) signalling pathways during HLF-MF transition (all P<0.05). Our data suggests that Ang-(1-7) decreases the expression of Col-I via TGF-ß1/Smad2/3 and subsequently inhibits HLF-MF transition.

Long-term efficacy and safety of bronchial thermoplasty in patients with moderate-to-severe persistent asthma: a systemic review and meta-analysis.

OBJECTIVE: To evaluate the long-term efficacy and safety of bronchial thermoplasty (BT) in the treatment of patients with moderate-to-severe persistent asthma. METHODS: We therefore performed a systematic literature review of peer-reviewed studies focusing on BT intervention in asthma control published between January 2000 and June 2014. Three randomized controlled studies and extension studies met the inclusion criteria (n = 6). Outcomes assessed after BT included spirometric data, adverse respiratory events, emergency room (ER) visits and hospitalization for respiratory illness. One-year and 5-year follow-up data were defined as V1 and V5, respectively. RESULTS: There were 249 BT-treated subjects in total who had a 1-year follow-up (V1), whereas 216 of them finished a 5-year follow-up (V5). No evidence of significant decline was found in pre-bronchodilator FEV1 (% predicted) (WMD = 0.75; 95% CI: 3.36 to 1.85; p = 0.57), or in post-bronchodilator FEV1 (% predicted) (WMD = 0.62; 95% CI: 3.32 to 2.08; p = 0.65) between V1 and V5. In addition, the frequency of respiratory adverse events was reduced significantly during the follow-up (RR = 3.41, 95% CI: 2.96-3.93, p < 0.00001). The number of ER visits for adverse respiratory events remained unchanged (RR = 1.06, 95% CI: 0.77-1.46, p = 0.71) after BT treatment. There was no statistically significant increase in the incidence of hospitalization for respiratory adverse events (V5 vs. V1, RR = 1.47, 95% CI: 0.69-3.12, p = 0.32). CONCLUSIONS: These data demonstrate long-term benefits of BT with regard to both asthma control and safety for moderate-to-severe asthmatic patients.

Levels of thioredoxin are related to the severity of obstructive sleep apnea: based on oxidative stress concept.

BACKGROUND: Oxidative stress is a typical feature of obstructive sleep apnea (OSA). Thioredoxin (TRX), as one of the oxidative stress biomarkers, is a potent protein disulfide reductase in antioxidant defense. Our study is designed to test whether thioredoxin could assess the severity of OSA. METHODS: Sixty-three adults suspected of having OSA were included in this study and were divided into four groups based on the results of polysomnography (PSG): control, mild, moderate, and severe. Subjects with chronic medical diseases (with the exception of essential hypertension) or taking any antioxidant medication were excluded. Blood samples were obtained within an hour after the overnight PSG test. Plasma TRX levels were detected by enzyme-linked immunosorbent assay. RESULTS: The plasma TRX level in severe group was obviously increased (8.62 ± 2.14, 13.33 ± 5.60, 14.71 ± 5.53, and 16.10 ± 7.34 ng/ml; p < 0.05). The TRX positively related to AHI (r = 0.313; p < 0.05), while negatively related to the lowest O(2) saturation (r = 0.266; p < 0.037). The OSA patients associated with hypertension showed elevated TRX level (17.70 ± 6.98 vs. 13.43 ± 5.83 ng/ml; t = 2.434, p < 0.018). The cutoff value of TRX for identifying OSA was 9.39 ng/ml (sensitivity 91 %, specificity 78 %), and its cutoff value for differentiating moderate-severe OSA from mild OSA was 11.79 ng/ml (sensitivity 75 %, specificity 65 %). CONCLUSION: These results suggest that plasma TRX level is associated with the severity of OSA. Therefore, TRX may be used as a severity indicator of OSA.

High-dose N-acetylcysteine in the prevention of COPD exacerbations: rationale and design of the PANTHEON Study.

Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation; from a pathophysiological point of view it involves many components, including mucus hypersecretion, oxidative stress and inflammation. N-acetylcysteine (NAC) is a mucolytic agent with antioxidant and anti-inflammatory properties. Long-term efficacy of NAC 600mg/d in COPD is controversial; a dose-effect relationship has been demonstrated, but at present it is not known whether a higher dose provides clinical benefits. The PANTHEON Study is a prospective, ICS stratified, randomized, double-blind, placebo-controlled, parallel-group, multi-center trial designed to assess the efficacy and safety of high-dose (1200 mg/daily) NAC treatment for one year in moderate-to-severe COPD patients. The primary endpoint is the annual exacerbation rate. Secondary endpoints include recurrent exacerbations hazard ratio, time to first exacerbation, as well as quality of life and pulmonary function. The hypothesis, design and methodology are described and baseline characteristics of recruited patients are presented. 1006 COPD patients (444 treated with maintenance ICS, 562 ICS naive, aged 66.27±8.76 yrs, average post-bronchodilator FEV1 48.95±11.80 of predicted) have been randomized at 34 hospitals in China. Final results of this study will provide objective data on the effects of high-dose (1200 mg/daily) long-term NAC treatment in the prevention of COPD exacerbations and other outcome variables.

[Characteristics of histone deacetylase 9 in peripheral blood of patients with bronchial asthma].

OBJECTIVE: To investigate the expression pattern of histone deacetylase 9 (HDAC9) in peripheral blood of asthmatics and its effect on immune cells (Th2, Th17, Tregs) involved in the pathogenesis of asthma. METHODS: Forty-seven asthmatics from Ruijin Hospital were recruited and assigned to intermittent, mild and moderate-severe groups. Lung function test and Asthma Control Questionnaire were performed to evaluate asthma control and severity. Twenty healthy donors were enrolled as controls. GATA3, IL-4, and HDAC9 mRNA expression levels were measured by SYRB Green Real-time PCR. The cytokine IL-17-mainly produced by Th17 cells and TGF-ß-mainly produced by Treg cells, were measured by ELISA. RESULTS: The GATA3 and IL-4 mRNA expression levels (28.12 ± 7.57 and 743.6 ± 312.8) were up-regulated in asthmatics as compared to the healthy controls [0.56 ± 0.22, 0.7 ± 0.8 (U = 16.00, 37.00, P < 0.01)]. The HDAC9 mRNA expression levels of intermittent, mild and moderate-severe groups were 3.20 ± 0.50, 89.6 ± 18.0, 323.0 ± 65.3, respectively, which were associated with the severity of disease (H = 11.32, P < 0.05). The level of IL-17 in asthmatic group was (83 ± 55) ng/L, which was up-regulated as compared to the healthy control [(34 ± 22) ng/L (U = 153.50, P < 0.01)]. The level of TGF-ß was decreased in the asthmatic groups as compared to the healthy control, but the difference did not reach significance. HDAC9 mRNA expression level was positively correlated with GATA3 mRNA expression level (r = 0.482, P < 0.05), and also with IL-4 mRNA expression (r = 0.432, P < 0.05) and IL-17 (r = 0.538, P < 0.05), but negatively correlated with TGF-ß (r = -0.417, P < 0.05). In patients with moderate-severe asthma, HDAC9 mRNA expression level was negatively correlated with FEV(1)% (r = -0.657, P < 0.05). CONCLUSION: HDAC9 mRNA expression was up-regulated in peripheral blood of asthmatics, which was not only associate with the Th2 master transcriptional factors GATA3, cytokine IL-4 mRNA, Th17 and Treg cell-related cytokines, but also with FEV(1)% in moderate-severe asthma.

Quantification of circulating cell-free DNA in the serum of patients with obstructive sleep apnea-hypopnea syndrome.

Serum cell-free DNA concentrations have been reported to increase in many acute diseases as well as in some chronic conditions such as cancer and autoimmune diseases. The aim of this study was to examine whether serum DNA concentrations were elevated in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). The effects of nasal continuous positive airway pressure (nCPAP) on serum DNA were also investigated. One hundred twenty-seven people diagnosed with OSAHS by polysomnography (PSG) were admitted into the OSAHS group, and 52 subjects without OSAHS were recruited for the control group. The OSAHS group was further divided into mild, moderate, and severe OSAHS subgroups based on their apnea-hypopnea index (AHI) during sleep. Ten patients with moderate and severe OSAHS were treated with nCPAP. Serum DNA, interleukin-6 (IL-6), and malonaldehyde (MDA) concentrations were measured and were found to be significantly higher in patients with moderate and severe OSAHS groups than those in the mild OSAHS and control groups (p < 0.05). Univariate analysis showed that serum DNA correlated positively with AHI, oxygen desaturation index (ODI), IL-6, and MDA, and negatively correlated with minimal oxygen saturation (miniSaO(2)) (all p < 0.05). In stepwise multiple regression analysis, only MDA and miniSaO(2) were suggested as significant independent predictors for the serum DNA concentrations. After 6 months of nCPAP therapy, serum concentrations of DNA, IL-6, and MDA were significantly decreased (p < 0.05). The increasing concentration of serum DNA in patients with OSAHS was positively correlated with disease severity. Serum DNA may become an important parameter for monitoring the severity of OSAHS and effectiveness of therapy.

[Characteristics of chronic obstructive pulmonary disease phenotypes based on high-resolution CT and the relationship with interleukin-6].

OBJECTIVE: To classify the high-resolution CT (HRCT) phenotypes of COPD, and to investigate the clinical characteristics of various phenotypes and the relationship with airway inflammation. METHODS: Chest HRCT and pulmonary function tests were performed in 84 COPD patients. The patients were classified into 3 phenotypes according to the visual HRCT findings. Exhaled breath condensate was gathered from 30 patients and the interleukin (IL)-6 level was measured by ELISA. RESULTS: The COPD patients were classified into 3 phenotypes: Phenotype A, absence of emphysema, with or without bronchial wall thickening (n = 34); Phenotype E, emphysema without bronchial wall thickening (n = 23); and Phenotype M, emphysema with bronchial wall thickening (n = 27). The 3 phenotypes of COPD showed different characteristics in several aspects. Patients with phenotype A showed a higher body mass index [(25.1 +/- 4.4) kg/m(2) vs phenotype E (22.5 +/- 4.1) kg/m(2) and phenotype M (21.3 +/- 3.4) kg/m(2), F = 6.732, P < 0.01]. The prevalence of patients with milder dyspnea was lower in phenotype A compared with others (15/34) vs phenotype E (2/23) and phenotype M (6/27), chi(2) = 9.097, P < 0.05. The patients who complained of severe expectoration in phenotype E were fewer than those in other groups (0/23) vs phenotype A (2/34) and phenotype M (4/27), chi(2) = 8.702, P < 0.05. The FEV(1)/FVC and FEV(1)% in phenotype M [(53 +/- 14)% and (51 +/- 25)%] were significantly lower as compared with those in other phenotypes [(67 +/- 11)% and (72 +/- 24)% in phenotype A, and (53 +/- 14)% and (52 +/- 26)% in phenotype E], F = 10.252, F = 6.508, P < 0.01. The ratio of inspiratory capacity to total lung capacity (IC/TLC) in phenotype A was higher [phenotype A (41 +/- 17)%, phenotype E (33 +/- 13)%, phenotype M (28 +/- 13)%, F = 5.964, P < 0.01], while the ratio of residual volume to total lung capacity (RV/TLC) was lower [phenotype A (37 +/- 9)%, phenotype E (44 +/- 10)%, phenotype M (45 +/- 8)%, F = 6.954, P < 0.01]. Patients with different phenotypes showed various levels of IL-6 in exhaled breath condensate [phenotype A (19.9 +/- 6.3) ng/L, phenotype E (16.7 +/- 2.1) ng/L, phenotype M (25.6 +/- 4.4) ng/L, F = 7.749, P < 0.01]. CONCLUSION: Various morphological phenotypes of COPD based on HRCT showed different clinical characteristics and airway inflammation.

[Atypical pathogens in adult patients admitted with community-acquired pneumonia].

OBJECTIVE: To investigate the current status of atypical pathogen associated infections in community-acquired pneumonia (CAP) in adults, and their clinical attributes. METHODS: Clinical data, sputum specimens from acute phase, and paired sera from acute- and convalescent-phases of CAP in 153 adult patients were collected from May 2005 to May 2008 in multiple medical centers. Chlamydia pneumoniae (Cpn) IgG antibody, and Legionella pneumophila (LP) mixed IgG, IgA and IgM antibodies were determined by indirect immuno-fluorescent assay. Mycoplasma pneumoniae (Mpn) mixed IgG, IgA and IgM antibodies were determined by passive agglutination assay. All the sputum specimens were routinely cultured for bacterial isolation. RESULTS: Fifty-two (34%) out of the 153 cases were diagnosed as atypical CAP per the paired serum-antibody assay. Forty-seven of the 52 atypical CAP cases were infected by one atypical pathogen, 38 with Cpn, 4 with Mpn, and 5 with LP, while 5 out of the 52 atypical CAP cases were infected by 2 pathogens, Cpn and Mpnin 2, Cpn and LP in 3 cases. Eleven cases (21.2%) out of the 52 patients with atypical pneumonia were complicated with bacterial infection. Except peripheral white blood count was significant increased in the group of typical (bacterial only) pneumonia (WBC > 10 × 109)/L, P = 0.03), all the other clinical parameters did not show statistically significant difference between the typical and the atypical pneumonia groups. CONCLUSIONS: Our data suggest that Chlamydia pneumoniae, Mycoplasma pneumoniae and Legionella pneumophila are common pathogens of adult CAP. Chlamydia pneumoniae might be the most frequent atypical pathogen associated with atypical CAP.

Different expression of mimecan as a marker for differential diagnosis between NSCLC and SCLC.

Mimecan mRNA was present in a limited number of mouse and human tissues, however, abundant mimecan mRNA was observed in the lung tissue. Therefore, we hypothesize that mimecan could serve as a biomarker for differentiating various histological types of lung cancers. In humans, the mimecan mRNA was found most abundant in ovary and less abundant in lung by using Northern blot analysis. Moreover, the mimecan was expressed strongly in the epithelial cells of the bronchial wall and weaker in the epithelial cells of the alveolar sacs by in situ hybridization and immunohistochemical analysis. Furthermore, the mimecan immunoreactivity was found in 103 (97.2%) of 106 non-small cell lung cancers (NSCLCs). Nevertheless, a large majority of small cell lung cancers (SCLCs) (50/56, 89.3%) showed negative immunoreactivity to mimecan polyclonal antibody. A significant difference of mimecan immunoreactivity was found between NSCLC and SCLC (P<0.00001). This is the first study showing that mimecan could serve as an excellent pathological biomarker to distinguish NSCLCs from SCLCs.

BMI is an independent risk factor for snoring in Chinese women aged over 30 years.

OBJECTIVE: The study was designed to analyze body mass index (BMI) as one of risk factors for snoring in Chinese women. MATERIALS AND METHODS: Totally, 2,938 women (2,423 available for evaluation of menstrual status) aged over 30 years from a population-based epidemiologic study were enrolled. RESULTS AND DISCUSSIONS: For those with regular menstrual status, BMI was the main risk factor with OR 3.906 (BMI >or=25 kg/m(2)) and 8.467 (BMI >or=30 kg/m(2)), respectively, compared with those of BMI 20-25 kg/m(2) (p < 0.001). For postmenopausal women, BMI was also indicated as a risk factor with OR 2.041 (BMI >or=25 kg/m(2)) and 2.884 (BMI >or=30 kg/m(2)) compared with those of BMI 20-25 kg/m(2) (p < 0.01). As for different BMI, menopause was the only risk factor for women with BMI < 20 kg/m(2) (OR = 10.568, p < 0.05). Whereas for those with BMI between 20 and 25 kg/m(2), the risk factors included post-menopause, family history, drinking, etc. CONCLUSION: In conclusion, the prevalence of snoring was correlated with BMI independent of menstrual status, and lower BMI is a protective factor against snoring in premenopausal women.

[Lipid frofile and hemorheology in obstructive sleep apnea-hypopnea syndrome.].

OBJECTIVE: To investigate whether there was a correlation between lipid level, hemorheology and the obstructive sleep apnea hypopnea syndrome. METHODS: Two hundred and thirty-one subjects in our sleep respiratory disease center between 2006 and 2009 were included. Eighty nine were obese OSAHS subjects, 62 were non-obese OSAHS subjects, 40 were obese subjects without OSAHS (obese group) and 40 were non-obese subjects without OSAHS (control group). We examined and compared the lipid profile and hemorheology in all subjects. RESULTS: In obese OSAHS group, the levels of triglyceride (TG) [(2.74 +/- 2.02) mmol/L], cholesterol (TC) [(5.14 +/- 0.96) mmol/L] were higher and HDL [(1.13 +/- 0.36) mmol/L], apoA-I [(1.20 +/- 0.20) mmol/L] were lower, compared to the non-obese OSAHS group (F = 7.77, 7.99, all P < 0.01). The level of the whole blood viscosity in obese OSAHS group was significantly higher than that in non-obese OSAHS group (F = 8.81-11.99, P < 0.05). There was no significant difference in blood lipid levels among the 2 study groups:non-obese OSAHS and control group, obese OSAHS and obese group (F = 6.42 - 11.99, P > 005). The levels of the whole blood viscosity and HCT were significantly higher in non-obese OSAHS group than in control group (F = 0.41 - 2.23, P < 0.05); obese OSAHS group were higher than obese group (F = 0.12 - 2.10, P < 0.05). No significant difference in blood lipid levels was noted among the 4 non-obese groups with different disease severity; similar result was also observed among obese OSAHS groups. CONCLUSIONS: Obesity is responsible for dyslipidemia in OSAHS. OSAHS has no significant correlation with lipid abnormalities, but it significantly correlates with hemorheology disorder.

Emphysema extent on computed tomography is a highly specific index in diagnosing persistent airflow limitation: a real-world study in China.

OBJECTIVE: The diagnostic value of emphysema extent in consistent air flow limitation remains controversial. Therefore, we aimed to assess the value of emphysema extent on computed tomography (CT) on the diagnosis of persistent airflow limitation. Furthermore, we developed a diagnostic criterion for further verification. MATERIALS AND METHODS: We retrospectively enrolled patients who underwent chest CT and lung function test. To be specific, 671 patients were enrolled in the derivation group (Group 1.1), while 479 patients were in the internal validation group (Group 1.2). The percentage of lung volume occupied by low attenuation areas (LAA%) and the percentile of the histogram of attenuation values were calculated. RESULTS: In patients with persistent airflow limitation, the LAA% was higher and the percentile of the histogram of attenuation values was lower, compared with patients without persistent airflow limitation. Using LAA% with a threshold of -950 HU >1.4% as the criterion, the sensitivity was 44.3% and 47.2%, and the specificity was 95.2% and 95.7%, in Group 1.1 and Group 1.2, respectively. The specificity was influenced by the coexistence of interstitial lung disease, pneumothorax, and post-surgery, rather than the coexistence of pneumonia, nodule, or mass. Multivariable models were also developed. CONCLUSION: The emphysema extent on CT is a highly specific marker in the diagnosis of persistent airflow limitation.

Gemcitabine and cisplatin treatment over a 3-week versus a 4-week dosing schedule: a randomized trial conducted in Chinese patients with nonsmall cell lung cancer.

BACKGROUND: Gemcitabine plus cisplatin is a standard treatment for stages IIIB and IV nonsmall cell lung cancer (NSCLC). This randomized phase II study evaluated a 3-week versus a 4-week schedule of gemcitabine-cisplatin as first line treatment for Chinese patients with advanced NSCLC. METHODS: Patients were randomized to receive cisplatin 75 mg/m(2) on day 1 plus either gemcitabine 1250 mg/m(2) on days 1 and 8 of a 21-day cycle (3-week group) or gemcitabine 1000 mg/m(2) on days 1, 8 and 15 of a 28-day cycle (4-week group). RESULTS: One hundred patients were enrolled in this study. The response rate was 24% (12/51 patients) in the 3-week group and 27% (13/49 patients) in the 4-week group. There were no statistically significant differences between the two treatment groups in survival (hazard ratio: 1.19; 95% CI: 0.68 - 2.09) with a median survival of 12.1 months and 13.8 months in the 3-week group and the 4-week group respectively. The rate of grade 3/4 toxicity in the 3-week group was 55% compared with 86% in the 4-week group (P = 0.001). The difference in the incidence of grade 3/4 haematological toxicities did not reach statistical significance (3-week: 37%, 4-week: 57%), however grade 3/4 drug related neutropenia (3-week: 27%, 4-week: 51%) and thrombocytopenia (3-week: 8%, 4-week: 31%) were significantly lower in the 3-week group. Grade 3/4 nonhaematological toxicities were less in the 3-week group (33% cf 63%; P = 0.005). CONCLUSIONS: The differences in the efficacy endpoints were all in favour of the 4-week schedule of gemcitabine plus cisplatin, however these differences did not reach statistical significance. Fewer grade 3/4 toxicities were observed in the 3-week group compared with the 4-week group.

[Expression of toll-like receptor 4 in human alveolar epithelial cells and its role in cellular inflammation].

OBJECTIVE: To investigate if type II alveolar epithelial cells express Toll-like receptor 4 (TLR4) and to investigate the role of TLR4 in airway inflammation of chronic obstructive pulmonary diseases (COPD). METHODS: A549, the line of human type II alveolar epithelial cells were cultured and divided into 3 groups: normal control group, E1A(+) group transfected with adenovirus E1A plasmid, E1A(-) group transferred with blank plasmid without adenovirus E1A. Lipopolysaccharide (LPS) of the concentrations of 0, 0.1, 1, and 10 microg/ml, IL-1 beta of the concentrations of 0, and 0.1 ng/ml, and cigarette smoking extract (CSE) of the concentrations of 0, 10%, 20%, and 40% were used to stimulated the A549 cells for 12 and 24 h. Reverse transcription polymerase chain reaction was used to detect the mRNA expression of IL-8 and TLR4. Western blotting was used to detect the protein expression of nuclear factor kappaB (NF-kappaB) subunit P65. RESULTS: Twenty-four hours after the stimulation of 10 microg/ml LPS, 0.1 ng/ml IL-1beta, and 20% CSE, the IL-8 mRNA expression of the E1A(+) group was 2.82, 1.87, and 4.70 respectively, all significantly higher than those of the normal control group (0.95, 0.78, and 1.02 respectively, all P < 0.05) and those of the E1A(-) group (0.97, 0.81, and 1.12 respectively, all P < 0.05). Twelve and twenty-four hours after the stimulation of 10 microg/ml of LPS, the TLR4 mRNA expression of the E1A+ group were 4.52 and 7.99, both significantly higher than those of the normal control group (1.91 and 3.81 respectively, both P < 0.05) and those of the E1A(-) group (2.00 and 3.88 respectively, both P < 0.05). IL-1beta increased the expression of TLR4 mRNA too, but CSE did not change the expression of TLR4 mRNA in all these groups. LPS, IL-1beta, and CSE all increased the expression levels of NF-kappaB subunit P65 protein. CONCLUSIONS: Pulmonary type II epithelial cells express TLR4. LPS and IL-1beta up-regulate the release of IL-8 which may be mediated via the activation of NF-kappaB induced by TLR4.

Effect of smoking cessation on airway inflammation of rats with chronic bronchitis.

BACKGROUND: Smoking is the major cause of airway inflammation in chronic obstructive pulmonary disease (COPD), and smoking cessation is regarded as one of the important strategies for prevention and treatment of the inflammation. The inflammation of the chronic airway may be present and deteriorated even if the COPD patients stop smoking. Whether and how early smoking cessation affects the progress of inflammation is still obscure. This study was conducted to find the appropriate time for smoking cessation to terminate the airway inflammation in rats with smoke-induced chronic bronchitis. METHODS: A rat model of COPD was established by passively inhaling smoke mixture. Fifty-four young male Sprague-Dawley rats were randomly divided into 9 groups with different periods of smoke exposure and different time points of cessation. The inflammation markers to be detected included inflammatory cells in the bronchoalveolar lavage fluid (BALF), the myeloperoxidose (MPO) activity, the morphologic changes and the expression of ICAM-1 on the airway epithelium. RESULTS: When smoking was terminated at early stage, the inflammatory markers and related indexes were different from those of the typical chronic bronchitis group (group M7) (P < 0.01). The pathologic score of group SC7 (2 weeks of smoking cessation after occurrence of typical chronic bronchitis) was not different from that of group M7, and the level of ICAM-1 was still up-regulated (compared to group M7, P > 0.05). Meanwhile, most of inflammatory cells in BALF were neutrophils compared to other groups (P < 0.01). When smoking was terminated, the MPO activity was significantly lower than that of group M7 (P < 0.01). CONCLUSIONS: Smoking cessation at early stage can effectively inhibit the inflammatory reaction of COPD. Once chronic bronchitis occurs, little could be improved by smoking cessation.

Validity of Asthma Control Test in Chinese patients.

BACKGROUND: So far, in China, there has been no effective or easy procedure to define the control of asthma. This study assesses the validity of Asthma Control Test in Chinese patients. METHODS: Three questionnaires (Asthma Control Test, Asthma Control Questionnaire and the 30 second asthma test) were administered to 305 asthma patients from 10 teaching hospitals across China. Spirometry was also used. Asthma specialists rated the control of asthma according to patients' symptoms, medications and forced expiratory volume in first second. The patients were divided into noncontrolled group and controlled group according to the specialists' rating. Reliability, empirical validity and screening accuracy were conducted for Asthma Control Test scores. Screening accuracy was compared among 3 questionnaires. The patients' self rating and the specialists' rating were also compared. RESULTS: The internal consistency reliability of the 5-item Asthma Control Test was 0.854. The correlation coefficient between Asthma Control Test and the specialists' rating was 0.729, which was higher than other instruments. Asthma Control Test scores discriminated between groups of patients differing in the percent predicted forced expiratory volume in first second (F = 26.06, P < 0.0001), the specialists' rating of asthma control (F = 88.24, P < 0.0001) and the Asthma Control Questionnaire scores (F = 250.57, P < 0.0001). Asthma Control Test showed no significant difference with Asthma Control Questionnaire in the percent correctly classified, while the percent correctly classified by Asthma Control Test was much higher than 30 second asthma test. The patients' self rating was the same as assessment of the specialists (t = 0.65, P = 0.516). CONCLUSION: The Asthma Control Test is an effective and practicable method for assessing asthma control in China.

[The influencing factors of Framingham cardiovascular risk score in patients with obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To compare the predictable value of different index in evaluating the risk of cardiovascular injury in the patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) by using Framingham Risk Score (FRS). METHODS: 120 OSAHS patients were divided into 2 groups with different levels of cardiovascular injury according to the FRS: low risk group (with the FRS < 10) and non-low risk group (with the FRS > or = 10). Data about medical history, gender, age, blood pressure, height, distribution, BMI, neck circumference (NC) Epworth sleepiness scale (ESS) SCORE were collected. Polysomnography (PSG) was used to measure the apnea-hypopnea index (AHI), oxygen desaturation index (ODI), lowest SaO(2) during sleep (LSaO(2)), time spent below 90% oxygen saturation (TS90). Peripheral blood samples were collected to examine the serum high-sensitivity C-reactive protein (hs-CRP). Correlation analysis was conducted. RESULTS: Except the traditional risk factors for coronary heart disease, the subjects with higher FRS were found with bigger NC [(40.48 +/- 2.80) cm vs (39.15 +/- 4.31) cm, P < 0.05], longer course of disease [(12.77 +/- 7.89) y vs (9.36 +/- 5.98) y, P < 0.05], higher AHI (47.61 +/- 25.63 vs 34.01 +/- 25.72, P < 0.01), lower LSaO(2) (73.85% +/- 11.10% vs 77.91 +/- 9.77%, P < 0.05), longer TS90 (23.46% +/- 24.46% vs 14.48% +/- 18.85%, P < 0.05), and higher ODI (49.62 +/- 23.75 vs 39.01 +/- 24.87, P < 0.05). Stepwise multivariate regression showed that FRS was positively correlated with AHI and ODI, and negatively correlated with LSaO(2). All the PSG index, AHI had the most important impact on FRS (t = 2.910, P = 0.004). There was no significant difference in hs-CRP level between different groups (P = 0.649). CONCLUSION: The cardiovascular injury in OSAHS patients is correlated with repeated hypoxia during sleep-time. AHI is the most important PSG index to predict this kind of damage.

[Pulmonary sclerosing hemangioma: report of 15 cases and review of the literature].

OBJECTIVE: To improve the understanding of pulmonary sclerosing hemangioma (PSH). METHODS: The clinical data of 15 cases of PSH were analyzed, and the literature was reviewed. The etiology, clinical manifestations, differential diagnosis, treatment and outcome of PSH were described. RESULTS: The etiology and histological origin of PSH were unclear. Most cases were asymptomatic or only with mild symptoms. The radiology of PSH often showed isolated nodule with distinct margin in the lung field. The characteristics of its pathological manifestation were as follows: (1) background of cell gathering or mucin matrix with scattered white blood cells; (2) proliferation of hemangioma with sclerosis of vessel wall; (3) papillary proliferation of small vessels intruding into the air space; (4) existence of hemorrhage or sclerosis zone. Immunohistological studies had not defined the correct histological origin of PSH. A pre-operation diagnosis of PSH was difficult. Thirteen cases had been misdiagnosed as malignancy. The outcome of the disease was good when early surgical resection was performed. CONCLUSIONS: PSH is an uncommon disease, and can be easily misdiagnosed. More attention should be paid to its clinical features and management.

MUC5AC expression up-regulation goblet cell hyperplasia in the airway of patients with chronic obstructive pulmonary disease.

OBJECTIVE: To determine the number of goblet cells, the change of MUC5AC expression in chronic obstructive pulmonary disease (COPD) patients and the relationship of smoking with goblet cell, MUC5AC, and lung function. METHODS: Eighteen patients undergoing lung resections for a solitary peripheral carcinoma were classified by lung function as having COPD. Twenty patients with normal lung function served as the control group. Normal lobe bronchioles far away from the lesion site were taken for paraffin section. Goblet cells were identified by AB/PAS staining and the expression of MUC5AC in the paraffin's section was tested by immunohistochemistry. RESULTS: Goblet cell hyperplasia was observed in the COPD group. The positive rate of goblet cell in COPD group (0.20% +/- 0.10%) was significantly higher than that in the normal lung function group (0.13% +/- 0.06%, P < 0.05). The positive rate of MUC5AC expression in the COPD group (0.27% +/- 0.09%) was higher than that in the normal lung function group (0.20% +/- 0.10%, P < 0.05). The positive rate of goblet cell in smokers (27.93% +/- 9.00%) of the COPD group and normal lung function group was higher than that in non-smokers (17.70% +/- 9.37%, P < 0.05), while MUC5AC expression had no significant difference between smokers and non-smokers (17.88% +/- 6.44% and 10.88% +/- 7.10%, respectively). CONCLUSION: For COPD patients with declined lung function, there were goblet cell hyperplasia and increased expression of MUC5AC. MUC5AC expression up-regulation may due to goblet cell hyperplasia. Smoking may be an important factor for goblet cell hyperplasia.