[Advances in research on impaired ventilatory efficiency in cardiopulmonary exercise testing and chronic obstructive pulmonary disease].

The investigation of the pathophysiological mechanisms and potential applications of impaired ventilatory efficiency in cardiopulmonary exercise testing has received considerable attention in the field of chronic obstructive pulmonary disease (COPD) research worldwide. A growing body of evidence supports the notion that impaired ventilatory efficiency is an important indicator of exertional dyspnea, reduced exercise capacity, and mortality in patients with COPD. As a result, ventilatory efficiency is emerging as a promising therapeutic target for alleviating dyspnea in COPD patients. This review aims to provide a comprehensive summary of the research progress into impaired ventilatory efficiency in patients with COPD. The primary objective of this review is to improve the understanding of COPD patients with impaired ventilatory efficiency, with the ultimate goal of facilitating the comprehensive assessment and management of COPD.

Association of pectoralis muscle area on computed tomography with airflow limitation severity and respiratory outcomes in COPD: A population-based prospective cohort study.

BACKGROUND: Previous studies have shown that patients with chronic obstructive pulmonary disease (COPD) of severe or very severe airflow limitation have a reduced pectoralis muscle area (PMA), which is associated with mortality. However, whether patients with COPD of mild or moderate airflow limitation also have a reduced PMA remains unclear. Additionally, limited evidence is available regarding the associations between PMA and respiratory symptoms, lung function, computed tomography (CT) imaging, lung function decline, and exacerbations. Therefore, we conducted this study to evaluate the presence of PMA reduction in COPD and to clarify its associations with the referred variables. METHODS: This study was based on the subjects enrolled from July 2019 to December 2020 in the Early Chronic Obstructive Pulmonary Disease (ECOPD) study. Data including questionnaire, lung function, and CT imaging were collected. The PMA was quantified on full-inspiratory CT at the aortic arch level using predefined -50 and 90 Hounsfield unit attenuation ranges. Multivariate linear regression analyses were performed to assess the association between the PMA and airflow limitation severity, respiratory symptoms, lung function, emphysema, air trapping, and the annual decline in lung function. Cox proportional hazards analysis and Poisson regression analysis were used to evaluate the PMA and exacerbations after adjustment. RESULTS: We included 1352 subjects at baseline (667 with normal spirometry, 685 with spirometry-defined COPD). The PMA was monotonically lower with progressive airflow limitation severity of COPD after adjusting for confounders (vs. normal spirometry; Global Initiative for Chronic Obstructive Lung Disease [GOLD] 1: ß=-1.27, P=0.028; GOLD 2: ß=-2.29, P<0.001; GOLD 3: ß=-4.88, P<0.001; GOLD 4: ß=-6.47, P=0.014). The PMA was negatively associated with the modified British Medical Research Council dyspnea scale (ß=-0.005, P=0.026), COPD Assessment Test score (ß=-0.06, P=0.001), emphysema (ß=-0.07, P<0.001), and air trapping (ß=-0.24, P<0.001) after adjustment. The PMA was positively associated with lung function (all P<0.05). Similar associations were discovered for the pectoralis major muscle area and pectoralis minor muscle area. After the 1-year follow-up, the PMA was associated with the annual decline in the post-bronchodilator forced expiratory volume in 1 s percent of predicted value (ß=0.022, P=0.002) but not with the annual rate of exacerbations or the time to first exacerbation. CONCLUSION: Patients with mild or moderate airflow limitation exhibit a reduced PMA. The PMA is associated with airflow limitation severity, respiratory symptoms, lung function, emphysema, and air trapping, suggesting that PMA measurement can assist with COPD assessment.

[Chronic exposure of biomass ambient particulate matter induces signal-regulatory protein α (SIRPα) and surfactant protein D expression in rat alveolar macrophages].

Objective: To observe the expression of signal-regulatory protein α (SIRPα), surfactant protein (SP) A, and SPD by, and the phagocytic function of alveolar macrophages (AMs) in the rats exposed to biomass ambient particulate matter (BMF). Methods: Seventy-two male SD rats were randomly divided into BMF group and clean air group. Protein levels of SIRPα, SPA, and SPD in AMs were determined by Western blotting and immunofluorescent assay after 4 days, 1 month, and 6 months of BMF exposure. Fluorescent labeled Glucose aureus and Pseudomonas aeruginosa were used to detect the phagocytic ability of AMs in rats at three time points. Results: After 4 days of BMF exposure, there was no significant difference in the protein levels of SIRPα and SPD compared with the clean air group (P>0.05). The relative levels of SIRPα and SPD were (1.73±0.64) and (2.01±0.78) at 1 month of BMF exposure, and those at 6 months of BMF exposure were (1.49±0.28) and (1.48±0.34), both of which were higher than those in the clean air group (P<0.05). The relative level of Staphylococcus aureus median fluorescence intensity (MFI) and Pseudomonas aeruginosa MFI at 1 month BMF group were (0.56±0.16) and (0.80±0.09), and those at 6 months BMF group were (0.67±0.11) and (0.76±0.16), both of which were lower than those in clean air group, and the difference was statistically significant (P<0.05). Conclusions: BMF induces upregulation of SIRPα and SPD in AMs and inhibits the phagocytosis of AMs.

OTX1 is a novel regulator of proliferation, migration, invasion and apoptosis in lung adenocarcinoma.

OBJECTIVE: Orthodenticle Homeobox 1 (OTX1) has been found to be closely related to the development of several human tumours. However, the function and underlying molecular mechanisms of OTX1 in non-small cell lung cancer (NSCLC) are unclear. This research was performed to investigate the effects of downregulating OTX1 gene expression on the proliferation, migration, invasion, cell cycle and apoptosis of human NSCLC cell lines. PATIENTS AND METHODS: Cultured NCI-H292 and XWLC cells were transfected with control small interfering RNA (siNC) or experimental siRNA (siOTX1). The mRNA levels were detected using a quantitative real-time PCR (RT-qPCR) assay. A Cell Counting Kit-8 (CCK-8) and a Real Time Cell Analyzer (RTCA) were used to determine cell activity. The RTCA and transwell chambers were used to assess cell migration and invasion. In addition, cell cycle progression and apoptosis were measured using flow cytometry, and the expression levels of key signalling pathway proteins were examined by Western blotting. RESULTS: The results revealed that compared with the control group, the experimental group exhibited significantly decreased cell activity (***p<0.001), significantly decreased migration and invasion abilities (***p<0.001), and cell cycle arrest in G2/M phase (*p<0.05). However, the number of apoptotic cells was higher in the experimental group than in the control group (*p<0.05). The Western blotting results were consistent with the functional experiment results. CONCLUSIONS: Silencing the OTX1 gene suppressed the proliferation, migration and invasion of NCI-H292 and XWLC cells, impeded the cell cycle transition from G2 to M phase, and accelerated apoptosis, revealing OTX1, a regulator of NSCLC, as a potential new therapeutic target.

Dust mite-derived Enterobacterial fimbriae H protein enforces the allergen specific immunotherapy in asthma mice.

BACKGROUND: The mite alimentary canal contains plenty of microbiota. It is accepted that some of the microbial products function as adjuvants to speed up immune responses. OBJECTIVES: We identified five bacterial proteins from dust mite, and Enterobacterial fimbriae H (FimH) was one of them. This study aims to test a hypothesis that the FimH protein enforces immunotherapy in asthmatic mice. METHODS: Asthmatic mice were treated by allergen specific immunotherapy (ASIT) with rDer f1/f2 or rDer f1/f2 plus FimH. Changes in inflammatory cell infiltration, airway hyperreactivity, frequency of Tregs, splenic CD4+IFN-γ+ cells, and serum levels of TGF-ß, IL-10, IL-13 and IL-17A of asthmatic mice were checked. RESULTS: ASIT with rDer f1/f2 plus FimH reduced inflammatory cell infiltration, airway hyperreactivity (AHR), and levels of IgE and IgG1 compared to ASIT with rDer f1/f2 alone, but the levels of IgG2a increased. Asthmatic mice that underwent ASIT with rDer f1/f2 plus FimH showed increased frequency of Tregs, splenic CD4+IFN-γ+ cells, serum levels of TGF-ß and IL-10; and deceased splenic CD4+IL-4+ cells, and serum levels of IL-13 and IL-17A. In vitro study showed FimH triggered IL-10 expression in a concentration dependent manner and facilitated the differentiation of Tregs. CONCLUSION: Used as an adjuvant, FimH enforces the effect of ASIT in asthmatic mice via augmenting Tregs.

Red blood cell distribution width is an independent predictor of mortality for an acute exacerbation of COPD.

BACKGROUND: The prognostic role of the red blood cell distribution width (RDW) on an acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is incompletely understood.OBJECTIVE: To investigate the effect of the RDW on in-hospital and 1-year mortality after an AECOPD.DESIGN: For 442 AECOPD patients, the RDW was measured and clinical characteristics, comorbidities and laboratory measurements were recorded. The RDW that discriminated survivors and non-survivors was determined using a receiver operator characteristic (ROC) curve. The risk factors for in-hospital and 1-year mortality were identified through logistic regression analysis and Cox regression analysis, respectively.RESULTS: Of 442 study patients, 31 died, and 411 survived while in hospital. The area under the ROC curve for RDW for in-hospital death was 0.726 (95%CI 0.631-0.822), with sensitivity of 0.71 and specificity of 0.64 for a cut-off point of 13.75%. An RDW ≥13.75% was a risk factor for in-hospital mortality (relative risk 4.30, 95%CI 1.98-9.58; P < 0.001). Univariate and multivariate Cox regression analysis showed that an RDW ≥13.75% was an independent risk factor for death at 1 year (univariate analysis, hazard ration [HR] 2.33, 95%CI 1.55-3.51; multivariate analysis, HR 1.64, 95%CI 1.08-2.50).CONCLUSION: The RDW was a strong and independent risk factor for in-hospital and 1-year death for AECOPD patients.

[The mechanism of nicotine on human bronchial smooth muscle cell contraction].

Objective: To investigate the molecular mechanism of contractility dysfunction of human bronchial smooth muscle cells induced by nicotine. Methods: Primary human bronchial smooth muscle cells were cultured in vitro. The cells were divided into a control group and a nicotine group which was treated with 10(-5) mol/L nicotine for 48 h and transfected with or without α7nAChR-siRNA (The siNC group, siNC + nicotine group and siα7nAChR + nicotine group). The effects of nicotine on the cell contractile function were examined by collagen gel shrinkage assay. The expressions of α7nAChR and TRPC6 protein in nicotine-treated human bronchial smooth muscle cells were detected by Western blotting. The change of intracellular calcium concentration by nicotine was detected by calcium ion imaging system.Data were analyzed by t test or single factor analysis of variance. Results: The area of collagen gel in the nicotine group (24±8)% was significantly lower than that in the control group (59±14)% (t=3.78, P<0.05). Compared with the control group, the expression of α7nAChR protein in nicotine-induced group (173±16)% was significantly higher than that of controls 100±0)%, t=-6.848, P<0.05. Compared with the siNC group [(72±10)%, (0.79±0.07), (0.41±0.04) and (0.17±0.02) respectively], the collagen gel area of siNC + nicotine group was significantly reduced by (37±10)%. However, the basal calcium level (1.04±0.02), store operated calcium entry level (SOCE, 0.68±0.03) and receptor operated calcium entry level (ROCE, 0.36±0.02) were remarkably elevated in the nicotine treated group (all P<0.05). Furthermore, compared with siNC + nicotine group, the area of collagen gel in siα7nAChR + nicotine group was significantly increased (62±10)%, and the basal calcium level (0.78±0.06), SOCE level (0.39±0.05) and ROCE level (0.15±0.02) were significantly reduced (all P<0.05). Conclusions: Nicotine can increase the expression of TRPC6 protein, SOCE and ROCE level, and increase the intracellular calcium concentration by upregulating the expression of α7nAChR protein, thereby promoting smooth muscle cell contraction.

[Preliminary analysis of lung function of population with biofuel smoke exposure].

Objective: To analyse the impaired lung functions of people with biofuel smoke exposure. Methods: Nonsmokers with biofuel smoke exposure were selected as research objects in a mountainous area of northern Guangdong where the families used biofuels as main energies and the nonsmokers without biofuel smoke exposure in the same area as control. Questionnaire interviews and spirometry tests were performed on all subjects. To analyse the differences of lung functions in both. Results: Seventy hundred and seventeen subjects were enro1led in this study.There were 530 nonsmokers with biofuel smoke exposure(observation group) including 442 women and 88 men, average age 54±10. There were 187 nonsmokers without biofuel smoke exposure(control group) including 141 women and 46 men, average age 54±10. There was no significant difference between two groups in age, height, weight, BMI, waist circumference, hip circumference and waist/hip ratio(P>0.05). The pulmonary ventilation function index(FEV(1)%Pred, FEV(1)/FVC) in the observation group was significantly less than that in control group [(100±18) vs.(106±25); (80±10) vs.(83±6) respectively, P<0.05]. Small airway function index(PEF25, PEF50, PEF75, MMPEF and MMPEF%Pred) was significantly less than that in control group(P<0.01). According to the univariate regression analysis and multivariate regression analysis, regression coefficients between BIOFUEL-INDEX and FEV/FVC was -0.1, 95%CI(-0.1, -0.1, P<0.01). According to the threshold analysis, the vertice of BIOFUEL-INDEX was 46.0, where the predicted Y value was 81.76, 95%CI (80.2, 83.33). When BIOFUEL-INDEX<46.0, the regression coefficient was 0, 95%CI (-0.1, 0.0)(P>0.05); when BIOFUEL-INDEX> 46.0, the regression coefficient 2 was -0.1, 95%CI (-0.2, -0.1)(P<0.01). The difference between coefficient 2 and 1 was -0.1, 95%CI (-0.2, 0.0), which was statistically significant (P<0.05). The Log-Likelihood ratio between Model I and Model Ⅱ had statistical significance (P=0.019). Conclusions: The biofuel smokes exposure causes damages in lung function.

[Establishment and application effect appraisement of community chronic obstructive pulmonary disease integrated management system].

Objective: To establish the COPD community integrated management system suitable for our national situation and assess its effects in the prevention and treatment for COPD. Methods: The COPD community integrated management system based on the electronic management system was established, including the functional modules of preliminary screening for COPD, electronic health record, grading management and dual referral system, ect. Two townships were randomly selected from the rural areas in north Guangdong as Observational Community and Control Community, respectively. Resident families were randomly selected from the two communities. One resident aged 40 or higher who was selected randomly from each family was enrolled in the trial and followed up for 2 years.Of a total of 460 participants from the Observational Community, 340 participants accomplished the two-years the follow-up, among whom there were 45 COPD patients, 117 high risk population, 178 common population. Of a total of 380 participants from the Control Community, 212 participants accomplished the follow-up, among whom there were 39 COPD patients, 68 high risk population, 105 common population.According to the COPD community integrated management system, the health cares including preliminary screening for COPD, grading management and dual referral, ect. were implemented in the Observational Community. Essential diagnosis and treatment services were performed in the Control Community. The effects of the system were appraised by comparisons of the pulmonary function change, acute exacerbation, quality of life and change of risk factors, ect. between the two communities. Results: After the intervention, the follow-up rate, smoking-quitting rate, the proportions of decline in current smoking, passive smoking and switching to clean energy for cooking in the Observational Community were significantly greater than those in the Control Community(73.9% vs. 55.8%, 70.8% vs. 9.1%, 24.2% vs. 7.1%, 32.6% vs. 3.5%, 67.8% vs. 3.2%, respectively, P<0.05). COPD knowledge rates of residents in the Observational Community, including "knowing about COPD" , "knowing about the symptoms of COPD" , "Whether COPD can be prevented and treated" and "lung function test" were significantly greater than before (84.7% vs.30.0%, 76.4% vs.7.6%, 71.5% vs.6.8%, 72.1% vs.27.4%, respectively, P<0.05) and greater than those in the Control Community(84.7% vs.73.6%, 76.4% vs.9.4%, 71.5% vs.7.1%, 72.1% vs.32.5%, P<0.05). In the Observational Community, FEV(1) and FEV(1) %Pred were significantly greater than before (1.88±0.71 vs. 1.74±0.64, 75.6±25.0 vs. 69.4±20.5, respectively, P<0.05). The values of the difference before and after the experiment in the patients of GOLD 1 grade COPD in the Observational Community were greater than those in the Control Community(P<0.05). In the Control Community, FEV(1)、FEV(1) %Pred had no significant difference before and after experiment(P>0.05). In the Observational Community, 6MWD, standard treatment rate and exercises>3 days per week were significantly greater than before(550.5±76.0 vs. 474.7±75.9, 64.4% vs. 8.9%, 100% vs. 22.2%, respectively, P<0.05) and greater than those in the Control Community(550.5±76.0 vs. 404.5±56.7, 64.4% vs. 10.3%, 100% vs. 30.8%, respectively, P<0.05), acute exacerbation was significantly less than before (4.4% vs. 17.8%, P<0.05). In the Control Unit, 6MWD was significantly less than before (404.5±56.7 vs. 469.8±58.5, P<0.05). Conclusions: The COPD community integrated management system can play a great role in community integrated prevention for COPD.

[PM2.5 from traffic-related ambient air and wood smoke induces epithelial-mesenchymal transition in human bronchial epithelial cells].

Objective: To observe if arterial traffic ambient PM2.5 (TAPM2.5) and wood smoke PM2.5(WSPM2.5) exposure can induce epithelial-mesenchymal transition (EMT) in human bronchial cells (HBEC). Methods: PM2.5 was collected from an arterial traffic road and a typical southern kitchen, and then the collections were extracted by DMSO. The viability of HBEC was measured by Cell Counting Kit (CCK-8) after culture with PM2.5-DMSO extracts for 24 hours. The expressions of EMT markers, including E-cadherin, cytokeratin, α-smooth muscle actin (α-SMA), vimentin and collagen typeⅠ (COL-Ⅰ) in HBEC were assayed by cell immunofluorescence and Western blot analysis after exposed to two different sources of PM2.5-DMSO extracts for 14 days. Results: The cell viability of HBEC increased at low concentrations (1, 2, 10 µg/ml and 1, 5, 10 µg/ml, corresponding to [(118.4±13.7)%, (118.2±8.0)%, (123.0±19.6)% and (112.4±4.1)%, (120±5.4)%, (117.8±7.0)%, respectively, all P<0.05], and then declined at high levels [20, 100, 200 µg/ml and 15, 20, 30, 40 µg/ml, corresponding to (100.7±12.1)%, (53.4±15.3)%, (9.4±1.7)% and (106.8±10.0)%, (93.8±7.9)%, (60.9±9.5)%, (46.2±3.6)%, respectively, P values were 0.923, 0.000, 0.000 and 0.231, 0.278, 0.000, 0.000, respectively] in both TAPM2.5-DMSO and WSPM2.5-DMSO incubation. After exposure for 14 days, the cells lost their typical cobblestone-like shape which implied that EMT might occur. The same treatment caused decreased positive signals of E-cadherin and cytokeratin in a small proportion of the cells. The decreased expressions of cytokeratin were verified by Western blot (TAPM2.5 and WSPM2.5 were 0.063±0.109 and 0.039±0.313, P values were 0.033 and 0.030, respectively), while α-SMA was only significantly upregulated in the WSPM2.5-DMSO group (7.853±4.784, P=0.049). The expressions of E-cadherin decreased in both groups but not statistically significant in Western blot (0.862±0.096 and 0.817±0.212, P values were 0.228 and 0.117, respectively). Another marker of EMT, COL-I, markedly increased in both PM2.5 treatment groups (2.549±1.037 and 3.658±1.207, P values were 0.034 and 0.001). Conclusions: Both PM2.5 from arterial traffic ambient air and wood smoke could induce EMT in human bronchial epithelial cells, while WSPM2.5 appeared to have a more significant influence on EMT in HBEC.

[Bone morphogenetic protein 4 increases canonical transient receptor potential protein expression by activating bone morphogenetic protein receptor â ¡/Smad signaling pathways in pulmonary arterial smooth muscle cells].

OBJECTIVE: To observe the effect of bone morphogenetic protein 4 (BMP4) on the Smad signaling pathway in rat distal pulmonary artery smooth muscle cells (PASMCs), and to explore the role of the transient receptor potential ion channel (TRPC) protein 1 and 6(TRPC1, 6) in rat distal PASMCs. METHODS: Distal pulmonary arteries were isolated from adult male Wistar rats(n=6, 280-300 g). The endothelium-denuded pulmonary artery tissue was digested using Collagenase and PASMCs were cultured. Activation of BMP4 signaling pathway in Smad was detected by Western blotting. Western blotting was used for the measurement of protein to determine the involvement of BMP4/BMPRⅡ signaling in BMP4-inducd TRPC1 and TRPC6 protein expression, and Smad signaling was inhibited by the specific BMPRⅡ small interfering RNA (BMPRⅡSiRNA). RESULTS: Rapid phosphorylation of Smad1/5/8 was seen after 15 min of stimulation with BMP4, which was reduced with time. The BMPR Ⅱ proteins was effectively down-regulated in the PASMCs after transfection with BMPRⅡ SiRNA, and the phosphorylation of Smad1/5/8 BMP4-induced was decreased in the PASMCs transfected with BMPR Ⅱ SiRNA compared to the normal PASMCs. In addition, transfection of BMPRⅡsiRNA also attenuated BMP4-induced TRPC1 and TRPC6 protein expression compared with transfection of NT-target siRNA in distal PASMCs. PASMCs transfected with BMPRⅡsiRNA showed a markedly decreased ability for BMP4 induction as assessed by gray value ratio of Western blotting, 2.7 times and 2.5 times by TRPC1/ß-actin and TRPC6/ß-actin respectively, compared with NT siRNA-treated cells(P<0.05). CONCLUSION: TRPC1 and TRPC6 protein expression can be up-regulated through Smad1/5/8 signaling activation by combination of BMP4 and BMPRⅡ in PASMCs.

Development and validation of a chronic obstructive pulmonary disease screening questionnaire in China.

OBJECTIVE: To develop a brief, reliable screening questionnaire for chronic obstructive pulmonary disease (COPD) for use in primary care settings. METHODS: We developed a COPD Screening Questionnaire (COPD-SQ) using data collected from 19,800 subjects aged ≥40 years obtained from an epidemiological study of COPD in China in 2002 (Phase I). A stepwise logistic regression method was adopted for item reduction and scoring. We then assessed the COPD-SQ through a cross-sectional study (Phase II) among 3231 subjects aged ≥40 years. RESULTS: The final COPD-SQ consisted of seven items: age, smoking pack-years, body mass index, cough, dyspnoea, family history of respiratory diseases and exposure to biomass smoke from cooking. Using the questionnaire to screen for COPD in Phase II, we obtained high classification accuracy with an area under the curve of 0.812 (95%CI 0.786-0.838). The sensitivity, specificity and correct classification rates for COPD diagnosis were respectively 60.6%, 85.2% and 82.7% at a cut-off score of 16. CONCLUSIONS: The COPD-SQ can be used in first-level screening for COPD.

Peak expiratory flow as a screening tool to detect airflow obstruction in a primary health care setting.

BACKGROUND: Peak expiratory flow (PEF) measurement is less expensive and requires fewer skills than spirometry testing. It is thus expected to be a reasonable substitute for spirometry in airflow obstruction screening when spirometry is unavailable. OBJECTIVES: To evaluate the validation of PEF measurement in the detection of airflow obstruction using newly established regression equations. METHODS: The PEFs of 553 'normal' participants aged 40-85 years were measured using mechanical devices. Based on these data, regression equations were generated to predict normal PEF values. Data were then collected from 3379 subjects. The specificity and sensitivity of the different predicted PEF cut-off points for detecting airflow obstruction were evaluated by spirometry, based on previously generated regression equations. RESULTS: Using newly established reference values for PEF, PEF had higher sensitivity and specificity than the questionnaire in detection of airflow obstruction. That PEF < 80% of predicted was more effective in the detection of airflow obstruction was confirmed by the lower limit of normal of forced expiratory volume in 1 second/forced vital capacity, Global Initiative for Chronic Obstructive Lung Disease (GOLD), and GOLD plus symptom, with a sensitivity of 78.7%, 76.8%, 85.3% and a specificity of 81.9%, 83.8%, 81.4%, respectively. CONCLUSIONS: Mechanical PEF may be a reasonable method of screening for airflow obstruction in settings where spirometry is unavailable.

Influence of environmental characteristics and climatic factors on mites in the dust of air-conditioner filters.

UNLABELLED: To investigate mites in the dust of air-conditioner filters (MACF) in China, a total of 652 dust samples were collected from six cities: Guangzhou (n = 129), Nanchang (n = 127), Shanghai (n = 113), Xian (n = 93), Beijing (n = 93), and Shenyang (n = 79). Tarsonemus granarius was the most dominant species (87.2%). Dermatophagoides pteronyssinus and Dermatophagoides farinae only represented 7.0 and 3.0% of total mites, respectively. With latitude increasing, both mite occurrence rate (P < 0.001) and density (mites/g dust) (P < 0.001) were significantly decreasing. Multivariate regression analysis suggested that the annual average temperature and minimum temperature in different cities had dominant influences on MACF density. The logistic regression analysis revealed that the presence of MACF was positively associated with air-conditioner age, utilization time and power. Wall and window type air-conditioner had higher risk of finding MACF than the floor type air-conditioner. As far as the cleaning interval time of ACF was concerned, higher risk ratio and the highest density of MACF were found in the time stage of >3, < or =12 months. It was also suggested that house type could influence the presence of MACF. A negative association between the house floor and the MACF prevalence was found as well. PRACTICAL IMPLICATIONS: Mites present in the dust of air-conditioner filters are potential indoor threat to asthma and allergy sufferers. In this study, we find that the storage mite Tarsonemus granarius is the predominant species of mites in the dust of air-conditioner filters (MACF). Thus, the possible clinical importance of T. granarius should cause more our attentions in the future. The abundance and distribution of MACF are also found significantly varied in different climatic regions of China. When we try to assess the possible risk of MACF, more attentions should be focused on subtropical region than temperate region. The influence analysis of environmental characteristics on the prevalence of MACF will shed light on the establishment of mite control strategy and the design of mite defense air-conditioner.

COPD in Chinese nonsmokers.

Little is known about chronic obstructive pulmonary disease (COPD) in Chinese nonsmokers. The present study aimed to investigate the profiles of COPD among nonsmokers based on the Chinese Epidemiological Survey of COPD (CESCOPD). In the CESCOPD, 20,245 subjects aged 40 yrs or older were interviewed with questionnaires and spirometry tests. Subjects with a post-bronchodilator forced expiratory volume in one second (FEV(1))/forced vital capacity (FVC) ratio of <0.70 were identified as having COPD. Data of 12,471 nonsmokers and 1,024 smoking COPD patients were analysed in the current study. The overall prevalence of COPD among nonsmokers was 5.2% (95% confidence interval 4.8-5.6). Being male, of advanced age, lower body mass index (BMI) and lower educational level, having exposure to environmental tobacco smoke, coal and/or biomass smoke, poor ventilation in the kitchen, a family history of respiratory disease and recurrent childhood cough were all independently associated with a higher risk of having COPD among nonsmokers. Nonsmokers with respiratory symptoms without airflow limitation showed a somewhat different pattern of risk factors. Nonsmokers with COPD were less likely to present with chronic productive coughs and lower BMI, while more likely to have received a physician diagnosis of asthma and respiratory diseases in childhood, than smokers with COPD. Chronic obstructive pulmonary disease is prevalent among Chinese nonsmokers, and nonsmoking chronic obstructive pulmonary disease may have different profiles from smoking chronic obstructive pulmonary disease.

Meta- and pooled analyses of the effect of glutathione S-transferase M1 and T1 deficiency on chronic obstructive pulmonary disease.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a complex polygenic disease in which gene-environment interactions are very important. A number of studies have investigated the genotypes of glutathione S-transferase M1 and T1 (GSTM1 and GSTT1) in relation to COPD susceptibility in different populations. However, the results of individual studies have been inconsistent. METHODS: To address the inconsistent findings in studies of the association of the polymorphism of the GSTM1 and GSTT1 genes with susceptibility to COPD, we performed a meta-analysis of the published data. We searched the Medline database for case-control studies published from 1966 to July 2008. Data were extracted and pooled, and ORs were calculated with their 95%CIs. RESULTS: Twelve eligible studies comprising 1697 patients with COPD and 1867 controls were included in the meta-analysis. The pooled result showed that the GSTM1 deficiency was associated with risk of COPD (OR 1.46, 95%CI 1.16-1.83). Subgroup analysis supported the results in smoking and non-Asian populations, but not in Asian populations. The GSTT1 deficiency was not associated with risk of COPD. CONCLUSIONS: The GSTM1 gene is a genetic contributor to overall COPD susceptibility in non-Asian populations, and the GSTT1 gene is not associated with COPD.

Chitosan microparticles loaded with mite group 2 allergen Der f 2 alleviate asthma in mice.

BACKGROUND: In recent years, nanoparticle materials have found wide applications in drug transport and release systems. Chitosan is a good carrier for proteins, peptides, and nucleic acids because of its favorable release properties and ability to increase membrane permeability. OBJECTIVE: To investigate the effect of chitosan microparticles loaded with the major epitope peptide of mite group 2 allergen Der f 2 from Dermatophagoides farinae (Der f 2-47-67) in alleviating asthma in mice. METHODS: Derf 2-47-67 was entrapped in chitosan to obtain Derf 2-47-67-loaded chitosan microparticles, which were injected intraperitoneally into BALB/c mice prior to an intranasal challenge with a Der f extract allergen. Airway hyperreactivity was measured via whole-body plethysmography, and bronchoalveolar lavage (BAL) fluid was collected to calculate total cell and eosinophil counts. Changes in lung histology were assessed after hematoxylin-eosin staining, and serum levels of Der f-specific immunoglobulin (Ig) G2a and IgE were determined by enzyme-linked immunoabsorbent assay. RESULTS: Mice immunized with Der f 2-47-67-loaded chitosan microparticles displayed decreased airway hyperreactivity, reduced numbers of eosinophils in BAL fluid, alleviated lung inflammation and mucus production, a reduced serum level of Der f-specific IgE and an increased serum level of Der f-specific IgG2a. CONCLUSION: Our data showed that Der f 2-47-67-loaded chitosan microparticles inhibited airway allergic inflammation.

Localization of Per a 3 allergen in the gut and faecal pellets of the American cockroach (Periplaneta americana).

Cockroach-derived materials are known to be a major source of potent aeroallergens, causing allergic respiratory diseases such as asthma and allergic rhinitis. The aim of this study was to determine the localization of the major allergen, Per a 3 (Cr-PI), within the American cockroach (Periplaneta americana), which might reveal the relative importance of excreted materials and nonexcreted cockroach components as allergen sources. American cockroaches (P. americana) and their faecal pellets were embedded in paraffin, and serial sections were cut and collected on glass slides. After being stained with mouse polyclonal antiserum against Per a 3, the sections were incubated sequentially with biotin-labelled sheep antimouse immunoglobulin G (IgG) and a preformed fluorescent isothiocyanate (FITC)-avidin complex. Finally, the sections were mounted and examined under a fluorescent microscope. Examination of Per a 3 immunoreactivity on the sections of the American cockroaches (P. americana) revealed that the midgut mucosa, gut contents and faecal pellets were all strongly labelled. Per a 3 immunoreactive products were not detected in any other internal organs of the American cockroaches. These results suggest that Per a 3 allergen might be synthesized in and secreted from the epithelia of the midgut mucosa and excreted from the body in the faecal pellets.

Increasing COPD awareness.

Early diagnosis and smoking cessation are the only available methods to stop the progression of chronic obstructive pulmonary disease (COPD). The aim of this study was to evaluate the effects of early detection of airflow limitation (AL) in a population with high risk for COPD, using spirometric screening. Smokers aged 40 yrs with a smoking history of 10 pack-yrs were invited to visit a local outpatient chest clinic for simple spirometry (forced expiratory volume in one second (FEV1) and forced vital capacity (FVC)). Smoking history was recorded, followed by smoking cessation advice relating the results of spirometry to the smoking behaviour. Subjects who did not fulfil the above criteria (younger and/or nonsmokers) were also screened. A total 110,355 subjects were investigated; they were aged 53.5+/-11.5 yrs and 58.2% were males. Of the total amount of subjects, 64% were current smokers, 25.1% were former smokers and 10.9% were lifelong nonsmokers. Spirometry tests were within normal values for 70.3%, and 20.3% showed signs of AL: this was mild in 7.6%, moderate in 6.7% and severe in 5.9%. The remaining 8.3% of subjects presented with a restrictive pattern of ventilatory impairment. Airflow limitation was found in 23% of smokers aged 40 yrs with a history of 10 pack-yrs. This study concluded that large-scale voluntary spirometry screening of the population with high risk for COPD detects a large number of subjects with AL.

An epidemiological study on children with syndromic hearing loss.

OBJECTIVES: To study the epidemiological factors in children with syndromic hearing loss. STUDY DESIGN: Interview based prospective study. SETTINGS: Govt. ENT Hospital, AYJNIHH, NIMH-SEC, and Schools for the Deaf-in Hyderabad and SecunderabadPatients: Children aged below 14 years, with hearing loss, their parents/guardians. INTERVENTION(S): The study revealed type and degree of hearing impairment. In high risk groups genetic counseling was offered. RESULTS: Epidemiological studies were carried out in 743 children below 14 years with hearing impairment and 138 (18.57%) were found to have syndromic deafness. Majority of the children with hearing loss have an association of ocular abnormality (22.46%, n=31) followed by skeletal anomalies 14.49% (n=20) and dental anomalies (10.86%). We observed 24 cases (3.21%) with genetically well recognized syndromes. CONCLUSION: Data is generated on epidemiological and etiology of Hearing Impairment. Hearing Impairment is due to both environmental and genetic causes. Environmental factors in 17 (13.77%), genetically inherited 21 cases (15.22%) and the cause is not known in the remaining cases. Such a data is required in order to offer genetic counseling to reduce the genetic burden.