Publications by authors named "Dunqiang Ren"

17 Publications

  • Page 1 of 1

Polyhexamethylene guanidine aerosol triggers pulmonary fibrosis concomitant with elevated surface tension via inhibiting pulmonary surfactant.

J Hazard Mater 2021 Jul 13;420:126642. Epub 2021 Jul 13.

Department of Environmental and Occupational Health, School of Public Health, Qingdao University, Qingdao 266071, China. Electronic address:

Environmental chemicals inhalation exposure could induce pulmonary fibrosis, which is characterized by the excessive proliferation of fibroblasts and accumulation of extracellular matrix components, in which surface tension usually plays vital roles. Polyhexamethylene guanidine (PHMG) was first recognized as a potential hazard ingredient in humidifier disinfectants, which caused an outbreak of pulmonary fibrosis in South Korea. However, the underlying mechanisms involved in PHMG-induced pulmonary fibrosis have not yet been fully elucidated. Therefore, this study mainly focuses on the effect of PHMG on surface tension to unveil the influence and involved mechanisms in PHMG-induced pulmonary fibrosis. C57BL/6J mice were exposed to sub-acute PHMG aerosol for 8 weeks. The results indicated that PHMG induced pulmonary fibrosis combined with elevated surface tension. Results from in vitro study further confirmed PHMG elevated surface tension by inhibited pulmonary surfactant. Mechanistically, PHMG suppressed the key surfactant protein SP-B and SP-C by inhibiting protein expression and block their active sites. The present study, for the first time, revealed the molecular mechanism of PHMG-induced pulmonary fibrosis based on pulmonary surfactant inhibition mediated surface tension elevated. And pulmonary surfactant may be a potential target for further intervention to prevent PHMG-induced fibrosis or alleviate the symptom of relevant patients.
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http://dx.doi.org/10.1016/j.jhazmat.2021.126642DOI Listing
July 2021

Immune checkpoint inhibitor-induced myocarditis in lung cancer patients: a case report of sintilimab-induced myocarditis and a review of the literature.

Ann Palliat Med 2021 Jan;10(1):793-802

Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China. Email:

Since its initial approval by the United States Food and Drug Administration (FDA) in 2014, the indications for the use of the immune checkpoint inhibitors (ICIs) in non-small cell lung cancer (NSCLC) patients has increased. However, to date, there has no report on immune myocarditis caused by the ICI sintilimab. In addition, there has been no literature review on ICI-induced myocarditis in lung cancer patients. This is a case report of an elderly male patient who presented with a productive cough and progressive dysphagia for 3 days. The symptoms started on day 6 after the third cycle of sintilimab treatment for his lung carcinoma. In accordance with his clinical manifestations of progressive dysphagia, a previous history of lung cancer, abnormal electrocardiograph, significantly increased serum myocardial enzyme levels, and normal coronary angiography results, sintilimab-induced myocarditis was diagnosed. Methylprednisolone (80-40 mg) was used to inhibit the immune injury and the patient was safely discharged on the 13th day following admission. Since ICI-induced myocarditis is rare and fatal, we summarized the characteristics of 20 cases of the disease in lung cancer patients to highlight to oncologists, respiratory experts, and cardiologists the serious side effects of the drug when they encounter lung cancer patients using ICIs. Like most ICIs, sintilimab induces severe immune myocarditis and requires corticosteroids therapy, and this should be recognized by doctors in multiple departments.
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http://dx.doi.org/10.21037/apm-20-2449DOI Listing
January 2021

Ambient air pollutants and hospital visits for pneumonia: a case-crossover study in Qingdao, China.

BMC Public Health 2021 01 7;21(1):66. Epub 2021 Jan 7.

Department of Occupational and Environmental Health, School of Public Health, Qingdao University, Qingdao, 266021, Shandong, China.

Background: Pneumonia is one of the principal reasons for incidence and death in the world. The former research mainly concentrated on specific sources of patients. Besides, due to the heterogeneity among regions, there are inconsistencies in the outcome of these surveys. To explore the relationship between atmospheric pollution and hospital visits for pneumonia under the climate and pollution conditions in Qingdao, we carried out this study.

Methods: The medical records of pneumonia patients were gathered from the affiliated hospital of Qingdao University during Jan 1st, 2014, and Dec 31st,2018. Daily concentrations of PM, PM, SO, NO, as well as CO, were collected from the national air quality monitoring stations in Qingdao. Case-crossover study design and conditional logistic regression model were used to estimate the associations. Daily temperature, relative humidity, and atmospheric pressure were adjusted as the covariates in all models. A principal component analysis was used to solve the multicollinearity between atmospheric pollutants and investigate the relationship between various air pollutants and pneumonia occurs.

Results: In the single pollutant model, with interquartile range increment of the density of PM, PM, NO and SO at the lag2 days, the odds ratio of hospital visits for pneumonia patients increased by 6.4% (95%CI, 2.3-10.7%), 7.7% (95%CI, 3.2-12.4%), 6.7% (95%CI, 1.0-12.7%), and 7.2% (95%CI, 1.1-13.5%). Stratified analysis showed that pollutants were more significant in the cold period. Besides, the impact of atmospheric particulates on different ages mainly occurs in the young child (0 to 3-year-old). The odds ratio was 1.042 (95%CI, 1.012-1.072) when the principal components of atmospheric pollutants were included in the conditional logistic model.

Conclusions: Our study found a significant relationship between short-term uncovering to PM, PM, NO, SO, and hospital visits for pneumonia in Qingdao. The effect of atmospheric pollutants mainly arose in a cold period. The particulate matter might be the principal reason in inducing hospital visits for pneumonia.
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http://dx.doi.org/10.1186/s12889-020-10065-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7791776PMC
January 2021

TGFβ/Smad mediated the polyhexamethyleneguanide areosol-induced irreversible pulmonary fibrosis in subchronic inhalation exposure.

Inhal Toxicol 2020 Sep - Oct;32(11-12):419-430. Epub 2020 Nov 4.

Department of Occupational and Environmental Health, School of Public Health, Qingdao University, Qingdao, China.

Aim: Polyhexamethylene guanidine (PHMG) is widely used as a disinfectant with broad spectra of bactericidal activity and low oral toxicity. However, inhalation of PHMG can cause pulmonary injury and severe pulmonary fibrosis. The mechanism underlying PHMG aerosol induced pulmonary fibrosis remains unclear. In this study, we aimed to examine the subchronic lung injury and determine potential cytokines involved in PHMG aerosol induced fibrosis.

Methods: C57BL/6N mice were exposed to 1.03 mg/m PHMG through aerosol inhalation for 3 weeks, or 3 weeks followed by other 3 weeks recovery.

Results: The results indicated that the expression of transforming growth factor-beta1 (TGF-β1) and extracellular matrix remodeling markers were up-regulated in the PHMG-treated mice and these parameters were aggravated after 3 weeks recovery. Bronchoalveolar lavage fluids (BALFs) analysis showed that the number of total cells was significantly decreased in exposure group. The percentage of macrophages in BALFs decreased significantly whereas the percentage of neutrophils and lymphocytes increased. Extensive collagen deposition was observed in the peribronchiolar and interstitial areas in the PHMG exposed lungs.

Conclusion: In conclusion, even low-does PHMG aerosol exposure could induce mice pulmonary local inflammation and irreversible fibrosis. In addition, TGF-β/Smad signaling pathway mediated the extracellular matrix remodeling involved in the development of pulmonary fibrosis.
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http://dx.doi.org/10.1080/08958378.2020.1836091DOI Listing
March 2021

[Advances in Exosomes in the Pathogenesis and Diagnosis of Lung Cancer].

Zhongguo Fei Ai Za Zhi 2020 Jul;23(7):589-596

Department of Respiratory and Critical Care Medcine, The Affiliated Hospital of Qingdao University, Qingdao 266000, China.

The incidence of lung cancer is high worldwide, and lung cancer is the leading cause of death from malignant tumors in both men and women. Early diagnosis of lung cancer can significantly improve the patient's prognosis. Therefore, searching for specific markers to assist in the early diagnosis of lung cancer is urgent question. Exosomes are nano-sized microvesicles and contain various biomaterial, including nucleic acids, proteins, and lipids. Exosomes are important carriers of these biomaterial, serve important roles in intracellular communications and signal transduction among tissues. Due to its unique enrichment mechanism, it has the stability and specificity as a biomarker. Exosomes are not only involved in the formation of tumor microenvironment and new blood vessels in lung cancer, but also involved in chemotherapy, targeted therapy response and prognosis assessment. Many research advances bring new hope for prolonging the survival of lung cancer patients. This article reviews the value of exosome specific protein and microRNA (miRNA) in lung cancer in the diagnosis and prognosis of lung cancer.
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http://dx.doi.org/10.3779/j.issn.1009-3419.2020.104.18DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406446PMC
July 2020

Association between air pollution and lung development in schoolchildren in China.

J Epidemiol Community Health 2020 10 11;74(10):792-798. Epub 2020 Jun 11.

Department of Occupational and Environmental Health, School of Public Health, Qingdao University, Qingdao, China

Background: China has been facing nationwide air pollution at unprecedented high levels primarily from fossil-fuel combustion in the past decade. However, few studies have been conducted on the adverse effect of severe air pollution on lung development in school-age children.

Methods: Using wellness check and air pollution data from 2014 to 2017, we conducted a retrospective analysis of lung development in 21 616 school-age children from Shijiazhuang and Qingdao from North China with severe vs mild air pollution. Linear mixed effects model was performed to assess the effect of air pollution on forced vital capacity (FVC) growth.

Results: Exposure to severe air pollution was associated with a dramatic reduction in annual FVC growth rate (-71.3 mL,  p< 0.001). In addition, every 10 μg/m increase in annual PM level was associated with a reduction of annual FVC growth by 12.2 mL ( p< 0.001). Sex discrepancy (boys vs girls) in FVC growth was greater in Qingdao (35.4 mL/year, 95% CI: 26.0 to 44.7) than in Shijiazhuang (19.8 mL/year, 95% CI: 9.3 to 30.3) (p for interaction=0.063). Exposure to indoor coal- or wood-burning stove heating (-79.4 mL,  p< 0.001) and secondhand smoke at home (-59.3 mL,  p= 0.003) were inversely associated with FVC growth.

Conclusion: Our study raised serious alarm over the threat of severe air pollution to lung development in school-age children. Sex discrepancy in lung development was reduced dramatically in heavily polluted area.
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http://dx.doi.org/10.1136/jech-2020-214283DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7577101PMC
October 2020

The efficacy and safety of fluticasone propionate/formoterol compared with fluticasone propionate/salmeterol in treating pediatric asthma: a systematic review and meta-analysis.

J Int Med Res 2020 Mar 18;48(3):300060519889442. Epub 2019 Dec 18.

Center of Diagnosis and Treatment of Breast Disease, The Affiliated Hospital of Qingdao University, Qingdao, China.

Objective: To evaluate the efficacy and safety of fluticasone propionate/formoterol (FP/FORM) versus fluticasone propionate/salmeterol (FP/SAL) in treating pediatric asthma during a 12-week treatment cycle.

Methods: Randomized controlled trials of FP/FORM compared with FP/SAL in treating pediatric asthma were searched systematically using Medline, Embase, and the Cochrane Controlled Trials Register.

Results: Two articles including 546 patients were evaluated. The FP/SAL group showed obvious improvements in pre-dose forced expiratory volume in 1 s (FEV) from day 0 to 84, asthma symptom scores, and sleep disturbance scores compared with the FP/FORM group; however, the FP/FORM group had improved peak expiratory flow rate (PEFR). In terms of 2-hour post-dose FEV from day 0 to 84, 2-hour forced expiratory flow at 25%, 50%, and 75%, and 2-hour forced vital capacity, we observed no significant differences between the two groups. For safety, including patients with at least one adverse event, bronchitis, cough, or pharyngitis, both groups had similar incidences, differing only in incidence of nasopharyngitis.

Conclusion: Compared with FP/FORM, FP/SAL showed a clear improvement in pre-dose FEV, asthma symptom scores, and sleep disturbance scores. However, FP/FORM resulted in improved PEFR with a lower incidence of nasopharyngitis.
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http://dx.doi.org/10.1177/0300060519889442DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7607222PMC
March 2020

A genetic variation in CHI3L1 is associated with bronchial asthma.

Arch Physiol Biochem 2021 Jun 11;127(3):279-284. Epub 2019 Jul 11.

Laborwatory of Cardiovascular Diseases, Nanfang Hospital, Guangzhou, China.

Background: This study was aimed to investigate the associations among Chitinase 3-like 1 ( polymorphisms, asthma and plasma YKL-40 levels in Chinese population.

Material And Methods: Four single nucleotide polymorphisms (SNPs) were genotyped. The YKL-40 level in plasma and eosinophil percentage in peripheral blood were quantified.

Results: A SNP (rs4950928) in the promoter was associated with elevated plasma YKL-40 levels ( = .02), asthma ( = .042) and lung function ( = .029 to .002) in this Chinese population. Plasma YKL-40 levels were significantly elevated in patients with asthma compared to those in control subjects ( < .05). Plasma YKL-40 levels were significantly correlated with forced expiratory volume per cent (FEV1%) measurements ( < .05). Although plasma YKL-40 levels were decreased after treatment, the correlation with FEV1% still existed.

Conclusions: locus is a risk factor for asthma in Chinese population.
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http://dx.doi.org/10.1080/13813455.2019.1634737DOI Listing
June 2021

[Clinical Features of EGFR Double Mutation in Non-small Cell Lung Cancer].

Zhongguo Fei Ai Za Zhi 2018 Aug;21(8):594-599

Department of Respiration, Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Background: The clinical features of patients with common single-mutation of epidermal growth factor receptor (EGFR) in non-small cell lung cancer (NSCLC) has been well characterized. There is a high adenocarcinoma incidence rate among female patients with none or shorter smoking history. Those patients have higher objective response rate (ORR) and progression free survival (PFS) treated with EGFR tyrosine kinase inhibitors (EGFR-TKIs). However, it is still unclear that the clinical features of patients with EGFR double mutation and the sensitivity towards EGFR-TKIs treatment.

Methods: We performed a retrospective cohort study of 1,238 primary NSCLC patients who had EGFR gene testing in Affiliated Hospital of Qingdao University from January 1, 2015 to December 31, 2016 and identified 603 patients with single mutation and 59 patients with double mutation. All genes were uniformly detected by using ARMS-PCR technology. We analyze the gene of 32 double-mutant patients with specific genotyping, and randomly selected 60 patients with single mutation and compared the clinical features with 59 patients with double mutation. Furthermore, we examined the efficacy of EGFR-TKIs treatment in lung cancer patients with double mutation and single mutation in EGFR.

Results: The rare single mutation gene is the most common in patients with double mutation of EGFR. There is no significant statistical difference in gender, smoking history, age, pathological type or tumor-node-metastasis (TNM) staging among patients with single and double EGFR mutantion. In the double mutation patients treated with EGFR-TKIs, the objective response rate was 36.80%, the disease control rate was 68.40%. The objective response rate was 60.00% and the disease control rate was 90.00% in the patients with single mutation. However, overall PFS was significantly higher in EGFR single mutation patients (P=0.003), with median PFS of 12.0 months compared with 6.0 months in EGFR double mutation patients.

Conclusions: There was no significant difference between the clinical features of patients with EGFR double mutation and single mutation. Patients with EGFR double mutation is associated with poor survival underwent the first generation of EGFR-TKIs treatment compared with patients with a single mutation.
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http://dx.doi.org/10.3779/j.issn.1009-3419.2018.08.05DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6105346PMC
August 2018

Immunomodulation by mesenchymal stem cells in treating human autoimmune disease-associated lung fibrosis.

Stem Cell Res Ther 2016 Apr 23;7(1):63. Epub 2016 Apr 23.

State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, P. R. China.

Background: Interstitial pneumonia in connective tissue diseases (CTD-IP) featuring inflammation and fibrosis is a leading cause of death in CTD-IP patients. The related autoimmune lung injury and disturbed self-healing process make conventional anti-inflammatory drugs ineffective. Equipped with unique immunoregulatory and regenerative properties, mesenchymal stem cells (MSCs) may represent a promising therapeutic agent in CTD-IP. In this study, we aim to define the immunopathology involved in pulmonary exacerbation during autoimmunity and to determine the potential of MSCs in correcting these disorders.

Methods: Lung and blood specimens, bronchoalveolar lavage fluid cells collected from CTD-IP patients, and human primary lung fibroblasts (HLFs) from patients pathologically diagnosed with usual interstitial pneumonia (UIP) and healthy controls were analyzed by histology, flow cytometry and molecular biology. T cell subsets involved in the process of CTD-IP were defined, while the regulatory functions of MSCs isolated from the bone marrow of normal individuals (HBMSCs) on cytotoxic T cells and CTD-UIP HLFs were investigated in vitro.

Results: Higher frequencies of cytotoxic T cells were observed in the lung and peripheral blood of CTD-IP patients, accompanied with a reduced regulatory T cell (Treg) level. CTD-UIP HLFs secreted proinflammatory cytokines in combination with upregulation of α-smooth muscle actin (α-SMA). The addition of HBMSCs in vitro increased Tregs concomitant with reduced cytotoxic T cells in an experimental cell model with dominant cytotoxic T cells, and promoted Tregs expansion in T cell subsets from patients with idiopathic pulmonary fibrosis (IPF). HBMSCs also significantly decreased proinflammatory chemokine/cytokine expression, and blocked α-SMA activation in CTD-UIP HLFs through a TGF-β1-mediated mechanism, which modulates excessive IL-6/STAT3 signaling leading to IP-10 expression. MSCs secreting a higher level of TGF-β1 appear to have an optimal anti-fibrotic efficacy in BLM-induced pulmonary fibrosis in mice.

Conclusions: Impairment of TGF-β signal transduction relevant to a persistent IL-6/STAT3 transcriptional activation contributes to reduction of Treg differentiation in CTD-IP and to myofibroblast differentiation in CTD-UIP HLFs. HBMSCs can sensitize TGF-β1 downstream signal transduction that regulates IL-6/STAT3 activation, thereby stimulating Treg expansion and facilitating anti-fibrotic IP-10 production. This may in turn block progression of lung fibrosis in autoimmunity.
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http://dx.doi.org/10.1186/s13287-016-0319-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4842299PMC
April 2016

Obstructive sleep apnoea and risks of all-cause mortality: preliminary evidence from prospective cohort studies.

Sleep Breath 2016 Mar 15;20(1):345-53. Epub 2016 Jan 15.

Department of Respiratory Medicine, XuZhou Central Hospital, The Affiliated XuZhou Hospital of Medical College of Southeast University, 199 South Jiefang Road, Xuzhou, Jiangsu, 221009, China.

Purpose: A meta-analysis of prospective cohort studies was conducted to clarify the association between obstructive sleep apnoea (OSA) and future risk of all-cause mortality.

Methods: Eligible studies were identified by searching the PubMed and EMBASE databases up to July 2015. Pooled hazard ratios (HRs) and their corresponding 95 % confidence intervals (CIs) were calculated to estimate the association between OSA and risk of all-cause mortality. Sources of heterogeneity were identified by subgroup and meta-regression analyses.

Results: Twelve prospective cohort studies involving 34,382 participants were included in this meta-analysis. The pooled HR of all-cause mortality was 1.262 (95 % CI 1.093-1.431) with significant heterogeneity. Subgroup analyses indicated that the pooled HRs of all-cause mortality in patients with mild, moderate and severe OSA were 0.945 (95 % CI 0.810-1.081), 1.178 (95 % CI 0.978-1.378) and 1.601 (95 % CI 1.298-1.902), respectively. OSA severity could be a possible sources of heterogeneity. Existing publication bias produced a minor contribution to effect size.

Conclusion: Severe, but not mild to moderate, OSA is significantly associated with increased risk of all-cause mortality.
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http://dx.doi.org/10.1007/s11325-015-1295-7DOI Listing
March 2016

Aptamer-Dendrimer Bioconjugates for Targeted Delivery of miR-34a Expressing Plasmid and Antitumor Effects in Non-Small Cell Lung Cancer Cells.

PLoS One 2015 25;10(9):e0139136. Epub 2015 Sep 25.

Department of Thoracic Surgery, The Affiliated Hospital of Qingdao University, Qingdao, P.R. China.

Metastasis and drug resistance are major barriers for the treatment of non-small cell lung cancer (NSCLC). To explore new therapeutic options, we successfully encapsulated MicroRNA-34a (miR-34a), a potent endogenous tumor suppressor in NSCLC into S6 aptamer-conjugated dendrimer to form lung cancer-targeted gene delivery nanoparticles (PAM-Ap/pMiR-34a NPs). PAM-Ap/pMiR-34a NPs had a diameter of 100-200 nm and Zeta potential of ~30 mV at applied N/P ratio. The aptamer conjugation significantly improved cellular uptake as well as gene transfection efficiency of PAM-Ap/pMiR-34a NPs in cultured NSCLC cells. We showed that PAM-Ap/pMiR-34a NPs enhanced the regulation of targeted genes, BCL-2 and p53 in vitro. In addition, we revealed PAM-Ap/pMiR-34a NPs significantly inhibited cell growth, migration, invasion and induced apoptosis of lung cancer cells compared with non-targeted NPs. The method provided a novel therapeutic strategy for the experimental treatment of NSCLC.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0139136PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4583438PMC
June 2016

Stem Cell and Idiopathic Pulmonary Fibrosis: Mechanisms and Treatment.

Curr Stem Cell Res Ther 2015 ;10(6):466-76

Department of Pediatrics and Adolescent Medicine Li Ka Shing Faculty of Medicine, The University of Hong Kong China.

Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease resulting from multiplex causes. Evidence indicates that stem/progenitor cells might play a key role in IPF pathogenesis and repair, which may provide some novel potential strategies for the future treatment of IPF. In this review, we first summarize the current understanding of the relationship between stem cells and IPF and then review the advancements made in recent clinical trials using stem/progenitor cells, especially mesenchymal stem cells, in treating IPF and their interpretations.
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http://dx.doi.org/10.2174/1574888x10666150519092639DOI Listing
July 2016

Effects of continuous positive airway pressure therapy on systemic inflammation in obstructive sleep apnea: a meta-analysis.

Sleep Med 2013 Nov 14;14(11):1139-50. Epub 2013 Aug 14.

Department of Radiotherapy, Xuzhou Central Hospital, Affiliated Xuzhou Hospital of Medical College of Southeast University, Xuzhou, China.

Objectives: Our meta-analysis was performed to estimate the effect of continuous positive airway pressure (CPAP) therapy on systemic inflammation in patients with obstructive sleep apnea (OSA).

Methods: A comprehensive literature search of PubMed and EMBASE was performed for literature published up to January 2013. Standardized mean difference (SMD) was calculated to estimate the treatment effects of pre- and post-CPAP therapy.

Results: A total of 35 studies involving 1985 OSA patients were included in the meta-analysis. Each study investigated one or more inflammatory markers: 24 studies on C-reactive protein (CRP), 16 studies on IL-6, 3 studies on IL-8, and 12 studies on tumor necrosis factor α (TNF-α). The results showed that the SMD (95% confidence interval [CI]) for CRP, IL-6, IL-8, and TNF-α were 0.452 (95% CI, 0.252-0.651), 0.299 (95% CI, 0.001-0.596), 0.645 (95% CI, 0.362-0.929), and 0.478 (95% CI, 0.219-0.736) in pre- and post-CPAP therapy, respectively. The subgroup analyses seemed to support better benefits with therapy duration of ≥3 months and more adequate compliance (≥4 h/night).

Conclusions: CPAP therapy could partially suppress systemic inflammation in OSA patients, and substantial differences were present among the various inflammatory markers.
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http://dx.doi.org/10.1016/j.sleep.2013.07.006DOI Listing
November 2013

[Effects of dexamethasone on expressions of IL-21 and its receptor in lungs of experimental asthma mice].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2013 Jun;29(6):561-4

Department of Respiratory Diseases, Nangfang Hospital, Southern Medical University, Guangzhou 510515, China.

Objective: To observe the expressions of IL-21 and its receptor (IL-21R) in the lungs of chronic asthmatic mice, and investigate the effects of dexamethasone (Dex) on their expressions.

Methods: Thirty-three specific pathogen free (SPF) BALB/c female mice were randomly divided into control group, asthmatic group and Dex treated group, 11 mice each group. The asthma model mice were induced by ovalbumin (OVA) with the classic method. The airway inflammation was evaluated by HE staining. The thicknesses of bronchial wall (Wat/Pbm) and airway smooth muscle (Wam/Pbm) were measured. The expressions of IL-21 and IL-21R proteins were detected by immunohistochemistry and Western blotting.

Results: Compared with the control group, the Wat/Pbm and Wam/Pbm in the asthmatic group significantly increased (P<0.01). The indexes in the Dex group were significantly reduced as compared with those in the asthmatic group (P<0.01). The expressions of IL-21 and IL-21R proteins in the asthmatic group were higher than those in the control group (P<0.05), but they were lower in the Dex group than in the asthmatic group (P<0.05).

Conclusion: The enhanced expressions of IL-21 and IL-21R in the asthmatic mice are found, and Dex can inhibit the expressions of IL-21 and IL-21R in the lung tissues of asthmatic mice.
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June 2013

Impact of continuous positive airway pressure on C-reactive protein in patients with obstructive sleep apnea: a meta-analysis.

Sleep Breath 2013 May 5;17(2):495-503. Epub 2012 Jun 5.

Guangzhou Institute of Respiratory Diseases, State Key Lab of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical College, 151 Yanjiang Road, Guangzhou, Guangdong 510120, China.

Purpose: C-reactive protein (CRP) is associated with the development of obstructive sleep apnea (OSA) and cardiovascular diseases. Continuous positive airway pressure (CPAP) is an effective treatment for OSA, but the impact of CPAP therapy on CRP levels in patients with OSA remains unclear. To obtain this information, we performed a meta-analysis to determine whether effective CPAP therapy could reduce serum CRP levels.

Methods: A comprehensive literature search was performed to identify studies that examined the impact of CPAP on serum CRP levels in OSA patients who were treated with CPAP for at least 4 weeks. Standardized mean difference (SMD) was used to analyze the summary estimates for CPAP therapy.

Results: Fourteen self-control design studies involving 1199 patients with OSA met the inclusion criteria. Meta-analysis indicated that the overall SMD for the CRP levels was 0.64 units (95 % confidence interval (CI) 0.40 to 0.88) before and after CPAP therapy; test for overall effect z = 5.27 (P = 0.000). Subgroup analysis showed that evolution of CRP decreased non-significantly in less than 3 months (SMD, 0.26, 95 % CI -0.08 to 0.60, P = 0.138), significantly decreased after 3 months (SMD, 0.68, 95 % CI 0.34 to 1.02, P = 0.000), and further declined after 6 months (SMD, 0.74, 95 % CI 0.43 to 1.05, P = 0.000).

Conclusions: The systemic inflammation, as measured by CRP, was present and significantly reduced by effective CPAP therapy in patients with OSA. The use of CRP levels may be clinically recognized as a valuable predictor for OSA treatment monitoring.
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http://dx.doi.org/10.1007/s11325-012-0722-2DOI Listing
May 2013

The PTEN tumor suppressor inhibits human airway smooth muscle cell migration.

Int J Mol Med 2010 Dec;26(6):893-9

Department of Respiratory Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China.

Airway remodeling in asthma is characterized by increased airway smooth muscle (ASM) mass, accompanied by cell migration. It is well known that the proliferation and migration of ASM cells (ASMCs) play a key role in airway remodeling, but the precise mechanism modulating these cellular events remains unclear. One of the genes most likely to be involved in this process is the phosphatase and tensin homolog (PTEN) gene, whose deletion from chromosome 10 can inhibit the proliferation and migration of many cell types. In this study, we investigated the effects of PTEN on human ASMCs. The cells were infected with recombinant adenovirus containing wild-type PTEN cDNA (Ad-PTEN), and the results were compared with those from the uninfected cells and those infected with the GFP-labeled adenovirus vector. Cell proliferation was measured using the MTT method. Cell migration was determined by wound-healing and transwell assays. The expressions of PTEN, phospho-Akt, Akt, phospho-ERK1/2, ERK1/2, phospho-focal adhesion kinase (FAK) and FAK, were examined by Western blot analysis. The results show that PTEN is expressed endogenously in ASMCs, and that Ad-PTEN inhibits the proliferation and migration of these cells. In addition, the Ad-PTEN treatment decreased the phosphorylation of Akt and FAK but not that of ERK1/2. In conclusion, this study demonstrates that PTEN overexpression inhibits the proliferation and migration of human ASMCs by down-regulating the activity of the Akt and FAK signaling pathways.
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http://dx.doi.org/10.3892/ijmm_00000539DOI Listing
December 2010
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