Obstructive sleep apnea and the risk of mortality in patients with lung cancer: a meta-analysis.

PURPOSE: Prior reports have examined the relationship between obstructive sleep apnea (OSA) and the mortality rate of lung cancer. However, the findings remain controversial. The present meta-analysis was performed to assess the relationship between OSA and increased risk of mortality in patients with lung cancer. METHODS: PubMed, Web of Science, and Embase were systematically searched for the correlative studies. Data were analyzed and pooled to evaluate odds ratios (ORs) of lung cancer mortality related to OSA. RESULTS: From 249 identified studies, 3 met inclusion criteria and were analyzed, including 67 patients with lung cancer and comorbid OSA and 45 patients with lung cancer and no OSA. The meta-analysis indicated that OSA was not significantly correlated with mortality rate in lung cancer (OR = 2.005, 95% CI = 0.703 to 5.715, z = 1.30, p = 0.193). There was no significant publication bias according to Begg's tests (p = 0.296) and Egger's tests (p = 0.097). CONCLUSION: This meta-analysis suggests that OSA is not significantly correlated with the mortality rate in lung cancer.

Astragaloside IV sensitizes non-small cell lung cancer cells to gefitinib potentially via regulation of SIRT6.

Astragaloside IV, the active component of Astragalus membranaceus, exhibits diverse biological roles including the anti-tumor activity. In this study, we evaluated the chemosensitive role of astragaloside IV in non-small cell lung cancer cells. Cell Counting Kit-8 analysis was performed to determine cell viability. Real-time polymerase chain reaction and western blot were used to measure the messenger RNA and protein expression. Results showed that astragaloside IV treatment could suppress the proliferation of non-small cell lung cancer cells. In addition, combined treatment with astragaloside IV remarkably enhanced the chemosensitivity to gefitinib in three non-small cell lung cancer cell lines including NCI-H1299, HCC827, and A549. Furthermore, compared with gefitinib-treated cells, the messenger RNA expression of SIRT6 was obviously increased in non-small cell lung cancer cells treated with gefitinib combined with astragaloside IV. In addition, downregulation of SIRT6 was accomplished using small interference RNA technology. As a result, SIRT6 inhibition abolished the sensitization role of astragaloside IV in non-small cell lung cancer cells. Taken together, these data demonstrated that astragaloside IV sensitized tumor cells to gefitinib via regulation of SIRT6, suggesting that astragaloside IV may serve as potential therapeutic approach for lung cancer.

ATF3 and extracellular matrix-related genes associated with the process of chronic obstructive pulmonary.

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is a major public health problem worldwide and is proved to be the number three cause of death in globally. The objective of this study was to explore the molecular mechanism of the progression of COPD. METHODS: Using the GSE1650 affymetrix microarray data accessible from Gene Expression Omnibus database, we first identified the differentially expressed genes (DEGs) between 18 COPD samples and 12 normal samples, followed by the GO / KEGG pathway analysis and gene interaction networks analysis of the DEGs. Our study identified 134 DEGs which involved in regulation of immune response, vesicle transport system, growth regulator and extracellular matrix (ECM)-related pathways. RESULTS: Gene interaction networks analysis showed that the sub-network involved by activating transcription factor-3 (ATF3) was the most significant sub-network in gene interaction networks. Furthermore, the investigation of extracellular matrix-related genes showed that genes like collagen and insulin-like growth factor binding protein could clearly distinguish the COPD and normal control. CONCLUSIONS: The genes regulated by ATF3 transcriptional activator as well as ECM-related genes may play an important role in the process of COPD. Our study provides a comprehensive bioinformatics analysis of genes and pathways which may be involved in the progression of COPD.

Expression of connective tissue growth factor and bone morphogenetic protein-7 in Pseudomonas aeruginosa-induced chronic obstructive pulmonary disease in rats.

Repeated intratracheal injection of Pseudomonas aeruginosa (PA) in male Wistar rats was used to investigate the role of chronic infection in the development of chronic obstructive pulmonary disease (COPD) and the possible involvement of connective tissue growth factor (CTGF) and bone morphogenetic protein-7 (BMP-7) in this process. Injections of PA or normal saline solution were given for 8 weeks and the rats observed for a further 8 weeks. In addition to arterial blood gas, lung function and lung pathology measurement during this time period, protein and mRNA expression of CTGF and BMP-7 were measured, and the correlation of expression of CTGF and BMP-7 with pathological changes in the lung was evaluated. Repeated intratracheal PA infection in rats caused reduction in body weight, hypoxia, carbon dioxide retention, compromised lung function, chronic inflammation, thickening of the tracheal and arterial walls, and emphysema, changes consistent with those of COPD. Rats with PA infection also had increased CTGF and decreased BMP-7 expression, suggesting that both CTGF and BMP-7 are involved in the occurrence and development of airway remodeling. Our findings suggest that repeated airway infection is not only a factor resulting in deterioration of COPD, but is also a risk factor for its development, and that CTGF and BMP-7 are involved in the pathogenesis of this condition.

[Inhibition of 1,25-(OH)2D3 on passively sensitized human airway smooth muscle cells].

OBJECTIVE: To investigate the effects of 1,25-(OH)(2)D(3) on the proliferation of passively sensitized human airway smooth muscle cells (HASMCs) and their expressions of MMP-9 and a disintegrin and metalloprotease 33(ADAM33). METHODS: HASMCs were passively sensitized with 10% serum from asthmatic patients. MTT colorimetry assay was used to examine the effect of 1,25-(OH)(2)D(3) on cell proliferation at different concentrations (10(-10) mol/L, 10(-9) mol/L, 10(-8) mol/L, 10(-7) mol/L).By this way, its optimal inhibitory concentration was determined. And then the effects of 1,25-(OH)(2)D(3) at the optimal concentration on cell proliferation was examined by the same MTT assay and cell cycle analysis by flow cytometry. The expressions of MMP-9 and ADAM33 in HASMCs were studied by real-time quantitative RT-PCR and Western blotting analysis. RESULTS: (1) Inhibition of cell proliferation by 1,25-(OH)(2)D(3) was barely detectable at 10(-10) mol/L. But with the increasing concentration ranging from 10(-9) mol/L to 10(-7) mol/L, 1,25-(OH)(2)D(3) markedly inhibited the cell proliferation concentration-dependently and reached the maximum effect at the concentration of 10(-7) mol/L. Accordingly, 10(-7) mol/L was chosen as the optimal concentration of 1,25-(OH)(2)D(3) for the following study. (2) At the concentration of 10(-7) mol/L, 1,25-(OH)(2)D(3) inhibited the cell proliferation of passively sensitized HASMCs in a time-dependent manner and hampered the G(1)/S transition. (3) 1,25-(OH)(2)D(3) pretreatment attenuated the MMP-9 and ADAM33 protein levels in passively sensitized HASMCs by (63.4 ± 3.6)% and (50.9 ± 2.9)%, respectively (P < 0.01). (4) 1,25-(OH)(2)D(3) significantly inhibited the MMP-9 and ADAM33 mRNA levels in passively sensitized HASMCs by (52.2 ± 2.5)% and (67.8 ± 3.2)%, respectively (P < 0.01). CONCLUSION: 1,25-(OH)(2)D(3) has a direct inhibitory effect on passively sensitized HASMCs in vitro, including the inhibition of cell proliferation and the expressions of MMP-9 and ADAM33, which maybe associated with the beneficial role of 1,25-(OH)(2)D(3) in the prevention and therapy of asthmatic airway remodeling.

[An experimental study on the safety of intratracheal drug administration].

OBJECTIVE: To explore whether injury and repair occur in the trachea and the lung after intra-tracheal administration of different drugs. METHODS: Wistar rats were randomly divided into 5 groups, a normal group, a blank control (BC) group, a normal saline (NS) group, a lidocaine (LD) group and an amikacin (AK) group. For the latter 3 groups, normal saline, lidocaine and amikacin were injected into trachea by needle puncture. Scanning electron microscope was used to observe the ultra-structural changes of the epithelium, and the percentage of the area of damage (PAD) in tracheal mucosa was calculated. Moreover, pathological changes of the mucous membrane of bronchioles and alveolar epithelial cells were also examined, and the degree of lung pathology was semi-quantified. RESULTS: Two hours after the injection of the 3 drugs, derangement and edema of the cilia were evident by scanning electron microscopy. The PAD of the NS group, the LD group and the AK group were (94.2 ± 3.2)%, (93.1 ± 3.0)% and (95.5 ± 1.8)%, respectively; all being significantly higher than that of the BC group (1.3 ± 0.3)%. For the NS group and the LD group, the PAD decreased significantly after 24 h, which were (73.7 ± 7.8)% and (81.0 ± 4.6)% respectively, and returned to normal at 48 h and 96 h. While for the AK group, the damage began to improve at 72 h [PAD (62.1 ± 5.2)%], and recovered at 96 h. Airway epithelial derangement and cell edema in the alveoli and the bronchioles also occurred 2 h after drug injection, and inflammatory cell infiltration became evident at 24 h. At this time, the score of pathology was 1.80 ± 0.84, 2.60 ± 0.55 and 2.80 ± 0.45 for the NS group, the LD group and the AK group, respectively; all being higher than that of the BC group (0). These pathological changes recovered totally after 72 h for the NS and the LD groups, and 96 h for the AK group. CONCLUSIONS: Intra-tracheal administration of normal saline, lidocaine and amikacin in rats led to reversible airway mucosal and lung tissue damages.

[Pulmonary cryptococcosis: analysis of 38 cases].

OBJECTIVE: To investigate the clinical features, radiology, diagnosis and treatment of pulmonary cryptococcosis. METHODS: A total of 38 cases of pulmonary cryptococcosis, confirmed by pathological examinations at Fuzhou General Clinical Medical College, Fujian Medical University from March 2003 to February 2010, were retrospectively studied. RESULTS: All of the cases were community-acquired. The patients consisted of 29 males and 9 females, aged from 21 to 70 years. There were no underlying diseases in 29 cases. The CD(4) cell numbers were normal in 20 patients. Radiological study showed that the majority of the lesions (35 cases) were close to the pleura. Lower lungs were often involved (left 21 and right 23). Pulmonary nodules, either solitary nodules (11 cases) or multiple nodules (16 cases), were the most common CT finding. The lesions had a higher standardized uptake value (SUV) in 4 patients with a PET-CT scan. The lung specimens of 33 cases were obtained by CT guided transthoracic needle aspiration biopsy. The disease was cured in 34 cases, and improved in 3 cases, but 1 died. CONCLUSIONS: Pulmonary cryptococcosis must be considered in the differential diagnosis of lesions of the lungs. The disease has some characteristics on radiology, such as multiple lesions, always close to the pleura and occurs frequently in the lower lungs. CT guided percutaneous biopsy is a safe and effective method for diagnosis.

Outbreak of mycoplasmal round pneumonia in an adult population: A case series.

BACKGROUND: Mycoplasmal pneumonia is a common type of adult community-acquired pneumonia in China, but round/spherical pneumonia caused by mycoplasma pneumoniae has rarely been reported. Here, we report an outbreak of mycoplasmal round pneumonia in a military dormitory in China. METHODS: We analysed epidemiological, clinical, imaging and laboratory data from a series of adults affected by an outbreak of mycoplasmal round pneumonia in the dormitory of a military hospital (Fuzhou General Hospital) in Fuzhou, China. The dormitory included 2 separate buildings. Mycoplasma antibody was detected using a passive agglutination assay. RESULTS: The first case in our series, a 23-year-old male intern, presented on July 16, 2015 with a 3-day history of low-grade fever, dizziness, fatigue and chest tightness. Chest computed tomography revealed spherical masses. Over the following 4 days, 11 individuals who had been in close contact with the first patient were found to have similar masses. All 12 cases were mildly symptomatic or asymptomatic, and fever was the only sign visible upon physical examination. Chest radiology revealed single, round consolidations in 3 cases and multiple round consolidations in 9 cases; consolidations ranged in size from 0.2 to 2.9 cm. Most cases had normal blood cell count, erythrocyte sedimentation rate and C reactive protein level. Nasopharyngeal swabs from all cases tested negative for 25 pathogens, including Mycoplasma pneumoniae, in a PCR-based assay performed on August 1, 2015. All 12 patients showed a 4-fold increase in the titre of anti-mycoplasmal pneumonia antibody in paired sera on August 13, 2015. Patients were given the antibiotic moxifloxacin or symptomatic treatment, and 11 of the 12 cases showed complete resolution of round pneumonia lesions within 4 weeks. CONCLUSION: This case series illustrates the diversity of clinical manifestations as well as imaging findings for mycoplasmal pneumonia, to which clinicians should pay more attention. Mycoplasmal round pneumonia should be included in differential diagnosis of multiple pulmonary nodules in adults in order to enable accurate clinical identification of disease and successful treatment and resolution.

miR-630 targets LMO3 to regulate cell growth and metastasis in lung cancer.

MicroRNAs (miRNAs) are a class of small non-coding RNAs that play key roles in cancer development and progression. Therefore, the discovery of miRNAs may provide a new and powerful tool for understanding the mechanism of carcinogenesis. In the present study, we aimed to investigate the functional significance of miR-630 and to identify its possible target genes in human non-small cell lung cancer (NSCLC). Our results showed that miR-630 was significantly down-regulated in NSCLC tissues and cell lines. The enforced expression of miR-630 was able to inhibit cell proliferation, migration, and invasion of NSCLC cells. Moreover, our results further revealed that LMO3, a nuclear LIM-only proteins, was identified as a target of miR-630. Restoration of LMO3 remarkably reversed the tumor-suppressive effects of miR-630 on cell proliferation, migration, and invasion in NSCLC cells. Therefore, we demonstrated that miR-630 suppressed the proliferation, migration, and invasion of NSCLC cells by down-regulating LMO3 expression, suggesting miR-630 as a potential therapeutic target for the treatment of human NSCLC in the future.

[A preliminary study of CTGF in bleomycin-induced mouse pulmonary fibrosis].

AIM: To investigate CTGF's role in bleomycin-induced pulmonary fibrosis. METHODS: Kunming mice were intratracheally administered with bleomycin to establish pulmonary fibrosis model. The expression of CTGF was studied by immunohistochemical method and RT-PCR. The degree of fibrosis was evaluated by pulmonary hydroxyproline assay. RESULTS: CTGF protein and mRNA were not expressed in normal mice. However, they were detected in pulmonary fibrotic mice from day 7 after bleomycin treatment, and increased as fibrosis developed (P <0.01). CTGF protein's expression was correlated with hydroxyproline content in lung tissue (r=0.92, P <0.01). CONCLUSION: CTGF plays a role in pulmonary fibrosis. Detection of CTGF may be an early and sensitive marker for evaluating the occurrence and development of pulmonary fibrosis.