Asthma control and severe exacerbations in patients with moderate or severe asthma in Jilin Province, China: a multicenter cross-sectional survey.

BACKGROUND: No systemic evaluation of asthma control in Jilin Province has been reported. Asthma control might provide the basis for asthma management in this region. A multicenter hospital-based cross-sectional study was performed to investigate the asthma control and related factors for severe asthma exacerbations in patients with moderate or severe asthma in Jilin Province, China. METHODS: The study enrolled 1546 patients in five grade one general hospitals from January to December 2013. Asthma medication, patient self-management, asthma control test (ACT) scores and frequency of severe asthma exacerbations during the follow-up (12 months) were collected via a follow-up questionnaire. RESULTS: In the study, 889 patients provided a complete follow-up questionnaire. Severe asthma exacerbations occurred in 54.89 % of patients. ACT score ≤15, asthma medication ≤ 3 months, severe asthma, income level lower than average Per Capita Disposable Income (PCDI) and a lower educational level were risk factors of a severe exacerbation. CONCLUSIONS: Poor adherence to asthma medication, poor asthma symptom control, lower income, a low educational level might be possible reasons for the high incidence of severe asthma exacerbations and poor asthma control in Jilin Province of China.

Promoter methylations of RASSF1A and p16 is associated with clinicopathological features in lung cancers.

UNLABELLED: Objection: The aim of this study is to investigate the association between promoter methylation of RASSF1A and p16 and the clinicopathological features in lung cancers. MATERIALS AND METHODS: PubMed, EBSCO, Ovid, Wiley, Web of Science, Wanfang, and VIP databases were searched using combinations of keywords related to RASSF1A, p16, methylation, and lung cancers. After screening for relevant studies, following a strict inclusion and exclusion criteria; the selected studies were incorporated into the present meta.analysis conducted using Comprehensive Meta Analysis 2.0. (CMA 2.0). RESULTS: We initially retrieved 402 studies, out which 13 studies met the inclusion and exclusion criteria for this meta.analysis, and contained a total of 1,259. patients with lung cancers. The results of this meta.analysis showed that the differences in promoter methylation ratio between the lung cancer patients in tumor, node, metastasis. (TNM) I.II and III.IV were not statistically significant. Based on histological types, patients with adenocarcinoma. (AC) and squamous cell carcinoma. (SCC) showed no significant differences in the promoter methylation ratios of RASSF1A, while the promoter methylation ratio of p16 was significantly higher in SCC patients compared to AC patients. Based on smoking status, the promoter methylation ratios of both RASSF1A and p16 was significantly higher in lung cancer patients with smoking history compared to nonsmokers. CONCLUSION: The present meta.analysis provides convincing evidence that the promoter methylation ratio of RASSF1A and p16 is associated with clinicopathological features in lung cancers, and could be used as effective biomarkers in early diagnosis in lung cancers.

Knockdown of HMGN5 expression by RNA interference induces cell cycle arrest in human lung cancer cells.

HMGN5 is a typical member of the HMGN (high mobility group nucleosome-binding protein) family which may function as a nucleosomal binding and transcriptional activating protein. Overexpression of HMGN5 has been observed in several human tumors but its role in tumorigenesis has not been fully clarified. To investigate its significance for human lung cancer progression, we successfully constructed a shRNA expression lentiviral vector in which sense and antisense sequences targeting the human HMGN5 were linked with a 9-nucleotide loop. Inhibitory effects of siRNA on endogenous HMGN5 gene expression and protein synthesis were demonstrated via real-time RT-PCR and western blotting. We found HMGN5 silencing to significantly inhibit A549 and H1299 cell proliferation assessed by MTT, BrdU incorporation and colony formation assays. Furthermore, flow cytometry analysis showed that specific knockdown of HMGN5 slowed down the cell cycle at the G0/G1 phase and decreased the populations of A549 and H1299 cells at the S and G2/M phases. Taken together, these results suggest that HMGN5 is directly involved in regulation cell proliferation in A549 and H1299 cells by influencing signaling pathways involved in cell cycle progression. Thus, our finding suggests that targeting HMGN5 may be an effective strategy for human lung cancer treatment.

[Adult hospital acquired pneumonia: a multicenter study on microbiology and clinical characteristics of patients from 9 Chinese cities].

OBJECTIVE: To investigate the etiology and clinical characteristics of hospital-acquired pneumonia (HAP) in China and to provide evidence for appropriate therapy. METHODS: We performed a prospective multicenter study in 13 Chinese urban tertiary hospitals. All HAP cases diagnosed at respiratory general ward and respiratory intensive care unit (RICU) from August 2008 to December 2010 were studied. Epidemiological data, etiology and clinical characteristics of enrolled patients were collected. Sputum or tracheal aspirate and blood cultures, Legionella antibodies and Streptococcus pneumoniae urinary antigen tests were performed. Bacteria to antimicrobial susceptibility test was performed. RESULTS: A total of 610 cases of HAP were diagnosed during the study, with an overall incidence of 1.4% among 42 877 hospitalized patients, while the incidence was 0.9% (362/41 261) in respiratory general ward and 15.4% (248/1616) in RICU. 93.9% (573 cases) of patients had at least one underlying disease, and 91.0% (555 cases) had exposure to at least one antimicrobial agent within 90 days prior to HAP diagnosis. Pathogens were identified in 487 patients, with Acinetobacter baumannii [30.0% (183/610)], Pseudomonas aeruginosa [22.0% (134/610)], Staphylococcus aureus [13.4% (82/610)] and Klebsiella pneumonia [9.7% (59/610)] being the most common pathogens. Eighteen patients (3.0%) had infection with fastidious bacteria. A. baumannii and S. aureus were the more frequent pathogens in the ventilator-associated pneumonia (VAP) cases [50.5% (97/192) and 21.4% (41/192)] as compared to non-VAP cases [20.6% (86/418) and 9.8% (41/418), P < 0.01]. A. baumannii and S. aureus were also frequent pathogens in cases with a score of more than 20 by the acute physiology and chronic health evaluation II (APACHEII) scoring [45.7% (69/151) and 20.5% (31/151)], as compared to cases with a score of less than 20 of APACHE II [24.8% (114/459) and 11.1% (51/459), P < 0.01]. A. baumannii showed high resistance rates to carbapenems [more than 70% (109/142)], and the susceptibility to cefoperazone/sulbactam, polymyxin B and tigecycline were 40.8% (58/142), 99.3% (141/142) and 95.8% (136/142) respectively. Resistance rates of P. aeruginosa to meropenem and imipenem were 48.8% (40/82) and 70.7% (58/82) respectively. Methicillin-resistant S. aureus (MRSA) accounted for 87.8% (43/49) in all strains of S. aureus. Mortality rate of VAP cases was 34.5% (61/177), significantly more than that of HAP patients [22.3% (135/605), P < 0.05]. The average hospital stay of patients with HAP was (23.8 ± 20.5) days, significantly more than that of the average for inpatients [(13.2 ± 13.6) days, P < 0.01] during the study period. Mean costs of HAP were (108 950 ± 116 608) yuan, significantly higher than the average hospital costs of respiratory inpatients (17 999 ± 33 364) yuan. CONCLUSIONS: Among Chinese patients hospitalized in urban tertiary medical centers, HAP incidence and mortality rate were high, which increased the patients' hospital stay and the medical costs. Common pathogens were A. baumannii, P. aeruginosa, S. aureus and K. pneumonia. The common bacteria of HAP in China showed high resistance rates to antibiotics.

[A multicentre retrospective study of pulmonary mycosis clinically proven from 1998 to 2007].

OBJECTIVE: To investigate the pathogens, clinical manifestations, prognosis of and the risk factors for pulmonary mycosis in China. METHODS: All cases of pulmonary mycosis from 16 centers in 10 cities from Jan. 1998 to Dec. 2007 that met the diagnostic criteria were included for clinical, microbiological and radiological analysis. RESULTS: Totally 474 cases of pulmonary mycosis were retrieved. The top 5 pulmonary mycosis was pulmonary aspergillosis (180 cases, 37.9%), pulmonary candidiasis (162 cases, 34.2%), pulmonary cryptococcosis (74 cases, 15.6%), pneumocystis carinii pneumonia (23 cases, 4.8%) and pulmonary mucormycosis (10 cases, 2.1%). The constituent ratio in the last 3 years was similar to that in the former 7 years. The main pathogens of pulmonary candidiasis were Candida albicans (308/474, 65.0%) and Candida tropicalis (57/474, 12.0%), which were sensitive to common azoles. Compared with bacterial pneumonia, pulmonary mycosis showed more symptoms of hemoptysis (147/474, 31.0%) and pleural effusion (95/474, 20.0%), and less radiological specificity. Classical halo sign (4/474, 0.8%) and crescentic sign (17/474, 3.6%) were only shown in several cases of pulmonary mycosis. The most common underlying diseases were tumor (including solid tumor and malignant hematological diseases) (94/474, 19.8%), chronic obstructive pulmonary disease (52/474, 11.0%), pulmonary tuberculosis (50/474, 10.5%) and diabetes (48/474, 10.1%). Compared with the other common pulmonary mycosis, pulmonary cryptococcosis affected younger patients, and more cases were community-acquired, but fewer cases with underlining diseases or compromised immune function, and had a better prognosis. CONCLUSION: The ahead five species of pulmonary mycosis in China were orderly pulmonary aspergillosis, pulmonary candidosis, pulmonary cryptococcosis, pneumocystis carinii pneumonia and pulmonary mucormycosis. The main pathogens of pulmonary candidosis were Candida albicans and Candida tropicalis, which were sensitive to common azoles. Compared with the other common pulmonary mycosis, pulmonary cryptococcosis catch younger patients, had more community-acquired cases, and had better prognosis.

[Three cases of pulmonary alveolar microlithiasis in a family and clinical analysis].

OBJECTIVE: To describe the characteristics of 3 cases of pulmonary alveolar microlithiasis in a family, and therefore to improve the understanding of the disease. METHODS: To analyze the clinical, laboratory and radiological data of three patients with pulmonary alveolar microlithiasis in a family and the relevant literatures were reviewed. RESULTS: There was a typical manifestation in these three cases of pulmonary alveolar microlithiasis: progressive dyspnoea, cough, family history. Chest X-ray and computed tomography demonstrate: the pulmones was full of high density reflection of intra-alveolar microliths especially in middle-lower lobe and posterior lobe. The etiology of these three cases is still unknown, consanguineous marriage of parents is possible reason. There was not effective therapies to them. CONCLUSION: Pulmonary alveolar microlithiasis is a disease without clear known etiology and effective therapy. For a patient with radiological features of high density intra-alveolar microliths and a positive family history, the diagnosis should be highly suspected.

[Preparation and identification of monoclonal antibodies against human DcR3].

AIM: To prepare monoclonal antibodies(mAbs) against human DcR3 and identify their characterization. METHODS: BALB/c mice were immunized with purified His-DcR3 protein, and mAbs against DcR3 which prepared by hybridoma technique were purified and identified by their specificity, subtype, titers via ELISA and Western blot. RESULTS: Five hybridoma cell lines secreting mAbs against human DcR3 were obtained, which were determined as IgG1 subtype and ascites titers of five mAbs against DcR3 reached 1x10(-5)-1x10(-7). Five mAbs were proved to recognize His-DcR3 protein specifically, one of which (1B1) could recognize SW480 cell. CONCLUSION: mAbs against DcR3 with high titers and specificity have been prepared and purified successfully, which laid a foundation for the study of DcR3 expression, distribution in tissu and development of ELISA kit.

[Detection of SLC34A2 in patients with pulmonary alveolar microlithiasis and the effect of SLC34A2 on transportation of calcium and phosphate in human alveolar epithelial cells].

OBJECTIVE: To detect the mutation of SLC34A2 in patients with pulmonary alveolar microlithiasis and to study the effect of SLC34A2 on transportation of calcium and phosphate in human alveolar epithelial cell (A549) cells. METHODS: The gene SLC34A2 was detected by segmentation-PCR and gene sequencing. RNA was obtained by Trizol from fresh lung tissues and the target gene was acquired by RT-PCR. Eukaryotic expression of recombinant pcDNA3.1(+)-SLC34A2 was constructed and SLC34A2 was transfected to A549 cells by liposome. The expression of SLC34A2 mRNA was detected by RT-PCR, and the content of calcium and phosphate of the extracellular fluid was measured by commercial kits. The cell experiments consisted of 3 groups including a control group (5 x 10(5)/well, one well), a blank group (5 x 10(5)/well, one well), a transfection group (5 x 10(5)/well, four wells). Every experiment was repeated 6 times. RESULTS: No mutation was found in patients with pulmonary alveolar microlithiasis. SLC34A2 cDNA was successfully amplified and the eukaryotic expression recombinant pcDNA3.1(+)-SLC34A2 was successfully constructed. The amount of SLC34A2 mRNA of the transfected cells was significantly higher (2.48 +/- 0.45), compared to the control cells (0.55 +/- 0.07) and the blank cells (0.60 +/- 0.06), q = 16.25, 15.78, all P < 0.01. The content of calcium and phosphate in the supernatant of the transfected cells was lower [(0.110 +/- 0.016) mmol/L, (3.8 +/- 0.4) mmol/L], compared with the control [(0.254 +/- 0.047) mmol/L, (7.3 +/- 0.8) mmol/L] and the blank (0.262 +/- 0.041) mmol/L, (7.1 +/- 0.4) mmol/L], q = 8.657 - 13.892, all P < 0.01. CONCLUSIONS: In human lung alveolar epithelial cells, the content of calcium and phosphate in cell supernatant decreased with increased amount of SLC34A2 mRNA. Mutation of SLC34A2 may not be at the DNA level.