Etiology and antimicrobial resistance of community-acquired pneumonia in adult patients in China / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Appropriate antimicrobial therapy of community-acquired pneumonia (CAP) is mainly based on the distribution of etiology and antimicrobial resistance of major pathogens. We performed a prospective observational study of adult with CAP in 36 hospitals in China.</p><p><b>METHODS</b>Etiological pathogens were isolated in each of the centers, and all of the isolated pathogens were sent to Zhongshan Hospital for antimicrobial susceptibility tests using agar dilution.</p><p><b>RESULTS</b>A total of 593 patients were enrolled in this study, and 242 strains of bacteria were isolated from 225 patients. Streptococcus pneumoniae (79/242, 32.6%) was the most frequently isolated pathogen, followed by Haemophilus influenzae (55/242, 22.7%) and Klebsiella pneumoniae (25/242, 10.3%). Totally 527 patients underwent serological tests for atypical pathogens; Mycoplasma pneumoniae and Chlamydia pneumoniae infections were identified in 205 (38.9%) and 60 (11.4%) patients respectively. Legionella pneumophila infections were identified in 4.0% (13/324) of patients. The non-susceptibility rate of isolated Streptococcus pneumoniae to erythromycin and penicillin was 63.2% and 19.1% respectively. Six patients died from the disease, the 30-day mortality rate was 1.1% (6/533).</p><p><b>CONCLUSIONS</b>The top three bacteria responsible for CAP in Chinese adults were Streptococcus pneumonia, Haemophilus influenza and Klebsiella pneumonia. There was also a high prevalence of atypical pathogens and mixed pathogens. The resistance rates of the major isolated pathogens were relatively low except for the high prevalence of macrolide resistance in Streptococcus pneumoniae.</p>

Effect of smoking cessation on airway inflammation of rats with chronic bronchitis / 中华医学杂志(英文版)

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

Expression of cellular phenotype switching markers-matrix protein Gla, mRNA and collagen I, III and V of human airway smooth muscle cells in vitro after TGF-beta1 stimulation / 中华儿科杂志

<p><b>OBJECTIVE</b>Bronchial asthma is a chronic inflammatory disorder. Long-term inflammation leads to varying degrees of structural changes in the airway wall known as airway reconstruction or remodeling. These structural changes are found in the airways of most patients with prolonged disease. After remodeling, the airway walls show the submucous membrane becomes thick with collagen deposition, and the smooth muscle cells show hyperplasia and hypertrophy. Smooth muscle cells are a vital component of the airway wall, and a major effector cell involved in the course of bronchial contraction. Smooth muscle cell hyperplasia and hypertrophy are important pathological changes in airway remodeling. This study investigated the expression of markers of human airway smooth muscle cells (ASMCs) phenotypic change, which were matrix Gla protein (MGP) and major fibrosis proteins, after in vitro treatment with transforming growth factor-beta(1) (TGF-beta(1)).</p><p><b>METHODS</b>Human ASMCs were subjected to primary culture in vitro. Ten groups of cells were treated with 100 microg/ml of TGF-beta(1), while the cells in the control groups were treated with 10% fetal bovine serum. After being cultured for 7 d, the cells of both groups were harvested. MGP mRNA expression was detected by RT-PCR. Protein levels of collagen I, III and V were determined by Western blot analysis.</p><p><b>RESULTS</b>Treated with TGF-beta(1), airway smooth muscle cells expressed MGP mRNA greater than controls [(62.3 +/- 13.1)% vs (27.4 +/- 11.4)%, P < 0.01]. Also, airway smooth muscle cells stimulated by TGF-beta(1) produced more collagen I, III and V than the control group (P < 0.01).</p><p><b>CONCLUSIONS</b>TGF-beta(1) induced expression of collagen III and V, which are early markers of the switch from a contractile to a synthetic phenotype in ASMCs. This induction is an indication that ASMCs have the potential to make this switch and that TGF-beta(1) is involved in airway remodeling.</p>

A heterozygous point mutation G13328A in antithrombin gene causes thrombosis / 中华血液学杂志

<p><b>OBJECTIVE</b>To identify the phenotype and the gene mutation in a kindred with antithrombin (AT) deficiency.</p><p><b>METHODS</b>Immuno-nephelometry and chromogenic assay were used to detect the plasma level of AT antigen (AT: Ag) and activity (AT: A), respectively. All the seven exons and intron-exon boundaries of AT gene from the propositus were amplified by PCR and direct sequencing of the PCR pro-ducts was performed. Corresponding PCR fragments from the kindred were also sequenced directly. Megaprimer method was used to construct the mutant AT cDNA expressing vector from normal plasmid pCRII AT cDNA. The normal and mutant AT plasmid were transiently transfected into Cos-7 cells and AT: Ag was detected in supernatant and lysate of transfected cell with ELISA.</p><p><b>RESULTS</b>The plasma level of AT: Ag and AT: A for the propositus were 179 mg/L and 42.3%, respectively. A heterozygous G13328A missense mutation in exon 6 was identified, which led to the substitution of Thr (ACC) 404 for Ala (GCC). The sequencing results from the pedigree suggested that three other members also had the mutation. The level of AT:Ag in supernatant and lysate from cells transfected with mutant AT cDNA was 40% and 68% of that of normal AT cDNA transfected cells.</p><p><b>CONCLUSION</b>This is an unreported AT gene mutation in China, which causes type I hereditary antithrombin deficiency and thrombosis in the proposita.</p>

Genetic polymorphism in matrix metalloproteinase-9 and the susceptibility to chronic obstructive pulmonary disease in Han population of south China / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>There are many candidate genes for chronic obstructive pulmonary disease (COPD). Matrix metalloproteinase-9 (MMP-9) plays an essential role in tissue remodeling and repair associated with development of COPD. In this study we investigated the correlation between MMP-9 gene polymorphism and COPD susceptibility in the Han population of South China.</p><p><b>METHODS</b>We examined the frequency of polymorphic genotypes of the MMP-9 promoter (-1562C/T) in 100 COPD patients and 98 healthy smokers by restriction fragment length polymorphism.</p><p><b>RESULTS</b>The frequencies of polymorphic genotypes in promoters of MMP-9 were C/C 86%, C/T 14% in COPD group; and C/C 98%, C/T 2% in the control group. There were significant differences between the two groups (P < 0.01). The allele frequencies were also significantly different between the COPD group and the control group (C allele frequency: 93% vs 99%, T allele frequency: 7% vs 1%, P < 0.05 respectively).</p><p><b>CONCLUSION</b>The genetic polymorphism in promoters of MMP-9 gene is associated with the susceptibility to COPD in the Han population of South China.</p>