Henan Provincial Chest Hospital

Henan’an, China

Henan Provincial Chest Hospital

Henan’an, China
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Xu X.-D.,Shanghai University | Liu S.-X.,Shanghai University | Liu X.,Henan Provincial Chest Hospital | Chen Y.,Henan Provincial Peoples Hospital | And 6 more authors.
Journal of Cardiology | Year: 2014

Background: Surgical repair is an effective method to treat ventricular septal defect (VSD) complicating acute myocardial infarction (AMI). However, the mortality rate remains high. This study was designed to assess the immediate and mid-term results of transcatheter closure of postinfarct muscular VSDs. Methods: Data were retrospectively collected from 42 AMI patients who underwent attempted transcatheter VSD closure between 2008 and 2012 in seven heart centers of China. Results: Nine patients underwent emergent VSD closure in the acute phase (within two weeks from VSD) while the others underwent elective closure. The time between VSD occurrence and closure in emergency group and elective group was 7.7. ±. 2.3 days and 35. ±. 14.5 days, respectively (p<. 0.01). The percentage of procedure success in the emergency group and elective group was 77.8% (7/9) and 97% (32/33), respectively (p= 0.048). The hospital mortality was higher for emergent closure in comparison to elective closure (66.7% vs. 6.1%, p<. 0.01). During a median follow-up of 25 months (0-58 months), two patients died at 8 and 29 months, respectively, and no serious complications occurred in other patients. Conclusion: Interventional postinfarct VSD closure is a safe and effective approach that can be performed with a high procedural success rate, with favorable outcomes if it can be undertaken >14 days postinfarct. © 2014 Japanese College of Cardiology.

PubMed | New Jersey Medical School, Henan Provincial Chest Hospital, Fudan University, International Tuberculosis Research Center and 2 more.
Type: Journal Article | Journal: Journal of clinical microbiology | Year: 2016

Extensively drug-resistant (XDR) tuberculosis (TB) cannot be easily or quickly diagnosed. We developed a rapid, automated assay for the detection of XDR-TB plus resistance to the drug isoniazid (INH) for point-of-care use. Using a simple filter-based cartridge with an integrated sample processing function, the assay identified a wide selection of wild-type and mutant sequences associated with XDR-TB directly from sputum. Four new large-Stokes-shift fluorophores were developed. When these four Stokes-shift fluorophores were combined with six conventional fluorophores, 10-color probe detection in a single PCR tube was enabled. A new three-phase, double-nested PCR approach allowed robust melting temperature analysis with enhanced limits of detection (LODs). Finally, newly designed sloppy molecular beacons identified many different mutations using a small number of probes. The assay correctly distinguished wild-type sequences from 32 commonly occurring mutant sequences tested in gyrA, gyrB, katG, and rrs genes and the promoters of inhA and eis genes responsible for resistance to INH, the fluoroquinolone (FQ) drugs, amikacin (AMK), and kanamycin (KAN). The LOD was 300 CFU of Mycobacterium tuberculosis in 1 ml sputum. The rate of detection of heteroresistance by the assay was equivalent to that by Sanger sequencing. In a blind study of 24 clinical sputum samples, resistance mutations were detected in all targets with 100% sensitivity, with the specificity being 93.7 to 100%. Compared to the results of phenotypic susceptibility testing, the sensitivity of the assay was 75% for FQs and 100% each for INH, AMK, and KAN and the specificity was 100% for INH and FQ and 94% for AMK and KAN. Our approach could enable testing for XDR-TB in point-of-care settings, potentially identifying highly drug-resistant TB more quickly and simply than currently available methods.

PubMed | Fudan University, U.S. National Institutes of Health and Henan Provincial Chest Hospital
Type: | Journal: Scientific reports | Year: 2015

Genetic heterogeneity of Mycobacterium tuberculosis (MTB) within a patient has caused great concern as it might complicate antibiotic treatment and cause treatment failure. But the extent of genetic heterogeneity has not been described in detail nor has its association with heterogeneous treatment response. During treatment of a subject with MDR-TB, serial computed tomography (CT) scans showed this subject had six anatomically discrete lesions and they responded to treatment with disparate kinetics, suggesting heterogeneous MTB population may exist. To investigate this heterogeneity, we applied deep whole genome sequencing of serial sputum isolates and discovered that the MTB population within this patient contained three dominant sub-clones differing by 10~14 single nucleotide polymorphisms (SNPs). Differential mutation patterns in known resistance alleles indicated these sub-clones had different drug-resistance patterns, which may explain the heterogeneous treatment responses between lesions. Our results showed clear evidence of branched microevolution of MTB in vivo, which led to a diverse bacterial community. These findings indicated that complex sub-populations of MTB might coexist within patient and contribute to lesions disparate responses to antibiotic treatment.

Shi R.,Henan Provincial Chest Hospital | Sugawara I.,The Research Institute of Tuberculosis
Tohoku Journal of Experimental Medicine | Year: 2010

Mycobacterium tuberculosis, the causative agent of tuberculosis, is a tenacious and remarkably successfulpathogen that has latently infected one third of the world's population, according to the World Health Organization (WHO) statistics. It is anticipated that 10% of these infected individuals will develop active tuberculosis at some point in their lifetime. The long-term use of the current drug regimen, the emergence of drug-resistant strains, and HIV co-infection have resulted in a resurgence of research efforts to address the urgent need for new anti-tuberculosis drugs. A number of potential candidate drugs with novel modes of action have entered clinical trials in recent years, and these are likely to be effective against antituberculosis drug-resistant strains. They include neuroquinolone derivatives, a modified ethambutol, nitroimidazole groups and so on. This mini-review summarizes the latest information about eight new antituberculosis drug candidates and describes their activities, pharmacokinetics, mechanisms of action, and mechanisms of drug-resistance induced by these drug candidates. © 2010 Tohoku University Medical Press.

Zhang B.-J.,Central Hospital of Xinxiang City | Gong H.-Y.,Xinxiang Medical University | Zheng F.,Xinxiang Medical University | Liu D.-J.,Zhengzhou University | Liu H.-X.,Henan Provincial Chest Hospital
International Journal of Clinical and Experimental Pathology | Year: 2014

Introduction: MicroRNAs (miRNAs) are noncoding RNAs that regulate multiple cellular processes during cancer progression. MiR-335 has recently been identified to be involved in tumorigenesis of several cancers such as ovarian cancer and gastric cancer. However, the regulation of miR-335 in esophageal squamous cell carcinoma (ESCC) has not been reported yet. Methods: Expression of miR-335 in tumor and their normal matched tissues was determined by quantitative real-time PCR in 67 ESCC patients and its association with overall survival of patients was analyzed by statistical analysis. Results: The expression level of miR-335 was reduced in malignant tissue samples in comparison to normal matched tissue (P < 0.05). It was also proved that miR-335 expression was associated with ESCC histological grade, lymph node metastasis, tumor stage and clinical stage (P < 0.05). In addition, the Kaplan-Meier survival curves revealed that low miR-335 expression was associated with poor prognosis in ESCC patients. Multivariate analysis showed that miR-335 expression was an independent prognostic marker of overall survival of ESCC patients. Conclusions: The study proves for the first time that miR-335 is down regulated in a majority of ESCC patients. Our results indicate that miR-335 expression is an independent prognostic factor for patients with esophageal cancer, which might be a potential valuable biomarker for ESCC.

Objective: To investigate the relationship between serum carcinoembryonic antigen (CEA) level and epidermal growth factor receptor (EGFR) gene mutations in non-small-cell lung cancer (NSCLC) patients and to analyze the influence of CEA level on postoperative survival time in lung cancer patients. Methods: A total of 296 patients who were treated in Thoracic Surgery Department of Henan Provincial Chest Hospital from September 2011 to September 2013 were recruited. The level of tumor markers, such as CEA, was determined before the surgery, and EGFR gene mutations were detected after surgery. Thereby, the relationship between tumor makers, including CEA, and EGFR mutation and its influence on prognosis could be investigated. Results: Among 296 patients, the positive rate of EGFR gene mutation was 37.84% (112/296); the mutation occurred more frequently in nonsmokers, adenocarcinoma patients, women, and patients aged <60 years (P<0.05). Both tumor markers and chemosensitivity indicators were related to the profile of EGFR mutations. Elevated squamous cell carcinoma and Cyfra21-1 as well as positively expressed ERCC1 were more common in patients with wild-type EGFR (P<0.05), whereas increased CEA level was observed more frequently in patients with EGFR gene mutation (P=0.012). The positive rate of EGFR gene mutations was higher as the serum CEA level increased, that is, the positive rate in patients with serum CEA level <5, 5–20, and >20 μg/L was 39.81%, 45.32%, and 65.47%, respectively (P=0.004). Logistic regression analysis showed that CEA level was an independent factor in predicting EGFR gene mutations, and serum CEA level was also an independent factor in affecting the prognosis of NSCLC patients, as the overall 2-year survival rate was 73.86% in elevated CEA group and 86.43% in normal group (P<0.01). Conclusion: The prognosis of NSCLC patients receiving resection can be predicted according to serum CEA level, which is associated with EGFR mutations in NSCLC patients and provides a preliminarily guidance for EGFR mutations. © 2016 Cai.

Wang X.,Henan Provincial Chest Hospital | Wang P.-F.,Henan Provincial Chest Hospital | Yuan W.-Y.,Henan Provincial Chest Hospital
Cell Biochemistry and Biophysics | Year: 2014

We sought to find the biological effects of MicroRNA-2 in suppressing Lewis lung cancer cells proliferation, invasion, and migration in tumor-bearing mice. MicroRNA-2 was transfected into Lewis lung cancer cells of tumor-bearing mice by gene transient transfection technique and these Lewis-microRNA-2 cells were taken as MicroRNA transfection group. At the same time, Lewis cells were taken as control group and Lewis-EGFP cells as empty plasmid group. The growth curves of cells in the three groups were drawn by manual counting method, while the invasiveness of cells in the three groups was compared by transmembrane cell invasion assay. The three kinds of cells were seeded into BALB/Nude SPF level nude mice to detect the formation of tumors and the number of metastases by Xenograft experiments. The result showed that the MicroRNA transfection group has the lowest vitality of cells proliferation, fewest cells passed through matrigel matrix protein layer, and lowest cells invasive rate. Mice with Lewis-microRNA-2 cells apparently had a longer time of tumor formation. The average tumor mass and the number of metastases were significantly lower than the other two groups. MicroRNA-2 significantly inhibited Lewis lung cancer cell proliferation, invasion and migration in tumor-bearing mice, which may be associated with the regulation of target genes PLK1 and TGF-β. © 2014, Springer Science+Business Media New York.

PubMed | Guilin Medical University and Henan Provincial Chest Hospital
Type: Journal Article | Journal: Experimental biology and medicine (Maywood, N.J.) | Year: 2016

DNA methylation is an epigenetic DNA modification catalyzed by DNA methyltransferase 1 (DNMT1). The purpose of this study was to investigate DNMT1 gene and protein expression and the effects of methylation status on tumor suppressor genes in human non-small cell lung cancer (NSCLC) cell lines grown invitro and invivo Human lung adenocarcinoma cell lines, A549 and H838, were grown invitro and inoculated subcutaneously into nude mice to form tumors and were then treated with the DNA methylation inhibitor, 5-aza-2-deoxycytidine, with and without treatment with the benzamide histone deacetylase inhibitor, entinostat (MS-275). DNMT1 protein expression was quantified by Western blot. Promoter methylation status of tumor suppressor genes (RASSF1A, ASC, APC, MGMT, CDH13, DAPK, ECAD, P16, and GATA4) was evaluated by methylation-specific polymerase chain reaction. Methylation status of the tumor suppressor genes was regulated by the DNMT1 gene, with the decrease of DNMT1 expression following DNA methylation treatment. Demethylation of tumor suppressor genes (APC, ASC, and RASSF1A) restored tumor growth in nude mice. The results of this study support a role for methylation of DNA as a potential epigenetic clinical biomarker of prognosis or response to therapy and for DNMT1 as a potential therapeutic target in NSCLC.

PubMed | Guangzhou University and Henan Provincial Chest Hospital
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

The majority of proteomic studies have focused on identifying atrial fibrillation (AF)-associated proteins in the right atrium (RA), thus potential differences in AFassociated proteins between the RA and left atrium (LA) remain unknown. The aim of the present study was to perform proteomic analysis to compare the potential differences in AFassociated proteins between the right atrial appendage (RAA) and left atrial appendage (LAA) in patients with rheumatic mitral valve disease (RMVD). RAA and LAA tissues were obtained from 18patients with RMVD (10 with AF) during mitral valve replacement surgery. Twodimensional fluorescence difference gel electrophoresis (2D DIGE) proteomics analysis was performed using these tissues to identify AFassociated proteins in RAA and LAA. Subsequently, the proteomics data was validated using western blot analysis of nine selected proteins. In RAA, 32AFassociated proteins were significantly dysregulated (15upregulated and 17 downregulated). In LAA, 31AFassociated proteins were significantly dysregulated (13upregulated and 18downregulated). Among these AFassociated proteins, 17were AFassociated in both RAA and LAA, 15were AFassociated only in RAA, and 14 were AFassociated only in LAA. Amongst the differentially expressed proteins, western blot analysis validated the results for 6AFassociated proteins, and demonstrated similar distributions in RAA and LAA compared with the 2D DIGE results. Of these proteins, 2proteins were AFassociated in both RAA and LAA, 2 were AFassociated only in RAA, and 2were AFassociated only in LAA. Additionally, the different distributions of AFassociated proteins in the RAA and LAA of patients with RMVD was analyzed, which may reflect the different regulatory mechanisms of the RA and LA in AF. These findings may provide new insights into the underlying molecular mechanisms of AF in patients with RMVD.

PubMed | Zhengzhou University and Henan Provincial Chest Hospital
Type: Journal Article | Journal: Journal of thoracic disease | Year: 2016

Lung cancer is the leading cause of cancer-related deaths worldwide; unfortunately, its prognosis is still very poor. Therefore, developing the target molecular is very important for lung cancer diagnosis and treatment, especially in the early stage. With this in view, spalt-like transcription factor 4 (In order to better investigate the association between the expression of The results of the study showed that females harbored more

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