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Cao B.,CAS Institute of Microbiology | Huang G.-H.,Chinese National Institute for Viral Disease Control and Prevention | Huang G.-H.,Xinjiang Medical University | Pu Z.-H.,YanTai Yu Huang Ding Hospital | And 16 more authors.
Chest | Year: 2014

Background: Since 2008, severe cases of emerging human adenovirus (HAdV) type 55 (HAdV-55) were reported sporadically in China. But no comparative studies had been conducted to discern the differences in epidemiologic and clinical abnormalities between HAdV-55 and other types (HAdV-7, HAdV-3, HAdV-14, HAdV-50, and HAdV-C). Methods: A multicenter surveillance study for adult and adolescent community-acquired pneumonia (CAP) was conducted prospectively in Beijing and Yan Tai between November 2010 and April 2012. A standardized data form was used to record clinical information. The viral DNA extracted from the clinical samples or adenovirus viral isolates was sequenced. Results: Among 969 cases, 48 (5%) were identified as adenovirus pneumonia. Six branches were clustered: HAdV-55 in 21, HAdV-7 in 11, HAdV-3 in nine, HAdV-14 in four, HAdV-50 in two, and HAdV-C in one. Most HAdV-55 cases were identified during February and March. All the hypervariable regions of the hexon genes of the 21 HAdV-55 strains were completely identical. Patients who had HAdV-55 were about 10 years older (P 5 .027) and had higher pneumonia severity index scores (P 5 .030) compared with those with other types (HAdV-7, HAdV-3, HAdV-14, HAdV-50, and HAdV-C). Systemic BP was also higher among patients in the HAdV-55 group (P 5 .006). Unilateral or bilateral consolidations were the most common radiologic findings in both patients with HAdV-55 and those with other types (57.9% vs 36%). More than one-half of the patients were admitted to hospital; oxygen therapy was given to 29.2% of the 48 patients, and two needed mechanical ventilation. Conclusions: HAdV-55 has established itself as a major pneumonia pathogen in the Chinese population, and further surveillance and monitoring of this agent as a cause of CAP is warranted. © 2014 American College of Chest Physicians.


Zhang S.,Capital Medical University | Zhang S.,Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders | Zhai Z.,Capital Medical University | Zhai Z.,Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders | And 15 more authors.
International Journal of Cardiology | Year: 2016

Venous thromboembolism (VTE) recurrence carries significant mortality and morbidity. Accurate risk assessment and effective treatment for patients with acute pulmonary embolism (PE) is important for VTE recurrence prevention. We examined the association of VTE recurrence with risk stratification and PE treatment. We enrolled 627 patients with a first episode of confirmed PE. Baseline clinical information was collected. PE severity was assessed by the European Society of Cardiology's (ESC) risk stratification, the simplified PE Severity Index (sPESI) and the Qanadli score of clot burden. Patients were followed for 1-5 years. The cumulative recurrent VTE and all-cause death were documented. The association between recurrent VTE and risk factors was analyzed. The cumulative incidences of recurrent VTE were 4.5%, 7.3%, and 13.9% at 1, 2, and 5 years of follow-up, respectively. The VTE recurrence was associated with higher (high- and intermediate-) risk stratification predicted by ESC model (HR 1.838, 95% CI 1.318-2.571, P < 0.001), as well as with unprovoked PE (HR 2.809, 95% CI 1.650-4.781, P b 0.001) and varicose veins (HR 4.747, 95% CI 2.634-8.557, P < 0.001). The recurrence was negatively associated with longer (≥ 6 months) anticoagulation (HR 0.473, 95% CI 0.285-0.787, P = 0.004), especially in patients with higher risk (HR 0.394, 95% CI 0.211-0.736, P = 0.003) and unprovoked PE (HR 0.248, 95% CI 0.122-0.504, P < 0.001). ESC high-risk and intermediate-risk PE, unprovoked PE and varicose veins increase recurrence risk. Longer anticoagulation treatment reduces recurrence, especially in higher risk and unprovoked PE patients. © 2014, Elsevier Ireland Ltd. All rights reserved.


Zhang S.,Capital Medical University | Zhang S.,Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders | Yang T.,Capital Medical University | Yang T.,Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders | And 11 more authors.
BMC Pulmonary Medicine | Year: 2015

Background: Oxidative stress (OS) and reduced nitric oxide (NO) bioavailability contribute to the pathogenesis of pulmonary hypertension (PH). Whether there are associations between OS and NO signaling biomarkers and whether these biomarkers are associated with the severity of PH remain unclear. Methods: Blood samples were collected from 35 healthy controls and 35 patients with pulmonary arterial hypertension (PAH, n = 12) or chronic thromboembolic pulmonary hypertension (CTEPH, n = 23). The mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance index (PVRI) were measured by right heart catheterization. We measured the derivative of reactive oxygen molecules (d-ROMs), biological antioxidant potential (BAP) and superoxide dismutase (SOD) by automatic biochemical analyzer, malondialdehyde (MDA) and asymmetric dimethylarginine (ADMA) by enzyme-linked immunosorbent assay. The relationship between oxidative-antioxidative biomarkers and ADMA, as well as their association with pulmonary hemodynamics, were analyzed. Results: Compared with age- and gender-matched controls, there was no significant difference of d-ROMs in PAH and CTEPH patients; MDA was increased in CTEPH patients (P = 0.034); BAP and SOD were decreased in PAH (P = 0.014, P < 0.001) and CTEPH patients (P = 0.015, P < 0.001); ADMA level was significantly higher in PAH (P = 0.007) and CTEPH patients (P < 0.001). No association between oxidative-antioxidative biomarkers and ADMA was found. Serum ADMA concentration was correlated with mPAP (r = 0.762, P = 0.006) and PVRI (r = 0.603, P = 0.038) in PAH patients. Conclusions: The antioxidative potential and NO signaling are impaired in PAH and CTEPH. Increased serum ADMA level is associated with unfavorable pulmonary hemodynamics in PAH patients. Thus, ADMA may be useful in the severity evaluation and risk stratification of PAH. © Zhang et al. 2015.


Wang N.,Capital Medical University | Wang N.,Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders | Hu X.,Capital Medical University | Liu C.,Capital Medical University | And 7 more authors.
Canadian Journal of Cardiology | Year: 2014

Background: The diagnostic accuracy of cardiovascular magnetic resonance (CMR) for pulmonary hypertension (PH) compared with right heart catheterization were assessed. The purpose of this systematic review was to comprehensively evaluate the diagnostic accuracy of CMR in evaluating PH. Methods: Published literature was obtained from PUBMED, Web of Knowledge, Cochrane library, Embase, Biosis Preview, China National Knowledge Infrastructure, and Chongqing VIP databases, and all studies were inclusive until December 2012. Studies relevant to PH and its imaging in CMR and right heart catheterization were included if correlation coefficient was elucidated clearly. Quality Assessment of Diagnostic Accuracy Studies 2 (QUADAS-2) score was used to assess the quality of studies. Sensitivity and specificity were pooled separately and compared with overall accuracy measures: diagnostic odds ratio and symmetric summary receiver operating characteristic. Results: Sixteen studies were included in the systematic review. Of all the studies, the most widely used index was ventricular mass index (VMI) of CMR. We performed a meta-analysis for VMI among 429 patients in 5 individual studies, which showed a modest diagnostic accuracy of VMI for PH with a summary sensitivity and specificity of 84% (95% confidence interval, 79%-87%) and 82% (95% confidence interval, 73%-89%), respectively. In addition, the summary positive likelihood ratio was 4.894, indicating that VMI of CMR allows a modest ability to distinguish PH patients from healthy subjects with a cutoff point of 0.45 using functional and structural measures. Conclusions: This systematic review and meta-analysis indicates that VMI seems to have a moderate sensitivity and specificity for detection of PH. The application values of other parameters still need further investigation. © 2014 Canadian Cardiovascular Society.


Liang L.R.,Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders | Liang L.R.,Capital Medical University | Lin Y.X.,Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders | Lin Y.X.,Capital Medical University | And 7 more authors.
Chinese Medical Journal | Year: 2014

Background Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide and has been the leading cause of death in China. Patients with COPD have significant decrements in their healthrelated quality of life (HRQL). It is necessary to identify the factors involved in worsening HRQL in order to improve the HRQL of COPD patients. However, evidence from longitudinal studies is limited. The aim of the study was to evaluate the determinants of the deterioration of HRQL in patients with COPD. Methods At baseline, a total of 491 patients with stable COPD received comprehensive assessments, including psychosocial and clinical variables, six minutes walk distance (6MWD), dyspnea grade measured by the 5-grade Medical Research Council (MRC) dyspnea scale, anxiety and depression measured by the hospital anxiety and depression scale and HRQL measured by St. George's Respiratory Questionnaire (SGRQ). Patients were then monitored monthly for 12 months to document COPD exacerbations. At the end of the study period, the SGRQ values were reassessed. A 1-year change in SGRQ total score ≥4 was defined as a deterioration of the HRQL and as the outcome. A total of 450 patients completed the 12-month follow-up and were analyzed in the present study. Results The age (mean±SD) was (65.0±10.6) years and 68.7% of subjects were men. The deterioration of the HRQL was 26.4%. In multivariate Logistic regression, independent and graded associations were found between the baseline MRC dyspnoea grade and the deterioration of HRQL (P=0.012), OR 3.03 (95% CI 1.11-8.24) for patients with MRC dyspnoea grade ≥4 versus patients with MRC dyspnoea grade =1. Similarly, the number of exacerbations during the follow-up was independently and gradually increased with the deterioration of HRQL (P <0.001), OR 3.03 (95% CI 1.9-5.6) for the participants with exacerbations ≥3 versus participants with no exacerbation. The 6MWD evaluated by quartiles was negatively associated with the deterioration of HRQL with borderline statistical significance. Conclusion MRC dyspnea grade and the number of exacerbations impair the HRQL of patients with COPD.


Huang J.,Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders
Experimental gerontology | Year: 2013

Aging is an inevitable process associated with immune imbalance, which is characterized by a progressive functional decline in major organs, including lung. However, effects of altered Th1/Th2 commitment on lung senescence are largely unknown. To examine effects of altered Th1/Th2 balance on lung aging, we measured proportions of Th1 and Th2 cells and expression of cytokines, chemokines, collagen deposition and other relevant physiological and pathological parameters in 2- and 20-months-old (mo) CXCR3-deficient (CXCR3(-/-)) C57BL/6J mice compared with wild-type (WT) mice. There was a significant weight-loss observed in 20-mo CXCR3(-/-) mice compared with the same aged WT group. Although lung function and structure changed with age in both groups, central airway resistance (Rn), tissue elastance (H) and damping (G) were significantly lower in 20-mo CXCR3(-/-) mice than those of WT mice. In contrast, the whole lung volume (V(L)), the mean linear intercept length of alveolar (L(m)), and the total lung collagen content were significantly elevated in 20-mo CXCR3(-/-) mice. With aging, the lungs of WT mice had typical Th1-type status (increased population of Th1 cells and concentrations of cytokine IFN-γ and CXCR3 ligands) while CXCR3(-/-) mice showed Th2-type polarization (decreased proportion of Th1 cells and concentrations of CXCR3 ligands but increased level of IL-4). Our data suggest that Immunosenescence is associated with lung aging, and that altered Th1/Th2 imbalance favors Th2 predominance in CXCR3(-/-) mice, which contributes to the process of accelerated lung aging in this model. Copyright © 2013 Elsevier Inc. All rights reserved.


Li Z.,Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders | Li Z.,Beijing Institute of Respiratory Medicine | Li Z.,Capital Medical University | Li J.,Capital Medical University | And 9 more authors.
Experimental Gerontology | Year: 2011

The p38 mitogen-activated protein kinase (p38 MAPK) pathway is a key regulator of pro-inflammatory cytokine biosynthesis, which may contribute to the chronic low-grade inflammation observed with aging. We hypothesize that aging up-regulates the activation of p38 MAPK as well as the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in mouse lung, and is accompanied by disturbances in oxidant-antioxidant status. In addition, the elevated protein levels of phosphorylated active form of p38 MAPK (phospho-p38 MAPK) with age are tissue-specific.To test this hypothesis, protein levels of phospho-p38 MAPK were determined using Western blot analysis in isolated lung, brain, heart, spleen, kidney and muscle of young (2-month-old) and aged (20-month-old) male C57BL/6J mice. Results show that phospho-p38 MAPK protein levels, not total-p38 MAPK, increased significantly (p<. 0.01, n = 8) in lung and brain of 20-month-old mice. The activation of p38 MAPK in other tissues was not altered with age. Immunostaining showed that epithelial cells and alveolar macrophages in lung parenchyma were the major cellular sources of phospho-p38 MAPK immunity. As measured by enzyme-linked immunosorbent assay (ELISA), TNF-α IL-1β and IL-6 in lung homogenates were elevated significantly with age, but there were no differences with age in serum levels except for IL-6. In addition, IL-1β and IL-6 were increased notably while TNF-α was not different with age in bronchoalveolar lavage fluid (BALF). Furthermore, the oxidant-antioxidant status was evaluated by measuring pro-oxidant malondialdehyde (MDA) levels and the activity of reactive oxygen species scavenging enzymes (i.e. superoxide dismutase (SOD) and glutathione (GSH)) in lung homogenates. The results showed that SOD and GSH decreased with age, while MDA did not change.In conclusion, our data demonstrate that p38 MAPK is activated during lung aging with a corresponding increase in pro-inflammatory cytokines and decrease in antioxidant capacity. © 2011 Elsevier Inc.


Yang S.Q.,Capital Medical University | Qu J.X.,Capital Medical University | Wang C.,Beijing Hospital | Wang C.,Capital Medical University | And 5 more authors.
Clinical Respiratory Journal | Year: 2014

Introduction: Comparisons of the characteristics between the influenza A (H1N1) pdm09 and common seasonal influenza are important for both clinical management and epidemiological studies. However, the differences between pandemic and seasonal influenza during the post-pandemic period are poorly understood. Objectives: The aim of our research was to investigate clinical and immune response differences between patients with influenza A (H1N1) pdm09 pneumonia and seasonal influenza A (H3N2) pneumonia in the post-pandemic period. Methods: During the first flu season in post-pandemic period, patients from Beijing Network for Adult Community-Acquired Pneumonia present A (H1N1) pdm09 or A (H3N2) influenza were compared concurrently in the aspects of clinical characteristics and inflammatory profile in acute phase. Result: Patients with A (H1N1) pdm09 influenza pneumonia showed a close mean age to A (H3N2) pneumonia (51±20 vs 53±16, mean±standard deviation, years) but tended to have more underlying diseases (32.8% vs 10%, P=0.036). Although clinical characteristics were similar, no statistical difference were found in pneumonia severity index (PSI) score or intensive care unit admission rate or mortality, patients in A (H1N1) pdm09 cohort present higher levels of aspartate aminotransferase, lactase dehydrogenase (P=0.006, 0.018, respectively) in blood and also longer duration of fever than A (H3N2) cohort. Levels of interleukin (IL)-10 and IL-12 (p70) were higher in A (H1N1) pdm09 cohort (P=0.031, 0.047, respectively). Conclusios: During the first post-pandemic flu season, patients with the A (H1N1) pdm09 pneumonia showed similar clinical characteristics but slightly higher disease severity and stronger systemic inflammatory response than A (H3N2) pneumonia. © 2013 The Authors. The Clinical Respiratory Journal published by John Wiley & Sons Ltd.


Zhang S.,Capital Medical University | Zhang S.,Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders | Zhai Z.,Capital Medical University | Zhai Z.,Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders | And 12 more authors.
Thrombosis Research | Year: 2015

Background As a special group in pulmonary embolism (PE), the baseline characteristics, better therapeutic strategy and prognosis of patients with concurrent malignancy need to be investigated. Long-term low-molecular-weight heparin (LMWH) is recommended for these patients, however, whether therapeutic strategy affects long-term prognosis remains unclear. Methods In this prospective study, acute symptomatic PE patients confirmed by imaging examinations, with/without malignancy, were enrolled and followed. Qanadli score was used to assess the embolic burden. The clinical endpoints included symptomatic recurrent venous thromboembolism (VTE), all-cause death and clinic relevant bleeding. Results In the 627 patients enrolled, 92 patients had malignancy at baseline. The median follow-up period was 36 months. The Qanadli score at baseline was lower in malignancy group than non-malignancy group (P = 0.003). 48.9% of patients with malignancy died, while 11.4% of non-malignancy group died (P < 0.001). Malignancy was a risk factor of death (HR 5.659, 95%CI 3.090-10.366, P < 0.001). In malignancy group, 56 patients used long-term LMWH and 36 patients received oral vitamin K antagonist (VKA). The median survival time was 30 months in LMWH group, significantly longer than 12.5 months in VKA group (P = 0.041). The mortality in the first 6 months was lower in LMWH group than VKA group (19.6% vs. 41.7%, P = 0.022). Conclusions PE patients with malignancy had much higher incidence of all-cause death in spite of less embolic burden compared with patients without malignancy. Anticoagulation using long-term LMWH could prolong the survival time of PE patients with malignancy, and it was more effective than VKA. © 2015 Elsevier Ltd.


PubMed | Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders
Type: Journal Article | Journal: Experimental gerontology | Year: 2011

The p38 mitogen-activated protein kinase (p38 MAPK) pathway is a key regulator of pro-inflammatory cytokine biosynthesis, which may contribute to the chronic low-grade inflammation observed with aging. We hypothesize that aging up-regulates the activation of p38 MAPK as well as the pro-inflammatory cytokines tumor necrosis factor- (TNF-), interleukin-1 (IL-1) and interleukin-6 (IL-6) in mouse lung, and is accompanied by disturbances in oxidant-antioxidant status. In addition, the elevated protein levels of phosphorylated active form of p38 MAPK (phospho-p38 MAPK) with age are tissue-specific. To test this hypothesis, protein levels of phospho-p38 MAPK were determined using Western blot analysis in isolated lung, brain, heart, spleen, kidney and muscle of young (2-month-old) and aged (20-month-old) male C57BL/6J mice. Results show that phospho-p38 MAPK protein levels, not total-p38 MAPK, increased significantly (p<0.01, n=8) in lung and brain of 20-month-old mice. The activation of p38 MAPK in other tissues was not altered with age. Immunostaining showed that epithelial cells and alveolar macrophages in lung parenchyma were the major cellular sources of phospho-p38 MAPK immunity. As measured by enzyme-linked immunosorbent assay (ELISA), TNF-, IL-1 and IL-6 in lung homogenates were elevated significantly with age, but there were no differences with age in serum levels except for IL-6. In addition, IL-1 and IL-6 were increased notably while TNF- was not different with age in bronchoalveolar lavage fluid (BALF). Furthermore, the oxidant-antioxidant status was evaluated by measuring pro-oxidant malondialdehyde (MDA) levels and the activity of reactive oxygen species scavenging enzymes (i.e. superoxide dismutase (SOD) and glutathione (GSH)) in lung homogenates. The results showed that SOD and GSH decreased with age, while MDA did not change. In conclusion, our data demonstrate that p38 MAPK is activated during lung aging with a corresponding increase in pro-inflammatory cytokines and decrease in antioxidant capacity.

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