Clinical Characteristics of Chlamydia psittaci Infection Diagnosed by Metagenomic Next-Generation Sequencing: A Retrospective Multi-Center Study in Fujian, China.

Objective: This study aimed to describe and compare the epidemiological, demographic, clinical, laboratory and radiological characteristics as well as the complications, treatments, and outcomes of these patients. Methods: We retrospectively investigated clinical data of patients with C. psittaci infection (psittacosis) in eight Grade IIIA hospitals of Fujian. Metagenomic next-generation sequencing (mNGS) was used identify C. psittaci in clinical samples of all included patients. Results: A total of 74 patients (39 severe/35 non-severe) was diagnosed with psittacosis, 25 (33.8%) of whom had history of poultry exposure. Common symptoms included high fever (98% [37/74]), fatigue (52.7% [39/74]), and dyspnea (51.4% [38/74]). Common manifestations in imaging included consolidation (89.2%), pleural effusion (77.0%), and air bronchogram (66.2%). Common complications included acute respiratory distress syndrome (55.4% [41/74]), type I respiratory failure (52.7% [39/74]), acute liver injury (41.9% [31/74]), and secondary infection (27.0% [20/74]). The in-hospital mortality rate was 8.11% (6/74). Conclusion: C. psittaci infection is represents an underestimated cause of CAP. For SCAP patients with poultry and bird contact history, specimens were encouraged to be sended for mNGS test in time. C. psittaci infection can lead to severe, multiple system involvement, and several complications. mNGS facilitate timely diagnosis of C. psittaci infection.

Alterations in nasal microbiota of patients with amyotrophic lateral sclerosis.

BACKGROUND: Links between alterations in gut microbiota composition and amyotrophic lateral sclerosis (ALS) have previously been reported. This study aimed to examine the microbiota in the nasal cavity of ALS. METHODS: Sixty-six ALS patients and 40 healthy caregivers who live in close proximity with patients were enrolled. High throughput metagenomic sequencing of the 16S ribosomal deoxyribonucleic acid (rDNA) gene V3-V4 region of nasal microbiota was used to characterize the alpha and beta diversity and relative abundance of bacterial taxa, predict function, and conduct correlation analysis between specific taxa and clinical features. RESULTS: The nasal microbiome of ALS patients showed lower alpha diversity than that of corresponding healthy family members. Genera Gaiella , Sphingomonas , Polaribacter _1, Lachnospiraceae _NK4A136_group, Klebsiella , and Alistipes were differentially enriched in ALS patients compared to controls. Nasal microbiota composition in ALS patients significantly differed from that in healthy subjects (unweighted UniFrac P = 0.001), while Linear discriminant analysis Effect Size (LEfSe) analysis indicated that Bacteroidetes and Firmicutes dominated healthy nasal communities at the phylum level, whereas Actinobacteria was the predominant phylum and Thermoleophilia was the predominant class in ALS patients. Genus Faecalibacterium and Alistipes were positively correlated with ALS functional rating scale revised (ALSFRS-R; rs = 0.349, P = 0.020 and rs = 0.393, P = 0.008), while Prevotella -9 and Bacteroides operational taxonomic units (OTUs) were positively associated with lung function (FVC) in ALS patients ( rs = 0.304, P = 0.045, and rs = 0.300, P = 0.048, respectively). Prevotella -1 was positively correlated with white blood cell counts (WBC, rs = 0.347, P = 0.021), neutrophil percentage (Neu%, rs = 0.428, P = 0.004), and neutrophil-to-lymphocyte ratio (NLR, rs = 0.411, P = 0.006), but negatively correlated with lymphocyte percentage (Lym%, rs = -0.408, P = 0.006). In contrast, Streptococcus was negatively associated with Neu% ( rs = -0.445, P = 0.003) and NLR ( rs = -0.436, P = 0.003), while positively associated with Lym% ( rs = 0.437, P = 0.003). No significant differences in nasal microbiota richness and evenness were detected among the severe and mild ALS patients. CONCLUSIONS: ALS is accompanied by altered nasal microbial community composition and diversity. The findings presented here highlight the need to understand how dysbiosis of nasal microbiota may contribute to the development of ALS.

Biogeography of the Respiratory Tract Microbiome in Patients With Malignant Tracheal Tumors.

BACKGROUND: This study aimed to characterize the bacterial microbiota in the oral cavity (OC), throat, trachea, and distal alveoli of patients with primary malignant tracheal tumors (PMTT), including squamous cell carcinoma (SCC) and salivary gland carcinoma patients (SGC), for comparison with a matched non-malignant tracheal tumor (NMTT) group. METHODS: Patients with pathological diagnosis of PMTT and NMTT were included in this study. Saliva, throat swab (TS), trachea protected specimen brush (PSB), and bronchoalveolar lavage fluid (BALF) samples were collected for 16S rRNA gene sequencing. The composition, diversity, and distribution of the microbiota were compared among biogeographic sampling sites and patient groups. The relationship between the genera-level taxon abundance and tracheal tumor types was also investigated to screen for candidate biomarkers. FINDINGS: The most represented phyla in the four sites were Bacteroidetes, Firmicutes, Proteobacteria, and Fusobacteria. In SCC patients, the relative abundance of Bacteroidetes and Firmicutes gradually decreased with increasing depth into the respiratory tract, while the relative abundance of Proteobacteria gradually increased. Bacterial communities at the four biogeographic sites formed two distinct clusters, with OC and TS samples comprising one cluster and PSB and BALF samples comprising the other group. Principal coordinate analysis showed that trachea microbiota in SCC patients were distinct from that of SGC or NMTT patients. In the trachea, AUCs generated by Prevotella and Alloprevotella showed that the abundance of these genera could distinguish SCC patients from both NMTT and SGC patients. INTERPRETATION: The structure of respiratory tract microbiota in PMTT patients is related to tumor type. Certain bacteria could potentially serve as markers of SCC, although verification with large-sample studies is necessary.

Effects of exogenous probiotics on the gut microbiota and clinical outcomes in critically ill patients: a randomized controlled trial.

BACKGROUND: Gut microbiota play an important role in the inflammation. This study aimed to investigate whether exogenous probiotics could improve the intestinal barrier function effect via attenuating inflammation and immunomodulation to improve the clinical outcomes in critically ill patients. METHODS: A single-blind, randomized controlled trial was performed in a respiratory intensive care unit (RICUs). Patients assigned to the intervention group received probiotics Clostridium butyricum until death or discharge. Stool and blood samples were collected on the 1st day and 15th day of administration. Primary clinical outcomes and clinical manifestations were recorded during the follow-up period. RESULTS: There were 61 patients in this study, with 28 patients receiving probiotics. There were no differences in the mortality and hospital stay between intervention group and control group. In addition, the duration of fever (% of hospital stays) was significantly shorter in the intervention group as compared to control group (4.85% vs. 12.94%, P=0.00). The incidence of constipation significantly reduced in the intervention group (17.86% vs. 42.42%, P=0.04). The overall ratio of gastrointestinal adverse effects was comparable between them. Bactericides significantly decreased after probiotic intervention (Δm=-0.69, P=0.048), while Escherichia coli and Enterococcus tended to decrease in the intervention group (Δm=-0.65, P=0.08; Δm=-0.52, P=0.22) on the day 15. No fluctuation was observed in the Bifidobacterium and Lactobacillus after probiotic intervention. CONCLUSIONS: Our study fails to show the beneficial effects of probiotics on the primary clinical outcomes in critically ill patients. The intestinal barrier is damaged, and probiotics may reduce the burden of Gm-bacteria from the gut.

Spliceosome-associated protein 130: a novel biomarker for idiopathic pulmonary fibrosis.

BACKGROUND: Spliceosome-associated protein 130 (SAP130), a novel danger-associated molecular pattern (DAMP), is involved in inflammatory disease. However, no data are available about SAP130 in idiopathic pulmonary fibrosis (IPF). Our study aimed to investigate SAP130 in the serum and lung tissue of patients with IPF and to determine its clinical significance. METHODS: SAP130 levels in the serum of 83 IPF patients and 38 healthy subjects were measured. Additionally, immunohistochemical staining for SAP130 was performed in lung specimens of IPF patients and control subjects. Correlation between serum SAP130 levels and clinical parameters were investigated. RESULTS: Serum SAP130 levels were elevated in IPF patients compared with healthy controls. In parallel, the expression of SAP130 in lung tissue was elevated in IPF. SAP130 levels were higher in patients with acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) than patients with stable IPF (P=0.0144). The area under curve (AUC) of the ROC curve for the diagnosis of IPF was 0.944 (95% CI, 0.810-0.997) for SAP130. The sensitivity (92.1%) and specificity (69.9%) were obtained for the cutoff value of 643.87 pg/mL. In patients with stable IPF, the SAP130 level correlated positively with fibrosis on high-resolution CT (HRCT) (r=0.4164, P=0.0029) and serum KL-6 (r=0.4564, P=0.0010), and inversely with FEV1 (r=-0.3562, P=0.0120) and DLCO (r=-0.5550, P<0.0001). In patients with AE-IPF, the SAP130 level correlated positively with fibrosis (r=0.3735, P=0.0296) and ground-glass opacity (r=0.4697, P=0.0051) on HRCT and serum Krebs von den Lungen 6 (KL-6) (r=0.5470, P= 0.0008). CONCLUSIONS: The study suggested that SAP130 was a potential noninvasive biomarker that correlates well with disease severity of IPF. A prospective, multicentre study is required to validate the clinical and pathophysiological utility of SAP130 in IPF.

Differences in the Clinical Characteristics of Early- and Late-Onset Asthma in Elderly Patients.

Differences between early-onset and late-onset asthma in elderly subjects have not been comprehensively described in China. We conducted a cross-sectional study to determine the phenotypic differences between early-onset asthma (EOA) and late-onset asthma (LOA) in elderly patients. We collected clinical and physiological data from 176 elderly patients with asthma. Participants were divided into two groups: EOA group and LOA group. Demographics, comorbidities, inflammatory parameters, lung function, severity, asthma control, and medication use among EOA and LOA elderly patients were compared. Elderly subjects with EOA had more atopic disease, a stronger positive family history of asthma, higher IgE, and exhaled nitric oxide levels as compared to those with LOA. In contrast, elderly subjects with LOA had lower lung function and more marked fixed airflow obstruction (FAO). Elderly subjects with LOA had a higher incidence of chronic obstructive pulmonary disease (COPD). No differences were observed in age, gender, BMI, history of smoking, severity, and asthma control between the two groups. Both similarities and differences exist between elderly subjects with EOA and those with LOA in China. Further work is required to determine the pathophysiological, clinical, and therapeutic implications for different asthma phenotypes in elderly subjects.

Protective effect of exogenous hydrogen sulfide on pulmonary artery endothelial cells by suppressing endoplasmic reticulum stress in a rat model of chronic obstructive pulmonary disease.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a multicomponent disorder characterized by inflammation, representing a significant leading cause of chronic morbidity and mortality. Reports have implicated hydrogen sulfide (H2S) in both the pathology and treatment of COPD. The present study aimed to explore the effects involved with exogenous H2S on endoplasmic reticulum stress (ERS) and pulmonary artery endothelial cells (PAECs) in a rat model of COPD. METHODS: Rat models of COPD were successfully established by means of passive smoke exposure and intratracheal injection with lipopolysaccharide (LPS). Pulmonary function tests were performed and histopathological changes were observed. The expression of ERS markers, glucose-regulated protein-78 (GRP78), and C/EBP homologous protein (CHOP) and caspase-12, associated with ERS-induced apoptosis, were determined by western blot and immunohistochemistry methods. TUNEL assay was applied to determine the apoptosis index (AI) in PAECs. RESULTS: Treatment with NaHS was followed by the exhibition of markedly increased forced expiratory volume over 0.3 s (FEV0.3)/forced vital capacity (FVC) and dynamic lung compliance as well as integral optical density (IOD), with decreased RI among COPD rats. Western blot analysis, immunohistochemistry and TUNEL assay results revealed there to be reduced expressions of GRP78, CHOP and caspase-12 in the lung tissues and AI of PAECs, post NaHS treatment. CONCLUSION: The key findings of the current study highlight ERS in COPD rats, as well as well as reduced apoptosis in PAECs in connection with exogenous H2S by suppressing ERS.

Effectiveness of meditative movement on COPD: a systematic review and meta-analysis.

BACKGROUND: The effectiveness of meditative movement (tai chi, yoga, and qigong) on COPD remained unclear. We undertook a systematic review and meta-analysis to determine the effectiveness of meditative movement on COPD patients. METHODS: We searched PubMed, Web of Science, EMBASE, and the Cochrane Center Register of Controlled Trials for relevant studies. The methods of standard meta-analysis were utilized for identifying relevant researches (until August 2017), quality appraisal, and synthesis. The primary outcomes were the 6-minute walking distance (6MWD), lung function, and dyspnea levels. RESULTS: Sixteen studies involving 1,176 COPD patients were included. When comparing with the control group, the 6MWD was significantly enhanced in the treatment group (3 months: mean difference [MD]=25.40 m, 95% CI: 16.25 to 34.54; 6 months: MD=35.75 m, 95% CI: 22.23 to 49.27), as well as functions on forced expiratory volume in 1 s (FEV1) (3 months: MD=0.1L, 95% CI: 0.02 to 0.18; 6 months: MD=0.18L, 95% CI: 0.1 to 0.26), and FEV1 % predicted (3 months: 4L, 95% CI: 2.7 to 5.31; 6 months: MD=4.8L, 95% CI: 2.56 to 7.07). Quality of life for the group doing meditative movement was better than the control group based on the Chronic Respiratory Disease Questionnaire dyspnea score (MD=0.9 units, 95% CI: 0.51 to 1.29) and fatigue score (MD=0.75 units, 95% CI: 0.42 to 1.09) and the total score (MD=1.92 units, 95% CI: 0.54 to 3.31). CONCLUSION: Meditative movement may have the potential to enhance lung function and physical activity in COPD patients. More large-scale, well-designed, multicenter, randomized controlled trials should be launched to evaluate the long-range effects of meditative movement.

Detection and analysis of apoptosis- and autophagy-related miRNAs of mouse vascular endothelial cells in chronic intermittent hypoxia model.

Endothelial dysfunction is the main pathogenic mechanism of cardiovascular complications induced by obstructive sleep apnea/hyponea syndrome (OSAHS). Chronic intermittent hypoxia (CIH) is the primary factor of OSAHS-associated endothelial dysfunction. The hypoxia inducible factor (HIF) pathway regulates the expression of downstream target genes and mediates cell apoptosis caused by CIH-induced endothelial injury. miRNAs play extensive and important negative regulatory roles in this process at the post-transcriptional level. However, the regulatory mechanism of miRNAs in CIH tissue models remains unclear. The present study established a mouse aortic endothelial cell model of CIH in an attempt to screen out specific miRNAs by using miRNA chip analysis. It was found that 14 miRNAs were differentially expressed. Of them, 6 were significantly different and verified by quantitative real-time PCR (Q-PCR), of which four were up-regulated and two were down-regulated markedly. To gain an unbiased global perspective on subsequent regulation by altered miRNAs, we established signaling networks by GO to predict the target genes of the 6 miRNAs. It was found that the 6 identified miRNAs were apoptosis- or autophagy-related target genes. Down-regulation of miR-193 inhibits CIH induced endothelial injury and apoptosis- or autophagy-related protein expression. In conclusion, our results showed that CIH could induce differential expression of miRNAs, and alteration in the miRNA expression pattern was associated with the expression of apoptosis- or autophagy-related genes.

Inhibition of microRNA-218 reduces HIF-1α by targeting on Robo1 in mice aortic endothelial cells under intermittent hypoxia.

OBJECTIVE: To investigate the effects of miR-218 on expression of hypoxia-inducible factors 1α (HIF-1α), vascular endothelial growth factor (VEGF) and cell apoptosis in normal mice aortic endothelial cells under intermittent hypoxia (IH) condition. METHODS: Anti-miR-218 inhibitor, miR-negative control and miR-218 mimic were used to tranfect the cells in different groups under IH condition. Both RT-PCR and Western blot were used to determine the expressions of HIF-1α and VEGF. Akt, p-Akt and cell apoptosis related proteins bcl-2, bax and caspase-3 and roundabout 1 (Robo1) were measured using Western blot. Cell apoptosis was evaluated by flow cytometry. Statistical analysis was performed using SPSS 18.0. RESULTS: Expression of miR-218 was significantly up-regulated in the IH group and was significantly inhibited when cells were transfected with miR-218 inhibitor. Down regulation of miR-218 could reduce the expression of HIF-1α and VEGF under intermittent hypoxia condition. In cells transfected with miR-218 mimic, expression of HIF-1α and VEGF significantly increased compared with the control. However, when treated with LY294002, the expression of HIF-1α and VEGF both decreased. Apoptosis assay showed that down regulation of miR-218 could inhibit intermittent hypoxia induced cell apoptosis, decrease expression of caspase-3 and bax and increase expression of bcl-2 under intermittent hypoxia condition. At last, silencing Robo1 could significantly enhance the expression of HIF-1α under IH condition. CONCLUSION: Inhibition of miR-218 could reduce the expression of HIF-1α and protect against IH-induced apoptosis in mice aortic endothelial cells. The effects were associated with PI3K/AKT pathway and might through targeting of Robo1.

Does high-flow nasal cannula oxygen improve outcome in acute hypoxemic respiratory failure? A systematic review and meta-analysis.

INTRODUCTION: To evaluate the efficacy of high-flow nasal cannula (HFNC) in the rate of intubation and mortality for patients with acute hypoxemic respiratory failure. METHODS: We searched Pubmed, EMBASE, and the Cochrane Library for relevant studies. Two reviewers extracted data and reviewed the quality of the studies independently. The primary outcome was the rate of intubation; secondary outcome was mortality in the hospital. Study-level data were pooled using a random-effects model when I2 was >50% or a fixed-effects model when I2 was <50%. RESULTS: Eight randomized controlled studies with a total of 1,818patients were considered. Pooled analysis showed that no statistically significant difference was found between groups regarding the rate of intubation (odds ratio [OR] = 0.79; 95% confidence interval [CI]: 0.60-1.04; P = 0.09; I2 = 36%) and no statistically significant difference was found between groups regarding hospital mortality (OR = 0.89; 95% CI: 0.62-127; P = 0.51; I2 = 47%). CONCLUSIONS: The use of HFNC showed a trend toward reduction in the intubation rate, which did not meet statistical significance, in patients with acute respiratory failure compared with conventional oxygen therapy (COT) and noninvasive ventilation (NIV). Moreover no difference in mortality. So, Large, well-designed, randomized, multi-center trials are needed to confirm the effects of HFNC in acute hypoxemic respiratory failure patients.

An irregular pulmonary nodule was confirmed diagnosis of aspiration pneumonia by finding plant cells through rapid on-site evaluation.

BACKGROUND: Rapid on-site evaluation (ROSE) is a method which is often used in quick-staining cytology in the tumour diagnostic field, and results in a significant decrease in diagnostic time and cost. However, we have not found any previous report on the ROSE method for diagnosing aspiration pneumonia. METHODS: We would like to discuss the case of a patient with an irregular pulmonary nodule in the left lower lobar bronchus who had a confirmed diagnosis of aspiration pneumonia through ROSE stained by Diff-Quik methods during bronchoscopy. RESULTS: Through ROSE, which we were able to perform within just 1 min, we observed the plant cells on the smear under the microscope. The Giemsa stain of the specimen, which would take much more time than Diff-Quik, also revealed the plant cells. CONCLUSION: ROSE for the specimen from the bronchoscopy could be done for the patient who has developed an unexplained pulmonary nodule and is helpful. If the non-human cells such as plant cells are found from the ROSE, aspiration pneumonia can be diagnosed immediately and the corresponding therapy may be performed, which may significantly shorten hospital stay, reduce hospital costs and improve patient outcomes.

Clinical analysis of non-AIDS patients pathologically diagnosed with pulmonary cryptococcosis.

BACKGROUND: Pulmonary cryptococcosis (PC) was not a rare infectious disease in non-AIDS patients. However, data on the immune status were lacking in southern China for comparative analysis of differences between immunocompromised and immunocompetent hosts. This study was to investigate the epidemiological, clinical, radiological, and treatment profiles for patients with PC. METHODS: We performed a retrospective review of 88 patients diagnosed with tissue-confirmed PC who were not HIV-infected from 2003 to 2013. RESULTS: Of 88 patients, 35(39.7%) were immunocompromised host. Fever and CNS symptom were significantly common in immunocompromised patients compared to immunocompetent patients (P=0.019 and P=0.036, respectively). The most frequent radiologic abnormalities were solitary or multiple pulmonary nodules, and masses or consolidations, and most lesions were located in the peripheral lung field. Cavitations and halo sign were significantly frequent in immunocompromised patients than in immunocompetent patients (P<0.05). The most frequently applied and reliable diagnostic procedure was CT-guided percutaneous translung biopsy. Treatment included antifungal drug alone in 20 patients, surgery alone in 20 including 3 treated by VATS, surgery plus antifungal drugs in 20 patients. CONCLUSIONS: PC was not rare in immunocompetent host in southern China. Special differences remained in clinical manifestation and radiological findings of PC between immunocompromised and immunocompetent patients. Future work on the mechanisms of possible differences is required.

WITHDRAWN: Detection and analysis of apoptosis- and autophagy-related miRNAs of vascular endothelial cells in a mouse chronic intermittent hypoxia model.

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The role of tissue factor and autophagy in pulmonary vascular remodeling in a rat model for chronic thromboembolic pulmonary hypertension.

BACKGROUND: Few reports have examined tissue factor (TF) and autophagy expression in chronic pulmonary thromboembolic hypertension (CTEPH) animal models. OBJECTIVES: To investigate the role of tissue factor (TF), autophagy and their interactions during chronic thromboembolic pulmonary hypertension (CTEPH) pathogenesis in a rat model. METHODS: Autologous blood clots were repeatedly injected into the left jugular vein of rats with injecting endogenous fibrinolysis inhibitor tranexamic acid (TXA). Mean pulmonary arterial pressure (mPAP), histopathology and TF, Beclin-1 and microtubule-associated protein 1 light chain (LC3) expression levels were detected. RESULTS: The mPAP and vessel wall area/total area (WA/TA) ratio in the experiment group increased significantly (P < 0.05). TF mRNA and protein expression levels in the experiment group increased significantly (P < 0.05). Beclin-1 and LC3B mRNA and protein expression levels were lower in the experiment group (P < 0.05). The mPAP had a positive correlation with WA/TA ratio (r = 0.955, P < 0.05). Beclin-1 and LC3B protein expression had a negative correlation with the WA/TA ratio (r = -0.963, P < 0.05, r = -0.965, P < 0.05, respectively). TF protein expression had a negative correlation with both Beclin-1 and LC3B protein expression (r = -0.995, P <0.05, r = -0972, P < 0.05, respectively). CONCLUSIONS: A rat model of CTEPH can be established by repeatedly introducing autologous blood clots into the pulmonary artery with injecting TXA. TF and autophagy may play a key role during CTEPH pathogenesis, especially in vascular remodeling.

Close concordance between pulmonary angiography and pathology in a canine model with chronic pulmonary thromboembolism and pathological mechanisms after lung ischemia reperfusion injury.

To investigate the pulmonary angiography and pathology in a canine model with chronic pulmonary thromboembolism (PTE). The cylindrical blood clots were selectively introduced into the left (n = 10) or right (n = 20) lower pulmonary arteries of dogs. Pulmonary arteriography (PA) was performed before or after embolization. The values after embolization and baseline of mean pulmonary arterial pressure, pulmonary vascular resistance, cardiac output had changed. After 1 or 2 weeks' embolization, local PA demonstrated the abrupt cut-off perfusion defects or webs, bands, and abrupt vascular narrowing. 2 weeks after embolization, the pathology showed that the fibrin networks of the thrombi had multiple recanalization channels, and pulmonary artery had the concentric, lamellar (onion-like) intimal hyperplasia, multilayered, irregular arrangements of endothelial cells, and the infiltration of inflammatory cells. After embolectomy-mediated reperfusion, 2 weeks' subgroup showed destroyed and incomplete alveolar structures, and a large number of exudative cells, primarily neutrophils, and exudate. There close concordance between pulmonary angiography and pathology in a canine model with chronic PTE. The LIRI mechanisms after embolectomy-mediated reperfusion involve the destroyed, incomplete alveolar structures, and infiltration of inflammatory cells, primarily neutrophils.

The role of mononuclear cell tissue factor and inflammatory cytokines in patients with chronic thromboembolic pulmonary hypertension.

Thrombosis and inflammation are two major factors underlying chronic thromboembolic pulmonary hypertension (CTEPH). Tissue factor (TF), C-reactive protein (CRP), tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein 1 (MCP-1) may play critical roles in the process of CTEPH thrombosis and pulmonary vascular remodeling. Ten patients with a confirmed diagnosis of CTEPH, 20 patients with acute pulmonary thromboembolism and 15 patients with other types of pulmonary hypertension were enrolled in this study, along with 20 healthy subjects as the control group. The immunoturbidimetric method was used to determine the plasma content of CRP. The plasma levels of TNF-α, MCP-1, and TF antigen were measured by an enzyme-linked immunosorbent assay, and TF activity was measured by the chromogenic substrate method. Percoll density gradient centrifugation was used to separate peripheral blood mononuclear cells from plasma. The level of monocyte TF mRNA was examined by reverse transcriptase-polymerase chain reaction. The correlations between all indices described above were analyzed. In CTEPH patients, the expression of CRP, TNF-α, and MCP-1 was significantly higher than that in controls (P < 0.05). The levels of TF activity, TF antigen, and TF mRNA in monocyte cells were increased in CTEPH patients when compared with control subjects, but only the TF antigen and TF mRNA levels were significantly different (P < 0.05). In CTEPH patients, levels of CRP, MCP-1, and TNF-α significantly correlated with the level of TF antigen in plasma. TF gene expression was increased in patients with CTEPH, suggesting that blood-borne TF mainly comes from mononuclear cells. TF expression significantly correlated with levels of CRP, TNF-α and MCP-1. These factors may play an important role in the development of CTEPH via the inflammation-coagulation-thrombosis cycle.

[The efficacy and safety of moxifloxacin in the treatment of patients with acute exacerbation of chronic obstructive pulmonary disease].

OBJECTIVE: To compare the effectiveness and safety of moxifloxacin and cefoperazone-sulbactam therapy in acute exacerbation of chronic obstructive pulmonary disease (COPD). METHODS: This was a prospective, randomized, multicentre study conducted between December 2011 and December 2012 involving 21 hospitals in Fujian. A total of 202 patients with AECOPD requiring antibiotic therapy were enrolled. Of these patients randomized to either treatments, 102 patients [male 60, female 42, (69.8 ± 6.5) y] received moxifloxacin (400 mg qd) and 100 [male 56, female 44, (69.6 ± 6.7) y] received cefoperazone-sulbactam (3.0 q 8 h). Clinical effectiveness, bacterial eradication and drug safety were evaluated. RESULTS: The clinical effectiveness rate was 90.2% (92/102) in the moxifloxacin group and 88.0% (88/100) in the cefoperazone-sulbactam group. The bacterial eradication rate was 51.9% (14/27) and 48.3% (14/29) in the 2 groups respectively. The differences between groups were not statistically significant in terms of clinical and microbiological effectiveness (χ² = 0.251, χ² = 0.072, both P > 0.05). The length of hospital stay and antibiotic-days were shorter in the moxifloxacin group [(8.7 ± 2.4) vs (11.7 ± 3.0) d; (6.7 ± 2.2) vs (8.7 ± 2.3) d], the differences being significant between the 2 arms. (t = 6.360, t = 7.732, P < 0.05). Both drugs were well tolerated with no significant differences in numbers of drug-related adverse events (P > 0.05). CONCLUSIONS: Moxifloxacin was equivalent to cefoperazone-sulbactam therapy for clinical success, bacteriologic eradication and showed superiority over the control group in shortening the length of hospital stay and antibiotic-days. Additionally, the drug safety of moxifloxacin was good.