Background Interstitial lung disease (ILD) is a common and potentially life-threatening complication for rheumatoid arthritis (RA) patients. However, there is a lack of clear prognostic factors in rheumatoid arthritis-associated interstitial lung disease (RA-ILD) patients. The purpose of this study was to complete a systematic review and meta-analysis of the factors associated with mortality in RA-ILD patients. Methods Medline, EMBASE and the Cochrane Library were searched up to September 1, 2020. The Newcastle–Ottawa Scale (NOS) was applied to assess the methodological quality of the eligible studies. Study characteristics and magnitude of effect sizes were extracted. Then, pooled hazard ratios (HRs) with the corresponding 95% confidence intervals (CIs) and pooled risk ratios (RRs) with 95% CIs were calculated to assess the factors associated with mortality in RA-ILD. Results Twenty-three of 3463 articles were eligible, and ten factors associated with mortality for RA-ILD were evaluated in the meta-analysis. Older age (HRs = 1.04, 95% CI 1.03–1.05), male sex (HRs = 1.44, 95% CI 1.21–1.73), having a smoking history (HRs = 1.42, 95% CI 1.03–1.96), lower diffusing capacity of the lung for carbon monoxide (DLCO)% predicted (HRs = 0.98, 95% CI 0.97–1.00), forced vital capacity (FVC)% predicted (HRs = 0.99, 95% CI 0.98–1.00), composite physiological index (CPI) (HRs = 1.04, 95% CI 1.02–1.06), usual interstitial pneumonia (UIP) pattern on HRCT (HRs = 1.88, 95% CI 1.14–3.10 and RRs = 1.90, 95% CI 1.50–2.39), emphysema presence (HRs = 2.31, 95% CI 1.58–3.39), and acute exacerbation of ILD (HRs = 2.70, 95% CI 1.67–4.36) were associated with increased mortality in RA-ILD, whereas rheumatoid factor (RF) positive status was not associated. Conclusions Through this systematic review and meta-analysis, we found that older age, male sex, smoking history, higher CPI, lower DLCO% predicted, lower FVC% predicted, UIP pattern on HRCT, emphysema presence and acute exacerbation of ILD were associated with an increased risk of mortality in RA-ILD.
Chronic obstructive pulmonary disease (COPD) has become a significant public health risk. Long non-coding RNAs (lncRNAs) have been identified as important factors involved in the proliferation, apoptosis and inflammatory cytokine expression of lung cells. Peripheral blood samples from 66 subjects (18 non-smokers, 24 smokers without COPD and 28 smokers with COPD) and HBE135-E6E7 cell treated with cigarette smoke extract (CSE) or not were used as the research object. The aim of the present study was to investigate the underlying mechanism of lncRNA maternally expressed gene 3 (MEG3) in COPD. Following transfection with microRNA (miR)-149-3p mimics, miR-negative control mimics, miR-149-3p inhibitor, miR-negative control inhibitor, small interfering (si)RNA targeting MEG3 (si-MEG3) and si-negative control (si-NC), levels of MEG3 and microRNA (miR)-149-3p were detected using reverse transcription-quantitative PCR, Proliferation and apoptosis were examined using the Cell Counting Kit-8 and flow cytometry assays, respectively. Enzyme-linked immunosorbent assay (ELISA) was performed to detect the expression of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Protein levels of B-cell lymphoma-2 (Bcl-2), cleaved-caspase-3, cleaved-caspase-9, phosphorylated (p)-p65, total (t)-p65, p-lkBα and t-lkBα were measured by western blotting. Luciferase assay was conducted to examine the relationship between MEG3 and miR-149-3p. LncRNA MEG3 was highly expressed, whereas miR-149-3p expression was downregulated in smokers with COPD peripheral blood samples, compared with non-smokers and smokers without COPD samples. Compared with untreated human bronchial epithelial (HBE) cells, MEG3 expression was increased in cigarette smoke extract (CSE)-treated HBE cells. Compared with CSE-treated HBE cells transfected with si-NC, MEG3 knockdown promoted cell proliferation and inhibited apoptosis in CSE-treated HBE cells transfected with si-MEG3, and it also decreased the levels of IL-6, TNF-α, Bcl-2 and increased cleaved-caspase-3 and cleaved-caspase-9 in CSE-treated HBE cells transfected with si-MEG3. The luciferase assay demonstrated that miR-149-3p has target sites for MEG3. MEG3 was demonstrated to regulate the NF-κB signaling pathway by sponging miR-149-3p in CSE-treated HBE cells. In conclusion, these findings suggested that MEG3 promoted proliferation and inhibited apoptosis by regulating the NF-κB signal pathway via miR-149-3p in CSE-treated HBE cells. These results provide an insight for further verification and understanding of the molecular basis of COPD.
The present study aimed to examine the effects of 2.5 µm particulate matter (PM2.5) on airway inflammation and to investigate the possible underlying mechanism. Specifically, the focus was on the imbalance of T helper (Th)1/Th2 cells and the dysregulated expression of transcription factors, including trans-acting T cell-specific transcription factor 3 (GATA3), runt-related transcription factor 3 (Runx3) and T-box transcription factor TBX21 (T-bet). In this study, ambient PM2.5 was collected and analyzed, male BALB/c mice were sensitized and treated with PBS, ovalbumin (OVA), PM2.5 or OVA + PM2.5. The effects of PM2.5 alone or PM2.5 + OVA on immunopathological changes, the expression of transcription factors GATA3, Runx3 and T-bet, and the imbalance of Th1/Th2 were investigated. It was found that PM2.5 + OVA co-exposure significantly enhanced inflammatory cell infiltration, increased higher tracheal secretions in lung tissue and upregulated respiratory resistance response to acetylcholine compared with PM2.5 or OVA single exposure and control groups. In addition, higher protein and mRNA expression levels of Th2 inflammatory mediators interleukin (IL)-4, IL-5 and IL-13 in bronchoalveolar lavage fluid were observed in PM2.5 + OVA treated mice, whereas the expression levels of GATA3 and STAT6 were exhibited in mice exposed to OVA + PM2.5 compared with the OVA and PM2.5 groups. By contrast, PM2.5 exposure decreased the protein and mRNA expression levels of Th1 cytokine interferon-γ and transcription factors Runx3 and T-bet, especially among asthmatic mice, different from OVA group, PM2.5 exposure only failed to influence the expression of T-bet. To conclude, PM2.5 exposure evoked the allergic airway inflammation response, especially in the asthmatic mouse model and led to Th1/Th2 imbalance. These effects worked mainly by upregulating GATA3 and downregulating Runx3. These data suggested that Runx3 may play an important role in PM2.5-aggravated asthma in BALB/c mice.
Background: Non-small cell lung cancer (NSCLC) is an intractable malignant lung cancer with high rates of metastasis and mortality. Currently, long noncoding RNA nuclear RNA host gene 7 (SNHG7) is recognized as a biomarker of multiple cancers. However, the role of SNHG7 in NSCLC requires further understanding. Methods: The expression of SNHG7, miR-449a and TGIF2 in NSCLC tumors and cells was examined by quantitative real time polymerase chain reaction (qRT-PCR). Cell viability was measured by MTT assay. Cell migration and invasion was conducted using transwell assay. Protein expression of TGIF2, vimentin, N-cadherin and E-cadherin was detected by western blot. The interaction between miR-449a and SNHG7 or TGIF2 was determined by luciferase reporter system, RIP and RNA pull-down assay, respectively. Xenograft mice models were established by subcutaneously injecting A549 cells transfected with sh-SNHG7 and sh-control. Results: SNHG7 expression was upregulated in NSCLC tumors and cells compared with normal tissues and cells. SNHG7 silencing repressed cell proliferation, migration, invasion and epithelial to mesenchymal transition (EMT) in NSCLC. Consistently, SNHG7 knockdown hindered tumor growth in vivo. The subsequent luciferase reporter system, RIP and RNA pull-down assay validated the interaction between miR-449a and SNHG7 or TGIF2. The rescue experiments displayed that miR-449a inhibitor counteracted SNHG7 silencing induced inhibition on proliferation, migration, invasion and EMT. Similarly, restoration of TGIF2 reversed miR-449a mediated inhibition on cell progression. In addition, the results indicated that SNHG7 could regulate cell progression by targeting miR-449a/TGIF2 axis. Conclusion: SNHG7 contributed to cell proliferation, migration, invasion and EMT in NSCLC by upregulating TGIF2 via sponging miR-449a, representing a novel targeted therapy method for NSCLC.
Objective Interstitial lung disease (ILD) is a common and potentially life‐threatening complication for individuals with systemic sclerosis (SSc). The purpose of this study was to complete a systematic review and meta‐analysis on prevalence and risk factors of SSc‐ILD in East Asia. Methods Medline, EMBASE, and Cochrane Library were searched up to January 22, 2021. The Reporting of Observational Studies in Epidemiology (STROBE) statement was applied to access the methodological quality of the eligible studies. Study characteristics and magnitude of effect sizes were extracted. Then, we calculated the pooled prevalence, weighted mean differences (WMDs), pooled odds ratios (ORs) with corresponding 95% confidence intervals (CIs), and performed subgroup analysis, sensitivity analysis, and publication bias with Egger's test. Results Twenty‐seven of 1584 articles were eligible and a total of 5250 patients with SSc were selected in the meta‐analysis. The pooled prevalence of SSc‐ILD in East Asia was 56% (95% CI 49%‐63%). The SSc‐ILD prevalence was higher in China (72%) than in Japan (46%) and Korea (51%). Longer disease duration (WMD = 1.97, 95% CI 0.55‐3.38), diffuse SSc (OR = 2.84, 95% CI 1.91‐4.21), positive anti‐topoisomerase I antibody (ATA) (OR = 4.92, 95% CI 2.74‐8.84), positive anti‐centromere body antibody (ACA) (OR = 0.14, 95% CI 0.08‐0.25), positive anti‐U3 ribonucleoprotein (RNP) antibody (OR = 0.17, 95% CI 0.04‐0.66), and higher erythrocyte sedimentation rate (ESR) (WMD = 6.62, 95% CI 1.19‐12.05) were associated with SSc‐ILD in East Asia. Conclusion Through this systematic review and meta‐analysis, we found that ILD occurs in up to approximately 56% of patients with SSc in East Asia. Longer disease duration, diffuse SSc, positive ATA, negative ACA, negative anti‐U3 RNP antibody, and higher ESR were risk factors for SSc‐ILD.
IntroductionAcute kidney injury (AKI) is a prevalent complication of coronavirus disease 2019 (COVID-19) and is closely linked with a poorer prognosis. The aim of this study was to develop and validate an easy-to-use and accurate early prediction model for AKI in hospitalized COVID-19 patients.MethodsData from 480 COVID-19-positive patients (336 in the training set and 144 in the validation set) were obtained from the public database of the Cancer Imaging Archive (TCIA). The least absolute shrinkage and selection operator (LASSO) regression method and multivariate logistic regression were used to screen potential predictive factors to construct the prediction nomogram. Receiver operating curves (ROC), calibration curves, as well as decision curve analysis (DCA) were adopted to assess the effectiveness of the nomogram. The prognostic value of the nomogram was also examined.ResultsA predictive nomogram for AKI was developed based on arterial oxygen saturation, procalcitonin, C-reactive protein, glomerular filtration rate, and the history of coronary artery disease. In the training set, the nomogram produced an AUC of 0.831 (95% confidence interval [CI]: 0.774–0.889) with a sensitivity of 85.2% and a specificity of 69.9%. In the validation set, the nomogram produced an AUC of 0.810 (95% CI: 0.737–0.871) with a sensitivity of 77.4% and a specificity of 78.8%. The calibration curve shows that the nomogram exhibited excellent calibration and fit in both the training and validation sets. DCA suggested that the nomogram has promising clinical effectiveness. In addition, the median length of stay (m-LS) for patients in the high-risk group for AKI (risk score ≥ 0.122) was 14.0 days (95% CI: 11.3–16.7 days), which was significantly longer than 8.0 days (95% CI: 7.1–8.9 days) for patients in the low-risk group (risk score <0.122) (hazard ratio (HR): 1.98, 95% CI: 1.55–2.53, p < 0.001). Moreover, the mortality rate was also significantly higher in the high-risk group than that in the low-risk group (20.6 vs. 2.9%, odd ratio (OR):8.61, 95%CI: 3.45–21.52).ConclusionsThe newly constructed nomogram model could accurately identify potential COVID-19 patients who may experience AKI during hospitalization at the very beginning of their admission and may be useful for informing clinical prognosis.
Background: Pulmonary lymphangitic carcinomatosis (PLC) is characterized by malignant infiltration into lung lymphatic channels from a primary site and is often observed in advanced malignant tumors. This study aimed to evaluate the diagnostic yield of transbronchial lung cryobiopsy in PLC guided by radial endobronchial ultrasound and virtual bronchoscopic navigation (VBN). Methods: This prospective study enrolled 40 patients with clinical and radiologic features indicating PLC.The radial endobronchial ultrasound probe was initially advanced to the region of interest of the desired lobe near the pleura with guidance by VBN. Transbronchial lung biopsy and transbronchial lung cryobiopsy were both performed in the same ROI of all patients with the obtained samples being sent to the pathology laboratory for diagnostic analysis. Procedural complications were recorded. Results: The average number of transbronchial lung biopsy and transbronchial lung cryobiopsy specimens were 4 (3 to 6) and 2 (1 to 3), respectively (t=10.43, P<0.01), with the corresponding mean diameters per biopsy being 3.7 and 8.7 mm (t=12.37, P<0.01). The diagnostic yields of transbronchial lung biopsy and transbronchial lung cryobiopsy were 70% (28/40) and 92.5% (37/40), respectively. The final positive predictive values of transbronchial lung cryobiopsy and transbronchial lung biopsy for PLC were 94.4% (34/36) and 77.8% (28/36), respectively (χ 2 =23.94, P<0.01). Further, 52.2% (12/23) and 81.5% (22/27) of the patients in the transbronchial lung biopsy and transbronchial lung cryobiopsy groups, respectively, were diagnosed with non-small lung cancer after further molecular analysis (χ 2 =19.56, P<0.01). Only 2 (5%) cases presented postoperative pneumothorax. Moreover, 0 (0%), 3 (7.5%), and 17 (42.5%) patients presented severe, moderate, and mild bleeding, respectively. There were no other adverse events or deaths.Conclusions: Transbronchial lung cryobiopsy with the guidance of radial endobronchial ultrasound and VBN without fluoroscopy has a good diagnostic yield for PLC; moreover, it allows one to obtain adequate and intact tissue samples for further molecular analysis.
Background. The aim of the study was to evaluate the utility of Endobronchial ultrasound (EBUS) features included elastography and B-mode features for differentiating malignant from benign lymph nodes(LNs). Methods. 84 patients with 151 enlarged mediastinal and hilar LNs underwent endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) were involved in the retrospective study from 1 January 2019 to 31 December 2019. Scores of EBUS elastography, EBUS B-mode features and final pathological results were recorded. Receiver operating characteristics, univariate and multivariate logistic regression analysis were used to evaluate the diagnostic yield of elastography and B-mode features for malignant LNs. Results. Total 84 patients of 151 LNs were enrolled in the single center retrospective study, which included 108 malignant nodes and 43 benign nodes obtained from 59/25 patients respectively. EBUS elastography score 4-5 differentiated malignant LNs from benign nodes with sensitivity, specificity, positive predictive value, negative predictive value and diagnostic accuracy 85.05%, 77.27%, 90.10%, 71.0% and 82.23% respectively. EBUS B-mode features round shape, heterogenenous echogenicity and absence of CHS showed statistical diagnostic yield by multivariate logistic analysis. ROC analysis suggested the combined AUC for elastography, round shape, absence of CHS and hetergeneous echogenicity was 0.849. Conclusions. EBUS features are effective for differentiating between benign and malignant LNs. This study was approved by the Ethics Committee of Qingdao medical college affiliated Yantai Yuhuangding Hospital (NO. 2014-111).
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