Publications by authors named "Surong Fang"

13 Publications

  • Page 1 of 1

Endobronchial Ultrasound Elastography Combined With Computed Tomography in Differentiating Benign from Malignant Intrathoracic Lymph Nodes.

Surg Innov 2020 Dec 18:1553350620978027. Epub 2020 Dec 18.

Department of Respiratory Medicine, 385685Nanjing First Hospital, Affiliated to Nanjing Medical University, China.

. This study was to combine endobronchial ultrasound elastography (UE) with computed tomography (CT) to identify benign and malignant thoracic lymph nodes (LNs) more objectively and accurately. A total of 42 patients with intrathoracic lymphadenopathy required for endobronchial ultrasound with real-time guided transbronchial needle aspiration (EBUS-TBNA) examination were enrolled. All patients were examined by enhanced chest CT, B-mode ultrasound, and endobronchial ultrasound (EBUS)-guided elastography before EBUS-TBNA. Each lymph node was assessed by describing the characteristics of CT image (short diameter, texture, shape, boundary, and mean CT value), B-mode ultrasound (short diameter, echo characteristic, shape, and boundary), and elastography (image type, grading score, strain rate, and blue area ratio). The pathological results were used as the gold standard. The characteristics were compared alone and in combination between benign and malignant LNs. . The blue area ratio of elastography combined with CT had better diagnostic value in differentiating benign and malignant LNs than elastography alone, with the accuracy, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) being 92%, 96%, 80%, 94%, and 86% vs 81%, 77%, 93%, 97%, and 56%, respectively. Elastography combined with B-mode ultrasound and CT characteristics showed the highest diagnostic value. Accuracy, sensitivity, specificity, PPV, and NPV were all 100%. . Endobronchial UE combined with CT and B-mode ultrasound imaging shows a greater diagnostic value in differentiating benign and malignant intrathoracic LNs than either imaging alone.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1177/1553350620978027DOI Listing
December 2020

Prognostic value of pretreatment platelet counts in lung cancer: a systematic review and meta-analysis.

BMC Pulm Med 2020 Apr 20;20(1):96. Epub 2020 Apr 20.

Department of Respiratory and Critical Care Medicine, Nanjing First Hospital, Nanjing Medical University, 68 Changle road, Nanjing, 210006, Jiangsu, China.

Background: The prognostic value of elevated pretreatment platelet counts remains controversial in lung cancer patients. We performed the present meta-analysis to determine its precise role in these patients.

Methods: We employed a multiple search strategy in the PubMed, EMBASE and Cochrane Library databases to identify eligible studies. Disease-free survival (DFS)/progression-free survival (PFS)/time to progression (TTP) and overall survival (OS) were used as outcomes with hazard ratios (HRs) and 95% confidence intervals (CIs). Heterogeneity among the studies and publication bias were also evaluated.

Results: A total of 40 studies including 16,696 lung cancer patients were eligible for the analysis. Overall, the pooled analysis showed that compared with normal platelet counts, elevated pretreatment platelet counts were associated with poorer OS (HR = 1.54, 95% CI: 1.37-1.72, P < 0.001) and poorer DFS/PFS/TTP (HR = 1.62, 95% CI: 1.33-1.98, P < 0.001) in patients with lung cancer. In subgroup analyses, elevated pretreatment platelet counts were also associated with poorer OS and DFS/PFS/TTP in most subgroups. There was no evidence of publication bias.

Conclusions: This meta-analysis revealed that elevated pretreatment platelet counts were an independent predictor of OS and DFS/PFS/TTP in lung cancer patients. Large-scale prospective studies and a validation study are warranted.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s12890-020-1139-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7171794PMC
April 2020

Lipoprotein-associated phospholipase A2 predicted cardiovascular disease in obstructive sleep apnea syndrome.

Respir Med 2020 03 28;163:105881. Epub 2020 Jan 28.

Department of Respiratory Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China. Electronic address:

Background: Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for cardiovascular disease (CVD). As a new inflammatory biomarker of CVD, rare attention has been paid to the roles of lipoprotein-associated phospholipase (Lp-PLA2) in OSAS studies. In this study, we aimed to investigate the correlation between Lp-PLA2 and concomitant CVD in OSAS patients.

Methods: In this prospective study, 152 OSAS patients were further divided into mild, moderate, and severe OSAS subgroups. They presented heart failure, coronary artery disease, or arrhythmia were confirmed with CVD. Thirty-one subjects without OSAS were recruited for the control group. The relationship between Lp-PLA2 and concomitant CVD in OSAS patients was analyzed.

Results: Serum Lp-PLA2 values were significantly higher in the severe and moderate OSAS group compared with mild OSAS and OSAS negative groups (P = 0.025). Significant increase was noticed in serum Lp-PLA2 levels in CVD patients compared with those without in severe-moderate-mild OSAS (P < 0.05). In logistic regression analysis, the level of Lp-PLA2 was proved as a significant independent predictor for CVD (OR = 1.117, P = 0.008). The ROC analysis indicated that the best cut-off value of Lp-PLA2 for predicting CVD in OSAS patients was 238.09 ng/ml. The positive and negative predictive values were 72.5% and 70.5%, respectively. The sensitivity was 46.8% and the specificity was 87.8%.

Conclusions: Lp-PLA2 might be associated with the severity of OSAS and the occurrence of CVD in OSAS patients. Lp-PLA2 is expected to be a promising biomarker candidate in predicting CVD in patients with OSAS due to test convenience.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.rmed.2020.105881DOI Listing
March 2020

The Molecular Mechanism of Metabolic Remodeling in Lung Cancer.

J Cancer 2020 13;11(6):1403-1411. Epub 2020 Jan 13.

Department of Respiratory Medicine, Nanjing First Hospital, Nanjing Medical University. No. 68 Changle Road, Qinhuai District, Nanjing 210001,People's Republic of China.

Metabolic remodeling is a key phenomenon in the occurrence and development of tumors. It not only offers materials and energy for the survival and proliferation of tumor cells, but also protects tumor cells so that they may survive, proliferate and transfer in the harsh microenvironment. This paper attempts to reveal the role of abnormal metabolism in the development of lung cancer by considering the processes of glycolysis and lipid metabolism, Identification of the molecules that are specifically used in the processes of glycolysis and lipid metabolism, and their underlying molecular mechanisms, is of great clinical and theoretical significance. We will focus on the recent progress in elucidating the molecular mechanism of metabolic remodeling in lung cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.7150/jca.31406DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6995370PMC
January 2020

Inhibition of FASN suppresses the malignant biological behavior of non-small cell lung cancer cells via deregulating glucose metabolism and AKT/ERK pathway.

Lipids Health Dis 2019 May 24;18(1):118. Epub 2019 May 24.

Department of Respiratory Medicine, Nanjing First Hospital, Nanjing Medical University, No. 68 Changle Road, Qinhuai District, Nanjing, 210001, People's Republic of China.

Background: Fatty acid synthase (FASN) is overexpressed in most human carcinomas, including non-small cell lung cancer (NSCLC), and contributes to poor prognosis. An increasing number of studies have highlighted the potential function of FASN as both a biomarker and therapeutic target for cancers. However, the underlying molecular mechanisms of FASN in glucose metabolism and the malignant biological behavior of NSCLC remain the subjects of intensive investigation.

Methods: FASN expression was depleted by FASN-siRNA in A549 and NCI-H1299 cell lines to detect the function of glucose metabolism and the malignant biological behavior of NSCLC cells. Western-blot and qPCR were applied to determine the expressions of FASN, t-AKT, p-AKT, t-ERK, p-ERK, PKM2, HK2 and AZGP1. ATP and lactate were detected to determine the activation of glucose metabolism. CCK8 and transwell assays were used to detect the proliferation, invasion, and migration capacity of the two types of NSCLC cells. The xenograft mouse model was used to evaluate tumor weights after suppression of FASN.

Results: LV-FASN-siRNA and its control lentiviral vector were successfully transfected into the two types of NSCLC cells (A549 and NCI-H1299). LV-FASN siRNA significantly suppressed FASN expression in both NSCLC cell types, and expressions of p-AKT, p-ERK, PKM2, and AZGP1 were also significantly decreased. Notably, the levels of ATP and lactate were significantly decreased after transfection with LV-FASN siRNA. The proliferation of both NSCLC cell types was decreased after suppression of FASN. The invasion and migration capacity of A549, but not NCI-H1299, were inhibited following down-regulation of FASN. In vivo, inhibition of FASN caused a marked animal tumor weight loss.

Conclusions: FASN was involved in glucose metabolism via down-regulation of the AKT/ERK pathway and eventually altered the malignant phenotype in lung cancer cells.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s12944-019-1058-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6533754PMC
May 2019

Increased Serum Romo1 Was Correlated with Lung Function, Inflammation, and Oxidative Stress in Chronic Obstructive Pulmonary Disease.

Inflammation 2019 Oct;42(5):1555-1560

Department of Respiratory Medicine, Nanjing First Hospital, Nanjing Medical University, No. 68, Changle Road, Qinhuai District, Nanjing, 210006, China.

Chronic obstructive pulmonary disease (COPD) is associated with abnormal inflammation and high oxidative stress. Studies suggest that reactive oxygen species modulator 1 (Romo1) involve in diseases associated with oxidative stress and inflammation. However, the relationship between COPD and Romo1 is still not clear. In this study, we compared serum Romo1 in 49 COPD patients and 34 health controls, and their correlation with lung function, systematic inflammation, and oxidative stress. In addition, serum levels of Romo1, C-reactive protein (CRP), and oxidative stress (measured by reactive oxygen species, ROS) were analyzed using commercial kits. Serum Romo1 was significantly higher in COPD patients than that of control (132.24 ± 10.34 vs. 93.26 ± 7.75 pg/ml, P < 0.05). Serum CRP and ROS were also significantly higher in COPD patients. Serum Romo1 was correlated inversely with FEV1% predicted in COPD patients (푟 = - 0.347, 푃 = 0.016), while it was correlated positively with CRP and ROS levels, respectively. These results suggest that serum Romo1 increase in COPD patients and that these levels are associated with lung function, inflammation, and oxidative stress in COPD.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10753-019-01017-xDOI Listing
October 2019

Prognostic Value of Plasma Fibrinogen in Lung Cancer Patients: A Meta-Analysis.

J Cancer 2018 10;9(21):3904-3911. Epub 2018 Oct 10.

Department of Respiration, Nanjing First Hospital, Nanjing Medical University, Nanjing, People's Republic of China.

The prognostic role of plasma fibrinogen in lung cancer remains controversial. The aim of this meta-analysis was to assess the prognostic value of plasma fibrinogen in lung cancer. We performed a systematic literature search to identify eligible studies in PubMed, Embase and the Cochrane Library database. The hazard ratios (HR) and their 95% confidence intervals (CI) were collected from these eligible studies and were used to assess the relationship between plasma fibrinogen and lung cancer. A total of 16 studies including 6,881 patients were selected in this meta-analysis. The results showed that elevated plasma fibrinogen in lung cancer patients was correlated with poor overall survival (OS) (HR = 1.38, 95% CI: 1.22-1.55, P < 0.001) and disease-free survival (DFS) / progress-free survival (PFS). (HR = 1.29, 95% CI: 1.01-1.65, P = 0.042). When stratified by cut-off value for OS and DFS/PFS, there was no significant heterogeneity. And the results of "cut-off value ≥ 400mg/dl" group showed that the high level of fibrinogen in serum was associated with worse OS and DFS/PFS of lung cancer. In further subgroup analysis by tumor histology, high plasma fibrinogen was also associated with worse OS in non-small cell lung cancer (NSCLC) (HR = 1.32, 95% CI: 1.14-1.53, P < 0.001). However, there was no significant association between high plasma fibrinogen and poor DFS in NSCLC patients (HR = 1.24, 95% CI: 0.97-1.57, P = 0.08). The Egger's regression test indicated evidence of publication bias for DFS/PFS. Elevated plasma fibrinogen, particularly defined as a plasma fibrinogen concentration of ≥ 400mg/dl, could be a promising indicator for worse OS in lung cancer patients, including NSCLC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.7150/jca.26360DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6218779PMC
October 2018

Serum Romo1 is significantly associated with disease severity in patients with obstructive sleep apnea syndrome.

Sleep Breath 2018 09 4;22(3):743-748. Epub 2018 Jan 4.

Department of Respiratory Medicine, Nanjing First Hospital, Nanjing Medical University, No. 68, Changle Road, Qinhuai District, Nanjing, 210006, China.

Purpose: We aim to evaluate reactive oxygen species modulator 1 (Romo1) levels in obstructive sleep apnea syndrome (OSAS) and analyze its possible relationships to OSAS severity, reactive oxygen species (ROS), and C-reactive protein (CRP). Additionally, we also investigated the effects of nasal continuous positive airway pressure (nCPAP) on serum Romo1.

Methods: One hundred and five patients diagnosed with OSAS were classified into the OSAS group, and 41 subjects without OSAS were recruited for the control group. The OSAS group was further divided into mild, moderate, and severe OSAS subgroups. Fifteen patients with moderate and severe OSAS were treated with nCPAP. Serum levels of Romo1, ROS, and CRP were also measured.

Results: Serum Romo1, ROS, and CRP were the lowest in normal subjects and increased across OSAS severities (P < 0.05). Univariate analysis showed that serum Romo1 was positively correlated with apnea-hypopnea index (AHI), oxygen desaturation index (ODI), time spent below 90% oxygen saturation (Ts90%), arousal index, ROS, and CRP, and was negatively correlated with minimal oxygen saturation (miniSaO) (all P < 0.05). Multiple linear regression analysis showed that serum Romo1 level was significantly associated with AHI and ODI, after adjusting for age, gender, BMI, and CRP. After 6 months of nCPAP therapy, serum Romo1, ROS, and CRP were significantly decreased (P < 0.05).

Conclusions: The increase of serum Romo1 in OSAS patients was positively correlated with disease severity. Serum Romo1 may be an important parameter for monitoring the severity of OSAS and treatment efficiency.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s11325-017-1606-2DOI Listing
September 2018

HE4 expression in lung cancer, a meta-analysis.

Clin Chim Acta 2017 Jul 9;470:109-114. Epub 2017 May 9.

Department of Respiration, Nanjing First Hospital, Nanjing Medical University, 68 Changle Road, Nanjing, Jiangsu 210006, People's Republic of China. Electronic address:

Background: The prognostic role of Human epididymis protein 4 (HE4) expression in lung cancer remains controversial. We performed this meta-analysis to assess the prognostic value of HE4 expression in lung cancer.

Methods: A systematic literature search was conducted to identify eligible studies in PubMed, Embase and Wanfang databases. The pooled hazard ratios (HRs) and their 95% confidence intervals (CIs) were used to assess the relationship.

Results: A total of 1412 patients from 8 studies were included in this meta-analysis. The results of univariate analysis (HR=1.73, 95% CI: 1.19-2.52, P=0.004) and multivariate analysis (HR=2.49, 95% CI: 1.89-3.28, P<0.001) demonstrated that high HE4 expression in lung cancer patients was correlated with poor overall survival (OS). We observed through further stratified analysis of the results of the univariate analysis that high HE4 expression was associated with worse OS in Asian lung cancer patients (HR=2.48, 95% CI: 1.88-3.26, P<0.001). However, there was no significant association between high HE4 expression and poor OS in Caucasian patients (HR=1.12, 95% CI: 0.80-1.55, P=0.513).

Conclusion: High serum HE4 level was a marker of poor prognosis in lung cancer patients, particularly in Asian patients with lung cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.cca.2017.05.007DOI Listing
July 2017

Increased risk of developing lung cancer in Asian patients carrying the TERT rs2736098 G>A polymorphism: evidence from 3,354 cases and 3,518 controls.

Onco Targets Ther 2015 30;8:2757-65. Epub 2015 Sep 30.

Department of Medical Oncology, Nantong University Affiliated Tumor Hospital, Nantong, People's Republic of China.

Background: The association between telomerase reverse transcriptase (TERT) rs2736098 G>A and risk of lung cancer (LC) remains inconclusive. To explore the association more precisely, we performed a comprehensive search and conducted a meta-analysis on all eligible case-control studies involving 3,354 cases and 3,518 controls.

Methods: The 95% confidence interval (95% CI) and the pooled odds ratio (OR) were calculated using a random or fixed effect model. Publication bias, heterogeneity, and sensitivity analysis were also explored.

Results: All studies were case-control studies on LC in patients of Asian descent, consisting of one Korean study and five Chinese studies. Overall, the variant A allele of TERT rs2736098 G>A was found to significantly increase the risk of LC in all genetic models (GA vs GG: OR =1.13, 95% CI =1.02-1.25, P=0.017; AA vs GG: OR =1.78, 95% CI =1.53-2.07, P<0.001; GA/AA vs GG: OR =1.25, 95% CI =1.14-1.38, P<0.001; AA vs

Ga/gg: OR =1.66, 95% CI =1.45-1.92, P<0.001). In the subgroup analysis, significant associations were found in Chinese group and hospital-based studies. Different genotype test methods showed no influence on the final results.

Conclusion: Our study identified that TERT rs2736098 G>A polymorphism significantly increased the risk of LC in Asian populations.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.2147/OTT.S87534DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4599062PMC
October 2015

Modulation of NF-κB/miR-21/PTEN pathway sensitizes non-small cell lung cancer to cisplatin.

PLoS One 2015 23;10(3):e0121547. Epub 2015 Mar 23.

Department of Respiratory Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.

Background: Platinum-based chemotherapy is a standard strategy for non-small cell lung cancer (NSCLC), while chemoresistance remains a major therapeutic challenge in current clinical practice. Our present study was aimed to determine whether inhibition of the NF-κB/miR-21/PTEN pathway could increase the sensitivity of NSCLC to cisplatin.

Methods: The expression of miR-21 in NSCLC tissues was determined using in situ hybridization. Next, the effect of miR-21 on the sensitivity of A549 cells to cisplatin was determined in vitro. Whether miR-21 regulated PTEN expression was assessed by luciferase assay. Furthermore, whether NF-κB targeted its binding elements in the miR-21 gene promoter was determined by luciferase and ChIP assay. Finally, we measured the cell viability and apoptosis under cisplatin treatment when NF-κB was inhibited.

Results: An elevated level of miR-21 was observed in NSCLC lung tissues and was related to a short survival time. Exogenous miR-21 promoted cell survival when exposed to cisplatin, while miR-21 inhibition could reverse this process. The RNA and protein levels of PTEN were significantly decreased by exogenous miR-21, and the 3'-untranslated region of PTEN was shown to be a target of miR-21. The expression of miR-21 was regulated by NF-κB binding to its element in the promoter, a finding that was verified by luciferase and ChIP assay. Hence, inhibition of NF-κB by RNA silencing protects cells against cisplatin via decreasing miR-21 expression.

Conclusion: Modulation of the NF-κB/miR-21/PTEN pathway in NSCLC showed that inhibition of this pathway may increase cisplatin sensitivity.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0121547PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370674PMC
February 2016

A liver-X-receptor ligand, T0901317, attenuates IgE production and airway remodeling in chronic asthma model of mice.

PLoS One 2014 28;9(3):e92668. Epub 2014 Mar 28.

Department of Respiratory Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.

The liver-X-receptors have shown anti-inflammatory ability in several animal models of respiratory disease. Our purpose is to investigate the effect of LXR ligand in allergen-induced airway remodeling in mice. Ovalbumin-sensitized mice were chronically challenged with aerosolized ovalbumin for 8 weeks. Some mice were administered a LXR agonist, T0901317 (12.5, 25, 50 mg/kg bodyweight) before challenge. Then mice were evaluated for airway inflammation, airway hyperresponsiveness and airway remodeling. T0901317 failed to attenuate the inflammatory cells and Th2 cytokines in bronchoalveolar lavage fluid. But the application of T0901317 reduced the thickness of airway smooth muscle and the collagen deposition. Meanwhile, T0901317 treatment evidently abolished the high level of OVA-specific IgE, TGF-β1 and MMP-9 in lung. So LXRs may attenuate the progressing of airway remodeling, providing a potential treatment of asthma.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0092668PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969355PMC
June 2015

Clinic significance of microRNA-99a expression in human lung adenocarcinoma.

J Surg Oncol 2013 Sep 24;108(4):248-55. Epub 2013 Jul 24.

Department of Respiratory Medicine, Nanjing First Hospital, Nanjing Medical University, No. 68 Changle Road, Jiangsu Province, Nanjing City, China.

Background: The purpose of this study was to investigate the clinical significance of microRNA-99a expression in lung adenocarcinoma.

Methods: qRT-PCR assay was performed to detect miR-99a expression in lung adenocarcinoma cells or tissues. The correlations of miR-99a expression with clinicopathological factors and prognosis of lung adenocarcinoma patients were analyzed. The effects of miR-99a expression on growth and apoptosis of lung adenocarcinoma cell line and its potential target gene were determined by MTT, flow cytometry, luciferase reporter, and Western blot assays.

Results: The relative miR-99a expression in lung adenocarcinoma cells was significantly lower than that in normal lung bronchial epithelium cell line. Also, miR-99a expression in lung adenocarcinoma tissues was significantly lower than that in corresponding nontumor tissues. Low miR-99a expression was found to be closely correlated with advanced clinical stage and lymph node metastasis. Kaplan-Meier survival and Cox regression analyses showed that the status of miR-99a expression was an independent prognosis factor for lung adenocarcinoma patients. Functional analyses showed that upregulation of miR-99a could inhibit growth and induce apoptosis in lung adenocarcinoma cells by targeting mTOR.

Conclusion: Low MiR-99a expression was a poor prognostic factor for patients with lung adenocarcinoma, and miR-99a functions as a tumor suppressor by targeting mTOR.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/jso.23381DOI Listing
September 2013