Publications by authors named "Yongjian Xu"

204 Publications

Green and sustainable cellulose-derived humidity sensors: A review.

Carbohydr Polym 2021 Oct 29;270:118385. Epub 2021 Jun 29.

Department of Chemical Engineering, University of New Brunswick, Fredericton, New Brunswick E3B 5A3, Canada. Electronic address:

Cellulose, as the most abundant natural polysaccharide, is an excellent material for developing green humidity sensors, especially due to its humidity responsiveness as a result of its rich hydrophilic groups. In combination with other components including carbon materials and polymers, cellulose and its derivatives can be used to design high-performance humidity sensors that meet various application requirements. This review summarizes the recent advances in the field of various cellulose-derived humidity sensors, with particular attention paid to different sensing mechanisms including resistance, capacitance, colorimetry and gravity, and so on. Furthermore, the roles of cellulose and its derivatives are highlighted. This work may promote the development of cellulose-derived humidity sensors, as well as other cellulose-based intelligent materials.
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http://dx.doi.org/10.1016/j.carbpol.2021.118385DOI Listing
October 2021

Association of fine particulate matter air pollution and its constituents with lung function: The China Pulmonary Health study.

Environ Int 2021 11 26;156:106707. Epub 2021 Jun 26.

Department of Respiratory and Critical Care Medicine, Beijing Hospital, Beijing, China; National Center of Gerontology, Beijing, China.

The associations of long-term exposure to various constituents of fine particulate matter (≤2.5 μm in aerodynamic diameter, PM) air pollution with lung function were not clearly elucidated in developing countries. The aim was to evaluate the associations of long-term exposure to main constituents of PM with lung function in China. This is a nationwide, cross-sectional analysis among 50,991 study participants from the China Pulmonary Health study. Multivariable linear regression models were used to obtain differences of forced expiratory volume in 1 s (FEV), forced vital capacity (FVC), FEV/FVC, peak expiratory flow (PEF), and forced expiratory flow at 25-75% of exhaled FVC (FEF) associated with an interquartile range (IQR) change of PM or its constituents. Residential annual PM levels varied from 26 μg/m to 92 μg/m (average: 53 μg/m). An IQR increase of PM concentrations was associated with lower FEV (19.82 mL, 95% CI: 11.30-28.33), FVC (17.45 mL, 95% CI: 7.16-27.74), PEF (86.64 mL/s, 95% CI: 59.77-113.52), and FEF (31.93 mL/s, 95% CI: 16.64-47.22). Black carbon, organic matter, ammonium, sulfate, and nitrate were negatively associated with most lung function indicators, with organic matter and nitrate showing consistently larger magnitude of associations than PM mass. This large-scale study provides first-hand epidemiological evidence that long-term exposure to ambient PM and some constituents, especially organic matter and nitrate, were associated with lower large- and small- airway function.
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http://dx.doi.org/10.1016/j.envint.2021.106707DOI Listing
November 2021

Treatment of steroid-resistant checkpoint inhibitor pneumonitis with pirfenidone: A case report.

Thorac Cancer 2021 08 18;12(15):2214-2216. Epub 2021 Jun 18.

Department of Pulmonary and Critical Care Medicine, Peking Union Medical Hospital, Chinese Academy of Medical Science & Peking Union Medical College, Beijing, China.

With the increased use of immune checkpoint inhibitors (ICIs) in lung cancer, which are of great benefit to patients, more and more immune-related adverse events (irAEs) are being reported. Checkpoint inhibitor pneumonitis (CIP) is one of the most challenging adverse events, which pose a huge challenge to clinical diagnosis and treatment, and its incidence in the real world is greatly underestimated. Currently, the treatment of CIP mainly depends on the use of glucocorticoids. As for steroid-resistant CIP, there is no unified standardized treatment strategy. Herein, we report a case of steroid-resistant CIP induced by pembrolizumab in a patient with advanced non-small cell lung cancer (NSCLC), in which their symptoms were successfully controlled with pirfenidone.
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http://dx.doi.org/10.1111/1759-7714.13921DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8327698PMC
August 2021

Local administration of liposomal-based Srpx2 gene therapy reverses pulmonary fibrosis by blockading fibroblast-to-myofibroblast transition.

Theranostics 2021 13;11(14):7110-7125. Epub 2021 May 13.

Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of National Health Commission, Key Site of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, 1095 Jiefang Ave, Wuhan 430030, China.

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive fatal interstitial lung disease characterized by abnormal transition and proliferation of fibroblasts. The uncontrolled transition of fibroblasts, commonly known as myofibroblasts, are the principal source of the enormous extracellular matrix (ECM) depositing in lung parenchyma, leading to gradual failure of gas exchange and mortality of the patients. However, up to now, rare effective therapeutic strategies have been developed to blockade fibroblast-to-myofibroblast transition (FMT) in IPF. We illustrated that the lungs originated from IPF patients and mice with pulmonary fibrosis are characterized by the overexpression of sushi-repeat-containing protein, X-linked 2 (SRPX2). Further functionality studies identified the pivotal role of SRPX2 in FMT. Mechanistically, SRPX2 was involved in a TGFβR1/SMAD3/SRPX2/AP1/SMAD7 positive feedback loop. Specifically, SRPX2 was upregulated by TGF-β1 in a TGFβR1/SMAD3-dependent manner, after which SRPX2 in turn repressed the expression of AP1, subsequently minimized SMAD7 expression, through which it reduced the formation of inhibitory complex with TGFβR1 and enhanced SMAD signaling pathway to promote FMT and exacerbate pulmonary fibrosis. Notably, intratracheal administration of siRNA-loaded liposomes could effectively suppress the expression of Srpx2 in the lung and remarkably protect mice against BLM-induced pulmonary fibrosis, concomitant with a significant reduction of FMT. Accordingly, these data indicate that Srpx2 plays an essential role in the pathogenesis of pulmonary fibrosis and suggests the strategy aiming at silencing Srpx2 could be a promising therapeutic approach against pulmonary fibrosis in clinical settings.
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http://dx.doi.org/10.7150/thno.61085DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8171094PMC
August 2021

Dopamine receptor agonists ameliorate bleomycin-induced pulmonary fibrosis by repressing fibroblast differentiation and proliferation.

Biomed Pharmacother 2021 Jul 23;139:111500. Epub 2021 Apr 23.

Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, 1095 Jiefang Ave, Wuhan 430030, China. Electronic address:

Idiopathic pulmonary fibrosis (IPF) is the most common fatal interstitial lung disease, with limited therapeutic options. The abnormal and uncontrolled differentiation and proliferation of fibroblasts have been confirmed to play a crucial role in driving the pathogenesis of IPF. Therefore, effective and well-tolerated antifibrotic agents that interfere with fibroblasts would be an ideal treatment, but no such treatments are available. Remarkably, we found that dopamine (DA) receptor D1 (D1R) and DA receptor D2 (D2R) were both upregulated in myofibroblasts in lungs of IPF patients and a bleomycin (BLM)-induced mouse model. Then, we explored the safety and efficacy of DA, fenoldopam (FNP, a selective D1R agonist) and sumanirole (SMR, a selective D2R agonist) in reversing BLM-induced pulmonary fibrosis. Further data showed that DA receptor agonists exerted potent antifibrotic effects in BLM-induced pulmonary fibrosis by attenuating the differentiation and proliferation of fibroblasts. Detailed pathway analysis revealed that DA receptor agonists decreased the phosphorylation of Smad2 induced by TGF-β1 in primary human lung fibroblasts (PHLFs) and IMR-90 cells. Overall, DA receptor agonists protected mice from BLM-induced pulmonary fibrosis and may be therapeutically beneficial for IPF patients in a clinical setting.
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http://dx.doi.org/10.1016/j.biopha.2021.111500DOI Listing
July 2021

Longitudinal Expression of Testicular from Prepuberty to Sexual Maturity in Congjiang Xiang Pigs.

Animals (Basel) 2021 Feb 8;11(2). Epub 2021 Feb 8.

College of Animal Science, Guizhou University, Guiyang 550025, China.

Testicular expression of taste receptor type 1 subunit 3 (T1R3), a sweet/umami taste receptor, has been implicated in spermatogenesis and steroidogenesis in mice. We explored the role of testicular T1R3 in porcine postnatal development using the Congjiang Xiang pig, a rare Chinese miniature pig breed. Based on testicular weights, morphology, and testosterone levels, four key developmental stages were identified in the pig at postnatal days 15-180 (prepuberty: 30 day; early puberty: 60 day; late puberty: 90 day; sexual maturity: 120 day). During development, testicular T1R3 exhibited stage-dependent and cell-specific expression patterns. In particular, T1R3 levels increased significantly from prepuberty to puberty ( < 0.05), and expression remained high until sexual maturity ( < 0.05), similar to results for phospholipase Cβ2 (PLCβ2). The strong expressions of T1R3/PLCβ2 were observed at the cytoplasm of elongating/elongated spermatids and Leydig cells. In the eight-stage cycle of the seminiferous epithelium in pigs, T1R3/PLCβ2 levels were higher in the spermatogenic epithelium at stages II-VI than at the other stages, and the strong expressions were detected in elongating/elongated spermatids and residual bodies. The message RNA (mRNA) levels of taste receptor type 1 subunit 1 (T1R1) in the testis showed a similar trend to levels of T1R3. These data indicate a possible role of T1R3 in the regulation of spermatid differentiation and Leydig cell function.
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http://dx.doi.org/10.3390/ani11020437DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7916009PMC
February 2021

Correction: IL-24 deficiency protects mice against bleomycin-induced pulmonary fibrosis by repressing IL-4-induced M2 program in macrophages.

Cell Death Differ 2021 Jan 5. Epub 2021 Jan 5.

The Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Key Cite of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, 1095 Jiefang Ave, Wuhan, 430030, China.

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http://dx.doi.org/10.1038/s41418-020-00721-8DOI Listing
January 2021

Suppressing Sart1 to modulate macrophage polarization by siRNA-loaded liposomes: a promising therapeutic strategy for pulmonary fibrosis.

Theranostics 2021 1;11(3):1192-1206. Epub 2021 Jan 1.

Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Key Site of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, 1095 Jiefang Ave, Wuhan 430030, China.

Idiopathic pulmonary fibrosis (IPF) is a chronic and diffuse form of interstitial lung disease of unknown etiology with a fatal outcome. Although various strategies for IPF have been developed over the last few decades, no significant positive impact on the prognosis of IPF has been observed. According to the current paradigm, macrophages have been recognized to play a significant role in IPF pathogenesis. Here, we report a potential nanomedicine-based gene therapy for IPF based on regulate macrophage polarization. C57BL/6 mice were obtained and used to establish a bleomycin (BLM)-induced pulmonary fibrosis animal model, and siRNA-loaded liposomes were designed for experiment. The experimental animals were administered BLM intratracheally on day 0 and treated with siRNA on days 14 and 17. In the experiment, we further examined the function of Sart1 in macrophages. Our data indicated that the liposomes could passively target the fibrotic area in the lung and efficiently accumulate in macrophages. The suppression of Sart1 by siRNA-loaded liposomes significantly protected mice against BLM-induced lung injury and fibrosis, which was attributed to attenuated M2 macrophage infiltration in the lung. Our study provides a valuable reference for modulating macrophage polarization and a promising strategy for the treatment of pulmonary fibrosis in clinical settings.
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http://dx.doi.org/10.7150/thno.48152DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7738894PMC
July 2021

The preventive and therapeutic effects of AAV1-KLF4-shRNA in cigarette smoke-induced pulmonary hypertension.

J Cell Mol Med 2021 01 20;25(2):1238-1251. Epub 2020 Dec 20.

Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

We found previously that KLF4 expression was up-regulated in cultured rat and human pulmonary artery smooth muscle cells (PASMCs) exposed to cigarette smoke (CS) extract and in pulmonary artery from rats with pulmonary hypertension induced by CS. Here, we aim to investigate whether CS-induced pulmonary hypertension (PH) is prevented and ameliorated by targeted pulmonary vascular gene knockdown of KLF4 via adeno-associated virus 1 (AAV1)-KLF4-shRNA in vivo in rat model. The preventive and therapeutic effects were observed according to the different time-point of AAV1-KLF4-shRNA intratracheal administration. We tested haemodynamic measurements of systemic and pulmonary circulations and observed the degree of pulmonary vascular remodelling. In the preventive experiment, KLF4 expression and some pulmonary circulation hemodynamic measurements such as right ventricular systolic pressure (RVSP), mean right ventricular pressure (mRVP), peak RV pressure rate of rise (dP/dt max) and right ventricle (RV) contractility index were increased significantly in the CS-induced PH model. While in the prevention group (AAV1-KLF4-shRNA group), RVSP, mRVP, dP/dt max and RV contractility index which are associated with systolic function of right ventricle decreased and the degree of pulmonary vascular remodelling relieved. In the therapeutic experiment, we observed a similar trend. Our findings emphasize the feasibility of sustained pulmonary vascular KLF4 gene knockdown using intratracheal delivery of AAV1 in an animal model of cigarette smoke-induced PH and determined gene transfer of KLF4-shRNA could prevent and ameliorate the progression of PH.
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http://dx.doi.org/10.1111/jcmm.16194DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812256PMC
January 2021

MBD2 serves as a viable target against pulmonary fibrosis by inhibiting macrophage M2 program.

Sci Adv 2021 01 1;7(1). Epub 2021 Jan 1.

The Center for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, 1095 Jiefang Ave., Wuhan 430030, China.

Despite past extensive studies, the mechanisms underlying pulmonary fibrosis (PF) still remain poorly understood. Here, we demonstrated that lungs originating from different types of patients with PF, including coronavirus disease 2019, systemic sclerosis-associated interstitial lung disease, and idiopathic PF, and from mice following bleomycin (BLM)-induced PF are characterized by the altered methyl-CpG-binding domain 2 (MBD2) expression in macrophages. Depletion of Mbd2 in macrophages protected mice against BLM-induced PF. deficiency significantly attenuated transforming growth factor-β1 (TGF-β1) production and reduced M2 macrophage accumulation in the lung following BLM induction. Mechanistically, Mbd2 selectively bound to the promoter in macrophages, by which it repressed Ship expression and enhanced PI3K/Akt signaling to promote the macrophage M2 program. Therefore, intratracheal administration of liposomes loaded with siRNA protected mice from BLM-induced lung injuries and fibrosis. Together, our data support the possibility that MBD2 could be a viable target against PF in clinical settings.
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http://dx.doi.org/10.1126/sciadv.abb6075DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7775789PMC
January 2021

A Model Using Support Vector Machines Recursive Feature Elimination (SVM-RFE) Algorithm to Classify Whether COPD Patients Have Been Continuously Managed According to GOLD Guidelines.

Int J Chron Obstruct Pulmon Dis 2020 4;15:2779-2786. Epub 2020 Nov 4.

Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences & Technology, Wuhan, People's Republic of China.

Purpose: Patients with chronic obstructive pulmonary disease (COPD) would have a poor prognosis if they were not continuously managed according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. We aim to develop a model to classify whether COPD patients have been continuously managed according to GOLD in the previous year.

Methods: The Managed group were COPD patients from a prospective cohort from November 2017 to November 2019, who have been continuously managed according to GOLD for 1 year. The Control group were COPD patients who were not continuously managed according to GOLD. They were from a retrospective cohort from October 2016 to October 2017 in the same hospitals as the Managed group. A synthetic minority over-sampling technique (SMOTE) algorithm was used to up-sample the Managed group in a training dataset. Features for classification were selected using a support vector machine recursive feature elimination (SVM-RFE) algorithm. The classification model was developed using LibSVM, and its performance was assessed on the testing dataset.

Results: The final analysis included 15 subjects in the Managed group and 191 in the Control group. SVM-RFE selects nine features including smoking history, post-bronchodilator (post-)FVC before management, and those after 1-year follow-up (BMI, moderate and severe AECOPD frequency in previous 12 months, mMRC score, post-FEV1, post-FEV1%pred, post-FVC, and post-FEV1/FVC). For our model, positive predictive value is 66.7%, F1 score is 0.978, and AUC is 0.987.

Conclusion: SVM classifier combined with SVM-REF feature selection algorithm could achieve good classification between COPD patients who are or are not continuously managed. This model could be applied in clinical practice to help doctors make decisions and enhance COPD patients' compliance with standard treatment.
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http://dx.doi.org/10.2147/COPD.S271237DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7649211PMC
June 2021

Exploration of plasma interleukin-27 levels in asthma patients and the correlation with lung function.

Respir Med 2020 12 29;175:106208. Epub 2020 Oct 29.

Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Respiratory Diseases, National Ministry of Health of the People's Republic of China and National Clinical Research Center for Respiratory Disease, Wuhan, China. Electronic address:

Background: IL-27 attenuates allergic inflammation and improves lung function in mouse models of allergic asthma. However, plasma IL-27 levels of asthma patients and the association with clinical features remain poorly understood.

Methods: This study examined plasma IL-27 protein expression in untreated asthma patients and controls, analyzed its correlation with Th2 inflammation and lung function, and evaluated the effect of corticosteroids on IL-27 expression.

Results: Plasma IL-27 levels were lower in untreated asthma patients compared to controls. Plasma IL-27 levels were inversely correlated with sputum IL-5 mRNA expression in Th2 group. The Th2IL-27 subgroup suffered from the highest airway hyperresponsiveness (AHR) and the worst pulmonary function. The patients in Th2IL-27 subgroup were less likely to be atopic and had the worst improvement of symptoms after four weeks of standard treatment. In vitro, dexamethasone could decrease the expression of IL-27 in THP-1 cell line. The majority of asthma patients had further decreased IL-27 levels after standard treatment, whereas patients with sustained high levels of IL-27 post-treatment had more blood neutrophils at baseline compared with those without.

Conclusions: The results indicate that low levels of IL-27 in peripheral blood are closely related to Th2 inflammation and lung function of asthma patients. Low IL-27 levels in combination with high Th2 inflammation identify an asthma phenotype with high AHR and substantial response to corticosteroids. Understanding of this interaction could help to elucidate the inherent inflammation heterogeneity of asthma.
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http://dx.doi.org/10.1016/j.rmed.2020.106208DOI Listing
December 2020

IL-24 deficiency protects mice against bleomycin-induced pulmonary fibrosis by repressing IL-4-induced M2 program in macrophages.

Cell Death Differ 2021 Apr 3;28(4):1270-1283. Epub 2020 Nov 3.

The Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Key Cite of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, 1095 Jiefang Ave, Wuhan, 430030, China.

Idiopathic pulmonary fibrosis (IPF) is the most common type of idiopathic interstitial pneumonia and has one of the poorest prognosis. However, the molecular mechanisms underlying IPF progression remain largely unknown. In this study, we determined that IL-24, an IL-20 subfamily cytokine member, was increased both in the serum of IPF patients and the bronchoalveolar lavage fluid (BALF) of mice following bleomycin (BLM)-induced pulmonary fibrosis. As a result, IL-24 deficiency protected mice from BLM-induced lung injury and fibrosis. Specifically, loss of IL-24 significantly attenuated transforming growth factor β1 (TGF-β1) production and reduced M2 macrophage infiltration in the lung of BLM-induced mice. Mechanistically, IL-24 alone did not show a perceptible impact on the induction of M2 macrophages, but it synergized with IL-4 to promote M2 program in macrophages. IL-24 suppressed IL-4-induced expression of suppressor of cytokine signaling 1 (SOCS1) and SOCS3, through which it enhanced signal transducer and activator of transcription 6/peroxisome proliferator-activated receptor gamma (STAT6/PPARγ) signaling, thereby promoting IL-4-induced production of M2 macrophages. Collectively, our data support that IL-24 synergizes with IL-4 to promote macrophage M2 program contributing to the development of pulmonary fibrosis.
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http://dx.doi.org/10.1038/s41418-020-00650-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8027679PMC
April 2021

Integrating phosphotungstic acid-assisted prerefining with cellulase treatment for enhancing the reactivity of kraft-based dissolving pulp.

Bioresour Technol 2021 Jan 20;320(Pt A):124283. Epub 2020 Oct 20.

College of Bioresources Chemical and Materials Engineering, Shaanxi Provincial Key Laboratory of Papermaking Technology and Specialty Paper Development, Shaanxi University of Science and Technology, Xi'an 710021, China; Department of Chemical Engineering, University of New Brunswick, Fredericton, New Brunswick E3B 5A3, Canada.

Viscosity control and reactivity enhancement are of practical importance for high-quality dissolving pulp manufacturing. In this work, we demonstrate a two-step activating process consisting of a phosphotungstic acid (PTA)-assisted prerefining (PTA/R pretreatment), followed by cellulase treatment for this purpose. The cellulase adsorption can increase from 29.1% to 49.7% as a result of PTA/R pretreatment (8000 r at 90 °C). The viscosity of the resultant pulp decreases from 665 to 430 mL/g, while its Fock reactivity increases from 31.5% to 74.4% under a low-loading cellulase treatment (0.5 mg cellulase /g odp), which mainly due to the fact that the PTA/R pretreatment can increase fiber accessibility and viscosity control, thus facilitating cellulase adsorption and reaction efficiency. Moreover, PTA also shows a high recyclability/ reusability (more than 86%) during the PTA/R pretreatment. Therefore, the new proposed two-step activating process provides a green, and efficient pathway for large-scale manufacturing of high-quality dissolving pulp.
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http://dx.doi.org/10.1016/j.biortech.2020.124283DOI Listing
January 2021

Serum Levels of Gamma-Glutamyltransferase During Stable and Acute Exacerbations of Chronic Obstructive Pulmonary Disease.

Med Sci Monit 2020 Oct 22;26:e927771. Epub 2020 Oct 22.

Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China (mainland).

BACKGROUND One of the most important factors in the pathogenesis of COPD (chronic obstructive pulmonary disease) is oxidative stress. GGT (gamma-glutamyltransferase) has been regarded as a novel marker of oxidative stress over the last few years. This study aimed to compare the serum levels of GGT during stable and acute exacerbations of COPD at a single center. MATERIAL AND METHODS The research included 117 patients with AECOPD (acute exacerbation of chronic obstructive pulmonary disease), 107 patients with stable COPD, and 112 control subjects. Serum GGT, spirometry function, and other clinical parameters (anthropometric and biochemical measurements) were evaluated and compared among the subjects. RESULTS Serum GGT was elevated in patients with stable COPD in comparison to the control subjects. Its level was inversely related to lung function. It was also significantly higher in AECOPD patients compared to stable COPD patients. We also found that a GGT level of 21.2 IU/L displays a reliable diagnostic prediction of COPD and that a GGT level of 26.5 IU/L can be applied to predict the exacerbation of COPD. CONCLUSIONS Our research demonstrates that serum GGT level is inversely associated with pulmonary function and may serve as a biomarker during the progression of COPD. The monitoring of GGT values can be applied to evaluating COPD and its exacerbation risk.
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http://dx.doi.org/10.12659/MSM.927771DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7590526PMC
October 2020

Changing Income-Related Inequality in Daily Nutrients Intake: A Longitudinal Analysis from China.

Int J Environ Res Public Health 2020 10 19;17(20). Epub 2020 Oct 19.

School of Public Policy and Administration, Xi'an Jiaotong University, Xi'an 710049, China.

Because of economic reform, dietary pattern in China changed rapidly during the past two decades. Meanwhile, the changes of income and nutrients intake had the same trend. This study aims to measure the income-related inequality in daily nutrients intake and its health-related income mobility over time. Data was sourced from four waves of China Health and Nutrition Survey. Concentration indexes and health-related income mobility indexes were employed to measure the income-related inequality of nutrients intake and its change over time. This study found that the daily protein intake, daily fat intake, daily energy intake, and proportion of energy from fat over 30% were more concentrated on the rich, whereas daily carbohydrates intake among the poor. The income-related inequalities were more severe than the cross-sectional perspective in the long run. The dynamic change of urbanisation indexes has resulted that over 30% of energy from fat was more concentrated among the rich and carbohydrates intake among the poor. The nutrition transition may bring about more severe disease economic burden to the poor in the future. This study recommends an approach to minimize gaps between rural and city areas by promoting rural revitalization to reduce the income-related inequality in daily nutrient intake.
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http://dx.doi.org/10.3390/ijerph17207627DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7588920PMC
October 2020

Indirubin alleviates bleomycin-induced pulmonary fibrosis in mice by suppressing fibroblast to myofibroblast differentiation.

Biomed Pharmacother 2020 Nov 11;131:110715. Epub 2020 Sep 11.

Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Key Cite of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, 1095 Jiefang Ave, Wuhan 430030, China. Electronic address:

Background And Objective: Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing interstitial lung disease with a poor prognosis. Indirubin, a compound obtained from indigo-bearing plants or mollusks of the family Muricidae, has various bioactivities, including anti-tumor activity and anti-inflammation effect. However, whether indirubin could mediate its therapeutic effects on bleomycin (BLM)-induced pulmonary fibrosis has not been addressed.

Methods: The impacts of indirubin on bleomycin (BLM)-induced pulmonary fibrosis were evaluated by pathological staining, western blot, RT-PCR and immunofluorescent staining. The effects of indirubin on fibroblast differentiation and related signaling were next investigated to demonstrate the underlying mechanisms.

Results: The results indicated that indirubin-treated mice exhibited a definitively improved survival rate than that of the BLM-induced mice in a dose-depend manner. Additionally, administration of indirubin significantly alleviated inflammatory cells infiltration in BLM mice. Importantly, indirubin provided protection for mice against BLM-induced pulmonary fibrosis as manifested by the attenuating expression of fibrotic hallmarks, including fibronectin, collagen I and α-smooth muscle actin (α-SMA). Subsequently, we providedin vitro evidence revealing that indirubin suppressed fibroblast to myofibroblast differentiation by repressed TGF-β/Smad signaling in a dose-dependent manner. Notably, our data showed that indirubin seemed to be safe in mice and fibroblasts.

Conclusion: Overall, indirubin could protect the mice against BLM-induced pulmonary fibrosis by alleviated fibroblast differentiation and may be therapeutically beneficial for IPF patients.
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http://dx.doi.org/10.1016/j.biopha.2020.110715DOI Listing
November 2020

Scutellarein inhibits BLM-mediated pulmonary fibrosis by affecting fibroblast differentiation, proliferation, and apoptosis.

Ther Adv Chronic Dis 2020 30;11:2040622320940185. Epub 2020 Jul 30.

Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Ave., Wuhan, 430030, China.

Introduction: Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible interstitial pulmonary disease that has a poor prognosis. Scutellarein, which is extracted from the traditional Chinese medicine , is used to treat a variety of diseases; however, the use of scutellarein for the treatment of pulmonary fibrosis and the related mechanisms of action have not been fully explored.

Methods: This study was conducted using a well-established mouse model of pulmonary fibrosis induced by bleomycin (BLM). The antifibrotic effects of scutellarein on histopathologic manifestations and fibrotic marker expression levels were examined. The effects of scutellarein on fibroblast differentiation, proliferation, and apoptosis and on related signaling pathways were next investigated to demonstrate the underlying mechanisms.

Results: In the present study, we found that scutellarein alleviated BLM-induced pulmonary fibrosis, as indicated by histopathologic manifestations and the expression levels of fibrotic markers. Further data demonstrated that the ability of fibroblasts to differentiate into myofibroblasts was attenuated in scutellarein-treated mice model. In addition, we obtained evidence that scutellarein inhibited fibroblast-to-myofibroblast differentiation by repressing TGF-β/Smad signaling, inhibited cellular proliferation by repressing PI3K/Akt signaling, and increased apoptosis of fibroblasts by affecting Bax/Bcl2 signaling.

Discussion: In general, scutellarein might exert therapeutic effects on pulmonary fibrosis by altering the differentiation, proliferation, and apoptosis of fibroblasts. Although scutellarein has been demonstrated to be safe in mice, further studies are required to investigate the efficacy of scutellarein in patients with IPF.
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http://dx.doi.org/10.1177/2040622320940185DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7418478PMC
July 2020

Advanced pneumonic type of lung adenocarcinoma: survival predictors and treatment efficacy of the tumor.

Tumori 2021 Jun 6;107(3):216-225. Epub 2020 Aug 6.

Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Purpose: To retrospectively explore the survival predictors and treatment efficacy of advanced pneumonic-type lung adenocarcinoma (P-ADC).

Methods: Retrospective analysis of clinical data and survival follow-up was undertaken on 41 patients with advanced P-ADC from January 1, 2009, to April 30, 2019. Analysis on tumor biomarkers such as carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), and the cytokeratin-19-fragment (Cyfra21-1) were undertaken. The patients in this study were divided into three groups based on usage of tyrosine kinase inhibitor (TKI): TKI therapy group (including combination with chemotherapy), non-TKI therapy group (chemotherapy alone), and palliative care group.

Results: More than half of the patients had higher levels of tumor biomarkers and the incidence of NSE was highest (81.8%), followed by CEA (74.4%) and Cyfra21-1 (74.1%). All patients had abnormal findings on chest computed tomography and with adenocarcinoma pathology. The overall survival (OS) time was 10.4 months in TKI group, 8.8 months in the non-TKI group, and 2.1 months in the palliative care group. Patients with higher level of serum Cyfra21-1 had insignificantly shorter survival time compared to those with normal Cyfra21-1 ( = 0.067). TKI therapy and non-TKI therapy provided a better prognosis prediction compared to palliative care. TKI therapy improved prognosis compared to non-TKI therapy. The comprehensive based TKI therapy provided improved OS vs the non-TKI therapy.

Conclusion: TKI-based therapy could improve the prognosis and OS for advanced P-ADC. This study recommends the analysis of mutations for all patients with advanced P-ADC.
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http://dx.doi.org/10.1177/0300891620947159DOI Listing
June 2021

Prevalence and risk factors of small airway dysfunction, and association with smoking, in China: findings from a national cross-sectional study.

Lancet Respir Med 2020 11 26;8(11):1081-1093. Epub 2020 Jun 26.

State Key Laboratory of Biotherapy of China and Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, China.

Background: Small airway dysfunction is a common but neglected respiratory abnormality. Little is known about its prevalence, risk factors, and prognostic factors in China or anywhere else in the world. We aimed to estimate the prevalence of small airway dysfunction using spirometry before and after bronchodilation, both overall and in specific population subgroups; assess its association with a range of lifestyle and environmental factors (particularly smoking); and estimate the burden of small airway dysfunction in China.

Methods: From June, 2012, to May, 2015, the nationally representative China Pulmonary Health study invited 57 779 adults to participate using a multistage stratified sampling method from ten provinces (or equivalent), and 50 479 patients with valid lung function testing results were included in the analysis. We diagnosed small airway dysfunction on the basis of at least two of the following three indicators of lung function being less than 65% of predicted: maximal mid-expiratory flow, forced expiratory flow (FEF) 50%, and FEF 75%. Small airway dysfunction was further categorised into pre-small airway dysfunction (defined as having normal FEV and FEV/forced vital capacity [FVC] ratio before bronchodilator inhalation), and post-small airway dysfunction (defined as having normal FEV and FEV/FVC ratio both before and after bronchodilator inhalation). Logistic regression yielded adjusted odds ratios (ORs) for small airway dysfunction associated with smoking and other lifestyle and environmental factors. We further estimated the total number of cases of small airway dysfunction in China by applying present study findings to national census data.

Findings: Overall the prevalence of small airway dysfunction was 43·5% (95% CI 40·7-46·3), pre-small airway dysfunction was 25·5% (23·6-27·5), and post-small airway dysfunction was 11·3% (10·3-12·5). After multifactor regression analysis, the risk of small airway dysfunction was significantly associated with age, gender, urbanisation, education level, cigarette smoking, passive smoking, biomass use, exposure to high particulate matter with a diameter less than 2·5 μm (PM) concentrations, history of chronic cough during childhood, history of childhood pneumonia or bronchitis, parental history of respiratory diseases, and increase of body-mass index (BMI) by 5 kg/m. The ORs for small airway dysfunction and pre-small airway dysfunction were similar, whereas larger effect sizes were generally seen for post-small airway dysfunction than for either small airway dysfunction or pre-small airway dysfunction. For post-small airway dysfunction, cigarette smoking, exposure to PM, and increase of BMI by 5 kg/m were significantly associated with increased risk, among preventable risk factors. There was also a dose-response association between cigarette smoking and post-small airway dysfunction among men, but not among women. We estimate that, in 2015, 426 (95% CI 411-468) million adults had small airway dysfunction, 253 (238-278) million had pre-small airway dysfunction, and 111 (104-126) million had post-small airway dysfunction in China.

Interpretation: In China, spirometry-defined small airway dysfunction is highly prevalent, with cigarette smoking being a major modifiable risk factor, along with PM exposure and increase of BMI by 5 kg/m. Our findings emphasise the urgent need to develop and implement effective primary and secondary prevention strategies to reduce the burden of this condition in the general population.

Funding: Ministry of Science and Technology of China; National Natural Science Foundation of China; National Health Commission of China.
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http://dx.doi.org/10.1016/S2213-2600(20)30155-7DOI Listing
November 2020

Absence of the MFG-E8 gene prevents hypoxia-induced pulmonary hypertension in mice.

J Cell Physiol 2021 01 27;236(1):587-600. Epub 2020 Jun 27.

Department of Respiratory and Critical Care Medicine, National Clinical Research Center of Respiratory Disease, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Pulmonary hypertension (PH) is a chronic vascular disease characterized by elevated pulmonary arterial resistance and vascular remodeling, and chronic hypoxia plays an important role in PH. Milk fat globule-EGF factor 8 (MFG-E8) is a glycoprotein that regulates cell proliferation and apoptosis, but its role in hypoxia-induced PH is unknown. The current study aimed to determine the function and fundamental mechanisms of MFG-E8 in hypoxia-induced PH. Herein, we exposed mice to hypoxia for 5 weeks, and MFG-E8 was found to be elevated in mouse lung tissues, arteries, and plasma. Compared with wild-type littermates, mice lacking MFG-E8 showed a significant increase in the ratio of pulmonary artery acceleration time to ejection time (PAT/PET), while they showed decreases in right ventricular systolic pressure, the Fulton's Index, percent medial wall thickness (%WT), and vascular muscularization in pulmonary arteries. In addition, MFG-E8 protein levels were also increased in the serum of patients with chronic PH. Similarly, we observed a higher expression of MFG-E8 in human pulmonary artery smooth muscle cells (PASMCs) in the presence of hypoxic stimulation than MFG-E8 in cells in normoxic conditions. Furthermore, MFG-E8 silencing resulted in partial inhibition of proliferation, migration and cell cycle progression in human PASMCs, and the possible mechanisms might involve the interaction between MFG-E8 and the p-Akt/cyclin D1 pathway. Collectively, our study suggests that the absence of MFG-E8 can attenuate the development of hypoxia-induced PH and vascular remodeling. MFG-E8 can be a potential therapeutic target or a biomarker for PH.
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http://dx.doi.org/10.1002/jcp.29885DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7689852PMC
January 2021

A multifunctional self-crosslinked chitosan/cationic guar gum composite hydrogel and its versatile uses in phosphate-containing water treatment and energy storage.

Carbohydr Polym 2020 Sep 29;244:116472. Epub 2020 May 29.

Department of Chemical Engineering, University of New Brunswick, Fredericton, New Brunswick E3B 5A3, Canada. Electronic address:

A new self-crosslinked composite hydrogel is prepared with chitosan (CS) and cationic guar gum (CGG), based on the imine and acetal chemistry for gelation. The CS/CGG hydrogel exhibits thermal/pH responsiveness, injectability, adhesiveness and good compressive strength. The hydrogel is effective in removing phosphate from wastewater through an adsorption process, during which KHPO is used as a phosphate model. The adsorption complies with the Freundlich model, indicating that it is a multilayered process with complex adsorption mechanisms. Considering their porous structure and nitrogen/phosphorus heteroatoms doping, the phosphate-adsorbed hydrogels are made into porous N,P doped carbon aerogels that can be potentially used as electrodes for a supercapacitor. The results indicate that these carbon aerogels possess excellent capacitive performance (best specific capacitance of 302.2 ± 4.9 F/g), as well as good cycling stability after 5000 times of charging/discharging.
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http://dx.doi.org/10.1016/j.carbpol.2020.116472DOI Listing
September 2020

Double-layer cellulose hydrogel solar steam generation for high-efficiency desalination.

Carbohydr Polym 2020 Sep 25;243:116480. Epub 2020 May 25.

College of Bioresources Chemical and Materials Engineering, Shaanxi University of Science & Technology, Xi'an, 710021, China; National Demonstration Center for Experimental Light Chemistry Engineering Education, Shaanxi University of Science & Technology, Xi'an, 710021, China; Shaanxi Provincial Key Laboratory of Papermaking Technology and Specialty Paper Development, China. Electronic address:

Solar steam generation is one of the most promising technologies for desalination. In order to further promote the development of solar steam generation, a double-layer cellulose hydrogel (DCH) was designed and used as solar steam generation for seawater desalination. Under one sun illumination intensity (1 kW·m), the average evaporation rate and the steam evaporation efficiency reaches 1.582 kg·m h and 91.4 %, respectively. The durability test was performed to verify the long-time durability and antifouling property. Outdoor experiment was carried out to prove the high steam evaporation efficiency and desalination performance of DCH. This paves a way for the cellulose-based hydrogel as a biodegradable, low-cost and promising solar steam generation.
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http://dx.doi.org/10.1016/j.carbpol.2020.116480DOI Listing
September 2020

Design of infrared radiation diagnostic calorimeter for the prototype radio frequency driven negative ion source for neutral beam injection.

Rev Sci Instrum 2020 Apr;91(4):043501

Institute of Plasma Physics, Chinese Academy of Sciences, Hefei 230031, China.

In order to study the generation and extraction of negative ions for neutral beam injection application, a prototype radio frequency driven negative ion source and the corresponding test bench are under construction at the Institute of Plasma Physics, Chinese Academy of Sciences. A new design of infrared radiation diagnostic calorimeter for testing beam characteristics is put forward. Compared with the conventional calorimeter, the calorimeter adopts the block structure (8 × 28 tungsten hexahedron blocks) and modularization design (4 modules), so it has higher precision and good scalability. The thermal performance of the calorimeter is assessed using a finite element method. Simulation results show that the design can be achieved to operate in the stable-state mode at the maximum thermal flux 6.45 MW/m and meet the full requirement of beam diagnosis.
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http://dx.doi.org/10.1063/1.5130717DOI Listing
April 2020

Circular RNA hsa_circ_0000326 acts as a miR-338-3p sponge to facilitate lung adenocarcinoma progression.

J Exp Clin Cancer Res 2020 Apr 5;39(1):57. Epub 2020 Apr 5.

Department of Respiratory and Critical Care Medicine, Wuhan Clinical Medical Research Center for Chronic Airway Medicine, NHC Key Laboratory of Pulmonary Diseases, Key cite of National Clinical Research Center for Respiratory Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences & Technology, 1095 Jiefang Ave, Wuhan, 430030, China.

Background: Circular RNAs (circRNAs) are a novel class of noncoding RNAs that regulate gene expression at the transcriptional or posttranscriptional level. According to recent studies, circRNAs are involved in the pathogenesis of cancer, but the roles of circRNAs in lung adenocarcinoma are largely unknown.

Methods: In this study, we identified a novel upregulated circRNA, hsa_circ_0000326, in human lung adenocarcinoma tissues using microarray analysis and qRT-PCR. We then explored the biological role of hsa_circ_0000326 using gain- and loss-of-function assays in adenocarcinoma cells. Bioinformatics databases were used to screen for potential target miRNAs and the luciferase reporter assays and RNA-FISH further validated the interaction. Downstream protein was detected by western blot. Finally, we established xenografts in nude mice to assess the function of hsa_circ_0000326 in vivo.

Results: We found that high expression of hsa_circ_0000326 was correlated with tumor size, regional lymph node status and differentiation in human lung adenocarcinoma. Additionally, we conducted gain- and loss-of-function assays and found that hsa_circ_0000326 acted as a positive regulator of cell proliferation and migration and a negative regulator of apoptosis. Mechanistic studies showed that hsa_circ_0000326 acted as a miR-338-3p sponge and altered the function of miR-338-3p, which in turn upregulated the expression of the downstream target RAB14 and affected the proliferation, migration and apoptosis of lung adenocarcinoma cells.

Conclusions: Collectively, our study results reveal crucial roles for hsa_circ_0000326 in the proliferation, migration and apoptosis of lung adenocarcinoma cells and suggest that hsa_circ_0000326 may represent a potential therapeutic target in patients with lung adenocarcinoma.
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http://dx.doi.org/10.1186/s13046-020-01556-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7132982PMC
April 2020

Tartrate-Resistant Acid Phosphatase 5/ACP5 Interacts with p53 to Control the Expression of SMAD3 in Lung Adenocarcinoma.

Mol Ther Oncolytics 2020 Mar 8;16:272-288. Epub 2020 Feb 8.

Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Key Site of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China.

Tartrate-resistant acid phosphatase 5 (TRAP/ACP5) has been shown to involve the development and prognosis of multiple tumors in previous studies; however, the mechanism in lung cancer is still unclear, and thus this study investigated the role of ACP5 in the progression of lung adenocarcinoma. After a series of and experiments, we observed that ACP5 expression was increased in lung adenocarcinomas (40/69, 57.97%); importantly, an increased ACP5 level was associated with patient age (p = 0.044) and lymph node metastasis (p = 0.0385). ACP5 overexpression significantly enhanced A549 and NCI-H1975 cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) and reduced cell apoptosis. Knocking down the expression of ACP5 could rescue the above cell phenotypes. Furthermore, enhancing ACP5 expression promoted lung adenocarcinoma cell hyperplasia and intrapulmonary metastasis in a mouse model. Additionally, mechanistic studies revealed that ACP5 might regulate p53 phosphorylation at Ser392, thereby enhancing the ubiquitination of p53, which then underwent degradation. Reducing the levels of p53 intensified the transcription of , which promotes EMT in lung adenocarcinoma cells. In summary, the present study provides a theoretical basis and important scientific evidence on the key role of ACP5 in lung adenocarcinoma progression by inducing EMT via the regulation of p53/SMAD3 signaling.
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http://dx.doi.org/10.1016/j.omto.2020.01.010DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066063PMC
March 2020

A New Sight into Bio-Based Polybenzoxazine: From Tunable Thermal and Mechanical Properties to Excellent Marine Antifouling Performance.

ACS Omega 2020 Feb 17;5(7):3763-3773. Epub 2020 Feb 17.

Ningbo Institute of Materials Technology and Engineering, Chinese Academy of Sciences, Ningbo 315201, PR China.

With the rapid development of bio-based polymers, polybenzoxazine derived from renewable resources has been widely investigated. However, there are few reports on the functional application of bio-based polybenzoxazine based on the special chemical structures of renewable compounds. In this work, an easy approach to prepare the polybenzoxazines with varied thermomechanical properties and excellent marine antifouling performance from renewable resources is presented. After a variety of main-chain-type benzoxazine polymers (MCBPs) were synthesized from the renewable daidzein, furfurylamine, polyetheramine, and paraformaldehyde, their chemical structures were identified by Fourier transform infrared spectroscopy and nuclear magnetic resonance spectroscopy (H NMR). Then, their curing behaviors were monitored by differential scanning calorimetry and rheological tests. Results revealed that the cross-linked MCBPs with varied thermomechanical properties could be easily prepared by adjusting the molar ratio of polyetheramine and furfuramine. Notably, these cured MCBP films demonstrated excellent antibacterial and algaecidal properties due to the presence of daidzein and furan units. This work first presents the new application prospect of bio-based MCBPs, for example, in marine antifouling coatings.
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http://dx.doi.org/10.1021/acsomega.0c00025DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7045792PMC
February 2020

A Nomogram for Predicting Severe Exacerbations in Stable COPD Patients.

Int J Chron Obstruct Pulmon Dis 2020 18;15:379-388. Epub 2020 Feb 18.

Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Key Cite of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, People's Republic of China.

Objective: To develop a practicable nomogram aimed at predicting the risk of severe exacerbations in COPD patients at three and five years.

Methods: COPD patients with prospective follow-up data were extracted from Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS) obtained from National Heart, Lung and Blood Institute (NHLBI) Biologic Specimen and Data Repository Information Coordinating Center. We comprehensively considered the demographic characteristics, clinical data and inflammation marker of disease severity. Cox proportional hazard regression was performed to identify the best combination of predictors on the basis of the smallest Akaike Information Criterion. A nomogram was developed and evaluated on discrimination, calibration, and clinical efficacy by the concordance index (C-index), calibration plot and decision curve analysis, respectively. Internal validation of the nomogram was assessed by the calibration plot with 1000 bootstrapped resamples.

Results: Among 1711 COPD patients, 523 (30.6%) suffered from at least one severe exacerbation during follow-up. After stepwise regression analysis, six variables were determined including BMI, severe exacerbations in the prior year, comorbidity index, post-bronchodilator FEV% predicted, and white blood cells. Nomogram to estimate patients' likelihood of severe exacerbations at three and five years was established. The C-index of the nomogram was 0.74 (95%CI: 0.71-0.76), outperforming ADO, BODE and DOSE risk score. Besides, the calibration plot of three and five years showed great agreement between nomogram predicted possibility and actual risk. Decision curve analysis indicated that implementation of the nomogram in clinical practice would be beneficial and better than aforementioned risk scores.

Conclusion: Our new nomogram was a useful tool to assess the probability of severe exacerbations at three and five years for COPD patients and could facilitate clinicians in stratifying patients and providing optimal therapies.
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http://dx.doi.org/10.2147/COPD.S234241DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7035888PMC
February 2021

Curdione ameliorates bleomycin-induced pulmonary fibrosis by repressing TGF-β-induced fibroblast to myofibroblast differentiation.

Respir Res 2020 Feb 19;21(1):58. Epub 2020 Feb 19.

Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Key Cite of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, 1095 Jiefang Ave, Wuhan, 430030, China.

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible disease characterized by excessive fibroblast to myofibroblast differentiation with limited therapeutic options. Curdione, a sesquiterpene compound extracted from the essential oil of Curcuma aromatica Salisb, has anti-inflammatory and anti-tumor effects. However, the role of curdione in IPF is still unclear.

Methods: The effects of curdione were evaluated in a bleomycin (BLM)-induced pulmonary fibrosis mouse model. C57BL/6 mice were treated with BLM on day 0 by intratracheal injection and intraperitoneal administered curdione or vehicle. In vitro study, expression of fibrotic protein was examined and the transforming growth factor (TGF)-β-related signaling was evaluated in human pulmonary fibroblasts (HPFs) treated with curdione following TGF-β1 stimulation.

Results: Histological and immunofluorescent examination showed that curdione alleviated BLM-induced lung injury and fibrosis. Specifically, curdione significantly attenuated fibroblast to myofibroblast differentiation in the lung in BLM induced mice. Furthermore, curdione also decreased TGF-β1 induced fibroblast to myofibroblast differentiation in vitro, as evidenced by low expression of α-SMA, collagen 1 and fibronectin in a dose dependent manner. Mechanistically, curdione suppressed the phosphorylation of Smad3 following TGF-β1 treatment, thereby inhibiting fibroblast differentiation.

Conclusions: Overall, curdione exerted therapeutic effects against pulmonary fibrosis via attenuating fibroblast to myofibroblast differentiation. As curdione had been shown to be safe and well-tolerated in BLM-induced mouse model, curdione might be useful for developing novel therapeutics for IPF.
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http://dx.doi.org/10.1186/s12931-020-1300-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031930PMC
February 2020

Surfactant protein A expression and distribution in human lung samples from smokers with or without chronic obstructive pulmonary disease in China.

Medicine (Baltimore) 2020 Feb;99(7):e19118

Department of Respiratory Medicine, Yiwu Fuyuan Hospital.

Cigarette smoking is considered the main risk factor for chronic obstructive pulmonary disease (COPD), although the mechanism remains unknown. surfactant protein A (SP-A) is thought to protect the lung from smoking-induced damage, but related studies performed in China are scarce. The aim of the study is to assess alterations of SP-A expression and distribution in lung samples from Chinese smokers with or without COPD.This cross-sectional study assessed 45 men in Wuhan Tongji Hospital after lobectomy for lung cancer in June 2010 to September 2010. Peripheral lung specimens were collected from control nonsmokers without airflow obstruction (nonsmoking group, n = 15), smokers without airflow obstruction (smoking group, n = 15), and patients with COPD (COPD group, n = 15). SP-A expression levels in lung tissue samples and its distribution in lung cells, type II pneumocytes (PNII), and alveolar macrophages (MACR) were determined by immunoblotting and immunohistochemistry.SP-A levels were significantly decreased in the COPD group (1.00 ± 0.25) compared with the smoking (2.31 ± 0.64) and nonsmoking (8.03 ± 2.80) groups; the smoking group also showed significantly reduced levels compared with the nonsmoking group (P < .05). PNII expressing SP-A were less abundant in the COPD group (39.3% ± 7.1%) compared with the smoking group (76.2% ± 29.8%), whereas SP-A MACR were more abundant (92.4% ± 7.1% vs 68.5% ± 20.2%) (all P < .05). Among the 30 smokers, forced expiratory volume in one second (% predicted) was positively correlated with SP-A levels (r = 0.739) and the rate of SP-A+ PNII (r = 0.811), and negatively correlated with the rate of SP-A+ MACR (r = -0.758) (all P < .05).Changes in SP-A expression and distribution in lung tissues may be involved in COPD pathogenesis in smokers.
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http://dx.doi.org/10.1097/MD.0000000000019118DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7035059PMC
February 2020
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