8 results on '"Chenting Zhang"'
Search Results
2. Visibility, wind speed, and dew point temperature are important factors in SARS‐CoV‐2 transmissibility
- Author
-
Dansha Zhou, Elizabeth W. Wang, Chi Hou, Jing Liao, Jiarui Zhang, Xin Fu, Jiyuan Chen, Yue Xing, Wei Hong, Zhe Zhang, Yuanwei Chen, Huazhuo Feng, Yilin Chen, Qifeng Yang, Huosheng Zhang, Zicong Li, Weici Feng, Ting Wang, Ziying Lin, Chenting Zhang, Kai Yang, Wenju Lu, Jian Wang, and Yuqin Chen
- Subjects
Alpha VOC ,Delta VOC ,meteorological factors ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 ,Diseases of the respiratory system ,RC705-779 - Abstract
Abstract The aim of this study is to provide evidence for the influencing factors of severe acute respiratory syndrome coronavirus 2 (SARS‐COV‐2) virus mutation by determining the impact of geographical and meteorological factors on SARS‐CoV‐2 transmission, and the different impacts of SARS‐CoV‐2 variant strains. From January 20 to March 10, 2020, we collected a number of daily confirmed new cases and meteorological factors in all cities and regions in China and Italy affected by the Alpha “variants of concern” (VOC). We also collected the daily confirmed cases of the Delta VOC infection in China and Italy from May 21 to November 30, 2021. The relationships between daily meteorological data and daily verified new cases of SARS‐CoV‐2 transmission were then investigated using a general additive model (GAM) with a log link function and Poisson family. The results revealed that latitude was substantially connected with daily confirmed new instances of the Alpha VOC, while there was no such correlation with Delta VOC transmission. When visibility is greater than 7 m, the propagation of the Alpha and Delta VOCs in Italy and China can be controlled. Furthermore, greater temperatures and increased wind speed reduce the transmission of the Alpha and Delta VOCs. In conclusion, geographical and meteorological factors play an important role in SARS‐CoV‐2 transmissibility and should be considered in virus mitigation strategies.
- Published
- 2022
- Full Text
- View/download PDF
3. Establishment and evaluation of chronic obstructive pulmonary disease model by chronic exposure to motor vehicle exhaust combined with lipopolysaccharide instillation
- Author
-
Jiaze Shu, Wenju Lu, Kai Yang, Qiuyu Zheng, Defu Li, Yi Li, Meidan Kuang, Hanwei Liu, Ziying Li, Yuqin Chen, Chenting Zhang, Xiaoyun Luo, Junyi Huang, Xiongting Wu, Haiyang Tang, and Jian Wang
- Subjects
chronic obstructive pulmonary disease ,lipopolysaccharide ,motor vehicle exhaust ,Physiology ,QP1-981 - Abstract
New Findings What is the central question of this study? In this study, by using motor vehicle exhaust (MVE) exposure with or without lipopolysaccharide (LPS) instillation, we established, evaluated and compared MVE, LPS and MVE+LPS treatment‐induced chronic obstructive pulmonary disease (COPD) models in mice. What is the main finding and its importance? Our study demonstrated that the combination of chronic exposure to MVE with early LPS instillation can establish a mouse model with some features of COPD, which will allow researchers to investigate the underlying molecular mechanisms linking air pollution and COPD pathogenesis. Abstract Although it is well established that motor vehicle exhaust (MVE) has a close association with the occurrence and exacerbation of chronic obstructive pulmonary disease (COPD), very little is known about the combined effects of MVE and intermittent or chronic subclinical inflammation on COPD pathogenesis. Therefore, given the crucial role of inflammation in the development of COPD, we wanted to establish an animal model of COPD using both MVE exposure and airway inflammation, which could mimic the clinical pathological changes observed in COPD patients and greatly benefit the study of the molecular mechanisms of COPD. In the present study, we report that mice undergoing chronic exposure to MVE and intratracheal instillation of lipopolysaccharide (LPS) successfully established COPD, as characterized by persistent air flow limitation, airway inflammation, inflammatory cytokine production, emphysema and small airway remodelling. Moreover, the mice showed significant changes in ventricular and vascular pathology, including an increase in right ventricular pressure, right ventricular hypertrophy and remodelling of pulmonary arterial walls. We have thus established a new mouse COPD model by combining chronic MVE exposure with early intratracheal instillation of LPS, which will allow us to study the relationship between air pollution and the development of COPD and to investigate the underlying molecular mechanisms.
- Published
- 2018
- Full Text
- View/download PDF
4. Airway delivery of <scp> Streptococcus salivarius </scp> is sufficient to induce experimental pulmonary hypertension in rats
- Author
-
Chenting Zhang, Tingting Zhang, Yue Xing, Wenju Lu, Jiyuan Chen, Xiaoyun Luo, Xuefen Wu, Shiyun Liu, Lishi Chen, Zizhou Zhang, Dansha Zhou, Ziying Lin, Yuqin Chen, Mingmei Xiong, Jason X.‐J. Yuan, Kai Yang, and Jian Wang
- Subjects
Pharmacology - Published
- 2023
5. Mitomycin C induces pulmonary vascular endothelial‐to‐mesenchymal transition and pulmonary veno‐occlusive disease via Smad3‐dependent pathway in rats
- Author
-
Yuqin Chen, Cheng Hong, Xiaoyun Luo, Haixia Chen, Shiyun Liu, Jiyuan Chen, Chunli Liu, Chenting Zhang, Dejun Sun, Yi Li, Wenju Lu, Haiyang Tang, Xuefen Wu, Qiuyu Zheng, Zizhou Zhang, Guoping Gu, Qian Jiang, Jian Wang, Liu Wenyan, Jing Liao, and Kai Yang
- Subjects
0301 basic medicine ,CD31 ,Pathology ,medicine.medical_specialty ,Hypertension, Pulmonary ,Mitomycin ,Vimentin ,Pathogenesis ,03 medical and health sciences ,0302 clinical medicine ,Von Willebrand factor ,Animals ,Humans ,Medicine ,Endothelium ,Smad3 Protein ,Pharmacology ,Lung ,biology ,business.industry ,Mesenchymal stem cell ,Endothelial Cells ,medicine.disease ,Pulmonary hypertension ,Rats ,030104 developmental biology ,medicine.anatomical_structure ,biology.protein ,Pulmonary Veno-Occlusive Disease ,business ,030217 neurology & neurosurgery - Abstract
Background and purpose Pulmonary veno-occlusive disease (PVOD) is a rare disease characterized by the obstruction of small pulmonary veins leading to pulmonary hypertension. However, the mechanisms underlying pulmonary vessel occlusion remain largely unclear. Experimental approach A mitomycin C (MMC)-induced PVOD rat model was used as in vivo animal model, and primarily cultured rat pulmonary microvascular endothelial cells (PMVECs) were used as in vitro cell model. Key results Our data suggested an endothelial-to-mesenchymal transition (EndoMT) may be present in the pulmonary microvessels isolated from either PVOD patients or MMC-induced PVOD rats. In comparison to the control vessels, vessels from both PVOD patients and PVOD rats had co-localized staining of specific endothelial marker von Willebrand factor (vWF) and mesenchymal marker α-smooth muscle actin (α-SMA), suggesting the presence of cells that co-express endothelial and mesenchymal markers. In both the lung tissues of MMC-induced PVOD rats and MMC-treated rat PMVECs there were decreased levels of endothelial markers (e.g. VE-cadherin and CD31) and increased mesenchymal markers (e.g. vimentin, fibronectin and α-SMA) were detected indicating EndoMT. Moreover, MMC-induced activation of the TGFβ/Smad3/Snail axis, while blocking this pathway with either selective Smad3 inhibitor (SIS3) or small interfering RNA (siRNA) against Smad3, dramatically abolished the MMC-induced EndoMT. Notably, treatment with SIS3 remarkably prevented the pathogenesis of MMC-induced PVOD in rats. Conclusions and implications Our data indicated that targeted inhibition of Smad3 leads to a potential, novel strategy for PVOD therapy, likely by inhibiting the EndoMT in pulmonary microvasculature.
- Published
- 2020
6. Dysregulation of BMP9/BMPR2/SMAD signalling pathway contributes to pulmonary fibrosis and pulmonary hypertension induced by bleomycin in rats
- Author
-
Tao Wang, Ran Ma, Haixia Chen, Wenju Lu, Shiyun Liu, Chenting Zhang, Yi Li, Zizhou Zhang, Kai Yang, Yuqin Chen, Cheng Hong, Jian Wang, Xiaoyun Luo, Qian Jiang, Chunli Liu, and Wenliang Guo
- Subjects
Male ,0301 basic medicine ,Pathology ,medicine.medical_specialty ,Hypertension, Pulmonary ,Pulmonary Fibrosis ,SMAD ,Pulmonary Artery ,Bone Morphogenetic Protein Receptors, Type II ,Bleomycin ,Vascular remodelling in the embryo ,Rats, Sprague-Dawley ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Right ventricular hypertrophy ,Pulmonary fibrosis ,medicine ,Animals ,Pharmacology ,Lung ,business.industry ,Endothelial Cells ,medicine.disease ,Pulmonary hypertension ,Rats ,BMPR2 ,030104 developmental biology ,medicine.anatomical_structure ,chemistry ,business ,030217 neurology & neurosurgery - Abstract
Background and purpose Pulmonary hypertension related to pulmonary fibrosis is classed as WHO Group III, one of the most common groups which lacks effective treatment options. In this study, we aimed to uncover the underlying mechanisms, particularly the involvement of the BMP9/BMPR2/SMAD signalling pathway, in this subtype of pulmonary hypertension. Experimental approach Male Sprague Dawley rats were used to establish a model of pulmonary hypertension with pulmonary fibrosis, induced by bleomycin. Haemodynamic and lung functions were measured, along with histological and immunohistochemical examinations. Primary cultures of rat pulmonary microvascular endothelial cells (PMVECs) were analysed with western blots, apoptosis assays and immunohistochemistry. Key results Early (7 days) after bleomycin treatment of rats, pulmonary arterial thickening and severe loss of pulmonary arterial endothelium were observed, followed (14 days) by increased right ventricular systolic pressure and right ventricular hypertrophy. Marked down-regulation of the BMP9/BMPR2/SMAD signalling pathway was markedly down-regulated in lung tissues from bleomycin-treated rats (throughout the 7- to 35-day treatment period) and bleomycin-treated rat PMVECs, along with excessive cell apoptosis and loss of pulmonary arterial endothelium. Treatment with recombinant human bone morphogenetic protein 9 (rhBMP9) attenuated these aspects of bleomycin-induced pulmonary hypertension, by restoring disrupted BMP9/BMPR2/SMAD signalling. Conclusion and implications In bleomycin-treated rats, early and persisting suppression of the BMP9/BMPR2/SMAD signalling pathway triggered severe loss of pulmonary arterial endothelium and subsequent pulmonary arterial vascular remodelling, contributing to the development of pulmonary hypertension. Therapeutic approaches reinforcing BMP9/BMPR2/SMAD signalling might be ideal strategies for this subtype of pulmonary hypertension. Linked articles This article is part of a themed issue on Risk factors, comorbidities, and comedications in cardioprotection. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.1/issuetoc.
- Published
- 2020
7. BRIP1 rs10744996C>A variant increases the risk of chronic obstructive pulmonary disease in the Mongolian population of northern China
- Author
-
Zili Zhang, Ke Hu, Jing Wang, Dejun Sun, Chenting Zhang, and Wenju Lu
- Subjects
China ,Physiology ,DNA repair ,DNA damage ,Population ,Single-nucleotide polymorphism ,030204 cardiovascular system & hematology ,Pulmonary Disease, Chronic Obstructive ,03 medical and health sciences ,0302 clinical medicine ,Smoke ,Physiology (medical) ,medicine ,Humans ,RNA, Messenger ,education ,Genotyping ,COPD ,education.field_of_study ,Nutrition and Dietetics ,business.industry ,BRIP1 ,Epithelial Cells ,General Medicine ,Odds ratio ,medicine.disease ,Fanconi Anemia Complementation Group Proteins ,A549 Cells ,Immunology ,business ,RNA Helicases ,030217 neurology & neurosurgery - Abstract
What is the central question of this study? What is the role of breast cancer type 1 interacting protein C-terminal helicase 1 (BRIP1) polymorphism in chronic obstructive pulmonary disease (COPD)? What is the main finding and its importance? Variant rs10744996CA of BRIP1 increases the susceptibility of the Mongolian population to COPD. The expression of BRIP1 was significantly reduced in cigarette smoke extract-treated airway epithelial cells.Cigarette smoke is a major environmental pollutant that can induce DNA damage in humans. The development and progression of chronic obstructive pulmonary disease (COPD) are known to be related to the impairment of DNA repair. Breast cancer type 1 interacting protein C-terminal helicase 1 (BRIP1) plays an important role in DNA interstrand crosslink repair and double-strand break repair. However, the role of BRIP1 polymorphisms in COPD has not been previously described. In this study, whole genome sequencing was used to identify mutations, and single nucleotide polymorphism (SNP) genotyping was used to verify the selected SNPs. In addition the BRIP1 expression levels in 16HBE and A549 airway epithelial cells treated with or without cigarette smoke extract (CSE) were measured using western blotting and RT-qPCR. Rs10744996CA in the 3'-untranslated region (3'UTR) of BRIP1 was then genotyped in 1296 COPD cases and 988 healthy control subjects from a Mongolian population in northern China. Significant differences in the distribution of rs10744996CA variants between COPD and control groups (P = 0.001) were identified. Rs10744996CA was found to be associated with significantly increased COPD risk (adjusted odds ratio = 1.60, 95% CI = 1.30-1.98, P 0.0001). Additionally, rs10744996A genotype was found to interact with a family history of cancer and a history of x-ray exposure (P = 0.028 and 0.009, respectively). BRIP1 expression levels in 16HBE and A549 cells treated with CSE were significantly lower compared to the control treated cells. The rs10744996CA variant of BRIP1 increased the COPD susceptibility of the Mongolian population cohort. BRIP1 mRNA and protein expression levels were significantly reduced in conjunction with CSE-induced DNA damage in 16HBE and A549 cells.
- Published
- 2020
8. Bone morphogenetic protein 4 inhibits liposaccharide-induced inflammation in the airway
- Author
-
Wenju Lu, Xuefang Gong, Yafei Qi, Xiaoming Xu, Defu Li, Zhengtu Li, Jian Wang, Hua Jiang, Kedong Zhang, Chun Tang, Nanshan Zhong, Chuyi Xu, Chenting Zhang, and Yan Wang
- Subjects
animal structures ,Lung ,Lipopolysaccharide ,Growth factor ,medicine.medical_treatment ,Immunology ,Inflammation ,respiratory system ,Lung injury ,Biology ,respiratory tract diseases ,chemistry.chemical_compound ,medicine.anatomical_structure ,Bone morphogenetic protein 4 ,chemistry ,embryonic structures ,medicine ,Cancer research ,Immunology and Allergy ,Tumor necrosis factor alpha ,Interleukin 8 ,medicine.symptom - Abstract
Bone morphogenetic protein 4 (BMP4) is a multifunctional growth factor that belongs to the TGF-β superfamily. The role of BMP4 in lung diseases is not fully understood. Here, we demonstrate that BMP4 was upregulated in lungs undergoing lipopolysaccharide (LPS)-induced inflammation, and in airway epithelial cells treated with LPS or TNF-α. BMP4 mutant (BMP4(+/-) ) mice presented with more severe lung inflammation in response to LPS or Pseudomonas aeruginosa, and lower bacterial load compared with that in BMP4(+/+) mice. Knockdown of BMP4 by siRNA increased LPS and TNF-α-induced IL-8 expression in 16HBE human airway epithelial cells and in primary human bronchial epithelial cells. Similarly, peritoneal macrophages from BMP4(+/-) mice produced greater levels of TNF-α and keratinocyte chemoattractant (KC) upon LPS treatment compared with cells from BMP4(+/+) mice. Administration of exogenous BMP4 attenuated the upregulation of TNF-α, IL-8, or KC induced by LPS and/or TNF-α in airway epithelial cells, and peritoneal macrophages. Finally, partial deficiency of BMP4 in BMP4(+/-) mice protected the animals from restrictive lung function reduction upon chronic LPS exposure. These results indicate that BMP4 plays an important anti-inflammatory role, controlling the strength and facilitating the resolution of acute lung inflammation; yet, BMP4 also contributes to lung function impairment during chronic lung inflammation.
- Published
- 2014
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.