Int Arch Allergy Immunol
August 2022
Background: Chitinase 3-like 1 (CHI3L1) is an important factor involved in the development of asthma. This meta-analysis assessed the association of the CHI3L1 polymorphisms rs4950928, rs10399931, rs883125, rs880633, and rs10399805 with asthma risk.
Methods: The literature searches were conducted in PubMed, Web of Science, Wanfang, and China National Knowledge Infrastructure up until September 4, 2021, for relevant studies.
Introduction: Given the evidence that the matrix metalloproteinases (MMPs) play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD), a number of case-control studies have attempted to assess the relationship between genetic polymorphisms in genes and COPD risk. However, reliable measures of these results are lacking.
Material And Methods: We assessed the published evidence for association of the -9 and polymorphisms with COPD risk using meta-analytic techniques.
Eur Arch Otorhinolaryngol
June 2018
Purpose: The aim of this study was to conduct a meta-analysis for single nucleotide polymorphisms (SNPs) in interleukin-13 (IL-13) and cluster of differentiation 14 (CD14) genes and the risk for allergic rhinitis (AR).
Methods: We screened studies identified through seven databases including Pubmed, Medline, Web of Science, Embase, China Biology Medicine disc, Wanfang, and China Academic Journal Network Publishing Database. The odds ratios (ORs) and 95% confidence intervals (CIs) were determined to assess the association under allelic, dominant and recessive models.
Background: Several recent studies have provided evidence that polymorphisms in the interleukin-1 (IL1) gene are implicated in tuberculosis (TB). However, results of different studies are inconsistent. The aim of this study was to perform a meta-analysis investigating the association of the IL1B (-511 and +3954) and IL1RN VNTR polymorphisms with TB risk.
View Article and Find Full Text PDFThe interleukin-1 (IL-1) gene polymorphisms have been implicated in chronic obstructive pulmonary disease (COPD) risk, but results are controversial. We aimed to conduct a meta-analysis to address this issue. Odds ratio (OR) and 95% confidence interval (CI) were used to investigate the strength of the association.
View Article and Find Full Text PDFZhonghua Jie He He Hu Xi Za Zhi
January 2012
Objective: To evaluate the changes of CD(4)(+)IL-17(+) T (Th17) and CD(4)(+)Foxp3(+) regulatory T (Treg) cells in peripheral blood and bronchoalveolar lavage fluid (BALF), and therefore to explore the role of Th17 and Treg in cigarette smoke-induced airway inflammation/COPD in rats.
Methods: Forty male Wistar rats were randomly divided into 4 groups: a 12 wk smoke-exposure group, a 24 wk smoke-exposure group, a 12 wk control group and a 24 wk control group (n = 10 each). Cells in BALF were collected and analyzed by absolute and differential cell counts.
Genet Test Mol Biomarkers
April 2012
Background And Objective: The tumor necrosis factor (TNF)-α-308G/A polymorphism has been implicated in susceptibility to obstructive sleep apnea (OSA). However, results from previous studies are inconsistent. A systematic review and meta-analysis of the published studies was performed to investigate this association.
View Article and Find Full Text PDFZhonghua Jie He He Hu Xi Za Zhi
September 2010
Objective: To evaluate the expression of Treg in a cigarette smoke-induced rat model of emphysema and after smoking cessation in the rats.
Methods: Fifty male Wistar rats were randomly divided into control group 1 (12 weeks), control group 2 (24 weeks), smoke-exposure group 1 (12 weeks), smoke-exposure group 2 (24 weeks) and smoking cessation group, with 10 rats in each group. Alveolar airspace enlargement was observed by hematoxylin-eosin (HE) staining.
Objective: to study the change of airway inflammation induced by Th1/Tc1 and the expression of CD4(+)CD25(+) regulatory T cells (Treg) in smoking cessation rats.
Methods: fifty healthy male Wistar rats were randomly divided into five groups: 12-week normal control (group A, n = 10), 24-week normal control (group B, n = 10), 12-week smoke exposure (group C, n = 10), 24-week smoke exposure (group D, n = 10) and smoking cessation (group E, n = 10). Groups C, D and E were exposed to cigarettes for 12 weeks.