16 research outputs found

    Impact of childhood wheezing on lung function in adulthood: A meta-analysis

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    <div><p>Background</p><p>A growing body of evidence shows that childhood wheezing may lead to recurrent or persistent symptoms in adulthood, such that persistent wheezing associated with lung function deficits often have their roots in the first few years of life.</p><p>Objectives</p><p>We summarized information from several prospective cohort studies following children with or without wheezing into adulthood, to estimate the effect of childhood wheezing on adulthood lung function.</p><p>Methods</p><p>Medical literatures were searched in the Medline, PubMed, ScienceDirect, Web of Science and Embase databases up to October 31, 2016. The adulthood lung function was selected as primary outcome, and chronic obstructive pulmonary disease (COPD) prevalence was selected as secondary outcome. The meta-analysis was performed with the Stata Version 14.0. A random-effects model was applied to estimate standardized mean difference (SMD) of lung function, and relative risk (RR) of COPD.</p><p>Results</p><p>Six articles enrolling 1141 and 1005 children with and without wheezing, respectively. Meta-analysis showed that childhood wheezing decreased adulthood lung function as compared with no-wheezing subjects (SMD = -0.365, 95% confidence interval (CI): -0.569~-0.161, P = 0.000). Subgroup analyses indicated that childhood atopic wheezing reduced adulthood FEV1/FVC and FEV1%pred when compared with no-wheezing subjects. In addition, childhood atopic wheezing was significantly associated with COPD prevalence (RR = 5.307, 95% CI:1.033~27.271, P = 0.046).</p><p>Conclusions</p><p>Our meta-analysis suggests that childhood wheezing may induce ongoing declined lung function that extends into adult life, as well as an increased risk of COPD prevalence when accompanied with atopy.</p></div

    Western blot analysis of BRM expression in HCC tissue and adjacent non-tumor tissues.

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    <p>(A) BRM expression for different BRM-1321 genotypes. (B) BRM expression for different haplotypes. Haplotype #1: −1321 del/del-741 ins/ins, Haplotype #2: −1321 del/del-741 del/del, Haplotype #3: −1321 ins/ins-741 ins/ins.</p

    BRM expression in HCC tumor tissues <i>vs.</i> non-tumor tissues and its correlations between BRM-1321 indel polymorphism as well as corresponding haplotypes.

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    <p>(<b>A</b>) Relative BRM expression in HCC tumor tissues <i>vs.</i> non-tumor tissues (n = 72); (<b>B</b>) Relative BRM expression in three genotypic groups of BRM-1321 (−1321 ins/ins, n = 10, −1321 ins/del, n = 32, −1321 del/del, n = 30); (<b>C</b>) Relative BRM expression in different haplotype groups (haplotype: −1321 ins/ins-741 ins/ins, n = 6, haplotype: −1321 del/del-741 del/del, n = 11, haplotype: −1321 del/del-741 ins/ins, n = 4); (<b>D</b>) Relative BRM expression in hepatoma cell lines with different haplotypes. Data represented as mean ± SEM. *indicates <i>P</i><0.01, **indicates <i>P</i><0.001 compared within the same group (HCC tissue or non HCC tissue).</p
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