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- Bousquet, J, et al.
(författare)
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Increased risk of asthma attacks and emergency visits among asthma patients with allergic rhinitis: a subgroup analysis of the improving asthma control trial
- 2005
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Ingår i: Clinical and Experimental Allergy. - : Wiley. - 1365-2222. ; 35:6, s. 723-727
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Tidskriftsartikel (refereegranskat)abstract
- Background Inadequately controlled allergic rhinitis (AR) in asthmatic patients can contribute towards increased asthma exacerbations and poorer symptom control, which may increase medical resource use. We assessed asthma-related medical resource use and attacks in asthmatic patients who did and did not have concomitant AR and were adding montelukast or salmeterol to baseline treatment with inhaled. fluticasone. Methods A post hoc resource use analysis of a 52-week, double-blind multicentre clinical trial (IMPACT: IMProving Asthma Control Trial) including 1490 adults with chronic asthma, aged 15 72 years, with FEV1 50-90% of predicted and >= 12% increase in FEV1 after salbutamol administration, treated with either montelukast 10mg daily or salmeterol 50 mu g twice daily in addition to. fluticasone 200 mg, was undertaken. Asthma- related medical resource use included medical visits ( defined as either an unscheduled visit [to a general practitioner, a specialist or a nonmedical provider] or a specialist visit), emergency room visits and hospitalizations during follow-up. Asthma attacks were defined as the worsening of asthma requiring unscheduled visit, emergency visit, hospitalization or oral/intravenous/intramuscular corticosteroids. Results A self-reported history of concomitant AR was identified in 60% of the patients (n=893). Univariate analysis suggests that significantly more patients with concomitant AR experienced emergency room visits (3.6% vs. 1.7%, P=0.029) and asthma attacks (21.3% vs. 17.1%, P=0.046). Multivariate analysis adjusting for treatment group, age and baseline asthma severity confirmed these results since the presence of concomitant AR in patients with asthma increases the likelihood of emergency room visit ( odds ratio ( OR) 52.35, 95% confidence interval (CI) = 1.12 - 4.80) and asthma attack (OR = 1.35, 95% CI = 1.03 - 1.77). Patients with asthma alone compared with patients with both conditions did not differ in terms of unscheduled or specialist visits and hospitalizations. Conclusions Presence of self-reported concomitant AR in patients with asthma resulted in a higher rate of asthma attacks and more emergency room visits compared with asthma patients without concomitant AR.
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- Gao, R, et al.
(författare)
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Resetting histone modifications during human prenatal germline development
- 2023
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Ingår i: Cell discovery. - : Springer Science and Business Media LLC. - 2056-5968. ; 9:1, s. 14-
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Tidskriftsartikel (refereegranskat)abstract
- Histone modifications play critical roles in regulating gene expression and present dynamic changes during early embryo development. However, how they are reprogrammed during human prenatal germline development has not yet been elucidated. Here, we map the genome-wide profiles of three key histone modifications in human primordial germ cells (hPGCs) from weeks 8 to 23 of gestation for the first time by performing ULI-NChIP-seq. Notably, H3K4me3 exhibits a canonical promoter-enriched pattern, though with relatively lower enrichment, and is positively correlated with gene expression in globally hypomethylated hPGCs. In addition, H3K27me3 presents very low enrichment but plays an important role in not only dynamically governing specific bivalent promoters but also impeding complete X chromosome reactivation in female hPGCs. Given the activation effects of both global DNA demethylation and H3K4me3 signals, repressive H3K9me3 and H3K27me3 marks are jointly responsible for the paradoxical regulation of demethylation-resistant regions in hPGCs. Collectively, our results provide a unique roadmap of three core histone modifications during hPGC development, which helps to elucidate the architecture of germ cell reprogramming in an extremely hypomethylated DNA environment.
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