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Atopic dermatitis (AD) is a chronic inflammatory skin disorder, with a highly variable prevalence worldwide. (R)-HTS-3 compound library inhibitor Recent evidence, however, has shown an increase in prevalence in the Asia Pacific region. Nevertheless, most of the published literature has focused mainly on Western populations, and only few clinical trials have included subgroups of other ethnic populations. Reasons for the observed ethnic and geographical differences in AD are not well established. This calls into question the need for a better understanding of AD pathogenesis and inter-ethnic differences in clinical and immuno-phenotypes. These differences may reflect inherent variability in disease mechanisms between populations, which in turn may impact upon treatment responses such as biologics that are currently tailored mainly to a specific immuno-phenotype (T-helper type 2 dominant). In this article, we reviewed existing literature on the prevalence of AD globally, highlighting differences, if any, in the clinical and immuno-phenotypes of AD between different ethnicities. We discussed genetic and environmental factors that affect AD in different populations and therapeutic considerations. Our review highlights AD as a disease with ethnic-dependent clinical and immunological heterogeneity and calls for greater inclusion of ethnic diversity in future research in order to develop targeted treatments.

Severe asthma exacerbations are a major cause of asthma morbidity and increased healthcare costs. Several studies have shown racial and ethnic differences in asthma exacerbation rates. We aimed to identify genetic variants associated with severe exacerbations in two high-risk populations for asthma.

A genome-wide association study of asthma in children and youth with severe exacerbations was performed in 1283 exacerbators and 2027 controls without asthma of Latino ancestry. Independent suggestive variants (P ≤ 5 × 10

) were selected for replication in 448 African Americans exacerbators and 595 controls. Case-only analyses were performed comparing the exacerbators with additional 898 Latinos and 524 African Americans asthma patients without exacerbations, while adjusting by treatment category as a proxy of asthma severity. We analyzed the functionality of associated variants with in silico methods and by correlating genotypes with methylation levels in whole blood in a subset of 473 Latinos.

We identifng genes.

Smell dysfunction is highly prevalent worldwide and has adverse effects on quality of life. Smell loss in rhinitis subjects is mainly caused by mechanical obstruction of odorant transmission due to mucosal type 2 inflammation. We determined the association of 25-hydroxyvitamin D (25[OH]D) levels with the severity of smell dysfunction in children.

We measured the olfactory threshold score in a total of 518 children (10-12 years old, 264 boys) using the Sniffin' Sticks kit, and the children were divided into tertiles according to olfactory threshold score. We also assessed serum 25[OH]D level, common aeroallergen-specific immunoglobulin E, rhinitis severity with visual analog scale, and the Total Four Symptom Score, and pre- and post-decongestant nasal patency with acoustic rhinometry.

The children with 25(OH)D deficiency had significantly reduced mean olfactory threshold scores when compared to those with 25(OH)D levels of ≥20.0 ng/mL (6.56 ± 3.54 and 7.28 ± 3.87, respectively, P = .036). The proportion of loss of smell function and pre-decongestant nasal patency significantly associated with low 25(OH)D levels (chi-square trend test, P for trend = .007). Likewise, after adjustment for confounders, children with smell loss (third tertile) were significantly associated with low 25(OH)D level (aβ=-0.062, 95% CI=-0.064 to -0.060, P = .009) independent of aeroallergen sensitization, and a low pre-decongestant nasal patency.

25-Hydroxyvitamin D is significantly associated with smell dysfunction independent of aeroallergen sensitization, nasal obstruction, and the presence of allergic rhinitis. This finding may provide insight into the mechanisms involved in the development of olfactory dysfunction.

25-Hydroxyvitamin D is significantly associated with smell dysfunction independent of aeroallergen sensitization, nasal obstruction, and the presence of allergic rhinitis. This finding may provide insight into the mechanisms involved in the development of olfactory dysfunction.

To analyze the results of different cut-off index (COI) values of Elecsys

HIV combi PT assay and to assess the role of COI in reducing the frequency of false-positive results.

We conducted a retrospective study of samples analyzed by Elecsys

HIV combi PT assay, a 4th-generation ECLIA, between 2016 and 2017. A total amount of 379122 samples were collected for HIV (Human Immunodeficiency Virus) screening.

A total of 379122 samples were analyzed. 2528 (0.67%) were positive by Elecsys

HIV combi PT. Of these, 468 were false-positive results, and most of them (94.87%) were in samples with 1<COI < 15. The false-positive rate was 0.12%. Patients with false-positive samples were more distributed in elder (P<.001) and female (P<.001) than true-positive specimens. The median COI in true-positive specimens was (385.20), which is significantly higher than false-positive specimens (2.08). The consistency between Elecsys

HIV combi PT assay and 3rd-generation and positive predictive value (PPV) increased with higher COI values. Cancer, infection, and neurological diseases were considered the potential confounding factors of HIV false-positive results (19.44%, 11.11%, and 6.62%, respectively).

Samples with low COI values, especially those contain confounding factors, need to be further scrutinized to determine whether the confounding factors may cause false-positive problem. In addition, the hypothesis that low COI values may predict false-positive results is valid.

Samples with low COI values, especially those contain confounding factors, need to be further scrutinized to determine whether the confounding factors may cause false-positive problem. In addition, the hypothesis that low COI values may predict false-positive results is valid.

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