Examination of Substance Use, Risk Factors, and Protective Factors on Student Academic Test Score Performance

BACKGROUND: School administrators and teachers face difficult decisions about how best to use school resources in order to meet academic achievement goals. Many are hesitant to adopt prevention curricula that are not focused directly on academic achievement. Yet, some have hypothesized that prevention curricula can remove barriers to learning and, thus, promote achievement. This study examined relationships between school levels of student substance use and risk and protective factors that predict adolescent problem behaviors and achievement test performance in Washington State. METHODS: Hierarchical Generalized Linear Models were used to examine predictive associations between school-averaged levels of substance use and risk and protective factors and Washington State students’ likelihood of meeting achievement test standards on the Washington Assessment of Student Learning, statistically controlling for demographic and economic factors known to be associated with achievement. RESULTS: Results indicate that levels of substance use and risk/protective factors predicted the academic test score performance of students. Many of these effects remained significant even after controlling for model covariates. CONCLUSIONS: The findings suggest that implementing prevention programs that target empirically identified risk and protective factors have the potential to positively affect students’ academic achievement

Mapping atopic dermatitis and anti-IL-22 response signatures to Type 2-low severe neutrophilic asthma

BACKGROUND: Transcriptomic changes in patients who respond clinically to biological therapies may identify responses in other tissues or diseases.OBJECTIVE: We sought to determine whether a disease signature identified in atopic dermatitis (AD) is seen in adults with severe asthma and whether a transcriptomic signature for patients with AD who respond clinically to anti-IL-22 (fezakinumab [FZ]) is enriched in severe asthma.METHODS: An AD disease signature was obtained from analysis of differentially expressed genes between AD lesional and nonlesional skin biopsies. Differentially expressed genes from lesional skin from therapeutic superresponders before and after 12 weeks of FZ treatment defined the FZ-response signature. Gene set variation analysis was used to produce enrichment scores of AD and FZ-response signatures in the Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes asthma cohort.RESULTS: The AD disease signature (112 upregulated genes) encompassing inflammatory, T-cell, T H2, and T H17/T H22 pathways was enriched in the blood and sputum of patients with asthma with increasing severity. Patients with asthma with sputum neutrophilia and mixed granulocyte phenotypes were the most enriched (P &lt; .05). The FZ-response signature (296 downregulated genes) was enriched in asthmatic blood (P &lt; .05) and particularly in neutrophilic and mixed granulocytic sputum (P &lt; .05). These data were confirmed in sputum of the Airway Disease Endotyping for Personalized Therapeutics cohort. IL-22 mRNA across tissues did not correlate with FZ-response enrichment scores, but this response signature correlated with T H22/IL-22 pathways. CONCLUSIONS: The FZ-response signature in AD identifies severe neutrophilic asthmatic patients as potential responders to FZ therapy. This approach will help identify patients for future asthma clinical trials of drugs used successfully in other chronic diseases.</p

Mapping atopic dermatitis and anti-IL-22 response signatures to Type 2-low severe neutrophilic asthma.

BACKGROUND Transcriptomic changes in patients who respond clinically to biological therapies may identify responses in other tissues or diseases. OBJECTIVE To determine whether a disease signature identified in atopic dermatitis (AD) is seen in adults with severe asthma (SA) and whether a transcriptomic signature for AD patients who respond clinically to anti-IL-22 (Fezakinumab, FZ) is enriched in SA. METHODS An AD disease signature was obtained from analysis of differentially expressed genes (DEGs) between AD lesional and non-lesional skin biopsies. DEGs from lesional skin from therapeutic super-responders before and after 12 weeks FZ treatment defined the FZ-response signature. Gene Set Variation Analysis (GSVA) was used to produce enrichment scores (ES) of AD and FZ-response signatures in the U-BIOPRED asthma cohort. RESULTS The AD disease signature (112 up-regulated genes) encompassing inflammatory, T-cell, Th2 and Th17/Th22 pathways was enriched in the blood and sputum of asthmatics with increasing severity. Asthmatics with sputum neutrophilia and mixed granulocyte phenotypes were the most enriched (p<0.05). The FZ-response signature (296 down-regulated genes) was enriched in asthmatic blood (p<0.05) and particularly in neutrophilic and mixed granulocytic sputum (p<0.05). These data were confirmed in sputum of the ADEPT (Airway Disease Endotyping for Personalized Therapeutics) cohort. IL-22 mRNA across tissues did not correlate with FZ-response ES, but this response signature correlated with Th22/IL-22 pathways. CONCLUSIONS The FZ-response signature in AD identifies severe neutrophilic asthmatics as potential responders to FZ therapy. This approach will help identify patients for future asthma clinical trials of drugs used successfully in other chronic diseases

Review of periodical literature published in 2011

Non peer reviewe