A Systematic Review of Patient- and Family-Level Inhaled Corticosteroid Adherence Interventions in Black/African Americans

Background: Inhaled corticosteroid (ICS) adherence rates are suboptimal among adult black/African Americans. Comprehensive studies characterizing the effectiveness and the methodological approaches to the development of interventions to improve ICS adherence in adult black/African Americans have not been performed. Objectives: Conduct a systematic review of patient/family-level interventions to improve ICS adherence in adult black/African Americans. Methods: We searched MEDLINE, EMBASE, Web of Science, and CINAHL from inception to August 2017 for English-language US studies enrolling at least 30% black/African Americans comparing patient/family-level ICS adherence interventions with any comparator. Two investigators independently selected, extracted data from, and rated risk of bias. We collected information on intervention characteristics and outcomes, and assessed whether studies were informed by behavior theory, stakeholder engagement, or both. Results: Among 1661 abstracts identified, we reviewed 230 full-text articles and identified 4 randomized controlled trials (RCTs) and 1 quasi-experimental (pre-post design) study meeting criteria. Study participants (N range, 17-333) varied in mean age (22-47 years), proportion black/African Americans studied (71%-93%), and sex (69%-82% females). RCTs evaluated problem-solving classes, self-efficacy training, technology-based motivational interviewing program, and the use of patient advocates. The RCT testing self-efficacy training was the only intervention informed by both behavior theory and stakeholder engagement. All 4 RCTs compared interventions with active control and rated as medium risk of bias. No RCTs found a statistically significant improvement in adherence. Conclusions: Few studies assessing asthma adherence interventions focused on adult black/African-American populations. No RCTs demonstrated improved ICS adherence in participants. Future studies that are informed by behavior change theory and stakeholder engagement are needed

Single Spin Asymmetry ANA_N in Polarized Proton-Proton Elastic Scattering at s=200\sqrt{s}=200 GeV

We report a high precision measurement of the transverse single spin asymmetry $A_N$ at the center of mass energy $\sqrt{s}=200$ GeV in elastic proton-proton scattering by the STAR experiment at RHIC. The $A_N$ was measured in the four-momentum transfer squared $t$ range $0.003 \leqslant |t| \leqslant 0.035$ \GeVcSq, the region of a significant interference between the electromagnetic and hadronic scattering amplitudes. The measured values of $A_N$ and its $t$-dependence are consistent with a vanishing hadronic spin-flip amplitude, thus providing strong constraints on the ratio of the single spin-flip to the non-flip amplitudes. Since the hadronic amplitude is dominated by the Pomeron amplitude at this $\sqrt{s}$, we conclude that this measurement addresses the question about the presence of a hadronic spin flip due to the Pomeron exchange in polarized proton-proton elastic scattering.Comment: 12 pages, 6 figure

Deleterious variants in CRLS1 lead to cardiolipin deficiency and cause an autosomal recessive multi-system mitochondrial disease

Mitochondrial diseases are a group of inherited diseases with highly varied and complex clinical presentations. Here, we report four individuals, including two siblings, affected by a progressive mitochondrial encephalopathy with biallelic variants in the cardiolipin biosynthesis gene CRLS1. Three affected individuals had a similar infantile presentation comprising progressive encephalopathy, bull’s eye maculopathy, auditory neuropathy, diabetes insipidus, autonomic instability, cardiac defects and early death. The fourth affected individual presented with chronic encephalopathy with neurodevelopmental regression, congenital nystagmus with decreased vision, sensorineural hearing loss, failure to thrive and acquired microcephaly. Using patient-derived fibroblasts, we characterized cardiolipin synthase 1 (CRLS1) dysfunction that impaired mitochondrial morphology and biogenesis, providing functional evidence that the CRLS1 variants cause mitochondrial disease. Lipid profiling in fibroblasts from two patients further confirmed the functional defect demonstrating reduced cardiolipin levels, altered acyl-chain composition and significantly increased levels of phosphatidylglycerol, the substrate of CRLS1. Proteomic profiling of patient cells and mouse Crls1 knockout cell lines identified both endoplasmic reticular and mitochondrial stress responses, and key features that distinguish between varying degrees of cardiolipin insufficiency. These findings support that deleterious variants in CRLS1 cause an autosomal recessive mitochondrial disease, presenting as a severe encephalopathy with multi-systemic involvement. Furthermore, we identify key signatures in cardiolipin and proteome profiles across various degrees of cardiolipin loss, facilitating the use of omics technologies to guide future diagnosis of mitochondrial diseases.Richard G. Lee ... Janice Fletcher ... et al

J/ψ polarization in p+p collisions at s=200 GeV in STAR

AbstractWe report on a polarization measurement of inclusive J/ψ mesons in the di-electron decay channel at mid-rapidity at 2<pT<6 GeV/c in p+p collisions at s=200 GeV. Data were taken with the STAR detector at RHIC. The J/ψ polarization measurement should help to distinguish between different models of the J/ψ production mechanism since they predict different pT dependences of the J/ψ polarization. In this analysis, J/ψ polarization is studied in the helicity frame. The polarization parameter λθ measured at RHIC becomes smaller towards high pT, indicating more longitudinal J/ψ polarization as pT increases. The result is compared with predictions of presently available models

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

J/ψ Production At Low Pt In Au+au And Cu+cu Collisions At Snn =200 Gev With The Star Detector

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