Quit4baby: Results from a pilot test of a mobile smoking cessation program for pregnant women

Background: Text messaging (short message service, SMS) programs have been shown to be effective in helping adult smokers quit smoking. This study describes the results of a pilot test of Quit4baby, a smoking cessation text messaging program for pregnant smokers that was adapted from Text2quit. Objective: The study aimed to demonstrate the feasibility and acceptability of Quit4baby for women currently enrolled in Text4baby, a perinatal health text messaging program. Methods: Pregnant women enrolled in Text4baby and who were current smokers or had quit within the last 4 weeks (n=20) were enrolled in Quit4baby. Those under the age of 18, not pregnant, not current smokers, those using nicotine replacement therapy, and those not interested in participating were ineligible. Participants were surveyed at baseline and at 2 and 4 weeks postenrollment. Results: Most participants responded to the program favorably. Highly rated aspects included the content of the program, skills taught within the program, and encouragement and social support provided by the program. Participants reported that the program was helpful in quitting, that the program gave good ideas on quitting, and that they would recommend the program to a friend. Suggestions for improvement included increasing the message dose and making the quitpal more interactive. Conclusions: This pilot test provides support for the feasibility and acceptability of Quit4baby. Future studies are needed to assess whether Quit4baby is effective for smoking cessation during pregnancy

Research-Based Web Design & Usability Guidelines [2006 edition]

The new edition of the U.S. Department of Health and Human Services’ (HHS) Research-Based Web Design and Usability Guidelines. These guidelines reflect HHS’ commitment to identifying innovative, research-based approaches that result in highly responsive and easy-to-use Web sites for the public. These guidelines help move us in that direction by providing practical, yet authoritative, guidance on a broad range of Web design and communication issues. Having access to the best available research helps to ensure we make the right decisions the first time around and reduces the possibility of errors and costly mistakes

Comparison of the Metabolic Effects of Ritonavir-Boosted Darunavir or Atazanavir Versus Raltegravir, and the Impact of Ritonavir Plasma Exposure: ACTG 5257

Background. Metabolic effects following combination antiretroviral therapy (cART) vary by regimen type. Changes in metabolic effects were assessed following cART in the AIDS Clinical Trials Group (ACTG) A5257 study, and correlated with plasma ritonavir trough concentrations (C24)

Comparison of the Metabolic Effects of Ritonavir-Boosted Darunavir or Atazanavir Versus Raltegravir, and the Impact of Ritonavir Plasma Exposure: ACTG 5257

Background. Metabolic effects following combination antiretroviral therapy (cART) vary by regimen type. Changes in metabolic effects were assessed following cART in the AIDS Clinical Trials Group (ACTG) A5257 study, and correlated with plasma ritonavir trough concentrations (C24)

Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation