Demonstrating the validity of the Video Game Functional Assessment-Revised (VGFA-R)

Problematic video play has been well documented over the course of the last decade. So much so the DSM-5 (APA, 2013) has included problematic video gaming as disorder categorized as Internet Gaming Disorder. The field of applied behavior analysis has been utilizing functional assessments for the last 30 years and has showed evidence of effective results across different populations and environments. Therefore, the purpose of this investigation (comprising three studies) was to validate an indirect functional assessment entitled the Video Game Functional Assessment-Revised (VGFA-R). Using academic experts in the field of video game addiction and applied behavioral analysis (n=6), the first study examined the content validity of the VGFA-R and was able to demonstrate the assessment exceeded the criterion for an established assessment. A second study comprising a survey of 467 gamers examined the factorability by using a confirmatory factor analysis, and found that VGFA-R had an overall variance above .60. Within the third laboratory-based study using gamers (n=11), the VGFA-R was examined for construct validity and found the VGFA-R was able to predict 85% of the appropriate function of behavior. Implications of the study are discussed along with the strengths and limitations of the study and future research directions

High-resolution microbiome analysis reveals exclusionary Klebsiella species competition in preterm infants at risk for necrotizing enterocolitis.

Intestinal colonization with Klebsiella has been linked to necrotizing enterocolitis (NEC), but methods of analysis usually failed to discriminate Klebsiella species or strains. A novel ~ 2500-base amplicon (StrainID) that spans the 16S and 23S rRNA genes was used to generate amplicon sequence variant (ASV) fingerprints for Klebsiella oxytoca and Klebsiella pneumoniae species complexes (KoSC and KpSC, respectively) and co-occurring fecal bacterial strains from 10 preterm infants with NEC and 20 matched controls. Complementary approaches were used to identify cytotoxin-producing isolates of KoSC. Klebsiella species colonized most preterm infants, were more prevalent in NEC subjects versus controls, and replaced Escherichia in NEC subjects. Single KoSC or KpSC ASV fingerprinted strains dominated the gut microbiota, suggesting exclusionary Klebsiella competition for luminal resources. Enterococcus faecalis was co-dominant with KoSC but present infrequently with KpSC. Cytotoxin-producing KoSC members were identified in most NEC subjects and were less frequent in controls. Few Klebsiella strains were shared between subjects. We conclude that inter-species Klebsiella competition, within an environment of KoSC and E. faecalis cooperation, appears to be an important factor for the development of NEC. Preterm infants seem to acquire Klebsiella primarily through routes other than patient-to-patient transmission

Efficacy of the Pentavalent Rotavirus Vaccine, RotaTeq (RV5), Between Doses of a 3-Dose Series and With Less Than 3 Doses (Incomplete Regimen)

Post-hoc analyses of the Rotavirus Efficacy and Safety Trial (RES T) were conducted to determine whether the pentavalent rotavirus vaccine (RV5) confers early protection against rotavirus gastroenteritis (RVGE) before completion of the 3-dose regimen. To evaluate the efficacy of RV5 between doses in reducing the rates of RVGE-related hospitalizations and emergency department (ED) visits in infants who ultimately received all 3 doses of RV5/placebo, events occurring from 2 weeks after the first and second doses to receipt of the subsequent dose (Analysis A) and events occurring from 2 weeks after the first and second doses to 2 weeks after the subsequent dose (Analysis B) were analyzed. In Analysis A, RV5 reduced the rates of combined hospitalizations and ED visits for G1-G4 RVGE or RVGE regardless of serotype between doses 1 and 2 by 100% [95% confidence interval (CI): 72-100%] or 82% (95% CI: 39-97%), respectively, and between doses 2 and 3, RV5 reduced the rates of combined hospitalizations and ED visits for G1-G4 RVGE or RVGE regardless of serotype by 91% (95% CI: 63-99%) or 84% (95% CI: 54-96%), respectively. Similar rate reductions were observed in Analysis B. These data suggest that RV5 provides a high level of protection between doses against hospitalizations and ED visits for RVGE starting as early as 14 days after the first dose

Replication protein A physically interacts with the Bloom's syndrome protein and stimulates its helicase activity.

Bloom's syndrome is a rare autosomal recessive disorder characterized by genomic instability and predisposition to cancer. BLM, the gene defective in Bloom's syndrome, encodes a 159-kDa protein possessing DNA-stimulated ATPase and ATP-dependent DNA helicase activities. We have examined mechanistic aspects of the catalytic functions of purified recombinant BLM protein. Through analyzing the effects of different lengths of DNA cofactor on ATPase activity, we provide evidence to suggest that BLM translocates along single-stranded DNA in a processive manner. The helicase reaction catalyzed by BLM protein was examined as a function of duplex DNA length. We show that BLM catalyzes unwinding of short DNA duplexes (/=259-bp). The presence of the human single-stranded DNA-binding protein (human replication protein A (hRPA)) stimulates the BLM unwinding reaction on the 259-bp partial duplex DNA substrate. Heterologous single-stranded DNA-binding proteins fail to stimulate similarly the helicase activity of BLM protein. This is the first demonstration of a functional interaction between BLM and another protein. Consistent with a functional interaction between hRPA and the BLM helicase, we demonstrate a direct physical interaction between the two proteins mediated by the 70-kDa subunit of RPA. The interactions between BLM and hRPA suggest that the two proteins function together in vivo to unwind DNA duplexes during replication, recombination, or repair

Mammal assemblage composition predicts global patterns in emerging infectious disease risk

As a source of emerging infectious diseases, wildlife assemblages (and related spatial patterns) must be quantitatively assessed to help identify high-risk locations. Previous assessments have largely focussed on the distributions of individual species; however, transmission dynamics are expected to depend on assemblage composition. Moreover, disease-diversity relationships have mainly been studied in the context of species loss, but assemblage composition and disease risk (e.g. infection prevalence in wildlife assemblages) can change without extinction. Based on the predicted distributions and abundances of 4466 mammal species, we estimated global patterns of disease risk through the calculation of the community-level basic reproductive ratio R0, an index of invasion potential, persistence, and maximum prevalence of a pathogen in a wildlife assemblage. For density-dependent diseases, we found that, in addition to tropical areas which are commonly viewed as infectious disease hotspots, northern temperate latitudes included high-risk areas. We also forecasted the effects of climate change and habitat loss from 2015 to 2035. Over this period, many local assemblages showed no net loss of species richness, but the assemblage composition (i.e. the mix of species and their abundances) changed considerably. Simultaneously, most areas experienced a decreased risk of density-dependent diseases but an increased risk of frequency-dependent diseases. We further explored the factors driving these changes in disease risk. Our results suggest that biodiversity and changes therein jointly influence disease risk. Understanding these changes and their drivers and ultimately identifying emerging infectious disease hotspots can help health officials prioritize resource distribution.Peer reviewe

Custom Integrated Circuits

Contains reports on seven research projects.U.S. Air Force - Office of Scientific Research (Contract F49620-84-C-0004)National Science Foundation (Grant ECS81-18160)Defense Advanced Research Projects Agency (Contract NOO14-80-C-0622)National Science Foundation (Grant ECS83-10941