5,922 research outputs found
Decrease in Free Computer Science Papers Found through Google Scholar
Purpose - Google Scholar was used to locate free full-text versions of computer science research papers to determine what proportion could be freely accessed.Design/methodology/approach - A sample of 1967 conference papers and periodical articles from 2003-2010, indexed in the ACM Guide to Computing Literature, was searched for manually in Google Scholar, using the paper or article title and the first author’s surname and supplementary searches as needed. Findings - Free full-text versions were found for 52% of the conference papers and 55% of the periodical articles. Documents with older publication dates were more likely to be freely accessible than newer documents, with free full-text versions found for 71% of items published in 2003 and 43% of items published 2010. Many documents did not indicate what version of the document was presented. Research limitations/implications - Results were limited to the retrieval of known computer science publications via Google Scholar. The results may be different for other computer science publications, subject areas, types of searches, or search engines. Practical implications - Users of Google Scholar for finding free full-text computer science research papers may be hindered by the lower access to recent publications. Because many papers are freely available, libraries and scholarly publishers may be better served by promoting services they provide beyond simple access to papers. Originality/value – Previous research showed lower levels of free access than we found for computer science, but the decline found in this study runs contrary to increases found in previous research
A Lifestyle Modification Program for Community Dwelling Adults with Obesity
Obesity is significantly rising among adults in the United States. The Center for Disease Control (CDC, 2009e), estimates that obesity increased by 15% to 32.9% within a 20 year span (1985 – 2008). Clinical obesity is defined as having a BMI 30 and over; it is correlated with secondary complications that include hypertension, type II diabetes, osteoarthritis, cardiovascular diseases, cancers, cerebral vascular accidents, sleep apnea, and respiratory illnesses (CDC, 2009d; World Health Organization [WHO], 2009). Beyond the many health consequences caused by obesity, there are also psychosocial, genetic, and discriminatory aspects of this disease that negatively impact the quality of life and participation in occupations (Clark, Reingold, & Salles-Jordan, 2006).
Occupational therapists can provide education and intervention focusing on lifestyle modification to increase participation in occupations, and improve quality of life (Blanchard, 2006; Clark, et al. 2006). The CDC (2009g) describes that 10-minute bouts of moderate to vigorous intensity in the form of meaningful activities such as lawn mowing, dancing, or biking to the store is adequate for raising heart rates and starting the path to physical fitness. This approach fits well with the role of occupational therapy.
A comprehensive literature review was conducted on obesity and the impact it has on activities of daily living. Key areas explored include medications, genetics, psychological impacts and discrimination, impact on activities of daily living, sedentary lifestyles, impact of socio-economic status on health, dietary modifications, as well as effective holistic intervention strategies.
The literature indicated a need for a lifestyle modification program for community dwelling adults who are overweight or obese. The Step It Up to A Better You is a lifestyle modification program consisting of one-hour educational sessions for 12-weeks. The overall goal is to gain a healthy lifestyle with enhanced quality of life and ability to participate in one’s meaningful daily activities. The sessions include educational resources on motivation, nutrition, physical activity, exploring community resources, psychosocial well-being, and a lifestyle maintenance plan
Regulation of Sphingosine-1-phosphate Lyase Gene Expression by Members of the GATA Family of Transcription Factors
Sphingosine-1-phosphate is a bioactive sphingolipid that regulates proliferation, differentiation, migration, and apoptosis. Sphingosine-1-phosphate is irreversibly degraded by the highly conserved enzyme sphingosine-1-phosphate lyase. Recent studies have suggested that sphingosine-1-phosphate lyase expression affects animal development and cell fate decisions. Despite its crucial role, mechanisms affecting expression of sphingosine-1-phosphate lyase remain poorly understood. In this study, regulation of sphingosine-1-phosphate lyase gene expression was investigated in Caenorhabditis elegans, where lyase expression is spatially restricted to cells of the developing and adult gut and is essential for normal development. Deletion analysis and generation of transgenic worms combined with fluorescence microscopy identified a 350-nucleotide sequence upstream of the ATG start site necessary for maximal lyase expression in adult worms. Site-specific mutagenesis of a GATA transcription factor-binding motif in the promoter led to loss of reporter expression. Knockdown of the gut-specific GATA transcription factor ELT-2 by RNA interference similarly led to loss of reporter expression. ELT-2 interacted with the GATA factor-binding motif in vitro and was also capable of driving expression of a Caenorhabditis elegans lyase promoter-{beta}-galactosidase reporter in a heterologous yeast system. These studies demonstrate that ELT-2 regulates sphingosine-1-phosphate lyase expression in vivo. Additionally, we demonstrate that the human sphingosine-1-phosphate lyase gene is regulated by a GATA transcription factor. Overexpression of GATA-4 led to both an increase in activity of a reporter gene as well as an increase in endogenous sphingosine-1-phosphate lyase protein
An Innovative Approach for Community Engagement: Using an Audience Response System
Community-based participatory research methods allow for community engagement in the effort to reduce cancer health disparities. Community engagement involves health professionals becoming a part of the community in order to build trust, learn from the community and empower them to reduce disparities through their own initiatives and ideas. Audience Response Systems (ARS) are an innovative and engaging way to involve the community and obtain data for research purposes using keypads to report results via power point. The use of ARS within communities is very limited and serves to widen the disparity gap by not delivering new advances in medical knowledge and technology among all population groups. ARS was implemented at a community town hall event sponsored by a National Institute on Minority Health and Health Disparities Exploratory Center of Excellence, the Center for Equal Health. Participants appreciated being able to see how everyone else answered and felt included in the research process. ARS is beneficial because the community can answer truthfully and provides instant research results. Additionally, researchers can collect large amounts of data quickly, in a non-threatening way while tracking individual responses anonymously. Audience Response Systems proved to be an effective tool for successfully accomplishing community-based participatory research
Body mass index throughout adulthood, physical activity, and risk of multiple myeloma: A prospective analysis in three large cohorts
TRIP/NOPO E3 Ubiquitin Ligase Promotes Ubiquitylation of DNA Polymerase η
We previously identified a Drosophila maternal effect-lethal mutant named ‘no poles’ (nopo). Embryos from nopo females undergo mitotic arrest with barrel-shaped, acentrosomal spindles during the rapid cycles of syncytial embryogenesis because of activation of a Chk2-mediated DNA checkpoint. NOPO is the Drosophila homolog of human TNF receptor associated factor (TRAF)-interacting protein (TRIP), which has been implicated in TNF signaling. NOPO and TRIP contain RING domains closely resembling those of known E3 ubiquitin ligases. We herein sought to elucidate the mechanism by which TRIP/NOPO promotes genomic stability by performing a yeast two-hybrid screen to identify potential substrates/interactors. We identified members of the Y-family of DNA polymerases that facilitate replicative bypass of damaged DNA (translesion synthesis) as TRIP interactors. We show that TRIP and NOPO co-immunoprecipitate with human and Drosophila Polη, respectively, from cultured cells. We generated a null mutation in Drosophila Polη (dPolη) and found that dPolη-derived embryos have increased sensitivity to ultraviolet irradiation and exhibit nopo-like mitotic spindle defects. dPolη and nopo interact genetically in that overexpression of dPolηn hypomorphic nopo-derived embryos suppresses nopo phenotypes. We observed enhanced ubiquitylation of Polη by TRIP and NOPO E3 ligases in human cells and Drosophila embryos, respectively, and show that TRIP promotes hPolη localization to nuclear foci in human cells. We present a model in which TRIP/NOPO ubiquitylates Polη to positively regulate its activity in translesion synthesis
Anomaly Inflow for Gauge Defects
Topological defects constructed out of scalar fields and possessing chiral
fermion zero modes are known to exhibit an anomaly inflow mechanism which
cancels the anomaly in the effective theory of the zero modes through an inflow
of current from the space in which the defect is embedded. We investigate the
analog of this mechanism for defects constructed out of gauge fields in higher
dimensions. In particular we analyze this mechanism for string (one-brane)
defects in six dimensions and for fivebranes in ten dimensions.}Comment: 23 pp (harvmac l
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Outcomes of Randomized Clinical Trials of Interventions to Enhance Social, Emotional, and Spiritual Components of Wisdom: A Systematic Review and Meta-analysis.
ImportanceWisdom is a neurobiological personality trait made up of specific components, including prosocial behaviors, emotional regulation, and spirituality. It is associated with greater well-being and happiness.ObjectiveTo evaluate the effectiveness of interventions to enhance individual components of wisdom.Data sourcesMEDLINE and PsycINFO databases were searched for articles published through December 31, 2018.Study eligibility criteriaRandomized clinical trials that sought to enhance a component of wisdom, used published measures to assess that component, were published in English, had a minimum sample size of 40 participants, and presented data that enabled computation of effect sizes were included in this meta-analysis.Data extraction and synthesisRandom-effect models were used to calculate pooled standardized mean differences (SMDs) for each wisdom component and random-effects meta-regression to assess heterogeneity of studies.Main outcomes and measuresImprovement in wisdom component using published measures.ResultsFifty-seven studies (N = 7096 participants) met review criteria: 29 for prosocial behaviors, 13 for emotional regulation, and 15 for spirituality. Study samples included people with psychiatric or physical illnesses and from the community. Of the studies, 27 (47%) reported significant improvement with medium to large effect sizes. Meta-analysis revealed significant pooled SMDs for prosocial behaviors (23 studies; pooled SMD, 0.43 [95% CI, 0.22-0.3]; P = .02), emotional regulation (12 studies; pooled SMD, 0.67 [95% CI, 0.21-1.12]; P = .004), and spirituality (12 studies; pooled SMD, 1.00 [95% CI, 0.41-1.60]; P = .001). Heterogeneity of studies was considerable for all wisdom components. Publication bias was present for prosocial behavior and emotional regulation studies; after adjusting for it, the pooled SMD for prosocial behavior remained significant (SMD, 0.4 [95% CI, 0.16-0.78]; P = .003). Meta-regression analysis found that effect sizes did not vary by wisdom component, although for trials on prosocial behaviors, large effect sizes were associated with older mean participant age (β, 0.08 [SE, 0.04]), and the reverse was true for spirituality trials (β, -0.13 [SE, 0.04]). For spirituality interventions, higher-quality trials had larger effect sizes (β, 4.17 [SE, 1.07]), although the reverse was true for prosocial behavior trials (β, -0.91 [SE 0.44]).Conclusions and relevanceInterventions to enhance spirituality, emotional regulation, and prosocial behaviors are effective in a proportion of people with mental or physical illnesses and from the community. The modern behavioral epidemics of loneliness, suicide, and opioid abuse point to a growing need for wisdom-enhancing interventions to promote individual and societal well-being
A conserved circadian function for the Neurofibromatosis 1 gene
Summary: Loss of the Neurofibromatosis 1 (Nf1) protein, neurofibromin, in Drosophila disrupts circadian rhythms of locomotor activity without impairing central clock function, suggesting effects downstream of the clock. However, the relevant cellular mechanisms are not known. Leveraging the discovery of output circuits for locomotor rhythms, we dissected cellular actions of neurofibromin in recently identified substrates. Herein, we show that neurofibromin affects the levels and cycling of calcium in multiple circadian peptidergic neurons. A prominent site of action is the pars intercerebralis (PI), the fly equivalent of the hypothalamus, with cell-autonomous effects of Nf1 in PI cells that secrete DH44. Nf1 interacts genetically with peptide signaling to affect circadian behavior. We extended these studies to mammals to demonstrate that mouse astrocytes exhibit a 24-hr rhythm of calcium levels, which is also attenuated by lack of neurofibromin. These findings establish a conserved role for neurofibromin in intracellular signaling rhythms within the nervous system. : Bai et al. show that the gene mutated in the disease Neurofibromatosis 1 is required for maintaining levels or cycling of calcium in circadian neurons in Drosophila and in mammalian cells. These effects likely account for effects of Nf1 on circadian behavior in Drosophila and may be relevant in explaining sleep phenotypes in patients. Keywords: circadian rhythms, neurofibromatosis 1, Drosophila, peptide signaling, cycling of calcium, mouse astrocyte
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