A Survey of Computer Anxiety Among Secondary English Teachers in St. Johns County

As a result, in part, of computer anxiety, many educators are not utilizing available computer technology, even though its innovations extend to the classroom. Forty-four secondary English teachers from st. Johns County, Florida were given the Computer Attitude Rating Survey (CARS) along with a follow-up questionnaire, to identify anxiety levels and possible correlations with gender, education level, computer experience, and in-service training for this sample. Results indicate that men have less computer anxiety than women, that computer experience and in-service training decrease anxiety, and that Masters degree students have lower anxiety scores than do Baccalaureate degree students. These findings mirror earlier results, and provide directional data for decreasing the computer anxiety of future educators

Population-based RNA profiling in Add Health finds social disparities in inflammatory and antiviral gene regulation to emerge by young adulthood

Health in later life varies significantly by individual demographic characteristics such as age, sex, and race/ethnicity, as well as by social factors including socioeconomic status and geographic region. This study examined whether sociodemographic variations in the immune and inflammatory molecular underpinnings of chronic disease might emerge decades earlier in young adulthood. Using data from 1,069 young adults from the National Longitudinal Study of Adolescent to Adult Health (Add Health)-the largest nationally representative and ethnically diverse sample with peripheral blood transcriptome profiles-we analyzed variation in the expression of genes involved in inflammation and type I interferon (IFN) response as a function of individual demographic factors, sociodemographic conditions, and biobehavioral factors (smoking, drinking, and body mass index). Differential gene expression was most pronounced by sex, race/ethnicity, and body mass index (BMI), but transcriptome correlates were identified for every demographic dimension analyzed. Inflammation-related gene expression showed the most pronounced variation as a function of biobehavioral factors (BMI and smoking) whereas type I IFN-related transcripts varied most strongly as a function of individual demographic characteristics (sex and race/ethnicity). Bioinformatic analyses of transcription factor and immune-cell activation based on transcriptome-wide empirical differences identified additional effects of family poverty and geographic region. These results identify pervasive sociodemographic differences in immune-cell gene regulation that emerge by young adulthood and may help explain social disparities in the development of chronic illness and premature mortality at older ages

Population-based RNA profiling in Add Health finds social disparities in inflammatory and antiviral gene regulation to emerge by young adulthood

Health in later life varies significantly by individual demographic characteristics such as age, sex, and race/ethnicity, as well as by social factors including socioeconomic status and geographic region. This study examined whether sociodemographic variations in the immune and inflammatory molecular underpinnings of chronic disease might emerge decades earlier in young adulthood. Using data from 1,069 young adults from the National Longitudinal Study of Adolescent to Adult Health (Add Health)—the largest nationally representative and ethnically diverse sample with peripheral blood transcriptome profiles—we analyzed variation in the expression of genes involved in inflammation and type I interferon (IFN) response as a function of individual demographic factors, sociodemographic conditions, and biobehavioral factors (smoking, drinking, and body mass index). Differential gene expression was most pronounced by sex, race/ethnicity, and body mass index (BMI), but transcriptome correlates were identified for every demographic dimension analyzed. Inflammation-related gene expression showed the most pronounced variation as a function of biobehavioral factors (BMI and smoking) whereas type I IFN-related transcripts varied most strongly as a function of individual demographic characteristics (sex and race/ethnicity). Bioinformatic analyses of transcription factor and immune-cell activation based on transcriptome-wide empirical differences identified additional effects of family poverty and geographic region. These results identify pervasive sociodemographic differences in immune-cell gene regulation that emerge by young adulthood and may help explain social disparities in the development of chronic illness and premature mortality at older ages

Socioeconomic inequalities in early adulthood disrupt the immune transcriptomic landscape via upstream regulators

Disparities in socio-economic status (SES) predict many immune system-related diseases, and previous research documents relationships between SES and the immune cell transcriptome. Drawing on a bioinformatically-informed network approach, we situate these findings in a broader molecular framework by examining the upstream regulators of SES-associated transcriptional alterations. Data come from the National Longitudinal Study of Adolescent to Adult Health (Add Health), a nationally representative sample of 4543 adults in the United States. Results reveal a network—of differentially expressed genes, transcription factors, and protein neighbors of transcription factors—that shows widespread SES-related dysregulation of the immune system. Mediational models suggest that body mass index (BMI) plays a key role in accounting for many of these associations. Overall, the results reveal the central role of upstream regulators in socioeconomic differences in the molecular basis of immunity, which propagate to increase risk of chronic health conditions in later-life

An ethical matrix for the reintroduction of trafficked primates:a platyrrhine case study

The illegal primate trade is one of the major drivers of the decline of nonhuman primate populations and a threat to their wellbeing. Thousands of trafficked primates enter rescue centers every year, and their destiny (release back into the wild, long-term captivity, or euthanasia) involves controversial decisions and complex ethical considerations. To navigate these issues, we developed an ethical matrix, an ethical framework previously used to address conservation-related issues. We gathered information from studies on the reintroduction of trafficked platyrrhines in Latin America from 1990 to 2022 to develop the matrix. We found 22 studies performed in eight Latin American countries, which included howler monkeys, spider monkeys, woolly monkeys, capuchin monkeys, squirrel monkeys, marmosets, and tamarins. We found that the reintroduction of trafficked platyrrhines may yield positive results for the welfare of individuals and for the conservation of their taxa and some of the potential negative effects, such as spillover of infectious agents to free-ranging populations or to human populations, or competition for resources between reintroduced monkeys and resident conspecifics have not yet been documented in the scientific literature, although this does not mean that they do not occur. We conclude that the ethical matrix is a useful method to consider the interests of all potential stakeholders and that the reintroduction of trafficked primates may be a viable management option if the individual welfare of the animals is considered, programs comply with the IUCN and government guidelines, and the objective and justification of the reintroduction are clear

Socioeconomic inequalities in early adulthood disrupt the immune transcriptomic landscape via upstream regulators

Disparities in socio-economic status (SES) predict many immune system-related diseases, and previous research documents relationships between SES and the immune cell transcriptome. Drawing on a bioinformatically-informed network approach, we situate these findings in a broader molecular framework by examining the upstream regulators of SES-associated transcriptional alterations. Data come from the National Longitudinal Study of Adolescent to Adult Health (Add Health), a nationally representative sample of 4543 adults in the United States. Results reveal a network-of differentially expressed genes, transcription factors, and protein neighbors of transcription factors-that shows widespread SES-related dysregulation of the immune system. Mediational models suggest that body mass index (BMI) plays a key role in accounting for many of these associations. Overall, the results reveal the central role of upstream regulators in socioeconomic differences in the molecular basis of immunity, which propagate to increase risk of chronic health conditions in later-life

Reduction of β-amyloid pathology by celastrol in a transgenic mouse model of Alzheimer's disease

<p>Abstract</p> <p>Background</p> <p>Aβ deposits represent a neuropathological hallmark of Alzheimer's disease (AD). Both soluble and insoluble Aβ species are considered to be responsible for initiating the pathological cascade that eventually leads to AD. Therefore, the identification of therapeutic approaches that can lower Aβ production or accumulation remains a priority. NFκB has been shown to regulate BACE-1 expression level, the rate limiting enzyme responsible for the production of Aβ. We therefore explored whether the known NFκB inhibitor celastrol could represent a suitable compound for decreasing Aβ production and accumulation <it>in vivo</it>.</p> <p>Methods</p> <p>The effect of celastrol on amyloid precursor protein (APP) processing, Aβ production and NFκB activation was investigated by western blotting and ELISAs using a cell line overexpressing APP. The impact of celastrol on brain Aβ accumulation was tested in a transgenic mouse model of AD overexpressing the human APP695sw mutation and the presenilin-1 mutation M146L (Tg PS1/APPsw) by immunostaining and ELISAs. An acute treatment with celastrol was investigated by administering celastrol intraperitoneally at a dosage of 1 mg/Kg in 35 week-old Tg PS1/APPsw for 4 consecutive days. In addition, a chronic treatment (32 days) with celastrol was tested using a matrix-driven delivery pellet system implanted subcutaneously in 5 month-old Tg PS1/APPsw to ensure a continuous daily release of 2.5 mg/Kg of celastrol.</p> <p>Results</p> <p><it>In vitro</it>, celastrol dose dependently prevented NFκB activation and inhibited BACE-1 expression. Celastrol potently inhibited Aβ_1-40and Aβ_1-42production by reducing the β-cleavage of APP, leading to decreased levels of APP-CTFβ and APPsβ. <it>In vivo</it>, celastrol appeared to reduce the levels of both soluble and insoluble Aβ_1-38, Aβ_1-40and Aβ_1-42. In addition, a reduction in Aβ plaque burden and microglial activation was observed in the brains of Tg PS1/APPsw following a chronic administration of celastrol.</p> <p>Conclusions</p> <p>Overall our data suggest that celastrol is a potent Aβ lowering compound that acts as an indirect BACE-1 inhibitor possibly by regulating BACE-1 expression level via an NFκB dependent mechanism. Additional work is required to determine whether chronic administration of celastrol can be safely achieved with cognitive benefits in a transgenic mouse model of AD.</p