Background Recent reports indicate racial disparities in the rates of infection and mortality from the 2019 novel coronavirus (coronavirus disease 2019 [COVID-19]). The aim of this study was to determine whether disparities exist in the levels of knowledge, attitudes and practices (KAPs) related to COVID-19. Methods We analyzed data from 1216 adults in the March 2020 Kaiser Family Foundation ‘Coronavirus Poll’, to determine levels of KAPs across different groups. Univariate and multivariate regression analysis was used to identify predictors of KAPs. Results In contrast to White respondents, Non-White respondents were more likely to have low knowledge (58% versus 30%; P < 0.001) and low attitude scores (52% versus 27%; P < 0.001), but high practice scores (81% versus 59%; P < 0.001). By multivariate regression, White race (odds ratio [OR] 3.06; 95% confidence interval [CI]: 1.70–5.50), higher level of education (OR 1.80; 95% CI: 1.46–2.23) and higher income (OR 2.06; 95% CI: 1.58–2.70) were associated with high knowledge of COVID-19. Race, sex, education, income, health insurance status and political views were all associated with KAPs. Conclusions Racial and socioeconomic disparity exists in the levels of KAPs related to COVID-19. More work is needed to identify educational tools that tailor to specific racial and socioeconomic groups.

Background Outbreaks of vector-borne diseases such as dengue, and malaria can overwhelm health systems in resource-poor countries. Environmental management strategies that reduce/eliminate vector breeding sites combined with improved personal prevention strategies can help to significantly reduce transmission of these infections. Objective This study was conducted to assess the knowledge, attitudes and practices (KAPs) of residents in Western Jamaica regarding control of mosquito vectors and protection from mosquito bites. Methods A cross-sectional study was conducted between May and August 2010 among patients or family members of patients waiting to be seen at hospitals in Western Jamaica. Participants completed an interviewer-administered questionnaire on sociodemographic factors and KAPs regarding vector-borne diseases. KAP scores were calculated and categorized as high or low based on number of correct/positive responses. Logistic regression analyses were conducted to identify predictors of KAP and linear regression analysis conducted to determine if knowledge and attitude scores predicted practice scores. Results Three-hundred and sixty-one people (85 males and 276 females) participated in the study. Most participants (87%) scored low on knowledge and practice items (78%). Conversely, 78% scored high on attitudes items. By multivariate logistic regression, housewives were 82% less likely to have high attitude scores than laborers, and homeowners were 65% less likely to have high attitude scores than renters. Participants from households with 1–2 children were 3.4 times more likely to have high attitude scores compared to those from households with no children. Participants from households ≥5 people were 65% less likely to have high practice scores compared to those from households with <5. By multivariable linear regression knowledge and attitude scores were significant predictors of practice score. Conclusion The study revealed poor knowledge of vector-borne diseases and poor prevention practices among participants. It identified specific groups that can be targeted with vector-control and personal protection interventions to decrease transmission of the infections.

Depending upon the stimulus, neuronal cell death can either be triggered from the cell body (soma) or the axon. We investigated the origin of the degeneration signal in amyloid β (Aβ) induced neuronal cell death in cultured in vitro hippocampal neurons. We discovered that Aβ1–42 toxicity-induced axon degeneration precedes cell death in hippocampal neurons. Overexpression of Bcl-xl inhibited both axonal and cell body degeneration in the Aβ-42 treated neurons. Nicotinamide mononucleotide adenylyltransferase 1 (Nmnat1) blocks axon degeneration in a variety of paradigms, but it cannot block neuronal cell body death. Therefore, if the neuronal death signals in Aβ1–42 toxicity originate from degenerating axons, we should be able to block neuronal death by inhibiting axon degeneration. To explore this possibility we over-expressed Nmnat1 in hippocampal neurons. We found that inhibition of axon degeneration in Aβ1–42 treated neurons prevented neuronal cell death. Thus, we conclude that axon degeneration is the key component of Aβ1–42 induced neuronal degeneration, and therapies targeting axonal protection can be important in finding a treatment for Alzheimer’s disease.

End-stage kidney disease is a terminal stage of chronic kidney disease, which is associated with a high incidence of cardiovascular disease. Cardiovascular disease frequently results from endothelial injury caused by carbamylated LDL (cLDL), the product of LDL modification by urea-derived cyanate. Our previous data suggested that cLDL induces mitogen-activated protein kinase-dependent mitotic DNA fragmentation and cell death. However, the mechanism of this pathway is unknown. The current study demonstrated that cLDL-induced endothelial mitotic cell death is independent of caspase-3. The expression of endonuclease G (EndoG), the nuclease implicated in caspase-independent DNA fragmentation, was significantly increased in response to cLDL exposure to the cells. The inhibition of EndoG by RNAi protected cLDL-induced DNA fragmentation, whereas the overexpression of EndoG induced more DNA fragmentation in endothelial cells. Ex vivo experiments with primary endothelial cells isolated from wild-type (WT) and EndoG knockout (KO) mice demonstrated that EndoG KO cells are partially protected against cLDL toxicity compared with WT cells. To determine cLDL toxicity in vivo, we administered cLDL or native LDL (nLDL) intravenously to the WT and EndoG KO mice and then measured floating endothelial cells in blood using flow cytometry. The results showed an increased number of floating endothelial cells after cLDL versus nLDL injection in WT mice but not in EndoG KO mice. Finally, the inhibitors of MEK-ERK1/2 and JNK-c-jun pathways decreased cLDL-induced EndoG overexpression and DNA fragmentation. In summary, our data suggest that cLDL-induced endothelial toxicity is caspase independent and results from EndoG-dependent DNA fragmentation.