Domestic Violence and Health Care: Opening Pandora¿s Box ¿ Challenges and Dilemmas

In this article we take a critical stance toward the rational progressive narrative surrounding the integration of domestic violence within health care. Whilst changes in recent UK policy and practice have resulted in several tangible benefits, it is argued that there may be hidden dilemmas and challenges. We suggest that the medical model of care and its discursive practices position women as individually accountable for domestic violence-related symptoms and injuries. This may not only be ineffective in terms of service provision but could also have the potential to reduce the political significance of domestic violence as an issue of concern for all women. Furthermore, it is argued that the use of specific metaphors enables practitioners to distance themselves from interactions that may prove to be less comfortable and provide less than certain outcomes. Our analysis explores the possibilities for change that might currently be available. This would appear to involve a consideration of alternative discourses and the reformulation of power relations and subject positions in health care

Reproductive biology of Cattleya eldorado, a species of Orchidaceae from the Amazonian white sand campinas

The orchid plants are highly prized for their lush exotic flowers. It is the largest plant family with more than 24000 species, which indicates a high diversity of forms and adaptations to different environments, including the capacity to attract, deceive and manipulate visitors involved in cross-pollination. Cattleya eldorado occurs in areas of white sand campinas, a typical vegetation type of the Amazon region, which is under strong anthropogenic pressure. This work's main objectives to know the biological processes of C. eldorado providing subsidies to maintain and manage it in its natural habitat. This study was conducted from 2000 to 2006 in the Campina Biological Reserve, during its flowering period. C. eldorado is an epiphytic orchid species that has the melittophyly syndrome and is adapted to its pollinator, the bee Eulaema mocsaryi recognizing their flowers by smell and by visual stimuli, through their color and reflection of ultraviolet light. C. eldorado is self-compatible, even if it requires a pollinating agent for the transfer of the pollinarium until its deposition in the stigmatic cavity of the flower.", 'enAs Orchidaceae são muito apreciadas por suas flores exóticas e exuberantes. É a maior família de plantas apresentando mais de 24000 espécies, o que denota uma alta diversidade de formas e adaptações a diferentes ambientes, como também para atração, engano e manipulação de visitantes na realização da polinização cruzada. Cattleya eldorado ocorre em áreas de campinas, que são formações vegetais típicas da região amazônica, que se encontram sob forte ação antrópica. Este trabalho tem como um de seus principais objetivos conhecer parte dos processos biológicos de C. eldorado fornecendo subsídios para conservá-la e manejá-la em seu habitat natural. Este estudo foi desenvolvido na Reserva Biológica de Campina, de 2000 a 2006, durante a sua floração. C. eldorado é uma espécie epifítica que apresenta a síndrome de melitofilia, estando adaptada ao seu polinizador, a abelha Eulaema mocsaryi, que reconhece suas flores pelo odor e pelo estímulo visual através de sua coloração e reflexão de luz ultravioleta. C. eldorado é uma espécie autocompatível, embora necessite de um agente polinizador para a transferência do polinário até sua deposição na cavidade estigmática da flor

Amyloid and tau pathology associations with personality traits, neuropsychiatric symptoms, and cognitive lifestyle in the preclinical phases of sporadic and autosomal dominant Alzheimer’s disease

Background Major prevention trials for Alzheimer’s disease (AD) are now focusing on multidomain lifestyle interventions. However, the exact combination of behavioral factors related to AD pathology remains unclear. In 2 cohorts of cognitively unimpaired individuals at risk of AD, we examined which combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle (years of education or lifetime cognitive activity) related to the pathological hallmarks of AD, amyloid-β, and tau deposits. Methods A total of 115 older adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomatic EValuation of Experimental or Novel Treatments for AD] cohort) underwent amyloid and tau positron emission tomography and answered several questionnaires related to behavioral attributes. Separately, we studied 117 mutation carriers from the DIAN (Dominant Inherited Alzheimer Network) study group cohort with amyloid positron emission tomography and behavioral data. Using partial least squares analysis, we identified latent variables relating amyloid or tau pathology with combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle. Results In PREVENT-AD, lower neuroticism, neuropsychiatric burden, and higher education were associated with less amyloid deposition (p = .014). Lower neuroticism and neuropsychiatric features, along with higher measures of openness and extraversion, were related to less tau deposition (p = .006). In DIAN, lower neuropsychiatric burden and higher education were also associated with less amyloid (p = .005). The combination of these factors accounted for up to 14% of AD pathology. Conclusions In the preclinical phase of both sporadic and autosomal dominant AD, multiple behavioral features were associated with AD pathology. These results may suggest potential pathways by which multidomain interventions might help delay AD onset or progression

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease