23 research outputs found
Tablet-based disclosure counselling for HIV-infected children, adolescents, and their caregivers: a pilot study
BACKGROUND:
Overwhelmed, under-trained medical staff working in resource-limited settings need efficient resources for HIV disclosure counselling. The objective of this study was to describe providers' experiences using tablet computers for disclosure-related counselling with HIV-infected children and their caregivers in western Kenya, with additional perspectives from adolescents.
METHODS:
A qualitative study design was implemented at three HIV clinics in western Kenya (Bumala, Busia and Port Victoria) within the Academic Model Providing Access to Healthcare (AMPATH) partnership. Twenty-one healthcare providers involved with paediatric disclosure were recruited and enrolled in the study. Initial interviews focused on understanding current disclosure practices and barriers. Tablets containing disclosure-related resources were distributed. Resources included short narrative videos created in this context to highlight issues relevant to child HIV disclosure.
RESULTS:
Providers reported tablets improved disclosure, child participation, and medication adherence. All reported that reviewing materials increased their knowledge and comfort with disclosure. The most frequently used materials were the narrative videos and an animated video explaining the importance of medication adherence. Time was a major barrier for using the tablet. Clinician self-education persisted at one-year follow-up. Adolescents expressed enjoyment from viewing the tablet resources and had a better understanding of the importance of medication adherence.
CONCLUSIONS:
Tablet computers containing resources for disclosure are an acceptable and potentially effective resource to help providers support families with disclosure. Further work is needed to train the clinical providers in using the resources in a developmentally appropriate manner, and to develop new resources on adolescent-specific and HIV-related topics
Obesity remodels activity and transcriptional state of a lateral hypothalamic brake on feeding
The current obesity epidemic is a major worldwide health concern. Despite the consensus that the brain regulates energy homeostasis, the neural adaptations governing obesity are unknown. Using a combination of high-throughput single-cell RNA sequencing and longitudinal in vivo two-photon calcium imaging, we surveyed functional alterations of the lateral hypothalamic area (LHA) - a highly conserved brain region that orchestrates feeding - in a mouse model of obesity. The transcriptional profile of LHA glutamatergic neurons was affected by obesity, exhibiting changes indicative of altered neuronal activity. Encoding properties of individual LHA glutamatergic neurons were then tracked throughout obesity, revealing greatly attenuated reward responses.These data demonstrate how diet disrupts the function of an endogenous feeding suppression system to promote overeating and obesity
Novel Cleft Susceptibility Genes in Chromosome 6q
Cleft lip/palate is a defect of craniofacial development. In previous reports, chromosome 6q has been suggested as a candidate region for cleft lip/palate. A multipoint posterior probability of linkage analysis of multiplex families from the Philippines attributed an 88% probability of harboring a cleft-susceptibility gene to a narrower region on bands 6q14.2-14.3. We genotyped 2732 individuals from families and unrelated individuals with and without clefts to investigate the existence of possible cleft-susceptibility genes in this region. We found association of PRSS35 and SNAP91 genes with cleft lip/palate in the case-control cohort and in Caucasian families. Haplotype analyses support the individual associations with PRSS35. We found Prss35 expression in the head and palate of mouse embryos at critical stages for palatogenesis, whereas Snap91 was expressed in the adult brain. We provide further evidence of the involvement of chromosome 6q in cleft lip/palate and suggest PRSS35 as a novel candidate gene