Development and Evaluation of a Smartphone-enabled, Carer-supported Educational Intervention for Management of Disabilities Following Stroke in India

Background The incidence and prevalence of stroke in India has reached epidemic proportions and is considered a major public health problem. Given the nature of the condition, affected individuals often become disabled, with profound effects on their quality of life. This study aimed to develop an educational intervention for management of post-stroke disability in India and to evaluate the feasibility and acceptability of delivering this intervention using Smartphone technology and caregiver support. Objectives:- To systematically develop a Smartphone-enabled, carer-supported, educational intervention that is multi-disciplinary, patient-centred and culturally-sensitive for management of disabilities following stroke in India. -To evaluate the feasibility and acceptability of the intervention by stroke survivors and their caregivers in the Indian context. Methodology The study was conducted in Chennai, India, and was implemented in three phases: Phase 1: Development of the intervention Phase 2: Field-testing and finalising of the intervention Phase 3: Piloting of the intervention and assessment of feasibility and acceptability. A mixed methods approach was used to develop and evaluate the intervention. Results The intervention was systematically developed and titled ‘Care for Stroke’. It was delivered through a web-based, Smartphone-enabled application. During field-testing, key uncertainties, such as issues with connectivity, video streaming, picture clarity, quality of the videos and functionality of the application, were identified. The intervention was reviewed, revised and finalised before pilot-testing. Findings from the pilot-testing showed that the ‘Care for Stroke’ intervention was feasible and acceptable in an Indian context. Over 90% of the study participants felt that the intervention was relevant, comprehensible and useful. About 95% of the stroke survivors and all the caregivers (100%) rated the intervention to be excellent, based on its overall credibility, usability and user-friendliness. Discussion ‘Care for Stroke’ is an innovative educational intervention that can empower stroke survivors and their families to be cognisant of their disability, ways to manage it and how to make appropriate decisions on their road to recovery. The current context for stroke rehabilitation provides a reasonable opportunity for public health practitioners to optimise interventions such as ‘Care for Stroke’ to efficiently bridge the gaps in accessibility of stroke rehabilitation services and enhance the continuum of care for stroke survivors worldwide. The intervention is specifically pertinent to India and many other Low and Middle-Income Countries (LIMCs) where resources for improving access to stroke rehabilitation services are inadequate. Conclusion ‘Care for Stroke’ is an innovative effort towards the global need for research to develop interventions that bridge the barriers to the provision of stroke rehabilitation services and meet the needs of affected individuals. This application and similar approaches that harness the potential of current technology need to be researched further to bridge the gaps in access to stroke services worldwide

Sex Differences in the uptake of health care services in persons with disabilities. Identifying barriers to health care access

Background Evidence suggests that disability is more common among vulnerable populations which include women, elderly and children. And people with disabilities face widespread barriers in accessing services in relation to health, education, employment and transport. This study looks at the barriers women with disability face in accessing heath care services. The present study was undertaken in two states of India - Andhra Pradesh (Medak district) and Karnataka (Bidar). This is a descriptive study with a nested case control for comparison of access to health, education and employment status among those with and without disability The study was funded by CBM South Asia Regional Office (SARO) and was technically supported by CBM SARO Aim The main aim of the study was to look into whether women with disability have equitable access to health care in India and if there are disparities in access, the underlying causes and reasons for the same

The non-pathogenic mycobacteria M. smegmatis and M. fortuitum induce rapid host cell apoptosis via a caspase-3 and TNF dependent pathway

<p>Abstract</p> <p>Background</p> <p>The HIV pandemic raised the potential for facultative-pathogenic mycobacterial species like, <it>Mycobacterium kansasii</it>, to cause disseminating disease in humans with immune deficiencies. In contrast, non-pathogenic mycobacterial species, like <it>M. smegmatis</it>, are not known to cause disseminating disease even in immunocompromised individuals. We hypothesized that this difference in phenotype could be explained by the strong induction of an innate immune response by the non-pathogenic mycobacterial species.</p> <p>Results</p> <p>A comparison of two rapid-growing, non-pathogenic species (<it>M. smegmatis </it>and <it>M. fortuitum</it>) with two facultative-pathogenic species (<it>M. kansasii </it>and <it>M. bovis </it>BCG) demonstrated that only the non-pathogenic bacteria induced strong apoptosis in human THP-1 cells and murine bone marrow-derived macrophages (BMDM) and dendritic cells (BMDD). The phospho-<it>myo</it>-inositol modification of lipoarabinomannan (PI-LAM) isolated from non-pathogenic species may be one of the cell wall components responsible for the pro-inflammatory activity of the whole bacteria. Indeed, PI-LAM induces high levels of apoptosis and IL-12 expression compared to the mannosyl modification of LAM isolated from facultative-pathogenic mycobacteria. The apoptosis induced by non-pathogenic <it>M. smegmatis </it>was dependent upon caspase-3 activation and TNF secretion. Consistently, BALB/c BMDM responded by secreting large amounts of TNF upon infection with non-pathogenic but not facultative-pathogenic mycobacteria. Interestingly, C57Bl/6 BMDM do not undergo apoptosis upon infection with non-pathogenic mycobacteria despite the fact that they still induce an increase in TNF secretion. This suggests that the host cell signaling pathways are different between these two mouse genotypes and that TNF is necessary but not sufficient to induce host cell apoptosis.</p> <p>Conclusion</p> <p>These results demonstrate a much stronger induction of the innate immune response by non-pathogenic versus facultative-pathogenic mycobacteria as measured by host cell apoptosis, IL-12 and TNF cytokine induction. These observations lend support to the hypothesis that the strong induction of the innate immune response is a major reason for the lack of pathogenicity in fast-growing mycobacteria.</p

Functional Dichotomy between NKG2D and CD28-Mediated Co-Stimulation in Human CD8+ T Cells

Both CD28 and NKG2D can function as co-stimulatory receptors in human CD8+ T cells. However, their independent functional contributions in distinct CD8+ T cell subsets are not well understood. In this study, CD8+ T cells in human peripheral blood- and lung-derived lymphocytes were analyzed for CD28 and NKG2D expression and function. We found a higher level of CD28 expression in PBMC-derived naïve (CD45RA+CD27+) and memory (CD45RA−CD27+) CD8+ T cells (CD28Hi), while its expression was significantly lower in effector (CD45RA+CD27−) CD8+ T cells (CD28Lo). Irrespective of the differences in the CD28 levels, NKG2D expression was comparable in all three CD8+ T cell subsets. CD28 and NKG2D expressions followed similar patterns in human lung-resident GILGFVFTL/HLA-A2-pentamer positive CD8+ T cells. Co-stimulation of CD28Lo effector T cells via NKG2D significantly increased IFN-γ and TNF-α levels. On the contrary, irrespective of its comparable levels, NKG2D-mediated co-stimulation failed to augment IFN-γ and TNF-α production in CD28Hi naïve/memory T cells. Additionally, CD28-mediated co-stimulation was obligatory for IL-2 generation and thereby its production was limited only to the CD28Hi naïve/memory subsets. MICA, a ligand for NKG2D was abundantly expressed in the tracheal epithelial cells, validating the use of NKG2D as the major co-stimulatory receptor by tissue-resident CD8+ effector T cells. Based on these findings, we conclude that NKG2D may provide an expanded level of co-stimulation to tissue-residing effector CD8+ T cells. Thus, incorporation of co-stimulation via NKG2D in addition to CD28 is essential to activate tumor or tissue-infiltrating effector CD8+ T cells. However, boosting a recall immune response via memory CD8+ T cells or vaccination to stimulate naïve CD8+ T cells would require CD28-mediated co-stimulation