We aim to investigate the obstacles faced by elderly indigenous individuals in the Chittagong Hill Tracts, Bangladesh when accessing healthcare services. A qualitative research approach was utilized, and data collection was carried out in three distinct regions of the aforementioned area. A total of 30 in-depth, semi-structured interviews and participant observations were conducted to achieve the research objectives. Thematic analysis utilizing both a deductive and inductive approach was employed to analyze the data. The Granheim method and Nvivo-12 software were utilized to process, analyze and code the data. The study's findings indicate that a lack of knowledge about healthcare needs, geographical barriers, poor financial conditions, higher cost of medical services, scarcity of hospitals nearby and communication barriers all contribute to inadequate access to healthcare services. By recognizing the factors that impede access to healthcare services in this region, this study offers valuable insight for policymakers and healthcare providers on how to enhance healthcare services for the indigenous population, especially the elderly. Furthermore, the government can adopt a more efficient approach to include these elderly individuals in various social safety net programs.
Glypican-3 (GPC3), a membrane-bound heparan sulfate proteoglycan, has long been found to be dysregulated in human lung adenocarcinomas (LUADs). Nevertheless, the function, mutational profile, epigenetic regulation, co-expression profile, and clinicopathological significance of the GPC3 gene in LUAD progression are not well understood. In this study, we analyzed cancer microarray datasets from publicly available databases using bioinformatics tools to elucidate the above parameters. We observed significant downregulation of GPC3 in LUAD tissues compared to their normal counterparts, and this downregulation was associated with shorter overall survival (OS) and relapse-free survival (RFS). Nevertheless, no significant differences in the methylation pattern of GPC3 were observed between LUAD and normal tissues, although lower promoter methylation was observed in male patients. GPC3 expression was also found to correlate significantly with infiltration of B cells, CD8+, CD4+, macrophages, neutrophils, and dendritic cells in LUAD. In addition, a total of 11 missense mutations were identified in LUAD patients, and ~1.4% to 2.2% of LUAD patients had copy number amplifications in GPC3. Seventeen genes, mainly involved in dopamine receptor-mediated signaling pathways, were frequently co-expressed with GPC3. We also found 11 TFs and 7 miRNAs interacting with GPC3 and contributing to disease progression. Finally, we identified 3 potential inhibitors of GPC3 in human LUAD, namely heparitin, gemcitabine and arbutin. In conclusion, GPC3 may play an important role in the development of LUAD and could serve as a promising biomarker in LUAD.