Medication adherence and environmental barriers to self-care practice among people with diabetes: A cross-sectional study in a lifestyle clinic in eastern India.

Objective: The study was conducted to estimate the prevalence of non-adherence to medications among patients with type 2 diabetes attending a lifestyle clinic in a tertiary care hospital in West Bengal, India; to identify the environmental barriers to self-care practices, including diet, exercise, glucose testing and medication; and to identify the socio-demographic and environmental determinants of medication non-adherence. Methods: A cross-sectional study was performed among the patients with type 2 diabetes taking oral hypoglycemic drugs and attending a lifestyle clinic of a teaching hospital in 2021. The participants were interviewed in clinical settings via a structured questionnaire in the local language. Medication adherence was assessed with Morisky Medication Adherence Scale-8 (MMAS), and environmental barriers were assessed with the Environmental Barrier Assessment Scale (EBAS). Results: Among 178 participants, a high level of adherence (MMAS score 8.0) was found among 3 (1.7%) participants, and moderate adherence (MMAS score 6.0 to 7.75) was found among 67 (37.6%; 95% CI 30.3%, 44.9%) participants. The prevalence of non-adherence was 60.7% (95% CI: 53.4%, 68.0%). The overall mean barrier score was 134 (SD 13). All environmental barrier components were distributed equally among the predictor variables except the diet score, which was lower among men (mean difference 1.3; 95% CI: 0.04, 2.5) and people with higher education (mean difference 1.8; 95% CI: 0.6, 3.1). Conclusion: The study indicated poor adherence to OHA in this population. Barriers to self-care practice and medication adherence were observed acrross all socio-economic strata. Poor medication adherence poses a major challenge to clinicians and public health experts in achieving treatment goals.

Modeling the neuron as a nanocommunication system to identify spatiotemporal molecular events in neurodegenerative disease.

AIM: In tauopathies such as Alzheimer's disease (AD), molecular changes spanning multiple subcellular compartments of the neuron contribute to neurodegeneration and altered axonal signaling. Computational modeling of end-to-end linked events benefit mechanistic analysis and can be informative to understand disease progression and accelerate development of effective therapies. In the calcium-amyloid beta model of AD, calcium ions that are an important regulator of neuronal function undergo dysregulated homeostasis that disrupts cargo loading for neurotrophic signaling along axonal microtubules (MTs). The aim of the present study was to develop a computational model of the neuron using a layered architecture simulation that enables us to evaluate the functionalities of several interlinked components in the calcium-amyloid beta model. METHODS: The elevation of intracellular calcium levels is modeled upon binding of amyloid beta oligomers (AßOs) to calcium channels or as a result of membrane insertion of oligomeric Aß1-42 to form pores/channels. The resulting subsequent Ca2+ disruption of dense core vesicle (DCV)-kinesin cargo loading and transport of brain-derived neurotrophic factor (BDNF) on axonal MTs are then evaluated. Our model applies published experimental data on calcium channel manipulation of DCV-BDNF and incorporates organizational complexity of the axon as bundled polar and discontinuous MTs. The interoperability simulation is based on the Institute of Electrical and Electronics Engineers standard association P1906.1 framework for nanoscale and molecular communication. RESULTS: Our analysis provides new spatiotemporal insights into the end-to-end signaling events linking calcium dysregulation and BDNF transport and by simulation compares the relative impact of dysregulation of calcium levels by AßO-channel interactions, oligomeric Aß1-42 pores/channel formation, and release of calcium by internal stores. The flexible platform of our model allows continued expansion of molecular details including mechanistic and morphological parameters of axonal cytoskeleton networks as they become available to test disease and treatment predictions. CONCLUSION: The present model will benefit future drug studies on calcium homeostasis and dysregulation linked to measurable neural functional outcomes. The algorithms used can also link to other multiscale multi-cellular modeling platforms to fill in molecular gaps that we believe will assist in broadening and refining multiscale computational maps of neurodegeneration.