Expanding surgical access in Africa through improved health insurance schemes: A review.

Surgical access remains a pressing public health concern in African nations, with a substantial portion of the population facing challenges in obtaining safe, timely, and affordable surgical care. This paper delves into the impact of health insurance schemes on surgical accessibility in Africa, exploring the barriers, challenges, and future directions. It highlights how high out-of-pocket costs, reliance on traditional healing practices, and inadequate surgical infrastructure hinder surgical utilization. Financing mechanisms often need to be more effective, and health insurance programs face resistance within the informal sector. Additionally, coverage of the poor remains a fundamental challenge, with geographical and accessibility barriers compounding the issue. Government policies, often marked by inconsistency and insufficient allocation of resources, create further obstacles. However, strategic purchasing and fund integration offer avenues for improving the efficiency of health insurance programs. The paper concludes by offering policy recommendations, emphasizing the importance of inclusive policies, streamlined financing mechanisms, coverage expansion, and enhanced strategic purchasing to bridge the surgical access gap in Africa. Decoupling entitlement from the payment of contributions, broadening the scope of coverage for outpatient medicines and related expenses, and enhancing safeguards against overall costs and charges, especially for individuals with lower incomes. Ultimately, by addressing these challenges and harnessing the potential of health insurance schemes, the continent can move closer to achieving universal surgical care and improving the well-being of its people.

Reversal of behavioral decline and neuropathology by a complex vitamin supplement involves modulation of key neurochemical stressors.

Metal ions are crucial for normal neurochemical signaling and perturbations in their homeostasis have been associated with neurodegenerative processes. Hypothesizing that in vivo modulation of key neurochemical processes including metal ion regulation (by transferrin receptor-1: TfR-1) in cells can improve disease outcome, we investigated the efficacy of a complex vitamin supplement (CVS) containing B-vitamins and ascorbic acid in preventing/reversing behavioral decline and neuropathology in rats. Wistar rats (eight weeks-old) were assigned into five groups (n = 8), including controls and those administered CVS (400 mg/kg/day) for two weeks before or after AlCl3 (100 mg/kg)-induced neurotoxicity. Following behavioral assessments, prefrontal cortex (PFC) and hippocampus were prepared for biochemical analyses, histology and histochemistry. CVS significantly reversed reduction of exploratory/working memory, frontal-dependent motor deficits, cognitive decline, memory dysfunction and anxiety. These correlated with CVS-dependent modulation of TfP-1 expression that were accompanied by significant reversal of neural oxidative stress in expressed superoxide dismutase, nitric oxide, catalase, glutathione peroxidase and malondialdehyde. Furthermore, CVS inhibited neural bioenergetics dysfunction, with increased labelling of glucokinase within PFC and hippocampus correlating with increased glucose-6-phosphate dehydrogenase and decreased lactate dehydrogenase expressions. These relates to inhibition of over-expressed acetylcholinesterase and increased total protein synthesis. Histological and Nissl staining of thin sections corroborated roles of CVS in reversing AlCl3-induced neuropathology. Summarily, we showed the role of CVS in normalizing important neurochemical molecules linking concurrent progression of oxidative stress, bioenergetics deficits, synaptic dysfunction and cellular hypertrophy during neurodegeneration.