RESUMEN
Global outdoor biomass burning is a major contributor to air pollution, especially in low- and middle-income countries. Recent years have witnessed substantial changes in the extent of biomass burning, including large declines in Africa. However, direct evidence of the contribution of biomass burning to global health outcomes remains limited. Here, we use georeferenced data on more than 2 million births matched to satellite-derived burned area exposure to estimate the burden of biomass fires on infant mortality. We find that each additional square kilometer of burning is associated with nearly 2% higher infant mortality in nearby downwind locations. The share of infant deaths attributable to biomass fires has increased over time due to the rapid decline in other important causes of infant death. Applying our model estimates across harmonized district-level data covering 98% of global infant deaths, we find that exposure to outdoor biomass burning was associated with nearly 130,000 additional infant deaths per year globally over our 2004 to 2018 study period. Despite the observed decline in biomass burning in Africa, nearly 75% of global infant deaths due to burning still occur in Africa. While fully eliminating biomass burning is unlikely, we estimate that even achievable reductions-equivalent to the lowest observed annual burning in each location during our study period-could have avoided more than 70,000 infant deaths per year globally since 2004.
Asunto(s)
Contaminantes Atmosféricos , Contaminación del Aire , Incendios , Lactante , Humanos , Biomasa , Mortalidad Infantil , Muerte del Lactante , Mortalidad , Contaminantes Atmosféricos/análisisRESUMEN
COVID-19, aka Coronavirus Disease 2019, triggered by new severe acute respiratory syndrome coronavirus-2 or SARS-CoV-2, is now a public health emergency due to its rapid spread, high transmission efficiency, and severe viral pandemic that is significantly increasing the number of patients and associated deaths. Currently, no specific treatment is available for this highly contagious virus. The unavailability of effective and specific treatments and the severity of this epidemic situation potentiate medicinal chemists' in supporting new prophylactic or therapeutic interventions against COVID-19. This study discusses the therapeutic potential of hesperidin, a traditionally used herbal medicine with an exceptional safety profile. Recent studies on hesperidin advocate its promising potential in the prevention and management of COVID-19. This paper also discusses the recent clinical studies based on the previously documented antiviral activity of hesperidin. Herein, we propose the detailed preclinical and clinical manifestations of hesperidin based on its multifaceted bioactivities to develop a novel anti-COVID-19 lead.
Asunto(s)
COVID-19 , Hesperidina , Humanos , SARS-CoV-2 , Hesperidina/farmacología , Hesperidina/uso terapéutico , Antivirales/farmacología , Antivirales/uso terapéutico , PandemiasRESUMEN
Nephropathy has become the most common reason for end-stage renal disease worldwide. The progression of end-stage renal disease occurs caused by decreased glomerular filtration rate, damage to capillaries in renal glomeruli or a higher risk of cardiovascular morbidity and mortality in diabetic patients. The involvement of mechanism in the development of nephropathy via generation of AGEs, the elevation of growth factors, altered hemodynamic and metabolic factors, inflammatory mediators, oxidative stress and dyslipidaemia. The prevalence of chronic kidney disease in India will rise from 3.7 million in 1990 to 7.63 million in 2020 becoming the main cause of mortality and morbidity. The pathogenesis of nephropathy mediates by various molecules that cause alterations in the structure and function of the kidney like growth factors, endothelins, transforming growth factor (TGF-ß), and Angiotensin-converting enzymes (ACE), fibronectin and proinflammatory cytokines, mast cells and dyslipidemia. Growth factors like VEGF, IGFs, PDGF, EGFR and TGF-ß contribute to excessive extracellular matrix accumulation, together with thickening of the glomerular and tubular basement membranes and an increase in the mesangial matrix, leading to glomerulosclerosis and tubulointerstitial fibrosis. Oxidative stress and inflammation factors like TNF-α, IL-1 and IL-6 are hypothesized to play a role in the development of pathological changes in nephropathy like renal hyperfiltration and hypertrophy, thickening of the glomerular basement membrane (GBM), glomerular lesion and tubulointerstitial fibrosis. Dyslipidemia is involved in the progression of nephropathy by impaired action of lipoprotein lipase, lecithincholesterol acyltransferase (LCAT) and cholesteryl ester transferase protein (CETP) resulting in the increased level of LDL-C, Triglyceride level and decrease HDL-C that enhance macrophage infiltration, excessive extracellular matrix production and accelerate inflammation with the development of proteinuria. Interruption in the RAS, oxidative stress and dyslipidemia have yielded much better results in terms of reno-protection and progression of nephropathy. In this review, we would focus on various factors that have been shown to contribute to renal injury in many experimental models of nephropathy.