Objective To analyse the process of implementing and enforcing smoke-free environments, tobacco advertising, tobacco taxes and health warning labels from Costa Rica's 2012 tobacco control law. Method Review of tobacco control legislation, newspaper articles and interviewing key informants. Results Despite overcoming decades of tobacco industry dominance to win enactment of a strong tobacco control law in March 2012 consistent with WHO's Framework Convention on Tobacco Control, the tobacco industry and their allies lobbied executive branch authorities for exemptions in smoke-free environments to create public confusion, and continued to report in the media that increasing cigarette taxes led to a rise in illicit trade. In response, tobacco control advocates, with technical support from international health groups, helped strengthen tobacco advertising regulations by prohibiting advertising at the point-of-sale (POS) and banning corporate social responsibility campaigns. The Health Ministry used increased tobacco taxes earmarked for tobacco control to help effectively promote and enforce the law, resulting in high compliance for smoke-free environments, advertising restrictions and health warning label (HWL) regulations. Despite this success, government trade concerns allowed, as of December 2015, POS tobacco advertising, and delayed the release of HWL regulations for 15 months. Conclusions The implementation phase continues to be a site of intensive tobacco industry political activity in low and middle-income countries. International support and earmarked tobacco taxes provide important technical and financial assistance to implement tobacco control policies, but more legal expertise is needed to overcome government trade concerns and avoid unnecessary delays in implementation.

ResumenObjetivo. Analizar la adopción de la ley de control del tabaco de 2012 en Costa Rica. Material y métodos. Revisión de la legislación, artículos de periódicos y entrevistas con informantes clave. Resultados. Los defensores del control del tabaco, en estrecha colaboración con grupos internacionales de salud pública y expertos nacionales, regionales e internacionales, reclutados para testificar en la Asamblea Legislativa, implementaron campañas de comunicación e incidencia política que resultaron en la aprobación en marzo de 2012 de una legislación fuerte y en consonancia con el Convenio Marco para el Control del Tabaco de la Organización Mundial de la Salud. Todo esto a pesar de los esfuerzos de la industria tabacalera que, por décadas, había logrado bloquear la aprobación de una legislación eficaz de control del tabaco en Costa Rica. Conclusión. La experiencia de Costa Rica ilustra cómo con recursos, una buena planificación estratégica, tácticas agresivas y perseverancia, los defensores del control del tabaco pudieron superar la oposición de la industria tabacalera en la Asamblea Legislativa y el Poder Ejecutivo. La adopción de una ley efectiva de control de tabaco ha posicionado a Costa Rica como un líder regional en el control de tabaco.

Functional status is considered the main determinant of healthy aging. Impairment in skeletal muscle and the cardiovascular system, two interrelated systems, results in compromised functional status in aging. Increased oxidative stress and inflammation in older subjects constitute the background for skeletal muscle and cardiovascular system alterations. Aged skeletal muscle mass and strength impairment is related to anabolic resistance, mitochondrial dysfunction, increased oxidative stress and inflammation as well as a reduced antioxidant response and myokine profile. Arterial stiffness and endothelial function stand out as the main cardiovascular alterations related to aging, where increased systemic and vascular oxidative stress and inflammation play a key role. Physical activity and exercise training arise as modifiable determinants of functional outcomes in older persons. Exercise enhances antioxidant response, decreases age-related oxidative stress and pro-inflammatory signals, and promotes the activation of anabolic and mitochondrial biogenesis pathways in skeletal muscle. Additionally, exercise improves endothelial function and arterial stiffness by reducing inflammatory and oxidative damage signaling in vascular tissue together with an increase in antioxidant enzymes and nitric oxide availability, globally promoting functional performance and healthy aging. This review focuses on the role of oxidative stress and inflammation in aged musculoskeletal and vascular systems and how physical activity/exercise influences functional status in the elderly.

In hyperphosphataemic CKD, a defective suppression of high PTH exacerbates HP-mediated osteogenic VSMC differentiation and reduces vascular levels of anti-calcifying sclerostin.

In mammalians, advancing age is associated with sarcopenia, the progressive and involuntary loss of muscle mass and strength. Hyperphosphatemia is an aging-related condition involved in several pathologies. The aim of this work was to assess whether hyperphosphatemia plays a role in the age-related loss of mass muscle and strength by inducing cellular senescence in murine myoblasts and to explore the intracellular mechanism involved in this effect. Cultured mouse C2C12 cells were treated with 10 mM beta-glycerophosphate (BGP] at different periods of time to induce hyperphosphatemia. BGP promoted cellular senescence after 24 h of treatment, assessed by the increased expression of p53, acetylated-p53 and p21 and senescence associated β-galactosidase activity. In parallel, BGP increased ILK expression and activity, followed by mTOR activation and autophagy reduction. Knocking-down ILK expression increased autophagy and protected cells from senescence induced by hyperphosphatemia. BGP also reduced the proliferative capacity of cultured myoblasts. Old mice (24-months-old] presented higher serum phosphate concentration, lower forelimb strength, higher expression of p53 and ILK and less autophagy in vastus muscle than young mice (5-months-old]. In conclusion, we propose that hyperphosphatemia induces senescence in cultured myoblasts through ILK overexpression, reducing their proliferative capacity, which could be a mechanism involved in the development of sarcopenia, since old mice showed loss of muscular strength correlated with high serum phosphate concentration and increased levels of ILK and p53.