Asunto(s)
Gastroenterología , Humanos , Cambio Climático , Tracto Gastrointestinal , Sociedades MédicasAsunto(s)
Huella de Carbono , Cambio Climático , Conservación de los Recursos Naturales , Gastroenterología , Enfermedades Gastrointestinales , Eliminación de Residuos Sanitarios , Residuos Sanitarios , Equipos Desechables , Equipo Reutilizado , Enfermedades Gastrointestinales/diagnóstico , Enfermedades Gastrointestinales/epidemiología , Enfermedades Gastrointestinales/terapia , Humanos , Residuos Sanitarios/efectos adversos , ReciclajeRESUMEN
Climate change has been described as the greatest public health threat of the 21st century. It has significant implications for digestive health. A multinational team with representation from all continents, excluding Antarctica and covering 18 countries, has formulated a commentary which outlines both the implications for digestive health and ways in which this challenge can be faced.
Asunto(s)
Cambio Climático , Gastroenterología , HumanosAsunto(s)
Salud Global , Efecto Invernadero , Rol del Médico , Política , Predicción , Humanos , LiderazgoRESUMEN
In normal human cells, telomeres shorten with successive rounds of cell division, and immortalization correlates with stabilization of telomere length. These observations suggest that human cancer cells achieve immortalization in large part through the illegitimate activation of telomerase expression. Here, we demonstrate that the rate-limiting telomerase catalytic subunit hTERT is expressed in cycling primary presenescent human fibroblasts, previously believed to lack hTERT expression and telomerase activity. Disruption of telomerase activity in normal human cells slows cell proliferation, restricts cell lifespan, and alters the maintenance of the 3' single-stranded telomeric overhang without changing the rate of overall telomere shortening. Together, these observations support the view that telomerase and telomere structure are dynamically regulated in normal human cells and that telomere length alone is unlikely to trigger entry into replicative senescence.