Resveralogues protect HepG2 cells against cellular senescence induced by hepatotoxic metabolites.

Progressive liver disease and dysfunction cause toxic metabolites including ammonia and unconjugated bilirubin to accumulate in plasma. As the population ages alternatives to liver transplantation become increasingly important. One approach for use as a bridge to transplant or recovery is the use of bioartificial liver systems (BALS) containing primary or immortalised hepatocytes as ex-vivo replacements or supports for endogenous liver function.

Correction: Population type influences the rate of ageing.

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Population type influences the rate of ageing.

Mutation accumulation is one of the major genetic theories of ageing and predicts that the frequencies of deleterious alleles that are neutral to selection until post-reproductive years are influenced by random genetic drift. The effective population size (N) determines the rate of drift and in age-structured populations is a function of generation time, the number of newborn individuals and reproductive value. We hypothesise that over the last 50,000 years, the human population survivorship curve has experienced a shift from one of constant mortality and no senescence (known as a Type-II population) to one of delayed, but strong senescence (known as a Type-I population).

Senescence in the aging process.

The accumulation of 'senescent' cells has long been proposed to act as an ageing mechanism. These cells display a radically altered transcriptome and degenerative phenotype compared with their growing counterparts. Tremendous progress has been made in recent years both in understanding the molecular mechanisms controlling entry into the senescent state and in the direct demonstration that senescent cells act as causal agents of mammalian ageing.