Cell Count

Normal human diploid cells, TIG-1, ceased to proliferate at about the 62 population doubling level (PDL). Transformed clones isolated from TIG-1 cells infected with wtSV40 and those with tsA900 SV40 cultured at 34 degrees C were subcultured up to about 80 PDL. When the culture temperature of tsA SV40-transformed cells was shifted from 34 to 39.5 degrees C at 51 PDL, the growth curve of these transformed cells changed to that of normal young cells.

An increasing number of people are living past the age of 100 years, but little is known about what differentiates centenarians from the rest of the population. In this study, brains from female subjects in 3 different age groups, 65-75 years (n = 8), 76-85 years (n = 8), and 94-105 years (n = 7), were examined to estimate the total number of neocortical neurons, astrocytes, oligodendrocytes, and microglia.

Cardiovascular (CV) diseases and related complications are the main causes of morbidity and mortality in the elderly. CV progenitor cells, including CD34+ cells, play a role in delaying the progression of atherosclerosis. In the present study we observed 100 octogenarians for seven years, in order to address the question of whether CD34+ cell number is a predictor of longevity in selected survivors.

Cellular senescence is a defense mechanism in response to molecular damage which accumulates with aging. Correspondingly, the number of senescent cells has been reported to be greater in older than in younger subjects and furthermore associates with age-related pathologies. Inter-individual differences exist in the rate at which a person ages (biological age). Here, we studied whether younger biological age is related to fewer senescent cells in middle-aged individuals with the propensity for longevity, using p16INK4a as a marker for cellular senescence.

An increasing number of people are living past the age of 100 years, but little is known about what differentiates centenarians from the rest of the population. In this study, brains from female subjects in 3 different age groups, 65-75 years (n = 8), 76-85 years (n = 8), and 94-105 years (n = 7), were examined to estimate the total number of neocortical neurons, astrocytes, oligodendrocytes, and microglia.

Insulin-like growth factor 1 (IGF-1) is a critical regulator of many physiological functions, ranging from longevity to immunity. However, little is known about the role of IGF-1 in natural killer cell development and function. Here, we identify an essential role for IGF-1 in the positive regulation of human natural killer cell development and cytotoxicity. Specifically, we show that human natural killer cells have the ability to produce IGF-1 and that differential endogenous IGF-1 expression leads to disparate cytotoxicity in human primary natural killer cells.

Ageing can have profound effects on the post-mitotic organ of behaviour, the brain. As yet the precise causes of these deleterious effects are unknown. However, clear insights into the putative mechanisms and consequences of ageing in the CNS have been achieved through the use of invertebrate models. It is now clear that ageing alters the endogenous properties of neurones, their morphology, the efficacy of the connections that the neurones make with their targets and may even lead to neurone loss.

How adult tissue stem and niche cells respond to the nutritional state of an organism is not well understood. Here we find that Paneth cells, a key constituent of the mammalian intestinal stem-cell (ISC) niche, augment stem-cell function in response to calorie restriction. Calorie restriction acts by reducing mechanistic target of rapamycin complex 1 (mTORC1) signalling in Paneth cells, and the ISC-enhancing effects of calorie restriction can be mimicked by rapamycin.