The biology of telomeres and telomerase has been the subject of intensive investigative effort since it became evident that they play a significant role in two important biological processes, the loss of cellular replicative capacity inherent to organismal ageing and the unrestricted cell proliferation characteristic of carcinogenesis. Telomere shortening in normal cells is a result of DNA replication events, and reduction beyond a critical length is a signal for cellular senescence.
Odontogenic keratocysts (OKC) present an aggressive course with a marked tendency to recurrence. The epithelium of OKC is thought to have an intrinsic growth potential and has been shown to present a higher rate of proliferation as compared to other types of cyst. bcl-2 has a role in the extension of cell survival. The objective of the present study was to evaluate the bcl-2 protein expression in different odontogenic cysts. A total of 19 dentigerous cysts (DC), 20 radicular cysts (RC) and 14 OKC were used in the present study. DC and RC showed an almost complete negativity for bcl-2.
The proliferative lifespan of normal mammalian cells is limited by intrinsic controls, which desensitize the cell-cycle machinery to extrinsic stimulation after a given number of cell divisions. One underlying clock driving this process of 'replicative senescence' is the progressive erosion of chromosome telomeres, which occurs with each round of DNA replication. This appears to trigger growth inhibition via activation of the tumour suppressor gene (TSG) product, p53, and the consequent up-regulation of the cell-cycle inhibitor p21WAF1.
Mutations in human CuZn superoxide dismutase (SOD) have been associated with familial amyotrophic lateral sclerosis (FALS). Although leading to many experimental advances, this finding has not yet led to a clear understanding of the biochemical mechanism by which mutations in SOD promote the degeneration of motorneurons that causes this incurable paralytic disease.
The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
The question of whether aging - the process that converts fit adults into frailer adults with a progressively increased risk of illness, injury, and death - is under genetic control is ambiguous, and its answer depends on what one means by aging. Natural selection can select for genes that retard aging, but only in species and niches where the value of prolonged survival outweighs its costs. Although the form aging takes can be affected by variations at many genetic loci the number of loci that moderate the pace of synchronized decay may be far smaller.
During the course of normal respiration, reactive oxygen species are produced which are particularly detrimental to mitochondrial function. This is shown by recent studies with a mouse that lacks the mitochondrial form of superoxide dismutase (Sod2). Tissues that are heavily dependent on mitochondrial function such as the brain and heart are most severely affected in the Sod2 mutant mouse.
Shortening of telomeres occurs with cell proliferation and correlates well with ageing in humans. Telomerase is a ribonucleoprotein, and is the body's most widely studied mechanism for extension of telomeres to circumvent cellular ageing. Telomerase levels remain at low or unmeasurable levels in most somatic cell populations with only a few exceptions. However, in transformed cell populations, upregulation of telomerase or some other mechanism for telomere extension is required for immortality.
Nihon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics
The potential link between aging and insulin signaling has attracted substantial attention since several decades ago, on the basis of evidence including age-related increase in incidence of insulin resistance, insulin resistance and type 2 diabetes in accelerated aging syndromes and lifespan extension by caloric restriction in rodents. In addition, the intensive investigations in C.
Caloric restriction (CR), undernutrition without malnutrition, remains the only experimental paradigm that has been shown consistently to extend lifespan and slow aging in short-lived species. Decades of research, mostly in laboratory rodents, have shown that CR consistently extends lifespan, reduces or delays the onset of many age-related diseases and slows aging in many physiological systems. In recent years gerontologists interested in CR have focused on two unanswered questions. 1) What is the relevance of this nutritional paradigm to human aging?
Radiographics: A Review Publication of the Radiological Society of North America, Inc
Computed tomographic (CT) cystography has been advocated in lieu of conventional cystography in the initial work-up of patients with suspected urinary bladder trauma. CT cystography was applied to a classification scheme for bladder injury based on the degree of wall injury and anatomic location and demonstrated characteristic imaging features for each type of injury. In bladder contusion (type 1), findings are normal.