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1.

001-es BibID:BIBFORM055220
Első szerző:Cutler, Richard G.
Cím:Concentration of RNA sequences complementary to specific oncogene probes as a function of age and tissue in C57BL/6J male mice / R. G. Cutler, S. Ma, I. Semsei
Dátum:1986
ISSN:0016-9013
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
Megjelenés:Gerontologist. - 26 : Special Issue (1986), p. 71A-72A. -
További szerzők:Ma, Shuyi Semsei Imre (1954-) (vegyész, gerontológus)
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2.

001-es BibID:BIBFORM053876
Első szerző:Cutler, Richard G.
Cím:Development, cancer and aging : possible common mechanisms of action and regulation / R. G. Cutler, I. Semsei
Dátum:1989
ISSN:0022-1422
Megjegyzések:The incidence of most types of cancer intensifies throughout an animal's life span. This correlation of cancer incidence with age raises the question of a possible causative link. Over the past few years there has been a rapid increase in our knowledge of genetic mechanisms of cancer initiation and propagation. In view of these advances, a reevaluation of the links between aging and cancer appears appropriate. This article attempts such a reevaluation and concludes that there is indeed much evidence indicating common causes of cancer and aging. This conclusion is primarily based on the positive correlation between aging rate of different species with their cancer rate and that both cancer and aging may be initiated and propagated by impairments of gene regulation driven by destabilizing processes affecting regulatory elements. Reduction of cancer incidence and aging rate would then be based on enhancing common mechanism acting to maintain proper gene regulation of differentiated cells.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Gerontology. - 44 : 6 (1989), p. 25-34. -
További szerzők:Semsei Imre (1954-) (vegyész, gerontológus)
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3.

001-es BibID:BIBFORM055216
Első szerző:Semsei Imre (vegyész, gerontológus)
Cím:Cancer and aging : possible common mechanisms of oxyradicals in destabilizing proper gene regulation / I. Semsei, R. G. Cutler
Dátum:1990
Tárgyszavak:Orvostudományok Klinikai orvostudományok könyvfejezet
Daganatok
Öregedés
Megjelenés:The Theoretical Bases of Aging Research / eds. Ladislas Robert, Gerhard Hofecker. - p. 141-144.
További szerzők:Cutler, Richard G.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM053875
Első szerző:Semsei Imre (vegyész, gerontológus)
Cím:Tissue and age specific expression of the myc proto-oncogene family throughout the life span of the C57BL/6J mouse strain / Imre Semsei, Shuyi Ma, Richard G. Cutler
Dátum:1989
ISSN:0950-9232
Megjegyzések:The expression of the proto-oncogene myc family (c, L and N) in terms of steady-state mRNA levels was determined in seven different normal non-cancerous tissues throughout the life span (seven different ages) of the C57BL/6J male mouse strain. C-myc oncogene expression was highest in prenatal and newborn ages and then decreased to its lowest levels at about 6 months of age. With further increase of age, a progressive pattern of increase in expression of c-myc was found in brain, liver, skin, and small intestine. However, for kidney, spleen and heart, little or no significant change was evident. Significant differential expression of c-myc was found in most tissues in animals of the same age, with highest expression consistently being found in spleen and liver at all ages. For the N-myc and L-myc oncogenes, expression was also highest in prenatal and newborn tissue as compared to the 6-month young adult, but little or no further change was found at older ages. However, substantial tissue-dependent differences in expression were also found, and no expression at all was detected at any age for N-myc in liver and for L-myc in heart, small intestine and liver. Taken together, these results indicate that the expression of the proto-oncogenes c-, L- and N-myc is dependent not only on tissue and embryonic development, as previously shown by other workers, but also on age past the young adult stage of life span. The age-dependent increase in expression of c-myc oncogene found in normal-appearing non-cancerous tissues is of particular interest as possibly reflecting tissue alterations related to both the aging process and the age-dependent increase in cancer incidence.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Oncogene. - 4 : 4 (1989), p. 465-471. -
További szerzők:Ma, Shuyi Cutler, Richard G.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM053847
Első szerző:Semsei Imre (vegyész, gerontológus)
Cím:The effects of idebenone on DNA and RNA contents as well as synthesis rates of total and poly(A)+ RNA in brain of normal, old C57BL/6J mice and in experimental partial cerebral ischemia of rats / I. Semsei, R. G. Cutler, I. Zs.-Nagy
Dátum:1990
ISSN:0167-4943
Megjegyzések:Effects of idebenone on RNA and DNA contents as well as on synthesis rates of total and poly(A)(+) RNA in the brain were measured in two animal models: (1) Normal young and old, male C57BL/6J mice (6 and 32 months). Idebenone suspended in 5% gum arabic was applied in 50 mg/kg/day dose to old mice for 1 month through a gastric tube. (2) Adult female CFY rats (14-18 months) in which experimental partial cerebral ischemia was induced by bilateral common carotid artery occlusion. Idebenone was administered intraperitoneally in two dose (10mg/kg and 100 mg/kg body weight) 30 min before the interruption of carotid blood flow. DNA content remained invariate during aging in the brain; idebenone treatment did not exert any influence on this parameter. RNA content as well as total and poly(A)(+) RNA synthesis rates, which were measured by incorporation of tritiated uridine into RNA, decreased significantly with age in brain. Idebenone treatment did not cause any essential change of the metabolism of RNA under the given conditions. The RNA and DNA contents of brain were influenced neither by experimental partial cerebral ischemia nor by treatment with idebenone during the ischemia. Partial cerebral ischemia decreased the rate of total and poly(A)(+) RNA synthesis in the brain about 15-45% depending on the methods and basis of expression. This decline could totally be prevented by intraperitoneal application of 10 mg/kg idebenone 30 min before the onset of the partial ischemia. The dose of 100 mg/kg idebenone also elevated the rate of RNA synthesis; however, this increase remained statistically insignificant.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Archives of Gerontology And Geriatrics. - 11 : 3 (1990), p. 293-306. -
További szerzők:Cutler, Richard G. Zs. Nagy Imre
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6.

001-es BibID:BIBFORM053874
Első szerző:Zs. Nagy Imre
Cím:Dysdifferentiation hypothesis of aging and cancer : a comparison with the membrane hypothesis of aging / I. Zs.-Nagy, I. R. G. Cutler, I. Semsei
Dátum:1988
ISSN:0077-8923
Megjegyzések:Our laboratories have been testing the basic concept that the age-dependent deterioration of the molecular components of living systems may be due in part to the biochemical effects of active oxygen species. The dysdifferentiation hypothesis of aging and cancer (DHAC) as well as the membrane hypothesis of aging (MHA) are discussed and compared to each other. These two hypotheses consider cellular mechanisms through which free radical-induced alterations may lead to the aging process. DHAC emphasizes the importance of the instability of the differentiated state of cells and how active oxygen species may interact with the genetic apparatus of cells, leading to improper gene regulation. The evidence supporting this hypothesis includes an age-dependent increase in the expression of specific genes that normally are expected to be repressed. Such evidence now includes the c-myc oncogene as well as an age-dependent decrease in the average methylation level of the entire genome in liver tissue of mice. The central concept of DHAC is that aging is a result of gene regulatory instability and that lifespan is governed by mechanisms acting to stabilize proper gene regulation. MHA is based on the concept that all cellular components are exposed to free-radical attacks, and that the damaging efficiency of the radicals is density-dependent. Compact structures like membranes are consequently more susceptible to damage than cytosolic components. In addition, the cell plasma membrane is exposed to another damaging effect called residual heat damage, which is due to the depolarization-induced discharge of the membrane during the action potential. MHA predicts that a key process of normal differentiation as well as aging is a continuous, age-dependent loss of the passive permeability of the cell membrane for potassium and probably also for water. This is due to a constant difference between the rates of damage and replacement of the membrane components and results in a gradual dehydration of the intracellular mass from the embryonic state to the aging state. The increasing intracellular density will eventually become rate-limiting for many different cellular functions, resulting in the cessation of growth and the beginning of aging. MHA also predicts an overall decrease of gene expression and protein turnover rate during aging. Pharmacological interventions on the cell membrane have supported the validity of MHA and have indicated specific mechanisms of how aging and dysdifferentiation may occur.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Annals of The New York Academy of Sciences. - 521 : 1 (1988), p. 215-225. -
További szerzők:Cutler, Richard G. Semsei Imre (1954-) (vegyész, gerontológus)
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