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Biomedical subjects

G Hofecker

Publications and source records attributed to G Hofecker.

59 records · Page 4Linked to original sources
PubMedDate not supplied

The effect of aging on laboratory values in dogs.

The main objective of this study was to examine age-associated changes in laboratory values in dogs in order to establish standard values for dogs of a certain age. These standard values could serve to judge the health status of individual dogs and possibly estimate their remaining life expectancy. Thus, haematological and immunological parameters, plasma constituents, kidney characteristics and the capacity of homeostasis were determined in German shephard dogs (0.5-13.5 years) and beagles (4-9 years). Significant changes were noted. We detected that the number of white blood cells declines with age. The change in a number of organ specific enzymes indicates organ involution and increased cell death. Increased plasma glucose levels and a decreased glucose tolerance point to a diminished sensitivity of tissue to concentrations change due to a decrease in organ production and changes in the immune system, which are also reflected in an impaired lymphocyte proliferation capacity. These factors lead to an increased blood sedimentation rate. Cortisol increases might reflect a reduced stress resistance. Age-related decreases in aldosterone concentration and PAH-clearance were also found.

Aging↗
PubMedDate not supplied

The change in the supply with reduction equivalents in different organs of the rat during aging.

The rate of metabolic kinetics and the frequency of biological cycles may be correlated with the rate of aging and the maximum life-span potential. Therefore, investigation either into changes with age of such parameters within one species or into differences between species may give some information about the genetic programming of the aging process. Male Sprague-Dawley rats aged 3.5, 7, 12, 17, 23, and 33 months (m) were used to determine the changes with age of those metabolic pathways mentioned in the title, using the liver (LI), kidney (KI), brain (BR), heart (HE) and the skeletal muscle (SM). The maximum percentage of glucose utilization via the pentose pathway, compared to the total glucose utilization, was calculated after intravenous administration of D-[1-14C]- and D-[6-14C]glucose by the determination of the trioses (as lipids) 3 hours after the application. Furthermore, in rats aged 13 and 25 m the kinetics of both glucoses was measured in liver, kidney, heart, brain, skeletal muscle, spleen (SP), and testes (TE) during the first 3 hours after application. Pentose pathway values were calculated. The results indicate a decrease in the glucose utilization via the pentose pathway in the course of aging in liver, kidney, heart and skeletal muscle and a decrease from 3.5 months on in brain, younger rats exhibit a higher rate of glucose utilization via the pentose pathway as do old ones, the reduction of the pentose pathway may possibly be the cause of higher lipofuscin accumulation in the cells of some organs, lacking sufficient reduction equivalents for lipid metabolism.

Aging↗
PubMedDate not supplied

[Physiosclerosis of various blood vessels in the rat].

The rat is notoriously resistant to atherosclerosis, however, physiosclerosis appears to develop in the rat in the same way as in man. Since physiosclerosis is very likely to set the stage for the development of atherosclerosis, there must be a fundamental difference in physiosclerosis between man and rat. In an investigation of this difference, we analyzed stress-strain curves of the aorta and determined the lipid and calcium content of several blood vessels of male Sprague-Dawley rats at various ages between 9 and 33 months. Physiosclerosis was mainly due to an increase in the amount and rigidity of collagen with no sign of early elastolysis. Lipid concentration paralleled increasing plasma level only in early senescence and decreased after an age of 18 months. Calcium obviously accumulates at the same speed as in man, dependent on the chronological rather than on the biological age. In the short-lived rat it, therefore, does not reach the high levels found in man (Fleckenstein, 1983), which may trigger changes in smooth muscle cells related to the onset of atherosclerosis.

Age Factors↗
PubMedDate not supplied

[Is selection for extended life expectancy possible by regularity in aging?].

To answer this question it is important to explain the mode of development of the different maximum life span potentials (MLP) during evolution. We know by empiric-historical investigations, that at least later in evolution appearing species of mammals possess a higher MLP. What does then mean a "regular process"? The aging process is a regular one, being a physiologic event, in the character of that what all we can determine at it, as far as it allows explanation and prediction. This did succeed in a high degree during the until now short tradition of experimental gerontology. We refer to experimental results not only from the literature but also from our own work on repair, genetic and metabolic changes and multivariate investigations into the biological age, to decide from two hypotheses of the causes of aging, how the title question can be answered: a) aging as a programmed event, brought about by aging genes, controlled by an intrinsic clock. These genes should restrict life expectancy or the replicative capacity of cells--hence the adaptive hypothesis; b) aging as a consequence of the accumulation of errors counteracted by antibiosenescent strategies (AS)--hence nonadaptive hypotheses, the most plausible one being that of the disposable soma. Later species are adapted better to changing environmental conditions by their other development, their ecological niches are larger, their environment contains specifically lesser dangers and risks, because they better cope with them--therefore it is worth while to spend more energy for the maintenance of their soma than for their reproduction: they develop better and more AS.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗