Biomedical subjects

S Finkelbrand

Publications and source records attributed to S Finkelbrand.

9 recordsLinked to original sources

PubMed1988

Age and exercise-related changes in myocardial mitochondria in mice.

A quantitative histochemical and an ultrastructural study was performed on the left ventricular myocardium of C57BL/6J female mice to evaluate the effects of aging and running exercise on mitochondrial structure and SDH activity. A comparison was made between 6-month-old ("young") and 27-month-old ("old") sedentary mice with age-matched mice subjected to running schedules (10 or 30 min/d) for 6 weeks. In longer-term studies, 27-month-old mice were given similar daily running schedules over a 10 month period ("long term runners"). No significant differences were found in SDH activity during the normal course of aging in mice (6 to 27 months of age), however, the response to running differed markedly in young versus old mice. "Young" trained mice showed significant increase in SDH activity compared with age-matched sedentary mice, whereas "old" trained mice showed significantly reduced SDH activity. Electron microscopy showed ultrastructural changes in mitochondria associated with aging including the development of large aggregations of mitochondria in subsarcolemmal and paranuclear sites. Running schedules, especially in aged runners, caused an increase in interfibrillar mitochondria hypertrophy, loss of matrix and cristae, incorporation of lipid inclusions and the formation of giant mitochondria. These abnormal mitochondrial changes are interpreted as being degenerative and possibly contributing to the reduced SDH levels found in cardiac myocytes of aged runners. Our results indicate that whereas regular exercise in young animals enhanced SDH activity, in aged mice it may be detrimental rather than beneficial.

Aging↗

PubMed1983

Morphometric analysis of aging skeletal muscle following endurance training.

Aging of skeletal muscle in the hindleg of the mouse is accompanied by a progressive increase in the amount of the interstitial tissue and especially that of lipid cells and fibroblasts. Quantitative analysis indicates that there was a nonsignificant increase in the total number of muscle fibers per unit area, perhaps due to a splitting process. The proportion of high oxidative fibers was decreased to a nonsignificant degree, and the remaining high oxidative fibers underwent a significant compensatory hypertrophy. Concomitantly, the number of low oxidative fibers increased significantly. This study revealed that endurance training in young animals induced morphometric changes very similar to those noticed in intact aging animals (i.e., splitting phenomenon, hypertrophy of high oxidative fibers, and an increased proportion of low oxidative fibers). It also became apparent that the skeletal muscle of old animals lacks the capacity to respond to enforced training, except for a further increase in the proportion of low oxidative fibers. It appears that aging muscle is unable to adapt to changing environmental circumstances.

Aging↗

PubMed1981

Changes in gastric parietal cells during prolonged intermittent corticosteroid treatment.

Immature A/J mice were treated for up to 7 weeks with intermittent doses of triamcinolone hexacetonide and were thereafter allowed to recover for 7 weeks. Structural examinations and morphological measurements were performed on the parietal cells in the gastric mucosa. By the 3rd injection a significant decrease was noted in the number of the above cells - a feature that lasted throughout the experimental period. In contrast, the diameter of the parietal cells increased. However, following recovery, the latter returned to their normal size.

Animals↗

PubMed1980

Masseter myopathy following systemic corticosteroid administration: an experimental study.

Immature A/J mice were treated with a series of alternate (every 4 days) doses of triamcinolone hexacetonide, a long-acting synthetic analogue of cortisol, and their masseter muscles were studied ultrastructurally. Various degrees of degenerative changes were found in most myofibers of triamcinolone-treated animals. These changes ranged from local alterations in the configuration of the Z discs to a complete disarray of the myofibrilar architecture. Severely affected myofibers revealed areas with total disintegration of myofilaments, loss of mitochondria, and an almost total depletion of glycogen. In addition, some nuclei were centrally located and an obvious enhancement of collagen fibrillogenesis was found in the endomysial spaces. The latter comprised a mixture of banded collagen fibrils and slender filaments which lacked any specific orientation of organization. Endothelial cells of intramuscular capillaries were hypertrophic, thus evoking a marked occlusion of the vascular lumen. Ultrastructural changes were also noted in axon terminals and in the sole-plate sarcoplasm: loss of synaptic vesicles along with shrinkage of axon terminals, partial loss of postsynaptic folds, and a decrease in the number of mitochondria within the sole-plate sarcoplasm. It is proposed that triamcinolone, even if administered on an alternate schedule, promotes myopathic changes in the masseter muscles of immature mice which, in turn, might possibly contribute to the hormone-retardive effect upon the growth potential of the developing mandible.

Animals↗

PubMed1980

Reversibility of systemic corticosteroid-induced mandibular osteoarthritis: an experimental study in A/J mice.

Immature A/J mice were treated for up to seven weeks with intermittent systemic doses of triamcinolone hexacetonide (4 mg/kg body weight) and were than allowed to recover for seven weeks. Morphological studies were performed on the mandibular condylar cortilage of treated and control animals. By the third dose, obvious structural changes were seen within the cartilaginous matrix. The latter appeared first in the midst of the condylar cartilage and, in the more severe cases, also involved the articular surface. The hormonal catabolic influence intensified progessively so that by the end of the experimental period, most condyles had undergone severe degenerative changes in the form of cartilage fibrillation and ulceration. After the recovery period, experimental condyles had regained their normal appearance. Thus, although intermittent systemic administration of corticosteroid hormone tends to induce osteoarthritic changes in the mandibular joint of the mouse, the mice possess the capacity to undergo full recovery shortly after the termination of the hormonal treatment.

Animals↗

PubMed1979

Long bone growth during prolonged intermittent corticosteroid treatment and subsequent rehabilitation.

Immature A/J mice were treated for up to 7 weeks intermittent doses of triamcinolone hexacetonide and were thereafter allowed to recover for 7 weeks. Qualitative and quantitative morphological measurements were performed on the epiphyseal cartilage plate and diaphyseal bone of the humerus. By the third injection significant structural changes were noted in the cartilaginous tissue followed by a complete cessation of bone growth. The hormonal inhibitory effect on long bone growth lasted throughout the experimental period. However, at the end of the recovery period the length of the humerus was 96% of the normal. In contrast, the humeral width at midshaft and the width of its medullary cavity revealed slower recovery, achieving only 80% of the control values. Following rehabilitation, the growth of experimental epiphyseal plates exceeded that of nontreated animals as their width and the number of hypertrophic chondrocytes were 131% and 125% of their controls respectively. Thus, in A/J mice (a highly susceptible inbred strain of mice) intermittent (every four days) administration of a long-acting corticosteroid hormone arrested endochondral and periosteal bone formation; the former, however, underwent full recovery following the termination of the hormonal treatment.

Animals↗

PubMed1978

Activity of phosphatases and succinic dehydrogenase in the trigeminal ganglion of the corticosteroid-treated mouse.

Immature mice were treated for 21 days with daily doses of triamcinolone diacetate. The trigeminal ganglion was studied enzymatically for the activity of alkaline phosphatase, acid phosphatase, ATPase and succinic dehydrogenase. It became apparent that the prolonged treatment with a potent corticosteroid hormone did not affect significantly the in vivo activity of the above enzymes. Some enzymes even appeared to have increased their intracellular activity. The heterogeneous effect of corticosteroid upon their peripheral target organs is discussed.

Acid Phosphatase↗

PubMed1978

The exocrine pancreas in triamcinolone-treated mice. A light and electron microscopy study.

6-week-old ICR strain female mice were given between 16 and 21 daily injections of the synthetic glucocorticoid, triamcinolone diacetate (8 mg/kg body weight). Portions of their pancreas were examined by light and electron microscopy and compared with untreated littermate controls. Despite marked variability from animal to animal and lobule to lobule, triamcinolone treatment induced increased zymogen depletion and also the development of large basal vacuoles in many acinar cells. At the ultrastructural level, acinar cells show pronounced mitochondrial swelling, which in many instances is accompanied by the development of myelin whorls. The number of cells with distended granular endoplasmic reticulum is increased as is the number of atrophying cells and cells apparently undergoing disintegration. In addition, there are indications of marked activation of interlobular perivascular macrophages which show marked vacuolation. Our observations suggest that pancreatic acinar cells show cytological changes as a result of experimental hypercorticoidism.

Animals↗

PubMed1976

Effect of long-term hyperglucocorticoidism on the neuronal morphology of the trigeminal ganglion of the mouse.

Immature mice were treated for up to 12 weeks with daily doses of triamcinolone diacetate. The trigeminal ganglion was studied histologically at regular intervals. By the tenth injection significant morphological changes were noted in the various nerve cells, followed by marked cellular deterioration in the form of lysis or pyknosis. A possible explanation for the above findings is discussed.

Animals↗