Biomedical subjects

M D Johnson

Publications and source records attributed to M D Johnson.

At least 109 records · Page 6Linked to original sources

PubMed1995

Effects of dietary restriction on the change in aortic alpha 1-adrenoceptor mediated responses during aging in Fischer 344 rats.

These studies examine changes in alpha 1-adrenoceptor-stimulated contraction, accumulation of inositol phosphates (IPs) and calcium influx during aging, and the effect of dietary restriction. The potency of norepinephrine (NE) at stimulating aortic contraction was highest in aortas from 1-month-old rats compared to 6- or 24-month-old rats, while the potency at stimulating IP accumulation was higher in 6- and 24-month-old rats. The fact that the NE potency for IP accumulation is not decreased with age and is even increased a little, indicates that PI hydrolysis is not limiting for contraction. The data from 24-month-old dietary restricted rats support the same idea. Dietary restriction greatly increased the potency of NE for IP accumulation in the old animals (by 20-fold), but did not restore potency for contraction. Nifedipine (1 microM), a calcium channel blocker, inhibited the NE-stimulated aortic contractile response by 28% in 1-month, 40% in 6-month, and 67% in 24-month-old rats. While nifedipine did not inhibit NE-stimulated IP accumulation in 1-month-old aortas, it inhibited by 30% in 6-month-old aortas and by 27% in 24-month-old aortas. Dietary restriction (DR) did influence the inhibitory effects of nifedipine. Nifedipine inhibition of NE-stimulated contraction in 24-month-old DR rats was comparable to the inhibition in 6-month-old ad libitum (ad lib) controls and was less than in 24-month-old controls. Furthermore, nifedipine was less effective at inhibiting NE-stimulated IP accumulation in aortas from 24-month-old DR rats compared to 24-month-old controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1995

Age-related changes in cardiac norepinephrine release: role of calcium movement.

The purpose of this study was to determine if the age-related decrease in norepinephrine (NE) release from cardiac adrenergic nerve terminals is due to a defect in Ca2+ movement into the nerve terminal or to an alteration in Ca2+ activation of intracellular events leading to NE release. NE release was assessed in cardiac synaptosomes prepared from 6- and 24-month-old male F344 rats. K(+)-induced NE release was significantly greater in young vs old rats. Raising extracellular [Ca2+] increased NE release, but NE release always remained higher in the younger animals. Ionomycin, a Ca2+ ionophore, induced NE release from cardiac synaptosomes, and there was no age difference in the response. The age-related reduction in NE release induced by K+ and the capacity of ionomycin to induce similar NE release in young and old cardiac synaptosomes points to a reduction in Ca2+ movement during depolarization.

Aging↗

PubMed1995

Gliomatosis cerebri presenting as intractable epilepsy during early childhood.

We review 160 cases of gliomatosis cerebri from the literature and report an additional three infants and young children who presented with intractable epilepsy, corticospinal tract deficits, and developmental delay in whom a pathologic diagnosis was made. The progressive nature of the encephalopathy in our cases was documented by serial clinical examination, electroencephalograms, magnetic resonance imaging, and positron emission tomographic scans. The natural history of gliomatosis cerebri was determined by a retrospective review of the literature of 160 cases in 85 reports. The most common neurologic symptoms and signs included corticospinal tract deficits (58%), dementia/mental retardation (44%), headache (39%), seizures (38%), cranioneuropathies (37%), increased intracranial pressure (34%), and spinocerebellar deficits (33%). The most commonly involved central nervous system structures were the centrum semiovale and cerebrum (76%), mesencephalon (52%), pons (52%), thalamus (43%), basal ganglia (34%), and the cerebellum (29%). Fifty-two percent of patients were dead within 12 months of onset. Different grades of glial neoplasm may also coexist within gliomatosis cerebri such as astrocytoma with anaplastic astrocytoma, atypical or anaplastic oligodendroglioma, and glioblastoma multiforme. Hypotheses regarding the pathogenesis of gliomatosis cerebri include blastomatous dysgenesis, diffuse infiltration, multicentric origin, in situ proliferation, and "field transformation." The biologic determinants of whether a transformed glial cell behaves as a relatively localized tumor mass or truly loses anchorage dependence to become migratory as well as proliferative are not understood.

Brain↗

PubMed1995