Biomedical subjects

J A Strong

Publications and source records attributed to J A Strong.

75 records · Page 5Linked to original sources

PubMedDate not supplied

The assessment of postmenopausal osteoporosis by total body neutron activation analysis.

Total body calcium (TBCa) was measured using a cyclotron for in vivo neutron activation analysis (IVNAA) in 20 healthy women, 15 women with vertebral compression fractures, and 8 women with wrist fractures. The precision of the technique, using phantoms, was 1.8% for a dose of 13 mSv. A formula for predicted TBCa (TBCap) was derived from the 20 normal women based on span and years postmenopause. The coefficient of variation of TBCa after normalization in the normal women was 6.6%. The mean TBCa values for the vertebral and wrist fracture groups were 69% and 84% of TBCap for women at the time of the menopause. The low TBCa in the wrist fracture group was attributable to post-menopausal bone loss. Of the low TBCa in the vertebral fracture group, about half the loss could be attributed to postmenopausal age and half to other factors.

Aged↗

PubMedDate not supplied

Enhancement of calcium current in Aplysia neurones by phorbol ester and protein kinase C.

One of the molecular mechanisms capable of regulating the physiological properties of neurones is the phosphorylation of ion channels and other cellular components by cyclic AMP-dependent protein kinase. Another protein kinase present in high concentrations in the mammalian brain is protein kinase C (a calcium/phosphatidylserine/diacylglycerol-dependent protein kinase), but there is no direct evidence, as yet, for the involvement of this enzyme in the control of neuronal excitability. We now present evidence that activation of endogenous protein kinase C by the tumour-promoting phorbol ester TPA (12-O-tetradecanoyl- phorbol-13-acetate), or intracellular injection of the purified enzyme, enhances the voltage-sensitive calcium current in bag cell neurones of the mollusc Aplysia.

Action Potentials↗

PubMedDate not supplied

Stimulation of protein kinase C recruits covert calcium channels in Aplysia bag cell neurons.

The modulation of voltage-activated calcium currents by protein kinases provides excitable cells with a mechanism for regulating their electrical behaviour. At the single channel level, modulation of calcium current has, to date, been characterized only in cardiac muscle, where beta-adrenergic agonists, acting through cyclic AMP-dependent protein kinase, enhance the calcium current by increasing channel availability and opening. We now report that enhancement of calcium current in the peptidergic bag cell neurons of Aplysia by protein kinase C occurs through a different mechanism, the recruitment of a previously covert class of calcium channel. Under control conditions, bag cell neurons contain only one class of voltage-activated calcium channel with a conductance of approximately 12 pS. After exposure to agents that activate protein kinase C, these neurons also express a second class of calcium channel with a different unitary conductance (approximately 24 pS) that is never seen in untreated cells.

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