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Biomedical subjects

G M Alexander

Publications and source records attributed to G M Alexander.

63 records · Page 4Linked to original sources
PubMed1983

Computer registration of radioactive indicator-dilution curves.

A system is described for recording indicator-dilution curves produced by gamma radiation-emitting tracers. The system consists of a flow-through cuvette in a well counter, appropriate commercially available gamma radiation-detecting equipment, an Apple II computer, and a two-channel pulse-counting interface of our own design. With the counting interface and the software described here, an investigator can simultaneously record two indicator-dilution curves produced by gamma emitters. Instead of having to wait hours or days for results, the investigator can watch the data being recorded and display the results in graphic form almost immediately after each injection.

Animals↗
PubMed1982

Pyrophosphate arthropathy: a study of metabolic associations and laboratory data.

105 consecutive patients with pyrophosphate arthropathy have been studied. Disease associations and metabolic abnormalities were compared with those of an age and sex matched group of 105 acute medical admissions, and with 48 patients presenting with uncomplicated osteoarthritis. Patients with pyrophosphate arthropathy had a higher incidence of hypothyroidism (10, hyperparathyroidism 92), and chronic steroid therapy (15) than did those in the comparative groups. Laboratory data showed abnormalities suggesting chronic inflammatory disease in many patients, but no other unexpected metabolic findings. Metabolic abnormalities were uncommon in pyrophosphate arthropathy, and extensive metabolic screening of patients was unrewarding.

Adrenal Cortex Hormones↗
PubMed1982

The methylphenidate-induced stereotypy in the awake rat: local cerebral metabolism.

The local cerebral metabolic rate for glucose (1=CMRg) was computed in rats with methylphenidate-induced stereotypy using the quantitative 14C-2-deoxyglucose (2-DG) technique. Four rats received methylphenidate 15 mg per kilogram IP. Compared to five control animals, treated rats showed statistically significant (p less than or equal to 0.05) increases in 1-CMRg in globus pallidus, ventral lateral nucleus of the thalamus, subthalamic nucleus, red nucleus, substantia nigra, entopeduncular nucleus, inferior olivary nucleus, and the lateral cerebellar cortex. Significantly, 1-CMRg decreased in area 4 of the motor cortex. The auditory system showed no change in 1-CMRg, demonstrating the specific action of methylphenidate in the rat brain. This technique allows evaluation of the functional anatomy of the entire central nervous system and may be helpful in understanding the mechanisms of methylphenidate-induced stereotypy.

Animals↗
PubMed1981

Quantitative measurement of local cerebral metabolic rate for glucose utilizing tritiated 2-deoxyglucose.

The [14C]2-deoxyglucose (2-DG) technique has been widely utilized for quantitative measurement of local cerebral metabolic for glucose (1CMRG) in animals. The technique as presently used is limited by the energy of 14C beta-particles, which can travel relatively great distances in tissue. This results in limited audioradiographic resolution and in computed 14C concentrations which are a function of tissue section thickness. [3H]2-DG has less energetic beta-particles; hence, autoradiographs have better resolution and optical densities are independent of tissue thickness for sections greater than 5 micrometer. We have developed a method for quantitation of 1CMRG in rats using [3H]2-DG and a newly developed ultrasensitive X-ray film. Autoradiographic tissue standards were prepared by injecting rats with [3H]2-DG and assaying micro-samples of brain for 3H concentration. Ten rats were used in this study. Five rats received [3H]2-DG (300 muCi/100 g) and 5 rats received [14C]2-DG (7.5 muCi/100 g). The mean 1CMRG values for selected areas of the central nervous system demonstrated no significant difference (P greater than 0.05) between the [14C]2-DG and the [3H]2-DG groups. Values for 1CMRG from the [3H]2-DG group showed no variation attributable to inadequate microtome precision. The improved resolution obtained by utilizing [3H]2-DG is especially evident where gray matter (high 1CMRG) is immediately adjacent to white matter (low 1CMRG).

Animals↗
PubMedDate not supplied

Evidence for neuromelanin involvement in MPTP-induced neurotoxicity.

Exposure to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) reproduces certain clinical, pathological, and neurochemical features of Parkinson's disease. MPTP is metabolized by monoamine oxidase Type B to 1-methyl-4-phenylpyridine (MPP+), which is selectively accumulated by high-affinity uptake mechanisms into dopaminergic neurons. Lyden et al. described low-affinity binding of MPTP to synthetic and retinal melanin. We showed that MPP+ binds to neuromelanin with high affinity, suggesting that in MPTP neurotoxicity, MPP+ enters nigral neurons by the dopamine uptake system and binds to neuromelanin, which serves as a depot, continuously releasing MPP+ until it destroys the cells. This model predicts that agents which compete with MPP+ binding to neuromelanin should partially protect the dopamine neurons from MPTP-induced toxicity. The most potent identified competitor for MPP+ binding to melanin is the antimalarial drug chloroquine, which has a high affinity for melanins. In the present study, chloroquine, administered to monkeys in conventional anti-malarial doses before MPTP, protects them from MPTP-induced parkinsonian motor abnormalities, dopamine depletion in the striatum, and neuropathological changes in the substantia nigra.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMedDate not supplied

Quantification of cerebral infarct size by creatine kinase BB isoenzyme.

Creatine Kinase BB isoenzyme (CKBB) has been shown to rise in the serum and CSF following acute cerebral injury. To test the hypothesis that brain infarct size could be estimated from the appearance and disappearance of CKBB in the serum and CSF, strokes of varying size were produced in twelve mongrel dogs by silastic emboli. The rate of disappearance, Kd of CKBB (-.00732 +/- 0.001 min-1 mean +/- SE, N = 8) was determined by injecting purified CKBB (25 IU) intravenously then measuring its disappearance. Following the embolic stroke, serum samples were taken hourly for 24 hours and then at intervals for up to 160 hours for measurement of CKBB by radioimmunoassay until the animals were sacrificed. The brains were then removed, fixed in formalin, cut in 2 mm sections and photographed. The area of the infarct was measured using high pad digitizer interfaced with an Apple computer. The infarct size was then calculated from the area and thickness. Using a one-compartment mathematical model, the infarct size was estimated from the amount of CKBB appearing in the serum, the Kd of CKBB, and the amount of CKBB depleted from tissue. The computed infarct size correlated well (r = 0.94) with the measured infarct size. This model may have value in testing therapeutic modalities in the intact animal.

Animals↗