PubMed Health⌕ Search

Biomedical subjects

H B Bosmann

Publications and source records attributed to H B Bosmann.

At least 19 recordsLinked to original sources
PubMed1989

Superoxide dismutase activity in Alzheimer's disease: possible mechanism for paired helical filament formation.

Activity of the free radical scavenging enzyme, superoxide dismutase (SOD-1), was determined in fibroblast cell lines derived from familial Alzheimer's patients, trisomy 21 patients and normal controls. In the present study, SOD-1 activity was significantly elevated by 30% in Alzheimer's cell lines when compared to normal euploid cell lines. As SOD-1 activity is known to be elevated about 50% in trisomy 21 patients, these cell lines were included as a control for tissue culture and assay conditions. In the present study, SOD-1 activity was significantly increased by 42 +/- 11% in trisomy 21 patients. The elevation in SOD-1 activity observed in the familial Alzheimer's patients supports the theory that paired helical filaments are synthesized in Alzheimer's disease by free radical hydroxylation of proline residues in paired helical filament precursor protein(s).

Adolescent↗
PubMed1987

Growth hormone response to edrophonium in Alzheimer's disease.

Neuropathologic data from patients with Alzheimer's disease indicate the presence of neurofibrillary tangles in hypothalamic regions associated with regulation of pituitary hormone release. The authors explored the hypothesis that cholinergic projections to hypothalamic nuclei controlling pituitary growth hormone (GH) release degenerate in Alzheimer's disease. Integrity of cholinergic regulation was tested by assaying the GH response to a presynaptic cholinergic challenge. After administration of the choline esterase inhibitor edrophonium, the peak GH response was 14 ng/ml in healthy elderly control subjects and only 2 ng/ml in Alzheimer's patients. The magnitude of GH blunting was correlated with cognitive and functional deficits. Possible implications of these data for enhanced accuracy in the diagnosis of dementia are discussed.

Aged↗
PubMed1986

Properties of a local anesthetic receptor in rat brain.

Saturable binding of local anesthetics in rat brain homogenates was demonstrated using (14C)-lidocaine and (3H)-bupivacaine. Saturation analyses revealed a single class of binding sites for lidocaine and bupivacaine. A series of drugs with local anesthetic properties inhibited this binding, while drugs without local anesthetic activity did not affect the specific binding. Specific binding of lidocaine and bupivacaine was maximal from pH 8 to 10; the pH versus binding profile was similar to that reported for local anesthetic blocking of peripheral nerve conduction. These characteristics suggest that binding of local anesthetics to this or similar sites mediates their pharmacological activity.

Anesthetics, Local↗
PubMed1985

Human platelet reactivity with intact segments of rabbit aorta and selected regions of rabbit, rat and human aorta.

A technique measuring platelet reactivity with vessel wall subendothelium has been modified to examine platelet reactivity with vessel pieces in place of intact segments of aorta of a specific diameter. This modification of Baumgartner's original technique (1) allows measurement of blood platelet reactivity with vessel pieces, 5 X 10 mm in size, mounted on perfusion chambers with "twist bands." Adhesion and aggregation of human platelets to deendothelialized surfaces of intact segments of rabbit aorta and pieces of rabbit, rat and human aorta, were equivalent. This modification will expand the use of Baumgartner's technique to investigations of platelet vessel wall interactions using blood platelets and vessels from numerous experimental animal models and humans. It will also facilitate examination of possible differences in thrombogenocity of selected areas of vessels such as those exhibiting stages of atherosclerotic plaque formation.

Animals↗
PubMed1979

Sialyltransferase activities of aging diploid fibroblasts.

Sialyltransferase activity and cell-cell adhesion rates of aging WI-38 cells were studied to determine the possible basis for a previously described decrease in membrane bound sialic acid and loss of proliferation of senescent cells. Ectosialyltransferase was demonstrated on the surface of both young and old WI-38 cells. The sialyltransferase assays consist of an enzyme source which is either the surface of intact cells (ectoenzyme) or a Triton X-100 cell homogenate, the nucleotide sialic acid donor (cytidine monophosphate-N-acetylneuraminic acid), and an asialo-acceptor which may be endogenous to the enzyme preparation or may be added exogenously. When sialyltransferase activity is measured in the absence of exogenous acceptors, there is a greater amount of sialic acid transferred by odl cells. However, when exogenous acceptors are provided, the amount of transfer is stimulated to a greater extent in young cells equalizing the amount of sialic acid incorporated into young and old cells. This suggests that there are fewer asialoglycoproteins and that acceptor concentration is a limiting factor in assays of young cell sialyltransferase. The end result of this may be the previously described decreased amount of membrane-bound sialic acid of old cells. A change in the adhesiveness of old cells is described which may be related to the altered cell surface.

Cell Adhesion↗
PubMed1979

Glycoprotein galactosyltransferase activity in synaptic junctional complexes isolated from rat forebrain.

A synaptosomal plasma membrane fraction and its junctional and nonjunctional subfractions were isolated and analyzed for glycoprotein galactosyltransferase activity. The nonjunctional components fraction had the highest specific activity in the presence of exogenous acceptor, suggesting an enrichment of enzyme in this fraction. The synaptic junctional complex fraction had the highest specific activity in the absence of added acceptor, suggesting that there is a relative enrichment of endogenous acceptors for this galactosyltransferase within the synaptic junctional complex.

Animals↗
PubMed1979

Increased specific binding of [3H]diazepam in rat brain following chronic diazepam administration.

Male rats (175 g) were given 30 mg of diazepam in their food daily for 35 days. The animals became drowsy and ataxic from this high dose of drug. After the 35-day dosing, the rats were killed daily, and specific binding of [3H]diazepam and [3H]flunitrazepam was determined in synaptosomal preparations from these and corresponding control rats. On days 3, 4, 6, and 7 after the treatment period the specific binding and specific binding of [3H]diazepam was double that of the control binding and specific binding of [3H]flunitrazepam was 1.67 times that of control. The data indicate that very high doses of diazepam, given for long periods, cause increased specific binding of radiolabeled ligand to brain subfractions. The possible mechanisms and implications are discussed. When lower doses or shorter dosage regimens are used, increased binding is not observed.

Animals↗