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Biomedical subjects

S A Hart

Publications and source records attributed to S A Hart.

10 recordsLinked to original sources
PubMed2001

Quantitative analysis of ER alpha and GAD colocalization in the hippocampus of the adult female rat.

Despite the many effects of estrogen in the hippocampus, there has been little evidence that hippocampal principal cells express nuclear estrogen receptors. In the hippocampus, the alpha form of the nuclear estrogen receptor (ER alpha) has been localized to sparsely distributed cells with the morphological characteristics of inhibitory interneurons. Because inhibitory neurons may be involved in the effects of estrogen on hippocampal principal cells, quantitative description of ER alpha expression in gamma-aminobutyric acid (GABA)ergic (inhibitory) and non-GABAergic cells of the hippocampus is a key step in understanding the mechanism(s) of estrogen action on hippocampal circuitry. We used single and double-label immunohistochemistry for ER alpha and glutamic acid decarboxylase (GAD; a marker of GABAergic neurons) to determine the numbers and distributions of hippocampal GABAergic and non-GABAergic neurons that express ER alpha in the adult female rat. We found many more ER alpha-expressing cells in the hippocampus than any previous study and observed distinct dorsal vs. ventral differences in hippocampal ER alpha expression. In the dorsal hippocampus, most ER alpha-positive cells were also GAD positive; however, ER alpha was expressed in only a subset of GAD-positive cells. Double-labeled cells were concentrated at the border between str. radiatum and str. lacunosum-moleculare. In the ventral hippocampus, we found a very high number of ER alpha-positive cells, the majority of which were not immunoreactive for GAD and are likely to be pyramidal cells. These findings suggest that ER alpha can mediate the effects of estrogen primarily in GABAergic neurons in the dorsal hippocampus and in both GABAergic and non-GABAergic neurons in the ventral hippocampus.

Animals↗
PubMed2001

Solvent-dependent stereoselectivity in a Still-Wittig rearrangement: an experimental and ab initio study.

[see reaction]. The Still-Wittig rearrangement gave opposite selectivities for (Z:E)-alkenes in THF (3:1) vs toluene (1:3) in the synthesis of serine-proline dipeptide amide isosteres. Four transition states leading to (Z)-and (E)-alkenes with THF and without (representing toluene) were identified by ab initio calculations at the 3-21G* level. The calculated (Z:E)-ratios with THF (4.7:1) and without THF (1:3.2) suggested that the transition state geometries and energies were well-represented by the calculations.

Dipeptides↗
PubMed2001

Estrogen increases synaptic connectivity between single presynaptic inputs and multiple postsynaptic CA1 pyramidal cells: a serial electron-microscopic study.

Dendritic spines are sites of the vast majority of excitatory synaptic input to hippocampal CA1 pyramidal cells. Estrogen has been shown to increase the density of dendritic spines on CA1 pyramidal cell dendrites in adult female rats. In parallel with increased spine density, estrogen has been shown also to increase the number of spine synapses formed with multiple synapse boutons (MSBs). These findings suggest that estrogen-induced dendritic spines form synaptic contacts with preexisting presynaptic boutons, transforming some previously single synapse boutons (SSBs) into MSBs. The goal of the current study was to determine whether estrogen-induced MSBs form multiple synapses with the same or different postsynaptic cells. To quantify same-cell vs. different-cell MSBs, we filled individual CA1 pyramidal cells with biocytin and serially reconstructed dendrites and dendritic spines of the labeled cells, as well as presynaptic boutons in synaptic contact with labeled and unlabeled (i.e., different-cell) spines. We found that the overwhelming majority of MSBs in estrogen-treated animals form synapses with more than one postsynaptic cell. Thus, in addition to increasing the density of excitatory synaptic input to individual CA1 pyramidal cells, estrogen also increases the divergence of input from individual presynaptic boutons to multiple postsynaptic CA1 pyramidal cells. These findings suggest the formation of new synaptic connections between previously unconnected hippocampal neurons.

Animals↗
PubMed1990

Patterns of surgical treatment of breast cancer in Victoria.

We analysed data on admissions to Victorian public hospitals for surgical treatment of breast cancer over the period July 1985 to December 1988. Of the 2993 women admitted, 28.7% received breast-preserving surgery. The probability of a woman being treated conservatively was dependent on age, with women aged less than 50 or more than 70 years more likely to receive breast-preserving surgery than women aged 50-69. There was an age-specific change, of marginal statistical significance, in the proportion of women receiving breast-preserving surgery over the period. The public hospitals admissions database is a potentially useful means of monitoring patterns of surgical treatment.

Adult↗
PubMed1987

Fine needle aspiration cytology in breast disease management--a 4 year experience.

At the Queen Victoria Medical Centre between 1981 and 1984, 2920 fine needle aspirates of the breast were examined with an overall diagnostic accuracy of 97% and a sensitivity of 80%. This high diagnostic accuracy combined with the ease and complication-free nature of the procedure has meant that fine needle aspiration (FNA) has become an important part of the investigation and management of breast disease within the breast service of the Queen Victoria Medical Centre.

Australia↗
PubMed1985

Recognition memory in Alzheimer's disease.

Recognition memory for several types of stimulus material was examined in patients clinically diagnosed as having early Alzheimer's disease and in normal elderly controls. Although performance deficits were demonstrated for verbal and abstract stimuli (geometric shapes and histology slides), memory for faces was relatively intact in the patient group. Patients made more false positive responses than controls, but this could not be accounted for by a general disinhibition of responding. It is suggested that a contextual processing deficit may explain the pattern of false positive responding and this is discussed in relation to previous findings of drug studies in Alzheimer's disease.

Alzheimer Disease↗