Search PubMed⌕ Search

Biomedical subjects

M B Harrison

Publications and source records attributed to M B Harrison.

At least 19 recordsLinked to original sources
PubMed1997

Maternal inheritance in Parkinson's disease.

To evaluate possible matrilineal factors in the inheritance of Parkinson's disease, we prospectively identified families in which a parent and multiple siblings had Parkinson's disease. In each of the 5 families identified, the affected parent was the mother (p < 0.03). The age at onset in the offspring generation in these 5 families was younger than the age at onset in the parental generation (p < 0.001). In addition, the age at onset in all patients with an affected mother (n = 18) was younger than the age at onset in the affected mothers (p < 0.001). No difference was found between the age at onset in patients with an affected father (n = 14) and the age at onset in the affected fathers. These results are consistent with a role for inherited abnormalities of mitochondrial DNA in the pathogenesis of at least some cases of Parkinson's disease.

Adult↗
PubMed1997

Clinical correlates of sleep benefit in Parkinson's disease.

The phenomenon of sleep benefit, a period of lessened disability or feeling "on" upon awakening from sleep in the morning, has received scant attention in the literature on Parkinson's disease. We interviewed 162 consecutive patients regarding disease onset, medication history, and symptoms, evaluated them using the Unified Parkinson's Disease Rating Scale, and assessed them as to the presence or absence of sleep benefit. Thirty-three percent reported experiencing sleep benefit. Compared with patients not having sleep benefit, patients with sleep benefit tended to be younger at disease onset, have longer disease duration, take higher total daily doses of levodopa, have longer duration of levodopa treatment, and exhibit less cognitive and physical disability. The findings of this study suggest that sleep benefit is a common phenomenon that may be anticipated in a subgroup of patients with Parkinson's disease. The mechanisms underlying sleep benefit do not appear to be simple and may be multifactorial. Clinicians need to be aware of the authenticity of patients' reports of sleep benefit and consider the existence of this phenomenon when prescribing or adjusting patients' medication schedules.

Animals↗
PubMed1996

Expression of m1 and m4 muscarinic receptor mRNA in the striatum following a selective lesion of striatonigral neurons.

Cholinergic stimulation has opposing effects on striatopallidal and striatonigral neurons. Most striatal projection neurons express m1 muscarinic receptor mRNA with m4 mRNA found in 40-50%. Expression of m4 mRNA is found in most preprotachykinin neurons but only a subset of preproenkephalin neurons, suggesting preferential localization of m4 receptors to striatonigral neurons. A volkensin lesion of striatonigral neurons reduced striatal m4 mRNA by 63% and m1 mRNA by only 18%, suggesting that preferential expression of m4 receptors by striatonigral neurons may contribute to their differential response.

Animals↗
PubMed1996

A D1 dopamine agonist stimulates acetylcholine release from dissociated striatal cholinergic neurons.

We tested the hypothesis that a D1 dopamine agonist could stimulate acetylcholine release directly from striatal cholinergic neurons. A suspension of viable dissociated striatal cells was made enzymatically and mechanically from normal adult male rats. The heterogeneous suspension was incubated in [3H]choline to allow synthesis of [3H]acetylcholine selectively by cholinergic neurons. Fractional [3H]acetylcholine release from the cholinergic cells in the suspension was recorded during continuous dynamic perifusion. The D1 agonist, 50 microM (+/-) SKF 38393, increased the basal rate of release from the cholinergic cells by 50% and the action was inhibited by the D1 antagonist, SKF 83566. Stimulation of [3H]acetylcholine secretion was recorded as low as 500 nM SKF 38393. The (S, -) SKF 38393 stereoisomer was significantly less effective than the (R, +) isomer in stimulating release. The D1-mediated stimulation of acetylcholine secretion was abolished in a low-calcium environment that also inhibited basal release. The data suggest that striatal cholinergic cells express D1 receptors functionally coupled to the regulation of acetylcholine release. These D1 actions in the absence of synaptic circuitry imply that such circuitry is not required in situ. In vivo however, indirectly mediated D1 actions and those of other transmitters may modify the manifestations of this direct cholinergic stimulation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1996

Practice guidelines for the prediction and prevention of pressure ulcers: evaluating the evidence.

Clinical practice guidelines for the prediction and prevention of pressure ulcer (Agency for Health Care Policy and Research [AHCPR], 1992) were evaluated in a Canadian, university-affiliated, acute care hospital. Through a prospective study, the prevalence of pressure ulcers was determined, and pressure ulcer incidence was tracked to evaluate the accuracy of the Braden Scale for risk assessment. The prevalence rate for stage II or greater pressure ulcers was 13.6%; the rate was 29.7% when stage I (persistent redness) was included. In evaluating the Braden Scale's accuracy in predicting risk, the findings from this study were less favorable than previous reports. The total Braden score that appeared to have the best balance of sensitivity (67%) and specificity (66%) was 19. Several factors should be considered: The scale was implemented and tested hospitalwide with a wide range of patient diagnoses, age, and severity; the study was a cross-section of an existing population; and the levels of nursing care and type of staff vary between units ranging from critical to long-term care. This study highlights the need for individual settings to evaluate the AHCPR Guidelines for the Prediction and Prevention of Pressure Ulcers.

Female↗
PubMed1996

Quality of life as an outcome measure in nursing research. "May you have a long and healthy life".

Quality of life has emerged as an important concept and outcome in health and health care. Policy-makers, researchers, clinicians, and the public at large consider perceived quality of life to be an important dimension of the health of a population or an individual. The nature of nursing is such that many of its anticipated outcomes relate to improvement in the quality of life of individuals and populations. There continues to be debate about the actual definition of quality of life, and a concept that is difficult to define will naturally pose challenges to measurement. This has not impeded the proliferation of quality-of-life instruments, since the concept is recognized as an increasingly important clinical and research outcome. Progress has been made in clarifying and operationalizing the concept. We propose a conceptual viewpoint that separates what quality of life is from what contributes to quality of life. This will assist nurse researchers planning to use quality of life as an outcome in evaluating nursing interventions. In clinical or research situations, for the purposes of measurement, an operational definition of quality of life stems from a definition of health. From this is drawn a definition of health-related quality of life (HRQL). For the purpose of outcome measurement, the operational definition relates to the domains important to the study population and the particular health intervention under study. Issues that arise in the measurement of HRQL are also presented.

Humans↗
PubMed1995

Acetylcholine release from dissociated striatal cells.

To study the regulation of striatal acetylcholine (ACH) release, adult male rat striata were dissociated and incubated with 3H-choline to synthesize 3H-ACH. Fractional 3H-ACH efflux per min during continuous perifusion was: (1) tightly regulated; (2) dependent on calcium influx; (3) stimulated by 10 mM K+ and 1 mM glutamate; and (4) comparable to ACH release detected by HPLC. Thus, acutely dissociated striata exhibit calcium-sensitive, voltage-dependent secretion of 3H-ACH and direct receptor-mediated stimulation of release through the glutamate receptor family. This new approach toward cholinergic secretory physiology will help clarify complex striatal circuitry.

Acetylcholine↗
PubMed1995

Acute dopamine depletion potentiates independent stimulatory and inhibitory D1 DA receptor-mediated control of striatal acetylcholine release in vitro.

Fractional release of [3H]ACh was evaluated under basal and evoked conditions in striatal slices from normal and acutely dopamine-depleted adult rats for the influence of D1- and D2-DA receptor agonists. The D1 ligand had no effect on normal slices but DA depletion unmasked two independent but simultaneous supersensitive responses: augmentation of K(+)-evoked and inhibition of glutamate-evoked release. The D2 ligand inhibited evoked release in normal slices and this effect was not potentiated. This is a new cholinergic model of acute D1 receptor supersensitivity.

Acetylcholine↗
PubMed1995

Opioid peptide expression in models of chronic temporal lobe epilepsy.

Expression of the opioid peptides dynorphin and enkephalin is altered within the first 24 h after acutely induced seizures in certain experimental models of epilepsy. Using in situ hybridization, we examined the expression of prodynorphin and preproenkephalin messenger RNA acutely following induction of kindling with recurrent seizures and in two models of chronic temporal lobe epilepsy: (i) rats fully kindled with rapidly recurring hippocampal seizures; and (ii) rats surviving after self-sustaining limbic status epilepticus induced with focal electrical stimulation of the hippocampus. In naive animals, a ventral-dorsal gradient was identified in the expression of both prodynorphin and preproenkephalin messenger RNA in the dentate gyrus and expression of prodynorphin message was demonstrated for the first time in the ventral portion of cornu Ammonis regio superior. After stimulation producing rapidly recurring hippocampal seizures, acute decreases in prodynorphin messenger RNA were seen in the dentate gyrus and cornu Ammonis regio superior at 24 h after the last seizure. In contrast, increases in preproenkephalin messenger RNA expression were seen acutely in the dentate gyrus, with a decrease seen in the entorhinal cortex. The change in prodynorphin message expression in cornu Ammonis regio superior persisted in kindled animals that were studied after one month seizure-free period. There were no changes in preproenkephalin message in kindled animals studied after the one month seizure-free interval. No statistically significant changes were found for either prodynorphin or preproenkephalin message in the post-self-sustaining limbic status epilepticus group at one month following induced seizures. Acute changes in peptide expression may contribute to increased excitation in the dentate gyrus during induction of kindling, while the chronic change identified in cornu Ammonis regio superior may contribute directly to persistently increased excitability in this region.

Animals↗
PubMed1995

Prolonged survival in carcinomatous meningitis associated with breast cancer.

We describe a patient who survived for more than 7 years after the diagnosis of meningeal carcinomatosis associated with breast cancer. Meningeal carcinomatosis occurs in 1% to 5% of patients with breast cancer. The median survival ranges from 3 to 7 months, but most reports include a small number of patients who survive considerably longer, with up to 11% surviving more than 1 year. Early diagnosis, aggressive treatment of neurologic involvement, limited systemic tumor burden, and varied rates of progression are factors that may relate to extended duration of survival in these patients with breast cancer. Our patient, with a hormonally responsive adenocarcinoma of the breast and without systemic metastases, illustrates that meningeal carcinomatosis, like other forms of breast cancer metastasis, can run an indolent course. In such patients the delayed sequelae of therapy for metastasis to the central nervous system can profoundly influence the course of the illness.

Adenocarcinoma↗
PubMed1993

Differential localization of A2a adenosine receptor mRNA with D1 and D2 dopamine receptor mRNA in striatal output pathways following a selective lesion of striatonigral neurons.

We have used the suicide transport agent volkensin to produce selective lesions of striatonigral neurons. By in situ hybridization histochemistry unilateral volkensin injections in the substantia nigra decreased the number of D1 receptor mRNA-expressing neurons in the ipsilateral striatum but did not change the number of D2 receptor and A2a adenosine receptor mRNA-expressing neurons. These findings confirm that striatonigral neurons express D1 receptors and suggest that D2-A2a receptor expressing neurons are predominantly localized to other neuronal populations within the striatum.

Animals↗
PubMed1993

A selective lesion of striatonigral neurons decreases presynaptic binding of [3H]hemicholinium-3 to striatal interneurons.

We have used the suicide transport agent, volkensin, to produce selective lesions of striatal efferent neurons projecting to the substantia nigra in the rat. In order to evaluate potential trans-synaptic effects, we examined cholinergic interneurons intrinsic to the striatum following destruction of striatonigral projection neurons by nigral injection of volkensin. There was no change in the number of large interneurons identified either by Nissl stain or by immunocytochemistry for choline acetyltransferase, indicating that volkensin was not directly toxic to this group of neurons. However, [3H]hemicholinium-3 binding to the choline re-uptake site on the presynaptic cholinergic terminals decreased. No change in [3H]hemicholinium-3 binding was seen after destruction of dopaminergic afferents with 6-hydroxydopamine. Striatonigral afferents to the cholinergic interneurons contain substance P which has been shown to stimulate acetylcholine release. The decrease in [3H]hemicholinium-3 binding may reflect loss of this afferent input. However, striatonigral neurons are an efferent target of the cholinergic interneuron as well, and a presynaptic effect due to loss of target neurons also may contribute.

Animals↗
PubMed1993

Phenytoin and dyskinesias: a report of two cases and review of the literature.

Dyskinesia is a recognized but uncommon side-effect of treatment with phenytoin. Two additional cases of dyskinesia during treatment with phenytoin are described; both had radiographically documented thalamic infarctions. The reported experience to date with movement disorders induced by phenytoin is reviewed and the clinical features summarized. The available experimental evidence addressing the mechanism underlying this side effect is discussed.

Aged↗
PubMed1993

Differential effects of suicide transport lesions of the striatonigral or striatopallidal pathways on subsets of striatal neurons.

In the basal ganglia, centrally active suicide transport agents produce apparently selective lesions of the striatopallidal and striatonigral pathways based on receptor binding and neuropeptide mRNA studies. In the present study we sought to determine the selectivity of suicide transport lesions for specific subsets of striatal neurons. Using immunohistochemical methods, the neostriata of adult rats were examined 10 days after an injection of volkensin into the substantia nigra or an injection of OX7-saporin into the globus pallidus. Ricin, a suicide transport agent active in the peripheral but not the central nervous system, was injected into each target as a control. Adjacent sections were processed for (1) Nissl stain to assess neuronal density, both overall and for large interneurons, (2) NADPH-diaphorase (NADPH-d) histochemistry, to mark medium-sized aspiny interneurons, (3) enkephalin immunocytochemistry, to label striatopallidal neurons, or (4) substance P immunocytochemistry, to label striatonigral neurons. Ricin injections produced no change in the densities of these subsets of striatal cells. In animals receiving volkensin or OX7-saporin injections, analyses of Nissl material revealed that the striata ipsilateral to the toxin injections appeared normal and did not exhibit shrinkage or gliosis; however, a quantitation analysis revealed a moderate decrease in cell density (12-16% loss, P < 0.01). The densities of both large and NADPH-d-containing striatal interneurons were unchanged after lesions in either target. Following nigral injections with volkensin, the density of striatal substance P-labeled cells decreased (26% loss, P < 0.01), while the density of enkephalin-labeled cells did not decrease significantly (11% decrease, P > 0.1). After pallidal injections with OX7-saporin, the density of striatal enkephalin-labeled cells decreased (20% loss, P < 0.01), while that of substance P-labeled cells remained unchanged. These data show that nigral volkensin and pallidal OX7-saporin injections differentially lesion striatonigral and striatopallidal projection neurons and spare striatal interneurons. This study provides further evidence for the selectivity, specificity, and utility of suicide transport agents to study brain structure and function.

Animals↗
PubMed1992

The time course of changes in D1 and D2 receptor binding in the striatum following a selective lesion of striatonigral neurons.

The suicide transport agent volkensin was used to produce a selective lesion of striatonigral projection neurons and the time course of changes in binding at striatal D1 and D2 receptors analyzed. Both show a time-dependent decrease with two-thirds of the total change occurring within the first 10 days and a greater decrease in D1 receptor density at all time points. Our results confirm selective localization of D1 receptors to striatonigral neurons and are consistent with localization of some striatal D2 receptors to striatonigral neurons.

Animals↗
PubMed1992

Changes in D2 but not D1 receptor binding in the striatum following a selective lesion of striatopallidal neurons.

We have used the immunotoxin OX7/saporin, a suicide transport agent, to selectively lesion striatopallidal neurons. Following injection of OX7/saporin into the globus pallidus, in situ hybridization for preproenkephalin mRNA was examined in the striatum to confirm successful retrograde neurotoxicity. Comparison of D1 and D2 receptor binding in the striatum demonstrated that D2 but not D1 receptor binding sites are localized to striatopallidal neurons.

Animals↗