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Biomedical subjects

P E Marshall

Publications and source records attributed to P E Marshall.

18 recordsLinked to original sources
PubMed1994

New and borrowed strategies for mental health systems in the decade of the 1990s.

Use of the paradigm shifts advocated by futurists and the supporters of total quality management can facilitate access to new options for mental health systems. New views and innovative systems, however, become difficult to maintain in the context of increasingly rapid and unexpected change occurring in the environment. One strategy that can be employed is the use of leverage, a term usually associated with finance or politics.

Community Mental Health Services↗
PubMed1992

The mental health HMO: capitation funding for the chronically mentally ill. Why an HMO?

Excesses associated with deinstitutionalization during the 1970s provided a legacy of homelessness, revolving door rehospitalization, and gridlock in metropolitan hospital emergency rooms. To allow for the seriously and persistently mentally ill to move planfully into community life, caregivers must utilize new and improved care models. One option is the HMO capitation model being tested in the Monroe/Livingston County Mental Health Demonstration in New York State. Experience indicates positive results for patients and lower than anticipated costs. Integrated Mental Health (IMH) is the local authority for this locally designed demonstration in New York State. Community Mental Health Centers (CMHCs) act as "Lead Agencies" to manage care and rehabilitation for seriously mentally ill patients previously dependent totally on the State hospitals' services. Both improvements in patient functioning and in reduced cost of appropriate community care are being documented by this demonstration project.

Chronic Disease↗
PubMed1989

Capitation plans.

Explore the source record for details and available documents.

Capitation Fee↗
PubMed1988

Somatostatin-like immunoreactive material in associational ganglion cells of human retina.

The retinal ganglion cell is classically viewed as the output cell of the retina, sending a single axon via the optic nerve to synapse in visual relay nuclei of the brain. However, some ganglion cells, termed associational ganglion cells, have axons which do not leave the retina and presumably serve intraretinal communication. Using high-affinity and specific monoclonal antibodies to somatostatin-14 and the avidin-biotin-peroxidase immunohistochemical procedure, somatostatin-immunoreactive associational ganglion cells are specifically stained in human retinas obtained at necropsy. These cells are more numerous in the inferior than the superior retina; they have dendrites which ramify in the inner plexiform layer; and they have sparsely branching axons, many of which can be traced over 1 cm. These axons do not enter the optic nerve. They follow remarkably straight courses at the border of the inner plexiform layer and ganglion cell layer and thereby form a gridwork of fibers covering the entire retinal area. These observations verify the existence of associational ganglion cells in the human and establish somatostatin as a neurotransmitter or neuromodulator candidate for these neurons. The morphology of these cells suggests that they are involved in long-distance interactions within the retina.

Humans↗
PubMed1986

Somatostatin immunocytochemistry in the rabbit retina.

In previous work, radioimmunoassay was used to document the presence of somatostatin-like immunoreactive material in the rabbit retina. The present study was undertaken to determine the cellular localization of that material by light microscopic immunocytochemistry. Rabbit retinas were fixed by immersion in paraformaldehyde-lysine-periodate and reacted, either as whole retinas or as 50 microns Vibratome cross-sections, with an antiserum directed against somatostatin-14. Consistent staining of neuronal perikarya was seen only in the retinas of rabbits that had been pretreated with intravitreal injections of colchicine. Specifically stained cell bodies are present in the ganglion cell layer; the cells give rise to fibers in both the innermost and outermost sublaminas of the inner plexiform layer. In retinal whole mounts, the cells possess two or three primary dendrites with sparse branching. The dendritic fields are up to 1 mm in diameter, and adjacent dendritic fields overlap. Many cells have a thin varicose process arising from the soma or a proximal primary dendrite; these processes branch repeatedly within the retina and resemble intraretinal axons. The somatostatin-reactive cells may be associational ganglion cells or displaced amacrine cells; it is less likely that they are ganglion cells with axons projecting to the brain.

Animals↗
PubMed1985

Excitotoxin lesions do not mimic the alteration of somatostatin in Huntington's disease.

Huntington's disease is accompanied by severe neuronal death in the striatum, but despite this cell loss, there is a marked increase in the striatal concentration of somatostatin-like immunoreactivity (SLI). We attempted to examine the mechanism of this increase by using kainic or ibotenic acid to effect a unilateral lesion in the rat neostriatum. Graded doses of toxin cause a proportional decrease in the concentration of somatostatin-like immunoreactivity to a maximum of 50% of control, which is stable over an interval of 3 months. The increased somatostatin-like immunoreactivity in Huntington's disease is not mimicked by the excitotoxin lesions in rats. In addition we find that unilateral kainic acid lesions in the striatum reduce SLI in the contralateral striatum as well, although histologic evidence and assay of choline acetyltransferase activity indicate that damage is confined to the injected side. Immunocytochemistry demonstrates a loss of somatostatin-containing neurons on the lesioned side but no discernible loss in the contralateral striatum. The bilateral decrease in SLI following unilateral lesions suggests damage to a somatostatin projection to the contralateral striatum or a compensatory interaction between the two striatal nuclei.

Animals↗
PubMed1985

Immunoreactive somatostatin in the rat retina: light microscopic immunocytochemistry and chromatographic characterization.

The retinas of adult, male Long-Evans rats contain somatostatin-like immunoreactive material (SLI) as detected by radioimmunoassay. The SLI co-chromatographs with synthetic somatostatin-14 on both gel permeation chromatography and reversed phase high performance liquid chromatography; no somatostatin-28-like material or higher molecular weight forms have been detected. Immunocytochemical methods detect SLI in at least two cell populations. The more abundant stained cells are at the inner margin of the inner nuclear layer and give off processes which form a dense meshwork of fine, varicose fibers at the outer border of the inner plexiform layer, as well as processes which pass into other sublaminas of the inner plexiform layer. Varicose immunoreactive fibers run vertically or obliquely through the inner nuclear layer and bifurcate at its outer margin, giving rise to horizontally running fibers in the outer plexiform layer. These observations are consistent with rat retinal SLI being contained within amacrine cells, at least some of which are interplexiform cells. With cholchicine pretreatment, a more sparse population of stained cells is detected in the ganglion cell layer. These cells give rise to processes which enter the inner plexiform layer. It is not known if these are ganglion cells or displaced amacrine cells.

Animals↗
PubMed1985

Huntington's disease is accompanied by changes in the distribution of somatostatin-containing neuronal processes.

The distribution of somatostatin-like immunoreactivity in the caudate, putamen, globus pallidus and ventral mesencephalon of the normal human brain has been studied with immunocytochemical techniques, and compared to that seen in Huntington's disease. Within the normal striatum, sparsely distributed varicose fibers and a population of medium-sized neurons were stained. In Huntington's disease, somatostatin immunoreactive striatal neurons appear to degenerate in proportion to the loss of striatal tissue, but there is an increase in the density of immunostained varicose fibers. In contrast, the pattern and amount of fiber staining in the substantia nigra appeared virtually unchanged from that seen in the normal brain. The morphology of striatal perikarya containing somatostatin-like immunoreactivity and the patterns of fiber staining in normal and Huntington's disease pallidum and substantia nigra suggest that striatal neurons containing somatostatin-like immunoreactivity are local circuit neurons.

Adult↗
PubMed1985

Ultrastructural study of cholecystokinin-immunoreactive cells and processes in area CA1 of the rat hippocampus.

We used light and electron microscopic immunocytochemical methods to examine the structure of neuronal perikarya and processes containing cholecystokinin-like immunoreactivity (CCK-IR) in area CA1 of the rat hippocampus. The morphology of stained perikarya, their positions within all laminae, and the orientation of their dendrites indicate that CCK-IR is located in interneurons. These cells were seen in the electron microscope to have deeply folded nuclei and to receive both symmetric and asymmetric synaptic junctions on their cell somata and dendritic shafts. Their dendrites are essentially spine-free, but form bulges at the site of some asymmetric synaptic junctions. Axonal varicosities containing CCK-IR make symmetric synaptic junctions with cell somata and dendritic shafts of both pyramidal and non-pyramidal neurons. In addition, CCK-IR varicosities form symmetric junctions with unstained non-pyramidal neurons and with CCK-IR cells, suggesting either recurrent innervation of one cell on itself or interaction between interneurons. The presence of CCK-IR varicosities and synaptic junctions on pyramidal cells is in agreement with physiological data which indicate that CCK has a direct postsynaptic action. The observation of CCK-IR varicosities forming synaptic junctions on non-pyramidal cells suggests that CCK might also modify the response of interneurons.

Animals↗
PubMed1984

Implications of neuropeptides in neurological diseases.

Neuropeptides are sufficiently stable to allow valid radioimmunoassay of peptide concentrations in post-mortem human nervous tissue and in human cerebrospinal fluid. Studies have now documented abnormalities of peptide concentrations in degenerative diseases of the brain. Somatostatin concentration is reduced in the hippocampus and neocortex of patients dying with Alzheimer's type dementia. In Huntington's disease, there are reduced concentrations of substance P, met-enkephalin and cholecystokinin in the basal ganglia; in contrast the concentrations of somatostatin and TRH are increased. Immunocytochemical and experimental lesion studies are underway in an attempt to localize the peptide-containing cells affected by these disorders; and the potential role of alterations in neuropeptide function in the pathogenesis, clinical manifestations and therapy of these illnesses is of great interest. Although alterations of CSF peptide concentrations have been reported in a variety of human diseases, interpretation of these results requires knowledge of the origin and disposition of CSF peptides. Future research into the pathology of peptidergic systems will depend on the development of specific peptide antagonists to probe dynamic aspects of peptide function and on the application of the tools of molecular biology, such as specific mRNA assays, to human material.

Alzheimer Disease↗
PubMed1984

Occupational allergy due to inhalation of ipecacuanha dust.

A number of workers packing ipecacuanha tablets were complaining of allergic symptoms. Skin-prick tests, RAST and an assessment of clinical history by interview were used to confirm the presence of work-related allergy. Specific IgE antibodies to ipecacuanha were detected and the occurrence of antibodies correlated with the incidence of allergic symptoms. The individuals with positive RAST scores had been employed, on average, longer than those with negative scores. It was found that atopy did not predispose the workers to work-related allergy and that there was no correlation between smoking and respiratory symptoms in this population.

Allergens↗
PubMed1983

Immunocytochemical studies of substance P and leucine-enkephalin in Huntington's disease.

The distribution of substance P and leucine-enkephalin in selected regions of brain obtained postmortem from patients with Huntington's disease and from neurologically normal persons has been studied with immunocytochemical techniques. In the normal brain, substance P immunoreactivity was identified in medium-sized neurons in the neostriatum, in neurons of the external segment of the globus pallidus, and in fine fibers in teh neostriatum, inner segment of the globus pallidus, and in the pars reticulata of the substantia nigra. Huntington's disease brains all exhibited a marked decrease in substance P fiber density in the substantia nigra and globus pallidus. A few medium-sized neurons with substance P immunoreactivity remained in the neostriatal remnant. Leucine-enkephalin immunoreactive processes were present throughout the neostriatum of normal brain, and were densely packed in the external segment of the globus pallidus and in the substantia nigra. A uniform population of medium-sized neurons containing immunoreactive leucine-enkephalin was present in the caudate and putamen. By contrast, in the Huntington's disease brains there was a marked diminution of fiber staining in the globus pallidus and substantia nigra. A few medium-size neurons and sparse fibers with leucine-enkephalin immunoreactivity persisted in the atrophic neostriatum. These observations are consistent with previous reports of regional peptide concentrations in both normal and Huntington's disease brain. Cells containing substance P and leucine-enkephalin immunoreactivity persist in the basal ganglia in brains from patients with Huntington's disease, and we have no evidence that cellular content of one or the other peptide is associated with disproportionate cell death or survival.

Adolescent↗
PubMed1980

Neuroregulatory and neuroendocrine GnRH pathways in the hypothalamus and forebrain of the baboon.

The distribution of neurons containing gonadotropin-releasing hormone (GnRH) in the baboon hypothalamus and forebrain was studied immunocytochemically by light and electron microscopy. GnRH was present in the perikarya, axonal and dendritic processes of immunoreactive neurons. Three populations of GnRH neurons could be distinguished. Most of the GnRH neurons which are assumed to directly influence the anterior pituitary were in the medial basal hypothalamus. Other cells that projected to the median eminence were found scattered throughout the hypothalamus. A second, larger population of neurons apparently was not involved with control of the anterior pituitary. These neurons were generally found within afferent and efferent pathways of the hypothalamus and forebrain, and may receive external information affecting reproduction. A few neurons projecting to the median eminence were also observed sending collaterals to other brain areas. Thus, in addition to their neuroendocrine role, these cells possibly have neuroregulatory functions. The inference is made that these bifunctional neurons, together with the widely observed GnRH-GnRH cellular interactions may help to synchronize ovulation and sexual behavior.

Animals↗
PubMed1978

Synaptic development in the rabbit superior colliculus and visual cortex.

The development of synapses in the visual cortex (VC) and superior colliculus (SC) of the rabbit has been examined with the electron microscope. In both areas, the number of synapses reaches adult levels by 20--25 days of postnatal age, but the development in the visual cortex is delayed in comparison to that in the superior colliculus. When S synapses (spheroidal vesicles, asymmetric thickening) are compared with F synapses (flattened vesicles, symmetric thickening), even greater differences are seen. In both the VC and SC, S synapses develop earlier than F synapses, though there is considerable overlap. Of interest is that fact that synapses in the visual cortex seem to overshoot their adult levels late in development, suggesting that an excess of synapses may be formed in this system. Multiple synapses, probably of retinal origin, increase in the first 3 weeks of synaptic development in the SC, but never are present in significant proportions in the VC. Synapse formation most often is characterized by formation of a junction and a postsynaptic thickening, followed by acquisition of synaptic vesicles. After 15 days, there is only a small number of such "non-vesicle synapses" in either the SC or VC.

Age Factors↗