Hospital case management: bridging acute and long-term care.
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Biomedical subjects
Publications and source records attributed to F G Williams.
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Like all health care services, case management is a process that relies on information. Based on the experiences in implementing computer information systems in six hospital-based case management programs, several financial, technical, and management issues are reviewed. These issues, which are also relevant for other specialized hospital-based programs, include information priorities, user acceptance, quantifying data, data entry methods, data security, and systems integration. The lessons learned regarding these issues are discussed, and categories of software alternatives are presented.
The periaqueductal grey (PAG) plays an important role in the descending modulation of nociception. Inhibitory influences of GABAergic terminals, located within the periaqueductal grey, are thought to play a role in antinociception by influencing the activity of neurons that project to the nucleus raphe magnus and adjacent reticular nuclei. The present study utilized electron microscopic immunocytochemistry to quantitate the normal neuronal associations of GABA-immunoreactive terminals, and to visualize the neuronal distribution of the GABAA receptor in the ventrolateral periaqueductal grey of the rat. Of particular interest was a quantitative description of the interaction between GABA-immunoreactive axon terminals and periaqueductal grey neurons that were retrogradely-labelled from the nucleus raphe magnus and adjacent medullary reticular nuclei. Most terminals were observed to be immediately apposed only to two or three dendrites, although axonal and perikaryal associations were also observed. In the ventrolateral periaqueductal grey, 37.5% of all GABA-immunoreactive terminals were adjacent to periaqueductal grey-nucleus raphe magnus and periaqueductal grey-reticular nucleus projection neurons. Symmetrical synapses with these retrogradely-labelled neurons were formed by 17% of GABA-immunoreactive terminals in the ventrolateral periaqueductal grey. We also noted that 13.2% of the GABA-immunoreactive terminals formed symmetrical synapses with GABA-immunoreactive dendrites in the periaqueductal grey, and occasionally those dendrites were retrogradely labelled. Only 0.8% of the GABA-immunoreactive terminals formed putative symmetrical synapses with other GABA-immunoreactive terminals. Consistent with these findings, GABAA receptor immunoreactivity was only associated with dendrites and perikarya in neurons of the ventrolateral PAG. These results are consistent with an inhibitory role for GABA on PAG neurons, a configuration required by hypothetical models for opoid disinhibitory circuitry within the PAG. In addition, the data further suggest that other kinds of GABAergic connections may be important in descending antinociception, and that a population of GABAergic PAG projection neurons exists that may be inhibitory within nucleus raphe magnus and the adjacent reticular nuclei.
The subcellular site where insulin is degraded by rat hepatocytes in vivo is controversial. While several potential insulin-degrading enzyme systems, each with its own characteristic cellular location, are known to exist in the liver, questions remain about which of them participates in the degradation of physiologic doses of insulin. These studies examine the proteases that degrade physiologic doses of [125I]-insulin in vivo to determine (1) when and where initial degradation occurs, and (2) which of the potential degradative enzymes is active. Following injection into the mesenteric veins of male rats, intact [125I]-insulin and its labeled degradation products were analysed by reverse-phase high-performance liquid chromatography (RP-HPLC) of biopsy homogenates. [125I]-insulin was rapidly degraded in vivo; the t 1/2 of degradation was approximately 2.7 minutes. To test for extracellular protease activity, an isolated perfused liver system was employed. [125I]-insulin (or [125I]-glucagon) uptake was controlled by changing the temperature of the perfusion medium. Five minutes after [125I]-insulin injection, surface-bound label was recovered in an acidic (pH 3.5) wash. In perfusion at 15 degrees C, both the internalization and degradation of [125I]-insulin were inhibited; 7.2% of unbound hormone was degraded and 5.1% of surface-bound insulin was degraded. Only 11.4% of unbound insulin and 17.4% of surface-bound insulin were degraded at 35 degrees C. In contrast, 95.5% of unbound glucagon and 89.9% of surface-bound glucagon were degraded at 35 degrees C. Thus, although glucagon degradation occurs at the sinusoidal plasmalemma of perfused livers, the same membrane does not mediate the rapid degradation of insulin observed in vivo. Analysis of the RP-HPLC [125I]-insulin elution profiles from liver biopsy homogenates, and comparison of them to profiles produced by purified proteases, suggested that insulin protease is responsible for most hepatic degradation of physiologic doses of insulin. Some cathepsin D-like activity was also observed in vivo, confirming that two pathways exist for insulin metabolism. The time course over which insulin was degraded was more rapid than previous studies in vitro would have predicted. This suggests that more insulin was receptor-bound at the time of its initial degradation, and that the active protease was soluble and was introduced into endocytic peripheral endosomes within seconds after their formation.
These studies describe the normal anatomical distribution of neurons containing the mRNA coding for neurotensin (proneurotensin/neuromedin N) in the rat forebrain and midbrain and examine how that distribution is altered by acute administration of the dopamine antagonist haloperidol. A novel fluorescence detection method was developed and employed with biotinylated oligonucleotides to permit the rapid, sensitive visualization of in situ hybridization. The hybridization was temperature-sensitive, eliminated by ribonuclease, and co-localized in neurotensin-immunoreactive perikarya in the midbrain. In the forebrain of control rats, proneurotensin mRNA-containing neurons were found in the dorsomedial and ventrolateral caudate/putamen, in the nucleus accumbens, in the ventral striatum including the olfactory tubercles, and in the septal nuclei. Haloperidol induced significant increases in the frequencies and distributions of hybridization-positive neurons in the striatum and septal nuclei. In the midbrain, the highest frequency of hybridization-positive neurons occurred in the substantia nigra and the superior colliculus. Prominent populations were also present in the dorsal and ventral periaqueductal gray, the oculomotor region, and the medial longitudinal fasciculus. Less prominent were populations of neurons in the dorsomedial deep mesencephalic nuclei and the ventral tegmental area. Haloperidol induced only modest increases in the frequency of pro-neurotensin mRNA-containing neurons in the ventral tegmental area, and had no effects elsewhere in the midbrain. These results show that the fluorescent detection techniques used in this analysis provide a very rapid, reliable method for localizing hybridized mRNA in the rat brain. This study also suggests that a subpopulation of striatal neurons begin to express proneurotensin mRNA in response to haloperidol treatment. This effect of haloperidol on striatal neurons contrasts with results from additional studies of enkephalin mRNA in the striatum, suggesting that the mechanisms of haloperidol stimulation may differ between neurotensin and enkephalin-containing neurons.
The periaqueductal gray plays an important role in the descending modulation of nociception. While the importance of endogenous opioids to periaqueductal gray circuits that modulate nociception is supported by many studies, the ultrastructural relationships between enkephalin-immunoreactive axon terminals and the surrounding periaqueductal gray neuropil have not been quantitated in the rat. Further, the possible interaction between enkephalin-immunoreactive axon terminals and periaqueductal gray neurons that project to the rostroventral medulla has not been described. The present study utilized electron microscopic immunocytochemistry to quantitate the normal neuronal associations of enkephalin-immunoreactive terminals in the caudal periaqueductal gray of the rat. A primary focus of this analysis was to ascertain whether any interaction exists between enkephalin-immunoreactive axon terminals and periaqueductal gray neurons that were retrogradely-labeled from the nucleus raphe magnus and adjacent medullary reticular nuclei. We examined the ventrolateral periaqueductal gray and the ventral periaqueductal gray immediately subjacent to the aqueduct and found that both the average terminal diameters and the volume fractions of enkephalin-immunoreactive terminals were very similar. In these two regions, most terminals were observed to be in close apposition to either two or three dendrites that were neither retrogradely-labeled nor enkephalin-immunoreactive, although axonal and perikaryal associations were also observed. In the ventrolateral periaqueductal gray, 22% of all enkephalin-immunoreactive terminals were adjacent to periaqueductal gray-nucleus raphe magnus and periaqueductal gray-reticular nucleus projection neurons. In the periaqueductal gray subjacent to the aqueduct, 32% of all enkephalin-immunoreactive terminals were adjacent to periaqueductal gray-nucleus raphe magnus and periaqueductal gray-reticular nucleus projection neurons. Symmetrical synapses with these retrogradely-labeled neurons were formed by 5.5% of enkephalin-immunoreactive terminals in the ventrolateral periaqueductal gray, and by 4.3% of enkephalin-immunoreactive terminals located subjacent to the aqueduct. We also noted that enkephalin-immunoreactive terminals formed symmetrical synapses with non-retrogradely-labeled, enkephalin-immunoreactive dendrites in the periaqueductal gray. Direct opioid input onto putative excitatory periaqueductal gray output neurons that are hypothesized to modulate nociception was an unexpected finding.(ABSTRACT TRUNCATED AT 400 WORDS)
Social work practitioners in health and social services are expected to develop and implement programs and client care plans that require cooperation and coordination with numerous other individuals and programs. Such cooperation and coordination often are accomplished through informal networking. As programs develop, these relationships may be formalized in written policy agreements. In this article, the authors examine four policies designed to improve cooperation and coordination at different levels in hospital-based case management systems. Implications for social work practice are discussed.
This article contains the initial findings of an ongoing evaluation of a hospital-based coordinated care demonstration. The goal of the demonstration is to investigate the appropriateness and feasibility of providing hospital-based case management services for extended periods to elderly individuals living in the community. The rationale for the demonstration is reviewed, and the structure of each participating hospital's coordinated care program is described. Data are presented on the characteristics of clients served by the programs during the first six months of the demonstration. The factors that influenced implementation and early operations of these programs are analyzed, and their implications for hospital managers are discussed.
The periaqueductal gray of the rat contains significant levels of the putative peptide neurotransmitter neurotensin. The profound anti-nociceptive effects of neurotensin injected into the periaqueductal gray may involve a population of periaqueductal gray neurons having descending projections to the rostral ventral medulla, including nucleus raphe magnus and adjacent reticular nuclei. In this study, electron microscopic immunocytochemistry was used to examine the ultrastructure of periaqueductal gray axon terminals containing neurotensin-like immunoreactive material and to obtain quantitative data regarding the relationship of such terminals to other elements of the neuropil. Of particular interest was the interaction between neurotensin-like immunoreactive terminals and retrogradely labeled neurons that project to nucleus raphe magnus and adjacent reticular nuclei. Within the periaqueductal gray, the sites of retrograde and immuno-labeling were consistent with previous reports. The neurotensin-immunoreactive structures were predominantly axon fibers and terminals. In the ventrocaudal periaqueductal gray, the mean diameter of neurotensin-containing terminals was 0.93 +/- 0.02 micron and they comprised a volume fraction of 0.0010. Most of the neurotensin-positive terminals examined (74.2%) were in contact with or closely apposed to dendrites. The most common anatomical configuration observed was a single neurotensin-immunoreactive terminal juxtaposed to three dendrites. Only 2% of immunoreactive terminals were apposed to perikarya. Neurotensin-immunoreactive terminals were observed to form symmetrical synapses and 96.4% of such terminals were axodendritic. Occasional multiple neurotensin-immunoreactive terminals associated with single dendrites were observed. Although neurotensin-like immunoreactive terminals were quite prominent, only a small percentage made synaptic contact with periaqueductal gray neurons that project to the nucleus raphe magnus and adjacent reticular formation. Among the population of periaqueductal gray neurons retrogradely-labeled from nucleus raphe magnus and adjacent reticular nuclei, the frequency of direct synaptic contact by neurotensin-immunoreactive terminals was 2%. These data suggest that the periaqueductal gray circuitry by which neurotensin ultimately affects descending pathways is complex and may involve a population of local circuit neurons whose transmitters and connections remain to be elucidated.
The gerontological service delivery system often fails to integrate the different types of services needed at different times by older clients. Social workers need to address the urgent and increasing need for communication among acute care hospitals that are diversifying into areas previously the domain of community-based providers of services for the aged. Coordinated care case management programs were developed in seven hospitals to determine whether hospitals could serve as a logical entry point of frail elderly persons into the system. Examination of the experiences of these hospitals illustrated the need for models of service integration and resulted in several approaches to comprehensive service delivery and coordination. Social work professionals in both acute and long-term care settings need to understand all aspects of the service delivery system to ensure that elderly clients receive appropriate levels and continuity of care in a complex and constantly changing system.
We developed a mouse monoclonal antibody against neurotensin (NT), termed NT8, for applications in immunohistochemistry and for ELISA analysis of NT. The antibody's paratope was determined by competitive ELISA using several peptide fragments of NT. That paratope requires intact peptide bonds between NT residues proline-7, arginine-8, and arginine-9. The antibody is of the IgG2B sub-isotype, having an IC50 for intact NT of approximately 3 nM when measured by competitive ELISA. Light microscopic immunohistochemical studies in the periaqueductal gray (PAG) and hypothalamus demonstrated staining patterns that agreed well with previous reports. Neuron perikarya were visualized even in the absence of colchicine pre-treatment, indicating that NT8 antibody is very sensitive in immunohistochemical applications. At the EM level, the antibody stained axon terminals, dendrites, and perikarya in the PAG. In lightly immunoreactive perikarya, rough endoplasmic reticula were visualized, suggesting that biosynthetic precursors to NT might be recognized by NT8.
Arizona is adding long-term care to its prepaid, capitated alternative to Medicaid. This article discusses the potential for this major cost-control experiment. Experience suggests that those able to quality for long-term care will fare better than the poor did in the previous system. However, limiting eligibility will be the primary means of controlling costs; significant price competition is not likely to develop. The bidding process will serve more to transfer risk to contract providers than to improve program efficiency. Potential cost savings will be more than offset by an increased identification of need.
Contract management is more than just an alternative form of financing. Contract management enables hospitals to avoid costly investments in time, personnel, and capital by using outside sources to provide clinical and support services. However, healthcare organizations that contract for a large number of services run the risk of becoming "hollow hospitals"--institutions where patient care is no longer the hospital's core activity. Hospitals can avoid this situation by carefully reviewing the advantages and risks of contract management in terms of their mission, quality, and organizational objectives.
This article examines the use of volunteers within hospital-based long-term care case management programs. As hospitals diversify into long-term care, the roles played by volunteers are also diversifying. A brief description of the involvement of volunteers with the frail elderly is followed by a comparison of the roles and relationships of volunteers within existing hospital auxiliaries and long-term care case management programs. Three models for structuring hospital-based volunteer programs that address the needs of the frail elderly within diverse communities are presented. Implications surrounding the involvement of volunteers beyond hospital walls are discussed.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Studies were conducted to examine the insulin and proinsulin synthetic response to glucose in the streptozotocin-nicotinamide--induced rat islet adenoma. Tumors responded to an increase from 3.8 mmol/L to 16.6 mmol/L glucose by increasing incorporation of [3H]-L-leucine into both proinsulin and insulin. Though this response was statistically significant, the stimulation was less than that noted in rat islets, and the variability of incorporation was greater. In addition, the conversion of proinsulin to insulin was generally slow, again with substantial intertumor variation. The recovery of insulin, as well as proinsulin, was significantly higher at the end of four hours of incubation in tumors incubated in 16.6 mmol/L glucose, implicating an insulin-degradative pathway modulated by glucose. Therefore, while the tumor will not replace conventional sources of tissue for insulin biosynthetic experiments, systems utilizing the tumor can serve as an addition to the methodology for studying previously unrecognized or poorly understood intracellular processes within the beta cell.