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Biomedical subjects

J M Levine

Publications and source records attributed to J M Levine.

At least 19 recordsLinked to original sources
PubMed1995

Progress toward a restraint-free environment in a large academic nursing facility.

OBJECTIVE: To review the implementation and evolution of a successful physical restraint reduction program in a large nursing facility. INTERVENTION AND MEASUREMENTS: An initiative to reduce physical restraint began in March of 1990 with formation of a Restraint Review Committee (RRC), which developed and guided a program of inservice education, policy change, and procedural innovation. Progress was measured by monthly prevalence surveys of restraint use, both unit-specific and facility-wide. PATIENTS AND SETTING: The study took place in an 816-bed not-for-profit nursing facility with academic affiliation and closed medical staff. Mean age of residents was 85.5; 74% were female and 26% male. RESULTS: Physical restraint prevalence in our facility was reduced from 39% to 4% over 3 years, with marked decrease in variation among nursing units. Prevalence initially decreased to 20% after policy modifications and inservice education programs. Further innovations in procedure and policy resulted in continued reduction of physical restraint to 4%. The facility-wide rate of falls and accident-related injuries did not change over the 3-year period. Decrease in physical restraint was not accompanied by a change in the percentage of residents prescribed psychotropic medications such as benzodiazepines and neuroleptics. CONCLUSIONS: In response to the mandate to provide a least-restrictive environment, our institution has developed a successful system resulting in a dramatic reduction in physical restraint use. Changes in institutional culture and barriers to change are discussed, as well as issues of cost and generalizability.

Academic Medical Centers↗
PubMed1995

Pressure ulcers: a strategic plan to prevent and heal them.

Pressure ulcers are common in frail, disabled, or acutely ill older patients in the home, hospital, or nursing home. Prevention is the most important aspect of pressure ulcer care, and physician and nurse share in this responsibility. A nosocomial pressure ulcer adds significantly to mortality, morbidity, and hospital length-of-stay. Risk factor assessment scales can help identify patients who need prevention efforts, such as pressure relief, incontinence care, and nutritional supplements. When an ulcer does occur, careful documentation is required, including staging, size and depth description, and review of the interdisciplinary care plan. Knowledge of wound biology and cost-effectiveness should guide the choice of wound healing products.

Aged↗
PubMed1994

A quality-oriented approach to pressure ulcer management in a nursing facility.

The Jewish Home and Hospital for Aged, Bronx Division, is an 816-bed nursing facility that has developed a strategy for pressure ulcer management which relies on documentation, data flow, and feedback. Our system incorporates principles of Quality Improvement, and has resulted in a remarkably low nosocomial ulcer prevalence rate of 3.1%. We discuss Quality Improvement in the nursing facility and examine the value of pressure ulcer prevalence as a quality indicator. We present details of our system, highlighting the flow of information which comprises the Quality Improvement infrastructure, and include a discussion of benefits and costs of our system.

Aged↗
PubMed1994

A historical perspective on specialty beds and other apparatus for treatment of invalids.

The bed environment and support surface have long been recognized as important in the care of the chronically ill. A review of specialty beds from the 19th and early 20th century was done from the collection of medical trade catalogs at the New York Academy of Medicine. It has been said "Past Is Prologue." Whether or not this is true, examination of selected examples of these historical beds can provide an unique and interesting perspective on contemporary practice.

Beds↗
PubMed1994

Inhibition of neurite growth by the NG2 chondroitin sulfate proteoglycan.

The chondroitin sulfate proteoglycans (CSPGs) have been implicated as both positive and negative modulators of axonal growth; however, the functional properties of only a few specific CSPGs have been investigated. Here we demonstrate that NG2, an integral membrane CSPG expressed on the surfaces of glial progenitor cells, inhibits neurite growth from neonatal rat cerebellar granule neurons when presented to the cells as a component of the substrate. Growth inhibition occurred when NG2 was mixed with either laminin or L1, two potent promoters of axonal extension. Moreover, when given a choice between surfaces coated with NG2 and laminin or L1, the axons of the cerebellar neurons extended preferentially on laminin or L1 and avoided areas of the substrate containing NG2. The NG2 proteoglycan inhibited neurite growth after digestion with chondroitinase ABC, demonstrating that the inhibitory activity is a property of the core protein and not the covalently attached chondroitin sulfate glycosaminoglycan chains. NG2 also inhibited neurite growth from embryonic rat dorsal root ganglia neurons on substrates containing laminin. However, when the sensory neurons were plated onto surfaces containing the L1 glycoprotein and NG2, neurite growth was not inhibited. These results demonstrate that the NG2 proteoglycan provides an unfavorable substrate for axonal growth. Cells that express this proteoglycan in vivo may participate in axonal guidance by defining areas of the developing CNS that are nonpermissive for axonal extension from specific classes of developing neurons.

Animals↗
PubMed1994

Increased expression of the NG2 chondroitin-sulfate proteoglycan after brain injury.

Injury to the adult mammalian CNS results in reactive changes among the glial cells surrounding the site of damage. Recently, an unusual class of glial cells has been identified within the intact adult rat cerebellum on the basis of the expression of the NG2 chondroitin-sulfate proteoglycan (Levine and Card, 1987). To determine whether the cells that express the NG2 proteoglycan show reactive changes after injury, small puncture lesions were made into the cerebelli of adult rats, and changes among astrocytes, microglia and NG2-positive cells were examined using immunohistochemical staining with cell type-specific marker antibodies. Beginning at 24 hr after lesion, NG2-positive cells immediately adjacent to the lesion site bound the anti-NG2 antibodies more heavily than cells within the undamaged areas of the cerebellum. This increase in anti-NG2 immunoreactivity was transient, reaching a maximum at 7 d postlesion and declining slowly thereafter. The increase in anti-NG2 immunoreactivity was accompanied by an increase in the levels of mRNA encoding the NG2 core protein as demonstrated by in situ hybridization. NG2-positive cells adjacent to the lesion site incorporated 3H-thymidine into their nuclei beginning at 24 hr postlesion and increased in number. Concurrent with these changes, microglia became activated and increased in number, monocytes invaded the damaged tissue, and an astrocytic scar formed. These observations demonstrate that the cells that express the NG2 proteoglycan are a reactive cell type that responds to brain injury. The increased expression of the NG2 chondroitin-sulfate proteoglycan may contribute to the failure of damaged CNS axons to regenerate successfully.

Animals↗
PubMed1992

Modulation of a Ca2+ signaling pathway by GM1 ganglioside in PC12 cells.

The effects of exogenous GM1 ganglioside on depolarization and ligand-induced Ca2+ signaling were investigated in PC12 cells. Cellular responses to K+ depolarization and bradykinin application in control and GM1-treated cells were examined with respect to: 1) changes in the intracellular Ca2+ concentration ([Ca2+]i) measured using fura-2 fluorescence in single cells, and 2) changes in Ca(2+)-dependent protein kinase activity as assayed by two-dimensional phosphopeptide analysis of the site-specific phosphorylation of tyrosine hydroxylase. Pretreatment of cells with GM1 (10 or 100 microM) enhanced K+ depolarization-stimulated increases in [Ca2+]i and in 32PO4 incorporation into tyrosine hydroxylase phosphopeptide T2, a Ca2+/calmodulin-dependent protein kinase II substrate. In contrast, GM1 treatment had no effect on the transient increases in [Ca2+]i evoked by bradykinin or on bradykinin-induced increases in the site-specific phosphorylation of tyrosine hydroxylase. The depolarization-induced and GM1-enhanced increases in [Ca2+]i and T2 phosphorylation were prevented by removal of external Ca2+ or pretreatment with 1 microM nitrendipine, suggesting that these increases result from Ca2+ entry through dihydropyridine-sensitive Ca2+ channels. The ability of exogenous gangliosides to potentiate increases in [Ca2+]i may underlie their diverse neuritogenic and neurotrophic actions in the nervous system.

Animals↗
PubMed1992

Historical perspective: the neurotrophic theory of skin ulceration.

Though nearly forgotten, the neurotrophic theory was very much a part of mainstream medical thinking during the mid-nineteenth century. This theory stated that all bodily organs are maintained by special nutritional factors secreted by the central nervous system. Development of skin ulceration in the face of neurologic injury became a model for the theory, and controversy involved two great neurologists of the time, Jean Martin Charcot and Edouard Brown-Séquard. As the neurotrophic theory fell into disfavor, interest in decubitus ulcers waned as well. Today, pressure sores remain a major epidemiologic problem for the growing population of frail elderly persons in both acute and long-term care settings. Because of the increased mortality, morbidity, and cost associated with these lesions, attention needs to be refocused on research and education concerning the decubitus ulcer.

Animals↗
PubMed1992

Historical notes on pressure ulcers: the cure of Ambrose Paré.

Ambrose Paré practiced surgery in 16th century France, and is considered a founding father of modern medical surgical practice. History books remember him mainly for innovations in treating war wounds, but few are aware of his treatment for skin ulcers. His textbooks contain instructions sounding quite similar to ours, including nutrition, pain relief, and debridement. Paré's autobiography relates the case of a wounded French aristocrat who developed a pressure ulcer and was successfully cured.

France↗
PubMed1991

Stimulation of a Ca(2+)-dependent protein kinase by GM1 ganglioside in nerve growth factor-treated PC12 cells.

We have investigated the ability of exogenous gangliosides to modulate nerve growth factor (NGF) signal transduction in PC12 cells. The effects of exogenous ganglioside GM1 on multiple protein kinase activities were assayed by analyzing site-specific serine phosphorylation of tyrosine hydroxylase (TyrOHase) by two-dimensional phosphopeptide mapping. In the presence of NGF, exogenous GM1 (1-10 microM) increased 32P incorporation into TyrOHase phosphopeptide T2, a Ca2+/calmodulin-dependent protein kinase substrate whose phosphorylation is not normally affected by NGF treatment. In the absence of NGF, GM1 treatment had no significant effects on TyrOHase phosphorylation. The removal of extracellular Ca2+ or blockade of dihydropyridine-sensitive Ca2+ channels prevented the GM1-induced increases in 32P incorporation into phosphopeptide T2. Exogenous GM1 also potentiated K+ depolarization-induced increases in the phosphorylation of TryOHase. These results suggest that the stimulatory effects of exogenous GM1 ganglioside on NGF actions may be due to its ability to potentiate a Ca(2+)-dependent signaling pathway.

Adrenal Gland Neoplasms↗
PubMed1990

Type II glucocorticoid receptors are expressed in oligodendrocytes and astrocytes.

Glucocorticoid hormones affect gene expression directly at the level of transcription via intracellular receptors that translocate to the nucleus in the presence of steroid. In the brain, two types of high-affinity receptors bind glucocorticoids, the type I, mineralocorticoid receptor and the type II, glucocorticoid receptor (GR). Both receptor types are expressed by many types of neurons. Although binding studies have suggested that glial cells may also express receptors, the expression of these receptors in specific classes of glia has not been studied previously. This immunocytochemical study was undertaken to determine which of the different classes of glial cells express type II GR. Primary cultures of mixed glial cells from rat cerebrum and cerebellum, purified oligodendrocytes and astrocytes, as well as two glial tumor cell lines were screened for the expression of glucocorticoid receptors using a mouse monoclonal antibody directed against rat liver GR (BuGR-2). Glial cell types were identified by morphology and immunoreactivity (IR) with antibodies directed against glial fibrillary acidic protein (GFAP), cyclic nucleotide phosphodiesterase (CNP), or myelin basic protein (MBP). Double immunofluorescence microscopy revealed that all GFAP-IR cells (type 1 and type 2 astrocytes), all CNP- or MBP-IR cells (oligodendrocytes), as well as immature and intermediate cell types expressed GR, although at different levels. C6 glioma and JScl1 Schwannoma cells were observed to express moderate to high levels of GR. Furthermore, cells grown in the absence of glucocorticoids had diffuse GR staining over the cytoplasm, whereas cells grown in the presence of the synthetic glucocorticoid dexamethasone had strong nuclear staining. These results demonstrate that, in vitro, all classes of glial cells express glucocorticoid receptors that can translocate to the nucleus in the presence of hormone. These observations suggest that glial cells are major targets for glucocorticoid-directed control of gene transcription in the nervous system.

Astrocytes↗
PubMed1990

Lectin binding identifies a subpopulation of neurons in chick dorsal root ganglia.

We screened a variety of lectins with different sugar specificates to determine whether subpopulations of dorsal root ganglion (DRG) neurons in the chick can be distinguished by the carbohydrates they express. Of the 15 lectins tested only those that recognize N-acetylgalactosamine (galNac) residues labeled a subset of DRG neurons. For example, Dolichos biflorus (DBA) labeled a population of small-diameter neurons in the dorsomedial DRG and their terminals in the dorsal horn in hatchling chicks. Staining of live neurons in vitro demonstrated that DBA was binding to the cell surface. Labeling first appeared in sensory neurons at about St.38 (E12) and in dorsal horn laminae 1 and 2 at about St.42 (E16). Fainter labeling appeared somewhat later in lamina 3, after hatching. Labeling of the tissue sections was eliminated by chloroform: methanol extraction and reduced by alpha-N-acetylgalactosaminidase digestion, but survived trypsinization. Together these results suggest that a subset of DRG neurons in the chick can be identified by the presence of a cell surface glycoconjugate, perhaps a glycolipid, containing terminal alpha-linked galNac residues.

Acetylgalactosamine↗
PubMed1990

Leg ulcers: differential diagnosis in the elderly.

Leg ulcers are a common problem encountered in the elderly. Because their origins are often multifactorial, it is essential for the primary care physician to have a sound knowledge of differential diagnosis to institute proper treatment. This review discusses salient historical points as well as bedside physical examination techniques useful in patients presenting with leg ulcer. Also discussed are pathophysiology of most common types of ulcer, including venous disease, arterial disease, diabetes, and physical agents. Less common causes of leg ulcer are also reviewed.

Aged↗
PubMed1989

Neuronal influences on glial progenitor cell development.

The role of cell-cell interactions in the development of bipotential glial progenitor cells in cultures of rat cerebellum and optic nerve was studied. In the cerebellar cultures, progenitor cells divide slowly and most of their progeny develop into additional progenitor cells. Progenitor cells isolated from postconfluent cultures of cerebellum, however, develop rapidly into oligodendrocytes when grown in a serum-free medium. Factors secreted or shed into the medium by young cerebellar interneurons stimulate optic nerve progenitor cells to divide and promote the survival of progenitor cells. These factors appear to alter the function of the internal clock that regulates the timing of oligodendrocyte differentiation. These results suggest that the neuronal microenvironment can influence the lineage decisions of multipotential glial progenitor cells.

Animals↗
PubMed1989

Pressure sores: a plan for primary care prevention.

Pressure sores are a preventable cause of increased morbidity, mortality, and treatment cost. Prevention begins with a knowledge of risk factors, both external and internal, and specific interventional measures for each. Management is best implemented using a team: the physician, nurse, nurse's aide, rehab nurse, physical therapist, dietitian, and occupational therapist, with an informed physician as team director. New management tools available include risk factor assessment scales to help in targeting resources.

Aged↗
PubMed1989

Atypical locations of pressure sores: presentation of two cases.

When we consider pressure sores, we usually think of their location in areas of contact with the bed or chair. However, in the presence of risk factors, any area of skin is subject to breakdown if exposed to constant pressure. This article presents two cases demonstrating unusual locations of pressure sores, and discusses underlying risk factors which contributed to their genesis. Vigilant attention to risk factor intervention by the multidisciplinary care team can prevent the incidence of this common complication of immobility. The use of a standardized risk factor assessment scale can be a useful guide to prevention planning.

Aged↗
PubMed1987

Light and electron microscopic localization of a cell surface antigen (NG2) in the rat cerebellum: association with smooth protoplasmic astrocytes.

Immunofluorescence and immunoperoxidase techniques were used to localize a cell surface chondroitin-sulfate proteoglycan antigen, termed NG2, in the developing and adult rat cerebellum. In the adult, both polyclonal and monoclonal anti-NG2 antibodies labeled cells throughout the cerebellar cortex, with the labeled cells being especially prominent in the molecular layer. The labeled cells had small, irregularly shaped cell bodies from which thin highly branched processes radiated in a stellate array. The NG2-labeled cells were not labeled with antibodies against glial fibrillary acidic protein (GFAP), vimentin, or S-100 protein, intracellular markers for astrocytes. However, electron microscopic immunocytochemical analysis of NG2 immunoreactive cells revealed a cell morphology consistent with that of protoplasmic astrocytes. Labeled cell bodies contained a thin rim of organelle-poor cytoplasm surrounding a euchromatic nucleus. Thick processes originating from the cell soma tapered to form thin branches with highly irregular surface contours that extended between adjacent neuronal elements. The labeled processes did not form synapses in the neuropil, and no synaptic profiles onto anti-NG2-labeled cell bodies or processes were observed. Thus, we conclude that the NG2 antigen is a cell surface marker for a class of smooth protoplasmic astrocytes. Immunoreactive cells were seen in the developing cerebellum beginning at embryonic day 16. The number of labeled cells increased during the early stages of cerebellar development, reaching a peak at about postnatal day (PND) 4 or 5 and declining thereafter. In the developing cerebellum, labeled cells lying within the forming molecular layer resembled the cells seen in the adult, whereas cells lying deeper within the folia had an immature appearance with fewer processes and less branching. This apparent gradient of morphological maturation suggests that an interaction with parallel fibers in the developing molecular layer may play a role in the terminal cytodifferentiation of the NG2-labeled smooth protoplasmic astrocytes.

Animals↗