Biomedical subjects

M Segal

Publications and source records attributed to M Segal.

At least 145 records · Page 8Linked to original sources

PubMed1993

Assessing selfcare status in quadriplegia: comparison of the quadriplegia index of function (QIF) and the functional independence measure (FIM).

The purpose of this study was to compare the quadriplegia index of function (QIF) to the functional independence measure (FIM) in assessing the daily performance of selfcare activities by individuals with cervical spinal cord injury. This study evaluated feeding, grooming and bathing activities in 22 C4-C7, Frankel A-D spinal cord injury patients between 3 and 12 months postinjury. The manual muscle test (MMT) was performed on 17 of these subjects during the same window of time as the QIF and the FIM. An upper extremity motor score (UEMS) was derived from the MMT. In order to relate motor power to functional ability, the UEMS was used as a measure of neurological function to test the hypothesis that the QIF scores are more highly correlated to motor power than are the FIM scores for this population. Spearman coefficients were calculated to correlate the QIF, the FIM and the UEMS. For the bathing and grooming categories, both the QIF and the FIM showed significant and similar correlations to the UEMS. For the feeding category, however, the QIF had a significantly better correlation to the UEMS than did the FIM (Rho = 0.90 vs 0.53, p < 0.01). Use of the QIF feeding scale may allow the detection of changes in function as individuals recover that the FIM scale would miss. Further evaluation of the remaining selfcare and mobility scales is needed. Modification of the FIM with more sensitive portions of the QIF would improve the discriminative ability of outcome studies and program evaluations.

Adolescent↗

PubMed1993

Chronic diffuse varioliform gastritis in a child. Total gastrectomy for acute massive bleeding.

Chronic diffuse varioliform gastritis is an uncommon, subacute, inflammatory gastric mucosal disease characterized by swollen congested rugae and disseminated mucosal erosions. The entity is exceptionally rare in children. The spectrum of reported symptoms is broad; frank hematemesis has never been reported in childhood. We present a child in whom the disease had a remarkably unusual clinical course. Because many caretakers were unaware of the existence of the disease in children, the patient had numerous hospitalizations and surgical procedures, until massive gastric bleeding resulted in unavoidable emergency total gastrectomy. Microscopical examination and immunofluorescent staining of the gastric mucosa confirmed the diagnosis of chronic diffuse varioliform gastritis.

Child↗

PubMed1993

Risk factors for ventilatory impairment among middle-aged and elderly men. The Normative Aging Study.

To evaluate the relationship of atopy and inflammation to the occurrence of ventilatory impairment, we studied 1,301 middle-aged and older men participating in the Normative Aging Study at the time of their 1984 to 1987 examination. Screening at entry to the study in the 1960s had excluded subjects with asthma and other chronic diseases at that time. After adjustment for smoking status and pack-years in this cross-sectional analysis, a weak inverse relationship between FEV1 and blood eosinophil count was not statistically significant, and FEV1 showed no relationship to blood eosinophil count as a percentage of total leukocytes. A weak inverse relationship between FEV1 and serum total IgE concentration was not statistically significant. Cutaneous immediate hypersensitivity to one or more common aeroallergens was not related to FEV1. A significant inverse relationship between FEV1 and blood total leukocyte count was observed in never and former smokers. FEV1 was significantly lower in subjects reporting usual phlegm production. These findings suggest that ventilatory impairment is not related to atopic status among middle-aged and older men without a history of asthma. The inverse relationship between total leukocyte count and FEV1 in this sample supports the hypothesis that nonallergic inflammation plays a role in the pathogenesis of chronic airflow obstruction in this group.

Aged↗

PubMed1993

Women & AIDS.

Explore the source record for details and available documents.

Acquired Immunodeficiency Syndrome↗

PubMed1993

Calcium and neuronal plasticity.

The proposed involvement of free intracellular calcium concentration ([Ca]i) in neuronal plasticity is examined. While it is generally believed that a rise of [Ca]i is necessary for the triggering of long-term modification of synaptic connections, there are many unresolved issues related to this dogma; it is not entirely clear what is the source of the elevated calcium, how much of a calcium rise is sufficient to produce the synaptic potentiation, where and for how long, and what are the relevant chemical consequences of the transient rise of [Ca]i. It is generally believed that the dendritic spine is the locus of synaptic modification, yet little evidence exists to support this view. High resolution calcium imaging studies may contribute to the clarification of some key issues in the field of neuronal plasticity.

Animals↗

PubMed1993

Bilateral localized Castleman disease of the retroperitoneum.

A case report of a 23-year-old patient with abdominal pain was found to have a bilateral, retroperitoneal localized form of Castleman disease. To the best of our knowledge, it is the first report of a bilateral form described in the literature. Surgical excision resulted in the disappearance of symptoms and both masses were found to be of the hyaline type. Follow-up computerized tomography revealed no pathological sequelae.

Adult↗

PubMed1992

Interaction between the Saccharomyces cerevisiae CDC25 gene product and mammalian ras.

In order to characterize the interaction between the Saccharomyces cerevisiae Cdc25 protein and Harvey-ras (p21H-ras), we have constructed a yeast strain disrupted at the RAS1 and RAS2 loci, expressing both p21H-ras and the catalytic domain of the bovine GTPase activating protein (GAP) and containing the cdc25-2 mutation. Such a strain exhibits a temperature-sensitive phenotype. The shift to the nonpermissive temperature is accompanied by the loss of guanyl nucleotide-dependent activity of adenylylcyclase in vitro. The temperature-sensitive phenotype can be rescued by CDC25 itself, as well as by a plasmid containing a truncated SDC25 gene. In addition, wild type CDC25 significantly improves the guanyl nucleotide response observed in the background of the cdc25ts allele at the permissive temperature in a dosage-dependent manner and restores the guanyl nucleotide response at the restrictive temperature. Both CDC25 and a truncated SDC25 also restored p21H-ras-dependent guanyl nucleotide response in a strain isogenic to the one described above but containing a disrupted CDC25 locus instead of the temperature-sensitive allele. These results suggest that the S. cerevisiae Cdc25 protein interacts with p21H-ras expressed in yeast by promoting GDP-GTP exchange. It follows that the yeast system can be used for characterizing the interaction between guanyl nucleotide exchangers of Ras proteins and mammalian p21H-ras.

Adenylyl Cyclases↗

PubMed1992

AF102B, a muscarinic M1 receptor agonist, mimics some effects of acetylcholine on neurons of rat hippocampus slices.

The putative muscarinic M1 receptor agonist, AF102B, was applied to rat hippocampal slices and the responses of intracellularly recorded pyramidal cells were examined. AF102B mimicked some effects of acetylcholine on these cells as follows: at low concentration, AF102B attenuated a slow after-hyperpolarization in response to a long depolarizing current pulse. This effect was blocked by the M1 antagonist, pirenzepine. At higher concentrations, AF102B also depolarized the cells and caused an increase in their input resistance. AF102B did not affect local excitatory postsynaptic potentials or reactivity to topically applied excitatory amino acid substances. These experiments indicate that AF102B acts as an agonist at some muscarinic M1 receptor subtypes in mammalian brain.

Acetylcholine↗

PubMed1992

Acetylcholine enhances NMDA-evoked calcium rise in hippocampal neurons.

The effects of acetylcholine (ACh) on changes in [Ca]i produced by the glutamate agonist N-methyl-D-aspartate (NMDA) were measured in cultured rat hippocampal neurons loaded with the fluorescent calcium indicator Fluo-3 in a confocal laser scanning microscope. NMDA produced a dose-dependent reversible rise in [Ca]i. ACh had a smaller and less consistent effect on [Ca]i but could cause a marked enhancement of the reactivity of neurons to NMDA. This effect was reversed by the presence of the muscarinic antagonist atropine. AMPA, another glutamate agonist which causes a rise in [Ca]i by activating voltage gated calcium influx was less affected by ACh. Caffeine, which releases calcium from intracellular stores also enhanced reactivity of these neurons to NMDA. It is suggested that ACh can enhance reactivity to NMDA by releasing calcium from internal stores.

Acetylcholine↗

PubMed1992

Acidic amino acids evoke a smaller [Ca2+]i rise in GABAergic than non-GABAergic hippocampal neurons.

Changes in intracellular calcium concentration ([Ca2+]i) in response to topical application of the glutamate agonists N-methyl-D-aspartate (NMDA), or amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) were measured in cultured rat hippocampal neurons loaded with Fluo-3 and visualized in a confocal laser scanning microscope. These neurons were subsequently stained for the presence of the enzyme marker for gamma-amino butyric acid (GABA), glutamate decarboxylase (GAD). GAD-positive, putative interneurons were less responsive to NMDA and AMPA than GAD-negative neurons. The time course of the rise and decay of [Ca2+]i was similar in the two groups of neurons. Also, there was no clear difference in the shape and size of these two neuron groups indicating that the difference between them is not due to diffusion distances. These data indicate that interneurons are probably more able to handle a calcium load than other neurons, a difference that may underly their resistance to treatments which cause degeneration of other neurons in the hippocampus.

Animals↗

PubMed1992

Serum beta 2-microglobulin and prediction of progression to AIDS in HIV infection.

Identification of laboratory tests that can help predict progression to acquired immunodeficiency syndrome (AIDS) in people infected with human immunodeficiency virus (HIV) is important for clinical management and counselling. We have assessed the usefulness of CD4 lymphocyte count, serum beta 2-microglobulin concentration, and the presence of p24 antigen as predictors of AIDS. We studied 214 homosexual and bisexual men with well-defined dates of HIV seroconversion. For each participant, we defined the baseline date as the earliest date before the development of AIDS on which the three laboratory tests were done. beta 2-microglobulin concentration at baseline was in all analyses an independent predictor of AIDS, even after stratification by baseline CD4 count, duration of HIV infection, or use of zidovudine before or at baseline. For example, among men with at least 0.5 x 10(9)/l CD4 cells who were negative for p24 antigen, the risks of AIDS at 12 months and 24 months were 1% and 5%, respectively, for those whose beta 2-microglobulin concentrations were below 4.0 mg/l, compared with 17% and 27%, respectively for those with beta 2-microglobulin concentrations above that cut-off point (p less than 0.001). Among men with an estimated duration of infection of 5 years or less, beta 2-microglobulin concentration was the strongest independent predictor of AIDS. Measurement of serum beta 2-microglobulin adds important prognostic information to CD4 count in determining the risk of progression to AIDS in HIV-infected subjects, including those whose CD4 cell count has not yet fallen.

Acquired Immunodeficiency Syndrome↗

PubMed1992

Excitatory inputs to layer V pyramidal cells of rat primary visual cortex revealed by acetylcholine activation.

Cells in layers II-III or VI were activated by microdrop application of acetylcholine (ACh), while monitoring the intracellular response of layer V pyramidal cells. This enabled the tracing of functional connections between the cells of layers II-III or VI with those of layer V. ACh activation of layer II-III or VI cells resulted in a small depolarization of these cells, accompanied by a burst of excitatory postsynaptic potentials (EPSPs) from layer V pyramidal cells. These effects of ACh were blocked by tetrodotoxin (TTX), suggesting the involvement of action potentials in their production. The input resistance of layer V pyramidal cells during and after the EPSP burst was not significantly different from control values, further suggesting an indirect effect of ACh on layer V pyramidal cells. Isolation of the supragranular layer, by horizontal cutting, did not prevent the EPSP burst evoked by ACh application to the lower layer VI, suggesting a direct input from layer VI to layer V pyramidal cells. ACh applied near pyramidal cells in layers II-III, V or VI caused transient hyperpolarization associated with a decrease in input resistance followed by a large depolarization, an increase in input resistance, and action potential discharges. The ACh-mediated hyperpolarization and the train of action potentials of layer II-III pyramidal cells were blocked by TTX. Thus the ACh-activated cells in layers II-III and VI make an excitatory synaptic contact with layer V pyramidal cells, producing the EPSP burst observed in layer V.

Acetylcholine↗

PubMed1992

Calcium dependence of serotonin-evoked conductance in C6 glioma cells.

Whole-cell membrane currents and imaging of intracellular calcium concentrations ([Ca2+]i) were used to investigate the role of calcium in a response to serotonin of C6 glioma cells. Activation of a high-affinity serotonin receptor induced a transient rise in calcium concentration in these cells and activated a predominantly potassium conductance, with a small chloride component. Perfusion of the cytoplasm with an internal solution containing high calcium concentration induced similar but prolonged increase of membrane conductance. The responsiveness of C6 cells to serotonin was negatively correlated with the concentration of the unbound calcium chelator BAPTA when BAPTA-buffered calcium-containing intracellular solutions were used. Responses to serotonin persisted in the absence of external calcium, decreased gradually, and then recovered partially after replenishment of extracellular calcium. These findings substantiate the direct role of intracellular calcium in mediating the serotonin response, and indicate that serotonin-induced release of calcium from intracellular stores is sufficient for the activation of conductance in the C6 glioma cell line.

Brain Neoplasms↗

PubMed1992

Spontaneous recovery of deficits in spatial memory and cholinergic potentiation of NMDA in CA1 neurons during chronic lithium treatment.

The therapeutic action of lithium in affective disorders is still unclear. One effect of lithium is to deplete membrane inositol and consequently to exhaust the phosphoinositide (PI) pathway. Under chronic lithium treatment, rats showed persistent performance deficits in an active avoidance task and in a visually cued maze. The same treatment, however, resulted in only a transient deficit in the performance of rats in a spatial memory task. Lithium treatment caused a similarly transient deficit in the ability of acetylcholine to potentiate responses to N-methyl-D-aspartate (NMDA) in neurons of the hippocampal slice. The authors propose that the development of compensatory mechanisms may account for the lack of severe memory impairments during lithium treatment. It is suggested that the effects of lithium on the PI pathway are not sufficient to explain the behavioral consequences of chronic lithium treatment.

Acetylcholine↗

PubMed1992

Neuropeptidergic innervation of intramuscular hemangiomas.

Intramuscular hemangiomas are idiopathic lesions which are either tumoral or developmental in origin. A close association of abnormal blood vessels with nerve fibers is found and may suggest that nerves have a primary inciting role in the development of these lesions. In the current study, the number of nerve fibers in different zones around the tumors, as well as the type of neuropeptides present in these fibers, was quantitatively assessed by computer-assisted image analysis of immunohistochemical staining of histological slides. The number of nerve fibers as determined by positive staining by anti-protein S-100 antibodies was found to be elevated in the immediate vicinity of the abnormal blood vessels. The density of the nerve fibers rapidly declined with increasing distance from the hemangiomas, reaching normal values at distances of over 2 mm. Furthermore, hemangiomas contain a significantly higher number of calcitonin gene-related peptide (CGRP), substance P, and Met-enkephalin-positive fibers. The most significant rise in number is that of CGRP-positive fibers. This neuropeptide is a known mitogen, which could be responsible for the growth of the hemangiomatous blood vessels. Substance P is a nociceptive neurotransmitter and its presence can explain the pain which often accompanies even tiny intramuscular hemangiomas.

Adolescent↗

PubMed1992

The inositol 1,4,5-trisphosphate pathway mediates cholinergic potentiation of rat hippocampal neuronal responses to NMDA.

1. The cellular mechanism by which acetylcholine (ACh) potentiates neuronal responses to N-methyl-D-aspartate (NMDA) was investigated in CA1 neurones of hippocampal slices using current- and voltage-clamp techniques. 2. Loading cells with 5'-guanylylimidodiphosphate (GppNHp) caused a gradual increase in response to NMDA. Pulses of ACh accelerated this increase. Guanosine 5'-O-(2-thiodiphosphate) (GDP beta S) blocked the potentiating effect of ACh on responses to NMDA. 3. Acute LiCl caused a gradual decrease in the potentiating effect of ACh, while the potentiation was completely prevented by 3 day chronic 6 mequiv/kg (I.P.) LiCl treatment and restored by acute treatment with 10 mM-inositol. 4. Loading cells with a general protein kinase inhibitor, H-7, enhanced the potentiating effect of ACh on responses to NMDA and blocked the effect of ACh on the after-hyperpolarization (AHP). 5. Ultraviolet irradiation of cells loaded with a photolabile inositol 1,4,5-trisphosphate (InsP3) caused a transient increase in responses to NMDA, while penetrating cells with active InsP3-containing pipettes caused a gradual BAPTA-sensitive increase in responses to NMDA. 6. Reducing the rate of InsP3 metabolism, with 2,3-diphosphoglyceric acid (DPG), caused an increase and prolongation of the potentiating effect of ACh, while blocking the InsP3 receptor with heparin prevented the cholinergic potentiation. 7. NMDA, by itself, potentiated subsequent responses to NMDA, an effect that was blocked when [Ca2+]i was chelated with BAPTA. NMDA and ACh were also found to compete in potentiating responses to NMDA. Finally, the cholinergic potentiation was blocked when cells were loaded with BAPTA. 8. We propose that activation of the InsP3 branch of the phosphoinositide pathway potentiated responses to NMDA and that InsP3 exerted this effect by elevating [Ca2+]i.

Acetylcholine↗

PubMed1992

Confocal microscopic imaging of [Ca2+]i in cultured rat hippocampal neurons following exposure to N-methyl-D-aspartate.

1. The confocal laser scanning microscope (CLSM) was used in conjunction with the calcium indicator dye Fluo-3 to record changes in free intracellular calcium concentration ([Ca2+]i) in cultured hippocampal neurons in response to superfusion of N-methyl-D-aspartate (NMDA). 2. NMDA caused a rapid rise in [Ca2+]i in all parts of the neuron. The rise in [Ca2+]i was dependent on activation of an NMDA receptor, was enhanced by the removal of Mg2+ and addition of glycine to the superfusion medium, and was dependent on normal [Ca2+]o. 3. The rise of [Ca2+]i was seen first near the membrane. A wave of elevated [Ca2+]i moved centripetally at a rate of 117 microns/s. 4. Dantrolene pre-incubation caused a significant reduction in the efficacy of the NMDA-induced rise in [Ca2+]i, indicating that at least part of the rise is caused by intracellular release of calcium. 5. The replacement of calcium by barium caused a reduction in the response to NMDA, but a significant response was still present in these cells, supporting the assumption that NMDA causes release of calcium from intracellular stores. 6. The removal of sodium from the superfusion medium prolonged the [Ca2+]i rise in response to NMDA indicating that the Na-Ca antiporter is instrumental in reducing [Ca2+]i. 7. These studies demonstrate the multiplicity of regulating mechanisms of [Ca2+]i following activation of NMDA receptors.

Animals↗

PubMed1992

Activation of protein kinase C suppresses responses to NMDA in rat CA1 hippocampal neurones.

1. The effects of 1-oleoyl-2-acetylglycerol (OAG), an activator of protein kinase C (PKC), on NMDA receptor-mediated responses were investigated in CA1 neurones of hippocampal slices using current- and voltage-clamp techniques. 2. Topical application of OAG caused a suppression of the slow, voltage-sensitive, NMDA receptor-mediated component of excitatory postsynaptic potentials (EPSPs) evoked by stimulating the schaffer-collateral commissural afferents and had no effect on the fast, voltage-insensitive, quisqualate/kainate component. 3. OAG suppressed the amplitude of inward current responses to NMDA down to about one-third of control responses. OAG could also increase the duration of the responses to NMDA by up to twofold. The effect of OAG on the duration but not on the amplitude of the response to NMDA was blocked by pre-loading cells with the K+ channel blocker, Cs+. Topical application of OAG had no significant effect on current responses to quisqualate. 4. An OAG isomer, which does not activate PKC, had no effect on responses to NMDA. Intracellular application of the kinase inhibitor, H-7, completely blocked the effect of OAG on the amplitude and duration of responses to NMDA, as well as on the slow EPSP. Finally, topical application of another activator of PKC, phorbol 12-myristate 13-acetate (PMA), also suppressed responses to NMDA. PMA reduced the slow component of synaptic responses in about half of the cells tested. 5. We propose that activation of PKC in CA1 hippocampal neurones suppresses NMDA receptor-mediated responses.

Action Potentials↗