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Biomedical subjects

R Lim

Publications and source records attributed to R Lim.

At least 109 records · Page 6Linked to original sources
PubMed1990

Complete amino acid sequence of bovine glia maturation factor beta.

The protein glia maturation factor beta, isolated from bovine brain, has been sequenced by automated Edman degradation and tandem mass spectrometry of overlapped peptide fragments generated by cyanogen bromide cleavage and enzymatic digestion with trypsin, chymotrypsin, and endoproteinases Asp-N and Lys-C. The protein has 141 amino acid residues and possesses no potential N-glycosylation sites. It contains three cysteines (at positions 7, 86, and 95), three methionines (at positions 33, 101, and 102), and one tryptophan (at position 132). The blocked amino terminus as determined by tandem mass spectrometry is an N-acetylated serine. The carboxyl terminus is a histidine. To our knowledge, the sequence shows no significant homology with other sequenced proteins. The molecular weight calculated from the sequence information is 16,582.

Amino Acid Sequence↗
PubMed1990

Antiproliferative function of glia maturation factor beta.

Recombinant human glia maturation factor beta (GMF-beta) reversibly inhibits the proliferation of neoplastic cells in culture by arresting the cells in the G0/G1 phase. This phenomenon is not target-cell specific, as neural and nonneural cells are equally inhibited. When tested simultaneously, GMF-beta suppresses the mitogenic effect of acidic fibroblasts growth factor (aFGF), but the two are synergistic in promoting the morphologic differentiation of cultured astrocytes. GMF-beta also counteracts the growth-stimulating effect of pituitary extract and cholera toxin on Schwann cells. The results underscore the regulatory role of GMF-beta and its intricate interaction with the mitogenic growth factors.

Animals↗
PubMed1990

Cell-surface expression of glia maturation factor beta in astrocytes.

Glia maturation factor beta (GMF-beta) is a 17-kDa acidic protein isolated from the brain. When added to cultured cells, GMF-beta promotes the phenotypic expression of glia and neurons and inhibits the proliferation of their respective tumors. Although astrocytes produce GMF-beta and store it inside the cells, they do not secrete the protein into the cultured medium. This poses a question as to how GMF-beta mediates intercellular communication. This paper provides an answer by demonstrating the presence of GMF-beta on the surface of astrocytes, using gold-labeled antibody enhanced with silver. It appears that cell-surface GMF-beta acts on the target cells at close range when cells are in direct contact. In contrast to astrocytes, we failed to detect GMF-beta on the surface of C6 glioma cells, although these cells, like astrocytes, possess endogenous intracellular GMF-beta and are also responsive to GMF-beta added to the medium. The lack of cell-surface expression of GMF-beta in C6 cells may reflect a breakdown in intercellular communication in these malignant cells.

Animals↗
PubMed1990

Abolition of electrocardiographic pattern of left ventricular aneurysm by posterior myocardial infarction.

We report a patient who presented with prominent gastrointestinal symptoms in whom a confident clinical diagnosis of acute posterior myocardial infarction was facilitated because the fresh electrocardiographic changes of true posterior myocardial infarction abolished the old pattern of left ventricular aneurysm. This interesting electrocardiographic phenomenon has not, to our knowledge, been previously reported.

Electrocardiography↗
PubMed1989

Glia maturation factor-beta promotes the appearance of large neurofilament-rich neurons in injured rat brains.

Adult rat brains were injured by partial decortication. Glia maturation factor-beta (GMF-beta) was applied to the wound cavity 3 times over a period of two months. At the end of the experiment, brain sections were prepared and immunostained for neurofilaments. Large, neurofilament-rich neurons were observed in clusters in the brain tissue adjacent to the wound cavity. These neurons displayed prominent apical dendrites, some of which grew out branches toward the direction of the wound. The results suggest that GMF-beta promotes the hypertrophy of selective neurons in the injured cerebral cortex and implies a role for GMF-beta in central nervous system regeneration.

Animals↗
PubMed1989

Purification and characterization of glia maturation factor beta: a growth regulator for neurons and glia.

A protein has been isolated from bovine brains by using a modification of the procedure used to purify glia maturation factor. The method consists of ammonium sulfate precipitation, chromatography with DEAE-Sephacel, Sephadex G-75, and hydroxylapatite columns, passage through a heparin-Sepharose column, and finally fractionation by reverse-phase HPLC with a C4 column. The isolated protein reacts strongly with the mouse monoclonal antibody G2-09 and has a molecular weight of approximately 17,000 and an isoelectric point of pH 4.9. The N terminus is blocked, but tryptic digestion releases 28 peptides, 8 of which have been sequenced. The total known residues add up to more than two-thirds of the entire 140-residue protein, estimated from amino acid composition, and show no sequence homology with any known protein. Reversible thermal renaturation greatly enhances its biological activity. The purified protein stimulates differentiation of normal neurons as well as glial cells. It inhibits the proliferation of the N-18 neuroblastoma line and the C6 glioma line while promoting their phenotypic expression. We designate this protein glia maturation factor beta.

Amino Acids↗
PubMed1989

Cardiac arrhythmias during acute exacerbations of chronic airflow limitation: effect of fall in plasma potassium concentration induced by nebulised beta 2-agonist therapy.

The effect on cardiac rhythm of the fall in plasma potassium concentration induced by nebulised beta2-agonist therapy was studied in 20 patients admitted to hospital with an acute exacerbation of their reversible chronic airflow limitation. Arrhythmias considered serious or potentially life-threatening were recorded in 13 patients (65%). However, there was no significant increase in these arrhythmias in the hour following administration of nebulised beta2-agonist despite a significant fall in plasma potassium concentration during this period.

Acute Disease↗
PubMed1989

Axonal signals regulate expression of glia maturation factor-beta in Schwann cells: an immunohistochemical study of injured sciatic nerves and cultured Schwann cells.

Glia maturation factor-beta (GMF-beta) is a 17 kDa protein purified and sequenced from bovine brains. Using the monoclonal antibody G2-09 directed against GMF-beta, we previously demonstrated endogenous GMF-beta in astroblasts, Schwann cells, and their tumors in culture. In the present study, we have used indirect immunofluorescence microscopy with G2-09 to examine the effects of transection, crush, and regeneration of sciatic nerve on the expression of GMF-beta in Schwann cells in situ and to study the time course of GMF-beta induction in Schwann cells in vitro. For comparison, a parallel study was carried out with monoclonal antibodies directed against nerve growth factor (NGF) receptor. We found that (1) neither GMF-beta nor NGF receptor was detectable in intact sciatic nerves, (2) all Schwann cells of the distal segment of the transected nerve expressed GMF-beta as early as 3 d after axotomy that persisted up to 3 weeks, (3) axonal regeneration repressed the Schwann cell expression of GMF-beta, (4) isolated Schwann cells derived from rat sciatic and adult human sural nerves developed intracellular GMF-beta in culture following an initial lag period, and (5) the induction of Schwann cell NGF receptor coincided temporally with that of GMF-beta in the transected nerve and in culture. These results show that the expression of GMF-beta in Schwann cells, as is the case with the NGF receptor, is induced by the loss of the normal axon-Schwann cell contact. We propose that the induction of GMF-beta, as well as NGF receptor, in Schwann cells after nerve injury plays a role in axonal regeneration.

Animals↗
PubMed1988

Prescription of oxygen concentrators for long term oxygen treatment: reassessment in one district.

When oxygen concentrators became available on form FP10 in 1985 the Department of Health and Social Security issued clear guidelines for their prescription for long term treatment. Reassessment of those patients prescribed a concentrator in one district showed that 29 out of 61 patients did not fulfil these criteria. Furthermore, in only 28 cases was the daily use of the machine appropriate, though this did not reflect poor patient cooperation but was a result of inadequate prescribing instructions. In addition, 12 out of 54 patients continued to smoke. Overall, in only 18 of the 61 cases was both the prescription appropriate and the concentrator properly used. These results suggest a need for better cooperation between general practitioner and hospital in the initial assessment of patients for long term oxygen treatment and better education of both doctor and patient in the use of oxygen concentrators.

Adult↗
PubMed1988

Endogenous immunoreactive glia maturation factor-like molecule in cultured rat Schwann cells.

Using the monoclonal antibody G2-09 raised against bovine glia maturation factor (GMF), we demonstrated that cultured rat Schwann cells and Schwannoma cells, but not their conditioned media, possessed endogenous GMF-like immunoreactivity. The presence of immunoreactive GMF correlated well with GMF bioactivity. The GMF-like factor in Schwann cells was characterized by immunodotting, immunofluorescence, immunoadsorption and immunoblotting. Immunofluorescence confirmed the intracellular location of GMF. Immunoadsorption completely eliminated the GMF-like bioactivity from the cell extracts. Immunoblotting identified a protein band with a molecular weight of 14,000. Thus, the evidence strongly supports the argument that the GMF-like factor in rat Schwann cells is identical with GMF from the bovine brain. The GMF-like molecule in Schwannoma cells showed properties similar to those in Schwann cells, but for unknown reasons was not detectable by immunofluorescence. The presence of GMF in cultured rat Schwann cells suggests that the factor may play a role in the peripheral nervous system.

Antibodies, Monoclonal↗
PubMed1988

Early release of glia maturation factor and acidic fibroblast growth factor after rat brain injury.

A major component of the healing response of the brain to injury is the induction of growth and trophic factors. In the rat brain, glia maturation factor (GMF) and acidic fibroblast growth factor (aFGF) are not extracellular. However, within the first hour following brain injury, the amount of GMF and aFGF in the wound cavity increased by 7- and 13-fold, respectively, compared to the tissue adjacent to the wound. A cascade of cellular and biochemical events, leading to glial proliferation, the arrest of secondary neuronal death and axonal sprouting, may be initiated by the sudden increase in the extracellular concentration of these factors.

Animals↗
PubMed1988

Schwann cell-conditioned medium supports neurite outgrowth and survival of spinal cord neurons in culture.

The effect of Schwann cell-conditioned medium (SCM) on the development in vitro of spinal cord neurons was studied. Spinal cord neurons from 18-day-old rat embryos were cultured in serum-free conditioned medium obtained from confluent rat Schwann cells. In cultures fed SCM, the cells developed typical neuronal morphology and were identified by indirect immunofluorescence using a monoclonal antibody to neurofilament protein. SCM stimulated neurite outgrowth and supported survival of spinal cord neurons. Preliminary characterization suggests that the neurotrophic factor in SCM appears to be a protein with a molecular weight greater than 8000 daltons.

Animals↗
PubMed1988

Clinical trial of foam cushions in the prevention of decubitis ulcers in elderly patients.

Polyurethane foam cushions in a slab form or a customized contoured form are commonly used in wheelchairs to prevent the development of decubitus ulcers (DU) in elderly chronically ill persons. Sixty-two consenting subjects, 60 years or older, were randomly assigned to sit on one of the two types of cushions for 3 or more hours daily for 5 months. A total of 72 DU developed in the 52 subjects who completed the study. These were mostly in the areas of ischial tuberosities, buttocks, and thighs; were of persistent erythema level in severity; and took an average of 6 to 8 weeks to heal. No statistically significant differences were found in the incidence, location, severity, or healing time of the sores that developed in the subjects who used the slab (N = 26) and those who used the contoured (N = 26) cushions. But, more severe sores did develop among the slab cushion group in the area of ischial tuberosities. It appears that foam customization for elderly persons could be justified only if DU have been a particular problem in this region. Incontinence as a contributory factor to DU formation should receive careful attention with respect to prevention. The trials described are being continued, using a larger number of subjects.

Aged↗