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Biomedical subjects

R Lim

Publications and source records attributed to R Lim.

At least 37 records · Page 2Linked to original sources
PubMed1991

Do routine clinic visits prevent de-stabilization in patients awaiting coronary revascularization?

We examined retrospectively the usefulness of routine clinic visits in preventing adverse cardiac events in 115 patients awaiting coronary surgery or angioplasty. Mean waiting time from angiography to revascularization was 126 days. A total of 126 visits were made by 80 patients. No deaths occurred, but one patient, despite three visits, suffered myocardial infarction at 316 days post-angiography. Eight patients required admission for unstable angina, five having been on the waiting list for less than 5 weeks. The mean number of clinic visits, number of diseased vessels and proportion on triple anti-ischaemic therapy were similar in the patients suffering such events and those remaining stable. In conclusion, the inherent unpredictability of coronary disease greatly limits the role of interim clinic visits in the prevention of adverse cardiac events in patients awaiting revascularization.

Adult↗
PubMed1990

Disulfide isoforms of recombinant glia maturation factor beta.

Recombinant human glia maturation factor beta (r-hGMF-beta) is a single-chain polypeptide (141 amino acid residues) containing three cysteines, at positions 7, 86 and 95. Nascent r-hGMF-beta exists in the reduced state and has no biological activity. The protein can be activated through oxidative refolding by incubation with a mixture of reduced and oxidized glutathione. Reverse-phase HPLC analysis of the refolded r-hGMF-beta shows the presence of four peaks, corresponding to the reduced form plus three newly generated intrachain disulfide-containing isoforms predicted from the number of cysteine residues. Only one isoform shows biological activity when tested for growth suppression on C6 glioma cells. We infer from the HPLC elution pattern that the active form contains the disulfide bridge Cys86-Cys95.

Animals↗
PubMed1990

Identification of injury-induced mitotic cells in adult rat cerebral cortex by neuron-specific markers.

Adult rat brains were injured by partial decortication. Four days later, the brains were examined for mitotic cells that were immunostained for neuronal markers: the neuron-specific enolase (NSE) and neurofilaments (NF). Of the 30 rats stained for NSE, 15 were found to have NSE-positive cells containing mitotic figures; of the 25 rats stained for NF, 12 possessed NF-positive cells in mitosis. Most of the mitotic neurons were granule cells and small- and medium-size pyramidal cells and were located in cortical layer III within 500 microns from the wound margin. Although a rare phenomenon, mitosis of neurons in the neocortex of mature mammalian brains may reflect neuronal plasticity in response to injury.

Animals↗
PubMed1990

Glia maturation factor beta regulates the growth of N18 neuroblastoma cells.

Glia maturation factor beta (GMF-beta) is a 17-kDa growth regulating protein isolated from the brain. The effect of bovine GMF-beta on neurons was tested on the neuroblastoma line N18 and the pheochromocytoma line PC12. GMF-beta inhibited the proliferation of N18 cells and promoted their neurite outgrowth, with an increase in neurofilament protein, but had no effect on PC12 cells. This was in contrast to nerve growth factor (NGF) which regulated PC12 but not N18. Acidic fibroblast growth factor (FGF), on the other hand, had a weak effect on PC12 but none on N18. Antisera against GMF-beta and NGF neutralized the biological activity of the corresponding growth factors but showed no cross-neutralization. Fluorescence visualization revealed the binding of GMF-beta to N18 cells but not to PC12 cells; the opposite was true with NGF.

Adrenal Gland Neoplasms↗
PubMed1990

Factors influencing the compliance of patients using oxygen concentrators for long-term home oxygen therapy.

A previous study in the Liverpool district on patients receiving long term oxygen treatment using a domiciliary oxygen concentrator showed that only 55% were both using oxygen therapy correctly and had stopped smoking. To try and identify which factors influence patient behaviour, all 55 patients in this district receiving long-term oxygen therapy for hypoxaemic chronic airflow limitation were studied. We found that those with more symptoms were more likely to comply with this therapy. The prescription of a concentrator on the advice of a hospital physician did not improve on the compliance rates attained in those patients assessed by the general practitioner alone.

Adult↗
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↗