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Biomedical subjects

R Lim

Publications and source records attributed to R Lim.

At least 127 records · Page 7Linked to original sources
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↗
PubMed1987

Rat astrocytes and Schwann cells in culture synthesize nerve growth factor-like neurite-promoting factors.

Neurite-promoting activity in feeding medium conditioned by rat astrocytes and Schwann cells in culture was examined. The conditioned medium (CM) from both types of glial cultures stimulated extensive neurite outgrowth from embryonic chick dorsal root ganglia (DRG) as well as pheochromocytoma (PC12) cells. Both the DRG and PC12 cells also produce neurite outgrowth in the presence of nerve growth factor (NGF). With the DRG, the neurite growth rates observed with the glial cell CM were identical to growth rates seen with NGF. Although anti-NGF antibody did not inhibit the neurite outgrowth produced by either of the glial CM, a nerve growth factor radioreceptor assay did detect an NGF-like molecule in both CM. Since the extensive neurite outgrowth stimulated by the glial CM was not mimicked by pure laminin alone, we conclude that the glial neurite promoting factors are distinct from laminin.

Adrenal Gland Neoplasms↗
PubMed1987

Endogenous immunoreactive glia maturation factor-like molecule in astrocytes and glioma cells.

Using the monoclonal antibody G2-09 raised against bovine glia maturation factor (GMF), we conducted a survey of GMF-like immunoreactivity in various cell types. Of all the normal and neoplastic cells tested, only extracts from astroblasts, gliomas, Schwann cells and schwannomas, but not their conditioned media, possessed endogenous GMF-like immunoreactivity. The presence of immunoreactive GMF correlated well with GMF bioactivity. Using the same monoclonal antibody, the GMF-like factor in astroblasts and C6 glioma cells was characterized by 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 having a mol. wt. of 14,000 Da. Thus, the evidence strongly supports the argument that the GMF-like factor in astroblasts and C6 cells is identical with GMF from the bovine brain. In order to explain the fact that astroblasts and C6 cells are both the source and targets of GMF, we propose the hypothesis that GMF functions as an injury signal, being released from the injured glia and serving as a stimulant for gliosis in the neighboring intact glia.

Animals↗
PubMed1987

Distribution of immunoreactive glia maturation factor-like molecule in organs and tissues.

Using the monoclonal antibody G2-09 raised against bovine glia maturation factor (GMF), we screened various rat organs and tissues for GMF-like immunoreactivity. In the adult animal, with the exception of the heart, GMF was found exclusively in the nervous system, with the cerebellum exhibiting higher specific activity than other brain regions. The nature of the immunoactivity in the heart is presently unclear. None of the body fluids collected from humans, including serum and cerebrospinal fluid, possessed detectable GMF immunoactivity. A phylogenetic comparison revealed the presence of GMF in the brain of al vertebrates studied, from fish to primates. GMF was absent from bacteria and yeast. An ontogenetic study on rats showed the highest GMF level in the fetal brain, with a gradual but steady decrease after birth. However, a substantial amount of GMF persisted even in older animals. GMF was localized in astrocytes and Bergmann glia in the rat brain, using immunostaining at the light microscopic level.

Age Factors↗
PubMed1987

Induction of cytoskeletal alterations in C6 glioma by glia maturation factor.

C6 rat glioma cells respond to glia maturation factor (GMF) with characteristic morphological alterations. Observed under phase-contrast microscopy, the cells changed from a rounded morphology in random formation to a spindle-shaped appearance in parallel arrays. Observed under scanning electron microscopy, GMF led to a decrease in the number of microvilli and cell surface knobs. Transmission electron microscopy demonstrated the appearance of numerous microtubules aligned with the long axis of the cells after GMF stimulation. The change in cell shape and histotypic pattern was inhibited by vinblastin, further implicating the involvement of microtubules. Immunofluorescence using anti-alpha-tubulin revealed a well-defined cytoskeletal system in GMF-stimulated cells but not in the control cells. Finally, an increase in tubulin was confirmed with enzyme-linked immunosorbent assay (ELISA) on extracts from these cultures. The findings indicate that morphological alterations induced by GMF are associated with changes in the quantity and arrangement of microtubules.

Animals↗
PubMed1987

Acute cholecystitis in pregnancy.

Thirty cases of acute cholecystitis in pregnancy were identified during a 12-year period. Twenty-one patients were successfully managed with medical therapy alone. Nine underwent surgical intervention, four after failing medical therapy and five as the initial approach to therapy. Surgical therapy was complicated by preterm labor and delivery in two patients undergoing surgery during the early third trimester. One patient underwent cholecystectomy during the first trimester and subsequently aborted. There were no serious complications in patients undergoing surgery during the second trimester. These data suggest that conservative medical management can be successfully used in most patients with acute cholecystitis in pregnancy.

Abortion, Spontaneous↗
PubMed1986

Suppression of glioma growth in vitro and in vivo by glia maturation factor.

Glia maturation factor (GMF), a 14,000 Mr acidic protein of the brain, is capable of promoting differentiation of cultured astroblasts. In this study we report the effect of GMF on two glioma cell lines: the C6 line, of rodent origin, and the HG-1 line, of human origin. When tested in culture, GMF promotes the initial growth of the two cell lines when the cells are sparse but limits proliferation by restoring contact inhibition when the cells are confluent. Cell cycle analysis confirms the arrest of the cells at the G0/G1 phase when the tumor cells are contact inhibited by GMF. When C6 cells are inoculated into the athymic (nude) mice at a s.c. site, a single solid tumor grows out with a 100% take. Intraperitoneal injection of GMF leads to the slowing down of tumor growth. That the in vivo effect of GMF is not due to cytotoxicity is evidenced by the lack of necrosis and by the appearance of more mature astrocytic cells in the tumors. The results lend support to the concept of GMF as a cellular regulator and suggest the therapeutic potential of GMF for brain tumors.

Animals↗
PubMed1985

Purification of bovine glia maturation factor and characterization with monoclonal antibody.

Glia maturation factor (GMF) is purified 100 000-fold to apparent homogeneity from bovine brains by a procedure consisting of ammonium sulfate precipitation, column chromatography with diethylaminoethyl-Sephacel, Sephadex G-75, and hydroxylapatite, and a final step using C4 reverse-phase high-performance liquid chromatography. The product shows a single protein band in sodium dodecyl sulfate-polyacrylamide gel. It has a molecular weight of 14 000 and an isoelectric point of pH 5.2. Purified GMF stimulates cultured astroblasts to proliferate and to grow out cell processes with half-maximal activity at 8 ng/mL. A monoclonal antibody raised against partially purified GMF adsorbs the activity of pure GMF and immunologically binds the putative GMF protein band.

Amino Acids↗
PubMed1985

Glia maturation factor influences recovery from injury in neonatal rat brains.

Newborn rats were injured with a puncture wound in one cerebral hemisphere. Experimental animals were treated with three i.p. injections of Glia Maturation Factor (GMF) at daily intervals starting from the time of injury, whereas control littermates were treated with equivalent amounts of bovine serum albumin. At 25 days old the size of the cerebral cortex at the plane of injury was measured on representative brain sections. In control rats the injured side was 18% smaller than the normal side whereas in GMF-treated animals the difference was only 1%. The results suggest a possible regulatory role of GMF in promoting tissue recovery from brain damage.

Animals↗
PubMed1985

Mitogenic activity of glia maturation factor. Interaction with insulin and insulin-like growth factor-II.

The mitogenic activity of glia maturation factor (GMF) was tested on sparse-cultured cells. GMF stimulates the growth rate of normal astroblasts and fibroblasts grown in the presence of fetal calf serum (FCS), and raises the saturation density of the cells over what is imposed by the corresponding serum concentrations. GMF has no mitogenic effect in the complete absence of serum. The mitogenicity of GMF is also demonstrable in defined media where certain serum components are present. In particular, GMF in combination with the defined medium N2 partially mimics the proliferative effect of serum alone. Insulin, an ingredient of N2, can substitute for the complete N2 formula. Insulin-like growth factor-II (IGF-II), in turn, can substitute for insulin. The interaction of GMF with insulin or IGF-II can be demonstrated in a sequential manner, suggesting that GMF is a competence factor. Since insulin is required at a concentration well above the physiologic serum level, and must be used at a dose 1000 times higher than IGF-II, we suspected that insulin acts on IGF-II receptors. This was substantiated by the demonstration of IGF-II receptors and the absence of detectable insulin receptors on the astroblasts. The combined effect of IGF-II and GMF mimics the combined effect of 10% FCS and GMF, in both growth rate and saturation density.

Animals↗