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Biomedical subjects

C Soh

Publications and source records attributed to C Soh.

9 recordsLinked to original sources
PubMed2006

In-vivo measurement of brain relaxation after lobectomies.

Very little data exists on the visco-elastic properties of the living human brain tissue and collection of such data is vital for mechanical modelling. The purpose of this study was to measure the rate of relaxation of brain that has been compressed by tumour after surgical decompression. Seven patients who underwent a lobectomy for an intracranial space occupying lesion were included in the study. All underwent two CT scans within the first 24 h after the surgery. Volumes of the residual void on the serial CT scan were calculated using tools in the image acquisition software. There was a rapid expansion of the brain to fill up the void space in the first 24 h after surgery. The average rate of relaxation of the compressed brain is 2.25(0.76 - 6.64) ml/h. The graphs plotted for the volume of the void space against the time after surgery when the CT scans were done can be used to further explore the dynamics of brain relaxation. The rate of brain relaxation in the first 24 h after removal of a mass lesion averages 2.25(0.76 - 6.64) ml/h in this study. Further studies using more frequent data collection would allow for more accurate definition of the rate of relaxation.

Aged↗
PubMed2006

Reversible cytotoxic cerebral edema in cerebral fat embolism.

We present a case of cerebral fat embolism (CFE) that demonstrated evidence of diffuse white matter cytotoxic edema on diffusion-weighted magnetic resonance imaging, in addition to punctate hyperintensities on T2-weighted and diffusion-weighted imaging. The case suggests that CFE represents a combination of occlusive arteriolar disease and secondary neurotoxicity.

Adolescent↗
PubMed2006

Reversible delayed posthypoxic leukoencephalopathy.

Hypoxic ischemic encephalopathy may cause early deep white matter abnormalities on MR imaging that usually progress to include gray matter and basal ganglia change. Toxic leukoencephalopathy due to heroin inhalation predominantly causes cerebellar and posterior cerebral radiologic change. Both conditions rarely present clinically and radiologically in a delayed manner with subsequent recovery. We report a case of reversible delayed posthypoxic/toxic leukoencephalopathy with no clinical or radiologic evidence of gray matter insult.

Adult↗
PubMed2001

The human endoplasmic reticulum molecular chaperone BiP is an autoantigen for rheumatoid arthritis and prevents the induction of experimental arthritis.

Rheumatoid arthritis (RA) is the most common, crippling human autoimmune disease. Using Western blotting and tandem mass spectroscopy, we have identified the endoplasmic reticulum chaperone BiP, a 78-kDa glucose-regulated protein, as a possible autoantigen. It preferentially stimulated increased proliferation of synovial T cells from patients with RA but not from patients with other arthritides. Mice with established collagen- or pristane-induced arthritis developed IgG Abs to BiP. Although BiP injected in CFA failed to induce arthritis in several strains of rats and mice, including HLA-DR4(+/-)- and HLA-DR1(+/+)-transgenic animals, it completely inhibited the development of arthritis when given i.v. 1 wk before the injection of type II collagen arthritis. Preimmunization with BiP suppressed the development of adjuvant arthritis in Lewis rats in a similar manner. This is the first report of a mammalian chaperone that is an autoantigen in human RA and in experimental arthritis and that can also prevent the induction of experimental arthritis. These findings may stimulate the development of new immunotherapies for the treatment of RA.

Adult↗
PubMed1999

In vivo resistance to corticosteroids in bronchial asthma is associated with enhanced phosyphorylation of JUN N-terminal kinase and failure of prednisolone to inhibit JUN N-terminal kinase phosphorylation.

BACKGROUND: Corticosteroid-resistant (CR) asthma is associated with increased in vitro activity of the proinflammatory transcription factor activating peptide (AP)-1 in PBMCs resulting from increased c-FOS synthesis. Increased AP-1 may sequester the glucocorticoid receptor to produce a CR state. Using the tuberculin-induced inflammatory responses in the skin, we have previously demonstrated that a therapeutically effective dose of prednisolone suppressed T-cell, macrophage, and eosinophil infiltration into purified protein derivative-induced lesional skin of corticosteroid-sensitive (CS), but not CR, individuals. OBJECTIVE: Skin biopsy specimens from a tuberculin-induced model of dermal inflammation have been evaluated for the effect of corticosteroids in regulating components of AP-1 in vivo. METHODS: Immunohistochemical analysis of the tuberculin-mediated cutaneous response has been performed on 9 subjects with CS asthma and 6 subjects with CR asthma for the regulatory components of AP-1 before and after 9 days of either 40 mg prednisolone or placebo. RESULTS: Significantly greater expression of c-FOS, phosphorylated c-JUN, and phosphorylated JUN N-terminal kinase (JNK) protein has been identified in CR than in CS subjects. Corticosteroids suppressed phosphorylation of c-JUN and JNK in the CS Group (P =.004 for both) but enhanced phosphorylation of c-JUN and JNK in the CR group (P =.031 for both). CONCLUSION: Resistance to corticosteroids in asthmatic subjects may be caused, at least in part, by failure to suppress JNK phosphorylation, leading to failure to suppress c-JUN N-phosphorylation. Increased JNK may be one of the mechanisms central to the mechanism of CR asthma.

Animals↗
PubMed1993

Structure/activity relationship of leukotriene B4 and its structural analogues in chemotactic, lysosomal-enzyme release and receptor-binding assays.

The biological activities of chemically synthesized leukotriene B4 and eight structural analogues have been studied using chemotaxis, lysosomal-enzyme release and receptor-binding assays on human neutrophils. The results show that increasing the number of double bonds between C14 and C20, having triple bonds at C6 or C14, substitution of the primary carboxyl group at C1, changing the geometry of the double bond at C6 from the cis to trans configuration and changing the chirality of the hydroxyl group at C12 from the R to the S configuration result in substantial loss of both biological activity and the capacity to bind to the LTB4 recognition site in parallel. We suggest that the functional epitopes of 5S,12R-dihydroxy-6,14-cis-8,10-trans-icosatetraenoic acid (LTB4) are either the same, or reside in the same domain as the binding site for the LTB4 receptor. Development of LTB4 antagonists to the high-affinity LTB4 receptor, based on the structure of LTB4, is unlikely to be successful.

Binding Sites↗
PubMed1993

Effects of exogenous eicosapentaenoic acid on generation of leukotriene C4 and leukotriene C5 by calcium ionophore-activated human eosinophils in vitro.

Exogenous eicosapentaenoic acid (EPA) has been compared with exogenous arachidonic acid (AA) for its ability to modulate the oxidative metabolism of membrane-derived arachidonic acid by the 5-lipoxygenase pathway in ionophore-activated human eosinophils, and for its suitability as a parallel substrate in this pathway. Products were quantitated by specific RIA and tetraene and pentaene leukotrienes (LT) were separated by reverse-phase HPLC. Eosinophils were preincubated with control buffer, exogenous EPA or AA and stimulated optimally with 10 microM calcium ionophore (A23187) for 15 min. Mean generation of LTC4 in the absence of fatty acid was 6.0 = 1.1 ng/10(6) eosinophils (mean = SEM, n = 5). In the presence of EPA, the amount of LTC4 generated rose to peak at 16.5 +/- 1.9 ng/10(6) eosinophils at 10 micrograms/ml EPA and then fell to 8.3 +/- 3.1 ng/10(6) cells at 40 micrograms/ml EPA. The EPA derivative, LTC5 was first detectable at 5 micrograms/ml EPA with 4.8 +/- 1.2 ng/10(6) cells and gradually rose with increasing dose of EPA to be maximal at 40 micrograms/ml with 12.7 +/- 2.2 ng/10(6) cells. Identity of the LTC5 was confirmed by an identical retention time to synthetic LTC5 standard, immunoreactivity to a specific antibody against LTC4 and LTC5 and a typical UV absorbance spectrum. When eosinophils were preincubated with AA and similarly stimulated, LTC4 generation gradually increased from a baseline of 6.7 +/- 0.7 ng/10(6) cells in the absence of fatty acid to reach a maximum of 12.9 +/- 0.8 ng/10(6) cells at 40 micrograms/ml of AA. Total LTC generation was nearly twofold more with cells incubated with EPA than with cells incubated with AA (p < 0.05). Thus, EPA does not suppress LTC generation from eosinophils but stimulates it at lower doses and is a substrate for LTC5 generation.

Arachidonic Acid↗
PubMed1992

Cutaneous histamine metabolism in chronic urticaria.

Impaired metabolism of histamine in the skin of patients with chronic idiopathic urticaria (CIU) might explain the observed enhanced and prolonged skin responses to intradermal histamine. Histamine metabolism was measured in homogenates from unaffected forearm skin in nine patients with CIU and in skin of age- and sex-matched control subjects with a radiochromatographic assay, and the results are expressed as nanograms of histamine metabolized per milligram of protein per hour. Endogenous histamine content was determined by RIA. There was a highly significant increase in endogenous histamine content in the skin of patients with urticaria (407.8 +/- 188.3 ng/mg of protein) compared with that in skin of control subjects (240.0 +/- 73.0 ng/mg of protein) (mean +/- 1 SD; p less than 0.02), which suggests either an increase in mast cell number or histamine concentration per cell. No significant difference was observed in the metabolism of histamine between patient and control group; therefore, an alternative mechanism may underlie differences in skin reactivity to histamine.

Chronic Disease↗