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Biomedical subjects

C S Koh

Publications and source records attributed to C S Koh.

At least 145 records · Page 8Linked to original sources
PubMed1988

[A case of chronic polyneuropathy associated with chronic type B hepatitis].

A case of chronic polyneuropathy associated with chronic type B hepatitis was described. A 31 year-old male was admitted to our hospital with a 2-year history of progressive weakness and sensory disturbances of all limbs. There was past history of acute type B post-transfusion hepatitis after subtotal gastrectomy. On examination there was generalized muscle weakness, particularly in movements of the hands and feet with areflexia. He had a steppage gait. Sensory examination revealed moderately decreased pinprick, light touch, vibration and position sense in the distal portion of all extremities. On admission, hepatitis associated antigen and antibody were negative and positive, respectively. The level of circulating immune complexes was high with the titer of 6.6 micrograms/ml by Clq assay and 16X by Raji cell assay. Liver biopsy revealed fibrosis and periportal inflammatory infiltrate compatible with the diagnosis of chronic viral hepatitis. Sural nerve biopsy showed marked loss of large myelinated fibers and epineural vasculitis with the thickened blood vessel wall and mononuclear cell infiltrates. There have been increasing evidences that extrahepatic manifestations are caused by vasculitis due to HBs antigen-antibody immune complex deposits. On the basis of findings in the literature it seems possible that chronic polyneuropathy may be related to the vasculitis due to HBs antigen-antibody complex deposits after hepatitis B virus infection.

Adult↗
PubMed1987

A new model for multiple sclerosis: chronic experimental allergic encephalomyelitis induced by immunization with cerebral endothelial cell membrane.

Multiple sclerosis is considered to be an autoimmune demyelinating disease of the central nervous system. Damage to the blood-brain barrier, of which endothelial cells are the main constituent, occurs in multiple sclerosis, probably due to immunological mechanisms. We report here the results of immune-mediated damage to these cells, produced by immunizing guinea pigs with an endothelial cell membrane fraction. The fraction was obtained from cerebral endothelial cells grown in vitro and was free from myelin basic protein. The immunized animals developed a chronic neurological illness with evidence of delayed hypersensitivity to the cell membrane fraction but not to myelin antigens. Histological examination of the brain in the acute stage showed mononuclear cell infiltrates around blood vessels, while in the chronic phase large areas of demyelination, especially in the periventricular region, were present. This bore a striking similarity to the brain in multiple sclerosis. This may prove to be a useful new animal model for the investigation of the human demyelinating disease.

Animals↗
PubMed1987

Suppression of clinical signs of cell-transferred experimental allergic encephalomyelitis and altered cerebrovascular permeability in Lewis rats treated with a plasminogen activator inhibitor.

The purpose of this study was to determine whether fibrinolysis resulting from activation of the clotting cascade in juxtaposition to endothelial cells of the central nervous system (CNS) microvasculature is important for development of clinical signs of experimental allergic encephalomyelitis (EAE) in recipient Lewis rats. Rats were injected with previously primed syngeneic lymph node cells, activated in vitro with guinea pig myelin basic protein, and subsequently treated daily with trans-4-(aminomethyl)cyclohexanecarboxylic acid (AMCA), a synthetic inhibitor of plasminogen activator. Clinical signs of EAE were significantly suppressed in AMCA-treated rats compared to saline-treated control recipient animals. Furthermore, suppression of clinical signs in AMCA-treated rats was accompanied by a significant curtailment in EAE-associated increased permeability of the blood-brain barrier (BBB). These findings provide evidence that CNS-associated deposition of fibrin and ensuing fibrinolysis, together with increased permeability of the BBB, are related prerequisite events for expression of clinical manifestations of EAE.

Animals↗
PubMed1987

Demyelinating neuropathy associated with hepatitis B virus infection. Detection of immune complexes composed of hepatitis B virus surface antigen.

We observed 4 patients with the Guillain-Barré syndrome (GBS) type of polyneuropathy and one patient with chronic relapsing polyneuropathy associated with hepatitis B virus infection, and examined the sera, cerebrospinal fluid (CSF) and sural nerve specimens from the patients in search of the pathogenetic factors involved. It was demonstrated that hepatitis B surface antigen(HBsAg)-immune complexes were significantly increased in both the sera and the CSF of the 4 patients with GBS. The serum levels of immune complexes were also closely related to the clinical status of these patients. In all patients, HBsAg-positive labelling of immunofluorescence was found around the endoneural small blood vessels and in the endoneurium. Electron-dense deposits, suggestive of immune complexes composed of hepatitis B virus, were demonstrated in the endoneurium of the patient with chronic relapsing polyneuropathy. These results suggest that HBsAg immune complexes may be of importance in the etiology of GBS or chronic relapsing polyneuropathy associated with hepatitis B virus infection.

Adult↗
PubMed1987

Studies of protease and protease inhibitors in familial amyloidotic polyneuropathy.

Serum levels of 6 protease inhibitors, alpha 1-antitrypsin, Cl inactivator, alpha 2-macroglobulin, antithrombin-3, alpha 1-antichymotrypsin and inter-alpha-trypsin inhibitor were measured in patients with familial amyloidotic polyneuropathy (FAP) and a control group without neurologic disease. No significant differences were observed between the 2 groups. The proteolytic effect of brinase, an enzyme from Aspergillus oryzae, on amyloid tissue sections from patients with FAP was also evaluated. Amyloid fibrils were degraded by brinase, while the tissue structure remained fairly intact.

Amyloid↗
PubMed1987

Anti-endothelial cell antibodies and circulating immune complexes in the sera of patients with multiple sclerosis.

Sera from patients with multiple sclerosis (MS) were examined for anti-endothelial cell antibodies and immune complexes by enzyme-linked immunosorbent assays (ELISAs) using cultured brain endothelial cells and Raji cells respectively. The concentrations of immunoglobulin (Ig) G which bound to cerebral endothelial cells and of immune complexes were significantly increased in the sera of patients with MS, especially those with an exacerbation. The levels of IgG binding to endothelial cells were still increased in the sera of exacerbated MS patients after blocking Fc receptors compared to those of controls. These findings indicate that IgG binding to endothelial cells may be mediated via an immunologically specific antigen-antibody interaction. The results show that anti-endothelial cell antibodies and immune complexes are present in cases of MS and they may play a pathogenetic role in the blood-brain barrier (BBB) damage.

Adult↗
PubMed1987

HLA and Graves' disease in Koreans.

The HLA-A, B, C and DR antigen distribution in 128 Korean patients with Graves' disease was compared with that in 220 controls. The frequency of HLA-B13, DR5 and DRw8 (relative risk 3.8, 4.4, and 2.3, respectively) was significantly increased in patients with Graves' disease. There was no significant correlation between the presence of these HLA antigens and the clinical features.

Female↗
PubMed1987

Chronic relapsing demyelinating polyneuropathy associated with hepatitis B infection.

We studied a patient with chronic relapsing polyneuropathy associated with immune complexes of hepatitis B virus. There were cycles of remission and exacerbation in parallel with liver dysfunction. Immunofluorescent deposits of hepatitis B antigen, immunoglobulin, and C3 component were detected in the vasa nervorum. Ultrastructural study revealed electron-dense deposits that might have been immune complexes composed of hepatitis B virus, both around the endoneural capillary and in the endoneurium. Immune complexes composed of hepatitis B virus may play a role in the pathogenesis of chronic relapsing polyneuropathy.

Adult↗
PubMed1987

Role of the clotting system in the pathogenesis of neuroimmunologic disease.

Experimental allergic encephalomyelitis (EAE) is a prototypic neuroautoimmune disease involving sensitization to central nervous system myelin basic protein (MBP). Our studies of the clotting system and ensuing fibrinolysis implicate coagulation and cleavage of fibrin within or on the luminal surface of the cerebrovasculature as events initiating the inflammation characterizing EAE. Among recipient rats injected with MPB-primed, cultured-activated lymph node cells, opening of the blood-brain barrier (BBB) and deposition of perivascular fibrin within the spinal cord occur in parallel 1 day before onset of clinical signs of EAE. Daily treatment of recipient rats with trans-4-(aminomethyl)cyclohexanecarboxylic acid, a synthetic product that specifically inhibits plasminogen activator derived from endothelial cells, results in marked reduction of increased permeability of the BBB and suppression of clinical signs of EAE. We postulate that the critical event precipitating EAE is binding of circulating MBP-reactive immune effector cells to MBP immunodeterminants on the surface of cerebrovascular endothelial cells. Coagulation and ensuing fibrinolysis occur at sites of binding of effector cells to cerebrovascular endothelium. Release of biologically active peptides cleaved from fibrin open the BBB, thereby setting the stage for the cascade of inflammatory events culminating in clinical manifestations of EAE.

Animals↗