Biomedical subjects

C S Koh

Publications and source records attributed to C S Koh.

At least 73 records · Page 4Linked to original sources

PubMed1995

Effect of growth factors on the expression of proto-oncogenes c-fos and c-myc in FRTL-5 cell line.

This study was performed to prove the hypothesis that oncogene expressions would have the same patterns with those of cellular growth to growth factors in FRTL-5 cells. Ribonucleic acids of FRTL-5 were extracted at 15', 30', 60' and 120' after administration of growth factors to quiescent FRTL-5, and blotted to the nitrocellulose membrane. They were hybridized with radiolabelled c-fos, c-myc and beta-actin probes. Hybridized dot blots were autoradiographed and the amount of radioactivity was measured by densitometry. Densitometric readings were used as the indices of oncogene expressions. Expressions of c-fos and c-myc were more prominent in combined administrations of TSH (10 mU/ml) and IGF-I (100 ng/ml) or IgG of Graves' disease (Graves' IgG; 1 mg/ml) and IGF-I than in combined administration of TSH and Graves' IgG. IgG of primary myxedema suppressed oncogene expressions by TSH or Graves' IgG, but not by IGF-I. From the above results, it was suggested that expressions of c-fos and c-myc to growth factors would have similar patterns with those of cell growth to growth factors in FRTL-5, and the actions of TSH and Graves' IgG would be manifested through same signal transduction system, but IGF-I would be manifested by its own.

Animals↗

PubMed1995

[Immunohistochemical analysis of adhesion molecules in directional coronary atherectomy specimens].

Chronic inflammatory cells are key components in the progression of atherosclerotic plaques and restenosis after coronary angioplasty. Adhesion molecules are fundamental in inflammatory processes. Therefore, the distributions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule (VCAM) were investigated in directional coronary atherectomy specimens obtained from 14 patients, in 6 with acute coronary syndromes (myocardial infarction and unstable angina within 1 month), 6 with old myocardial infarction and 2 with stable effort angina. There were eight primary lesions and six restenotic lesions. Atherectomy tissue fragments were snap frozen and cut into 4 microns thick cryostat sections for immunohistochemical staining by avidin-biotin complex immunoperoxidase techniques using adhesion molecule specific monoclonal antibodies BBIG-I1 (ICAM-1) and BBIG-V1 (VCAM). The cells of lesions were characterized in sequential sections by macrophage marker KP1 (CD68), endothelial marker JC/70A (CD31), and smooth muscle cell marker 1A4 (alpha-smooth muscle actin). Four restenotic lesions that had undergone a prior balloon angioplasty within a few months consisted of intimal proliferation and the other lesions were atherosclerotic plaque. Macrophage-rich areas were seen in the lesions from acute coronary syndromes and/or early restenotic lesions. Expression of ICAM-1 or VCAM was strongly associated with macrophage-rich areas, but VCAM staining was weaker than ICAM-1 except in one restenotic lesion. Macrophages that express ICAM-1 and/or VCAM may be important in the unstable plaques and restenotic lesions related to disease activity of ischemic heart disease.

Aged↗

PubMed1995

[A case of multiple myeloma complicated by acute transverse myelopathy due to epidural abscess].

A 51-year-old man developed fever and lumbago followed by rapidly progressive bilateral sensory disturbance below the 9th thoracic spinal cord level, flaccid paraplegia, urinary obstruction and constipation. Based on radiological examinations and laboratory findings, a diagnosis of transverse myelopathy due to epidural abscess was made. A series of MRI studies revealed multiple abscess formation in the paravertebral muscles. Hypergammaglobulinemia with M protein was observed continuously, and further examination revealed multiple myeloma in the early stage. Since it has been reported that several different immunosuppressive mechanisms precede the development of bone lesions in multiple myeloma, these mechanisms may have played an important role in the rapid progression of the abscess in this patient. Multiple myeloma is not only important as one of the disorders underlying epidural abscess of unknown etiology, but important in predisposing to severe infection as a result of the immunosuppressive mechanisms present starting in the early stage of the disease.

Abscess↗

PubMed1995

Technetium-99m-labeled antigranulocyte antibody bone marrow scintigraphy.

UNLABELLED: Although bone scintigraphy is a sensitive method for detecting skeletal metastases, it is often equivocal for metastases due to poor specificity. This study evaluates 99mTc-antigranulocyte antibody (AGA) bone marrow scintigraphy in differentiating malignant from benign lesions, in 42 patients with skeletal tumors who had equivocal bone scans. METHODS: AGA scans performed approximately 1 wk after 99mTc-MDP bone imaging were visually assessed for the presence of concordant marrow defects. Final diagnoses were made from radiological results, follow-up bone scans or clinical evaluation for 12 mo or longer. RESULTS: The final diagnoses were: skeletal metastasis (19 patients), no metastasis (20 patients) and unconfirmed (3 patients). AGA scans could not determine the presence of a concordant defect in three patients because of overlying liver activity or previous irradiation of the region. Seventeen patients had bone marrow defects concordant with bone scan lesions, whereas 15/19 patients without metastasis had normal AGA scans. The sensitivity and specificity of AGA for detecting skeletal metastases were 100% and 79%, respectively. CONCLUSION: AGA scans had a low incidence of skeletal metastases in patients who had equivocal bone scans. Although a concordant marrow defect increases the possibility of metastasis, further radiological investigation to exclude benign disease is warranted.

Antibodies, Monoclonal↗

PubMed1995

[Comparative study of the efficacy of plasma exchange, immunoadsorption plasmapheresis and corticosteroid administration in the treatment of Guillain-Barré syndrome].

We have retrospectively compared the efficacy of plasma exchange (PE), immunoadsorption plasmapheresis therapy (IAPP), corticosteroid administration and no treatment in the treatment of the Guillain-Barré Syndrome (GBS). Forty-two patients with GBS and clinical functional grades of more than Hughes 3 were admitted to Shinshu University Hospital, Nagano Red-cross Hospital and Saku General Hospital between 1978 and 1994. These patients were treated with either PE, IAPP, corticosteroids or no therapy. Eight were treated with PE, eleven with IAPP, twelve with corticosteroids and eleven were untreated. None of the patients were received combined therapy. The four groups of patients were compared on the following points; duration of the deteliocation in symptoms, duration of the worst symptoms, period of the ability to walk after onset, minimum motor nerve conduction velocity (MCV) over the course, maximum cerebrospinal fluid (CSF) protein concentration over the course, and CSF protein concentration improvement 6 weeks after onset as compared with 2 weeks after onset. The results revealed that the duration of the worst symptoms was shortened more in the IAPP-treated and PE-treated groups than in the other groups. Decreases in CSF protein concentration were more significant in the IAPP-treated and PE-treated groups than in the other groups. There were no significant differences in the other parameters among the groups. Furthermore the clinical symptoms of GBS improved more rapidly with PE and IAPP than with supportive care alone or corticosteroid therapy, especially in the early phase of the disease. IAPP and PE are equally effective.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1995

[A patient with a relapse of myasthenia gravis after a 13-year remission following successful treatment by mediastinal irradiation and corticosteroid therapy].

We report a patient with myasthenia gravis who experienced a relapse 13 years after apparently successful treatment by mediastinal irradiation and corticosteroid therapy. A 20-year-old male was admitted to Shinshu University Hospital with a chief complain double vision and drooping eyelids. These symptoms had appeared 2 months prior to admission. They tended to be more severe late in the day, and varied from day to day. Prior to this admission the patient had been healthy for the 13 years since undergoing 45-Gy mediastinal irradiation and corticosteroid therapy. MRI and CT studies revealed no thymic hyperplasia. Total thymectomy was performed, and his myasthenic symptoms, including the opthalmoplegia, improved. Histological examination of the resected thymus revealed an active thymus with germinal centers. Immunohistological studies showed an abundance of intracellular adhesion molecule-1 (ICAM-1) in the germinal centers and thymic medullary epithelium, and the presence of lymphoid function-associated antigen-1 (LFA-1) in thymic lymphocytes. ICAM-1 and LFA-1 are ligand of adhesion molecules which interact with each other and play an important role in antigen presentation. Acetylcholine receptor (ACh-R) antigen is known to be present in the thymus. The presence of both ICAM-1 and LFA-1 in the active thymus in this patient suggests that these adhesion molecules may have a role in ACh-R antigen presentation, causing myasthenia. These findings suggest that patients with myasthenia gravis who do not undergo total thymectomy have a risk of recurrence, even after long-term remission.

Adult↗

PubMed1995

[The detection of factors that may promote the hepatocyte proliferation in the serum of a patient with crow-fukase syndrome].

We reported a case of Crow-Fukase syndrome and examined the mechanism of hepatomegaly in Crow-Fukase syndrome. A 67-year-old woman was presented with polyneruopathy, hepatosplenomegaly, pericardial effusion and M proteinemia. On examination, all laboratory data and clinical symptoms were compatible with Crow-Fukase syndrome. The patient was treated with prednisolone and immunoadsorption plasmaphresis therapy. All the clinical manifestations including hepatomegaly gradually improved. In order to examine whether some factors that promote the prolifelation of hepatocyte may exist in the patient's serum, we cultured mouse hepatocyte in the presence of patient's or control serum together. Though the number of hepatocytes decreased after 2 days culture, the number of hepatocytes cultured with patient's serum in active disease stage remained significantly greater than of hepatocytes cultured with either control serum or patient's serum in healing stage. There were no abnormal pathological findings in biopsied liver. Liver suggesting that hepatomegaly was the results of normal hepatocytes proliferation. Taken together, these findings suggest there were some factors that may promote the proliferation of hepatocytes or may have protective effect of hepatocyte in patient's serum. Though the level of human hepatocyte growth factor (h-HGF) in patient's serum in active disease stage was slightly increased, hepatomegaly cannot be attributable solely to h-HGF. Organomegaly is one of the important symptoms of the Crow-Fukase syndrome, however, in so far as we are aware its mechanism is not examined. In this report it is suggested that several unknown factors other than h-HGF may contribute the hepatomegaly of the Crow-Fukase syndrome.

Aged↗

PubMed1994

A hippocampal protein associated with paraneoplastic neurologic syndrome and small cell lung carcinoma.

A hippocampal 38 kd autoantigen recognized by an autoantibody from the serum of a patient with paraneoplastic limbic encephalitis (PLE) and small cell lung carcinoma (SCLC) was isolated by screening a human hippocampal cDNA library. The 1,991-nucleotide ple21 clone was obtained and the deduced 350-residue protein encoded by the ple21 cDNA clone was found to be highly homologous to the neuron-specific RNA recognition motifs (RRMs)-containing proteins. The homologies were confined to the RRMs and the RRM connecting region. The presence of RRM in the antigenic protein may be important in the pathogenesis of SCLC-associated paraneoplastic neurologic syndrome.

Amino Acid Sequence↗

PubMed1994

Suppression of experimental allergic encephalomyelitis in Lewis rats by administration of gangliosides.

Gangliosides (GA) are known to suppress T cell responses to mitogens and alloantigens. GA treatment (more than 50 mg/kg/rat subcutaneously every 12 hr) significantly suppressed clinical signs and histologic lesions of both actively induced and cell-transferred experimental allergic encephalomyelitis (EAE) in Lewis rats in a dose-dependent manner: P < 0.01, in actively induced EAE; P < 0.001 (100 mg/kg) or P < 0.005 (50 mg/kg), in cell-transferred EAE. Lymph node cells from guinea pig myelin basic protein (GPMBP)-sensitized rats were stimulated in vitro with the specific sensitizing antigen, GPMBP, or with Con A. Purified bovine brain GA significantly suppressed GPMBP-induced proliferation in a dose-dependent manner (P < 0.01). GA treatment during sensitization phase (from Day -5 to Day 4) did not suppress actively induced EAE. There were no significant differences in T cell subsets of peripheral blood or spleen cells between GA-treated rats and controls by flow cytometry analysis. Taken together, these findings indicate that GA primarily act on the immune effector phase of EAE.

Animals↗

PubMed1994

The effect of obesity on fibrinolytic activity and plasma lipoprotein (a) levels in patients with type 2 diabetes mellitus in Korea.

To determine whether previously reported abnormalities in fibrinolytic activity and plasma lipoprotein (a) levels could reflect obesity rather than diabetes per se, plasma concentrations of tissue-type plasminogen activator (t-PA), type 1 plasminogen activator inhibitor (PAI-1), and lipoprotein (a) (Lp (a)) were investigated in sixty-four type 2 diabetic patients (56.1 +/- 9.5 years; body mass index, 24.6 +/- 3.3 kg/m2) and thirty-two control subjects (57.9 +/- 8.9 years; body mass index, 24.6 +/- 3.4 kg/m2). Both the plasma t-PA and PAI-1 antigen levels were similar between the diabetic group (10.6 +/- 3.8 ng/ml; 27.7 +/- 11.6 ng/ml) and the control group (12.2 +/- 3.5 ng/ml; 27.7 +/- 9.6 ng/ml). The PAI-1 levels were evenly distributed from 5.93 to 52.7 ng/ml in diabetic patients. The difference of Lp (a) levels between the two groups was negligible (the diabetic group, median 11 mg/dl (range 0-72 mg/dl); the control group, median 13 mg/dl (range 0-55 mg/dl)). Significant correlations between PAI-1 levels and body mass index (BMI) were observed in both groups. In the diabetic group, PAI-1 levels also correlated with fasting C-peptide levels (r = 0.54, P < 0.01) and serum triglyceride levels (r = 0.28, P < 0.05). However, we could not find a significant association between either t-PA or PAI-1 levels and Lp (a) levels in the diabetic and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Primary cutaneous plasmacytosis: report of three cases and review of the literature.

BACKGROUND: Cutaneous plasmacytosis is a rare disease characterized by peculiar multiple eruptions and hypergammaglobulinemia. More than 40 cases have been reported, mainly in Japan, although information concerning the disorder was limited to individual case reports. OBJECTIVE AND METHODS: To clarify the clinicopathological and laboratory features, we reviewed 41 cases. RESULTS: All patients were Japanese and the male-to-female ratio was 1:0.6. The onset ages ranged from 20 to 62 years, with a mean and median of 37 and 37 years. A superficial lymphadenopathy was detected in 58% (22/38), and polyclonal hypergammaglobulinemia was found in 93% (38/41). No cases were associated with any apparent underlying diseases. The course was chronic without spontaneous remission. Four patients died, 3 of whom succumbed to leukemia, respiratory failure or renal failure, respectively. CONCLUSION: The results suggest that the condition appears to be a variant of reactive plasmacytic disorders of unknown origin.

Adult↗

PubMed1994

Expression of intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1 in the spinal cord of rats during acute experimental allergic encephalomyelitis.

We investigated the expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) by cells in the central nervous system (CNS) of Lewis rats during acute experimental allergic encephalomyelitis (EAE). A few endothelial cells in the CNS of normal rats expressed ICAM-1, whereas during the active phase of EAE, ICAM-1 was present on many endothelial cells. This alteration was detectable the day before clinical symptoms. Since histopathological studies showed few detectable mononuclear cells or inflammatory foci in any section of the preclinical rats, the expression of ICMA-1 was considered to be important at least in the early stage of inflammation. LFA-1 was seen on perivascular infiltrating cells. An increase in either ICAM-1- or LFA-1-positive cells was initially seen in the lumbosacral portion of the spinal cord, which then extended to the thoracic portion. The number of either ICAM-1- or LFA-1-positive cells peaked on the day of clinical onset in the lumbosacral portion. In contrast, in the thoracic portion, a peak in the number of either ICAM-1- or LFA-1-positive cells was observed on the day after clinical onset. This ascending extension of either ICAM-1- or LFA-1-positive cells was correlated with the progression of neurologic signs. It is suggested that increased expression of ICAM-1 and LFA-1 in the CNS of rat EAE may promote the extravasation of lymphocytes across the blood-brain barrier and be related to progression of the disease.

Acute Disease↗

PubMed1994

Poor renal uptake of technetium-99m-DMSA and technetium-99m-MDP in a patient with Fanconi syndrome and near normal glomerular filtration rate.

We present a patient with Fanconi syndrome who demonstrated poor renal uptake of 99mTc-DMSA and high urinary concentration of the tracer. A 99mTc-DTPA scan was normal and the creatinine clearance only minimally decreased. These findings suggest that 99mTc-DMSA may be accumulated in the kidney by glomerular filtration and subsequent tubular reabsorption, with the nonabsorbed fraction appearing in the urine. In Fanconi Syndrome the tubular reabsorption of DMSA may also be reduced, thus explaining the poor renal uptake in this patient. A 99mTc-MDP bone scan showed faint renal uptake and diffuse high uptake mainly in the spine, demonstrating that the metabolic bone disease associated with Fanconi Syndrome can be another mechanism for poor renal visualization on bone scan.

Fanconi Syndrome↗

PubMed1994

The tumor necrosis factor beta * 1 allele is linked significantly to HLA-DR8 in Koreans with atrophic autoimmune thyroiditis who are positive for thyrotropin receptor blocking antibody.

The localization and functional characteristics of tumor necrosis factor(TNF) beta gene raise the possibility that it may be involved in the susceptibility to autoimmune thyroid diseases. To investigate whether a TNF beta gene polymorphism is associated with autoimmune thyroiditis, we analyzed the TNF beta gene polymorphism with the restriction enzyme NcoI in 48 Korean patients with atrophic autoimmune thyroiditis [23 were found to be thyrotropin binding inhibitor immunoglobulin(TBII) positive, 25 TBII negative], 52 goitrous autoimmune thyroiditis, and 129 healthy controls. Two TNF beta alleles were identified from the restriction fragment length polymorphism studies of amplified genomic DNA. In atrophic autoimmune thyroiditis patients positive for TBII, 7 of 23 patients were homozygous for the TNF beta * 1 allele, 3 were homozygous for the TNF beta * 2 allele, and 13 were TNF beta * 1/2 heterozygous compared to controls(P = 0.20). Also, there were no associations between the TNF beta gene polymorphism and either TBII-negative atrophic autoimmune thyroiditis or goitrous autoimmune thyroiditis. Of the HLA-class II antigens, the frequency of HLA-DR8 was significantly greater among the 23 Korean patients with TBII-positive atrophic autoimmune thyroiditis compared to control subjects (Pc = 0.003). When the HLA-DR8 positive patients with TBII-positive atrophic autoimmune thyroiditis and controls were analyzed separately, the DR8 positive patients with TBII-positive atrophic autoimmune thyroiditis had more homozygotes for the TNF beta * 1 allele(6/12, 50.0%) and no homozygotes for the TNF beta * 2 allele, as compared to the DR8 negative patients with TBII-positive atrophic autoimmune thyroiditis and DR8 positive controls(P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗

PubMed1994

[A study on subpopulation of helper T cells in chronic inflammatory demyelinating polyneuropathy].

Chronic inflammatory demyelinating polyneuropathy (CIDP) is thought to be an inflammatory autoimmune disease against peripheral myelin. Recently several animal models have suggested that preferential activation of Th1 cell response is central to the pathogenesis of this disease. We studied the function of CD4 positive T cell subsets, Th1 cells and Th2 cells by analyzing their representative secreting cytokines. Th1 cells secrete Interferon gamma (IFH gamma) and Th2 cells secrete Interleukin 4 (IL4). Using enzyme linked immunospot (ELISPOT) assay, a very sensitive single cell analysis system, we enumerated IFN gamma and IL4 secreting peripheral blood lymphocytes in patients with CIDP. Also we examined these cytokines in supernatants of cultured peripheral blood lymphocytes by a very sensitive enzyme linked immunosorbent assay (ELISA), Immunodot assay and westernblot assay. In culture supernatants of CIDP patients' peripheral blood lymphocytes, the levels of both IFN gamma and IL4 were higher during the exacerbation stage than the remission stage. In the remission period, though the levels of IFN gamma and IL4 were low in the supernatants, the ELISPOT assay revealed that the number of IL4 secreting cells was elevated compared with that of IFN gamma secreting cells. Our results suggest that the switch from Th1 to Th2 might play an important role in inducing the remission stage in patients with CIDP.

Adult↗

PubMed1994

[Characterization of infiltrating mononuclear cells in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis (EAE)].

Mononuclear cells (MNCs) infiltrating in spinal cords (SCs) of Lewis rats with EAE were isolated in order to permit flow cytometric (FCM) analysis of these cell populations, using monoclonal antibody to T cell, CD4, CD8. MHC class II antigen (Ia), intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function associated antigen-1 (LFA-1). The number of MNCs isolated from SC varied from 5 to 620 x 10(4). They were increased and reached a peak on day 2 post clinical onset, and subsequently declined through the clinical course. The increase of infiltrating cells in SC paralleled the severity of the disease development. The surface phenotypes of MNCs from rats on the day of clinical onset were determined by flow cytometry. The phenotypes found in these rats were as follows: T cells (70.3%); CD4 + (58.3%); CD8 + (40.3%); Ia (51.9%); ICAM-1 (62.6%); LFA-1 (75.8%). These findings suggest that high proportion of ICMA-1 and LFA-1 expression may be important in antigen presentation in the inflammatory lesions of SC and in promoting lymphocyte extravasation across the blood-brain barrier during the disease. The approach we employed offered more sophisticated and quantitative analysis of CNS inflammatory cells, which is unobtainable by tissue section staining.

Animals↗

PubMed1994

[Inflammatory mechanisms in nervous system].

Experimental autoimmune encephalomyelitis (EAE), is a neuroautoimmune inflammatory disease, involving sensitization to central nervous system myelin basic protein (MBP). Our studies of the coagulation 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 MBP-primed, cultured-activated lymph node cells, "opening" the blood-brain barrier (BBB) and deposition of perivascular fibrin within the spinal cord occur in parallel one day before onset of clinical signs of EAE. The critical event precipitating EAE is a binding of circulating MBP-reactive immune effector cells to MBP immunodeterminants on the surface of cerebrovascular endothelial cells. Coagulation and ensuring fibrinolysis occur at sites of binding of effector cells to cerebrovascular endothelium. Release of biologically active peptides, cleaved from fibrin, "open" the BBB. Once BBB is opened, even transiently, the stage is set for a complex cascade of immunologically-nonspecific inflammatory events, which plays an important role in the development of tissue damage, including demyelination.

Animals↗

PubMed1994

[A pathogenic study of chronic inflammatory demyelinating polyradiculoneuropathy in a patient with hepatitis B infection].

We immunologically examined the pathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy in a patient with HB hepatitis. A 41-year-old male clerk has been suffered from muscle weakness, tingling and numbness in the distal portion of all limbs. All symptoms were compatible with the typical patterns of chronic inflammatory demyelinating polyradiculoneuropathy. We examined the patient's serum and biopsied sural nerve, using histochemical and immunological techniques. We detected the band that reacted with anti-HBs antibody in the sural nerve in western blotting. The result indicated that HBs antigen was expressed on the peripheral nerves in the patient. There were no anti-peripheral nerve antibodies neither in the sural nerve or serum. There was no increase of immune complex in the serum. No deposition of immunoglobulins and complements were detected in the sural nerve. Immunoadsorption therapy had no effect on this patient, but administration of prednisolone improved his symptoms drastically. These findings suggest that a cytotoxic T cell may had played a more important role than humoral factors in this patient's nerve injury. Though the pathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy remains unclear, our findings seem to be very interesting in that they go some way toward clarifying the pathogenesis of this disease.

Adult↗