OBJECTIVES: There have been several evidences that the central nervous system defect is one of the etiologic factors in schizophrenia and high nailfold plexus visibility can reflect indirectly. These are particularly related to the negative symptoms of schizophrenia. In this study, we examined the relationship between nailfold plexus visibility and various clinical variables in schizophrenia. METHODS: Forty patients(20 males, 20 females) satisfying the DSM-IV criteria for schizophrenia and forty normal controls(20 males, 20 females) were measured for Plexus Visualization Score(PVS) by using capillary microscopic examination. We used Positive and negative Syndrome Scale(PANSS). Uimann-Giovannoni Process-Reactive Questionnaire(PRQ), Phillips Premorbid Adjustment Scale(PAS). Continuous Performance Test, and Backward Masking for psychopathology and clinical variables. RESULTS: There was no significant relationship between schizophrenic subjects and normal controls in PVS. PVS was correlated with PANSS positively except negative symptom subscore. PVS was correlated with PRQ score negatively, and with PAS score positively. CONCLUSIONS: This study shows high PVS are associated with more severe psychotic symptoms and with clinical variables, such as disease process and premorbid adjustment, in some schizophrenics.
Adult* ; Capillaries ; Central Nervous System ; Diagnostic and Statistical Manual of Mental Disorders ; Humans ; Male ; Masks ; Psychopathology ; Schizophrenia

To elucidate the complex of insulin-like growth factor binding proteins (IGF-BPs) in short stature patients, we carried out a prospective study on three patients who were diagnosed as complete GH deficiency at the department of pediatrics from July 1992 to June 1993. The results were summarized as follows: 1) Two circulating IGFs complexed to specific binding protein existed in normal serum. Binding activity was found to be in the 150,000 molecular weight area (the large complex) and 50~60,000 molecular weight area (the small complex). 2) Binding activity for the large complex was seen to be dependent on advancing age, level of large IGF-BP3 complex peacked at the age of 15~16 years. 3) The binding activity for large complex diminished in three GH deficient patients and increased after hGH injection to near or above normal level. 4) Increased growth rate after GH treatment in GH deficient patient was closely related with increasing level of the large IGF-BP3 complex. Therefore we suggest that the large IGF-BP3 complex is regulated by GH. Estimating its serum level is useful for screening of GH deficiency and the monitoring of response to GH therapy.
Carrier Proteins ; Growth Hormone* ; Humans ; Insulin-Like Growth Factor Binding Proteins ; Insulin-Like Growth Factor I* ; Mass Screening ; Molecular Weight ; Pediatrics ; Prospective Studies

BACKGROUND: Pemphigus is an autoimmune bullous disease with circulating desmosomal autoantibodies of IgG. In direct IF studies with perilesional tissue, IgA or IgM antibodies can be seen in addition to IgG. OBJECTIVE: We examined sera of patients with pemphigus for the presence/frequency of IgA autoantibodies as well as IgG by indirect IF and immunoblot assay. Patients: Twenty patients of pemphigus (PV 10, PF 10) who showed positive findings in indirect IF examinations. METHODS: Indirect IF study with normal human skin substrates and immunoblot analysis using A431 cell extracts (with multi-step immunostaining) were performed with patients sera. RESULTS: In indirect IF, IgA autoantibodies that bind to the epidermal keratinocyte antigens were detected in 4 cases among the 20 patients (PV 2 and PF 2). In immunoblot analysis IgA bands reacting to PV/PF antigens were observed in 7 cases from the 20 patients with pemphigus (PV 3, PF 4). The serum titers of IgA autoantibodies were lower than those of IgG in every single case. CONCLUSION: In patients with pemphigus (PV/PF), 35% of cases have serum IgA autoantibodies as well as IgG autoantibodies specific to the pemphigus antigens (Dsg 1/Dsg 3). However, pathogenic roles of the associated IgA autoantibody are not clear.
Antibodies ; Autoantibodies ; Cell Extracts ; Humans ; Immunoglobulin A* ; Immunoglobulin G ; Immunoglobulin M ; Keratinocytes ; Pemphigus* ; Skin

Homeostasis of multicellular organism is controlled by proliferation and differentiation of cells as well as by cell death. The defects in programmed cell death contribute to the pathogenesis of rheumatoid arthritis (RA) and systemic lupus erythematous. RA is considered to be a proliferating disorder of synovial tissue which is accompanied by inflammatory cell infiltration and bone erosion. The aim of the study was to find whether potent inducers of apoptosis could be induced apoptosis in RA synovial cells. We examined the effects of drugs, such as dexamethasone, methotrexate, hydrogen peroxide, and ceramide on induction of apoptosis in cultured RA synovial cells. Used drugs did not induced apoptosis in RA synovial cells. Finally Fas antigen-mediated apoptosis of RA synovial cells was investigated by the addition of anti-Fas antibody. To examine the ICE (interleukin-1p-convertase; caspase-1) expression in synovial cells, RT-PCR of caspase-1 gene was performed. In synovial cells of RA, Fas induces that caspase-1 activation cause apoptosis.
Apoptosis* ; Arthritis, Rheumatoid* ; Cell Death ; Dexamethasone ; Homeostasis ; Humans ; Hydrogen Peroxide ; Ice ; Methotrexate

OBJECTIVES: Human osteoarthritis is a heterogeneous and multifactorial disease characterized by the progressive deterioration of the cartilage of diarthrodial joints. In some instances, there is an identifiable cause, such as trauma or congenital malformation, but, mostly the etiology remains unknown. Since familial aggregation is seen, genetic factors may be important, particularly in osteoarthritis of the hand. METHODS: Blood samples from patients and controls were obtained for DNA analysis. Exon 31 of type II procollagen gene was amplified by polymerase chain reaction, and screening for the mutation was undertaken using a restriction enzyme digestion (Dsa I). RESULTS: The patients phenotype represented typical, but earlyonset and family history, osteoarthritis. No mutation in exon 31 of type II procollagen gene could be identified. CONCLUSION: Screening of the 31 exon did not, however, reveal any mutation. It needs further evaluation in other sites of type II procollagen genes.
Cartilage ; Collagen Type II ; Digestion ; DNA ; Exons ; Hand ; Humans ; Joints ; Mass Screening ; Osteoarthritis* ; Phenotype ; Polymerase Chain Reaction ; Procollagen*

OBJECTIVES:Nitric Oxide(NO) is a toxic, inorganic, gaseous free radical produced during the metabolism of L-Arginine by NO synthase(NOS). It has been implicated in a rapidly growing number of physiological and pathophysiological processes such as cytotoxic effects against microbes and tumor cells, blood vessel dilation and neurotransmitter. Recently there is growing evidence implicating NO in immune regulation, inflammation, autoimmunity, and arthritis. We performed this study to determine a role for nitric oxide in inflammatory arthritis especially rheumatoid arthritis(RA). METHODS: We measured (1) the concentrations of nitrite, a breakdown product of nitric oxide, in serum and synovial fluid from patients with RA and osteoarthritis(OA) and in the serum of controls (2) the concentrations of nitrite in the supernatant of cultured synovial tissue with RA and OA and (3) determined whether human chondrocytes and synoviocytes can synthesize nitric oxide and if so, how production is regulated by cytokines and antirheumatic drugs. RESULTS: 1) Serum nitrite concentrations in patients with RA and OA were higher than in controls. In both disease groups synovial fluid nitrite was higher than serum nitrite. Serum and synovial fluid nitrite concenrations in RA were higher than those in OA. However, those findings are not statistically significant. 2) Although these findings are not statistically significant, the concentration of nitrite in the supernatant of cultured synavial tissue with RA was higher than that in OA. 3) IL-1beta and TNF-alpah induced the biosynthesis of NO by chondrocytes and synoviocytes. IGF-1 and TGF-beta failed to provoke the production of NO. The biosynthesis of NO required an induction period of approximately 6 hours and was inhibited by L-NMMA and cycloheximide. Dexamethasone, indomethacin, gold sodium thiomalate and methotrexate had no effect on the induction of NO biosynthesis. CONCLUSION: These results suggest a role for nitric oxide as an inflommatory mediator in inflammatory arthritis.
Antirheumatic Agents ; Arginine ; Arthritis* ; Arthritis, Rheumatoid ; Autoimmunity ; Blood Cells ; Chondrocytes ; Cycloheximide ; Cytokines ; Dexamethasone ; Gold Sodium Thiomalate ; Humans ; Indomethacin ; Inflammation ; Insulin-Like Growth Factor I ; Metabolism ; Methotrexate ; Neurotransmitter Agents ; Nitric Oxide ; omega-N-Methylarginine ; Synovial Fluid ; Transforming Growth Factor beta

OBJECTIVE: Angiogenesis is central role to both the proliferation and metastasis of malignant tumor. The intense interest in angiogenesis has also lead to a re-examination of the activity of established cytotoxic agents which are known to be an antiangiogenic effect anecdotally. In this study, anti-angiogenic effect of cisplatin, paclitaxel and thalidomide was evaluated in human ovarian cancer cell lines and cervical cancer cell line. METHODS: Human ovarian cancer cell line A2780, cisplatin resistant human ovarian cancer cell line A2780-CDDP, human breast cancer cell line MCF-7, and squamous cell uterine cervical carcinoma cell line SiHa were used to evaluate the level of mRNA and protein expression of VEGF, bFGF and TSP-1, 2 before and after the treatment with cisplatin, paclitaxel, and thalidomide using RT-PCR, protein extraction, and Western blot. The results were analyzed with Wilcoxon signed rank test in the SAS ver 8.1. RESULTS: Targeted mRNAs were synthesized as 212 bp VEGF, 238 bp bFGF, and 492 bp band sized except mRNA of TSP-2 via RT-PCR. The protein of VEGF and bFGF were appeared as 21KDa and 17 KDa size, however, the protein of TSP-1 was not appeared through western blot. No effect of cisplatin on protein expression was measured in these cell lines, but paclitaxel influenced the expression of bFGF in MCF-7 cell line and the expression of TSP-1 in MCF-7 and SiHa cell lines. TSP-1 expression was influenced by thalidomide in A2780 cell line. The protein expression of VEGF and bFGF were not influenced following treatment with cisplatin, paclitaxel, and thalidomide. CONCLUSION: These results were suggested that bFGF and TSP-1 will be used as a target gene for the assay of antiangiogenic effect of paclitaxel in breast and uterine cervical cancer tissue and TSP-1 will be used as that of thalidomide in ovarian cancer. Furthermore, thalidomide will be tried as an adjunctive agent for the improvement of the survival in the case of the patient with ovarian cancer.
Blotting, Western ; Breast ; Breast Neoplasms ; Cell Line* ; Cisplatin ; Cytotoxins* ; Humans ; MCF-7 Cells ; Neoplasm Metastasis ; Ovarian Neoplasms ; Paclitaxel ; RNA, Messenger* ; Thalidomide ; Thrombospondin 1 ; Uterine Cervical Neoplasms ; Vascular Endothelial Growth Factor A

BACKGROUND/AIMS: Tamoxifen is a widely used anticancer drug for breast cancer with frequent gastrointestinal side effects. Changes in gastrointestinal motility is associated with altered activities of membrane ion channels. Ion channels have important role in regulating membrane potential and cell excitability. This study was performed to investigate the effects of tamoxifen on the membrane ionic currents in colonic smooth muscle cells. METHODS: Murine colonic smooth muscle cells were isolated from the proximal colon using collagenase, and the membrane currents were recorded using a whole-cell patch clamp technique. RESULTS: Two types of voltage-dependent K+ currents were recorded (A-type and delayed rectifier K+ currents). Tamoxifen inhibited both types of voltage-dependent K+ currents in a dose-dependent manner. However, tamoxifen did not change the half-inactivation potential and the recovery time of voltage-dependent K+ currents. Chelerythrine, a protein kinase C inhibitor or phorbol 12, 13-dibutyrate, a protein kinase C activator did not affect the voltage-dependent K+ currents. Guanosine 5'-O-(2-thio-diphosphate) did not affect the tamoxifen-induced inhibition of voltage-dependent K+ currents. Tamoxifen inhibited voltage-dependent Ca2+ currents completely in whole-test ranges. CONCLUSIONS: These results suggest that tamoxifen can alter various membrane ionic currents in smooth muscle cells and cause some adverse effects on the gastrointestinal motility.
Animals ; Antineoplastic Agents, Hormonal/*pharmacology ; Calcium Channels/drug effects ; Colon/*drug effects/physiology ; English Abstract ; In Vitro ; Membrane Potentials ; Mice ; Myocytes, Smooth Muscle/*drug effects/physiology ; Potassium Channels/*drug effects ; Tamoxifen/*pharmacology

OBJECTIVE: Expressions of P-glycoprotein, the multidrug resistance-associated protein (MRP) and the lung resistance protein (LRP) with the MDR phenotype widely divergent in human cancer cell lines. This study focused on the altered gene expression related drug transport. METHODS: To examine correlations between MDR-associated genes and PKC isozyme with cisplatin resistance on the level of the mRNA expression, we analyzed MDR-associated gene (LRP, MDR1/P-gp and MRP) expression and PKC isozyme, topoisomerase II alpha and beta in cisplatin-sensitive ovarian cancer cell line A2780 and cisplatin - resistant cell line A2780cp using cDNA-PCR approach. RESULTS: LRP mRNA levels were significantly increased in A2780cp compared to the drug sensitive variant. In contrast, MRP mRNA levels were not significantly correlated with drug sensitivity. A modest increase in PKC(eta) and MDR1/P-gp mRNA expression activity was also observed in ovarian cancer A2780cp cell lines that were resistant to CDDP. The level of topoisomerase II alpha and beta were not affected. CONCLUSION: These results showed that MDR1/P-gp expression may be an important determinant of the MDR phenotype in cell lines intrinsically resistant to cancer chemotherapeutic agents and a multifactorial emergence of MDR phenotype of tumor with a possible involvement of the PKC isozymes may be associated with CDDP resistant ovarian cancer cell line.
Cell Line* ; Cisplatin ; DNA Topoisomerases, Type II ; Drug Resistance, Multiple* ; Gene Expression ; Humans ; Isoenzymes ; Lung ; Multidrug Resistance-Associated Proteins ; Ovarian Neoplasms* ; P-Glycoprotein ; Phenotype ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger

BACKGROUND: Left ventricular hypertrophy (LVH) has been known as an important predictor of prognosis of cardiovascular disease. Carboxy-terminal propeptide of procollagen type I (PIP) is related with myocardial fibrosis. We sought to analyze the differences in the characteristics of LVH, myocardial fibrosis, and LV functions among hypertension (HBP), diabetes mellitus (DM) and chronic renal failure (CRF). METHODS: We enrolled consecutive patients with LVH. Patients were grouped as HBP (n=50), DM (n=41), CRF (n=31). Age and sex-matched normal control was also enrolled (n=32). Echocardiography and blood sampling for serum PIP level measuring was performedin all participants. RESULTS: There were no differences in baseline characteristics except systolic blood pressure among four groups. In three patients groups, their LV mass indices were significantly increased than control. Serum PIP level in CRF was much higher than others (CRF 1505.5 vs. HBP 868.7 vs. DM 687.5 vs. control 826.4, p<0.0001). LV diastolic and systolic function evaluated by E', E/E, S' and midwall fractional shortening was significantly decreased in three patients groups. However, LAVi was significantly elevated and LV ejection fraction was significantly decreased in CRF compared to others. In correlation analysis, indices of diastolic function were weakly, but statistically correlated with PIP (E': r=0.234, p=0.006; LAVi: r=0.231, p=0.006). CONCLUSION: In CRF, LV function was more deteriorated and serum PIP was more elevated when compared to HBP or DM. Therefore, myocardial fibrosis may play an important role to LV dysfunction as well as LV hypertrophy in CRF in some degree.
Blood Pressure ; Cardiovascular Diseases ; Collagen Type I ; Diabetes Mellitus ; Echocardiography ; Fibrosis ; Humans ; Hypertension ; Hypertrophy ; Hypertrophy, Left Ventricular ; Kidney Failure, Chronic ; Prognosis