No abstract available.
Population Characteristics* ; Thyroid Gland* ; Thyroiditis*

No abstract available.
Adenylyl Cyclases* ; Graves Disease* ; Humans ; Thyroid Gland*

Pseudomembranous colitis (PMC) is a frequent cause of morbidity and mortality among hospitalized patients. Although diarrhea is the most common manifestation, PMC may be associated with intraperitoneal fluid accumulation in the severe cases. And a few cases showing both ascites and pleural effusion have been reported in patients with PMC. We report a case of PMC who showed elevated serum and ascites levels of carcinoembryonic antigen (CEA) with a normal CEA level in pleural effusion and who successfully recovered after oral administration of metronidazole. After treatment, the serum CEA level returned to the reference range.
Administration, Oral ; Ascites ; Carcinoembryonic Antigen* ; Diarrhea ; Enterocolitis, Pseudomembranous* ; Humans ; Metronidazole ; Mortality ; Pleural Effusion ; Reference Values

No abstract available.
Foreign Bodies* ; Pulmonary Artery*

BACKGROUND: TSH stimulates both the adenyl cyclase and phospholipase C (PLC) pathways by binding to a single cell surface receptor that is coupled to G protein, and we examined crosstalk between these two signaling pathways. METHODS: FRTL-5 rat thyroid cells were grown in 6H medium, then incubated with 5H medium before the stimulation. Then cells were incubated for 24 hours with 5H mix containing 1 mCi/L myo-(2-N-3H) inositol. After pretreatment of 100 microM Rp-cAMP, 100 microM forskolin, 50 nM staurosporine, or 100 nM PMA (phorbol-12-myristate-13-acetate), TSH were added in different experiments. After 30 min at 37 degrees C, cells were disrupted and IP formation was determined. RESULTS: Stimulation with 100 microU/mL TSH resulted in a 1.65 fold increase in IP generation. In pursuing the possibility that the two post-receptor events might be linked in some way, we examined the effect of exogenously administrated Rp-cAMP, protein kinase A antagonist, and forskolin, a direct stimulant of protein kinase A, on IP generation achieved at a dose of 100 microU/mL TSH. The pretreatment of 100 M Rp-cAMP at a concentration sufficient to inhibit protein kinase A enhanced TSH-induced IP production. This effect of Rp-cAMP was dose-dependent. Forskolin attenuatedTSH-stimulated increases in phosphatidylinositide turnover. PMA, a protein kinase C (PKC) activator and staurosporine, a PKC inhibitor did not affect TSH-induced IP generation. CONCLUSION: These data suggested that activation of adenylate cyclase/cAMP post-receptor signalling casacde, which results in the protien kinase A activation, has an inhibitory effect on IP turnover activated by TSH.
Adenylyl Cyclases ; Animals ; Colforsin ; Cyclic AMP-Dependent Protein Kinases ; GTP-Binding Proteins ; Inositol ; Phosphotransferases ; Protein Kinase C ; Rats ; Receptors, Thyrotropin* ; Signal Transduction* ; Staurosporine ; Thyroid Gland ; Type C Phospholipases

BACKGROUND: In patients with myocardial infarction (MI) and chronic stable angina, the coronary flow reserve (CFR) is reduced not only in the region of myocardium perfused by the ischemia-related artery but also in the regions supplied by angiographically normal coronary arteries. The effect of myocardial stunning on the remote CFR is unknown, however. METHODS: In ten open-chest anesthetized dogs, left circumflex coronary artery was occluded for 15 minutes (myocardial stunning group, n=5) or for 30 minutes (MI group, n=5) and was followed by a reperfusion for 60 minutes. Before coronary occlusion and at 30 minutes and at 60 minutes after reperfusion, resting coronary blood flow (CBF) and maximal CBF after IV injection of each of adenosine (ADE) and acetylcholine (Ach) was measured with electromagnetic flow probe located in the proximal left anterior descending coronary artery. CFR was calculated as the ratio of maximal and resting CBF. RESULTS: At 30 minutes and 60 minutes after reperfusion, the remote resting CBF were significantly increased in both groups and the remote CFR was significantly decreased in both groups. The CFR of the MI group was lower than myocardial stunning group. The coronary vasodilator response to Ach was significantly lower than the response to ADE in both groups. CONCLUSION: After MI and myocardial stunning, there was severe coronary vasodilator abnormality in the remote myocardium and that was more marked after MI. The coronary vasodilator response to Ach was significantly lower than the response to ADE in both groups, suggesting endothelial dysfunction in remote myocardium.
Acetylcholine ; Adenosine ; Angina, Stable ; Animals ; Arteries ; Coronary Occlusion ; Coronary Vessels ; Dogs ; Humans ; Magnets ; Myocardial Infarction ; Myocardial Stunning* ; Myocardium ; Reperfusion

No abstract available.
Humans ; Infant, Newborn* ; Mass Screening*

BACKGROUND: It has been known that most of thyroid stimulating antibodies (TSAbs) may interact with epitopes near N-terminal, and thyroid stimulation blocking antibodies (TSBAbs) near C-terminal on the extracellular domain of TSH receptor. However, many authors have reported different results about epitopes reacting with TSH receptor autoantibody (TRAb). TSBAbs inhibit thyroid stimulation of TSH and TSAbs at the receptor level. However, it has been reported that there are some TSBAbs which bind to the other sites, not TSH receptor, or block post-reeeptor process. These findings raise the possibility that TRAbs may be heterogeneous according to the mechanism of action. In order to investigate the heterogeneity of TRAb, we undertook immuno-precipitation using synthetic peptides of TSH receptor and measured TRAb activities by FRTL-5 cells and chimeric CHO cells. METHODS: We studied 102 patients with autoimmune thyroid disease (Graves disease 32, Hashimotos thyroiditis 29, atrophic thyroiditis 41) and 35 healthy persons. Three synthetic peptide fragments of TSH receptor were used to perform immunoprecipitation with serum or IgG of patients and healthy persons, TSAb and TSBAb activities were measured by FRTL-5 cells and CHO cells transfected with wild-type and 2 mutant TSH receptor cDNA (Mc2, Mc1+2). Mc2 and Mcl+2 were rnade to substitute amino acid residues of 90-165, 8-165 of the TSH receptor with corresponding residues of LH/CG receptor, respectively. RESULTS: Two out of 10 IgGs extracted from Graves disease and 2 out of 9 IgGs from atrophic thyroiditis had specific bidings over 0.84% in immunoprecipitation with peptide I (amino acid residue 35-50). Four out of 18 IgGs from Graves disease, 9 out of 41 IgGs from atrophic thyroiditis, and 6 out of 14 IgGs from Hashimotos thyroiditis had specific bidings over 0.84% in immunoprecipitation with peptide II (amino acid residue 317-332). Only 2 out of 10 IgGs from Graves disease had specific bidings over 0.84% in immunoprecipitation with peptide III (amino acid residue 341-358). When 10 IgGs extracted from Graves disease were reacted with wild-type, Mc2, and Mcl+2 CHO cells, 7 IgGs in wild-type and 4 IgGs in Mc2 had positive for TSAb activities. In 10 IgGs from atrophic thyroiditis, 5 in wild-type, 5 in Mc2, and 3 in Mcl+2 CHO cells had positive for TSBAb activities. In Hashimoto's thyroiditis, only 1 with hyperthyroidism had positive for TSAb activity in wild-type and 1 with hypothyroidism had positive for TSBAb activities in both of wild-type and Mc2 CHO cells. Therefore, patients with Graves disease were divided into at least 3 groups according to the TSAb activities measured by wild-type, Mc2, Mcl+ 2 CHO cells and TBII activities. And patients with atrophic thyroiditis were divided into at least 4 groups according to the TBII activities, TSBAb activities by wild-type, Mc2, Mcl+2 CHO cells and FRTL-5 cells. CONCLUSION: From these results, epitopes of TSH receptor reacting with TSAb or TSBAb in autoimmune thyroid disease may be scattered in the TSH receptor, although epitopes of TSAb tend to be near N-terminal and those of TSBAb near C-terminal. Graves disease or atrophic thyroiditis were divided into 3 or 4 groups according to the TBII and TRAb activities. Therefore, TRAb detected in autoimmune thyroid disease may be heterogenous.
Animals ; Antibodies, Blocking ; Autoantibodies* ; CHO Cells ; Cricetinae ; DNA, Complementary ; Epitopes ; Graves Disease ; Humans ; Hyperthyroidism ; Hypothyroidism ; Immunoglobulin G ; Immunoglobulins, Thyroid-Stimulating ; Immunoprecipitation ; Peptide Fragments ; Peptides ; Population Characteristics* ; Receptors, Thyrotropin* ; Thyroid Diseases* ; Thyroid Gland* ; Thyroiditis

OBJECT: This study was carried out to evaluate immunologic difference between baseline and after 4 weeks drug treatment with atypical antipsychotics (rispreidone) by measurement of serum concentration of 6 cytokines. METHODS: The subjets were composed of 25 patients who are admitted at Dajeon St's Marys hospital of psychiatry department and diagnosed as schizophrenia by DSM-IV diagnositc criteria. We measured serum IL-1beta, IL-2, IL-6, IL-12, INF-gamma, TNF-alpha concenatrations by quantitative ELISA method using ELISA kit (Endogen Inc., Woburn, MA, USA).The two psyciatrists performed PANSS examination between baseline and after 4 weeks risperidone treatments. RESULTS: The serum level of IL-12 was increased significantly after medication of 4 weeks and the serum concentration of IFN-gamma showed the tendency of decreasement but not significant. The serum level of the other cytokines showed no significant change. CONCLUSIONS: We spectulate that the increasement of IL-12 may contribute to role of activation of immune response by treatment of antipsychotic medication (risperidone). This study is first trial of IL-12 study in neuropsychiatric field and IL-12 which play important role of immune response becomes interesting subjects in immune research.
Antipsychotic Agents ; Cytokines* ; Diagnostic and Statistical Manual of Mental Disorders ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-12 ; Interleukin-2 ; Interleukin-6 ; Interleukins ; Risperidone* ; Schizophrenia* ; Tumor Necrosis Factor-alpha

Background: A lifelong thyroxine therapy is indicated in all patients who have hypothyroidism as a result of autoimmune thyroiditis. However, it has been reported that some hypothyroid patients with autoimmune thyroiditis have spontaneous remission with restriction of iodine intake instead of thyroxine therapy. The purpose of study was to investigate how many hypothyroid patients with autoimmune thyroiditis can recover from hypothyroidism with restriction of iodine intake instead of thyroxine therapy and which factors predict recovery from hypothyroidism. Methods: We studied 64 patients with autoimmune thyroiditis(goitrous autoimmune thyroiditis 56, atrophic autoimmune thyroiditis 8). Thyroxine therapy was discontinued in patients with goitrous autoimmune thyroiditis on the way(group 1, n=32) or from the beginning(group 2, n=24) and atrophic autoimmune thyroiditis on the way(group 3, n-8). All patients were asked to avoid iodine-rich foods and thyroid function was monitored every one to two months for up to 35 months. Serum T3, T4, TSH concentrations, antithyroglobulin and antimicrosomal antibodies were measured by radioimmunoassay(RIA). TSH binding inhibitor immunoglobulin(TBII) was measured in serum using radioreceptor assay. Two hundred micrograms of thyrotropin releasing hormone (TRH) were given as intravenous bolus and TSH levels were measured in blood samples taken at 0, 30, and 60 minutes. All values were expressed as mean+-SEM. Statistical analysis was done with paired or non-paired t-test, ANOVA, and the Chi-square test. Statistical significance was defined as p-value below 0.05. Results: Thirteen(40.6%) of 32 patients in group 1 remained euthyroid after 12-35 months of discontinuation of thyroxine therapy. The other 19(59.4%) patients in group 1 had recurrences of hypothyroidism within 3 months after discontinuation of thyroxine therapy. In 11(45.8%) out of 24 patients in group 2, serum TSH concentrations declined below 5 mU/L within 3 months without thyroxine therapy. The other 13(54.2%) patients in group 2 remained hypothyroid till 2-16 months and the thyroxine was given. In contrast, all 8 patients in group 3 had recurrences of hypothy- roidism within 3 months after stopping thyroxine therapy. When we compared the recovered patients of goitrous autoimmune thyroiditis with the non-recovered patients of goitrous autoimmune thyroiditis, regardless of thyroxine therapy from the beginning, age at onset of disease of the 24 recovered patients was significantly younger than the 32 non-recovered patients(30.1+2.0 years vs. 40.2+ 2.4 years; p=0.004). Concl#usion: These findings suggest that 42.9% of hypothyroid patients with goitrous autoim- mune thyroiditis remain or become spontaneously euthyroid with restriction of iodine intake instead of thyroxine therapy. Young age may be a predicting factor of recovery from hypothyroidism in goitrous autoimmune thyroiditis.
Age of Onset ; Antibodies ; Humans ; Hypothyroidism ; Iodine ; Radioligand Assay ; Recurrence ; Remission, Spontaneous ; Thyroid Gland ; Thyroiditis ; Thyroiditis, Autoimmune ; Thyrotropin-Releasing Hormone ; Thyroxine