[Anti-IgE autoantibody in patients with parasite infection].
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Biomedical subjects
Publications and source records attributed to T Koike.
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IgG subclass distributions of anticardiolipin (aCL), anti-ssDNA, and anti-dsDNA antibodies in sera of patients with systemic lupus erythematosus were determined by an enzyme linked immunoassay (ELISA) method, using mouse monoclonal antihuman IgG subclass antibodies. IgG aCL activity consisted mainly of the IgG1 subclass, and to some extent, the IgG3 subclass. Definite amounts of aCL activity were also detected in IgG2 in sera from 25% of the patients. Anti-ssDNA antibody activity was relatively equally distributed among IgG1, IgG2 and IgG3, but was poorly distributed in IgG4. In contrast, anti-dsDNA antibody activity consisted mainly of IgG1 and IgG3.
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The effects of the phorbol ester, 12-O-tetradecanoylphorbol 13-acetate (TPA) on stimulus-evoked dopamine release were studied in PC12 cells. Pretreatment of the cells with TPA resulted in an enhancement of dopamine release which could be further stimulated by high concentrations of K+, A23187, but not with carbamylcholine. TPA-dependent, high-K+ -evoked enhancement of dopamine release was studied in detail: a maximum release was observed (169% of control) in response to 50 mM KCl upon treatment with 10(-7) M TPA for 5 min at 37 degrees C. This enhancement of dopamine release was associated with the concomitant reduction of the concentration rise of intracellular Ca2+ ([Ca2+]i) induced by a high concentration of K+ monitored by a fluorescent indicator, fura2. Thus, these data provide an example for alteration in the efficiency of stimulus-secretion coupling as pointed out in our previous paper. Moreover, we have shown that nicardipine, CdCl2, and CoCl2 inhibit high-K+ -evoked dopamine release more effectively in TPA treated cells than that of untreated cells, and that the TPA-dependent, high-K+ -evoked dopamine release observed in TPA treated cells is completely abolished by the presence of nicardipine, Cd2+ or Co2+, but is only partially inhibited in the presence of verapamil. These relevant findings suggest the possible involvement of protein kinase C in regulating the efficiency of a high-K+ -evoked dopamine release through the modification of nicardipine-sensitive Ca2+ channels.
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The effect of fibroblast growth factor (FGF) on the growth of chondrocytes in soft agar was examined. FGF induced colony formation by chick embryo and rabbit chondrocytes. The colony-forming efficiency of FGF-exposed chondrocytes was similar to that of Rous sarcoma virus-transformed chondrocytes (15-20%). Other mitogenic agents tested, such as epidermal growth factor, insulin, insulin-like growth factor-l, and platelet-derived growth factor, induced very low levels of colony formation. The induction of growth in soft agar of chondrocytes by FGF was not due to cells' phenotypic transformation, because chondrocytes grown in soft agar with FGF retained the ability to synthesize cartilage-characteristic proteoglycan. FGF did not induce growth in soft agar of chondrocytes whose phenotypic expression was suppressed by retinoic acid or 5-bromodeoxyuridine. In addition, FGF did not induce growth in soft agar of primary fibroblasts and normal rat kidney (NRK) cells. These results suggest that FGF selectively stimulates growth of differentiated chondrocytes in soft agar.
An IgM antibody cytotoxic to normal human lymphocytes was found in 46.2% (male: 61.5%; female: 30.8%) of sera from chronic schizophrenics by means of a complement-dependent cytotoxicity test. The relationship between this antibody and the immunological manifestations of schizophrenia is discussed.
The tentorial artery is a branch of the meningohypophyseal trunk originating from the internal carotid artery; this artery sometimes becomes an enlarged feeding artery in patients with tentorial lesions, especially tentorial meningiomas. We experienced a case of a cerebellopontile angle meningioma whose angiogram revealed the disappearance of a feeding artery arising from the tentorial artery after embolization of the external carotid artery. We report this case and discuss the mechanism of this phenomenon.
A high-performance liquid chromatographic method using solid-phase dansylation on alumina for precolumn fluorescence label has been developed for the determination of catecholamines (norepinephrine, epinephrine, and dopamine) in various rat tissues. After alumina treatment of the tissue homogenate, catecholamines adsorbed on the alumina were dansylated by solid-phase reaction. Both the excess reagent and fluorescent degradation products produced during dansylation were washed out from the alumina. Dansylated catecholamines were eluted from the alumina and separated by reversed-phase high-performance liquid chromatography. The four catecholamine derivatives, including the internal standard, were separated within 17 min, and no major interfering peak could be detected on any chromatograms. The calibration graph showed a good linearity in a range of 10 to 500 pmol for each catecholamine per sample. This method was applied to different rat tissues, and both the recovery and the reproducibility for all samples proved to be satisfactory. The present study provides a simple, sensitive, and selective method useful for routine pharmacological experiments of the determination of catecholamines.
Nerve growth factor(NGF)-mediated neurite outgrowth of PC12 pheochromocytoma cells was potentiated in medium containing high concentrations of extracellular K+. The binding of iodinated NGF to the cells was also enhanced by raising the concentration of K+ in medium up to 100 mM; the enhancement was saturated at 50 mM K+. Although the mechanism by which NGF-mediated neurite outgrowth is potentiated in high K+ medium remains to be largely unknown, high K+-induced alterations in the NGF binding are suggested to play a role in this phenomenon.
Infection with human parvovirus (HPV) B19 was diagnosed in persons with hereditary spherocytosis during an outbreak of erythema infectiosum. A 10-year-old boy had an aplastic crisis of the bone marrow and a maculopapular rash. His mother also had an aplastic crisis, fever, rash and a transiently acellular marrow. Another boy had an aplastic crisis, leucopenia and fever, but did not have a rash. Aplastic crisis and a rash have rarely before been observed together and attributed to infection with HPV.
The effect of vanadate on proteoglycan synthesis by cultured rabbit costal chondrocytes was examined. Rabbit chondrocytes were seeded at low densities and grown to confluency in medium supplemented with 10% fetal bovine serum, and then the serum concentration was reduced to 0.3%. At the low serum concentration, chondrocytes adopted a fibroblastic morphology. Addition of 4 microM vanadate to the culture medium induced a morphologic differentiation of the fibroblastic cells to spherical chondrocytes, and increased by two- to threefold incorporation of [35S]sulfate and [3H]glucosamine into large, chondroitin sulfate proteoglycans. The stimulation of incorporation of labeled precursors reflected real increases in proteoglycan synthesis, in that chemical analyses showed increases in the accumulation of macromolecules containing hexuronic acid and hexosamine in vanadate-maintained cultures. However, vanadate had only a marginal effect on [35S]sulfate incorporation into small proteoglycans and [3H]glucosamine incorporation into hyaluronic acid and chondroitinase AC-resistant material. These results provide evidence that vanadate selectively stimulates the synthesis of proteoglycans characteristically found in cartilage by rabbit costal chondrocyte cultures.
The binding and internalization of 125I-nerve growth factor (NGF) by PC12 pheochromocytoma cells was studied as a function of extracellular potassium concentration. Both surface-bound and internalized fractions of 125I-NGF associated with the cells under depolarizing conditions (50 mM K+) increased to 144 +/- 28% (average +/- SEM, six different cell preparations) and to 176 +/- 12% (n = 6), respectively, of those observed at 6.0 mM K+. Scatchard-type analysis of the data indicates increased sites for the binding and internalization of iodinated NGF by the cells. Similar enhancement was observed for cells treated with NGF as well. This voltage-dependent phenomenon was reversible, and also observed in the presence of veratridine. Moreover, withdrawal of extracellular Ca2+ abolished high K+-induced modulation of 125I-NGF binding and internalization, indicating that this effect may be mediated by Ca2+.
We report the long term results of the treatment of 23 intracranial ruptured aneurysms by coating. Twenty-three patients treated by coating were followed for a mean period of 11.2 years. The mean interval between the last hemorrhage and the operation was 22.4 days. Ten aneurysms underwent total coating, 9 with Biobond and 1 with Aron Alpha. Thirteen aneurysms underwent partial coating, 11 with Biobond and 2 with Aron Alpha. Six aneurysms were reinforced partially by other materials, but no aneurysm was wrapped totally with these materials. Rebleeding occurred in 6 patients, of whom 5 died. The mean interval between coating and rebleeding was 4 years. All patients suffering rebleeding had been treated with Biobond, and 3 patients had undergone total coating of aneurysms. The risk of recurrent hemorrhage after total coating with Biobond was 33%. One rebleeding patient underwent a second operation 10.5 years after total coating of the aneurysm. Biobond was found only at the tip of the aneurysmal sac. From these results, reinforcement of ruptured aneurysms with Biobond seems to be of little value, and a more reliable method must be developed for aneurysms that cannot be clipped.
Two-dimensional gel electrophoresis revealed two protein spots, a (molecular weight 70,000, pI 4.6) and b (molecular weight 69,000, pI 4.4) in PC-12 cells (rat pheochromocytoma cells). When the cells were induced to differentiate with nerve growth factor, the amount of protein in spot a, and later spot b increased with time, then the amount in both spots gradually decrease to undetectable level. These spots were not detected in adult rat brain nor in other cell lines of rat and mouse. Thus, these proteins can be used as markers to follow the differentiation of PC-12 cells.
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