[Binding of bilirubin to serum albumin in Crigler-Najjar syndrome, type I].
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Biomedical subjects
Publications and source records attributed to T Aoki.
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The stereostructure of the archaebacterial C40 diol has been established as (3R,7R,11R,15S,18S,22R,26R,30R)-3,7,11,15,18,22,26,30- octamethyldotriacontane-1,32-diol by stereorational total synthesis. This provides the final evidence necessary to establish the structure of an archaebacterial membrane substance that is a 72-membered-ring tetraether with 18 stereocenters.
A large sample of carriers of human T-lymphotropic retrovirus type I (HTLV-I) in Niigata Prefecture was examined for the detection of natural antibodies to HTLV-I-related antigens in sera using both indirect immunofluorescence microscopy (IFM) and enzyme-linked immunosorbent assay (ELISA). The present findings are based on multiple surveys, using each assay technique at least twice. Although Niigata Prefecture has been considered a non-endemic region for HTLV-I, Sado Island has been proven by this study to be a relatively endemic pocket within this non-endemic area. Seropositivity was highest in residents of Sado Island; 97/1, 117 (8.7%) by IFM and 33/1,061 (3.1%) by ELISA; followed by Niigata City, 18/650 (2.8%) by IFM and 16/638 (2.5%) by ELISA; and lowest in the remaining areas, 57/2,631 (2.2%) by IFM and 20/2,551 (0.8%) by ELISA. Seropositivity was demonstrated in 172/4,398 (3.9%) by IFM and 69/4,250 (1.6%) by ELISA in Niigata Prefecture taken as a whole. In general, the incidence of seropositive residents increased gradually with age. The sex difference was not significant. The serum samples tested were categorized into 4 groups; (1) IFM and ELISA both positive, (2) IFM positive but ELISA negative, (3) IFM negative but ELISA positive, and (4) IFM and ELISA both negative. By absorption tests, IFM and ELISA seemed to recognize different specific antibodies in sera; IFM recognized antibodies to HTLV-I-related cellular antigens in addition to HTLV-I viral antigens, but ELISA recognized antibodies to HTLV-I viral antigens alone. Thus, IFM detected a broader spectrum of antigens, resulting in recognition of more positive sera than those detected by ELISA.
Subcutaneous (s.c.) administration of compound 48/80 (3.0 mg/kg) to conscious rats produced a time-dependent long-lasting increase of plasma renin activity (PRA). A dose-related increase of the hematocrit was also observed after injection of compound 48/80. The onset of the hematocrit increase preceded that of PRA increase. Pretreatment with a dose of more than 20 mg/kg of histamine H1-receptor antagonists such as tripelennamine or diphenhydramine prior to the injection of compound 48/80 (3.0 mg/kg s.c.) attenuated or abolished the effects of compound 48/80 on PRA, hematocrit and plasma extravasation. Pretreatment with cimetidine (histamine H2-receptor antagonist, 40 mg/kg i.p.) had no effect on these plasma variables. The increase of PRA caused by s.c. administration of compound 48/80 was not affected by the pretreatment with propranolol (beta-adrenoceptor antagonist, 10 mg/kg i.p.), which completely inhibited the isoproterenol (0.5 mg/kg s.c.)-induced PRA increase. Administration of compound 48/80 did not induce a significant PRA increase in the nephrectomized rats although the increase of hematocrit following s.c. administration of compound 48/80 persisted despite the absence of kidneys. S.c. administration of compound 48/80 (3.0 mg/kg) led to a significant decrease of histamine content at the site of injection and to a significant increase in plasma histamine concentration without affecting arterial blood pressure. The present data suggest that s.c. administration of compound 48/80 stimulates the release of histamine from cutaneous mast cells, which cause an increase in vascular permeability to plasma protein via the stimulation of histamine H1-receptors, then leads to hypovolemia. The resulting hypovolemia may directly stimulate the juxtraglomerular cells of the kidney to release renin.
The effect of the anti-tumor, anti-glutamine drug acivicin, L-(alpha S,5S)-alpha-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid, was determined on the activity of the rate-limiting enzyme of de novo pyrimidine biosynthesis, carbamoyl-phosphate synthetase II (glutamine-hydrolyzing) (EC 6.3.5.5), in human colon carcinoma. The synthetase II activity in human colon carcinoma was elevated 2- to 3-fold over values of the normal colon mucosa, and the substrate kinetic constants were similar for the enzyme in normal and neoplastic colon. The Km for glutamine was 17 microM (colon carcinoma) and 23 microM (normal mucosa), whereas the Km for ATP was 2.1 and 1.7 mM in tumor and mucosa respectively. The synthetase II activity in colon carcinoma was inhibited to a similar extent by UMP, UDP and UTP (36-41%). The three uracil nucleotides were also equally effective in inhibiting the enzyme from normal mucosa (39-46%). Both enzymes were activated by PRPP (63 and 57%) in mucosa and carcinoma respectively. Acivicin in vitro selectively inactivated the glutamine-dependent synthetase II from human colon carcinoma, and it did not affect the ammonia-dependent activity. The acivicin inactivation constant (Kinact) was 100 microM, and the minimum inactivation half-time (T) was 0.7 min. Acivicin most likely exerts its effect against human colon synthetase II by acting as an active site directed affinity analogue of L-glutamine.
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In mechanically skinned fibers of the semitendinosus muscle of bullfrogs, we examined the role of membrane sulfhydryl groups on Ca2+ release from the sarcoplasmic reticulum (SR). Hg2+, a sulfhydryl reagent (20-100 microM), induced a repetitive contracture of skinned fibers, and this contracture did not occur in skinned fibers in which the SR had been disrupted by treatment with a detergent (Brij 58). Procaine (10 mM), Mg2+ (5 mM), or dithiothreitol (1 mM) blocked the Hg2+-induced contracture. Ag+ or p-chloromercuribenzenesulfonic acid produced similar contractures to that induced by Hg2+. We conclude that Hg2+ releases Ca2+ from SR of a skinned fiber by modifying sulfhydryl groups on the SR membrane, and suggest that the Ca2+ released by Hg2+ may trigger a greater release of Ca2+ from SR to develop tension.
We investigated the hypothesis that a persistent viral infection of the thymus gland might trigger the autoimmune disease myasthenia gravis (MG). Thymus glands of nine patients with recent onset of MG were studied by a variety of techniques to detect the presence of occult viruses. No evidence of viral infection was found.
An inventory form for the personality description based on the principle of the three traits theory for the work curve of the Uchida-Kraepelin psychodiagnostic test was investigated from the factor-analytic point of view. Three kinds of analyses were performed. First of all, the 66 items of the present form were administrated and a tentative orthogonal factor solution was obtained. Secondly, the 20 items for a simplified pattern in the sense of "simple structure" were selected based on the result of the first factor rotation, and the further orthogonal factor rotation was applied to the data based on the selected items so that the assumption for the three traits, primacy (A), variability (B), and, recency (C) were confirmed factor-analytically. Finally, in order to increase the number of items for providing an extended form for academic and practical use, more 10 items were added to the 20 items of the second analysis after applying the third orthogonal factor rotation so that the new form consisting of 30 items was obtained. Some relationships between the present work and the one of Eysenck and Eysenck (1968) were discussed.
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Sera from 50 Japanese hemophiliacs were screened for antibodies to human T-lymphotropic retrovirus types I and III (HTLV-I and -III). As a whole, antibody to HTLV-I, antibody to HTLV-III, and antibodies to HTLV-I and -III were detected in sera from 2, 17, and 6 hemophiliacs, respectively. Among them, two hemophiliacs developed acquired immunodeficiency syndrome who were positive for both antibodies to HTLV-I and -III in sera. All of the others were asymptomatic. Most of the blood products transfused into these hemophiliacs were imported from abroad, whence the source of HTLV-III infection presumably originated. However, since quite a high percentage of these antibody-positive hemophiliacs was positive for antibody to HTLV-I, even though they are native residents in HTLV-I nonendemic areas of Japan, some special factors may have participated in HTLV-I infection. These special factors should be investigated in the future.
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This paper describes a non-invasive mathematical method for estimating the locations and sizes of myocardial infarction using body surface electrocardiographic mappings. The inverse calculation is the theoretical basis of our method of estimation. First, the boundary integral equations were used to relate body surface and epicardial potential distributions. Next, a spherical harmonic expansion was used to solve the equations in order to obtain the epicardial potentials from the body surface potentials. The validity of the method was assessed by animal experiments and the clinical application. Body surface potentials were recorded using a 128 channel electrocardiographic mapping device equipped with a 16 bit microprocessor. In the animal study, the epicardial potentials were recorded by another potential mapping device simultaneously with body surface potential recordings. In the animal study, 60 epicardial electrodes and a freezing unit were mounted on a elastic fabric sack and attached to the heart. After completion of open chest surgery, freezing myocardial injury was incurred by perfusing -50 degrees C acetone-dry ice cryogen into the freezing unit. Twenty minutes after the start of freezing, ST elevations of the body surface and epicardial potentials were simultaneously recorded. An ST subtraction map was compiled as the difference between the maps before and after the myocardial freezing injury. Then, an inverse calculation was applied to the ST subtraction potentials to estimate the epicardial ST elevation. The geometric parameters of each electrode were determined from stereometry using two-dimensional X-ray images. In the clinical study, the body surface potentials of a patient with old myocardial infarction were recorded. The abnormal Q subtraction map was calculated as the difference between the measured and standard potentials of a normal subject. In the inverse calculation, the geometric shape of the heart and the body surface were determined from cross-sectional body images of computed tomography. The location of the infarction was estimated independently using coronary arteriography and left ventriculography. The results obtained were as follows: Experimentally, the estimated epicardial ST elevations correlated well with the measured ones. The area of estimated ST elevation included the portion of the myocardial injury produced by the freezing procedure, although the area estimated was relatively small compared with the actual one. Clinically, the estimated abnormal Q area correlated well with the area of the left anterior descending artery in which severe stenosis was detected by coronary arteriography.(ABSTRACT TRUNCATED AT 400 WORDS)
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