Single amino acid substitution in the V3 domain of CD4 is responsible for OKT4 epitope deficiency.
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Biomedical subjects
Publications and source records attributed to S Kishi.
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Three steroidal saponins 3, 4 and 5a were newly isolated from Anemarrhenae Rhizoma. Compounds 3 and 4 were identical with desgalactotigonin and F-gitonin, respectively. Compound 5a was established as (25S)-26-O-beta-D-glucopyranosyl-22-hydroxy-5 beta-furostane-3 beta,26-diol 3-O-beta-D-glucopyranosyl-(1----2)-O-beta-D-galactopyranoside on the basis of chemical and spectroscopic evidence.
Although it is well-known that Leu3a-epitope on CD4 molecule functions as a receptor for human immunodeficiency virus (HIV), the function of OKT4-epitope is still obscure. In order to learn the significance of OKT4-epitope, we performed immunological and functional studies on lymphocytes obtained from individuals with incomplete/complete OKT-4 epitope deficiency. Their lymphocytes did not show any abnormality in their susceptibility to HIV infection, the internalization of CD4 molecules by TPA-treatment, the capability of producing IL-2 in vitro or the expression of IL-2R (alpha/beta-chain) by PHA-stimulation. By flow cytometric analysis it was demonstrated that quantity of OKT4-epitopes in the incomplete deficiency was approximately one-half less than that of normal individuals. Coupled with this fact and DNA analysis previously reported, individuals with incomplete/complete OKT4-epitope deficiency were considered to be heterozygote and homozygote, respectively. These results led us to the conclusion that OKT4-epitope deficiency was inherited as an autosomal codominant trait. Individuals with complete OKT4-epitope deficiency were found in 7 cases out of 1486 random samples (0.47%), from which individuals with incomplete OKT4-epitope deficiency were estimated to account for 12.8%.
The patient was a 72-year-old woman who had advanced carcinoma of the stomach. She presented massive ascites due to peritonitis carcinomatosa. The cytology of ascites was class V and the CEA level of ascites was elevated. Since renal function was low, we injected 300 mg of carboplatin intraperitoneally 2 times in 8 weeks. The amount of ascites was significantly diminished and the CEA level of ascites was decreased. The result suggested the effectiveness of intraperitoneal injection of carboplatin for the therapy of peritoneal metastasis of gastric cancer.
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We examined the vitreous of 37 eyes of 31 patients with macular holes of various stages. There was no posterior vitreous detachment (PVD) in 18 of 18 impending and 19 of 20 newly formed macular holes. In newly formed macular holes, the operculum was located either at the level of or immediately anterior to the retinal surface. The gel component of the vitreous was always separated from the posterior fundus by intervening liquefied lacuna, simulating PVD. However, the cortical vitreous was located posterior to the liquefied lacuna and remained attached to the retina. PVD failed to develop in all of 15 eyes during the follow-up period of 3 months after formation of a macular hole. The incidence of PVD increased in the eyes with macular holes lasting for 1 year or longer. In our present series, PVD in its classical sense did not contribute to the pathogenesis of macular holes as it developed after formation of the latter. Instead, a subtle anterior displacement of vitreous cortex strictly confined to the area of the fovea seemed to trigger the development of idiopathic macular holes.
We examined the vitreous of 84 human autopsy eyes by biomicroscopy after staining the gel component with fluorescein and immersing the specimen in water. A noteworthy finding was the presence of a posterior precortical vitreous pocket that was basically located immediately anterior to the posterior fundus surrounded by the temporal vascular arcades. The posterior wall of the posterior precortical vitreous pocket was composed of a thin layer of vitreous cortex. The anterior border was contoured by the formed vitreous. The posterior precortical vitreous pocket seemed to expand or become confluent with adjacent lacunae in the vitreous. The posterior precortical vitreous pocket was present in all of 48 eyes with no or incomplete posterior vitreous detachment and in 19 of 36 eyes with posterior vitreous detachment. An oval-shaped defect of the premacular cortical vitreous was seen in 10 of 36 eyes with posterior vitreous detachment. The posterior precortical vitreous pocket was consistently present in front of the macula regardless of the type of vitreous liquefaction.
Human liver guanase was purified and a specific antibody against it was raised in rabbits. The antiserum formed a single precipitin line with human liver extract, and also completely inhibited the activity of the liver enzyme. An immunoblotting study showed that the antibody bound specifically to one band of protein with guanase activity and not to other proteins. Therefore, we concluded that this antiserum against the liver enzyme was suitable for use in immunohistochemical demonstration of guanase. In tissue sections, the immunohistochemical reaction with this antibody was positive in the same locations as the histochemical guanase reaction with DAB (3,3'-diaminobenzidine tetrahydrochloride).
Histochemical studies of human guanase (guanine deaminase) have seldom been undertaken, in part because of technical difficulties which result in heavy background staining. We reported a modified procedure for histochemical demonstration of guanase in human tissues involving hydrolytic deamination of the substrate guanine to xanthine via guanase, and then oxidation of xanthine to uric acid, with concomitant reduction of nitrotetrazolium blue (NBT). In this report, we describe a modification of this method for cytochemical demonstration of guanase at the fine structural level using yellow tetrazolium in place of NBT for determination of the intracellular distribution of guanase in human hepatocytes. In the hepatocytes, the reaction products were seen to be concentrated in the nucleus, in mitochondria, cisternae of the smooth and/or rough-surfaced endoplasmic reticulum, and lysosomes. The precise locations of the reaction product in the cisternae of the nuclear envelope, chromosomes, and nucleus could not be determined. However, the reaction products in the mitochondria were clearly seen to be located in the spaces of cristae. This information of the intracellular distribution of guanase in normal hepatocytes will be useful in determining the physiological role of this enzyme and in further studies on diseased hepatocytes including those in non-A non-B hepatitis.
We studied the effect of vitamin B complex (vitamin B1, B6 and B12 complex) on the immune responsiveness in gastric cancer patients who underwent surgery. The depression of blastogenic responses to both PHA and PWM was observed 2 weeks after surgery in half of the patients treated with Vitamedin but the degree was significantly less than that in the control patients without vitamin B treatment whose lymphocyte responses were depressed. Moreover, the blastogenic responses were induced by vitamin B administration 2 or 4 weeks after surgery in 5 of the 8 stage III-IV patients whose lymphocytes had not responded prior to surgery. Four weeks after surgery, the patients without vitamin B treatment showed only a tendency of recovery of their lymphocyte responses, whereas the recovery of blastogenic responses in the patients treated with vitamin B was significant. Essentially similar results were obtained with skin reactions to PHA and PPD. These results suggest that the administration of vitamin B1, B6 and B12 complex is useful for the protection against and the recovery of immune dysfunction produced by surgery in cancer patients.
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We performed a scanning electron microscopic observation of the posterior retinal surface of 59 autopsy eyes with spontaneous vitreous detachment. In 26 eyes (44%), there were remnants of the posterior vitreous membrane in the foveal area. These vitreous cortex remnants formed three basic patterns. They appeared either as disc-shaped collagenous membranes covering the fovea, as rings along the foveal margin, or forming a structure that resembles a cyst. Each of these patterns seemed to have a counterpart to various known clinical situations. These findings imply that remnants of the vitreous cortex membrane frequently remain attached to the fovea after apparent complete posterior vitreous detachment. The observed features would provide morphological basis for the interpretation of several clinical conditions that take place along the vitreoretinal interface at the fovea.
We examined the retinal surface of 28 autopsy eyes by scanning electron microscopy (SEM). Glialike cells or their processes, arranged in rows, were observed along retinal vessels in 22 eyes. Additionally, there were clusters of glialike cells over retinal vessels in 8 eyes. These proliferations ranged from focal to extensive ones, the latter resulting in distinct preretinal membranes. Focal defects of the superficial retina along the vessel were noted in 6 of 28 eyes. Transmission electron microscopic study in 2 surgically enucleated eyes with normal retinae revealed epivascular retinal degeneration and thinning of Müller cells. Glial processes appeared to be covering the defect of the internal limiting membrane and some projections of these cells continued inwards. These findings were consistent with the SEM findings of epivascular glialike structure. Our conclusions are that epivascular glialike structures and paravascular surface defects appear as a common finding in normal senile eyes, and that occasionally membranous formations arise from the epivascular area.
An elevated type of gastric ulcer scar (EUS) (A) was noted in 8 out of 227 ulcer patients treated with cimetidine. These were compared with 15 patients with EUS (B), not treated with cimetidine and the etiology of the lesion was discussed. The incidence of EUS (3.5%) and the average age of the patients were higher (61 years) in the A group than in the B group. The scar was seen all over the stomach in the A group. The period from detection of gastric ulcer to confirmation of EUS averaged 4 weeks, and there was no difference between the two groups. No difference was seen in the histological findings of elevated lesions either. In the A group, it appears that EUS was induced by rapid tissue regeneration due to the strong anti-ulcer effect of cimetidine in ulcer lesions, since it was noted in the regions where it had previously been considered unlikely to occur.