Biomedical subjects
Publications and source records attributed to S Tsuji.
The "New Coccine Standard (C.I. 16255)" for the Dye Standard of the National Institute of Hygienic Sciences was prepared. The content of this Dye Standard determined by the titanium trichloride method was 97.5% on the average. The ultraviolet-visible absorption and infrared spectra of the Dye Standard were also measured.
The "Acid Red Standard (C.I. 45100)" for the Dye Standard of the National Institute of Hygienic Sciences was prepared. The content of this Dye Standard determined by the titanium trichloride method was 96.4% on the average. The ultraviolet-visible absorption and infrared spectra of the Dye Standard were also measured.
The "Indigo Carmine Standard (C.I. 73015)" for the Dye Standard of the National Institute of Hygienic Sciences was prepared. The content of this Dye Standard determined by the titanium trichloride method was 97.0% on the average. The ultraviolet-visible absorption and infrared spectra of the Dye Standard were also measured.
Explore the source record for details and available documents.
Genetic linkage studies of familial Alzheimer's disease (FAD) have suggested that some form of early-onset FAD is linked to proximal long arm of chromosome 21. It has been also suggested that some form of late-onset FAD is linked to long arm of chromosome 19. Goate et al have identified a mis-sense mutation (Val to Ile) in exon 17 of the amyloid precursor protein (APP) gene in 2 of 16 early-onset FAD families, and have shown that the FAD locus in an FAD family is tightly linked to the mis-sense mutation. To determine if the mis-sense mutation is observed in different ethnic origine, we have studied some early-onset FAD families. Two early-onset FAD families showed the existence of the mutation. As the mutation has been identified in different ethnic origine and the mutation has not been observed in normal individuals, it strengthen hypothesis that the mutation is pathogenic. Recently, Val to Phe and Val to Gly mutations have been also identified at the same codon (Codon 717) of the APP gene.
Using polymerase chain reaction (PCR), a rapid and highly sensitive method was developed for the diagnosis of tuberculous meningitis. The mycobacterium tuberculosis (M. tuberculosis) genome was detected in CSF of 5 of 6 patients with clinically diagnosed tuberculous meningitis, but not present in CSF from 10 patients with other types of meningitis and 10 normal controls. Furthermore, we detected M. tuberculosis in CSF of 2 of 24 patients with clinically possible tuberculous meningitis. This is highly useful method for the rapid diagnosis of tuberculous meningitis over other conventional method.
A 47-year-old woman with myasthenia gravis for last 11 years was admitted because of relapsed muscle weakness, hypermenorrhea and thrombocytopenia. Physical and neurological examinations revealed diplopia, proximal muscle weakness and purpuras on the left arm and bilateral legs. Repeated hematological examinations revealed cyclic fluctuation of platelet counts which spontaneously changed from the nadir levels of 12-27 x 10(3)/microliters to the peak levels of 150-400 x 10(3)/microliters. The platelet count reached a nadir at the onset of menstruation. Platelet-associated IgG (PAIgG) was within normal level when platelet count was at an increasing phase. Survival time of autologous platelets was normal when platelet count was at an increasing phase. Megakaryocytes in the bone marrow were apparently normal at the nadir phase. The patient's serum obtained at the nadir of platelet count significantly suppressed megakaryocyte colony forming unit (Meg-CFU) formation in comparison with that after the stabilization of platelet count, suggesting that this cyclic thrombocytopenia was secondary to cyclic hypoproduction of megakaryocytes caused by a suppressive factor. On the other hand muscle weakness showed no cyclic fluctuation. Administration of 60 mg/day prednisolone stabilized the platelet count at about 280 x 10(3)/microliters, abolished hypermenorrhea and gradually improved muscle weakness. These findings suggested autoimmune mechanism in the production of a Meg-CFU-suppressive factor might be involved in the pathogenesis of thrombocytopenia.
Explore the source record for details and available documents.
An A to G transition at nucleotide position 8,344 in tRNALys of mitochondrial DNA has been recently identified as a causative mutation of myoclonus epilepsy associated with ragged-red fibers (MERRF). To investigate if the degree of heteroplasmy of mitochondrial DNA is correlated with the severity of MERRF, we have developed a novel method for quantitation of the mutant mitochondrial DNA by polymerase chain reaction using a mismatched primer. With the method, populations of mutant mtDNAs from 5 cases of MERRF carrying the tRNALys mutation were analyzed. The tight linkage of the severity of symptoms and the degree of heteroplasmies is not necessarily observed for all cases, though there is a tendency that patients with less wild type mtDNAs show severer clinical symptoms and earlier onset.
We established a MAb N-25 reacted with a minor unknown antigen (AgX) in a commercially available GQ1b sample. It also recognized minor antigens in bovine brain (X-1, 2, 3, 4 and 5) and cultured neural cell lines (X-1). AgX is identical to X-5. X-5 is sialidase sensitive and has the common structure as X-1, which is resorcinol positive. These results suggested that novel gangliosides exist in bovine brain and neural cell lines.
Sialidase isolated from human placenta is associated with several proteins including acid beta-galactosidase, carboxypeptidase, N-acetyl-alpha-galactosaminidase, and others. These proteins are thought to form an aggregated complex during isolation of sialidase. One of the proteins of 60 kDa was recently identified by Potier et al. (Biochem. Biophys. Res. Comm. 173, 449-456, 1990) as a sialidase protein: this protein also cross-reacted with anti-prosaposin antibodies. We have isolated this protein and from the following evidence identified it as a heavy chain component of immunoglobulin G and not sialidase or a derivative of prosaposin. On gel filtration HPLC, sialidase activity and the 60 kDa protein were clearly separated from one another. The 60 kDa protein cross-reacted not only with antibodies raised against human saposins A, C, and D, but also with second antibody (goat anti-rabbit immunoglobulin G antibody) alone. This 60 kDa protein strongly cross-reacted with anti-human immunoglobulin G antibodies. The sequence of the initial 15 amino acids from the N-terminus of the 60 kDa protein was identical to the sequence of an immunoglobulin G heavy chain protein Tie (gamma 1).
High-resolution computed tomography (HR-CT) was performed on 20 patients with pyrophilitosis. Small nodular opacities in these patients could be divided by HR-CT into two types, namely, tiny irregular branching structures (TIB) and small round opacities (SRO). TIB had a centrilobular distribution and were characteristic of pyrophillitosis. SRO had both centrilobular and perilobular distributions and were considered to be changes modified by the aspiration of silica. Large opacities (LO) of pyrophillitosis were classified into three types, that is, spherical type, flat type parallel to the bronchus and flat type parallel to the thoracic wall. The spherical type was seen in patients exposed to both pyrophillite and silica, while the flat types were seen in patients exposed to only pyrophillite and were characteristic opacities of pyrophillitosis. Pulmonary emphysema was found in only one patient with pyrophillitosis, whereas mediastinal lymph node swelling and calcification were seen in most patients with pyrophillitosis. HR-CT is useful in making a more accurate evaluation of these lesions.
Explore the source record for details and available documents.
Expression of distamycin A-inducible rare fragile sites by AT-specific DNA-ligands was examined in lymphoblastoid cell lines derived from heterozygous carriers for the fra(8)(q24), fra(16)(p12), and fra(16)(q22) sites. The sensitivity of fragile site expression to the inducers was different at these fragile sites. The expression of fra(8)(q24) was induced markedly by Hoechst 33258, but not by distamycin A or berenil. An increased expression of fra(16)(p12) was found following treatment with Hoechst 33258 or berenil, but not with distamycin A. At fra(16)(q22), distamycin A markedly induced the fragile site, but Hoechst 33258 and berenil did not. Since their response to the different inducers was similar to that found in cultured lymphocytes, lymphoblastoid cell lines appear to retain their inherent properties. Although BrdUrd alone did not induce any fragile sites, concomitant treatment with BrdUrd plus the inducer was synergistically effective in inducing all the fragile sites. An increased frequency of sister chromatid exchanges was observed at fra(16)(p12) following simultaneous treatment with BrdUrd and berenil, mainly when the site was expressed as an isochromatid gap. Thus, the induced fra(16)(p12) site is a hot spot for the formation of sister chromatid exchanges, as found in other reported fragile sites.
Immunohistochemical localization of substance P (SP), CGRP, VIP, neuropeptide Y (NPY), and somatostatin (SOM) in the carotid labyrinth were compared in some species of amphibians using the peroxidase-antiperoxidase method. Immunoreactivity of SP, CGRP, VIP, and NPY was found in the nerve fibers distributed in the intervascular stroma of the carotid labyrinth. SP, CGRP, and VIP immunoreactive varicose fibers were densely distributed in the peripheral portion of the carotid labyrinth. Some SP-immunoreactive fibers were distributed similarly to CGRP-immunoreactive fibers. The density of NPY and SOM immunoreactive varicose fibers was low. No immunoreactivity of enkephalins was observed in the labyrinth. The intensities of these peptides were varied from species to species. No glomus cells showed immunoreactivity for any of the 7 peptides studied. These results suggest that the vascular regulatory function, which is one of the possible functions of the carotid labyrinth, is controlled by the peptidergic mechanisms in addition to regulation through intimate apposition of glomus and smooth muscle cells (g-s connection).
The effects of ethanol on gastric vasculature in isolated vascularly perfused rabbit stomach was investigated. The isolated stomach was perfused with Krebs-Henseleit solution containing 3% dextran bubbled with 95% O2 and 5% CO2 at a rate of 12 ml/min. After mixture and perfusion of 10 mM to 400 mM of ethanol, perfusion pressure and endothelin-1 concentration in effluent from gastric vasculature were measured. Perfusion pressure and endothelin-1 concentration in effluent increased in a dose-dependent manner with increasing ethanol concentrations. In conclusion, the data suggest that ethanol may stimulate the release of endothelin from gastric vasculature and may cause gastric ischemia due to vasoconstriction resulting in acute gastric mucosal injury.
Neurodegenerative diseases are characterized by neuronal degeneration of specific neurons, e.g., degeneration of motoneurons in amyotrophic lateral sclerosis. As an approach to understand molecular mechanisms of neuronal degeneration of human spinal cord motoneurons in various motor neuron diseases, we have constructed a human spinal cord cDNA library and developed a strategy for isolating spinal cord-specific genes by subtractive cloning. We constructed human spinal cord and brain cDNA libraries from postmortem human spinal cord and brain. To isolate human spinal cord-specific cDNAs, a spinal cord-enriched [32P]cDNA probe was generated by the phenol emulsion reassociation technique. Forty-eight cDNA clones out of 10,000 colonies gave strong signals with the subtracted probe, and individual spinal cord cDNA clones were isolated. Northern blotting analysis confirmed that two spinal cord cDNA clones are, in fact, more abundant in spinal cord compared to brain.
We studied the metabolism of radioactive fatty acids in cultured skin fibroblasts from patients with adrenoleukodystrophy (ALD) and Zellweger syndrome (ZS) to clarify the physiological significance of the fatty acid elongation system in the accumulation of very long chain fatty acids (VLFA) in ALD. A substantial amount of radioactive C26:0 was synthesized from [18-14C]stearic acid by ALD and ZS fibroblasts, whereas radioactive C26:0 was not detected in control fibroblasts. Kinetic studies demonstrated that the production of radioactive C24:0 and C26:0 in ALD fibroblasts is higher than that of ZS fibroblasts, which suggests that the fatty acid elongation activity plays an important role for the accumulation of VLFA in ALD, in addition to the decreased VLFA oxidation activities. The addition of monounsaturated fatty acids including oleic acid and erucic acid specifically lowered the formation rate of VLFA without any significant effect on degradation activities of VLFA both in ALD and control fibroblasts. The results suggest that the mechanism of decrease of VLFA by administration of monounsaturated fatty acids is based on the inhibition of fatty acid elongation activity.