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T Katagiri

Publications and source records attributed to T Katagiri.

At least 19 recordsLinked to original sources
PubMed1992

Marked increase in cerebrospinal fluid ubiquitin in Creutzfeldt-Jakob disease.

We have established the radioimmunoassay for ubiquitin in the cerebrospinal fluid (CSF) and measured the ubiquitin concentration in CSF from 4 cases of neuropathologically verified Creutzfeldt-Jakob disease (CJD), 10 cases of multi-infarct dementia (MID), 7 cases of senile dementia of Alzheimer type (SDAT), and 18 controls. The normal values were determined to range from 7.3 to 21.0 ng/ml, 14.3 +/- 1.1 ng/ml in the mean +/- S.E.M. The CSF ubiquitin levels in the cases of MID and SDAT were 16.6 +/- 6.4 ng/ml and 21.3 +/- 6.1 ng/ml, respectively. In the cases of CJD, the CSF ubiquitin was markedly increased at the early and middle stages of the disease (230.6 ng/ml in Case 1, 107.6 ng/ml in Case 2, 212.5 ng/ml in Case 3, and 377.0 ng/ml in Case 4) and these gradually decreased as the disease progressed. The measurement of CSF ubiquitin seems useful to make an early diagnosis of CJD.

Aged↗
PubMed1992

Phosphorylation of multiple CD3 zeta tyrosine residues leads to formation of pp21 in vitro and in vivo. Structural changes upon T cell receptor stimulation.

T lymphocyte activation resulting from antigen recognition involves a protein tyrosine kinase pathway which triggers phosphorylation of several cellular substrates including the CD3 zeta subunit of the T cell receptor (TCR) to form pp21. The homologous TCR-associated protein, CD3 eta, is an alternatively spliced product of the same gene locus as CD3 zeta. CD3 eta lacks one of six cytoplasmic tyrosine residues (Tyr-132) found in CD3 zeta and is itself not phosphorylated. Site-directed mutagenesis in conjunction with in vitro and in vivo phosphorylation studies herein demonstrates that Tyr-132 is required for the formation of pp21. Moreover, the differential phosphorylation of CD3 zeta versus CD3 eta is not due to a selective association of the known TCR-associated protein tyrosine kinase, p59fyn; p59fyn but not p56lck or p62yes is associated with each of the three TCR isoforms containing CD3 zeta 2, or CD3 eta 2, or CD3 zeta-eta. This association occurs through components of the TCR complex distinct from CD3 zeta or CD3 eta. In addition, we show that pp21 formation is not only dependent on Tyr-132 but results from concomitant phosphorylation of other CD3 zeta residues including Tyr-121. Mutation of Tyr-90, -121, or -132 does not alter primary signal transduction as shown by the ability of individual CD3 zeta Tyr----Phe mutants to produce interleukin-2 upon TCR stimulation. Thus, the substantial structural changes in CD3 zeta upon TCR stimulation as reflected by alteration in its mobility in sodium dodecyl sulfate-polyacrylamide gel electrophoresis may affect subsequent events such as receptor desensitization, receptor movement, and/or protein associations.

Amino Acid Sequence↗
PubMed1992

Tetraparental mice reveal complex cellular interactions of the mutant, autoimmunity-inducing lpr gene.

Lpr is a murine recessive autosomal mutant gene that, in conjunction with the background genes of different inbred mouse strains, produces varied syndromes of lymphadenopathy and autoantibody production. We have investigated the cellular basis of the lpr determined phenomena by constructing allophenic (tetraparental) chimeras of MRL/Mp-lpr/lpr combined with C57BL/6 and MRL/+ combined with C57BL/6-lpr/lpr. The appearance of lymphadenopathy, lpr atypical T cells, and autoantibodies was found to depend on the relative amounts +/+ and lpr tissue. The failure of these three abnormalities to correlate in certain animals suggested different pathways of lpr gene action. Furthermore, in the lpr predominant animals, both the lymphadenopathy and autoantibodies were essentially entirely contributed by the lpr donor. The expression of the lpr gene within the same cells expressing the MRL or B6 background determined the pathologic and serologic manifestations characteristic of the disease of that lpr strain, despite the presence of +/+ cells of the other background in the same individual. The lpr syndrome thus depends on the intracellular interaction of the lpr and background genes, and on positive signalling between different lpr cell populations.

Animals↗
PubMed1992

Human glial fibrillary acidic protein (GFAP): molecular cloning of the complete cDNA sequence and chromosomal localization (chromosome 17) of the GFAP gene.

We isolated three glial fibrillary acidic protein (GFAP) cDNA clones from a glioma cell line, U-251 MG. One clone isolated from a U-251 MG cDNA library was long, but lacked both ends. Using poly(A)+ RNA and primers synthesized according to the sequence of this clone, we used the polymerase chain reaction-assisted rapid amplification of cDNA ends (PCR-RACE) method, which is a strategy to isolate cDNA ends, and obtained cDNA clones for the 5' and 3' ends. From the sequences of these overlapping clones, the complete nucleotide sequence of human GFAP cDNA was established. The start (ATG) and the stop (TGA) signals were seen at nucleotide positions 15 and 1311, respectively, and divided the entire sequence of 3027 bp into 14 bp of 5' non-coding, 1296 bp of coding and 1717 bp of 3' non-coding regions. Using cDNA probes made from both the coding and the 3' non-coding regions, Northern blot hybridization was performed with two different stringencies on RNAs from human and rodent brains and human GFAP-positive and -negative cells. It was shown that the 3' non-coding region probe was more specific for human GFAP than the coding region probe which was specific only under higher stringency conditions. This was also suggested by homology analysis of the sequence with those of various intermediate filament proteins. Based on these findings, we performed spot blot hybridization of sorted human chromosomes and Southern blot hybridization of PCR-amplified DNAs of a panel of hamster-human somatic cell hybrids and localized the human GFAP gene to chromosome 17.

Amino Acid Sequence↗
PubMed1992

Modulation of monocytic differentiation of HL-60 cells by inhibitors of protein tyrosine kinases.

We showed previously that the expressions of various src family protein tyrosine kinases (PTKs) were induced independently during the monocytic differentiation of HL-60 cells. The role of PTKs was further assessed in the present study by investigating the effects of PTK inhibitors on the differentiation. It was demonstrated that PTK inhibitors such as genistein and herbimycin A modulated monocytic differentiation of HL-60 cells; they inhibited the differentiation induced by TPA, while promoting that induced by vitamin D3 (D3). Immunoblotting analysis of protein molecules which had been phosphorylated on their tyrosine residues demonstrated that TPA induced phosphorylation of certain molecules different from those induced by D3 in HL-60 cells. PTK inhibitors blocked the phosphorylation and modulated differentiation driven by the inducers. These data suggest that PTKs are involved both promotively and suppressively in signaling events that induce monocytic differentiation of HL-60 cells.

Antibiotics, Antineoplastic↗
PubMed1992

Structure and expression of human and rat D2 dopamine receptor genes.

D2 dopamine receptor may be related with the pathogenesis of Parkinson's disease and schizophrenia. Furthermore, the antipsychotic drugs have high affinity for D2 dopamine receptor. We carried out the cloning of the genomic DNA for human D2 dopamine receptor and clarified the structure of this gene. Our isolated gene spans about 15 kbp and consists of seven exons interrupted by six introns. However, putative first exon was not yet identified. Spot blot hybridization analysis of cell sorter fractionated human chromosomal DNA with D2 receptor genomic DNA revealed the localization of this gene in the chromosome 11 fraction. We analyzed human genomic DNA by Southern blot hybridization with D2 dopamine receptor genomic DNA as a probe, but so far we could not find RFLP. Northern blot analyses of brain RNA of several animals and rat brain RNA after various treatments were carried out. Developmental changes of D2 dopamine receptor mRNA were observed in the rat brains.

Aging↗
PubMed1992

Tumor-specific T cell lines: capacity to proliferate and produce interleukin 2 in response to various forms of tumor antigens.

Anti-tumor proliferative T cell lines were established from cultures of lymph node cells from BALB/c mice immunized to syngeneic CSA1M fibrosarcoma with the CSA1M tumor cell membrane. The cultures were maintained throughout in the absence of exogenous interleukin 2 (IL2). Cell surface phenotypes of all T cell lines established were Thy-1+, Ig-, L3T4+ and Lyt-2-. Their proliferation was induced in a tumor antigen dose-dependent fashion and a tumor antigen-specific way. Such proliferative responses were inhibited by the addition to cultures of anti-class II H-2d (anti-I-Ad) or anti-L3T4 but not of anti-class I H-2d or anti-Lyt-2 monoclonal antibody. None of the T cell lines exhibited any cytotoxic T lymphocyte activity but they all produced IL2 upon stimulation with CSA1M tumor antigens, indicating that they represent helper-type T cell (Th) lines. The activation of these tumor-specific Th lines was induced with either CSA1M tumor cells themselves, or their membrane or detergent-solubilized fraction depending on the presence of antigen-presenting cells (APC). Most importantly, activation was also inducible by membranous tumor antigen-pulsed APC, which were capable of producing potent anti-tumor protective immunity when administered in vivo into syngeneic BALB/c mice. These results indicate that the tumor-specific Th lines established here can be activated with various forms of tumor antigens for their expression of helper function. Since Th lines of this type have not been described previously, our Th lines provide an intriguing tool for investigating the cellular and molecular mechanisms by which tumor-specific Th recognize tumor antigens.

Animals↗
PubMed1992

The binding of basic fibroblast growth factor to ischaemic neurons in the rat.

Transient occlusion of the right middle cerebral artery for 15 min produced a small ischaemic lesion in the dorsal portion of the right striatum in rats as seen on days 3, 7 and 14 post-operatively. The lesions consisted mainly of reactive astrocytes and 'ischaemic neuron's with chromatin-condensed (pyknotic) nuclei and homogenously eosinophilic cytoplasm. The incubation of tissue sections with basic fibroblast growth factor (bFGF) followed by anti-bFGF, or with biotinylated bFGF without anti-bFGF, labelled virtually all ischaemic neurons, indicating that bFGF had bound to the latter. The pretreatment of sections with heparitinase prevented the binding of bFGF to these cells, suggesting that the chemical substrate for the bFGF binding was heparan sulphate. In light of the findings that many normal-looking neurons were observed in the corresponding portion of the right striatum in most rats on post-operative days 28 and 90, the appearance of bFGF-binding sites in ischaemic neurons may contribute to the repair process of injured neurons.

Animals↗
PubMed1992

Study on reperfusion injury on sarcoplasmic reticulum in acute myocardial ischemia.

Reperfusion injury in early myocardial ischemia was studied in the dog with special reference to sarcoplasmic reticulum (SR) and contraction bands. Acute myocardial ischemia (I) was induced by occlusion of the left anterior descending coronary artery (LAD) for 10, 20 and 30 min followed by reperfusion for 15 min (R). Ca(++)-ATPase activity of SR in 10-min-R-Group was significantly reduced to 60% of control activity, but activity of 10-min-I-Group remained near the control level in subendomyocardium (Endo). ATPase activity in 30-min-I-Group diminished to 60% of control activity in Endo and it was similar for 30-min-R-Group. In ischemic myocardium, composition of major ATPase protein decreased significantly in 30-min-I-Group and similar reduction was observed in 20-min-R-Group in Endo. In morphology proportion of appearance of contraction bands in Endo was significantly increased in 20-min or longer-R-Groups. These results suggest that reperfusion injury is likely to occur when coronary artery is reflowed after 10 min of ischemia. This may be caused by increased intracellular Ca++ at a very early stage of reperfusion period, and reperfusion injury may be induced due to acceleration in the necrotic process of the membrane system in the myocytes during ischemia.

Animals↗
PubMed1992

Impairment of sarcolemmal permeability in the acute ischemic myocardium--a study with ionic lanthanum probe method.

Impairment of sarcolemmal permeability after the initiation of acute ischemic myocardial injury was studied using an ionic lanthanum (La3+) probe in electron microscopy. Acute ischemic myocardium was induced by ligation of the left anterior descending coronary artery in dogs. In normal cardiac myocytes La is localized exclusively in the extracellular space. i.e. on the glycocalyx, in the T-system and in intercalated discs, with normal fine structures. In ischemic myocardial cells, La deposits were found in the cytosolic space in 22% of subendocardial cells with mild to moderate, but non-necrotic, fine structural changes as early as 30 min. The number of myocytes with La deposition increased with advancing ischemic injury, and necrotic fine structural changes were recognized following ischemia for 60 min. These results indicate that deposition of La occurs before the appearance of irreversible morphologic alterations in ischemic myocardial cells, and suggest an increased permeability of the sarcolemma for Ca2+ and the development of degradation of plasma membrane integrity.

Animals↗
PubMed1992

[A clinical study of postinfarction angina (PIA): the significance of electrocardiographic ST segment changes during anginal attacks].

We studied the clinical significance of electrocardiographic ST segment changes during PIA attacks. Of 478 AMI patients admitted to the CCU of our hospital within 48 hours after onset, we evaluated 73 (15.3%) with PIA. According to electrocardiographic ST segment changes during PIA attacks, the patients were divided into three groups, namely ST elevation at the same infarction site (same site elevation group), ST depression at the same site (same site depression group), and ST depression at other sites (other site depression group), and their pathological condition was studied. There were 33 patients (45.2%) in the same site elevation group, 19 (26.0%) in the same site depression group, and 21 (28.8%) in the other site depression group. The predominant infarction areas were anteroseptal and inferior wall in the same site elevation group, NTMI in the same site depression group, and inferior wall in the other site depression group. PIA usually occurred within 4 days after the onset of infarction in the same site elevation group, and within 5-7 days in the other site depression group, but no uniform trend was observed in the same site depression group. With respect to the number of vessels showing disease, cases of single-vessel disease tended to predominate in the same site elevation group, while cases of three-vessel disease tended to predominate in the same site depression group and the other site depression group. Stenosis rates in the vessels responsible for infarction were high in the same site elevation group in the acute period. Prognoses were poorest in the same site depression group.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1992

[A case of adult onset hypophosphatemic vitamin D resistant osteomalacia].

A case of adult onset hypophosphatemic vitamin D resistant osteomalacia is described. A 40-year-old female who complained of thorax and lumbar pain and gait disturbance was admitted to our hospital on 7 November, 1988. The patient had hypophosphatemia with normal plasma calcium, parathyroid hormone and 25-hydroxy vitamin D3 concentrations, but had decreased tubular reabsorption of phosphate and decreased plasma 1, 25-dihydroxy vitamin D3 concentrations. The iliac crest bone biopsy showed osteomalacic changes. The 99mTc-MDP bone scintigram showed evidence of increased bone turnover with raised plasma alkaline phosphatase concentrations. After treatment with oral 1 alpha-hydroxy vitamin D3 (3-6 micrograms/day) and intravenous or oral phosphate supplement (0.47-1.74g/day), the subjective and clinical findings improved.

Adult↗
PubMed1992

[The dysfunction of human peripheral blood dendritic cells on concanavalin A-induced T cell responses in patients with systemic lupus erythematosus].

The accessory cell (AC) functions of peripheral blood dendritic cells (PDC) in concanavalin A (Con A)-induced T cell proliferation were investigated in patients with systemic lupus erythematosus (SLE). In Con A-induced T cell proliferation using added autologous PDC, AC activity was present in SLE patients (p less than 0.01). The Con A-induced T cell proliferation, however, was significantly lower in SLE patients than in normal subjects (p less than 0.01), and the level of decrease became greater with increased activity of the disease (p less than 0.01). In investigating the Con A-induced T cell proliferation using added allogeneic PDC, we compared T cells from SLE patients + PDC from normal subjects or T cells from normal subjects + PDC from SLE patients with T cells + allogeneic PDC both from normal subjects. The former two combinations showed significantly reduced T cell proliferation in active SLE (p less than 0.01 for each), while no significant differences were found for inactive SLE. The above results suggest that the reduced function of PDC as AC may be involved in reduced Con A-induced T cell proliferation in patients with active SLE.

Adult↗
PubMed1992

[A case of sarcoidosis associated with Sjögren's syndrome].

A 49-year-old woman, who has had a past history of Raynaud's phenomenon since 1981, dry mouth since 1987 and dry eyes since 1990, was admitted to our hospital complaining of general fatigue, bilateral gonalgia, and shortness of breath in April 1991. Physical examinations revealed bilateral parotid gland enlargement and bilateral uveitis. Her family history included mixed connective tissue disease in her eldest daughter. Laboratory findings indicated an elevated erythrocyte sedimentation rate, hypergammaglobulinemia, and elevation of serum lysozyme and angiotensin converting enzyme levels. Antinuclear antibodies, anti-SSA antibodies, anti-SSB antibodies were positive, while tuberculin test was negative. Chest X-rays showed bilateral hilar lymphadenopathy and small nodular shadows in both lung fields. Increases in lymphocytes and the CD4/CD8 ratio of T cells were noted in alveolar lavage fluid. Renal biopsy revealed non-caseous granulomas. Other remarkable findings included positive Schirmer's test, apple tree lesions by sialography and chronic sialoadenitis by biopsy of the labial minor salivary gland. On the basis of all these findings, we diagnosed her as suffering from sarcoidosis with Sjögren's syndrome. After oral administration of prednisolone, her shortness of breath, hilar lymphadenopathy and small nodular shadows in the lung field disappeared, but the patient was transferred to the department of urology due to the onset of hydronephrosis. This case is noteworthy because sarcoidosis associated with Sjögren's syndrome has been reported in only 11 cases in the literature.

CD4-CD8 Ratio↗
PubMed1992

Nephritogenicity of the lprcg gene on the MRL background.

The novel lymphoproliferative and autoimmune lprcg gene, originally discovered in the CBA/K1Jms (CBA) strain of mice, was transferred onto the MRL/MpJ (MRL) strain background, and the resultant partially congenic MRL-lprcg/lprcg carrying 93% or more MRL genomes on average were examined for immune-complex glomerulonephritis and serological aberrations. Ordinary histological studies revealed that MRL-lprcg/lprcg mice developed glomerulonephritis histologically indistinguishable from that in MRL-lpr/lpr but at a lower frequency than in MRL-lpr/lpr mice. Glomerular immune complex deposition was almost the same in MRL-lprcg/lprcg and MRL-lpr/lpr mice. The levels of serum Ig, circulating immune complexes and autoantibodies in MRL-lprcg/lprcg were comparable to or even higher than those in MRL-lpr/lpr mice. Comparison of the serological abnormalities between MRL-lprcg/lprcg with glomerulonephritis and CBA-lprcg/lprcg without it evidenced the enhanced class switch from IgM to IgG responses in both class-specific autoantibody responses and serum Ig levels in MRL-lprcg/lprcg as in MRL-lpr/lpr mice. These results taken together indicate that the lprcg gene functions in much the same manner as lpr in induction of glomerulonephritis and serological abnormalities on the MRL background as expected from the allelism between the two mutant genes.

Animals↗
PubMed1992

A crucial role of the thymus in induction by the lprcg gene of lymphadenopathy with autoimmunity in the mouse.

The new mutation at the lpr locus, lprcg, induces massive lymphoproliferation characterized by the selective expansion of CD4-, CD8-, B220+, Thy-1+ cells or double-negative T lymphocytes and production of autoantibodies as does lpr. The thymus is necessary for the induction of anomalous double-negative T lymphocytes and autoimmune symptoms by lpr. To determine whether or not the thymus is also indispensable to expression of the function of lrpcg, lprcg homozygous athymic nude mice (lprcg/lprcg nu/nu; lprcg nudes) were constructed by crossing CBA/KlJms-lprcg/lprcg (CBA-lprcg) and DDD/l-nu/nu mice and observed for lymphoid organ hyperplasia and autoantibody production with or without thymus grafts from various strains of mice including CBA-lprcg. Neither lymphoproliferation nor significantly increased production of autoantibodies was observed in unmanipulated lprcg nudes. In contrast, thymus grafts of both +/+ and lprcg/lprcg genotypes caused lymphoid organ hyperplasia composed of anomalous double-negative T lymphocytes and significantly augmented the production of antibodies against single-stranded DNA (ssDNA). Interestingly, serum Ig and anti-ssDNA antibody levels rose in response to thymus grafts only in IgG but not in IgM classes. These results indicate that the thymus plays a crucial role in the induction of abnormal T-cell differentiation by lprcg and that thymic genotype is irrelevant.

Animals↗
PubMed1991

Calcitonin gene-related peptide immunoreactivity in familial amyotrophic lateral sclerosis.

The lumbar cords from 3 cases of familial amyotrophic lateral sclerosis (fALS), one case of vincristine neuropathy, and two control cases were examined with an antiserum to calcitonin gene-related peptide (CGRP). The anti-CGRP intensely labelled the spinal posterior horns in all cases. In the anterior horns, several perikarya and cord-like neuritic swellings, mostly axons, were labelled with the antibody in the fALS cases, whereas CGRP-positive structures were extremely rare in the cases other than fALS. It is possible that the accumulation of CGRP in the proximal axonal swellings and perikarya may result from entrapment of CGRP during the anterograde axonal transport, causing loss of, or decrease in, CGRP at the neuromuscular junction and producing weakness and atrophy of the muscles.

Adult↗