[Trans-catheter diagnosis].
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Cardiac Catheterization↗
Biomedical subjects
T Katagiri
Publications and source records attributed to T Katagiri.
[A case of cervical spondylitis mimicking motor neuron disease].
The patient was a 65-year-old man who had noted mild weakness of the right hand since summer, 1990. In October, 1990, he had fever and developed apparent weakness of the upper extremities. Neurological examination on admission revealed distal dominant muscle weakness and atrophy of the upper extremities with fasciculation. Deep tendon reflexes were diminished in the upper limbs and exaggerated in the lower ones. No sensory disturbance or cerebellar signs were recognized. Laboratory examination of his blood showed leukocytosis and elevated levels of acute reactants. The needle EMG showed a neurogenic pattern. MRI study of the neck disclosed narrowing of the intervertebral space between C7 and Th1 and a low signal intensity of these vertebral bodies on T1 weighted image. Treatment with antibiotics improved his neurological symptoms and the abnormal MRI findings. The present case was diagnosed as having cervical spondylitis. Neurological symptoms and signs associated with cervical spondylitis have been reported to be paraplegia or quadriplegia. Like the present case, however, cervical spondylitis should also be considered as one of the diseases which could show symptoms and signs very similar to those of motor neuron disease.
Aged↗
Induction of CD45 isoform switch in murine B cells by antigen receptor stimulation and by phorbol myristate acetate and ionomycin.
In this study, we examined whether CD45 isoform can be switched in murine mature B cells and what signals are responsible for the process. Stimulation of murine splenic B cells with lipopolysaccharide did not reduce the expression of CD45RA-, B-, and C-exon-dependent epitopes or a CD45 common epitope, but rather enhanced the expression. Stimulation with goat antimouse IgM antibody did not significantly reduce CD45 expression but caused a partial reduction in the expression of CD45RA-, B-, and C-exon-dependent epitopes. Phorbol myristate acetate (PMA) alone did not significantly alter the expression of CD45 but the combination of PMA and ionomycin induced a strong reduction in the expression of CD45RA-, B-, and C-exon-dependent epitopes without affecting the level of CD45 common epitope expression. Reverse transcription and polymerase chain reaction analysis demonstrated that CD45 isoform switch induced by anti-IgM or PMA plus ionomycin is indeed mediated by alternative splicing of A-, B-, and C-exon-derived mRNA. These results suggest that CD45 isoform of murine mature B cells can be switched by antigen receptor-mediated signals, and the process seems to be regulated at least in part by protein kinase C activation and mobilization of calcium ions.
Alternative Splicing↗
Distinctive expression of lprcg in the heterozygous state on different genetic backgrounds.
Much knowledge of the etiopathogenesis of human autoimmune diseases has been obtained from the mutant mouse models carrying lpr and gld. These autoimmune genes have been regarded as autosomal recessive. The novel lymphoproliferative and autoimmune mutation lprcg is unique in its interaction with gld despite their different chromosomal locations: chromosomes 19 and 1, respectively. Both lprcg and lpr mutations are shown to be the defects in the Fas antigen gene that controls apoptosis. Evidence has been provided for the partial expression of lpr in the heterozygous state and the significant influences of background genes on lpr-induced autoimmune disorders. To investigate the expression of the heterozygous lprcg and the effects of background genes on it, anatomical, serological, and pathological manifestations were compared among lprcg/lprcg,lprcg/+, and +/+ mice on both MRL/MpJ (MRL) and CBA/KlJms (CBA) backgrounds. On the MRL background, lymph nodes (LN) and spleens of lprcg/+ were significantly larger in weight than those of +/+, but far lower than those of lprcg/lprcg mice. In accord with this, these lprcg/+ mice had intermediate levels of anti-single-stranded DNA antibodies, circulating immune complexes, and serum Igs between those of lprcg/lprcg and +/+ mice and were similar to lprcg/lprcg mice in severity of glomerulonephritis. However, accumulation of anomalous CD4-8- T cells characteristic of the lpr disease was not proved in the enlarged lprcg/+ LN. On the CBA background, the LN and spleen weight increases in lprcg/+ were statistically significant compared to +/+ mice but were minimal, being regarded as clinically insignificant. In support of this, lprcg/+ mice were not different from +/+ mice in any of the serological and pathological parameters examined. The results clearly demonstrate that the lprcg gene can function to induce autoimmune disorders in the heterozygous state on the MRL but not on the CBA background.
Animals↗
Tyrosine-phosphorylation of tubulin during monocytic differentiation of HL-60 cells.
We have demonstrated that the 53- and 55-kDa proteins were markedly phosphorylated at tyrosine residues during tetradecanoyl phorbol acetate (TPA)-induced monocytic differentiation of HL-60 cells and that the inhibition of such phosphorylation resulted in suppression of the differentiation. Western blotting, using antiphosphotyrosine antibody PY-20, of antitubulin immunoprecipitate from the lysate of TPA-treated HL-60 cells revealed that tubulin was tyrosine-phosphorylated in TPA-treated HL-60 cells, but not in nontreated HL-60 cells. The tyrosine-phosphorylated 53- and 55-kDa proteins in TPA-treated HL-60 cells were absorbed with antitubulin antibody indicating that the predominantly tyrosine-phosphorylated proteins during the monocytic differentiation were tubulins. By combination of immunoprecipitation and in vitro kinase assay, the protein tyrosine kinases, Fyn and Lyn, which were abundantly induced during monocytic differentiation of HL-60 cells, were demonstrated to be associated with tubulin in the cells. The reorganization of microtubules was observed by immunostaining using rhodamine-conjugated anti-mouse Ig and mouse anti-alpha-tubulin mAb. These data suggest that tyrosine-phosphorylation of tubulin, in which Fyn and Lyn might involve, regulate monocytic differentiation through alteration of microtubule assembly.
Cell Differentiation↗
Heparin sulfate-like immunoreactivity in the spinal cord in motor neuron disease.
The spinal cords from eight autopsy cases of sporadic motor neuron disease (MND) and two control cases were immunohistochemically examined using antibodies directed to neurofilament proteins (anti-Nf) and to heparan sulfate (HepSS-1). Variable numbers of spheroids were observed in the anterior horns in the MND cases. In one case of MND, one third to half of the remaining anterior horn cells contained conglomerate inclusions in their perikarya. These pathological structures were not encountered in the control cases. The immunohistochemical study revealed that both anti-Nf and HepSS-1 intensely labelled all spheroids and conglomerate inclusions in the MND cases. The colocalization of heparan sulfate with neurofilamentous accumulation suggests that heparan sulfate is required for the aggregation of neurofilaments, resulting in the formation of spheroids and conglomerate inclusions in MND.
Aged↗
Macrophages release melanocyte dendrite extension factor in response to ultra-violet ray.
Mammalian melanocytes in epidermis extend their dendrites in response to UV ray in vivo in addition to proliferation and pigmentation. We found that cultured macrophages exert a factor in response to UV irradiation and that this factor induces the extension of dendrites of melanocyte. We designated this factor as dendrite extension factor (DEF) and characterized it as a protein. Our results indicate that the molecular weight of DEF is 30,000-100,000 and that it is heat-labile. Macrophages release DEF through transcription and translation. DEF seems to be a novel factor that enhances melanogenesis by UV irradiation.
Amanitins↗
Neuron-specific enolase (NSE) and non-neuronal enolase (NNE) mRNAs are co-expressed in neurons of the rat cerebellum: in situ hybridization histochemistry.
Using in situ hybridization histochemistry, we analysed the localization of mRNAs for neuron-specific enolase (NSE) and non-neuronal enolase (NNE) in the rat cerebellum at various postnatal developmental stages. Synthetic 45 meric oligonucleotides corresponding to partial sequences of the non-coding region of rat NSE or NNE mRNA were 35S-labeled to approximately the same specific activity and used as hybridization probes. On examination of the adult rat cerebellum, both NSE and NNE signals were detected in all identified and presumed neurons which included Purkinje cells, internal granule cells and presumed stellate/basket cells in the cerebellar cortex and neurons of the dentate nucleus. Examination of the cerebellum during postnatal development also revealed coexistence of NSE and NNE signals in these neurons from early stages. During development, both signals coincidentally increased in Purkinje cells and neurons of the dentate nucleus, while only NSE signals showed a gradual increase in the internal granule cells in which NNE signals remained at the same level from early postnatal to adult stages. The external granule cells showed NNE signals until postnatal day 7 but thereafter the signals became less distinct, especially in cells if the inner zone of the external granule cell layer. Thus, it was shown that NSE and NNE were commonly coexpressed at the mRNA level in various neurons of the cerebellum except for very undifferentiated external granule cells which expressed only NNE mRNA.
Aging↗
A novel metalloprotease/disintegrin-like gene at 17q21.3 is somatically rearranged in two primary breast cancers.
From chromosomal region 17q21.3, where a tumour suppressor gene(s) for breast and ovarian cancers is thought to be present, we have isolated a novel gene from a cosmid clone that revealed somatic rearrangements in two breast cancers. The gene (MDC) encodes a 524-amino acid metalloprotease-like, disintegrin-like and cysteine-rich protein with sequence similarity to members of the snake-venom metalloprotease/disintegrin family and guinea-pig sperm-surface protein PH-30. These proteins have been implicated in cell-cell or cell-extracellular matrix interactions. Rearrangements in both tumours involve multiple exons and disrupt the coding region of the new MDC.
Amino Acid Sequence↗
Chromosomal assignment of the gene for protein tyrosine phosphatase HPTP delta.
Protein tyrosine phosphatase (PTP) negatively regulates the effect of protein tyrosine kinases and is implicated in the regulation of a variety of biological phenomena such as cell activation, differentiation and neoplastic transformation. To gain insight into the role of PTPs, we cloned the human receptor-type PTP gene and assigned the chromosome harboring the gene for HPTP delta by using DNAs from human-mouse hybrid cell lines and by fluorescence in situ hybridization. The results clearly demonstrated that HPTP delta gene maps to human chromosome 9p24.
Animals↗
Transforming growth factor-beta (TGF-beta)-mediated immunosuppression in the tumor-bearing state: enhanced production of TGF-beta and a progressive increase in TGF-beta susceptibility of anti-tumor CD4+ T cell function.
The present study deals with the effect of transforming growth factor-beta (TGF-beta) on anti-tumor immune responsiveness at various stages of the tumor-bearing state. Spleen cells from BALB/c mice bearing a syngeneic tumor (CSA1M) 1-3 wk after inoculation with CSA1M cells produced interleukin-2 (IL-2) and macrophage-activating factor (MAF)/interferon-gamma (IFN-gamma) upon in vitro culture without addition of exogenous tumor antigens. This lymphokine production was achieved through collaboration between anti-CSA1M CD4+ T cells and antigen-presenting cells that had been pulsed with CSA1M tumor antigens in vivo in the tumor-bearing state. The IL-2-producing capacity of CD4+ T cells reached the maximal level as early as one week after tumor implantation but decreased with the progress of tumor-bearing stages. In contrast, the capacity of CD4+ T cells to produce MAF/IFN-gamma was not affected but was maintained at high levels even late in the tumor-bearing state. The addition of recombinant TGF-beta (rTGF-beta) to cultures of spleen cells from various tumor-bearing stages resulted in the suppression of lymphokine production. However, the magnitude of the TGF-beta-induced suppression varied depending on which tumor-bearing stages of splenic cells were tested as a responding cell population; it was slight in cells from early (1-3 wk) tumor-bearing stages but increased in cells from donor mice at later tumor-bearing stages. Thus, spleen cells from late tumor-bearing stages with weak but significant IL-2-producing and considerable MAF/IFN-gamma producing capacities failed to produce these lymphokines when rTGF-beta was present in cultures. A progressive increase in the TGF-beta susceptibility was also observed for IL-4-producing Th2 as well as IL-2/MAF-producing Th1 cells. In addition, increased levels of TGF-beta were detected in plasma from tumor-bearing mice at late stages. Taken together, these results indicate that tumor-bearing mice exhibit enhanced production of TGF-beta as well as a progressive increase in the susceptibility of anti-tumor CD4+ T cells to TGF-beta-induced suppressive mechanisms.
Animals↗
MPTP delta, a putative murine homolog of HPTP delta, is expressed in specialized regions of the brain and in the B-cell lineage.
Protein tyrosine phosphatases (PTPs), together with protein tyrosine kinases (PTKs), are involved in the regulation of cell activation, growth, and differentiation. To further elucidate the fine tuning of cell growth and differentiation through tyrosine phosphorylation, we tried to isolate mouse receptor-type PTP (RPTP) cDNA clones by screening mouse brain cDNA libraries with mouse CD45 PTP domain probes under reduced-stringency conditions. Characterization of isolated cDNA clones for RPTP showed that the cytoplasmic region contains two tandem repeats of PTP domain of about 230 amino acids with intrinsic phosphatase activity. The extracellular region was composed of immunoglobulin (Ig)-like domains and fibronectin type III (FN-III)-like domains. The gene was highly homologous to human PTP delta (HPTP delta) and thus was named MPTP delta (murine counterpart of HPTP delta). The MPTP delta gene appeared to generate at least three species of mRNA, which differ in the composition of the extracellular domain: type A, one Ig-like and four FN-III-like domains; type B, one Ig-like and eight FN-III-like domains; and type C, three Ig-like and eight FN-III-like domains. Interestingly, the 5' untranslated region and the leader peptide of types A and B were completely different from those of type C. Northern (RNA) blot analysis demonstrated that brain, kidney, and heart cells express three mRNA species of about 7 kb. Antibody directed against part of the extracellular domain of type A MPTP delta recognized a 210-kDa protein in brain and kidney lysates. In situ hybridization of brain samples revealed that MPTP delta mRNA is present in the hippocampus, thalamic reticular nucleus, and piriform cortex, where some Src family PTKs have been also demonstrated to exist. Although MPTP delta mRNA was not detected in lymphoid tissues, all of the pre-B-cell lines tested and one of three B-cell lines tested expressed MPTP delta mRNA, whereas antibody-producing B-cell hybridomas and T-cell and macrophage lines did not. Finally, the MPTP delta locus was tightly linked to the brown (b) locus on mouse chromosome 4.
Amino Acid Sequence↗
The biological roles of the third component of complement in osteoclast formation.
We previously reported that 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25-(OH)2D3] tissue-specifically stimulated the production of the third component of complement (C3) in bone in vitro and in vivo. In the present study, we examined the possible roles of C3 in bone using bone marrow cultures with antibodies against C3 and C3 receptors (Mac 1, 8C12, and 7G6) and the purified mouse C3 protein. The C3 protein produced preferentially by stromal cells in response to 1 alpha,25-(OH)2D3 was distributed in macrophage-like mononuclear cells and small cells with few nuclei. Adding anti-C3 antibody together with 1 alpha,25-(OH)2D3 to bone marrow cultures greatly inhibited not only the appearance of tartrate-resistant acid phosphatase (TRAP)-positive mononuclear and multinucleated cells, but also the growth of macrophage-like mononuclear cells and stromal cells. The inhibitory effect of anti-C3 antibody on osteoclast-like cell formation was most prominent when it was added between days 2-4 of the 6-day culture period, which corresponded to the late proliferative phase and the early differentiation phase of osteoclast development. Adding anti-C3 receptor antibodies also inhibited osteoclast-like cell formation induced by 1 alpha,25-(OH)2D3. When C3 receptors were detected by the binding of C3-coated sheep red blood cells or immunostaining, the localization of C3 receptor-positive cells coincided exactly with that of C3 protein-positive cells. C3 receptors were expressed mainly in macrophage-like mononuclear cells, TRAP-positive mononuclear cells, and TRAP-positive small cells with few nuclei. TRAP-positive large cells with many nuclei were totally negative for C3 receptors. When macrophage-colony-stimulating factor (M-CSF), the purified C3 protein, and 1 alpha,25-(OH)2D3 were added to bone marrow methylcellulose cultures, separately or in combination, M-CSF-dependent colony formation was strikingly inhibited by 1 alpha,25-(OH)2D3, but the inhibition was prevented by simultaneously adding C3. These results provide additional evidence that osteoclast progenitors are indeed cells of the monocyte-macrophage lineage. It is likely that the C3 produced by stromal cells in response to 1 alpha,25-(OH)2D3 is somehow involved in osteoclast development by potentiating M-CSF-dependent proliferation of bone marrow cells and induction of osteoclast differentiation.
Acid Phosphatase↗
Sequence in DNA synthetic phase ratio of spontaneous hypertensive rat (SHR) myocardium--study on development of cardiomegaly.
We studied the relative synthetic phase (S-phase) ratio of cardiac myocytes of spontaneously hypertensive rats (SHR) utilizing monoclonal antibody to 5-bromo 2'-deoxyuridine (BrdU), a halogen derivative of thymidine. BrdU was administered intraperitoneally to SHR and Wistar Kyoto rats at 66.7 mg/kg/day for 3 consecutive days. The rats were sacrificed 1 week after the first injection of BrdU. Using anti-BrdU antibody, myocardial tissue was stained by the avidin biotinylated peroxidase complex method. We assessed the ability of the nuclei to synthesize DNA. The percentage of BrdU-labeled myocytes was higher in SHR than in control rats at 9 weeks. The hyperplastic phase of heart growth in rats was presumed to occur about 3 weeks after birth. From these results, the ability of the myocardial cell to synthesize DNA is probably enhanced under the load of high blood pressure in the early hypertrophic phase following hyperplasia.
Aging↗
[Successful treatment with lobenzarit disodium in case of Churg-Strauss syndrome].
In this case the patient was a 62-year-old male with a chief complain of sensory disturbance of the extremities. In January 1987 he was diagnosed as having bronchial asthma by a neighboring doctor and began to receive prednisolone (PSL) therapy at his hospital on an ambulatory basis. Later on, in January 1990, he developed dyspnea, epigastralgia, ecchymoses and muscle weakness of the lower extremities, with which he was admitted to the neighboring hospital, where he was started on treatment of asthmatic attacks with 30 mg/day of PSL. However, because muscle weakness of his extremities became gradually worse, he was transferred to our hospital. Physical examination on admission revealed an absence of knee and ankle jerk, sensory loss in the bilateral hands, legs and feet and diminished muscle strength of the extremities. Significant laboratory findings included leukocytosis, eosinophilia (4743/mm) and elevated serum IgE concentration (4900 IU/ml). Histologic evidence of vasculitis with an associated infiltration by eosinophils was noted on skin biopsy. These findings led to a diagnosis of Churg-Strauss syndrome. Treatment was started with PSL at 40 mg/day. However, as asthmatic attacks and eosinophilia were refractory to the conventional therapies, concomitant lobenzarit disodium (CCA), 240 mg/day was initiated. On increasing the dosage of CCA to 320 mg/day because of unsatisfactory symptomatic responses elicited at the initial dose level, the patient became free from an asthmatic attack with a return to normal of his eosinophilic count. He was discharged virtually asymptomatic while being placed on a regimen of PSL at 5 mg/day.
Churg-Strauss Syndrome↗
The dysfunction of peripheral blood dendritic cells in patients with mixed connective tissue disease.
The morphological findings and functions of peripheral blood dendritic cells (DC) from patients with mixed connective tissue disease (MCTD) were compared with those of DC from normal subjects. DC from both groups possessed typical dendritic processes and showed HLA-DR antigens and C3bi receptor. The autologous mixed lymphocyte reaction (MLR) and autologous concanavalin A (Con A)-induced T cell proliferation using DC as stimulating cells and accessory cells were significantly depressed in patients with MCTD. In the allogeneic MLR and allogeneic Con A responses, DC from patients with MCTD were poorer stimulating cells and accessory cells. The dysfunction of DC also, as one of the various immune abnormalities, must play a role in the appearance of clinical features.
Adolescent↗
[Jaccoud's type arthritis in a patient with unclassified connective tissue disease complicated with alveolar cell carcinoma].
The association between Jaccoud's type arthritis and systemic lupus erythematosus (SLE) is well recognized. Myositis, various arthropathy, and an assortment of miscellaneous connective tissue disorders have been described in association with malignancies. To date however Jaccoud's type arthritis has not been reported in unclassified connective tissue disease (UCTD) complicated with alveolar cell carcinoma (ACC). We describe a UCTD patient who presented LE cells, fluorescent antinuclear antibody (FANA), developing nonerosive, deforming arthritis and ACC. The case is a 59-year-old female who was admitted to our department in November, 1991 for exacerbated exertional dyspnea. She presented with UCTD of six years duration, characterized during follow-up by no history of rheumatic fever or Sjögren's syndrome, nor SLE. Five years later from onset of UCTD, her fingers developed a marked ulnar deviation, as well as pronounced swan-neck deformities. However, radiology did not show the marginal erosions of rheumatoid arthritis. A chest radiograph revealed a reticulogranular shadow in allover lung field, and a lung scintigram showed perfusion dominant mismatched defect in bilateral lower lung field. A transbronchial lung biopsy of B8a was diagnostic for ACC.
Adenocarcinoma, Bronchiolo-Alveolar↗