Search PubMed⌕ Search

Biomedical subjects

S Imamura

Publications and source records attributed to S Imamura.

At least 253 records · Page 14Linked to original sources
PubMed1992

Extensive variant of cutaneous amyloidosis: report of a case with electron-microscopic and immunohistochemical studies of the basement membrane zone at sites of amyloid production.

A 60-year-old Japanese female developed widespread lichenoid eruptions with pigmentation, which initially appeared in preceding erythematous skin lesions due to dermatomyositis. Thioflavine T and Dylon stainings, electron microscopy and immunohistochemistry revealed that thick amyloid deposits were present in the papillary dermis particularly beneath the epidermis. Autopsy showed no evidence of systemic amyloidosis. Electron microscopy of the lesional skin disclosed the disturbance of lamina densa formation in the epidermal basement membrane zone (BMZ). There was disruption and dissociation of the lamina densa from the basal cell, and a lamina-densa-like substance was found in the amyloid deposits. Immunofluorescence and immunoelectron microscopy showed that type IV and VII collagens, LDA-1 antigen (a noncollagenous component of the BMZ) and laminin were distributed in irregular thick deposits along the BMZ and were also present within the amyloid itself. These findings indicate that morphological and immunohistochemical abnormalities of the lamina densa may be involved in amyloid production at the interface of the epidermis and dermis, at least in this case.

Amyloidosis↗
PubMed1992

Effect of caffeine on expression of cardiac myosin heavy chain gene in adult hypothyroid and fetal rats.

Changes in cardiac myosin heavy chain (MHC) gene expression and isozyme transitions have been shown to be caused by developmental changes, hemodynamic overload, or the activity of various hormones. In this study, to examine whether caffeine, which has teratogenic effects on the fetal cardiovascular system, causes the distribution of cardiac MHC phenotype and, if so, to evaluate the mechanisms of the distribution of cardiac MHC phenotype by caffeine, we examined the effects of caffeine, theophylline, and cAMP on the cardiac MHC isoform transitions at the gene and protein levels using hypothyroid adult rats. Furthermore, we examined the expression of alpha- and beta-MHC gene in cardiac muscles of fetuses whose dams had received caffeine. The results showed that caffeine, theophylline, and cAMP caused accumulations of alpha-MHC mRNA and MHC isozyme V1. Furthermore, in the fetal hearts, it was recognized that caffeine induced an accumulation of alpha-MHC gene expression, as was also seen in the dams. However, this effect of caffeine on the heart was stronger in the fetus than in the dam. Intracellular cAMP concentration was increased by the administration of caffeine, theophylline, or cAMP, and the levels showed a positive correlation with those of alpha-MHC mRNA. These results suggest that the induction of alpha-MHC mRNA expression by the administration of caffeine may be induced by an increase in intracellular cAMP concentration.

Aging↗
PubMed1992

Comparison of the effects of halothane and propranolol on the effective refractory period and the ventricular activation in a canine myocardial infarction model.

The effects of halothane on the effective refractory period (ERP) and the ventricular activation were examined in a canine myocardial infarction model, and compared with those of propranolol. Halothane reduced the heart rate and prolonged the ERP in both normal and infarcted zones. A prolongation of ERP with halothane was also observed during atrial pacing at the same rate as in control, but the effect was less than during sinus rhythm. Halothane (1 MAC) further delayed or blocked the delayed activation in the infarcted zones with only slight effects on the activation of the normal zones. Propranolol (0.2 mg/kg) prolonged ERP during sinus rhythm, but it did not affect either the ERP or ventricular activation during atrial pacing. In conclusion, halothane produced a selective depression of the delayed activation and the prolongation of ERP, which may be caused by both direct effects on the myocardium and secondary effects such as a reduction of the heart rate. These effects of halothane may contribute to its antiarrhythmic effects in the myocardial infarction model which have been previously reported.

Animals↗
PubMed1992

Molecular cloning and expression of a Streptomyces sarcosine oxidase gene in Streptomyces lividans.

A genomic library of Streptomyces sp. KB210-8SY, prepared in the plasmid vector pACYC184, was screened to obtain the gene encoding sarcosine oxidase with probes based on the amino acid sequence of the protein. A plasmid pSOXS13, which was isolated from a clone identified by hybridization with the probes, contained a 8.4-kb insert of Streptomyces DNA. When the 2.0-kb MIuI/EcoRV DNA fragment of pSOXS13 was inserted into the Streptomyces vector pIJ680 and introduced into S. lividans, the transformants produced 100-fold more sarcosine oxidase intracellularly than KB210-8SY. The nucleotides of the 1.7-kb fragment containing the sarcosine oxidase gene were sequenced. An open reading frame encoded a mature sarcosine oxidase consisting of 388 amino acids, with a calculated molecular mass of 42,107 daltons.

Amino Acid Sequence↗
PubMed1992

Prophylactic use of ofloxacin in granulocytopenic patients with hematological malignancies during post-remission chemotherapy.

The prophylactic efficacy of ofloxacin (OFLX) therapy was evaluated in 51 granulocytopenic episodes in 22 patients with hematological malignancies during post-remission chemotherapy in a prospective, randomized, controlled trial. Oral administration of OFLX plus amphotericin-B (AMPH) and polymyxin-B (PL) reduced episodes of fever and infection more than did the control regimen with PL and AMPH alone (p less than 0.01), and the reduction in the incidence of infection was evident even in patients showing severe granulocytopenia (p less than 0.01). Furthermore, the first fever after the onset of granulocytopenia in the OFLX regimen developed later than that in the control regimen (p less than 0.05). Clinically, the prophylactic efficacy was 92% for the OFLX regimen and 40% for the control regimen (p less than 0.01). These findings suggest that OFLX is a promising prophylactic agent following post-remission chemotherapy. Patient hemomyelogram findings similar to those of patients with other malignancies may imply that OFLX is widely effective in granulocytopenic patients taking aggressive chemotherapy.

Adolescent↗
PubMed1992

A case of xeroderma pigmentosum group A diagnosed with a polymerase chain reaction (PCR) technique. Usefulness of PCR in the detection of point mutation in a patient with a hereditary disease.

BACKGROUND: The gene responsible for the xeroderma pigmentosum (XP) group A gene was recently identified and isolated. Preliminary study with fibroblasts from patients with XP group A revealed that most of the Japanese patients with XP group A have a point mutation at the 3' splice acceptor site of intron 3. This mutation site in the XP group A-complementing gene can be recognized by a restriction enzyme, AlwNI. This article describes the usefulness of the polymerase chain reaction diagnosis on XP group A. OBSERVATIONS: We tried a polymerase chain reaction diagnosis on genomic DNA from a sporadic case of XP group A and this child's parents. AlwNI restriction fragment length polymorphism of the polymerase chain reaction product showed three bands for his father's and mother's DNA, one corresponding to normal and two corresponding to a point-mutated gene, respectively. A DNA sample from our patient showed two fragments indicating that only he has the mutated gene. CONCLUSIONS: This study demonstrated that we can know that this patient has group A XP without a complementation test that needs a lot of time. Moreover, our study revealed that we can detect the hidden mutated XP group A-complementing gene in the pedigree in which there is no patient with XP. Furthermore, it may be available soon for prenatal diagnosis.

Amino Acid Sequence↗
PubMed1992

[Ataxic cerebral palsy and brain imaging].

Five cases diagnosed as having ataxic cerebral palsy were presented with their brain imaging. Case 1, a 3-year-old-girl had been floppy since 7 months of age and began ataxic walk with spastic legs from 18 months of age. MRI revealed generalized atrophy of cerebellum (especially in anterior superior part) and slight atrophy of pons. Her mother also had ataxia with spastic legs of early onset. She and her mother were thought to have an early-onset inherited non-progressive cerebellar ataxia syndrome. Case 2, a 8-year-old-girl had ataxic walk since 17 months of age. MRI revealed cerebellar atrophy especially in anterior superior part. Case 3, a 10-year-old boy was floppy since 4 months of age and suspected as ataxic at 4 years of age. He could walk only with cruches. He had dwarfism and cataracts since 4 years of age. CT and MRI revealed generalized spino-ponto-cerebellar atrophy. Final diagnosis was Marinesco-Sjörgren syndrome. Case 4, a 10-year-old girl had opisthotonus and floppiness since 4 months of age. She could walk only with cruches. CT and MRI revealed generalized spino-ponto-cerebellar atrophy. Case 5, a 8-year-old boy showed head nodding and nystagmus since 4 months of age. He started ataxic gait at 8 years of age. He could vocalize only single sound for speech. MRI revealed cranium bifida and agenesis of anterior medullar velum. Ataxic cerebral palsy is the term often used to describe very different conditions, the clinical picture starts as hypotonia and changes into the ataxic symptoms in a few years.(ABSTRACT TRUNCATED AT 250 WORDS)

Ataxia↗
PubMed1992

[Inhibition of acute rejection of heart graft in rats without immunosuppressants after intrathymic myocardial cell inoculation in the neonatal period].

There have been no successful cases reported of organ transplantation in application of neonatal immunological tolerance. Isolated myocardial cells from Lewis (LEW/Crj) rat hearts were inoculated into the thymus of incompatible King (WKAH/Hkm) rats. Ten weeks later the heart from LEW donor was transplanted heterotopically to the WKAH rat that had inoculated intrathymic myocardial cells without immunosuppression (n = 4, Group 1). Group 2 was made up of 4 isografts of heart transplantation (nontreated isograft). Group 3 was made up 4 allografts of heart transplantation (nontreated allograft). The animals were killed 7 days after transplantation, and early rejection was evaluated by accumulation of iodine-125 (125I)-labeled antimyosin antibody (AMA) uptake and confirmed by histological examination. In Group 1 & 2, the value of I-125 AMA uptake ratio was small (Group 1; RV: 1.28 +/- 0.28, IVS: 1.29 +/- 0.28, LV: 1.43 +/- 0.25, Group 2: RV: 1.14 +/- 0.07, IVS: 0.95 +/- 0.06, LV: 1.16 +/- 0.21). This level of the value indicates that the rejection does not occur. On the other hand, in Group 3, the value was high (RV: 4.63 +/- 1.92, IVS: 4.42 +/- 1.75, LV: 4.45 +/- 1.73) compared with Group 1 & 2. This level indicate that the rejection is severe. In the histological studies, Group 3 showed necrosis of myocardial cells, while Group 1 with neonatal immunological tolerance showed only very mild lymphocytic infiltration. The histology of thymic tissue in Group 1, the LEW myocardial cells are surviving in the WKAH rat thymus.

Animals↗
PubMed1991

Analysis of N-methyl-N-nitrosourea-induced mutations in a shuttle vector plasmid propagated in mouse O6-methylguanine-DNA methyltransferase-deficient cells in comparison with proficient cells.

A shuttle vector plasmid, pYZ289, was constructed from the pZ189 plasmid and polyoma virus DNA. The plasmid contains a supF gene as a marker of mutation and can replicate in both Escherichia coli and mouse cells. The pYZ289 plasmids treated with N-methyl-N-nitrosourea were passed through mouse cells originating from skin tumors, which are either proficient (HL18) or deficient (HL8) in O6-methylguanine-DNA methyltransferase activity, and mutations in the supF gene were analyzed. In the repair-deficient HL8 cells, N-methyl-N-nitrosourea-treated pYZ289 showed lower plasmid survival and higher mutation frequency than in the repair-proficient HL18 cells. DNA sequence analysis in the mutated supF gene revealed that most mutations occurred in G:C base pairs (86% for HL8, 76% for HL18), and the frequency of G:C----A:T transition was higher in HL8 cells (69%) than in HL18 cells (31%). G:C----T:A transversions occurred more frequently in HL18 cells (31%) than in HL8 cells (12%). Mutations occurred frequently at the base pair positions of 123 and 159 of supF gene in HL18 cells and at 169 in HL8 cells. Analysis of the bases neighboring the mutations appeared to be related to the mutability of the base pairs with the sequence of 5'-purine-G-G-3' being the most frequently mutated. These results show that the new pYZ289 plasmid is useful for the analysis of mutations and that a deficiency in O6-methylguanine-DNA methyltransferase enhances the N-methyl-N-nitrosourea-induced mutation with significant specificity.

Animals↗
PubMed1991

Molecular cloning and primary structure of rat thyroxine-binding globulin.

Rat thyroxine-binding globulin (TBG) cDNAs were isolated from a rat liver cDNA library by using a human TBG cDNA as a probe. From two overlapping cDNA inserts, an aligned cDNA sequence of 1714 nucleotides was obtained. There was 70% homology with human TBG cDNA over the span of 1526 nucleotides. In order to confirm that the cloned cDNA encodes rat TBG and to localize the NH2-terminal amino acid of the mature molecule, the protein was purified by affinity chromatography and subjected to direct protein microsequencing. The NH2-terminal amino acid sequence was identical with that deduced from the nucleotide sequence. The rat TBG cDNA sequenced consisted of a truncated leader sequence (35 nucleotides), the complete sequence encoding the mature protein (1194 nucleotides) and the 3'-untranslated region (485 nucleotides), containing two polyadenylation signals. It was deduced that rat TBG consists of 398 amino acids (Mr = 44,607), three NH2-terminal residues more than human TBG, with which it shares 76% homology in primary structure. Of the six potential N-glycosylation sites, four are located in conserved positions compared to human TBG. Northern blot analysis of rat liver revealed an approximately 1.8-kilobase TBG mRNA. Its amount increased markedly following thyroidectomy and decreased with thyroxine treatment in a dose-dependent manner.

Amino Acid Sequence↗
PubMed1991

Calcium-induced intracellular cross-linking of lipocortin I by tissue transglutaminase in A431 cells. Augmentation by membrane phospholipids.

Covalently cross-linked multimers of lipocortin I are shown to be present in human epidermoid carcinoma A431 cells treated with epidermal growth factor or the calcium ionophore A23187. This intracellular cross-linking of lipocortin I is suggested to be mediated by the action of tissue transglutaminase, a Ca2(+)-dependent protein cross-linking enzyme. Cross-linking of lipocortin I competes with proteolytic digestion of the protein, and pretreatment of the cells with inhibitors for calpain (Ca2(+)-dependent intracellular protease) markedly enhanced the cross-linking of lipocortin I. Cross-linked lipocortin I is shown to be present in the soluble fraction of A431 cells as well as in the particulate fraction; a 34-kDa fragment of lipocortin I was solubilized successfully by plasmin digestion of the latter fraction. Immunofluorescence microscopy using specific antilipocortin-I antibody showed that cross-linked lipocortin I forms an envelope-like structure, which is not extracted with [ethylenebis(oxyethylenenitrilo)]tetraacetic acid (EGTA) or Triton X-100. In vitro incubation of purified lipocortin I with tissue transglutaminase resulted in the formation of covalently cross-linked lipocortin I dimer, tetramer, and so on. Amine incorporation and cross-linking studies using lipocortin I and its N-terminal truncated derivatives indicated that the cross-linking site is localized within the plasmin-susceptible N-terminal 29 amino acids of lipocortin I. The cross-linking of lipocortin I is shown to be accelerated more than 10 times by the addition of phosphatidylserine vesicles, on which lipocortin I molecules are most likely aligned in a conformation suitable for cross-linking. Collectively, these findings suggest that an increase of intracellular calcium concentration results in the attachment of lipocortin I onto the plasma membrane phospholipids through the C-terminal domain of the molecule where the membrane-bound lipocortin I is cross-linked by the action of tissue transglutaminase through the N-terminal domain.

Annexins↗
PubMed1991

1-2B7B: monoclonal antibody reacting to the 120 kDa polypeptide component of human epidermal hemidesmosomes.

Immunohistochemical and immunochemical analyses were performed on a monoclonal antibody designated 1-2B7B which was derived from immunizing mice with human prostate epithelial tissue. The 1-2B7B antigen was expressed not only along the acinous basement membrane zone (BMZ) of the prostate and testis, but also along the BMZ of the epithelia of several other organs including the skin, oesophagus, urinary bladder, ureter, stomach, intestine and bile duct. The antigenic epitope was not expressed in these tissues of lower mammals. Immunoelectron microscopic studies on normal human skin revealed that the 1-2B7B antigen was localized mainly just beneath the hemidesmosomes of basal keratinocytes, but not beneath melanocytes. Indirect immunofluorescence and immunoelectron microscopic studies on 1 M NaCl-split skin confirmed that this antigen was not separated from the cytoplasmic membrane of basal cells after salt treatment. SDS polyacrylamide gel electrophoresis of immunochemically purified protein from the epidermis demonstrated the molecular weight of the antigen to be 120 kDa. 1-2B7B monoclonal antibody should be a useful probe for studying the pathomechanism of some blistering diseases, as well as the assembly and function of the epidermal-dermal junction.

Animals↗
PubMed1991

Stimulation of anti-RNP antibody binding to cultured keratinocytes by estradiol.

Antibodies to extractable nuclear antigens (ENA) are frequently demonstrated in the serum of patients with cutaneous lupus erythematosus. To gain a better understanding of the influence of sex hormones on cutaneous lupus, we investigated the in vitro binding of anti-ENA antibodies to cultured human keratinocytes. Estradiol-beta augmented the binding of anti-RNP, anti-SS-A/Ro, and anti-SS-B/La antibodies to cultured cells, but produced no enhancement of the binding of anti-Sm antibodies. In addition, we examined the effects of 16-alpha-hydroxyestrone, a highly estrogenic metabolite, on the binding of anti-ENA antibodies to cultured cells. This agent did not produce any augmentation of binding. Based on these experiments, we discuss the influence of estradiol on cutaneous lupus.

Antibodies, Antinuclear↗
PubMed1991

A subpopulation of Langerhans cells (CD1a+Lag-) increased in the dermis of plaque lesions of mycosis fungoides.

The population of CD1a+ cells and the quantity of Birbeck granules were evaluated in comparison with the population of T lymphocytes in a variety of clinical lesions of mycosis fungoides. Anti-CD1a and Lag antibodies that specifically react with Birbeck granules and related structures of human Langerhans cells were used immunohistochemically. CD1a+ cells in the dermis of lesions of mycosis fungoides significantly increased in plaques of the plaque stage and in plaques of the tumor stage. They were most frequent in lesions with CD4+ cells ranging in number from 100 to 150/mm2. These lesions were suspected to be progressing from the plaque to the tumor stage. During the course of the disease, most of the dermal CD1a+ cells had few Lag antigens. These results suggest that dermal CD1a+Lag- cells may promote the progression of mycosis fungoides from the plaque to the tumor stage.

Antibodies, Monoclonal↗
PubMed1991

Survival period of tumor-bearing mice is prolonged after the interferon-gamma-producing gene transfer.

A highly tumorigenic keratinocyte-derived carcinoma cell line, designated as Pam-T, was established from a Pam212 line. The intradermal injection of more than 10(5) of these cells into syngeneic BALB/c mice induced substantial tumors. The tumors progressively enlarged and then invaded the peritoneal cavity leading to the death of the host mice. To comprehensively investigate the effects of interferon-gamma on tumorigenicity, we manufactured interferon-gamma-producing PamT cells by interferon-gamma gene transfer and examined the characteristics of the tumors induced by these cells in syngeneic mice. Interferon-gamma producing cells exhibited an apparently similar in vitro cell growth pattern and in vivo tumor formation to control cells, but the mean survival of the mice with the interferon-gamma-producing cells was significantly longer compared with control mice.

Animals↗