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Biomedical subjects

S Nagata

Publications and source records attributed to S Nagata.

At least 415 records · Page 23Linked to original sources
PubMed1994

Modification of the stages in total reconstruction of the auricle: Part I. Grafting the three-dimensional costal cartilage framework for lobule-type microtia.

Total auricular reconstruction for microtia is dependent on the fabricated three-dimensional costal cartilage framework, with all the auricular features and the skin flaps formed and utilized to cover the three-dimensional framework, in which extreme caution is required. Furthermore, other factors, such as contraction of the skin graft, use of the remnant ear cartilage in construction of the tragus, and the number of surgeries required, all affect the final results of total auricular reconstruction for microtia, especially with reference to the contour of the constructed ear, morphologic locations of the auricular features, contraction, circulatory dysfunction, resorption, etc. The grafting of the three-dimensional framework is the first stage of a two-stage surgical method for total auricular reconstruction without resorting to skin grafts, free composite grafts, and additional surgical procedures.

Cartilage↗
PubMed1994

Modification of the stages in total reconstruction of the auricle: Part II. Grafting the three-dimensional costal cartilage framework for concha-type microtia.

Among the microtic disorders, those with the remnant ear, ear lobule, concha, acoustic meatus, tragus, and incisura intertragica are classified as concha-type microtia. From these characteristic factors, concha-type microtia has been thought to be a milder form of microtic disorder in comparison with lobule-type microtia. The constructed modified three-dimensional costal cartilage framework is grafted to the superior portion of the auricle and fixed to the inferior remnant cartilage of the auricle (conchal portion). This may appear to be a simple procedure in comparison with the other microtic disorders, but it is extremely difficult to fix the modified three-dimensional framework to the remnant auricular cartilage so that a smooth configuration is attained at the seam. In this paper, the modification stages for total reconstruction of the auricle for concha-type microtia are discussed.

Cartilage↗
PubMed1994

Modification of the stages in total reconstruction of the auricle: Part III. Grafting the three-dimensional costal cartilage framework for small concha-type microtia.

The characteristic features of small concha-type microtia are the existence of the remnant ear and lobule and a small indentation representing the concha. Presently, the microtic disorder known as hypoplasia of the middle third of the auricle has the featured characteristics of a well-developed lobule, scapha, and helix and the existence of a small concha. Therefore, from these clinical aspects and features, the major criterion for classification for this particular type of microtia (small concha-type microtia) is the presence of the small concha. The modification stages involved in total reconstruction of the auricle for small concha-type microtia are described and discussed in this paper.

Cartilage↗
PubMed1994

Modification of the stages in total reconstruction of the auricle: Part IV. Ear elevation for the constructed auricle.

The contour of the constructed structures of the anterior surface of the auricle tends to diminish after ear elevation; thus it is extremely difficult to obtain the proper projection of the constructed ear without destroying the contour of these structures. There have been numerous articles concerned with ear elevation, even though most methods or procedures are plagued with problems. The major factors concerned with ear elevation have been described and stated in a previous article. This paper will discuss the major modification and refinement stages involved in attaining the present ear elevation method.

Cartilage↗
PubMed1994

Alcoholic pancreatic injury: alterations of pancreatic autonomic nerves and microcirculation.

Alteration of microcirculatory status and aberration of the autonomic nervous activity are thought to play an important role in the pathogenesis of ethanol-induced organ damages. Recently, the significant roles of nitric oxide and endothelin in the regulation of the pancreatic microcirculatory system and its disturbances have also been discovered. The present study was undertaken to clarify the histochemical and biochemical alteration of the cholinergic and adrenergic nerves. NADPH diaphorase and nitric oxide synthase activities, markers of nitroxergic nerves, and endothelin immunoreactivity as well as binding sites of 125 I-endothelin, were also studied in the pancreas of rats fed for three months with the Lieber-DeCarli's ethanol-containing liquid diet. In the rats fed ethanol, the histochemical and biochemical activities of the cholinergic nerves gradually increased, compared with the control rats. Monoamine fluorescence and NADPH diaphorase histochemical activity were also markedly enhanced in the ethanol-treated group. The results suggest that the activation of cholinergic and adrenergic nerves and increased NO synthesis are involved in the pathogenesis of ethanol-induced pancreatic injury.

Acetylcholinesterase↗
PubMed1994

Expression of gamma-glutamyl transpeptidase mRNA after depletion of glutathione in rat liver.

Gamma-glutamyl transpeptidase (gamma-GT) is the enzyme in the gamma-glutamyl cycle which mediates the first step of glutathione degradation. Recently, it has been reported that diethyl maleate, a glutathione-depleting agent, enhanced hepatic gamma-GT activity. In this study, we examined how gamma-GT mRNA was expressed after the depletion of glutathione by using the RT-PCR method and in situ hybridization technique with digoxigenin-labeled oligonucleotide probe. We could detect hepatic gamma-GT mRNA in the epithelial cell of bile duct and the cytoplasm of hepatocytes in the periportal area, even in control rats. Furthermore, we found that the expression of gamma-GT mRNA was expanded to hepatocytes of a whole lobule 12 hr after depletion of glutathione by diethyl maleate, followed by the return to the pretreatment condition under which gamma-GT mRNA appears to be controlled in correlation with hepatic glutathione levels. These results suggest that the depletion of glutathione may induce hepatic gamma-GT activity through an increased synthesis of its mRNA.

Animals↗
PubMed1993

Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family.

The Fas antigen (Fas) belongs to the tumor necrosis factor (TNF)/nerve growth factor receptor family, and it mediates apoptosis. Using a soluble form of mouse Fas, prepared by fusion with human immunoglobulin Fc, Fas ligand was detected on the cell surface of a cytotoxic T cell hybridoma, PC60-d10S. A cell population that highly expresses Fas ligand was sorted using a fluorescence-activated cell sorter, and its cDNA was isolated from the sorted cells by expression cloning. The amino acid sequence indicated that Fas ligand is a type II transmembrane protein that belongs to the TNF family. The recombinant Fas ligand expressed in COS cells induced apoptosis in Fas-expressing target cells. Northern hybridization revealed that Fas ligand is expressed in activated splenocytes and thymocytes, consistent with its involvement in T cell-mediated cytotoxicity and in several nonlymphoid tissues, such as testis.

Amino Acid Sequence↗
PubMed1993

Unidirectional cross-phosphorylation between the granulocyte colony-stimulating factor and interleukin 3 receptors.

The mouse interleukin-3 (IL-3)-dependent hemopoietic precursor cell line 32DC13 responds to granulocyte colony-stimulating factor (G-CSF) for proliferation and differentiation. We established a subline (32D-FH) of the 32DC13 cells which has lost the ability to respond to G-CSF. When murine G-CSF receptor cDNA was introduced into the 32D-FH cell line, the transformants responded to G-CSF as well as to IL-3 for proliferation. Adding G-CSF to the transformants rapidly induced tyrosine phosphorylation not only of the G-CSF receptor but also of both subtypes of the IL-3 receptor beta-chain (AIC2A and AIC2B molecules). On the other hand, stimulation of the transformants with IL-3 induced tyrosine phosphorylation of the AIC2A and AIC2B but not of the G-CSF receptor. These results indicate that the tyrosine kinase activated through the G-CSF receptor interacts with the IL-3 receptor beta-chains but not vice versa. This unidirectional cross-phosphorylation between the G-CSF and IL-3 receptors may play a role in granulopoiesis induced by G-CSF.

Amino Acids↗
PubMed1993

Simultaneous determination of bile acids in rat bile and serum by high-performance liquid chromatography.

A method for the simultaneous determination of bile acids in rat bile and serum by high-performance liquid chromatography with a post-column enzymic reaction and fluorescence detection has been developed. Without prior fractionation and alkaline hydrolysis, 26 unconjugated, glycine- and taurine-conjugated bile acids were determined. They were separated on a reversed-phase column using a linear gradient solvent system of 200 mM dibasic ammonium phosphate buffer (pH 7.9)-acetonitrile-methanol (73:19:8, v/v/v) and 20 mM dibasic ammonium phosphate buffer (pH 7.9)-acetonitrile-methanol (2:1:2, v/v/v). The limits of detection were 1-5 pmol, and calibration curves were linear for concentrations between 10 and 4000 pmol. This rapid and reliable method is effective for measuring bile acid levels in the bile and serum not only of rats but also of patients with hepatobiliary and other diseases.

Animals↗
PubMed1993

In vivo and in vitro suppression of primary B lymphocytopoiesis by tumor-derived and recombinant granulocyte colony-stimulating factor.

Transplantation of a granulocytosis-inducing murine CE mammary carcinoma into mice suppresses primary B lymphopoiesis in the marrow. The mechanisms of this tumor-induced B-cell suppression were investigated using Whitlock-Witte-type lymphoid cultures. When seeded with normal marrow progenitors, stromal cells of tumor-bearing mice supported the production of B220+ cells as well as did either stomal cells derived from control mice or the stromal cell line S17. Cultured over normal stroma, marrow cells of tumor-bearing mice depleted of adherent cells and B220+ cells generated B220+ cells as effectively as a similar cell population from control mice. However, interleukin-7-responsive progenitors, were completely depleted from the marrow of tumor-bearing mice. When conditioned medium (CM) of cloned CE tumor cells known to produce granulocyte colony-stimulating factor (G-CSF) and macrophage-CSF, or recombinant murine G-CSF was added to the cultures established with S17 cells, B220+ cell production was significantly diminished. Antiserum to murine G-CSF blocked these effects. These in vitro observations were corroborated by the elimination of marrow B220+ cells in mice injected with G-CSF. These in vitro and in vivo studies suggest that G-CSF plays an inhibitory role in primary B lymphopoiesis by blocking stromal cell-mediated differentiation of early B-cell progenitors into phenotypically recognizable B220+ pre-B cells.

Animals↗
PubMed1993

Growth and differentiation signals mediated by different regions in the cytoplasmic domain of granulocyte colony-stimulating factor receptor.

Granulocyte colony-stimulating factor (G-CSF) is a cytokine that regulates the proliferation and differentiation of neutrophils. The G-CSF receptor (G-CSFR) is a member of the hemopoietic growth factor receptor family. A G-CSFR expression plasmid was introduced into interleukin-3 (IL-3)-dependent mouse myeloid precursor FDC-P1 cells that normally do not respond to G-CSF. G-CSF stimulated proliferation of the transformants, down-regulated Thy-1 and F4/80 antigens on the cell surface, and induced expression of neutrophil-specific genes such as myeloperoxidase (MPO) and leukocyte elastase. On the other hand, neither granulocyte/macrophage colony-stimulating factor (GM-CSF) nor IL-3 induced MPO gene expression, but they inhibited G-CSFR-mediated MPO gene expression. These results suggested that the G-CSFR, but not the IL-3/GM-CSF receptors, transduced the neutrophilic differentiation signal into cells. Mutational analysis of the G-CSFR indicated that the N-terminal region of its cytoplasmic domain is sufficient to transduce the proliferation signal into cells, while the C-terminal region plays an essential role in transducing the differentiation signal.

Animals↗
PubMed1993

Elevated serum alpha-fetoprotein level of nude mice bearing hepatoma cells by treatment with monoclonal antibodies to alpha-fetoprotein.

This study was carried out to clarify the reason for elevation of serum alpha-fetoprotein (AFP) level of nude mice bearing hepatoma cells after treatment with monoclonal antibodies (MoAbs) to AFP. MoAbs to AFP showed no effect on the cumulative amounts of AFP secreted from human hepatoma cell line, HuH-7, in vitro. However, the treatment of nude mice bearing HuH-7N cells (HuH-7 xenograft) with MoAbs to AFP led to elevation of the serum AFP level in spite of the fact that the growth curve of HuH-7N cells was similar to that for PBS treatment. This apparent elevation of the serum AFP level is thought to be due to the slow elimination of AFP-MoAb immune complexes with little lattice structure from circulation, but not the enhancement of AFP secretion of HuH-7N cells. Thus, when using a MoAb alone or MoAb-drug conjugate, the serum AFP level should only be cautiously used as a tumor marker for evaluating the targeting immunotherapy.

Animals↗
PubMed1993

Increased fragmentation of urinary fibronectin in cancer patients detected by immunoenzymometric assay using domain-specific monoclonal antibodies.

Monoclonal antibodies (MoAbs) recognizing the distinct domains of human fibronectin had previously been established and they were used to construct several sandwich immunoenzymometric assays (IEMAs) for the structural analysis of fibronectin found in the urine of cancer patients. Urinary fibronectin (UFN) was immunodetectable only with FN12-8 and FN30-8 MoAbs against cell-binding domains and was less reactive with other IEMAs using MoAbs directed to terminal domains, indicating that UFN was almost completely fragmented and consisted mainly of cell-binding regions. The IEMA using MoAbs against cell-binding domains had sufficient immunoreactivities with the antigen fragmented by artificial proteolysis, but these fragments could hardly be detected by other IEMAs. UFN levels were significantly elevated in various cancer patients and extremely elevated in some patients with distant metastasis. It is presumed that UFN fragments which increase in cancer patients are generated by extracellular matrix destruction. Thus UFN levels and the ratio of the fragmented UFN level to the non-fragmented UFN level appear to be informative clinical indicators of tumor malignancy or metastatic ability in cancer patients.

Animals↗
PubMed1993

Lethal effect of the anti-Fas antibody in mice.

During mammalian development, many cells are programmed to die most mediated by apoptosis. The Fas antigen coded by the structural gene for mouse lymphoproliferation mutation (lpr), is a cell surface protein belonging to the tumour necrosis factor/nerve growth factor receptor family, and mediates apoptosis. The Fas antigen messenger RNA is expressed in the thymus, liver, heart, lung and ovary. We prepared a monoclonal antibody against mouse Fas antigen, which immunoprecipitated the antigen (M(r) 45K) and had cytolytic activity against cell lines expressing mouse Fas antigen. We report here that staining of mouse thymocytes with the antibody indicated that thymocytes from the wild-type and lprcg mice expressed the Fas antigen, whereas little expression of the Fas antigen was found in lpr mice. Intraperitoneal administration of the anti-Fas antibody into mice rapidly killed the wild-type mice but neither lpr nor lprcg mice. Biochemical, histological and electron microscope analyses indicated severe damage of the liver by apoptosis. These findings suggest that the Fas antigen is important in programmed cell death in the liver, and may be involved in fulminant hepatitis in some cases.

Animals↗
PubMed1993

Identification of the product of the murine ST2 gene.

The murine ST2 gene is expressed in growth-stimulated BALB/c-3T3 cells. This gene encodes a protein that is similar to the extracellular portions of the interleukin-1 receptors (types 1 and 2). In this study, we prepared a polyclonal antibody against the recombinant ST2 protein produced in Escherichia coli. This antibody detected recombinant ST2 protein in the culture fluid of COS7 cells transfected with a mammalian expression vector (pEF-BOS) carrying ST2 cDNA. Using this antibody, we could detect the ST2 protein in the culture fluid of growth-stimulated BALB/c-3T3 cells, and in the medium of continuously growing cells, but not in that of growth-arrested cells. ST2 proteins produced in COS7 cells and BALB/c-3T3 cells were N-glycosylated as predicted from nine putative N-glycosylation sites in its deduced amino-acid sequence.

3T3 Cells↗
PubMed1993

Effect of bcl-2 on Fas antigen-mediated cell death.

Fas Ag is a cell surface protein that can mediate apoptosis and belongs to the TNF receptor family. The product of protooncogene bcl-2, a membrane-associated protein, has been shown to inhibit apoptosis in various hematopoietic cells including B cells and T cells. To examine the possible interaction of the Fas Ag and bcl-2, we coexpressed human Fas Ag and bcl-2 cDNA in murine IL-3-dependent FDC-P1 cell line and murine lymphoma WR19L. FDC-P1 transformants expressing bcl-2 showed a prolonged survival to IL-3 depletion. FDC-P1 transformants expressing the Fas Ag alone were killed by anti-Fas antibody in the presence of IL-3. Overexpression of bcl-2 in FDC-P1 resulted in a partial inhibition of Fas-induced cell death. WR19L transformants expressing bcl-2 were partially resistant to the cytolytic activities of the TNF-alpha and anti-Fas antibody treatment. These results suggest that the Fas Ag and TNF receptor may share the same signaling pathway, and that bcl-2 interferes with the apoptotic process mediated by the Fas Ag and TNF receptor.

Antigens, Surface↗
PubMed1993

[Stress-induced immune changes, and brain-immune interaction].

It is commonly known that psychosocial stress influences the immune system. Recent progress in neuroscience and immunology has elucidated the mechanism of stress induced immune changes, as well as brain-immune interactions. Numerous studies suggest that psychosocial stress increases the susceptibility to bacterial and viral infections. Stressful life events, inappropriate coping behavior and disturbed emotional states are associated with decreased phagocytosis, reduced lymphocyte response to mitogen, diminished natural killer cell activity, and with the risk of developing neoplasm. There is increasing evidence for a bidirectional communication system between the immune system and the brain through common receptors and biologically active substances such as cytokines and neuropeptides. Research has demonstrated the direct regulatory effect of the autonomic nervous system on the immune system, as well as the hypothalamic-pituitary-adrenal axis. It has also been shown that immune and allergic reactions can be classically conditioned, cytokines have an effect on the central nervous system, and that lymphocytes can produce neuropeptides. In this article, stress induced immune changes and brain-immune interactions are reviewed and discussed using pertinent literature, including studies by the authors.

Animals↗