Characterization of B cells producing xenoreactive natural antibodies in humans.
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Antibodies, Heterophile↗
Biomedical subjects
M Satake
Publications and source records attributed to M Satake.
Enzyme-assisted synthesis of disaccharides to inhibit binding of human anti-alpha Gal antibody.
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Antibodies, Heterophile↗
Human platelet alloantigen (HPA)-5a/b mismatch decreases disease-free survival in unrelated bone marrow transplantation.
Matching of human platelet alloantigen (HPA) systems 2-6 was retrospectively investigated in 715 unrelated bone marrow transplantations. Of the five HPA systems studied, HPA-5 mismatching was found to have a significant effect on the disease-free survival rate of recipients following transplantation in the HLA-A, -B, -C, and -DR allele-matched donor-recipient pairs. The effect of the HPA-5 mismatch was most significant in the recipient group possessing the HLA haplotype A*2402-B*5201, which is a highly frequent haplotype among the Japanese population. However, the probability of development of acute graft-versus-host disease (GVHD) was not increased significantly by the HPA-5 mismatching. These findings suggest that the HPA-5 mismatching decreases the recipient's survival by a mechanism different from that in the case of mismatching of minor antigens found often in transplant recipients developing GVHD.
Antigens, Human Platelet↗
Xenograft rejection of fetal porcine islet-like cell clusters in the rat: effects of active and passive immunization.
The process of islet xenograft rejection is still poorly understood. To elucidate further possible mechanism(s) involved in xenograft rejection, the effect of different immunization protocols was investigated. Fetal porcine islet-like cell clusters (ICCs) were transplanted under the kidney capsule in otherwise untreated rats, rats pre-immunized by s.c. injections of ICCs and in rats passively immunized with immune serum. The rejection process was evaluated with regard to antibody and complement deposition in the graft, as well as to morphology and phenotype of the infiltrating cells. In otherwise untreated animals, a moderate perigraft mononuclear cell infiltrate was seen after 3 days. Graft destruction became evident on day 6 with marked intragraft infiltration by macrophages (ED1 positive), whereas T cells were in the minority and mainly located in the perigraft area. In contrast to the findings in non-immunized rats, the rejection process in pre-immunized rats was characterized by marked intragraft infiltration by macrophages 3 days after transplantation. Moreover, both T cells and macrophages heavily infiltrated the adjacent kidney parenchyma, and major histocompatibility complex (MHC) class II expression in surrounding kidney tubular cells was concomitantly enhanced. Syngeneic rat islets mixed with porcine ICCs escaped the rejection process in non-immunized rats but were affected in pre-immunized animals. Thus, the specificity of the rejection process in non-immunized animals seems to be lost in pre-immunized animals. The early macrophage infiltration was also accelerated in rats passively immunized with immune serum, but no early switch from perigraft to intragraft infiltration or subsequent cellular infiltration in the adjacent kidney parenchyma was seen. Circulating xenoreactive antibodies of the IgG isotype increased after transplantation in normal and otherwise untreated rats. No distinct IgG deposition in the ICC xenografts was observed until day 12 after transplantation in untreated rats, whereas perigraft deposition of IgG was found 1 day after transplantation in pre-immunized rats and in rats given immune serum. No deposition of complement was observed within the ICC xenograft in any of the groups during the observation period. The dependence on T cells, the massive infiltration of macrophages with a unique phenotype, the cellular distribution, and the loss of specificity (bystander killing) of the rejection process in immunized rats suggest that ICC xenograft rejection shares some of its main characteristics with a delayed type hypersensitivity-like (DTH) immune response.
Animals↗
Haemodynamic changes in non-alcoholic (viral) liver cirrhosis studied by computed tomography (CT) arterial portography and CT arteriography.
AIMS: To evaluate haemodynamic and vascular changes in non-alcoholic (viral) cirrhosis on conventional computed tomography (CT), CT arteriography (CTA) and CT arterial portography (CTAP), and to determine the cause of the observed reticular stain on angiography. METHODS: Using surgically resected liver specimens from 31 patients with viral hepatitis associated hepatocellular carcinoma, images of conventional CT, CTA, CTAP and the sinusoidal phase of hepatic arteriography were retrospectively analysed and compared with pathology of the non-cancerous portion of the liver. RESULTS: Computed tomography arteriography showed inhomogeneous enhancement (diffuse, low-density nodules) in a total of 16 samples (52%); in eight of 10 (80%) cirrhotic livers, three of six (50%) precirrhotic livers, five of 12 (42%) livers with chronic active hepatitis and none of three with no active liver disease. The frequency of inhomogeneous enhancement became significantly higher with increasing severity of parenchymal damage (P < 0.05). In contrast, conventional CT and CTAP showed homogeneous enhancement in all 31 (100%) patients. There was no correlation between inhomogeneous enhancement on CTA and reticular staining on sinusoidal-phase hepatic angiograms. Inhomogeneous enhancement was frequently seen in patients with hepatitis B surface antigen and/or anti-hepatitis C virus antibody compared with those without them (P < 0.05). CONCLUSION: The CTA was much more sensitive in detecting haemodynamic changes in the cirrhotic liver than CTAP, conventional CT and sinusoidal-phased hepatic angiography. Further study is required to clarify the mechanism of inhomogeneous enhancement on CTA and homogeneous enhancement on CTAP seen in cirrhosis.
Adult↗
Optimal injection protocol for CT evaluation during hepatic arterial infusion chemotherapy.
OBJECTIVE: As an imaging modality for follow-up during continuous or repeated hepatic arterial infusion chemotherapy using a hepatic intra-arterial indwelling catheter, the usefulness of CT while infusing contrast through the indwelling catheter (reservoir port) was examined. METHODS: Using reservoir ports implanted in eight patients with hepatic metastasis from colon cancer, radioisotope perfusion scintigraphy (RI), CT (three rates of infusion of contrast were used), and digital subtraction angiography (AG) were performed to compare the modalities' ability to visualize the intrahepatic and abnormal extrahepatic distributions. RESULTS: CT (infusion rate 0.1 mL/sec) was superior to AG and RI in terms of the ability to visualize intrahepatic distribution, particularly in small areas, and facilitated 3D delineation of the distribution. In evaluating extrahepatic distribution, CT also outperformed the other modalities. CONCLUSIONS: For imaging study follow-up during hepatic arterial infusion chemotherapy, CT proved to be more useful than conventional RI and AG.
Aged↗
Axonal and perikaryal involvement in chronic inflammatory demyelinating polyneuropathy.
OBJECTIVES: To assess the extent of loss of myelinated nerve fibres and spinal motor neuron loss in chronic inflammatory demyelinating polyneuropathy (CIDP), a clinicopathological study was conducted on biopsied sural nerves and necropsied spinal cords from patients with CIDP. METHODS: The myelinated fibre pathology of 71 biopsied sural nerves and motor neuron pathology of nine necropsied spinal cords at L4 levels in patients with CIDP were quantitatively and immunohistochemically assessed. RESULTS: Myelinated nerve fibre density was significantly diminished to 65.4% of the control values (p <0.0001), correlating inversely with the extent of segmental demyelination and remyelination (r = -0.43, p < 0.0005) and duration of illness (r = -0.31, p < 0.01). Numbers of large spinal motor neurons in CIDP were variably but significantly diminished (range from 46.0 to 97.6% of the age matched control value (p < 0.005)), and reactive astrogliosis was evident in the ventral horn in CIDP. The frequency of ventral horn neurons exhibiting central chromatolysis and the accumulation of phosphorylated high molecular weight neurofilament protein was significantly higher in CIDP than in controls (p<0.01 and p<0.05). CONCLUSIONS: The loss of nerve axons and spinal motor neurons is common in CIDP, and extensive in some cases. These neuronal and axonal losses may influence the functional prognosis in CIDP.
Adolescent↗
Definitive chemoradiotherapy for T4 and/or M1 lymph node squamous cell carcinoma of the esophagus.
PURPOSE: To investigate the efficacy and feasibility of concurrent chemoradiotherapy for locally advanced carcinoma of the esophagus. PATIENTS AND METHODS: Fifty-four patients with clinically T4 and/or M1 lymph node (LYM) squamous cell carcinoma of the esophagus were enrolled. Patients received protracted infusion of fluorouracil 400 mg/m(2)/24 hours on days 1 to 5 and 8 to 12, 2-hour infusion of cisplatin 40 mg/m(2) on days 1 and 8, and concurrent radiation therapy at a dose of 30 Gy in 15 fractions over 3 weeks. Filgrastim was prophylactically administered to 35 patients. This schedule was repeated twice every 5 weeks, for a total radiation dose of 60 Gy, followed by two courses of fluorouracil (800 mg/m(2)/24 hours for 5 days) and cisplatin (80 mg/m(2) on day 1). RESULTS: There were 21 patients with T4M0 disease, one with T2M1 LYM, 17 with T3M1 LYM, and 15 withT4M1 LYM. Forty-nine patients (91%) completed at least the chemoradiotherapy segment. The 18 patients (33%) who achieved a complete response included nine (25%) of the 36 with T4 disease and nine (50%) of the 18 with non-T4 disease. Major toxicities were leukocytopenia and esophagitis; there were four (7%) treatment-related deaths. Prophylactic filgrastim reduced the incidence of grade 3 or worse leukopenia without improving dose-intensity or response. With a median follow-up duration of 43 months, median survival time was 9 months. The 3-year survival rate was 23%. CONCLUSION: Despite its significant toxicity, this combined modality seemed to have curative potential even in cases of locally advanced carcinoma of the esophagus.
Adult↗
A novel sesterterpenoid, nitiol, as a potent enhancer of IL-2 gene expression in a human T cell line, from the Peruvian folk medicine "Hercumpuri" (Gentianella nitida).
A novel sesterterpenoid designated as nitiol (1), possessing enhancement activity of IL-2 gene expression in a human T cell line, was isolated from the Peruvian folk medicine "Hercampuri" (Gentianella nitida). The structure was elucidated by extensive spectroscopic investigation.
Cells, Cultured↗
Monoamine oxidase inhibitory naphthoquinone and/or naphthalene dimers from Lemuni Hitam (Diospyros sp.), a Malaysian herbal medicine.
From the extract of a Malaysian herbal medicine, Lemuni Hitam (Diospyros sp.), which exhibited monoamine oxidase (MAO) inhibition, three new naphthoquinone and/or naphthalene dimers (lemuninols A-C, 1-3) were isolated together with 4,6-dihydroxy-5-methoxy-2-methyl-naphthalene (8) and six known monomers (4-7, 9 and 10). The structures were determined by spectroscopic methods including 2D-NMR techniques. Among them, lemuninol A showed 45% inhibition of MAO (mouse liver) at 5.0 x 10(-6) g/ml, and lemuninols B and C and a naphthoquinone (9) indicated weak activity. Some related quinones were also tested for their MAO inhibitory activities.
Animals↗
[Tight junctional permeability of intestinal epithelium and its regulation by food factors].
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Cell Membrane Permeability↗
[Geobotanical studies on the island of Tanegashima (affinity of world property island Yakushima)].
A list was drawn up of wild plants growing on Tanegashiama island that were identified in our field work, and the list was compared with the flora of the rest of Japan and the flora of Taiwan. There were 166 families and 1,218 species consisting of 23 families and 159 species of Pteridophyta, 4 families and 7 species of Gymnosperma, 113 families and 700 species of the dicotyledous Angiosperma, and 26 families and 353 species of monocotyledous Angiosperma. There are 229 families and 5,500 species of plants in Japan, 196 families and 3,019 species in Kyushu, and 228 families and 3,477 species in Taiwan. There are 11 species of endemic plants on Tanegashima and Yakushima, and the best known of them is Pinus armandii Francht. var. amamiana Hatsushima. There are 181 species of flora of flora limited to the northern element, including several important medicinal plants, such as Akebia quinata Decaisne and Zanthoxylum piperitum DC. The 69 species of flora limited to the southern element include several important tropical plants, such as Messerschmidia argentea Johnston and Clerodendrum inerme Gaertn. Most of these plants are distributed on both island, but some of are distributed only Tanegashima. We concluded that one of the temperate borderlines of Japanese flora in the temperate zone is the islands of Tokara. The flora of Tanegashima and Yakushima are having a closely affinity of plant species and having the rich plant species.
Botany↗
Evaluation of perioperative administration of methylprednisolone sodium succinate and urinary trypsin inhibitor for prevention of surgical stress.
The authors could confirm that the laparoscopy-assisted cholecystectomy (LAC) elicited less postoperative biological responses compared to the ordinary cholecystectomy under laparotomy (OCL), when granulocyte elastase (GE)-alpha1-protease inhibitor complex (GEcomplex), interleukin-6, pancreatic secretory trypsin inhibitor (PSTI) and alpha1-antitrypsin (alpha1-AT) were used as biological response markers. Perioperative administrations of methylprednisolone sodium succinate (MPSL: 10 mg/kg body weigh) or MPSL with urinary trypsin inhibitor (UTI) could suppress such postoperative reactions after OCL down to the levels after LAC, especially immediately after surgery. Preoperative MPSL followed by continuous infusion of UTI for 3 days exerted the most prominent suppressive effects on these markers compared to the effect of the preoperative MPSL alone as well as the preoperative administration of MPSL followed by UTI infusion for only one hour. Bolus administration of MPSL induced no lymphocytopenia. Decreased plasma level of alpha1-AT immediately after operation is thought to be due to consumption in binding to GE as well as other lysosomal enzymes, while production of rapid turn over proteins are still not accelerated in the liver. In early postoperative phase after administration of MPSL, administration of UTI was efficacious to prevent fluctuation of biological response markers. Clinical applications of these drugs might be approved especially for those patients with poor risk.
Adult↗
Typing for human platelet alloantigens.
Antibodies to platelet alloantigens, and sometimes to isoantigens, induce severe clinical problems such as neonatal alloimmune thrombocytopenia (NAIT), post-transfusion purpura (PTP) and refractoriness to platelet transfusions (PTR). For example, NAIT affects approximately 1 in 5,000 live births. It is essential, therefore, to screen pregnant women for platelet antibodies in order to save babies' lives. Almost 40 years ago, two platelet alloantigen systems were discovered using relatively simple methods, namely the platelet agglutination test and the complement fixation test. However, these methods were not sensitive enough to identify all antibodies in mothers and patients, even in those with severe clinical problems. Tremendous effort has been devoted to establish more sensitive and reliable methods. In recent years, excellent new serological and immunochemical methods have been established and several new platelet antigen systems have been discovered. Simultaneously, newly developed molecular genetic techniques have been introduced for the typing and analysis of human platelet alloantigen systems. These methods allow DNA typing for cases in which serological typing is not available. In this article, the history of studies on human platelet alloantigen systems and isoantigens, the nomenclature of platelet alloantigen systems and their alleles, the present status of antibody detection and typing techniques and, finally, ethnic variations in platelet antigen profiles are reviewed.
Alleles↗
AML1(-/-) embryos do not express certain hematopoiesis-related gene transcripts including those of the PU.1 gene.
The AML1 and PEBP2beta/CBFbeta genes encode the DNA-binding and non-binding subunits, respectively, of the heterodimeric transcription factor, PEBP2/CBF. Targeting each gene results in an almost identical phenotype, namely the complete lack of definitive hematopoiesis in the fetal liver on embryonic day 11.5 (E11.5). We examined and compared the expression levels of various hematopoiesis-related genes in wild type embryos and in embryos mutated for AML1 or PEBP2beta/CBFbeta. The RNAs were prepared from the yolk sacs of E9.5 embryos, from the aorta-gonad- mesonephros regions of E11.5 embryos and from the livers of E11.5 embryos and RT-PCR was performed to detect various gene transcripts. Transcripts were detected for most of the hematopoiesis-related genes that encode transcription factors, cytokines and cytokine receptors, even in tissues from homozygously targeted embryos. On the other hand, PU.1 transcripts were never detected in any tissue of AML1(-/-) or PEBP2beta/CBFbeta(-/-) embryos. In addition, transcripts for the Vav, flk-2/flt-3, M-CSF receptor, G-CSF receptor and c-Myb genes were not detected in certain tissues of the (-/-) embryos. The results suggest that the expression of a particular set of hematopoiesis-related genes is closely correlated with the PEBP2/CBF function.
Animals↗
Overexpression of AML1 renders a T hybridoma resistant to T cell receptor-mediated apoptosis.
The AML1 gene, which encodes the DNA binding subunit of the heterodimeric transcription factor, PEBP2/CBF, is involved in several types of chromosomal translocations associated with human acute myeloid leukemia, and has been shown by gene targeting to be essential for the development of definitive hematopoiesis in the murine fetal liver. In addition, the gene is expressed abundantly in T lymphocytes and has been implicated in T cell specific gene expression. In the present study we examined the function of AML1 in T cell receptor (TCR)-mediated, Fas/Fas-ligand dependent apoptosis of a T hybridoma line, DO11.10. Several independent cell clones overexpressing the AML1 protein were isolated by transfecting AML1 cDNA into these cells. These clones possessed an increased level of PEBP2/CBF DNA binding activity and were found to be resistant to apoptosis induced by anti-CD3 antibody treatment. Northern blot analysis revealed that induction of the Fas-ligand transcript was markedly suppressed in the anti-CD3 treated clones. Instead, expression of IL-2 receptor alpha subunit (IL-2R alpha), which is a manifestation of proliferative TCR signaling, was induced. This was in contrast to the parental, anti-CD3 treated DO11.10 cells where induction of Fas-ligand but not of IL-2R alpha was observed. Resistance of the AML1 overexpressing cell clones to TCR-mediated apoptosis is most likely attributable to the lack of Fas-ligand induction, since simultaneous treatment with anti-CD3 and anti-Fas antibodies caused apoptosis of the clones. The overall results suggest that the AML1 protein may play a pivotal role in switching TCR signaling between apoptosis and cell proliferation in T lymphocytes.
Animals↗
The chimeric protein, PEBP2 beta/CBF beta-SMMHC, disorganizes cytoplasmic stress fibers and inhibits transcriptional activation.
The chromosomal inversion 16(p13;q22) associated with human acute myeloid leukemia generates the chimeric PEBP2 beta/CBF beta-SMMHC gene. The PEBP2 beta/CBF beta portion of the chimeric polypeptide harbors most of the amino acid sequence of the PEBP2 beta/CBF beta protein, the non-DNA binding subunit of the heterodimeric transcription factor, PEBP2/CBF, whereas the SMMHC portion of the chimera consists of the rod domain of the smooth muscle myosin heavy chain molecule. In this study we examined the subcellular localization of the chimeric protein and its effect both on stress fibers and transcriptional activation by transfecting cDNA into tissue culture cells. The localization of the chimera was investigated by immunocytochemical staining of cells and was found to be both cytoplasmic and nuclear. One aspect of the effect of expression of the chimera was a drastic alteration of cell morphology. The cells appeared elongated and possessed long cytoplasmic processes. Double fluorescent labeling revealed disorganization of the stress fibers and an altered F-actin staining pattern in the transfected cells. Studies using a deletion mutant showed that both the PEBP2 beta/CBF beta and SMMHC domains are necessary for the induction of the morphological alteration. A significant proportion of the chimeric protein was retained in the cytoskeleton after detergent extraction of the cells and could be recuperated as a membrane fraction, suggesting that this is one of the probable sites of action of the PEBP2 beta/CBF beta-SMMHC protein. Another effect of the chimeric protein was inhibition of transcriptional activation dependent on the PEBP2/CBF binding DNA sequence. However, deregulation of PEBP2/CBF site dependent transcription by itself was not sufficient to induce cell morphological changes. Taken together, these results indicate that the PEBP2 beta/CBF beta-SMMHC chimeric protein acts at two levels, at the level of stress fiber organization and at the level of transcriptional activation. We suggest that the action of PEBP2 beta/CBF beta-SMMHC depends to a great extent on whether it is located in the cytoplasm or in the nucleus.
Acute Disease↗
Mutations of connexin32 in Charcot-Marie-Tooth disease type X interfere with cell-to-cell communication but not cell proliferation and myelin-specific gene expression.
Connexin32 (Cx32) is a gap junction protein and its mutations are responsible for X-linked Charcot-Marie-Tooth disease. We examined the functional abnormality of C6 glioma cells transfected with mutant (C53S and P172R) Cx32 genes. Nontransfected C6 did not express Cx32. Northern and Western blot analyses showed Cx32 mRNA and protein in cells with the wild-type gene as well as with the mutant Cx32 genes. An immunocytochemical study of cells with the wild-type gene showed the immunoreactive spots in the cell membrane. In cells with C53S or P172R mutant gene, however, the immunoreactivity was found in the cytoplasm. The scrape-loading method produced effective dye transfer in cells with the wild-type gene but not in those with mutant genes. A cell proliferation assay showed no differences in nontransfected cells, cells with the wild-type gene and those with the mutant genes. Messenger RNA expression for proteolipid protein did not change. These findings suggest that Cx32 gene mutation results in loss of cell-to-cell communication because of failure to incorporate Cx32 protein in the cell membrane. The mutations do not, however, interfere with cell proliferation or myelin-specific gene expression, at least myelin proteolipid protein expression in C6 glioma cells.
Blotting, Northern↗