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Biomedical subjects

M Isobe

Publications and source records attributed to M Isobe.

At least 199 records · Page 11Linked to original sources
PubMed1996

Radiofrequency catheter ablation of supraventricular tachycardias in patients with hypertrophic cardiomyopathy.

Supraventricular tachycardias, as well as ventricular tachycardia, are critical patients with hypertrophic cardiomyopathy. Anti-arrhythmic agents often induce arrhythmias, known as pro arrhythmia. Radiofrequency catheter ablation has become a well-established therapy for the treatment of supraventricular tachycardia. The reported success rate is over 90%, although catheter mapping in the left ventricle is difficult in patients with hypertrophic cardiomyopathy because of the marked left ventricular wall thickening associated with bizarre myocardial hypertrophy with disorganization, the abundant capillary muscle networks, and annoying ventricular arrhythmias. This report documents catheter mapping technique of radio frequency ablation in patients with hypertrophic cardiomyopathy and supraventricular tachycardias.

Adult↗
PubMed1996

The role of cell adhesion molecules in allograft rejection after penetrating keratoplasty in mice. Clinical and immunohistochemical study.

BACKGROUND: It has been reported that adhesion molecules play an important role in immunological rejection after organ transplantation. In the present study, we examined the role of ICAM-1/ LFA-1 adhesion molecules in corneal allograft rejection and evaluated the immunological specificity of monoclonal antibodies (mAbs) in preventing allograft rejection in mice. METHODS: The allografted mice were intraperitoneally injected with 100 micrograms/day of the following mAbs: a control mAb, anti-ICAM-1 mAb, anti-LFA-1 mAb, or a mixture of anti-ICAM-1 and anti-LFA-1 mAbs from 1 day before to 7 days after surgery. The expression of ICAM-1 and LFA-1 molecules in the grafted cornea was studied immunohistochemically. The corneas from a syngeneic donor or a third-party strain were transplanted 4 weeks after the initial keratoplasty onto the mice treated with both anti-ICAM-1 and anti-LFA-1 mAbs. RESULTS: The allografts treated with anti-LFA-1 mAb alone or both anti-ICAM-1 and anti-LFA-1 mAbs remained transparent for more than 2 weeks, and the survival rate at 8 weeks was 40% in both groups. ICAM-1 was expressed on the mononuclear cells, keratocytes and endothelial cells in the allografts without treatment. The second corneal grafts syngeneic to the initial donor remained transparent at 2 weeks, whereas those from the third party were rejected. CONCLUSIONS: ICAM-1 and LFA-1 adhesion molecules play a crucial role in the pathophysiology of corneal transplant rejection. The immunosuppressive effects of anti-ICAM-1 and anti-LFA-1 mAbs are highly allospecific. The administration of mAbs to the adhesion molecules represents a new means of suppressing allograft rejection after penetrating keratoplasty.

Animals↗
PubMed1996

Monoclonal antibody against lymphocyte function-associated antigen 1 inhibits the formation of primary biliary cirrhosis-like lesions induced by murine graft-versus-host reaction.

Interaction between intercellular adhesion molecule 1 (ICAM-1) and lymphocyte function-associated antigen 1 (LFA-1) might be involved in the pathogenesis of liver diseases. We investigated whether monoclonal antibodies (mAbs) against these two adhesion molecules could inhibit the formation of primary biliary cirrhosis (PBC)-like lesions in an animal model using graft-versus-host reaction (GVHR) with major histocompatibility complex class II disparity. PBC-like hepatic lesions such as cellular infiltration of portal area and nonsupprative destructive cholangitis (NSDC) were generated by injecting spleen T cells of C57BL/6 (B6) mice into (B6. C-H-2bm12 X B6) F1 mice. In the liver of these mice, increased number of LFA-1-positive cells and enhanced expression of ICAM-1 on sinusoidal endothelial cells and bile duct epithelial cells were observed immunohistochemically, when compared with F1 mice without GVHR. Hepatic lesions of these mAb-treated mice were almost completely inhibited in these mice compared with GVHR mice. Furthermore, we studied to determine which anti-LFA-1 mAb or anti-ICAM-1 mAb was essential to inhibit the hepatic lesions. Mice solely treated with anti-LFA-1 mAb showed significant inhibition of hepatic lesions, whereas treatment with anti-ICAM-1 mAb could not inhibit the lesions. Despite the inhibition of hepatic lesions, induction of GVHR and production of antimitochondrial antibodies were not impaired in mAb-treated mice. We conclude that LFA-1 mediates cell infiltration into the liver in this murine model of GVHR and suggest a possible therapeutic role of mAbs to this adhesion molecule in selective autoimmune liver diseases.

Animals↗
PubMed1996

18S ribosomal RNA gene sequences of three Panax species and the corresponding ginseng drugs.

Total DNA was extracted from the fresh underground parts of three Panax separate species. The 18S rRNA regions of extracted DNA were amplified by the polymerase chain reaction (PCR) and their sequences were determined. In each species, the sequences were found to be of 1809 base pairs (bps) but with different gene sequences. Different base substitutions were observed at nucleotide positions 497, 499, 501 and 712. The same procedure was performed on commercial samples of Ginseng Radix, Panacis Japonici Rhizoma and American Ginseng. Each sequence completely corresponded with that of each original plant, namely P. ginseng, P. japonicus and P. quinquefolius, respectively. This is the first time that 18S rRNA gene sequencing on Panax species was carried out. Previously, Ginseng drugs have been identified mainly by their external and internal structure. Thus this method will be useful in identifying Ginseng drugs at the gene level.

Base Sequence↗
PubMed1996

[Allo-cytotoxic T lymphocyte responses in corneal allografted mice treated with monoclonal antibodies to adhesion molecules].

Corneal transplantation was performed by grafting C3H/He donor corneas into BALB/c corneal beds. The allografted mice were injected either with 0.5 mg/day of anti-very late antigen (VLA)-4 antibody, anti-leukocyte function-associated antigen (LFA)-1 antibody, or 0.25 mg/day each of both antibodies on days -2, 0, 1, 3, 5, and 7. After 3 weeks, cytotoxic T lymphocyte (CTL) responses to donor alloantigens were assessed. Splenocytes in the allografted mice without treatment demonstrated greater CTL responses that those in naive mice. CTL responses were depressed in mice treated with either anti-LFA-1 alone or a combination of anti-LFA-1 and anti-VLA-4 antibodies as compared with splenocytes from allografted mice without treatment. These data suggest that CTLs play significant roles in eliciting immune response to corneal allografts.

Animals↗
PubMed1996

Staging of cardiac rejection by simultaneous administration of 123I-antimyosin and 111In-anti MHC class II antibodies.

Noninvasive diagnosis of cardiac rejection before the advent of myocyte necrosis is important in clinical management of cardiac transplantation. Mice with abdominal heart transplants were studied to determine whether a dual scintigraphy using antimyosin and anti-major histocompatibility complex (MHC) class II antigen monoclonal antibody (mAb) labeled with different isotopes allows to detect early rejection just before myocyte necrosis. Allografts from BALB/c donors were transplanted into C3H/He recipients. Mice were intravenously injected with 100 microCi each of 123I labeled antimyosin and 111In labeled anti-MHC class II mAbs and were sacrificed for gamma counting from 2 to 9 days after transplantation. Localization of two different isotopes was compared with histological degree of acute rejection. Uptake of 111In labeled anti-MHC class II mAb increased from the fourth day after transplantation, however, that of 123I labeled antimyosin mAb was shown only 9 days after transplantation. Induction of MHC class II antigen develops preceding the development of myocyte necrosis, and this difference in time course can be identified by the dual scintigraphy. Thus, dual scintigraphy using anti-myosin and anti-MHC class II mAbs is potentially useful in staging of cardiac rejection.

Animals↗
PubMed1996

Cadmium injures tube formation by cultured human vascular endothelial cells.

The effect of cadmium chloride (Cd; CdCl2) on the tube formation by cultured human umbilical vascular endothelial cells (HUVEC) was examined. HUVEC were collected by enzymatic digestion with collagenase. Tube formation was studied by culturing the cells on a gelled basement membrane matrix (Matrigel). Treatment of HUVEC with 0.1 microM-1.0 mM Cd for 24 hours inhibited tube formation dose-dependently. The cadmium concentration inhibiting tube formation by 50% relative to untreated cells was about 150 microM. The length of tube formation decreased time-dependently with 150 microM Cd. The treatment of HUVEC by 50 nM of beta-phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C, increased tube formation. However, the inhibitory effect of Cd on tube formation was not affected by the addition of PMA. The pretreatment of the Matrigel by Cd inhibited tube formation similarly to the results of Cd treatment. These findings suggest that Cd inhibits the formation of a capillary network by HUVEC, and that the Cd-inhibitory effect on tube formation may have been dependent in this study on the degeneration of Matrigel by Cd.

Cadmium Chloride↗
PubMed1995

TCL1 oncogene activation in preleukemic T cells from a case of ataxia-telangiectasia.

The TCL1 oncogene on human chromosome 14q32.1 is involved in chromosome translocations [t(14;14)(q11;q32.1) and t(7;14)(q35;q32.1)] and inversions [inv14(q11;q32.1)] with TCR alpha/beta loci in T-cell leukemias, such as T-prolymphocytic (T-PLL). It is also involved in T-acute and -chronic leukemias arising in cases of ataxia-telangiectasia (AT), an immunodeficiency syndrome. Similar chromosomal rearrangements occur also in the clonally expanded T cells in AT patients before the appearance of the overt leukemia. We have analyzed the expression of TCL1 mRNA and protein in peripheral blood lymphocytes (PBLs) from four AT cases and from healthy controls. We found that the TCL1 gene was overexpressed in the PBLs of an AT patient with a large clonal T-cell population exhibiting the t(14;14) translocation but not in the lymphocytes of the other cases. Fluorescence in situ hybridization of the TCL1 genomic locus to lymphocyte metaphases from the AT patient with the T-cell clonal expansion showed that the breakpoint of the t(14;14) translocation lies within the TCL1 locus and is accompanied by an inverted duplication of the distal part of chromosome 14. These data indicate that TCL1 is activated in preleukemic clonal cells as a consequence of chromosome translocation involving sequences from the TCR locus at 14q11. Deregulation of TCL1 is the first event in the initiation of malignancy in these types of leukemias and represents a potential tool for clinical evaluation.

Adolescent↗
PubMed1995

A novel dodecadepsipeptide, cereulide, is an emetic toxin of Bacillus cereus.

A vacuole-formation substance, cereulide of Bacillus cereus, is an emetic toxin in animals. Both oral administration and intraperitoneal injection of cereulide caused dose-dependent emesis in Suncus murinus, a new animal model of emesis. Vagotomy or a 5-HT3 receptor antagonist completely abolished this emetic effect. Therefore, cereulide causes emesis through the 5-HT3 receptor and stimulation of the vagus afferent. We also found that our purified cereulide caused swelling of mitochondria of HEp-2 cells.

Animals↗
PubMed1995

Inhibition of specific binding of okadaic acid to protein phosphatase 2A by microcystin-LR, calyculin-A and tautomycin: method of analysis of interactions of tight-binding ligands with target protein.

Several groups have reported that okadaic acid (OA) and some other tight-binding protein phosphatase inhibitors including microcystin-LR (MCLR), calyculin-A and tautomycin prevent each other from binding to protein phosphatase 2A (PP2A). In this paper, we have introduced an improved procedure for examining to what extent the affinity of an enzyme for a labelled tight-binding ligand is reduced by binding of an unlabelled tight-binding, ligand to the enzyme. Using this procedure, we have analysed the dose-dependent reduction of PP2A binding of [24-3H]OA by addition of OA, MCLR, calyculin-A and tautomycin. The results indicate that the binding of the unlabelled inhibitors to the PP2A molecule causes a dramatic (10(6)-10(8)-fold) increase in the dissociation constant associated with the interaction of [24-3H]OA and PP2A. This suggests that OA and the other inhibitors bind to PP2A in a mutually exclusive manner. The protein phosphatase inhibitors may share the same binding site on the PP2A molecule. We have also measured values of the dissociation constant (Ki) for the interaction of these toxins with protein phosphatase 1 (PP1). For MCLR and calyculin-A, the ratio of the Ki value obtained for PP1 to that for PP2A was in the range 4-9, whereas it was 0.01-0.02 for tautomycin. The value of tautomycin is considerably smaller than that (0.4) calculated from previously reported Ki values.

Antifungal Agents↗
PubMed1995

Immunosuppressive effect of monoclonal antibodies to ICAM-1 and LFA-1 on peripheral nerve allograft in mice.

This study evaluated the immunosuppressive effect of monoclonal antibodies against cell surface molecules in a murine peripheral nerve allograft model. After nerve allografting, 18 recipients were treated with both anti-intercellular adhesion molecule-1 (ICAM-1) and anti-lymphocyte function-associated molecule-1 (LFA-1) monoclonal antibodies in low or high dose. Nerve allografts were harvested at 8 weeks for histologic and morphometric evaluation. Recipients were subsequently challenged with skin grafts at 9 weeks and a cytotoxic assay at 12 weeks. The majority of the antibody-treated allografts (13 of 18) showed excellent regeneration comparable to the autografts with preservation of the normal nerve architecture and scant cellular infiltrate. All untreated allografts demonstrated severe structural disorganization with cellular infiltrate consistent with acute rejection. In the high dose group, the mean skin graft survival time from nerve donor mice, but not third-party mice, was significantly prolonged. (17.5 vs. 11.3 days). Similarly, the cytotoxic activity against nerve donor alloantigen was significantly suppressed. These preliminary findings suggest that antibody therapy alone can facilitate nerve regeneration in a murine nerve allograft model.

Animals↗
PubMed1995

Cerebral hemodynamics and "re-build-up" phenomenon on electroencephalogram in children with moyamoya disease.

"Re-build-up" phenomenon, induced by hyperventilation, is a characteristic finding on electroencephalogram (EEG) in children with moyamoya disease, and suggests close correlation with cerebral ischemic attack. Its mechanism, however, remains obscure. In this study, we examined the relationship between the cerebral hemodynamics and this phenomenon before and after vascular reconstructive surgery. Regional cerebral blood flow and its reactivity to acetazolamide were analyzed using the xenon-133 inhalation method and single photon emission computed tomography in six children with moyamoya disease. These results were compared with the EEG. Regional vasoreactivity to acetazolamide was significantly lower in "re-build-up" -positive regions than in "re-build-up" -negative regions. Postoperative studies revealed a significant improvement of reactivity in the regions where the "re-build-up" phenomenon disappeared after surgery. These results suggest that the "re-build-up" phenomenon represents a focal reduction of the cerebral perfusion reserve in moyamoya disease.

Acetazolamide↗
PubMed1995

Intercellular adhesion molecule-1 induction: a sensitive and quantitative marker for cardiac allograft rejection.

OBJECTIVES: Rats with abdominal heterotopic heart transplants were studied to determine whether cardiac allograft rejection could be assessed by immunoscintigraphy targeting intercellular adhesion molecule-1 (ICAM-1), which was induced on allografted organ cells in association with rejection. BACKGROUND: It is important to detect early rejection before development of myocyte necrosis. Although a variety of methods for the detection of cardiac rejection have been investigated, histologic inspection of biopsied samples is still used routinely for clinical diagnosis of rejection. METHODS: DA rat (RT-1a) hearts were transplanted into PVG rats (RT-1c). Immunohistologic examination of the allografts demonstrated that ICAM-1 induction on vascular endothelial cells was observed as early as 4 days after transplantation in this combination. Thirty-nine allografted rats and seven isografted rats were studied. One day after injection of 100 microCi of 111Inlabeled anti-ICAM-1 monoclonal antibody (1A29), planar images were obtained. RESULTS: Rejecting allografts showed increased radiotracer uptake and could be identified on the images as early as 5 days after transplantation. In contrast, nonrejecting cardiac allografts and isografts did not show specific uptake. Mildly rejecting allografts, with mononuclear cell infiltration but without significant myocyte necrosis, could be scintigraphically identified, and the level of radiotracer uptake reflected the histologic severity of rejection. Accumulation of 111In-labeled monoclonal antibody of isotype-matched irrelevant specificity was not detected in the rejecting allografts. CONCLUSIONS: These data indicate that ICAM-1 induction can be assessed quantitatively by radioimmunoscintigraphy. Radioimmunoscitigraphy is a sensitive method for early detection and assessment of cardiac allograft rejection.

Abdomen↗