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Biomedical subjects

J Abe

Publications and source records attributed to J Abe.

At least 109 records · Page 6Linked to original sources
PubMed1993

Angiotensin converting enzyme inhibitors or DuP753 prevent neointimal formation following balloon injury with single topical or multiple systemic application.

Angiotensin II plays an important role in neointimal formation after vascular injury. Our objectives were 1) to investigate the difference between angiotensin converting enzyme inhibitors (captopril, delapril) and an angiotensin II subtype 1 (AT1) receptor antagonist (DuP753) in suppressing neointimal proliferation; and 2) to investigate the antiproliferative effects of these drugs given topically to the injured vessels. All these treatments effectively prevented neointimal formation (p < 0.01). Even a single topical application of either type of drug with F127 pluronic gel to be injured vessel after ballooning is found to be significantly effective probably due to the inhibition of smooth muscle cell migration (p < 0.01). Multiple systemic application of angiotensin converting enzyme inhibitors was more effective than that of DuP753 at the same blood pressure level. The effectiveness of topical application of these drugs suggests clinical usefulness after angioplasty or vascular surgery.

Administration, Topical↗
PubMed1993

Evidence for superantigen production by Yersinia pseudotuberculosis.

Yersinia pseudotuberculosis is an enteric pathogen that induces a variety of clinical symptoms, fever, scarlatiniform rash, diarrhea, vomiting, and arthritis. Characteristic histopathologic findings in Y. pseudotuberculosis infection such as lymphoid hyperplasia, typically seen in mesenteric lymph nodes, suggest that the stimulation of a large proportion of T lymphocytes may be involved in the pathogenesis of this infection. In this study, we assessed the mitogenic activity of culture supernatants of the clinical isolates of Y. pseudotuberculosis and investigated the mechanism by which these culture sups activate T cells. The culture sups, as well as partially purified fractions obtained by gel filtration, were found to selectively stimulate T cells bearing V beta 3, V beta 9, V beta 13.1, and V beta 13.2 compared with stimulation by anti-CD3. Furthermore, fibroblasts transfected with different HLA class II molecules, either HLA-DPw9, -DQw6, -DR1, or -DR4 Dw15, were capable of presenting Y. pseudotuberculosis culture supernatants to purified T cells. The T cell response to this sup was not restricted by donor HLA-DR types and was not neutralized by antibodies against the known staphylococcal superantigens, Staphylococcal enterotoxin (SE)A, SEB, SEC2, SED, SEE, and TSST1. These results suggest that Y. pseudotuberculosis produces superantigenic toxins that may mediate some of the systemic illnesses associated with infection by this organism.

Animals↗
PubMed1993

Arginine is essential for the alpha-amylase inhibitory activity of the alpha-amylase/subtilisin inhibitor (BASI) from barley seeds.

Treatment of barley alpha-amylase/subtilisin inhibitor (BASI) with reagents specific for arginine, histidine, methionine and tyrosine residues and amino and carboxyl groups indicates that an arginine residue(s) is essential for its action on the target enzyme barley alpha-amylase 2. Phenylglyoxal modified eight out of 12 arginine residues in BASI. Kinetic analysis shows that the inactivation of BASI follows a pseudo-first-order reaction and is due to reaction with one molecule of phenylglyoxal; the second-order rate constant is determined to be 2.95 M-1.min-1. At pH 8.0, BASI and barley alpha-amylase 2 form an inactive 1:1 complex. The Ki value of this association is 2.2 x 10(-10) M. The alpha-amylase protects four arginine residues and also the alpha-amylase inhibitory activity of BASI against phenylglyoxal. When BASI from the phenylglyoxal-modified target enzyme-inhibitor complex is isolated and subjected to a second treatment with phenylglyoxal, four additional arginine residues are modified, with concomitant loss of the inhibitory activity. These results are discussed in relation to a three-dimensional model of BASI based on the known structure of the corresponding inhibitor from wheat.

Arginine↗
PubMed1993

Characterization of T cell repertoire changes in acute Kawasaki disease.

Kawasaki disease (KD) is an acute multisystem vasculitis of unknown etiology that is associated with marked activation of T cells and monocyte/macrophages. Using a quantitative polymerase chain reaction (PCR) technique, we recently found that the acute phase of KD is associated with the expansion of T cells expressing the V beta 2 and V beta 8.1 gene segments. In the present work, we used a newly developed anti-V beta 2 monoclonal antibody (mAb) and studied a new group of KD patients to extend our previous PCR results. Immunofluorescence analysis confirmed that V beta 2-bearing T cells are selectively increased in patients with acute KD. The increase occurred primarily in the CD4 T cell subset. The percentages of V beta 2+ T cells as determined by mAb reactivity and flow cytometry correlated linearly with V beta expression as quantitated by PCR. However, T cells from acute KD patients appeared to express proportionately higher levels of V beta 2 transcripts per cell as compared with healthy controls or convalescent KD patients. Sequence analysis of T cell receptor beta chain genes of V beta 2 and V beta 8.1 expressing T cells from acute KD patients showed extensive junctional region diversity. These data showing polyclonal expansion of V beta 2+ and V beta 8+ T cells in acute KD provide additional insight into the immunopathogenesis of this disease.

Acute Disease↗
PubMed1993

Myocardial reperfusion can be predicted by myoglobin/creatine kinase ratio of a single blood sample obtained at the time of admission.

To evaluate noninvasive markers for determining the reperfusion status without coronary angiography (CAG) or serial blood sampling in patients with acute myocardial infarction (AMI), two markers were examined: (1) serum myoglobin (Mb) level and (2) serum myoglobin/creatine kinase ratio (Mb/CK). Before emergency CAG a blood sample was drawn from 72 AMI patients within 6 hours after the onset of AMI. CAG revealed thrombolysis in myocardial infarction grades (TIMI) 0 to 1 in 56 and TIMI 2 to 3 in 16 patients (spontaneous reperfusion). No patients had received thrombolytic therapy before admission. TIMI 0 to 1 patients were characterized with lower Mb levels than TIMI 2 to 3 patients at admission (346 +/- 476 vs 1558 +/- 2005, mean +/- SD, p < 0.001). Furthermore, the mean Mb0/CK0 ratio in TIMI 2 to 3 patients, who had already achieved the reperfusion at admission, was significantly higher than that in patients with TIMI 0 to 1 patients (6.5 +/- 3.9 vs 2.1 +/- 1.8, mean +/- SD, p < 0.0001). When Mb0/CK0 > 5.0 was assumed to indicate the sufficient reperfusion at admission, the sensitivity, specificity, and accuracy evaluating the reperfusion status were 75%, 96%, and 92%, respectively. It can be concluded that the reperfusion status can be predicted satisfactorily by a single blood sample obtained at the time of admission without CAG.

Aged↗
PubMed1993

L-arginine inhibits neointimal formation following balloon injury.

Nitric oxide (NO)-generating vasodilators inhibit the mitogenesis and proliferation of cultured vascular smooth muscle cells. We investigated the role of NO in the vascular response to arterial injury by administering L-arginine (precursor of NO), D-arginine or N-nitro L-arginine methylester (NAME; an inhibitor of NO synthesis) to a rat model of balloon catheter-induced left carotid artery injury. Two weeks after the balloon injury, animals that received both oral (1.25 g/l water) and local (10mg in gel) administration of L-arginine showed suppression of neointimal proliferation with no change in systolic blood pressure. Medial proliferation was potentiated in NAME-treated animals with a higher blood pressure. Tissue cGMP content (representative of NO generation) of the injured arteries was similar to that of normal arteries with intact endothelium. These findings suggest that a higher local concentration of NO produced from L-arginine can inhibit the migration and proliferation of smooth muscle cells in the injured vascular wall.

Animals↗
PubMed1993

Pokeweed mitogen induces IgE synthesis in the presence of a blocking antibody to the interferon-gamma receptor.

BACKGROUND: Although pokeweed mitogen (PWEM) can induce peripheral blood mononuclear cells (PBMCs) to synthesize IgG, IgA, and IgM, such cultures fail to induce IgE synthesis. The present study examined the possibility that the stimulation of interferon-gamma (IFN-gamma) production plays a role in the failure of PWM to induce IgE synthesis. METHODS: We examined PBMCs from eight normal control subjects for IFN-gamma and IL-4 production. Since IFN-gamma synthesis is known to inhibit IgE synthesis, we also examined the effect of a neutralizing anti-IFN-gamma antibody and of two anti-IFN-gamma receptor antibodies, monoclonal antibody (mAb) GIR208, which blocks cellular binding of IFN-gamma, and mAB GIR94.5, which binds to the IFN-gamma receptor but does not block the binding of IFN-gamma to its receptor on PWM-stimulated PBMCs. RESULTS: After stimulation with PWM, culture supernatants contained significantly more IFN-gamma (p = 0.001) and IL-4 (P = 0.001) compared with supernatants from nonstimulated cultures. PWM-stimulated PBMCs also expressed higher levels of IFN-gamma and IL-4 gene transcripts than unstimulated cells. When cultured in the presence of anti-IFN-gamma, supernatants from PWM-stimulated cultures also induced CD23 on Ramos B cells in an IL-4-dependent manner. In the presence of mAB GIR208 and a neutralizing anti-IFN-gamma antibody, but not mAb GIR94.5, PWM stimulated PBMCs from eight normal control subjects and six patients with atopic dermatitis to produce IgE. Monoclonal antibody GIR208, however, did not enhance IgG synthesis. Furthermore, the exogenous addition of IFN-gamma inhibited the IgE-stimulatory effect of mAb GIR208. Monoclonal antibody GIR208 was unable to induce purified B cells to synthesize IgE in the presence of IL-4. CONCLUSIONS: Thus unlike anti-CD40, mAb GIR208 does not act as a second signal for the induction of IgE synthesis. These results demonstrate that the induction of IFN-gamma production contributes to the failure of PWM to stimulate synthesis of IgE in PBMCs from atopic and nonatopic donors.

Adult↗
PubMed1993

Effect of barbiturate therapy on phenytoin pharmacokinetics.

OBJECTIVE: To evaluate the effect of high-dose pentobarbital therapy on phenytoin pharmacokinetics. DESIGN: A prospective, clinical study. SETTING: The intensive care unit of a university hospital. PATIENTS: Ten adult patients with cerebral lesions requiring anticonvulsants and control of intracranial pressure. INTERVENTIONS: Each patient received phenytoin sufficient to maintain a plasma concentration at 15 micrograms/mL (60 mumol/L) both before and after barbiturate therapy. Plasma concentrations of total phenytoin, unbound phenytoin, and the major metabolite of phenytoin, 5-(p-hydroxyphenyl)-5-phenylhydantoin, were measured, and pharmacokinetic variables obtained before and after barbiturate therapy were compared. MEASUREMENTS AND MAIN RESULTS: Plasma concentrations of total phenytoin remained within the therapeutic range during the 12-hr period preceding barbiturate therapy. After barbiturate therapy, plasma concentrations of both total and unbound phenytoin were significantly less than those concentrations before barbiturate therapy. For total phenytoin, maximum metabolic velocity was increased by 62% (1.09 +/- 0.62 to 1.77 +/- 0.52 mg/L/hr, 1.20 +/- 0.68 to 1.95 +/- 0.57 nmol/L/sec, p < .05), and area under the plasma concentration-time curve (0 to infinity) and mean residence time were each decreased by 73% (32.5 +/- 20.0 to 8.7 +/- 3.1 min.mg/mL, 2.14 +/- 1.25 to 0.57 +/- 0.19 sec.mmol/L, p < .01, and 135,000 +/- 69,000 to 37,000 +/- 11,000 secs, p < .005, respectively) after barbiturate therapy. The plasma concentration of the principal metabolite of phenytoin, 5-(p-hydroxyphenyl)-5-phenylhydantoin, was significantly increased after barbiturate therapy. CONCLUSIONS: Phenytoin metabolism is increased by barbiturate therapy, and supplemental doses of phenytoin and frequent drug monitoring may be required after barbiturate therapy.

Adult↗
PubMed1993

22-Oxacalcitriol: dissection of 1,25(OH)2D3 receptor-mediated and Ca2+ entry-stimulating pathways.

22-Oxa-1,25-dihydroxyvitamin D3 (oxacalcitriol, or OCT) is a bioactive analogue of 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] with lower calcemic activity than the parent compound. We investigated the ability of OCT to stimulate 1) genomic pathways mediated by nuclear receptors for 1,25(OH)2D3 versus 2) nongenomic pathways mediated by voltage-sensitive Ca2+ channels in growth phase rat osteosarcoma cells (ROS 17/2.8) and in chick intestine. Effects on nuclear receptor-mediated pathways were evaluated by measuring the ability of OCT to compete with [3H]1,25(OH)2D3 for soluble receptors. We also measured the ability of OCT to increase mRNA encoding osteoblast marker proteins osteopontin (OPN) and osteocalcin (OCN), which are both increased by 1,25(OH)2D3. Effects on Ca2+ entry into osteoblasts were measured using 45Ca2+ influx assays. The rapid stimulation of calcium absorption (transcaltachia) in chick intestine treated with OCT also was measured. We found that OCT bound to the nuclear receptor with lower binding affinity [relative competitive index (RCI) = 48.1 for ROS 17/2.8; RCI = 14.8 for chick intestine] than 1,25(OH)2D3 (RCI = 100). Like 1,25(OH)2D3, OCT increased mRNA levels of OPN and OCN in ROS 17/2.8 cells over a 48-h period. In contrast, OCT had no effect on transmembrane influx of 45Ca2+ across ROS cell membranes, whereas uptake was stimulated within 1 min by 1 nM 1,25(OH)2D3. In transcaltachia assays in perfused duodenum, OCT stimulated absorption with a maximum response at 6.5 nM.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Genetic study on HLA class II and class III region in the disease associated with IgA nephropathy.

Increased frequency of C4 gene deletions in IgA nephropathy and Henoch-Schönlein purpura nephritis. To determine the frequency of complement 4 (C4) deficiency among the patients with IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN), C4 and factor B protein allotypes and the DNA restriction fragment length polymorphism (RFLP) of C4, steroid 21-hydroxylase (21OHase), HLA DQ beta and DR beta chain genes were studied. Genomic DNA from 32 patients with IgAN, 24 patients with HSPN and 143 controls was digested with restriction enzyme TaqI or BamHI and subjected to Southern analysis. The frequency of C4 gene deletions was significantly increased in the patients (16.1 vs. 2.8%, p = 0.002). The serum C4 concentration in patients with C4 gene deletion was significantly lower than in patients without gene deletion (11.4 +/- 2.4 vs. 19.7 +/- 5.2 mg/dl, p = 0.001). DNA-RFLP typing of DQB/BamHI and DRB/TaqI showed increased frequency of 10.26 kb of D-DQw4/8/9 (87.5 vs. 64.5%, p = 0.004) and 5.22 kb of D-DR4 (66.1 vs. 41.7%, p = 0.03) among the patients. Segregation analysis showed that the association of the D-DQw4/8/9 and D-DR4 with the diseases was not responsible for the increased frequency of C4 gene deletion in the patients. The decreased concentration of C4 in sera in C4 gene-deleted patients might be directly involved in the pathogenesis of IgAN and HSPN.

Child↗
PubMed1993

Immunohistochemical analysis of myoblast proliferation and differentiation in experimental skeletal muscle regeneration.

We investigated the onset and duration of DNA synthesis and differentiation of muscle precursor cells in the early stage in muscle regeneration after bupivacaine induced muscle necrosis using monoclonal anti-PCA and anti-desmin antibodies. The first positive PCNA reaction indicating the commencement of proliferating cycle of muscle precursor cells appeared at 24 hours after injury, and were most prominent at 60-72 hours after injury. Thereafter the reaction for PCNA disappeared as the maturation of regenerated myofibers progressed. Some nuclei of regenerated myotubes in the early stage were positive for PCNA contrary to the generally accepted concept that myonuclei after fusion were out of cell cycle. The first desmin expression was observed in mononuclear presumptive myoblasts at 48 hours after injury, some of which were also positive for PCNA in the double immunostained sections for desmin and PCNA. This result suggested that differentiation of presumptive myoblasts could already initiate during their proliferative phase.

Animals↗
PubMed1993

[A case of gliosarcoma associated with large cyst].

A case of gliosarcoma with a large cyst is reported. A 22-year-old female was admitted to our hospital with complaints of blurred vision and headache. Plain skull x-ray films showed a radiolucent area in the right frontal area. Computed tomography (CT) revealed an iso-dense mass in the right frontal lobe with a large cyst. After administration of contrast medium, the solid part and cyst wall were well enhanced and the content of the cyst was slightly enhanced. CT number of the cyst fluid was increased from 64.2 to 83.5 Hounsfield units, after administration of the contrast medium. Axial T1-weighted magnetic resonance image (MRI) revealed an iso-intense mass with marked enhancement by Gd-DTPA in the same area. A large cyst was shown to be located in the dorsal part of the mass. A small round protrusion, 10 mm in diameter, was found on the anterior portion of the mass on this MRI. Right carotid angiogram showed a tumor stain fed by the frontopolar artery. Right frontal lobectomy including the tumor was carried out with a preoperative diagnosis of glioblastoma. The patient received radiation therapy of 60Gy (whole brain 40Gy; focal 20Gy) and chemotherapy postoperatively. Histologically, necrosis, hemorrhage and endothelial hyperplasia were revealed at the tumor lesion. The tumor was composed of proliferation of glial and mesenchymal elements. The glial element appeared as fibrillary astrocytoma and polar spongioblastoma. The mesenchymal element showed sarcoma. As mentioned above, this tumor was diagnosed as gliosarcoma. It was difficult to make a diagnosis of gliosarcoma preoperatively because of the complex findings similar to malignant gliomas in conventional neuroradiological imaging.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Barley malt-alpha-amylase. Purification, action pattern, and subsite mapping of isozyme 1 and two members of the isozyme 2 subfamily using p-nitrophenylated maltooligosaccharide substrates.

Isoforms AMY1, AMY2-1 and AMY2-2 of barley alpha-amylase were purified from malt. AMY2-1 and AMY2-2 are both susceptible to barley alpha-amylase/subtilisin inhibitor. The action of these isoforms is compared using substrates ranging from p-nitrophenylmaltoside through p-nitrophenylmaltoheptaoside. The kcat/Km values are calculated from the substrate consumption. The relative cleavage frequency of different substrate bonds is given by the product distribution. AMY2-1 is 3-8-fold more active than AMY1 toward p-nitrophenylmaltotrioside through p-nitrophenylmaltopentaoside. AMY2-2 is 10-50% more active than AMY2-1. The individual subsite affinities are obtained from these data. The resulting subsite maps of the isoforms are quite similar. They comprise four and six glucosyl-binding subsites towards the reducing and the non-reducing end, respectively. Towards the non-reducing end, the sixth and second subsites have a high affinity, the third has very low or even lack of affinity and the first (catalytic subsite) has a large negative affinity. The affinity declines from moderate to low for subsites 1 through 4 toward the reducing end. AMY1 has clearly a more negative affinity at the catalytic subsite, but larger affinities at both the fourth subsites, compared to AMY2. AMY2-1 has lower affinity than AMY2-2 at subsites adjacent to the catalytic site, and otherwise mostly higher affinities than AMY2-2. Theoretical kcat/Km values show excellent agreement with experimental values.

Electrophoresis, Polyacrylamide Gel↗
PubMed1992

Selective expansion of T cells expressing T-cell receptor variable regions V beta 2 and V beta 8 in Kawasaki disease.

Kawasaki disease (KD) is an acute vasculitis complicated by the development of coronary artery abnormalities. The etiology of KD is unknown. Based on the observation that KD is associated with marked activation of T cells and monocyte/macrophages, we hypothesized that KD may be caused by a superantigen [e.g., a bacterial toxin that stimulates T cells expressing particular T-cell receptor beta chain variable (V beta) gene segments]. Peripheral blood T cells from patients in the acute and convalescent phases of KD and from various control groups were analyzed for T-cell receptor V beta gene expression by using a quantitative PCR technique and cytofluorographic analysis with available anti-V beta monoclonal antibodies. Patients with acute KD demonstrated significantly elevated levels of circulating V beta 2+ and V beta 8.1+ T cells compared to the other control groups. none of the other 20 V beta populations analyzed by quantitative PCR were found to be significantly elevated. Using flow cytometry, we confirmed a significant elevation of T cells reactive with anti-V beta 8.1 and the lack of change in several other V beta subsets--i.e. V beta 5.1, -5.2, -6.7, and -12. During the convalescence phase of KD, there was a reduction in the abnormal levels of V beta 2+ and V beta 8.1+ T cells. These observations suggest that KD may be caused by a superantigen and may provide insight into the nature of the etiologic agent.

Gene Expression↗
PubMed1992

Decreased interferon gamma and increased interleukin-4 production in atopic dermatitis promotes IgE synthesis.

The mechanism(s) responsible for increased IgE synthesis in atopic dermatitis (AD) are unknown, but they may be related to either decreased interferon gamma (IFN-gamma) and/or increased interleukin (IL)-4 production. In this study we examined peripheral blood mononuclear cells (PBMCs) from 21 patients with AD, six patients with psoriasis, and 22 nonatopic healthy controls for IFN-gamma and IL-4 production after stimulation with concanavalin A (Con A). The Con A-induced proliferative response of AD PBMCs was similar to the response of healthy controls (p = 0.9). After mitogen stimulation, however, AD culture supernatants contained significantly less IFN-gamma (p = 0.001) but increased IL-4 (p = 0.001) compared with supernatants from nonatopic controls. In contrast, PBMCs from patients with psoriasis produced normal levels of IFN-gamma and IL-4 in vitro. Since IL-4 is known to decrease IFN-gamma synthesis, we examined the effect of neutralizing anti-IL-4 on IFN-gamma production. Anti-IL-4 significantly increased IFN-gamma production in patients with AD (p = 0.008) and nonatopic controls (p = 0.02) but did not normalize IFN-gamma production by AD PBMCs. Supernatants from AD PBMCs, but not supernatants from nonatopic PBMCs, induced IgE synthesis in PBMCs from nonatopic donors (p = 0.02). When an anti-IFN-gamma receptor antibody, which blocks cellular binding of IFN-gamma, was added to supernatants from nonatopic controls their capacity to induce IgE synthesis was significantly greater (p = 0.03). These results demonstrate an imbalance of IL-4 and IFN-gamma production, which may contribute to increased IgE synthesis in AD.

Dermatitis, Atopic↗
PubMed1992

An autopsy case of Kawasaki disease with reference to occurrence of acute coronary thrombosis in the convalescent stage.

A one-year, four month-old boy who had suffered from Kawasaki disease died suddenly during convalescence despite intensive gamma-globulin treatment. Autopsy revealed a) sausage-like aneurysms of the left and right coronary arteries and fresh thrombosis in the right coronary aneurysm, b) fresh transmural myocardial necrosis in the whole wall of the left ventricle and the anterior part of the wall of the right ventricle, and c) swelling of the cervical lymph nodes and thymus (60 g). Histologically, fibrocellular thickening of the intima and destruction of the media and internal elastic lamina were conspicuous in the area of the aneurysm, but those of the intima and media in the areas adjacent to the aneurysm were mild. Abrupt narrowing of the lumen at the border between the aneurysm and periphery of the right coronary artery was detected, and this may have been responsible for formation of the thrombus in the right coronary aneurysm. In the systemic arteries, perivascular fibrosis was very noticeable despite less severe injury to the intima and media. These findings suggest that severe inflammation of the periarterial regions was present in the acute phase. The lymph system still showed inflammation, supporting the infectious or toxic nature of Kawasaki disease.

Acute Disease↗
PubMed1992

Neuronal hyaline inclusions observed in an autopsy case of Behçet's disease.

An autopsy case of Behçet's disease is reported. The patient, a 59-year-old Japanese woman, died of intestinal bleeding after a 34-year clinical course of Behçet's disease. She also suffered from recurrent oral aphthous ulcers, erythema nodosum-like cutaneous lesions and genital ulcerated lesions. Autopsy revealed marked atherosclerosis of the aorta and multiple deep ulcerations in the terminal ileum with no significant vascular lesions. Lewy bodies and globular hyaline inclusions in the neurons of the central nervous system were noted, although there were no clinical symptoms of Parkinson's disease throughout the clinical course. These findings appear to suggest that the patient was probably in the preclinical or early stage of Parkinson's disease. However, the presence of Lewy bodies in the 6th decade without any accompanying symptoms is very rare. This case seems to draw attention to the presence of these neuronal inclusions in Behçet's disease.

Autopsy↗