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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 379 records · Page 21Linked to original sources
PubMed1992

[Use of diltiazem in the anesthetic management of epinephrine predominant pheochromocytoma].

This report describes a case of epinephrine predominant pheochromocytoma successfully managed intraoperatively with an infusion of diltiazem. A 50-yr-old woman with a 10-yr history of diabetes mellitus was admitted to the hospital because of thirst and general fatigue. A cystic left adrenal tumor was found on computed tomographic scan. Although resting plasma catecholamine levels were normal, plasma norepinephrine and epinephrine levels obtained from the left adrenal vein were 1.6 ng.ml-1 (normal, 0.04-0.35) and 6.2 ng.ml-1 (normal, less than 0.12), respectively. Diltiazem was administered i. v. at a rate of 3 micrograms.kg-1.min-1 before induction of anesthesia. Anesthesia was induced with enflurane 2-3% and nitrous oxide in oxygen, followed by tracheal intubation facilitated with vecuronium. Anesthesia was maintained with enflurane 1-3% and nitrous oxide in oxygen. Paralysis was maintained with vecuronium. Hypertension during the manipulation of the tumor was controlled by increasing the inspired concentration of enflurane or by increasing the infusion rate of diltiazem to 5 micrograms.kg-1.min-1. There was no tachyarrhythmia. The infusion of diltiazem was continued until the draining vein from the tumor had been ligated. Hypotension, after removal of the tumor, was treated by the rapid infusion of fluid. Plasma norepinephrine and epinephrine levels during tumor manipulation were 1.18 ng.ml-1 and 6.57 ng.ml-1, respectively.

Adrenal Gland Neoplasms↗
PubMed1992

[Systemic plasmacytosis with polyclonal hypergammaglobulinemia and numerous plasma cells in the blood].

We report a patient with systemic plasmacytosis with polyclonal hyperimmunoglobulinemia who at presentation showed a blood and bone marrow picture suggestive of plasma cell leukemia. A 78-year-old woman was admitted to our hospital because of marked hepatosplenomegaly and generalized lymphadenopathy. She had leukocytosis with 42% plasmacytes, and plasma cells were increased also in her bone marrow (32.6%). She had marked polyclonal hyperimmunoglobulinemia with increased IgG, IgA and IgE. IgM and IgD were normal. She complained of cough and dyspnea. Her general condition was too poor to remove a lymph node for pathological examination. After treatment with daunorubicin, vincristine and prednisolone (DVP), her lymphadenopathy diminished rapidly, the immunoglobulins decreased and the plasma cells in her blood disappeared. She achieved a complete remission and has been in good condition without further treatment for 24 months.

Aged↗
PubMed1992

[Hypertrophic cardiomyopathy with rapid development of giant negative T-wave within a year: a case report].

A 61-year-old female was admitted to our hospital, presenting hypertension and giant negative T-wave (GNT) on an electrocardiogram (ECG). The ECG taken one year prior to the admission showed left ventricular hypertrophy (LVH) without GNT. Hypertension had been poorly treated during the year previous to her admission. These had been almost no administration of antihypertensive drugs. Echocardiograms, left ventriculograms and magnetic resonance imaging revealed concentric and diffuse LVH. Endomyocardial biopsy of bilateral ventricles disclosed a degeneration of myocytes and their bizarre hypertrophy with disorganization. This pathologic finding was compatible with that of hypertrophic cardiomyopathy (HCM). Although GNT has frequently been noted in apical type of HCM, the alteration from normal T-wave to GNT within a year has rarely been reported. The present case exhibited GNT on an ECG which showed no apical hypertrophy. Since GNT had developed within a year while hypertension was poorly treated, the rapid development of GNT might have been precipitated by hypertension, which possibly altered the hypertrophic pattern of the left ventricle.

Cardiomyopathy, Hypertrophic↗
PubMed1992

In situ demonstration of proliferating cells in the rat central nervous system during experimental autoimmune encephalomyelitis. Evidence suggesting that most infiltrating T cells do not proliferate in the target organ.

Experimental autoimmune encephalomyelitis (EAE) was induced in Lewis rats and the bromodeoxyuridine (BrdU)-incorporating cells were demonstrated immunohistochemically in lesions in the central nervous system (CNS) to assess the extent of T cell proliferation during EAE. In active EAE, BrdU+ cells were most numerous on day 12 postimmunization, when both clinical signs and inflammation detected by histologic examination were most severe; they declined thereafter although a considerable number of inflammatory foci remained in some rats. In passive EAE, BrdU+ cells were most numerous 2 days before the full-blown EAE and then rapidly decreased in number. On day 6 post-transfer, the CNS showed the most severe histologic changes but virtually no inflammatory cells in the lesions were labeled with BrdU. Double immunofluorescence staining with T cell (OX52) and macrophage/microglia (OX42) markers showed that about half of the BrdU+ cells were labeled with OX52 at the peak of EAE. The proportion of BrdU+OX52+ T cells at later stages was about 20%. BrdU+OX42+ cells ranged between 50 and 80% throughout the course of the disease. Furthermore, serial pulsing experiments during passive EAE revealed that inflammatory cells that had been labeled with BrdU outside the CNS and found later in the CNS were 15 times more numerous than those labeled in situ in the CNS. Taken together, these findings indicate that the majority of T cells involved in EAE undergo DNA synthesis outside the CNS and then infiltrate into the CNS, and that T cells labeled in situ in the CNS are few, and decrease rapidly in number. Since interleukin-2-receptor-positive cells detected by mAb OX39 outnumbered BrdU+ T cells at these later stages, we postulate that an unresponsive state instead of T-cell proliferation was induced in the CNS.

Animals↗
PubMed1991

Endothelium-independent and -dependent contractions induced by endothelin-1 in canine basilar arteries.

Endothelium-dependence of contractile responses to endothelin-1 was examined in isolated canine basilar arteries. Within 2 hrs after mounting tissue preparations, endothelin-1 (10(-9) M) caused a monophasic tonic contraction that developed very slowly and was sustained in intact and endothelium-removed arteries. More than 5 hrs after tissue mounting, endothelin-1 (10(-9) M) caused a biphasic contraction consisting of phasic and tonic components in intact arteries, and caused a monophasic tonic contraction in endothelium-removed arteries. This phasic component was significantly decreased by aspirin (5 x 10(-5) M,), OKY-046 (10(-5) M) (a TXA2 synthetase inhibitor) and ONO-3708 (10(-8) M) (a TXA2 antagonist). The present experiments demonstrate that endothelin-1 causes an endothelium-independent tonic contraction and an endothelium-dependent phasic contraction in canine basilar arteries, and suggest that TXA2 plays a role as an endothelium-derived contracting factor.

Animals↗
PubMed1991

Vasoinhibitory effect of NP-252, a new dihydropyridine derivative, in canine cerebral artery.

The vasoinhibitory effect of NP-252, a 1,4-dihydropyridine derivative Ca++ antagonist, was examined in canine cerebral artery, and this effect was compared with that of nifedipine. NP-252 (10(-7)M) and nifedipine (10(-6) M) nearly abolished the contraction induced by addition of Ca++ to Ca(++)-free medium containing KC1. NP-252 (10(-6)M) and nifedipine (10(-6)M) attenuated the contraction produced by thromboxane A2 agonist (STA2) in normal medium, and the resultant contractions were 22% (n = 6) and 35% (n = 6) of the control contraction, respectively. The vasoinhibitory effects of NP-252 were significantly stronger than those of nifedipine in canine cerebral artery. NP-252 (10(-7) and 10(-6) M) dose-dependently attenuated nifedipine-resistant Ca(++)-contraction in the presence of STA2 in both canine cerebral and coronary arteries. The inhibitory effect of combined treatment with NP-252 (10(-6) M) and nitroglycerin (10(-6) M) on nifedipine-resistant Ca(++)-contraction in the cerebral artery was additive. These results indicate that NP-252 possesses a stronger vasoinhibitory effect than that of nifedipine in canine cerebral artery.

Animals↗
PubMed1991

L3T4+ T cells induce hepatic lesions resembling primary biliary cirrhosis in mice with graft-versus-host reactions due to major histocompatibility complex class II disparity.

We had shown that the appearance of hepatic lesions such as epithelioid granulomas and chronic nonsuppurative destructive cholangitis (CNSDC)-like bile duct changes characteristic of primary biliary cirrhosis (PBC) in mice undergoing MHC class II-disparate graft-versus-host reactions (GVHR). To further examine the pathogenesis of the disease, we examined in the present study which T cell subset, i.e., L3T4+ or Lyt-2+ T lymphocytes, had an ability to induce such hepatic lesions. (B6 x bm12)F1 recipients were injected with unseparated T cells, L3T4+, or Lyt2+ T cells of B6 mice and on various days postinjection liver specimens were obtained. At Day 14 postinjection, livers of mice injected with whole T cells or L3T4+ T cells showed PBC-like histological changes, but none of the lesions were induced by Lyt-2+ T cells. Immunohistochemical studies revealed that Lyt-2+ as well as L3T4+ T cells were detected around bile ducts and some of them were infiltrating among bile duct epithelial cells. Kinetic studies showed that shortly after injection of L3T4+ T cells, L3T4+ T cells appeared around bile ducts and then Mac-1+ cells emerged. Lyt-2+ T cells and surface IgM+ B cells were detected on Day 5 and increased thereafter. Hepatic granulomas consisted of both L3T4+ and Lyt-2+ T cells with a few B cells. The aberrant expression of MHC class II (Ia) antigen was detected mainly at the lateral surface of bile duct epithelial cells by Day 14 postinjection. Based on these findings, the developmental mechanism of PBC-like hepatic lesions induced in mice with GVHR was discussed.

Animals↗
PubMed1991

Induced dipole moment of purple membranes. Theoretical analysis.

The induced dipole moment of a purple membrane parallel to the membrane surface was analysed based on the two-dimensional fluctuation theory of counterions. The observed polarizability previously measured by electric dichroism and its dependence on the membrane size were derived from theory for the case where the interaction between counterions was screened. The screening effect of salts on the induced dipole moment was estimated from the theory on diffuse double layers.

Journal Article↗
PubMed1991

Induction of cutaneous graft-versus-host disease by local injection of unprimed T cells.

The skin is a major target organ in human graft-versus-host disease (GVHD) after bone-marrow transplantation. GVHD can be induced in mice by i.v. injection of T cells into unirradiated semi-allogeneic or lethally irradiated allogeneic recipients. However, in the murine systemic GVHD model, cutaneous lesions occur only in lethally irradiated recipients. Since lethal irradiation itself might induce the epidermal cell damage, several investigators have employed another murine model of cutaneous GVHD, in which cutaneous lesions were induced by intradermal injection of alloreactive T cell clones. Using this system, it has been reported that both MHC class I- and II-reactive T cell clones can induce cutaneous GVHD in non-irradiated or sublethally irradiated recipients. However, it has remained unknown whether or not freshly prepared T cells are able to induce cutaneous GVHD after local injection into non-irradiated recipients. We show that unprimed T cells can induce cutaneous GVHD after local injection into unirradiated MHC class II- or I + II-disparate recipients. In contrast to alloreactive T cell clones, unprimed T cells could elicit only mild cutaneous lesions in MHC class I-disparate recipients. Since sublethal irradiation of MHC class I-disparate recipients did not result in the manifestation of cutaneous lesions after injection of unprimed T cells, host anti-donor responses by radiosensitive cells could not be responsible for this phenomenon. This experimental system provides a useful model for analysis of the regulation mechanisms in the induction of GVHD by unprimed T cells.

Animals↗
PubMed1991

Myelodysplastic syndrome with myelofibrosis: myelodysplastic syndrome as a major primary disorder for acute myelofibrosis.

Seven cases of myelodysplastic syndrome with myelofibrosis, which is defined using the following criteria: (1) pancytopenia with less than 5% blasts in the peripheral blood; (2) minimal or no splenomegaly; (3) myelofibrosis with cellular marrow; (4) absence of diffuse proliferation of blasts in the bone marrow; and (5) presence of myelodysplastic features of bone marrow or peripheral blood cells, are presented. They were in the range of 52-82 years old and consisted of 3 males and 4 females. Six out of 7 cases developed into acute leukaemia after 5 to 8 months from the onset and died from between 2 weeks to 8 months from the evolution to leukaemia. The type of leukaemia was acute myeloblastic in 3 patients, and acute myelo-megakaryoblastic in 3 patients. Another patient died of severe hepatic injury after 5 months from the onset of the disease. These findings revealed that the complication of myelofibrosis in the patients with myelodysplastic syndrome was an indicative sign of rapid progression to overt leukaemia or otherwise poor prognosis for survival. In addition myelodysplastic syndrome is thought to be major primary disorder for acute myelofibrosis. Myelodysplastic syndrome with myelofibrosis is closely associated with the neoplastic proliferation of megakaryoblasts in a considerable number of patients.

Acute Disease↗
PubMed1991

Characterization of tumor-infiltrating mononuclear cells in renal cell cancer: quantitative analysis by immunoperoxidase staining.

In order to determine whether tumor-infiltrating mononuclear cells (TIM) of renal cell cancer (RCC) is suitable for adoptive immunotherapy, their number and characteristics were examined immunohistologically. TIM consisted of T cells and a smaller number of macrophages. Among T cells, CD8-positive cells were the dominant population which was reported to be more potent for the lysis of tumor cells. The number of T cells was variable: in 5 tumors no T cells were observed and in an other 5 the number of T cells were less than 2 x 10(6) cells/cm3. These results suggest that the TIM of RCC might be favorable for adoptive immunotherapy but TIM could not be available in some cases because of their small number.

Adult↗
PubMed1991

Characteristics of giant cells and factors related to the formation of giant cells in myocarditis.

Giant cell myocarditis is a serious and frequently fatal inflammatory heart disease of which the etiology remains unknown. In the present study, we investigated the origin of multinucleated giant cells in myocarditis with the use of an experimental model. We also examined the factors relating to the formation of giant cells in myocarditis. Severe myocarditis characterized by the appearance of multinucleated giant cells was induced in Lewis rats by immunization with cardiac myosin in complete Freund's adjuvant. Two types of giant cells, foreign body giant cell-like and myocytelike, were observed in this myocarditis. Immunohistochemical studies revealed that both types of multinucleated giant cells were stained with OX42 and ED1 (macrophage markers) and were not stained with anti-desmin antibody and HHF35 (markers for muscle fibers). Therefore, it is likely that multinucleated giant cells in this myocarditis are derived from macrophages. During the course of the disease, the appearance of multinucleated giant cells was restricted to a period corresponding with the fulminant phase of inflammation. When the severity of the disease was modulated by immunization with various doses of the antigen, multinucleated giant cells appeared only in severe myocarditis after inoculation of a large dose of the antigen. Administration of immunoadjuvants also affected the formation of giant cells. Most of the rats injected with cardiac myosin in complete Freund's adjuvant developed giant cell myocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Cardiac muscle cell damage through autoimmune mechanism--can cardiac proteins provoke autoimmune myocarditis?

In this paper, the ability of human cardiac myosin to provoke autoimmune myocarditis was investigated. Myosin fractions were immunized into A.SW. mice, Lewis rats or Hartley guinea pigs. All of the immunized rats displayed overt symptoms of myocarditis and, in a few cases, died from it. The hearts of these rats were enlarged and discolored. Histologically, the muscles of the heart were characterized by remarkable cell infiltration, extensive myofiber necrosis and the appearance of polynuclear giant cells. Neither mice nor guinea pigs showed such disease profile. In this novel experimental model, the disease state was transferable by T lymphocytes. Thus, cardiac myosin was shown to provoke muscle cell damage through a T cell mediated autoimmune process.

Animals↗
PubMed1991

Effects of chronic administration of carteolol on beta-adrenoceptors in spontaneously hypertensive rat heart.

We studied the effects of chronic administration of beta-adrenoceptor antagonists with and without intrinsic sympathomimetic activity (ISA): carteolol (with ISA) and propranolol (without ISA), respectively, on the heart of spontaneously hypertensive rat (SHR) and Wistar Kyoto rat (WKY). Six-week-old SHRs and WKYs were orally given carteolol or propranolol for ten weeks. The heart rate was reduced in propranolol-treated SHR, but not in carteolol-treated ones. In WKY, carteolol-treatment increased the heart rate. The number and affinities of beta-adrenoceptors were analyzed using [3H]dihydroalprenolol as a ligand. Propranolol at 30 mg/kg increased the number of cardiac beta-adrenoceptors in both SHR and WKY. In contrast, 10 mg/kg carteolol significantly decreased the number of cardiac beta-adrenoceptors in SHR, but not in WKY. These data indicate that carteolol, a beta-adrenoceptor antagonist with ISA, does not cause up-regulation of the number of cardiac beta-adrenoceptors in the rat and suggest that this fact is related to a possible lack of "rebound phenomena" after sudden discontinuation of chronic carteolol-therapy in humans.

Aging↗
PubMed1991

Epithio-11,12-methano-thromboxane A2 stimulates inositol phosphates accumulation in isolated canine mesenteric artery strips.

Epithio-11,12-methano-thromboxane A2 (STA2), a stable analog of thromboxane A2 (TXA2), stimulated inositol phosphates (IPs) accumulation in canine mesenteric artery strips, but not in cerebral (basilar) artery strips. When canine mesenteric artery strips were incubated with 0.1 microM [3H]myo-inositol for 15 min and then stimulated with 10 microM STA2 for 30 min, there was a significant increase in 3H-IPs accumulation as measured by anion exchange chromatography (2,028 +/- 204 and 3,526 +/- 210* dpm/mg protein for basal and stimulated accumulations, respectively; means +/- S.E.M., n = 3, *P less than 0.01, significantly different from the basal value). This effect of STA2 was dose-dependent with an EC50 value of 1.6 +/- 0.2 microM. The presence of equimolar concentrations of TXA2 receptor antagonists, either ONO-3708 (9,11-dimethylmethano-11,12-methano-13,14-dihydro-13-aza-14-oxo-15 -cyclopental- 16,17,18,19,20-pentanor-15-epi-thromboxane A2) or S-1452 (5Z-7-(3-endo-phenylsulfonylamino-(2.2.1)-bicyclohept- 2-exo-yl)heptenoic acid), completely blocked the effect of STA2. These results suggest the presence of TXA2 receptors coupled with IPs accumulation in canine mesenteric artery strips. The exact location of the TXA2 receptor-IPs system, however, remains unknown.

Animals↗