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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 289 records · Page 16Linked to original sources
PubMed1995

Concentric fibrosis and cellular infiltration around bile ducts induced by graft-versus-host reaction in mice: a role of CD8+ cells.

We report in this paper on obvious fibrotic lesions in the liver of mice undergoing specified graft-versus-host reaction (GVHR). B6 CD8+ splenocytes were transferred into (bm 12 x bm 1)F1 mice to induce GVHR. Recipient mice had been thymectomized and administrated with anti-CD8 monoclonal antibody (mAb) to deplete CD8+ cells from the hosts. Two weeks after the mAb administration, recipient mice were injected with B6 CD8+ cells and sacrificed further two or four weeks later for analyzing hepatic lesions histopathologically. Light microscopic analyses revealed the presence of concentric fibrosis around both small and large duct levels and the infiltration of mononuclear cells into portal areas. Focal necrosis of hepatocytes was also detected electron-microscopically. These findings suggest that CD8+ T lymphocytes might play an important role in the induction of fibrotic lesions in the liver.

Animals↗
PubMed1995

Recipient-derived T cells participate in autoimmune-like hepatic lesions induced by graft-versus-host reaction.

Autoimmune-like hepatic lesions were induced by injection of CD4+ T cells from B10.Thy-1.1 mice into MHC class II-disparate (B10.Thy-1.1 x bm12)F1 mice. Hepatic lesions characterized by mononuclear cell accumulation in the portal area of the central vein and around interlobular bile ducts were observed in these recipients. The morphologic features of the lesions resembled primary biliary cirrhosis. The origin of T cells invading at the site of the hepatic lesions was immunohistochemically analyzed. It was shown that many recipient-derived T cells were present at the lesions and that some of them infiltrated the bile duct epithelia. Furthermore, the lesions were weakened when recipient-type T cells were depleted by thymectomy and the administration of anti-Thy-1.2 monoclonal antibody. Recipient-derived T cells were observed to take part in the formation of autoimmune hepatic lesions. These findings suggest the possibility that the tolerance of self-reactive T cells is abrogated by the graft-versus-host reaction.

Animals↗
PubMed1995

[Acute myocardial infarction during sport].

Thirty patients with acute myocardial infarction which occurred during sport were investigated to identify the type of sport, prodromata, situations at the onset of disease, habit of exercise, preceding medical evaluation, coronary risk factors, and coronary angiographic findings. Infarction occurred during golf in 12 patients, bowling in 4, gateball in 4, jogging or running in 5, baseball in 2, and tennis or table tennis in 3. The majority of the patients were playing ball games. Twenty-seven patients were men (90%) and 3 were women (10%). All patients had played the same kind of sport for several years. Twenty-four patients had one or more coronary risk factors, and especially 18 patients smoked cigarettes. Nine patients had experienced anterior chest pain but only two patients had received medical evaluation. Coronary angiography was performed in 25 patients (83.3%), revealing single-vessel disease in 14, two-vessel disease in 6, three-vessel disease in 4, and disease of all left main coronary trunks in 1. The acute episode of infarction occurred mainly in spring or fall. Many patients with acute myocardial infarction occurring during sport participate in sports of low or moderate dynamic and low static exercises which are generally regarded safe. Many patients had enjoyed their sports regularly for a long time. Though many patients had coronary risk factors, only a few had received a medical check before their heart attack.

Adult↗
PubMed1995

Increased excretion of taurine, hypotaurine and sulfate after hypotaurine loading and capacity of hypotaurine metabolism in rats.

Hypotaurine was intraperitoneally injected into rats and urinary taurine, hypotaurine and sulfate were determined. Taurine excretion increased dose-dependently when 1 to 7 mmol of hypotaurine per kg of body weight was administered. The total excretion and the increased excretion (difference of those before and after the loading) were 2328 +/- 219 and 1948 +/- 153 mumol per kg of body weight per day, respectively, at 7 mmol of hypotaurine loading. Hypotaurine excretion was negligible in the normal rat urine. However, it increased when hypotaurine was loaded. Hypotaurine excretion at 7 mmol of hypotaurine loading was 2282 +/- 258 mumol per kg per day. These results indicate that the capacity of hypotaurine oxidation to taurine in rats is more than 2 mmol per kg per day under the present experimental conditions. Sulfate excretion increased significantly when more than 3 mmol of hypotaurine per kg of body weight was injected. When 5 and 7 mmol of hypotaurine was loaded, the increased excretion of sulfate was 619 +/- 205 and 632 +/- 118 mumol per kg per day, respectively. It was confirmed that in vitro incubation of hypotaurine and 2-oxoglutarate with rat liver homogenate results in the formation of L-glutamate and sulfate. Present findings indicate that hypotaurine in vivo was mainly oxidized to taurine and that it was partly metabolized to sulfate via transamination reaction.

Animals↗
PubMed1995

[Effect of cilazapril on exercise tolerance and neurohumoral factors in patients with asymptomatic chronic heart failure after myocardial infarction].

The effects of cilazapril on exercise tolerance and neurohumoral factors were investigated in old myocardial infarction (OMI) patients with asymptomatic heart failure and reduced left ventricular ejection fraction. Cilazapril (0.5 mg) was administered once daily to OMI patients (n = 20) [NYHA class I, sinus rhythm, ejection fraction by radionuclide scanning < 50% (36.8 +/- 9.1%, mean +/- SD)]. Two weeks later, five patients were excluded from the study because of cough or hypotension, and 15 patients received 1.0 mg cilazapril once daily for the next 6 weeks. Exercise tolerance, neurohumoral factors and ejection fraction were measured in OMI patients before and after administration of cilazapril. Seven age-matched healthy adults served as the controls. OMI patients had latent heart failure because their exercise tolerance values and aldosterone levels were lower and alpha-atrial natriuretic polypeptide levels were higher than those in healthy subjects. In OMI patients, 8 weeks after cilazapril administration, exercise duration increased from 545 +/- 59 to 590 +/- 74 sec (p < 0.05), anaerobic threshold from 17.5 +/- 3.2 to 20.1 +/- 2.8 ml/min/kg (p < 0.05), peak-VO2 from 23.5 +/- 4.7 to 27.1 +/- 4.4 ml/min/kg (p < 0.05), plasma renin activity from 1.34 +/- 1.13 to 5.82 +/- 5.47 ng/ml/hr (p < 0.01) and alpha-atrial natriuretic polypeptide decreased from 100.7 +/- 44.3 to 80.5 +/- 28.0 pg/ml (p < 0.05). In patients with asymptomatic left ventricular dysfunction after myocardial infarction, 8 week's cilazapril administration improved exercise tolerance and neurohumoral conditions.

Aged↗
PubMed1995

[Exocrinopathy resembling Sjögren's syndrome induced by a murine retrovirus].

Recently, retrovirus is suggested to participate in the pathogenesis of Sjögren's syndrome (SjS). During the course of our study on mice infected with LP-BM5 murine leukemia virus, we found SjS-like systemic exocrinopathy in those mice. This virus is known to induce murine acquired immunodeficiency syndrome (MAIDS) in sensitive strains of mice. Most cells infiltrating into the glands were composed of CD3+ T cells (CD4-dominant), Mac-1+ cells and also B220+ cells. The virus genome was detected in the submandibular glands by immunohistochemistry or by PCR and the retroviral particles were also detected by electron microscopy. This mice might become an animal model for SjS and provide us with valuable informations for analysing the mechanism of how a retrovirus could induce SjS.

Animals↗
PubMed1995

[Coronary artery spasm as a cause of perioperative myocardial infarction and stunned myocardium].

We report a male patient who had recurrent coronary artery spasm on withdrawal from cardiopulmonary bypass, which led to myocardial infarction and stunned myocardium. The spasm responded to conventional medication. Transesophageal echocardiogram showed no remarkable asynergy during the operation. However, MB fraction of creatine kinase was 132 IU.l-1 and electrocardiogram showed new Q waves. After stopping intravenous catecholamines, hypokinesis of the anteroseptal segment appeared in the echocardiogram. Spotty myocardial necrosis and stunned myocardium might have resulted from recurrent coronary artery spasm.

Aged↗
PubMed1995

[Anesthetic management of patients with Young's syndrome].

Young's syndrome is characterized by chronic sinopulmonary infections and obstructive azoospermia due to systemic mucociliary transport failure. We gave anesthesia to four adult male patients with Young's syndrome for microsurgical epididymovasostomy or epididymal sperm aspiration. Preoperatively, all patients had no or mild clinical manifestation of the lung disease. Intraoperatively, however, three of four patients had voluminous tracheal discharge and two of them showed low arterial oxygen tension. Postoperatively, massive sputa secretion continued. In anesthesia for the patients with Young's syndrome, although they show no or little respiratory symptoms before anesthesia, attention should be paid to lung complication during and after anesthesia.

Adult↗
PubMed1994

Release of endogenous ATP from the caudal artery in rats with arteriosclerosis.

Noradrenaline significantly increased (by a prazosin-sensitive mechanism) the overflow of ATP and its metabolites from the caudal arteries of rats treated with excess vitamin D2 and a high-cholesterol diet (arteriosclerotic rats), although the amount of the overflow was smaller than that in the normal rats. The arteries from the arteriosclerotic rats showed a marked increase in the calcium content and there was a significant negative correlation between the noradrenaline-induced overflow of ATP and the arterial calcium content. These findings indicate that ATP release from arteriosclerotic rat caudal arteries mediated by alpha 1-adrenoceptors is impaired in proportion to the extent of arterial calcification.

Adenosine Diphosphate↗
PubMed1994

Influence of H-2 class II antigens on the development of murine AIDS.

Inbred strains of mice differ markedly in their relative susceptibility to the development of lymphoproliferation and immunodeficiency, a syndrome termed mouse AIDS (MAIDS), after infection with the LP-BM5 mixture of murine leukemia viruses (MuLV). The etiologic virus in this mixture is replication defective (BM5def) and encodes only a variant gag protein. Genetic determinants of resistance and susceptibility to induction of MAIDS reside both within and outside the MHC. In strains with C57BL background genes, the MHC haplotypes associated with resistance to disease include d and a, whereas haplotypes b, s, and q are associated with sensitivity. Previous studies showed that MHC class I genes (H-2Dd, H-2Ld) mapping in the D end of H-2 and other genes mapping proximal to the D end determine resistance to MAIDS. This paper examines the nature of these non-D end MHC genes using assays of MHC recombinant and transgenic mice. We demonstrate that expression of E alpha d confers significant resistance to MAIDS, even in mice that do not express H-2Dd/H-2Ld. Unexpectedly, we found that E alpha polymorphisms can significantly influence resistance, with H-2b mice bearing E alpha d as a transgene having greater resistance to MAIDS than mice bearing an E alpha k transgene. E alpha d-mediated resistance to MAIDS was associated with decreased levels of the BM5def genome in splenic DNA, suggesting that E alpha genes exert their effect by enhancing antiviral activity.

Animals↗
PubMed1994

NG-nitro-L-arginine-resistant endothelium-dependent relaxation induced by acetylcholine in the rabbit renal artery.

Studies were designed to determine the extent of the involvement of endothelium-derived relaxing factor(s) other than nitric oxide (NO) in vascular relaxation in response to acetylcholine (ACh) in the rabbit renal artery. ACh (10(-9)-10(-6) M) induced concentration-dependent relaxation of isolated endothelium-intact arterial rings preconstricted with noradrenaline. NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, partly inhibited the ACh-induced endothelium-dependent relaxation, whereas it almost completely abolished the production of cyclic-3', 5'-guanosine monophosphate (cGMP) in these rings in response to ACh. Methylene blue, an inhibitor of guanylate cyclase, had an essentially similar effect to L-NAME on the relaxation. Indomethacin, an inhibitor of cyclooxygenase, had no effect. High concentrations of potassium chloride (to inhibit endothelium-dependent hyperpolarization), tetraethylammonium (TEA) or 4-aminopyridine (4-AP), a voltage-dependent or Ca(2+)-dependent K+ channel blocker, partly inhibited the relaxation while, in contrast, glibenclamide, an ATP-sensitive K+ channel blocker, had no effect. Ouabain, an inhibitor of Na+, K(+)-ATPase, also partly inhibited the ACh-induced relaxation, especially the higher concentration effect. Application of L-NAME together with ouabain, TEA, or a high concentration of potassium chloride completely abolished the relaxation. These results suggest that ACh-induced endothelium-dependent relaxation in the rabbit renal artery is mediated by NO, and by an other factor(s), which relaxes the vascular smooth muscle through opening K+ channels other than ATP-sensitive ones, and/or through the activation of a Na+, K(+)-pump.

Acetylcholine↗
PubMed1994

Uchida rat (rSey): a new mutant rat with craniofacial abnormalities resembling those of the mouse Sey mutant.

A new mutant rat with small eyes (rSey) which was found in the course of breeding Sprague-Dawley rats is described. Genetic analysis demonstrates that rSey is inherited as an autosomal dominant mutation. Heterozygotes (rSey/+) have small eyes, while homozygotes (rSey/rSey) do not develop lens and nasal placodes, resulting in lack of eyes and the nose and perinatal death. rSey does not affect any other cranial regions including the maxilla, mandible, hyoid arch and otic vesicles. The genetics and phenotype of the mutant rat closely resemble the Sey mutation in the mouse, suggesting that rSey is the rat counterpart of the Sey mouse. Tissue recombination studies indicate that ectoderm from homozygotes (rSey/rSey) never differentiates into lens tissue even if it is cultured with normal optic vesicles from rSey/+ or +/+ embryos. In contrast, lens differentiation occurs when ectoderm from rSey/+ or +/+ as well as rSey/rSey embryos. These results suggest that the failure of head ectoderm from rSey/rSey embryos to differentiate into lens results from defects in the early differentiation signaling from the neural plate or underlying mesenchyme before the optic vesicle grows out to contact the head ectoderm.

Abnormalities, Multiple↗
PubMed1994

Butyrate enhances the in vitro anti-SRBC (sheep red blood cell) antibody responses in murine splenocytes.

Butyrate at concentrations of 200-600 microM markedly enhanced the in vitro antibody productions against sheep red blood cells (SRBC) in murine splenocytes. However, other saturated short-chain fatty acids, including acetate, propionate and valeric acid, and 4-carbon compounds such as butanol, acetoacetate and beta- and gamma-hydroxybutyrate had no such effects. The presence of butyrate in the early phase of the cell culture was crucial for enhancement of the response. Butyrate also augmented the antibody production in T-cell-depleted splenocytes supplemented with the culture supernatant of concanavalin A (Con A)-stimulated lymphocytes. Interleukin (IL)-2 secreted from splenocytes in response to SRBC was increased by adding butyrate to the culture, but IL-1 secretion was not affected. On the other hand, Con A or lipopolysaccharide-stimulated proliferation of splenocytes was partly depressed by the addition of butyrate, while Con A-induced IL-2 production was not effected. These findings suggest that butyrate may act on T and B cells to promote their differentiation during the process of antibody production.

Animals↗