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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 307 records · Page 17Linked to original sources
PubMed1994

Olfactory mucosal findings and clinical course in patients with olfactory disorders following upper respiratory viral infection.

Seventy patients with olfactory disorders following upper respiratory viral infection (URVI) were studied clinically, and the olfactory mucosa of 13 patients was biopsied using special biopsy forceps. The specimens were examined using immunohistochemical staining for neuron-specific enolase (NSE), S-100 protein (S-100), cytokeratin (CK), and proliferating cell nuclear antigen (PCNA). Although the clinical course of URVI-olfactory disorders was not very good, overall a high proportion of Alinamin intravenous injection test-positive patient's recovered their sense of smell. Immunohistochemical study of the biopsy specimens revealed a decrease in the number of olfactory receptor cells and nerve bundles. In a few cases the olfactory neuroepithelium was replaced by metaplastic squamous epithelium. Sometimes different types of degeneration were found in the same specimen. No PCNA-immunoreactivity was detected in the olfactory epithelium. The result generally correlated with the degree of degeneration of the olfactory mucosa, because regeneration of the olfactory receptor cells is suspected to be extremely slow or rare in humans. Alinamin test-positive patients had many olfactory receptor cells. These findings suggest that olfactory mucosal biopsy and the Alinamin intravenous injection test are useful methods of determining the prognosis in post-URVI olfactory disorders.

Adult↗
PubMed1994

Suppressive effect of cyclophosphamide on the progression of lethal graft-versus-host disease in mice--a therapeutic model of fatal post-transfusion GVHD.

In this paper, we examine in a murine system whether cyclophosphamide (CY) could prevent the development of fatal GVHD and furthermore whether it could be used to treat on-going GVHD. (C57BL/6xDBA/2)F1 (BDF1) mice were injected with spleen cells from B6 donors and their thoraces were opened to mimic cardiac operation. These mice lost body weight gradually and most of them died during 2-4 weeks post-transfusion. They showed splenomegaly, thymic atrophy and marked bone-marrow aplasia. When CY was administered at 100 mg kg-1 on days 0, 2, 7 and 9, all mice were relieved of GVHD and their organs were almost free of signs of GVHD. CY (100 mg kg-1) administered on days 7 and 9 also save mice from lethal GVHD. Moreover, CY administered at a dose of 20 mg kg-1 on days 9 and 11 when GVHD became apparent was also effective. These data suggest that CY might be used as a therapeutic agent for lethal post-transfusion GVHD.

Animals↗
PubMed1994

Parasitological and clinical studies on Wuchereria bancrofti infection in Chuuk (formerly Truk) State, Federated States of Micronesia.

A total of 2193 people in 14 villages on 9 islands was examined for microfilaria (mf). The average mf rate of those examined was 2.6%. High mf rates of 7-10% were obtained in 3 villages on 3 islands. Analysed by sex and age, the highest mf rates were observed among males of age > or = 20 years (6-10%). A clinical study conducted on 466 adult males of age > or = 15 years showed that the average hydrocele rate was 3.4% and that of elephantiasis 0.4%. For the ages > or = 50 years the hydrocele rate was nearly 10%, indicating that filariasis is an important public health problem. Filariasis in Chuuk seems to be decreasing, but some endemic villages found in the study imply the existence of many unknown and thus unattended foci of filariasis in Pacific islands.

Adolescent↗
PubMed1994

Expansion of intermediate T-cell receptor cells in mice with autoimmune-like graft-versus-host disease.

Chronic graft-versus-host disease (GVHD) following bone marrow transplantation often gives rise to a severe autoimmune-like state. To investigate the immunopathogenesis of this diseased state, mice receiving a transplant of lymphocytes with major histocompatibility complex (MHC) class II disparity (the simplest model of chronic GVHD) were examined. (B10.Thy-1.1 x B6.C-H-2bm12) F1 mice were injected with parental B10.Thy-1.1 CD4+ splenic T cells. These mice showed intensive lymphocyte infiltration of the target organs, including the liver, salivary glands and pancreas. Indeed, the cell numbers yielded from the spleen and liver were increased, and polyclonal B-cell activation was induced by 14 days after injection. More strikingly, more than 80% of such expanding lymphocytes in the target organs became T cells with T-cell receptors (TCR) of intermediate intensity (i.e. intermediate TCR cells) that carried the properties of extrathymic origin. Despite the homogeneous expansion of intermediate TCR cells in GVHD mice, these T cells were polyclonal in terms of V beta usage. These results, in conjunction with the data using the thymectomized mice as recipients, suggested that extrathymic, intermediate TCR cells possibly of recipient origin might be intimately related to the pathogenesis of the autoimmune-like state resulting from chronic GVHD.

Animals↗
PubMed1994

Preventive effects of magnesium on raised serum lipid peroxide levels and aortic cholesterol deposition in mice fed an atherogenic diet.

We examined the effects of various levels of magnesium intake on serum lipid levels and aortic cholesterol deposition in mice fed for 14 weeks on an atherogenic diet containing 10 per cent linoleic acid. During that time, the mice were given MgCl2.6H2O in drinking water at magnesium doses of 10, 50, 100, or 200 mg/kg/d. A magnesium dose of 50 mg/kg/d is approximately equivalent to the amount consumed in the normal daily diet. Throughout the experimental period, levels of both serum total cholesterol and lipid peroxides decreased relative to increases in the dose of magnesium, while levels of serum phospholipid, triglyceride, and high density lipoprotein (HDL)-cholesterol were unaffected. Levels of aortic cholesterol, particularly cholesteryl ester, decreased as the dose of magnesium increased. These findings indicate that adequate magnesium intake prevents cholesterol deposition in the aortas of mice fed an atherogenic diet, and that this was due to the inhibitory effect of magnesium on lipid peroxidation and its hypocholesterolaemic effect, suggesting in turn, that the antioxidative action of this element plays an important role in creating a defence against the development of atherosclerosis.

Animals↗
PubMed1994

[Analysis of fibroblast growth factor receptor genes expressed in the retinal pigment epithelium of chick embryos by reverse transcription polymerase chain reaction].

To characterize the mechanism by which retinal pigment epithelial cells (RPE) respond to fibroblast growth factors (FGFs), reverse transcription polymerase chain reaction (RT-PCR) was performed on 7.5-day chick embryonic RPE. We amplified and cloned tyrosine kinase related sequences from chick embryonic RPE messenger RNA and characterized the partial complementary DNA (cDNA) by nucleic acid sequencing. Three different FGF receptor (FGFR) genes were found to be expressed in 7.5-day chick embryonic RPE; two of them were cek 2 (FGFR3) and cek 3 (FGFR2), and the third one, named chick pigment epithelium derived FGFR (CPE-FGFR), has not been previously identified. The deduced amino acid sequence of CPE-FGFR is more than 70% identical with each previously characterized FGFR. It appears that the effect of FGFs on differentiation of RPE are mediated by several types of FGFRs.

Amino Acid Sequence↗
PubMed1994

[Analysis of fibroblast growth factor receptor genes expressed in the retinal pigment epithelium of chick embryos by in situ hybridization].

To study the expression pattern of fibroblast growth factor receptor (FGFR) genes cek 1, cek 2, cek 3, and a novel FGFR (chick pigment epithelium derived FGFR, CPE-FGFR) in the retinal pigment epithelium (RPE) during chick eye development, in situ hybridization was performed on sections of chick embryos. cek 1 and CPE-FGFR were expressed, but neither cek 2 nor cek 3 were expressed in 3-day, 4-day, or 5.5-day chick embryonic RPE. Four subtypes of FGFR were expressed in 7-day and 9-day chick embryonic RPE. CPE-FGFR was expressed not only in RPE but also in whole embryos. The differential expression of FGFR subtypes in RPE at different stages suggests the possibility that FGFs influence the differentiation of RPE through the control of FGFR expression.

Animals↗
PubMed1994

[A case of congenital protein C deficiency with pulmonary thromboembolism].

A 47-year-old woman, with a history of recurrent venous thrombosis in her lower limbs (1988 and June, 1992), was admitted because of pulmonary thromboembolism in the right middle lung lobe. She was given anti-coagulant therapy with warfarin. The consolidation in the right middle lobe disappeared within two months. Hematological examinations concerning the coagulation and fibrinolytic system showed a significant decrease in both the serum concentration and the activity of protein C, a vitamin K-dependent hepatic protein which acts as an anticoagulant by shutting off fibrin formation and stimulating fibrinolysis. Since a sister of the patient also has a history of venous thrombosis, several members of her family were tested for protein C deficiency. The familial study revealed that her sister and mother had both a decreased concentration and depressed activity of protein C, indicating that this is a case of congenital protein C deficiency. Warfarin therapy has been continued to reduce the prothrombin time to 70% of the normal control level, resulting in no further episodes of thrombosis.

Female↗
PubMed1994

De novo Ph-negative acute T-lymphoblastic leukemia with BCR gene rearrangement.

We herein report a rare case of Ph chromosome-negative acute T-lymphoblastic leukemia (T-ALL) with a classical BCR rearrangement seen in chronic myelogenous leukemia (CML). There were no clinical or morphologic features to suggest a previous chronic phase of CML. The importance of a full analysis of the BCR gene in the case of adult acute lymphoblastic leukemia (ALL), especially in T-ALL, are discussed.

Adult↗
PubMed1994

Mechanism of the induction of autoimmune disease by graft-versus-host reaction. Role of CD8+ cells in the development of hepatic and ductal lesions induced by CD4+ cells in MHC class I plus II-different host.

BACKGROUND: We previously reported that primary biliary cirrhosis (PBC)-like hepatic lesions were induced in (bm12xB6)F1 mice undergoing graft-versus-host reaction with major histocompatibility complex class II disparity. In this paper, we report on a new experimental system, enabling establishment of more progressed stages of PBC-like lesions and clarification of the role of CD8+ cells in the development of the lesions. EXPERIMENTAL DESIGN: Recipient (bm12xbm1)F1 mice were thymectomized and administered anti-Lyt-2 monoclonal antibodies intraperitoneally to deplete host CD8+ cells as completely as possible. The treatment was necessary to induce autoimmune hepatic lesions in this type of F1 mice. Recipients were divided into five groups: group 1 received B6 CD4+ cells on day 0 and 2 weeks later, B6 CD8+ cells; group 2, only B6 CD4+ cells on day 0; group 3, only B6 CD8+ cells on day 14; group 4, B6 CD4+ on day 0 plus F1 CD8+ cells 14 days later. Cell transfer was not done in group 5. All of the mice were killed on day 28 for examination by light and electron microscopy and also by immunohistochemistry. RESULTS: PBC-like hepatic lesions without tissue destruction were induced in the mice of group 2, as was previously reported. In addition to similar lesions to group 2, destruction of hepatocytes and bile duct epithelia was induced in the mice of group 1. Weak lymphocytic infiltration and periductal concentric fibrosis were observed in the mice of group 3. PBC-like hepatic lesions without tissue destruction were induced in mice of group 4 as were those of group 2. However, the cellular infiltration was much weaker. CONCLUSIONS: For the animal model of PBC, we have devised a new experimental system in which the role of donor or host type CD8+ cells is assessable. Tissue-destructive lesions were induced only in mice that received donor CD4+ cells followed by CD8+ cells. The PBC-like lesions were suppressed by host type CD8+ cells. These results suggest that destructive hepatic lesions of PBC might progress through CD8+ cells in cooperation with CD4+ cells, and that host type CD8+ cells could act as "regulatory" T cells for the progression of the lesions.

Animals↗
PubMed1993

Plasma-free and sulfoconjugated MHPG in major depressive disorders: differences between responders to treatment and nonresponders.

The plasma levels of free and sulfoconjugated forms of 3-methoxy-4-hydroxyphenylglycol (MHPG) were examined before and after treatment in 16 patients with unipolar major depressive disorders without melancholia. The patients were treated with intravenous administration of clomipramine for 4 weeks. Seven depressive disorder patients who showed marked improvement (the improvement group) revealed significant reduction in their plasma sulfoconjugated MHPG levels. In 6 depressive disorder patients who showed no improvement (the no-improvement group), the plasma sulfoconjugated MHPG levels showed no significant change after treatment. The remaining 3 patients, who showed ambiguous change after treatment, were excluded from the analysis. Levels of plasma-free MHPG showed significant change after treatment in neither the improvement group nor in the no-improvement group. It is suggested that levels of plasma sulfoconjugated MHPG may serve as an indicator of brain noradrenergic activity.

Adolescent↗
PubMed1993

Immunomodulation of experimental autoimmune encephalomyelitis by staphylococcal enterotoxin D.

Staphylococcal enterotoxins (SEs) can bind major histocompatibility antigens and stimulate T cells which bear particular types of T cell receptor. Therefore, it has been postulated that SEs may trigger or modulate the development of autoimmune diseases caused by T cells. In the present study, we examined the effects of SEs on rat encephalitogenic T cells and the clinical manifestation of experimental autoimmune encephalomyelitis (EAE). SED, but not other SEs, stimulated encephalitogenic T cells. Furthermore, culture of lymphoid cells from myelin basic protein (MBP)-immunized rats with SED augmented the clinical manifestation of passively transferred EAE, whereas SEA and SEB showed no significant EAE-transfer ability. Flow cytometric analysis demonstrated that in vitro SED stimulation of T cells from MBP-immunized rats, but not from normal rats, resulted in selective expansion of V beta 8.2+ T cells. Consistent with in vitro findings, in vivo administration of SED modulated EAE elicited by immunization with MBP. SED given after the immunization augmented clinical manifestation, especially at low doses. On the other hand, SED given 7 days before the immunization suppressed the development of EAE in a dose-dependent manner. Interestingly, the same toxin given at a dose of 20 micrograms to thymectomized rats induced enhanced EAE regardless of the timing of administration. It has already been established that SEs stimulate T cells bearing a particular type of TCR V beta chain and subsequently induce unresponsiveness of these T cells. The present results suggest that a similar mechanism may operate in rats after the toxin treatment and MBP immunization. However, in vitro assay showed that the proliferative responses of T cells from EAE-suppressed rats to MBP and SED were not eliminated, suggesting that SED-induced suppressor T cells may also play some roles in EAE suppression. The present study has shown that SED, one of the superantigens, modulates an autoimmune disease. More importantly, its effects are not uniform, but instead are closely related to the dose of the toxin, timing of toxin exposure, and the status of hosts.

Amino Acid Sequence↗
PubMed1993

Toxoplasma gondii: induction of toxoplasmic encephalitis in mice with chronic infection by inoculation of a murine leukemia virus inducing immunodeficiency.

Infection with the avirulent Fukaya strain of Toxoplasma gondii induced few inflammatory responses in the brain of C57BL/6 mice. When mice with chronic infection with the Fukaya strain were challenged with murine leukemia virus (MuLV) LP-BM5, which is known to induce a remarkable immunodeficiency in mice, those mice suffered from a severe encephalitis. Infiltration of mononuclear cells was remarkable in both meninges and parenchyma in those mice. Numerous sites of acute focal inflammation were noted in the brain and the presence of tachyzoites and Toxoplasma antigens was demonstrable in those areas by immunoperoxidase staining using rabbit anti-Toxoplasma IgG antibodies. All mice infected with both T. gondii and LP-BM5 MuLV died from 9 to 14 weeks after the virus infection, whereas no mice died in the infection with either T. gondii or the virus alone. Spleen cells from the mice with coinfection failed to respond to both T cell (Con A) and B cell mitogens (LPS) in vitro in contrast to the cells from mice infected with T. gondii alone that responded to those mitogens just as cells from normal mice did. Mice chronically infected with T. gondii and challenged with LP-BM5 MuLV appears to provide a good animal model of toxoplasmic encephalitis which is a major cause of morbidity and mortality in AIDS patients.

Animals↗
PubMed1993

Relative efficiencies of the maximum likelihood, maximum parsimony, and neighbor-joining methods for estimating protein phylogeny.

The relative efficiencies of the maximum likelihood (ML), maximum parsimony (MP), and neighbor-joining (NJ) methods for protein phylogeny in obtaining the correct tree topology were studied by using computer simulation. Furthermore, the robustness of the methods against departures from the assumed underlying model was studied. The following conclusions were suggested: (1) While the MP method is sensitive to the violation of constant evolutionary rate among lineages, the ML and NJ methods are robust. (2) The NJ method is efficient even if the evolutionary rate differs among lineages, but it is prerequisite to estimate the distance matrix correctly in this case. (3) The ML method is generally (with some exceptions) robust with respect to violations of the assumed model for amino acid substitution. (4) The ML and MP methods are robust to heterogeneity of evolutionary rate among sites, while the NJ method is sometimes not efficient in the heterogeneous case, unless the heterogeneity is taken into account in estimating the multiple-hit effect.

Amino Acid Sequence↗
PubMed1993

Endothelium-dependent contraction produced by acetylcholine and relaxation produced by histamine in monkey basilar arteries.

The present experiments were carried out to investigate endothelium-dependence of the responses to ACh, arachidonic acid and histamine in monkey basilar arteries. As we reported previously (1), ACh (10(-7) M) and arachidonic acid (5 x 10(-7) M) caused endothelium-dependent contraction (EDC) in both monkey and canine basilar arteries. The endothelium-derived contracting factor (EDCF) is probably TXA2, since the EDC was attenuated by a cyclooxygenase inhibitor (aspirin, 5 x 10(-5) M), thromboxane A2 (TXA2) synthetase inhibitors (OKY-046, 10(-5) M; RS-5186, 10(-6) M) and TXA2 antagonists (ONO-3708, 10(-8) M; S-145, 5 x 10(-9) M). Histamine caused endothelium-dependent relaxation (EDR) in monkey basilar arteries and EDC in canine basilar arteries. The EDR in monkey basilar arteries was attenuated by nitric oxide synthetase inhibitor, NG-monomethyl-L-arginine (L-NMMA) in a concentration-dependent manner and the EDC in canine basilar arteries was attenuated by aspirin, TAX2 synthetase inhibitors and TXA2 antagonists. The EDR and EDC were antagonized by tripelennamine (10(-6) M) but not by cimetidine (10(-5) M), indicating that they are mediated by H1-receptors. From these results, we suggest that in the monkey basilar artery, either there are two types of endothelium, an EDCF type for ACh and arachidonic acid and an EDRF type for histamine, or there is single type of endothelium with two types of signalling processes, one for EDC and one for EDR.

Acetylcholine↗