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Biomedical subjects

R Yoneda

Publications and source records attributed to R Yoneda.

At least 19 recordsLinked to original sources
PubMed2002

Heavy metals in emergent trees and pioneers from tropical forest with special reference to forest fires and local pollution sources in Sarawak, Malaysia.

Leaf samples of tropical trees, i.e. Dryobalanops lanceolata (Kapur paji), Dipterocarpaceae and Macaranga spp. (Mahang), Euphorbiaceae were analyzed for 21 chemical elements. The pioneer Macaranga spp. exhibited higher concentrations for the majority of elements compared to the emergent species of Dryobalanops lanceolata, which was attributed to the higher physiological activity of the fast growing pioneer species compared to emergent trees. Lead showed rather high concentrations in several samples from the Bakam re-forestation site. This is suggested to be caused by emissions through brick manufacturing and related activities in the vicinity. A comparison of Dryobalanops lanceolata samples collected in 1993, 1995 and 1997 in the Lambir Hills National Park revealed that certain heavy metals, i.e. Co, Cu, Mn, Ni, Pb and Ti showed higher values in 1997 compared to the previous years, which could indicate an atmospheric input from the haze caused by the extensive forest fires raging in Borneo and other parts of Southeast Asia.

Ecosystem↗
PubMed2000

Bilateral interstitial pneumonic shadows caused by perivascular fibrosis and extramedullary megakaryopoiesis of the lung in a case of advanced agnogenic myeloid metaplasia and myelofibrosis.

A 59-year-old man with progressive and advanced agnogenic myeloid metaplasia, also called idiopathic myelofibrosis, had complications showing bilateral interstitial pneumonic shadows. Pathological assessment of transbronchial biopsy revealed pulmonary perivascular fibrosis and infiltration of megakaryocytes. Autopsy 3 months later showed extramedullary megakaryopoiesis and fibrosis in lung, pleura, kidney, liver and spleen. Histopathological analysis for platelet-derived growth factor (PDGF) and PDGF-receptor revealed an abnormally high expression of the PDGF-receptor-beta gene in pulmonary fibroblasts. This is the first description of an association between pulmonary fibrosis and PDGF in idiopathic myelofibrosis.

Cell Movement↗
PubMed1999

A case of acute pancreatitis complicating Salmonella enteritis.

We report a case of acute pancreatitis complicating Salmonella enteritis. A 43-yr-old woman who was admitted to our department because of Salmonella enteritis developed clinical acute pancreatitis with laboratory and radiographic signs on the fourth hospital day. She was free from symptoms on the eighth hospital day, but her elevated serum amylase and lipase levels persisted for more than 2 m.o. In this case, clinical acute pancreatitis was a complication of bacterial enteritis caused by Salmonella enteritidis, and it was characterized by onset a few days after the onset of enteritis and by sustained elevation of serum pancreatic enzyme levels.

Acute Disease↗
PubMed1998

[Pathologic reconsideration on allergic bronchopulmonary aspergillosis and mycosis].

We examined lung specimens that fulfilled the pathological criteria of Bosken and were obtained from 5, patients with allergic bronchopulmonary aspergillosis/mycosis (ABPA/M). A finding common to all 5 was the presence of hard mucous plugs containing numerous eosinophils and fungal hyphae in the bronchi, showing central bronchiectasis. Bronchocentric granulmatosis with tissue eosinophilia (4 cases), xanthogranulomatous lesions (3 cases), eosinohilic pneumonia (2 cases) and organizing pneumonia (3 cases) were recognized only in bronchi distal to the mucous plugs (BMP). Almost normal lung parenchyma could be seen in some areas distal to the BMP. We found clusters of degenerated eosinophils (CDE) showing a "fir-tree like structure" and fungal hyphae in both the mucous plugs and the peripheral lesions. Most CDEs were free in the exudate and were not engulfed by macrophages. The presence of fungi in the mucous plugs may have caused marked inflammation in the wall around the BMP, which may have made the walls fragile and caused central bronchiectasis. The fungi in the mucous plugs may have caused the peripheral lesions via aerogenous dissemination. For this reason, we conclude that ABPA/M is an infectious disease, and that the primary lesion in ABPA/M is the formation of mucous plugs. Therefore, the presence of mucous plugs containing fungi and many eosinophils is diagnostic of ABPA/M.

Aged↗
PubMed1997

CD8 cytotoxic T-cell clone rapidly transfers autoimmune diabetes in very young NOD and MHC class I-compatible scid mice.

A CD8 T-cell clone (YNK1.3) generated from acutely diabetic NOD mouse islets, showed proliferation and cytotoxicity when challenged with NOD and BALB/c islet cells and NOD-derived insulinoma cells. When 1-2 x 10(7) YNK1.3 cells were administered to 7-10-day-old NOD mice, the cells transferred overt diabetes very rapidly in each of the 16 recipients within 4 days of cell transfer. However, of 14 recipients receiving YNK 1.3 cells above 14 days of age none became diabetic. Fluorescent dye-labelled YNK1.3 cells extensively accumulated in the islets by 36 h after transfer in 7-day-old NOD recipients, while no significant insulitis was seen in 21-day-old recipients. Over half of NOD-scid recipients (5/9) rapidly became diabetic within 5 days after transfer of 1-2 x 10(7) YNK1.3 cells at 7 days of age, whereas only one of 12 recipients over 14 days of age became diabetic. Furthermore, YNK1.3 cells also transferred diabetes to H-2Kd-matched very young BALB/c-scid and CB17-scid mice, but not to C57BL/6-scid mice. Thus, optimally activated islet-specific CD8 T-cell clones are able to rapidly transfer diabetes to NOD and MHC class I compatible scid mice when a large enough number is administered at 7 days of age. Administration of monoclonal antibodies against adhesion molecules involved in the trafficking of lymphocytes from the circulation into the inflammatory tissues, could not prevent the cellular infiltration of YNK1.3 cells into the islets in 7-day-old NOD recipients. The results indicate that islet cells in the mouse around 7 days of age are generally susceptible to cytotoxic CD8 T cells, suggesting, therefore, that CD8 T cells may play an important role in the initiation of autoimmune diabetes in NOD mice.

Adoptive Transfer↗
PubMed1997

Efficient and beta-stereoselective synthesis of 4(5)-methyl-5(4)-(5-amino-5-deoxy-beta-D-ribofuranosyl)imidazole and related compounds exhibiting antiulcer activity.

The reaction of 2,3,5-tri-O-benzyl-D-ribose with the lithium salt of an imidazole derivative gave an adduct 17RS. Treatment of 17RS with 1.5N HCl in refluxing tetrahydrofuran gave the beta-4(5)-ribofuranosylimidazole 19 (35%) and the ribosylimidazole 18 (51%). The latter was converted into beta-19 in 86% yield by the Mitsunobu cyclization. This synthetic method produced only the desired beta-anomer. Protection of the imidazole nitrogen of 19 with an ethoxycarbonyl group followed by debenzylation gave 21, which was successively derived to the 5'-amino derivative 1 via the 5'-substituted phthalimide 23, followed by hydrazine degradation in excellent yield. Compound 1 was then converted into the 5'-cyanoguanidine 2 in 79% yield. The 5'-amino derivatives 3-9 lacking a methyl group were efficiently synthesized. Among them, the cyanoguanidine 5 and phenylthiourea 8 exhibited antiulcer activities with half the efficacy of cimetidine. The molecular conformation of 5 was determined by X-ray structure analysis.

Animals↗
PubMed1997

[Pathology of bronchopulmonary aspergillosis].

This paper concerns the morphology of 3 types of bronchopulmonary aspergillosis: saprophytic aspergillosis (SPA), invasive aspergillosis (IVA) and allergic bronchopulmonary aspergillosis (ABPA)/allergic bronchopulmonary mycosis (ABPM). To know whether Aspergillus (ASP) in SPA only colonizes in preexisting cavities or presents significant pathogenecity, we examined 38 surgical specimens of SPA and 10 post-tuberculous open cavities (PT-OC). Macroscopically, SPA cavities had macroscopic ulcers (81.6%) and bronchi originating from the cavities (68.4%), in contrary to PT-OC that had neither of them. Microscopically, SPA cavities showed shallow ulcers (100%), coagulation necrosis (42.1%) and granulomatous reaction (52.6%), although ASP invasion to the viable lung tissue couldn't be discovered. The lung tissue around the SPA cavities showed various inflammation caused by transbronchial ASP dissemination from the cavities. We concluded that (1) SPA should be considered chronic destructive infection by ASP, but not colonization, (2) SPA couldn't be differentiated in quality from semi-invasive/chronic necrotizing pulmonary aspergillosis, and both should be categorized into secondary bronchopulmonary aspergillosis. Respecting IVA, we investigated 10 autopsy cases. In those cases, the disease was brought about in the lungs having no preexisting lesions. Three forms were distinguished; (1) 5 cases in that coagulation necrosis was a main feature (CN-IVA). (2) 2 cases having lung balls in cavitary lesions (LB-IVA), and (3) 3 cases showing suppurative lesions (SP-IVA). In CN-IVA and LB-IVA cases, ASP invaded to the viable lung tissue. But in 2 cases of SP-IVA, fungal hyphae were identified only in necrotic lesions but not in the viable tissue. Because the "invasive" was vague in definition, we should categorized these cases into primary bronchopulmonary aspergillosis. To determine the primary lesion of ABPA/ABPM, 5 lobectomy specimen were examined. All cases had hard or firm mucous plugs in the proximal bronchi, peripheral to which we found inflammation with tissue eosinophilia (bronchocentric granulomatosis with tissue eosinophilia : 5 cases, xanthogranuloma-like lesions : 2 cases, eosinophilic pneumonia : 2 cases and organizing pneumonia : 4 cases). Conglomerates of degenerated eosinophils, sometimes showing fir-structure, and fungal hyphae were recognized in both of mucous plugs and the peripheral lesions. We concluded that the mucous plug was the primary lesion of ABPA/ABPM.

Aged↗
PubMed1996

Induction of tolerance in murine autoimmune diabetes by transient blockade of leukocyte function-associated antigen-1/intercellular adhesion molecule-1 pathway.

The present study demonstrated that a short-term administration of mAbs against leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) at critical periods resulted in complete protection of autoimmune diabetes in non-obese diabetic (NOD) mice. When these mAbs were administered for only 6 days at 2 wk of age, neither diabetes nor insulitis was observed at 30 wk of age. It appears that the tolerance against beta cell Ag(s) was induced by this transient blockade of the LFA-1/ICAM-1 pathway. Protective suppressor activity was not enough to prevent diabetes because co-transfer of splenocytes from female NOD mice, which had received these mAbs at 2 wk of age, resulted in only a short delay of the diabetic onset caused by adoptive transfer of splenocytes from acutely diabetic NOD mice. Transfer of these splenocytes to young NOD mice could not also abrogate the spontaneous diabetes and insulitis. Furthermore, cyclophosphamide treatment could not abrogate the protection. When splenocytes from the treated NOD mice were transferred to NOD-SCID mice, none of the recipient mice developed significant insulitis and subsequent overt diabetes, suggesting the absence or the inactivation of diabetogenic effector T cells. However, splenic T cells from the insulitis-free NOD mice that had received the mAb treatment preserved proliferative responses to both islet cells and 65-kDa glutamic acid decarboxylase (GAD65) in vitro. These results suggest that a unique peripheral tolerance was induced by the transient blockade of the LFA-1/ICAM-1 pathway in an early age of NOD mice.

Adoptive Transfer↗
PubMed1996

Effects of continuous and intermittent cold (SART) stress on sympathoadrenal system activity in rats.

We compared sympathoadrenal responses to intermittent cold (SART) stress (in which cold exposure is interrupted by 4-hourly intervals daily at room temperature) with those to continuous cold (-3 degrees C) stress. Plasma levels of dihydroxyphenylalanine (DOPA), catecholamines and their metabolites as well as tyrosine hydroxylase (TH) activities in sympathetically innervated tissues were examined in rats exposed to each stressor for 1 day or for 5 days. Neither SART nor continuous exposure to cold for 1 day or 5 days altered plasma epinephrine (EPI) levels. However, norepinephrine (NE) and dihydroxyphenylglycol (DHPG) levels increased markedly during exposure to these stressors. On the first day of SART or continuous cold stress, NE levels were increased similarly, but the increments in DHPG levels were greater during SART stress. Since DHPG is formed in neurons, neural reuptake of NE may be more enhanced on the first day of SART stress than on the first day of continuous cold stress. After 5 days of SART stress plasma NE levels were significantly higher than those found after 5 days of continuous cold exposure. Plasma levels of DHPG were elevated to the same extent in both 5 days SART- and continuously cold-stressed rats, whereas plasma levels of methoxyhydroxyphenylglycol (MHPG) increased only by 5 days SART stress. Even at 1 h after the removal from 5 days SART stress, increased plasma levels of NE, DHPG and MHPG were still evident. These results suggest that 5 days SART stress elevates extraneuronal O-methylation of DHPG, and that NE turnover is more greatly increased by SART stress than by continuous cold stress. Plasma levels of DOPA, dopamine, dihydroxyphenylacetic acid and homovanillic acid also increased after either SART or continuous cold stress for 1 day and 5 days. Adrenal TH activities were significantly increased in rats exposed to SART or continuous cold stress for 1 day and 5 days, but in brown fat TH activity was elevated only in rats exposed to 5 days of continuous cold. Both SART and continuous cold stress are selective and potent stimuli for activation of the sympathoneural system, apparently without significant adrenomedullary EPI release. The increase of TH activity in the brown fat pad as well as of plasma NE and its metabolites is probably a result of adaptation to cold. It appears that even short intervals of return to a normal environmental temperature, as in SART, are sufficient to diminish sympathetic adaptation to cold.

3-Methoxy-4-hydroxyphenylethanol↗
PubMed1996

Meisenheimer rearrangement of azetopyridoindoles. VIII. Synthesis and antiviral activities of 12-carbaeudistomin analogs.

Eudistomins, isolated from the colonial tunicate Eudistoma olivaceum, have been a synthetic target due to their strong antiviral activity against Herpes simplex virus (HSV-1) and activities against certain types of tumors in vivo. In order to examine the structure-activity relationship of eudistomins, 12-carbaeudistomin analogs were synthesized and their activities against influenza A and B virus, HSV-1, HSV-2 and human cytomegalovirus were investigated. Among them, racemic 6-methoxy-12-carbaeudistomin showed similar activity to (-)-debromoeudistomin K, synthesized as a control compound.

Animals↗
PubMed1995

Administration of monoclonal antibodies against vascular cell adhesion molecule-1/very late antigen-4 abrogates predisposing autoimmune diabetes in NOD mice.

The interaction of vascular cell adhesion molecule-1 and very late antigen-4 (alpha 4 beta 1-integrin) has been recently known to be profoundly involved in the trafficking of lymphocytes from the circulation into the inflammatory tissues. To elucidate the role of these molecules in the development of autoimmune diabetes, the expression of these adhesion molecules on inflamed islets and the effects of administration of monoclonal antibodies to these molecules on insulitis and overt diabetes were evaluated in nonobese diabetic (NOD) mice. Immunohistochemical study revealed the overexpression of vascular cell adhesion molecule-1 on vascular endothelium near or within inflamed islets and alpha 4-integrin on islet-infiltrating mononuclear cells. Either anti-vascular cell adhesion molecule-1 or anti-alpha 4-integrin monoclonal antibody prevented the transfer of diabetes in irradiated NOD mice which received spleen cells from acutely diabetic NOD mice. When both monoclonal antibodies were administrated to NOD mice during 2-30 weeks of age, neither lymphocytic infiltration to islets nor overt diabetes was observed. Furthermore, administration of these antibodies even from 10 weeks of age could inhibit the development of insulitis and diabetes, whereas administration during 2-5 weeks of age could not. Splenocytes obtained from these treated mice showed no significant change of cytokine production and preserved the ability to transfer diabetes into NOD scid/scid mice. This suggests that treatment with antibodies against these adhesion molecules can inhibit insulitis and diabetes without affecting the Th1/Th2 balance or effector T cells. The blockade of vascular cell adhesion molecule-1/very late antigen-4 interaction would be suitable for therapeutical treatment of the predisposing and latent type I (insulin-dependent) diabetic subjects.

Animals↗
PubMed1995

A novel function of islet-derived CD8+T cells in initiating and developing autoimmune insulin-dependent diabetes mellitus in non-obese diabetic (NOD) mice.

Accumulated studies revealed that CD4+T cells were initially required for diabetes in NOD mice, whereas interaction of CD4+T/CD8+T cells is not fully understood. To address this question, we established islet-derived CD4+T cells and CD8+T cells from NOD mice. One NOD neonate that received CD4+T cells developed diabetes and insulitis with CD8+T cells. Administration of cyclophosphamide to non-diabetic recipients accelerated the development of diabetes, while none of the mice with anti-CD8 antibody did so. Similarly, it was observed that neonates that received islet-derived CD8+T cells developed diabetes and obvious insulitis mainly with CD4+T cells. Administration of anti-CD4 antibody with transfer of CD8+T cells inhibited insulitis. These results imply that CD8+T cells function as an initial element to recruit CD4+T cells to islets as well as a final effector.

Animals↗
PubMed1995

Occupational hypersensitivity pneumonitis in Japan: data on a nationwide epidemiological study.

OBJECTIVES: Diagnostic criteria were prepared for hypersensitivity pneumonitis (HP) and a nationwide survey was conducted to investigate epidemiological and clinical characteristics of HP in Japan. The results are presented with special focus on occupational HP and on the key to the diagnosis of HP. METHODS: A questionnaire was completed by 185 doctors from 185 hospitals (response rate 89.5%). All cases were verified according to diagnostic criteria; 835 cases were classified as HP (653 definite and 182 probable). These 835 cases (total HP) and 99 possible cases of HP diagnosed during the 1980s were analysed and presented as a case series study. RESULTS: Occupational HP was noted in 115 cases (13.8%). 21 occupations, and 20 aetiological antigens were listed. Farmer's lung: 68 cases (59% of occupational HP) was the most prevalent diagnosis followed by 19 industrial workers who handled chemicals (for example, isocyanate) and 10 office workers. Unique cases of mushroom, greenhouse, and silkworm farmers, and a new type of bagassosis are also described. Adverse environmental conditions, immunological findings on examination, antigen challenge, and pathological findings were all significantly lower for possible than for total HP. This was not true for clinical findings. The differences in antibody analysis (6% positive of possible HP v 59% of total HP) and environmental challenge (3% v 74%) were notable. CONCLUSION: These data suggest that a careful interview about the environment and an antigen panel matched to variations in exposure are the key to the diagnosis.

Alveolitis, Extrinsic Allergic↗
PubMed1995

Expression of intercellular adhesion molecule 1 on pancreatic beta-cells accelerates beta-cell destruction by cytotoxic T-cells in murine autoimmune diabetes.

Intercellular adhesion molecule 1 (ICAM-1) plays an important role in the pathogenesis of insulin-dependent diabetes mellitus (IDDM) by being involved in the extravasation of lymphocytes from the circulation into the inflamed pancreas. However, the mechanism of beta-cell destruction by which expression of ICAM-1 on beta-cells may facilitate adhesion of effector cells still remains to be elucidated. Several lines of evidence suggest that this adhesion molecule is involved in the destruction of pancreatic beta-cells by killer lymphocytes in the NOD mouse, which shows an autoimmune diabetic syndrome similar to that of human IDDM. Immunohistochemical study under light microscopy demonstrated that all of the mononuclear cells infiltrating the islets strongly expressed ICAM-1 and leukocyte function-associated antigen 1 (LFA-1), a counterreceptor of ICAM-1, whereas ICAM-1 expression on islet cells was not apparent. However, immunohistochemical staining under electron microscopy revealed that islet beta-cells adjacent to infiltrating lymphocytes were clearly stained by an anti-ICAM-1 monoclonal antibody (mAb). Flow cytometric analysis showed that the ICAM-1 expression on NOD islet cells and NOD-derived insulinoma cells (MIN6N8a) was inducible by interferon (IFN)-gamma or tumor necrosis factor-alpha. These cytokines had an additive effect on the ICAM-1 induction. Susceptibility of MIN6N8a cells to lysis by a NOD islet-derived CD8+ cytotoxic T-cell clone was greatly enhanced by IFN-gamma pretreatment, and this enhancement was abolished by anti-ICAM-1 and anti-LFA-1 mAbs. When both mAbs were administered into NOD mice with spontaneous or adoptively transferred diabetes, the development of diabetes was significantly prevented.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Prevention of autoimmune insulin-dependent diabetes in non-obese diabetic mice by anti-LFA-1 and anti-ICAM-1 mAb.

Diverse adhesion molecules participate in many important responses and thus would be implicated in the pathogenesis of various autoimmune diseases. However, there is little evidence for the role of these molecules in autoimmune insulin-dependent diabetes mellitus. Here we present several lines of evidence suggesting that leukocyte function-associated antigen-1 (LFA-1) and its counter-receptor intercellular adhesion molecules (ICAM-1), one of the most important pairs among these adhesion molecules, are involved in the development of autoimmune diabetes in the non-obese diabetic (NOD) mouse. Immunohistochemical study showed the hyperexpression of ICAM-1 on islet-infiltrating mononuclear cells and vascular endothelium in NOD pancreas. In vivo administration of anti-LFA-1 or anti-ICAM-1 mAb from 5 to 30 (or 12) weeks of age exerted a very strong preventative effect on the development of spontaneous diabetes with a marked reduction of insulitis, whereas both antibodies, even combined to use simultaneously, could not prevent cyclophosphamide-induced diabetes. Adoptive transfer of insulitis and diabetes to young NOD mice following the injection of islet-derived mononuclear cells from diabetic donors was completely blocked by administration of both antibodies to recipients. The present study, therefore, provides the first evidence that immunointervention to LFA-1-ICAM-1 interaction has a strong prophylactic effect on autoimmune diabetes in NOD mice.

Animals↗
PubMed1994

Meisenheimer rearrangement of azetopyridoindoles, VI. Synthesis of 12-carbaeudistomin and related compounds.

For structure-activity relationship investigation of eudistomins 1, 12-carbaeudistomin 3, its 1,10-trans isomer 4, and 11,12-didehydro-12-carbaeudistomin 5 have been synthesized. The [2,3]-Meisenheimer rearrangement of the corresponding N-oxide of the 2-vinylazetopyridoindole 12a bearing a benzenesulfonyl group as a protective group of the indole nitrogen atom afforded the oxazepino ester 14, which was easily isomerized to 20a. Compounds 3 and 4 were synthesized from 14 and 20a, respectively, according to the following reaction sequences [hydrogenation of the double bond (Pd-C/H2), desulfonylation (Mg in MeOH), hydrolysis (AlBr3-EtSH), and Curtius rearrangement (a mixed anhydride method using NaN3), followed by debenzylation (Pd-C/H2)]. The Curtius reaction of the carboxylic acid 27 using DPPA gave the carbamate 29, which was subjected to debenzylation (AlBr3-EtSH) followed by desulfonylation (LiAlH4) to afford 5. Evaluation of anti-influenza virus activities of the amino compounds 3, 4, and 5 revealed that 12-carbaeudistomin 3 possesses a specific activity against influenza virus B.

Antiviral Agents↗