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Biomedical subjects

E Yamaguchi

Publications and source records attributed to E Yamaguchi.

At least 91 records · Page 5Linked to original sources
PubMed1994

[Angiotensin-converting enzyme (ACE) polymorphism and serum ACE activities in sarcoidosis].

Recently, a genetic control of serum ACE (SACE) levels has been suggested by the identification of an insertion/deletion (I/D) polymorphism of the ACE gene by Rigat et al. We have also confirmed significant association between ACE gene polymorphism and SACE activities both in controls and sarcoidosis and established the new reference intervals of SACE activities for each genotype. The new reference intervals improved discrimination between normal and abnormal SACE activities. The frequencies of two alleles (I/D) in Japanese were quite different from those in whites and the insertion allele was dominant in Japanese. This genetic variation may affect the pathogenesis and prognosis of various diseases such as sarcoidosis and ischemic heart diseases.

Alleles↗
PubMed1993

Two independent macrophage receptors for acetylated high-density lipoprotein.

We previously demonstrated that acetylated human high-density lipoprotein (acetyl-HDL) was recognized by a scavenger receptor of rat sinusoidal liver cells (Murakami, M., Horiuchi, S., Takata, K. and Morino, Y. (1987) J. Biochem. (Tokyo) 101, 729-741). The present study describes the interaction of acetyl-HDL with rat peritoneal macrophages in vitro. Acetylation of HDL enhanced its cell-association by 2-fold and cellular degradation by > 25-fold. The cell-association of [125I]acetyl-HDL was effectively inhibited by unlabeled acetyl-HDL (> 85%), whereas the inhibition by HDL or acetylated human low-density lipoprotein (acetyl-LDL) was partial (60% and 50%, respectively). However, when both HDL and acetyl-LDL were present, the cell-association of [125I]acetyl-HDL was effectively inhibited by > 80%, a level identical or closely similar to that by acetyl-HDL. The cellular degradation of [125I]acetyl-HDL was effectively suppressed by acetyl-LDL whereas the effect of HDL was much weaker. These findings indicate that acetyl-HDL is endocytosed by both the HDL receptor and the scavenger receptor for acetyl-LDL in which the ligands bound to the latter might be subjected to lysosomal degradation.

Acetylation↗
PubMed1993

Correlation of GM-CSF mRNA in bronchoalveolar fluid with indices of clinical activity in sarcoidosis.

BACKGROUND: Granulocyte-macrophage colony stimulating factor (GM-CSF) has several proinflammatory effects, some of which potentially favour granuloma formation. Its mRNA expression by the inflammatory cells recovered from lungs of patients with pulmonary sarcoidosis has been previously reported. In this study an association between GM-CSF expression and manifestations of the disease was explored. METHODS: GM-CSF mRNA was detected by reverse transcription polymerase chain reaction in the cells of bronchoalveolar lavage (BAL) fluid of 20 patients with pulmonary sarcoidosis. RESULTS: GM-CSF mRNA expression was positive in 15 of 20 patients with sarcoidosis. Fourteen of the 15 patients with positive mRNA expression had worsening or unchanged disease during the year preceding this study, on the basis of radiographic or physical findings, or both, whereas all five "negative" patients were judged to be improving. Similarly, serum levels of angiotensin converting enzyme, the proportion of lymphocytes in BAL fluid, and the CD4+/CD8+ ratio of lymphocytes in BAL fluid were significantly higher in the positive patients. CONCLUSIONS: There was an association between the presence of GM-CSF mRNA in the cells in BAL fluid and other indices of disease activity in sarcoidosis.

Adult↗
PubMed1993

Release of tumor necrosis factor-alpha from human alveolar macrophages is decreased in smokers.

It is known that smoking affects the development and maintenance of certain types of granulomatous lung diseases. To explore this mechanism(s), we measured tumor necrosis factor (TNF)-alpha concentrations in the culture supernatants of lipopolysaccharide (LPS)-stimulated alveolar macrophages (AMs) in 13 healthy nonsmokers, 13 healthy smokers, 13 nonsmoking sarcoid patients, and 16 smoking sarcoid patients. We found that the capacity of smokers' AMs to release TNF-alpha was significantly decreased both in the normal and sarcoid groups. We also confirmed the previous observation that there was an exaggerated TNF release in patients with pulmonary sarcoidosis. These results indicate a significant role of TNF-alpha in the pathogenetic mechanisms of pulmonary sarcoidosis and suggest the possible involvement of TNF in the mechanisms by which smoking modulates local immune phenomena.

Adult↗
PubMed1993

Acute rise in serum immunoglobulin E concentration in pulmonary thromboembolism.

Events mediated by immunoglobulin E (IgE) may be related to platelet activation and aggregation, and there may be an association between IgE and pulmonary thromboembolism (PTE). Fourteen patients with PTE were studied with regard to serum concentrations of IgE, IgA, IgG, IgM, fibrinogen, and D-dimer and with regard to blood neutrophil, lymphocyte, platelet, and eosinophil counts during acute and recovery phases. The serum IgE concentration increased during the acute phase to 402 +/- 310 IU/ml and decreased afterwards in all patients. The increase in serum IgE concentration lagged a few days behind that of the serum D-dimer concentration, indicating later IgE production than thrombus formation and lysis. Infarction and pleural fluid accumulation developed in patients with a high initial serum IgE concentration. These results indicated a relationship between serum IgE concentration and the pathophysiology of PTE. Serum IgE may be an indicator of the severity of PTE and provide insight into its pathogenesis, thereby facilitating the diagnosis of PTE.

Adult↗
PubMed1993

[A case of interferon-alpha-induced pneumonitis].

We report a case of interferon-alpha-induced pneumonitis. A 61-year-old man was diagnosed as having recurrence of renal cell carcinoma and treated with 3 x 10(6) unit of interferon-alpha daily for 8 weeks. On the 55th injection, he presented with a high fever and mild dyspnea, and his chest CT films revealed diffuse reticulonodular shadows in both lung fields. We suspected interstitial pneumonitis due to interferon-alpha, and started steroid therapy. He showed rapid improvement of symptoms and diffusing capacity, and the pulmonary infiltrates in his chest CT were markedly reduced. Transbronchial lung biopsy (TBLB) revealed slightly thickened alveolar walls and small granulomatous-like lesions. These granulomatous-like lesions showed marked accumulation of macrophages. To our knowledge, this is the first report of interferon-alpha-induced pulmonary injury in Japan.

Carcinoma, Renal Cell↗
PubMed1993

A follow-up study of resected stomach cancer patients with special emphasis on the incidence of second primary cancers.

The causes of death in long-term survivors of stomach cancer after a gastrectomy have been investigated in a follow-up study of 320 such patients, with special focus on the postoperative development of a second primary cancer. The five- and 10-year overall survival rates of early stomach cancer patients were 87.5 and 75.8%, respectively, and of advanced stomach cancer patients, 44.2 and 37.5%, respectively. A multivariate analysis identified the patient's age and stage of cancer at the time of diagnosis as separate prognostic factors for overall survival. During the observation period, 15 (4.7%) patients developed a second primary cancer, so that no significantly elevated risk of developing a second primary cancer was demonstrated. During the same observation period, however, 48 (15%) of the patients died of a non-cancerous disease, 12 succumbing to an acute myocardial infarction and/or heart failure. Given these results, it is felt that continued follow-up of long-term stomach cancer survivors should be pursued to prevent or impede the development of a non-cancerous disease and/or a second primary cancer, so that the life of such former patients can be prolonged.

Adult↗
PubMed1993

[Studies on the responsiveness of alveolar T cells to proliferative stimuli and on surface antigens].

Lymphocyte alveolitis which can be detected by bronchoalveolar lavage is a characteristic feature of pulmonary sarcoidosis and has been thought to be a latent or preceding pathogenetic process of granuloma formation in the lung. To explore the mechanism of this lymphocyte accumulation, the capacity of alveolar T cells obtained from patients with pulmonary sarcoidosis to release interleukin-2 (IL-2) was assessed and compared with that of autologous peripheral blood T cells. Contrary to previous reports, spontaneous production of IL-2 by unstimulated alveolar T cells was not observed. When stimulated with phytohemagglutinin (PHA), alveolar T cells released considerable amounts of IL-2, however, still less than blood T cells. We next measured intracytoplasmic free calcium ion concentrations ([Ca2+]i) which are intimately related to cell activation triggered by proliferative stimuli. Alveolar T cells in patients with pulmonary sarcoidosis showed lowered responses of [Ca2+]i than blood T cells when stimulated with PHA, thus, demonstrating PHA-hyporesponsiveness at the second messenger level. Meanwhile, [Ca2+]i response of alveolar T cells stimulated with anti-CD3 antibody was higher than that of blood T cells. To investigate mechanisms underlying this unique responsiveness of alveolar T cells, we first examined cell surface expression of alpha beta T cell receptor (TCR). Flow cytometric analysis showed reduced expression of TCR by alveolar T cells compared with blood T cells, a phenomenon commonly called modulation. Since modulation of TCR/CD3 molecular complex is reportedly associated with T cell hyporesponsiveness to lectins, modulation appeared to account, in part, for the reduced IL-2 release by PHA-stimulated alveolar T cells. On the other hand, the present study revealed that memory T cells were dominant among alveolar T cells. This fact also seemed to be responsible for contrasting responses of [Ca2+]i to PHA and anti-CD3 antibody mentioned above, since mitogenic response of memory T cells coincide well with [Ca2+]i response of alveolar T cells. Interestingly and importantly enough, both modulation and memory T cell-dominancy in alveolar T cells were also observed in normal subjects. Accordingly, these findings suggest that responsiveness of alveolar T cells to mitogenic stimuli observed for patients with sarcoidosis is a feature shared by alveolar T cells in health and disease. Thus, present study revealed characteristics of alveolar T cells in general taking advantage of investigation of IL-2 production by alveolar T cells in sarcoidosis.

Adult↗
PubMed1992

Lack of linkage between atopy and locus 11q13.

Atopy as defined in terms of IgE responsiveness was reported to be controlled by a single gene in British families, and this concept was further supported by a significant linkage between atopy and restriction fragment length polymorphism (RFLP) detected by a DNA probe specific to chromosome 11q13. To confirm this observation in a Japanese population, segregation and linkage analyses were done in four large families. Although segregation patterns of atopy were in agreement with the pattern of autosomal dominant inheritance, there was no significant linkage between atopy and locus 11q13. Alterations in the definitions of atopy did not affect the results. These findings suggested the presence of heterogeneity in genetic elements of atopy, even though atopy may be determined mainly by a single dominant gene.

Adolescent↗
PubMed1992

Administration of alpha 1-proteinase inhibitor ameliorates bleomycin-induced pulmonary fibrosis in hamsters.

The effect of alpha 1-proteinase inhibitor (alpha 1Pi) administration on the acute lung injury and subsequent fibrosis induced by bleomycin (BLM) was examined in hamsters. Pulmonary lesions were quantitatively reduced in alpha 1Pi-administered BLM-treated (BLM-alpha 1Pi) animals compared with animals treated by BLM alone (BLM-control) at both 7 days (acute stage) and 30 days (fibrotic stage) after BLM treatment. Analysis of intraalveolar cells from bronchoalveolar lavage (BAL) fluid revealed that neutrophils and lymphocytes were significantly decreased in the BLM-alpha 1Pi animals at 7 days after BLM treatment and that 30 days after BLM treatment macrophages as well as neutrophils and lymphocytes were remarkably decreased in the BLM-alpha 1Pi animals. The elastase activity in supernatants of BAL fluid during 7 days following BLM treatment was detected, but there was no difference between the two groups. In vitro studies on neutrophil responsiveness to stimulation of BAL fluid at 3 days after BLM treatment revealed noticeable chemotaxis and generation of superoxide anion of isolated neutrophils, but alpha 1Pi did not show any inhibitory effects on neutrophil responsiveness. We suggest that alpha 1Pi administration ameliorates pulmonary fibrosis preceded by acute lung injury induced by BLM treatment in hamsters and that the inhibitory effects of alpha 1Pi on lung injury may not be brought about by altered elastase activity, chemotaxis, or superoxide generation in neutrophils. Alternative mechanisms are discussed.

Animals↗
PubMed1992

Functional upper airway obstruction. Psychogenic pharyngeal constriction.

A 15-year-old boy, known to have asthma, developed acute inspiratory airway obstruction with marked stridor. Spirometry indicated extrathoracic airway obstruction and a bronchofiberoptic examination disclosed narrowing in the hypopharynx. After administration of sedatives, the stridor suddenly disappeared. Psychotherapy decreased the frequency of subsequent stridor attacks. It is suggested that psychogenic pharyngeal constriction may have caused the upper airway obstruction with respiratory distress.

Adolescent↗
PubMed1992

Abnormalities in platelets and vascular endothelial cells induced by glycated lipoproteins.

We studied the effects of glycated lipoproteins of low- and high-density (LDL and HDL) on platelets and vascular endothelial cells. After pretreatment for 5 minutes at 37 degrees C, the thrombin-induced synthesis of thromboxane B2 in washed platelets was significantly increased by glycated LDL as compared with native LDL (198.9 +/- 16.2 vs 90.3 +/- 29.4 ng/10(9) platelets, n = 8, p less than 0.01). Platelet aggregation was also increased by glycated LDL as compared with native LDL. After treatment with platelet-rich plasma for 5 hours at 37 degrees C, these values were suppressed by native HDL vs the control (buffer), but not by glycated HDL. Abnormalities in the release of 6-keto prostaglandin F1 alpha and lactate dehydrogenase from vascular endothelial cells were also induced by glycated LDL and/or HDL. These observations suggest that abnormalities induced in platelets and vascular endothelial cells by glycated lipoproteins may play an important role in the development of atherosclerosis in patients with diabetes mellitus.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

[Alveolar macrophages and granuloma formation].

We measured intracytoplasmic free calcium ion concentration ([Ca3+]i) of alveolar macrophages (AMs) in order to elucidate the mechanism(s) of lipopolysaccharide (LPS)-hyperresponsiveness of AMs in patients with sarcoidosis at the second messenger level. Resting [Ca2+]i was higher in patients with sarcoidosis than in normal subjects. [Ca2+]i increase responses were also elevated in patients with sarcoidosis when AMs were stimulated with either anti-CD14 (a LPS/LPS-binding protein complex receptor) antibody, anti-CD64 (Fc gamma receptor I), antibody or platelet activating factor. After incubation with interferon-gamma, resting [Ca2+]i and increase in [Ca2+]i induced by anti-CD14 antibody stimulation were higher in patients with sarcoidosis as compared with values before incubation. Thus, these data suggest that activation of AMs at the second messenger level induced by IFN gamma, at least in part, accounts for LPS-hyperresponsiveness in sarcoidosis.

Acute-Phase Proteins↗
PubMed1992

Photochemical deoxyribose C2' oxidation in 5-iodouracil-containing hexanucleotide.

To investigate photochemistry of 5-iodouracil (IU) in DNA, photoreaction of IU-containing oligonucleotides was examined. It was found that d(GCAIU G C) 2 undergoes selective photochemical C1' and C2' oxidation at the 5' side of IU residue to provide ribonolactone-containing hexamer 1 and erythrose-containing hexamer 2. Upon heating under alkaline conditions, erythrose-containing hexamer 2 was found to undergo retro aldol condensation to provide two fragments having glycolaldehyde termini.

Deoxyribose↗
PubMed1992

[Case report of collagen lung in SLE presenting with cough variant asthma: relation between the localization of responsible receptors and cough].

A 27-year-old nonsmoking woman complained of cough and chest oppression for two years since an episode of pneumonia. Clinical tests showed decrease in FEV1.0 during attacks of coughing and evidence of bronchial hypersensitivity. While these events fitted the picture of bronchial asthma, the nonwheezing cough suggested cough variant asthma. Antinuclear antibody and anti-ds DNA antibody were increased and leukopenia was recognized, suggesting the diagnosis of systemic lupus erythematosus (SLE). Bronchoalveolar lavage showed lymphocytic alveolitis and decreased T4/T8. These results were suggestive of collagen lung induced by SLE. Inhalation challenge with capsaicin and rapid intravenous injection of lobelin and alinamin indicated that peripheral c-fiber receptors were involved in the induction of coughing. We conclude that the peripheral lesion of collagen lung stimulates the peripheral c-fiber receptors, leading to cough variant asthma.

Adult↗