PubMed Health⌕ Search

Biomedical subjects

Y Taguchi

Publications and source records attributed to Y Taguchi.

At least 37 records · Page 2Linked to original sources
PubMed1992

[Assessment of liver graft function after cold preservation using 31P and 23Na NMR spectroscopy].

We investigated the functional damages of cytoplasm and cell membrane of liver grafts in male WKY rats after 24hr- or 48hr-cold preservation using a UW solution in vitro. 10mM fructose or 50mM NH4Cl was added to the perfusate, and synthesis of fructose-1-phosphate (F-1-P) and Na(+)- and H(+)-ion transports through the cell membrane were evaluated with 31P-MRS and 23Na-MRS. After 30 minutes of reperfusion, beta-ATP/(inorganic phosphate: Pi) of the 48hr-preserved liver was significantly lower than those of the other groups. In the control and the 24hr-preserved liver, the changes of F-1-P were almost the same, but F-1-P synthesis was lower in the 48hr-preserved liver than those of the other groups. Intracellular pH began to drop after cessation of NH4Cl loading, and then recovered to the previous level. At the same time Nain was increased in the control group. However, in the other two groups, the increasing rates of Nain were lower, and the recoveries of Nain were worse. In conclusion, the function of cell membrane was more fragile than that of mitochondria and cytoplasmic sugar metabolism in the liver graft.

Adenosine Triphosphate↗
PubMed1992

Hemagglutination and graft-versus-host disease in the severe combined immunodeficiency mouse lymphoproliferative disease model.

In the course of evaluating the severe combined immunodeficiency mouse-human peripheral blood lymphocyte (SCID-PBL) model of lymphoproliferative disease, we noted hemagglutination occurring in peripheral blood smears of mice with serum human immunoglobulin levels greater than 1.0 mg/ml. The hemagglutinating process was mediated by human anti-mouse red cell antibodies of the IgM class, peaked at five to seven weeks post-transfer of 5 to 7 x 10(7) human PBL and was generally self limiting. However, death resulted in some mice when serum immunoglobulin levels were greater than 3.0 mg/ml. The most severely affected mice had hemagglutination induced congestion of liver, lungs and spleen. Several mice also had lesions consistent with graft-versus-host disease (GVHD) including focal hepatic necrosis and destruction of mouse splenic hematopoietic elements. The lesions associated with hemagglutination and GVHD in SCID-PBL mice are distinct from those associated with EBV-induced lymphoproliferation. Recognition of these pathologic processes are required for a thorough understanding of the SCID-PBL model.

Animals↗
PubMed1991

SCID mouse model of Epstein-Barr virus-induced lymphomagenesis of immunodeficient humans.

Immunodeficient humans are at very high risk of developing Epstein-Barr virus (EBV)-induced lymphomagenesis. Severe combined immunodeficient mice (SCID) have been shown to develop lymphoproliferative disease (LPD) following transfer of peripheral blood leukocytes (PBL) with latent EBV. To study mechanisms of lymphomagenesis, we compared results of engraftment of PBL from normal donors and immunodeficient donors with X-linked lymphoproliferative disease (XLP). Graft-versus-host disease (GVHD) developed in 6 of 10 SCID mice 4 to 8 weeks following transfer of PBL from normal donors. In contrast, none of 9 mice engrafted with PBL from XLP patients with T-cell defects showed GVHD. LPD developed in mice regardless of the immune competence of the donors. The expression of EBV-encoded proteins, results of immunophenotyping, and karyotyping of the LPD lesions revealed lethal oligoclonal LPD owing to transfer of latent EBV in B cells in mice engrafted with PBL from seropositive donors. Polyclonal LDP developed in mice engrafted with PBL from seronegative patients which were infected with B95-8 virus 6 weeks after transfer of the cells. This model is useful for investigating mechanisms of EBV-induced LDP in immunodeficient patients.

Animals↗
PubMed1991

Role of type III homology repeats in cell adhesive function within the cell-binding domain of fibronectin.

Recombinant fibronectin (FN) fragments and their mutant proteins were produced to elucidate the role of type III homology repeats in cell adhesive activity within the cell-binding domain of FN. Cell adhesive activity of the 11.5-kDa fragment, the cell attachment site of the cell-binding domain, was less than 0.1% that of native FN despite the presence of the Arg-Gly-Asp-Ser sequence. The activity increased as type III homology repeats were added to the N terminus of the 11.5-kDa fragment, and a 52-kDa fragment with four additional type III repeats had almost the same activity of native FN. Deletion of Arg-Gly-Asp from the fully active fragments completely abolished the cell adhesive activity. Deletion of one or two repeats from the 52-kDa fragment affected the extent of the cell adhesive activity, the degree of the effect being inversely correlated with the distance of the deletion from the type III repeat containing Arg-Gly-Asp-Ser. Rearrangement of type III repeats caused much loss of activity. These results suggest that the number and kinds of type III repeats and their correct alignment rather than the putative synergistic site decide the extent of the specific cell adhesive activity.

Amino Acid Sequence↗
PubMed1991

Production and characterization of functional domains of human fibronectin expressed in Escherichia coli.

An efficient expression system was constructed in Escherichia coli that produced a 33-kDa fragment, C-274, of human fibronectin with a strong cell-adhesive activity. The entire sequence of the heparin-binding domain with 271 amino acids, H-271, was also expressed. Deletion analysis of the type III repeats showed that the heparin-binding site was at type III-13. The cell-adhesive activity of a fusion protein, CH-271, containing the cell- and the heparin-binding domains was twice that of C-274 when BHK but not B16-F10 melanoma cells were tested; H-271 alone was inactive. Recombinant proteins containing the CS1 sequence of the IIICS region were more active than C-274 and CH-271 with B16-F10. However, H-296, which contained both H-271 and CS1, was almost inactive with BHK. CH-296, which contained CS1 at the C-terminus of CH-271, was more active with B16-F10 than H-296 and C-CS1, which was produced by the deletion of H-271 from CH-296. Thus, the cell-binding domain was active with both kinds of cells. The heparin-binding domain promoted the adhesion of both kinds of cells only when linked to the cell-binding domain or CS1. CS1 was specific for the adhesion of B16-F10 but was not essential.

Animals↗
PubMed1991

Hematopathologic features of Epstein-Barr virus-induced human B-lymphoproliferation in mice with severe combined immunodeficiency. A model of lymphoproliferative diseases in immunocompromised patients.

The anatomical distribution, morphology, and clonality, of 'non-Hodgkin's lymphomas' in immunocompromised patients are usually distinctly different from NHL occurring in the general population. Mosier DE, Gulizia RJ, Baird SM, Wilson DB: Nature (London) 335:256, 1988 have described lymphoproliferative disease (LPD) of human B cell origin in mice with severe combined immunodeficiency (scid mice) after transfer of human peripheral blood mononuclear cells from Epstein-Barr virus-seropositive individuals. Reported herein is detailed information regarding the morphology, phenotypes, and clonality of LPD lesions in 10 of 18 scid mice that had developed LPD after transfer of peripheral blood mononuclear cells. These lesions were diffuse and monomorphic proliferations of immunoblastoid cells. They were invasive in their growth and often necrotic. Human B cell-related and activation-associated antigens were found on the LPD lesions, although the numbers of cells with the latter antigens were relatively small. Immunofixation electrophoresis for human immunoglobulins in sera of the majority of mice revealed oligoclonal populations, however, phenotypic and cytogenetic analyses showed no definite monoclonality. This scid mouse model is beneficial for understanding the early phases in the pathogenesis of LPD in immunocompromised patients.

Animals↗
PubMed1991

[Etiological examination of idiopathic interstitial pneumonia and lung cancer in autopsy cases].

In order to investigate the etiology of usual interstitial pneumonia (UIP) and UIP with lung cancer (LC), autopsy findings in 18 cases of UIP with LC and 11 cases of uncomplicated UIP were clinicopathologically compared with the environmental factors of smoking habits and occupation. UIP with LC was highly correlated with smoking, especially heavy smoking and with occupations in which dust is inhaled, such as electrical installation and ceramic production, indicating that these environmental factors are important background factors in the complication of UIP with IC. Pathologic examination of cases of UIP with LC (6 squamous cell carcinomas, 5 small cell carcinomas, 4 adenocarcinomas, and 3 large cell carcinomas, 2 of which showed pulmonary double carcinoma revealing a slight correlation between fibrosis and primary site of LC and a slightly greater correlation of squamous cell carcinoma and small cell carcinoma to smoking habits and inhalation of dust. In terms of the correlation between UIP and LC among autopsy cases, the environmental factors proved to be more significant than the fibrotic findings. These environmental factors are thought to merit consideration as common predisposing factors in the development of LC and its complication with UIP.

Aged↗
PubMed1991

[Clinicopathological features of metastatic pulmonary calcinosis with malignant neoplasm].

Metastatic pulmonary calcinosis is a rare complication seen in malignancies accompanied by hypercalcemia, or chronic renal failure. We reviewed the clinicopathological findings of 8 cases of metastatic pulmonary calcinosis accompanied malignancy revealed at autopsy. The underlying diseases were malignant lymphoma in 3 cases (adult T cell lymphoma in 2 cases), multiple myeloma in 2, lung cancer in 2, and acute myelocytic leukemia in 1, all cases were complicated by hypercalcemia and renal failure. Chest X-ray revealed almost normal findings in 2 cases, bilateral diffuse infiltrates in 4, bilateral infiltrates in the apex in 1, and right atelectasis in 1. Bone scintigraphy was performed in 4 cases, and revealed warm pulmonary uptake in 1 patient with multiple myeloma and 1 with lung cancer, but normal findings in the 2 other cases. Histopathological examination revealed diffuse alveolar septal edema and fibrosis due to calcium deposition, which were considered to be the cause of respiratory failure. Metastatic pulmonary calcinosis is a rare but a serious complication in malignancies accompanied by hypercalcemia and renal failure, and bone scintigraphy seems to be a useful method for its diagnosis.

Adolescent↗
PubMed1991

[Clinicopathological study of methicillin-resistant Staphylococcus aureus detected by pulmonary microbial culture in autopsied cases].

Microbial culture of lung specimens from 569 autopsied cases from 1986 to 1989 revealed methicillin-resistant Staphylococcus aureus (MRSA) in 28 cases, which were subsequently analyzed clinicopathologically. The number of MRSA positive cases has markedly increased in recent years (2 cases in 1986, 2 in 1987, 6 in 1988, 18 in 1989). The most frequent underlying disease was neoplasm, which was seen in 17 cases. Of non-neoplastic diseases, liver cirrhosis and diffuse panbronchiolitis were prevalent. Twenty-four cases had received a course of antibiotic therapy. Antibiotics frequently administered were third-generation Cephem and Imipenem/cilastatin sodium (used in 20 cases). Antibiotics o which MRSA was sensitive were administered in only one case (minocycline). Sputum culture was performed in only 10 cases, 5 of which were MRSA positive. MRSA had acquired resistance to fosfomycin and ofloxacin. Histological examination revealed complication by pneumonia in 19 cases. In 7 of these 19 cases, MRSA was the only pathogen detected. Pulmonary MRSA infection detected at autopsy is frequently seen in patients with terminal stage cancer, but it is frequently not diagnosed and is undertreated. This may be a factor responsible for the recent marked increase in the proportion of MRSA in pathogens causing infection within medical institutions.

Cross Infection↗
PubMed1991

[Old pulmonary embolism causing intrabronchial bleeding].

A 51-year-old man was admitted because of hemoptysis. Physical examinations and chest XP revealed no abnormal findings. Fiberoptic bronchoscopy showed pulsatile bleeding at the orifice of right B6. Right bronchial arteriography showed a markedly dilated and tortous bronchial artery and shunting to the pulmonary arterial system in the middle and lower lobes. Pulmonary arteriography showed complete obstruction of the right middle lobar and lower lobe segmental arteries (A6, 9, 10). The hemoptysis was thought to be due to increased blood flow of the right bronchial artery, which compensated for reduced right pulmonary arterial flow. Right middle and lower lobe resection was done to prevent further hemoptysis. The resected specimen revealed old thromboemboli in the right middle and lower lobe pulmonary arteries. In this case old pulmonary embolism should be considered as a cause of intrabronchial bleeding.

Bronchial Arteries↗
PubMed1991

[Cellular interstitial pneumonia and follicular bronchiolitis diagnosed by open lung biopsy in a patient with rheumatoid arthritis].

A 54-year-old woman under treatment for rheumatoid arthritis was admitted because of aggravation of dyspnea on effort and restrictive pulmonary dysfunction. Although chest X-ray revealed no marked change, the symptoms progressively worsened, necessitating open lung biopsy for diagnosis and treatment. Based on the histopathological findings of the biopsied tissue, the patient was diagnosed as having active rheumatoid lung complicated with cellular interstitial pneumonia and follicular bronchiolitis. The patient responded well to adrenocorticosteroid and immunosuppressor therapy, and is now being followed up as an outpatient. Rheumatoid arthritis can be complicated by diverse lung diseases. Among them one important disease is interstitial pneumonia, which serves as a prognostic factor. When cellular interstitial pneumonia is treated with adrenocorticosteroid therapy, it responds well and its prognosis is good. Therefore, its early detection and appropriate adrenocortical therapy are essential. Patients with rheumatoid arthritis presenting with dyspnea on effort and pulmonary dysfunction should be examined for cellular interstitial pneumonia, follicular bronchiolitis and other lung diseases, even when no marked change is visible on chest X-ray films.

Arthritis, Rheumatoid↗
PubMed1990

Modulation of haptotactic migration of metastatic melanoma cells by the interaction between heparin and heparin-binding domain of fibronectin.

We utilized recombinant fibronectin polypeptides with cell-binding domain and heparin-binding domains (referred to as C-274 and H-271, respectively) and their fusion polypeptide (CH-271) to examine the role of sulfated polysaccharide heparin and/or the functional domains of fibronectin in modulating tumor cell behavior. Both C-274 and CH-271 polypeptides with cell-binding domains promoted the adhesion and migration of B16-BL6 melanoma cells, whereas H-271 did not. Heparin bound to the immobilized polypeptides with heparin-binding domain (H-271, CH-271, and a mixture of C-274 and H-271 or fibronectin) but did not affect the tumor cell adhesion to the substrates. At the same time, heparin or two monoclonal antibodies against the heparin-binding domain were able to inhibit the haptotactic migration to CH-271 or fibronectin, though not to C-274 or a mixture of C-274 and H-271. This suggests that although heparin did not affect tumor cell adhesion to the cell-binding domain near the heparin-binding domain in CH-271 or fibronectin, it did lead to a modulation of cell motility. It seems likely that the regulatory mechanism may depend on interaction between heparin-like molecules on the cell surface and the heparin-binding domain in fibronectin, rather than on simple steric hindrance or on the masking of the cell-binding domain caused by the binding of heparin to heparin-binding domain.

Animals↗
PubMed1990

Interferon induction by human herpesvirus 6 in human mononuclear cells.

Interferon (IFN) production after inoculation with human herpesvirus 6 (HHV-6) was studied in peripheral blood mononuclear cells from 10 HHV-6-seropositive healthy adults and five samples of cord blood mononuclear cells. When the cells were exposed to HHV-6 at a multiplicity of infection of 10(-2) 50% tissue culture infectious doses/cell, IFN activity was detected as early as 12 h after exposure to HHV-6, plateaued at days 2-5, and gradually decreased thereafter. IFN was also induced by ultraviolet-inactivated but not heat-inactivated HHV-6. The response of cord blood mononuclear cells was lower than that of the cells from healthy adults. The activity of all IFN samples was stable to acid and exclusively neutralized by anti-human IFN-alpha. The IFN-producing cell population was mainly non-T cells and monocytes. Furthermore, exogenous IFN suppressed HHV-6 replication. Production of IFN-alpha may be an important part of the host response to HHV-6.

Cell Separation↗
PubMed1990

Inhibition of lung metastasis by synthetic and recombinant fragments of human fibronectin with functional domains.

We have investigated the antimetastatic effect of synthetic or recombinant peptides containing the functional domains of fibronectin on experimental and spontaneous lung metastases of murine tumor cells. CS1 peptide which is present within type III homology connecting segment (IIICS) as well as C-274 (cell-binding domain) were able to inhibit experimental lung metastasis when co-injected intravenously (iv) with B16-BL6 melanoma cells, while H-271 (heparin-binding domain) could not. In the spontaneous metastasis model, multiple iv administrations of CS1 or C-274 after surgical excision of primary tumors caused a significant reduction of metastatic colonies in the lung. Both CS1 and C-274 significantly inhibited cell adhesion and migration to fibronectin-coated substrates when added freely in solution. CS1 peptide also inhibited the cell adhesion and migration to laminin-coated substrates, but C-274 did not. H-271 did not have any inhibitory effect on cell adhesion or migration to either of the substrates. Similarly, CS1 inhibited tumor invasion to both Matrigel/fibronectin- and Matrigel/laminin-coated filters, whereas C-274 inhibited the invasion to only Matrigel/fibronectin-coated filter. These results indicate that CS1 peptide of fibronectin, lacking the Arg-Gly-Asp-containing domain, actively inhibits tumor metastases in spontaneous and experimental metastasis models. The use of such a peptide might offer a promising therapeutic approach for combatting or preventing cancer metastasis.

Amino Acid Sequence↗