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Biomedical subjects

S Ohdama

Publications and source records attributed to S Ohdama.

At least 19 recordsLinked to original sources
PubMed1999

Expression of tissue factor in non-small-cell lung cancers and its relationship to metastasis.

Tissue factor (TF) is an initiator of the extrinsic cascade of blood coagulation. Although recent studies have revealed a relationship between metastatic properties and TF expression in some neoplastic cells, the significance of TF in lung cancer, especially in non-small-cell lung cancer (NSCLC), is still unclear. In this study, TF was detected in NSCLC cell lines by functional study, Western blot analysis and immunocytochemical staining. TF levels in eight NSCLC cell lines were also quantitated by enzyme-linked immunosorbent assay (ELISA), and TF expression was evaluated in 55 specimens of surgically resected NSCLCs. NSCLC cell lines derived from metastatic lesions produced high levels of TF (48.3+/-23.5 ng 10(-6) cells, mean +/- s.e.m.), whereas those derived from primary lesions produced low levels of TF (0.2+/-0.1 ng 10(-6) cells). Immunohistochemical studies disclosed significantly stronger staining for TF in cells from NSCLC patients with metastasis than in those without metastasis. Among the 28 patients with metastasis, ten were strongly positive, 16 were moderately positive and two were negative for TF. In contrast, among the 27 patients without metastasis, only two were strongly positive, 18 were moderately positive and seven were negative for TF. Therefore, malignant cells from patients with lung cancer produce various levels of TF, and TF may play an important role in the metastatic process.

Biomarkers, Tumor↗
PubMed1995

Alveolar basement membrane breaks down in diffuse alveolar damage: an immunohistochemical study.

Sequential structural changes of the alveoli in diffuse alveolar damage (DAD) were examined by immunohistochemical methods. Lung specimens obtained at autopsy from 52 patients with DAD were stained with antibodies to laminin, 7S collagen (7S) and type IV collagen (type IV) for alveolar basement membrane, to von Willebrand factor, CD-31 and thrombomodulin (TM) for the alveolar capillary endothelial cell, and to epithelial membrane antigen and surfactant apo-protein (PE-10) for the alveolar epithelium. Forty-two of the patients had the exudative form of DAD; 10 of the patients had the proliferative form of DAD. The results were summarized as follows: (i) laminin was most easily impaired both in the epithelial and capillary basement membrane in the early exudative stage; (ii) following laminin, 7S and type IV in the capillary basement membrane were also injured in the early exudative stage, and recovered in the proliferative stage; (iii) subsequently, 7S and type IV in the epithelial basement membrane were also impaired in the late exudative stage, and remained impaired even in the proliferative stage; and (iv) alveolar epithelium regenerated almost completely in the late exudative stage, but staining for TM in the alveolar capillary recovered in the proliferative stage. Because the alveolar basement membrane must govern the homeostasis of alveolar tissue architecture, it was concluded that its preservation is necessary to avoid the abnormal remodeling of the alveoli in the reparative stage of DAD, if the patient survives the acute episodes of the disease.

Adolescent↗
PubMed1995

Determination of a common clonal origin of gastric and pulmonary mucosa-associated lymphoid tissue lymphomas presenting five years apart.

Mucosa-associated lymphoid tissue (MALT) lymphoma is often mis-diagnosed as a benign tumor. Dissemination to other sites occurs in MALT lymphoma. We report a 60-year-old man with gastric and pulmonary tumors of MALT lymphoma which occurred 5 years apart. Initially, the gastric tumor had been diagnosed as reactive lymphoreticular hyperplasia. To determine whether the two tumors arose from the same malignant clone, we amplified and sequenced the complementarity-determining region 3 of the immunoglobulin heavy chain gene using the polymerase chain reaction (PCR). The sequences were identical except for 11-nucleotide difference, suggesting identical clonality.

Base Sequence↗
PubMed1994

Plasma thrombomodulin as an indicator of thromboembolic disease in systemic lupus erythematosus.

We serially measured the plasma thrombomodulin (TM) levels in systemic lupus erythematosus (SLE) patients and assessed them clinically. The patients who responded to medical treatment experienced a decrease in plasma TM levels. Patients who developed exacerbations of SLE, thrombotic thrombocytopenic purpura or thrombosis, displayed increased plasma TM levels. There was no significant difference between the plasma TM levels of the lupus anticoagulant-positive (LAC-positive) patients and the LAC-negative patients or between the plasma TM levels of the anticardiolipin antibody-positive (aCL-positive) patients and the aCL-negative patients. While LAC and aCL titers did not always coincide with improvement in the patients' clinical course or with aggravation of the disease, the TM values correlated well with the patients' clinical condition. Plasma TM values may be used to evaluate disease activity and may predict the occurrence of thrombosis in SLE.

Antibodies, Anticardiolipin↗
PubMed1994

Plasma thrombomodulin as a marker of vascular injuries in collagen vascular diseases.

Thrombomodulin, a thrombin receptor on the vascular endothelial cell surface, is released into circulating blood. The plasma concentrations in patients with collagen vascular diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis, juvenile rheumatoid arthritis, Sjögren's syndrome, systemic sclerosis, polymyositis and/or dermatomyositis (PM/DM), Behçet's disease, and Wegener's granulomatosis, were measured and compared with those of healthy persons. The mean plasma thrombomodulin concentrations in patients with juvenile rheumatoid arthritis, systemic sclerosis, PM/DM, Wegener's granulomatosis, and active states of SLE, rheumatoid arthritis, and Beçhet's disease were significantly higher than those in the control group. Patients with Wegener's granulomatosis showed the highest mean value. The mean values in patients with inactive states of the diseases and Sjögren's syndrome were not significantly different from the values in the control group. In cases of juvenile rheumatoid arthritis, systemic sclerosis, PM/DM, and Wegener's granulomatosis, patients with active interstitial pneumonitis or extensive pulmonary lesions frequently showed higher values of plasma thrombomodulin than those without overt pulmonary involvement. Elevated plasma thrombomodulin values were decreased along with amelioration of the diseases by treatment. These results may indicate that plasma thrombomodulin measurement may be helpful for evaluating vascular injury in patients with collagen diseases.

Adult↗
PubMed1994

Determination of plasma tissue factor antigen and its clinical significance.

To investigate the clinical significance of determination of plasma tissue factor (TF) antigen, we have developed a highly sensitive enzyme-linked immunosorbent assay (ELISA) for plasma TF, using two different monoclonal antibodies against TF apoprotein, 6B4 (catching antibody) and 5G9 (detecting antibody), and tetramethyl benzidine/H2O2 as substrates. Titration curves of recombinant human TF in buffer containing Triton X-100 were linear within the range from 50 to 2000 pg/ml. The total assay time was 3 h. Ultracentrifugation and immunoblot analysis indicated that human plasma and urine contained 50,000 g sedimentable and non-sedimentable forms of TF, both of which were detected by our ELISA method. Plasma and urine concentrations of TF in healthy subjects and patients with various diseases were measured by the ELISA method. In healthy subjects, plasma and urinary TF levels were found to be 149 +/- 72 pg/ml (n = 30) and 175 +/- 60 pg TF/urine creatinine mg (n = 95), respectively. TF was increased in plasma of patients with disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura, vasculitis associated with collagen diseases, diabetic microangiopathy and chronic renal failure receiving haemodialysis, but not in the plasma of endotoxaemic patients without DIC. The plasma TF/serum creatinine ratio did not show a positive correlation. Measurement of TF antigen in plasma may be useful for evaluating the endothelial damage and cell destruction in TF-containing tissues.

Adult↗
PubMed1994

Plasma thrombomodulin in Wegener's granulomatosis as an indicator of vascular injuries.

OBJECTIVE: To compare the concentrations of thrombomodulin (TM) and titers of antineutrophil cytoplasmic antibodies (ANCA) in plasma of patients with Wegener's granulomatosis (WG). PATIENTS: Nine patients with WG were diagnosed according to the clinical criteria and histologic findings of biopsy specimens. MEASUREMENTS AND RESULTS: The concentrations of plasma TM were measured by enzyme-linked immunosorbent assay (ELISA). Titers of ANCA were determined by immunofluorescence technique (cANCA) and by ELISA (anti-PR-3 Ab). The mean plasma TM concentration in patients with WG at an active stage was significantly higher than that of normal control, but that in remission was not significantly different from the normal value. More organs were involved, higher plasma TM levels were observed. The elevated plasma levels of TM returned to normal when the patients were treated successfully and in remission. The cANCA and anti-PR-3 Ab did not correlate with the severity of vasculitis in patients with active WG, although the antibodies determined by both methods were always negative in patients with inactive WG. Postmortem examination of one patient, who died of respiratory failure resulting from diffuse pulmonary hemorrhage, revealed pulmonary capillaritis with the total absence of TM in the lesions involved, suggesting that TM had been released totally from injured capillary endothelial cells. CONCLUSIONS: These results suggest that the plasma TM level may be a useful indicator of the extent of vascular injury in WG.

Adult↗
PubMed1994

[Metastasis of an adenocarcinoma of unknown origin to mediastinal lymph nodes, and transient regression].

A 67-year-old woman was admitted to our hospital because of fever. Chest roentgenogram showed an enlargement of mediastinal lymph nodes. Despite thorough examination, no definite diagnosis could be made. The mediastinal lymph nodes got smaller over the next 3 weeks and a chest roentgenogram taken 4 months later showed no mediastinal lymphadenopathy. The mediastinal lymphadenopathy and fever recurred 5 months later. She underwent thoracotomy and the mediastinal lymph nodes were excised. Microscopic examination of pretracheal lymph node specimens showed invasion of poorly differentiated adenocarcinoma associated with abundant tumor-infiltrating lymphocytes. The other lymph nodes showed sarcoid reaction. Although she has been followed for one year and 11 months, no primary site of the cancer has been found. Metastasis of cancer of unknown origin to mediastinal lymph nodes is extremely rare. It is also interesting that the lymph node swelling diminished spontaneously. The tumor-infiltrating lymphocytes and sarcoid reactions may have been immunological responses to the cancer and may have caused the transient regression.

Adenocarcinoma↗
PubMed1994

[Blood concentrations of thrombomodulin in patients with various diseases].

Concentrations of thrombomodulin in blood plasma were measured by a one-step sandwich enzyme immunoassay (EIA). The concentrations in normal healthy subjects were 9.9 +/- 2.9 ng/ml. The concentrations were found to be significantly higher in patients with SLE, RA and other collagen diseases in their active stages than at their non-active stages. The concentrations increased in patients with DIC, and significantly higher levels were observed when DIC was complicated by multiple organ failure. These findings indicate that plasma concentrations of thrombomodulin may be a useful parameter for vascular injuries caused by inflammatory processes or coagulation/fibrinolysis reactions.

Adult↗
PubMed1994

[A case of crescentic glomerulonephritis associated with anti-myeloperoxidase antibody presenting as alveolar hemorrhage].

A 77-year-old man was admitted because of hemoptysis. Chest roentgenograms initially showed progressive infiltrative shadows, which improved spontaneously in 3 months. Transbronchial lung biopsy specimens obtained during the first admission revealed alveolar hemorrhage with neither granuloma nor vasculitis. Alveolar hemorrhage associated with renal dysfunction recurred 9 months later. Serum creatinine level was elevated to 3.5 mg/dl. No other organ than lungs or kidneys was involved. Renal biopsy was performed to confirm the pathological diagnosis of crescentic glomerulonephritis. Anti-basement-membrane antibody was negative, whereas anti-neutrophil-cytoplasmic antibody was positive for perinuclear pattern (P-ANCA) by indirect immunofluorescent (IF) method. He was diagnosed as having idiopathic crescentic glomerulonephritis complicated with alveolar hemorrhage, and the presence of anti-myeloperoxidase (MPO) antibody in serum was anticipated. Anti-MPO antibody level in his serum evaluated by ELISA was markedly elevated. Although myeloperoxidase has been considered as a common antigen to P-ANCA and anti-MPO antibody, the determination of P-ANCA has been clinically unreliable because of equivocal results. In contrast, the presence of anti-MPO antibody is highly specific for idiopathic crescentic glomerulonephritis complicated with alveolar hemorrhage or its incomplete variant case. Also, it is a better index of disease activity. Therefore, there is a possibility that those patients diagnosed as having idiopathic pulmonary hemosiderosis or pulmonary-renal syndrome may be categorized into the one disease, anti-MPO antibody-associated disease, and the measurement of anti-MPO antibody may lead to prompt treatment prior to the histological diagnosis.

Aged↗
PubMed1993

[A case of surgically resected primary pulmonary lymphoma with IgG-paraproteinemia: gene analysis was effective for establishing its diagnosis].

A 69-year-old woman was hospitalized because of abnormal lung shadow and IgG-lambda paraproteinemia. She was otherwise healthy and asymptomatic. Chest roentgenogram showed a consolidation in the right lower lobe. Chest CT showed a tumour in S8 and subpleural interstitial shadow in S10. No intrathoracic lymphadenopathy was found. Serum IgG was 6,109 mg/dl. The cell count obtained by bronchoalveolar lavage (BAL) was 44.5% plasma cells and 17.5% lymphocytes. CD19-positive lymphocytes were prominent. The IgG/albumin ratio was 13 times higher, and IL-6/albumin ratio was 29 times higher in lavage fluid than in serum. Transbronchial lung biopsy (TBLB) specimen showed interstitial infiltration of plasma cells and lymphocytes. Right lower lobectomy was performed, and serum IgG subsequently decreased to about 4,000 mg/dl. DNA was extracted from the surgical specimen, and analyzed by Polymerase Chain Reaction (PCR) method. A rearrangement band was amplified with Fr3a & VLJH primers (immunoglobulin heavy chain gene). The infiltrated cells were proved to be monoclonal B-cells. This case was diagnosed as small lymphocytic lymphoma, plasmacytoid. Most primary pulmonary lymphomas are well differentiated B-cell type, and the histopathological findings resemble those of LIP or pseudolymphoma. Gene analysis may thus be an effective procedure for the distinction between inflammatory and neoplastic cell proliferation, such as LIP and lymphoma.

Aged↗
PubMed1992

[A case of pulmonary alveolar proteinosis and disseminated atypical mycobacteriosis complicating chronic myelogenous leukemia].

A 47-year-old woman with chronic myelogenous leukemia was treated with daily busulfan (total dose approximately 500 mg) from December 1988 to January 1990. The disease thereafter remained stable with no evidence of blastic transformation. In February 1990 she developed productive cough and abnormal acinar lung shadows appeared transiently on her chest X-ray. In October 1990, productive cough and linear and abnormal acinar lung shadows reappeared. Expectorated sputa contained acid-fast bacilli (Gaffky 6, 10). Antituberculous therapy was started, which caused severe liver dysfunction. She was admitted to our hospital for evaluation of abnormal lung shadows. Transbronchial lung biopsy revealed pulmonary alveolar proteinosis with thickening of alveolar septa. The alveolar septal thickening was suspected to be a pathological change following pulmonary alveolar proteinosis. Cultures from sputum, cerebrospinal fluid, and bone marrow aspiration specimens revealed atypical mycobacterium (M. avium complex), and the diagnosis of disseminated atypical mycobacteriosis was established. The pathogenesis of the disseminated atypical mycobacteriosis was considered to be superinfection by mycobacteria.

Busulfan↗
PubMed1991

Pentoxifylline prevents tumor necrosis factor-induced suppression of endothelial cell surface thrombomodulin.

Thrombomodulin (TM) expression has been reported to be down-regulated by cytokines (endotoxin, interleukin-1, and tumor necrosis factor). We report, in the present study, up-regulation of surface TM antigen of human umbilical vein endothelial cells (HUVECs) by pentoxifylline (PTX) which is one of the agents that can increase intracellular cyclic AMP in HUVECs at therapeutic concentrations. Surface TM antigen was measured by an enzyme immunoassay. PTX increased surface TM antigen and intracellular cAMP in HUVECs in a dose dependent manner. Upregulation of TM by PTX was due to de novo synthesis of TM protein resulting from increased TM mRNA levels. PTX counterbalanced the TNF-induced suppression of TM expression. These results suggest that protein kinase A may be involved in cellular regulatory mechanism for TM expression and PTX may protect partially against TNF-induced endothelial cell injury and restore anticoagulant state of endothelium.

Antibodies↗