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Biomedical subjects

K Eguchi

Publications and source records attributed to K Eguchi.

At least 91 records · Page 5Linked to original sources

Carcinomatous lymphangitis mimicking pulmonary thromboembolism.

A 41-year-old woman was admitted with rapidly worsening dyspnea. Echocardiography disclosed interventricular septal flattening and a markedly decreased left ventricle, although left ventricular contraction remained normal. Computed tomography of the chest demonstrated slightly dilated main pulmonary arteries and fine reticulonodular densities in the lung. Examination of a transbronchial lung biopsy specimen revealed carcinomatous lymphangitis, and the patient died 7 days after admission. The clinical presentation of this patient was difficult to discriminate from that seen with pulmonary thromboembolism.

Adenocarcinoma↗

Pulmonary nocardiosis associated with idiopathic thrombocytopenic purpura.

A 69-year-old woman with idiopathic thrombocytopenic purpura, who was regularly followed and treated with prednisolone and danazol, was admitted to our hospital because of shortness of breath. Chest roentgenogram showed a large amount of left-sided pleural effusion. Gram-positive branching rods, subsequently identified as Nocardia farcinica, were isolated from the fluid. Antibiotic treatment together with pleural drainage with an intercostal catheter resulted in complete remission of pyothorax. Pulmonary nocardiosis is a rare disease, but recognition of the disease in immunocompromised patients and the prompt initiation of appropriate treatments based on isolation of the pathogen can lead to a successful outcome.

Aged↗

Apoptosis in autoimmune diseases.

Over the past decade, our understanding of apoptosis, or programmed cell death, has increased greatly, with the identification of some of the major components of the apoptotic program and the processes regulating their activation. Although apoptosis is an intrinsic process present in all cells, it can be regulated by extrinsic factors, including growth factors, cell surface receptors, cellular stress and hormones. Apoptotis plays an important role in autoimmune diseases. Normal thyrocytes could induce apoptosis of infiltrating activated T cells and protect against attack by such cells, i.e., the normal thyroid tissues act as an immune privileged site. In Hashimoto's thyroiditis (HT), Fas-mediated apoptosis of thyrocytes in a section of tissues is due to at least two separate mechanisms, the first by infiltrating activated T cells, and the other by FasL-positive thyrocytes in a suicidal or fratricidal fashion. A common feature of autoimmune diseases such as systemic lupus erythematosus (SLE) is the breakdown of tolerance of self antigens, a consequence of which is the production of autoantibodies reactive with multiple self proteins. Evidence is accumulating that modifications of autoantigens during apoptosis lead to the development of autoantibodies by bypassing the normal mechanisms of tolerance. Tissue homeostasis is maintained through a balance between cell proliferation and apoptotic cell death. Rheumatoid arthritis (RA) is characterized by pronounced hyperplasia of the synovial tissue, cell infiltration and periarticular osteoporosis. Enhanced Bcl-2 expression and NF-kappaB nuclear translocation of synovial cells are induced by inflammatory cytokines and/or growth factors. These synovial cells become resistant toward apoptosis triggered by various stimuli. The infiltrated cells which are defect in activation-induced cell death can cause autoimmunity by allowing the survival of autoreactive T and B cells. These data suggest that apoptosis might be implicated with the pathogenesis of autoimmunity, whereas the mechanisms might be distinct in each autoimmune disease.

Animals↗

Mixed connective tissue disease associated with von Recklinghausen's neurofibromatosis.

We report a 42-year-old Japanese woman with Recklinghausen's neurofibromatosis 1 (NF1) who developed mixed connective tissue disease (MCTD). Previously experiencing good health without an increase in subcutaneous nodules, she presented with Raynaud's phenomenon, swollen hands and polyarthralgia Clinical examination revealed a high titer of anti-RNP antibody, and she was thus diagnosed as having MCTD. She was treated with oral prednisolone (10 mg/day) and her symptoms improved rapidly. Since the association of MCTD and NF1 has not been reported previously, we concluded that this association is rare. We also discussed the association of NF1 and autoimmune diseases including MCTD.

Adult↗

Clinical features of fulminant hepatitis in Nagasaki Prefecture, Japan.

OBJECTIVE: Fulminant hepatitis is a rare but fatal disease. In the present study, we examined the changes in etiology and prognosis of fulminant hepatitis in Nagasaki Prefecture, Japan between 1980 to 1999. METHODS: Eighty-one patients with fulminant hepatitis admitted to our hospitals from 1980 to 1999 were examined with respect to the etiology and prognosis. RESULTS: Fulminant hepatitis was due to hepatitis A virus in 2 (12%) cases, hepatitis B virus in 18 (22%) cases, unknown etiology in 50 (62%) cases, and drug-induced in 11(14%) cases. The number of cases in the first half of the study (1980-1989) was 47 and that of the latter half (1990-1999) was 34 cases. The incidence of fulminant hepatitis type B also decreased from 14 cases (30%) to 4 cases (12%) during these periods. The overall survival rate of fulminant hepatitis was 32%; it was equal in fulminant hepatitis type B, fulminant hepatitis of unknown etiology and fulminant drug-induced hepatitis. The survival rate of fulminant hepatitis type A was 100%, though only two cases were identified. Retrospectively, the survival rate in patients with a pre-encephalopathy period of < or = 10 days and aged < or = 39 years was significantly higher than in patients > or = 40 years of age (p<0.01). There was no difference between the two age groups when pre-encephalopathy period was > or = 11 days. CONCLUSIONS: The incidence of fulminant hepatitis especially that of fulminant hepatitis type B in Nagasaki Prefecture has decreased in recent years. The survival rate is significantly higher in younger patients with a short pre-encephalopathy period.

Adolescent↗

[Long distance air transport by helicopter of a patient with severe head damage].

A report of a case of a patient with severe head trauma with pneumonia and cerebral infarction transported by helicopter. An eighty-year-old male was referred to our hospital because of dyspnea after a fall during sightseeing at Hiroshima. He was lucid at first, but, after two days presented restlessness due to brain contusional hemorrhage and edema. Moreover, he developed pneumonia and cerebral infarction during the period of his hospitalization. He was intubated and received central venous routing. While being transported, his consciousness showed moderate disturbance, aphasia and right hemiplegia. His family asked that therapy be continued near his house in Osaka. We selected transport by helicopter because of his bad general condition and because transport time would be much shorter. He was transported by helicopter to Osaka one month after admission. First, he was transported by ambulance to the airport of Hiroshima. He was carried to the helicopter at the airport. An oxygen cylinder was connected to the incubation tube via an ambu bag because direct connection between the oxygen cylinder and the intubation tube was impossible. Just before the take off, O2 saturation was checked by the pulse oximeter of the ambulance. In the helicopter, there were six men; two pilots, two rescue men, one doctor and the patient. Suction was applied only once and there was no trouble during the flight. The weather was fine and the helicopter experienced almost no rolling during the flight. The flight time was only one hour and twenty minutes. The helicopter safely landed at an emergency heliport in Osaka. The patient was carried to a waiting ambulance and transported to the hospital. Total transport time was only two hours and thirty minutes. This is a case showing a helicopter could safely transport a patient with severe brain damage over a long distance in a short time.

Aged↗

[Decompressive craniectomy for massive infarction of middle cerebral artery territory].

There is continuing controversy about the benefits of decompressive craniectomy for the treatment of massive infarction of middle cerebral artery (MCA) territory. Under conservative therapy, the mortality rate for this stroke is reported to be up to 80%. So the authors have actively carried out decompressive craniectomy since 1997, and have compared the outcome with patients who were admitted before 1997 and, consequently treated with conservative therapy. Fifteen consecutive victims of massive infarction of MCA territory were studied. Seven patients (male: 1, female: 6, mean age: 79.8 years) were treated with conservative therapy, and 8 patients (male: 3, female: 5, mean age: 71.8 years) were treated with decompressive craniectomy. There were no significant differences in age and consciousness level distribution between the two groups. Mortality rate in the conservative therapy group was 85.7% against 12.5% in the surgery group (p < 0.05). Functional performance, which was evaluated by activity in daily life (ADL), was also better in the surgery group e.g. 3 patients in ADL 3, and 3 in ADL 4 (1 patient died from a non-neurological cause). Even among the patients with speech-dominant hemispheric stroke, all except one were able to communicate in some way and understand language. Even though patients in this study were elderly, decompressive craniectomy reduced mortality and improved functional performance, so it seems that this surgery should be aggressively considered for massive infarction of MCA territory.

Aged↗

Protein kinase C inhibits insulin-induced Akt activation in vascular smooth muscle cells.

Protein kinase C (PKC) activation, enhanced by hyperglycemia, is associated with many tissue abnormalities observed in diabetes. Akt is a serine/threonine kinase that mediates various biological responses induced by insulin. We hypothesized that the negative regulation of Akt in the vasculature by PKC could contribute to insulin resistant states and, may therefore play a role in the pathogenesis of cardiovascular disease. In this study, we specifically looked at the ability of PKC to inhibit Akt activation induced by insulin in cultured rat aortic vascular smooth muscle cells (VSMCs). Activation of Akt was determined by immunoblotting with a phospho-Akt antibody that selectively recognizes Ser473 phosphorylated Akt. A PKC activator, phorbol 12-myristate 13-acetate (PMA), inhibited insulin-dependent Akt phosphorylation. However, PMA did not inhibit platelet-derived growth factor (PDGF)-induced activation of Akt. We further showed that the PKC inhibitor, G06983, blocked the PMA-induced inhibition of Akt phosphorylation by insulin. In addition, we demonstrated that PMA inhibited the insulin-induced tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1). From these data, we conclude that PKC is a potent negative regulator of the insulin signal in the vasculature, which indicate an important role of PKC in the development of insulin resistance in cardiovascular disease.

Animals↗

Computed tomography screening for lung carcinoma in Japan.

BACKGROUND: In Japan, lung carcinoma is the leading cause of cancer-related deaths. Adenocarcinoma accounts for roughly half of all lung carcinomas. Earlier detection of lung carcinoma is expected to reduce mortality rates. Computed tomography (CT) provides higher contrast resolution and greater visualization of chest compartments that are difficult to view with chest radiography, such as the mediastinum. CT further permits the detection of minute peripheral nodules. At present, several institutions and research groups are evaluating the utility of low dose spiral CT for lung carcinoma screening. METHODS: From September 1993 to December 1998, 1669 individuals underwent a biannual screening program for lung carcinoma. The program included posteroanterior radiograph, sputum cytology, and low dose spiral CT at a for-profit organization: The Anti-Lung Cancer Association (ALCA). A total of 9993 examinations were carried out. The low dose spiral CT parameters used were 120 kvP, 50 mA, 10-mm collimation, and 2:1 pitch. RESULTS: Peripheral lung carcinoma was detected in 31 of 9993 examinations (0.3%). Of the 31 cases, 24 tumors (77%) were detected by low dose spiral CT but were not visible on standard chest radiography. Twenty-two of the 24 tumors were Stage IA (T1N0M0, according to staging system revised in 1997). CONCLUSIONS: Low dose spiral CT shows promise for lung carcinoma screening. The effectiveness of the technique for the detection of minute lung lesions remains to be established. Routine use of the technique will require resolution of several issues. These issues include the establishment of CT diagnostic criteria, the development of a diagnostic support system, the establishment of methods for definite diagnosis, and assessments of efficacy.

Humans↗

Attenuation of expression of gamma-glutamylcysteine synthetase by ribozyme transfection enhance insulin secretion by pancreatic beta cell line, MIN6.

Low levels of intracellular antioxidant enzyme activities as well as glutathione (GSH) concentrations have been described in pancreatic beta cells. We examined the effects of intracellular GSH depletion on insulin secretion and the role of intracellular GSH in signal transduction in beta cell line, MIN6 cells. Anti-gamma-glutamylcysteine synthetase (gamma-GCS) heavy subunit ribozyme was stably transfected to MIN6 cells to reduce intracellular GSH concentration. In the presence of 10 mM glucose, ribozyme-transfected cells (RTC) increased insulin secretion from 0.58 microg/10(6) cells/h in control cells (CC) to 1.48 microg/10(6) cells/h. This was associated with increased intracellular Ca(2+) concentration in RTC, detected by fluo-3 staining. Our results demonstrated that intracellular GSH concentration might influence insulin secretion by MIN6 cells, and suggest that enhanced insulin secretion by beta cells conditioned by chronic depletion of GSH is mediated by increased intracellular Ca(2+) concentration.

Adenosine Triphosphate↗

Bronchiolitis obliterans organizing pneumonia syndrome in breast-conserving therapy for early breast cancer: radiation-induced lung toxicity.

PURPOSE: Breast-conserving surgery and postoperative radiotherapy have played important roles in the treatment of early breast cancer. Bronchiolitis obliterans organizing pneumonia (BOOP) syndrome has recently been reported to be one of the complications of adjuvant radiotherapy. The purpose of this study was to determine the incidence of and risk factors for BOOP syndrome in breast cancer patients. METHODS AND MATERIALS: Between January 1996 and December 1998, 157 patients with breast cancer underwent radiotherapy after breast-conserving surgery. The criteria used for the diagnosis of BOOP syndrome were as follows: 1) radiation therapy to the breast within 12 months, 2) general and/or respiratory symptoms lasting for at least 2 weeks, 3) radiographic lung infiltrates outside the radiation port, and 4) no evidence of a specific cause. RESULTS: BOOP syndrome developed in 4 (2.5%) patients, who had fever and nonproductive cough, with patchy infiltrative shadows on chest roentgenograms which emerged between 5 and 6 months after radiotherapy. The symptoms and pulmonary infiltrates were rapidly improved by treatment with prednisone (40 mg/day), which was tapered over 2- to 5-month periods. However, BOOP syndrome relapsed in all cases during the tapering period or after withdrawal of prednisone. The eosinophil and neutrophil counts were increased and the ratios of CD4+ to CD8+ lymphocytes were elevated in bronchoalveolar lavage fluid in all four cases. There were no differences in proportions of patients by age, irradiated breast site, use of tamoxifen and/or chemotherapy, or radiation dose between those with and without BOOP syndrome. CONCLUSIONS: BOOP syndrome is considered an intractable form of lung toxicity after radiotherapy to the breast. An immunologic reaction mediated by eosinophils, neutrophils, and lymphocytes may be responsible for the development of this syndrome. Methods of prevention of BOOP syndrome should be established.

Adult↗

Protein expression and functional difference of membrane-bound and soluble receptor activator of NF-kappaB ligand: modulation of the expression by osteotropic factors and cytokines.

A variety of humoral factors modulate the osteoclastogenesis. Receptor activator of NF-kappaB ligand (RANKL) expressed on osteoblast/stromal lineage cells plays a pivotal role to transduce an essential differentiation signal to osteoclast lineage cells through binding to its receptor, RANK, expressed on the latter cell population; however, the difficulty to detect RANKL protein expression hampers us in investigating the regulation of RANKL expression by humoral factors. To determine protein expression of RANKL, we have established a new method, named as a ligand-receptor precipitation (LRP) Western blot analysis, which can specifically concentrate the target protein by the use of specific binding characteristic between RANKL and RANK/osteoprotegrin (OPG). RANKL protein expression in the postnuclear supernatant was not detected by common Western blotting, but LRP Western blot analysis clearly showed that RANKL is produced as a membrane-bound protein on murine osteoblasts/stromal cells, and cleaved into a soluble form by metalloprotease. Cytokines stimulating the osteoclastogenesis, such as IL-1beta, IL-6, IL-11, IL-17, and TNF-alpha, increased the expression of RANKL with decrease of OPG expression in osteoblasts/stromal cells. In contrast, cytokines inhibiting the osteoclastogenesis, such as IL-13, INF-gamma, and TGF-beta1 suppressed the expression of RANKL and/or augmented OPG expression. Functional difference between membrane-bound and soluble RANKL was demonstrated, which showed that membrane-bound RANKL works more efficiently than soluble RANKL in the osteoclastogenesis developed from murine bone marrow cell culture. The present study indicates the usefulness of LRP Western blot analysis, which shows that the modulation of osteoclastogenesis by humoral factors is achieved, in part, by regulation of the expression of RANKL and OPG in osteoblast/stromal lineage cells.

Animals↗

Regulation of rheumatoid synovial cell growth by ceramide.

Overgrowth of rheumatoid synoviocytes, which results in joint destruction, is due to impaired balance between cell proliferation and cell death (apoptosis). Ceramide is an important lipid messenger involved in mediating a variety of cell functions including apoptosis. We investigated the effects of ceramide on growth-promoting anti-apoptotic signals in rheumatoid synovial cells. Human synovial cells isolated from patients with rheumatoid arthritis (RA) were stimulated with platelet-derived growth factor (PDGF) in the presence or absence of C2-ceramide. The kinase activity of Akt, MEK, and ERK1/2 was analyzed in PDGF-stimulated synovial cells by Western blot analysis. Pretreatment with C2-ceramide completely inhibited PDGF-induced cell cycle progression of rheumatoid synovial cells. PDGF stimulation induced phosphorylation and activation of Akt, MEK, and ERK1/2 in rheumatoid synovial cells. C2-ceramide inhibited the activation of Akt, MEK and ERK1/2 in PDGF-stimulated synovial cells. Our data demonstrated that inhibition of anti-apoptotic kinases, such as Akt and ERK1/2, may play an important role in ceramide-mediated apoptosis of rheumatoid synovial cells.

Apoptosis↗

Induction of COX-2 expression by nitric oxide in rheumatoid synovial cells.

Prostaglandins formed by cyclooxygenase (COX) enzymes are important mediators of inflammation. The contribution of inducible COX-2 in the rheumatoid synovium is well documented. In this study, we evaluated the contribution of nitric oxide (NO) to COX-2 expression in rheumatoid synovial cells. Exposure of rheumatoid synovial cells to a NO donor, SNAP, induced COX-2 protein expression in a dose-dependent manner. RT-PCR analysis also demonstrated that COX-2 mRNA was induced in SNAP-treated synovial cells. Dexamethasone at therapeutic concentrations markedly inhibited this NO-mediated COX-2 expression in synovial cells. In contrast to its effect on COX-2 expression, SNAP did not affect the constitutive expression of COX-1 in rheumatoid synovial cells. Our findings suggest that NO is an important modulator of COX-2 expression and that glucocorticoids exert their anti-inflammatory action in rheumatoid synovium, at least in part, by suppression of COX-2 induction.

Arthritis, Rheumatoid↗

Combination of nedaplatin and vindesine for treatment of relapsed or refractory non-small-cell lung cancer.

PURPOSE: A phase II study of nedaplatin and vindesine was conducted to evaluate their efficacy and safety for treatment of relapsed or refractory non-small-cell lung cancer (NSCLC). METHODS: Between August 1996 and September 1998, 48 patients who had previously received chemotherapy, thoracic radiotherapy, and/or surgery were enrolled in the study. Patients were required to have an Eastern Cooperative Oncology Group performance status of 0 to 2 and an age between 20 and 79 years. Treatment consisted of nedaplatin (80 mg/m2, day 1) and vindesine (3 mg/m2, days 1 and 8) every 3 to 4 weeks. RESULTS: Of 48 patients, 7 (14.6%) exhibited an objective response. Four (50%) of eight chemotherapy-naive patients had a partial response. However, of the 40 patients who had received prior chemotherapy, a partial response was observed in only 3 (7.5%). At a median follow-up time of 85.1 weeks, the median survival time was 43.6 weeks (95% confidence interval 34.4-52.7) for patients who had received chemotherapy, with a survival rate of 40% at 1 year. Grade 3 or 4 neutropenia occurred in 43 of 48 patients (90%), and neutropenic fever was observed in 3 of the 43 patients, one of whom died of sepsis. Pharmacokinetic and pharmacodynamic analyses of platinum were performed in 43 patients during the first cycle of chemotherapy. Percent reduction in absolute neutrophil count was correlated not only with the area under the plasma ultrafilterable platinum concentration versus time curve (r = 0.41, P = 0.007) but also with the duration of ultrafilterable platinum concentration above 1 microg/ml (r = 0.41, P = 0.007). Patients with progressive disease exhibited a shorter duration of ultrafilterable platinum concentration over 1 microg/ml (P = 0.046) than those with other responses. CONCLUSION: A combination of nedaplatin and vindesine was unsatisfactory as second-line chemotherapy for NSCLC, although the combination was well tolerated. The duration of ultrafilterable platinum concentration above 1 microg/ml was an important pharmacokinetic parameter for predicting both chemotherapy-induced neutropenia and treatment outcome.

Adult↗