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Biomedical subjects

Y Kawabata

Publications and source records attributed to Y Kawabata.

At least 73 records · Page 4Linked to original sources
PubMed2000

[Erdheim-Chester disease presenting with pulmonary lesion].

A 49-year-old man first visited our hospital in 1991 for further examination of abnormal pulmonary shadows. A chest radiograph and computed tomographic (CT) scan showed diffuse reticular shadows in both lung fields. The findings from a transbronchial lung biopsy specimen were not conclusive. Although there was little change in the abnormal pulmonary shadows, the patient's lung functions gradually deteriorated, indicating an obstructive defect. The patient was admitted in 1998 with the chief complaint of increasing dyspnea on exertion. A thoracoscopic lung biopsy specimen revealed proliferation of histiocytes with fibrosis in the pleura and perivascular interstitium. Immunohistochemically, the histiocytic cells were CD68-positive, alpha 1-antichymotripsin-positive, S100 protein-negative, and CD1a-negative. A bone scintigram and magnetic resonance images showed symmetrical diametaphyseal bone lesions in the distal femurs and the proximal tibiae; however, the epiphyses were spared. These findings were consistent with Erdheim-Chester disease. This is the first reported case of Erdheim-Chester disease with pulmonary involvement in Japan.

Antigens, CD↗
PubMed2000

[A questionnaire survey of surgical lung biopsy in patients with diffuse lung diseases].

A nationwide questionnaire survey was conducted to investigate the indications, diagnostic yield, complications, outcome, and benefit of surgical lung biopsy for diffuse lung diseases. Surgical lung biopsies were performed in 410 patients at 132 institutes in 1998, 94% of them as video-assisted thoracoscopic surgery (VATS). Interstitial lung diseases of unknown etiology formed the largest diagnostic group, and consisted of 194 patients. The clinical diagnosis prior to lung biopsy was inconsistent with the final diagnosis in 32.8%. Complications were seen in 32 patients, and mortality was 1.2%. Acute exacerbation of the underlying disease was seen in 9 patients, four of whom died. Patients with nonspecific interstitial pneumonia and even usual interstitial pneumonia who were treated following biopsy showed better outcomes than those untreated. The physician in charge judged that 82.2% of the patients received clinical benefits from the biopsy procedure. We concluded that VATS lung biopsies are indicated in more cases to confirm diagnoses and as a reference for treatments in patients with diffuse lung disease.

Adolescent↗
PubMed2000

[Familial summer-type hypersensitivity pneumonitis in a grandfather and his two-and-a-half-year-old grandson].

We encountered a family in which two of the six members, the grandfather and his grandson, had summer-type hypersensitivity pneumonitis in late summer. Chest computed tomography of these patients showed small, diffuse nodular shadows in both lung fields, with mosaic-like opacities in the grandfather and ground glass opacity of both lung fields in the grandson. Bronchoalveolar lavage fluid from the grandfather disclosed high total cell counts, high percentages of lymphocytes, and a low ratio of CD 4+ cells to CD 8+ cells. Transbronchial lung biopsy specimens obtained from the same patient revealed alveolitis with non-caseous epithelioid cell granulomas in the interstitium and Masson bodies in the alveolar septa. These two patients recovered spontaneously after hospital admission. They had positive results in provocation tests for their home and were positive for serum anti-Trichosporon cutaneum (T. asahii, T. mucoides) antibodies. Both cases were accordingly diagnosed as summer-type hypersensitivity pneumonitis.

Aged↗
PubMed1999

Defective apoptotic signal transduction pathway downstream of caspase-3 in human B-lymphoma cells: A novel mechanism of nuclear apoptosis resistance.

Mitochondria play a central role in controlling apoptosis, and activation of the caspase cascade appears to be crucial event during the apoptotic process. Human B lymphoma Raji cells are resistant to nuclear apoptosis induced by various stimuli. Using this cell line, we have asked whether reduction of the mitochondrial transmembrane potential and activation of caspase-3 are sufficient to induce DNA fragmentation during the apoptotic process. After stimulation with cell-permeable C2-ceramide or mitochondrial permeability transition (PT) inducers, not only apoptosis-sensitive cell lines (HL-60, Jurkat, and Daudi cells), but also Raji cells showed reduction of the mitochondrial transmembrane potential (triangle uppsim), activation of caspase-3, and loss of clonogenic potential. However, Raji cells did not show detectable levels of nuclear apoptosis (DNA degradation). In a cell-free system, cell lysates from tetra-butylhydroperoxide (t-BHP)-treated HL-60 cells induced DNA degradation of Raji nuclei, whereas cell lysates from t-BHP-treated Raji cells failed to induce DNA degradation in either apoptosis-sensitive cell lines or apoptosis-resistant Raji cells. Cleavage of DFF-45, which is a downstream target molecule for caspase-3, was observed in Raji cells as well as in apoptosis-sensitive Daudi cells. These results indicate that there is a defective apoptotic pathway in the cytoplasm downstream of caspase-3 in Raji cells.

Alkylating Agents↗
PubMed1999

Molecular characteristics of poorly differentiated adenocarcinoma and signet-ring-cell carcinoma of colorectum.

In a series of 45 poorly differentiated adenocarcinomas (por) and 7 signet-ring-cell carcinomas (sig) of the colorectum, K-ras gene mutation, p53 immunostaining and microsatellite instability (MSI) were analyzed for a comparison with 46 cases of colorectal carcinomas of the well or moderately differentiated type (well/mod). In addition, the mutations of simple repeated sequences in the transforming-growth-factor-beta type-II receptor (T beta R-II) gene and the BAX gene were analyzed as possible targets for DNA replication errors. Mutation of the K-ras gene in the por, sig and well/mod specimens was detected in, respectively, 22%, 11% and 48%, positive immunostaining for p53 in 41.8%, 28.6% and 60.3%, and MSI in 36%, 30% and 4%. Frameshift mutation of the T beta R-II gene was detected in 27.5% of the por and none of the sig specimens, while corresponding figures for mutation of the BAX gene were 15.7% and 0%. Significant differences between the por and well/mod tumors were found in the occurrence of K-ras mutation at codons 12 and 13, and MSI. Clinicopathologically, the tumor status of por with MSI was found to significantly correlate with the tumor's location in the proximal colon. In cases without MSI and sig, no frameshift mutation of either the T beta R-II or the BAX gene was found. These results suggest that poorly differentiated and signet-ring-cell carcinomas have a genetic background different from that of well or moderately differentiated carcinomas of the colorectum, and that DNA-replication error is at least partly involved in the carcinogenesis of these specific types of colorectal carcinomas.

Adenocarcinoma↗
PubMed1999

Angiotensin II subtype-1 receptor antagonists improve hemodynamic and renal changes without affecting glucose metabolisms in genetic rat model of non-insulin-dependent diabetes mellitus.

The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is a new genetic model of non-insulin-dependent diabetes mellitus (NIDDM). We investigated whether treatment with an angiotensin II (ANGII) subtype-1 receptor antagonist delays the onset of NIDDM and attenuates diabetic nephropathy in the OLETF rat. OLETF rats fed a regular chow were treated with ANGII subtype-1 receptor antagonists (E4177 or TA606) for 22 weeks. Hemodynamic changes, glucose metabolism, and the effects on diabetic nephropathy were examined. Systolic blood pressure increased in OLETF rats in an age-dependent manner. OLETF rats exhibited increases in plasma concentrations of glucose and insulin and developed glucosuria at the age of 28 weeks. The changes in glucose metabolism were associated with proteinuria and an increase in urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG). Morphologic investigation revealed nodular lesions in glomeruli in the OLETF rats. The ANGII receptor antagonist treatment abolished the blood pressure elevation. However, the treatment did not affect plasma glucose and insulin levels and did not significantly reduce glucosuria. Nodular lesions in glomeruli were not improved by the treatment. However, the receptor antagonists significantly reduced proteinuria and urinary NAG excretion. Multivariate analyses revealed that proteinuria was determined by systolic blood pressure, lipid metabolism, and glucose levels in plasma. ANGII subtype-1 antagonism does not improve glucose metabolism in the OLETF rat model of NIDDM, which has abnormalities in the glucose-uptake system. Blood pressure elevation and part of the proteinuria associated with NIDDM depends on the renin-angiotensin system rather than glucose metabolisms per se.

Acetylglucosaminidase↗
PubMed1999

Association of plasma fibrinogen level and blood pressure with diabetic retinopathy, and renal complications associated with proliferative diabetic retinopathy, in Type 2 diabetes mellitus.

AIM: To clarify the association of several clinical parameters, including plasma fibrinogen level, with diabetic retinopathy in patients with Type 2 diabetes mellitus (DM). METHODS: A total of 294 Japanese patients with Type 2DM were studied; 53 patients with no diabetic retinopathy (NDR), 90 with background diabetic retinopathy (BDR), and 151 with proliferative diabetic retinopathy (PDR). Multiple logistic regression analysis was performed to assess variables independently associated with diabetic retinopathy in two settings: presence of retinopathy of any severity and presence of advanced retinopathy. RESULTS: The following parameters were identified as independent factors associated with the presence of diabetic retinopathy (NDR vs. BDR + PDR): type of therapy (P<0.0005), log-transformed plasma fibrinogen level (P < 0.05), mean blood pressure (P < 0.05), and duration of diabetes (P < 0.05). The independent variables associated with advanced retinopathy were type of therapy (P<0.00005), age (P<0.0005) and nephropathy (P<0.05). Body mass index, smoking and hypertensive status, HbA1c and total cholesterol levels were not independently associated. CONCLUSIONS: These data suggest that in patients with Type 2 DM, an increased blood viscosity due to high fibrinogen level as well as an elevated intravessel pressure play a role in the development of diabetic retinopathy, and that the progression to PDR is influenced or accompanied by the deterioration of renal status.

Aged↗
PubMed1999

High salt intake potentiates the renal vascular and glomerular damage caused by low doses of angiotensin II in uni-nephrectomized rats.

OBJECTIVE: We recently reported that the renin-angiotensin system plays an important role in the progression of vascular and kidney injuries, even in Dahl salt-sensitive rats with volume-dependent hypertension. In this study, we investigated whether a high-salt diet increases susceptibility to kidney injury induced by angiotensin II in normotensive, uni-nephrectomized Sprague-Dawley rats, which mimics the condition of salt-volume repletion and blunted renin-angiotensin system. METHODS: The rats were fed either a low-salt (0.3% NaCl) or a high-salt (4% NaCl) diet and divided into five groups: two control groups with a low-salt or a high-salt diet without angiotensin II infusion (saline infusion), and three angiotensin II groups (angiotensin II infusion, 10 or 50 ng/kg per min with high-salt diet, 50 ng/kg per min with low-salt diet, subcutaneously). The rats were kept on these regimes for 8 weeks. The blood pressure was measured every week. Functional and morphological alterations in the kidney were assessed at the end of the experiment RESULTS: There were no differences in the arterial blood pressures of the five experimental groups. However, angiotensin II infusion increased the weights of the heart and aortic walls in a dose-dependent manner in the high-salt groups. There was also a dose-dependent increase in proteinuria, N-acetyl-beta-D-glucosaminidase activity (NAG) excretion, and additional glomerular and arterial injuries in the kidney, associated with angiotensin II infusion in the high-salt groups. In the rats given a higher dose of angiotensin II, the high-salt diet significantly increased the weights of the heart and aortic walls and exacerbated the renal function and morphological injuries, compared to the low-salt group. High-salt diet alone increased the kidney and heart weights. However, it did not significantly influence the results of the morphological and functional study. On the other hand, angiotensin II infusion on a low-salt diet showed a trend towards glomerular damage; however, the effects were small and not significant. Similarly, there were few effects of angiotensin II infusion on morphology and functional study on a low-salt diet CONCLUSION: These data clearly show that a high-salt intake increases susceptibility of the kidney to injuries induced by low doses of angiotensin II in normotensive, uni-nephrectomized rats.

Angiotensin II↗
PubMed1999

Complement-dependent accumulation and degradation of platelets in the lung and liver induced by injection of lipopolysaccharides.

We found unique behaviors among platelets within a few minutes of the intravenous injection of lipopolysaccharide (LPS) into mice. Platelets accumulated primarily in the liver at lower doses of LPS, but at higher doses they accumulated largely in the lungs. When the platelets accumulated in these organs were degraded, there was a rapid anaphylactoid shock. The platelet response depended on the strain of mouse and on the source of LPS. Of various LPSs tested, the LPS from the smooth type of Klebsiella O3 (KO3-S LPS) was the most potent at inducing the platelet response and shock. K-76 monocarboxylic acid, an inhibitor of complement C5, effectively prevented the KO3-S LPS-induced degradation (but not accumulation) of platelets and the ensuing rapid shock in BALB/c mice. Moreover, in DBA/2 mice (which are deficient in complement C5), platelets accumulated in the lungs and liver in response to KO3-S LPS but soon returned to the circulation without degradation, and there was no rapid shock. The LPS from the rough type of KO3 induced an accumulation of platelets in the liver and lungs but not a degradation of platelets. On the basis of these results and those reported by other investigators, we propose that in the platelet response to LPS, the lectin pathway to form C3 convertase from C4 and C2 is involved in the rapid accumulation of platelets in the liver and lungs and that the pathway from C5 to C9 is involved in the destruction of platelets and the consequent anaphylactoid shock.

Anaphylaxis↗
PubMed1999

Regression of glomerular injury by kallikrein infusion in Dahl salt-sensitive rats is a bradykinin B2-receptor-mediated event.

AIMS: We investigated whether kallikrein infusion attenuates renal injury in Dahl salt-sensitive rats with hypertension and assessed the role of bradykinin-nitric oxide axis in the renal protection using HOE-140, the bradykinin type-2 (B2) receptor specific antagonist. METHODS: Subdepressor dose of purified rat urinary kallikrein (RUK) (400 ng/day) was continuously infused through the jugular vein by an osmotic mini-pump for 4 weeks in Dahl salt-sensitive (Dahl S) rats fed a high-salt (2% NaCl) diet. RESULTS: Blood pressure increased in a time-dependent manner in Dahl S rats fed a high-salt diet. The RUK infusion did not influence the elevation of blood pressure in Dahl S rats. However, the RUK infusion significantly decreased urinary protein excretion, and increased glomerular filtration rate, as compared with untreated high-salt Dahl S rats. Morphological investigation disclosed that the RUK infusion significantly attenuated glomerulosclerosis and arterial and tubular injuries in the kidney of hypertensive Dahl S rats. The RUK infusion produced an increase in urinary excretions of nitric oxide and cyclic guanosine monophosphate. In addition, the RUK infusion enhanced the generation of nitric oxide from the kidney slices. The functional and morphological effects of the RUK infusion on the kidney were completely lessened by co-administration of the bradykinin B2-receptor antagonist, HOE-140. CONCLUSION: Long-term infusion of subdepressor dose of rat urinary kallikrein attenuates functionally and morphologically the progression of renal injury in Dahl rats susceptible to salt-induced hypertension, and that the protection is mediated by stimulation of bradykinin B2 receptor.

Animals↗
PubMed1999

Long-term inhibition of renin-angiotensin system sustains memory function in aged Dahl rats.

The Dahl salt-sensitive (DS) rat, a genetic model of salt-induced hypertension in humans, is more likely to develop severe vascular injuries than a rat with spontaneous hypertension. We designed an experiment to scrutinize the effects of renin-angiotensin inhibition on cognitive dysfunction in the aged, normotensive DS with a passive avoidance test. Eighteen months of treatment with a very low dose of the angiotensin-converting enzyme (ACE) inhibitor cilazapril (2.5 microg/mL in drinking water) or the angiotensin II type 1 receptor antagonist E4177 did not reduce blood pressure throughout the experiment, although in the low dose cilazapril group (12.5 microg/mL in drinking water), blood pressure dropped within 6 months after treatment began. The cilazapril treatments dose-dependently improved memory function in the aged, normotensive DS fed a low-salt diet compared with the untreated, control rats. This improvement was associated with significant increases in hippocampal CA1 cells and capillary densities in the CA1 regions compared with those in the untreated DS. Similarly, E4177 slightly improved the memory dysfunction observed in the aged DS. The cells in the hippocampal CA1 region were restored slightly, but the capillary densities were not influenced by the receptor antagonist. On the other hand, the ACE inhibitor and receptor antagonist both attenuated urinary protein excretions with an improvement of glomerular sclerosis. These data suggest that long-term treatment with an ACE inhibitor improves memory dysfunction probably through restoration of capillary and hippocampal cells. The effects are due to the inhibition of the angiotensin II type 1 receptor and probably to the enhancement of the kallikrein-kinin system.

Aging↗
PubMed1999

[A case of advanced gallbladder cancer responding to neoadjuvant intra-arterial chemotherapy].

The patient was a 52-year-old female who had been diagnosed as advanced gall bladder cancer by various imaging studies. The cancer responded to neoadjuvant intra-arterial chemotherapy and was curatively resected. Since cancer had invaded the median widely, the posterior and the lateral segments of the liver according to CT imaging, neoadjuvant chemotherapy was used. The combination chemotherapy included intra-arterial chemotherapy (CDDP 10 mg + 5-FU 250 mg/day/week x5 times, EPI 10 mg + 5-FU 250 mg/day/week x3 times) through the hepatic artery and oral chemotherapy (UFT 300 mg/day for 106 days). No severe side effects were found during this chemotherapy. Imaging studies after the chemotherapy showed a partial response (PR) and curative resection (hepato-pancreato-duodenectomy with regional lymph nodes dissection) could be performed successfully. She has been disease-free without any sign of recurrence for 18 months after surgery. We conclude that this combination chemotherapy will be useful for advanced gall bladder cancer if the appropriate combinations, dosages, and administration routes are chosen.

Adenocarcinoma↗
PubMed1999

[Seven cases of marked pulmonary fibrosis in the upper lobe].

We report on 7 patients with marked idiopathic pulmonary fibrosis in the upper lung lobes. The patients were generally characterized by the following pathological and clinical features: (1) marked subpleural pulmonary opacities and reticular shadows mainly in the upper lobes, with a progressive reduction in lung volume; (2) nonspecific fibrosis (subpleural, zonal, rather well-defined fibrosis with small cysts and honeycomb lesions) in 5 patients and interstitial pneumonia in 2, mainly in the upper lobes; and (3) a slender build, and a family history of recurrent spontaneous pneumothorax. Clinically, all 7 cases resembled idiopathic upper-lobe fibrosis as described by Amitani in 1992. Further clinical and experimental research will be required to delineate the characteristics of idiopathic fibrosis affecting primarily the upper lobes.

Adult↗
PubMed1999

[Interstitial pneumonia, pulmonary thrombotic microangiopathy, and hyperimmunoglobulinemia associated with Basedow's disease].

A 44-year-old man with a history of Basedow's disease complained of dry cough and lymphadenopathy. Polyclonal hypergammaglobulinemia (IgG level: 5,839 mg/dl) was present, and the patient's serum was positive for lupus anticoagulant. Chest radiography disclosed irregular thickening of bronchovascular bundles, centrilobular granular and branching opacities, and small cystic changes in both lung fields. Examination of a thoracoscopic biopsy specimen revealed fibrous thickening of the pleura, interlobular septum, and peribronchiolar/perivascular connective tissue, with mild round-cell infiltration. Lymphoid follicle formation and pulmonary thrombotic microangiopathy were also observed. Corticosteroid therapy was ineffective for hypergammaglobulinemia and diffuse opacities disclosed by chest computed tomographic scans. This case differed from multicentric Castleman's disease with respect to the pathological findings of a lymph nodes biopsy, and also was not consistent with any known collagen vascular disease, (e.g., Sjögren's syndrome). We suspect this case may be representative of a new form of collagen vascular disease.

Adult↗
PubMed1999

[Pronounced progression of interstitial pneumonia in a precious metal worker].

A 43-year-old man who had been engaged in the precious-metal processing industry for 18 years was admitted to our hospital because of shortness of breath on exertion. Chest roentgenograms disclosed ground glass opacities and annular-nodular shadows in the basal area of the right lung field and almost all of the left lung field. A video-assisted thoracoscopic lung biopsy was performed, and histologic examination disclosed usual interstitial pneumonia (UIP). Mineral analysis revealed high modes of silicon and aluminum, two elements consistent with the materials used in the patient's factory. The histopathological findings indicated interstitial pneumonia caused by the inhalation of dust particles. After corticosteroid therapy, computed tomographic scans disclosed that the ground glass opacities had subsided, but that honeycomb shadows remained. A chest roentgenogram taken 2 years earlier demonstrated only minute granular lesions in the basal area of right lung field. The interstitial shadows had progressed significantly over the intervening 2-year span. The findings in this case should be of value to the etiologic study of UIP.

Adult↗
PubMed1999

[Interstitial pneumonia induced by the inhalation of hard metal].

A 51-year-old man visited Okayama Rousai Hospital with the chief complaints of dyspnea and emaciation. His occupational history included 23 years as a hard-metal polisher for a shipyard. Physical examination disclosed digital clubbing and fine crackles audible in the inferior posterior lung fields. Laboratory examination revealed hypoxemia and a remarkably reduced vital capacity of the lungs. Chest x-ray films and computed tomograms disclosed interstitial pneumonia predominantly in the upper lung lobes. Lung fibrosis progressed rapidly, and the patient died of exacerbation of chronic respiratory failure 2 years after his first visit to our hospital. The histopathologic findings from tissue specimens obtained by open lung biopsy and necropsy revealed mixed patterns of atypical and usual interstitial pneumonia, but no giant cell interstitial pneumonia. X-ray analysis detected tungsten in the lung tissue and mediastinal lymph nodes, but no cobalt was found. The interstitial pneumonia observed in this patient was thought to be induced by the occupational inhalation of hard metal.

Air Pollutants, Occupational↗
PubMed1999

[Idiopathic pulmonary fibrosis of the upper lobe: a case report].

A 26-year-old man was admitted to our hospital complaining of exertional dyspnea. Chest x-ray films disclosed reticulonodular shadows predominantly in the upper fields of both lungs, but no apical cap. Lung biopsy specimens obtained from the upper lobe by video-assisted thoracoscopy revealed subpleural elasto-fibrosis. Also, specimens obtained from the lower lobes disclosed micro-honeycombing due to peri-lobular fibrosis resembling usual interstitial pneumonia. Although pneumothorax occurred repeatedly, the lungs reinflated on each occasion without artificial intervention. Similar radiographic findings had been obtained on the patient's father, who died of idiopathic pulmonary fibrosis at the age of 56. Idiopathic pulmonary upper lobe fibrosis was conclusively diagnosed because the patient exhibited most of the features originally described by Amitani et al.

Adult↗