Biomedical subjects

Y Kawabata

Publications and source records attributed to Y Kawabata.

At least 145 records · Page 8Linked to original sources

PubMed1995

Possible linkage between renal injury and cardiac remodeling in Dahl salt-sensitive rats treated with the calcium channel antagonist benidipine.

Interest in cardiovascular protection by calcium channel antagonists has grown over the past decade. We investigated the prevention of cardiac remodeling and renal injury by the long-acting calcium channel antagonist benidipine using 12 week-old Dahl salt-sensitive (Dahl S) rats fed a high-salt (4% NaCl) diet. Six-week benidipine treatment (10 mg/kg chow) decreased systolic blood pressure by 22% in Dahl S rats. This blood pressure reduction was associated with decreases in cardiac mass and weight of the aortic wall. Collagen content in the left ventricle tended to decline with benidipine treatment. In addition, glomerular filtration rate increased by 33% and arterial and glomerular lesions improved morphologically with this treatment. Regression of cardiac mass and collagen content in the left ventricle was due mainly to blood pressure reduction; however, collagen content in the low-pressure right ventricle was not only related to systemic blood pressure but to the severity of renal lesions. These data suggest that the calcium channel antagonist benidipine attenuates cardiac and renal injury in hypertensive Dahl S rats, and that part of the cardiac hypertrophy is due to a non-hemodynamic mechanism that might be responsible for, or be a consequence of, the lesions in the kidney.

Animals↗

PubMed1995

A rapidly progressive case of interstitial pneumonia.

We treated a 51-year-old woman who had rapidly progressive respiratory distress with an interstitial shadow on chest roentgenogram. Pathologically, open lung biopsy specimens showed an acutely changed lesion such as interstitial inflammatory thickening, polypoid intraluminal organizing exudates, and also honeycombing which was not recognized on chest computed tomogram. These findings were considered unconformable to acute interstitial pneumonia (AIP), bronchiolitis obliterans organizing pneumonia (BOOP), and also usual interstitial pneumonia, although the clinical diagnosis was AIP or BOOP. We diagnosed a rapidly progressive interstitial pneumonia showing an acute lung injury pattern like AIP and BOOP. She showed significant recovery with corticosteroid and cyclophosphamide.

Acute Disease↗

PubMed1995

[Clinical features of subacute interstitial pneumonia--clinico-pathological study based on open lung biopsy findings].

A clinico-pathological study was done to elucidate characteristic features of subacute interstitial pneumonia. The patients were four men and mine women, with a mean age of 60 years. In ten patients, the disease was idiopathic, three had collagen vascular disease, (and one was undergoing gold therapy for rheumatoid arthritis). The time interval between onset of symptoms and open lung biopsy was 80 +/- 40 days. Eleven patients had progressive dyspnea, seven had coughing, and only one complained of fever. Fine crakles were heard in ten patients. Mild increases in CRP were observed in all cases. Mild increases in total serum IgG concentration were observed in five of eight cases. Multiple patchy infiltration or diffuse interstitial shadows, located predominantly in the lower fields of both lungs were the characteristic chest roentgenographic findings. The average %VC was 62.7 +/- 17% and the average PaO2 was 68.3 +/- 10 Torr. Bronchoalveolar lavage was done in nine patients, and the mean total cell count was 16.5 +/- 10.2 x 10(4)/ml. A moderate increase in lymphocytes (30.8 +/- 18.6%) with a low CD4/8 ratio (0.48 +/- 0.57), a mild increase in neutrophils (6.2 +/- 9.1%), and a mild increase in eosinophils (2.3 +/- 3.7%) were observed. Pathologically, interstitial cellulo-fibrous changes associated with alveolar space closure due to organization of exudate were the main features. Patients were given steroid pulse therapy or oral steroids. The results were mild to marked improvements in chest roentgenographic findings and lung function.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1995

[A case of allergic broncho-pulmonary mycosis with degranulation of eosinophils in the necrotic focus].

A 55-year-old asthmatic woman was first found to have an abnormal shadow on chest radiograph in 1986. Since then she was followed for wandering pulmonary infiltrates observed on radiographs. Open lung biopsy was done when she developed chest pain and bloody sputum. Histological examination of the surgical specimen revealed bronchocentric granulomatosis with infiltration of eosinophils and filaments of fungus. From clinical and histological findings, allergic bronchopulmonary mycosis (ABPM) was diagnosed. Immunohistological staining using monoclonal secretory form of eosinophilic cationic protein antibody was diffusely positive in the eosinophils and also revealed marked degranulation into the necrotic area. We suspect that granules of eosinophils relate to pathogenesis of the disease.

Alveolitis, Extrinsic Allergic↗

PubMed1995

Subpressor dose of angiotensin II increases susceptibility to the haemodynamic injury of blood pressure in Dahl salt-sensitive rats.

OBJECTIVE: To investigate the effects of subpressor doses of angiotensin II (Ang II) on the progression of renal injuries in Dahl salt-sensitive (Dahl-S) rats with hypertension. METHODS: Rats were fed a high-salt (4% NaCl) diet and given an Ang II infusion (10 or 50 ng/kg per min, subcutaneously) for 4 weeks. RESULTS: The plasma Ang II concentration achieved in the high-dose Ang II infusion was lower than that in low-salt (0.3% NaCl) normotensive rats. The Ang II infusion did not affect systolic blood pressure, cardiac hypertrophy or weight of thoracic aorta. However, the high-dose Ang II infusion increased proteinuria by 58%, enhanced the urinary N-acetyl-beta-D-glucosaminase index by 77% and reduced the glomerular filtration rate by 37%. The impaired renal function was associated with a progression of glomerulosclerotic lesions. Neither tubular nor arterial lesions were exacerbated. The infusion did not influence prostacyclin production or urinary cyclic GMP excretion. CONCLUSION: A subpressor dose of Ang II infusion impairs renal function with progression of glomerulosclerosis, and these alterations may be due to increased susceptibility of the glomerulus in Dahl-S rats to Ang II-induced injuries. Such a mechanism might underlie a predisposition to hypertension-induced organ damage seen in Dahl-S rats with salt-induced hypertension.

Angiotensin II↗

PubMed1995

[A case of extramedullary plasmacytoma of the lung associated with nodular deposit of amyloid].

A 63-year-old man underwent left upper lobectomy because of a 35-mm tumor in the lingula. Microscopic findings showed that the tumor was composed of a proliferation of plasma cells, and that in some areas eosinophilic amorphous material had been deposited between the tumor cells. By immunoperoxidase staining, the tumor cells were positive for IgG and kappa chain, but they were negative for lambda chain. In addition to the tumor in the lingula, another nodule was found in the left lower lobe and was resected at thoracotomy. The nodule was composed of diffuse eosinophilic amorphous material, which was found to be amyloid after Congo red staining and observation in polarized light. In and around the nodule, a few plasma cells were noted and these cells were also positive for IgG and kappa chain, but negative for lambda chain immunoperoxidase staining. In serum taken from the patient before surgery, M-protein was not detected by immuno electrophoresis but polyclonal hypergammaglobulinemia was noted, and it continued after the thoractomy. Bone marrow examination and a bone scintigram revealed no abnormality. In this case, a pulmonary plasmacytma co-existed with nodular pulmonary amyloidosis. We could not determine which lesion developed first, but the results of the immunoperoxidase staining of plasma cells in both lesions indicate that the origin of the plasmacytoma was probably the same as that of the nodular amyloid.

Amyloidosis↗

PubMed1995

[Relations between chest CT and pathologic findings in pulmonary infarction associated with lung cancer].

Chest radiographic (mainly CT), and pathological findings in pulmonary infarction associated with lung cancer were studied to obtain information useful for the interpretation of CT findings, and to help determine the cause of infarction. Sixteen cases of lung infarction were chosen from among 518 cases of lung cancer. All patients were operated on between January 1980 and December 1990. Sixteen surgical cases and one autopsy case all with evidence of lung cancer and infarction were chosen. There were 13 men and 4 women with a mean age of 56 years. Adenocarcinoma was found in 8 cases, squamous cell carcinoma in 6, adenosquamous carcinoma in 2, and small cell carcinoma in 1. Chest radiographs and CT revealed infarction shadows in 8 of the 16 cases. Typical CT findings for pulmonary infarction were: shadows located in the same lobe and periphery as the cancer; ill-defined, 10-25 mm nodular shadows; and lesions located both in the subpleural zone and apart from the pleura. Lesion counts in each area were about the same. Observation of one patient for 2 months revealed a decrease in the size of the nodular shadows and clarification of their margins. In most cases, centrally extended cancer resulted in vascular stenosis and infarction.

Adenocarcinoma↗

PubMed1995

Role of Epstein-Barr virus in pleural lymphomagenesis.

Longstanding inflammation in chronic pyothorax (CP) plays a role in the development of pleural lymphoma; therefore, in 1987, the term pyothorax-associated lymphoma (PAL) was proposed. A recent study showed in the tumor cells of a limited number of patients, the presence of the Epstein-Barr virus (EBV) genome together with the expression of latent infection genes in the tumor cells of PAL. The purpose of the present study is to evaluate an association of EBV with PAL in a large number of patients. In addition, the presence of the EBV genome was examined in cases with CP without PAL. Histologic, immunohistochemical studies, and analyses by polymerase chain reaction (PCR) and in situ hybridization method for EBV were performed on 34 PAL and 16 CP collected by nationwide study. Median age of the patients in both diseases was approximately 70 years with a marked preponderance in men. Mean duration of CP in patients with CP alone and with CP complicated with PAL was 33 and 37 years, respectively. Histologically all PAL were non-Hodgkin's lymphoma, with immunoblastic type being the most common. Immunohistochemistry revealed 28 of 34 PAL to be B-cell type. Combined PCR, in situ hybridization method, and immunohistochemistry showed that the EBV genome was detected in lymphoma cells in 85% of PAL with almost constant expression of latent membrane protein-1. The EBV genome was detected by PCR in only one of 16 CP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Effect of perchloroethylene inhalation on nasal mucosa in mice.

An experimental group of 16 male pure-bred mice was exposed to perchloroethylene gas at 300 ppm for 6h daily for 5 days. Histopathological study of the nasal mucosa was performed sequentially 1, 2, 4, and 7 days after exposure. Erosion of the olfactory epithelium and dilatation of Bowman's glands were observed from 1 to 7 days after exposure. Atrophy of the olfactory nerves was observed from 4 to 7 days after exposure. At 4 days after exposure, regenerating epithelial cells were observed, indicating that these cells represented the first step of the repair process after exposure. Nonetheless, epithelial degeneration in the nasal mucosa without erosion was observed for 4-7 days after exposure. Such epithelial lesions were more severe in the olfactory mucosa and appeared earlier than in other sites in the respiratory mucosa. The present study revealed that perchloroethylene gas exerted a more potent harmful action on the olfactory mucosa than on the general respiratory mucosa.

Administration, Inhalation↗

PubMed1994

Temporal integration at equiluminance and chromatic adaptation.

The present study showed that at equiluminance the critical duration of temporal integration became shorter as the chromatic saturation of an adaptation field was increased. These results suggest that the chromatic coding system (which is assumed to posses poorer temporal resolution or larger temporal integration time than the luminance coding system) can change its temporal integrating organization with its own adaptation level, independently of the luminance system.

Adaptation, Ocular↗

PubMed1994

Spatial integration in human vision with bichromatically-mixed adaptation field.

The present study showed that the spatial integration area was expanded even if the background energy was increased, provided that the background consisted of the two colors which were opponent to each other (red/green). This expansion was not found for the subjects with dichromatic color vision even though the same condition was utilized. It was suggested that polarization and its release (the change of adaptation level) of the chromatically-opponent red/green system were involved in control of spatial integration area.

Adaptation, Ocular↗

PubMed1994

Effects of a novel cardiotonic agent (+-)-6-[3-(3,4-dimethoxybenzylamino)-2-hydroxypropoxy]-2(1H)-quinolino ne (OPC-18790) on contractile force, cyclic AMP level, and aequorin light transients in dog ventricular myocardium.

We studied the effects of a novel cardiotonic agent OPC-18790 [(+-)-6-[3-(3,4-dimethoxybenzylamino)-2-hydroxypropoxy]-2(1H)- quinolinone] on isometric contractions, intracellular aequorin light transients, and cyclic AMP levels in isolated dog ventricular trabeculae. The positive inotropic effect (PIE) of OPC-18790 (1-30 microM) was consistently associated with an abbreviation of contractions and an increase in the amplitude of aequorin light transients. The maximum responses of Ca2+ transients and force to OPC-18790 were approximately 40% of the isoproterenol-induced maximum. Carbachol (3 microM) markedly attenuated the increases in force, light transients, and cyclic AMP accumulation induced by OPC-18790. These results indicate that OPC-18790 is a cardiotonic agent with moderate effectiveness, and that the PIE of OPC-18790 may be produced mainly by an increase in intracellular Ca2+ transients induced by cyclic AMP accumulation. For a given increase in amplitude of Ca2+ transients, OPC-18790 produced a more pronounced increase in force of contraction (FOC) than did isoproterenol, suggesting that OPC-18790 does not produce as great a decrease in Ca2+ sensitivity of contractile proteins as does isoproterenol. These observations indicate that among cardiotonic agents acting through cyclic AMP pathway, regulation of contractility produced by the selective cyclic AMP phosphodiesterase III (PDE-III) inhibitor OPC-18790 is qualitatively different from the regulation induced by isoproterenol that acts on cyclic AMP generation in intact myocardial cells.

Aequorin↗

PubMed1994

Vasoconstrictors and renal protection induced by beta 1-selective adrenoceptor antagonist bisoprolol.

We investigated the role of the vasoconstrictors endothelin-1 (ET-1) and thromboxane in renal protection by the beta 1-selective adrenoceptor antagonist, bisoprolol, in Dahl salt-sensitive rats (Dahl S) and salt-resistant rats (Dahl R). Six-week bisoprolol treatment (20 mg/kg chow) reduced systolic blood pressure (SBP) by 14% in Dahl S rats fed a high-salt (4% NaCl) diet. This BP reduction was accompanied by a decrease in aortic wall thickness. ET-1 and thromboxane released from renal cortex was significantly decreased by 17 and 30% with bisoprolol, respectively. Other prostaglandin synthesis was unaffected. Renal function such as proteinuria, N-acetyl-beta-D-glucosaminidase (NAG) excretion, and glomerular filtration rate (GFR) was not influenced by bisoprolol. Morphologic investigation showed that bisoprolol significantly improved glomerular sclerosis by 29% and attenuated arterial damage by 71%, although tubular injury was not affected. The more severe the glomerulosclerotic lesions, the greater the generation of thromboxane and ET. The arterial lesions were positively correlated to thromboxane generation. These data indicate that long-term bisoprolol treatment reduces vasoconstrictive ET-1 and thromboxane generation and that these alterations may be partly responsible for the amelioration of glomerular and arterial injury in Dahl S rats.

Adrenergic beta-1 Receptor Antagonists↗

PubMed1994

New dihydropyridine calcium channel antagonist, pranidipine, attenuates hypertensive renal injury in Dahl salt-sensitive rats.

Interest in the cardiovascular protective effects of calcium channel antagonists has increased in the past decade. We investigated prevention of vascular wall remodeling by the long-acting calcium channel antagonist pranidipine in 12-week-old Dahl salt-sensitive (SS) rats with high-salt-induced (4% NaCl) hypertension. Six-week pranidipine treatment (60 mg/kg chow) decreased systolic blood pressure (SBP) by 22% in SS rats. This BP reduction was associated with decreases in cardiac mass and weight of the aortic wall. Glomerular filtration rate (GFR) was increased by 33%, but this did not lead to a decrease in urinary protein or NAG excretion. Morphologic investigation demonstrated striking resolution of arterial injury (medial necrosis and/or hyperplasia, inflammatory cell infiltration, and thrombus formation) by 87% after pranidipine treatment. Glomerular sclerosis was also attenuated by 61%, whereas tubular injury was improved by only 28%. These morphologic changes were reflected in the findings that the capacity of kidney homogenate for generating lipid peroxides was significantly decreased and that collagen levels and pattern type became similar to those of normotensive salt-resistant (SR) rats. Pranidipine also attenuated hypertensive vasculopathy in small arteries of the middle cerebral arteries. Thus, the calcium channel antagonist pranidipine can attenuate the vascular injury that occurs in salt-induced hypertension, a promising property that implicates its clinical usage, particularly in essential hypertension with cardiovascular complications.

Animals↗

PubMed1994

Guinea pigs prepared with various bacteria and their components to induce a necrotic reaction provoked with muramyldipeptide.

Guinea pigs were given a preparatory injection of heat-killed Mycobacterium tuberculosis in a water-in-mineral oil emulsion into the footpads. A provocative injection of muramyldipeptide given 3-8 weeks later into the flanks, caused severe inflammation, with hemorrhage and necrosis and necrosis at the footpads. In this study, we determined the features of the preparatory injection required to prepare the necrotic reaction. Most mycobacteria-related and Gram-negative bacteria were capable of preparing guinea pigs for the necrotic reaction upon provocative injection with muramyldipeptide, whereas Gram-positive bacteria did not. Boivin- and Morrison-type lipopolysaccharides, which have a high content of bacterial protein, induced the susceptibility, whereas Westphal-type lipopolysaccharide, which has a low level of the protein, did not. Moreover, the latter adjuvant-active lipopolysaccharide and muramyldipeptide together with ovalbumin also exerted the activity. The development of delayed-type hypersensitivity to the protein antigen seemed to be important for inducing the necrotic reaction. Mice, rats, rabbits and monkeys were injected in the same way as the guinea pigs. The necrotic reaction occurred in the flanks of the monkeys, but not in the other animals. A similar necrotic reaction also occurred in the flanks of guinea pigs given live BCG cells in phosphate-buffered saline as well as the heat-killed M. tuberculosis in water-in-mineral oil emulsion upon provocative injection with muramyldipeptide. These findings suggested that the induction is associated with the development of delayed-type hypersensitivity to the protein antigen administered in the preparatory injection [corrected].

Acetylmuramyl-Alanyl-Isoglutamine↗

PubMed1994

Immunobiological activities of a 55-kilodalton cell surface protein of Prevotella intermedia ATCC 25611.

A protein was extracted from whole cells of Prevotella intermedia ATCC 25611 with sodium lauroylsarcosine and purified by chromatography on a DEAE-Sepharose fast-flow column. The The apparent molecular weight of the protein was 55,000. A mouse polyclonal antibody specific for the protein recognized the cell surface structure of P. intermedia and also reacted with proteins in lysates of other black-pigmented anaerobic bacteria, such as Porphyromonas endodontalis and Prevotella melaninogenica, but not with those in lysates of Porphyromonas gingivalis or with the purified fimbriae of P. gingivalis 381. The N-terminal sequence of the 55-kDa protein showed only low homology with the cell surface proteins of any black-pigmented bacteria reported to date. The level of immunoglobulin G antibody to the antigen was higher in the sera of patients with periodontitis than in the sera of healthy volunteers. The protein induced interleukin-1 alpha, -1 beta, -6, and -8 and tumor necrosis factor alpha in human peripheral blood mononuclear cell cultures and interleukin-1 beta and -6 in human umbilical vascular endothelial cell and gingival fibroblast cultures. The protein induced interleukin-6 and tumor necrosis factor alpha activities in peritoneal macrophages from C3H/HeJ as well as from C3H/HeN mice and also induced cytokine activities in the sera of both strains of mice primed with muramyldipeptide.

Amino Acid Sequence↗

PubMed1994

Antihypertensive property and renal protection by shichimotsu-koka-to extract in salt-induced hypertension in Dahl strain rats.

We determined whether or not the kampo formula, Shichimotsu-koka-to extract, attenuates the development of salt-induced hypertension and provides renal protection against hypertensive injury in Dahl salt-sensitive (Dahl S) rats. A six-week treatment using this formula dose-dependently decreased the systolic blood pressure in Dahl S rats fed a high-salt (2% NaCl) diet. This blood pressure reduction was associated with a decrease in the thickness of the aortic wall. Renal function was not altered with this treatment; however, glomerular sclerotic lesions in the kidney were significantly attenuated. Neither arterial nor tubular lesions were affected. These data suggest that Shichimotsukoka-to extract exhibits an antihypertensive effect which is associated with partial resolution of glomerular sclerosis in the kidney.

Animals↗

PubMed1994

Long-term infusion of kallikrein attenuates renal injury in Dahl salt-sensitive rats.

We investigated whether long-term infusion of kallikrein would attenuate renal injury in salt-induced hypertension in Dahl salt-sensitive rats. A subdepressor dose of purified rat urinary kallikrein (700 ng/d IV) was infused by osmotic minipump for 4 weeks in male Dahl salt-sensitive rats fed a high salt (2% NaCl) diet. This dose did not affect the time-dependent elevation of blood pressure; however, urinary protein excretion was significantly decreased, and glomerular filtration rate was increased. These beneficial effects were reflected morphologically by an attenuation of glomerulosclerotic lesions and tubular injury seen in the hypertensive Dahl salt-sensitive rats. Kallikrein infusion increased urinary excretion of bradykinin and stimulated excretion of cyclic GMP, suggesting that the kallikrein-kinin-prostaglandin and nitric oxide axes were enhanced by rat urinary kallikrein infusion. The alterations induced by kallikrein infusion were potentiated by the concomitant administration of the angiotensin-converting enzyme inhibitor alacepril. These studies indicated that long-term replacement with rat tissue kallikrein attenuates renal injury in hypertensive Dahl salt-sensitive rats.

Angiotensin-Converting Enzyme Inhibitors↗