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Biomedical subjects

S Haraoka

Publications and source records attributed to S Haraoka.

At least 19 recordsLinked to original sources
PubMed1995

The induction of cell differentiation and polarity of tracheal epithelium cultured on the amniotic membrane.

We have developed a culture system of guinea pig tracheal epithelial cells using the epithelium-denuded human amnion as a source of basement membrane. Culture medium fluid over the epithelial cells was replaced by air after 7-day immersion culture and thereafter maintained for 2 weeks. Electron microscopical observations revealed that the height of epithelial cells and the ratio of ciliated epithelial cells looked like that of normal guinea pigs epithelium growth in 2 weeks after the air interface, but that no goblet cells could be found. In order to study cell polarity, we measured endothelin-1 levels in the media of apical and basal sides of the epithelial cell monolayer by means of the enzyme-linked immunosorbent assay. The endothelin-1 content of the submucosal side was over 30 times higher than that of the apical side. These findings suggest that ET-1 would be mainly released from airway epithelial cells toward the submucosal side.

Amnion↗
PubMed1995

Participation of T lymphocytes in atherogenesis: sequential and quantitative observation of aortic lesions of rats with diet-induced hypercholesterolaemia using en face double immunostaining.

Using en face double immunostaining coupled with electron microscopy, we studied the temporal and spatial distribution of T lymphocytes and macrophages during the development of atherosclerosis in a diet-induced rat model fed an atherogenic diet for 2-40 weeks. T lymphocytes and macrophages adhered to the aortic surface by 2 weeks on the diet, with subsequent migration under the endothelium, and formed a fatty streak-like lesion. Analysis of the cellular components revealed that infiltration of T lymphocytes was most prominent in the incipient phase of lesion formation accounting for 60%, 29% and 34% of mononuclear cells appearing in 2-week lesions of the superior thoracic, inferior thoracic and abdominal segments of the aorta, respectively. After the incipient phase, the relative number of T lymphocytes in the three segments of the aorta showed a slow decline; the proportion of T lymphocytes to macrophages was approximately 1:3 to 1:4 in 10- to 20-week lesions. An overall view of the lesional cells often demonstrated direct cellular contact between T lymphocytes and macrophages. Further, OX6/ED1 double immunostaining demonstrated that Ia antigen was expressed on most macrophages. In later stages, breakdown of foamy macrophages occurred, and the extracellular accumulation of lipids and cell debris became prominent. The results demonstrated that in the diet-induced rat model, together with macrophages, large numbers of T lymphocytes participated in all stages of aortic lesions, initially adhering to the surface at prelesional stages and later as the principal component of the atherosclerotic lesion. It is possible that the method described here will provide a good tool for examining the role of T lymphocytes in atherogenesis.

Animal Feed↗
PubMed1995

Morphological fate and sequelae of human atherosclerosis: evaluation of immune mechanisms in atherogenesis through immunohistological and ultrastructural analysis.

Modern techniques of investigation have revealed several similarities between atherosclerosis and chronic inflammation, and that immune mechanisms seem to operate in the incipient and subsequent phases of atherosclerosis. In the present study, the fate and morphogenesis of human atherosclerosis was considered, and the immune aspects of atherogenesis were analysed, using fresh human aorta obtained from autopsy cases. One of the earliest changes in the grossly normal, lesion-prone area of the aorta from young cases (prelesional changes) was the infiltration of blood-borne T lymphocytes and monocytes/macrophages beneath the endothelium. Cell-populated lesions abounding in T lymphocytes and macrophages, often bearing signs of activation, with or without cytoplasmic lipids were found in the fatty streaks, cap and shoulder regions of more advanced atheromatous plaques. The ultrastructural observation of cell-rich areas suggested that cognate cell-to-cell interaction plays a pivotal role in atherosclerosis, as well as cytokine-mediated paracrine or autocrine mechanisms. From an immunological perspective, the areas where both cell types are especially numerous and in close proximity are considered to be the areas with an index of disease activeness or progressiveness. Also, the present authors show evidence of clonal expansion of T lymphocytes. It is most likely that the increase of intimal cells was caused by the recruitment of immunocompetent cells from the blood-stream into the intima and by the clonal expansion of T lymphocytes. In addition, dead or dying cells were identified in areas of different stages ranging from prelesional areas to atheromatous plaques. Thus, the initiation and progression of human atherosclerosis appears to be punctuated by brief episodes of immunological events related to cell infiltration, proliferation and death.

Adolescent↗
PubMed1995

[The evaluation of systolic right ventricular pressure and right ventricular hypertrophy using body surface mapping (isointegral map, isochrone map)].

We studied QRS and QRST isointegral maps, and isochrone map for the diagnosis of right ventricular hypertrophy and its severity in atrial septal defects and primary pulmonary hypertensions. The discriminant analysis in QRS isointegral map showed better results for differential diagnosis between atrial septal defects and both normal subjects and incomplete right bundle branch block patients than these in QRST isointegral map and isochrone map. Three parameters (Qp/Qs, systolic right ventricular pressure, right ventricular ejection fraction) for right ventricular overload showed significant correlation with QRS isointegral map and QRS isopotential map. Thus body surface map was an useful method for the evaluation of right ventricular hypertrophy.

Body Surface Potential Mapping↗
PubMed1995

[Myoglobin].

Explore the source record for details and available documents.

Humans↗
PubMed1995

Xanthogranulomatous cholecystis. Cell composition and a possible pathogenetic role of cell-mediated immunity.

Thirty-three cases of xanthogranulomatous cholecystitis (XGC) exhibiting the typical morphologic features were studied by light and electron microscopy and immunohistochemical techniques. Incidence of XGC was 4.2% of the surgically resected gallbladder diseases. Histologically, the granulomatous lesion of XGC principally consisted of accumulations of foam cells and lymphocytes. Variable numbers of multinucleated giant cells, granulocytes and fibroblastic cells were also noted. With respect to the origin of foam cells, it was considered that the vast majority of foam cells were derived from monocytes/macrophages because they were invariably positive for KP1, HAM56, CD11b and CD68. Interspersed among macrophage foam cells, many T lymphocytes were identified. The subtyping of T cells indicated a heterogenous population composed of both CD4+ and CD8+ lymphocytes typically in a ratio of 1:2. Macrophages and T lymphocytes demonstrated a marked expression of HLA-DR antigen. Electron microscopic and immunohistochemical double-staining observation demonstrated intimate apposition of T lymphocytes to macrophages or macrophage foam cells. The results indicate that XGC is a granulomatous disorder characterized by accumulations of macrophage foam cells and T cells. Delayed type hypersensitivity reaction of cell-mediated immunity may be implicated in the pathogenesis of XGC.

Adult↗
PubMed1994

Endothelial cell heterogeneity in experimentally-induced rabbit atherosclerosis. Demonstration of multinucleated giant endothelial cells by scanning electron microscopy and cell culture.

We investigated the aortic endothelial cells of cholesterol-fed rabbits, using scanning electron microscopy and a cell culture technique. Rabbits were given a 1% cholesterol diet intermittently for up to 40 weeks. In these animals, the area of endothelial cells was increased and the cells showed polymorphism in relation to the progression of atherosclerosis. In animals fed the cholesterol diet for 12, 28 and 40 weeks, the average area of the endothelial cells was 436 +/- 15, 762 +/- 153, and 836 +/- 165 microns2, respectively. In the cholesterol-fed 40-week group, in particular, giant endothelial cells, measuring more than 1200 microns2, accounted for 14% of the population. In animals fed a standard diet there was no significant difference in endothelial cell morphology between control 0-week and control 40-week groups; in both, the luminal surface of the thoracic aorta formed a homogeneous sheet covered by small rhomboidal endothelial cells, the area of most being less than 400 microns2. Primary cultured endothelial cells harvested from those control groups were mononuclear typical small cells with a centrally located nucleus; the proportion of binucleated cells was less than 2% and no multinucleated giant cells with three or more nuclei were detected. Endothelial cells from the cholesterol-fed groups, however, contained larger numbers of binucleated cells, with the number increasing in proportion to the duration of cholesterol feeding. The major distinguishing feature of the endothelial cells in the cholesterol-fed groups was the presence of multinucleated giant cells with three or more nuclei; these accounted for 2.3% and 3.3% of the total cell population in the cholesterol-fed 28- and 40-week groups, respectively. No bromodeoxyuridine uptake was found in the nuclei of the cultured multinucleated giant cells. Heterogeneity of endothelial cells, with the concomitant appearance of multinucleated giant cells, emerges with the progression of diet-induced atherosclerosis. The morphological alterations of endothelial cells observed in the present study intimately reflect changes in their function associated with the progression of atherosclerotic lesions.

Animals↗
PubMed1994

An unusual presentation of spontaneous pneumoperitoneum secondary to the rupture of a gas-containing pyogenic liver abscess: report of a case.

We describe a rare case of spontaneous pneumoperitoneum secondary to the rupture of a gas-containing pyogenic liver abscess in a 59-year-old man. The patient was diagnosed as having a hollow viscus perforation based on a sudden onset of acute abdominal pain along with radiological evidence of bilateral subphrenic feee air (pneumoperitoneum), and underwent an emergency laparotomy. Contrary to expectations, the surgery revealed no perforations of the hollow viscus, but instead a ruptured liver abscess at the dome of the right hepatic lobe was identified associated with suppurative peritonitis. To the best of our knowledge, such a case of spontaneous pneumoperitoneum secondary to the rupture of a gas-containing liver abscess is extremely rare.

Abdomen, Acute↗
PubMed1994

Role of endothelium-derived nitric oxide and adenosine in functional myocardial hyperemia.

To investigate the role of endothelium-derived nitric oxide (EDNO) and adenosine in functional myocardial hyperemia, we examined the effect of NG-nitro-L-arginine (L-NNA) and 8-p-sulfophenyltheophylline (8-SPT) on coronary vasodilation in response to increased myocardial oxygen consumption in pentobarbital sodium-anesthetized dogs. L-NNA significantly attenuated the increase in coronary conductance from 28 +/- 6 to 16 +/- 2% with atrial pacing, from 69 +/- 5 to 36 +/- 6% with isoproterenol, and from 25 +/- 6 to 9 +/- 4% with constriction of the aorta. 8-SPT given alone attenuated the increase in coronary conductance to the same extent as L-NNA. The combined administration of L-NNA and 8-SPT did not further change coronary conductance. These findings suggest that EDNO and adenosine play an important role in functional hyperemia. EDNO-induced functional hyperemia appears to be dependent on adenosine receptor activation.

Adenosine↗
PubMed1994

Effects of nipradilol on venous hemodynamics: evaluation with a Doppler blood flow method.

Nipradilol is a newly synthesized beta-blocker which has a propranolol-like structure and contains a nitrate moiety. To examine the effect of nipradilol on venous blood flow, a single oral dose of nipradilol (6 mg) and propranolol (20 mg) was administered in the same 15 normal volunteers on separate days. Peak flow velocities, flow velocity integrals, and the diameter of the right brachiocephalic vein were measured before and 2 h after drug administration using Doppler echocardiography. These two beta-blockers significantly decreased systolic blood pressure to the same extent as they did heart rate. Nipradilol dilated the venous diameter by 8% and decreased peak flow velocity by 8% during systole and 9% during diastole. The flow velocity integral in one cardiac cycle also decreased significantly by 14%. Propranolol, however, failed to modify these parameters. These results suggest that nipradilol decreased venous return through its nitroglycerin-like direct vasodilating action.

Adult↗
PubMed1993

Generation of cells with morphological and antigenic properties of microglia from cloned EBV-transformed lymphoid progenitor cells derived from human fetal liver.

Single-cell clones from the Epstein Barr virus transformed lymphoid progenitor-like cell line established from human fetal liver at 8-week gestation, have been derived and characterized. These clones retained immunoglobulin (Ig) and T cell receptor (TCR) genes in their germ line configuration. They expressed HLA-DR and some B lymphoid markers such as CD19, CD20, and in some, the T lymphoid marker, CD2. They did not express surface Igs, CD3, CD4, CD8 or TCRs (alpha/beta, gamma/delta). A sensitive RT-PCR assay revealed that they did not express mRNA for a recombination activating gene-1, which is expressed after commitment to lymphoid cells. These results suggest that the established cloned lines are very early lymphoid progenitors that have not yet been committed to lymphoid cell lineage. In one of the lines, FL8.2.1.4, a marked morphological change that resembled microglia was induced when the cells were cultured in the presence of phorbol myristate acetate (PMA). After 72 hr of culture, 5-10% of FL8.2.1.4 cells developed a microglial morphology when stimulated with 10 to 100 ng/ml PMA. The newly generated cells with microglial morphology expressed HLA-DR and stained with Recinus communis agglutinin-1, which has been reported to bind specifically to brain microglia. In contrast, expression of lymphoid markers on cells with microglia-shaped morphology was remarkably diminished by PMA stimulation. Thus, the early lymphoid progenitor cells have the capacity to differentiate into cells with the morphological and antigenic properties of microglia cells. This system might be useful for further understanding of the characteristics and functions of microglia cells distributed in the central nerve system.

Antigens, CD↗
PubMed1993

Monocyte-endothelial cell interactions in vitro, with reference to the influence of interleukin-1 and tumor necrosis factor.

The interaction between monocytes and endothelial cells plays an important role in normal vascular biology and the pathogenesis of several vascular diseases. In the present study, interactions of freshly isolated human monocytes (Mos) and cultured umbilical vein endothelial cells (ECs) were quantitatively analyzed by a time lapse microcinematographic optical video system in vitro, with reference to Mo locomotion, adherence, and cytokine influence on these processes. The interaction between Mos and ECs was found to be a dynamic process. Without any stimulation of ECs, Mos generally possessed higher binding capacity to ECs and more active motile property than neutrophils and lymphocytes. The binding ratio of Mos to ECs varied from 0 to 8. Mos crawled over the surface of ECs or along the intercellular boundary areas of ECs by extending pseudopodia as long as 60 microns in length to traverse several ECs. Mos migrated into the subendothelium and could cause the disruption of the EC monolayer. In contrast, neutrophils or lymphocytes showed less adhesiveness to ECs and exhibited less dislocation when they moved on the ECs. Pretreatment of ECs with either human recombinant interleukin-1 beta (IL-1 beta) or tumor necrosis factor (TNF) (10-20 U/ml for 4-8 h) significantly increased adhesion rates of both Mos and neutrophils. Furthermore, the increased adhesion of neutrophils to stimulated ECs was accompanied by incremental increases in the rate of cellular movements. These phenomena were found to be associated with activation of EC surface adhesion molecules. In addition, by using the Boyden chamber assay, we found that IL-1 and TNF did not produce any chemotactic activity for Mos with a concentration range of 10(-3) to 10(3) U/ml. These results indicate that, in comparison with neutrophils and lymphocytes, Mos exhibited active adhesive and motive properties even on unstimulated EC surfaces, which could potentially interfere with the integrity of ECs. Upon exposure to cytokine stimulation, ECs increase the expression of adhesion molecules thereby enhancing both adhesion and locomotion of leukocytes. The distinctively higher affinity for binding to cultured ECs of blood Mos and their active motility relative to other circulating leukocytes may have great consequences in various physiological and pathological processes in vivo, including atherogenesis.

Cell Communication↗
PubMed1993

Effects of oral theophylline on sick sinus syndrome.

OBJECTIVES: We sought to determine the effect of theophylline on cardiac pauses in sick sinus syndrome. BACKGROUND: Sick sinus syndrome, a relatively benign condition, is usually treated with pacemaker implantation without any proved effectiveness. Thus, an appropriate pharmacologic therapy would be useful. METHODS: Theophylline (200 to 400 mg/day for 1 month) was initially administered orally to 17 patients with sick sinus syndrome, which is manifested by sinus pauses of > 2.5 s. Eleven of the 17 patients subsequently received theophylline for an additional 8 to 37 months. Twenty-four-hour Holter recordings were obtained before treatment, at the end of 1 month of treatment and then at 6-month intervals. RESULTS: Theophylline decreased the frequency of sinus pauses from 256 +/- 230 to 23 +/- 62 pauses per 24 h and decreased the duration of the longest pauses from 4.7 +/- 1.8 to 2.2 +/- 0.97 s after 1 month of treatment. Subjective symptoms associated with cardiac pauses disappeared in 16 of 17 patients. Ventricular premature beats increased in frequency but did not last longer than two beats. Three patients experienced adverse effects. Nine of the 11 patients receiving long-term treatment had a good outcome, but 2 patients required a pacemaker because of the reappearance of long sinus pauses. CONCLUSIONS: The results suggest that oral theophylline may be beneficial for the treatment of patients with sick sinus syndrome.

Administration, Oral↗
PubMed1993

Relationship between pressure-rate product and myocardial oxygen consumption of normal and hypertrophic right ventricles in open-chest dogs.

There are few reports on the relationship between right ventricular performance and its myocardial oxygen consumption (RVMVO2). The present study was conducted to investigate the relationship between RVMVO2 and the mechanical performance of normal and hypertrophic right ventricles in open-chest dogs. Right ventricular hypertrophy (RVH) was induced by producing chronic right ventricular pressure overload by banding the pulmonary arteries of 8 puppies for 6 months. The experiment was performed under basal conditions and after increasing the RVMVO2 in the eight dogs with RVH as well as in 20 normal dogs. The RVMVO2 showed significant positive relationships with right coronary (RCA) flow, right ventricular systolic pressure, and right ventricular pressure-rate product (PRP) in both the normal right ventricle and RVH hearts. However, the slope between the PRP and RVMVO2 was significantly steeper in the normal right ventricle (RV) than in the hypertrophic RV. When the PRP was normalized for the thickness of the right ventricular free wall, the slope of the two regression lines merged into a single line of fit. These results suggest that the pressure-rate product can be used to predict myocardial oxygen demand not only in the normal RV but also in well-compensated, hypertrophic RV. Isoproterenol induced smaller increases in cardiac output in the dogs with RVH than in those with normal RV. It also appears that the cardiac output of the hypertrophic RV is less sensitive to beta-adrenoceptor stimulation than that of the normal RV.

Animals↗
PubMed1993

Intravenous injection of adenosine triphosphate for assessing sinus node dysfunction in patients with sick sinus syndrome.

The clinical value of rapid intravenous injection of adenosine triphosphate (ATP, Adephos Kowa # L3, CAS 56-65-5) for assessing sinus node function was examined in 5 patients with sick sinus syndrome (SSS) and 6 normal controls. All patients with SSS showed cardiac pauses longer than 3 s on a 24-h Holter ECG monitoring. First, after prophylactic insertion of a temporary pacemaker in the right ventricle, overdrive suppression test was conducted using the standard technique, and sinus node recovery time (SNRT) was observed to evaluate the sinus node function. Then, 10 min later, 10 mg of ATP was rapidly injected intravenously, and body surface and intracavitary ECG were continuously recorded until the basal state was regained. The rapid injection of ATP resulted in a slight inhibition of sinus node automaticity in normal subjects, but marked inhibition was in patients with SSS associated with suppression of AV conduction. The longest post ATP atrial cycle (AA interval in the intracavitary ECG showed a close inverse relationship with SNRT corrected for basal sinus length (CSNRT), according to the following formula: longest AA interval (ms) = 3.32 x CSRT (ms) +254.4 (r = 0.91, p < 0.001). The results suggest that rapid intravenous injection is a useful tool for the diagnosis of SSS.

Adenosine Triphosphate↗
PubMed1993

Effects of inosine on adenosine-induced coronary vasodilation in the open chest dog.

The effects of inosine (CAS 58-63-9) on adenosine-induced coronary vasodilation were studied in open-chest dogs. Inosine and hypoxanthine were infused into the coronary artery at a rate to obtain respective calculated coronary plasma concentrations of 10(-5) mol/l, and the dose-coronary flow response of adenosine was recorded with and without inosine or hypoxanthine infusion. When the maximum coronary dilation was obtained, 10 ml of 2 x 10(-3) mol/l 8-phenyltheophylline (8-PT) solution was injected into the femoral vein. Additionally, adenosine deaminase activity was measured in vitro in the presence of various concentrations of either inosine or hypoxanthine. It was found that inosine, but not hypoxanthine, intensified the coronary vasodilatory effect of adenosine, which was abolished by 8-PT injection: EC50 of adenosine was reduced from 10(-5.43) mol/l to 10(-5.90) mol/l by inosine. Inosine and hypoxanthine did not affect adenosine deaminase activity at concentrations of 10(-4) mol/l or less. These findings indicate that inosine intensifies the coronary vasoactivity of adenosine, independent of inhibition of adenosine deaminase activity.

Adenosine↗
PubMed1993

[A case of an idiopathic enlargement of the right atrium, lacking in prominent right atrium contour and mimicking left pericardial defect on the chest X ray].

A 47-year-old man was admitted for evaluation of heart murmur in 1982. On admission, two-dimensional echocardiogram showed a giant right atrium with mild tricuspid regurgitation, but a chest X ray showed no prominent right atrium contour. Echocardiographic finding at various postures and chest X ray with artificial pneumothorax indicated little likelihood of left pericardial defect. An angiocardiogram and computed tomography showed the dilated right atrium with clockwise rotation. There was no indication of right atrial overload. Therefore, we made the diagnosis of an idiopathic enlargement of the right atrium. For about 10 years after discharge, we have followed up this patient. He has received no treatment and has been asymptomatic. On the other hand, echocardiography shows that the right atrium has gradually enlarged. Electrocardiogram has clearly revealed only a tall and slender peaked P wave in chest leads for the last 5 years. This may indicate not only an increasing load on the right atrium but also that the enlarged atrium is getting closer to the walls of the chest. We report this case of an idiopathic enlargement of the right atrium lacking in prominent right atrium contour, and mimicking left pericardial defect on chest X ray.

Cardiomegaly↗