Biomedical subjects
Publications and source records attributed to T Fukuhara.
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An intrasplenic injection (i.s.) of BALB/c bone marrow cells induces a higher survival rate than an intravenous injection (i.v.) in irradiated C3H/He recipients. Coculture experiments revealed the presence of alloantigen-specific and nonspecific suppressor cells in the spleens of mice injected i.s. and i.v. Suppressor activity decreased 50-60 days after bone marrow transplantation in i.v. chimeras, while there was no decrease in i.s. chimeras. In vitro suppressor activity was correlated with in vivo activity. Histopathological changes in the liver were examined. A total of 28% of the i.v. chimeras showed severe changes compared with 6% of the i.s. chimeras. The spleen indices of i.v. and i.s. chimeras were compared. Although there was no statistically significant difference between the spleen indices of i.v. chimeras and those of i.s. chimeras, spleen indices of i.v. chimeras tended to be higher than those of i.s. chimeras. These results show that suppressor cells in i.s. chimeras appear to inhibit graft-versus-host reactions more efficiently. Furthermore, an adoptive transfer assay showed that suppressor cells detected in i.s. chimeras were effective in vivo. We therefore suggest that suppressor cells detected in vitro correlate with in vivo activity and may play some role in the induction and maintenance of transplantation tolerance.
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We determined the effect of the calcium antagonistic agent, diltiazem hydrochloride upon ischemia-reperfusion injury in the dog. Ischemia was produced by occluding the left anterior descending artery for 40 min. Subsequent reperfusion was accomplished for 120 min by virtue of removal of the occlusion. Sixteen of the dogs studied were randomly assigned to diltiazem (D)-treated group (n = 8) and saline (S)-treated group (n = 8). D in saline was intravenously infused at a concentration of 3 mcq/kg/min starting 15 min after the occlusion. Myocardial blood flow (MBF) was measured using hydrogen gas clearance method. Infarct size was quantified as percent myocardium at risk by triphenyltetrazolium chloride staining. D administration caused a slight decline in mean aortic pressure, heart rate, and heart rate X systolic blood pressure throughout the periods of occlusion and reperfusion. However, there was no significant difference observed in both groups of dogs. MBF to ischemic myocardium was not significantly enhanced by D during ischemia. After 5 min of reperfusion subepicardial MBF was increased in group S, indicating a tendency towards reactive hyperemia. After 120 min of reperfusion there was a significant reduction in subendocardial MBF in group S and the transmural blood flow ratio was 1.23 +/- 0.59 in group D as compared with 0.53 +/- 0.39 in group S (p less than 0.05). The infarcted area as a percentage of the risk area was considerably smaller in group D than in group S (27.5 +/- 3.0 vs 47.0 +/- 6.5%, p less than 0.05). D markedly reduced the elevation of tissue calcium especially in the subendocardium. These findings suggest that D reduces the ultimate infarct size through the beneficial effect on ischemia-reperfusion injury.
An analysis using vectorcardiography and left ventriculography was made on forty patients, 17 of whom had dilated cardiomyopathy (DCM), 14 with triple vessel coronary artery disease (CAD) and 9 control subjects. QRS deflection area vector (Aqrs) was directed the most posteriorly in the DCM group and the second most posteriorly in the CAD group. Ventricular gradients (G) were smaller in the DCM and CAD groups than in the control group and directed more posteriorly in the DCM group than in the CAD and control groups. G/Aqrs was the smallest in the DCM group and the second smallest in the CAD group. Aqrs-At Angle was the widest in the DCM group and the second widest in the CAD group. Left ventricular ejection fraction (EF) showed high correlations with the azimuth of Aqrs (r = 0.659), with the magnitude of G (r = 0.720), with G/Aqrs (r = 0.785) and with Aqrs-At Angle (r = -0.855). From this evidence, we conclude that the magnitude of G, G/Aqrs and Aqrs-At Angle have a definable relationship with the impairment of left ventricular function and the Aqrs-At Angle is an especially useful parameter to detect the grade of myocardial damage in both the DCM and CAD groups.
We assessed the histochemical, ultrastructural and cytochemical effects of reperfusion on ischemic myocardial cells during the early and late reperfusion phases in two groups of dogs. Group A were 8 dogs undergoing 1 hour occlusion of LAD, and Group B were 14 dogs undergoing 1 hour occlusion of LAD followed by 2 hour reperfusion period. The results of the histochemical study (PAS stain) demonstrated that in Group A, a patchy distribution of glycogen occurred primarily in the subepicardial region. Three-dimensional analysis of this distribution revealed peninsulas of glycogen running parallel with a vessel. The cells in Group B, mainly subepicardium, showed a moderate glycogen content which was more extensive than those in Group A. The ultrastructural changes were assessed after a 60-minute ischemia and subsequent recovery (after 5 minutes and 120 minutes of reflow) using transmural biopsy specimens. Each myocardial cell was graded from 0-4 according to the degree of ischemic injury and recovery. The degree of ischemic damage varied in intensity from slight to severe, in both the subepicardium and the subendocardium. Ca++-ATPase activity was examined cytochemically in myocardial cells of Group B. After 60-minute occlusion, the moderately ischemic cells (especially in the subepicardium) that were without amorphous dense bodies or marked sarcolemmal lifting-off made significantly greater ultrastructural recovery (p less than 0.05) with restoration of Ca++-ATPase activity on sarcoplasmic reticulum and mitochondria after 120 minutes of reflow. This occurred even though after 5 minutes of reflow the cell showed temporary deterioration such as contraction bands, vacuoles and severe destruction of some mitochondria.
Molsidomine was administered intraduodenally to anesthetized dogs which were instrumented for measurements of aortic and left ventricular (LV) pressures, coronary perfusion pressure, intramyocardial pressure in the subendocardium, and subendocardial and subepicardial myocardial blood flow in the ischemic and non-ischemic regions. The dogs were divided into two groups: group M (n = 9) was administered molsidomine (0.2 mg/kg), group S (n = 10), saline only. Maximum LV systolic pressure decline was 20% in group M and 3% in group S (p less than 0.05). Maximum LV end-diastolic pressure decline was 63% and 35% in groups M and S, respectively (p less than 0.05). There was no difference between mean aortic pressure and coronary perfusion pressure between the two groups. The subepicardial blood flow in the ischemic region was decreased (-23% in group M vs 5% in group S; p less than 0.05), but subendocardial blood flow in the ischemic region increased only slightly in group M. The ratio of subendocardial to subepicardial blood flow increased at 15 and 30 min after administration of molsidomine in the ischemic area (67% in group M vs -10% in group S; p less than 0.05), but did not show any change in the non-ischemic region. Intramyocardial pressure at systole did not show any change but it decreased at end-diastole, (-32% in group M vs -7% in group S; p less than 0.05). Thus molsidomine redistributed the myocardial blood flow from the subepicardium to the subendocardium and from the non-ischemic to the ischemic region. This redistribution was associated with a reduction in both LV end-diastolic pressure and intramyocardial pressure at end-diastole.
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A comparative study of rat and human mammary tumors was undertaken to clarify the mechanism of hormone dependency by the PAP method. In normal mammary glands, histological estrogen receptor ER (+) cells were observed in the ductal epithelium and acinal cells, while only ER (-) cells were noted in HAN. After overiectomy, 55.6% of the ER (+) cells changes to ER (-). Furthermore, histological changes were glandular atrophy, anaplastic changes, (with) the remaining ER (+) cells (being in the) insular group. Those ER (+) cancer cells seem to be different in hormone sensitivity. As for human mammary glands, proliferation of ER (+) cells was observed in papillary lesions as duct papillomatosis. In the cancer tissues as a whole, ER (+) and ER (-) cancer cells were mixed, showing a so-called mosaic pattern.
Chemically produced prostaglandin E1 (PGE1) was administered in clinical cases of orthodontic tooth movement. In the first phase, lingual arch springs were applied on both sides of the maxilla to upper first premolars which were scheduled for extraction. One side received submucosal injections of PGE1 and the other received vehicle injections. The rate of tooth movement in the buccal direction approximately doubled on the side of several PGE1 injections as compared to the control side. In the second phase, the PGE1 injections were applied in canine-retraction cases for up to 3 weeks in first-premolar-extraction cases. The rate of distal canine movement was almost double on the side receiving PGE1 injections as compared to the vehicle-injected side. In the third phase, the PGE1 injections were applied on routine canine retraction in first-premolar-extraction cases. The rate of distal canine movement was almost 1.6-fold on the side of PGE1 injections as compared to the vehicle-injected side. Throughout this study, no side effects were observed macroscopically in the gingiva and roentgenographically in the alveolar bone, except for a slight pain reaction consistent with orthodontic tooth movement.
To identify and characterize the border zone, anesthetized dogs were subjected to 1-hour occlusion of the left anterior descending coronary artery with (Group R) or without (Groups A and B) 2 hours of subsequent reperfusion. Histochemical analysis of glycogen distribution, biochemical determination of lactate and adenosine triphosphate (ATP), and ultrastructural examination were carried out. In Group A, the epicardial edge of cyanosis was clearly visible and the sharply demarcated glycogen-depleted area contained peninsulas of cells with varying amounts of glycogen in its epicardial half, which were suggested to depend on collateral blood flow by intracoronary dye injection. In Group B, the edge of cyanosis was obscure and the glycogen-depleted area contained above-mentioned peninsulas at its lateral edge also. In Group R, although the edge of cynaosis was clear on occlusion, the peninsulas were numerous at the lateral edge as well as in the subepicardium after reperfusion. Lactate accumulation and ATP degradation corresponded well to glycogen decrease in all groups and were reduced significantly by reperfusion (p less than 0.005). Ultrastructural examination confirmed these findings. Therefore epicardial, and in some cases also lateral, salvageable border zones may exist and be composed of peninsulas of normal and intermediately injured cells dependent on collateral blood flow.
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Distal Surgical margin, required in the sphincter preserving operation for rectal cancer was studied histologically on the 78 resected specimens. The extramural cancer spread, examined by clearing method, was found in 20.5%, and was more frequent and expansive compared to intramural spread of cancer. No distal spread was found in cancer limited to the rectal wall. Length of the spread by 3 cm in lower rectal cancer and 4 cm in the upper rectal cancer. Postoperative anal function showed a good or fair in patients with internal sphincteric function preserved. Postoperative dysuria and male sexual disturbance showed a close relation to the pelvic nodes dissection. Ro-dissection was followed by 20% of dysuria, while RI and R 2 46.7%, R 3 1.8%.
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