[Operative technic for aortic arch aneurysm using profound hypothermic cerebral circulatory arrest with intermittent retrograde cerebral perfusion through the superior vena cava].
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Biomedical subjects
Publications and source records attributed to Y Ueda.
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Sixty-six children aged between 8 months and 15 years (average age 5.5 +/- 3.8 years) underwent mitral reconstructive operations for congenital mitral regurgitation between June 1969 and February 1987. The pathologic findings of the mitral valves were annular dilatation in 37 patients, cleft of the leaflet in eight, hypoplasia of the leaflet in 44, perforation of the leaflet in one, chordal elongation in 22, chordal absence in 16, and chordal shortening in seven. The methods of repair consisted of asymmetric annuloplasty (Kay-Reed method) in 61 patients, De Vega-type annuloplasty in one, plication of redundant leaflet in 15, and closure of cleft or perforation in nine. The single operative death (1.5%) was due to heart block. Follow-up data were available over 373.8 patient-years (average 5.7 years). The four late deaths (6.0%) were due to heart failure in two patients, pneumonia in one, and hepatitis in one. The actuarial survival rate was 93.1% +/- 3.1% at 7 years and 88.4% +/- 5.1% after 17 years. Valvuloplasty failed in 19 of the long-term survivors. One of these patients underwent mitral valve replacement 11 years after initial operation. The rate of freedom from reoperation was 86% +/- 10% after 17 years. The rate of freedom from valvuloplasty failure was 80% +/- 6.7% after 5 years, 67% +/- 7.2% after 10 years, and 44% +/- 11.9% after 15 years.
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SRCA was performed using surgically removed fresh tissues in 26 cases of lung cancer. The histological examination of day 6 xenograft showed that only a few xenografts contained tumor cells because of the host cell infiltration and stroma. For the assay considered as evaluable, we defined that control mice needed to show delta tumor size larger than -0.5 OMU and histological presence of tumor cell more than 50% in the day 6 xenograft. The evaluable assay rate (EAR) was no more than 25% (4/16). By the pretreatment with X-ray irradiation of 3 Gy, host cell infiltration was significantly suppressed. With this procedure however, only 40% (4/10) of EAR was gained. The reason for this low EAR was due to the difficulty to obtain the specimens enriched with tumor cells because of stroma and necrotic tissue. Then we used specimen obtained from the human lung cancer line xenografted in nude mice, which resulted in a high EAR of 84% (16/19). We concluded that SRCA for fresh surgical materials was still difficult. However SRCA for lung cancer line was feasible, especially for in vivo preclinical chemosensitivity test for new agents and decision for new drug combination. SRCA as a disease oriented chemosensitivity test is expected to develop in the future.
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In order to clarify the onset of insulin secretion and the regulatory mechanism of its receptor induction in fetus, blood glucose, serum insulin and its hepatic receptor in situ in fetal rats (D18-D21) were measured and the changes of the levels of insulin and its receptor after the direct injection of glucose (1g/kg) to fetal rats in utero were investigated. In fetal rats (D18-D21), both serum insulin and glucose levels increased as pregnancy progresses and specific binding of insulin in fetal liver microsomal membranes increased on D21 of gestation, mainly due to the increase in binding affinity rather than binding capacity. After the direct injection of glucose to the fetus in utero, the rapid increase in serum insulin and the rapid decrease in insulin specific binding to liver microsomal membranes were observed in a part of D20 and all of D21 fetal rats, which was mainly due to the decrease of binding capacity. This suggests that the acute elevation of endogenous insulin level followed by the decrease of insulin specific binding in fetal rat liver is based on the down regulation mechanism of insulin receptor, because the amounts of insulin separated from liver microsomal membranes were less than one twentieth of the insulin concentration which are enough to decrease the binding capacity of hepatic receptor theoretically. In addition, the dissociation of 125I-insulin from liver microsomal membranes of glucose-treated rats were indistinguishable from that of control. From these results, it can be concluded that the onset of glucose-stimulated insulin secretion appears in fetal rats on D20 of gestation and the elevation of endogeneous insulin rapidly down-regulates the number of hepatic insulin receptor in fetal rats.
In 38 patients with aortic regurgitation (AR) associated with ventricular septal defect (VSD), indications for aortic valvuloplasty (AVP) or aortic valve replacement (AVR) were investigated by assessing AR ratio, which was measured by electromagnetic flowmetry of the ascending aorta during the operation. Residual AR was evaluated by auscultation postoperatively. Patients were assigned to group A if they underwent VSD closure alone and to group B if they underwent AVP in addition to VSD closure; patients who had no postoperative AR were assigned to group I and those with persistence of AR to group II. Thus, the patients were separated into 4 subgroups; A-I (9 patients), A-II (5 patients), B-I (20 patients) and B-II (4 patients). In subgroup A-I, mean AR ratio decreased from 9% to 7% postoperatively, in A-II from 19% to 16% (p less than 0.1), in B-I from 36% to 9% (p less than 0.01) and in B-II from 44% to 20% (p less than 0.05). An AR ratio of more than 25% should be regarded as an absolute indication for AVP or AVR. If the AR ratio is between 20 and 25%, the indication of AVP is determined by inspection of the aortic valve. A good correlation was found between AR ratio and the AR rate determined by the aortic angiographic findings (Sellers classification): grade I AR corresponded to an AR ratio of 5 to 15%, grade II to 20 to 35%, grade III to 25 to 50% and grade IV to 45% or higher (r = 0.87, p less than 0.01).
We studied the afferent sources of Leu-enkephalin (ENK) -like immunoreactive (ENKI) fibers in the anteroventral thalamic nucleus (AV) of the rat using experimental immunohistochemistry. These fibers were markedly fewer on the operated side after the destruction of the medial mammillary nucleus pars medialis where a number of ENKI cells were observed. This strongly suggests that these ENKI cells project ipsilaterally to the AV. ENKI fibers seemed to reach the AV via the mammillothalamic tract.
As congenital malformations may be caused by perturbations of glycolytic flux on early embryogenesis [16], effects of hypoglycaemia were investigated by using rat embryo organ culture. Nine and one-half day old rat embryos were grown in vitro for 48 h (day 9 1/2 to 11 1/2) in the presence of hypoglycaemic serum for different hours during the culture period. Hypoglycaemic serum was obtained from rats given insulin intraperitoneally. On exposure to hypoglycaemic serum during the first 24 h of culture (day 9 1/2 to 10 1/2), embryos showed marked growth retardation and had increased frequencies of neural lesions (42.7% versus 0%, p less than 0.01), in contrast to hypoglycaemic exposure during the second 24 h of culture (day 10 1/2 to 11 1/2), where only minor growth retardation and low frequencies of neural lesions (2.4% versus 0%, NS) were seen. Even exposure to hypoglycaemic serum for a relatively short period (8 h) during the first 24 h of culture resulted in neural lesions at the frequency of 9.3-13.3%. The embryos exposed to hypoglycaemia demonstrated decreased glucose uptake and lactic acid formation, indicating decreased energy production via glycolysis that constitutes the principal energy pathway at this stage of embryonic development. These results suggest that hypoglycaemia during critical periods of embryogenesis has adverse effects on the development of the embryo and these effects might be mediated through metabolic interruption of embryogenesis.