Change of electronic structures with carrier doping in the highly correlated electron system Y1-xCaxTiO3.
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Biomedical subjects
Publications and source records attributed to Y Taguchi.
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To analyze the RSF1010-specific priming mechanism, a library of randomly mutagenized ssiA sequences was constructed by chemical synthesis using mixed nucleotide phosphoramidites. Synthetic ssiA sequences with the single base-substitutions were assayed for the SSI activity in E. coli JM109 expressing RepB' primase. It was demonstrated that the activity of ssiA was damaged markedly by single base-substitutions within the possible stem-loop structure and its 3'-flanking region. It is conceivable that these domains are critical in recognition and primer synthesis by RepB' primase.
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The interface between bone and a bioactive glass cement--a mixture of bioactive glass powder and ammonium phosphate solution, previously reported on by the authors--was evaluated quantitatively and histologically. The materials tested were (1) the original bioactive glass cement (BCI cement); (2) an improved type of bioactive glass cement (BCII cement); (3) polymethylmethacrylate (PMMA) bone cement; and (4) a bioactive, apatite-wollastonite-containing, glass ceramic (A-WGC). Hardened cylindrical specimens of each cement were inserted loosely into canine femora and the interfacial shear strengths were measured using a push-out test. The interfacial strength values of the bioactive glass cements increased with prolonged implantation time. At each postimplantation time studied (8, 12, and 24 weeks), the interfacial strength value of BCI cement did not differ significantly from that of A-WGC. BCII cement interfacial strength was greater than that of BCI cement, whereas the interfacial strength of PMMA bone cement remained at a very low level throughout the study. Histological examinations revealed that direct bonding of both bioactive glass cements to bone had occurred without pathologic degradation. After 24 weeks, the defects between the bone and the bioactive glass cements had been filled with mature lamellar bone. Because the bioactive glass cement system developed by the authors, especially BCII cement, shows excellent osteoconductivity and bonds to bone tightly, we consider it to be a promising material for fixing prostheses into bone.
We immunized AKR/n (H-2k) spleen cells in BALB/c (H-2d) mice via the portal vein (pv) and investigated the role of hepatic mononuclear cells (MNC) in the induction of alloantigen-specific immune tolerance. MNC in the liver and spleen of pv-administered mice were demonstrated to abrogate the responses to AKR/n alloantigens in allogeneic MLR. On the contrary, MNC in the liver and spleen of mice administered subcutaneously with the same antigens showed greater responses than those of control mice. The tolerance induced by pv administration was alloantigen-specific and appeared earlier in hepatic MNC than in splenic MNC. Furthermore, hepatic MNC of pv-administered mice had a suppressive effect when these cells were added to allogeneic MLR, in which mitomycin C (MMC)-treated AKR/n splenic MNC were used as stimulator and control BALB/c splenic MNC were used as responder. Splenic MNC of pv-administered mice and hepatic MNC of control mice did not show such suppressive effects. Such suppression was alloantigen-specific, since no suppression was induced when hepatic MNC of pv-administered mice were added to a system using MMC-treated C57BL/6 (H-2b) splenic MNC. The alloantigen-specific suppression induced by hepatic MNC was abrogated by a depletion of TcR-alpha beta + cells but not of CD4+, CD8+, nor B220+ cells from hepatic MNC. These results suggested that alloantigen-specific suppressor cells appeared predominantly in the hepatic MNC of pv-administered mice and displayed the phenotype of TcR-alpha beta +CD4-8- double-negative T cells, although alloantigen-specific tolerance was induced in both hepatic and splenic MNC.
The relationship between late ventricular potentials (LP) and myocardial ischemic changes or ventricular arrhythmias was investigated in patients with Duchenne muscular dystrophy (DMD). Twenty-six DMD patients aged 10-33 years (mean 18.2 years) and 27 age-matched healthy volunteers were studied. Ventricular arrhythmias were detected by 24-h Holter ECGs and LPs were determined using signal-averaged ECGs. In DMD patients filtered QRS duration, late duration, and low-amplitude signal under 40 microV were significantly prolonged compared with those of the controls. The root mean square voltage of the f-QRS complex in the last 40 ms was lower in DMD patients than in the controls. None of the control subjects had LP. However, LP was detected in 8 (31%) of the 26 DMD patients. The patients with LP had more frequent ST-T depression and ventricular arrhythmias than the patients without LP. LP had 60% sensitivity and 87% specificity for documented ventricular arrhythmias. It is concluded that LP in DMD patients indicates the presence of substrate for ventricular arrhythmias associated with local myocardial fibrosis, and is useful in identifying those at high risk for malignant ventricular arrhythmias.
Intravenous pyelography is the standard first-line investigation for suspected renal trauma. A faint, and/or delayed visualization, or nonvisualization of the damaged renal unit is not uncommon. Low-dose dopamine (3 micrograms/kg/min) increases renal blood flow without deleterious side effects. An experimental rat model was developed to evaluate the effects of low-dose dopamine on intravenous pyelograms in animals with unilateral renal trauma. A consistent and significant improvement in the visualization of the injured kidney was noted in the dopamine-treated animals compared with controls that received equivalent volumes of normal saline.
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PURPOSE: The clinical significance of abnormal signal averaged ECG (SA-ECG) determined by time and frequency domain analyses was assessed in tetralogy of Fallot patients after surgical repair, and the methods of analysis were compared. MATERIALS AND METHODS: SA-ECG was performed in 42 patients (mean age, 9.4 years) after radical surgical repair of tetralogy of Fallot, and in 11 preoperative patients (mean age, 2.6 years). Abnormal SA-ECGs were defined by time domain analysis (vector magnitude method) and frequency domain analysis (fast Fourier transformation). RESULTS: Abnormal SA-ECGs were recognized in 10 postoperative, patients (3 by time domain and 9 by frequency domain, analysis), but in none of the preoperative patients. Three patients with abnormal SA-ECGs had nonsustained ventricular tachycardia, 5 others had premature ventricular contractions, and the remaining 2 had no ventricular tachyarrhythmias documented by 24 h Holter monitoring. Patients with abnormal SA-ECGs more commonly had ST-T segment depression on standard ECG during exercise (8/10 versus 8/32, p < 0.001), a history of resection of a hypertrophic septoparietal muscle band (8/10 versus 2/32, p < 0.001) and histologically documented myocardial fibrosis at radical surgical repair (9/10 versus 5/19, p < 0.002). CONCLUSION: A Combination of time and frequency domain analyses was necessary to detect abnormal SA-ECGs in postoperative patients because of ventricular conduction disturbance. This technique might increase our ability to identify patients at risk of ventricular tachyarrhythmia, or those with underlying myocardial abnormalities.
Recent studies have revealed that altered mineral and vitamin D metabolism is observed in diabetic patients with the complication of osteopenia. In order to elucidate the role of parathyroid hormone-related peptide (PTHrP) on calcium homeostasis in diabetes, we have measured the serum level and urinary excretion of PTHrP as well as other serum calcium-regulating hormones in 106 patients with non-insulin-dependent diabetes mellitus (NIDDM) and 43 control subjects. The serum concentration of intact PTH was 2.34 +/- 0.13 (mean +/- SEM) pmol/l in NIDDM patients, which is significantly lower than the value of 3.11 +/- 0.14 pmol/l in the controls (p < 0.01). Both serum calcium and calcitonin, however, were not statistically different from controls. On the other hand, circulating PTHrP in NIDDM was 40.1 +/- 1.4 pmol/l, which is significantly elevated when compared to 27.3 +/- 1.3 pmol/l in the controls (p < 0.01). Moreover, urinary excretion of PTHrP also was significantly higher in NIDDM (p < 0.01). In the present study, the circulating calcium level was well preserved in NIDDM patients, although the PTH levels were shown to be decreased. The elevated serum PTHrP might, therefore, have a physiologically compensatory role on the calcium regulatory systems in NIDDM. Furthermore, this elevation is most likely due to the excess production of this peptide and not to the decrease in urinary excretion.
It is important to distinguish proximal right bundle branch block (RBBB) from distal RBBB because patients with both proximal RBBB and left bundle branch block may progress to a late atrioventricular conduction disturbance. Signal-averaged electrocardiograms (SAECGs) were investigated in 35 patients with RBBB following surgical correction of tetralogy of Fallot or ventricular septal defect in order to determine the block site of RBBB noninvasively using a SAECG. The site of RBBB was first identified by a body surface map; 12 patients had proximal RBBB (group 1), and 23 had distal RBBB (group 2). The control groups consisted of 8 patients with RBBB without congenital heart disease (group 3) and 20 normal subjects (group 4). The mean of the filtered QRS duration in the group 1 patients was significantly longer than in the other 3 groups (p < 0.01). The number of fragmented signals in group 1 was significantly greater than that in the other 3 groups (p < 0.01). A filtered QRS pattern was divided into 4 different types (whole, early, late, and normal) according to the successive fragmented signals; the "whole" type was the most common in group 1 (83%). SAECG is successful in identifying those patients with proximal RBBB according to the following indices: a filtered QRS duration equal to or longer than 160 msec, a fragmented signal number greater than 10 and a "whole" type filtered QRS pattern. In conclusion, SAECG is a useful tool for distinguishing proximal RBBB from distal RBBB.
A large supratentorial tumor associated with an extraparenchymatous cyst and multiloculated intraparenchymatous cysts occurred in a 14-month-old infant. This case had all the characteristic features of desmoplastic infantile ganglioglioma both clinically and histologically. The notable difference was the extraparenchymatous cyst. The extraparenchymatous cyst was probably caused by entrapment of cerebrospinal fluid in the subarachnoid space by some check-valve mechanism because the leptomeninges were commonly involved in the tumor. A similar mechanism may explain the etiology of the intraparenchymatous, disproportionately large cyst in desmoplastic infantile gangliogliomas.
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We reviewed 224 patients, who underwent kidney transplantation to investigate relationship between aseptic necrosis (AN) and administration of steroid, Cyclosporin A (CsA), body weight gain. We classified patients into 4 groups by the type of immunosuppressant: the AP group had received Azathioprine (AZ) + Prednisolone (Pre); the CP group, CsA + Pre; the ACP group, AZ + CsA + Pre; and others. There were total 24 AN patients (10.7%). The incidences of AN is 18% in the CP group, 9.3% in the AP group and 0% in the ACP group. In the AP group, weight gain at 1 and 2 month after transplantation and cumulative steroid dose at 3, 4, 5 and 6 month after transplantation correlated with AN. In the patients with AN of the CP and ACP groups, CsA doses per kilogram of body were higher than those in patients without AN at 5, 6 and 12 month after transplantation. In the CP group, the incidence of AN is significantly higher, and administration dose of CsA was higher than that in the ACP group. However steroid dose and body weight gain were lower in the CP group. Therefore AN was associated with CsA in the CP group. In contrast, AN correlated with weight gain and early high cumulative steroid dose administration in the AP group.
To improve the diagnostic accuracy and understanding of the pathogenesis of lymphoproliferative diseases (LPDs) occurring in immunosuppressed transplant recipients (post-transplantation LPD), clonality of Epstein-Barr virus-induced human LPDs in mice with severe combined immunodeficiency was examined by analyzing: 1) human immunoglobulin genes and their products, 2) the clonality of Epstein-Barr virus DNA, and 3) genetic alteration of c-myc or bcl-2 genes. A spectrum of clonality was found in the LPDs comparable with that reported for post-transplantation LPDs, although rearrangements of c-myc or bcl-2 genes were not detected. It is confirmed that this system is useful in terms of clonality for understanding the early phases in the pathogenesis of post-transplantation LPD or LPD in immune deficient patients.
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