Long-term results in human T-cell leukemia virus type 1-positive renal transplant recipients.
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Adult↗
Biomedical subjects
K Tanabe
Publications and source records attributed to K Tanabe.
Effect of interferon-alfa treatment in renal transplant recipients with chronic hepatitis C.
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Adult↗
Recurrence of membranoproliferative glomerulonephritis in renal allografts.
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Adolescent↗
Isolation of a MX-guanosine adduct formed at physiological conditions.
3-Chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX), a highly potent mutagen present in chlorine-disinfected drinking water, was allowed to react with adenosine, guanosine, and cytidine in aqueous solutions. HPLC analyses, with detection at 254 and 310 nm, showed that a clearly detectable base adduct was formed in the reaction with guanosine. This substance was isolated by C18 column chromatography and characterized by UV absorbance, 1H NMR spectroscopy, and mass spectrometry. The compound was identified as 10-formyl-1, N2-benzoquinone propenoguanosine (I), and the yield was estimated to be approximately 0.1% in reactions performed at pH 7.4 and 37 degrees C.
Fresh Water↗
Alternative expression of Shc family members in nerve-injured motoneurons.
Expression of Shc family protein (Shc/ShcA, SCK/ShcB and N-Shc/ShcC) and Grb2 mRNAs in the hypoglossal motoneurons after axotomy was examined by in situ hybridization. In normal hypoglossal motor neurons, N-Shc mRNA was expressed predominantly, whereas the Shc mRNA level is very low. Rat hypoglossal nerve injury reversed the expressions of these two molecules in hypoglossal motoneurons. Shc mRNA expression was up-regulated markedly whereas N-Shc was down-regulated after nerve injury. Expression levels of SCK, another Shc family member, and Grb2 were unaffected by nerve injury. These results suggest that, whereas the N-Shc-mediated pathway dominates under normal conditions, an alternative Shc-mediated pathway is utilized in the event of nerve injury. By changing the expression of the Shc family members, the signaling pathway can be altered and various responses induced for nerve regeneration.
Adaptor Proteins, Signal Transducing↗
Improved visualization of the left atrial appendage by transthoracic 2-dimensional tissue harmonic compared with fundamental echocardiographic imaging.
We compared fundamental and tissue harmonic transthoracic echocardiographic imaging for the delineation of the left atrial appendage (LAA) in 32 subjects. The LAA images recorded in the parasternal short-axis view were divided into 4 segments and 2 observers independently graded for each segment using a visual scoring system ranging from 0 to 3 (0 = no, 3 = clearly visible over the entire length of the segment). For the 128 segments, the averaged segment scores were significantly increased after switching to harmonic imaging (1.32 +/- 0.69 versus 1.60 +/- 0.81 for fundamental and tissue harmonic imaging, respectively; P <.0005 for observer 1, and 1.38 +/- 0.65 versus 1.61 +/- 0.82, respectively; P <.001 for observer 2). In a patient with LAA thrombus, the image contrast of the thrombus was improved in harmonic compared with fundamental imaging. These data suggest that tissue harmonic imaging significantly improves image quality of the LAA.
Adult↗
Autotransfusion supported by erythropoietin therapy in transurethral resection of the prostate.
We investigated the collection and transfusion of autologous blood after treatment with EPO in 68 BPH patients (including 10 controls) who were scheduled to undergo TUR-P. All patients received oral and/or intravenous iron supplements. Assessments were made based on the preoperative increase in blood hemoglobin levels including autologous blood predonation (deltaHb). The deltaHb in patients undergoing collection of 600 ml of blood were as follows: control group: -0.36 +/- 0.57 g/dl; EPO group, 9 x 3000 units intravenously: 1.15 +/- 0.83 g/dl; EPO group, 6 x 6000 units intravenously: 0.79 +/- 0.80 g/dl; EPO group, 3 x 12,000 units subcutaneously: 1.47 +/- 0.62 g/dl. In patients undergoing collection of 800 ml of blood, the results were as follows: EPO group, 3 x 12,000 units subcutaneously: 1.80 +/- 0.69 g/dl; EPO group, 3 x 24,000 units subcutaneously: 2.03 +/- 0.77 g/dl. All EPO-treated patients successfully underwent surgery using their own blood, and none of them required homologous transfusion. The increase of Hb was greater in the patients treated with EPO than in controls, allowing safe preoperative blood collection even in elderly patients. In patients with relatively severe BPH, homologous transfusion could be avoided and surgery was performed safely.
Aged↗
Inhibitory effects of propofol on intracellular signaling by endothelin-1 in aortic smooth muscle cells.
BACKGROUND: Blood pressure decreases when propofol is administered. However, the exact mechanism underlying the vascular effects of propofol has not yet been elucidated. Endothelin produced by vascular endothelial cells is a potent vasoactive peptide that elicits prolonged contraction of vascular smooth muscle cells. The effects of propofol on endothelin-1-induced intracellular signaling in an aortic smooth muscle cell line, A10 cells, were examined. METHODS: Cultured A10 cells were pretreated with propofol for 20 min and then stimulated with endothelin-1. The effect of propofol on the endothelin-1-induced Ca2+ influx into A10 cells was evaluated by measuring intracellular 45Ca2+. The effects of propofol on the endothelin-1-induced activation of phosphatidylinositol-hydrolyzing phospholipase C and phosphatidylcholine-hydrolyzing phospholipase D were evaluated by measuring the formation of inositol phosphates and choline, respectively. The effect of propofol on endothelin-1 binding to its receptor was determined by an [125I] endothelin-1-binding assay. RESULTS: Propofol inhibited the endothelin-1-induced Ca2+ influx, but this was significant only at supuraclinical concentrations. The endothelin-1-stimulated formation of inositol phosphates was significantly suppressed by propofol. However, propofol had no effect on the formation of inositol phosphates induced by NaF, an activator of heterotrimeric guanosine triphosphate (GTP)-binding proteins. Propofol inhibited the endothelin-1-induced formation of choline. Propofol had no effect on the binding of endothelin-1 to its receptor. CONCLUSIONS: These results suggest that propofol inhibits endothelin-1-induced intracellular signaling in vascular smooth muscle cells. The inhibitory effect of propofol might be exerted at a point between the endothelin-1 receptor and its GTP-binding protein. However, because all significant effects are observed at high concentrations, clinical relevance is unclear.
Anesthetics, Intravenous↗
Effect of GR144053, a fibrinogen-receptor antagonist, on thrombus formation and vascular patency after thrombolysis by tPA in the injured carotid artery of the hamster.
The antithrombotic effect of GR144053, which inhibits platelet aggregation by binding to the fibrinogen receptor (glycoprotein IIb/IIIa), was investigated in vitro and in vivo by using hamsters. This compound inhibited the platelet aggregation induced by adenosine diphosphate (ADP; 2.5 microM) with a mean inhibitory concentration (IC50) value of 2.2 +/- 0.4 x 10(-5) M. Vascular injury was inflicted in one carotid artery by using a modified catheter to produce endothelial denudation. In the control group, arterial blood flow was interrupted 4.4 +/- 2.3 min (n = 12) after the injury. When GR144053 continuously infused intravenously at doses of 0 (saline) 0.1, 0.3, and 1.0 mg/kg/h (n = 8, each), the time that elapsed before the vessel became completely obstructed was prolonged in a dose-dependent manner. In separate experiments, reperfusion could be obtained by continuous infusion of tissue-type plasminogen activator (tPA; 0.52 mg/kg) starting 30 min after the initiation of thrombus formation. When GR144053 (0.3 and 1.0 mg/kg/h) was infused in addition to tPA, the incidence of reperfusion and the later patency of the reperfused artery were much improved as compared with tPA alone. The bleeding time at the end of tPA infusion was significantly prolonged in the presence of the highest dose of GR144053. Next, neointima formation was evaluated 2 weeks after the vascular injury. When GR144053 (0.3 mg/kg/h) was continuously infused i.v. by an implanted osmotic pump for 14 days, the neointimal area was significantly reduced. In separate hamsters, the proliferating index of smooth muscle cells (SMCs) by using bromodeoxyuridine (BrdU) was investigated, and treatment with both tPA and GR144053 significantly decreased the SMC proliferation index in vivo. However, in the in vitro experiments using a hamster SMC line, GR144053 did not have an inhibitory effect on SMC proliferation. These findings suggest that GR144053 inhibits platelet activation on the injured artery and improves vascular patency after thrombolysis with tPA, which furthermore results in suppression of neointima formation.
Animals↗
Inhibition of cyclin D1 expression and induction of apoptosis by inostamycin in small cell lung carcinoma cells.
Previously, we demonstrated that inostamycin, an inhibitor of phosphatidylinositol turnover, caused cell cycle arrest at the G1 phase, inhibiting the expression of cyclins D1 and E in normal cells. In the present study, we examined the effects of inostamycin on cell cycle progression and apoptosis in human small cell lung carcinoma Ms-1 cells. Treatment of exponentially proliferating Ms-1 cells with low concentrations of inostamycin caused cells to accumulate in the G1 phase. We found that inostamycin decreased cyclin D1, and increased cyclin-dependent kinase inhibitors such as p21WAF1 and p27KIP1 in Ms-1 cells. On the other hand, higher concentrations of inostamycin induced morphological apoptosis and DNA fragmentation in Ms-1 cells without affecting the expression of p53, Bcl-2 and Bax. Inostamycin-induced apoptosis was suppressed by an inhibitor of caspase-3, and a 17 kDa fragment of activated caspase-3 was detected following inostamycin treatment. Therefore, caspase-3(-like) would appear to be involved in inostamycin-induced apoptosis. On the other hand, an inhibitor of caspase-3(-like) proteases did not affect the inhibitory effect of inostamycin on cyclin D1 expression, suggesting that caspase-3(-like) proteases were not responsible for inostamycin-induced G1 arrest.
Anti-Bacterial Agents↗
Potentiation of paclitaxel cytotoxicity by inostamycin in human small cell lung carcinoma, Ms-1 cells.
In the present study, we found that inostamycin increased the ability of paclitaxel to induce apoptosis in Ms-1 cells. A considerably higher concentration of paclitaxel was required for the induction of apoptosis in Ms-1 cells than in other cell lines tested. Treatment of Ms-1 cells with inostamycin, an inhibitor of phoshatidylinositol (PI) synthesis, reduced the dosage of paclitaxel required to induce cell death by apoptosis. This effect of inostamycin is specific to Ms-1 cells, and inostamycin did not increase the cytotoxicity of other antitumor drugs such as adriamycin, vinblastine, methotrexate, cisplatin, etoposide, or camptothecin in Ms-1 cells. Addition of inostamycin to paclitaxel-treated cells caused a significant increase in the sub G1 peak, representing apoptosis, which was accompanied by a decrease in the G2/M peak seen in paclitaxel-treated Ms-1 cells, without affecting paclitaxel-inhibited tubulin depolymerization. Moreover, paclitaxel did not enhance inostamycin-inhibited PI synthesis. The expression levels of Bcl-2, Bax, and Bcl-XL were not changed following the co-treatment with inostamycin plus paclitaxel, whereas the activated form of caspase-3 was markedly increased. Thus, inostamycin is a chemosensitizer of paclitaxel in small cell lung carcinoma Ms-1 cells.
Antineoplastic Combined Chemotherapy Protocols↗
Renal transplantation into augmented bladders.
BACKGROUND: Urinary bladder augmentation is gaining popularity for the treatment of dysfunctional bladders in renal transplant patients. Although reported cases of adult and pediatric transplants into the augmented bladder have been favorable, the potential risk of urinary tract infection and graft failure under immunosuppression is still disputable. We report our experiences with 4 patients who underwent renal transplantation into an augmented bladder. METHODS: Between 1971 and 1996, 1275 renal transplants were performed at our institution. Of these transplants, 4 patients underwent renal transplantation into an augmented urinary bladder. Augmentation cystoplasty was performed before transplantation in 3 patients and 7 years after transplantation in the other patient. The bladder was augmented with an ileal segment in 3 patients and a ureter in the fourth patient. Graft function was assessed by the serum creatinine level. Fluorocystometrograms were performed in all patients at fixed intervals. RESULTS: Posttransplant renal function was satisfactory overall and no patient exhibited proteinuria. All patients except 1 acquired a large capacity low pressure bladder and remained continent with clean intermittent catheterization. One patient who underwent ureterocystoplasty is still incontinent because of his relatively small bladder capacity. Posttransplant pyelonephritis was documented in 3 patients during the follow-up period, but no other complications were observed. CONCLUSIONS: Our study demonstrates that renal transplantation into extensively reconstructed bladders can be safely performed with good success. Although urinary tract infection is a major consideration, we recommend pretransplant reconstruction not only to preserve graft function, but also to achieve urinary continence.
Adult↗
Efficacy of oral magnesium administration on decreased exercise tolerance in a state of chronic sleep deprivation.
We have previously reported that chronic sleep deprivation causes a deficiency of intracellular magnesium (Mg) and decreased exercise tolerance. The aim of this study was to clarify whether oral administration of Mg could be effective in restoring the exercise tolerance that is decreased by chronic sleep deprivation. A bicycle ergometer cardiopulmonary exercise test was performed by 16 healthy volunteers (mean age 21.9 years). They were divided into 2 groups: 8 received doses of 100 mg of Mg orally per day for 1 month (Mg group) and the remaining 8 received no Mg and served as the control group. The study conditions were designed as follows: (1) the usual state (good sleep); and (2) the sleep-deprived state (sleeping time up to 60% less than the usual state for 1 month). The ratio of intracellular Mg content of the sleep-deprived state to the usual sleep state was significantly higher in the Mg group (p<0.05) than the untreated control group. There was no difference between the sleep-deprived state and the usual state with regard to anaerobic threshold and peak oxygen uptake in the Mg group, whereas both of these decreased in the sleep-deprived state in the control group. These results indicate that decreased exercise tolerance observed in the sleep-deprived state could be improved by oral Mg administration.
Administration, Oral↗
Influence of aerobic exercise training on brain natriuretic peptide secretion in patients in the chronic phase of myocardial infarction.
Brain natriuretic peptide (BNP) secretion increases after myocardial infarction (MI); its plasma level may reflect the degree of left ventricular dysfunction. This study examines how aerobic exercise therapy for MI influences BNP secretion. Subjects included 70 patients (mean age, 62.0+/-11.3 years) who were divided into four groups: (1) 20 patients with an anterior MI and exercise training; (2) 20 patients with an anterior MI and no exercise training; (3) 15 patients with an inferior MI and exercise training; and (4) 15 patients with an inferior MI and no exercise training. The training groups performed aerobic exercise 3 times a week for 2 months. Exercise intensity was defined as a heart rate of anaerobic threshold (AT), derived from the treadmill cardiopulmonary exercise testing at 1 month after the onset of MI. The subjects underwent cardiopulmonary exercise testing again at 3 months after the onset of MI. To measure BNP, blood samples were obtained in the resting state and immediately after the peak exercise. AT and peak oxygen uptake increased in the training group with anterior MI and in both the training and nontraining groups with inferior MI. Significant serial change in plasma BNP level was not observed in the inferior MI groups. Plasma BNP level decreased longitudinally only in the nontraining anterior MI group. It was concluded that exercise training in patients with an anterior MI could delay the recovery of left ventricular function, but will increase exercise tolerance.
Aged↗
Image enhancement by noncontrast harmonic echocardiography. Part II. Quantitative assessment with use of contrast-to-speckle ratio.
OBJECTIVE: To ascertain whether "harmonic imaging"--use of ultrasound signals with the frequency twice that of the transmitted signal for ultrasound image generation--can improve image contrast while reducing noise. METHODS: Technically difficult echocardiograms (nonvisualization of 2 or more endocardial segments in a 16-segment model) from 25 patients were analyzed. Corresponding fundamental and harmonic images of the left ventricle in the apical four-chamber, two-chamber, and long-axis views were divided into basal, mid, and apical regions. The difference in image quality between fundamental and harmonic scans was assessed by using the muscle-to-cavity contrast-to-speckle ratio (CSRmc). RESULTS: The mean CSRmc values of pooled data revealed significant image enhancement by harmonic scanning (CSRmc increased from 0.84 to 1.06; P < 0.0001). Regression analysis showed that harmonic imaging improved the CSRmc values in 68% of all scans. Regional analysis indicated the most enhancement in basal regions (CSRmc increased from 0.96 to 1.34; P < 0.0001), followed by the mid (CSRmc increased from 0.84 to 1.04; P < 0.0001) and apical (CSRmc increased from 0.68 to 0.74; P = 0.0138) left ventricular regions. CONCLUSION: Noncontrast harmonic imaging significantly enhances suboptimal echocardiographic images, particularly in the regions distant from the transducer.
Adult↗
Allelic diversity at the merozoite surface protein-1 locus of Plasmodium falciparum in clinical isolates from the southwestern Brazilian Amazon.
Nucleotide sequences of each variable block in the Plasmodium falciparum merozoite surface protein-1 gene (PfMSP-1) may be grouped into one of two or three possible allelic types, named after the reference isolates MAD20, K1, and RO33. Allelic diversity at this locus basically results from different combinations of allelic types in variable blocks. We used a polymerase chain reaction (PCR)-based strategy to type the variable blocks 2, 4a, 4b, and 10 of the PfMSP-1 gene of P. falciparum isolates from 54 symptomatic malaria patients living in Rondonia, a hypoendemic area in the southwestern Brazilian Amazon. Ten different PfMSP-1 gene types, defined as unique combinations of allelic types in variable blocks, were identified among the 54 isolates. Twenty-one isolates (39%) harbored more than one gene type and two had at least three genetically distinct clones. Hybrid sequences, with a MAD20-type sequence in the 5' segment (4a) and a K1-type sequence in the 3' segment (4b), were quite common in block 4. Direct sequencing of block 4 PCR products revealed a new putative recombination site in four isolates. In contrast with previous studies, the observed distribution of gene types does not deviate significantly from that expected under the null hypothesis of random association between allelic types detected in each variable block. These contradictory data are discussed with reference to the immunoepidemiologic features prevailing in distinct malaria-endemic areas.
Adolescent↗
A PCR method for molecular epidemiology of Plasmodium falciparum Msp-1.
Merozoite surface protein-1 (MSP-1) of Plasmodium falciparum is a strong malaria vaccine candidate. However, MSP-1 exhibits extensive antigenic polymorphism, an issue which may compromise the development of effective vaccine based on this molecule. Since polymorphic nature of MSP-1 has not been fully understood in endemic areas of malaria, variation of the MSP-1 gene (Msp-1) must be studied in detail in natural parasite populations. Here, a PCR-based method for determination of P. falciparum Msp-1 haplotype is described, which can detect up to 24 different haplotypes per infected person. The method can be applied to various purposes of molecular epidemiology of not only Msp-1 haplotype but the genetic structure of P. falciparum populations.
Animals↗
Multiple inhibition of platelet activation by aurintricarboxylic acid prevents vascular stenosis after endothelial injury in hamster carotid artery.
Activated platelets are instrumental in restenosis due to their role in thrombus formation. Aurintricarboxylic acid (ATA) has been reported to prevent platelet activation by inhibiting von Willebrand factor binding to platelet glycoprotein (GP)Ib. We investigated the effects of ATA in vitro and in vivo in hamsters. ATA inhibited the in vitro platelet aggregation induced by ADP, botrocetin and thrombin, but not by collagen. The IC50 values during the ex vivo platelet aggregation by ADP, botrocetin and thrombin were 8.2 +/- 1.8 microM, 0.9 +/- 0.4 microg/ml and 2.4 +/- 0.8 unit/ml, respectively. The platelet retention time to collagen-coated beads of hamster blood samples was inhibited by ATA (0.1, 0.3 and 1.0 mg/kg per hour) in a dose-dependent manner. Continuous administration of ATA (0, 0.1, 0.3, 1.0, 3.0 and 10.0 mg/kg per h) via an infusion pump produced dose-dependent antithrombotic effects: the time to occlude the carotid artery after vascular injury with a modified catheter was prolonged. Only when infused at doses of 3.0 and 10.0 mg/kg per hour, bleeding times were significantly prolonged. The continuous treatment with ATA (1.0 mg/kg per h) using a 2ML1 Alzet infusion pump for 2 weeks, resulted in a decrease in neointimal area by 22.2 +/- 6.8% when measured 2 weeks after injury induction. DNA synthesis using DDT1MF2 hamster SMCs was decreased by ATA in a dose-dependent manner. ATA reduced the number of platelets adhering on the injured area, as detected by electron microscopy. These results indicated that treatment with ATA inhibited platelet adhesion but also SMC proliferation. These observations may explain the effect of ATA on neointima formation.
Animals↗