[Unilateral visual disturbance].
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Biomedical subjects
Publications and source records attributed to Y Taguchi.
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We present a case of chronic granulomatous disease with an angiographically proven pseudosequestration of the lung. The patient was a 15-year-old boy who was admitted to the hospital with symptoms of fever, cough, hemoptysis and a subcutaneous abscess. Aspergillus fumigatus was isolated from the sputum and the abscess. During treatment, angiography demonstrated on anomalous blood supply to the right middle lobe. The therapeutic implications of pseudosequestration of the lung for the treatment of chronic granulomatous disease are discussed.
In order to investigate the relationship between urinary excretion of sialic acid and the severity of diabetic microangiopathy, urinary levels of sialic acid were determined in patients with non-insulin-dependent diabetes mellitus. The urinary molar ratio of sialic acid to creatinine in the diabetic patients was significantly higher than in the healthy controls (p < 0.01). Moreover, the urinary ratio was found to be gradually increased with the degree of diabetic microangiopathy. Urine molar ratio of sialic acid to creatinine in patients with proliferative diabetic retinopathy was significantly higher than in patients without retinopathy (p < 0.01). Urinary excretion in patients with macroproteinuria was also significantly higher than in patients without nephropathy (p < 0.01). Since urinary levels of sialic acid are proportionally increased with the severity of diabetic microangiopathy, the measurement of urinary sialic acid could become a useful biochemical means to monitor the degree of diabetic microangiopathy.
We have isolated a Schizosaccharomyces pombe gene, bfr1+, which on a multicopy plasmid vector, pDB248', confers resistance to brefeldin A (BFA), an inhibitor of intracellular protein transport. This gene encodes a novel protein of 1,531 amino acids with an intramolecular duplicated structure, each half containing a single ATP-binding consensus sequence and a set of six transmembrane sequences. This structural characteristic of bfr1+ protein resembles that of mammalian P-glycoprotein, which, by exporting a variety of anticancer drugs, has been shown to be responsible for multidrug resistance in tumor cells. Consistent with this is that S. pombe cells harboring bfr1+ on pDB248' are resistant to actinomycin D, cerulenin, and cytochalasin B, as well as to BFA. The relative positions of the ATP-binding sequences and the clusters of transmembrane sequences within the bfr1+ protein are, however, transposed in comparison with those in P-glycoprotein; the bfr1+ protein has N-terminal ATP-binding sequence followed by transmembrane segments in each half of the molecule. The bfr1+ protein exhibited significant homology in primary and secondary structures with two recently identified multidrug resistance gene products of Saccharomyces cerevisiae, Snq2 and Sts1/Pdr5/Ydr1. The bfr1+ gene is not essential for cell growth or mating, but a delta bfr1 mutant exhibited hypersensitivity to BFA. We propose that the bfr1+ protein is another member of the ATP-binding cassette superfamily and serves as an efflux pump of various antibiotics.
We report the case of a male infant with a variant of congenital dyserythropoietic anemia (CDA), who developed severe hyperbilirubinemia on the day of birth, subsequent severe anemia, and hyperferritinemia. Bone marrow and laboratory examinations revealed features of CDA including trilineage myelodysplasia and erythroblasts with a binucleated nuclear morphology and ineffective erythropoiesis. The CDA in this patient was assumed to be a new variant type because of: the lack of internuclear chromatin bridges in the erythroblasts with abnormal nuclear morphology; a negative acid serum test; the presence of erythrocyte antigen I, and the effect of splenectomy. Trilineage myelodysplasia in CDA is not known. An abnormality in the stem cells was suggested to be the cause of CDA in this case.
UNLABELLED: In the liver transplantation one of the causes of primary graft nonfunction is likely associated with lipid peroxidation at reperfusion after cold preservation. In this study, we investigated whether free radicals produced in mitochondrial electron transport system would result in lipid peroxidation after cold preservation in UW solution. MATERIALS AND METHODS: Under anesthesia, the liver of male Wistar rat was flushed via the portal vein with cold Ringer lactate, and then placed in 4 degrees C UW solution for 24 hr. After cold preservation, we examined mitochondrial respiratory control ratio (RCR), free radicals (O2-) from mitochondrial electron transport system by MCLA induced chemiluminescence, and lipid peroxidation by chemiluminescence (CL) after reoxygenation. RESULTS: RCR gradually decreased up to 24 hr preservation. O2- generation from mitochondrial electron transport system was not recognized at any length of the time after cold preservation up to 24 hr. At 6 hr, CL values were slightly higher than those of the control, but significantly decreased at 24 hr. CONCLUSION: O2(-)-generated in electron transport system of mitochondria did not increase with cold preservation up to 24 hr, therefore, the radical from mitochondria did not cause a lipid peroxidation at reperfusion injury.
In this study, the authors investigated enhancing the results of autoclaved autograft bone by combining it with a vascularized bone graft and supplementing it with autogenous bone marrow for replacement of a 2-cm tibial defect in the rabbit model. The study was divided into 4 groups. Group I consisted of autoclaved autograft bone only; Group II, autoclaved autograft bone and vascularized bone graft; Group III, autoclaved autograft bone and autogenous bone marrow; and Group IV, autoclaved bone and autogenous bone marrow and vascularized bone graft. The vascularized bone graft was provided by the ipsilateral fibula, pedicled on the peroneal vessels, and transposed to sit alongside the autoclaved bone. In Group I, all grafts had nonunion at 16 weeks. In Group II, new bone formation was seen at the proximal and distal site of the autoclaved bone, host bone, and vascularized fibular graft junction as early as 2 weeks, and bony union occurred at the 16th week. The autogenous bone marrow-supplemented groups (III and IV) had new bone formation along the entire length of the autoclaved bone. Bony union at the proximal and distal junction was seen as early as 4 weeks, extending to the entire autoclaved bone by the eight week (98% of the cases with 1 case of infection). Histologic examination showed revascularization and capillary ingrowth into the autoclaved bone at 16 weeks, with a significantly improved torsional stiffness when compared with the groups without autogenous bone marrow supplementation. The addition of vascularized bone graft resulted in an improved union rate as compared with the autoclaved bone alone. Autogenous bone marrow supplementation, in addition to the vascularized bone graft, resulted in rapid new bone formation all around the autoclaved bone, early revascularization and incorporation of the autoclaved bone, and a significantly improved torsional stiffness of the reconstruction.
A 72-year-old woman was admitted to our hospital because of a mass shadow in the left upper lobe on chest roentgenograms. She had noticed floaters in both visual fields 2 months before admission. Percutaneous aspiration of the lung lesion was done, and revealed poorly differentiated squamous cell carcinoma. Metastatic tumors were noted in the choroid of both eyes and in both kidneys. These lesions responded partially to systemic chemotherapy and the floaters disappeared. There have been few reports of metastatic choroidal tumors, but most cite the lung and the breast as the primary sites. We should pay attention to ophthalmologic findings because lung cancer may metastasize to the choroid.
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Thrombocytopenia has been shown to be an initial maternal response to conception. We investigated a potent bioactive lipid, platelet-activating factor (PAF), as one of the candidates derived from embryos to induce the decrease of platelet counts in maternal blood. First, we examined the potential of murine embryos to liberate PAF. In brief, twenty to thirty murine two-cell embryos of C57BL/6 mice were cultured in Whitten's medium for 24 h. The supernatant of the medium was collected and the total was extracted. After developing the lipid on thin-layer chromatography, the area corresponding to authentic PAF was scraped off and the lipid was extracted. The embryo-derived PAF was quantified by platelet aggregation using rabbit whole blood, and the presence of PAF was further confirmed by the addition of a PAF-receptor antagonist, SRI63-441. The results showed that a significant amount of PAF (ca. 10 ng/ml) was recovered from the lipid extract, whereas little platelet-aggregating activity was observed in the presence of SRI63-441. Second, the physiological function of murine platelets was examined using authentic PAF. When PAF (up to 83 micrograms/ml) was added to the murine platelets suspended in the whole blood, it neither induced platelet aggregation nor reduced the number of platelets. Considering these results, it is considered that PAF released from the embryos does not directly act on maternal platelets, but transduces its signal to the maternal host via some other bioactive substance.
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The broad host-range plasmid RSF1010 contains two oppositely oriented priming signals, ssiA and ssiB, for DNA synthesis dependent on the origin of vegetative DNA replication (oriV). If either ssiA or ssiB was deleted or inverted, the RSF1010 miniplasmids containing engineered oriVs were maintained at low copy numbers, replicated abnormally as dimers, and accumulated specific single strands in the Escherichia coli strain supplying the three RSF1010-encoded RepA, RepB', and RepC proteins. Interestingly, an additional intracellular supply of the Sog primase (the sog gene product of plasmid CoIIb-P9) reversed the replication deficiency of these miniplasmids with respect to all three aspects described above. These were also true for the RSF1010 miniplasmids in which either ssiA or ssiB was replaced by the primosome assembly site (PAS) or by the G4-type ssi signal (G site). Furthermore, comparative analysis of the functional contribution of the two oppositely oriented ssi signals to the DNA replication of RSF1010 showed that, irrespective of their types, ssi signals conducting the initiation of DNA chain elongation away from the iterons were functionally more important than ones in the inverted orientation. We consider that this functional difference reflects the inherent properties of the initiation mechanism of RSF1010 DNA replication.
We developed an improved determination method of mitochondrial proton adenosine triphosphatase (ATPase) activity in the liver. The activity was measured fluorometrically with a 3,3'-dipropylthiodicarbocyanine iodide (diS-C3(5)), which is excited at 625 nm and emits fluorescence at 670 nm. This dye transmits the electric potential across the inner mitochondrial membrane. The fluorescence intensity of diS-C3(5) with mitochondria (100 microliters, 4-16 mg/ml protein) in a 2 ml potassium buffer (pH 7.4) was regarded as a standard electric potential. After confirming the activity of the mitochondrial electron transport chain by succinic acid (9 mumol), we inhibited the chain by antimycin A (1.25 micrograms). Fluorescence intensity decreased by adenosine 5'-triphosphate (ATP) (2 mumol) and oligomycin (25 micrograms) inhibited this depression. The value of mitochondrial proton ATPase activity was calculated as a percentage of the fluorescence intensity change by ATP per the standard electric potential. The activity of mitochondrial proton ATPase in the normal fresh rat livers was 50.3 +/- 2.2%. Good correlation (r2 = 0.807) between two methods for mitochondrial proton ATPase activity, our newly developed method and a conventional colorimetric method, was obtained in the rat livers with various conditions. This method has advantages that the proton ATPase activity can be measured in intact mitochondria, and all procedures can be completed within 40 min. It is suitable for the determination of mitochondrial viability of liver graft in the hepatic resections and transplantations.
The broad host range plasmid RSF1010 requires for its replication in Escherichia coli three plasmid-encoded proteins and specific nucleotide sequences ssiA, ssiB, and iterons in the oriVRSF1010. In Pseudomonas aeruginosa, a recombinant mini-RSF1010 plasmid lacking ssiB lost its replication ability, but a miniplasmid lacking ssiA or carrying a primosome assembly site in place of ssiA could replicate. Moreover, ssiA, as a sole ssi signal, in the orientation that ssiB had originally taken was sufficient for replication of the miniplasmid. These results indicated that only one RSF1010-specific ssi signal in the orientation that ssiB takes in wild-type oriVRSF1010 was essential for replication of RSF1010. Replication of the miniplasmids was dependent on the three plasmid-encoded proteins, RepA, B', and C, as in E. coli.
The objective was to detect chronic hepatitis C virus infection in recipients of blood products using retrospective analysis by recall and enrollment of recipients. 226 patients who received blood products for open heart surgery from January 1983 to June 1992 were examined for HCV antibody by using a second generation assay and liver function test. 22 (14%) of the 161 patients who received blood products before November 1989 had detectable HCV antibody, but none of the 65 recipients receiving blood products after 1990, the year the Japanese blood bank began to screen for HCV-antibody. Abnormal alanine aminotransferase (ALT) levels, more than 25 iu/L, during the chronic phase of HCV infection was recognized in nine of 22 (41%) seropositive patients. The liver function test and second generation HCV antibody in the serum are effective markers to screen for chronic hepatitis C in blood product recipients transfused before 1990.