[A 65-year-old woman presenting with a left hilar mass].
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Biomedical subjects
Publications and source records attributed to T Mitani.
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We compared the imaging capability of magnetic resonance angiography (MRA) with that of conventional coronary angiography in a patient with coronary-pulmonary fistulae. Using the latter procedure, it is difficult to measure abnormal tortuous blood vessels in one section. However, the course of blood vessels could be evaluated quite well by rearranging serial cross-sectional MRA images using multiplanar reconstruction (MPR). This procedure allowed us to determine the anatomic positional relationship of these vessels to the peripheral cardiac great vascular system. MPR may detect sites of influx and outflow of abnormal blood vessels.
We report a 23-year-old woman who developed ascites 3 years after ventriculoperitoneal shunting. Revision of the shunt to ventricular drainage followed by ventriculo-atrial shunting was required for resolution of ascites. In our patient the pathophysiology of this rare shunt complication most likely involved impaired absorption of fluid within the peritoneum associated with multiple shunt reconstructions and tube extensions resulting in chronic inflammation. Cerebrospinal ascites must be suspected irrespective of post-shunt intervals in similar patients.
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The muscarine receptor agonist SK-946, an aniline derivative with a characteristic bicyclo amine, was found. We describe a new synthetic method for 1-azabicyclo[3.3.0]octane and describe the biological activity of SK-946.
To establish practical, effective medical digital image filing systems, various problems remain to be solved. The authors focused on 2 such problems of great importance: image data compression and standard specifications for digital data storage. From a variety of image compression algorithms now available, 2D-Color Doppler image compression was clinically investigated using the Joint Photographic Expert Group (JPEG) method. In low grade compression, the images decompressed showed no significant alterations in image quality, however, in higher grades of compression attained through irreversible coding in the JPEG method, the images showed subtle but significant alterations: emergence of 2 kinds of artifact, i.e., borderline-artifact produced in the DCT procedures and pseudo color spots. The reproducibility of colors was found to be altered by changing the quantization table in the JPEG procedure. It was thought necessary to choose a proper quantization table and examine the DC coefficients (number of pixels) in the DCT procedure to attain practical 2D-Color Doppler image compression by the JPEG method. Although attempts in Japan are being made to establish common standards for electronic data storage, based on MEDIS, in an effort to promote standardization there are many problems to be solved before practical use is possible. To ensure common availability as required by the technical standards, it is necessary to organize minimum-required specifications into common standards and make them open to the public.
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The effect of ethanol on cells infected with mouse hepatitis virus (MHV) was investigated. After MHV infection of competent cells, NCTC1469, ethanol was added to the culture at various concentrations, and the viability of cells was measured using 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide. To examine the possible involvement of the ethanol metabolite, acetaldehyde, alcohol dehydrogenase activity was measured in NCTC1469 cells. Ethanol alone did not show cytotoxicity against NCTC1469 cells at concentrations from 0.125% to 2%. After infection with MHV, the viability of cells decreased, and this decrease was further enhanced, dose-dependently, by the addition of ethanol. The activity of alcohol dehydrogenase in the cells was below the detectable level. The same phenomena were also demonstrated in cells infected with influenza virus and Herpes simplex virus. These results demonstrate that ethanol enhances MHV-mediated cytotoxicity; this exacerbation of cytotoxicity by ethanol is suggested to be an effect common to cytopathic virus-infected cells.
We have isolated suppressor mutants that suppress temperature-sensitive colony formation and anucleate cell production of a mukB mutation. A linkage group (smbB) of the suppressor mutations is located in the rne/ams/hmp gene encoding the processing endoribonuclease RNase E. All of the rne (smbB) mutants code for truncated RNase E polypeptides lacking a carboxyl-terminal half. The amount of MukB protein was higher in these rne mutants than that in the rne+ strain. These rne mutants grew nearly normally in the mukB+ genetic background. The copy number of plasmid pBR322 in these rne mutants was lower than that in the rne+ isogenic strain. The results suggest that these rne mutations increase the half-lives of mukB mRNA and RNAI of pBR322, the antisense RNA regulating ColE1-type plasmid replication. We have demonstrated that the wild-type RNase E protein bound to polynucleotide phosphorylase (PNPase) but a truncated RNase E polypeptide lacking the C-terminal half did not. We conclude that the C-terminal half of RNase E is not essential for viability but plays an important role for binding with PNPase. RNase E and PNPase of the multiprotein complex presumably cooperate for effective processing and turnover of specific substrates, such as mRNAs and other RNAs in vivo.
Chitosan-amino acid conjugates were prepared by coupling amino acid esters to the carboxyl group of glyoxylic acid-substituted chitosan. The removal of heavy metals (Cu, Ni, Co and Mn) was increased by introduction of amino acids to chitosan, especially for Mn. Heavy metals were almost completely removed by chitosan-amino acid conjugates from solutions at an initial concentration of 100 parts per million.
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The MukB protein is essential for chromosome partitioning in Escherichia coli and consists of 1484 amino acid residues (170 kDa). We have determined the base changes at the mutated sites of the mukB106 mutant and a newly isolated mutant, mukB33. These mutant mukB genes were each found to carry a single base-pair transition which leads to an amino acid substitution; a serine residue at position 33 was changed to phenylalanine in the case of mukB106, and an aspartic acid residue at position 1201 was changed to asparagine in the case of mukB33.
Dynamic 3-dimensional Fourier transformation (3 DFT)-FISP MR imaging was performed in 30 patients with 49 liver tumors (hepatocellular carcinoma 26, hemangioma 13, cholangiocellular carcinoma 2, metastatic liver tumor 8) to evaluate characteristic enhancement patterns. MR images of 3 DFT-FISP (TR/TE/flip angle/slab thickness/partition/slice thickness, 20 msec/8 msec/30 degree/21-75 mm/7 or 15/3-5 mm) were obtained before, just after (early phase), 1 min after (late phase 1) and 2-4 min after (late phase 2) the administration of 0.1 mmol/kg of Gd-DTPA. Twenty-three of the 26 (88%) hepatocellular carcinomas showed total hyperintense enhancement relative to surrounding liver parenchyma in the early phase, and isointense or total hypointense enhancement in the late phase. Eleven of 13 (85%) hemangiomas showed peripheral hyperintense enhancement in the early phase, and peripheral or total hyperintense enhancement in the late phase. Cholangiocellular carcinomas were enhanced gradually from the early to the late phase. Metastatic liver tumors showed doughnut-like ring enhancement in all 8 lesions in the early phase. We concluded that 3 DFT-FISP dynamic MR imaging was useful in the differential diagnosis of liver tumor.
The 5-year cumulative survival rate of 443 patients who underwent transcatheter chemoembolization (TCE) for non-resectable hepatocellular carcinoma (HCC) before December 1986 was 8.0%, and 29 patients survived for 5 years or more. Of these 29 patients, 25 were men and 4 were women; their mean age was 63.9 years. Macroscopic classification showed lesions of the single nodular type in 16 cases, the multiple nodular type in 10 cases, and the massive type in 3 cases; 12 of the single nodular lesions measured 5 cm or less in size. The TNM classification showed lesions of stage I in 3 cases, stage II in 14 cases, stage III in 6 cases, and stage IV in 6 cases. Lesions classified as Child A were found in 23 patients, and they were thus much more common than Child B lesions (2 patients) and Child C lesions (1 patient). The response was analyzed in relation to the use of iodized oil (Lipiodol). It was used in 215 of the patients, and the 5-year cumulative survival rate of those patients was 12.9% (23 of them survived for 5 years or more). Lipiodol was not used in 228 patients, and they showed a 5-year cumulative survival rate of 3.4%, with 6 patients surviving for 5 years or more. The 6 patients with stage III disease and the 6 with stage IV disease received Lipiodol. TCE with Lipiodol thus contributed greatly in prolonging the survival of patients with HCC complicated by intrahepatic metastases or intraportal tumor thrombi.
The mukB gene codes for a 177 kDa protein, which might be a candidate for a force-generating enzyme in chromosome positioning in Escherichia coli. The mukB106 mutant produces normal-sized, anucleate cells and shows a temperature-sensitive colony formation. To identify proteins interacting with the MukB protein, we isolated three multicopy suppressors (msmA, msmB, and msmC) to the temperature-sensitive colony formation of the mukB106 mutation. The msmA gene, which could not suppress the production of anucleate cells, was found to be identical to the dksA gene. The msmB and msmC genes suppressed the production of anucleate cells as well as the temperature-sensitive colony formation. However, none of them could suppress both phenotypes in a mukB null mutation. DNA sequencing revealed that the msmB gene was identical to the cspC gene and that the msmC gene had not been described before. A homology search revealed that the amino acid sequences of both MsmB and MsmC possessed high similarity to proteins containing the cold-shock domain, such as CspA of E. coli and the Y-box binding proteins of eukaryotes; this suggests that MsmB and MsmC might be DNA-binding proteins that recognize the CCAAT sequence. Hence, the msmB and msmC genes were renamed cspC and cspE, respectively. Possible mechanisms for suppression of the mukB106 mutation are discussed.