[Real-time ultrasonically guided percutaneous transhepatic cholangiography(UGPTC) and percutaneous transhepatic bile drainage(UGPTBD): indication for the first-puncture UGPTBD].
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Biomedical subjects
Publications and source records attributed to T Okuno.
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The effects of three types of angiotensin-converting enzyme inhibitor, SQ 14225 (captopril), SQ 20881 (teprotide) and SA 446 (Santen, Osaka, Japan), on the vascular contraction induced by norepinephrine were studied in the perfused rat mesenteric vascular bed. (1) SQ 14225 attenuated in the vascular contraction induced by norepinephrine, but SQ 20881 and SA 446 revealed no effect on vascular reactivity. (2) The effect of SQ 14225 was not altered in the presence of bradykinin or angiotensin II in the perfusate. On the basis of these results it is suggested that the attenuating effect on the vascular response to norepinephrine may be limited to SQ 14225 and that its effect is not mediated through the renin-angiotensin or kallikrein-kinin system.
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Ultrastructure of alcoholic hyaline (AH) in alcoholic hepatitis was observed to demonstrate the relationship between AH filaments and intermediate filaments (IFs). Type 1, Type 2 and Type 3 AH were noted in hepatocytes, and the filaments in these types of AH showed similar ultrastructural findings as already reported. Two different kinds of filaments were noted in the Type 2 AH. The large on showed 160 to 200 A in a diameter and the small one showed around 100 A in diameter. Of the 29 cases with alcoholic hepatitis, a new type of AH was noted in the rosette forming hepatocytes in 2 cases of alcoholic hepatitis. The filaments of this AH in rosette forming hepatocytes showed 40 to 60 A in diameter and shorter length compared with Type 2 AH. These filaments with 40 to 60 A diameter were quite different from IFs. Our results indicate that AH in alcoholic hepatitis is not induced by the simple accumulation of the IFs.
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Varicella-zoster virus (VZV), labelled with [35S]methionine or [14C]glucosamine, was purified by centrifugation through sucrose gradients followed by equilibrium centrifugation in CsCl, and analysed by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). At least 32 polypeptides ranging in mol. wt. from approx. 280 X 10(3) to 21.5 X 10(3) (280K to 21.5K) and six glycopeptides ranging in mol. wt. from approx. 115K to 45K (gp1 to gp6) were found in the virion. The immunological relationship of VZV and herpes simplex virus (HSV) was investigated. In neutralization (NT) tests, no cross-neutralization was observed between VZV and HSV-1 or -2. In fluorescent antibody staining, however, a cross-reaction was observed between VZV- and HSV-1-infected human embryonic lung (HEL) cells and heterologous antiserum. When cross-reactions were investigated by immunoprecipitation followed by SDS-PAGE, several cross-reacting polypeptides were discovered. Cross-reacting glycopeptides of 64K (gp3) and 55K (gp5) were isolated from VZV-infected cell lysates by affinity column chromatography to immobilized HSV-1 antibodies.
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A case of multiple, computed tomographic areas of hypodensity in the cerebral white matter was diagnosed as acute disseminated encephalomyelitis. The low density area regressed, and the 5-year-old patient improved after steroid treatment.
The electroencephalographic (EEG) and cranial computed tomographic (CCT) findings of 41 children with hemiplegic cerebral palsy were analyzed. There was a positive correlation between EEG abnormalities and the affected side of the body in 25 (61%), while there was a positive correlation between CCT abnormalities and the affected side of the body in 37 (90%). In 24 cases (59%), there was a positive correlation between EEG and CCT laterality. However, in 13 of the patients with dominant abnormalities in the cerebral hemisphere contralateral to the palsy, EEgs did not show the same laterality as the CCT. In two of these cases, dominant seizure discharges were present on the side opposite to the CCT abnormalities. CCT was more useful than EEG in determining the side of maximal brain damage in hemiplegic cerebral palsy (p less than 0.01).
Meningeal involvement in multiple myeloma is a rare occurrence. We report a case of IgG myeloma with neoplastic cell infiltration into the cerebrospinal fluid as determined by a protein A plaque-forming cell assay. Electrophoresis of the cerebrospinal fluid revealed a monoclonal band in the same position as the monoclonal band in the serum. Meningeal involvement may probably be more common at the terminal stage in multiple myeloma than has been previously considered.
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Effect of disodium cromoglycate (DSCG) on hemolysis of rat erythrocytes was studied. The heat-induced hemolysis was remarkably inhibited by DSCG. This effect was not affected by normal rat serum and was maintained for longer than 60 min similar to the activity in clinical use, although the inhibitory effect of DSCG on reagin-induced histamine release from mast cell disappeared rapidly in 5 min after administration. Non-steroidal anti-inflammatory drugs such as flufenamic acid or phenylbutazone which are known to inhibit the hemolysis depending on their protein stabilizing activities inhibited both of the heat-induced hemolysis and albumin denaturation, but DSCG did not inhibit the albumin denaturation. Furthermore, it was also observed that DSCG inhibited the hemolysis induced by lipophilic agents such as saponin, linoleic acid or phospholipase C. These findings suggest that DSCG has a certain membrane stabilizing activity, in addition to the inhibitory effect on reagin-induced histamine release, and that the activity may be probably related to membrane lipids rather than membrane-proteins.
In the perfused rat mesenteric vascular bed, the effects of captopril and prostaglandin I2 (PGI2) on the vasoconstrictor responses to norepinephrine or potassium chloride were studied. Captopril or PGI2 in the perfusate attenuated the vascular responses to norepinephrine in a dose-related manner, while these substances had no effect on the vascular contractions induced by potassium chloride. In preparations treated with indomethacin, the inhibitory effect of captopril on the vascular response to norepinephrine was similar to that found in the untreated preparations. These results suggest that, although the effects of captopril on the vascular reactivity is similar to that of PGI2, the direct vascular action of captopril is not mediated by the synthesis of prostaglandins in the vascular bed.