[Study on the nicotinic acid loading test in patients with various liver diseases].
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Biomedical subjects
Publications and source records attributed to T Okuno.
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In 1963, Klein et al. first described two girls with normokalemic periodic paralysis and cardiac arrhythmia. We have observed a 15-year-old girl with cardiac arrhythmia and normokalemia but with some features of hyperkalemic, periodic paralysis. The patient showed a waddling gait and Gower's sign. She had atrophy of the proximal muscles and deep tendon reflexes were reduced. Her ECG showed bigeminy with multifocal premature ventricular contractions. At the start of an episode of muscle weakness, the serum potassium concentration rose from 3.1 to 4.4 mEq/l. Muscle weakness was not provoked by intravenous administration of 45 g glucose or of 72 g glucose followed by 10 units of regular insulin. Muscle weakness was evoked by the ingestion of 4 g potassium chloride. During the provoked muscle weakness, the ECG showed normal sinus rhythm temporarily.
A retrospective study of 307 patients with chronic active hepatitis (CAH) was conducted to assess the prognostic significance of bridging necrosis (BN). BN was encountered in 70 (22.8%) of 307 patients with CAH. Twenty six cases of CAH with BN and 40 of CAH without BN were followed up with repeated liver biopsies for periods of from 6 months to 12 years. Twelve (46.1%) of the 26 CAH cases with BN developed cirrhosis including 4 cases of early cirrhosis. Seven cases had no sequential histologic changes. Histologic improvement to CAH or to chronic inactive hepatitis (CIH) was seen in 3. On the other hand, one (2.5%) of 40 CAH cases developed cirrhosis and 3 early cirrhosis. Another 3 cases histologically showed aggravation to CAH with BN, two of which developed in a short period after the initial biopsy and the possibility of sampling error in the initial biopsy cannot be ruled out. There were no sequential histologic changes in 26 of the 40 cases. Histologic improvement to nonspecific reactive hepatitis or to CIH was seen in 7. From these findings, it may be concluded that the presence of BN in CAH holds prognostic implications.
Varicella-Zoster virus (VZV) contains four major glycoproteins designated as gp 1(115K), gp 2(100-80K), gp 3(64K), and gp 5(55K) (K. Shiraki, T. Okuno, K. Yamanishi, and M. Takahashi, J. Gen. Virol. 61, 255-269, 1982). The present studies focused on the synthesis and processing of these glycoproteins using monoclonal antibodies. Twenty-seven hybridomas secreting monoclonal antibodies against VZV proteins have been established. The antibodies were characterized further by radioimmunoprecipitation with [35S]-methionine, [3H]glucosamine, [125I]labeled viral antigens followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Twelve clones of these hybridomas produced antibodies to glycosylated polypeptides of VZV, which could be classified into three groups on the basis of the electrophoretic patterns. The first group reacted specifically with polypeptides with apparent molecular weights of 94K and 83K (both presumed to correspond to gp 2) in infected cells, on the surface membrane of infected cells, and on the virions. The second group precipiated polypeptides with molecular weights of 94K, 83K, 55K (corresponding to gp 5) in infected cells, and 94K, 83K, 55K, 45K on the surface membrane of infected cells, and 94K, 83K, and 55K on the virions. Finally, the third group reacted with polypeptides with molecular weights of 116K, 106K, and 64K corresponding to gp 3) in infected cells, 64K on the surface membrane of infected cells, and on the virions. By pulse-chase experiments, antibodies from the former two groups precipitated new polypeptides with molecular weights of 75K and 49K, respectively, which were presumed to be precursor proteins. These data suggest that the precursor proteins of gp 2, gp 3, and gp 5 are synthesized in infected cells, glycosylated, and the product proteins are expressed on the surface membrane of infected cells as well as on the virions. It was also found that a glycoprotein of 45K detected in culture fluid of infected cells (K. Shiraki and M. Takahashi, J. Gen. Virol. 61, 271-275, 1982) was derived from the polypeptide with molecular weight of 55K (gp 5).
A 2-year-old girl developed encephalitis following influenza A virus infection. Brain computed tomography (CT) showed symmetrical hypodense areas in the putamina. Contrast enhancement was noted surrounding the hypodense areas 2 days after the onset of encephalitis. These localized lesions demonstrated on CT have not been reported in the literature of postinfluenzal encephalitis.
L(O)cl 3 and L(K)cl 1 cells, biochemically transformed by varicella-zoster virus (VZV), were labelled with L-[35S]methionine and [32P]orthophosphate. Cell extracts were immunoprecipitated with anti-VZV monkey serum and analysed by SDS-polyacrylamide gel electrophoresis. Four polypeptides of apparent mol. wt. 135000 (135K), 48K, 44K and 35K were detected in the L-[35S]methionine-labelled extracts, and, of these, the 35K band showed marked intensity. However, this band was not detected in extracts from cells infected with a VZV tk- strain (Kanno strain). Also, the 35K polypeptide showed very low intensity when immunoprecipitated from extracts of transformed cells grown in non-selective (NS) medium, i.e. cells that had a very low thymidine kinase (tk) activity. In the case of [32P]orthophosphate-labelled cells, polypeptides of apparent mol. wt. 180K, 81K, 48K, 44K and 37K were obtained. In both instances, the 44K polypeptide was not immunoprecipitated from L(K)cl 1 cell extracts. From our data it is postulated that the expression of the 35K polypeptide is correlated with the VZV-specific tk activity of the cells.
Sequential CT studies were performed in 24 patients with infantile spasms, before, during and after ACTH therapy, in order to analyze the relationship between the dose of ACTH and changes in CT scan findings. In six cases CT scans did not return to their original state after ACTH therapy. Two illustrative cases are reported. There was a good correlation between the total dose of ACTH and the percentage decrease of brain parenchyma. It is concluded that 'cerebral atrophy' on CT scans may represent an accumulative effect of ACTH and that ACTH should be given with the utmost discretion, and in as low a dose as possible.
To determine whether impaired arginine vasopressin (AVP) release occurs when DOCA-NaCl hypertension is prevented following chemical sympathectomy with 6-hydroxydopamine (6-OHDA), male Sprague-Dawley rats treated with intraventricular injections of 6-OHDA (250 micrograms X 2) or Merlis solution received deoxycorticosterone acetate (DOCA) implants (100 mg/kg) and drank 0.5% saline. Systolic blood pressure in the 6-OHDA-treated DOCA/NaCl group (139 +/- 4 mmHg) was lower (P less than 0.001) than in the Merlis-DOCA/NaCl group (183 +/- 7 mmHg). 6-OHDA treatment produced widespread catecholamine depletion throughout the central nervous system, including the supraoptic and paraventricular nuclei, the cells of which are known to produce AVP, but hypothalamic, pituitary, and plasma AVP levels were similar in both experimental groups, the latter values averaging 1.5-2 times those of controls. Both groups of rats suppressed AVP secretion appropriately when water loaded. Such suppression, however, had no effect on blood pressure in the hypertensive animals and, furthermore, administration of the AVP antagonist d(CH2)5Tyr(Me)AVP produced small decrements in mean blood pressure of both groups that were not significantly different from responses seen in control normotensive rats. These data demonstrate that 6-OHDA does not prevent DOCA-NaCl hypertension by decreasing AVP levels and suggest that AVP is not necessary for the maintenance of hypertension in this model.
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A boy with a peculiar face and slight psychomotor retardation was found to have a tandem duplication of segment 14q13-22. The karyotype was described as 46,XY, dir dup (14)(pter-q22::q13-q22::q22-qter), being trisomic for the segment. His parents were normal both phenotypically and cytogenetically. The clinical features of the propositus were compared with those of previously reported cases of trisomy 14q involving segment 14q13-22.
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