[A case of fusiform aneurysm of the intrahepatic portal vein with tumor thrombus].
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Biomedical subjects
Publications and source records attributed to Y Imamura.
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This paper reports two cases of crossed dextral aphasia. The first patient was a 60-year-old right-handed male with no family history of sinistrality. He experienced sudden onset of left hemiplegia and loss of consciousness. A CT scan showed high-density area in the right fronto-parietal region. An angiography revealed an arteriovenous malformation (AVM) in the right parietal lobe. It was fed by a branch of the middle cerebral artery and drained through a cortical vein. Neuropsychological examination one week after the surgery showed severe defects of all language moderalities. He was alert and cooperative, but completely mute. He recognized common words by auditory and visual stimuli, but could not perform simple command. He wrote some meaningless letters when asked to write his own name. Auditory and reading comprehension gradually improved thereafter, but Broca's type of aphasia with non-fluent hesitant and effortful output was still present four months after the surgery. The second patient was a 38-year-old right-handed male. All members of this family are right-handed except for one sister who is left-handed. He suddenly suffered left hemiparesis and loss of consciousness. A CT scan disclosed a right parietal intracerebral hematoma. And an AVM which was fed by the angular artery and drained through a cortical vein was angiographically demonstrated in the same area. Postoperatively the left hemiparesis rapidly disappeared, but left homonymous hemianopsia and anomic type of aphasia still persisted. His speech was fluent and daily communication was possible in spite of circumlocutory paraphasic output.(ABSTRACT TRUNCATED AT 250 WORDS)
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We have developed a sensitive enzyme immunoassay (EIA) for the quantification of argininosuccinate synthetase (ASS) in the range of 0.05-1 ng/tube using a Fab'-peroxidase conjugate prepared with maleimide compound devised by Ishikawa et al. Amounts of hepatic ASS in control subjects were determined by this method with the purified enzyme as a standard and their specific activities were calculated to be 1.3-1.4 mumol product/min (U)/mg of ASS, which was quite similar to that of the purified enzyme. Amounts of ASS in the liver of patients with three types of citrullinemia, type I, II and III according to our arbitrary classification, were determined by the EIA method. The following results were obtained: hepatic ASS from a patient diagnosed as type I citrullinemia because of its abnormally large Km values for citrulline and aspartate was calculated to have a specific activity of 0.18 U/mg of ASS, indicating that the enzyme is a variant; specific activities of ASS in the hepatic extract of type II citrullinemic patients were 1.2-1.3 U/mg of ASS, confirming the finding obtained by single radial immunodiffusion method that the decrease of the activity in type II is caused by a decrease in the total amount of ASS protein; a very small amount of immune cross-reactive material was detected in the liver of a patient diagnosed as type III citrullinemia based on findings of undetectable ASS activity in the liver and cultured skin fibroblast.
Dosulepin, 11-(3-dimethylaminopropylidene)-6,11-dihydrodibenzo [b,e]thiepin hydrochloride, is a thio analogue of amitriptyline and is used for the treatment of anxiety and affective disorders. The present study developed a simple and sensitive procedure for the determination of this compound and its metabolite, northiaden, by a combination of high-performance liquid chromatography with electrochemical detection. Hydrodynamic voltammograms demonstrated an optimal applied potential at 1300 mV for both dosulepin and northiaden. A mobile phase consisting of 0.1 M acetate buffer-acetonitrile-perchloric acid-trichloroacetic acid (50:50:2:1.5) provided the best separation of the drugs. The extraction procedure, which used a heptane-isoamyl alcohol (99:1) mixture, was successfully applied with a recovery of over 90%. A preliminary pharmacokinetic study was performed by the proposed method.
The fluorescence of phenprocoumon is greatly enhanced on binding to a single site on alpha 1-acid glycoprotein (alpha 1-AGP). Advantage is taken of this phenomenon to estimate a binding constant for the binding of phenprocoumon to alpha 1-AGP. The fluorescence intensity and binding constant of the phenprocoumon: alpha 1-AGP complex decreased with pH from 6.5 to 8.5, suggesting that phenprocoumon binding to alpha 1-AGP is significantly affected by microenvironmental change in alpha 1-AGP. A variety of drugs, including chlorpromazine and dicumarol, significantly inhibited phenprocoumon binding to alpha 1-AGP. Fatty acids seem to displace phenprocoumon from its binding site on alpha 1-AGP, whereas the addition of neutral salts and sialic acid did not cause the displacement of phenprocoumon. It is concluded that the phenprocoumon binding site is located in the hydrophobic protein structure of alpha 1-AGP.
Wave forms of ML-AEP were studied in 21 healthy subjects and in 4 cases with well localized lesions in the brain. In order to obtain and define the constant wave form we used 5 mg of diazepam in these subjects. In awake state (before administration of diazepam) two types of muscle activity were observed. Postauricular muscle reflex (PMR), which follows high amplitude Na, Pa and Nb potentials, decreases its amplitude and seems to disappear when No and Po come out in light sleep (after administration of diazepam). The other type of muscle activity is derived from facial and other extracranial muscles associated with face or neck movements and deforms wave form in which we are unable to identify each component. These muscle activities cause the variability of wave form in awake state. In light sleep, wave forms were classified as follows: A, includes all components of ML-AEP; B, no Nb component; C, no No and Po components. The most constant waves are Na and Pa potentials and No, Po are variable in appearance. Sequential recordings from awake to light sleep suggested that No, Po are the remnants of PMR in light sleep. Studies of ML-AEP in 4 cases revealed attenuated or absent Na, Pa and Nb potentials. No and Po are variable in appearance in these cases in spite of different locations of lesions in the brain. These studies seemed to support the idea that No and Po are remnants of PMR in light sleep and the constant wave form of ML-AEP consists of Na, Pa and Nb potentials.
The nucleotide sequence of DNA clones complementary to the genomic RNA of an extremely avirulent strain D26 of Newcastle disease virus was analyzed, and the sequence of 2102 nucleotides directly following F gene reported previously (Sato et al., 1987, Virus Res. 7, 241-255), and corresponding to HN0 gene was determined. A long open reading frame coding for the HN0 peptide of 616 amino acid residues was found in this sequence. It was flanked by the consensus sequences N1 and N2 (Ishida et al., 1986, Nucleic Acids Res. 14, 6551-6564), and the former was shown by the primer extension method to serve as the transcriptional initiation site. The deduced amino acid sequence of the HN0 peptide was highly homologous to that of the HN peptides of strains Beaudette C and B1, but had a carboxyl terminal extension of 39 amino acid residues with a potential glycosylation site in it. The terminal extension is likely to be excised during the processing, and this is consistent with the observation that unglycosylated HN0 is larger in size than unglycosylated HN. A microheterogeneity among the cDNA clones in the nucleotide sequence was also noted which may be relevant to the synthesis of a small amount of an HN-sized peptide in strain D26-infected cells.
Molecular cloning of most if not all of the genome of an avirulent strain D26 of Newcastle disease virus (NDV) was carried out. cDNA clones were aligned by mutual hybridization and restriction map analysis. The nucleotide sequence of 3672 bases which completed the partial sequence of P gene reported in our previous paper (Ishida, N. et al., 1986, Nucleic Acids Res. 14, 6551-6564), and also covered M and F genes, was determined. Each gene contained one long open reading frame which could code for polypeptides of 395, 364, and 553 amino acid residues, respectively. The deduced amino acid sequences of P and M gene products showed little homology to those of other paramyxoviruses. In contrast, comparison of the amino acid sequence of the F gene product revealed highly conserved regions including the amino terminal sequence of the F1 portion following the putative processing site. There was only one basic amino acid residue at the putative processing site, which would explain the low virulence of this strain.
Glucocorticoid receptor levels of myeloma cells were quantitated in 7 patients with multiple myeloma. In 4 patients, glucocorticoid receptor levels were less than 10 fmol/10(6) cells. In 3 patients, receptor levels were from 17.6 to 21.4 fmol/10(6) cells. We further examined the correlation between glucocorticoid receptor levels and effect of dexamethasone on 14C-thymidine incorporation and cell viability using 2 myeloma cell lines, OPM-1 and OPM-2, established from a patient with multiple myeloma. Glucocorticoid receptor levels of OPM-1 and OPM-2 were 8.5 fmol/10(6) cells and 63.2 fmol/10(6) cells, respectively. The sensitivity of OPM-1 to dexamethasone in these studies was lower than that of OPM-2. These results suggest the possibility that the low level of glucocorticoid receptor in myeloma cells may be important for predicting a poor response to glucocorticoid therapy.