Three-dimensional computed tomography in orbital osteoma.
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Biomedical subjects
Publications and source records attributed to M Takeda.
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We studied accommodation and vergence eye movements in a patient with a left middle cerebral artery embolism. Accommodation was monitored by an infrared optometer with the accommodative target being controlled by a microcomputer. Computed tomography showed low-density areas in the left cortex, with intact brainstem. The patient had convergence palsy and accommodation abnormalities. The amplitude of the accommodative responses was reduced and the accommodation velocity was markedly lowered. Our results further substantiate the neurologic relationship between the cerebral cortex and accommodation and convergence.
Rabbits were injected intracerebrally with aluminum salt leading to experimental neurofibrillary change formation as a model of Alzheimer neurofibrillary change. Eleven days after the injection, the brain tissues were excised from the cortex, hippocampus, and cervical region of spinal cord. Five lysosomal enzymes (cathepsin D, beta-glucuronidase, acid phosphatase, acid DNase, alkaline DNase) were assayed and compared with the control. Cathepsin D, acid DNase and beta-glucuronidase activities increased significantly in all 3 areas of aluminum-injected brain. On the other hand, acid phosphatase and alkaline DNase activities remained at the same level. The results showed the lysosomal enzymes did not change in parallel after aluminum administration, suggesting a role of the increased enzymes in the brain with neurofibrillary changes.
The effect of cathepsin D on bovine neurofilament protein was studied biochemically, immunologically, and morphologically. Degradation products of each neurofilament triplet by bovine brain cathepsin D at neutral pH were identified by electrophoresis and immunoblotting with anti-neurofilament antibodies. The 68-kDa subunit was the most susceptive to cathepsin D proteolysis among the triplet proteins. All of the triplet gave rise to partial degradates of the 50-kDa size. The reconstituted fiber from neurofilament triplet proteins and the 68-kDa subunit protein were attacked by cathepsin D and the mode of disruption of the fiber structure was studied by electronmicroscopy.
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Nickel (II)-substituted myoglobin (Mb), hemoglobin (Hb) and horseradish peroxidase (HRP) were oxidized with iridate to examine whether porphyrin pi-cation radical is formed or not in these hemoproteins. It was found that Ni (II)-porphyrin pi-cation radical is formed in all of these hemoproteins as confirmed by UV-visible and ESR spectra, although the porphyrin pi-cation radical in Mb and Hb was less stable than in HRP. These results are discussed in relation to the different features of higher oxidation states of native Mb and HRP.
Two type 2A protein phosphatases, phosphatases I (Mr = 180,000) and III (Mr = 177,000), were purified to near homogeneity from human erythrocyte cytosol. Phosphatase I was composed of alpha (34 kDa), beta (63 kDa), and delta (74 kDa) subunits in a ratio of 1:1:1. Phosphatase III comprised alpha, beta, and gamma (53 kDa) subunits in the same ratio. Heparin-Sepharose column chromatography converted most of phosphatase I and 20% of phosphatase III into alpha 1 beta 1 which were indistinguishable from phosphatase IV (Usui, H., Kinohara, N., Yoshikawa, K., Imazu, M., Imaoka, T., and Takeda, M. (1983) J. Biol. Chem. 258, 10455-10463). The catalytic subunit alpha and the beta subunit of phosphatases I, III, and IV displayed identical V8 and papain peptide maps, respectively, while the peptide maps of the alpha, beta, gamma, and delta subunits were clearly distinct. The molar ratio of phosphatases I, III, and IV in erythrocyte cytosol was estimated to be 6:1:14. Comparison of molecular activities of alpha, alpha 1 beta 1, alpha 1 beta 1 delta 1, and alpha 1 beta 1 gamma 1 revealed that beta suppressed phosphorylase and P-H2B histone phosphatase activities of alpha but stimulated the P-H1 histone phosphatase activity, and delta suppressed all the phosphatase activities of alpha 1 beta 1. The gamma subunit stimulated the P-histone phosphatase activity of alpha 1 beta 1 but inhibited the phosphorylase and P-spectrin phosphatase activities. The beta subunit increased the Mg2+ or Mn2+ requirement for P-H2B histone phosphatase activity of alpha, an effect which was counteracted by delta. The effects of heparin, H1 histone, protamine, and polylysine on the phosphorylase phosphatase activity of phosphatases I, III, IV, and alpha were described and discussed in connection with the functions of the subunits.
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Nine heterozygous patients with familial hypercholesterolemia (FH) were treated by low density lipoprotein (LDL)-apheresis using dextran sulfate cellulose columns. After more than 3 procedures of LDL-apheresis without drug therapy, combination therapy with LDL-apheresis and CS-514 (eptastatin), an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme (HMG-CoA) reductase, at a dose of 10 mg twice daily was started. Pre- and post-apheresis serum cholesterol levels were decreased significantly by CS-514, from 289 +/- 24 mg/dl (mean +/- SEM) to 247 +/- 25 mg/dl and from 118 +/- 7 mg/dl to 106 +/- 9 mg/dl, respectively. Pre- and post-apheresis apolipoprotein B levels decreased significantly on CS-514 from 160 +/- 9 mg/dl to 138 +/- 8 mg/dl and from 58 +/- 6 mg/dl to 45 +/- 6 mg/dl, respectively. No adverse effects were observed during the combination therapy. Thus, the addition of an inhibitor of HMG-CoA reductase to LDL-apheresis is a useful method for further reducing serum cholesterol and apolipoprotein B levels in FH heterozygotes.
The presence of apo E-containing HDL in familial hypercholesterolaemia was investigated and its removal by LDL-apheresis using a dextran sulphate cellulose column was demonstrated by measurement of the apo E/apo A-I molar ratio of serum and by nondenaturing polyacrylamide gel electrophoresis followed by immunoblotting. The molar ratios of apo E/apo A-I in the density greater than 1.063 kg/l fraction of serum obtained from two homozygous patients with familial hypercholesterolaemia were higher (0.021 and 0.030) than that from normal subjects (mean +/- SE 0.011 +/- 0.002) (P less than 0.05). Polyacrylamide gel electrophoresis and immunoblotting showed an increase in apo E-containing HDL similar to HDL2, in the plasma obtained from the homozygous patient with familial hypercholesterolaemia. The increased amounts of apo E-enriched HDL were removed from plasma by adsorption with a dextran-sulphate cellulose column. These results suggested that LDL-apheresis using the dextran-sulphate cellulose column, may cause an increase in the turnover rate of the apo E-containing HDL and thus facilitate cholesterol removal from the peripheral tissues.
Specific activities of tyrosine tubulin kinase in the particulate fractions from rat cerebellum, medulla oblongata, hypothalamus, striatum, midbrain, and cerebral cortex ranged within 30% of each other and more than 3 times higher than those in the soluble fractions. In the cerebral cortex, tyrosine protein kinase activity toward tubulin and tyrosine-glutamate (1:4) copolymers was mainly distributed in the plasma membrane and the microsome fractions. The kinase activity in cerebral cortex particulate fractions was quantitatively solubilized and separated into two peaks, kinase I and kinase II, by Sephacryl S-300 gel filtration in the presence of 0.2% Nonidet P-40 and 0.2 M NaCl. Kinases I and II were each resolved into 5 active peaks (I-1----5 and II-1----5) by casein-Sepharose column chromatography. The molecular weights of these kinases were estimated from the s20,w values to be 59,000-65,000. The Km values of II-1----5 for tubulin were nearly 10 times higher than those of I-1----5. However, the Km values of the two groups of kinases for tyrosine-glutamate copolymers were not so significantly different. About 60% of the copolymers kinase activity in I-3, I-4, II-3, and II-4 was immunoprecipitable with a saturating amount of monoclonal antibody against pp60c-src. Incubation of the immunoprecipitates with ATP resulted in the autophosphorylation of a 60 kDa protein in I-3 and I-4, and a 52 kDa protein in II-3 and II-4. Immunoblotting also indicated I-3 and I-4 as 60 kDa bands and II-3 and II-4 as 52 kDa bands on SDS-polyacrylamide gels.(ABSTRACT TRUNCATED AT 250 WORDS)
For elucidating the nonvisual eye position control system, we studied the accuracy of saccades toward the remembered position (memory-guided saccades) in a patient with ocular lateropulsion having tonic bias of the eye position. Although the saccadic dysmetria caused by ocular lateropulsion was recorded during memory-guided saccades in the same manner as visually guided saccades, the eyes reached precisely the intended position by corrective saccades. The mean latency of corrective saccades was significantly longer than that of corrective saccades observed for visually guided saccades. This long latency of corrective saccades supports the assumption that feedback information of the eye position is a signal generated by orbital afferents rather than a copy of the motor command.
The reactivity and specificity of commonly used non-steroidal anti-inflammatory drugs (NSAID) towards two major intracellular aspartic proteinases, cathepsins D and E, were investigated. Of the different drugs tested, indomethacin and flufenamic acid were shown to be potent inhibitors of cathepsin D. Sodium salicylate (SA) and aspirin also inhibited cathepsin D, although the apparent inhibition was observed at the concentrations of 5 mM or above. The inhibitions by these drugs were pH-dependent. The maximal inhibitory potencies of indomethacin and aspirin against cathepsin D activity were observed at pH values below 4.0, whereas that of flufenamic acid was at pH values above 7.0. The Lineweaver-Burk plots showed that the inhibition of cathepsin D by these drugs was of a non-competitive type. On the other hand, all NSAID tested, except for SA, had no inhibitory effect on cathepsin E. SA alone inhibited cathepsin E at concentrations above 50 mM. The inhibition of cathepsin E by SA was of the non-competitive type. Of the three monohydroxy benzoates, the inhibitory potency of the ortho isomer (SA) against cathepsin E was greater than those of the meta and para isomers.
This study used an isolated right atrial preparation, cross-perfused with arterial blood from a support dog. We investigated the effects of dibutyryl cyclic AMP (DBcAMP) on heart rate and arterial blood pressure of the support dog and on the sinus rate and atrial contractile force of the isolated perfused atrium. DBcAMP was injected into the external jugular vein of the support dog or into the sinus node artery of the isolated atrium. DBcAMP to the support dog induced a small increase and/or decrease in arterial blood pressure at a dose of 3 or 10 mg/Kg i.v. It produced a decrease, with or without an increase in blood pressure, at a dose of 30 mg/Kg i.v., and a dose-dependent increase in heart rate in the support dog. In the isolated atrium, positive chronotropic and inotropic effects were observed. Direct injection of DBcAMP (3-30 mg) into the sinus node artery of the isolated atrium induced positive chronotropic and inotropic effects, after initial brief negative effects, in a dose-dependent manner. DBcAMP did not change norepinephrine-induced positive chronotropic and inotropic effects in the isolated atrium. These results demonstrate that DBcAMP induces a decrease in systemic arterial blood pressure with increases in sinus rate and atrial contractile force, and acts additively with the norepinephrine-induced positive cardiac effects in the dog heart.
The intermediate filaments in mouse taste bud cells were studied by immunocytochemistry using antikeratin antibodies, and by conventional electron microscopy. Taste bud cells (types I, II, and III) possessed less densely aggregated bundles of intermediate filaments than the surrounding epithelial cells. Type III cells, however, contained more densely aggregated bundles than type I or II cells. Basal cells in the taste buds showed aggregations of filaments as dense as those seen in the epithelial cells, although their bundles were more slender than those of the epithelial cells. The antibodies to keratins from the bovine muzzle and human stratum corneum stained all types of the taste bud cells as well as the surrounding epithelial cells. PKK2 antibody reacted with the surrounding epithelial cells, but did not react with the taste bud cells. These results show that keratins are present in both taste bud and surrounding epithelial cells, although the keratin subtype differs between those cells. This finding has led us to the supposition that all cell types comprising the taste buds--including type III (receptor) cells--originate from the epithelial cells surrounding the taste buds. It is also suggested that both keratin subtypes and aggregation patterns of intermediate filament bundles change during differentiation from surrounding epithelial cells to taste bud cells, and from basal cells in the taste buds to types I, II, or III cells.
Short-latency somatosensory evoked potentials (SSEPs) and brainstem auditory evoked potentials (BAEPs) were recorded in 30 patients with Parkinson's disease (mean age 66.3 years), 17 patients with vascular parkinsonism (mean age 70.5 years) and 22 normal subjects (mean age 66.7 years). In patients with vascular parkinsonism, the interpeak latencies between N13 and N20(CCTs) were significantly longer than those of patients with Parkinson's disease and normal subjects (p less than 0.005 and p less than 0.001, respectively). Patients with Parkinson's disease and normal subjects did not show any significant differences with regard to CCT. The significant differences between left and right CCT were revealed between patients with vascular parkinsonism and patients with Parkinson's disease or normal subjects (p less than 0.001 and p less than 0.001, respectively). Patients with vascular parkinsonism disclosed significant prolongation of interpeak latencies between waves I and V (I-V IPLs) compared to patients with Parkinson's disease and normal subjects (p less than 0.005 and p less than 0.001, respectively). Furthermore, the I-V IPLs in patients with Parkinson's disease were significantly longer than those of the normal subjects (p less than 0.01). The mean left-right differences of I-V IPLs in patients with vascular parkinsonism were longer than those of the other two groups. Present results indicate that there were some differences between Parkinson's disease and vascular parkinsonism from the electrophysiological aspects and suggest that assessments of SSEPs and BAEPs may be helpful in differentiating Parkinson's disease from vascular parkinsonism.
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