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Biomedical subjects

Y Yoshida

Publications and source records attributed to Y Yoshida.

At least 1,189 records · Page 66Linked to original sources
PubMed1990

[Polycythemia vera terminating in myelodysplastic syndrome].

A 77-year-old male, who had been treated with carboquone and busulfan for polycythemia vera (PV), developed myelodysplastic syndrome (MDS) 8 years later. On admission the peripheral blood revealed pancytopenia, but blastoid cells were not noted. The bone marrow showed hypercellularity, and functional and morphological abnormalities in trilineages of hemocytes. Cytogenetic study showed complex abnormalities involving chromosomes 5 and 7. We diagnosed this case as secondary MDS to alkylating agents. He was treated with 1, 25 (OH)2 vitamin D3. However, it was not effective and the percentage of myeloblasts increased to 14.4%. In spite of supportive therapy, he died of sepsis due to urinary tract infection.

Aged↗
PubMed1990

[Bleeding time and volume in vitro by THROMBOSTAT].

We tested an in vitro system simulating bleeding time reported by Kratzer et al. Primary hemostasis was studied perfusing an artificial vessel with citrated blood under a constant pressure of 40 mmHg, measuring the blood volume perfused (bleeding volume) and the time until blood flow stopped (bleeding time). The artificial vessel consists of a glass capillary simulating arteriole and a filter covered with collagen type I to provide a surface for the adhesion of platelets. The bleeding volume (mean +/- SD microliters) was 317.7 +/- 93.8 in controls (n = 19), 487.3 +/- 242.1 in idiopathic thrombocytopenic purpura (n = 9), 666.8 +/- 224.1 in aplastic anemia and paroxysmal nocturnal hemoglobinuria (n = 4), greater than 820 in von Willebrand's disease (n = 3), 231.0 +/- 74.5 in hemophilia A (n = 3), 499.0 +/- 269.4 in liver cirrhosis (n = 6), and 457.7 +/- 229.0 in myeloproliferative disorders (n = 11). When citrated blood was applied to this system after incubation with monoclonal antibodies (MoAb) to von Willebrand factor or platelet membrane glycoprotein Ib (GPIb), bleeding volume was significantly increased while no effects were observed after incubation with MoAb to GPIIb/IIIa, factor VIII: CAg and factor XIIIa. These data suggest that in vitro model of primary hemostasis could be used for not only diagnosing bleeding disorders although 'time' is not reliable, but also investigating the mechanisms of hemostasis.

Antibodies, Monoclonal↗
PubMed1990

[Prognostic factors in aplastic anemia. A statistical analysis of 105 cases].

We analyzed 105 cases of aplastic anemia diagnosed between 1958 and 1985 to clarify the variables that are related to prognosis. The most significant variable at diagnosis was reticulocyte count, followed in order by percent bone marrow lymphocyte, red cell turnover rate, T-score severity grade, iron utilization and aplastic anemia study group (AASG) severity grade. Reticulocyte count was the single significant variable in multivariate analysis. Three months after diagnosis, the most significant variable was still the reticulocyte count, followed by AASG severity grade. Changes of variables during the 3 months were not correlated to prognosis. Our result reconfirmed that reticulocyte count was the most important variable related to prognosis.

Adolescent↗
PubMed1990

[A case of spinal dural arteriovenous malformation associated with the broad lesion within spinal cord--diagnostic value of MRI with Gd-DTPA enhancement].

A 70-year-old man, with slowly progressive gait disturbance, numbness in his lower limbs and dysuria, was admitted to our hospital in July, 1988. Neurological examination revealed flaccid paraparesis, hyperesthesia below the level of Th-10 combined with the disturbance of pain and temperature sensations below the level of Th-11, and neurogenic bladder. Midsagittal Tl-weighed image of MRI did not reveal any abnormal finding except for a mild enlargement of the conus medullaris. With Gadolinium (Gd)-DTPA injection, however, the spinal cord was diffusely enhanced below the level of the 9th thoracic spine. This enhancement effect was particularly remarkable at the periphery of the spinal image showing several high intensity spots in the posterior aspect of the spinal cord, which was thought to be incompatible with the spinal cord neoplasm. The angiographic examination of the selective Th-7 intercostal artery on the left showed vascular malformation lying adjacent to the 7th intervertebral foramen with markedly dilated tortuous spinal veins going upwards and downwards, which was compatible with spinal dural arteriovenous malformation (AVM). After the artificial embolization, draining veins as well the nidus of AVM had completely disappeared on angiogram. There was an improvement on his neurological findings and Gd-DTPA enhancement had been diminished on MRI. It was suggested that Gd-DTPA enhancement on MRI was due to the dilated and remarkably congestive spinal veins, and that both the elevated venous pressure and reduction of intramedullary arteriovenous pressure gradient were the cause of the development of clinical symptoms.

Aged↗
PubMed1989

Purification and characterization of a protease from Xenopus embryos.

A proteolytic enzyme was purified from Xenopus embryos. The purification procedure consisted of fractionation of an extract of embryos with acetone, gel filtration of Sephadex G-75 and chromatography on carboxymethyl-cellulose and hydroxylapatite. The preparation of enzyme appeared to be homogeneous as judged by electrophoresis in polyacrylamide gels. This protease had a molecular mass of 43-44 kDa and was composed of two subunits with molecular masses of 30 kDa and 13 kDa. The optimal pH of the reaction catalysed by the protease was approximately 4.0. This proteolytic activity was inhibited by antipain, leupeptin and iodoacetic acid; it was not affected by phenylmethylsulfonyl fluoride and pepstatin; and it was enhanced by dithiothreitol. In the presence of RNA, the optimal pH was shifted from pH 4.0 to pH 4.5. The protease was activated by addition of total RNA from Xenopus embryos, by poly(rU) or poly(rG). In contrast, after addition of tRNA or poly(rC), no activation of the protease was observed.

Animals↗
PubMed1989

The 3-hydroxy group of lanosterol is essential for orienting the substrate site of cytochrome P-450(14DM) (lanosterol 14 alpha- demethylase).

Interaction of lanosterol, 3-epilanosterol, 3-oxolanosta-8,24-diene, 3-methylenelanost-8-ene and lanosterol acetate with cytochrome P-450(14DM) were studied. The cytochrome mediated the 14alpha-demethylation of 3-epilanosterol with nearly the same activity as lanosterol but could not mediate the 14alpha-demethylation of the 3-methylene derivative and the 3-acetate. The cytochrome catalyzed the 14alpha-demethylation of the 3-oxo derivative with low rate. Based on these and some additional observations the hydrogen bond formation between the 3-hydroxy group of lanosterol and the specific amino acid residue in the substrate site is assumed to be essential for orienting the substrate in the substrate site of the cytochrome.

Chemical Phenomena↗
PubMed1989

Deformylation of 32-oxo-24,25-dihydrolanosterol by the purified cytochrome P-45014DM (lanosterol 14 alpha-demethylase) from yeast evidence confirming the intermediate step of lanosterol 14 alpha-demethylation.

32-Oxo-24,25-dihydrolanosterol (32-oxo-DHL) was deformylated to 4,4-dimethylcholesta-8,14-dien-3 beta-ol, the product of 14 alpha-demethylation of 24,25-dihydro-lanosterol (DHL), by the reconstituted lanosterol 14 alpha-demethylase system consisting of cytochrome P-45014DM and NADPH-cytochrome P-450 reductase of yeast. Affinity of 32-oxo-DHL to the cytochrome was considerably higher than those of lanosterol and DHL, and the rate of deformylation of 32-oxo-DHL was faster than the rate of demethylation of lanosterol and DHL. Spectral analysis of the 32-oxo-DHL complex of cytochrome P-45014DM suggested the interaction between the 32-aldehyde group and the heme iron. These observations, together with our preceding findings on the metabolism of 32-hydroxy-24,25-dihydrolanosterol (Aoyama, Y., Yoshida, Y., Sonoda, Y., and Sato, Y. (1987) J. Biol. Chem. 262, 1239-1243), indicate that the 14 alpha-demethylation of lanosterol catalyzed by cytochrome P-45014DM proceeds with three step monooxygenations via the 32-hydroxy and 32-oxo intermediates, and the cytochrome mediates this sequential reaction without releasing the intermediates.

Binding, Competitive↗
PubMed1989

Frontal decortication decreases the affinity of N-(1-[2-thienyl]cyclohexyl)[3H]piperidine binding to rat striatum.

Bilateral ablation or transection of the corticostriatal pathways of the rat caused a reduction in N-(1-[2-thienyl]cyclohexyl)[3H]piperidine ([3H]TCP) binding to the striatum at 5-7, but not 3 and 14-28, days postlesion with a persistent decrease in striatal glutamate content 3-28 days after the decortication. This reduction was found to be due to an increase in Kd without changes in Bmax of the [3H]TCP binding. The present findings suggest that interruption of striatal glutamatergic transmission following frontal decortication may produce a temporal reduction in the affinity of phencyclidine receptor in the striatum.

Animals↗
PubMed1989

Effect of combination of 5-fluorouracil, epirubicin and mitomycin C (FEM) on advanced gastric carcinoma.

Fifteen patients with advanced gastric carcinoma were treated with the combination of 5-Fluorouracil (5-FU), Epirubicin (EPI) and Mitomycin C (MMC). Twelve of 15 patients were evaluable. Three patients showed partial response (25%) and 4 showed no change (33%) according to the criteria of Japan Society for Cancer Therapy. Mean survival time for responders, nonresponders and all evaluable patients were 14. 3, 3.6 and 6.3 months, respectively. Two patients with partial response lived over 18 months. Major toxicities included myelosuppression, nausea and vomiting, and alopecia. These were mild in general and reversible by discontinuance. No cardiotoxicity developed. It was concluded that this combination therapy is beneficial in patients with advanced gastric carcinoma because it showed measurable clinical effectiveness with less toxicity than FAM therapy (a combination of 5-FU, Doxorubicin and MMC).

Adult↗
PubMed1989

Increases in vascular alpha 1-adrenoceptor affinity and PI turnover in DOCA-salt hypertensive rats.

The pD2 value for norepinephrine and the pA2 value for prazosin in mesenteric larger resistance vessels from deoxycorticosterone acetate (DOCA)-salt hypertensive rats were significantly higher than the values of normotensive rats, suggesting that alpha 1-adrenoceptors have a higher affinity in hypertensive rats. The accumulation of [3H]inositol monophosphate induced by norepinephrine was significantly greater in the mesenteric artery from hypertensive rats than in the mesenteric artery from normotensive rats. These results suggest that the enhanced phosphatidylinositol turnover seen in DOCA-salt hypertensive rats may contribute, at least partly, to the higher affinity of alpha 1-adrenoceptors.

Animals↗
PubMed1989

Differential down-regulation of protein kinase C isozymes.

Types I, II, and III protein kinase C have been shown to be products of, respectively, gamma, beta, and alpha genes of this enzyme family (Huang, F. L., Yoshida, Y., Nakabayashi, H., Knopf, J. L., Young, W. S., III, and Huang, K.-P. (1987) Biochem. Biophys. Res. Commun. 149, 946-952). Incubation of the highly purified rat brain protein kinase C isozymes with trypsin (kinase/trypsin (w/w) = 100) under identical conditions results in a preferential degradation of types I and II enzymes, whereas the type III enzyme was relatively resistant to tryptic proteolysis. Degradation of the type III enzyme by trypsin could be facilitated with the addition of Ca2+, phosphatidylserine, and dioleoylglycerol; none of these components alone was effective. Limited proteolysis of the three protein kinase C isozymes generated distinctive fragments for each isozyme, indicating that each isozyme has different trypsin-sensitive sites. Tryptic digestion of the type III protein kinase C was used as a model to determine the effects of various modulators on protein kinase C degradation. While Ca2+ and phosphatidylserine together were sufficient to convert the type III protein kinase C from a trypsin-insensitive to a -sensitive form, addition of dioleoylglycerol greatly reduced the Ca2+ requirement for such a conversion. Among the various phospholipids tested, in the presence of either dioleoylglycerol or phorbol ester, phosphatidylserine, cardiolipin, and phosphatidic acid were the most effective, and phosphatidylcholine and phosphatidylethanolamine were the least effective in supporting the digestion of type III protein kinase. Other acidic phospholipids, such as lysophosphatidylserine and phosphatidylinositol, were also effective in supporting the degradation in the presence of phorbol ester but not in the presence of dioleoylglycerol. The relevance of these proteolytic reactions to physiological responses was assessed with phorbol ester on rat basophilic leukemia RBL-2H3 cells, which contained both types II and III protein kinase C. Immunoblot analysis with the isozyme-specific antibodies revealed that phorbol ester induced a faster degradation of type II than that of type III isozyme in these cells. The results demonstrate that the various protein kinase C isozymes have different susceptibilities to proteolysis in vitro, when tested with trypsin, as well as to endogenous proteases in intact cells.

Animals↗
PubMed1989

Role of the 8-double bond of lanosterol in the enzyme-substrate interaction of cytochrome P-450(14DM) (lanosterol 14 alpha-demethylase).

The role of the 8-double bond of lanosterol in the enzyme-substrate interaction of yeast cytochrome P-450(14DM) (lanosterol 14 alpha-demethylase) was studied by analyzing metabolism of 8-lanostene-3 beta,32-diol, 7-lanostene-3 beta,32-diol, 6-lanostene-3 beta,32-diol and lanostane-3 beta,32-diol by the cytochrome. 8-Lanostene-3 beta,32-diol was actively metabolized by cytochrome P-450(14DM) and converted to the 32-nor-14-unsaturated metabolite. 7-Lanostene-3 beta,32-diol was also metabolized by the cytochrome, but the rate of metabolism was low. However, the cytochrome failed to catalyze the conversion of 6-lanostene-3 beta,32-diol and lanostane-3 beta,32-diol to their 32-nor metabolites. Spectral analysis of the sterol-cytochrome complexes and kinetics of cytochrome P-450(14DM) reduction in the presence of the sterols indicated that 6-lanostene-3 beta,32-diol and lanostane-3 beta,32-diol could not interact with the substrate site of the cytochrome. These results revealed that the 8-double bond of lanosterol plays an important role in the enzyme-substrate interaction of cytochrome P-450(14DM).

Cytochrome P-450 Enzyme System↗