A monogalactosyl diacylglycerol from a cultured marine dinoflagellate, Scrippsiella trochoidea.
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Biomedical subjects
Publications and source records attributed to Y Oshima.
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Binding characteristics among three catalytic components of rat liver branched-chain 2-oxo acid dehydrogenase complex (BCKADH) were investigated by ELISA. Dihydrolipoamide dehydrogenase (E3) was bound to solid-phase dihydrolipoamide acyltransferase (E2). The binding curve was hyperbolic giving a calculated half-maximal binding concentration of 167 ng/ml for E3. Specificity of the binding of E3 to E2 was certified by a competition experiment measuring binding of biotin-labeled E3 in the presence of unlabeled E3. The decarboxylase component (E1), which is the other catalytic component of the complex, prevented the E3 binding to E2. The specific binding between E2 and E3 was verified in the opposite direction with immobilized E3. E2 also bound to solid-phase E1 in a specific manner, and addition of E3 prevented the E2 binding to E1. No binding between E1 and E3 was observed. Thus, E1 and E3 prevented each other's binding to E2, suggesting that E1 and E3 may recognize overlapped binding sites on the E2 polypeptide or that they may, at least in part, sterically interact with each other on their binding to E2. The reconstitution experiment of the complex also supported such a mutually exclusive binding of E1 and E3 to the E2 core.
1. Myotoxin alpha (MYTX), a polypeptide toxin purified from the venom of prairie rattlesnakes (Crotalus viridis viridis) induced Ca2+ release from the heavy fraction (HSR) but not the light fraction of skeletal sarcoplasmic reticulum at concentrations higher than 1 microM, followed by spontaneous Ca2+ reuptake by measuring extravesicular Ca2+ concentrations using the Ca2+ electrode. 2. The rate of 45Ca2+ release from HSR vesicles was markedly accelerated by MYTX in a concentration-dependent manner in the range of concentrations between 30 nM and 10 microM, indicating the most potent Ca2+ releaser in HSR. 3. The Ca2+ dependency of MYTX-induced 45Ca2+ release has a bell-shaped profile but it was quite different from that of caffeine, an inducer of Ca(2+)-induced Ca2+ release. 4. 45Ca2+ release induced by MYTX was remarkable in the range of pCa between 8 and 3, whereas that by caffeine was prominent in the range of pCa, i.e., between 7 and 5.5. 5. MYTX-induced 45Ca2+ release consists of both early and late components. The early component caused by MYTX at low concentrations (30-300 nM) completed within 20 s, while the late component induced by it at higher concentrations (> 0.3 microM) was maintained for at least 1 min. 6. Both the components were almost completely inhibited by inhibitors of Ca2+ such as Mg2+, ruthenium red and spermine. 7. 45Ca2+ release induced by caffeine or beta,gamma-methyleneadenosine 5'-triphosphate (AMP-PCP) was completely inhibited by high concentrations of procaine. Procaine abolished the early component but not the late one, suggesting that at least the early component is mediated through Ca(2+)-induced Ca2+ release channels. 8. On the basis of these results, the character of Ca2+ release induced by MYTX was quite different from that caused by caffeine or AMP-PCP, suggesting that MYTX induces Ca2+ release having novel properties in HSR. MYTX is the first polypeptide Ca2+ inducer and has become a useful pharmacological tool for clarifying the mechanism of Ca2+ release from skeletal muscle SR.
A simple measuring system for the frequency of recombinant clones generated by R-protein mediated recombination was constructed. By applying the system, the frequencies of recombinant clones due to site-specific recombination between two loci on one or two different nonhomologous chromosome(s) were monitored during cultivation. Subsequently, it was found that the frequencies increase nearly in proportion to the culture period and are different among the individual two selected loci. Thus, the system is thought to be a candidate for analyzing physicochemical situations, such as folding and localization, of chromosomes in the nucleus.
A 14-year-old female with ulcerative colitis developed right anterior cervical pain and high fever. Cervical contrast-enhanced computed tomography (CE-CT) showed a wall thickness of the right common carotid artery which suggested aortitis. Her pulmonary angiography demonstrated a narrowing of the pulmonary arteries and she was diagnosed as having Takayasu's disease associated with ulcerative colitis. HLA analysis showed Bw52 and DR2 haplotype, which is frequently found in patients with Takayasu's disease associated with ulcerative colitis.
We experienced three patients who have collagen diseases with respiratory failure accompanied by hyponatremia. They were one systemic lupus erythematosus patient with interstitial pneumonia, one rheumatoid arthritis patient with acute pneumonitis, and one dermatomyositis patient with pulmonary fibrosis and organizing pneumonia. In all 3 patients, hyponatremia appeared along with a decrease in arterial O2 partial pressure (PaO2) and the hyponatremia tended to improve when the PaO2 increased after inhalation of oxygen, even though their respiratory failure were not improved. In dermatomyositis patient, serum Na levels were over-corrected after increase in PaO2. The serum and urine osmolality, serum antidiuretic hormone (ADH) levels and clinical pictures demonstrated a presence of inappropriate secretion of ADH (SIADH) in all 3 cases when hyponatremia and hypoxia appeared. A close association between hyponatremia and hypoxia observed in 3 patients strongly suggested that their SIADH were associated with hypoxia since SIADH could be demonstrated by hypoxia. Therefore, it is important to realize that hypoxia-induced hyponatremia will be promptly corrected to hypernatremia by an oxygen inhalation, which could cause a lethal central pontine myelinolysis.
The following points on polyarteritis nodosa (PN) were presented: definition, difference between PN and vascular lesions in other collagen disease, diagnostic criteria, clinical symptoms and laboratory findings, clinical type, histologic stage, therapy and three case reports with two active vasculitis and one scarred vasculitis.
A 33-day-old girl was transferred to our hospital because of severe cyanosis and tachypnea. The diagnosis of aortopulmonary window and interrupted aortic arch was established by echocardiogram and cineangiocardiogram. Reconstruction of aortic arch by extended direct anastomosis and simple patch closure of aortopulmonary window were performed by means of profound hypothermia and circulatory arrest on 36 days of age. Her postoperative clinical course was uneventful, but at 2 months after operation, stenosis of the ascending aorta was noticed by echocardiographic examination. As her physical growth had been satisfactory, she was managed under close observation at outpatient clinic. At seven months after operations, she fell into progressive left heart failure, and emergency operation was carried out for the relief of stenosis of the ascending aorta, but she could not come off bypass. A stenosis of the ascending aorta is a fatal complication that may occur after one-stage repair of interrupted aortic arch with aortopulmonary window consisting of extended direct anastomosis and simple patch closure. We now consider that division of ascending aorta and pulmonary artery and repair of both of the defect is indispensable for the correction of aortopulmonary window, especially in neonate and small infant with this lesion associated with interrupted aortic arch.
In the last 14 years, 7 consecutive patients with supravalvular aortic stenosis (SVAS) underwent surgical treatment for SVAS and/or for associated lesions. There were 5 male and 2 female patients ranging in age from 3 months to 12 years. Six of them had associated other cardiac anomalies; two had severe multiple peripheral pulmonary stenoses (PPS) and one each had ventricular septal defect (VSD), valvular pulmonary stenosis, coarctation of aorta with patent ductus arteriosus (PDA), total anomalous pulmonary venous return (TAPVR) with pulmonary branch stenosis, PPS and left lower pulmonary venous obstruction. The type of SVAS were localized in all and 5 of them underwent successful surgical repair of SVAS (3 with extended aortoplasty and 2 with patch aortoplasty). In 2 patients with VSD or valvular pulmonary stenosis, associated cardiac anomalies and SVAS were repaired simultaneously. Four patients had undergone previous operations, which included repair of severe multiple PPS by extended peripheral pulmonary arterioplasty (case 4, 6), repair of coarctation of aorta and division of PDA (case 5), repair of TAPVR (Ia + IIa) and pulmonary branch stenosis (case 7). There was no operative death and one patient died late postoperatively (case 7) due to right heart failure in a follow up period of 3 to 14 years. In conclusion, it is important to select the appropriate surgical treatment according to the location and the severity of associated other cardiac anomalies as well as the severity of SVAS, and extended peripheral pulmonary arterioplasty is considered to be a recommended method for the relief of severe multiple PPS associated with SVAS.
We have studied bronchopulmonary lesions that developed in 3 allogeneic bone marrow recipients between days 120 and 250 post-transplant. Two cases had extensive chronic GVHD at the time of onset. All patients complained of low-grade fever, dry cough, and shortness of breath. The bronchopulmonary lesions were characterized by hypoxemia with increased AaDO2 and bilateral multiple noncircumscribed interstitial shadows on chest CT scan. Broncho-alveolar lavage (BAL) showed elevated numbers of lymphocytes in BAL fluid in all cases. BAL fluid was negative for CMV, pneumocystis carinii cysts, bacteria and fungi in all cases. The results of transbronchial lung biopsy (TBLB) showed interstitial infiltration of lymphocytes in all 3 cases. The bronchopulmonary lesions were improved by either starting or increasing the dose of immunosuppressants. These findings and clinical courses suggest that the bronchopulmonary lesions in these patients were related to chronic GVHD.
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Between 1981 and 1992, 38 consecutive patients underwent initial operation for pulmonary atresia with intact ventricular septum. Transpulmonary valvotomy using balloon occlusion of RV outflow was carried out in 24 patients at a mean age of 20 days. An additional Blalock-Taussig shunt was required in 4 patients early in the series. Based on a retrospective review on the patients early in the series, initial palliative procedure had been decided in conformity with the value of an index of RV development (RVDI) = RVEDV% x TVD% x RVODmm/BSAm2 x 10(-5), and recent 3 patients with RVDI < 0.35 and patent RV outflow underwent concomitant valvotomy and Blalock-Taussig shunt. Fourteen patients with muscular atresia of RV outflow or major sinusoidal coronary artery communication underwent Blalock-Taussig shunt. There were 1 operative and 3 late deaths and second Blalock-Taussig shunt was required in 6 patients. Definitive repair was carried out in 20 patients between 1985 and 1994. Fifteen patients with RVEDV > 30% of normal had biventricular repair (partial closure of ASD in 6) and 5 underwent Fontan type repair. In terms of the definitive procedures, when the RV.TV index (= RVEDV% x TVD% x 10(-4)) is greater than 0.4, complete repair should be performed. When the index is between 0.2 and 0.4, the atrial septal defect should only be partially closed when the outflow tract is reconstructed. In those cases with an index of less than 0.2, the Fontan procedure seems to be a procedure of choice.
Crystals have been obtained of the DNA-binding domain of the yeast transcription factor PHO4 in complexes with several synthetic fragments of DNA with appropriate cognate sequences. Crystals suitable for X-ray diffraction studies were produced in the case of a complex of the protein with a 17 base-pair fragment of DNA from a solution in polyethylene glycol and calcium chloride. The crystals have the space group of P4(1)2(1)2 or P4(3)2(1)2 with unit cell dimensions a = b = 56.7 A, c = 447.8 A. The diffraction data at 3 A resolution were collected using synchrotron radiation with a Weissenberg camera for macromolecular crystallography.
The smp2 mutant of Saccharomyces cerevisiae shows increased stability of the heterologous plasmid pSR1 and YRp plasmids. A DNA fragment bearing the SMP2 gene was cloned by its ability to complement the slow growth of the smp2 smp3 double mutant (smp3 is another mutation conferring increased stability of plasmid pSR1). The nucleotide sequence of SMP2 indicated that it encodes a highly charged 95 kDa protein. Disruption of the genomic SMP2 gene resulted in a respiration-deficient phenotype, although the cells retained mitochondrial DNA, and showed increased stability of pSR1 like the original smp2 mutant. The fact that the smp2 mutant is not always respiration deficient and shows increased pSR1 stability even in a rho0 strain lacking mitochondrial DNA suggested that the function of the Smp2 protein in plasmid maintenance is independent of respiration. The SMP2 locus was mapped at a site 71 cM from lys7 and 21 cM from ilv2/SMR1 on the right arm of chromosome XIII.
A cis-acting locus, Z, of plasmid pSR1 functions in stable maintenance of the plasmid in the native host, Zygosaccharomyces rouxii. The Z locus was shown to be located in a 482 bp sequence in the 5' upstream region of an open reading frame, P, by subcloning various DNA fragments in a plasmid replicating via the ARS1 sequence of the Saccharomyces cerevisiae chromosome. Northern analysis revealed that the Z region is not transcribed in either the native host Z. rouxii or the heterologous host S. cerevisiae. The Z region is protected from micrococcal nuclease attack in Z. rouxii but not in S. cerevisiae, its protection depending on the product of the S gene encoded by pSR1. Gel retardation assays suggested that a factor present in nuclear extracts of Z. rouxii cells, irrespective of the presence or absence of a resident pSR1 plasmid, binds to a 111 bp RsaI-SacII sequence in the Z region. These findings suggest that a host protein binds to the Z locus and that the S product interacts with this DNA-protein complex and stabilizes pSR1.
The PHO81 gene encoding one of the regulators of the phosphatase regulon in Saccharomyces cerevisiae was mapped 9.8 centimorgans distal from the ser2 locus on the right arm of chromosome VII. Determination of the nucleotide sequence of cloned PHO81 DNA revealed a 3537 bp open reading frame encoding a 134 kDa protein. This protein has six repeats of a 33-amino acid sequence homologous to the ankyrin repeat and an asparagine-rich region. Transcription of PHO81 is activated by Pho4 protein in cooperation with Pho2 (i.e., Bas2/Grf10) protein under the influence of the inorganic phosphate (Pi) concentration in the medium, through the PHO regulatory system. Major transcription initiation sites of PHO81, determined by primer extension analysis, are at nucleotide positions -66 and -65 relative to the ATG codon. Deletion analysis showed that a 95 bp region from nucleotide position -385 to -291 is essential for response to the Pi signals. Purified Pho4 protein protected a 19 bp region (positions -350 to -332) in the 95 bp fragment from DNase I digestion in vitro and the protected region includes the core sequence 5'-CACGTG-3', which is also observed in other genes of phosphate metabolism.
We report the long-term results after systemic-to-pulmonary artery shunts using the internal mammary arteries in 2 patients. The systemic-to-pulmonary artery shunts using the internal mammary arteries were created in 2 children. Both of them are doing well 11 years and 7 years after operation. This procedure could be a reasonable alternative to classic Blalock-Taussig shunt for patients with diminutive pulmonary arteries as it offered good long-term palliation.
A mechanism of antidepressant activity of beta-amyrin palmitate was studied using the forced swimming method in mice. Beta-amyrin palmitate (10 mg/kg) reduced the increase in the duration of immobility induced by tetrabenazine (100 and 200 mg/kg), but showed no effect on that in mice treated with alpha-methyl-para-tyrosine (500 mg/kg). Beta-amyrin palmitate (5 and 10 mg/kg) decreased the duration of immobility in mice treated with desipramine plus 6-hydroxy-dopamine (50 micrograms/mouse), but did not affect that induced by nomifensine plus 6-hydroxydopamine. The decreased immobility produced by desipramine (15 mg/kg) was not affected by beta-amyrin palmitate. A study of norepinephrine release in mouse brain synaptosomes indicated that beta-amyrin palmitate caused a release of [3H]norepinephrine. The results of the present study suggest that beta-amyrin palmitate might release norepinephrine from newly synthesized pools, and thus, it might activate noradrenergic activity.