Biomedical subjects

S Iida

Publications and source records attributed to S Iida.

At least 379 records · Page 21Linked to original sources

PubMed1985

Origin of human triosephosphate isomerase isozymes: further evidence for the single structural locus hypothesis with Japanese variants.

Four electrophoretic variants of human erythrocyte triosephosphate isomerase (TPI) have been studied to investigate the origin of the multiple forms of human TPI, in particular the constitutive TPI-B isozyme and the cell division-associated TPI-A isozyme. The variant phenotype expressed by the constitutive TPI-B isozyme in both erythrocytes and peripheral lymphocytes was also expressed by the cell division-associated isozymes in mitogen-stimulated lymphocytes and hair root cells. These results strongly support the hypothesis of Decker and Mohrenweiser (1981) that TPI-B and TPI-A originated from the same structural gene. We also found that the isozyme e is different from TPI-A with respect to both its electrophoretic mobility and heat stability. This finding is in contrast to the recent conclusion of Yuan et al. (1981) that both the isozyme e and TPI-A are deamidation products of TPI-B.

Carbohydrate Epimerases↗

PubMed1985

An active variant of the prokaryotic transposable element IS903 carries an amber stop codon in the middle of an open reading frame.

The prokaryotic mobile genetic element IS903.B is an active variant of IS903. It differs from IS903 and IS102 by 34 and 61 nucleotide substitutions, respectively. The large open reading frame (ORFI) which probably encodes the transposase is conserved in all three IS elements, whereas the smaller open reading frame (ORFII), which codes on the opposite DNA strand and entirely overlaps ORFI, contains an amber stop codon past the middle of ORFII in IS903.B. Experiments using Escherichia coli K12 strains permissive or non-permissive for amber mutations revealed no difference in the cointegration frequency mediated by IS903.B. Therefore, a possible peptide encoded by ORFII on the IS903-related element is unlikely to be necessary for transposition.

Base Sequence↗

PubMed1985

Reversion of a truncated gene for ampicillin resistance by genetic rearrangements in Escherichia coli K12.

The composite transposon Tn2672 is a derivative of the Tn3-related transposon Tn902 whose bla gene providing ampicillin resistance had been inactivated by the insertion of the IS1-flanked multiple drug resistance transposon Tn2671. Most ampicillin resistant revertants of Tn2672 are due to precise excision of Tn2671. However, a rare Bla+ revertant which still retains all the previously acquired drug resistance markers was isolated. On this revertant, the 5' part of the split bla gene on Tn2672 has converted to an intact, active bla gene, and the entire Tn902 is structurally restored. In contrast, the adjacent IS1b element belonging to Tn2671 has its terminal 142 base pairs deleted. Despite of this rearrangement, the split 3' part of bla and its adjacent sequences have remained unchanged. Models are presented to explain the observed DNA rearrangements, and their similarity with gene conversion events is discussed.

Ampicillin↗

PubMed1985

Gene organization and target specificity of the prokaryotic mobile genetic element IS26.

The 820-bp mobile genetic element IS26 loses its ability to promote transpositional cointegration (1) by short deletions near the middle of the element causing shifts in both reading frames ORFI (left to right) and ORFII (right to left) and (2) by deletions causing substitutions of the C-terminus of ORFI but not affecting ORFII. The 702-bp ORFI is thus likely to code for the IS26 transposase. An 82-bp long sequence from the left end of IS26 contains a promoter-like structure in front of the start of ORFI at coordinate 64. In appropriately constructed plasmids, this sequence promotes the expression of the galK structural gene. The observation provides additional evidence for the functional relevance of ORFI. Neither the presence nor the absence of an intact IS26 element on the same plasmid affects measurably the degree of the galK gene expression by the IS26 promoter. Sequence comparison of 14 independent integration sites of IS26 and its relatives reveals no striking rules for target selection by the element, and the distrubtion of integration sites of IS26 on small multicopy plasmids is nearly random and independent of the local AT-content.

Base Sequence↗

PubMed1985

Direction of splenic venous flow assessed by pulsed Doppler flowmetry in patients with a large splenorenal shunt. Relation to spontaneous hepatic encephalopathy.

We studied the direction of blood flow in the splenic vein, using a combined ultrasonic system consisting of an electronic sector scanner and a pulsed Doppler flowmeter, in 21 patients with a large spontaneous splenorenal shunt demonstrated by angiography. Pulsed Doppler flowmetry revealed hepatofugal flow in the splenic vein in all 11 patients with chronic spontaneous hepatic encephalopathy, and hepatopetal flow in 10 patients without encephalopathy. In the former, hepatofugal flow of part of the superior mesenteric venous blood into the splenorenal shunt was corroborated by the venogram obtained after superior mesenteric arteriography. In 5 patients without a history of hepatic encephalopathy, superior mesenteric arteriography demonstrated hepatofugal flow of part of the superior mesenteric venous blood into the splenorenal shunt. Pulsed Doppler flowmetry, however, revealed hepatopetal flow in all of these patients, suggesting that the angiographic finding of hepatofugal flow may have represented an artifact.

Arteriovenous Malformations↗

PubMed1985

Crossover sites cix for inversion of the invertible DNA segment C on the bacteriophage P7 genome.

The bacteriophage P7 genome contains an invertible DNA segment called C which determines its host range. P7 C(+) phages produce plaques on Escherichia coli K12. The C segment consists of a 3-kb unique sequence and 0.62-kb inverted repeats of which one carries an internal 0.2-kb deletion. This deletion has been mapped within the right inverted repeat in the C(+) orientation. The crossover sites cix for inversion of the C segment do not map at the inside boundaries of the inverted repeats, as had been proposed. They are localized at the external ends of these repeats. Thus organization of the C segment in phage P7 is analogous to that in the related phage P1.

Base Sequence↗

PubMed1985

Expression of the bacteriophage P1 cin recombinase gene from its own and heterologous promoters.

The cin recombinase of bacteriophage P1, a protein that catalyses site-specific DNA inversions, has been identified and its structural gene has been cloned under the control of different promoters. One of the DNA sequences used for the site-specific recombination, cixL, overlaps with the 3' end of the gene, but we show that the presence of this site does not affect cin gene expression from strong promoters. To assay cin activity we have constructed plasmids that carry antibiotic resistance genes within the invertible segment that are transcribed from promoters outside the segment. DNA inversion switches on or off genes for chloramphenicol or kanamycin resistance. These tester plasmids are used to study cin-mediated DNA inversion both in vivo and in vitro.

Base Sequence↗

PubMed1985

Pathogenesis of precirrhotic portal hypertension in alcohol-fed baboons.

To study mechanisms and anatomic correlates of precirrhotic portal hypertension, we measured portal pressure either at laparotomy (in the portal vein) or by hepatic vein catheterization (wedge pressure) in 24 pairs of baboons fed 50% of energy either as ethanol or isocaloric carbohydrate (controls) for 4 mo-9 yr. On liver biopsy 7 had simple fatty liver; none had portal pressure exceeding the control range (2.7-13.0 cmH2O). The remaining 17 alcohol-fed baboons had fibrous tissue deposition around the terminal hepatic venules and adjacent sinusoids. The mean portal pressure was significantly increased (15.0 +/- 1.4 cmH2O) compared with the value in baboons with fatty liver (9.6 +/- 0.9 cmH2O) and in controls (8.0 +/- 0.6 cmH2O), with 8 animals exceeding the control range. Estimated hepatic blood flow was unchanged. Alcohol feeding resulted in increased hepatocyte size in both the fatty liver and fatty liver with fibrosis group; however, portal pressure did not correlate with alterations of cell size, liver volume, hepatic triacylglycerol, and protein contents. By contrast, for veins of comparable size, there was a significant correlation (r = 0.6666, p less than 0.01) between the thickness of the perivenular fibrous rim and portal pressure. Perivenular fibrosis was commonly associated with adjacent perisinusoidal fibrosis and this lesion also correlated with portal pressure. Furthermore, if one postulates that increased cell size causes enhanced pressure with secondary fibrosis, the latter should have first occurred "upstream," in the mid and portal zones. Sequential biopsy specimens, however, showed that fibrosis first appeared in the perivenular areas, suggesting that, in most instances, increased pressure is in fact secondary to the perivenular fibrosis.

Animals↗

PubMed1985

Site-specific DNA inversion is enhanced by a DNA sequence element in cis.

A segment of the bacteriophage P1 genome, called the C segment, can be inverted by site-specific recombination; the two different orientations of the invertible segment confer different host ranges to the phage. Inversion is catalyzed by the product of the cin gene which is adjacent to one of the crossover sites flanking the C segment. The Cin-catalyzed recombination can be measured in trans by using tester plasmids in which inversion switches on antibiotic-resistance genes. We show here that an additional sequence, distinct from the two crossover sites, is needed in cis for efficient inversion. This sequence is part of the cin structural gene and stimulates recombination more than 100-fold. We have localized the major enhancer sequence on a 72-base-pair fragment and found its activity to be largely independent of the orientation or position of the sequence with respect to the crossover sites.

Journal Article↗

PubMed1985

Transposable element IS1 intrinsically generates target duplications of variable length.

Target duplication during transposition is one of the characteristics of mobile genetic elements. IS1, a resident insertion element of Escherichia coli K-12, was known to generate a 9-base-pair target duplication, while an IS1 variant, characterized by a nucleotide substitution in one of its terminal inverted repeats, was reported to duplicate 8 base pairs of its target during cointegration. We have constructed a series of transposons flanked by copies of either the normal or the variant IS1. The analysis of their transposition products revealed that transposons with normal termini as well as those with variant termini can intrinsically generate either 9- or 8-base-pair target duplications. We also observed that a normal IS1 from the host chromosome generated an 8-base-pair repeat. The possible relevance of the observation for the understanding of transposition processes and models to explain the variable length of target duplications are discussed.

Base Sequence↗

PubMed1985

Bacteriophage P1 derivatives unaffected in their growth by a large inversion or by IS insertions at various locations.

Several plaque-forming phage P1 derivatives carrying DNA rearrangements associated with IS elements are described. They have IS1, IS3 and IS5 inserted in four distinct locations, all of which are non-essential regions for phage P1 propagation. One derivative carries a genome segment, inverted relative to the one in the P1 wild-type genome, between two inverted copies of IS1. The inverted DNA segment spans about 23 kb of the 90 kb long P1 genome and it includes the invertible C segment. This phage is as viable as an isomeric P1 which carries the relevant segment in its original orientation. These results are discussed with regard to the genome organization of phage P1.

Coliphages↗

PubMed1985

Unaltered stimulation of pituitary adrenocorticotrophin secretion by corticotrophin-releasing factor following sodium valproate administration in a patient with Nelson's syndrome.

A 53-year-old woman with Nelson's syndrome was treated with 600 mg sodium valproate daily. Her plasma ACTH was effectively decreased, whilst the response of plasma ACTH to corticotrophin-releasing factor (CRF) was unaltered. The result of the CRF test suggested that sodium valproate, at least in the present patient, acted at the hypothalamic level.

Adrenocorticotropic Hormone↗

PubMed1985

Organization of the Tn6-related kanamycin resistance transposon Tn2680 carrying two copies of IS26 and an IS903 variant, IS903. B.

The kanamycin resistance transposon Tn2680, which originates from the R plasmid Rts1, is homologous to Tn6 and carries two directly repeated copies of IS26, one at each end. The kanamycin resistance gene codes for type I aminoglycoside-3'-phosphotransferase. Tn2680 also contains, in the middle of the transposon, an additional IS element homologous to IS903. This element, designated IS903.B, is flanked by a 9-base-pair direct target duplication. A novel kanamycin resistance transposon. Tn2681, can be generated from Tn2680 by IS903.B-mediated cointegration and subsequent reciprocal recombination between the directly repeated IS26 sequences. Tn2681 carries a single IS26 element in the middle of the transposon and is flanked by two directly repeated copies of IS903.B. Possible evolutionary relationships between Tn2680 and other kanamycin resistance transposons such as Tn903 and Tn2350 are discussed, based on the gene organization and DNA sequences.

Base Sequence↗

PubMed1985

Portal venous hemodynamics in chronic liver disease: effects of posture change and exercise.

Changes of portal hemodynamics with the progression of chronic liver disease and changes caused by body posture and physical exercise were investigated using an ultrasonic pulsed Doppler flowmeter in healthy adults and in patients with chronic persistent hepatitis, chronic active hepatitis, and cirrhosis. Portal venous velocity was significantly reduced in patients with chronic active hepatitis, cirrhosis without a large splenorenal shunt, and cirrhosis with a large splenorenal shunt, compared with normal subjects and patients with chronic persistent hepatitis. Portal venous flow, by contrast, was significantly reduced only in patients with cirrhosis and a large splenorenal shunt compared with normal subjects and with the other three groups; there was no significant difference in portal venous flow among the latter four groups. Both portal venous velocity and flow showed a tendency toward further reduction in patients with cirrhosis who had hepatofugal flow of part of the superior mesenteric venous blood into the splenic vein and a large splenorenal shunt. Both exercise and posture change from supine to sitting significantly reduced portal venous velocity and portal venous flow in normal subjects, as well as in the patients with chronic liver disease.

Adolescent↗

PubMed1985

Primary cortisol resistance accompanied by a reduction in glucocorticoid receptors in two members of the same family.

This report describes studies of a man suspected of having primary cortisol resistance. This conclusion is based on his high plasma cortisol levels and high 24-h urinary 17-hydroxycorticosteroid and cortisol excretion, plus the fact that he had no manifestations of Cushing's syndrome. Among family members tested, his mother also had hypercortisolemia. Both mother and son had high levels of unbound plasma cortisol, but their plasma ACTH concentrations were within the normal range. Both were partially resistant to dexamethasone adrenal suppression, and both had mild hypertension without hypokalemia. To study this apparent end-organ resistance to cortisol, we examined the glucocorticoid receptors in peripheral mononuclear cells. Using whole cell assays, glucocorticoid receptors in both patients were found to have reduced total binding capacity. We conclude that these two patients, members of the same family, have primary cortisol resistance accompanied by a reduced number of glucocorticoid receptors.

17-Hydroxycorticosteroids↗

PubMed1985

[Ouabain binding and the conformational change in Na+, K+ -ATPase].

The addition of ouabain to the Na+, K+-ATPase [EC.3.6.1.3] of pig kidney modified with N-[p-(2-benzimidazolyl) phenyl] maleimide gradually increased the fluorescence and the amount of phosphoenzyme from Pi with the same time course in the presence of 0.43 mM Mg2+, 16 mM Na+, 27 microM ADP and 27 microM Pi. The extent of the increment of the fluorescence intensity was dependent on the concentration of ouabain. A Hill plot of the data showed that n (Hill coefficient) and K1/2 (apparent affinity) were equal to 0.27 and 0.84 microM, respectively. Addition of ouabain to give 93 microM increased the intensity to the highest level, similar to that of K+-sensitive phosphoenzyme (E2P), and increased the extent of phosphorylation to half the amount of E2P formed with Mg2, Na+ and ATP. ADP inhibited the phosphorylation from Pi without affecting the binding of ouabain. The extent of the fluorescence intensity induced by ouabain in the presence of 0.43 mM Mg2+, 16 mM Na+ and 27 microM ADP was the same irrespective of the presence of 27 microM Pi. Addition of inorganic phosphate to give 2.6 mM accelerated the rate of fluorescence increase and 27 microM ADP retarded it without affecting the extent of the increment. The addition of ouabain to the Na+-bound enzyme increased the fluorescence with time to a level similar to that of E2P. These results and those of others indicate that ouabain can bind to nonphosphorylated Na+, K+-ATPase, and the relative fluorescence intensity of ouabain bound Na+, K+-ATPase was similar to that of E2P irrespective of the phosphorylation.

Adenosine Diphosphate↗

PubMed1985

[Effect of 4-(o-benzylphenoxy)-N-methylbutylamine hydrochloride (bifemelane hydrochloride, MCI-2016) on cerebral glucose metabolism].

To predict the influence of MCI-2016 on cerebral energy metabolism, the activity of MCI-2016 on uptake of 2-deoxy-D-[14C]glucose ([14C]-DG) into the brain under normal or hypoxic conditions, formation of 14CO2 from 14C-glucose in the brain, and local cerebral glucose utilization (LCGU) were examined. Cerebral uptake of [14C]-DG in mice were significantly enhanced by 6 day repeated administration of MCI-2016 (25 mg/kg, i.p.) and Ca-hopantenate (100 mg/kg, i.p.). The two drugs showed a slight enhancing effect on [14C]-DG uptake after single administration. As an index of cerebral glucose metabolism, 14CO2 formation from 14C-glucose was also stimulated by 6 day repeated administration of MCI-2016 (100 mg/kg, p.o., mice and rats) and Ca-hopantenate (250 mg/kg, i.p., rats). MCI-2016 moderately attenuated the decreased [14C]-DG uptake under the hypoxic condition in rats after 6 day repeated administration (100 mg/kg, p.o.). In addition, local cerebral glucose utilization (LCGU) in rats was also significantly potentiated by MCI-2016 (100 mg/kg, p.o., 6 days) in the areas of the visual cortex, thalamus ventral nucleus and uvula. From these results, MCI-2016 may be suggested to have a moderate activating effect on cerebral energy metabolism.

Administration, Oral↗

PubMed1985

Gamma-MSH and its related peptides do not augment ACTH-induced steroidogenesis in isolated rat adrenal cells.

In a sensitive ACTH bioassay system using isolated rat adrenal cells, we tested the effect of gamma-MSH related peptides on ACTH-induced steroidogenesis. Peptides, including synthetic gamma1-, gamma2-, gamma3- and Lys-gamma3-MSH, exerted no effect in augmenting ACTH-induced steroidogenesis. None of the 16 kilodalton fragment of ACTH/beta-lipotropin precursor and its cleaved fragment had such an activity. The results are in contrast with previous reports concerning ACTH-potentiating activity of gamma-MSH related peptides and, therefore, indicate the necessity of further investigation of the principle involved in this unique biological activity.

Adrenal Glands↗