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Biomedical subjects

S Iida

Publications and source records attributed to S Iida.

At least 325 records · Page 18Linked to original sources
PubMed1987

Portal hemodynamics in idiopathic portal hypertension (Banti's syndrome). Comparison with chronic persistent hepatitis and normal subjects.

A comparative study of portal hemodynamics was made in 17 patients with idiopathic portal hypertension, 5 patients with chronic persistent hepatitis having no portal hypertension, and 21 healthy adults who served as the control for certain measurements. Venous pressures were measured by portal and hepatic vein catheterizations, blood flow by the pulsed Doppler flowmeter, organ volume by computed tomography, and intrahepatic shunt index by 99mTc-macroaggregated albumin instilled in the portal vein. The patients with idiopathic portal hypertension were divided into two groups: group A (n = 8) and group B (n = 9), consisting of those who respectively had portal venous flow per liver volume above and below the mean + 2 SD of healthy adults. In group A, portal vein pressure was moderately elevated, portal venous flow was significantly increased compared with the control, and portal vascular resistance was not much altered. In group B, portal vein pressure was markedly elevated above that of control, portal venous flow was comparable, and portal vascular resistance was significantly elevated. Splenic venous flow measured in the splenic vein between the left and short gastric veins was markedly increased in groups A and B, the increase being greater in the former. It was concluded that in some patients with idiopathic portal hypertension, increased portal venous flow, partly a result of increased splenic venous flow secondary to splenomegaly of an undetermined process, is the main contributor initially to the elevation of portal vein pressure; in others, possibly later, increased portal vascular resistance plays an important role.

Adult↗
PubMed1987

Prospective controlled trial of elective endoscopic sclerotherapy in comparison with percutaneous transhepatic obliteration of esophageal varices in patients with nonalcoholic cirrhosis.

The results of a prospective randomized controlled trial of elective endoscopic intravariceal sclerotherapy carried out over a 36-mo period in comparison with elective percutaneous transhepatic obliteration of varices (PTO) are presented. Sixty-six patients with nonalcoholic cirrhosis were randomized after they had stabilized, usually between 7 and 14 days after variceal bleeding had stopped following medical treatment (balloon tamponade and vasopressin infusion). Thirty-three patients were assigned to the sclerotherapy group and the other 33 patients were assigned to the PTO group. The mean follow-up period was similar in both groups. There was no significant difference in demographic, clinical, and laboratory data between the two groups. Six patients (18%) in the sclerotherapy group and 21 (64%) in the PTO group had at least one episode of gastrointestinal bleeding during the follow-up period (p less than 0.005). Three patients in the sclerotherapy group and 1 patient in the PTO group bled from lesions other than varices; therefore the incidence of variceal bleeding was 9% in the former and 61% in the latter (p less than 0.005). The cumulative variceal bleeding rate was significantly lower in the sclerotherapy group than the PTO group (p less than 0.05). Five patients in the sclerotherapy group died during the follow-up period but none died of recurrent variceal bleeding. Nineteen patients in the PTO group died and 10 of them died of bleeding from varices. The cumulative survival rate was significantly better in the sclerotherapy group (p less than 0.05). These results indicate that elective endoscopic intravariceal sclerotherapy is superior to elective PTO in the prevention of recurrent variceal hemorrhage and mortality in nonalcoholic cirrhosis.

Clinical Trials as Topic↗
PubMed1987

Quantitative aspects of portal-systemic and arteriovenous shunts within the liver in cirrhosis.

To estimate vascular changes in chronic liver disease, we quantitated intrahepatic arteriovenous and portal-systemic shunts in 12 patients with cirrhosis and arteriovenous shunts alone in 4 patients with cirrhosis. An index was obtained for intrahepatic arteriovenous shunts by instilling technetium 99m-macroaggregated albumin into the proper hepatic artery and portal-systemic shunts, by the same procedure done in the portal trunk, near the porta hepatis on different days. Counts were taken over the liver and both lungs in the anterior as well as the posterior view for calculation of the shunt index: cpm in lungs divided by cpm in liver and lungs X 100%. In the 12 patients with cirrhosis in whom both shunts were measured, intrahepatic arteriovenous shunting was significantly lower compared with intrahepatic portal-systemic shunting (1.4% +/- 1.1% vs. 36.0% +/- 29.0%, p less than 0.001). Thus, it seems that in patients with cirrhosis, the development of intrahepatic arteriovenous shunts is not as great as that of portal-systemic shunts, which were found in this study to be considerable and variable in degree.

Adult↗
PubMed1987

Portal venous hemodynamics in hepatocellular carcinoma. Effects of hepatic artery embolization.

Portal hemodynamics were studied in 55 patients with hepatocellular carcinoma in comparison with 41 normal subjects, using the duplex system that consists of an electronic sector scanner and a pulsed Doppler velocitometer. Changes of portal hemodynamics after transcatheter hepatic artery embolization were also investigated in 15 of the patients with hepatocellular carcinoma. The duplex system showed that 9 of the 55 had no Doppler signal in the portal trunk, suggesting portal vein thrombosis, 2 had hepatofugal flow in the portal trunk indicative of arterioportal shunts, and 44 had hepatopetal flow in the portal trunk. One of the 9 patients with no significant portal venous flow showed hepatopetal flow in collateral veins at the porta hepatis, suggesting cavernous transformation of the portal vein. All of these ultrasound findings were confirmed by subsequent celiac-mesenteric angiography. In 44 of the 55 patients there was no tumor invasion in the portal trunk, and portal venous flow was found to be close to that of normal subjects regardless of the stage or size of tumor, and tumor invasion into relatively large portal branches. After transcatheter hepatic artery embolization, portal venous flow was increased, even on the next day, and it remained increased for at least 2 wk. Thus, the duplex system is useful to study qualitative and quantitative changes of portal hemodynamics in hepatocellular carcinoma. Our observations suggest that the portal venous flow is kept relatively constant by some homeostatic mechanism even in advanced hepatocellular carcinoma until the tumor invades into the portal trunk, and that it increases when hepatic arterial flow is occluded.

Adult↗
PubMed1987

Two DNA antirestriction systems of bacteriophage P1, darA, and darB: characterization of darA- phages.

Bacteriophage P1 is only weakly restricted when it infects cells carrying type I restriction and modification systems even though DNA purified from P1 phage particles is a good substrate for type I restriction enzymes in vitro. Here we show that this protection against restriction is due to the products of two phage genes which we call darA and darB (dar for defense against restriction). Each of the dar gene products provides protection against a different subset of type I restriction systems. The darA and darB gene products are found in the phage head and protect any DNA packaged into a phage head, including transduced chromosomal markers, from restriction. The proteins must, therefore, be injected into recipient cells along with the DNA. The proteins act strictly in cis. For example, upon double infection of restricting cells with dar+ and dar- P1 phages, the dar+ genomes are protected from restriction while the dar- genomes are efficiently restricted.

Coliphages↗
PubMed1987

Expression and proteolytic processing of the darA antirestriction gene product of bacteriophage P1.

The darA gene coding for one of the two bacteriophage P1 antirestriction functions is expressed late after infection or induction. The protein is made as a high-molecular-weight soluble precursor. This is proteolytically cleaved to the mature form, which is a structural component of the phage head. Defective mutants of the phage have been found in which the synthesis of gpdarA is normal but processing does not take place. These mutations all map to the same region of the P1 genome and we propose that they lie in the structural gene for the processing protease.

Coliphages↗
PubMed1987

Optimization of [11C]HCN production and no-carrier-added [1-11C]amino acid synthesis.

The optimal conditions for the catalytic production of [11C]HCN from [11C]CO2 were investigated. [11C]CO2 was reduced to [11C]CH4 with H2 on Ni and then converted to [11C]HCN by reaction with NH3 on Pt in a radiochemical yield of more than 95% under the optimized conditions of an NH3 concentration of 5 vol%, a Pt furnace temperature of 920 degrees C, and a reaction gas flow rate of over 200 mL/min. Absorbers were used to remove O2 and H2O from the reaction gas. The synthesis of no-carrier-added [1-11C]amino acids from [11C]HCN via [11C]aminonitriles was successfully carried out. This method is suitable for automation of [1-11C]amino acid production.

Amino Acids↗
PubMed1987

In vitro studies of skin fibroblasts from a patient with a new type of primary cortisol resistance: glucocorticoid receptor status and glucocorticoid effect on DNA synthesis.

Studies made on cultured skin fibroblasts obtained from a patient with primary cortisol resistance are described. Whole cell in vitro assays, using the patient's fibroblasts revealed a reduction in the dexamethasone binding capacity (7.86 +/- 0.73 fmol/micrograms DNA, mean +/- SD, n = 3; normal: 15.2 +/- 1.90 fmol/micrograms DNA, n = 8) and an apparently normal dissociation constant (3.69 +/- 0.15 nM; normal: 3.74 +/- 0.40 nM). In addition, the effects of glucocorticoids on DNA synthesis in these cells were examined. DNA synthesis was inhibited by dexamethasone both in normal fibroblasts and in the patient's cells, but the patient's cells were less sensitive to this inhibition, indicating resistance of the cells to glucocorticoid in vitro. These results suggest that the resistance of target tissues to glucocorticoids is due to the reduction in receptor number and that this is the primary defect in this new type of primary cortisol resistance in man.

Adult↗
PubMed1987

Lethal and mutagenic effects of 252Cf radiation in cultured human cells.

HeLa MR cells were exposed to radiation emitted from a man-made spontaneously fissioning isotope, californium-252. The neutron to gamma-ray ratio in the radiation dose was measured to be 2.0. The extrapolation number of the dose-survival curve was 1.3 and the Do was 200 cGy. A dose-dependent increase in mutation to 6-TGr (6-thioguanine resistant) was observed. The relative biological effectiveness (r.b.e.) for cell killing of the neutrons from 252Cf, calculated relative to high-dose-rate X-rays, was 2.6 at 50 per cent survival. The r.b.e. for mutation induction was 2.7 at a mutation frequency of 5 X 10(-5) per surviving cell.

Californium↗
PubMed1987

Amplification of drug resistance genes flanked by inversely repeated IS1 elements: involvement of IS1-promoted DNA rearrangements before amplification.

Tn2653 contains one copy of the tet gene and two copies of the cat gene derived from plasmid pBR325 and is flanked by inverted repeats of IS1. Transposed onto the P1-15 prophage, it confers a chloramphenicol resistance phenotype to the Escherichia coli host. Because the prophage is perpetuated as a plasmid at about one copy per host chromosome, the host cell is still tetracycline sensitive even though P1-15 is carrying one copy of the tet gene. We isolated P1-15::Tn2653 mutants conferring a tetracycline resistance phenotype, in which the whole transposon and variable flanking P1-15 DNA segments were amplified. Amplification was most probably preceded by IS1-mediated DNA rearrangements which led to long direct repeats containing Tn2653 sequences and P1-15 DNA. Subsequent recombination events between these direct repeats led to amplification of a segment containing the tetracycline resistance gene in tandem arrays.

Chloramphenicol↗
PubMed1987

Familial renal hypouricemia with intact reabsorption of uric acid.

Three patients with renal hypouricemia in the same family are described. Serum urate levels in the mother were in the low normal range and were below normal in her 2 sons. In all 3 patients, the ratios of renal urate clearance to creatinine clearance were abnormally elevated. Clear responses to either pyrazinamide or probenecid administration were observed in these ratios. These results suggest that these 3 patients had renal hypouricemia with normal reabsorption of urate as judged by the criteria for differentiating abnormalities in renal urate handling. This corresponds to the previously postulated mechanism as renal urate hypersecretion. Possible limitations to the diagnostic use of probenecid and pyrazinamide are also discussed.

Adult↗
PubMed1987

The influence of plasma membrane cholesterol on the response of adrenal cells to adrenocorticotropin.

The concentration of cholesterol in plasma membranes of Y-1 cells was altered between values of the molar ratio of cholesterol to phospholipids (C/P) of 0.6:1.6 to study the influence of plasma membrane cholesterol on the response to ACTH. Increasing concentrations of membrane cholesterol (C/P) were associated with an increase in the number of ACTH receptors and, hence, production of cAMP and steroids without affecting the nature of binding (Kd) of ACTH to its receptor. Binding studies revealed spare ACTH receptors at all concentrations of membrane cholesterol. However, production of cAMP and steroids by Y-1 cells were tightly coupled. Studies with cholera toxin showed that extreme changes in C/P were without influence on the activity of Ns or that of the cyclase itself. It was also shown that production of steroids in the absence of ACTH and that in response to cholera toxin involve some effect of membrane cholesterol not dependent on cAMP.

20-alpha-Dihydroprogesterone↗
PubMed1987

The effect of polymyxin B on steroidogenesis from adrenocortical cells.

The action of the cyclic peptide polymyxin B (a well known inhibitor of protein kinase C) on adrenal steroid synthesis was examined with Y-1 adrenal tumor cells. Polymyxin B produces a biphasic effect on the stimulation of steroid synthesis by 2 nM ACTH in these cells, with inhibition at low concentrations (less than 10 microM) and a return to control levels at high concentrations (greater than 100 microM). Polymyxin B does not inhibit the stimulatory effect of Bu2cAMP on steroidogenesis. Inhibition of the steroidogenic response to ACTH by a fixed concentration (20 microM) of polymyxin B is overcome by high concentrations of ACTH. Polymyxin B causes a concentration-dependent stimulation of steroid synthesis by Y-1 cells and, over the same concentration range, increases the production of cAMP by these cells. Polymyxin B also partially inhibits the increased production of the cyclic nucleotide produced by ACTH. In addition, polymyxin B inhibits binding of [125I](Phe2,Nle4)ACTH-(1-38) to Y-1 cells. Polymyxin B, like ACTH, promotes rounding of Y-1 cells and partially inhibits rounding produced by ACTH. These effects of polymyxin B are specific to the extent that polymyxins E1 and E2 do not exert similar effects. The actions of polymyxin B are not confined to transformed cells, since responses similar to those seen with Y-1 cells were also observed with cultured rat fasciculata cells. On the other hand, the effect of polymyxin B is specific for adrenal cells, since the cyclic peptide does not influence the steroidogenic response of rat Leydig cells to LH. It is concluded that polymyxin B is a partial agonist of ACTH which is likely to prove useful in studying the molecular basis of the interaction between ACTH and its adrenal receptor.

20-alpha-Dihydroprogesterone↗
PubMed1987

Effect of peptide bond splitting on ouabain sensitive conformational changes in Na+,K+-ATPase treated with N-[p-(2-benzimidazolyl)phenyl]maleimide.

Trypsin treatment of N-[p-(2-benzimidazolyl)phenyl]maleimide modified enzyme caused a marked reduction in Na+,K+-ATPase activity and in the amount of the alpha-chain, which contains the phosphorylation and ouabain binding sites. However, these preparations retained nearly 90% of the ouabain binding capacity and showed ouabain sensitive dynamic fluorescence changes accompanying the hydrolysis of ATP. The data showed that the three dimensional structure of Na+,K+-ATPase, which is important in the dynamic fluorescence change, is little affected in spite of extensive covalent bond splitting in the alpha-chain of Na+,K+-ATPase.

Electrophoresis, Polyacrylamide Gel↗
PubMed1987

Changes in fluorescence energy transfer between sulfhydryl fluorescent residues during ouabain sensitive Na+,K+-ATP hydrolysis.

Na+,K+-ATPase from pig kidney was sequentially modified with two different sulfhydryl fluorescent reagents, N-[p-(2-benzimidazolyl)phenyl]maleimide (BIPM) and N-[7-dimethylamino 4-coumarinyl]maleimide (DACM). The preparation thus obtained contained 3 and 2 moles of each residue in the alpha-chain. When the BIPM residues were excited at 313 nm, ouabain sensitive decrease and increase in the fluorescence intensity at not only 365 nm (BIPM fluorescence) but also 455 nm (DACM fluorescence) were observed, which were dependent on the amounts of reaction intermediates accumulated. When DACM residues were excited directly at 390 nm, only the decrease in the fluorescence intensity was observed irrespective of the intermediates accumulated. The data suggest that at least two DACM residues which differently change their microenvironments during ouabain sensitive Na+,K+-ATPase reaction are present. One is located close enough and the other is located too far to accept the energy from BIPM residue(s) in the three dimensional structure of Na+,K+-ATPase. Addition of sodium dodecyl sulfate (SDS) remarkably inhibited the energy transfer from BIPM to DACM residues. Limited proteolysis suggested that BIPM residues are located mainly in the peptides which are assumed to contain ATP binding sites and that DACM residues are located near the phosphorylation sites.

Adenosine Triphosphate↗