Observation of ultracold-neutron production by 9-Å cold neutrons in superfluid helium.
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Biomedical subjects
Publications and source records attributed to K Sakai.
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Synthesis of alginate by Pseudomonas aeruginosa correlates with its pathogenicity in the lungs of patients suffering from cystic fibrosis (CF). Alginate synthesis-encoding genes (alg) in P. aeruginosa are normally silent, but are specifically triggered in the CF lung environment. The promoter for the algD gene, located at the upstream end of the alg cluster, is activated by environmental factors such as high osmolarity, nutrient limitation and dehydration. Several regulatory proteins are known to control transcription from the algD promoter. Among these proteins is AlgR1 which is homologous to the phosphorylation-dependent response regulators of the two-component signal transduction system. In this paper, we report that AlgR2, an 18-kDa protein which in cooperation with AlgR1 regulates the algD promoter, undergoes phosphorylation in the presence of ATP. The phosphate group acquired by AlgR2 is then transferred to AlgR1. In addition, we show that AlgR1 can be phosphorylated by an AlgR2-analog in Escherichia coli. AlgR1 is isolated in a phosphorylatable 80-kDa complex in association with AlgR2 in P. aeruginosa and the AlgR2-analog in E. coli.
A protein liquid membrane composed of coacervated alpha-elastin, a chemical fragmentation product of the biological elastic fiber protein, functioned as an amphoteric liquid ion-exchange membrane. Ionic permselectivities of the alpha-elastin coacervate membrane to a series of metal chlorides were investigated for the concentration-cell systems by the ordinary electrochemical measurements. Effects of pH on the transmembrane potential responses for NaCl, CaCl2, and MgCl2 systems were examined. Only in the Ca(2+)-containing system did potential responses stay at constant levels against the pH changes, whereas in the other systems, increasing pH caused potential changes, indicating an improvement of cationic permselectivity across the alpha-elastin coacervate membrane. It was suggested that the characteristic Ca2+ transport mechanisms across the alpha-elastin coacervate membrane are related in some way to the polypeptide backbone interactions specific and selective to Ca2+ ions.
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When an aqueous solution of plasmid DNA at a constant low concentration of 5 micrograms/cm3 was irradiated with 60Co gamma-rays, D37 dose of single-strand breaks was decreased from 18 Gy at a dose-rate of 6.77 Gy/h of acute irradiation to 2.3 Gy at a dose-rate of 0.00212 Gy/h. Or G value was increased from 0.0010 to 0.0081. Similar dose-rate dependency of D37 dose and G value were also found when the plasmid DNA solution was treated with various concentrations of tritiated water at various dose-rates, ranging from 5.13 Gy/h to 0.000118 Gy/h. RBE of tritium beta-rays for single-strand breaks was ranged from 0.3 to 0.5 in a wide range of dose-rates. When the DNA solution was saturated with argon to remove oxygen, the dose-rate dependency of gamma-rays was abolished and that of tritium beta-rays was significantly suppressed. When the DNA solution in air was kept at 4 degrees C for 50 h or 25 days after acute irradiation, the G value of DNA breaks was the same as that kept at -20 degrees C for the same period, but much lower than that of the solution irradiated for the same period at a lower dose-rate to give the same total doses. This shows that the inverse dose-rate effect could not be induced from the different exposure periods but from continuous irradiation of different dose-rates. The inverse dose-rate effect for inactivation of transforming activity of DNA irradiated with tritiated water was also observed in the range from 0.0588 Gy/h to 0.00118 Gy/h.
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We studied the echocardiographic findings and clinical features of left ventricular pseudoaneurysm after mitral valve replacement. From December 1979 to March 1991, 1050 patients underwent mitral valve replacement at our institute, and eight patients (0.8%) had left ventricular pseudoaneurysm. In all eight patients, left ventricular pseudoaneurysm developed after the second mitral valve replacement. The incidence of left ventricular pseudoaneurysm among 253 patients who had had previous mitral valve surgery was 3.1%. Seven of the eight patients were still alive and were followed up from 5 to 136 months (mean, 57 months) after the development of left ventricular pseudoaneurysm; these patients had no complications. One patient died as a result of low cardiac output after mitral valve replacement in spite of repair of the left ventricular pseudoaneurysm. This patient had a long and wide myocardial laceration near the left ventricular pseudoaneurysm. In the other seven patients, transthoracic echocardiography demonstrated a large extraventricular cavity along the posterobasal left ventricle. In five of these patients, a turbulent flow in the neck of the left ventricular pseudoaneurysm was recorded both in systole and diastole by pulsed and color Doppler echocardiography. Transesophageal echocardiography clearly showed the narrow neck of the left ventricular pseudoaneurysm and an abnormal flow between the left ventricle and the left ventricular pseudoaneurysm. Generally, when left ventricular pseudoaneurysm develops after mitral valve replacement, surgical repair is the first choice of therapy. Our study demonstrated, however, that the development of left ventricular pseudoaneurysm was not always associated with a poor prognosis without surgical intervention.(ABSTRACT TRUNCATED AT 250 WORDS)
Stable transfection of H4 neuroglioma cells with the Epstein-Barr virus-based eucaryotic CD4 expression vector pKS286 generated the cell line, H4/CD4, in which greater than 90% of cells express surface CD4 receptors. Optimal conditions for infection of H4/CD4 cells with HIV-1 were determined; these included a cocultivation with growth-arrested, chronically infected T cells. Under these conditions, 3-days after infection up to 50% of H4/CD4 cells expressed HIV-1 antigens as detected by immunofluorescence assay, the number of intracellular HIV-1 RNA copies reached 10(3) molecules per cell as determined by liquid hybridization, and virus production ranged from 0.2 to 1.0 micrograms HIV-1 p24 core antigen per ml of culture supernatant, comparable to that measured under the same conditions in HIV-1 infected T cells. Giant cells and cytolysis were common. Inhibition of HIV-1 infection by nucleoside analogues in H4/CD4 cells was comparable to that in T cells, suggesting that the early stages of HIV-1 infection were similar in both cell systems. Infection in the presence of soluble CD4 reduced HIV-1 expression to the levels determined in CD4-negative H4 cells. This system may be useful for screening of drugs intended to block HIV-1 replication in the brain and for the evaluation of the HIV-1 life cycle in brain cells.
Long-term results of a randomized series of 27 vascularized and 22 conventional sural nerve grafts in patients with comparable upper extremity injuries are reported. Recovery speed and outcome depended on (1) whether or not there was an overlying skin defect, (2) how the defect was closed, and (3) which nerve was injured and at what level. Generally, a vascularized nerve graft is indicated when the nerve gap is more than 6 cm and is associated with a massive skin defect or the graft is performed after reimplantation. Otherwise, results achieved with a conventional graft are equally good.
A severed head which had been wrapped in seven plastic bags and set in concrete in an airtight insulated plastic box was found approximately 22 months after the occurrence of death. Ammonium magnesium phosphate had formed and on the basis of this and other observed postmortem changes, time elapsed after death was estimated to be from 2 weeks to 6 months. The absence of oxygen is thought to have contributed significantly to the great discrepancy between estimated and actual time elapsed after death.
We have isolated and sequenced complementary DNA (cDNA) for the human 80K-L protein, a major substrate for protein kinase C and the human homologue of an 80- to 87-kDa bovine protein named MARCKS (myristoylated alanine-rich C kinase substrate). The human 80K-L cDNA encodes a protein of 332 amino acids with a calculated molecular weight of 31,534. Homology comparisons of the nucleotide sequences of the cDNAs indicated that their 3'-untranslated regions are more homologous than the coding regions. Spot blot hybridization using flow-sorted human chromosomes indicated that the gene encoding the 80K-L protein, designated MACS, maps to the q15----qter region of human chromosome 6, and it also suggested that a genomic region with a sequence homologous to the 3'-untranslated region of the 80K-L mRNA exists on chromosome 21.
Most patients who receive multiple blood or platelet transfusions do not develop graft-versus-host disease (GVHD) in spite of the transfusion of donor white cells--cells that are capable of engraftment and subsequent GVHD. The object of this study was to search for the factors responsible for resistance to GVHD in such patients. Some sera from patients who have received multiple platelet transfusions inhibit the proliferation of alloreactive T-cell clones that function as an in vitro model of donor-derived proliferating T cells recognizing recipient alloantigens. The humoral factor in such sera was capable of binding to the T-cell clones, but not to stimulator cells. Further analysis revealed that the humoral factor in such sera was IgG, which specifically bound to membrane molecules of the T-cell clones. The antibody competed with WT31, a monoclonal antibody (MoAb) to T-cell receptor (TCR), in binding to TCR of the T-cell clones. It did not compete with CD3 or CD2 MoAb. These observations strongly favor the view that the antibody against TCR exists in the sera of multiple transfusion recipients. It is suggested that the TCR antibody binds to TCR of the T-cell clones, thus blocking the interaction of the T-cell clone with alloantigens of stimulator cells and resulting in inhibition of the proliferation of T-cell clones. Furthermore, in view of T-cell clone-specific binding of the antibody in sera, it might be concluded that the antibody is anti-idiotypic.
The phospholipid (PL) content was 4-fold higher while the triacylglycerol (TG) content tended to be 65% lower in human breast cancer tissues as compared with non-cancerous reference parts from excised breast tissues. The variation in TG content among breast tissues was very large while that of PL was relatively small. The fatty acid compositions of PL were significantly different between the cancer and reference tissues; the proportions of octadecenoate (18:1), docosahexaenoate (22:6n-3), the total n-3 fatty acids and the n-3/n-6 ratio, but not the proportion of arachidonate (20:4n-6), were significantly higher in the major PL of cancer tissues as compared with those of the reference tissues. No significant differences were observed in the proportion of the major fatty acids of TG in these tissues. The turnover of lipids was faster in the cancer tissues than in the reference tissues. The turnover of TG was faster than that of PL in the cancer tissues, whereas the opposite was true in the reference tissues, indicating significant differences in lipid metabolism between these tissues. A striking difference in the n-3 and n-6 fatty acids of the reference tissues noted for Japanese and Finnish women is discussed in relation to the roles of eicosanoids and eicosanoid precursors in mammary carcinogenesis.
N-isopropyl-p-[I-123] iodoamphetamine (I-123 IMP) SPECT studies were performed on a 75-year-old patient who could be clinically classified as subcortical arteriosclerotic encephalopathy (Binswanger's disease). Regional cerebral blood flow (rCBF) was quantitatively measured by a microsphere model, and was diffusely decreased in the whole brain (mean rCBF: 36 ml/100 g/minute). After a ventriculoperitoneal shunt operation, his clinical symptoms were markedly improved, and the improvement was validated by a 32% increase of mean rCBF. However, MRI and CT images showed no significant interval changes before and after the shunt operation. Regional rCBF measurement by I-123 IMP SPECT should be performed and plays an important role in the evaluation of Binswanger's disease.
The structural features required for xyloglucan oligosaccharides to inhibit 2,4-dichlorophenoxyacetic acid-stimulated elongation of pea stem segments have been investigated. A nonasaccharide (XG9) containing one fucosyl-galactosyl side chain and an undecasaccharide (XG11) containing two fucosyl-galactosyl side chains were purified from endo-beta-1,4-glucanase-treated xyloglucan, which had been isolated from soluble extracellular polysaccharides of suspension-cultured sycamore (Acerpseudoplatanus) cells and tested in the pea stem bioassay. A novel octasaccharide (XG8') was prepared by treatment of XG9 with a xyloglucan oligosaccharide-specific alpha-xylosidase from pea seedlings. XG8' was characterized and tested for its ability to inhibit auxin-induced growth. All three oligosaccharides, at a concentration of 0.1 microgram per milliliter, inhibited 2,4-dichlorophenoxyacetic acid-stimulated growth of pea stem segments. XG11 inhibited the growth to a greater extent than did XG9. Chemically synthesized nona- and pentasaccharides (XG9, XG5) inhibited 2,4-dichlorophenoxyacetic acid-stimulated elongation of pea stems to the same extent as the same oligosaccharides isolated from xyloglucan. A chemically synthesized structurally related heptasaccharide that lacked a fucosyl-galactosyl side chain did not, unlike the identical heptasaccharide isolated from xyloglucan, significantly inhibit 2,4-dichlorophenoxyacetic acid-stimulated growth.
Using ethanolic phosphotungstic acid staining, we studied the development of synaptic junctions in the brains of mice subjected to total asphyxia. One-day-old mice, Std:ddY strain, were put into a chamber continuously flushed with 100% CO2-gas for 35 min. The surviving mice (28.1%) were used as experimental models, while unasphyxiated littermates served as controls. The synaptic junctions in the frontal motor cortex and hippocampal cortex were studied at 20 and 60 days of age using E-PTA staining, and the numbers of synaptic junctions in both areas were counted. In comparison with the control animals, the frontal motor cortex of the subject mice showed a smaller increase in the number of synaptic junctions, both at 20 and at 60 days of age. In the hippocampal cortex, the number of synaptic junctions seen in the experimental mice brains was similar to that in the controls at 20 days of age; however, the number of synaptic junctions in the treated mice brains showed a slower rate of increase than in the controls at 60 days of age.
Twelve-hour urinary sodium excretion, the number of sodium pump sites (Bmax) and the Na/K flux ratio in erythrocytes were measured in 13 previously diagnosed hypertensive subjects. At the time of the study, six subjects were still hypertensive and showed a significantly lower Na/K flux ratio in erythrocytes than the remaining seven subjects who were normotensive. Bmax was also lower in the hypertensive group compared to the normotensive group, although this was not statistically significant. Urinary Na excretion did not show any significant difference between the two groups. These findings suggest that a cell membrane sodium transport defect may have a role in the development of essential hypertension in adult life.
The feasibility of using a ferrofluidic actuator for an artificial heart was studied. A ferrofluidic actuator directly drives magnetic fluids simply by applying a magnetic field to the ferrofluids and does not require a bearing. Magnetic fluid in a U-shaped glass cylinder was placed in an air gap of a solenoid. When a magnetic flux of 0.32 T was applied to the interface of the ferrofluid and air, the ferrofluid was displaced and a pressure of 7.58 kPa (57 mm Hg) was obtained. An array of three poles of solenoids was mounted near the U-shaped glass cylinder. The solenoids were sequentially activated and deactivated. A pressure of 9.98 kPa (75 mm Hg)/-1.33 kPa (-10 mm Hg) was obtained. Calculations indicate that a magnetic flux of 0.49 T is enough to obtain a pressure of 13.3 kPa (100 mm Hg). A ferrofluidic actuator is promising for use with an implantable artificial heart.