Search PubMed⌕ Search

Biomedical subjects

T Tsuchiya

Publications and source records attributed to T Tsuchiya.

At least 757 records · Page 42Linked to original sources
PubMed1982

[LE cell test].

Explore the source record for details and available documents.

Humans↗
PubMed1982

Na+-coupled transport of melibiose in Escherichia coli: analysis of mutants with altered cation specificity.

Melibiose transport via the melibiose transport system of Escherichia coil utilizes either H+ or Na+ as a coupling cation. This system may represent a evolutional transition state between H+-substrate cotransport (bacteria type) and Na+-substrate cotransport (animal type). We have isolated mutants which showed altered cation specificity for melibiose transport. The melibiose carrier of the mutants has lost the ability to recognize H+. This communication describes the properties of the melibiose transport system and the properties of the mutants.

Adenosine Triphosphatases↗
PubMed1981

The average number of distinct sites visited by a one-dimensional random walker and its application to isotope exchange in polypeptides.

The average number of distinct sites visited by a random walker moving with arbitrary transition probability on a one-dimensional lattice is calculated. Asymptotic forms of this quantity for both asymmetric and symmetric random walks are determined, and an exact solution for the latter case is also given for any number of steps. The average number of sites visited is then analyzed for intermediate numbers of steps by introducing an exponent. This approach is applied to explain the results of isotope exchange experiments in polypeptides, and applications of asymmetric random walks to other biological problems are briefly discussed.

Journal Article↗
PubMed1981

Theoretical aspects of translocation on DNA: adenosine triphosphatases and treadmilling binding proteins.

The basic kinetic and bioenergetic theory is outlined for two kinds of translocation on DNA: (i) helicases that use ATP to move along single-stranded DNA or to move on and invade double-stranded DNA at a replication fork; and (ii) DNA-binding proteins (not ATPases) that form bound aggregates on single-stranded DNA and facilitate replication by steady-state treadmilling of molecules between the ends of the aggregate. The respective resemblances to myosin--actin in muscle and to steady-state treadmilling in solution of actin or tubulin are pointed out.

Adenosine Triphosphatases↗
PubMed1981

Isotonic velocity transients in frog muscle fibres following quick changes in load.

1. The isotonic velocity transients following quick changes in load were studied on tetanized frog skeletal muscle fibres with special reference to those following quick increases in load. 2. When the load was increased quickly from the maximum isometric force P0 to 1.05-1.3 P0, the fibres exhibited markedly oscillatory length changes with distinct reversal in the direction of movement before starting to lengthen with a nearly constant velocity. 3. The period of the oscillatory length changes increased with increasing magnitude of the load step, and decreased with increasing temperature. The amplitude of oscillatory length changes never exceeded 0.5% of the slack length L0, i.e. about 50 A per half-sarcomere. 4. If the load was increased quickly from P0 to 1.3-1.6 P0, the fibres lengthened continuously with velocities decreasing with time. 5. The response of fibres, shortening isotonically under a large load (about 0.8 P0), to quick increases in load was qualitatively similar to that of isometrically contracting fibres. 6. When quick increases in load were applied during isotonic shortening under a moderate or small load (0.1-0.6 P0), the fibres showed initial transient lengthening before starting to shorten against a new load, indicating a decrease in the ability of the fibres to sustain a load after a period of isotonic shortening and its restoration during the transient lengthening. 7. The extent of decrease in load-sustaining ability as well as its subsequent restoration process was dependent on both the amount of load and the duration of preceding isotonic shortening. 8. The decrease in the load-sustaining ability during the course of isotonic shortening appeared to be complete within 30-50 msec after the beginning of shortening. 9. These results are discussed in relation to the kinetic properties of the crossbridges responsible for muscle contraction.

Animals↗
PubMed1981

Enhancement of mechanical performance in frog muscle fibres after quick increases in load.

1. The change in the ability of frog skeletal muscle fibres to sustain a load was studied during the course of oscillatory length changes or continuous isotonic lengthening following quick increases in load, by applying "test' load steps and measuring the initial velocity of resulting isotonic motion. 2. When quick decreases in load were applied during oscillatory length changes or continuous isotonic lengthening, the fibres were found to shorten against a load above the maximum tension (P0), indicating an increase in load-sustaining ability after quick increases in load. 3. If quick increases in load were applied at various times after preceding quick increase in load, the initial velocity of resulting isotonic lengthening decreased with time, also indicating an increase in load-sustaining ability. 4. An increase in load-sustaining ability was also observed during the course of rapid isotonic lengthening under a load of 1.6-1.7 P0, in which the fibres lengthened with increasing velocity. 5. The increase in load-sustaining ability after quick increases in load was associated with a shift of the force-velocity curve towards higher force values, while no significant change was observed in the maximum shortening velocity at zero load. 6. The stiffness of muscle fibres was estimated by measuring quick length changes coincident with load steps. It decreased with decreasing isotonic load below P0, approaching a certain finite value as the load tended to zero. For isotonic load below P0, approaching a certain finite value as the load tended to zero. For isotonic loads above P0, the stiffness increased with increasing isotonic load up to 1.6-1.7 P0, when step decreases in load were used for stiffness measurements. 7. The mechanism of enhancement of mechanical performance of the fibres after quick increases in load is discussed in relation to the sliding filament/cross bridge hypotheses of muscle contraction.

Animals↗
PubMed1981

Role of inducer exclusion in preferential utilization of glucose over melibiose in diauxic growth of Escherichia coli.

The role of inducer exclusion in diauxic growth of Escherichia coli on glucose and melibiose was investigated. The amounts of glucose and melibiose in the culture medium were determined during the diauxie. Glucose was consumed during the first growth cycle of the diauxie, and melibiose was consumed during the second cycle. The addition of adenosine 3',5'-cyclic monophosphate to the culture medium released both transient and catabolite repressions on the melibiose operon by glucose. Biphasic growth without a transient lag phase was observed in the presence of adenosine 3',5'-cyclic monophosphate. Preferential utilization of glucose over melibiose was observed even under such conditions. Thus, it is clear that inducer exclusion alone is sufficient to ensure the preferential utilization of glucose over melibiose. Similar results were obtained from a glucose-lactose diauxie. Inducer exclusion itself was not affected by adenosine 3',5'-cyclic monophosphate.

Biological Transport↗
PubMed1981

Proton translocation coupled to trimethylamine N-oxide reduction in anaerobically grown Escherichia coli.

Proton translocation coupled to trimethylamine N-oxide reduction was studied in Escherichia coli grown anaerobically in the presence of trimethylamine N-oxide. Rapid acidification of the medium was observed when trimethylamine N-oxide was added to anaerobic cell suspensions of E. coli K-10. Acidification was sensitive to the proton conductor 3,5-di-tert-butyl-4-hydroxybenzylidenemalononitrile (SF6847). No pH change was shown in a strain deficient in trimethylamine N-oxide reductase activity. The apparent H+/trimethylamine N-oxide ratio in cells oxidizing endogenous substrates was 3 to 4 g-ions of H+ translocated per mol of trimethylamine N-oxide added. The addition of trimethylamine N-oxide and formate to ethylenediaminetetraacetic acid-treated cell suspension caused fluorescence quenching of 3,3'-dipropylthiacarbocyanine [diS-C3-(5)], indicating the generation of membrane potential. These results indicate that the reduction of trimethylamine N-oxide in E. coli is catalyzed by an anaerobic electron transfer system, resulting in formation of a proton motive force. Trimethylamine N-oxide reductase activity and proton extrusion were also examined in chlorate-resistant mutants. Reduction of trimethylamine N-oxide occurred in chlC, chlG, and chlE mutants, whereas chlA, chlB, and chlD mutants, which are deficient in the molybdenum cofactor, could not reduce it. Protons were extruded in chlC and chlG mutants, but not in chlA, chlB, and chlD mutants. Trimethylamine N-oxide reductase activity in a chlD mutant was restored to the wild-type level by the addition of 100 microM molybdate to the growth medium, indicating that the same molybdenum cofactor as used by nitrate reductase is required for the trimethylamine N-oxide reductase system.

Anaerobiosis↗
PubMed1981

Syntheses of 9-substituted josamycin, 13-substituted isojosamycin and their tetrahydro derivatives.

Derivatives of josamycin and isojosamycin modified at C-9 and C-13 have been prepared by reaction sequences involving treatment of josamycin with alcohols, phenol or 1-methyl-1H-tetrazol-5-ylthiol in acidic media. Several tetrahydro derivatives of josamycin and isojosamycin have also been prepared by reaction sequences involving catalytic hydrogenation. From the 1H NMR studies, it was found that the conformation of the macro-lactone portion of 13-O-methylisojosamycin dimethylacetal, a key intermediate, is flexible and changeable with variation of the solvent.

Anti-Bacterial Agents↗