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Biomedical subjects

I Matsubara

Publications and source records attributed to I Matsubara.

At least 37 records · Page 2Linked to original sources
PubMed1989

Structural changes in the thin filament during activation studied by X-ray diffraction of highly stretched skeletal muscle.

The actin layer-lines were recorded from a frog semitendinosus muscle stretched to a sarcomere length greater than 4.4 microM. On activation of the muscle, the equator, the second layer-line at 1/18 nm-1 and the 5.9 nm layer-line increased in integrated intensity. On the other hand, the integrated intensity of the first layer-line at 1/36 nm-1 decreased markedly on activation. This decrease was not fully attributable to shifts of tropomyosin strands and therefore suggested a structural change in the actin subunit. The decrease may account for the apparent lack of an intensity increase of this layer-line on activation at normal muscle lengths where attachment of myosin heads to actin increases the intensities of other layer-lines.

Actins↗
PubMed1989

Cross-bridge movement in rat cardiac muscle as a function of calcium concentration.

1. By applying the X-ray diffraction method to chemically skinned papillary muscles of the rat, the transfer of myosin heads from the thick to the thin filaments was studied as a function of Ca2+ concentration. 2. No significant transfer of the heads occurred when the Ca2+ concentration was below the threshold of contraction (pCa 6.2). 3. During the maximum isometric contraction at pCa 4.4, 80% of the myosin heads were transferred to the thin filament. 4. When the muscle was activated isometrically at low Ca2+ concentrations (pCa 6.2-5.8), where the average tension was less than 20% of the maximum, a disproportionately large number of myosin heads were transferred to the thin filament. 5. It was concluded that a significant fraction of the heads transferred at the low Ca2+ concentrations does not produce tension.

Animals↗
PubMed1989

Measurement of sarcomere length in situ.

The laser diffraction method was applied to a whole, unisolated muscle of the mouse in order to study the changes in sarcomere length caused by passive movements of joints. The accuracy of measurement of sarcomere lengths in situ by this method was +/- 5.6%. The site-to-site variation in sarcomere length within resting muscle was not affected by stretching of the muscle and the sarcomere length varied in direct proportion to the muscle length (correlation coefficient = 0.805, p less than 0.01). These results agreed with previous observations on resting muscles in vitro.

Animals↗
PubMed1989

In situ observation of adjustment of sarcomere length in skeletal muscle under sustained stretch.

Adjustment of sarcomere length to sustained stretch was studied in situ by the light diffraction method applied to the extensor digitorum longus muscle of the mouse. The muscle was stretched maximally (with the ankle and toes in full plantar flexion) and immobilized by a plaster cast: the sarcomere length immediately after stretch was 2.98 microns. After 1, 3, 5, 7, and 14 days of immobilization, the sarcomere length was 2.94, 2.86, 2.83, 2.77 and 2.78 microns, respectively. This shows how a muscle under sustained stretch adapts itself to a new length and explains why the efficiency of muscle function is maintained after limb lengthening.

Animals↗
PubMed1989

[Clinical course and prognosis of primary biliary cirrhosis--multivariant analysis on cases of national survey].

In order to predict prognosis and clinical course of BPC, theory quantification was applied and the discriminated rate was calculated concerning the cases of PBC national survey in Japan. We examined the prediction of three and five year's survival about all cases, the prediction of appearance of symptoms about asymptomatic PBC and that of jaundice about asymptomatic PBC and symptomatic PBC alone with pruritus. The useful items for the prediction of prognosis were serum bilirubin, albumin and the presence of esophageal varices at first medical examination. Fairly good discriminated rate was obtained on the prediction of three and five year's survival. However poor results were obtained concerning the prediction of appearance of symptoms. In conclusion we can predict the prognosis of PBC based on clinical features.

Aged↗
PubMed1988

Can blood gas analysis indicate when mechanical ventilation should start in patients with acute myocardial infarction?

Arterial blood gas analysis of 69 patients with acute myocardial infarction were evaluated to provide a basis for respiratory care. Patients were divided into two groups: group A which received oxygen therapy only (n = 38) and group B which received oxygen therapy with mechanical ventilation (n = 31). The patients in group B were further divided into surviving cases (n = 14) and fatal cases (n = 17). On admission patients assigned to group B had lower PaO2 values than those placed in group A. In group B, there was no difference in the P/F value before mechanical ventilation of the surviving and the fatal cases, but the survivors demonstrated an improvement of the P/F value and an increase in cardiac index after mechanical ventilation. It may be reasonable to assume that a P/F value of less than 250 serves as an indicator for the initiation of mechanical ventilation. An increase in the P/F value after mechanical ventilation seems to be a valuable index to estimate prognosis in respiratory failure.

Blood Gas Analysis↗
PubMed1988

Changes in the 5.9 nm actin layer-line on activation of frog skeletal muscles.

The intensity changes of the actin layer-lines during activation of sartorius and overstretched semitendinosus muscles were measured by using a two-dimensional X-ray detector. In both muscles, the intensity of the 5.9 nm layer-line increased without a detectable shift in the peak position. The intensity of the second layer-line increased in both muscles by a similar amount. In semitendinosus muscle, a large intensity decrease of the first actin layer-line was observed. Model calculations suggest that these results are difficult to explain in terms of a simple steric blocking model of regulation involving only a movement of tropomyosin on the actin helix.

Actins↗
PubMed1988

[Non-clostridial gas-producing brain abscess in a brain death patient--report of a case].

A 46 year old female was admitted to our emergency room because of cardiopulmonary arrest by hanging. After ten minutes cardiopulmonary resuscitation, she was resuscitated but her consciousness did'nt recover. CT-scans on the day of admission showed no abnormalities but on the second hospital day it showed symmetrical low density areas within the basal ganglia, the thalamus, the hippocampus, and the occipital lobe. There were marked enhanced effect in cerebral sulci due to cytotoxic edema of hypoxic encephalopathy. She was comatose for a week, her pupils were dilated, light reflex and other brain stem reflex were absent. CT-scans on the sixth hospital day showed marked brain swelling with disappearance of the ventricular systems (so called brain tamponade). Brain death was confirmed on the basis of Japanese Criteria on the seventh and tenth day of admission. She had been suffering from pneumonia and urinary tract infection with an elevation of temperature since the fourth hospital day. We detected Enterobacter Cloacae (E. Cloacae), Klebsiella Oxytoca from the cultures of sputum and urine. On the tenth hospital day her temperature was running up to 39.4 degrees C and blood count revealed a peripheral blood leucocytosis of 40,300/mm3 with a shift to the left. E. Cloacae was also detected from the cultures of blood. Skull roentgenogram showed multiple gas collections in the ventricular systems. CT-scans on the fourteenth hospital day showed multiple gas-containing brain abscess. The etiology of this infection was considered due to septicemia of E. Cloacae. She died from acute renal failure on the fifteenth hospital day. Consent for autopsy was not accepted.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Abscess↗
PubMed1985

Lateral filamentary spacing in chemically skinned murine muscles during contraction.

A mouse toe muscle was chemically skinned with saponin and the 1,0 spacing of the hexagonal myofilament lattice at a sarcomere length of 2.5 micron was measured with the X-ray-diffraction method. In the relaxed state, the 1,0 spacing was 40.8 nm. When the muscle was maximally activated at pCa 4.4, the spacing decreased to 38.4 nm. During contractions at lower calcium concentrations, the spacing decreased less. In rigor, the spacing decreased to almost the same extent as during maximum contraction, although the rigor tension was only 8% of the maximum tension. When the spacing in relaxed muscle had been adjusted osmotically to about 38 nm, activation caused no further decrease in the spacing. The results support the view that the force responsible for the lattice shrinkage during contraction is produced by cross-bridges displaced from their optimum lateral positions.

Animals↗
PubMed1985

Movements of cross-bridges during and after slow length changes in active frog skeletal muscle.

The cross-bridge movements underlying the tension responses of active muscle to slow length changes were studied by a time-resolved X-ray diffraction method. During an isometric tetanus at 2 degrees C, the meridional reflexion at 1/14.3 nm-1 was 55% more intense than in the resting state, suggesting that the myosin heads maintain the 14.3 nm periodicity of the thick filament. When active muscle was stretched by 7% at a constant speed of 0.03-0.70 muscle lengths s-1, the intensity of the meridional reflexion decreased progressively as the tension increased continuously during the stretch. This suggests that the myosin heads spread out along the thick filament. During stress relaxation after a stretch, the intensity returned gradually toward the active isometric level, suggesting a rearrangement of the myosin heads. The meridional intensity changed in a similar manner when active muscle was released by 7% at the same speeds; it decreased progressively during the release and returned gradually to the isometric level after completion of the release. The intensity decrease during a release was smaller than that during a stretch, provided the speed was low (0.03-0.09 muscle lengths s-1). It was concluded that the tension responses to slow length changes are due to shifts of the myosin heads along the thick filament, and that the elastic element responsible for tension production is located in the myosin molecules.

Animals↗
PubMed1984

Changes in the lateral filament spacing of skinned muscle fibres when cross-bridges attach.

When a skinned fibre prepared from frog skeletal muscle goes from the relaxed to the rigor state at a sarcomere length of about 2.2 micron, the 1, 0 transverse spacing of the filament lattice, measured by X-ray diffraction, decreases by about 11%. In measurements at various sarcomere lengths, the decrease in the spacing was approximately proportional to the degree of overlap between the thick and thin filaments. This suggests that the shrinkage of the lattice is caused by a lateral force produced by cross-bridges. In order to estimate the magnitude of the lateral force, the decrease of spacing between relaxed and rigor states was compared with the shrinkage caused osmotically by adding a high molecular weight polymer, polyvinylpyrrolidone, to the bathing solution. The results indicate that the lateral force produced per unit length of thick filament in the overlap zone is of the same order of magnitude as the axially directed force produced during maximum isometric contraction (10(-10) to 10(-9) N/micron). Experiments in the presence of a high concentration of polyvinylpyrrolidone (100 g/l) show that when the lattice spacing is decreased osmotically beyond a certain value, the lateral force produced when the fibre goes into rigor changes its direction, causing the lattice to swell. This result can be explained by assuming that there is an optimum interfilament spacing at which the cross-bridges produce no lateral force. At other spacings, the lateral force tends to displace the filament lattice toward that optimum value.

Animals↗
PubMed1984

Lateral shrinkage of the myofilament lattice in chemically skinned muscles during contraction.

A toe muscle was isolated from a hind limb of the mouse and treated with saponin to make the sarcolemma more permeable to the solutes of the bathing medium. The equatorial X-ray diffraction pattern was recorded to determine the 1,0 spacing of the hexagonal myofilament lattice. The spacing in relaxed muscle at a sarcomere length of 2.5 microns was 408 A. When the muscle was maximally activated at pCa 4.4, a steady isometric tension of 1.3 kg/cm2 was produced and the spacing decreased to 384 A. A decrease in spacing of the same magnitude was observed when a relaxed muscle went into rigor, although the rigor tension was only 0.1 kg/cm2, 8% of the maximum contractile tension. From the intensity ratio of the 1,0 and 1,1 reflections the number of myosin heads transferred radially to the vicinity of the thin filament was calculated. During the maximum activation at pCa 4.4 the amount of the radial transfer was 96% of that in rigor. When the muscle was activated at a lower calcium concentration, the lattice shrinkage was smaller and the radial transfer was also smaller. These findings suggest that the lateral force underlying the lattice shrinkage may be due to lateral elasticity of cross-bridges.

Actins↗
PubMed1984

Cross-bridge movements during a slow length change of active muscle.

Tension changes caused by slow stretch or release of actively contracting muscle are accompanied by axial displacements of myosin heads (i.e., cross-bridges) from the positions characteristic of isometric contraction. The direction of the axial displacement appears to affect the rate of cross-bridge detachment or reattachment during muscle-length changes.

Animals↗
PubMed1982

The state of cardiac contractile proteins during the diastolic phase.

The molecular events underlying contraction and relaxation of heart muscle were studied by the X-ray diffraction method. In quiescent heart muscle most myosin heads were in the vicinity of the thick filaments. When heart muscle contracted, myosin heads moved to the vicinity of the thin filaments to react with actin. On relaxation of muscle, myosin heads returned to the thick filaments. However, in cyclically contracting heart muscle a significant fraction of myosin heads remained in the vicinity of the thin filaments until the end of the diastolic phase. Therefore, the molecular state during the diastolic phase was considerably different from that in the quiescent state. Paired-pulse stimulation, which enhanced the tension development, increased the number of myosin heads near the thin filaments not only during the systolic phase but also during the diastolic phase. Thus the diastolic molecular state was modified by inotropic intervention. These findings suggest that the diastolic phase should be regarded as a dynamic phase rather than a static phase.

Animals↗
PubMed1981

Changes of thick filament structure during contraction of frog striated muscle.

The strongest myosin-related features in the low-angle axial x-ray diffraction pattern of resting frog sartorius muscle are the meridional reflections corresponding to axial spacings of 21.4 and 14.3 nm, and the first layer line, at a spacing 42.9 nm. During tetanus the intensities of the first layer line and the 21.4-nm meridional decrease by 62 and 80% respectively, but, when the muscle is fresh, the 14.3-nm meridional intensity rises by 13%, although it shows a decrease when the muscle is fatigued. The large change in the intensity of the 21.4-nm meridional reflection suggests that the projected myosin cross-bridge density onto the thick filament axis changes during contraction. The model proposed by Bennett (Ph.D. Thesis, University of London, 1977) in which successive cross-bridge levels are at 0,3/8, and 5/8 of the 42.9-nm axial repeat in the resting muscle, passing to 0, 1/3, and 2/3 in the contracting state, can explain why the 21.4-nm reflection decreases in intensity while the 14.3-nm increases when the muscle is activated. The model predicts a rather larger increase of the 14.3-nm reflection intensity during contraction than that observed, but the discrepancy may be removed if a small change of shape or tilt of the cross-bridges relative to the thick filament axis is introduced. The decrease of the intensity of the first layer line indicates that the cross-bridges become disordered in the plane perpendicular to the filament axis.

Animals↗