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Biomedical subjects

M Kano

Publications and source records attributed to M Kano.

At least 253 records · Page 14Linked to original sources

Development of spike potentials in skeletal muscle cells differentiated in vitro from chick embryo.

The development of spike potential mechanisms during cell differentiation was studied in chick myotubes formed in vitro from trypsin-dissociated myoblasts. The spike potential and its rate of rise were measured in myotubes from 4-14 day old cultures. A depolarizing current pulse was delivered to evoke the spike potential after the steady membrane potential had been adjusted to a standard level of -80 mV in all cases. This gives the greatest maximum rate of rise of the spike potential and eliminates variation due to differences in the resting membrane potential of the myotubes. The size and maximum rate of rise of the spike potential increased significantly during the period examined. The spike potential was blocked by tetrodotoxin in almost all myotubes. These results suggest that during differentiation myotubes develop the ability to generate a spike potential due to an inward current carried by sodium ions.

Animals↗

Development of action potential in larval muscle fibers in Drosophila melanogaster.

In the presence of tetraethylammonium or barium ions, the larval muscle fibers of Drosophila melanogaster were found to produce an all-or-none action potential operated by the calcium channels. The development of this distinctive membrane property during the maturation of muscle cells was studied by measuring the maximum rate of rise of the action potential in the larval muscle fibers at different stages of development from the sixteenth to ninety-sixth hours after hatching. The value increased significantly with age until a peak was reached at the sixty-fourth hour, although it became lower again as puparium formation neared at about the ninety-sixth hour. This suggests that during larval development the muscle fibers develop the ability to generate an action potential due to an inward current through the calcium channels, although the ability became lower at the later stage of larval development.

Action Potentials↗

Polycythemia vera and transient monocular blindness. Observation of the platelet embolic phenomena in the ocular fundus.

Transient monocular blindness in the patient with polycythemia vera has generally been considered to be caused by retinal arteriospasm. In the present case with complaints of frequent monocular blindness, ophthalmoscopic observation and serial photographs of the ocular fundus were made. During these acute attacks, microembolic phenomena were noticed in the retinal arteries. Laboratory examination showed abnormal platelet aggregability, increased platelet adhesiveness and a significantly decreased platelet count during attacks. It is suggested that transient monocular blindness is caused by platelet emboli. The cause of intermittent cerebral ischemic attacks in the patient with polycythemia vera is probably platelet emboli.

Acute Disease↗

Effect of immunization with an allogeneic tumor on the growth of primary methylcholanthrene-induced sarcomas in rats.

Making use of common antigenicity among allogeneic tumors, the immunotherapy against primary 3-methylcholanthrene(MCA)-induced sarcomas in rats was attempted. At the time when MCA-induced sarcomas reached approximately 1 cm in diameter, allogeneic Usubuchi sarcoma cells were injected 5 times into the subcutaneous tissue of rats. In most cases, inhibitory effect on the growth of the tumor was observed in the early period, but none of 29 cases treated resulted in final regression. Twenty-nine non-treated cases showed uniformly progressive growth from the beginning. This result seems to indicate the possibility of using allogeneic tumor(s) for the immunotherapy against human cancer.

Animals↗

Development of excitability in embryonic chick skeletal muscle cells.

During embryonic and early postnatal development, the chick leg muscle cells undergo a series of changes in their electrical responses in the following sequence: passive response, plateau response, plateau plus spike response and spike response. This suggests that the electrogenetic mechanism of muscles matures during development; a mechanism producing the plateau may first be induced, and then that producing the spike. The plateau is sensitive to manganese or cobalt ions, while the spike to tetrodotoxin. This suggests that the plateau is related to the increase in permeability to calcium ions, while the spike to sodium ions.

Animals↗

Histologic host response to primary methylcholanthrene-induced sarcomas in rats immunized with allogeneic tumors.

Lymphocytic infiltration was observed in 44 of 51 (86%) 3-methylcholanthrene (MCA)-induced sarcomas in rats which had been intensively immunized with allogeneic tumors. Eleven of 29 (38%) tumors with intense lymphocytic infiltration and 5 of 15 (33%) tumors with moderate lymphocytic infiltration were "negative" in autologous transplantation. On the other hand, all of 7 tumors accompanied with slight or no lymphocytic infiltration were "positive".

Animals↗

[Penetration of cephaloridine and cephalothin into the cerebrospinal fluid-clinical study (author's transl)].

There were 35 cases, treated with Cephaloridine or Cephalothin after neurosurgical operation. Neurological surgeon always troubled with passage of blood-brain barrier when drug was given. Antibiotics was not exceptionally, therefore we, neurological surgeon, must select the effective drug to bacterium, that which penetrated enough to the intracranial organ through the blood-brain barrier. In this paper, we measured the concentration of Cephaloridine and Cephalothin into cerebrospinal fluid in the cases with non inflammatory meninges. We collected the cerebrospinal fluid from continued ventricle tap and serum, then measured the concentration of the drug with bioassay. Cephaloridie treated cases. 22 cases. 1) 1 g intramuscular injection. 4 cases. Serum level got to highest value, 64 mug/ml (mean value) 1 hour after injection. CSF level got to maximum concentration 46.8 mug/ml. (mean value) serum mean level 21.5 mug/ml. CSF mean level 0.73 mug/ml. 2) 1 g 3 minutes-intravenous injection 5 cases. Serum level got to highest value 67.5 mug/ml. CSF maximum level was 5.25 mug/ml. Serum mean level 19.74 mug/ml. CSF mean level 0.61 mug/ml. 3) 1 g 1 hour-intravenous drip. 9 cases. Serum maximum level 121.0 mug/ml. CSF maximum level 2.30 mug/ml. Serum mean level 20.08 mug/ml. CSF mean level 0.67 mug/ml. 4) 1 g 8 hours-intravenous drip. 3 cases. Serum maximum level 61.0 mug/ml. CSF maximum level 1.36 mug/ml. Serum mean level 14.78 mug/ml. CSF mean level 0.47 mug/ml. Cephalothin treated cases, 12 cases. 1) 1 g 8 hours-intravenous drip, 4 cases. In fact we could detect the drug only in one case, in CSF, and we could not in other three cases. In KF - 4 case, serum maximum concentration was 26.0 mug/ml, CSF maximum concentration was 0.07 mug/ml. Serum mean level 16.97 mug/ml. CSF mean level 0.01 mug/ml 2) 2 g 1 hour-intravenous drip, 9 cases. Serum maximum level 690.0 mug/ml. CSF maximum level 2.03 mug/ml. Serum mean level 29.59 mug/ml. CSF mean level 0.06 mug/ml. In cephaloridine cases, the tendency was observed, that which, as concentration of the drug in CSF increased, cell count and protein decreased, and, as concentration of the drug decreased, cell count and protein increased. CSF/serum concentration ratio of Cephaloridine increased, when time passed, in intramuscular, 3 minutes intravenous, and 1 hour-intravenous drip group. Then only in 8-hours-intravenous prip group. Then only in 8-hours-intravenous drip group, concentration ratio decreased. In Cephaloridine group, mean value of CSF/serum ratio showed. 1 g i.m. 0.084 1 g 3 minutes-i.v. 0.098 1 g 1 hour-i.v. 0.194 1 g 8 hours-i.v. 0.044.

Adolescent↗