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Biomedical subjects

M Takata

Publications and source records attributed to M Takata.

At least 325 records · Page 18Linked to original sources
PubMed1979

A case of hypogonadotropic eunuchoidism associated with familiar periodic paralysis--induction of paralytic attacks by testosterone administration.

A case report was made of a 24-year-old man suffering from hypogonadotropic eunuchoidism associated with a hypokalemic type of familiar periodic paralysis. The attacks were observed only during the period of continual administration of the oil solution of 115.7 mg of testosterone enanthate and 20.0 mg of testosterone propionate, intramuscularly as a depot. From the findings on this patient, it was concluded that testosterone might possibly play a role in the occurrence of attacks in the case of periodic paralysis.

Adult↗
PubMed1979

Postsynaptic potentials in the hypoglossal motoneurons set up by hypoglossal nerve stimulation.

In nembutalized cats intracellular potentials were recorded from hypoglossal motoneurons innervating either protruder or retractor muscles of the tonge (protruder and retractor motoneurons: P-Mns and R-Mns). Responses to stimulation of the hypoglossal nerve were explored and found to consist of an antidromic spike followed by an afterhyperpolarization (AHP) and a postsynaptic potential (PSP). When hypoglossal nerve stimulation was made with an intensity three times as large as the threshold for the hypoglossal motor fibers, the PSPs became evident under blockage of soma-dendritic invasion of the antidromic spike. In most of P-Mns or R-Mns, the PSPs were IPSPs, independent of the side of peripheral stimulation. The latencies were about 12 msec. Even when the cell membrane was hyperpolarized by injecting a hyperpolarizing current of up to 16 nA, the reversal point of the IPSP was difficult to find. In a small fraction of hypoglossal motoneurons the PSPs to hypoglossal nerve stimulation were EPSPs with latencies of 10 to 12 msec.

Afferent Pathways↗
PubMed1978

Afterhyperpolarization mechanism in the dorsal spinocerebellar tract cells of the cat.

1. The longlasting afterhyperpolarization (a.h.p.) following single or short trains of spikes in dorsal spinocerebellar tract (DSCT) neurons of the cat has been studied with intracellular recording techniques. 2. The a.h.p. amplitude was found to be potential dependent, increasing with depolarization and decreasing with hyperpolarization of the membrane. With large membrane hyperpolarization, the a.h.p. could be reversed in direction, the estimated reversal level being around 30 mV more negative than the threshold potential for spike initiation. The a.h.p. amplitude was also little affected by Cl- ions injected into the cell. 3. The a.h.p. was associated with an increase in the membrane conductance, as measured with short current pulses. The major part of the conductance change was related to the a.h.p. itself and not secondary to the hyperpolarization, i.e. to an anomalous rectification. A conductance change was also found when the membrane potential was polarized close to the a.h.p. reversal level. There was a clear correlation between the a.h.p. amplitude and the measured conductance changes. 4. It is concluded that the a.h.p. in DSCT neurones, as in spinal motoneurones, is caused primarily by an increase in membrane conductance to potassium ions. 5. The time course of the conductance change underlying the a.h.p. was calculated from the a.h.p. voltage and a mathematical expression describing this time course is given. The properties of the a.h.p. in DSCT cells are compared with those in spinal motoneurones and the functional significance of the differences is discussed briefly.

Action Potentials↗
PubMed1977

Triglyceride metabolism in the lung.

Experiments were carried out to examine whether the lung acts as a depot for circulating lipid, especially that absorbed from the intestine. When 0.5 ml of triolein was administered orally to rats, the triglyceride content of the lung increased 2-3 hr later, but its increase in the lungs 2-3 hr later was only of about 1/10 of that in the liver. In the fed state the triglyceride content of the lung was only about 1/8 of that of the liver. When [3H]palmitic acid was administered orally to mice its uptake by the lung 1 and 2 hr later was 1/25-40 of that by the liver. In the lung, it was incorporated into phospholipid more than into triglyceride, but in the liver it was predominatly incorporated into triglyceride. Most of the lipase activity in both the microsomal and soluble fractions of rat lung appeared to be due to lipoprotein lipase. Fasting did not decrease the lipoprotein lipase activity in either fraction. It was concluded that the lung is not important in removal of triglyceride from the blood, even during fat absorption from the intestine, and that the lung takes up circulating lipid for its own metabolism rather than for storage.

Animals↗
PubMed1975

[Determination of conjugated and free estrogen in male plasma (authors transl)].

Radioimmunoassay for conjugated and free estrone (E1), estradiol-17beta(E2) and estriol (E3) in male plasma was investigated, while no precise determination of conjugated estrogen in male plasma had been established. Each tritiated estrogen glucuronides for determining the recovery was added to 3 ml of plasma samples. These plasma samples were extracted with acetone, hydrolyzed with 15 vol% HCl at 100 degrees C for 60 minutes, and resulting free estrogens were extracted with ether. These extracts were washed with 1% NaOH and 1% NaHCO3, and applied to microcolumn of Sephadex LH-20. Then they were determined by the radioimmunoassay as the same method of evaluation for free estrogen. Each mean values of plasma free and conjugated estrogen in 10 normal adult males was as follows: 36.0 +/- 9.81 pg/ml(free E1), 29.5 +/- 11.0 pg/ml(free E2), 1.80 +/- 1.27 pg/ml (free E3), 31.0 +/- 12.6 pg/ml (conjugated E1), 36.0 +/- 14.2 pg/ml (conjugated E2), 30.6 +/- 8.35 pg/ml (conjugated E3). Conjugated estrogen to free estrogen ratio was 1.45.

Adult↗
PubMed1975

Inhibition of hypoglossal motoneurons by stimulation of the jaw-opening muscle afferents.

The synaptic linkage of jaw-opening muscle afferents with the retractive and the protrusive motoneurons (R-Mns and P-Mns) in the hypoglossal motor nucleus was explored in anesthetized cats. It was found that stimulation of low-threshold afferents arising in the jaw-opening muscles (m. mylohyoideus and m. digastricus) evoked IPSPs in both R-Mns and P-Mns with about 10 to 15 msec latencies. By injecting Cl ions into R-Mns or P-Mns, the hyperpolarizing postsynaptic potentials evoked by jaw-opening muscle afferent impulses were reversed to depolarizing potentials. The lingual-IPSPs of hypoglossal motoneurons were concluded to be dependent on increase of Cl conductance. Stimulation of low threshold lingual afferents evoked a reflex discharge in the retractive nerve fibers with a 6.0 msec latency and in the protrusive nerve fibers with a 5.5 msec latency. Inhibition of the linguohypoglossal reflex by stimulation of the jaw-opening muscle afferents was completely removed by an intravenous injection of strychnine (0.1 mg/kg) or picrotoxin (6 mg/kg). It is concluded that the low threshold afferents arising in the jaw-opening muscles are connected to both R-Mns and P-Mns and P-Mns through inhibitory synapses via a polysynaptic pathway.

Animals↗