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Biomedical subjects

K Tajima

Publications and source records attributed to K Tajima.

At least 523 records · Page 29Linked to original sources

The acute toxicity of butylated hydroxytoluene and its metabolites in mice.

the acute toxicity of butylated hydroxytoluene (BHT) and four of its metabolites, 2,6-di-tert-butyl-4-hydroperoxy-4-methyl-2,5-cyclohexadien-1-one (BHT-OOH), 2,6-di-tert-butyl-4-hydroxy-4-methyl-2,5-cyclohexadien-1-one (BHT-OH), 2,6-di-tert-butyl-p-benzoquinone (DBQ), and 2,6-di-tert-butyl-4-[(methylthio)methyl]phenol (BHT-SCH3) was studied in young male mice following intraperitonel administration. The i.p. LD50 values of BHT, BHT-OOH, BHT-OH, DBQ, and BHT-SCH3 wee 3550, 190, above 1600, 2270, and 1840 mg/kg, respectively. These results suggest that BHT-OOH probably is the most toxic metabolite of BHt.

Animals↗

Comparative study of the effects of 4-aminopyridine and tetraethylammonium on neuro-effector transmission in the guinea-pig vas deferens.

1 Effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA) on the neuro-effector junction of the guinea-pig vas deferens were investigated by microelectrode and double sucrose gap techniques. 2 4-AP (0.05 to 0.5 mM) or TEA (0.5 to 1 mM) did not alter the membrane potential, or the membrane input resistance of the smooth muscle cell. 3 The amplitude and frequency of the miniature junction potentials (m.e.j.ps) were not modified by treatment with 4-AP (0.05 to 0.5 mM) or TEA (1 mM). 4 4-AP (1 mM) increased the membrane input resistance, enhanced the spike amplitude of the smooth muscle cells and thereby augmented the amplitude of twitch contraction. 5 4-AP (.05 to 0.5 mM) or TEA (1 mM) markedly increased the amplitude of excitatory junction potentials (e.j.ps), but the facilitation phenomena produced by repetitive stimulation were not affected. 6 The duration of the extracellularly recorded action potential from the small nerve bundle was prolonged by 4-AP (0.5 mM). 7 The amplitude of the e.j.p. was dependent on the external concentration of calcium. A straight line was produced when the amplitude of the e.j.p. and [Ca]o was plotted on a double log scale. Application of 4-AP resulted in a parallel shift of this line to the left. 8 These results indicate that 4-AP (0.05 to 0.5 mM) and TEA (0.5 to 1.0 mM) prolonged the action potential generated from the sympathetic nerve terminal thus enhancing the amplitude of the e.j.p. due to an increase in the Ca-influx. However, in the concentrations used, these compounds did not modify the Ca-mobilization in the nerve terminal or the postsynaptic membrane during the resting state.

4-Aminopyridine↗

Action of morphine on the neuro-effector transmission in the guinea-pig ileum and in the mouse vas deferens.

Effects of morphine on the neuro-effector junction of the guinea-pig ileum or mouse vas deferens were investigated by the micro-electrode and double sucrose gap methods. 1. Morphine (10(-8)-10(-5) M) did not change the membrane potential, membrane resistance and electrical threshold required to produce the action potential of smooth muscle cells of guinea-pig ileum or mouse vas deferens. 2. Morphine (10(-8)-10(-7) M) markedly suppressed the amplitude of excitatory junction potential (e.j.p.) of ileum or that of vas deferens. However the same concentration of morphine did not suppress the inhibitory junction potential recorded from the guinea-pig ileum or the facilitation phenomena observed with repetitive stimulation in the mouse vas deferens. In addition, this opiate (3.5 x 10(-5) M) did not alter the amplitude or the frequency of miniature excitatory junction potential recorded from the mouse vas deferens. 3. Naloxone (3.5 x 10(-7) M), itself, exerted no effect on the membrane potential and amplitude of the e.j.p. After pretreatment with naloxone, however, the inhibitory action of morphine on the e.j.p. was suppressed. 4. The extracellularly recorded action potential from the small nerve bundle innervating the mouse vas deferens was not affected by morphine (3.5 x 10(-5) M). 5. The amplitude of the e.j.p. of the guinea-pig ileum was dependent on the concentration of [Ca]o. When [Ca]o and the relative amplitude of e.j.p. were plotted on a double logarithmic scale, the above relation yielded a straight line with a slope of 1.7. Application of morphine resulted in a reduction in the slope of the straight line to 1.0. 6. These results indicate that morphine probably suppresses the influx of Ca during spike electrogenesis in the nerve terminal, however, there is no modification of the action of Ca in nerve terminals.

Animals↗

Some problems on the histopathological diagnosis of non-Hodgkin's malignant lymphoma -- a proposal of a new type.

A new classification for non-Hodgkin's malignant lymphoma is proposed as the one suited for the Lymphomas in Japan, which is to provide a new subtype "pleomorphic" for those more or less rapid-growing lymphomas of peripheral T-cell nature, along with another subtype lymphoblastic, after Nathwani et al. for those of central T-cell nature. The proposal is based on the result of the investigation by the Study Group for Histopathological Diagnosis on Malignant Lymphoma that (1) the presence of a significant number of T-cell lymphomas with peculiar "pleomorphism" is responsible for the very low reproducibility rate of histopathological diagnosis on the diffuse, mixed L&H type of Rappaport classification, and (2) the relative incidence of lymphoms as peripheral T-cell nature including the so-called adult T-cell leukemia is much higher in Japan than in the Western countries.

B-Lymphocytes↗

An electrophysiological analysis of the actions of prostaglandin on neuromuscular transmission in the guinea-pig vas deferens.

Effects of prostaglandins (PGs) on the neuromuscular junction of the guinea-pig vas deferens were investigated by the micro-electrode and double sucrose gap methods. 1. PGE1, PGE2 or PGF2 alpha (10(-10) to 10(-7) g/ml.) did not change the membrane potential, membrane resistance and electrical threshold required to produce the action potential. 2. PGs markedly suppressed the amplitude of excitatory junction potential (e.j.p.) but the facilitation phenomena seen with repetitive stimulation were not affected. PGs did not change the amplitude and frequency of the miniature e.j.p. 3. The action potential recorded from the small nerve bundle with the aid of an extracellular micro-electrode method was not affected by PGS. 4. The amplitude of the e.j.p. was dependent on the external concentration of Ca. When plotted against [Ca]o on a double log scale, the above relation yielded a straight line with a slope of 1.0. Application of PGs resulted in a parallel shift of this relation to the right. 5. From the concentrations of [Ca]o to produce a given e.j.p. in the absence and presence of various concentrations of PGE1, the linear relation was observed from double logarithmic plot between [[Ca]o ratio -1] and [PGE1]o. However the slope of the line was too small (-0.37) to indicate a simple competition between [PGE1]o and [Ca]o. 6. Indomethacin (10(-6) g/ml.) had no effect on the amplitudes of e.j.p. produced by repetitive stimulation. 7. These results indicate that a low concentration of PGs interact with [Ca]o at the activated nerve terminals, but that there is no modification of the actions of Ca in the nerve terminals required for release of chemical transmitter.

Action Potentials↗

Equilibrium studies of lecithin-cholesterol interactions. II. Phase relations in surface films: analysis of the "condensing" effect of cholesterol.

From measurements of the equilibrium spreading pressure pie for dispersions of lecithin--dimyristoyl (DML) or dioleoyl (DOL)--and cholesterol (CHOL) in water, we have deduced the phase relations in both the aqueous dispersions and the equilibrium surface films. At 29.5 degrees C, when the mole fraction of cholesterol in the dispersion chi(CHOL) is 0 chi(CHOL) less than chi(CHOL) less than 0.33, pie is constant and equal to the value for pure lecithin (DOL or DML). The phase rule predicts than two bulk lipid phases coexist; these are pure lecithin and lecithin:cholesterol 2:1 complex. The equilibrium surface film contants only lecithin and therefore lecithin and 2:1 complex are immiscible in surface films. When 0.33 less than chi/CHOL) less than 1.0, pie is also contant with a value intermediate between that for pure lecithin and cholesterol. In this range of lipid composition two bulk lipid phases also coexist: lecithin:cholesterol 2:1 complex and pure cholesterol. However, the equilibrium surface film contains only the 2:1 complex and, therefore, 2:1 complex is also immiscible with cholesterol in surface films. When pi less than pie, as in the case of spread films, we deduce that two surface phases may coexist; the composition of the phases will depend on chi(CHOL). When 0 less than chi(CHOL) less than 0.33, both lecithin and 2:1 complex coexist, and when 0.33 less than chi(CHOL) less than 1.0, 2:1 complex and cholesterol coexist. The "condensing" effect of cholesterol in lecithin surface films is reexamined. The effect is attributed to formation of the lecithin:cholesterol 2:1 complex and nonequilibrium conditions in the two-phase surface film.

Cholesterol↗