Search PubMed⌕ Search

Biomedical subjects

Y Sakurai

Publications and source records attributed to Y Sakurai.

At least 703 records · Page 39Linked to original sources
PubMed1977

Enhancement of anti-tumor activity of 1-beta-D-arabinofuranosylcytosine by encapsulation in liposomes.

1-beta-D-Arabinofuranosylcytosine (ara-C) was encapsulated in four different types of unsonicated artificial vesicles of phospholipid (liposomes) to compare the anti-tumor effect on mouse leukemia L1210 inoculated in CD2F, mice with that of free ara-C. The anti-tumor activity of ara-C was markedly enhanced by encapsulation in liposomes when given in a single IP injection. Among the four types of liposomes, a physically stable and positively charged liposome consisting of sphingomyelin, stearylamine and cholesterol (20:2:15 molar ratio) most effectively enhanced the effect of ara-C. A single IP dose of 50 mg/kg of ara-C, encapsulated in this kind of liposome exhibited high activity, producing a survival rate of 60% of the treated mice at 60 days. This enhanced effect of ara-C encapsulated in liposomes was also demonstrated when the drug was administered either IV or SC, and the range between the minimum effective and the maximum tolerable doses was wide enough to allow the safe use of the encapsulated ara-C. Intraperitoneal administration of encapsulated ara-C induced a more prolonged survival of mice inocualted with L1210 than did free ara-C, regardless of whether it was given in single or multiple doses.

Administration, Oral↗
PubMed1977

Maximum rate of tension fall during isometric relaxation at end-systolic fiber length in canine papillary muscle.

We measured the characteristics of the decline in tension during isometric relaxation of canine papillary muscle. In the intact heart, relaxation begins with the isovolumic phase, but in experiments on papillary muscle previously reported the isotonic phase preceded the isometric phase during the course of relaxation. In our experiments, however, the isotonic bar was locked at the instant the muscle reached the end-systolic fiber length in order to hold the fiber at the length during the succeeding relaxation process. Therefore, we obtained a relaxation process similar to that occurring in the intact heart. The major results of these experiments are: (1) Maximum rate of the decline in tension (-dT/dtmax) is linearly related to the magnitude of total load. (2) -dT/dtmax is augmented by positive inotropic interventions and diminished by negative inotropic interventions. (3) An increase in preload results in only a slight increase in -dT/dtmax. (4) End-systolic fiber length itself is not a principal determinant of -dT/dtmax. (5) -dT/dtmax divided by total load is independent of the amount of muscle shortening. We, therefore, suggest that -dT/dtmax divided by total load cand be a useful index of the relaxation characteristics of cardiac muscle.

Animals↗
PubMed1977

Effect of spironolactone on urinary kallikrein excretion in patients with essential hypertension and in primary aldosteronism.

Urinary kallikrein excretion was measured before and after administration of spironolactone in 12 patients with essential hypertension (including 7 patients with low renin and 5 patients with normal renin) and 6 patients with primary aldosteronism. In low renin essential hypertension, two types of urinary kallikrein excretion were observed. In one type, urinary kallikrein decreased from 6.2+/-2.1 (S.E.) EU/day to 2.7+/-0.3 EU/day after the treatment. In another type, urinary kallikrein increased from 3.1+/-0.5 EU/day to 6.4+/-1.0 EU/day. In the former, plasma aldosteron showed high levels (12.3+/-2.1 ng/100 ml), while in the latter, it was normal (3.2+/-0.5 ng/100 ml). In normal renin essential hypertension, urinary kallikrein excretion did not alter after the treatment. In primary aldosteronism, urinary kallikrein showed moderate decrease after the spironolactone treatment from 8.5+/-1.6 EU/day to 4.2+/-1.6 EU/day. Spironolactone is said to compete directly with the effect of aldosterone at renal distal tubules. The present investigation suggests that urinary kalikrein excretion is related to the effective levels of aldosterone at renal distal tubules, and alteration of aldosterone levels mediates the release of kallikrein, and that there are different mechanisms in the renal handling of sodium and kallikrein in low renin essential hypertension, in normal renin essential hypertension, and in primary aldosteronism.

Adult↗
PubMed1977

Effects of 1-Sar-8-Ile-angiotensin II on urinary prostaglandin excretion in patients with essential hypertension.

To investigate the interaction between the renin angiotensin aldosterone system and the renal prostaglandin (PG), urinary excretion of PGE, urinary excretion of main urinary metabolite (MUM) of PGF2a, urinary excretion of aldosterone, and plasma renin activity were measured before and after infusion of 1-Sar-8-Ile-Angiotensin II, a specific competitive inhibitor of angiotensin II, in 18 patients with essential hypertension under normal and low sodium diets. The values of urinary sodium excretion in these patients before the infusion of the peptide were 160.8 +/- 13.3 and 27.0 +/- 2.7 mEq per day on normal and low sodium diet, respectively. On normal sodium diet, urinary excretion of PGE was found to correlate with the level of plasma renin activity before the infusion (r = 0.6977, p less than 0.01), and it was decreased slightly from 0.37 +/- 0.05 ng/min to 0.26 +/- 0.04 ng/min after the infusion of the antagonist. On low sodium diet, urinary excretion of PGE was not significantly changed by the infusion of the peptide and showed no correlation with the level of plasma renin activity before the infusion, while urinary excretion of PGE showed a significant correlation with the excretion of urinary aldosterone (r = 0.6719, p less than 0.02). Excretion of PGF2aMUM decreased after the infusion of this peptide on both sodium diets, but the changes were not statistically significant. The present data suggest that angiotensin II influences the synthesis or release of renal PG in patients with essential hypertension on normal sodium diet, but not when they are on low sodium diet.

Adolescent↗
PubMed1977

Role of DNA repair in natural resistance of rat ascites hepatomas to nitrogen mustard.

Mechanism of natural resistance of rat ascites hepatomas to nitrogen mustard was examined with tumors, especially AH-13 and AH-44, sensitive and resistant to the chemical, respectively. There was found little difference in the uptake and binding of the chemical among the two lines. In contrast, DNA repair activity of the resistant line was higher than that of the sensitive line. This result suggested that natural resistance of AH-44 to the drug may be, at least partially, due to its higher activity of repairing DNA damage.

Animals↗
PubMed1977

Induction of resistance to L1210 leukemia in BALB/c X DBA/2Cr F1 mice, with L1210 cells treated with glutaraldehyde and concanavalin A.

Immunization with L1210 mouse leukemia cells treated with glutaraldehyde and concanavalin A resulted in the induction of leukemia-specific immune resistance in BALB/c X DBA/2Cr F1 mice. This was measured by survival of the mice after challenge either with the intact cells or with modified leukemia cells of less malignancy. Factors involved in the induction of immunoprophylaxis were analyzed. To produce an immune response against L1210 cells, preincubation with both glutaraldehyde and concanavalin A was required. Repeated sensitization with this combination produced higher incidences of survivors upon subsequent challenge with L1210 cells than did a single sensitization by equivalent or larger doses. However, the sensitization was rendered less effective by repetition of the immunization process five times.

Aldehydes↗