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A nickel and aluminium system including monodentate oxazoline ligands catalyzed the regioselective cyclotrimerization of enones and alkynes.

A 74 year old female was admitted to our hospital because of bradycardia caused by digitalis intoxication. The patient had undergone percutaneous transvenous mitral commissurotomy four years ago. The left atrial pressure decreased to 12 mm Hg at the end of the procedure and no continuous murmur was heard. On physical examination a grade 3/6 continuous murmur was heard over the fifth intercostal space at the right sternal border besides …

Much discussion has been made as to whether vibration syndrome is a peripheral or systemic disorder. We studied plasma and urine norepinephrine and epinephrine, and plasma cortisol under resting and cold exposure conditions (7 degrees C cold room for 30 min). The subjects were 20 patients with vibration syndrome and with a history of Raynaud's phenomenon, 20 patients with vibration syndrome without a history of Raynaud's phenomenon, and 20 healthy controls. They were all males and the three groups were matched by age. The following results were obtained. 1. Mean temperatures of finger skin in the patient groups under resting and cold exposure conditions were lower than in the control group. Mean systolic and diastolic blood pressures in the patient groups under both conditions were higher than in the control group. Mean values of blood pressure change produced by cold exposure in the patient groups were lower than in the control group. Some of these differences were statistically significant (p less than 0.05 or p less than 0.01). 2. Mean levels of plasma norepinephrine in the patient groups under resting and cold exposure conditions were significantly higher (p less than 0.01 or p less than 0.05) than in the control group. This finding indicates that the patients with vibration syndrome had hyperfunction of the sympathetic nervous system. Mean levels of urine norepinephrine in the patient groups were not significantly different from the control group. 3. Mean levels of plasma epinephrine in the patient groups under resting and cold exposure conditions were lower than in the control group. The differences between the patient groups and the control group were significant (p less than 0.05 or p less than 0.01) in the cold exposure condition. This finding suggests that the patients with vibration syndrome had hypofunction of the adrenomedullar system. Urine epinephrine in the patient groups was not significantly different from the control group. 4. Mean levels of cortisol in the patient groups were higher than in the control group. The difference in cortisol level between the group of patients without Raynaud's phenomenon and the control group was significant (p less than 0.01) in the resting condition. This finding may suggest that the patients with vibration syndrome had hyperfunction of the adrenocortex. The foregoing data support the hypothesis that vibration syndrome is a systemic dysfunction, which includes disorders of the sympathetic-adrenomedullar system and adrenocortex.

Background: Activated partial thromboplastin time (aPTT) is recommended for monitoring anticoagulant activity in dabigatran-treated patients; however, there are limited data in Japanese patients. To clarify the relationship between plasma dabigatran concentration and aPTT, we analyzed plasma dabigatran concentration and aPTT at various time points following administration of oral dabigatran in a Japanese hospital. Methods: We enrolled 149 patients (316 blood samples) with non-valvular atrial fibrillation (NVAF) who were taking dabigatran. Patients had a mean age of 66.6±10.0 years (range: 35–84) and 66% were men. Plasma dabigatran concentrations and aPTT were measured using the Hemoclot® direct thrombin inhibitor assay and Thrombocheck aPTT-SLA®, respectively. Samples were classified into eight groups according to elapsed times in hours since oral administration of dabigatran. Results: Significantly higher dabigatran concentrations were observed in samples obtained from patients with low creatinine clearance (CLCr) (CLCr

We investigated the effect of atrial natriuretic factor (ANF) on aldosterone receptors in the kidney cytosol, because the binding of aldosterone to aldosterone receptors in the cytosol is considered a critical step of its action. Rat atriopeptin III was injected into male Sprague-Dawley rats (200-250 g) via the femoral vein while under pentobarbital anesthesia, and aldosterone receptors in the kidney cytosol were determined. The maximum binding capacity and dissociation constant were calculated by the Scatchard analysis. Maximum binding capacity of both types of aldosterone receptor (Type I, high affinity and low binding capacity and Type II, low affinity and high binding capacity) gradually decreased after ANF injection, reached the lowest level after 2 hours, and then slightly recovered. When more than 2.5 micrograms/kg of rat atriopeptin III was injected, the density of aldosterone receptors significantly decreased. Injection of 12.5 micrograms/kg of rat atriopeptin III decreased maximum binding capacity of Type I receptor from 42.3 +/- 2.4 (mean +/- SD, n = 6) to 22.8 +/- 3.2 femtomole/mg protein (n = 6) (p less than 0.01), and that of Type II receptor decreased from 388 +/- 46 to 285 +/- 30 fmol/mg protein (p less than 0.01). Dissociation constant of both types of receptors did not change significantly after ANF injection. Plasma aldosterone concentration showed no significant change after ANF injection, and a significant change was noted after ANF administration on aldosterone receptors in the experiments on adrenalectomized rats 7 days after operation. Furosemide had no significant effect on aldosterone receptors in both normal and adrenalectomized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Taurine is a sulfur-containing amino acid abundant in many mammalian organs and reported to have some important roles1. However, physiological meaning is not fully understood. We have been investigating the antihypertensive effects of taurine, especially in relation to natriuresis2. The taurine natriuresis is supposed to be mainly concerned to the activation of the kallikrein-kinin system. This mechanism will be discussed in detail in another chapter in this review by our colleague, Dr. N. Kohashi. By the way, it became realized that atrial natriuretic peptide(ANP) may play some important roles in water-electrolyte balances and the potent natriuretic activity of ANP has been focused recently3,4, because ANP became to be able to be synthesized more easily, after amino acid sequence of ANP was determined5-8. So it may be increasingly important and neccessary to discuss the action of the natriuretic agents such as taurine in relation to ANP. The purpose of this paper is to examine how ANP takes part in the natriuresis induced by taurine and then assess the interaction of ANP and the activated kallikrein-kinin system induced by taurine. According to this purpose, we designed the following three experiments. 1 Effect of long term taurine administration on urinary kallikrein, atrial and plasma ANP. 2 Acute effect of ANP on natriuresis on rats with long term taurine administration. 3 Natriuresis of ANP in taurine administered rats with inhibiting kallikrein activity by aprotinin.