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Biomedical subjects

K Sakurai

Publications and source records attributed to K Sakurai.

At least 325 records · Page 18Linked to original sources

Management of atrial fibrillation in the post-thyrotoxic state.

This study was designed to investigate the appropriate timing for cardioversion in patients with chronic atrial fibrillation who had been rendered euthyroid from a thyrotoxic state. We carried out a retrospective study of 163 patients with thyrotoxic atrial fibrillation, with a mean follow-up of 34 months. With control of thyroid function alone, 101 patients had spontaneous reversion of atrial fibrillation to sinus rhythm and 62 patients had persistent atrial fibrillation. In those with spontaneous reversion, the longest duration of atrial fibrillation prior to the euthyroid state was 13 months. In those with persistent fibrillation, the shortest duration of atrial fibrillation prior to the euthyroid state was eight months. Almost three-quarters of those with spontaneous reversion had conversion to sinus rhythm within three weeks of becoming euthyroid. No spontaneous reversion occurred if atrial fibrillation was still present after the patients had been in a euthyroid state for four months. This study suggests that spontaneous reversion of atrial fibrillation to sinus rhythm is highly unlikely if the duration of atrial fibrillation before the euthyroid state is achieved exceeds 13 months, or if it is still present after the patient has been in a euthyroid state for four months, Cardioversion should be performed at about the 16th week after the euthyroid state is achieved.

Adult↗

A new method for colony formation in vitro by leukemic cells in acute nonlymphocytic leukemia with PHA-stimulated lymphocyte conditioned medium as stimulating factor.

A new agar culture system to clone specifically acute nonlymphocytic leukemia (ANLL) is described, which consists of two phases: an initial liquid phase in the presence of PHA-stimulated lymphocyte conditioned medium (PHA-LCM) and a semi-solid phase. By preincubation of leukemic cells with PHA-LCM in a liquid phase, leukemic cells were found to be more sensitive to forming colonies and clusters in agar medium. In addition, this PHA-two step assay could eliminate colony formation by T cell progenitors. The leukemic origin of the colonies was proven by electron-microscopic analysis, which demonstrated the presence of nuclear blebs and abnormal perinuclear fibril formation. Morphological studies also indicated myeloid differentiation of the cells in the leukemic colonies, although considerable variation was observed among patients. The wide range of linearity between the number of cells plated and the number of colonies grown permits quantitative assay of colony-forming leukemic cells (L-CFU). This assay should be valuable for studies of chemotherapy, growth regulation, and differentiation of L-CFU.

Acute Disease↗

Influences of prostaglandins on electrophoretic mobility and aggregation of rabbit platelets.

Influences of prostaglandin (PG)s on electrophoretic mobilities and aggregation of rabbit platelets were studied. The PGs studied (PGI2, PGE1, PGD2, PGF2 alpha, PGA2 and PGA1) had no effect on platelet electrophoretic mobility. However, both PGE1 and PGI2 in 0.3 and 3.0 muM inhibited ADP-induced aggregation and ADP-induced decrease in the mobility. PGD2 in 0.3 and 3.0, and PGE2 in 30 microM inhibited the aggregation but did not depress the ADP-induced decrease in the mobility. PGF2 alpha, PGA2 and PGA1 had no effect on the decrease in electrophoretic mobility and on the aggregation caused by ADP.

Adenosine Diphosphate↗

Inhibitory effect of tiaramide of aggregation in vivo and on electrophoresis of rabbit platelets.

Effects of tiaramide, aspirin an indomethacin were studied on rabbit platelet aggregation in vivo and on platelet electrophoretic mobility. When tiaramide (6 mg/kg), aspirin (30 mg/kg) or indomethacin (1.3 mg/kg) was injected into the ear vein of rabbit during 60 sec, tiaramide only inhibited ADP-induced aggregation, 20 min after the injection. All three drugs prevented collagen-induced aggregation 20 and 120 min after the injection. Tiaramide and aspirin prevented aggregation 24 hours later. The inhibitory effects on the aggregation of tiaramide are presumably independent of prostaglandin synthesis, because malondialdehyde (a metabolite of PGG2) production was not influenced. Tiaramide reduced cyclic AMP levels in platelets after 20 min incubation, despite the ability of this agent to inhibit platelet aggregation. Tiaramide, aspirin and indomethacin per se has no effect on platelet electrophoretic mobility, while tiaramide prevented the decrease in the mobility produced by ADP. Tiaramide and aspirin also depressed the decrease in the mobility produced by collagen.

Adenosine Diphosphate↗