Biomedical subjects

T Sakamaki

Publications and source records attributed to T Sakamaki.

131 records · Page 8Linked to original sources

PubMed1975

Rapidly labeled intermediates in DNA replication in higher plants.

In detached Vicia embryos, the incorporation of [3-H] thymidine into DNA starts at about 25 h after the beginning of imbibition and reaches maximum at about 33 h. The DNA synthesized during the first replication phase was extracted. Alkaline sucrose density-gradient analyses of the DNA indicated the occurrence of several short pieces of rapidly labeled DNA having sedimentation values of approx. 10 S and 14 S, after a pulse for 5 to 10 min. Prolonged labeling and chase incubation led to a shift of the shorter fragments to longer ones of 19 S and 22 S or more, thus indicating the nature of intermediates during DNA replication of these short fragments.

Centrifugation, Density Gradient↗

PubMedDate not supplied

Follow-up study of slipped capital femoral epiphysis.

We studied 50 hips in 46 patients with slipped capital femoral epiphysis (SCFE). Seven patients with acute cases were treated by closed reduction with excellent results and without any known complication. The cases in the remaining 39 patients were of the chronic type. The method of treatment was determined according to the posterior tilting angle: in situ pinning for angles less than 30 degrees, intertrochanteric osteotomy for angles between 30 and 60 degrees, and subcapital wedge osteotomy for angles greater than 60 degrees. Chondrolysis was observed in one case treated with intertrochanteric osteotomy, and chondrolysis and avascular necrosis occurred in one case of subcapital wedge osteotomy.

Activities of Daily Living↗

PubMedDate not supplied

Humoral factor in pressor hyperresponsiveness in renal prehypertensive rabbits.

Prehypertensive rabbits with renal artery stenosis of 3 days' duration (one-kidney, one clip) are known to have increased pressor responses to norepinephrine and vasopressin; this pressor hyperresponsiveness is restored to normal by the angiotensin II (AII) antagonist, [ Sar1, Ile8 ] AII, even though plasma renin activity (PRA) and plasma AII concentrations are not elevated. In the present study, the cross-circulation of blood between conscious one-kidney, 3-day renal artery stenosis rabbits and conscious normal rabbits resulted in the transfer of pressor hyperresponsiveness to the normal rabbits, although both groups of rabbits had normal values for PRA. A similar cross-circulation of blood between one-kidney rabbits without renal artery stenosis and normal rabbits did not alter the pressor responsiveness of the normal rabbits to norepinephrine. It was concluded that a circulating humoral factor is involved in mediating pressor hyperresponsiveness in 3-day renal artery stenosis rabbits. To evaluate the interrelationship between AII and the hormonal hyperresponsiveness factor, an additional experiment was performed in which blood was cross-circulated between one-kidney, 3-day renal artery stenosis rabbits and normal rabbits, with the normal rabbits receiving [ Sar1, Ile8 ] AII immediately following cross-circulation. Administration of this AII antagonist to the normal rabbits prevented them from showing pressor hyperresponsiveness following the cross-circulation of blood. It is concluded that in this prehypertensive renal artery stenosis model the humoral hyperresponsiveness factor exerts its effect through AII mechanisms, rather than AII acting to increase the release or secretion of the hyperresponsiveness factor.

1-Sarcosine-8-Isoleucine Angiotensin II↗

PubMedDate not supplied

Pressor hyperresponsiveness in saline-infused rabbits.

Conscious rabbits infused intravenously (i.v.) with isotonic saline at 1.5 to 1.8 ml/min for 24 hours had greater pressor responses to norepinephrine (NE) than did normal control rabbits. Infusion of the angiotension II (ANG II) antagonist [Sar1, Ile8] ANG II did not decrease the exaggerated pressor responses to NE in saline-infused rabbits. Measurements of cardiac output (CO) as well as the pressor responses to NE before and after saline infusion revealed that, although saline infusion increased the CO and decreased total peripheral resistance (TPR), CO did not change during NE infusion either before or after saline infusion, but NE produced significantly greater increases in mean arterial pressure (MAP) and TPR after saline infusion than before the saline infusion. The cross-circulation of blood at 10 ml/min for 5 minutes between saline-infused donor rabbits and normal recipient rabbits resulted in pressor hyperresponsiveness to NE in the normal recipients. Similar cross-circulation experiments between pairs of normal rabbits did not alter the pressor responses to NE. These studies provided direct evidence that expansion of body fluid volumes by saline infusion results in pressor and vascular hyperresponsiveness. There was no evidence to indicate that ANG II was involved in the mechanisms producing this pressor hyperresponsiveness. Some circulating hormonal factor, however, was involved in mediating the pressor hyperresponsiveness following saline infusion. The results of this study are compatible with the concept that natriuretic hormone may play a role in promoting pressor hyperresponsiveness in saline-expanded animals.

Angiotensin II↗

PubMedDate not supplied

Follow-up study of the subcapital wedge osteotomy for severe chronic slipped capital femoral epiphysis.

Fifteen patients (18 hips) whose hips underwent subcapital wedge osteotomy for severe chronic slipped capital femoral epiphysis were studied. The results of 14 patients were excellent, and the patients themselves believed the results of the operation to be excellent. One patient had both avascular necrosis and cartilage necrosis. The postoperative follow-up period ranged from 2 to 17 years (average 10 years 3 months).

Adolescent↗