Factor X in freeze-dried factor- VIII reference plasma.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to I Robertson.
Explore the source record for details and available documents.
The stability of prothrombin and factor VII was studied using accelerated degradation tests in three preparations of freeze-dried pooled normal plasmas. In a previous report (Brozović, Gurd, Robertson, and Bangham, 1971) factor X was shown to be relatively unstable in these preparations of freeze-dried plasma: it was calculated that up to 8% of the original factor X activity would be lost after 10 years at -20 degrees C, up to 54% at 4 degrees C, and up to 90% at room temperature. The losses of factor VII activity were estimated to be negligible at -20 degrees C, between 2 and 18% at 4 degrees C, and between 20 and 70% of the original activity at 20 degrees C, after 10 years of storage. Prothrombin was found to be less stable than factor VII: the expected loss in 10 years at -20 degrees C may be up to 4%, at 4 degrees C up to 30%, and at 20 degrees C up to 83% of the initial activity. These findings indicate that in freeze-dried plasma prothrombin as well as factor X may be insufficiently stable for plasma to serve as long-term reference material for the standardization of the one-stage prothrombin time. Moreover, the loss of prothrombin and factor X in freeze-dried plasma stored at 4 degrees C may be so high that when it is required to preserve these factors it may be necessary to store freeze-dried plasma at lower temperatures.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Nadolol is a nonselective beta-adrenergic receptor antagonist used on a long-term basis for therapy of angina and hypertension. It has been reported to increase renal blood flow in humans. Theoretically, this could lead to an increase in glomerular filtration rate and improved renal sodium handling. The present study was designed to test whether patients receiving long-term nadolol therapy exhibited changes in whole-body composition that might arise as a consequence. Nine nadolol recipients with angina were followed for up to one year, and serial assessments were made of glomerular filtration rates and whole-body composition using in vivo neutron activation analysis to assess nitrogen, oxygen, sodium, potassium, chlorine, phosphorous, and calcium. No significant changes in these elements were observed. We conclude that any effect of nadolol on renal blood flow in short-term studies is not associated with significant changes in body composition measured over a period of one year.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Cognitive remediation programmes were delivered by microcomputer to three patients showing visual neglect using single-case experimental methodology with multiple-baseline across-function designs. The patients included one head injury case and two cases of cerebrovascular accident. Clear differences were produced in target functions. The most likely mechanism for this change was the learning of new verbal regulation strategies, although other, non-verbal, mechanisms may have been involved.
Three young men with attentional problems after severe head injury were given microcomputer based training involving a variety of tasks designed to ameliorate attentional problems. A multiple baseline across function single case experimental design showed these procedures to be effective in producing change specifically in the targetted function.
There remains controversy over the effects of angiotensin-converting enzyme inhibitors on renal function in patients with heart failure. Accordingly, we investigated the effects of long-term captopril therapy on renal function in 14 patients with congestive heart failure in a double-blind fashion. Creatinine clearance declined (from 61 +/- 21 to 56 +/- 21 ml/min; p less than 0.01), and both serum urea and creatinine rose. Glomerular filtration rate estimated radioisotopically also fell (from 53 +/- 19 to 48 +/- 18 ml/min), although this was not statistically significant. Effective renal plasma flow estimated radioisotopically increased (from 241 +/- 72 to 287 +/- 100 ml/min; p less than 0.05). Thus, filtration fraction--the ratio of glomerular filtration rate to effective renal plasma flow--fell. Because blood pressure also fell, the rise in renal plasma flow indicates a fall in calculated renal vascular resistance. Whole body sodium and chlorine, measured by total body in vivo neutron activation analysis, were unchanged, indicating no long-term natriuresis, despite evidence of clinical improvement. While converting enzyme inhibition causes symptomatic improvement in cardiac failure, there is a concomitant loss of compensatory direct effects of angiotensin II within the kidney, and hence usually some decline in renal function.