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J D Sweeney

Publications and source records attributed to J D Sweeney.

64 records · Page 4Linked to original sources

An implantable micropower command receiver for telemetry battery power switching.

Command receivers that control the functioning of additional implanted circuitry can be useful in many medical telemetry applications. The authors have designed and constructed a thick-film hybrid command receiver system that directly interfaces with the second-generation ICP telemetry system. This command receiver controls telemetry on/off state through enabling/disabling the telemetry pulse generator stage. Lithium battery powering of the implant is made practical through use of this command receiver. An automatic power shutdown feature is incorporated to guard against accidental battery drain. The unit uses two commercial CMOS integrated circuits, a transistor, a resistor and an RF coil.

Electric Power Supplies↗

p Phenotype in an Ecuadorian family.

The red cell phenotype 'p' is reported in an Ecuadorian family of Spanish descent. There are no previous confirmed reports of Ecuadorian individuals with this rare allele. The proband was not the product of a consanguineous marriage. This factor together with certain geographical and historical considerations support speculation that there may be a small cohort of homozygous 'p' individuals in the region.

Adolescent↗

Aprotinin, cardiac surgery, and factor V Leiden.

BACKGROUND: Aprotinin has been shown to reduce blood transfusion in cardiac surgery. Aprotinin inhibits activated protein C (APC). Patients with factor V (FV) Leiden have an inherited resistance to APC proteolysis. If the inhibition of APC by aprotinin contributes to its beneficial effect in cardiac surgery, then patients with FV Leiden undergoing cardiac surgery might be expected to require less transfusion than patients without FV Leiden. However, the use of aprotinin in such patients also could compromise the protein C regulatory pathway and precipitate a clinical thrombotic event. STUDY DESIGN AND METHODS: Patients undergoing cardiac surgery were studied for the presence of the FV Leiden defect by the use of a Russell's viper venom clot-based assay and polymerase chain reaction. The total amount of blood transfused was recorded for each patient. The effect of aprotinin on the plasma of normal and FV Leiden patients was studied. Further studies were performed on the direct inhibition of APC by aprotinin. RESULTS: Over an 18-month period, 162 patients were studied, of whom 13 (8%; 95% CI, 4.3-13.3%) were positive for FV Leiden. These 13 had a smaller requirement for blood transfusion than the to 13 matched controls. In vitro, aprotinin induced a FV Leiden defect in normal plasma and exacerbated the defect in the plasma of FV Leiden patients. Aprotinin inhibited APC in a dose-dependent manner, and kinetic analysis showed competitive inhibition with an inhibition constant of 4.5 microM (250 Kallikrein inhibitor units/mL). CONCLUSION: The inhibition of APC by aprotinin may contribute to its hemostatic effect. The use of aprotinin in patients with FV Leiden could cause extreme dysfunction of the protein C regulatory pathway, which could result in clinical thrombosis.

Aged↗

Progressive pressure expansion in skeletal muscle ventricle conditioning.

Skeletal muscle ventricle (SMV) conditioning typically results in reduced muscle performance. This study investigated the effects of progressive SMV resting pressure expansion and dynamic muscle training on SMV pumping capability. SMVs were formed from latissimus dorsi muscle in five goats. Three experimental SMVs were conditioned against a compliant pneumatic implant system. SMV resting pressure was progressively increased as the SMV adapted to each increment. Resting pressure rose from 40 to 100-120 mmHg over an 8 week period of time. Two control SMVs were conditioned against a non expanded incompressible implant. Both experimental and control SMVs were electrically burst stimulated for at least 6 weeks after an initial 2 week vascular delay interval. Results demonstrate that 1) experimental SMVs increased in volume; 2) SMV passive and active (evoked isovolumetric pressure) pressure-volume curves adapted to the increasing or static resting volume; and 3) two of three experimental SMVs generated greater stroke volumes than control SMVs across a range of counterpulsation pressures and electrical stimulation parameters. Progressive pressure expansion using a compliant implant system improved final SMV pumping performance and merits further investigation.

Adaptation, Physiological↗

Quality of platelet concentrates.

Despite the current emphasis in transfusion medicine on regulatory compliance and cost containment, there is continuing activity in quality improvement of blood products. Quality can be assessed by measuring both benefit and risk. High quality products are those in which the benefit is maximized and the risk minimized. Risk, in the context of platelet transfusions, is minimized by reducing infectious agents, sources of allergic reactions, and other factors likely to cause adverse reactions in recipients. Benefit can be better described as potency. Potency is the ability to produce a desired effect. For platelet concentrates, potency has both quantitative [platelet yield] and qualitative [platelet viability, survival, and function] components. There are many activities which may influence the potency of the final transfused platelet product and these are summarized in Figure 1. It is helpful to review each step in order to assess the potential impact on the potency of the final transfused product.

Blood Platelets↗