17 research outputs found

    Simulating the Gradually Deteriorating Performance of an RTG

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    Degra (now in version 3) is a computer program that simulates the performance of a radioisotope thermoelectric generator (RTG) over its lifetime. Degra is provided with a graphical user interface that is used to edit input parameters that describe the initial state of the RTG and the time-varying loads and environment to which it will be exposed. Performance is computed by modeling the flows of heat from the radioactive source and through the thermocouples, also allowing for losses, to determine the temperature drop across the thermocouples. This temperature drop is used to determine the open-circuit voltage, electrical resistance, and thermal conductance of the thermocouples. Output power can then be computed by relating the open-circuit voltage and the electrical resistance of the thermocouples to a specified time-varying load voltage. Degra accounts for the gradual deterioration of performance attributable primarily to decay of the radioactive source and secondarily to gradual deterioration of the thermoelectric material. To provide guidance to an RTG designer, given a minimum of input, Degra computes the dimensions, masses, and thermal conductances of important internal structures as well as the overall external dimensions and total mass

    End-Stage Heart Failure with Multiple Intracardiac Thrombi: A Rescue Strategy

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    The use of ventricular assist devices as a bridge to transplantation has become a widely used option for patients with end-stage heart failure. In contrast to total artificial hearts, ventricular assist devices support the failing heart by bypassing one or both ventricles. In certain cases (myocardial tumors, graft failure, transplant rejection, endocarditis, intracardiac thrombus formation), however, it may be advantageous to excise the heart and replace it with an artificial device. Total artificial hearts are intracorporeal devices designed for this purpose. Unfortunately, some patients are too small or are, for other reasons, ineligible for a total artificial heart. We describe the case of a 55-year-old woman who had ischemic cardiomyopathy and thrombus formation in all 4 cardiac chambers. To reduce the risk of thromboembolic events, we elected to replace her heart completely with 2 extracorporeal ventricular assist devices. The heart was excised via a median sternotomy approach, and the outflow cannulae (from device to patient) were connected to both atrial remnants. The 2 inflow cannulae (from patient to device) were anastomosed end-to-end to the aorta and the pulmonary artery, respectively. After attaining a flow of more than 5 L, the 2 extracorporeal assist devices effectively and efficiently performed the work of the native heart. Thus re-established, organ perfusion was improved by this mechanically driven circulation, as signified by an initial decrease in creatinine and blood urea nitrogen levels. The patient, however, did not recover from postoperative neurological dysfunction and died of respiratory insufficiency and multiple-organ failure on the 26th postoperative day

    Organ-specific regulation of pro-inflammatory molecules in heart, lung, and kidney following brain death

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    Nonspecific inflammatory events following brain death may increase the intensity of the immunological host response. The present study investigated the course of pro-inflammatory molecules in heart, lung, kidney, and plasma after brain death induction. Brain death was induced in five pigs by inflation of an intracranial Foley catheter and five pigs were sham-operated as controls. Each experiment was terminated 6 h after brain death/sham operation and the organs were harvested. We measured the mRNA and protein levels for TNF-α, IL-1β, and IL-6 in heart, lung, kidney, and plasma. Additionally, the mRNA expression for IL-6R, ICAM-1, MCP-1, and TGF-β was determined in each organ. After 6 h, the plasma cytokine levels were higher in the brain-dead animals than in the sham-operated. In heart, lung, and kidney there was an increase in IL-6 and IL-1β following brain death, while TNF-α was up-regulated in lung only ( P < 0.05). MCP-1 and TGF-β were significantly higher in heart and lung and IL-6R increased in heart after brain death ( P < 0.05). Brain death was associated with non-uniform cytokine expression patterns in the investigated organs. These expression patterns may cause variable pro-inflammatory priming resulting in different degrees of damage and explain the organ-specific variation in outcomes after transplantations
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