The Effects of Cyclophosphamide on the Pharmacokinetics of Triiodothyronine in the Male Rat

In the present study, the possibility that cyclophosphamide or a cyclophosphamide metabolite may be accelerating the clearance of triiodothyronine has been examined. Following administration of exogenous triiodothyronine to saline-and cyclophosphamide-treated rats, the area under the plasma-concentration time curve (AUC), apparent clearance (CL_app) and half-life of triiodothyronine were measured. AUC (34.43 ± 12.34 compared with 33.32 ± 9.92 nmol hL^?1), CL_app (36.30 ± 12.89 compared with 37.51 ± 11.16 mLh^?1) and half-life (7.50 ± 1.39 compared with 6.40 ± 0.96 h) were not significantly different in the control rats compared with the cyclophosphamide-treated rats. As cyclophosphamide does not appear to alter the elimination of triiodothyronine, it is likely that cyclophosphamide or a cyclophosphamide metabolite is acting at the hypothalamo-pituitary axis, reducing the synthesis or release of thyroid stimulating hormone and consequently decreasing the levels of triiodothyronine and thyroxine.     

Stability of the Defibrillation Probability Curve with the Development of Ventricular Dysfunction in the Canine Rapid Paced Model

Most patients with implantable defibrillators have diminished cardiac function. Progressive heart failure might impair defibrillation efficacy, leading to interpreted device, failure. This study sought to determine the effect of ventricular dysfunction on defibrillation energy using a biphasic endocardial system. Eleven dogs were ventricularly paced at 225 pulses/min for 2 weeks to induce ventricular dysfunction, and five control dogs remained unpaced. Dose response defibrillation probability curves were generated for each animal at baseline, after 2 weeks (at which time the pacemakers were turned off in the paced group), and then 1 week later. The defibrillation thresholds, ED₂₀, ED₅₀, and ED₈₀ (the 20%, 50%, and 80% effective defibrillation energies, respectively) were determined for each dog at each study. In the paced dogs, the mean ejection fraction fell from 55% to 25% after pacing (P < 0.0001), and rose to 46% after its discontinuation (P = 0.0002). The defibrillation threshold, ED20, ED₅₀, and ED80 remained unchanged in both the control and paced groups for all three studies, even after adjustment for dog weight or left ventricular mass. Rapid pacing produced no change in left ventricular mass. It induced ventricular cavity dilatation and wall thinning, which had opposing effects on defibrillation energy requirements, resulting in no net change of the ED₅₀ in heart failure. In conclusion, the defibrillation efficacy of a biphasic transvenous system is not changed by the development of heart failure using the rapid paced canine model.     

Hyperglycaemia and mortality from acute stroke

Hyperglycaemia has been observed after acute stroke, and isassociated with a poor prognosis. It is not known whether thisis due to the stress response of the acute illness or whetherhyperglycaemia is, in itself, harmful to ischaemic nervous tissue.Seventy-one patients admitted to hospital with acute strokeand no history of diabetes or other acute illness were recruited,and fasting blood sampling was carried out within 24 h of symptomonset, for plasma glucose and stress hormones and levels ofhaemoglobin A1c (HbA1c). Computerized tomography of the brainwas carried out on 77% of the subjects. The subjects were followedup for 3 months or until death. Glucose levels were higher insubjects who died during the course of the study (p=0.025),but this relationship became non-significant after age (p<0.001) and cortisol (p= 0.001) levels were taken into accountwith multivariate analysis. The correlation between serum cortisoland the volume of the lesion on CT scan was also stronger thanthe relation of glucose with volume. Haemoglobin A1c had norelationship with either mortality or lesion volume. These findingssuggest that the hyperglycaemia seen after an acute stroke issecondary to a stress response and they do not support the theoryof hyperglycaemia being harmful to ischaemic nervous tissue.These findings have implications for the treatment of acutestroke with hypoglycaemic agents.     

Inhibition of 3,3',4,4',5-Pentachlorobiphenyl-Induced Chicken Embryotoxicity by 2,2',4,4',5,5'-Hexachlorobiphenyl

3,3',4,4',5-Pentachlorobiphenyl (pentaCB) caused a dose-dependentinduction of chicken embryolethality, malformations, edema,and liver lesions at doses ranging from 0.5 to 12.0 µg/kg.In contrast, no embryotoxicity was observed after treatmentwith 10, 25, or 50 mg/kg 2,2',4,4',5,5'-hexaCB. In eggs cotreatedwith 2.0 µ/kg, 3,3',4,4',5-pentaCB plus 10, 25, or 50mg/kg 2,2',4,4',5,5'-hexaCB, there was significant protectionfrom 3,3',4,4',5-pentaCB-induced embryo malformations, edema,and liver lesions, whereas no inhibition of embryolethalitywas observed. These results further extend the response-specificnonadditive interactions of binary mixtures of polychlorinatedbiphenyls (PCBs) and should be considered in the developmentof approaches for hazard assessment of PCB mixtures and relatedcompounds.     

What Can Health Communication Science Offer for ACA Implementation? Five Evidence-Informed Strategies for Expanding Medicaid Enrollment

Context: Implementing the Affordable Care Act (ACA) in 2014 will require effective enrollment and outreach efforts to previously uninsured individuals now eligible for coverage.Methods: From 1996 to 2013, the Health Communication Research Laboratory conducted more than 40 original studies with more than 30,000 participants to learn how to improve the reach to and effectiveness of health information for low-income and racial/ethnic minority populations. We synthesized the findings from this body of research and used them to inform current challenges in implementing the ACA.Findings: We found empirical support for 5 recommendations regarding partnerships, outreach, messages and messengers, life priorities of low-income individuals and families, and the information environment. We translated these into 12 action steps.Conclusions: Health communication science can inform the development and execution of strategies to increase the public''s understanding of the ACA and to support the enrollment of eligible individuals into Medicaid or the Health Insurance Marketplace.