A Practical Approach to the Oncology Patient With Heart Failure.

Left ventricular systolic dysfunction is a significant cause of morbidity among cancer patients in whom this unfortunate complication develops. Investigation and management of chemotherapy- and radiation-induced cardiomyopathy in the emerging field of cardio-oncology involves a multidisciplinary approach between cardiology and oncology departments. The purpose of this article is to provide a practical approach to the cardiologist's assessment and management of cancer treatment-related cardiomyopathies.

Eating disorder behaviors and depression: a minimal relationship beyond social comparison, self-esteem, and body dissatisfaction.

Existing literature fails to comprehensively identify factors contributing to the comorbid relationship between eating disorder (ED) behaviors and unipolar depression. Maladaptive social comparison, body dissatisfaction, and low self-esteem are disruptive psychological patterns common to both constructs. It is unclear whether a unique relationship exists between depression and eating disorder behaviors beyond the effects exerted by this negative cognitive triad. The purpose of the present study is to examine whether a unique relationship exists between depression and ED behaviors after controlling for maladaptive social comparison, body dissatisfaction, and low self-esteem. We predict minimal unique variance in ED behaviors will be explained by depression after controlling for this negative cognitive triad.

Inhibition of apoB secretion from HepG2 cells by insulin is amplified by naringenin, independent of the insulin receptor.

Hepatic overproduction of apolipoprotein B (apoB)-containing lipoproteins is characteristic of the dyslipidemia associated with insulin resistance. Recently, we demonstrated that the flavonoid naringenin, like insulin, decreased apoB secretion from HepG2 cells by activation of both the phosphoinositide-3-kinase (PI3-K) pathway and the mitogen-activated protein kinase/extracellular-regulated kinase (MAPK(erk)) pathway. In the present study, we determined whether naringenin-induced signaling required the insulin receptor (IR) and sensitized the cell to the effects of insulin, and whether the kinetics of apoB assembly and secretion in cells exposed to naringenin were similar to those of insulin. Immunoblot analysis revealed that insulin stimulated maximal phosphorylation of IR and IR substrate-1 after 10 min, whereas naringenin did not affect either at any time point up to 60 min. The combination of naringenin and submaximal concentrations of insulin potentiated extracellular-regulated kinase 1/2 activation and enhanced upregulation of the LDL receptor, downregulation of microsomal triglyceride transfer protein expression, and inhibition of apoB-100 secretion. Multicompartmental modeling of apoB pulse-chase studies revealed that attenuation of secreted radiolabeled apoB in naringenin- or insulin-treated cells was similar under lipoprotein-deficient or oleate-stimulated conditions. Naringenin and insulin both stimulated intracellular apoB degradation via a kinetically defined rapid pathway. Therefore, naringenin, like insulin, inhibits apoB secretion through activation of both PI3-K and MAPK(erk) signaling, resulting in similar kinetics of apoB secretion. However, the mechanism for naringenin-induced signaling is independent of the IR. Naringenin represents a possible strategy for reduction of hepatic apoB secretion, particularly in the setting of insulin resistance.