Treating PTSD Within the Context of Heightened Suicide Risk

Because posttraumatic stress disorder (PTSD) is one of the few psychological conditions that predict suicidal behavior among those who think about suicide, many patients with PTSD present clinically with elevated suicide risk. Expert consensus and practice guidelines recommend against trauma-focused treatments for patients with elevated suicide risk, however. Research aimed at understanding the common mechanisms that underlie the association of PTSD and suicide risk has led to several advances in the effective care of suicidal patients diagnosed with PTSD. Based on these results, various combinations and sequences of suicide-focused treatments, risk management procedures, and trauma-focused treatments are implicated.     

Mature dendritic cells use endocytic receptors to capture and present antigens

In response to inflammatory stimuli, dendritic cells (DCs) trigger the process of maturation, a terminal differentiation program required to initiate T-lymphocyte responses. A hallmark of maturation is down-regulation of endocytosis, which is widely assumed to restrict the ability of mature DCs to capture and present antigens encountered after the initial stimulus. We found that mature DCs continue to accumulate antigens, especially by receptor-mediated endocytosis and phagocytosis. Internalized antigens are transported normally to late endosomes and lysosomes, loaded onto MHC class II molecules (MHCII), and then presented efficiently to T cells. This occurs despite the fact that maturation results in the general depletion of MHCII from late endocytic compartments, with MHCII enrichment being typically thought to be a required feature of antigen processing and peptide loading compartments. Internalized antigens can also be cross-presented on MHC class I molecules, without any reduction in efficiency relative to immature DCs. Thus, although mature DCs markedly down-regulate their capacity for macropinocytosis, they continue to capture, process, and present antigens internalized via endocytic receptors, suggesting that they may continuously initiate responses to newly encountered antigens during the course of an infection.     

Rethinking surgical technique and priorities for pediatric tonsillectomy

The past 100 years have witnessed dramatic shifts in the concept of ideal surgical goals and operative technique in tonsil surgery. Surgeons are reviving a technique of intracapsular tonsillectomy with increasing precision thanks to modern technology. With intracapsular tonsillectomy, pediatric patients recover faster, use less pain medication, and have a lower risk of dehydration and hemorrhage. Various considerations will dictate the adoption of this technology in the coming years. This current review explores concepts and controversies surrounding tonsillectomy with a focus on quality improvement.     

Myasthenia Gravis—An Unexpected Cause of Respiratory Failure and Reversible Left Ventricular Dysfunction after Cardiac Surgery

Abstract We report a case of postpericardiotomy myasthenia gravis. A 68‐year‐old male patient without prior history of neuromuscular or autoimmune disorders presented with respiratory failure and severe left ventricular dysfunction four weeks after mitral valve replacement. Markedly elevated acetylcholine receptor antibodies were noted, and the patient responded promptly to immunologic therapy. Awareness of this rare but potentially fatal consequence of cardiac surgery may allow the early institution of specific treatment. (J Card Surg 2010;25:662‐664)     

Kappa and delta opioid receptor signaling is augmented in the failing heart

The opioidergic system, an endogenous stress pathway, modulates cardiac function. Furthermore, opioid peptide and receptor expression is altered in a number of cardiac pathologies. However, whether the response of myocardial opioid receptor signaling is altered in heart failure progression is currently unknown. Elucidating possible alterations in and effects of opioidergic signaling in the failing myocardium is of critical importance as opioids are commonly used for pain management, including in patients at risk for cardiovascular disease. A hamster model of cardiomyopathy and heart failure (Bio14.6) was used to investigate cardiac opioidergic signaling in heart failure development. This study found an augmented negative inotropic and lusitropic response to administration of agonists selective for the kappa opioid receptor and delta opioid receptor in the failing heart that was mediated by a pertussis toxin-sensitive G-protein. The augmented decrease in cardiac function was manifested by increased inhibition of cAMP accumulation and the amplitude of the systolic Ca²⁺ transient. Furthermore, increased depression of cardiac function and of two important second messengers, cAMP and intracellular Ca²⁺, were independent of changes in cardiac opioid peptide or receptor expression. Thus, the cardiomyopathy-induced failing heart experiences increased cardiac depressant effects following opioid receptor stimulation which could exacerbate diminished cardiac function in end-stage heart failure. As cardiac function is already depressed in heart failure patients, administration of opioids could exacerbate the degree of cardiac dysfunction and worsen disease progression.