Managing Friends and Foes: Sanctioning Mutualists in Mixed-Infection Nodules Trades off With Defense Against Antagonists.

Successful plant growth requires plants to minimize harm from antagonists and maximize benefit from mutualists. However, these outcomes may be difficult to achieve simultaneously, since plant defenses activated in response to antagonists can compromise mutualism function, and plant resources allocated to defense may trade off with resources allocated to managing mutualists. Here, we investigate how antagonist attack affects plant ability to manage mutualists with sanctions, in which a plant rewards cooperative mutualists and/or punishes uncooperative mutualists.

Integrated hepatic transcriptomics and metabolomics identify Pck1 as a key factor in the broad dysregulation induced by vehicle pollutants.

Background: Exposure to air pollution is associated with worldwide morbidity and mortality. Diesel exhaust (DE) emissions are important contributors which induce vascular inflammation and metabolic disturbances by unknown mechanisms. We aimed to determine molecular pathways activated by DE in the liver that could be responsible for its cardiometabolic toxicity.

Extramedullary Hematopoiesis in Serous Cavity Fluids: A Closer Look at This Rare Phenomenon With Diagnostic Pitfalls and Prognostic Significance.

Background: Extramedullary hematopoiesis (EMH) is usually seen in the reticuloendothelial system such as the spleen and liver; however, there have been rare case reports when EMH is seen in serous fluids (SFs). The aim of this study included analyzing the cytomorphological features of EMH in SFs in correlation with various clinicopathologic parameters and recognizing potential diagnostic pitfalls as well as their prognostic significance.

Methods: Clinicopathologic parameters and radiologic and pathologic information from the patients with a cytologic diagnosis of EMH were evaluated with cytology slides.

Conditional ablation of MCU exacerbated cardiac pathology in a genetic arrhythmic model of CPVT.

Background: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a genetic arrhythmic syndrome caused by mutations in the calcium (Ca) release channel ryanodine receptor (RyR2) and its accessory proteins. These mutations make the channel leaky, resulting in Ca-dependent arrhythmias. Besides arrhythmias, CPVT hearts typically lack structural cardiac remodeling, a characteristic often observed in other cardiac conditions (heart failure, prediabetes) also marked by RyR2 leak.