Training curriculum in minimally invasive emergency digestive surgery: 2022 WSES position paper.

Background: Minimally invasive surgery (MIS), including laparoscopic and robotic approaches, is widely adopted in elective digestive surgery, but selectively used for surgical emergencies. The present position paper summarizes the available evidence concerning the learning curve to achieve proficiency in emergency MIS and provides five expert opinion statements, which may form the basis for developing standardized curricula and training programs in emergency MIS.

Methods: This position paper was conducted according to the World Society of Emergency Surgery methodology.

Inactivation of platelet-derived TGF-β1 attenuates aortic stenosis progression in a robust murine model.

Aortic stenosis (AS) is a degenerative heart condition characterized by fibrosis and narrowing of aortic valves (AV), resulting in high wall shear stress (WSS) across valves. AS is associated with high plasma levels of transforming growth factor-β1 (TGF-β1), which can be activated by WSS to induce organ fibrosis, but the cellular source of TGF-β1 is not clear. Here, we show that platelet-derived TGF-β1 plays an important role in AS progression.

Platelet TGF-β1 deficiency decreases liver fibrosis in a mouse model of liver injury.

Transforming growth factor-β1 (TGF-β1) signaling in hepatic stellate cells (HSCs) plays a primary role in liver fibrosis, but the source of TGF-β1 is unclear. Because platelets are rich in TGF-β1, we examined the role of platelet TGF-β1 in liver fibrosis by challenging wild-type (WT) mice and mice deficient in platelet TGF-β1 ( with carbon tetrachloride (CCl), an inducer of acute hepatic injury and chronic fibrosis. CCl elicited equivalent hepatic injury in WT and mice based on loss of cytochrome P450 () expression, observed at 6 hours and peaking at 3 days after CCl challenge; mice exhibited less liver fibrosis than control mice.

HIV protease inhibitor-induced cardiac dysfunction and fibrosis is mediated by platelet-derived TGF-β1 and can be suppressed by exogenous carbon monoxide.

Human immunodeficiency virus (HIV) infection is an independent risk factor for cardiovascular disease. This risk is magnified by certain antiretrovirals, particularly the protease inhibitor ritonavir, but the pathophysiology of this connection is unknown. We postulated that a major mechanism for antiretroviral-associated cardiac disease is pathologic fibrosis linked to platelet activation with release and activation of transforming growth factor (TGF)-β1, and that these changes could be modeled in a murine system.

The impact of ionic mercury on antioxidant defenses in two mercury-sensitive anaerobic bacteria.

While the toxicological effects of mercury (Hg) are well studied in mammals, little is known about the mechanisms of toxicity to bacterial cells lacking an Hg resistance (mer) operon. We determined that Shewanella oneidensis MR-1 is more sensitive to ionic mercury [Hg(II)] under aerobic conditions than in fumarate reducing conditions, with minimum inhibitory concentrations of 0.25 and 2 μM respectively.