Does increased experience with laparoscopic cholecystectomy yield more complex bile duct injuries?

Background: Two decades since the advent of laparoscopic cholecystectomy, the rate of bile duct injuries still remains higher than in the open cholecystectomy era.

Methods: The rate and complexity of bile duct injuries was evaluated in 83,449 patients who underwent laparoscopic cholecystectomy between 1995 and 2008 in the Kaiser Permanente Northern California system. Fifty-six surgeons who performed a laparoscopic cholecystectomy in the past were surveyed to determine factors that predispose to bile duct injuries.

Heparin protects against septic mortality via apoE-antagonism.

Background: Apolipoprotein E (apoE), a component of plasma lipoproteins, increases septic mortality in a rodent model of sepsis, presumably by enhancing lipid antigen presentation to antigen-presenting cells via the low-density lipoprotein receptor (LDLR). Downstream, this culminates in natural killer T (NKT) cell activation and cytokine secretion. To determine whether apoE antagonism would protect against septic mortality in mice, apoE-LDLR binding was antagonized using heparin, which can inhibit apoE's LDLR-binding site.

Chylomicrons combined with endotoxin moderate microvascular permeability.

Triglyceride-rich lipoprotein-bound endotoxin (CM-LPS) inhibits the host innate immune response to sepsis by attenuating the hepatocellular response to pro-inflammatory cytokine stimulation. This 'cytokine tolerance' in hepatocytes is a transient, receptor-dependent process that correlates with internalization of CM-LPS via low density lipoprotein (LDL) receptors. Since endothelial cells are integral to the immune response and similarly express LDL receptors, we hypothesized that CM-LPS could be internalized and ultimately attenuate the deleterious effects of pro-inflammatory molecules like tumor necrosis factor-α (TNF-α) and platelet activating factor (PAF) on endothelial permeability.