Remifentanil and glucose suppress inflammation in a rat model of surgical stress.

Purpose: Postoperative stress produces an inflammatory response. Recent studies have shown that narcotic analgesics suppress the immune system. Nutritional management during perioperative care has also been reported to affect inflammation.

Vitamin E derivative ETS-GS reduces liver ischemia-reperfusion injury in rats.

Background: Ischemic liver injury is often the result of surgical procedures such as liver transplantation and hepatic resection. Liver damage occurs after reperfusion, leading to increased systemic inflammation. Recent studies have reported that vitamin E and glutathione can ameliorate ischemia-reperfusion (I/R) injury.

Alternate day calorie restriction improves systemic inflammation in a mouse model of sepsis induced by cecal ligation and puncture.

Background: Calorie restriction (CR) exerts cytoprotective effects by up-regulating survival factors, such as mammalian target of rapamycin (mTOR), sirtuin, and peroxisome proliferator-activated receptor-γ co-activator 1α (PGC-1α). These survival factors have well-established roles in attenuating the inflammatory response. However, it is unclear whether CR affects sepsis-related inflammation.

Total parenteral-nutrition-mediated dendritic-cell activation and infiltration into the small intestine in a rat model.

Purpose: Total parenteral nutrition (TPN) is commonly carried out in the clinical setting. However, effects of TPN on the immune system, including dendritic cells (DC), are not well understood. The purpose of this study was to determine whether TPN affects DC activation and infiltration into the intestinal barrier.

Dendritic cell activation in response to ischemia-reperfusion injury of the small intestine.

Purpose: Recent studies have increased our understanding of the important role that the immune system plays in ischemia-reperfusion (I/R) injury. Although dendritic cells (DCs) are important regulators of intestinal immunity, their role in the response to intestinal I/R injury is not well understood. The aim of this study was to determine whether I/R injury affects DC infiltration into the intestinal barrier.

Heat shock protein 72 protects insulin-secreting beta cells from lipopolysaccharide-induced endoplasmic reticulum stress.

Purpose: Hyperthermia-induced activation of stress response proteins allows cells to withstand metabolic insults. In this study we set out to determine whether insulin secretion by pancreatic beta cells was affected by the acute inflammatory response, systemic inflammation-induced hyperglycaemia, and whole-body hyperthermia. Given that systemic-inflammation induces ER stress, we further examined whether hyperthermia can attenuate the extent of LPS-induced ER stress.

Hyperglycemia contributes to cardiac dysfunction in a lipopolysaccharide-induced systemic inflammation model.

Objectives: Hyperglycemia is frequently observed in nondiabetic patients during acute illness. Furthermore, intensive insulin therapy significantly reduces mortality and morbidity due to several critical illnesses, including cardiac or infectious diseases. The purpose of this study was to determine whether cardiac function is affected by hyperglycemia and its treatment with insulin.

Danaparoid sodium prevents cerulein-induced acute pancreatitis in rats.

Systemic inflammatory mediators, including the protein high-mobility group box 1 (HMGB1), play an important role in the development of acute pancreatitis. Anticoagulants such as danaparoid sodium (DA) may be able to inhibit sepsis-induced inflammation, but the mechanism of action is not well understood. We hypothesized that DA would act as an inhibitor of inflammation and prevent cerulein-induced acute pancreatitis.

High-dose intravenous immunoglobulin G improves systemic inflammation in a rat model of CLP-induced sepsis.

Objective: Intravenous immunoglobulin therapy has been proposed as an advanced treatment for sepsis. Yet, its benefit remains unclear and the mechanism of action is poorly understood. One key mediator in the development of sepsis is high mobility group box 1 (HMGB1).