[Ultrasound-guided umbilical venous catheterisation: A cost-effectiveness analysis].

Introduction: Although the use of ultrasound for the insertion of central catheters has proven to be cost-effective in adults, it is not known if this is the case in the neonatal population. This study compared the cost-effectiveness of ultrasound-guided umbilical venous catheterisation with conventional catheterisation in a neonatal intensive care unit of a Public University Hospital.

Patients And Methods: A retrospective observational study was conducted on newborns that required an umbilical venous catheter before completing their first 24hours of extra-uterine life.

Gemfibrozil attenuates the inflammatory response and protects rats from abdominal sepsis.

Sepsis is a serious condition characterized by an infectious process that induces a severe systemic inflammatory response. In this study, the effects of gemfibrozil (GFZ) on the inflammatory response associated with abdominal sepsis were investigated using a rat model of cecal-ligation and puncture (CLP). Male Wistar rats were randomly divided into three groups: Sham-operated group (sham), where laparotomy was performed, the intestines were manipulated, and the cecum was ligated but not punctured; control group, subjected to CLP; and GFZ group, which received GFZ prior to undergoing CLP.

Hepatic ischemia/reperfusion injury is diminished by atorvastatin in Wistar rats.

Background And Aims: Temporal occlusion of the hepatoduodenal ligament (HDL) is often used during liver surgeries in order to reduce blood loss, resulting in ischemia/reperfusion injury (I/R). The aim of the study was to investigate the effects of atorvastatin (ATOR) on hepatic I/R injury and on serum levels of tumor necrosis factor-alpha (TNF-α), endothelin-1 (ET-1), antithrombin III (ATIII) and intracellular adhesion molecule-1 (ICAM-1).

Methods: Liver ischemia was induced in Wistar rats by clamping the HDL for 60 min, followed by either 60 or 180 min reperfusion.

Temporal relationship of serum markers and tissue damage during acute intestinal ischemia/reperfusion.

Objective: It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate.

Arachidonic acid derivatives and their role in peripheral nerve degeneration and regeneration.

After peripheral nerve injury, a process of axonal degradation, debris clearance, and subsequent regeneration is initiated by complex local signaling, called Wallerian degeneration (WD). This process is in part mediated by neuroglia as well as infiltrating inflammatory cells and regulated by inflammatory mediators such as cytokines, chemokines, and the activation of transcription factors also related to the inflammatory response. Part of this neuroimmune signaling is mediated by the innate immune system, including arachidonic acid (AA) derivatives such as prostaglandins and leukotrienes.

Comparative effects of triflusal, S-adenosylmethionine, and dextromethorphan over intestinal ischemia/reperfusion injury.

Ischemia/reperfusion (I/R) is a condition that stimulates an intense inflammatory response. No ideal treatment exists. Triflusal is an antiplatelet salicylate derivative with anti-inflammatory effects.

Ketamine reduces intestinal injury and inflammatory cell infiltration after ischemia/reperfusion in rats.

Purpose: Intestinal ischemia reperfusion (I/R) induces severe injury and significant mortality. New therapeutic interventions are needed; ketamine is an anesthetic with anti-inflammatory properties, which has shown protective effects on I/R in various organs. This study investigated effects of ketamine on intestinal I/R injury.

Molecular inflammatory mediators in peripheral nerve degeneration and regeneration.

Wallerian degeneration, the self-destructive set of cellular and molecular processes by which degenerating axons and myelin are cleared after injury, is initiated by macrophages and Schwann cells. Molecular inflammatory mediators such as cytokines (IL-1, IL-6, IL-10, and TNF-alpha, among others), transcription factors (NF-kappaB, c-Jun), the complement system and arachidonic acid metabolites have been shown to modulate these processes in various studies. However, the exact role that each of these mediators plays during axonal degeneration and regeneration has not been fully established.

Effect of sulfasalazine on renal ischemia/reperfusion injury in rats.

Renal ischemia/reperfusion (I/R) occurs during shock and transplant procedures, greatly affecting outcome. A definitive treatment has not been found. One of the pathophysiological bases of renal I/R injury is the activation of the transcription factor nuclear factor-kappaB (NF-KappaB).

The effects of NMDA receptor antagonists over intestinal ischemia/reperfusion injury in rats.

Intestinal ischemia/reperfusion causes severe injury and alters motility. N-methyl-D-aspartate (NMDA) receptor antagonists have been shown to reduce ischemia/reperfusion injury in the nervous system, and in other organs. In this study, we set out to investigate the effects of NMDA receptor antagonists over intestinal ischemia/reperfusion injury.

Different patterns of intestinal response to injury after arterial, venous or arteriovenous occlusion in rats.

Aim: To investigate the differences in injury patterns caused by arterial, venous or arteriovenous mesenteric occlusion.

Methods: Male Wistar rats were separated equally into four groups. Occlusion was performed by clamping the superior mesenteric artery (A), the mesenteric vein (V) or both (AV) for 30 min, followed by 60 min of reperfusion.

Celecoxib accelerates functional recovery after sciatic nerve crush in the rat.

The inflammatory response appears to be essential in the modulation of the degeneration and regeneration process after peripheral nerve injury. In injured nerves, cyclooxygenase-2 (COX-2) is strongly upregulated around the injury site, possibly playing a role in the regulation of the inflammatory response. In this study we investigated the effect of celecoxib, a COX-2 inhibitor, on functional recovery after sciatic nerve crush in rats.