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Aims Cardiac arrest (CA) is a major cause of mortality and survivors often develop neurologic deficits. The objective of this study was to determine the effect of CA and cardiopulmonary resuscitation (CPR) in mice on the EEG and neurologic outcomes, and identify biomarkers that can prognosticate poor outcomes. Main methods Video-EEG records were obtained at various periods following CA-CPR and examined manually to determine the presence of spikes and sharp-waves, and seizures. EEG power was calculated using a fast Fourier transform (FFT) algorithm. Key findings Fifty percent mice died within 72 h following CA and successful CPR. Universal suppression of the background EEG was observed in all mice following CA-CPR, however, a more severe and sustained reduction in EEG power occurred in the mice that did not survive beyond 72 h than those that survived until sacrificed. Spikes and sharp wave activity appeared in the cortex and hippocampus of all mice, but only one out of eight mice developed a purely electrographic seizure in the acute period after CA-CPR. Interestingly, none of the mice that died experienced any acute seizures. At 10 days after the CA-CPR, 25% of the mice developed spontaneous convulsive and nonconvulsive seizures that remained restricted to the hippocampus. The frequency of nonconvulsive seizures was higher than that of convulsive seizures. Significance A strong association between changes in EEG power and mortality following CA-CPR were observed in our study. Therefore, we suggest that the EEG power can be used to prognosticate mortality following CA-CPR induced global ischemia.

Glutamine (GLN) has been shown to be a key pharmaconutrient in the body's response to stress and injury. It exerts its protective effects via multiple mechanisms, including direct protection of cells and tissue from injury, attenuation inflammation, and preservation of metabolic function. Data support GLN as an ideal pharmacologic intervention to prevent or treat multiple organ dysfunction syndrome after sepsis or other injuries in the intensive care unit population. A large and growing body of clinical data shows that in well-defined critically ill patient groups GLN can be a life-saving intervention.

Purpose of review A growing body of data has revealed that specific nutrient deficiencies contribute to microvascular and cellular dysfunction following critical illness. Further, targeted administration of these 'pharmaconutrients' may reverse or improve this dysfunction and improve clinical outcome. Recent findings Specific nutrient therapy with glutamine protects cellular metabolism and vascular function via induction of heat shock proteins, which are key proteins found to be deficient following acute illness. Arginine becomes rapidly deficient following trauma and surgery. This leads to significant immunosuppression, which when treated by arginine administration significantly reduces postoperative infection. Omega-3 fatty acids attenuate the inflammatory response and provide for resolution of ongoing inflammatory injury via production of resolvins/protectins. Antioxidants (vitamin C and selenium) and trace elements (zinc) become rapidly depleted in critical illness and replacement appears vital to ensure optimal cellular and microvascular function. Data on targeted metabolic (mitochondrial) therapies (i.e. co-enzyme Q10) show promise to improve myocardial function following cardiac surgery. Summary These specific nutrients have newly discovered vital mechanistic roles in the optimization of cellular and microcirculatory function in critical illness and injury. A growing body of literature is demonstrating that correction of key nutrient deficiencies via therapeutic administration of these pharmaconutrients can improve clinical outcome in critically ill patients.

This study was designed to quantify and identify differences in protein levels between tumor and adjacent normal breast tissue from the same breast in 18 women with stage I/II ER positive/Her2/neu negative invasive breast cancer. Eighteen separate difference gel electrophoresis (DIGE) gels were run (1 gel per patient). Relative quantification was based on DIGE analysis. After excision and tryptic digestion, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and peptide mass mapping were used to identify protein spots. Two hundred and forty-three spots were differentially abundant between normal and cancer tissues. Fifty spots were identified: 41 were over abundant and nine were less abundant in cancers than in normal breast tissue. Western blotting provided independent confirmation for three of the most biologically and statistically interesting proteins. All 18 gels were replicated by another technician and 32% of the differentially abundant proteins were verified by the duplicate analysis. Follow-up studies are now examining these proteins as biomarkers in blood.

Activation of the coagulation system was evaluated in 30 patients with familial hyperlipoproteinemia (types II and IV), by measurement of high molecular weight fibrin(ogen) derivatives (HMWFD). These HMWFD can be separated from fibrinogen and its derivatives X, D, and E by gel filtration of plasma on 4% agarose columns. Type II patients had a higher plasma concentration of HMWFD (31.6% of total plasma fibrinogen-like material) than type IV patients (19.8%) or normal subjects (3.2%). The HMWFD were shown to consist at least in part of crosslinked fibrin by polyacrylamide gel electrophoresis. Serum fibrin(ogen) degradation products (FDP) were assayed by staphylococcal clumping test and tanned red cell hemagglutination inhibition immunoassay and were found to be normal in type II and type IV patients. Our data show that type II patients have increased circulating HMWFD, while type IV patients have lesser increases in these soluble fibrin complexes.