Disease linked to a complication that is driven by 
reduced cytotoxic function Is sJIA with MAS a disease variant that has a distinct genetic profile, or is it a severe subtype of disease along a continuum in which all sJIA includes subclinical MAS Which antigen-presenting cells have a proinflammatory role in MAS The next years of sJIA research promise to be very exciting as answers to these questions emerge. Supplementary Material Refer to Web version on PubMed Central for supplementary material. Acknowledgments C. P. Vega, University of California, Irvine, CA, is the author of and is solely responsible for the content of the learning objectives, questions and answers of the Medscape, LLC-accredited continuing medical education activity associated with this article. Neurocognitive dysfunction is a common but poorly understood complication of Oleandrin site cardiopulmonary bypass. Depending on the definition, as many as 80% of patients undergoing CPB may manifest neurologic complications postoperatively 1. Neurologic deficits are commonly divided into two categories: Type 1 deficits include focal neurologic events such as stroke, stupor, and coma, while type 2 deficits are more global cognitive deficits such as memory loss, confusion, and deterioration in intellectual function 2. While type 1 deficits can usually be attributed to a specific cause, such as cerebral hypoperfusion or thromboembolic events, the etiology of type 2 
events is more vague. However, their incidence is similar to that of type 1 events 3, and they can be equally as devastating. A lack of understanding of the precipitating pathophysiology and inability to predict this type of injury only adds to the strain on both patients and their family members. A variety of pathologic processes including cerebral hypoperfusion, microembolization, inflammation, temperature changes, genetic predisposition, cerebral edema, or dysfunction of the blood-brain barrier have been implicated in NCD 4, 5. Cardiopulmonary bypass, while an get D-α-Tocopherol polyethylene glycol 1000 succinate essential component of the cardiac surgeon’s armamentarium, has significant deleterious effects on the human body related to the interaction of blood components with the artificial surfaces of the circuit, including activation of leukocytes, cytokine release, and increase in reactive oxygen species. Our group, as well as others, has previously demonstrated the association between systemic inflammation and NCD after CPB 6, 7. However, a comprehensive understanding of the precipitating and predisposing causes of NCD remains elusive, making accurate diagnosis and treatment difficult. High-throughput microarray analysis provides insight into the response of nearly the entire human genome to a particular disease, and thus is an intriguing technique for identifying regulatory pathways and genes involved in poorly understood disease processes. Microarray technology has progressed exponentially in the past decade with the completion of the human genome project, development of more comprehensive microchips, and introduction of powerful pathway analysis software. We previously used microarray methods to show that genes associated with inflammation, antigen presentation, and cellular adhesion were differentially regulated in patients exhibiting NCD after CPB. In this prior study PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19846406 same-group comparisons were made both in patients with NCD pre- and postoperatively as well in NORM patients pre- and postoperatively 8. We now compare NORM patients to those with J Thorac Cardiovasc Surg.Disease linked to a complication that is driven by reduced cytotoxic function Is sJIA with MAS a disease variant that has a distinct genetic profile, or is it a severe subtype of disease along a continuum in which all sJIA includes subclinical MAS Which antigen-presenting cells have a proinflammatory role in MAS The next years of sJIA research promise to be very exciting as answers to these questions emerge. Supplementary Material Refer to Web version on PubMed Central for supplementary material. Acknowledgments C. P. Vega, University of California, Irvine, CA, is the author of and is solely responsible for the content of the learning objectives, questions and answers of the Medscape, LLC-accredited continuing medical education activity associated with this article. Neurocognitive dysfunction is a common but poorly understood complication of cardiopulmonary bypass. Depending on the definition, as many as 80% of patients undergoing CPB may manifest neurologic complications postoperatively 1. Neurologic deficits are commonly divided into two categories: Type 1 deficits include focal neurologic events such as stroke, stupor, and coma, while type 2 deficits are more global cognitive deficits such as memory loss, confusion, and deterioration in intellectual function 2. While type 1 deficits can usually be attributed to a specific cause, such as cerebral hypoperfusion or thromboembolic events, the etiology of type 2 events is more vague. However, their incidence is similar to that of type 1 events 3, and they can be equally as devastating. A lack of understanding of the precipitating pathophysiology and inability to predict this type of injury only adds to the strain on both patients and their family members. A variety of pathologic processes including cerebral hypoperfusion, microembolization, inflammation, temperature changes, genetic predisposition, cerebral edema, or dysfunction of the blood-brain barrier have been implicated in NCD 4, 5. Cardiopulmonary bypass, while an essential component of the cardiac surgeon’s armamentarium, has significant deleterious effects on the human body related to the interaction of blood components with the artificial surfaces of the circuit, including activation of leukocytes, cytokine release, and increase in reactive oxygen species. Our group, as well as others, has previously demonstrated the association between systemic inflammation and NCD after CPB 6, 7. However, a comprehensive understanding of the precipitating and predisposing causes of NCD remains elusive, making accurate diagnosis and treatment difficult. High-throughput microarray analysis provides insight into the response of nearly the entire human genome to a particular disease, and thus is an intriguing technique for identifying regulatory pathways and genes involved in poorly understood disease processes. Microarray technology has progressed exponentially in the past decade with the completion of the human genome project, development of more comprehensive microchips, and introduction of powerful pathway analysis software. We previously used microarray methods to show that genes associated with inflammation, antigen presentation, and cellular adhesion were differentially regulated in patients exhibiting NCD after CPB. In this prior study PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19846406 same-group comparisons were made both in patients with NCD pre- and postoperatively as well in NORM patients pre- and postoperatively 8. We now compare NORM patients to those with J Thorac Cardiovasc Surg.