The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · Jan 2002
ReviewConsensus-based method for risk adjustment for surgery for congenital heart disease.
The aim was to develop a consensus-based method of risk adjustment for in-hospital mortality among children younger than 18 years after surgery for congenital heart disease (designated RACHS-1). ⋯ The RACHS-1 method should adjust for baseline risk differences and allow meaningful comparisons of in-hospital mortality for groups of children undergoing surgery for congenital heart disease.
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J. Thorac. Cardiovasc. Surg. · Jan 2002
Methicillin-resistant Staphylococcus aureus infection in a cardiac surgical unit.
Increased antibiotic resistance of common bacteria is attributed in part to the widespread use of various antibiotic agents. Prophylactic and therapeutic antibiotic treatments are routinely used in cardiac surgical units, and it is no surprise that methicillin-resistant Staphylococcus aureus infection is becoming a major cause of surgical infections in cardiac patients. ⋯ Mediastinal and other infections caused by methicillin-resistant Staphylococcus aureus have a significant morbidity in cardiac surgical patients. After an outbreak of methicillin-resistant Staphylococcus aureus mediastinal infections, several preventive measures to control methicillin-resistant Staphylococcus aureus contamination of surgical patients were implemented (nasal screening, preventive isolation, application of mupirocin, prophylaxis with vancomycin and alcohol gels) and were effective in decreasing the incidence of methicillin-resistant Staphylococcus aureus infection and mediastinitis after cardiac surgery.
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J. Thorac. Cardiovasc. Surg. · Jan 2002
Enhancement of Apo2L/TRAIL (tumor necrosis factor-related apoptosis-inducing ligand)-induced apoptosis in non-small cell lung cancer cell lines by chemotherapeutic agents without correlation to the expression level of cellular protease caspase-8 inhibitory protein.
Apo2L/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential anticancer drug that promotes apoptosis specifically in tumor cells. Because not all cancer cells are susceptible to Apo2L/TRAIL, the aim of our study was to determine whether non-small cell lung cancer cells can be sensitized by chemotherapeutic agents for Apo2L/TRAIL-induced apoptosis. In addition, endogenous expression levels of the caspase-inhibiting cellular protease caspase-8 inhibitory protein (C-FLIP) were measured to investigate partial resistance to Apo2L/TRAIL. ⋯ Apo2L/TRAIL-induced apoptosis in non-small cell lung cancer cell lines is significantly enhanced by chemotherapeutic agents. Resistance and sensitization to Apo2L/TRAIL are not correlated with the endogenous expression level of cellular protease caspase-8 inhibitory protein, implying that in non-small cell lung cancer other mechanisms are responsible for inhibition of the Apo2L/TRAIL pathway. Even though the molecular mechanism remains unclear, the combination of Apo2L/TRAIL with chemotherapy may be a promising treatment modality for non-small cell lung cancer.
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J. Thorac. Cardiovasc. Surg. · Jan 2002
Soluble Fas may be a proinflammatory marker after cardiopulmonary bypass in children.
Ischemia-reperfusion injury after cardiopulmonary bypass is known to provoke an inflammatory response, which can be attenuated with steroid pretreatment. Cardiopulmonary bypass is also known to stimulate apoptosis. Induction of the cellular apoptotic cascade occurs via interaction between two membrane receptors: Fas and Fas ligand. Both molecules also exist in soluble forms, whose significance remains undetermined; however, both may have a proinflammatory role. We aimed to document the temporal profile of soluble Fas and soluble Fas ligand after cardiopulmonary bypass and to investigate whether steroid pretreatment alters this response. ⋯ Release of soluble Fas and soluble Fas ligand follows a markedly different temporal profile after cardiopulmonary bypass. The similarity between soluble Fas and interleukin 6, together with the attenuation of both with steroids, may suggest a role for soluble Fas as a proinflammatory marker.