In addition protects the underlying tissues and thereby facilitating invasion. Patients suffering from COPD, for example, are frequently colonized by large numbers of Gram-negative or Grampositive bacteria, which produce and release large quantities of LPS, PG and LTA. Although the PAMP concentration required to elicit increased gliotoxin production in our experiments might be high as compared to typical systemic concentrations of bacteria infected patients, the local concentrations of PAMPs on the infected mucosal surfaces of the lung is likely to be much higher. In summary, we propose a theory that would explain how a bacterial infection possibly aggravates the mold co-infection rather than the traditional view that the mold infection clears a path for subsequent bacterial co-infections. In support of this, a recent study of aspergillosis patients showed that a systemic antibacterial treatment targeting the frequent co-infecting Pseudomonas aeruginosa, had a side effect of significantly diminishing the presence of Asperigillus fumigatus in the lungs. These results therefore advocate further investigation of the need to prioritize preventive suppression of pulmonary bacterial colonization in patients that have a high risk of contracting aspergillosis. Despite significant advances in anesthetic and surgical techniques, postoperative atrial fibrillation remains the most common complication after cardiac surgery. The incidence of POAF varies from 11% to 40%, depending on the definition and the method of monitoring. Although this arrhythmia is usually benign and self-limiting, it may result in hemodynamic Isoacteoside instability, a longer hospital stay, and increased health care costs. Given the clinical consequences a ributable to POAF, its prevention is of great importance. To date, many pharmacologic approaches have been a empted to prevent POAF, for example, b-blockers, amiodarone, and magnesium. Most reviews reflect a growing consensus in favor of the prophylactic administration of b-blockers for cardiac surgery patients. In addition, updated American College of Cardiology/American Heart Association 2006 guidelines recommend bblockers for the prevention of POAF. Despite the extensive studies, the exact pathophysiology of POAF is for the moment far from being fully elucidated. A growing body of evidence suggests that markers of inflammation and oxidative injury are elevated in atrial fibrillation patients. Carvedilol, a non-selective badrenergic blocking agent approved for use in heart failure cases, has a number of ancillary activities including antiinflammatory and antioxidant properties. Moreover, unlike other beta-blockers, carvedilol antagonizes the rapiddepolarizing sodium channel, the human ether-a-go-go-related gene potassium channel, and the L-type calcium channel, which suggests a pharmacologic profile similar to amiodarone, a proven anti-arrhythmic agent for the prevention of POAF. Theoretically, this should reduce the incidence of arrhythmia, including POAF. All these properties of carvedilol have generated interest in its use as a prophylactic agent for POAF. Recently, several Coptisine-chloride relevant studies regarding prophylactic carvedilol in preventing POAF have been published. However, the role of carvedilol in preventing POAF remains unknown.