Within the confines of the SAE definitions used, use of anesthesia professionals does not appear to bring a safety benefit to patients receiving colonoscopy and is associated with an increased SAE risk for ASA I, II, and III patients undergoing EGD.

Our results show that epicardial-level of I(to) acts as a negative, rather than positive regulator of myocyte mechanical properties in canine ventricular myocytes.

The Extended Observer's Assessment of Alertness and Sedation (or EOAA/S) extends the range of the widely used MOAA/S score to include truly noxious stimulation, thereby enabling the identification of drug-induced central nervous system depression representative of surgical anaesthesia.

Background:Laparoscopic surgery is increasingly replacing the open procedure because of its many patient-related benefits that are well aligned with policies and programs that seek to optimize health system performance. However, widespread adoption of laparoscopic surgery has been slow, in part, because of the complexity of laparoscopic suturing. The objective of this study was to review the clinical and economic impacts of laparoscopic suturing in key procedures and to assess its role as a barrier to the broader adoption of laparoscopic surgery.Database:A medical literature search of MEDLINE, EMBASE, and BIOSIS from January 2010 through June 2016 identified 47 relevant articles.Conclusion:Laparoscopic suturing and intracorporeal knot tying may result in extended surgical time, complications, and surgeon errors, while improving patient quality of life through improved cosmesis, diet toleration, and better bowel movements. Despite advancement in surgical techniques and the availability of newer surgical tools, the complexity of laparoscopic suturing continues to be a barrier to greater adoption of MIS. The results of the study underscore the need for development of proficiency in laparoscopic suturing, which may help improve patient outcomes and reduce healthcare costs.

Ischemic heart disease is a common cause of end-stage heart failure and has persisted as one of the main causes of end stage heart failure requiring transplantation. Maladaptive myocardial remodeling due to ischemic injury involves multiple cell types and physiologic mechanisms. Pathogenic post-infarct remodeling involves collagen deposition, chamber dilatation and ventricular dysfunction. There have been significant improvements in medication and revascularization strategies. However, despite medical optimization and opportunities to restore blood flow, physicians lack therapies that directly access and manipulate the heart to promote healthy post-infarct myocardial remodeling. Strategies are now arising that use bioactive materials to promote cardiac regeneration by promoting angiogenesis and inhibiting cardiac fibrosis; and many of these strategies leverage the unique advantage of cardiac surgery to directly visualize and manipulate the heart. Although cellular-based strategies are emerging, multiple barriers exist for clinical translation. Acellular materials have also demonstrated preclinical therapeutic potential to promote angiogenesis and attenuate fibrosis and may be able to surmount these translational barriers. Within this review we outline various acellular biomaterials and we define epicardial infarct repair and intramyocardial injection, which focus on administering bioactive materials to the cardiac epicardium and myocardium respectively to promote cardiac regeneration. In conjunction with optimized medical therapy and revascularization, these techniques show promise to upregulate pathways of cardiac regeneration to preserve heart function.

Phospholamban (PLN), the reversible inhibitor of the sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA2a), is a key regulator of myocyte Ca(2+) cycling with a significant role in heart failure. We previously showed that the single amino acid difference between human and mouse PLN results in increased inhibition of Ca(2+) cycling and cardiac remodeling and attenuated stress responses in transgenic mice expressing the human PLN (hPLN) in the null background. Here we dissect the molecular and electrophysiological processes triggered by the superinhibitory hPLN in the mouse. Using a multidisciplinary approach, we performed global gene expression analysis, electrophysiology, and mathematical simulations on hPLN mice. We identified significant changes in a series of Na(+) and K(+) homeostasis genes/proteins (including Kcnd2, Scn9a, Slc8a1) and ionic conductance (including L-type Ca(2+) current, Na(+)/Ca(2+) exchanger, transient outward K(+) current). Simulation analysis suggests that this electrical remodeling has a critical role in rescuing cardiac function by improving sarcoplasmic reticulum Ca(2+) load and overall Ca(2+) dynamics. Furthermore, multiple structural and transcription factor gene expression changes indicate an ongoing structural remodeling process, favoring hypertrophy and myogenesis while suppressing apoptosis and progression to heart failure. Our findings expand current understanding of the hPLN function and provide additional insights into the downstream implications of SERCA2a superinhibition in the mammalian heart.

Anesthesiologists determined arterial oxygenation to be the most important physiological variable in assessing sedation risk and the potential for adverse clinical outcomes. AUCDesat, a composite index that incorporates duration, incidence, and depth of oxygen desaturation, was better correlated to the Likert scores. AUCDesat, given that it is a single numerical variable, is an ideal end point for assessment of risk of adverse clinical outcomes in clinical sedation studies. Future studies using AUCDesat and actual physiological outcomes may be useful in further defining this end point.

The Brugada syndrome (BrS) is a right ventricular (RV) arrhythmia that is responsible for up to 12% of sudden cardiac deaths. The aims of our study were to determine the cellular mechanisms of the electrical abnormality in BrS and the potential basis of the RV contractile abnormality observed in the syndrome. Tetrodotoxin was used to reduce cardiac Na(+) current (I(Na)) to mimic a BrS-like setting in canine ventricular myocytes. Moderate reduction (<50%) of I(Na) with tetrodotoxin resulted in all-or-none repolarization in a fraction of RV epicardial myocytes. Dynamic clamp and modeling show that reduction of I(Na) shifts the action potential (AP) duration-transient outward current (I(to)) density curve to the left and has a biphasic effect on AP duration. In the presence of a large I(to), I(Na) reduction either prolongs or collapses the AP, depending on the exact density of I(to). These repolarization changes reduce Ca(2+) influx and sarcoplasmic reticulum load, resulting in marked attenuation of myocyte contraction and Ca(2+) transient in RV epicardial myocytes. We conclude that I(Na) reduction alters repolarization by reducing the threshold for I(to)-induced all-or-none repolarization. These cellular electrical changes suppress myocyte excitation-contraction coupling and contraction and may be a contributing factor to the contractile abnormality of the RV wall in BrS.