Over the past decade and a half, homogenous gold catalysis has emerged as a diverse and rich field of research resulting in the continuous development of new methods for organic synthesis. The activation of alkynes towards nucleophilic attack by Au(I) and Au(III) complexes is a well-established mode of reactivity and the gold-catalyzed hydration and hydroalkoxylation of alkynes are two of the more well-explored reaction pathways. Although these classes of reactions have seen continuous development since their initial reports, achieving regioselectivity persists as one of the most challenging issues for this chemistry. This article aims to draw attention to the general problem of regioselectivity in these reactions. A select set of examples is presented to highlight the challenges and survey some of the strategies employed to address this problem.

Full-body patient simulators provide the technology and the environment necessary for excellent clinical education while eliminating risk to the patient. The extension of simulator-based training into management of basic and critical situations in complex patient populations is natural. We describe the derivation of an infant cardiovascular model through the redefinition of a complete set of parameters for an existing adult model. Specifically, we document a stepwise parameter estimation process, explicit simplifying assumptions, and sources for these parameters. The simulated vital signs are within the target hemodynamic variables, and the simulated systemic arterial pressure wave form and left ventricular pressure volume loop are realistic. The system reacts appropriately to blood loss, and incorporation of aortic stenosis is straightforward. This infant cardiovascular model can form the basis for screen-based educational simulations. The model is also an essential step in attaining a full-body, model-driven infant simulator.

Full-body patient simulators provide a technological basis for clinical education without risk to real patients. In a previous study, we described a model for educational simulation of infant cardiovascular physiology. Using essentially the same methodology, we derive a mathematical model for the cardiovascular system of a healthy 1-week-old neonate. Computer simulations of this model result in vital signs that are close to target hemodynamic variables. Simulated systemic arterial pressure waveform and left ventricular pressure-volume loop are realistic, and the system reacts appropriately to blood loss. We also adapt the model structure and change its parameters to reflect the congenital heart defects: patent ductus arteriosus, tetralogy of Fallot, complex coarctation of the aorta with patent foramen ovale, and transposition of the great arteries. Simulated vital signs are again close to target hemodynamic variables. The resulting model for neonatal cardiovascular pathophysiology is an essential step in attaining a full-body, model-driven neonatal acute care simulator.