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个人简介
My research career was characterized by focus on two territories, including basic and clinical area. Recently, using bibliometric tools, we describe the current research activities of anesthesiology discipline and revealed the trend of academic publication activity in anesthesiology from 1995 to 2014 (Asian Journal of Anesthesiology).
In the basic research area, the major emphasis of my research is on the mechanism underlying different type of IV anesthetics for rhythmic sympathetic nerve activity. Our work uses an in vitro nerve-cord preparation or an in vitro nerve-brainstem-spinal cord preparation. One advantage in using these in vitro preparations to study sympathetic regulation is that the nutrition-supply and oxygen-supply have evaded blood circulation. Therefore, it is possible to exclude the influence of changes in hemodynamic conditions, which inevitably would alter central sympathetic outflow. Another advantage is that it permits the researcher to analyze drug effects with a precise control of extracellular drug concentrations on sympathetic activity in anesthetic-free and muscle relaxant-free conditions. In a series of studies, I and my colleagues showed that activating intraspinal adenosine A1 receptors, not A2 or A3 receptors, could down-regulate sympathetic outflow (European Journal of Pharmacology). In addition, by using blind whole cell, patch-clamp techniques to record splanchnic sympathetic preganglionic neuron, we demonstrated that baclofen activated intraspinal GABAB receptors and suppressed sympathetic nerve activity via a mixture of ion events that link to a change in Ca2+ conductance (Journal of Applied Physiology). We also showed that ketamine attenuated spinal sympathetic activity through mechanisms not mediated by N-methyl-D-aspartate receptors (Anesthesia and Analgesia). By using this in vitro nerve-cord preparation that allowed a better control of drug concentrations, we compared the effects of propofol and midazolam at sedative concentrations on sympathetic tone generation. These findings suggested that administration of 9-19 μM propofol or 0.7-0.9 μM midazolam, the clinically relevant concentrations for sedation, did not alter central sympathetic outflow at the spinal cord levels; however, propofol at a concentration of 86 μM, which could be achieved by a single-bolus loading dose to induce sedation, would depress central sympathetic activity (Acta Anaesthesiologica Scandinavica). Moreover, we showed that spinal sympathetic nerve discharge genesis is initiated from some spontaneously active sympathetic preganglionic neurons, which are capable of TTX- or MECA-resistant c-Fos expression (Journal of Biomedical Science). We also showed a novel computational solution of spike overlapping using data-based subtraction algorithms to resolve synchronous sympathetic nerve discharge (Frontiers in Computational Neuroscience); using this computational solution to prove that fine-tuning of ionotropic glutamate receptor activities in the spinal cord may serve as a simple way for heterogeneous regulation of various sympathetic-targeting tissues (Autonomic Neuroscience: Basic and Clinical). Recently, our data suggest that NO orchestrates a repertoire of excitatory and inhibitory neurotransmissions and thus, alters sympathetic firing in a manner of power-law firing modulations (Frontiers in Physiology).
In the clinical research area, the major emphasis of my research is on the mechanism underlying dexamethasone and antiemetic. In a series of clinical research, I and my colleagues investigated the clinical application of the antiemetic action of dexamethasone; our results demonstrated that dexamethasone could reduce vomiting after thyroidectomy (Anesthesia and Analgesia), laparoscopic operations (British Journal of Anaesthesia, British Journal of Anaesthesia), tympanomastoid surgery (Laryngoscope), and epidural morphine (Anesthesia and Analgesia). In a series of animal studies, we explored the antiemetic mechanism of dexamethasone; our result demonstrated that dexamethasone reduced xylazine-induced emesis in cats (American Journal of Veterinary Research). Most importantly, by using the methodology of stereotaxic microinjection, we demonstrated that bilateral nuclei tractus solitarius could be the sites of the antiemetic action of dexamethasone and glucocorticoid receptor might play the pivotal part in this mechanism (Anesthesia and Analgesia). In summary, we published two review articles about dexamethasone prevents postoperative nausea and vomiting: benefit versus risk (Acta Anaesthesiologica Taiwan) and the cellular mechanisms of the antiemetic action of dexamethasone (European Journal of Pharmacology).
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