Even though robotic technology holds great potential for performing spinal surgery and advancing neurosurgical techniques, it is of utmost importance to establish its practicality and to demonstrate better clinical outcomes compared with traditional techniques, especially in the current cost-effective era. Several systems have proved to be safe and reliable in the execution of tasks on a routine basis, are commercially available, and are used for specific indications in spine surgery. However, workflow, usability, interdisciplinary setups, efficacy, and cost-effectiveness have to be proven prospectively. This article includes a short description of robotic structures and workflow, followed by preliminary results of a randomized prospective study comparing conventional free-hand techniques with routine spine navigation and robotic-assisted procedures. Additionally, we present cases performed with a spinal robotic device, assessing not only the accuracy of the robotic-assisted procedure but also other factors (eg, minimal invasiveness, radiation dosage, and learning curves). Currently, the use of robotics in spinal surgery greatly enhances the application of minimally invasive procedures by increasing accuracy and reducing radiation exposure for patients and surgeons compared with standard procedures. Second-generation hardware and software upgrades of existing devices will enhance workflow and intraoperative setup. As more studies are published in this field, robot-assisted therapies will gain wider acceptance in the near future.

Minute-by-minute ICP/MABP data contain relevant information for autoregulation monitoring. In this study, the authors' new method based on minute-by-minute data resolution allowed for CPPopt calculation in nearly the entire monitoring time. This will facilitate the use of pressure reactivity monitoring in all ICUs.

The stimulation of cell proliferation by insulin like growth factor IGF-1 has previously been shown to depend on activation of voltage gated K(+) channels. The signaling involved in activation of voltage gated K(+) channel Kv1.3 includes the phosphatidylinositol-3 (PI3) protein kinase, 3-phosphoinositide dependent protein kinase PDK1 and the serum and glucocorticoid inducible kinase SGK1. However, nothing is known about mechanisms mediating the stimulation of Kv1.3 by SGK1. Most recently, SGK1 has been shown to phosphorylate and thus inactivate the ubiquitin ligase Nedd4-2. The present study has been performed to explore whether the regulation of Kv1.3 involves Nedd4-2. To this end Kv1.3 has been expressed in Xenopus oocytes with or without coexpression of Nedd4-2 and/or constitutively active (S422D)SGK1. In oocytes expressing Kv1.3 but not in water injected oocytes, depolarization from a holding potential of -80 mV to +20 mV triggers rapidly inactivating currents typical for Kv1.3. Coexpression of Nedd4-2 decreases, coexpression of (S422D)SGK1 enhances the currents significantly. The effects of either Nedd4-2 or of SGK1 are abrogated by destruction of the respective catalytic subunits ((C938S)Nedd4-2 or (K127N)SGK1). Further experiments revealed that wild type SGK1 and SGK3 and to a lesser extent SGK2 are similarly effective in stimulating Kv1.3 in both, presence and absence of Nedd4-2. It is concluded that Kv1.3 is downregulated by Nedd4-2 and stimulates by SGK1, SGK2, and SGK3. The data thus disclose a novel mechanism of Kv1.3 channel regulation.

The serum and glucocorticoid inducible kinase (SGK1) is well known to up-regulate the renal epithelial Na⁺ channel ENaC. Excessive SGK1 activity would be expected to cause renal Na⁺ retention and blood pressure increase. Certain polymorphisms of the SGK1 gene (E8CC/CT;I6CC) are indeed associated with moderately enhanced blood pressure. We have recently disclosed another function of SGK1, i.e. the stimulation of the slowly activating K⁺ channel KCNE1/KCNQ1. Among the functions of this channel is the repolarisation of cardiac myocytes. Accordingly, defective KCNE1 and/or KCNQ1 lead to long QT syndrome, a disorder causing fainting and sudden cardiac death. In the present study we demonstrate that coexpression of SGK1 in Xenopus oocytes increases KCNQ1/KCNE1 induced current without significantly altering voltage dependence, activation and deactivation kinetics. To test for the relevance of SGK1 in human cardiac repolarization, we analysed the ECG of monozygotic (MZ) (126 pairs) and dizygotic (DZ) (70 pairs) twin subjects and parents of DZ twins. The E8CC/CT;I6CC polymorphism was indeed significantly (p<0.025) associated with shortened age and gender corrected QT interval. No significant differences were observed in any other ECG parameter, including heart rate, P, PQ and QRS. We conclude that the regulation of KCNE1/KCNQ1 by SGK1 is similarly relevant for the repolarization of cardiac myocytes as for regulation of renal ENaC activity and blood pressure control.

Human ether-a-go-go (HERG) channels participate in the repolarization of the cardiac action potential. Loss of function mutations of HERG lead to delayed cardiac repolarization reflected by prolonged QT interval. HERG channels are regulated through a signaling cascade involving phosphatidylinositol 3 (PI3) kinase. Downstream targets of PI3 kinase include the serum and glucocorticoid inducible kinase (SGK) and protein kinase B (PKB) isoforms. The present study has been performed to explore whether SGK1 and SGK3 participate in the regulation of HERG channel activity. HERG was expressed in Xenopus oocytes with or without additional expression of SGK1 or SGK3. Chemiluminescence was employed to determine HERG plasma membrane protein abundance. Coexpression of SGK3 but not of SGK1 in Xenopus oocytes resulted in an increase of steady state current (I_HERG) and enhanced cell membrane protein abundance without affecting gating kinetics of the channel. Replacement of serine by alanine at the two SGK consensus sites decreased I_HERG but neither mutation abolished the stimulating effect of SGK3. In conclusion, SGK3 participates in the regulation of HERG by increasing HERG protein abundance in the plasma membrane and may thus modify the duration of the cardiac action potential.