Device, system and method for obtaining vital sign related information of a living being

The present invention relates to a device, system and method for obtaining vital sign related information of a living being (3). The proposed device comprises an input unit (12) for receiving an input signal (32) generated from light (31) received in at least one wavelength interval reflected from a skin region (2) of a living being (3), said input signal representing vital sign related information from which a vital sign of the living being can be 5 derived, a processing unit (14) for processing the input signal (32) and deriving vital sign related information (36) of said living being from said input signal (32), an orientation estimation unit (16) for estimating the orientation of said skin region (2), and a control unit (18) for controlling an illumination unit (40) for illuminating said skin region (3) with light (41) to illuminate said skin region (2) based on the estimated orientation of said skin region 10 (2) and/or for controlling said processing unit to derive vital sign related information (36) from said input signal obtained during time intervals selected based on the estimated orientation of said skin region (2).</p

System and method for obtaining vital sign related information of a living being

The present invention relates to a device, system and method for obtaining vital sign related information of a living being. The proposed device comprises an input unit for receiving an input signal generated from light received in at least one wavelength interval reflected from a skin region of a living being, said input signal representing vital sign related information from which a vital sign of the living being can be derived, a processing unit for processing the input signal and deriving vital sign related information of said living being from said input signal, an orientation estimation unit for estimating the orientation of said skin region, and a control unit for controlling an illumination unit for illuminating said skin region with light to illuminate said skin region based on the estimated orientation of said skin region and/or for controlling said processing unit to derive vital sign related information from said input signal obtained during time intervals selected based on the estimated orientation of said skin region.</p

Effect of helium pre- or postconditioning on signal transduction kinases in patients undergoing coronary artery bypass graft surgery

Background: The noble gas helium induces pre- and postconditioning in animals and humans. Volatile anesthetics induce cardioprotection in humans undergoing coronary artery bypass graft (CABG) surgery. We hypothesized that helium induces pre-and postconditioning in CABG-patients, affecting signaling molecules protein kinase C-epsilon (PKC-epsilon), p38 mitogen activated protein kinase (p38 MAPK), extracellular signal-regulated kinase 1/2 (ERK-1/2) and heat shock protein 27 (HSP-27) within cardiac tissue, and reducing postoperative troponin levels. Methods: After ethical approval and informed consent, 125 elective patients undergoing CABG surgery were randomised into this prospective, placebo controlled, investigator blinded, parallel arm single-centre study. Helium preconditioning (3 x 5 min of 70 % helium and 30 % oxygen) was applied before aortic cross clamping; postconditioning (15 min of helium) was applied before release of the aortic cross clamp. Signaling molecules were measured in right atrial appendix specimens. Troponin-T was measured at 4, 12, 24 and 48 h postoperatively. Results: Baseline characteristics of all groups were similar. Helium preconditioning did not significantly alter the primary outcome (molecular levels of kinases PKC-e and HSP-27, ratio of activated p38 MAPK or ERK 1/2). Postoperative troponin T was 11 arbitrary units [5, 31; area-under-the-curve (interquartile range)] for controls, and no statistically significant changes were observed after helium preconditioning [He-pre: 11 (6, 18)], helium postconditioning [He-post: 11 (8, 15)], helium pre-and postconditioning [He-PP: 14 (6, 20)] and after sevoflurane preconditioning [APC: 12 (8, 24), p = 0.13]. No adverse effects related to study treatment were observed in this study. Conclusions: No effect was observed of helium preconditioning, postconditioning or the combination thereof on activation of p38 MAPK, ERK 1/2 or levels of HSP27 and PKC-e in the human heart. Helium pre-and postconditioning did not affect postoperative troponin release in patients undergoing CABG surgery

European implementation of the '2014 ESC/ESA guideline on non-cardiac surgery: cardiovascular assessment and management'

BACKGROUND: Substandard implementation of a guideline is a major factor contributing to poor guideline adherence and has the potential to result in preventable patient harm. This study aims to quantify the uptake of the European guideline on non-cardiac surgery by European anesthetists. METHODS: This is a questionnaire-based cross-sectional study. Data was collected during Euroanaesthesia, the annual congresses of the Dutch Society of Anaesthesiology, European Association of Cardiothoracic Anaesthesiologists and European Society for Regional Anaesthesia and Pain Therapy in 2015. Primary endpoints were the implementation and knowledge scores derived from the questionnaires. RESULTS: The implementation score from 488 questionnaires was excellent in 4%, good in 14%, average in 22%, poor in 32% and very poor in 28% of the cases. The knowledge score was excellent in 1%, good in 27%, moderate in 49%, poor in 18% and very poor in 5% of the cases. CONCLUSIONS: Current implementation and knowledge of the guideline on non-cardiac surgery in Europe needs to be improved

Esophageal sphincter device for gastroesophageal reflux disease

BACKGROUND Patients with gastroesophageal reflux disease who have a partial response to proton-pump inhibitors often seek alternative therapy. We evaluated the safety and effectiveness of a new magnetic device to augment the lower esophageal sphincter. METHODS We prospectively assessed 100 patients with gastroesophageal reflux disease before and after sphincter augmentation. The study did not include a concurrent control group. The primary outcome measure was normalization of esophageal acid exposure or a 50% or greater reduction in exposure at 1 year. Secondary outcomes were 50% or greater improvement in quality of life related to gastroesophageal reflux disease and a 50% or greater reduction in the use of proton-pump inhibitors at 1 year. For each outcome, the prespecified definition of successful treatment was achievement of the outcome in at least 60% of the patients. The 3-year results of a 5-year study are reported. RESULTS The primary outcome was achieved in 64% of patients (95% confidence interval [CI], 54 to 73). For the secondary outcomes, a reduction of 50% or more in the use of proton-pump inhibitors occurred in 93% of patients, and there was improvement of 50% or more in quality-of-life scores in 92%, as compared with scores for patients assessed at baseline while they were not taking proton-pump inhibitors. The most frequent adverse event was dysphagia (in 68% of patients postoperatively, in 11% at 1 year, and in 4% at 3 years). Serious adverse events occurred in six patients, and in six patients the device was removed. CONCLUSIONS In this single-group evaluation of 100 patients before and after sphincter augmentation with a magnetic device, exposure to esophageal acid decreased, reflux symptoms improved, and use of proton-pump inhibitors decreased. Follow-up studies are needed to assess long-term safety. (Funded by Torax Medical; ClinicalTrials.gov number, NCT00776997.

Morphine induces preconditioning via activation of mitochondrial KCa channels

PURPOSE: Mitochondrial calcium sensitive potassium (mK(Ca)) channels are involved in cardioprotection induced by ischemic preconditioning. In the present study we investigated whether morphine-induced preconditioning also involves activation of mK(Ca) channels. METHODS: Isolated rat hearts (six groups; each n = 8) underwent global ischemia for 30 min followed by a 60-min reperfusion. Control animals were not further treated. Morphine preconditioning (MPC) was initiated by two five-minute cycles of morphine 1 muM infusion with one five-minute washout and one final ten-minute washout period before ischemia. The mK(Ca) blocker, paxilline 1 muM, was administered, with and without morphine administration (MPC + Pax and Pax). As a positive control, we added an ischemic preconditioning group (IPC) alone and combined with paxilline (IPC + Pax). At the end of reperfusion, infarct sizes were determined by triphenyltetrazoliumchloride staining. RESULTS: Infarct size was (mean +/- SD) 45 +/- 9% of the area at risk in the Control group. The infarct size was less in the morphine or ischemic preconditioning groups (MPC: 23 +/- 8%, IPC: 20 +/- 5%; each P < 0.05 vs Control). Infarct size reduction was abolished by paxilline (MPC + Pax: 37 +/- 7%, P < 0.05 vs MPC and IPC + Pax: 36 +/- 6%, P < 0.05 vs IPC), whereas paxilline alone had no effect (Pax: 46 +/- 7%, not significantly different from Control). CONCLUSION: Cardioprotection by morphine-induced preconditioning is mediated by activation of mK(Ca) channel