Data_Sheet_1_Desflurane is risk factor for postoperative delirium in older patients’ independent from intraoperative burst suppression duration.pdf

BackgroundPostoperative Delirium (POD) is the most frequent neurocognitive complication after general anesthesia in older patients. The development of POD is associated with prolonged periods of burst suppression activity in the intraoperative electroencephalogram (EEG). The risk to present burst suppression activity depends not only on the age of the patient but is also more frequent during propofol anesthesia as compared to inhalative anesthesia. The aim of our study is to determine, if the risk to develop POD differs depending on the anesthetic agent given and if this correlates with a longer duration of intraoperative burst suppression.MethodsIn this secondary analysis of the SuDoCo trail [ISRCTN 36437985] 1277 patients, older than 60 years undergoing general anesthesia were included. We preprocessed and analyzed the raw EEG files from each patient and evaluated the intraoperative burst suppression duration. In a logistic regression analysis, we assessed the impact of burst suppression duration and anesthetic agent used for maintenance on the risk to develop POD.Results18.7% of patients developed POD. Burst suppression duration was prolonged in POD patients (POD 27.5 min ± 21.3 min vs. NoPOD 21.4 ± 16.2 min, p ConclusionWe found a significantly increased risk to develop POD after desflurane anesthesia in older patients, even though burst suppression duration was shorter under desflurane anesthesia as compared to propofol anesthesia. Our finding might help to explain some discrepancies in studies analyzing the impact of burst suppression duration and EEG-guided anesthesia on the risk to develop POD.</p

MOESM1 of Accuracy, reliability, feasibility and nurse acceptance of a subcutaneous continuous glucose management system in critically ill patients: a prospective clinical trial

Additional file 1: Supplementary Method. CGM Device. Supplementary Tables. Table S1. The local insulin protocol. Table S2. Detection of dysglycemic events. Table S3a. Confounding factors on MARD. Table S3b. Spearman´s correlation of paO2, temperature, lactate, pH-value, hemoglobin, potassium and SOFA-Score and MARD. Supplementary Figures. Fig. S1. Correlation of blood glucose variability per patient and MARD per patient. Fig. S2. MARD after time-shifting the reference a fixed amount (1 up to 30 minutes). Fig. S3. Nurse questionnaire

Additional file 3: Figure S2. of Critical illness polyneuropathy in ICU patients is related to reduced motor nerve excitability caused by reduced sodium permeability

MEMFIT data showing best fit of current changes in % for critical illness polyneuropathy patients. GKfl, internodal fast K conductance; GKfN, nodal fast K conductance; GKsN, nodal slow K conductance; PNa p (%), percent of persistent Na; P Na N, nodal sodium permeability; GLkN, nodal leak conductance; IPumpNI, pump currents; GKsI, internodal slow K conductance). (TIF 112 kb

Additional file 1: Table S1. of Critical illness polyneuropathy in ICU patients is related to reduced motor nerve excitability caused by reduced sodium permeability

Electrophysiological data. neCMAP, nerve evoked compound muscle action potential amplitude; SNAP, sensory nerve action potential amplitude; dmCMAP, direct muscle evoked compound muscle action potential amplitude. p value compares ICU controls versus CIP patients (Mann-Whitney U). Values are given as mean ± SD. Table S2. Laboratory data p value compares ICU controls with CIP patients. pCO, partial arterial pressure of carbon dioxide; pO2, partial arterial pressure of oxygen; HCO3, bicarbonate; Na, sodium; K, potassium; Ca, calcium. (DOC 52 kb

The Role of Excitation Energy in Photobrightening and Photodegradation of Halide Perovskite Thin Films

We study the impact of excitation energy on the photostability of methylammonium lead triiodide (CH₃NH₃PbI₃ or MAPI) perovskite thin films. Light soaking leads to a transient increase of the photoluminescence efficiency at excitation wavelengths longer than 520 nm, whereas light-induced degradation occurs when exciting the films with wavelengths shorter than 520 nm. X-ray diffraction and extinction measurements reveal the light-induced decomposition of CH₃NH₃PbI₃ to lead iodide (PbI₂) for the high-energy excitation regime. We propose a model explaining the energy dependence of the photostability that involves the photoexcitation of residual PbI₂ species in the perovskite triggering the decomposition of CH₃NH₃PbI₃

Apoptosis in the retina is restricted to the S334ter rat model.

<p>The analysis of BAX expression, mitochondrial cytochrome c release, activation of caspase-9 and -3 shows essentially no positive detection in 9 out of 10 animal models for hereditary retinal degeneration. The notable exception was the S334ter transgenic rat which harbours a mutation in the rhodopsin gene leading to a truncated protein and in which many photoreceptors were positive for apoptosis. In all other animal models, while there were cells displaying clear evidence for apoptosis, their numbers were within the wild-type levels, indicating that this was related to physiological, developmental cell death, which is characteristic for the postnatal rodent retina. Importantly, the numbers of apoptotic cells did not match the numbers of mutation-induced dying cells as evidenced by the TUNEL assay. Scale bar 20 µm.</p

List of antibodies used in this study.

<p>List of antibodies used in this study.</p

Cell death in hereditary retinal degeneration is predominantly non-apoptotic.

<p>In 10 out of 10 animal models for hereditary retinal degeneration, large numbers of photoreceptors display cGMP accumulation, HDAC and PARP activity, PAR accumulation, and calpain activity, respectively. Intriguingly, these non-apoptotic markers are prominent even in the S334ter retina, concomitant with this also showing signs of apoptosis. This suggests that in S334ter retina two different cell death mechanisms may run in parallel while in all other studied RD models the mutation-induced cell death followed a non-apoptotic mechanism. Scale bar 20 µm.</p

Two routes to cell death.

<p>Classical apoptosis, such as it occurs in S334ter transgenic photoreceptors, involves a mutation-induced up-regulation and translocation of BAX protein to form the mitochondrial permeability transition pore (MPTP). This leads to leakage of cytochrome c from the mitochondria to the cytoplasm, where it combines with apoptotic protease activating factor (APAF) and caspase-9 to form the apoptosome, which in turn activates down-stream executioner caspases, including caspase-3. In 9/10 RD animal models investigated here, photoreceptor death followed a different route: mutation-induced up-regulation of cGMP on the one hand causes activation of the CNG channel, leading to Ca2+ influx and calpain activation. On the other hand cGMP-dependent activation of protein kinase G (PKG) is associated with histone deacetylase (HDAC) and poly-ADP-ribose-polymerase (PARP) activation. Importantly, this alternative, non-apoptotic cell death mechanism offers a number of novel targets for neuroprotection of photoreceptors.</p

Progression of cell death in inherited RD models.

<p>Depending on the causative genetic insult, the temporal development of retinal degeneration is highly variable in the different animal models. The quantification of dying, TUNEL-positive photoreceptor cells in the outer nuclear layer (ONL) allowed determination of the evolution and the peak of photoreceptor death for each of these animal models (<b>A</b>). The peak was taken as reference point for the ensuing analysis of cell death mechanisms. The bar graph (<b>B</b>) shows a comparison of maximum peak heights for all ten RD models studied. Note the different scales in line graphs. Values are mean ± SEM from at least three different animals. See also <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0112142#pone.0112142.s004" target="_blank">Table S1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0112142#pone.0112142.s005" target="_blank">S2</a>.</p