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"text": "\n13548\nSodium intake does not influence bioimpedance-derived extracellular volume loss in head-down rest.\n\nHinghofer-Szalkay, HG\n\nLászló, Z\n\nPassath, H\n\nPilz, K\n\nRössler, A\n\nJezova, D\n\nScharfetter, H\n\nBeiträge in Fachzeitschriften\nISI:000225503000003\n15619857.0\nNone\nNone\nINTRODUCTION: There is disagreement regarding the impact of dietary sodium on alterations in extracellular volume during head-down bed rest (HDBR). The primary purpose of this study was to assess the effects of salt intake on extracellular volume (ECV) during HDBR. METHODS: We performed whole-body bioimpedance spectroscopy with controlled sodium intake during 4 d of ambulation and 8 d of -6 degrees HDBR in 10 normotensive men. Each subject performed an initial 12-d familiarization run with moderate sodium (246 +/- 12 mmol x L(-1) x d(-1) excreted) during which no measurements were made. They then participated in treatment runs involving low sodium (LS: 143 +/- 10 mmol x L(-1) x d(-1) Na+ excreted) and high sodium (HS: 434 +/- 17 mmol x L(-1) x d(-1) Na+ excreted). The different treatments were separated by > or =1 mo and the order of LS and HS was balanced among the subjects. These treatments were based on controlled food and drink supplies as prepared by a dietitian. We monitored sodium output and measured aldosterone, plasma renin activity (PRA), and vasopressin. Bioimpedance was measured every second day in supine position using tetrapolar electrodes. RESULTS: Based on exponential data fitting, we calculated an ECV decrease of 0.79 +/- 0.32 L (-5.8%; p = 0.018) in LS, and 1.21 +/- 0.31 L (-4.0%; p = 0.002) in HS during HDBR. LS and HS were not different (p > 0.1); 4 d pre-HDBR sodium adjustment produced a fall in ECV in the LS group only (-3.7%, p = 0.023). Hormone levels were not changed by HDBR. Plasma aldosterone was lower in HS (69 +/- 7 pg x ml(-1)) than in LS (180 +/- 24 pg x ml(-1)). DISCUSSION: Our bioimpedance data confirm that low sodium intake decreases ECV in ambulatory conditions and indicate that 8 d of HDBR produce a loss of ECV of about 5% (p < 0.05). The loss did not seem to be influenced by sodium intake between approximately 3 and approximately 10 g x d(-1).\n\nHinghofer-Szalkay, Helmut\n\nRössler, Andreas\n\n\n"
},
{
"text": "\n60685\nPro- and supination impairments due to torsional deformities of the radial diaphysis before and after ulna osteotomy\n\nKasten, P\n\nKrefft, M\n\nSchneider, S\n\nHesselbach, J\n\nWeinberg, AM\n\nBeiträge in Fachzeitschriften\nISI:000221017900010\n15141672.0\n10.1007/s00132-003-0544-9\nNone\nThe aim of this experimental study was to measure the exact influence of torsional deformities at the middle third of the radial shaft before and after osteotomy of the ulnar shaft on the rotation of the forearm. Intact and fresh cadaver specimens were fixed in a newly developed apparatus that allowed free pronation and supination. A ring fixator was applied to the radial shaft with K wires that allowed torsional deformities to be stabilized in steps of 10 degrees. The middle of the radial shaft was osteotomized via a small soft tissue window leaving the other soft tissues including the interosseous membrane intact. Supination and pronation were measured using a goniometer in a standardized fashion. The mean supination value before osteotomy of the radius was 71.6 degrees [standard deviation (SD)15.2 degrees], the mean pronation value was 64.5 degrees (SD 12.4 degrees). Radial osteotomy caused no significant difference in the range of motion prior to creation of torsional deformities. Supination torsional deformities greater than 30 degrees showed a significant loss of pronation and pronation torsional deformities greater than 30 degrees resulted in a significant loss of supination in 14 fresh cadavers, respectively. The amount of mean rotational loss was approximately the same in the respective pronation and supination torsional deformities. In the next step the influence of an ulna osteotomy on the range of motion was evaluated in different torsional deformities. In the four cadavers measured, there was an increase of the range of motion in the direction of the torsional deformity. These values were not significant when compared to values before ulna osteotomy, but there were significant changes to the non deformity (p=0.004 for pronation, p=0.003 for supination). Impairment of range of motion in the opposite direction of the deformity showed a similar appearance as values before ulna osteotomy. Again, there were significant changes to the non deformity (p=0.003 for pronation, p=0.005 for supination).\n\nWeinberg, Annelie-Martina\n\n\n"
},
{
"text": "\n140234\nOptimum binary cut-off threshold of a diagnostic test: comparison of different methods using Monte Carlo technique.\n\nReibnegger, G\n\nSchrabmair, W\n\nBeiträge in Fachzeitschriften\nISI:000345866600001\n25421000.0\n10.1186/s12911-014-0099-1\nPMC4253606\nUsing Monte Carlo simulations, we compare different methods (maximizing Youden index, maximizing mutual information, and logistic regression) for their ability to determine optimum binary cut-off thresholds for a ratio-scaled diagnostic test variable. Special attention is given to the stability and precision of the results in dependence on the distributional characteristics as well as the pre-test probabilities of the diagnostic categories in the test population.\n Fictitious data sets of a ratio-scaled diagnostic test with different distributional characteristics are generated for 50, 100 and 200 fictitious "individuals" with systematic variation of pre-test probabilities of two diagnostic categories. For each data set, optimum binary cut-off limits are determined employing different methods. Based on these optimum cut-off thresholds, sensitivities and specificities are calculated for the respective data sets. Mean values and SD of these variables are computed for 1000 repetitions each.\n Optimizations of cut-off limits using Youden index and logistic regression-derived likelihood ratio functions with correct adaption for pre-test probabilities both yield reasonably stable results, being nearly independent from pre-test probabilities actually used. Maximizing mutual information yields cut-off levels decreasing with increasing pre-test probability of disease. The most precise results (in terms of the smallest SD) are usually seen for the likelihood ratio method. With this parametric method, however, cut-off values show a significant positive bias and, hence, specificities are usually slightly higher, and sensitivities are consequently slightly lower than with the two non-parametric methods.\n In terms of stability and bias, Youden index is best suited for determining optimal cut-off limits of a diagnostic variable. The results of Youden method and likelihood ratio method are surprisingly insensitive against distributional differences as well as pre-test probabilities of the two diagnostic categories. As an additional bonus of the parametric procedure, transfer of the likelihood ratio functions, obtained from logistic regression analysis, to other diagnostic scenarios with different pre-test probabilities is straightforward.\n\nReibnegger, Gilbert\n\nSchrabmair, Walter\n\n\n"
},
{
"text": "\n140641\nFive-year outcome of catheter ablation of persistent atrial fibrillation using termination of atrial fibrillation as a procedural endpoint.\n\nScherr, D\n\nKhairy, P\n\nMiyazaki, S\n\nAurillac-Lavignolle, V\n\nPascale, P\n\nWilton, SB\n\nRamoul, K\n\nKomatsu, Y\n\nRoten, L\n\nJadidi, A\n\nLinton, N\n\nPedersen, M\n\nDaly, M\n\nO'Neill, M\n\nKnecht, S\n\nWeerasooriya, R\n\nRostock, T\n\nManninger, M\n\nCochet, H\n\nShah, AJ\n\nYeim, S\n\nDenis, A\n\nDerval, N\n\nHocini, M\n\nSacher, F\n\nHaissaguerre, M\n\nJais, P\n\nBeiträge in Fachzeitschriften\nISI:000349873000006\n25528745.0\n10.1161/CIRCEP.114.001943\nNone\nThis study aimed to determine 5-year efficacy of catheter ablation for persistent atrial fibrillation (AF) using AF termination as a procedural end point.\n One hundred fifty patients (57±10 years) underwent persistent AF ablation using a stepwise ablation approach (pulmonary vein isolation, electrogram-guided, and linear ablation) with the desired procedural end point being AF termination. Repeat ablation was performed for recurrent AF or atrial tachycardia. AF was terminated by ablation in 120 patients (80%). Arrhythmia-free survival rates after a single procedure were 35.3%±3.9%, 28.0%±3.7%, and 16.8%±3.2% at 1, 2, and 5 years, respectively. Arrhythmia-free survival rates after the last procedure (mean 2.1±1.0 procedures) were 89.7%±2.5%, 79.8%±3.4%, and 62.9%±4.5%, at 1, 2, and 5 years, respectively. During a median follow-up of 58 (interquartile range, 43-73) months after the last ablation procedure, 97 of 150 (64.7%) patients remained in sinus rhythm without antiarrhythmic drugs. Another 14 (9.3%) patients maintained sinus rhythm after reinitiation of antiarrhythmic drugs, and an additional 15 (10.0%) patients regressed to paroxysmal recurrences only. Failure to terminate AF during the index procedure (hazard ratio 3.831; 95% confidence interval, 2.070-7.143; P<0.001), left atrial diameter≥50 mm (hazard ratio 2.083; 95% confidence interval, 1.078-4.016; P=0.03), continuous AF duration≥18 months (hazard ratio 1.984; 95% confidence interval, 1.024-3.846; P<0.04), and structural heart disease (hazard ratio 1.874; 95% confidence interval, 1.037-3.388; P=0.04) predicted arrhythmia recurrence.\n In patients with persistent AF, an ablation strategy aiming at AF termination is associated with freedom from arrhythmia recurrence in the majority of patients over a 5-year follow-up period. Procedural AF nontermination and specific baseline factors predict long-term outcome after ablation.\n © 2014 American Heart Association, Inc.\n\nManninger-Wünscher, Martin\n\nScherr, Daniel\n\n\n"
},
{
"text": "\n142589\nBone marrow or peripheral blood stem cell transplantation from unrelated donors in adult patients with acute myeloid leukaemia, an Acute Leukaemia Working Party analysis in 2262 patients.\n\nRingdén, O\n\nLabopin, M\n\nBeelen, DW\n\nVolin, L\n\nEhninger, G\n\nFinke, J\n\nGreinix, HT\n\nKyrcz-Krzemien, S\n\nBunjes, D\n\nBrinch, L\n\nNiederwieser, D\n\nArnold, R\n\nMohty, M\n\nRocha, V\n\nAcute Leukaemia Working Party of European Group for Blood and Marrow Transplantation (EBMT)\n\nBeiträge in Fachzeitschriften\nISI:000310388100007\n22519980.0\n10.1111/j.1365-2796.2012.02547.x\nNone\nNo survival benefit of using blood stem cells instead of bone marrow (BM) has been shown in matched unrelated donor (MUD) transplantation.\n In a retrospective registry analysis, we compared the use of blood stem cells (n = 1502) and BM (n = 760) from unrelated donors in patients aged 18-60 years with acute myeloid leukaemia (AML) undergoing myeloablative conditioning between 1997 and 2008. The blood stem cell recipients were older (P < 0.01), had more advanced disease (P < 0.0001) and received less total body irradiation (P < 0.0001) and more antithymocyte globulin (P = 0.01).\n Recovery of neutrophils and platelets was faster with blood stem cells (P < 0.0001). The incidence of acute graft-versus-host disease (GVHD) was similar, but there was more chronic GVHD in the blood stem cell group [hazard ratio (HR) = 1.29, P = 0.02]. There were no significant differences in nonrelapse mortality (NRM), relapse incidence and leukaemia-free survival (LFS) between the two groups amongst patients with AML in remission. In patients with advanced leukaemia, NRM was lower (HR = 0.61, P = 0.02) and LFS was prolonged (HR = 0.67, P = 0.002) when blood stem cells were used. At 3 years, LFS for all patients, regardless of remission status, was 41% for both treatment groups. The outcome was not affected after multivariable analysis adjusted for confounders.\n Blood stem cells compared with BM in MUD transplantation for patients with AML in remission resulted in the same rates of LFS. In patients with advanced leukaemia, the blood stem cell group had reduced NRM and improved LFS.\n © 2012 The Association for the Publication of the Journal of Internal Medicine.\n\nGreinix, Hildegard\n\n\n"
},
{
"text": "\n144359\nEffects of vitamin D on blood pressure and cardiovascular risk factors: a randomized controlled trial.\n\nPilz, S\n\nGaksch, M\n\nKienreich, K\n\nGrübler, M\n\nVerheyen, N\n\nFahrleitner-Pammer, A\n\nTreiber, G\n\nDrechsler, C\n\nÓ Hartaigh, B\n\nObermayer-Pietsch, B\n\nSchwetz, V\n\nAberer, F\n\nMader, J\n\nScharnagl, H\n\nMeinitzer, A\n\nLerchbaum, E\n\nDekker, JM\n\nZittermann, A\n\nMärz, W\n\nTomaschitz, A\n\nBeiträge in Fachzeitschriften\nISI:000354364900011\n25801871.0\n10.1161/HYPERTENSIONAHA.115.05319\nNone\nVitamin D deficiency is a risk factor for arterial hypertension, but randomized controlled trials showed mixed effects of vitamin D supplementation on blood pressure (BP). We aimed to evaluate whether vitamin D supplementation affects 24-hour systolic ambulatory BP monitoring values and cardiovascular risk factors. The Styrian Vitamin D Hypertension Trial is a single-center, double-blind, placebo-controlled study conducted from June 2011 to August 2014 at the endocrine outpatient clinic of the Medical University of Graz, Austria. We enrolled 200 study participants with arterial hypertension and 25-hydroxyvitamin D levels below 30 ng/mL. Study participants were randomized to receive either 2800 IU of vitamin D3 per day as oily drops (n=100) or placebo (n=100) for 8 weeks. Primary outcome measure was 24-hour systolic BP. Secondary outcome measures were 24-hour diastolic BP, N-terminal-pro-B-type natriuretic peptide, QTc interval, renin, aldosterone, 24-hour urinary albumin excretion, homeostasis model assessment-insulin resistance, triglycerides, high-density lipoprotein cholesterol, and pulse wave velocity. A total of 188 participants (mean [SD] age, 60.1 [11.3] years; 47% women; 25-hydroxyvitamin D, 21.2 [5.6] ng/mL) completed the trial. The mean treatment effect (95% confidence interval) for 24-hour systolic BP was -0.4 (-2.8 to 1.9) mm Hg (P=0.712). Triglycerides increased significantly (mean change [95% confidence interval], 17 [1-33] mg/dL; P=0.013), but no further significant effects were observed for secondary outcomes. Vitamin D supplementation in hypertensive patients with low 25-hydroxyvitamin D has no significant effect on BP and several cardiovascular risk factors, but it was associated with a significant increase in triglycerides.\n URL: http://www.clinicaltrials.gov. Unique identifier: NCT02136771.\n © 2015 American Heart Association, Inc.\n\nAberer, Felix\n\nFahrleitner-Pammer, Astrid\n\nLerchbaum, Elisabeth\n\nMader, Julia\n\nMärz, Winfried\n\nMeinitzer, Andreas\n\nObermayer-Pietsch, Barbara\n\nPilz, Stefan\n\nScharnagl, Hubert\n\nTheiler-Schwetz, Verena\n\nTreiber, Gerlies\n\nVerheyen, Nicolas Dominik\n\n\n"
},
{
"text": "\n148969\nSerum amyloid A: high-density lipoproteins interaction and cardiovascular risk.\n\nZewinger, S\n\nDrechsler, C\n\nKleber, ME\n\nDressel, A\n\nRiffel, J\n\nTriem, S\n\nLehmann, M\n\nKopecky, C\n\nSäemann, MD\n\nLepper, PM\n\nSilbernagel, G\n\nScharnagl, H\n\nRitsch, A\n\nThorand, B\n\nde las Heras Gala, T\n\nWagenpfeil, S\n\nKoenig, W\n\nPeters, A\n\nLaufs, U\n\nWanner, C\n\nFliser, D\n\nSpeer, T\n\nMärz, W\n\nBeiträge in Fachzeitschriften\nISI:000366492300012\n26248570.0\n10.1093/eurheartj/ehv352\nNone\nHigh-density lipoproteins (HDLs) are considered as anti-atherogenic. Recent experimental findings suggest that their biological properties can be modified in certain clinical conditions by accumulation of serum amyloid A (SAA). The effect of SAA on the association between HDL-cholesterol (HDL-C) and cardiovascular outcome remains unknown.\n We examined the association of SAA and HDL-C with mortality in the Ludwigshafen Risk and Cardiovascular Health (LURIC) study, which included 3310 patients undergoing coronary angiography. To validate our findings, we analysed 1255 participants of the German Diabetes and Dialysis study (4D) and 4027 participants of the Cooperative Health Research in the Region of Augsburg (KORA) S4 study. In LURIC, SAA concentrations predicted all-cause and cardiovascular mortality. In patients with low SAA, higher HDL-C was associated with lower all-cause and cardiovascular mortality. In contrast, in patients with high SAA, higher HDL-C was associated with increased all-cause and cardiovascular mortality, indicating that SAA indeed modifies the beneficial properties of HDL. We complemented these clinical observations by in vitro experiments, in which SAA impaired vascular functions of HDL. We further derived a formula for the simple calculation of the amount of biologically 'effective' HDL-C based on measured HDL-C and SAA from the LURIC study. In 4D and KORA S4 studies, we found that measured HDL-C was not associated with clinical outcomes, whereas calculated 'effective' HDL-C significantly predicted better outcome.\n The acute-phase protein SAA modifies the biological effects of HDL-C in several clinical conditions. The concomitant measurement of SAA is a simple, useful, and clinically applicable surrogate for the vascular functionality of HDL.\n Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.\n\nMärz, Winfried\n\nScharnagl, Hubert\n\nSilbernagel, Günther\n\n\n"
},
{
"text": "\n155886\nDistinct effects of surgical denervation on hepatic perfusion, bowel ischemia, and oxidative stress in brain dead and living donor porcine models.\n\nGolling, M\n\nJahnke, C\n\nFonouni, H\n\nAhmadi, R\n\nUrbaschek, R\n\nBreitkreutz, R\n\nSchemmer, P\n\nKraus, TW\n\nGebhard, MM\n\nBüchler, MW\n\nMehrabi, A\n\nBeiträge in Fachzeitschriften\nISI:000245596400021\n17394167.0\n10.1002/lt.21069\nNone\nThe liver function and perfusion following brain death is mainly influenced by the sympathetic nerves and hormones. We examined the specific influence of surgical liver denervation on systemic and hepatic perfusion parameters, bowel ischemia and oxidative stress in hemodynamically stable BD and control (living donor [LD]) pigs. Brain death was induced in 8 pigs via saline infusion into the balloon of an epidural Tieman-catheter (1 mL/15 minutes) and compared to the control group (n = 6) over 4 hours. At 2 hours postoperatively, complete liver denervation was initiated. We analyzed systemic cardiocirculatory parameters (mean arterial pressure, aortic flow, bowel ischemia (endotoxin, and endotoxin-neutralizing capacity) and oxidative stress (total glutathione in erythrocytes [tGSH(E)]) and compared them to local/hepatic perfusion parameters (hepatic artery and portal venous flow, liver blood flow index, and microperfusion), local bowel ischemia (intramucosal pH [pHi] of stomach [pHi(S)]/colon[pHi(C)]), and liver oxidative stress (glutathione [rGSH(L), GSSG(L)]). Following brain death, the parameters including mean arterial pressure, aortic flow, pHi, endotoxin, and tGSH(E) showed no significant changes at 2 hours. Portal venous flow and microperfusion were decreased significantly and hepatic arterial buffer response was ineffective. Hepatic oxidative stress was increased in BD animals (decrease rGSH(L), increase GSSG(L)). Surgical denervation/manipulation increased portal venous flow significantly, hepatic arterial buffer response became effective, and stomach pHi decreased (BD and LD groups). Hepatic oxidative stress was reduced in the BD group (increase rGSH(L)/GSSG(L); P < 0.001) while it was increased in the LD group (decrease rGSH(L)/GSSG(L); P < 0.001). In conclusion, denervation reduces hepatic oxidative stress in BD only in contrast to the LD. The reciprocal effect of denervation depends on the state of neural activation and postulates a potential benefit of surgical denervation before organ harvesting in brain death.\n\nSchemmer, Peter\n\n\n"
},
{
"text": "\n159116\nAssessment of cardiac fibrosis: a morphometric method comparison for collagen quantification.\n\nSchipke, J\n\nBrandenberger, C\n\nRajces, A\n\nManninger, M\n\nAlogna, A\n\nPost, H\n\nMühlfeld, C\n\nBeiträge in Fachzeitschriften\nISI:000400355800011\n28126909.0\n10.1152/japplphysiol.00987.2016\nNone\nFibrotic remodeling of the heart is a frequent condition linked to various diseases and cardiac dysfunction. Collagen quantification is an important objective in cardiac fibrosis research; however, a variety of different histological methods are currently used that may differ in accuracy. Here, frequently applied collagen quantification techniques were compared. A porcine model of early stage heart failure with preserved ejection fraction was used as an example. Semiautomated threshold analyses were imprecise, mainly due to inclusion of noncollagen structures or failure to detect certain collagen deposits. In contrast, collagen assessment by automated image analysis and light microscopy (LM)-stereology was more sensitive. Depending on the quantification method, the amount of estimated collagen varied and influenced intergroup comparisons. PicroSirius Red, Masson's trichrome, and Azan staining protocols yielded similar results, whereas the measured collagen area increased with increasing section thickness. Whereas none of the LM-based methods showed significant differences between the groups, electron microscopy (EM)-stereology revealed a significant collagen increase between cardiomyocytes in the experimental group, but not at other localizations. In conclusion, in contrast to the staining protocol, section thickness and the quantification method being used directly influence the estimated collagen content and thus, possibly, intergroup comparisons. EM in combination with stereology is a precise and sensitive method for collagen quantification if certain prerequisites are considered. For subtle fibrotic alterations, consideration of collagen localization may be necessary. Among LM methods, LM-stereology and automated image analysis are appropriate to quantify fibrotic changes, the latter depending on careful control of algorithm and comparable section staining.NEW & NOTEWORTHY Direct comparison of frequently applied histological fibrosis assessment techniques revealed a distinct relation of measured collagen and utilized quantification method as well as section thickness. Besides electron microscopy-stereology, which was precise and sensitive, light microscopy-stereology and automated image analysis proved to be appropriate for collagen quantification. Moreover, consideration of collagen localization might be important in revealing minor fibrotic changes.\n Copyright © 2017 the American Physiological Society.\n\nManninger-Wünscher, Martin\n\n\n"
},
{
"text": "\n161746\nReproducibility and clinical significance of exercise-induced increases in cardiac troponins and N-terminal pro brain natriuretic peptide in endurance athletes.\n\nScharhag, J\n\nUrhausen, A\n\nSchneider, G\n\nHerrmann, M\n\nSchumacher, K\n\nHaschke, M\n\nKrieg, A\n\nMeyer, T\n\nHerrmann, W\n\nKindermann, W\n\nBeiträge in Fachzeitschriften\nISI:000241026600015\n16926669.0\n10.1097/00149831-200606000-00015\nNone\nCardiac troponins I and T and brain natriuretic peptide are the accepted standards to serologically identify myocardial necrosis and elevated wall stress. In addition, they allow risk stratification in cardiovascular patients. The clinical significance of increases in cardiac markers after strenuous endurance exercise in obviously healthy athletes is unclear.\n We therefore examined the reproducibility and clinical significance of exercise-induced increases in cardiac troponins I and T and N-terminal pro brain natriuretic peptide after two standardized endurance exercise trials in healthy endurance athletes with prior competition-induced elevations of cardiac troponins (I, 0.08-1.93 mug/l; T, 0.01-0.56 mug/l).\n Twenty male athletes (36+/-7 years; VO2max: 60+/-5 ml/min per kg) completed a 1-h and a 3-h exercise study (exercise intensities 100 and 75%, respectively, of the individual anaerobic threshold) on two different days in randomized order to determine cardiac markers before, 30 min and 3 h after exercise. In addition to pre- and post-exercise echocardiography including tissue Doppler imaging, delayed enhancement magnetic-resonance-imaging was performed after a 3-h exercise study to detect myocardial necrosis.\n A marginal increase in cardiac troponin I was documented after both exercise trials (from 0.02 to 0.03 mug/l; P < 0.001). Cardiac troponin T remained without significant changes. N-terminal pro brain natriuretic peptide increased by 9 and 30 ng/l after 1-h and 3-h exercise studies, respectively (P < 0.001). In contrast to cardiac troponins, increases in N-terminal pro brain natriuretic peptide after competition correlated with those after 1-h exercise study (rho = 0.88) and 3-h exercise-study (rho = 0.82). No pathologies were demonstrated by echocardiography or delayed-enhancement magnetic resonance imaging.\n Due to the missing reproducibilty and evidence of myocardial damage, exercise-induced increases in cardiac troponins may represent a physiologic reaction under special conditions and seem to be without pathological significance in healthy athletes.\n\nHerrmann, Markus\n\n\n"
},
{
"text": "\n169258\nDiagnostic and Clinical Management of Skull Fractures in Children.\n\nArneitz, C\n\nSinzig, M\n\nFasching, G\n\nBeiträge in Fachzeitschriften\nNone\n28028451.0\n10.4103/2156-7514.194261\nPMC5157005\nThe indications of routine skull X-rays after mild head trauma are still in discussion, and the clinical management of a child with a skull fracture remains controversial. The aim of our retrospective study was to evaluate our diagnostic and clinical management of children with skull fractures following minor head trauma.\n We worked up the medical history of all consecutive patients with a skull fracture treated in our hospital from January 2009 to October 2014 and investigated all skull X-rays in our hospital during this period.\n In 5217 skull radiographies, 66 skull fractures (1.3%) were detected. The mean age of all our patients was 5.9 years (median age: 4.0 years); the mean age of patients with a diagnosed skull fracture was 2.3 years (median age: 0.8 years). A total of 1658 children (32%) were <2 years old. A typical boggy swelling was present in 61% of all skull fractures. The majority of injuries were caused by falls (77%). Nine patients (14%) required a computed tomography (CT) scan during their hospital stay due to neurological symptoms, and four patients had a brain magnetic resonance imaging. Nine patients (14%) showed an intracranial hemorrhage (ICH; mean age: 7.3 years); one patient had a neurosurgery because of a depressed skull fracture. Nine patients (14%) were observed at our pediatric intensive care unit for a mean time of 2.9 days. The mean hospital stay was 4.2 days.\n Our findings support previous evidence against the routine use of skull X-rays for evaluation of children with minor head injury. The rate of diagnosed skull fractures in radiographs following minor head trauma is low, and additional CT scans are not indicated in asymptomatic patient with a linear skull fracture. All detected ICHs could be treated conservatively. Children under the age of 2 years have the highest risk of skull fractures after minor head trauma, but do not have a higher incidence of intracranial bleeding. Neuroobservation without initial CT scans is safe in infants and children following minor head trauma and CT scans should be reserved for patients with neurological symptoms.\n\nArneitz, Christoph\n\n\n"
},
{
"text": "\n169497\nGenome-wide association study of 23,500 individuals identifies 7 loci associated with brain ventricular volume.\n\nVojinovic, D\n\nAdams, HH\n\nJian, X\n\nYang, Q\n\nSmith, AV\n\nBis, JC\n\nTeumer, A\n\nScholz, M\n\nArmstrong, NJ\n\nHofer, E\n\nSaba, Y\n\nLuciano, M\n\nBernard, M\n\nTrompet, S\n\nYang, J\n\nGillespie, NA\n\nvan der Lee, SJ\n\nNeumann, A\n\nAhmad, S\n\nAndreassen, OA\n\nAmes, D\n\nAmin, N\n\nArfanakis, K\n\nBastin, ME\n\nBecker, DM\n\nBeiser, AS\n\nBeyer, F\n\nBrodaty, H\n\nBryan, RN\n\nBülow, R\n\nDale, AM\n\nDe Jager, PL\n\nDeary, IJ\n\nDeCarli, C\n\nFleischman, DA\n\nGottesman, RF\n\nvan der Grond, J\n\nGudnason, V\n\nHarris, TB\n\nHomuth, G\n\nKnopman, DS\n\nKwok, JB\n\nLewis, CE\n\nLi, S\n\nLoeffler, M\n\nLopez, OL\n\nMaillard, P\n\nEl Marroun, H\n\nMather, KA\n\nMosley, TH\n\nMuetzel, RL\n\nNauck, M\n\nNyquist, PA\n\nPanizzon, MS\n\nPausova, Z\n\nPsaty, BM\n\nRice, K\n\nRotter, JI\n\nRoyle, N\n\nSatizabal, CL\n\nSchmidt, R\n\nSchofield, PR\n\nSchreiner, PJ\n\nSidney, S\n\nStott, DJ\n\nThalamuthu, A\n\nUitterlinden, AG\n\nValdés Hernández, MC\n\nVernooij, MW\n\nWen, W\n\nWhite, T\n\nWitte, AV\n\nWittfeld, K\n\nWright, MJ\n\nYanek, LR\n\nTiemeier, H\n\nKremen, WS\n\nBennett, DA\n\nJukema, JW\n\nPaus, T\n\nWardlaw, JM\n\nSchmidt, H\n\nSachdev, PS\n\nVillringer, A\n\nGrabe, HJ\n\nLongstreth, WT\n\nvan Duijn, CM\n\nLauner, LJ\n\nSeshadri, S\n\nIkram, MA\n\nFornage, M\n\nBeiträge in Fachzeitschriften\nISI:000445607500016\n30258056.0\n10.1038/s41467-018-06234-w\nPMC6158214\nThe volume of the lateral ventricles (LV) increases with age and their abnormal enlargement is a key feature of several neurological and psychiatric diseases. Although lateral ventricular volume is heritable, a comprehensive investigation of its genetic determinants is lacking. In this meta-analysis of genome-wide association studies of 23, 33 healthy middle-aged to elderly individuals from 26 population-based cohorts, we identify 7 genetic loci associated with LV volume. These loci map to chromosomes 3q28, 7p22.3, 10p12.31, 11q23.1, 12q23.3, 16q24.2, and 22q13.1 and implicate pathways related to tau pathology, S1P signaling, and cytoskeleton organization. We also report a significant genetic overlap between the thalamus and LV volumes (ρgenetic = -0.59, p-value = 3.14 × 10-6), suggesting that these brain structures may share a common biology. These genetic associations of LV volume provide insights into brain morphology.\n\nHofer, Edith\n\nSABA, Yasaman\n\nSchmidt, Helena\n\nSchmidt, Reinhold\n\n\n"
},
{
"text": "\n169835\nBinding of CD40L to Mac-1's I-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis--but does not affect immunity and thrombosis in mice.\n\nWolf, D\n\nHohmann, JD\n\nWiedemann, A\n\nBledzka, K\n\nBlankenbach, H\n\nMarchini, T\n\nGutte, K\n\nZeschky, K\n\nBassler, N\n\nHoppe, N\n\nRodriguez, AO\n\nHerr, N\n\nHilgendorf, I\n\nStachon, P\n\nWillecke, F\n\nDuerschmied, D\n\nvon zur Muhlen, C\n\nSoloviev, DA\n\nZhang, L\n\nBode, C\n\nPlow, EF\n\nLibby, P\n\nPeter, K\n\nZirlik, A\n\nBeiträge in Fachzeitschriften\nISI:000296872200014\n21998326.0\n10.1161/CIRCRESAHA.111.247684\nPMC3291815\nCD40L figures prominently in chronic inflammatory diseases such as atherosclerosis. However, since CD40L potently regulates immune function and hemostasis by interaction with CD40 receptor and the platelet integrin GPIIb/IIIa, its global inhibition compromises host defense and generated thromboembolic complications in clinical trials. We recently reported that CD40L mediates atherogenesis independently of CD40 and proposed Mac-1 as an alternate receptor.\n Here, we molecularly characterized the CD40L-Mac-1 interaction and tested whether its selective inhibition by a small peptide modulates inflammation and atherogenesis in vivo.\n CD40L concentration-dependently bound to Mac-1 I-domain in solid phase binding assays, and a high-affinity interaction was revealed by surface-plasmon-resonance analysis. We identified the motif EQLKKSKTL, an exposed loop between the α1 helix and the β-sheet B, on Mac-1 as binding site for CD40L. A linear peptide mimicking this sequence, M7, specifically inhibited the interaction of CD40L and Mac-1. A cyclisized version optimized for in vivo use, cM7, decreased peritoneal inflammation and inflammatory cell recruitment in vivo. Finally, LDLr(-/-) mice treated with intraperitoneal injections of cM7 developed smaller, less inflamed atherosclerotic lesions featuring characteristics of stability. However, cM7 did not interfere with CD40L-CD40 binding in vitro and CD40L-GPIIb/IIIa-mediated thrombus formation in vivo.\n We present the novel finding that CD40L binds to the EQLKKSKTL motif on Mac-1 mediating leukocyte recruitment and atherogenesis. Specific inhibition of CD40L-Mac-1 binding may represent an attractive anti-inflammatory treatment strategy for atherosclerosis and other inflammatory conditions, potentially avoiding the unwanted immunologic and thrombotic effects of global inhibition of CD40L.\n\nZirlik, Andreas\n\n\n"
},
{
"text": "\n175347\nSource Environments of the Microbiome in Perennially Ice-Covered Lake Untersee, Antarctica.\n\nWeisleitner, K\n\nPerras, A\n\nMoissl-Eichinger, C\n\nAndersen, DT\n\nSattler, B\n\nBeiträge in Fachzeitschriften\nISI:000467619000001\n31134036.0\n10.3389/fmicb.2019.01019\nPMC6524460\nUltra-oligotrophic Lake Untersee is among the largest and deepest surface lakes of Central Queen Maud Land in East Antarctica. It is dammed at its north end by the Anuchin Glacier and the ice-cover dynamics are controlled by sublimation - not melt - as the dominating ablation process and therefore surface melt during austral summer does not provide significant amounts of water for recharge compared to subsurface melt of the Anuchin Glacier. Several studies have already described the structure and function of the microbial communities within the water column and benthic environments of Lake Untersee, however, thus far there have been no studies that examine the linkages between the lake ecosystem with that of the surrounding soils or the Anuchin Glacier. The glacier may also play an important role as a major contributor of nutrients and biota into the lake ecosystem. Based on microbial 16S rRNA amplicon sequencing, we showed that the dominant bacterial signatures in Lake Untersee, the Anuchin Glacier and its surrounding soils were affiliated with Actinobacteria, Bacteroidetes, Cyanobacteria, Firmicutes, and Proteobacteria. Aerosol and local soil depositions on the glacier surface resulted in distinct microbial communities developing in glacier ice and cryoconite holes. Based on a source tracking algorithm, we found that cryoconite microbial assemblages were a potential source of organisms, explaining up to 36% of benthic microbial mat communities in the lake. However, the major biotic sources for the lake ecosystem are still unknown, illustrating the possible importance of englacial and subglacial zones. The Anuchin Glacier may be considered as a vector in a biological sense for the bacterial colonization of the perennially ice-covered Lake Untersee. However, despite a thick perennial ice cover, observed "lift-off" microbial mats escaping the lake make a bidirectional transfer of biota plausible. Hence, there is an exchange of biota between Lake Untersee and connective habitats possible despite the apparent sealing by a perennial ice cover and the absence of moat areas during austral summer.\n\nMoissl-Eichinger, Christine\n\n\n"
},
{
"text": "\n179680\nDe novo Prograf versus de novo Advagraf: are trough level profile curves similar?\n\nSarvary, E\n\nWagner, L\n\nTelkes, G\n\nGaman, G\n\nVarga, M\n\nGaal, I\n\nMathe, Z\n\nChmel, R\n\nFehervari, I\n\nLanger, RM\n\nBeiträge in Fachzeitschriften\nISI:000341076800126\n25131131.0\n10.1016/j.transproceed.2014.05.061\nNone\nAccording to the clinical trials, Advagraf (ADV) has efficacy and safety profile similar to Prograf (PROG). The aim of this study was to compare the graft functions, dosages, and tacrolimus (TAC) trough level profile curves of patients on de novo PROG and ADV therapy.\n The ADV group included 39 de novo renal cases who had received initial immunosuppression (IS) with once-daily TAC (1 × 0.2 mg/kg from day1 after transplantation). We compared them with a PROG group of 38 transplant patients who received equivalent IS with twice-daily TAC (2 × 0.1 mg/kg from day1). In both groups, the IS was combined with antimetabolites and steroids. The mean follow-up time was similar (13.5 ± 7 days) in both groups after renal transplantation until the emission of the patients from our clinic.\n TAC mean total daily dose was reduced and whole-blood trough levels decreased over the time in early postoperative days. Only on day 3 and day 4 after transplant, a significant higher adjustment in the ADV dosage was necessary to achieve sufficient TAC trough levels. The average TAC trough level profile curves were similar in PROG and ADV groups, but the individual curves were very different. Mainly in patients on ADV therapy, the initial concentrations were often >30 ng/mL, and in some cases on the 9th posttransplant day decreased to <5 ng/mL, then slowly increased into the required therapeutic range.\n The results demonstrate that patients after renal transplantation can be safely treated de novo with ADV. Setting the required therapeutic TAC blood levels may require more attention to avoid the "fluctuations" of trough level profile curve during the early postoperative period. Our data suggest that dose adjustment of ADV can be carried out more carefully compared with PROG on the basis of clinical symptoms and the value of TAC blood levels to avoid acute rejection and toxicity.\n Copyright © 2014 Elsevier Inc. All rights reserved.\n\n\n"
},
{
"text": "\n182470\nExternal validation of the prognostic relevance of the advanced lung cancer inflammation index (ALI) in pancreatic cancer patients.\n\nBarth, DA\n\nBrenner, C\n\nRiedl, JM\n\nPrinz, F\n\nKlocker, EV\n\nSchlick, K\n\nKornprat, P\n\nLackner, K\n\nStöger, H\n\nStotz, M\n\nGerger, A\n\nPichler, M\n\nBeiträge in Fachzeitschriften\nISI:000555250800019\n32537935.0\n10.1002/cam4.3233\nPMC7402815\nThe advanced lung cancer inflammation index (ALI) was first introduced for prognosis prediction in lung cancer patients and since then evaluated in several other malignancies. However, in pancreatic cancer (PC) the ALI and its prognostic utility were only investigated in a comparably small and specific cohort of locally advanced PC patients treated with chemoradiotherapy.\n In our single-center cohort study, we included 429 patients with histologically verified PC who were treated between 2003 and 2015 at our academic institution. The ALI was defined as body mass index (BMI; kg/m2 ) × serum albumin levels (g/dL)/neutrophil-lymphocyte ratio (NLR) and we defined the optimal cutoff for biomarker dichotomization by ROC-analysis. Kaplan-Meier method as well as uni- and multivariate Cox regression Hazard proportional models were implemented to assess the prognostic potential of ALI in PC patients. We considered cancer-specific survival (CSS) as the primary endpoint of the study.\n The ALI showed a significant negative correlation with CA19-9 levels and C-reactive protein levels whereas we found an association with localized tumor stage and better performance status (P < .05 for all mentioned variables). As opposed to patients with a high ALI, decreased ALI was significantly associated with shorter CSS (HR = 0.606, 95% CI: 0.471-0.779, P = .001). Multivariate analysis demonstrated tumor grade, tumor stage, chemotherapy, C-reactive protein levels, and CA19-9 levels to independently predict for CSS (all P < .05). In contrast the ALI failed to independently predict for CSS in the performed multivariate models (HR = 0.878, 95% CI: 0.643-1.198, P = .411).\n In this large cohort of PC patients, the ALI did not complement existing clinicopathological factors for outcome determination.\n © 2020 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.\n\nBarth, Dominik Andreas\n\nGerger, Armin\n\nKlocker, Eva Valentina\n\nKornprat, Peter\n\nLackner, Karoline\n\nPichler, Martin\n\nPrinz, Felix\n\nRiedl, Jakob\n\nStoeger, Herbert\n\n\n"
},
{
"text": "\n184663\nMolecular repertoire of Deinococcus radiodurans after 1 year of exposure outside the International Space Station within the Tanpopo mission.\n\nOtt, E\n\nKawaguchi, Y\n\nKölbl, D\n\nRabbow, E\n\nRettberg, P\n\nMora, M\n\nMoissl-Eichinger, C\n\nWeckwerth, W\n\nYamagishi, A\n\nMilojevic, T\n\nBeiträge in Fachzeitschriften\nISI:000590592000002\n33121542.0\n10.1186/s40168-020-00927-5\nPMC7597052\nThe extraordinarily resistant bacterium Deinococcus radiodurans withstands harsh environmental conditions present in outer space. Deinococcus radiodurans was exposed for 1 year outside the International Space Station within Tanpopo orbital mission to investigate microbial survival and space travel. In addition, a ground-based simulation experiment with conditions, mirroring those from low Earth orbit, was performed.\n We monitored Deinococcus radiodurans cells during early stage of recovery after low Earth orbit exposure using electron microscopy tools. Furthermore, proteomic, transcriptomic and metabolomic analyses were performed to identify molecular mechanisms responsible for the survival of Deinococcus radiodurans in low Earth orbit.\n D. radiodurans cells exposed to low Earth orbit conditions do not exhibit any morphological damage. However, an accumulation of numerous outer-membrane-associated vesicles was observed. On levels of proteins and transcripts, a multi-faceted response was detected to alleviate cell stress. The UvrABC endonuclease excision repair mechanism was triggered to cope with DNA damage. Defense against reactive oxygen species is mirrored by the increased abundance of catalases and is accompanied by the increased abundance of putrescine, which works as reactive oxygen species scavenging molecule. In addition, several proteins and mRNAs, responsible for regulatory and transporting functions showed increased abundances. The decrease in primary metabolites indicates alternations in the energy status, which is needed to repair damaged molecules.\n Low Earth orbit induced molecular rearrangements trigger multiple components of metabolic stress response and regulatory networks in exposed microbial cells. Presented results show that the non-sporulating bacterium Deinococcus radiodurans survived long-term low Earth orbit exposure if wavelength below 200 nm are not present, which mirrors the UV spectrum of Mars, where CO2 effectively provides a shield below 190 nm. These results should be considered in the context of planetary protection concerns and the development of new sterilization techniques for future space missions. Video Abstract.\n\nMoissl-Eichinger, Christine\n\n\n"
},
{
"text": "\n186628\nLate-Gadolinium Enhancement Interface Area and Electrophysiological Simulations Predict Arrhythmic Events in Patients With Nonischemic Dilated Cardiomyopathy.\n\nBalaban, G\n\nHalliday, BP\n\nPorter, B\n\nBai, W\n\nNygåard, S\n\nOwen, R\n\nHatipoglu, S\n\nFerreira, ND\n\nIzgi, C\n\nTayal, U\n\nCorden, B\n\nWare, J\n\nPennell, DJ\n\nRueckert, D\n\nPlank, G\n\nRinaldi, CA\n\nPrasad, SK\n\nBishop, MJ\n\nBeiträge in Fachzeitschriften\nISI:000629470800014\n33602406.0\n10.1016/j.jacep.2020.08.036\nPMC7900608\nThis study sought to investigate whether shape-based late gadolinium enhancement (LGE) metrics and simulations of re-entrant electrical activity are associated with arrhythmic events in patients with nonischemic dilated cardiomyopathy (NIDCM).\n The presence of LGE predicts life-threatening ventricular arrhythmias in NIDCM; however, risk stratification remains imprecise. LGE shape and simulations of electrical activity may be able to provide additional prognostic information.\n Cardiac magnetic resonance (CMR)-LGE shape metrics were computed for a cohort of 156 patients with NIDCM and visible LGE and tested retrospectively for an association with an arrhythmic composite endpoint of sudden cardiac death and ventricular tachycardia. Computational models were created from images and used in conjunction with simulated stimulation protocols to assess the potential for re-entry induction in each patient's scar morphology. A mechanistic analysis of the simulations was carried out to explain the associations.\n During a median follow-up of 1, 11 (interquartile range: 881 to 2, 41) days, 16 patients (10.3%) met the primary endpoint. In an inverse probability weighted Cox regression, the LGE-myocardial interface area (hazard ratio [HR]: 1.75; 95% confidence interval [CI]: 1.24 to 2.47; p = 0.001), number of simulated re-entries (HR: 1.40; 95% CI: 1.23 to 1.59; p < 0.01) and LGE volume (HR: 1.44; 95% CI: 1.07 to 1.94; p = 0.02) were associated with arrhythmic events. Computational modeling revealed repolarization heterogeneity and rate-dependent block of electrical wavefronts at the LGE-myocardial interface as putative arrhythmogenic mechanisms directly related to the LGE interface area.\n The area of interface between scar and surviving myocardium, as well as simulated re-entrant activity, are associated with an elevated risk of major arrhythmic events in patients with NIDCM and LGE and represent novel risk predictors.\n Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.\n\nPlank, Gernot\n\n\n"
},
{
"text": "\n4187\nSubplasmalemmal endoplasmic reticulum controls K(Ca) channel activity upon stimulation with a moderate histamine concentration in a human umbilical vein endothelial cell line.\n\nFrieden, M\n\nMalli, R\n\nSamardzija, M\n\nDemaurex, N\n\nGraier, WF\n\nBeiträge in Fachzeitschriften\nISI:000174999200009\n11927670.0\n10.1113/jphysiol.2002.017053\nPMC2290214\nThis study was designed to elucidate the role of the subplasmalemmal endoplasmic reticulum (sER) in autacoid-induced stimulation of Ca(2+)-dependent K(+) channels in the umbilical vein endothelial cell-derived cell line EA.hy926. Cells were transfected with the Ca(2+) probe cameleon targeted to the ER for visualization of the ER network. A patch pipette was then placed close to or far (> 5 microm away) from the sER, single channel recordings (patch clamp technique) were monitored simultaneously with measurements of either ER Ca(2+) concentration (using the Ca(2+) probe Cam4-ER) or cytosolic free Ca(2+) concentration ([Ca(2+)](i); using fura-2) using a deconvolution imaging device. A voltage-dependent, large conductance Ca(2+)-dependent K(+) channel (BK(Ca); single channel conductance (gamma), 250 pS) was found. At membrane potentials of +40 and -40 mV, the EC(50) for Ca(2+) was 2.7 and 49.7 microM, respectively. In the vicinity of the sER, the BK(Ca) channel activity induced by 10 microM histamine was 32 times higher (open probability (P(o)) = 0.083 +/- 0.026) than in areas away from the sER (P(o) = 0.0026 +/- 0.002). However, at supramaximal histamine stimulation (100 microM), BK(Ca) channel activation was similar in patches in the vicinity of or away from the sER (P(o) = 0.18 +/- 0.09 and 0.25 +/- 0.07, respectively). In contrast to BK(Ca) channel activity, ER Ca(2+) depletion (Cam4-ER) and elevation of [Ca(2+)](i) in response to 10 and 100 microM histamine were not influenced by the pipette position. We conclude that in endothelial cells, the activation of BK(Ca) channels in response to moderate histamine concentration essentially depends on the proximity of the sER domains to the mouth of this K(+) channel. These findings further support our concept of the subplasmalemmal Ca(2+) control unit (SCCU) and add the local activation of Ca(2+)-activated K(+)-channels to the function of the SCCU.\n\nGraier, Wolfgang\n\nMalli, Roland\n\n\n"
},
{
"text": "\n4873\nSingle channel analysis of the regulation of GIRK1/GIRK4 channels by protein phosphorylation.\n\nMüllner, C\n\nYakubovich, D\n\nDessauer, CW\n\nPlatzer, D\n\nSchreibmayer, W\n\nBeiträge in Fachzeitschriften\nISI:000183123700063\n12547819.0\nNone\nPMC1302715\nG-Protein activated, inwardly rectifying potassium channels (GIRKs) are important effectors of G-protein beta/gamma-subunits, playing essential roles in the humoral regulation of cardiac activity and also in higher brain functions. G-protein activation of channels of the GIRK1/GIRK4 heterooligomeric composition is controlled via phosphorylation by cyclic AMP dependent protein kinase (PKA) and dephosphorylation by protein phosphatase 2A (PP(2)A). To study the molecular mechanism of this unprecedented example of G-protein effector regulation, single channel recordings were performed on isolated patches of plasma membranes of Xenopus laevis oocytes. Our study shows that: (i) The open probability (P(o)) of GIRK1/GIRK4 channels, stimulated by coexpressed m(2)-receptors, was significantly increased upon addition of the catalytic subunit of PKA to the cytosolic face of an isolated membrane patch. (ii) At moderate concentrations of recombinant G(beta1/gamma2), used to activate the channel, P(o) was significantly reduced in patches treated with PP(2)A, when compared to patches with PKA-cs. (iii) Several single channel gating parameters, including modal gating behavior, were significantly different between phosphorylated and dephosphorylated channels, indicating different gating behavior between the two forms of the protein. Most of these changes were, however, not responsible for the marked difference in P(o) at moderate G-protein concentrations. (iv) An increase of the frequency of openings (f(o)) and a reduction of dwell time duration of the channel in the long-lasting C(5) state was responsible for facilitation of GIRK1/GIRK4 channels by protein phosphorylation. Dephosphorylation by PP(2)A led to an increase of G(beta1/gamma2) concentration required for full activation of the channel and hence to a reduction of the apparent affinity of GIRK1/GIRK4 for G(beta1/gamma2). (v) Although possibly not directly the target of protein phosphorylation/dephosphorylation, the last 20 C-terminal amino acids of the GIRK1 subunit are required for the reduction of apparent affinity for the G-protein by PP(2)A, indicating that they constitute an essential part of the off-switch.\n\nPlatzer, Dieter\n\nSchreibmayer, Wolfgang\n\n\n"
}
]
}