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"text": "\n128592\nDabigatran versus warfarin in the treatment of acute venous thromboembolism.\n\nSchulman, S\n\nKearon, C\n\nKakkar, AK\n\nMismetti, P\n\nSchellong, S\n\nEriksson, H\n\nBaanstra, D\n\nSchnee, J\n\nGoldhaber, SZ\n\nRE-COVER Study Group\n\nBeiträge in Fachzeitschriften\nISI:000272547600008\n19966341.0\n10.1056/NEJMoa0906598\nNone\nBackground: The direct oral thrombin inhibitor dabigatran has a predictable anticoagulant effect and may be an alternative therapy to warfarin for patients who have acute venous thromboembolism. Methods: In a randomized, double-blind, noninferiority trial involving patients with acute venous thromboembolism who were initially given parenteral anticoagulation therapy for a median of 9 days (interquartile range, 8 to 11), we compared oral dabigatran, administered at a dose of 150 mg twice daily, with warfarin that was dose-adjusted to achieve an international normalized ratio of 2.0 to 3.0. The primary outcome was the 6-month incidence of recurrent symptomatic, objectively confirmed venous thromboembolism and related deaths. Safety end points included bleeding events, acute coronary syndromes, other adverse events, and results of liver-function tests. Results: A total of 30 of the 1274 patients randomly assigned to receive dabigatran (2.4%), as compared with 27 of the 1265 patients randomly assigned to warfarin (2.1%), had recurrent venous thromboembolism; the difference in risk was 0.4 percentage points (95% confidence interval [CI], -0.8 to 1.5; P<0.001 for the prespecified noninferiority margin). The hazard ratio with dabigatran was 1.10 (95% CI, 0.65 to 1.84). Major bleeding episodes occurred in 20 patients assigned to dabigatran (1.6%) and in 24 patients assigned to warfarin (1.9%) (hazard ratio with dabigatran, 0.82; 95% CI, 0.45 to 1.48), and episodes of any bleeding were observed in 205 patients assigned to dabigatran (16.1%) and 277 patients assigned to warfarin (21.9%; hazard ratio with dabigatran, 0.71; 95% CI, 0.59 to 0.85). The numbers of deaths, acute coronary syndromes, and abnormal liver-function tests were similar in the two groups. Adverse events leading to discontinuation of the study drug occurred in 9.0% of patients assigned to dabigatran and in 6.8% of patients assigned to warfarin (P=0.05). Conclusions: For the treatment of acute venous thromboembolism, a fixed dose of dabigatran is as effective as warfarin, has a safety profile that is similar to that of warfarin, and does not require laboratory monitoring. (ClinicalTrials.gov number, NCT00291330.) N Engl J Med 2009;361:2342-52.\n\nPilger, Ernst\n\n\n"
},
{
"text": "\n142306\nRetinal hemodynamic effects of antioxidant supplementation in an endotoxin-induced model of oxidative stress in humans.\n\nTold, R\n\nPalkovits, S\n\nSchmidl, D\n\nBoltz, A\n\nGouya, G\n\nWolzt, M\n\nNapora, KJ\n\nWerkmeister, RM\n\nPopa-Cherecheanu, A\n\nGarhöfer, G\n\nSchmetterer, L\n\nBeiträge in Fachzeitschriften\nISI:000335913100027\n24576874.0\n10.1167/iovs.13-13784\nNone\nThe Age-Related Eye Disease Study 1 (AREDS 1) has shown that nutritional supplementation with antioxidants and zinc modifies the natural course of AMD. It is presumed that the supplements exert their beneficial effects by ameliorating oxidative stress due to the scavenging of reactive oxygen species (ROS). We have shown in a human model that under oxidative stress induced by administration of lipopolysaccharide (LPS) the vasoconstrictor response of retinal vessels to oxygen breathing is diminished. This reduced vascular response to hyperoxia was previously shown to be normalized by the AREDS 1 supplements. In the present study, we tested the hypothesis that the response can also be restored by a different antioxidant formulation.\n This randomized, double-masked, placebo-controlled parallel group study included 40 healthy volunteers. On each study day, retinal red blood cell (RBC) flow and the reactivity of retinal RBC flow to hyperoxia were investigated in the absence and presence of 2 ng/kg LPS. Between the two study days, subjects received either the supplement or placebo for 14 days.\n Before supplementation LPS reduced retinal arterial vasoconstriction (P < 0.001) and reactivity of retinal RBC flow (P = 0.03) in response to 100% oxygen breathing. Two weeks of supplementation did not affect baseline retinal RBC flow, but normalized the LPS-induced change in the response to hyperoxia. The arterial vasoconstrictor response during LPS and 100% oxygen breathing was 4.1 ± 1.0% after administration of placebo and 10.6 ± 0.9% after supplementation (P = 0.005). The response of RBC flow to 100% oxygen breathing during LPS was 52.2 ± 2.1% after administration of placebo and 59.5 ± 2.0% after supplementation (P = 0.033).\n Our data show that the supplement used in the present study can normalize the response of retinal RBC flow to hyperoxia under LPS administration. This indicates that supplementation can prevent endothelial dysfunction induced by oxidative stress, which is assumed to play a role in the pathophysiology of AMD. (ClinicalTrials.gov number, NCT00914576.).\n\n\n"
},
{
"text": "\n155842\nCytosolic and nuclear caspase-8 have opposite impact on survival after liver resection for hepatocellular carcinoma.\n\nKoschny, R\n\nBrost, S\n\nHinz, U\n\nSykora, J\n\nBatke, EM\n\nSinger, S\n\nBreuhahn, K\n\nStremmel, W\n\nWalczak, H\n\nSchemmer, P\n\nSchirmacher, P\n\nGanten, TM\n\nBeiträge in Fachzeitschriften\nISI:000329029500001\n24209510.0\n10.1186/1471-2407-13-532\nPMC3834100\nAn imbalance between proliferation and apoptosis is one of the main features of carcinogenesis. TRAIL (TNF-related apoptosis-inducing ligand) induces apoptosis upon binding to the TRAIL death receptors, TRAIL receptor 1 (TRAIL-R1) and TRAIL-R2, whereas binding to TRAIL-R3 and TRAIL-R4 might promote cell survival and proliferation. The anti-tumor activity of TRAIL-R1 and TRAIL-R2 agonists is currently investigated in clinical trials. To gain further insight into the regulation of apoptosis in hepatocellular carcinoma (HCC), we investigated the TRAIL pathway and the regulators of apoptosis caspase-8, Bcl-xL and Mcl-1 in patients with HCC regarding patient survival.\n We analyzed 157 hepatocellular carcinoma patients who underwent partial liver resection or orthotopic liver transplantation and healthy control liver tissue using immunohistochemistry on tissue microarrays for the expression of TRAIL-R1 to TRAIL-R4, caspase-8, Bcl-xL and Mcl-1. Immunohistochemical data were evaluated for potential associations with clinico-pathological parameters and survival.\n Whereas TRAIL-R1 was downregulated in HCC in comparison to normal liver tissue, TRAIL-R2 and -R4 were upregulated in HCC, especially in G2 and G3 tumors. TRAIL-R1 downregulation and upregulation of TRAIL-R2 and TRAIL-R4 correlated with tumor dedifferentiation (G2/G3). TRAIL-R3, Bcl-xL and Mcl-1 showed no differential expression in tumor tissue compared to normal tissue. The expression levels of TRAIL receptors did not correlate with patient survival after partial hepatectomy. Interestingly, in tumor tissue, but not in normal hepatocytes, caspase-8 showed a strong nuclear staining. Low cytosolic and high nuclear staining intensity of caspase-8 significantly correlated with impaired survival after partial hepatectomy, which, for cytosolic caspase-8, was independent from tumor grade.\n Assessment of TRAIL-receptor expression patterns may have therapeutic implications for the use of TRAIL receptor agonists in HCC therapy. Tumor-specific nuclear localisation of caspase-8 in HCC suggests an apoptosis-independent function of caspase-8 and correlates with patient survival.\n\nSchemmer, Peter\n\n\n"
},
{
"text": "\n161082\nDefinition of a tolerable upper intake level of niacin: a systematic review and meta-analysis of the dose-dependent effects of nicotinamide and nicotinic acid supplementation.\n\nMinto, C\n\nVecchio, MG\n\nLamprecht, M\n\nGregori, D\n\nBeiträge in Fachzeitschriften\nISI:000403350500006\n28541582.0\n10.1093/nutrit/nux011\nNone\nNicotinic acid and nicotinamide are soluble compounds of the vitamin B group, widely used to regulate the lipid profile in hyperlipidemic individuals. Higher doses of nicotinic acid are associated with adverse effects, especially flushing. A unique tolerable upper intake level (UL) of nicotinic acid has not been defined.\n This meta-analysis aims to evaluate adverse effects and their incidence after supplementation with different doses of nicotinic acid and nicotinamide, comparing results with current ULs in Europe and the United States.\n PubMed was searched for articles providing detailed information about nicotinic acid or nicotinamide supplementation and related outcomes.\n A total of 2670 citations were selected for screening. Two primary outcomes were considered: occurrence of adverse effects following nicotinic acid or nicotinamide supplementation, and dose at which adverse effects occurred.\n Details on study population, type and duration of treatment, dosage of vitamins, association with lipid-influencing drugs, length of follow-up, and incidence and type of adverse events were extracted.\n After screening, 47 articles involving 11 741 individuals were included. Meta-analysis was based on estimation of benchmark doses for the probability of adverse effects after supplementation. In individuals with dyslipidemia or cardiovascular disease, nicotinic acid monotherapy seems to be protective against any adverse effects considered, as adverse events occurred at doses above those used with other treatments. In healthy individuals treated with nicotinic acid alone, major adverse effects occurred at doses below 1000 mg/d.\n Results may indicate a high degree of conservativeness in the UL of nicotinic acid, fixed at 35 mg/d in United States and 10 mg/d in Europe. Reconsideration of the UL of nicotinic acid for nutritional supplements, possibly differentiating between ULs in healthy and unhealthy individuals, may be warranted.\n © The Author(s) 2017. Published by Oxford University Press on behalf of the International Life Sciences Institute. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.\n\n\n"
},
{
"text": "\n164993\nEstimating Global Burden of Disease due to congenital anomaly: an analysis of European data\n\nBoyle, B\n\nAddor, MC\n\nArriola, L\n\nBarisic, I\n\nBianchi, F\n\nCsaky-Szunyogh, M\n\nde Walle, HEK\n\nDias, CM\n\nDraper, E\n\nGatt, M\n\nGarne, E\n\nHaeusler, M\n\nKallen, K\n\nLatos-Bielenska, A\n\nMcDonnell, B\n\nMullaney, C\n\nNelen, V\n\nNeville, AJ\n\nO'Mahony, M\n\nQueisser-Wahrendorf, A\n\nRandrianaivo, H\n\nRankin, J\n\nRissmann, A\n\nRitvanen, A\n\nRounding, C\n\nTucker, D\n\nVerellen-Dumoulin, C\n\nWellesley, D\n\nWreyford, B\n\nZymak-Zakutnia, N\n\nDolk, H\n\nBeiträge in Fachzeitschriften\nISI:000419372700005\n28667189.0\n10.1136/archdischild-2016-311845\nPMC5750368\nTo validate the estimates of Global Burden of Disease (GBD) due to congenital anomaly for Europe by comparing infant mortality data collected by EUROCAT registries with the WHO Mortality Database, and by assessing the significance of stillbirths and terminations of pregnancy for fetal anomaly (TOPFA) in the interpretation of infant mortality statistics.\n EUROCAT is a network of congenital anomaly registries collecting data on live births, fetal deaths from 20 weeks' gestation and TOPFA. Data from 29 registries in 19 countries were analysed for 2005-2009, and infant mortality (deaths of live births at age <1 year) compared with the WHO Mortality Database. Eight EUROCAT countries were excluded from further analysis on the basis that this comparison showed poor ascertainment of survival status.\n According to WHO, 17%-42% of infant mortality was attributed to congenital anomaly. In 11 EUROCAT countries, average infant mortality with congenital anomaly was 1.1 per 1000 births, with higher rates where TOPFA is illegal (Malta 3.0, Ireland 2.1). The rate of stillbirths with congenital anomaly was 0.6 per 1000. The average TOPFA prevalence was 4.6 per 1000, nearly three times more prevalent than stillbirths and infant deaths combined. TOPFA also impacted on the prevalence of postneonatal survivors with non-lethal congenital anomaly.\n By excluding TOPFA and stillbirths from GBD years of life lost (YLL) estimates, GBD underestimates the burden of disease due to congenital anomaly, and thus declining YLL over time may obscure lack of progress in primary, secondary and tertiary prevention.\n © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.\n\n\n"
},
{
"text": "\n180683\nInsulin-like growth factor 1 (IGF-1), IGF-1 density, and IGF-1/PSA ratio for prostate cancer detection.\n\nDjavan, B\n\nBursa, B\n\nSeitz, C\n\nSoeregi, G\n\nRemzi, M\n\nBasharkhah, A\n\nWolfram, R\n\nMarberger, M\n\nBeiträge in Fachzeitschriften\nISI:000082792700005\n10510914.0\n10.1016/s0090-4295(99)00280-0\nNone\nRecent studies suggest an association between increased serum levels of insulin-like growth factor 1 (IGF-1) and an increased risk of prostate cancer (PCa). We prospectively analyzed the value of IGF-1, IGF-density (IGFD), and IGF-1/prostate-specific antigen (PSA) ratio for early detection of prostate cancer.\n IGF-1, IGFD, and IGF-1/PSA ratio were determined prospectively during an 11-month period in the serum from 245 consecutive white men with PSA levels between 2.5 and 15 ng/mL. Octant biopsy (including transition zone biopsy) was performed. A second biopsy was performed 6 weeks later if the first biopsy was negative. Prostate volume was measured using transrectal ultrasound and the prolate ellipsoid method. Receiver operating characteristic curves were performed to compare tests.\n No evidence of malignancy was found in 174 patients (71%), and PCa was found in 71 (29%). The mean age for patients with no evidence of malignancy and those with PCa was 67.7+/-9 and 65.7+/-6 years, respectively (P = 0.17). IGF-1, IGFD, IGF-1/PSA ratio, and PSA were significantly higher in patients with PCa than in those with benign disease (P = 0.03, P = 0.045, P = 0.001, and P = 0.018, respectively). The area under the curve value derived from the receiver operating characteristic curves for IGF-1/PSA ratio, PSA, IGFD, and IGF-1 was 71%, 61%, 60%, and 58%, respectively. At 95% sensitivity, the specificity of the IGF-1/PSA ratio was significantly greater than that of all other parameters (P<0.0001 ). An IGF-1/PSA cutoff value of 25 afforded a 95% sensitivity for detecting PCa and would have avoided unnecessary biopsies in 24.1% of patients.\n Although IGF-1 and IGFD were unable to enhance the performance of PSA in our study, the IGF-1/PSA ratio significantly improved PCa detection over the use of PSA alone. Thus, increased IGF-1 levels (i.e., the IGF-1/PSA ratio) may not only be associated with an increased PCa risk but may also be a useful tool for early detection.\n\n\n"
},
{
"text": "\n186958\nScreening for delirium with the Intensive Care Delirium Screening Checklist (ICDSC): Symptom profile and utility of individual items in the identification of delirium dependent on the level of sedation.\n\nBoettger, S\n\nMeyer, R\n\nRichter, A\n\nFernandez, SF\n\nRudiger, A\n\nSchubert, M\n\nJenewein, J\n\nNuñez, DG\n\nBeiträge in Fachzeitschriften\nISI:000460290900012\n29792239.0\n10.1017/S1478951518000202\nNone\nThe importance of the proper identification of delirium, with its high incidence and adversities in the intensive care setting, has been widely recognized. One common screening instrument is the Intensive Care Delirium Screening Checklist (ICDSC); however, the symptom profile and key features of delirium dependent on the level of sedation have not yet been evaluated.\n In this prospective cohort study, the ICDSC was evaluated versus the Diagnostic and Statistical Manual, 4th edition, text revision, diagnosis of delirium set as standard with respect to the symptom profile, and correct identification of delirium. The aim of this study was to identify key features of delirium in the intensive care setting dependent on the Richmond Agitation and Sedation Scale levels of sedation: drowsiness versus alert and calmness.ResultThe 88 delirious patients of 225 were older, had more severe disease, and prolonged hospitalization. Irrespective of the level of sedation, delirium was correctly classified by items related to inattention, disorientation, psychomotor alterations, inappropriate speech or mood, and symptom fluctuation. In the drowsy patients, inattention reached substantial sensitivity and specificity, whereas psychomotor alterations and sleep-wake cycle disturbances were sensitive lacked specificity. The positive prediction was substantial across items, whereas the negative prediction was only moderate. In the alert and calm patient, the sensitivities were substantial for psychomotor alterations, sleep-wake cycle disturbances, and symptom fluctuations; however, these fluctuations were not specific. The positive prediction was moderate and the negative prediction substantial. Between the nondelirious drowsy and alert, the symptom profile was similar; however, drowsiness was associated with alterations in consciousness.Significance of resultsIn the clinical routine, irrespective of the level of sedation, delirium was characterized by the ICDSC items for inattention, disorientation, psychomotor alterations, inappropriate speech or mood and symptom fluctuation. Further, drowsiness caused altered levels of consciousness.\n\nJenewein, Josef\n\n\n"
},
{
"text": "\n187051\nWhat stresses parents most after the loss of an extremely preterm child? A qualitative study\n\nJenewein, J\n\nFauchere, JC\n\nGlaser, A\n\nMorgeli, HP\n\nBuchi, S\n\nBeiträge in Fachzeitschriften\nISI:000240549600004\nNone\n10.1055/s-2005-872980\nNone\nBackground and Aims: Sudden and unexpected extreme prematurity, the subsequent stay and treatment of the newborn in a Neonatal Intensive Care Unit (NICU), and finally the loss of the child is a very stressful situation for parents and may constitute risk factors for their psychological health. The aim of this study was first to analyse the most stressful factors for parents; secondly, to determine whether there are differences between parents' assessment of stressful factors and that of staff. Participants and Methods: 52 answers from parents and 14 answers from members of staff to the question "What was the most stressful factor during the birth, treatment in the NICU and death of the child?" were analysed by qualitative content analysis. Results: Content analysis showed five stressful factors overall: about 1/3 of parents' statements (30%) referred to the death of the child whereas about 2/3 referred to stressful circumstances or emotions like helplessness (30.7%), treatment in hospital (16.5%), behaviour of the environment (13.4%), and guilt (9.5%). Statements referring to treatment in hospital and guilt were significantly higher in mothers than in fathers. Analysis of the answers of the staff showed helplessness (40%), death (28.9%), and guilt (25.5%) to be the most stressful factors. Treatment in hospital per se was not rated as a stressful factor. Conclusions: There is evidence that after the death of an extremely preterm child parents not only suffer from the loss of their baby, but also from traumatic circumstances of the loss. These parents are at risk of developing long-lasting psychiatric disorders. Parents therefore should receive all the information they need and, particularly, fathers should be more involved in treatment to reduce their feelings of helplessness/isolation. Special attention should be paid to the high burden of the treatment itself As parents still have symptoms of distress even six years after the loss, general practitioners and other caregivers should be informed in order to be sensitised to potential sequelae like anxiety disorders or depression.\n\nJenewein, Josef\n\n\n"
},
{
"text": "\n2001\nPolymorphisms of apolipoproteins A-IV and E in a Turkish population living in Germany.\n\nMalle, E\n\nPfeiffer, KP\n\nDugi, K\n\nPfeiffer, C\n\nGlaum, M\n\nOezcueruemez, M\n\nKloer, HU\n\nSteinmetz, A\n\nBeiträge in Fachzeitschriften\nISI:A1996VA11500006\n8707295.0\n10.1007%2Fs004390050208\nNone\nHuman apolipoproteins (apo) E and apo A-IV are polymorphic with significantly different allele frequencies among different ethnic groups. Whereas the variation at the apo E gene locus affects plasma cholesterol levels in all populations studied so far and is associated with longevity in Caucasians, the influence of the common apo A-IV polymorphism on plasma lipoproteins has not been unanimously accepted. We have therefore determined the common apo E and apo A-IV polymorphisms by isoelectric focusing, calculated the respective allele frequencies and studied their effects on plasma lipoproteins in a random sample of 240 nonrelated Turkish subjects (141 males, 99 females) living in Germany and originating from central and eastern Anatolia. When compared with the German population and other Caucasians in Europe a prominence of the apo epsilon 3 allele frequency (0.885) was accompanied by a decrease in the frequencies of both the apo epsilon 2 allele (0.048) and the apo epsilon 4 allele (0.067). Thus, the Turkish population studied here clustered with populations mainly from southern Europe and Japan, which have low epsilon 2 and epsilon 4 allele frequencies. Also, the frequency of the A-IV-1 allele was higher (0.967) and that of the A-IV-2 allele lower (0.033) in the Turkish subjects studied than in other populations. At an average level of total cholesterol of 194.5 +/- 45 mg/dl, no significant influence of the A-IV alleles on plasma lipoproteins was seen. However, apo E and apo B differed significantly between apo E phenotypes, with high levels of apo E and low levels of cholesterol and apo B in carriers of the epsilon 2 allele, and vice versa for the epsilon 4 allele. The average cholesterol excess for the epsilon 2 allele was -7.95 mg/dl, for the epsilon 3 allele, -1.34, and for the epsilon 4 allele, + 14.15 mg/dl. Thus, despite the unusual frequency distribution of the apo E alleles, their effects on plasma lipoproteins are within the range reported for other populations in Europe.\n\nMalle, Ernst\n\n\n"
},
{
"text": "\n2381\nSodium chloride-citrate beverages attenuate hypovolemia in men resting 12 h at 2800 m altitude.\n\nGreenleaf, JE\n\nFarrell, PA\n\nLoomis, JL\n\nFedele, MJ\n\nWest, J\n\nRössler, A\n\nHinghofer-Szalkay, H\n\nBeiträge in Fachzeitschriften\nISI:000076125400002\n9773893.0\nNone\nNone\nBACKGROUND: The mechanism for reduction and restoration of total body water and plasma volume (PV) during initial exposure to acute altitude (ALT) is not clear but may involve involuntary dehydration; i.e., delayed voluntary fluid intake. METHOD: Ten men (24 +/- SD 3 yr, 180.8 +/- 8.1 cm height, 78.8 +/- 12.8 kg weight, 1.99 +/- 0.19 m2 surface area, and 12.2 +/- 4.0% body fat) were in a semi-reclining position for 12 h in a chamber at 2800 m (539 mmHg) ALT or at 321 m (732 mmHg; ground). They ate a controlled breakfast (450 kcal + 3 ml x kg(-1) H2O) on the ground, and lunch and dinner at ALT (or on the ground) for a total daily intake of 2850 kcal (14% PRO, 67% CHO, 16% fat, 2.6g NaCl). At hour 10 they consumed fluid-electrolyte beverages or water (12 ml x kg(-1), 948 ml x d(-1)) in 4 sessions at weekly intervals. Beverage compositions were: a) 185 mEq x L(-1) Na+, 283 mOsm x kg(-1); b) 21.6 mEq x L(-1) Na+, 365 mOsm x kg(-1); c) water at ALT; and d) water on the ground. RESULTS: After 10 h at ALT % deltaPV (Hb-Hct) decreased (p < 0.05) by: a) 9.0 +/- SE 1.5%; b) 6.2 +/- 1.7%; c) 7.4 +/- 2.2%; and d) by 9.0 +/- 2.4%, respectively. After drinking from 1000-1030 h, PV at 1200 h changed by: a) +8.3 +/- SE 2.0% (p < 0.05); b) +2.8 +/- 2.7% (NS); c) -0.9 +/- 1.5% (NS); and d) by +0.8 +/- 3.5% (NS), respectively. The similar ground-induced hypovolemia suggests a response to confinement rather than an ALT effect and involuntary dehydration does not appear to be implicated. CONCLUSION: The significant increase in PV after consuming the (a) NaCl-NaCitrate beverage indicates that drink ionic composition appears to be more important than its osmolality for restoring PV in these conditions. Practical considerations: Because this hypovolemia was probably due to the confinement rather that reduced ambient pressure, appropriate countermeasures could be consumption of isotonic beverages, elastic stockings, leg exercise, and leg elevation.\n\nHinghofer-Szalkay, Helmut\n\nRössler, Andreas\n\n\n"
},
{
"text": "\n22643\nERK and STAT3 phosphorylation in sensory neurons during capsaicin-induced impairment and nerve growth factor treatment.\n\nDonnerer, J\n\nLiebmann, I\n\nSchicho, R\n\nBeiträge in Fachzeitschriften\nISI:000232489400002\n16141720.0\n10.1159/000088015\nNone\nDistinct signal transduction pathways have been shown to regulate injury responses and regeneration in peripheral nerves. In the present investigation, the time courses of the induction of phospho-MAPK/ERK1/2 and of phospho-STAT3 were investigated in the dorsal root ganglia (DRG) and in the sciatic nerve of rats following a systemic capsaicin treatment without or with concomitant intraplantar NGF injections. Western blots were probed with polyclonal antibodies that specifically detect phosphorylated ERK 1/2 and STAT3. Phosphorylation of ERK clearly peaked in the sciatic nerve and in the lumbar DRGs at 6 and 10 h after the capsaicin treatment. In the following 8 days phospho-ERK decreased to very low levels and was found recovered to basal values at the time point 16 days. An additional intraplantar nerve growth factor (NGF) injection at time points 20, 44 and 92 h after the capsaicin treatment, and collection of tissues 4 h later, markedly increased the level of phospho-ERK in the sciatic nerve as well as in the DRG, as compared to the samples taken from rats at the same time points with a capsaicin treatment only. Posphorylated STAT3, which was almost non-detectable in the control sciatic nerve, clearly peaked at 6 h after the capsaicin treatment and decreased again during the following days to almost undetectable levels. The intraplantar NGF injections slightly stimulated phosho-STAT3 in the sciatic nerve. A basal level of phosphorylated STAT3 was present in DRGs of control animals, it remained at a high level up to 6 h after the capsaicin treatment, then markedly decreased and recovered on day 8 and day 16. NGF increased STAT3 phosphorylation in DRG on day 1 and day 2 above the level observed in samples taken from rats at the same time points with a capsaicin treatment only. The present study demonstrates that a capsaicin impairment of small diameter primary sensory neurons followed by an NGF treatment evokes a characteristic pattern of ERK and STAT3 activation indicative of neuronal degeneration and regeneration.\n\nDonnerer, Josef\n\nSchicho, Rudolf\n\n\n"
},
{
"text": "\n72318\nMultidrug-resistance gene 1-type p-glycoprotein (MDR1 p-gp) inhibition by tariquidar impacts on neuroendocrine and behavioral processing of stress.\n\nThoeringer, CK\n\nWultsch, T\n\nShahbazian, A\n\nPainsipp, E\n\nHolzer, P\n\nBeiträge in Fachzeitschriften\nISI:000251698100019\n17881135.0\n10.1016/j.psyneuen.2007.08.001\nNone\nThe multidrug-resistance gene 1-type p-glycoprotein (MDR1 p-gp) is a major gate-keeper at the blood-brain barrier (BBB), protecting the central nervous system from accumulation of toxic xenobiotics and drugs. In addition, MDR1 p-gp has been found to control the intracerebral access of glucocorticoid hormones and thus to modulate the activity of the hypothalamic-pituitary-adrenocortical (HPA) system. In view of the implication of glucocorticoids in the control of behavior, we examined how acute pharmacological inhibition of MDR1 p-gp at the BBB by tariquidar (XR9576; 12 mg/kg, PO) impacts the neuroendocrine and behavioral processing of stress in C57BL/6JIcoHim inbred mice. Inhibition of MDR1 p-gp at the BBB did not alter emotional behavior at baseline. However, mice that were sensitized by water-avoidance stress, a mild psychological stressor, displayed significantly reduced anxiety-related behavior in the elevated plus-maze test when treated with tariquidar. Tariquidar, however, had no effect on stress-coping performance assessed in the forced swim test. Investigating the impact of acute MDR1 p-gp inhibition on the glucocorticoid system, we observed a significant attenuation of the mild stress-induced increase of plasma corticosterone after tariquidar administration. In order to examine whether the anti-anxiety effect of tariquidar in sensitized animals is mediated by glucocorticoids, the animals were treated with corticosterone (1mg/kg, SC) immediately after exposure to water-avoidance stress. Corticosterone caused a significant anxiolytic-like effect in this stress-related anxiety protocol, whereas tariquidar could not further enhance corticosterone's anti-anxiety effects. The current data show for the first time that pharmacological inhibition of MDR1 p-gp at the murine BBB by tariquidar alters emotional behavior and HPA axis activity. By facilitating the entry of corticosterone into the brain, tariquidar enhances feedback inhibition of the HPA system and in this way improves anxiety-related stress processing. These findings highlight a novel approach to the treatment of stress-related affective disorders in humans.\n\nHolzer, Peter\n\n\n"
},
{
"text": "\n91031\nExit-site care in austrian peritoneal dialysis centers -- a nationwide survey.\n\nKopriva-Altfahrt, G\n\nKonig, P\n\nMundle, M\n\nPrischl, F\n\nRoob, JM\n\nWiesholzer, M\n\nVychytil, A\n\nBeiträge in Fachzeitschriften\nISI:000266247800020\n19458307.0\nNone\nNone\nBackground: Catheter-associated infections markedly contribute to treatment failure in peritoneal dialysis (PD) patients. There is much controversy surrounding prophylactic strategies to prevent these infections. Methods: In this nationwide multicenter study we analyzed strategies to prevent catheter-associated infections as performed in Austrian PD centers in 2006. A questionnaire was sent to all 23 PD centers in Austria. Results: Ten different catheter models were used in the 332 patients being treated in the 23 Austrian PD centers. Systemic antibiotics prior to catheter placement were given by 17 of the 23 PD centers (glycopeptides, n = 7; cephalosporins, n = 10). Nasal swabs were taken preoperatively by 17 PD centers; nasal Staphylococcus aureus carriers were treated prophylactically with mupirocin cream in 15 of these centers. Dressing change was routinely performed in 318 of 332 chronic PD patients (nonocclusive film dressing, n = 58; gauze dressing, n = 260). Disinfectants for chronic exit-site care included povidone iodine (n = 155), sodium hypochlorite (n = 31), povidone iodine + sodium hypochlorite together (n = 102), and octenidine dihydrochloride/phenoxyethanol (n = 17). Water + non-disinfectant soap or 0.9% sodium chloride was administered as a cleansing agent to the exit site by 27 patients. Routine S. aureus screening (nasal and/or exit-site swabs) in chronic PD patients was performed in 12 PD centers; carriers were treated with mupirocin cream in 11 of these centers. Dialysis staff members were screened for S. aureus in 8 PD centers and spouses were screened for S. aureus in 5 PD centers. The overall exit-site infection rate was 1 episode/43.9 patient-months, tunnel infection rate was 1 episode/88.9 patient-months, and peritonitis rate was 1 episode/51.0 patient-months. Patients of centers that have installed a prophylaxis protocol for treating S. aureus carriers had lower mean infection rates compared with those not using such a protocol. Conclusion: Various individual prophylactic strategies are used to prevent catheter-associated infections in Austrian PD centers. Infection rates are within the range reported in the literature. There is still scope for improvement in some centers (e. g., by establishing a prophylaxis protocol).\n\n\n"
},
{
"text": "\n106179\nUrinary collagen fragments are significantly altered in diabetes: a link to pathophysiology.\n\nMaahs, DM\n\nSiwy, J\n\nArgilés, A\n\nCerna, M\n\nDelles, C\n\nDominiczak, AF\n\nGayrard, N\n\nIphöfer, A\n\nJänsch, L\n\nJerums, G\n\nMedek, K\n\nMischak, H\n\nNavis, GJ\n\nRoob, JM\n\nRossing, K\n\nRossing, P\n\nRychlík, I\n\nSchiffer, E\n\nSchmieder, RE\n\nWascher, TC\n\nWinklhofer-Roob, BM\n\nZimmerli, LU\n\nZürbig, P\n\nSnell-Bergeon, JK\n\nBeiträge in Fachzeitschriften\nISI:000282210700021\n20927192.0\n10.1371/journal.pone.0013051\nPMC2946909\nThe pathogenesis of diabetes mellitus (DM) is variable, comprising different inflammatory and immune responses. Proteome analysis holds the promise of delivering insight into the pathophysiological changes associated with diabetes. Recently, we identified and validated urinary proteomics biomarkers for diabetes. Based on these initial findings, we aimed to further validate urinary proteomics biomarkers specific for diabetes in general, and particularity associated with either type 1 (T1D) or type 2 diabetes (T2D).\n Therefore, the low-molecular-weight urinary proteome of 902 subjects from 10 different centers, 315 controls and 587 patients with T1D (n = 299) or T2D (n = 288), was analyzed using capillary-electrophoresis mass-spectrometry. The 261 urinary biomarkers (100 were sequenced) previously discovered in 205 subjects were validated in an additional 697 subjects to distinguish DM subjects (n = 382) from control subjects (n = 315) with 94% (95% CI: 92-95) accuracy in this study. To identify biomarkers that differentiate T1D from T2D, a subset of normoalbuminuric patients with T1D (n = 68) and T2D (n = 42) was employed, enabling identification of 131 biomarker candidates (40 were sequenced) differentially regulated between T1D and T2D. These biomarkers distinguished T1D from T2D in an independent validation set of normoalbuminuric patients (n = 108) with 88% (95% CI: 81-94%) accuracy, and in patients with impaired renal function (n = 369) with 85% (95% CI: 81-88%) accuracy. Specific collagen fragments were associated with diabetes and type of diabetes indicating changes in collagen turnover and extracellular matrix as one hallmark of the molecular pathophysiology of diabetes. Additional biomarkers including inflammatory processes and pro-thrombotic alterations were observed.\n These findings, based on the largest proteomic study performed to date on subjects with DM, validate the previously described biomarkers for DM, and pinpoint differences in the urinary proteome of T1D and T2D, indicating significant differences in extracellular matrix remodeling.\n\n\n"
},
{
"text": "\n121621\nA high-throughput resequencing microarray for autosomal dominant spastic paraplegia genes.\n\nDufke, C\n\nSchlipf, N\n\nSchule, R\n\nBonin, M\n\nAuer-Grumbach, M\n\nStevanin, G\n\nDepienne, C\n\nKassubek, J\n\nKlebe, S\n\nKlimpe, S\n\nKlopstock, T\n\nOtto, S\n\nPoths, S\n\nSeibel, A\n\nStolze, H\n\nGal, A\n\nSchols, L\n\nBauer, P\n\n\n\nBeiträge in Fachzeitschriften\nISI:000307520500004\n22552817.0\n10.1007/s10048-012-0329-6\nNone\nHereditary spastic paraplegias (HSP) are a heterogeneous group of neurological disorders. Insidiously progressive spastic weakness of the lower extremities is the common criterion in all forms described. Clinically, HSP is differentiated into pure (uncomplicated) and complex (complicated) forms. While pure HSP is predominantly characterized by signs and symptoms of pyramidal tract dysfunction, additional neurological and non-neurological symptoms occur in complicated forms. Autosomal dominant, autosomal recessive, and X-linked modes of inheritance have been described and at least 48 subtypes, termed SPG1-48, have been genetically defined. Although in autosomal dominant HSP families 50-60% of etiologies can be established by genetic testing, genotype predictions based on the phenotype are limited. In order to realize high-throughput genotyping for dominant HSP, we designed a resequencing microarray for six autosomal dominant genes on the Affymetrix CustomSEQ array platform. For validation purposes, 10 previously Sanger sequenced patients with autosomal dominant HSP and 40 positive controls with known mutations in ATL1, SPAST, NIPA1, KIF5A, and BSCL2 (32 base exchanges, eight small indels) were resequenced on this array. DNA samples of 45 additional patients with AD spastic paraplegia were included in the study. With two different sequencing analysis software modules (GSEQ, SeqC), all missense/nonsense mutations in the positive controls were identified while indels had a detection rate of only 50%. In total, 244 common synonymous single-nucleotide polymorphisms (SNPs) annotated in dbSNP (build 132) corresponding to 22 distinct sequence variations were found in the 53 analyzed patients. Among the 22 different sequence variations (SPAST n = 15, ATL1 n = 3, KIF5A n = 2, HSPD1 n = 1, BSCL2 n = 1, NIPA1 n = 0), 12 were rare variants that have not been previously described and whose clinical significance is unknown. In SPAST-negative cases, a genetic diagnosis could be established in 11% by resequencing. Resequencing microarray technology can therefore efficiently be used to study genotypes and mutations in large patient cohorts.\n\n\n"
},
{
"text": "\n124046\nDevelopmental dysplasia of the hip: impact of sonographic newborn hip screening on the outcome of early treated decentered hip joints-a single center retrospective comparative cohort study based on Graf's method of hip ultrasonography.\n\nTschauner, C\n\nFürntrath, F\n\nSaba, Y\n\nBerghold, A\n\nRadl, R\n\nBeiträge in Fachzeitschriften\nNone\n23205143.0\n10.1007/s11832-011-0366-y\nPMC3221760\nPURPOSE/BACKGROUND/INTRODUCTION: The aim of this study was to retrospectively evaluate the impact of neonatal sonographic hip screening using Graf's method for the management and outcome of orthopaedic treatment of decentered hip joints with developmental dysplasia of the hip (DDH), using three decades (1978-2007) of clinical information compiled in a medical database.\n Three representative cohorts of consecutive cases of decentered hip joints were selected according to different search criteria and inclusion and exclusion parameters: (1) cohort 1 (1978-1982; n = 80), without sonographic screening; (2) cohort 2.1 (1994-1996; n = 91), with nationwide established general sonographic screening according to the Graf-method; (3) cohort 2.2 (2003-2005; n = 91), with sonographic screening including referred cases for open reduction from non-screened populations. These three cohorts were compared for the following parameters: age at initial treatment, successful closed reduction, necessary overhead traction, necessary adductor-tenotomy, rate of open reduction, rate of avascular necrosis (AVN) and rate of secondary acetabuloplasty.\n The age at initial treatment was reduced from 5.5 months in the first cohort to 2 months in the two subsequent two cohorts and the rate of successful closed reduction increased from 88.7 to 98.9 and 95.6%, respectively. There was a statistically significant improvement in six out of seven parameters with sonographic hip screening; only the rate of secondary acetabuloplasty did not improve significantly.\n Compared to the era before the institution of a sonographic hip screening programme according to the Graf-method in Austria in 1992, ultrasound screening based-treatment of decentered hip joints has become safer, shorter and simpler: "safer" means lower rate of AVN, "shorter" means less treatment time due to earlier onset and "simpler" means that the devices are now less invasive and highly standardized.\n\nBerghold, Andrea\n\nRadl, Roman\n\nSABA, Yasaman\n\n\n"
},
{
"text": "\n126226\nCommon Variants Within Oxidative Phosphorylation Genes Influence Risk of Ischemic Stroke and Intracerebral Hemorrhage.\n\nAnderson, CD\n\nBiffi, A\n\nNalls, MA\n\nDevan, WJ\n\nSchwab, K\n\nAyres, AM\n\nValant, V\n\nRoss, OA\n\nRost, NS\n\nSaxena, R\n\nViswanathan, A\n\nWorrall, BB\n\nBrott, TG\n\nGoldstein, JN\n\nBrown, D\n\nBroderick, JP\n\nNorrving, B\n\nGreenberg, SM\n\nSilliman, SL\n\nHansen, BM\n\nTirschwell, DL\n\nLindgren, A\n\nSlowik, A\n\nSchmidt, R\n\nSelim, M\n\nRoquer, J\n\nMontaner, J\n\nSingleton, AB\n\nKidwell, CS\n\nWoo, D\n\nFurie, KL\n\nMeschia, JF\n\nRosand, J\n\non behalf of the International Stroke Genetics Consortium\n\nBeiträge in Fachzeitschriften\nISI:000315447400013\n23362085.0\n10.1161/STROKEAHA.112.672089\nPMC3582722\nBackground and Purpose-Previous studies demonstrated association between mitochondrial DNA variants and ischemic stroke (IS). We investigated whether variants within a larger set of oxidative phosphorylation (OXPHOS) genes encoded by both autosomal and mitochondrial DNA were associated with risk of IS and, based on our results, extended our investigation to intracerebral hemorrhage (ICH).\nMethods-This association study used a discovery cohort of 1643 individuals, a validation cohort of 2432 individuals for IS, and an extension cohort of 1476 individuals for ICH. Gene-set enrichment analysis was performed on all structural OXPHOS genes, as well as genes contributing to individual respiratory complexes. Gene-sets passing gene-set enrichment analysis were tested by constructing genetic scores using common variants residing within each gene. Associations between each variant and IS that emerged in the discovery cohort were examined in validation and extension cohorts.\nResults-IS was associated with genetic risk scores in OXPHOS as a whole (odds ratio [OR], 1.17; P=0.008) and complex I (OR, 1.06; P=0.050). Among IS subtypes, small vessel stroke showed association with OXPHOS (OR, 1.16; P=0.007), complex I (OR, 1.13; P=0.027), and complex IV (OR, 1.14; P=0.018). To further explore this small vessel association, we extended our analysis to ICH, revealing association between deep hemispheric ICH and complex IV (OR, 1.08; P=0.008).\nConclusions-This pathway analysis demonstrates association between common genetic variants within OXPHOS genes and stroke. The associations for small vessel stroke and deep ICH suggest that genetic variation in OXPHOS influences small vessel pathobiology. Further studies are needed to identify culprit genetic variants and assess their functional consequences. (Stroke. 2013;44:612-619.)\n\nSchmidt, Reinhold\n\n\n"
},
{
"text": "\n127107\nChanges in the prevalence, treatment and control of hypertension in Germany? A clinical-epidemiological study of 50.000 primary care patients.\n\nLabeit, AM\n\nKlotsche, J\n\nPieper, L\n\nPittrow, D\n\nEinsle, F\n\nStalla, GK\n\nLehnert, H\n\nSilber, S\n\nZeiher, AM\n\nMärz, W\n\nWehling, M\n\nWittchen, HU\n\nBeiträge in Fachzeitschriften\nISI:000313051500025\n23284945.0\n10.1371/journal.pone.0052229\nPMC3532113\nIntroduction: Medical societies have developed guidelines for the detection, treatment and control of hypertension (HTN). Our analysis assessed the extent to which such guidelines were implemented in Germany in 2003 and 2001.\nMethods: Using standardized clinical diagnostic and treatment appraisal forms, blood pressure levels and patient questionnaires for 55, 18 participants from the cross-sectional Targets and Essential Data for Commitment of Treatment (DETECT) study (2003) were analyzed. PhysicianANDapos;s diagnosis of hypertension (HTNdoc) was defined as coding hypertension in the clinical appraisal questionnaire. Alternative definitions used were physicianANDapos;s diagnosis or the patientANDapos;s self-reported diagnosis of hypertension (HTNdoc, at), physicianANDapos;s or patientANDapos;s self-reported diagnosis or a BP measurement with a systolic BP ANDgt;= 140 mmHg and/or a diastolic BP ANDgt;= 90 (HTNdoc, at, p) and diagnosis according to the National Health and Nutrition Examination Survey (HTNNHANES). The results were compared with the similar German HYDRA study to examine whether changes had occurred in diagnosis, treatment and adequate blood pressure control (BP below 140/90 mmHg) since 2001. Factors associated with pharmacotherapy and control were determined.\nResults: The overall prevalence rate for hypertension was 35.5% according to HTNdoc and 56.0% according to NHANES criteria. Among those defined by NHANES criteria, treatment and control rates were 56.0% and 20.3% in 2003, and these rates had improved from 55.3% and 18.0% in 2001. Significant predictors of receiving antihypertensive medication were: increasing age, female sex, obesity, previous myocardial infarction and the prevalence of comorbid conditions such as coronary heart disease (CHD), hyperlipidemia and diabetes mellitus (DM). Significant positive predictors of adequate blood pressure control were CHD and antihypertensive medication. Inadequate control was associated with increasing age, male sex and obesity.\nConclusions: Rates of treated and controlled hypertension according to NHANES criteria in DETECT remained low between 2001 and 2003, although there was some minor improvement.\n\nMärz, Winfried\n\n\n"
},
{
"text": "\n135989\nThe Freedom SOLO valve: mid-term clinical results with a stentless pericardial valve for aortic valve replacement.\n\nHorst, M\n\nEaso, J\n\nHölzl, PP\n\nEichstaedt, HC\n\nKronberg, K\n\nNordmeyer, P\n\nDapunt, OE\n\nBeiträge in Fachzeitschriften\nISI:000306675200014\n22655502.0\nNone\nNone\nThe study aim was to evaluate the Freedom SOLO pericardial stentless valve prosthesis implanted in a subcoronary or supra-annular position, using a single running suture, over a follow up period of up to five years. The clinical data obtained after aortic valve replacement (AVR) were analyzed retrospectively for validation.\n Between April 2004 and September 2009, a total of 143 patients (81 males, 62 females; mean age 71 +/- 7 years; range: 41-87 years) underwent primary AVR using the Freedom SOLO valve, implanted with a supra-annular subcoronary technique. Isolated AVR was performed on 120 patients, while 23 patients required additional surgery that included coronary artery bypass grafting (n = 5), ascending aorta replacement (n = 1), atrial fibrillation surgery (n = 9), and mitral valve repair (n = 1). Clinical investigations were performed before, during and after surgery; the follow up was 100% complete. A subgroup of patients (70%) was investigated echocardiographically during the follow up period to analyze the hemodynamic performance of the prosthesis.\n For all procedures the mean ischemia time was 66 +/- 15 min, and the mean cardiopulmonary bypass (CPB) time 88 +/- 20 min. For isolated AVR, the mean cross-clamp time was 65 +/- 14 min, and the mean CPB time 85 +/- 17 min. The predominant implanted valve size was 25 mm (42%). Operative mortality was 4.9% (7/143), with an overall mortality of 10.5% (15/143) at 4.7 years of follow up. The mean follow up was 1.8 +/- 1.4 years, and the total follow up 257 patient-years. At postoperative follow up the mean valve gradient was 10.6 mmHg, while the effective orifice area was 1.9 +/- 0.6 cm2 at one month and 1.9 +/- 0.6 cm2 at 12 months.\n The Freedom SOLO valve was implanted in a cohort of patients, using a simplified, supra-annular subcoronary technique, with no technical problems. Subsequently, the valve demonstrated an excellent clinical performance for up to five years. Further long-term follow up will be required to confirm the performance of the prosthesis with regards to structural and nonstructural valve stability.\n\n\n"
},
{
"text": "\n137447\nTreat-to-target in systemic lupus erythematosus: recommendations from an international task force.\n\nvan Vollenhoven, RF\n\nMosca, M\n\nBertsias, G\n\nIsenberg, D\n\nKuhn, A\n\nLerstrøm, K\n\nAringer, M\n\nBootsma, H\n\nBoumpas, D\n\nBruce, IN\n\nCervera, R\n\nClarke, A\n\nCostedoat-Chalumeau, N\n\nCzirják, L\n\nDerksen, R\n\nDörner, T\n\nGordon, C\n\nGraninger, W\n\nHoussiau, F\n\nInanc, M\n\nJacobsen, S\n\nJayne, D\n\nJedryka-Goral, A\n\nLevitsky, A\n\nLevy, R\n\nMariette, X\n\nMorand, E\n\nNavarra, S\n\nNeumann, I\n\nRahman, A\n\nRovensky, J\n\nSmolen, J\n\nVasconcelos, C\n\nVoskuyl, A\n\nVoss, A\n\nZakharova, H\n\nZoma, A\n\nSchneider, M\n\nBeiträge in Fachzeitschriften\nISI:000335362100009\n24739325.0\n10.1136/annrheumdis-2013-205139\nNone\nThe principle of treating-to-target has been successfully applied to many diseases outside rheumatology and more recently to rheumatoid arthritis. Identifying appropriate therapeutic targets and pursuing these systematically has led to improved care for patients with these diseases and useful guidance for healthcare providers and administrators. Thus, an initiative to evaluate possible therapeutic targets and develop treat-to-target guidance was believed to be highly appropriate in the management of systemic lupus erythematosus (SLE) patients as well. Specialists in rheumatology, nephrology, dermatology, internal medicine and clinical immunology, and a patient representative, contributed to this initiative. The majority convened on three occasions in 2012-2013. Twelve topics of critical importance were identified and a systematic literature review was performed. The results were condensed and reformulated as recommendations, discussed, modified and voted upon. The finalised bullet points were analysed for degree of agreement among the task force. The Oxford Centre level of evidence (LoE, corresponding to the research questions) and grade of recommendation (GoR) were determined for each recommendation. The 12 systematic literature searches and their summaries led to 11 recommendations. Prominent features of these recommendations are targeting remission, preventing damage and improving quality of life. LoE and GoR of the recommendations were variable but agreement was >0.9 in each case. An extensive research agenda was identified, and four overarching principles were also agreed upon. Treat-to-target-in-SLE (T2T/SLE) recommendations were developed by a large task force of multispecialty experts and a patient representative. It is anticipated that 'treating-to-target' can and will be applicable to the care of patients with SLE.\n\nGraninger, Winfried\n\n\n"
}
]
}