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"text": "\n125635\nTreatment of stress urinary incontinence after radical prostatectomy: adjustable transobturator male system - results of a multicenter prospective observational study].\n\nHoda, MR\n\nPrimus, G\n\nSchumann, A\n\nFischereder, K\n\nvon Heyden, B\n\nSchmid, N\n\nMoll, V\n\nHamza, A\n\nKarsch, JJ\n\nSteinbach, F\n\nBrössner, C\n\nBauer, W\n\nFornara, P\n\nBeiträge in Fachzeitschriften\nISI:000310999500010\n22836942.0\n10.1007/s00120-012-2950-2\nNone\nThe adjustable transobturator male system (ATOMSA (R)) is a new method for the treatment of male stress urinary incontinence. This article presents the results of a prospective multicenter observational study with this system. Between March 2009 and March 2011 a total of 124 patients with persistent stress urinary incontinence after radical prostatectomy received the ATOMS system. Postoperative adjustments via the implanted port chamber were performed after 6 weeks and thereafter when necessary. Postoperative evaluation consisted of medical history, mictionary protocol, 24-h pad tests, 24-h pad counts and sonography. The mean age of the patients was 71.2 +/- 5.5 years (range 58-85 years). Previous incontinence surgery had been carried out in 36.3% of patients while 34.5% of patients had a previous history of radiation treatment. The mean operation time was 48.3 +/- 11.2 min (range 36-116 min) and the mean hospital stay was 3.8 +/- 1.2 days (range 2-6 days). No intraoperative urethral or bladder injuries occurred. After removal of the transurethral catheter on the first postoperative day, temporary urinary retention occurred in 3 patients who were conservatively treated. Transient perineal/scrotal pain or dysesthesia was observed in 75 patients (60.5%) and resolved after 3-4 weeks of non-opioid analgesics. There were no perineal infections; however, infections at the port site occurred in 3 patients (2.4%) leading to explantation of the system in all cases. The average number of adjustments to achieve the desired result was 4.3 +/- 1.8 (range 2-7). After a mean follow-up of 19.1 +/- 2.2 months (range 12-36 months), there was a significant reduction in the mean number of pads/24 h from 8.8 to 1.8 (p < 0.001). The overall success rate was 93.8% with 61.6% of the patients being dry and 32.2% of the patients showing improvement. The results of the study demonstrate the safety and efficacy to date of the ATOMS system for treatment of stress urinary incontinence after radical prostatectomy.\n\n\n"
},
{
"text": "\n127110\nA variant in the ABO gene explains the variation in soluble E-selectin levels-results from dense genotyping in two independent populations.\n\nKarakas, M\n\nBaumert, J\n\nKleber, ME\n\nThorand, B\n\nDallmeier, D\n\nSilbernagel, G\n\nGrammer, TB\n\nRottbauer, W\n\nMeisinger, C\n\nIllig, T\n\nMärz, W\n\nKoenig, W\n\nBeiträge in Fachzeitschriften\nISI:000313051500011\n23300549.0\n10.1371/journal.pone.0051441\nPMC3532506\nElevated soluble (s) E-selectin levels have been associated with various cardiovascular diseases. Recently, genetic variants in the ABO blood group have been related to E-selectin levels in a small cohort of patients with type 1 diabetes. We evaluated whether this association is reproducible in two large samples of Caucasians.\n Data of the present study was drawn from the population-based MONICA/KORA Augsburg study (n = 1, 82) and the patients-based LURIC study (n = 1, 46). A high-density genotyping array (50K IBC Chip) containing single-nucleotide polymorphisms (SNPs) from E-selectin candidate genes selected on known biology of E-selectin metabolism, mouse genetic studies, and human genetic association studies, was used for genotyping. Linear regression analyses with adjustment for age and sex (and survey in KORA) were applied to assess associations between gene variants and sE-selectin concentrations. A number of 12 SNPs (in KORA) and 13 SNPs (in LURIC), all from the ABO blood group gene, were significantly associated with the log-transformed concentration of E-selectin. The strongest association was observed for rs651007 with a change of log-transformed sE-selectin per one copy of the minor allele of -0.37 ng/ml (p = 1.87×10(-103)) in KORA and -0.35 ng/ml (p = 5.11×10(-84)) in LURIC. Inclusion of rs651007 increased the explained sE-selectin variance by 0.256 in KORA and 0.213 in LURIC. All SNPs had minor allele frequencies above 20% showing a substantial gene variation.\n Our findings in two independent samples indicate that the genetic variants at the ABO locus affect sE-selectin levels. Since distinct genome-wide association studies linked the ABO gene with myocardial infarction (MI) in the presence of coronary atherosclerosis and with coronary artery disease, these findings may not only enhance our understanding of adhesion molecule biology, but may also provide a focus for several novel research avenues.\n\nMärz, Winfried\n\nSilbernagel, Günther\n\n\n"
},
{
"text": "\n142553\nMolecular disease eradication is a prerequisite for long-term remission in patients with t(8;21) positive acute myeloid leukemia: a single center study.\n\nMitterbauer, M\n\nMitterbauer-Hohendanner, G\n\nSperr, WR\n\nKalhs, P\n\nGreinix, HT\n\nFonatsch, C\n\nHaas, OA\n\nJäger, U\n\nMannhalter, C\n\nLechner, K\n\nBeiträge in Fachzeitschriften\nISI:000220063900015\n15291357.0\n10.1080/10428190310001638913\nNone\nAssociation of long-term clinical remission and molecular disease-eradication is well established in acute myeloid leukemia (AML) patients with t(15;17) and inv(16). In patients with t(8;21) positive AML no consensus exists over the disappearance of the AML1/ETO fusion transcript during the course of disease and most studies reported reverse transcriptase polymerase chain reaction (RT-PCR) positivity as a common finding after consolidation chemotherapy, autologous and allogeneic stem cell transplantation (alloSCT). In our single center study, we performed RT-PCR monitoring in 14 patients with t(8;21) in CR1 (n = 13) and/or CR2 (n = 4). The median number of bone marrow (BM) and/or peripheral blood (PB) samples per patient was 18 (range, 2-43). In 5 out of 6 cases relapse occurred after persistence of minimal residual disease (MRD) in CR for 4-14 months. The sixth patient relapsed despite molecular remission (MR) in BM and PB for 3 months, molecular relapse preceded hematological relapse for 7 months. Eleven patients with a median follow-up of 7.8 (range, 1.5-15.4) years are in persistent CR and MR after consolidation chemotherapy (n = 7). mainly with repetitive cycles of high-dose Ara-C, autologous (n = 1) or myeloablative allogeneic (n = 3) stem cell transplantation. Molecular remission was attained immediately after alloSCT, but after 6-26 months in CR in patients with consolidation chemotherapy. In 7 patients, MRD was only studied in long-term remission. In conclusion, long-term CR was associated with persistent molecular disease-eradication. In our patients, molecular remission was a prerequisite but not a guarantee for long-term disease-free survival. Hematological relapse never occurred without prior molecular relapse. Due to the slow kinetics of AML1/ETO after consolidation chemotherapy the value of qualitative RT-PCR to predict early relapse is limited. In this situation quantitative RT-PCR might help to define individual relapse risk and to improve as well as facilitate clinical decision-making.\n\nGreinix, Hildegard\n\n\n"
},
{
"text": "\n145655\nEpigenetic down-regulation of integrin α7 increases migratory potential and confers poor prognosis in malignant pleural mesothelioma.\n\nLaszlo, V\n\nHoda, MA\n\nGaray, T\n\nPirker, C\n\nGhanim, B\n\nKlikovits, T\n\nDong, YW\n\nRozsas, A\n\nKenessey, I\n\nSzirtes, I\n\nGrusch, M\n\nJakopovic, M\n\nSamarzija, M\n\nBrcic, L\n\nKern, I\n\nRozman, A\n\nPopper, H\n\nZöchbauer-Müller, S\n\nHeller, G\n\nAltenberger, C\n\nZiegler, B\n\nKlepetko, W\n\nBerger, W\n\nDome, B\n\nHegedus, B\n\nBeiträge in Fachzeitschriften\nISI:000360913200007\n26011651.0\n10.1002/path.4567\nNone\nMalignant pleural mesothelioma (MPM) is a devastating malignancy characterized by invasive growth and rapid recurrence. The identification and inhibition of molecular components leading to this migratory and invasive phenotype are thus essential. Accordingly, a genome-wide expression array analysis was performed on MPM cell lines and a set of 139 genes was identified as differentially expressed in cells with high versus low migratory activity. Reduced expression of the novel tumour suppressor integrin α7 (ITGA7) was found in highly motile cells. A significant negative correlation was observed between ITGA7 transcript levels and average displacement of cells. Forced overexpression of ITGA7 in MPM cells with low endogenous ITGA7 expression inhibited cell motility, providing direct evidence for the regulatory role of ITGA7 in MPM cell migration. MPM cells showed decreased ITGA7 expressions at both transcription and protein levels when compared to non-malignant mesothelial cells. The majority of MPM cell cultures displayed hypermethylation of the ITGA7 promoter when compared to mesothelial cultures. A statistically significant negative correlation between ITGA7 methylation and ITGA7 expression was also observed in MPM cells. While normal human pleura samples unambiguously expressed ITGA7, a varying level of expression was found in a panel of 200 human MPM samples. In multivariate analysis, ITGA7 expression was found to be an independent prognostic factor. Although there was no correlation between histological subtypes and ITGA7 expression, importantly, patients with high tumour cell ITGA7 expression had an increased median overall survival compared to the low- or no-expression groups (463 versus 278 days). In conclusion, our data suggest that ITGA7 is an epigenetically regulated tumour suppressor gene and a prognostic factor in human MPM.\n Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.\n\nBrcic, Luka\n\nPopper, Helmuth\n\n\n"
},
{
"text": "\n151830\nAugmentation of phosphate-induced osteo-/chondrogenic transformation of vascular smooth muscle cells by homoarginine.\n\nAlesutan, I\n\nFeger, M\n\nTuffaha, R\n\nCastor, T\n\nMusculus, K\n\nBuehling, SS\n\nHeine, CL\n\nKuro-O, M\n\nPieske, B\n\nSchmidt, K\n\nTomaschitz, A\n\nMaerz, W\n\nPilz, S\n\nMeinitzer, A\n\nVoelkl, J\n\nLang, F\n\nBeiträge in Fachzeitschriften\nISI:000378442700015\n27001421.0\n10.1093/cvr/cvw062\nNone\nReduced homoarginine plasma levels are associated with unfavourable cardiovascular outcome in chronic kidney disease (CKD). Cardiovascular events in CKD are fostered by vascular calcification, an active process promoted by hyperphosphatemia and involving osteo-/chondrogenic transformation of vascular smooth muscle cells (VSMCs). The present study explored the effect of homoarginine on phosphate-induced osteo-/chondrogenic signalling and vascular calcification.\n Experiments were performed in hyperphosphatemic klotho-hypomorphic mice (kl/kl), in subtotal nephrectomy and vitamin D3-overload mouse calcification models and in primary human aortic smooth muscle cells (HAoSMCs). As a result, plasma homoarginine levels were lower in kl/kl mice than in wild-type mice and in both genotypes significantly increased by lifelong treatment with homoarginine. Surprisingly, homoarginine treatment of kl/kl mice and of mice with renal failure after subtotal nephrectomy augmented vascular calcification and enhanced the transcript levels of plasminogen activator inhibitor 1 (Pai1) and of osteogenic markers Msx2, Cbfa1, and Alpl. Similarly, homoarginine treatment of HAoSMCs increased phosphate-induced calcium deposition, ALP activity, as well as PAI1, MSX2, CBFA1, and ALPL mRNA levels. Homoarginine alone up-regulated osteo-/chondrogenic signalling and indicators of oxidative stress in HAoSMCs. Furthermore, homoarginine reduced citrulline formation from arginine by nitric oxide (NO) synthase (NOS) isoforms. NO formation by NOS was reduced when using homoarginine as a substrate instead of arginine. The osteoinductive effects of homoarginine were mimicked by NOS inhibitor L-NAME and abolished by additional treatment with the NO donors DETA-NONOate and PAPA-NONOate or the antioxidants TEMPOL and TIRON. Furthermore, homoarginine augmented vascular calcification and aortic osteo-/chondrogenic signalling in mice after vitamin D3-overload, effects reversed by the NO donor molsidomine.\n Homoarginine augments osteo-/chondrogenic transformation of VSMCs and vascular calcification, effects involving impaired NO formation from homoarginine.\n Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2016. For permissions please email: journals.permissions@oup.com.\n\nMärz, Winfried\n\nMeinitzer, Andreas\n\nPilz, Stefan\n\n\n"
},
{
"text": "\n167049\nGlenohumeral Function of the Long Head of the Biceps Muscle: An Electromyographic Analysis.\n\nChalmers, PN\n\nCip, J\n\nTrombley, R\n\nCole, BJ\n\nWimmer, MA\n\nRomeo, AA\n\nVerma, NN\n\nBeiträge in Fachzeitschriften\nNone\n26535304.0\n10.1177/2325967114523902\nPMC4555617\nOptimal treatment of superior labral anterior-posterior (SLAP) tears is controversial, in part because the dynamic role of the long head of the biceps muscle (LHBM) in the glenohumeral joint is unclear. The aim of this study was to determine dynamic LHBM behavior during shoulder activity by studying (1) the electromyographic activity of the LHBM during shoulder motion, (2) the effect of elbow immobilization on this activity, and (3) the effect of a load applied to the distal humerus on this activity.\n The LHBM would not play a significant role in active glenohumeral range of motion.\n Controlled laboratory study.\n Thirteen normal volunteers underwent surface electromyography (EMG) measurement of the LHBM, short head biceps muscle (SHBM), deltoid, infraspinatus, and brachioradialis during shoulder motion from the neutral position (0° of rotation, flexion, and abduction) to 45° of flexion, 90° of flexion, 45° of abduction, and 90° of abduction. These motions were repeated both with and without splint immobilization of the forearm and elbow at 100° of flexion and neutral rotation and with and without a 1-kg weight placed on the lateral distal humerus.\n Mean EMG activity within the LHBM and the SHBM was low (≤11.6% ± 9.1%). LHBM activity was significant increased by flexion and abduction (P < .049 in all cases), while SHBM activity was not. EMG activity from the middle head of the deltoid was significantly increased by loading with the shoulder positioned away from the body (ie, in abduction or flexion). When compared with the unloaded state, the addition of a distal humeral load significantly increased LHBM activity in 45° of abduction (P = .028) and 90° of flexion (P = .033) despite forearm and elbow immobilization. The SHBM showed similar trends.\n In normal volunteers with forearm and elbow immobilization and application of a load to the distal humerus, LHBM EMG activity is increased by both glenohumeral flexion and abduction, suggesting that this muscle plays a dynamic role in glenohumeral motion with higher demand activities.\n Biceps tenodesis may result in dynamic change within the glenohumeral joint with higher demand activities.\n\n\n"
},
{
"text": "\n170050\nInterventions to increase hand hygiene compliance in a tertiary university hospital over a period of 5 years: An iterative process of information, training and feedback.\n\nHoffmann, M\n\nSendlhofer, G\n\nPregartner, G\n\nGombotz, V\n\nTax, C\n\nZierler, R\n\nBrunner, G\n\nBeiträge in Fachzeitschriften\nISI:000458362400019\n30357973.0\n10.1111/jocn.14703\nNone\nTo explore whether an iterative process of information and training paired with a feedback system to observed healthcare professionals and the respective management improves hand hygiene (HH) compliance.\n Healthcare-associated infections are a major risk for patient safety, and adherence to the "My five moments" (M5M) for HH varies significantly within organisations as well as within healthcare professional groups. Identified barriers in a baseline survey revealed the need of more information, training, repetitive compliance measurements and feedback to all healthcare professionals.\n A quality improvement project using the method of direct observation of healthcare professionals in nonsurgical and surgical wards.\n Between 2013 and 2017, 6, 09 healthcare professionals were informed and trained, and HH compliance measurements were performed by hygiene experts. Compliance measurement results were documented in an online tool to give an immediate feedback to observed healthcare professionals. Additionally, a report was forwarded to the management of the respective department to raise awareness. Compliance rates per year were descriptively summarised. The research and reporting methodology followed SQUIRE 2.0.\n In total, 84 compliance measurements with 19, 95 "M5M for HH" were observed in 49 wards. Overall, mean HH compliance increased from 81.9 ± 5.2% in 2013 to 94.0 ± 3.6% in 2017. Physicians' HH compliance rate improved from 69.0 ± 16.6% to 89.3 ± 6.6%, that of nurses from 86.0 ± 6.9% to 96.4 ± 3.1%, and that of others from 60.5 ± 27.9% to 83.8 ± 20.2%. All M5M for HH (#1-#5) increased over the study period (#1: +16.9%; #2: +20.5%; #3: +7.6%; #4: +5.9%; #5: +12.7%).\n Results demonstrated that an iterative process of information, training, observation and feedback over a period of 5 years can be successful in increasing HH compliance. Positive trends were observed for HH compliance rates across all healthcare professional groups as well as for all M5M for HH.\n © 2018 The Authors. Journal of Clinical Nursing Published by John Wiley & Sons Ltd.\n\nBrunner, Gernot\n\nHoffmann, Magdalena\n\nPregartner, Gudrun\n\nSendlhofer, Gerald\n\n\n"
},
{
"text": "\n171424\nActivation of protein phosphatase 1 by a selective phosphatase disrupting peptide reduces sarcoplasmic reticulum Ca<sup>2+</sup> leak in human heart failure.\n\nFischer, TH\n\nEiringhaus, J\n\nDybkova, N\n\nSaadatmand, A\n\nPabel, S\n\nWeber, S\n\nWang, Y\n\nKöhn, M\n\nTirilomis, T\n\nLjubojevic, S\n\nRenner, A\n\nGummert, J\n\nMaier, LS\n\nHasenfuß, G\n\nEl-Armouche, A\n\nSossalla, S\n\nBeiträge in Fachzeitschriften\nISI:000453600400011\n30191648.0\n10.1002/ejhf.1297\nNone\nDisruption of Ca2+ homeostasis is a key pathomechanism in heart failure. CaMKII-dependent hyperphosphorylation of ryanodine receptors in the sarcoplasmic reticulum (SR) increases the arrhythmogenic SR Ca2+ leak and depletes SR Ca2+ stores. The contribution of conversely acting serine/threonine phosphatases [protein phosphatase 1 (PP1) and 2A (PP2A)] is largely unknown.\n Human myocardium from three groups of patients was investigated: (i) healthy controls (non-failing, NF, n = 8), (ii) compensated hypertrophy (Hy, n = 16), and (iii) end-stage heart failure (HF, n = 52). Expression of PP1 was unchanged in Hy but greater in HF compared to NF while its endogenous inhibitor-1 (I-1) was markedly lower expressed in both compared to NF, suggesting increased total PP1 activity. In contrast, PP2A expression was lower in Hy and HF compared to NF. Ca2+ homeostasis was severely disturbed in HF compared to Hy signified by a higher SR Ca2+ leak, lower systolic Ca2+ transients as well as a decreased SR Ca2+ load. Inhibition of PP1/PP2A by okadaic acid increased SR Ca2+ load and systolic Ca2+ transients but severely aggravated diastolic SR Ca2+ leak and cellular arrhythmias in Hy. Conversely, selective activation of PP1 by a PP1-disrupting peptide (PDP3) in HF potently reduced SR Ca2+ leak as well as cellular arrhythmias and, importantly, did not compromise systolic Ca2+ release and SR Ca2+ load.\n This study is the first to functionally investigate the role of PP1/PP2A for Ca2+ homeostasis in diseased human myocardium. Our data indicate that a modulation of phosphatase activity potently impacts Ca2+ cycling properties. An activation of PP1 counteracts increased kinase activity in heart failure and successfully seals the arrhythmogenic SR Ca2+ leak. It may thus represent a promising future antiarrhythmic therapeutic approach.\n © 2018 The Authors. European Journal of Heart Failure © 2018 European Society of Cardiology.\n\nHolzer, Senka\n\n\n"
},
{
"text": "\n177418\nIs Pelvic Floor Dysfunction Associated With Development of Transient Low Back Pain During Prolonged Standing? A Protocol.\n\nBussey, MD\n\nAldabe, D\n\nRibeiro, DC\n\nMadill, S\n\nWoodley, S\n\nHammer, N\n\nBeiträge in Fachzeitschriften\nNone\n31205437.0\n10.1177/1179562X19849603\nPMC6537301\nProlonged standing has been associated with an increased prevalence of low back pain (LBP) and is recognized as a potential workplace hazard for employees such as retail staff, assembly line workers, and healthcare personnel. Low back pain is more prevalent in women than in men, and disability due to LBP is worse in women with severe urinary incontinence. However, it is unclear whether pelvic floor dysfunction observed in stress urinary incontinence is a risk factor for LBP. The main purpose of this study is to determine whether co-activation patterns between the pelvic floor and abdominal muscles during a 2-hour prolonged standing task predict transient LBP in women with and without stress urinary incontinence.\n In this is prospective cohort study, 60 female volunteers will stand in a confined area for 2 hours (120 minutes) while performing tasks such as, 'computer work' and 'small object assembly'. The primary outcome measure is transient LBP, which will be monitored every 10 minutes using a numeric pain rating scale. Surface electromyography (EMG) will be collected from the gluteus medius and internal oblique/transverse abdominis muscles, and an intravaginal electrode will be used to monitor pelvic floor muscle activity. The EMG signals will be divided into 12 10-minute blocks to assess changes in co-activation over time. Cross-correlation analyses will be used to quantify co-activation between the muscle pairs (e.g. pelvic floor and internal oblique/transverse abdominis), and the coefficient of co-activation will be expressed as a percentage for each block. A mixed-model regression analysis will be used to determine whether co-activation patterns can predict transient LBP during the prolonged standing task.\n The primary objective of this research is to improve current understanding regarding the role of pelvic floor muscles in the onset of LBP and the potential association between stress urinary incontinence and LBP. These findings have the potential to inform prevention and rehabilitation programmes for women with stress urinary incontinence and LBP.\n ACTRN12618000446268 [Protocol Version 2].\n\nHammer, Niels\n\n\n"
},
{
"text": "\n178033\nNovel phenotypes observed in patients with <i>ETV6</i>-linked leukaemia/familial thrombocytopenia syndrome and a biallelic <i>ARID5B</i> risk allele as leukaemogenic cofactor.\n\nKarastaneva, A\n\nNebral, K\n\nSchlagenhauf, A\n\nBaschin, M\n\nPalankar, R\n\nJuch, H\n\nHeitzer, E\n\nSpeicher, MR\n\nHöfler, G\n\nGrigorow, I\n\nUrban, C\n\nBenesch, M\n\nGreinacher, A\n\nHaas, OA\n\nSeidel, MG\n\nBeiträge in Fachzeitschriften\nISI:000538112700010\n31704777.0\n10.1136/jmedgenet-2019-106339\nNone\nBackground. The phenotypes of patients with the recently discovered, dominant, ETV6-linked leukaemia predisposition and familial thrombocytopenia syndrome are variable, and the exact mechanism of leukaemogenesis remains unclear. Patients and Methods. Here, we present novel clinical and laboratory phenotypes of seven individuals from three families with ETV6 germline mutations and a refined genetic analysis of one child with additional high-hyperdiploid acute lymphoblastic leukaemia (HD-ALL), aiming to elucidate second oncogenic hits. Results. Four individuals from two pedigrees harboured one novel or one previously described variant in the central domain of ETV6 (c.592C>T, p.Gln198* or c.641C>T, p.Pro241Leu, respectively). Neutropenia was an accompanying feature in one of these families that also harboured a variant in RUNX1 (c.1098_1103dup, p.Ile366_Gly367dup), while in the other, an autism-spectrum disorder was observed. In the third family, the index patient suffered from HD-ALL and life-threatening pulmonary mucor mycosis, and had a positive family history of 'immune' thrombocytopenia. Genetic analyses revealed a novel heterozygous mutation in the ETS domain of ETV6 (c.1136T>C, p.Leu379Pro) along with absence of heterozygosity of chromosome (10)(q21.2q21.3), yielding a biallelic leukaemia risk allele in ARID5B (rs7090445-C). The neutrophil function was normal in all individuals tested, and the platelet immune histochemistry of all three pedigrees showed delta-storage-pool defect-like features and cytoskeletal defects. Conclusions. Our clinical observations and results of high-resolution genetic analyses extend the spectrum of possible phenotypes cosegregating with ETV6 germline mutations. Further, we propose ARID5B as potential leukaemogenic cofactor in patients with ETV6-linked leukaemia predisposition and familial thrombocytopenia syndrome.\n © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.\n\nBenesch, Martin\n\nHeitzer, Ellen\n\nHöfler, Gerald\n\nJuch, Herbert\n\nKarastaneva, Anna\n\nSchlagenhauf, Axel\n\nSeidel, Markus\n\nSpeicher, Michael\n\nUrban, Ernst-Christian\n\n\n"
},
{
"text": "\n179999\nNon-invasive diagnosis of cirrhosis and long-term disease monitoring by transient elastography in patients with Wilson disease.\n\nPaternostro, R\n\nPfeiffenberger, J\n\nFerenci, P\n\nStättermayer, AF\n\nStauber, RE\n\nWrba, F\n\nLongerich, T\n\nLackner, K\n\nTrauner, M\n\nFerlitsch, A\n\nReiberger, T\n\nWeiss, KH\n\nBeiträge in Fachzeitschriften\nISI:000508627500001\n31898387.0\n10.1111/liv.14368\nPMC7187206\nThe value of liver stiffness measurement (LSM) by transient elastography (TE) for non-invasive fibrosis staging and disease monitoring has not been established in patients with Wilson disease (WD).\n Liver stiffness measurement by TE and non-invasive fibrosis scores (APRI, FIB-4) were analysed from 188 WD patients with liver biopsy (LBX). Longitudinal LSM was performed in 128 (68.1%) patients.\n One hundred and eighty-eight patients (mean age: 35 ± 14 years, 54.8% women; 27.1% with histological cirrhosis) were studied. Forty-four[23.4%] patients were recently diagnosed with WD, while 144[76.6%] were previously diagnosed (>1 year between LBX and LSM). Overall, LSM (11.3 vs 6.1 kPa, P < .001), APRI (0.72 vs 0.38, P < .001) and FIB-4 (1.54 vs 0.89, P < .001) were higher in cirrhotic than in non-cirrhotic patients. This was even more pronounced in recently diagnosed patients (35.2 kPa vs 6.4 kPa, P < .001). Accuracy for diagnosing cirrhosis at an LSM cut-off ≥9.9 kPa was better in recently diagnosed (PPV: 74%, NPV: 100%) vs previously diagnosed (PPV: 53%, NPV: 82%) patients. Recently diagnosed patients had higher Area Under the Curve (AUC) for APRI (0.79 vs 0.61) and FIB-4 (0.84 vs 0.65) than previously diagnosed patients. At APRI <1.5 and FIB-4 <3.25 cirrhosis was ruled out with a specificity of 93% and 95% respectively. During a median follow-up of 46 (24-66) months, only 5.9% (5/85) of non-cirrhotic WD patients showed progression to cirrhotic LSM values, while 30.8% (4/13) of cirrhotic WD patients showed LSM suggestive of cirrhosis regression.\n TE-based LSM ≥9.9 kPa accurately identifies cirrhosis in WD patients. Next to TE-LSM <9.9 kPa, APRI <1.5 and FIB-4 <3.25 values assist to non-invasively rule out cirrhosis. LSM remains stable in most non-cirrhotic patients on WD therapy, while one-third of cirrhotic patients present clinically relevant decreases in LSM.\n © 2020 The Authors. Liver International published by John Wiley & Sons Ltd.\n\nLackner, Karoline\n\nStauber, Rudolf\n\n\n"
},
{
"text": "\n183029\nHerbal therapy treatment in thromboangiitis obliterans: a retrospective clinical study.\n\nLi, G\n\nZefr, C\n\nYang, B\n\nHe, C\n\nHafner, F\n\nPang, H\n\nBeiträge in Fachzeitschriften\nISI:000555045100039\n32692190.0\n10.21037/apm-19-578\nNone\nCritical limb ischemia in patients with thromboangiitis obliterans (TAO, Buerger's disease) is associated with refractory rest pain, gangrene, and increased rates of amputation. Tuoju lotion was prepared by the Pharmacy Department of Dongfang Hospital. The focus of the study is to elicit the efficacy of the addition of Herbal therapy treatment to conventional treatment in TAO patients with severe extremity pain and to assess any statistically significant benefits in patient's pain control at rest. We fund that the addition of herbal therapy treatment can augment conventional treatments in TAO patients by improving or eliminating intermittent claudication symptoms, prolonging claudication distance, and reducing total blood viscosity. At the same time, Tuoju lotion can improve microcirculation status in the short term. The purpose of this study was to investigate the effect of topical Herbal therapy treatment on patient outcomes in patients with TAO.\n Seventy patients with TAO treated between January 2009 and July 2019 were included in a retrospective analysis of a single university hospital vascular center. Forty patients received topical herbal treatment in addition to conventional therapy and were compared to a control group who received standard treatment alone (n=30).\n Patients in both, the experimental and control group, were matched according to age and gender. There was no significant difference in course of disease and past medical history between the two groups. The mean ankle brachial index (ABI), toe pressure, and blood viscosity were also similar in both groups. Rest pain score (baseline VAS 4.76±2.87, post-treatment 3.32±1.29) and walking distance (baseline 169.7±23.6 m, post-treatment 284.5±32.3 m) significantly improved in the herbal treatment group. ABI values improved and total blood viscosity decreased in both groups with no significant difference between the herbal and conservative treatment arms. However, the arterial blood pressure ratio in the lower extremity stage showed no difference between the superficial femoral artery and the popliteal artery.\n The addition of Herbal therapy treatment to conventional treatment in TAO patients with severe extremity pain was associated with a reduction of rest pain and intermittent claudication.\n\nHafner, Franz\n\n\n"
},
{
"text": "\n4298\nEstimating phosphate removal in haemodialysis: an additional tool to quantify dialysis dose.\n\nGutzwiller, JP\n\nSchneditz, D\n\nHuber, AR\n\nSchindler, C\n\nGutzwiller, F\n\nZehnder, CE\n\nBeiträge in Fachzeitschriften\nISI:000176090900017\n12032194.0\n10.1093%2Fndt%2F17.6.1037\nNone\nBACKGROUND: Half of the dialysis population suffers from hyperphosphataemia, which is now recognized as a major factor of haemodialysis (HD) morbidity and mortality. Current control is focussed on reducing dietary phosphate intake and diminishing absorption using phosphate binders, whereas control and quantification of phosphate removal by HD is undervalued. The aim of this prospective study was to develop a simple, bedside formula to estimate dialytic phosphate removal in stable HD patients. METHODS: This was a prospective, randomized trial. Phosphate and urea elimination were assessed in a representative group of patients at two dialysis centres using randomly different dialysers (1.3-2.4 m(2)). Quantification was performed by partial dialysate collection, concentration measurements in blood and effluent dialysate spot samples, and Kt/V(urea) during standard high-flux HD. Multiple linear regression analyses were used in 77% of all data sets to generate an equation to predict phosphate removal. The formula was validated in the remaining 23% of data sets, in the same group of patients using a large capillary filter, and in diabetic patients treated with a small dialyser at different blood flows (200, 250, and 300 ml/min). RESULTS: A formula allowing quantification of phosphate removal within one HD session was developed in 18 of 74 patients during 41 treatments (137 out of 177 data sets) and was determined as: M(PO4pred)=0.1t -17+50c(ds60)+11c(b60), where t is treatment time in min, c(ds60) and c(b60) are phosphate concentrations in dialysate and plasma measured 60 min into HD in mmol/l, and M(PO4pred) is estimated phosphate removed in mmol. The precision was remarkable (r(2)=0.92-0.94). The comparison of phosphate and Kt/V(urea) showed a significant association (r(2)=0.28), albeit with remarkable scatter. CONCLUSIONS: We present the first approach to quantify phosphate removal during high-flux HD by a bedside formula. Only 28% of the variation in phosphate removal was explained by Kt/V(urea). It appears that other factors not adequately accounted for by Kt/V(urea) affect phosphate removal. Therefore, we propose an individual control and quantification of phosphate removal in HD.\n\nSchneditz, Daniel\n\n\n"
},
{
"text": "\n73146\nTeledermatological monitoring of leg ulcers in cooperation with home care nurses.\n\nBinder, B\n\nHofmann-Wellenhof, R\n\nSalmhofer, W\n\nOkcu, A\n\nKerl, H\n\nSoyer, HP\n\nBeiträge in Fachzeitschriften\nISI:000251684600005\n18086999.0\n10.1001/archderm.143.12.1511\nNone\nOBJECTIVES: To examine the feasibility and acceptance of teledermatology for wound management for patients with leg ulcers by home care nurses and evaluate the reduction of costs and the acceptance of teledermatology by patients and home care nurses. DESIGN: Case series of telemonitored patients with leg ulcers including cost-effectiveness analysis. SETTING: Home monitoring by home care nurses. PATIENTS: Sixteen patients with 45 leg ulcers of different origin were included. MAIN OUTCOME MEASURES: After an initial outpatient visit when the leg ulcers were assessed and classified, teledermatological follow-up was done by home care nurses. Relevant clinical information and 1 to 4 digital images of the wound and surrounding skin were transmitted weekly via a secure Web site to an expert at the wound care center, who assessed the wound and made therapeutic recommendations. RESULTS: Of the 707 images transmitted for teleconsultation, in 644 (89%) the quality of the images was excellent or sufficient and the experts were confident in giving therapeutic recommendations. Of the 45 ulcers, 32 (71%) decreased in size and 14 (31%) healed completely, whereas 10 of the 45 ulcers (22%) increased slightly in size despite the teledermatological monitoring. In 3 ulcers (7%), no measurement was possible owing to the overly large size of the ulcers. The acceptance of telemedicine was very good by most patients. Of 15 home care nurses working in the district, 7 were very satisfied with teledermatological monitoring of wound care. There was a reduction of 46% in transportation costs for the insurance companies as well as for the patients owing to a significant decrease in the number of visits to general physicians or the wound care center. CONCLUSIONS: The acceptance of teledermatological monitoring of wound care was very high by patients, home care nurses, and wound experts. Decreased health care costs by reducing the number of visits to wound care centers or specialist physicians and improvement in quality of life for patients with leg ulcers using telemedicine seems possible. Teledermatology offers great potential for long-term wound care.\n\nBinder, Barbara\n\nHofmann-Wellenhof, Rainer\n\nKerl, Helmut\n\nSalmhofer, Wolfgang\n\n\n"
},
{
"text": "\n106004\nPlerixafor and granulocyte-colony-stimulating factor (G-CSF) in patients with lymphoma and multiple myeloma previously failing mobilization with G-CSF with or without chemotherapy for autologous hematopoietic stem cell mobilization: the Austrian experience on a named patient program.\n\nWorel, N\n\nRosskopf, K\n\nNeumeister, P\n\nKasparu, H\n\nNachbaur, D\n\nRuss, G\n\nNamberger, K\n\nWitt, V\n\nSchloegl, E\n\nZojer, N\n\nLinkesch, W\n\nKalhs, P\n\nGreinix, HT\n\nBeiträge in Fachzeitschriften\nISI:000290267700013\n20880037.0\n10.1111/j.1537-2995.2010.02896.x\nNone\nPlerixafor in combination with granulocyte-colony-stimulating factor (G-CSF) has been shown to enhance stem cell mobilization in patients with multiple myeloma, non-Hodgkin's lymphoma, and Hodgkin's disease who demonstrated with previous mobilization failure. In this named patient program we report the Austrian experience in insufficiently mobilizing patients.\n Twenty-seven patients from eight Austrian centers with a median (range) age of 58 (19-70) years (18 female, nine male) were included in the study. Plerixafor was limited to patients with previous stem cell mobilization failure and was given in the evening of Day 4 of G-CSF application.\n A median increase of circulating CD34+ cells within 10 to 11 hours from administration of plerixafor by a factor of 4.7 over baseline was noted. Overall, 20 (74%) patients reached more than 10 × 10(6) CD34+ cells/L in the peripheral blood, resulting in 17 (63%) patients collecting at least 2 × 10(6) CD34+ cells/kg body weight (b.w.; median, 2.6 × 10(6) CD34+ cells/kg b.w.; range, 0.08 × 10(6) -8.07 × 10(6) ). Adverse events of plerixafor were mild to moderate and consisted of gastrointestinal side effects and local reactions at the injection site. Thirteen (48%) patients underwent autologous transplantation receiving a median of 2.93 × 10(6) CD34+ cells/kg (range, 1.46 × 10(6) -5.6 × 10(6) ) and showed a trilinear engraftment with a median neutrophil recovery on Day 12 and a platelet recovery on Day 14.\n Our study confirms previous investigations showing that plerixafor in combination with G-CSF is an effective and well-tolerated mobilization regimen with the potential of successful stem cell collection in patients with previous mobilization failure.\n © 2010 American Association of Blood Banks.\n\nGreinix, Hildegard\n\nNeumeister, Peter\n\n\n"
},
{
"text": "\n113007\nActivation of mitogen-activated protein kinase by the A(2A)-adenosine receptor via a rap1-dependent and via a p21(ras)-dependent pathway.\n\nSeidel, MG\n\nKlinger, M\n\nFreissmuth, M\n\nHöller, C\n\nBeiträge in Fachzeitschriften\nISI:000082554200088\n10464324.0\n10.1074/jbc.274.36.25833\nNone\nThe A(2A)-adenosine receptor, a prototypical G(s)-coupled receptor, activates mitogen-activated protein (MAP) kinase in a manner independent of cAMP in primary human endothelial cells. In order to delineate signaling pathways that link the receptor to the regulation of MAP kinase, the human A(2A) receptor was heterologously expressed in Chinese hamster ovary (CHO) and HEK293 cells. In both cell lines, A(2A) agonist-mediated cAMP accumulation was accompanied by activation of the small G protein rap1. However, rap1 mediates A(2A) receptor-dependent activation of MAP kinase only in CHO cells, the signaling cascade being composed of G(s), adenylyl cyclase, rap1, and the p68 isoform of B-raf. This isoform was absent in HEK293 cells. Contrary to CHO cells, in HEK293 cells activation of MAP kinase by A(2A) agonists was not mimicked by 8-bromo-cAMP, was independent of Galpha(s), and was associated with activation of p21(ras). Accordingly, overexpression of the inactive S17N mutant of p21(ras) and of a dominant negative version of mSos (the exchange factor of p21(ras)) blocked MAP kinase stimulation by the A(2A) receptor in HEK 293 but not in CHO cells. In spite of the close homology between p21(ras) and rap1, the S17N mutant of rap1 was not dominant negative because (i) overexpression of rap1(S17N) failed to inhibit A(2A) receptor-dependent MAP kinase activation, (ii) rap1(S17N) was recovered in the active form with a GST fusion protein comprising the rap1-binding domain of ralGDS after A(2A) receptor activation, and (iii) A(2A) agonists promoted the association of rap1(S17N) with the 68-kDa isoform of B-raf in CHO cells. We conclude that the A(2A) receptor has the capacity two activate MAP kinase via at least two signaling pathways, which depend on two distinct small G proteins, namely p21(ras) and rap1. Our observations also show that the S17N version of rap1 cannot be assumed a priori to act as a dominant negative interfering mutant.\n\nSeidel, Markus\n\n\n"
},
{
"text": "\n117942\nflt3 ligand in cooperation with transforming growth factor-beta1 potentiates in vitro development of Langerhans-type dendritic cells and allows single-cell dendritic cell cluster formation under serum-free conditions.\n\nStrobl, H\n\nBello-Fernandez, C\n\nRiedl, E\n\nPickl, WF\n\nMajdic, O\n\nLyman, SD\n\nKnapp, W\n\nBeiträge in Fachzeitschriften\nISI:A1997XR21800010\n9269760.0\n10.1182/blood.V90.4.1425.1425_1425_1434\nNone\nUsing a recently described serum-free culture system of purified human CD34+ progenitor cells, we show here a critical cooperation of flt3 ligand (FL) with transforming growth factor-beta1 (TGF-beta1) in the induction of in vitro dendritic cell/Langerhans cell (DC/LC) development. The addition of FL to serum-free cultures of CD34+ cells supplemented with TGF-beta1, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor alpha, and stem cell factor strongly increases both percentages (mean, 36% +/- 5% v 64% +/- 4%; P = .001) and total numbers (4.4- +/- 0.8-fold) of CD1a+ dendritic cells. These in vitro-generated CD1a+ cells molecularly closely resemble a particular type of DC known as an epidermal Langerhans cell. Generation of DC under serum-free conditions was found to strictly require supplementation of culture medium with TGF-beta1. Upon omission of TGF-beta1, percentages of CD1a+ DC decreased (to mean, 10% +/- 8%; P = .001) and, in turn, percentages of granulomonocytic cells (CD1a- cells that are lysozyme [LZ+]; myeloperoxidase [MPO+]; CD14+) increased approximately threefold (P < .05). Furthermore, in the absence of TGF-beta1, FL consistently promotes generation of LZ+, MPO+, and CD14+ cells, but not of CD1a+ cells. Serum-free single-cell cultures set up under identical TGF-beta1- and FL-supplemented culture conditions showed that high percentages of CD34+ cells (mean, 18% +/- 2%; n = 4) give rise to day-10 DC colony formation. The majority of cells in these DC-containing colonies expressed the Langerhans cell/Birbeck granule specific marker molecule Lag. Without TGF-beta1 supplementation, Lag+ colony formation is minimal and formation of monocyte/macrophage-containing colonies predominates. Total cloning efficiency in the absence and presence of TGF-beta1 is virtually identical (mean, 41% +/- 6% v 41% +/- 4%). Thus, FL has the potential to strongly stimulate DC/LC generation, but has a strict requirement for TGF-beta1 to show this costimulatory effect.\n\nStrobl, Herbert\n\n\n"
},
{
"text": "\n135926\nThe Freedom SOLO valve for aortic valve replacement: clinical and hemodynamic results from a prospective multicenter trial.\n\nBeholz, S\n\nRepossini, A\n\nLivi, U\n\nSchepens, M\n\nEl Gabry, M\n\nMatschke, K\n\nTrivedi, U\n\nEckel, L\n\nDapunt, O\n\nZamorano, JL\n\nBeiträge in Fachzeitschriften\nISI:000274764900015\n20329497.0\nNone\nNone\nThe study aim was to investigate the early results, hemodynamics and left ventricular remodeling after aortic valve replacement (AVR) with the Freedom SOLO valve, a bovine pericardial valve bioprosthesis, using a single running suture line in a supra-annular position.\n Between July 2004 and September 2006, a total of 256 patients (116 males; 140 females; mean age 74.5 +/- 6.4 years; range: 41-89 years) who underwent AVR with the Freedom SOLO valve in nine European institutions were enrolled in the study. The indications for AVR were stenosis in 182 patients, regurgitation in 15, and combined in 57. Preoperatively, 37%, 59% and 4% of the patients were in NYHA classes I-II, III, and IV, respectively. Concomitant procedures were performed in 91 patients (36%). A patient subgroup underwent echocardiography preoperatively (n=192), and at one (n=194) and 12 (n=165) months postoperatively.\n The early mortality was 2.3% (n=6). There were 18 late deaths (6.2%/pt-yr). After 12 months, 82% of the patients were in NYHA class I-II. Linearized rates were 0.69%/pt-yr for bleeding, 0.34%/pt-yr for thromboembolism, 0.0%/pt-yr for structural degeneration and thrombosis, 1.37%/pt-yr for paravalvular leak, and 2.06%/pt-yr for endocarditis. Five patients required reoperation. Twelve-month transprosthetic regurgitation was graded as absent in 92% of cases. The mean gradient was 42.3 +/- 20.2 mmHg preoperatively, 6.5 +/- 3.8 mmHg at one month, and 6.7 +/- 4.1 mmHg at 12 months. The effective orifice area was improved from 0.78 +/- 0.35 cm2 preoperatively to 1.90 +/- 0.56 cm2 at one month and 1.89 +/- 0.56 cm2 at 12 months. The left ventricular mass was decreased by 23%, from 217.8 +/- 77.2 g/m2 preoperatively to 167.4 +/- 68.2 g/m2 at one year. The mean left ventricular ejection fraction was 65.5 +/- 14.2% preoperatively, and 64.5 +/- 12.5% and 66.0 +/- 10.6% at one month and at 12 months, respectively.\n The data obtained suggest that the Freedom SOLO stentless bioprosthesis shows excellent early clinical and hemodynamic results, resulting in a significant regression of left ventricular hypertrophy and improvement in left ventricular systolic function.\n\n\n"
},
{
"text": "\n138710\nInterleukin 10-coated nanoparticle systems compared for molecular imaging of atherosclerotic lesions.\n\nAlmer, G\n\nSummers, KL\n\nScheicher, B\n\nKellner, J\n\nStelzer, I\n\nLeitinger, G\n\nGries, A\n\nPrassl, R\n\nZimmer, A\n\nMangge, H\n\nBeiträge in Fachzeitschriften\nISI:000341113100001\n25214785.0\n10.2147/IJN.S66830\nPMC4159402\nAtherosclerosis (AS) is one of the leading causes of mortality in high-income countries. Early diagnosis of vulnerable atherosclerotic lesions is one of the biggest challenges currently facing cardiovascular medicine. The present study focuses on developing targeted nanoparticles (NPs) in order to improve the detection of vulnerable atherosclerotic-plaques. Various biomarkers involved in the pathogenesis of atherosclerotic-plaques have been identified and one of these promising candidates for diagnostic targeting is interleukin 10 (IL10). IL10 has been shown to be a key anti-inflammatory responding cytokine in the early stages of atherogenesis, and has already been used for therapeutic interventions in humans and mice. IL10, the targeting sequence, was coupled to two different types of NPs: protamine-oligonucleotide NPs (proticles) and sterically stabilized liposomes in order to address the question of whether the recognition and detection of atherosclerotic-lesions is primarily determined by the targeting sequence itself, or whether it depends on the NP carrier system to which the biomarker is coupled. Each IL10-targeted NP was assessed based on its sensitivity and selectivity toward characterizing atherosclerotic-plaque lesions using an apolipoprotein E-deficient mouse as the model of atherosclerosis. Aortas from apolipoprotein E-deficient mice fed a high fat diet, were stained with either fluorescence-labeled IL10 or IL10-coupled NPs. Ex vivo imaging was performed using confocal laser-scanning microscopy. We found that IL10-targeted proticles generated a stronger signal by accumulating at the surface of atherosclerotic-plaques, while IL10-targeted, sterically stabilized liposomes showed a staining pattern deeper in the plaque compared to the fluorescence-labeled IL10 alone. Our results point to a promising route for enhanced in vivo imaging using IL10-targeted NPs. NPs allow a higher payload of signal emitting molecules to be delivered to the atherosclerotic-plaques, thus improving signal detection. Importantly, this allows for the opportunity to visualize different areas within the plaque scenario, depending on the nature of the applied nanocarrier.\n\nAlmer, Gunter\n\nGries, Anna\n\nKellner, Josef\n\nLeitinger, Gerd\n\nMangge, Harald\n\nPrassl, Ruth\n\nStelzer, Ingeborg\n\n\n"
},
{
"text": "\n153982\nβ-Defensin 2 is a responsive biomarker of IL-17A-driven skin pathology in patients with psoriasis.\n\nKolbinger, F\n\nLoesche, C\n\nValentin, MA\n\nJiang, X\n\nCheng, Y\n\nJarvis, P\n\nPeters, T\n\nCalonder, C\n\nBruin, G\n\nPolus, F\n\nAigner, B\n\nLee, DM\n\nBodenlenz, M\n\nSinner, F\n\nPieber, TR\n\nPatel, DD\n\nBeiträge in Fachzeitschriften\nISI:000397295800025\n27502297.0\n10.1016/j.jaci.2016.06.038\nNone\nIL-17A is a key driver of human autoimmune diseases, particularly psoriasis.\n We sought to determine the role of IL-17A in psoriasis pathogenesis and to identify a robust and measurable biomarker of IL-17A-driven pathology.\n We studied 8 healthy subjects and 8 patients with psoriasis before and after administration of secukinumab, a fully human anti-IL-17A mAb, and used a combination of classical techniques and a novel skin microperfusion assay to evaluate the expression of 170 proteins in blood, nonlesional skin, and lesional skin. For validation, we also tested stored sera from 601 patients with a variety of autoimmune diseases.\n IL-17A was specifically expressed in lesional compared with nonlesional psoriatic skin (9.8 vs 0.8 pg/mL, P < .001). Proteomic and gene transcription analyses revealed dysregulated antimicrobial peptides, proinflammatory cytokines, and neutrophil chemoattractants, levels of which returned to normal after treatment with secukinumab. β-Defensin 2 (BD-2) was identified as a biomarker of IL-17A-driven pathology by comparing protein expression in patients with psoriasis versus that in healthy subjects (5746 vs 82 pg/mL in serum, P < .0001; 2747 vs <218 pg/mL in dermis, P < .001), responsiveness to secukinumab therapy, and synergistic induction by IL-17A and TNF-α in epidermal keratinocytes. In a validation set of sera from 601 patients with autoimmune diseases thought to be IL-17A driven, we found that BD-2 levels are most highly increased in patients with psoriatic skin lesions, and in patients with psoriasis, BD-2 levels correlated well with IL-17A levels (r = 0.70, n = 199, P < .001) and Psoriasis Area and Severity Index scores (r = 0.53, n = 281, P < .001).\n IL-17A is a primary driver of skin pathology in patients with psoriasis, and serum BD-2 is an easily measurable biomarker of IL-17A-driven skin pathology.\n Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.\n\nPieber, Thomas\n\nSadoghi, Birgit\n\nSinner, Frank Michael\n\n\n"
}
]
}