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"text": "\n7750\nThree-dimensional structure determination of antibodies. Primary structure of crystallized monoclonal immunoglobulin IgG1 KOL, I\n\nSchmidt, WE\n\nJung, HD\n\nPalm, W\n\nHilschmann, N\n\nBeiträge in Fachzeitschriften\nISI:A1983QW04500038\n6884994.0\n10.1515/bchm2.1983.364.1.713\nNone\nThe crystallizable myeloma immunoglobulin IgG1 KOL [allotype Gm(-1, ), (gamma 1, gamma)2] which is well characterized in its three-dimensional structure by X-ray diffraction analysis of high resolution has been proved to be homogenous by polyacrylamide gel electrophoresis. The H- and L-chains were separated by gel filtration after complete reduction and carboxymethylation and were characterized by amino acid analysis, end group determination and polyacrylamide gel electrophoresis, respectively. The intact IgG1 KOL was cleaved by cyanogen bromide and all CNBr-fragments were isolated and characterized. The reduced and carboxymethylated H-chain was digested by trypsin and the tryptic hydrolysate was separated by ion-exchange chromatography. Using different procedures of rechromatography 35 out of 37 tryptic H-chain peptides could be isolated in sufficient amounts, the missing 2 peptides were produced by tryptic digestion of 2 CNBr-fragments. The amino acid sequences of all tryptic peptides were determined using a modified Edman degradation method after separation of the enzymatic cleavage products by high-performance liquid chromatography (HPLC). The complete primary structure of the VH-part of the H-chain was established by isolation and partial sequence determination of overlapping peptides obtained from cleavage of the intact H-chain by Staphylococcus aureus proteinase. The gamma 1-H-chain KOL comprises 455 amino acid residues and belongs to subgroup III. The switch from the variable to the constant part occurs at position 126/127, thus making VH-KOL one of the longest variable parts among the yet known immunoglobulin H-chains. This is due to the hypervariable region Hhv4 which is made up by 17 amino acid residues (4-9 residues more compared with other VH-parts). Within this region a so far not described additional intrapeptidal disulfide bridge could be localized (Cys 105-Cys 110) that creates a short loop with antiparallel running peptide strains in beta-pleated sheet conformation. Its role in the three-dimensional structure of the antigen-binding site of the IgG1 KOL molecule is discussed using the data obtained from X-ray diffraction analysis.\n\n\n"
},
{
"text": "\n11789\nRadiation therapy in stage III ovarian cancer following surgery and chemotherapy: prognostic factors, patterns of relapse, and toxicity: a preliminary report.\n\nArian-Schad, KS\n\nKapp, DS\n\nHackl, A\n\nJuettner, FM\n\nLeitner, H\n\nPorsch, G\n\nLahousen, M\n\nPickel, H\n\nBeiträge in Fachzeitschriften\nISI:A1990EF79100006\n2227572.0\n10.1016/0090-8258(90)90397-4\nNone\nTwenty patients with FIGO stage III epithelial ovarian cancer who had undergone maximum cytoreductive surgery (including pelvic and paraaortic lymph node dissection) and combination chemotherapy (4-10 cycles, median 6) were treated with irradiation to the abdomen and pelvis with 30 Gy followed by diaphragmatic/paraaortic and pelvis boost fields to 42 and 51.6 Gy, respectively. Second-look laparotomy was not performed. Seventeen of 20 patients completed the planned course of radiation. In 2 cases, failure to complete treatment was related to acute hematologic toxicity, and 1 patient refused further treatment. Five patients (29%) required treatment breaks ranging from 8 to 16 days (median, 12 days) due to pancytopenia. Actuarial overall survival and relapse-free survival at 3 years for the 17 patients who completed radiation was 69 and 47%, respectively, with follow-up ranging from 19 to 53 months (median: 24, mean: 27.6 months). Seven patients (41%) relapsed within the abdomen alone and 2 patients developed extraabdominal lymph node metastasis as their sole site of failure. The prognostic factors evaluated for correlation with relapse-free survival included histologic subtype, grade, amount of residual disease at the time of surgery, and nodal involvement; only residual tumor at surgery (none vs less than or equal to 2 cm or greater than 2 cm) was found to be statistically significant (P less than 0.01). Three-year overall survival correlated with amount of residual disease following the initial cytoreductive surgery. It was 100% for patients with no residual disease, 66.7% for less than or equal to 2 cm, and 26.7% for those with greater than 2 cm residual disease, respectively. Radiation treatment was well tolerated, with only one patient developing treatment-related bowel obstruction 7 months after radiation therapy. The results of this planned trimodality treatment approach compare favorably with those reported following surgery and chemotherapy, particularly in patients who have been maximally cytoreduced.\n\nSmolle-Juettner, Freyja-Maria\n\n\n"
},
{
"text": "\n14079\nPlatelet-activating factor acetylhydrolase activity indicates angiographic coronary artery disease independently of systemic inflammation and other risk factors: the Ludwigshafen Risk and Cardiovascular Health Study.\n\nWinkler, K\n\nWinkelmann, BR\n\nScharnagl, H\n\nHoffmann, MM\n\nGrawitz, AB\n\nNauck, M\n\nBöhm, BO\n\nMärz, W\n\nBeiträge in Fachzeitschriften\nISI:000227302900006\n15710755.0\n10.1161/01.CIR.0000156457.35971.C8\nNone\nBACKGROUND: Platelet-activating factor acetylhydrolase (PAF-AH), also denoted as lipoprotein-associated phospholipase A2, is a lipoprotein-bound enzyme that is possibly involved in inflammation and atherosclerosis. This study investigates the relationship of PAF-AH activity to angiographic coronary artery disease (CAD), the use of cardiovascular drugs, and other established risk factors. METHODS AND RESULTS: PAF-AH activity, lipoproteins, sensitive C-reactive protein (sCRP), fibrinogen, serum amyloid A, and white blood cell count were determined in 2454 subjects with angiographically confirmed CAD and in 694 control subjects. PAF-AH activity was highly correlated with LDL cholesterol (r=0.517), apolipoprotein B (r=0.644), and non-HDL cholesterol (r=0.648) but not with sCRP or fibrinogen. PAF-AH activity was lower in women than in men and was affected by the intake of lipid-lowering drugs (-12%; P<0.001), aspirin (-6%; P<0.001), beta-blockers (-6%; P<0.001), and digitalis (+7%; P<0.001). Unlike sCRP, fibrinogen, and serum amyloid A, PAF-AH activity was not elevated in unstable angina, non-ST-elevation myocardial infarction, or ST-elevation myocardial infarction. When nonusers of lipid-lowering drugs were examined, PAF-AH activity was associated with the severity of CAD and the number of coronary vessels with significant stenoses. In individuals not taking lipid-lowering drugs and after adjustment for use of aspirin, beta-blocker, and digitalis, the odds ratio for CAD associated with increasing PAF-AH activity was 1.39 (95% CI 1.26 to 1.54, P<0.001), a finding that was robust against further adjustments. CONCLUSIONS: PAF-AH activity is not an indicator of the systemic inflammation that accompanies acute coronary syndromes. PAF-AH activity is affected by a number of cardiovascular drugs; however, after such medication use was accounted for, PAF-AH activity was associated with angiographic CAD, complementary to sCRP and independently of established risk factors such as LDL cholesterol.\n\nMärz, Winfried\n\nScharnagl, Hubert\n\n\n"
},
{
"text": "\n22036\nInvasion of cytotrophoblastic (JEG-3) cells is up-regulated by interleukin-15 in vitro.\n\nZygmunt, M\n\nHahn, D\n\nKiesenbauer, N\n\nMünstedt, K\n\nLang, U\n\nBeiträge in Fachzeitschriften\nISI:000077464600004\n9870075.0\nNone\nNone\nPROBLEM: Trophoblast invasion into the uterus is controlled by many factors. Some cytokines (interleukin [IL]-1, IL-6, and IL-10) have been shown previously to play an important role in placentation. The human placenta is an important source of IL-15, although the cellular source of IL-15 in the placenta has not yet been specified. IL-15 influences cell adhesion and migration by redistributing adhesion molecules in lymphocytes and has been shown to have effects on endothelial cells and in some human tumors. METHOD OF STUDY: To study the role of IL-15 in trophoblast invasion, we investigated the effect of IL-15 (concentrations, 1-10 ng/ml) in a trophoblast invasion model (JEG-3 with matrigel-coated filters). Cell invasion was assessed using matrigel-coated filters and was expressed as the quotient of invading cells in comparison with the number of cells that had passed the control membrane. Cell migration was studied by examining the number of cells that had passed the filters without matrigel. Cell proliferation was quantified by a tetrazolium salt WST-1 cleavage assay. Matrix metalloproteinase (MMP)-1, MMP-2, and MMP-9 activities were measured by specific enzyme assays. RESULTS: IL-15 significantly (P < 0.05) increased the in vitro invasion of cytotrophoblastic (JEG-3) cells in a dose-dependent manner. There was a fourfold increase in the invasion at a concentration of 10 ng/ml of IL-15. Migration also was increased by a factor of 2.3 (P < 0.05). Cell proliferation, however, remained unchanged. The collagenolytic activity of cytotrophoblastic (JEG-3) cells was increased by IL-15 stimulation. A significant increase in MMP-1 concentration occurred after the incubation of JEG-3 cells with IL-15. No changes appeared in MMP-2, MMP-9, and tissue inhibitor of metalloproteinase-1 concentrations. CONCLUSIONS: Trophoblast invasion and migration, but not proliferation, are enhanced by IL-15. Our results suggest a role for IL-15 in the modulation of MMP-1 secretion by JEG-3 cells. Furthermore, we speculate, that IL-15 might be related to the changes of cell adhesion molecule phenotype during the process of invasion.\n\n\n"
},
{
"text": "\n93990\nAcute administration of GPR40 receptor agonist potentiates glucose-stimulated insulin secretion in vivo in the rat.\n\nDoshi, LS\n\nBrahma, MK\n\nSayyed, SG\n\nDixit, AV\n\nChandak, PG\n\nPamidiboina, V\n\nMotiwala, HF\n\nSharma, SD\n\nNemmani, KV\n\nBeiträge in Fachzeitschriften\nISI:000263882400011\n19217448.0\n10.1016/j.metabol.2008.10.005\nNone\nRecently, several in vitro studies have shown that GPR40 receptor activation by free fatty acids (FFAs) results in glucose-dependent insulin secretion. However, whether GPR40 receptor activation results in glucose-dependent insulin secretion in vivo in rats is not known. Therefore, we evaluated the effect of synthetic GPR40 receptor agonist (compound 1) on glucose tolerance test (GTT) in fed, fasted, and insulin-resistant rats. In oral GTT, intraperitoneal GTT, and intravenous GTT, GPR40 receptor agonist improved glucose tolerance, which was associated with increase in plasma insulin level. Interestingly, in GTTs, the rise in insulin levels in agonist-treated group was directly proportional to the rate of rise and peak levels of glucose in control group. Although glibenclamide, a widely used insulin secretagogue, improved glucose tolerance in all GTTs, it did not display insulin release in intraperitoneal GTT or intravenous GTT. In the absence of glucose load, GPR40 receptor agonist did not significantly change the plasma insulin concentration, but did decrease the plasma glucose concentration. Fasted rats exhibited impaired glucose-stimulated insulin secretion (GSIS) as compared with fed rats. Compound 1 potentiated GSIS in fasted state but failed to do so in fed state. Suspecting differential pharmacokinetics, a detailed pharmacokinetic evaluation was performed, which revealed the low plasma concentration of compound 1 in fed state. Consequently, we examined the absorption profile of compound 1 at higher doses in fed state; and at a dose at which its absorption was comparable with that in fasted state, we observed significant potentiation of GSIS. Chronic high-fructose (60%) diet feeding resulted in impaired glucose tolerance, which was improved by GPR40 receptor agonist. Therefore, our results demonstrate for the first time that acute GPR40 receptor activation leads to potentiation of GSIS in vivo and improves glucose tolerance even in insulin-resistant condition in rats. Taken together, these results suggest that GPR40 receptor agonists could be potential therapeutic alternatives to sulfonylureas.\n\n\n"
},
{
"text": "\n107643\nDownregulation of FGFRL1 Contributes to the Development of the Diaphragmatic Defect in the Nitrofen Model of Congenital Diaphragmatic Hernia.\n\nDingemann, J\n\nDoi, T\n\nRuttenstock, EM\n\nPuri, P\n\nBeiträge in Fachzeitschriften\nISI:000287446200012\n20938900.0\n10.1055/s-0030-1262853\nNone\nIntroduction: The nitrofen model of Congenital Diaphragmatic Hernia (CDH) displays a diaphragmatic defect of the Bochdalek-type and has been widely used to investigate the pathogenesis of CDH. However, the exact pathomechanism of the diaphragmatic defect is still poorly understood. Fibroblast growth factor (FGF) receptor-like 1 (FGFRL1), a member of the FGF receptor family, plays a key role in physiological diaphragmatic development. FGFRL1 is expressed in the fetal diaphragm at low levels in early gestation and its expression steadily increases, becoming most pronounced in later gestational stages. It has been reported that FGFRL1 homozygous null mice have thin, partially amuscular diaphragms and die at birth due to respiratory failure. The aim of this study was to investigate the hypothesis that FGFRL1 gene expression in the diaphragm is downregulated during the later gestational stages in the nitrofen CDH model. Material and Methods: Timed pregnant rats were exposed to either olive oil or 100 mg nitro-fen on day 9 of gestation (D9). Cesarean section was performed on D18 or D21. Fetal diaphragms (n = 40) were micro-dissected and divided into CDH group and controls. Total RNA was extracted from the diaphragms and the mRNA levels of FGFRL1 were determined using real-time PCR. Immunohistochemistry was performed to evaluate diaphragmatic protein expression of FGFRL1. Student's t-test and Mann-Whitney test were used, where appropriate. Statistical significance was considered for p < 0.05. Results: Relative mRNA expression levels of FGFRL1 were significantly decreased in the CDH group compared to controls on D18 (3.63 +/- 1.65 vs. 6.04 +/- 3.12, p < 0.05) and D21 (1.36 +/- 1.01 vs. 2.57 +/- 1.34, p < 0.05). Immunoreactivity of FGFRL1 was markedly decreased in the diaphragms of the CDH group compared to controls on D18 and D21. Conclusion: Our data provide strong evidence that downregulation of the FGFRL1 gene during the late stages of gestation may contribute to the development of the diaphragmatic defect in nitrofen-induced CDH.\n\n\n"
},
{
"text": "\n126035\nPermanent cardiac pacing in children: choosing the optimal pacing site: a multicenter study.\n\nJanoušek, J\n\nvan Geldorp, IE\n\nKrupičková, S\n\nRosenthal, E\n\nNugent, K\n\nTomaske, M\n\nFrüh, A\n\nElders, J\n\nHiippala, A\n\nKerst, G\n\nGebauer, RA\n\nKubuš, P\n\nFrias, P\n\nGabbarini, F\n\nClur, SA\n\nNagel, B\n\nGaname, J\n\nPapagiannis, J\n\nMarek, J\n\nTisma-Dupanovic, S\n\nTsao, S\n\nNürnberg, JH\n\nWren, C\n\nFriedberg, M\n\nde Guillebon, M\n\nVolaufova, J\n\nPrinzen, FW\n\nDelhaas, T\n\nWorking Group for Cardiac Dysrhythmias and Electrophysiology of the Association for European Pediatric Cardiology\n\nBeiträge in Fachzeitschriften\nISI:000314691700015\n23275383.0\n10.1161/CIRCULATIONAHA.112.115428\nNone\nBackground-We evaluated the effects of the site of ventricular pacing on left ventricular (LV) synchrony and function in children requiring permanent pacing. Methods and Results-One hundred seventy-eight children (aged < 18 years) from 21 centers with atrioventricular block and a structurally normal heart undergoing permanent pacing were studied cross-sectionally. Median age at evaluation was 11.2 (interquartile range, 6.3-15.0) years. Median pacing duration was 5.4 (interquartile range, 3.1-8.8) years. Pacing sites were the free wall of the right ventricular (RV) outflow tract (n=8), lateral RV (n=44), RV apex (n=61), RV septum (n=29), LV apex (n=12), LV midlateral wall (n=17), and LV base (n=7). LV synchrony, pump function, and contraction efficiency were significantly affected by pacing site and were superior in children paced at the LV apex/LV midlateral wall. LV dyssynchrony correlated inversely with LV ejection fraction (R=0.80, P=0.031). Pacing from the RV outflow tract/lateral RV predicted significantly decreased LV function (LV ejection fraction < 45%; odds ratio, 10.72; confidence interval, 2.07-55.60; P=0.005), whereas LV apex/LV midlateral wall pacing was associated with preserved LV function (LV ejection fraction >= 55%; odds ratio, 8.26; confidence interval, 1.46-47.62; P=0.018). Presence of maternal autoantibodies, gender, age at implantation, duration of pacing, DDD mode, and QRS duration had no significant impact on LV ejection fraction. Conclusions-The site of ventricular pacing has a major impact on LV mechanical synchrony, efficiency, and pump function in children who require lifelong pacing. Of the sites studied, LV apex/LV midlateral wall pacing has the greatest potential to prevent pacing-induced reduction of cardiac pump function. (Circulation. 2013;127:613-623.)\n\n\n"
},
{
"text": "\n128579\nStent Placement versus Balloon Angioplasty for the Treatment of Obstructive Lesions of the Popliteal Artery: A Prospective, Multi-centre, Randomized Trial.\n\nRastan, A\n\nKrankenberg, H\n\nBaumgartner, I\n\nBlessing, E\n\nMüller-Hülsbeck, S\n\nPilger, E\n\nScheinert, D\n\nLammer, J\n\nGißler, M\n\nNoory, E\n\nNeumann, FJ\n\nZeller, T\n\nBeiträge in Fachzeitschriften\nISI:000320916900017\n23694965.0\n10.1161/CIRCULATIONAHA.113.001849\nNone\nBackground Stenting has been shown to improve patency after femoral artery revascularization compared with balloon angioplasty. Limited data are available evaluating endovascular treatment for obstructive lesions of the popliteal artery. Methods and Results This prospective, randomized, multicenter trial compared primary nitinol stent placement to percutaneous transluminal balloon angioplasty in patients with peripheral artery disease Rutherford-Becker class 2 to 5 who had a de novo lesion in the popliteal artery. The primary study end point was 1-year primary patency, defined as freedom from target-lesion restenosis (luminal narrowing of 50%) as detected by duplex ultrasound. Secondary end points included target-lesion revascularization rate and changes in Rutherford-Becker class. Provisional stent placement was considered target-lesion revascularization and loss of primary patency. Two hundred forty-six patients were included in this trial. The mean target-lesion length was 42.3 mm. One hundred ninety-seven patients were available for the1-year follow-up. The 1-year primary patency rate was significantly higher in the group with primary nitinol stent placement (67.4%) than in the percutaneous transluminal balloon angioplasty group (44.9%, P=0.002). Target-lesion revascularization rates were 14.7% and 44.1%, respectively (P=0.0001); however, when provisional nitinol stent placement was not considered target-lesion revascularization and loss in patency, no significant differences prevailed between the study groups (67.4% versus 65.7%, P=0.92 for primary patency). Approximately 73% of patients in the percutaneous transluminal balloon angioplasty group and 77% in the nitinol stent group showed an improvement of 1 Rutherford-Becker class (P=0.31). Conclusions Primary nitinol stent placement for obstructive lesions of the popliteal artery achieves superior acute technical success and higher 1-year primary patency only if provisional stenting is considered target-lesion revascularization. Provisional stenting as part of a percutaneous transluminal balloon angioplasty strategy has equivalent 1-year patency and should be preferred over primary stenting.\n\nPilger, Ernst\n\n\n"
},
{
"text": "\n133105\nA retrospective analysis of securing autologous split-thickness skin grafts with negative pressure wound therapy in paediatric burn patients.\n\nHoeller, M\n\nSchintler, MV\n\nPfurtscheller, K\n\nKamolz, LP\n\nTripolt, N\n\nTrop, M\n\nBeiträge in Fachzeitschriften\nISI:000341898400007\n24438740.0\n10.1016/j.burns.2013.12.007\nNone\nDeep dermal and full-thickness burn wounds are excised and grafted with split-thickness skin grafts. Especially in less compliant patients such as young children, conventional fixing methods can often be ineffective due to high mobility rates in this age group. The aim of this retrospective single-centre study was to give an overview of our experience in the fixation of autologous split-thickness skin grafts (ASTSGs) on burn wounds by negative pressure wound therapy (NPWT) in paediatric patients.\n A retrospective analysis describing 53 paediatric patients with burns or burn-related injuries who were treated as 60 individual cases were conducted. All patients received ASTSGs secured by NPWT.\n Of the individual cases, 60 cases with a mean age of 8±6 years (the youngest was 3 months, the eldest was 24 years old) were treated in a single procedure with ASTSG and NPWT. Total burn surface area (TBSA) was, median (med) 4.5% (3.0-12.0%). The TBSA of deep dermal thickness to full-thickness (IIb-III°) burns was med 4.0% (2.0-6.0%). The TBSA treated with ASTSG and NPWT was med 3.5% (2.0-6.0%). Take rate was, med 96% (90-99%) with a total range of 70-100%. The only significant correlation that could be found was between the grafted TBSA and the take rate. The smaller the grafted TBSA the better the take rate resulted, as expected. In three cases, major complications were noted.\n To sum up our experience, the NPWT system has developed itself to be a constant, well-implemented and useful tool in securing ASTSGs to the wound bed. The main advantage of the technique is a much higher mobility of the patient compared to conventional fixation methods. The high compliance rate of an often challenging group of patients such as children recompenses possible higher costs compared to conventional fixation methods.\n Copyright © 2013 Elsevier Ltd and ISBI. All rights reserved.\n\nKamolz, Lars-Peter\n\nPfurtscheller, Klaus\n\nSchintler, Michael\n\nTripolt, Norbert\n\nTrop, Marija\n\n\n"
},
{
"text": "\n137867\nReference intervals for insulin-like growth factor-1 (igf-i) from birth to senescence: results from a multicenter study using a new automated chemiluminescence IGF-I immunoassay conforming to recent international recommendations.\n\nBidlingmaier, M\n\nFriedrich, N\n\nEmeny, RT\n\nSpranger, J\n\nWolthers, OD\n\nRoswall, J\n\nKörner, A\n\nObermayer-Pietsch, B\n\nHübener, C\n\nDahlgren, J\n\nFrystyk, J\n\nPfeiffer, AF\n\nDoering, A\n\nBielohuby, M\n\nWallaschofski, H\n\nArafat, AM\n\nBeiträge in Fachzeitschriften\nISI:000342339800054\n24606072.0\n10.1210/jc.2013-3059\nNone\nMeasurement of IGF-I is a cornerstone in diagnosis and monitoring of GH-related diseases, but considerable discrepancies exist between analytical methods. A recent consensus conference defined criteria for validation of IGF-I assays and for establishment of normative data.\n Our objectives were development and validation of a novel automated IGF-I immunoassay (iSYS; Immunodiagnostic Systems) according to international guidelines and establishment of method-specific age- and sex-adjusted reference intervals and analysis of their robustness.\n We conducted a multicenter study with samples from 12 cohorts from the United States, Canada, and Europe including 15 014 subjects (6697 males and 8317 females, 0-94 years of age).\n We measured concentrations of IGF-I as determined by the IDS iSYS IGF-I assay.\n A new IGF-I assay calibrated against the recommended standard (02/254) and insensitive to the 6 high-affinity IGF binding proteins was developed and rigorously validated. Age- and sex-adjusted reference intervals derived from a uniquely large cohort reflect the age-related pattern of IGF-I secretion: a decline immediately after birth followed by an increase until a pubertal peak (at 15 years of age). Later in life, values decrease continuously. The impact of gender is small, although across the lifespan, women have lower mean IGF-I concentrations. Geographical region, sampling setting (community or hospital based), and rigor of exclusion criteria in our large cohort did not affect the reference intervals.\n Using large cohorts of well-characterized subjects from different centers allowed construction of robust reference ranges for a new automated IGF-I assay. The strict adherence to recent consensus criteria for IGF-I assays might facilitate clinical application of the results.\n\nObermayer-Pietsch, Barbara\n\n\n"
},
{
"text": "\n146778\nFasting-induced G0/G1 switch gene 2 and FGF21 expression in the liver are under regulation of adipose tissue derived fatty acids.\n\nJaeger, D\n\nSchoiswohl, G\n\nHofer, P\n\nSchreiber, R\n\nSchweiger, M\n\nEichmann, TO\n\nPollak, NM\n\nPoecher, N\n\nGrabner, GF\n\nZierler, KA\n\nEder, S\n\nKolb, D\n\nRadner, FP\n\nPreiss-Landl, K\n\nLass, A\n\nZechner, R\n\nKershaw, EE\n\nHaemmerle, G\n\nBeiträge in Fachzeitschriften\nISI:000357991700021\n25733154.0\n10.1016/j.jhep.2015.02.035\nPMC4518503\nAdipose tissue (AT)-derived fatty acids (FAs) are utilized for hepatic triacylglycerol (TG) generation upon fasting. However, their potential impact as signaling molecules is not established. Herein we examined the role of exogenous AT-derived FAs in the regulation of hepatic gene expression by investigating mice with a defect in AT-derived FA supply to the liver.\n Plasma FA levels, tissue TG hydrolytic activities and lipid content were determined in mice lacking the lipase co-activator comparative gene identification-58 (CGI-58) selectively in AT (CGI-58-ATko) applying standard protocols. Hepatic expression of lipases, FA oxidative genes, transcription factors, ER stress markers, hormones and cytokines were determined by qRT-PCR, Western blotting and ELISA.\n Impaired AT-derived FA supply upon fasting of CGI-58-ATko mice causes a marked defect in liver PPARα-signaling and nuclear CREBH translocation. This severely reduced the expression of respective target genes such as the ATGL inhibitor G0/G1 switch gene-2 (G0S2) and the endocrine metabolic regulator FGF21. These changes could be reversed by lipid administration and raising plasma FA levels. Impaired AT-lipolysis failed to induce hepatic G0S2 expression in fasted CGI-58-ATko mice leading to enhanced ATGL-mediated TG-breakdown strongly reducing hepatic TG deposition. On high fat diet, impaired AT-lipolysis counteracts hepatic TG accumulation and liver stress linked to improved systemic insulin sensitivity.\n AT-derived FAs are a critical regulator of hepatic fasting gene expression required for the induction of G0S2-expression in the liver to control hepatic TG-breakdown. Interfering with AT-lipolysis or hepatic G0S2 expression represents an effective strategy for the treatment of hepatic steatosis.\n Copyright © 2015 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.\n\nKolb, Dagmar\n\n\n"
},
{
"text": "\n148989\nSubtype Classification of Lung Adenocarcinoma Predicts Benefit From Adjuvant Chemotherapy in Patients Undergoing Complete Resection.\n\nTsao, MS\n\nMarguet, S\n\nLe Teuff, G\n\nLantuejoul, S\n\nShepherd, FA\n\nSeymour, L\n\nKratzke, R\n\nGraziano, SL\n\nPopper, HH\n\nRosell, R\n\nDouillard, JY\n\nLe-Chevalier, T\n\nPignon, JP\n\nSoria, JC\n\nBrambilla, EM\n\nBeiträge in Fachzeitschriften\nISI:000366019300015\n25918286.0\n10.1200/JCO.2014.58.8335\nPMC4606061\nThe classification for invasive lung adenocarcinoma by the International Association for the Study of Lung Cancer, American Thoracic Society, European Respiratory Society, and WHO is based on the predominant histologic pattern-lepidic (LEP), papillary (PAP), acinar (ACN), micropapillary (MIP), or solid (SOL)-present in the tumor. This classification has not been tested in multi-institutional cohorts or clinical trials or tested for its predictive value regarding survival from adjuvant chemotherapy (ACT).\n Of 1, 66 patients in the IALT, JBR.10, CALGB 9633 (Alliance), and ANITA ACT trials included in the LACE-Bio study, 725 had adenocarcinoma. Histologies were reclassified according to the new classification and then collapsed into three groups (LEP, ACN/PAP, and MIP/SOL). Primary end point was overall survival (OS); secondary end points were disease-free survival (DFS) and specific DFS (SDFS). Hazard ratios (HRs) and 95% CIs were estimated through multivariable Cox models stratified by trial. Prognostic value was estimated in the observation arm and predictive value by a treatment effect interaction with histologic subgroups. Significance level was set at .01 for pooled analysis.\n A total of 575 patients were included in this analysis. OS was not prognostically different between histologic subgroups, but univariable DFS and SDFS were worse for MIP/SOL compared with LEP or ACN/PAP subgroup (P < .01); this remained marginally significant after adjustment. MIP/SOL patients (but not ACN/PAP) derived DFS and SDFS but not OS benefit from ACT (OS: HR, 0.71; 95% CI, 0.51 to 0.99; interaction P = .18; DFS: HR, 0.60; 95% CI, 0.44 to 0.82; interaction P = < .01; and SDFS: HR, 0.59; 95% CI, 0.42 to 0.81; interaction P = .01).\n The new lung adenocarcinoma classification based on predominant histologic pattern was not predictive for ACT benefit for OS, but it seems predictive for disease-specific outcomes.\n © 2015 by American Society of Clinical Oncology.\n\nPopper, Helmuth\n\n\n"
},
{
"text": "\n166425\nEffect of Additional Treatments Combined with Conventional Therapies in Pregnant Patients with High-Risk Antiphospholipid Syndrome: A Multicentre Study.\n\nRuffatti, A\n\nTonello, M\n\nHoxha, A\n\nSciascia, S\n\nCuadrado, MJ\n\nLatino, JO\n\nUdry, S\n\nReshetnyak, T\n\nCostedoat-Chalumeau, N\n\nMorel, N\n\nMarozio, L\n\nTincani, A\n\nAndreoli, L\n\nHaladyj, E\n\nMeroni, PL\n\nGerosa, M\n\nAlijotas-Reig, J\n\nTenti, S\n\nMayer-Pickel, K\n\nSimchen, MJ\n\nBertero, MT\n\nDe Carolis, S\n\nRamoni, V\n\nMekinian, A\n\nGrandone, E\n\nMaina, A\n\nSerrano, F\n\nPengo, V\n\nKhamashta, MA\n\nBeiträge in Fachzeitschriften\nISI:000429100700003\n29490410.0\n10.1055/s-0038-1632388\nNone\nThe effect of additional treatments combined with conventional therapy on pregnancy outcomes was examined in high-risk primary antiphospholipid syndrome (PAPS) patients to identify the most effective treatment strategy. The study's inclusion criteria were (1) positivity to lupus anticoagulant alone or associated with anticardiolipin and/or anti-β2 glycoprotein I antibodies; (2) a history of severe maternal-foetal complications (Group I) or a history of one or more pregnancies refractory to conventional therapy leading to unexplained foetal deaths not associated with severe maternal-foetal complications (Group II). Two different additional treatments were considered: oral-low-dose steroids (10-20 mg prednisone daily) and/or 200 to 400 mg daily doses of hydroxychloroquine and parenteral-intravenous immunoglobulins at 2 g/kg per month and/or plasma exchange. The study's primary outcomes were live birth rates and pregnancy complications. A total of 194 pregnant PAPS patients attending 20 tertiary centres were retrospectively enrolled. Hydroxychloroquine was found to be linked to a significantly higher live birth rate with respect to the other oral treatments in the Group II patients. The high (400 mg) versus low (200 mg) doses of hydroxychloroquine (p = 0.036) and its administration before versus during pregnancy (p = 0.021) were associated with a significantly higher live birth rate. Hydroxychloroquine therapy appeared particularly efficacious in the PAPS patients without previous thrombosis. Parenteral treatments were associated with a significantly higher live birth rate with respect to the oral ones (p = 0.037), particularly in the Group I patients. In conclusion, some additional treatments were found to be safe and efficacious in high-risk PAPS pregnant women.\n Schattauer GmbH Stuttgart.\n\nMayer-Pickel, Karoline Ilse\n\n\n"
},
{
"text": "\n168597\nLong-term survivors of childhood cancer: cure and care-the Erice Statement (2006) revised after 10 years (2016).\n\nJankovic, M\n\nHaupt, R\n\nSpinetta, JJ\n\nBeck, JD\n\nByrne, J\n\nCalaminus, G\n\nLackner, H\n\nBiondi, A\n\nOeffinger, K\n\nHudson, M\n\nSkinner, R\n\nReaman, G\n\nvan der Pal, H\n\nKremer, L\n\nden Hartogh, J\n\nMichel, G\n\nFrey, E\n\nBardi, E\n\nHawkins, M\n\nRizvi, K\n\nTerenziani, M\n\nValsecchi, MG\n\nBode, G\n\nJenney, M\n\nde Vathaire, F\n\nGarwicz, S\n\nLevitt, GA\n\nGrabow, D\n\nKuehni, CE\n\nSchrappe, M\n\nHjorth, L\n\nparticipants in PanCare\n\nBeiträge in Fachzeitschriften\nISI:000445241100004\n29946794.0\n10.1007/s11764-018-0701-0\nNone\nThe number of persons who have successfully completed treatment for a cancer diagnosed during childhood and who have entered adulthood is increasing over time, and former patients will become aging citizens.\n Ten years ago, an expert panel met in Erice, Italy, to produce a set of principles concerning the cure and care of survivors of childhood and adolescent cancer. The result was the Erice Statement (Haupt et al. Eur J Cancer 43(12):1778-80, 2007) that was translated into nine languages. Ten years on, it was timely to review, and possibly revise, the Erice Statement in view of the changes in paediatric oncology and the number and results of international follow-up studies conducted during the intervening years.\n The long-term goal of the cure and care of a child with cancer is that he/she becomes a resilient and autonomous adult with optimal health-related quality of life, accepted in society at the same level as his/her age peers. "Cure" refers to cure from the original cancer, regardless of any potential for, or presence of, remaining disabilities or side effects of treatment. The care of a child with cancer should include complete and honest information for parents and the child.\n Some members of the previous expert panel, as well as new invited experts, met again in Erice to review the Erice Statement, producing a revised version including update and integration of each of the ten points. In addition, a declaration has been prepared, by the Childhood Cancer International Survivors Network in Dublin on October 2016 (see Annex 1).\n\nLackner, Herwig\n\n\n"
},
{
"text": "\n175632\nEndothelial lipase increases antioxidative capacity of high-density lipoprotein.\n\nSchilcher, I\n\nLedinski, G\n\nRadulović, S\n\nHallström, S\n\nEichmann, T\n\nMadl, T\n\nZhang, F\n\nLeitinger, G\n\nKolb-Lenz, D\n\nDarnhofer, B\n\nBirner-Gruenberger, R\n\nWadsack, C\n\nKratky, D\n\nMarsche, G\n\nFrank, S\n\nCvirn, G\n\nBeiträge in Fachzeitschriften\nISI:000480664300009\n31220617.0\n10.1016/j.bbalip.2019.06.011\nPMC6699986\nEndothelial lipase (EL) is a strong determinant of structural and functional properties of high-density lipoprotein (HDL). We examined whether the antioxidative capacity of HDL is affected by EL. EL-modified HDL (EL-HDL) and control EV-HDL were generated by incubation of HDL with EL- overexpressing or control HepG2 cells. As determined by native gradient gel electrophoresis, electron microscopy, and small-angle X-ray scattering EL-HDL is smaller than EV-HDL. Mass spectrometry revealed an enrichment of EL-HDL with lipolytic products and depletion of phospholipids and triacylglycerol. Kinetics of conjugated diene formation and HPLC-based malondialdehyde quantification revealed that EL-HDL exhibited a significantly higher resistance to copper ion-induced oxidation and a significantly higher capacity to protect low-density lipoprotein (LDL) from copper ion-induced oxidation when compared to EV-HDL. Depletion of the lipolytic products from EL-HDL abolished the capacity of EL-HDL to protect LDL from copper ion-induced oxidation, which could be partially restored by lysophosphatidylcholine enrichment. Proteomics of HDL incubated with oxidized LDL revealed significantly higher levels of methionine 136 sulfoxide in EL-HDL compared to EV-HDL. Chloramine T (oxidizes methionines and modifies free thiols), diminished the difference between EL-HDL and EV-HDL regarding the capacity to protect LDL from oxidation. In absence of LDL small EV-HDL and EL-HDL exhibited higher resistance to copper ion-induced oxidation when compared to respective large particles. In conclusion, the augmented antioxidative capacity of EL-HDL is primarily determined by the enrichment of HDL with EL-generated lipolytic products and to a lesser extent by the decreased HDL particle size and the increased activity of chloramine T-sensitive mechanisms.\n Copyright © 2019 The Author(s). Published by Elsevier B.V. All rights reserved.\n\nBirner-Grünberger, Ruth\n\nCvirn, Gerhard\n\nDarnhofer, Barbara\n\nFrank, Sasa\n\nHallström, Seth\n\nKratky, Dagmar\n\nLedinski, Gerhard\n\nLeitinger, Gerd\n\nMadl, Tobias\n\nMarsche, Gunther\n\nRadulovic, Snjezana\n\nWadsack, Christian\n\nZhang, Fangrong\n\n\n"
},
{
"text": "\n177660\nCardiac power output accurately reflects external cardiac work over a wide range of inotropic states in pigs.\n\nAbawi, D\n\nFaragli, A\n\nSchwarzl, M\n\nManninger, M\n\nZweiker, D\n\nKresoja, KP\n\nVerderber, J\n\nZirngast, B\n\nMaechler, H\n\nSteendijk, P\n\nPieske, B\n\nPost, H\n\nAlogna, A\n\nBeiträge in Fachzeitschriften\nISI:000490455900001\n31615415.0\n10.1186/s12872-019-1212-2\nPMC6792198\nCardiac power output (CPO), derived from the product of cardiac output and mean aortic pressure, is an important yet underexploited parameter for hemodynamic monitoring of critically ill patients in the intensive-care unit (ICU). The conductance catheter-derived pressure-volume loop area reflects left ventricular stroke work (LV SW). Dividing LV SW by time, a measure of LV SW min- 1 is obtained sharing the same unit as CPO (W). We aimed to validate CPO as a marker of LV SW min- 1 under various inotropic states.\n We retrospectively analysed data obtained from experimental studies of the hemodynamic impact of mild hypothermia and hyperthermia on acute heart failure. Fifty-nine anaesthetized and mechanically ventilated closed-chest Landrace pigs (68 ± 1 kg) were instrumented with Swan-Ganz and LV pressure-volume catheters. Data were obtained at body temperatures of 33.0 °C, 38.0 °C and 40.5 °C; before and after: resuscitation, myocardial infarction, endotoxemia, sevoflurane-induced myocardial depression and beta-adrenergic stimulation. We plotted LVSW min- 1 against CPO by linear regression analysis, as well as against the following classical indices of LV function and work: LV ejection fraction (LV EF), rate-pressure product (RPP), triple product (TP), LV maximum pressure (LVPmax) and maximal rate of rise of LVP (LV dP/dtmax).\n CPO showed the best correlation with LV SW min- 1 (r2 = 0.89; p < 0.05) while LV EF did not correlate at all (r2 = 0.01; p = 0.259). Further parameters correlated moderately with LV SW min- 1 (LVPmax r2 = 0.47, RPP r2 = 0.67; and TP r2 = 0.54). LV dP/dtmax correlated worst with LV SW min- 1 (r2 = 0.28).\n CPO reflects external cardiac work over a wide range of inotropic states. These data further support the use of CPO to monitor inotropic interventions in the ICU.\n\nAlbori, Jochen\n\nMächler, Heinrich\n\nManninger-Wünscher, Martin\n\nZirngast, Birgit\n\nZweiker, David\n\n\n"
},
{
"text": "\n178864\nPlatelet-derived factors impair placental chorionic gonadotropin beta-subunit synthesis.\n\nForstner, D\n\nManinger, S\n\nNonn, O\n\nGuettler, J\n\nMoser, G\n\nLeitinger, G\n\nPritz, E\n\nStrunk, D\n\nSchallmoser, K\n\nMarsche, G\n\nHeinemann, A\n\nHuppertz, B\n\nGauster, M\n\nBeiträge in Fachzeitschriften\nISI:000503677000001\n31863152.0\n10.1007/s00109-019-01866-x\nPMC7007904\nDuring histiotrophic nutrition of the embryo, maternal platelets may be the first circulating maternal cells that find their way into the placental intervillous space through narrow intertrophoblastic gaps within the plugs of spiral arteries. Activation of platelets at the maternal-fetal interface can influence trophoblast behavior and has been implicated in serious pregnancy pathologies. Here, we show that platelet-derived factors impaired expression and secretion of the human chorionic gonadotropin beta-subunit (βhCG) in human first trimester placental explants and the trophoblast cell line BeWo. Impaired βhCG synthesis was not the consequence of hampered morphological differentiation, as assessed by analysis of differentiation-associated genes and electron microscopy. Platelet-derived factors did not affect intracellular cAMP levels and phosphorylation of CREB, but activated Smad3 and its downstream-target plasminogen activator inhibitor (PAI)-1 in forskolin-induced BeWo cell differentiation. While TGF-β type I receptor inhibitor SB431542 did not restore impaired βhCG production in response to platelet-derived factors, Smad3 inhibitor SIS3 interfered with CREB activation, suggesting an interaction of cAMP/CREB and Smad3 signaling. Sequestration of transcription co-activators CBP/p300, known to bind both CREB and Smad3, may limit βhCG production, since CBP/p300 inhibitor C646 significantly restricted its forskolin-induced upregulation. In conclusion, our study suggests that degranulation of maternal platelets at the early maternal-fetal interface can impair placental βhCG production, without substantially affecting morphological and biochemical differentiation of villous trophoblasts. KEY MESSAGES: Maternal platelets can be detected on the surface of the placental villi and in intercellular gaps of trophoblast cell columns from gestational week 5 onwards. Platelet-derived factors impair hCG synthesis in human first trimester placenta. Platelet-derived factors activate Smad3 in trophoblasts. Smad3 inhibitor SIS3 interferes with forskolin-induced CREB signaling. Sequestration of CBP/p300 by activated Smad3 may limit placental hCG production.\n\nForstner, Desiree\n\nGauster, Martin\n\nGüttler, Jacqueline\n\nHeinemann, Akos\n\nHuppertz, Berthold\n\nLeitinger, Gerd\n\nMarsche, Gunther\n\nMoser, Gerit\n\nNonn, Olivia\n\nPritz, Elisabeth\n\n\n"
},
{
"text": "\n179493\nVitamin D deficiency 2.0: an update on the current status worldwide.\n\nAmrein, K\n\nScherkl, M\n\nHoffmann, M\n\nNeuwersch-Sommeregger, S\n\nKöstenberger, M\n\nTmava Berisha, A\n\nMartucci, G\n\nPilz, S\n\nMalle, O\n\nBeiträge in Fachzeitschriften\nISI:000508321500001\n31959942.0\n10.1038/s41430-020-0558-y\nPMC7091696\nVitamin D testing and the use of vitamin D supplements have increased substantially in recent years. Currently, the role of vitamin D supplementation, and the optimal vitamin D dose and status, is a subject of debate, because large interventional studies have been unable to show a clear benefit (in mostly vitamin D replete populations). This may be attributed to limitations in trial design, as most studies did not meet the basic requirements of a nutrient intervention study, including vitamin D-replete populations, too small sample sizes, and inconsistent intervention methods regarding dose and metabolites. Vitamin D deficiency (serum 25-hydroxyvitamin D [25(OH)D] < 50 nmol/L or 20 ng/ml) is associated with unfavorable skeletal outcomes, including fractures and bone loss. A 25(OH)D level of >50 nmol/L or 20 ng/ml is, therefore, the primary treatment goal, although some data suggest a benefit for a higher threshold. Severe vitamin D deficiency with a 25(OH)D concentration below <30 nmol/L (or 12 ng/ml) dramatically increases the risk of excess mortality, infections, and many other diseases, and should be avoided whenever possible. The data on a benefit for mortality and prevention of infections, at least in severely deficient individuals, appear convincing. Vitamin D is clearly not a panacea, and is most likely efficient only in deficiency. Given its rare side effects and its relatively wide safety margin, it may be an important, inexpensive, and safe adjuvant therapy for many diseases, but future large and well-designed studies should evaluate this further. A worldwide public health intervention that includes vitamin D supplementation in certain risk groups, and systematic vitamin D food fortification to avoid severe vitamin D deficiency, would appear to be important. In this narrative review, the current international literature on vitamin D deficiency, its relevance, and therapeutic options is discussed.\n\nAmrein, Karin\n\nHoffmann, Magdalena\n\nKöstenberger, Markus\n\nMalle, Oliver\n\nNeuwersch-Sommeregger, Stefan Matthias\n\nPilz, Stefan\n\nTmava-Berisha, Adelina\n\n\n"
},
{
"text": "\n181818\nCirculating uromodulin inhibits vascular calcification by interfering with pro-inflammatory cytokine signalling.\n\nAlesutan, I\n\nLuong, TTD\n\nSchelski, N\n\nMasyout, J\n\nHille, S\n\nSchneider, MP\n\nGraham, D\n\nZickler, D\n\nVerheyen, N\n\nEstepa, M\n\nPasch, A\n\nMaerz, W\n\nTomaschitz, A\n\nPilz, S\n\nFrey, N\n\nLang, F\n\nDelles, C\n\nMüller, OJ\n\nPieske, B\n\nEckardt, KU\n\nScherberich, J\n\nVoelkl, J\n\nBeiträge in Fachzeitschriften\nISI:000637025500035\n32243494.0\n10.1093/cvr/cvaa081\nNone\nUromodulin is produced exclusively in the kidney and secreted into both urine and blood. Serum levels of uromodulin are correlated with kidney function and reduced in chronic kidney disease (CKD) patients, but physiological functions of serum uromodulin are still elusive. This study investigated the role of uromodulin in medial vascular calcification, a key factor associated with cardiovascular events and mortality in CKD patients.\n Experiments were performed in primary human (HAoSMCs) and mouse (MOVAS) aortic smooth muscle cells, cholecalciferol overload and subtotal nephrectomy mouse models and serum from CKD patients. In three independent cohorts of CKD patients, serum uromodulin concentrations were inversely correlated with serum calcification propensity. Uromodulin supplementation reduced phosphate-induced osteo-/chondrogenic transdifferentiation and calcification of HAoSMCs. In human serum, pro-inflammatory cytokines tumour necrosis factor α (TNFα) and interleukin-1β (IL-1β) co-immunoprecipitated with uromodulin. Uromodulin inhibited TNFα and IL-1β-induced osteo-/chondrogenic signalling and activation of the transcription factor nuclear factor kappa-light-chain-enhancer of activated β cells (NF-kB) as well as phosphate-induced NF-kB-dependent transcriptional activity in HAoSMCs. In vivo, adeno-associated virus (AAV)-mediated overexpression of uromodulin ameliorated vascular calcification in mice with cholecalciferol overload. Conversely, cholecalciferol overload-induced vascular calcification was aggravated in uromodulin-deficient mice. In contrast, uromodulin overexpression failed to reduce vascular calcification during renal failure in mice. Carbamylated uromodulin was detected in serum of CKD patients and uromodulin carbamylation inhibited its anti-calcific properties in vitro.\n Uromodulin counteracts vascular osteo-/chondrogenic transdifferentiation and calcification, at least in part, through interference with cytokine-dependent pro-calcific signalling. In CKD, reduction and carbamylation of uromodulin may contribute to vascular pathology.\n Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.\n\nMärz, Winfried\n\nPilz, Stefan\n\nVerheyen, Nicolas Dominik\n\n\n"
},
{
"text": "\n183924\nSex-Related Differences in the Long-Term Outcomes of Patients with Femoropopliteal Arterial Disease Treated with the IN.PACT Drug-Coated Balloon in the IN.PACT SFA Randomized Controlled Trial: A Post Hoc Analysis.\n\nKohi, MP\n\nBrodmann, M\n\nZeller, T\n\nMicari, A\n\nBaumgartner, I\n\nWang, H\n\nWall, B\n\nRazavi, MK\n\nBeiträge in Fachzeitschriften\nISI:000577351600008\n32868016.0\n10.1016/j.jvir.2020.05.012\nNone\nTo evaluate sex-related disparities in long-term outcomes of patients with peripheral artery disease (PAD) treated with IN.PACT drug-coated balloon (DCB) or percutaneous transluminal angioplasty (PTA).\n A post hoc analysis of the IN.PACT SFA trial was performed. Participants with Rutherford Clinical Classification 2-4 PAD and femoropopliteal artery lesions up to 18 cm long were randomly assigned to treatment with DCB (n = 220) or PTA (n = 111). Effectiveness outcomes were evaluated, including 36-month primary patency (freedom from binary restenosis and freedom from clinically driven [CD] target lesion revascularization [TLR]).\n In the DCB group, women were significantly older (69.4 y ± 9.9) than men (66.4 y ± 9.1; P = .025). Mean reference vessel diameter (RVD) was significantly smaller in women (4.4 mm ± 0.68) compared with men (4.8 mm ± 0.89, P < .001). Primary patency was 65.4% in women and 71.8% in men (P = .302). Freedom from CD-TLR was 81.1% in women and 86.4% in men (P = .285). Women treated with PTA were older (70.4 y ± 8.3) than men (66.9 y ± 9.5; P = .063). Mean RVD was significantly smaller in women (4.2 mm ± 0.77) compared with men (4.9 mm ± 0.77, P < .001). Primary patency was 42.3% in women and 46.7% in men (P = .551). Freedom from CD-TLR was 59.4% in women and 75.5% in men (P = .109). No significant differences were noted in safety and mortality outcomes.\n In both groups, women were older and had smaller vessels. Particularly in the PTA group, women had worse clinical outcomes, though not reaching statistical significance. Further evaluation is necessary to understand the disparate nature of disease progression and outcomes following endovascular treatment in women compared with men.\n Copyright © 2020 SIR. Published by Elsevier Inc. All rights reserved.\n\nBrodmann, Marianne\n\n\n"
}
]
}