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"text": "\n159322\nA comprehensive fracture prevention strategy in older adults: The European union geriatric medicine society (EUGMS) statement\n\nBlain, H\n\nMasud, T\n\nDargent-Molina, P\n\nMartin, FC\n\nRosendahl, E\n\nvan der Velde, N\n\nBousquet, J\n\nBenetos, A\n\nCooper, C\n\nKanis, JA\n\nReginster, JY\n\nRizzoli, R\n\nCortet, B\n\nBarbagallo, M\n\nDreinhofer, K\n\nVellas, B\n\nMaggi, S\n\nStrandberg, T\n\nAlvarez, MN\n\nAnnweiler, C\n\nBernard, PL\n\nBeswetherick, N\n\nBischoff-Ferrari, HA\n\nBloch, F\n\nBoddaert, J\n\nBonnefoy, M\n\nBousson, V\n\nBourdel-Marchasson, I\n\nCapisizu, A\n\nChe, H\n\nClara, JG\n\nCombe, B\n\nDelignieres, D\n\nEklund, P\n\nEmmelot-Vonk, M\n\nFreiberger, E\n\nGauvain, JB\n\nGoswami, N\n\nGuldemond, N\n\nHerrero, AC\n\nJoel, ME\n\nJonsdottir, AB\n\nKemoun, G\n\nKiss, I\n\nKolk, H\n\nKowalski, ML\n\nKrajcik, S\n\nKutsal, YG\n\nLauretani, F\n\nMacijauskiene, J\n\nMellingsaeter, M\n\nMorel, J\n\nMourey, F\n\nNourashemi, F\n\nNyakas, C\n\nPuisieux, F\n\nRambourg, P\n\nRamirez, AG\n\nRapp, K\n\nRolland, Y\n\nRyg, J\n\nSahota, O\n\nSnoeijs, S\n\nStephan, Y\n\nThomas, E\n\nTodd, C\n\nTreml, J\n\nAdachi, R\n\nAgnusdei, D\n\nBody, JJ\n\nBreuil, V\n\nBruyere, O\n\nBurckardt, P\n\nCannata-Andia, JB\n\nCarey, J\n\nChan, DC\n\nChapuis, L\n\nChevalley, T\n\nCohen-Solal, M\n\nDawson-Hughes, B\n\nDennison, EM\n\nDevogelaer, JP\n\nFardellone, P\n\nFeron, JM\n\nPerez, AD\n\nFelsenberg, D\n\nGlueer, C\n\nHarvey, N\n\nHiligsman, M\n\nJavaid, MK\n\nJorgensen, NR\n\nKendler, D\n\nKraenzlin, M\n\nLaroche, M\n\nLegrand, E\n\nLeslie, WD\n\nLespessailles, E\n\nLewiecki, EM\n\nNakamura, T\n\nPapaioannou, A\n\nRoux, C\n\nSilverman, S\n\nHenriquez, MS\n\nThomas, T\n\nVasikaran, S\n\nWatts, NB\n\nWeryha, G\n\nBeiträge in Fachzeitschriften\nISI:000393044000011\nNone\n10.1016/j.eurger.2016.04.012\nNone\nPrevention of fragility fractures in older people has become a public health priority, although the most appropriate and cost-effective strategy remains unclear. In the present statement, the Interest group on falls and fracture prevention of the European union geriatric medicine society (EUGMS), in collaboration with the International association of gerontology and geriatrics for the European region (IAGG-ER), the European union of medical specialists (EUMS), the Fragility fracture network (FFN), the International osteoporosis foundation (IOF) - European society for clinical and economic aspects of osteoporosis and osteoarthritis (ECCEO), outlines its views on the main points in the current debate in relation to the primary and secondary prevention of falls, the diagnosis and treatment of bone fragility, and the place of combined falls and fracture liaison services for fracture prevention in older people. (C) 2016 Published by Elsevier Masson SAS.\n\nGoswami, Nandu\n\n\n"
},
{
"text": "\n165815\nPersonalized Therapy Against Preeclampsia by Replenishing Placental Protein 13 (PP13) Targeted to Patients With Impaired PP13 Molecule or Function.\n\nMeiri, H\n\nOsol, G\n\nCetin, I\n\nGizurarson, S\n\nHuppertz, B\n\nBeiträge in Fachzeitschriften\nISI:000425900600033\n29034064.0\n10.1016/j.csbj.2017.09.002\nPMC5633742\nHypertensive disorders affect about one third of all people aged 20 and above, and are treated with anti-hypertensive drugs. Preeclampsia (PE) is one form of such disorders that only develops during pregnancy. It affects ten million pregnant women globally and additionally causes fetal loss and major newborn disabilities. The syndrome's origin is multifactorial, and anti-hypertensive drugs are ineffective in treating it. Biomarkers are helpful for predict its development. Generic drugs, such as low dose aspirin, were proven effective in preventing preterm PE. However, it does not cure the majority of cases and many studies are underway for fighting PE with extended use of additional generic drugs, or through new drug development programs. This review focuses on placental protein 13 (PP13). This protein is only expressed in the placenta. Impaired PP13 DNA structure and/or its reduced mRNA expression leads to lower blood PP13 level that predict a higher risk of developing PE. Two polymorphic PP13 variants have been identified: (1) The promoter PP13 variant with an "A/A" genotype in the -98 position (versus "A/C" or "C/C"). Having the "A/A" genotype is coupled to lower PP13 expression, mainly during placental syncytiotrophoblast differentiation and, if associated with obesity and history of previous preeclampsia, it accurately predicts higher risk for developing the disorder. (2) A thymidine deletion at position 221 causes a frame shift in the open reading frame, and the formation of an early stop codon resulting in the formation of DelT221, a truncated variant of PP13. In pregnant rodents, both short- and long- term replenishment of PP13 causes reversible hypotension and vasodilation of uterine vessels. Long-term exposure is also accompanied by the development of larger placentas and newborns. Also, only w/t PP13 is capable of inducing leukocyte apoptosis, providing maternal immune tolerance to pregnancy. Based on published data, we propose a targeted PP13 therapy to fight PE, and consider the design and conduct of animal studies to explore this hypothesis. Accordingly, a new targeted therapy can be implemented in humans combining prediction and prevention.\n\nHuppertz, Berthold\n\n\n"
},
{
"text": "\n181971\nThe DALI vitamin D randomized controlled trial for gestational diabetes mellitus prevention: No major benefit shown besides vitamin D sufficiency.\n\nCorcoy, R\n\nMendoza, LC\n\nSimmons, D\n\nDesoye, G\n\nAdelantado, JM\n\nChico, A\n\nDevlieger, R\n\nvan Assche, A\n\nGaljaard, S\n\nTimmerman, D\n\nLapolla, A\n\nDalfra, MG\n\nBertolotto, A\n\nHarreiter, J\n\nWender-Ozegowska, E\n\nZawiejska, A\n\nKautzky-Willer, A\n\nDunne, FP\n\nDamm, P\n\nMathiesen, ER\n\nJensen, DM\n\nAndersen, LLT\n\nTanvig, M\n\nHill, DJ\n\nJelsma, JG\n\nSnoek, FJ\n\nKöfeler, H\n\nTrötzmüller, M\n\nLips, P\n\nvan Poppel, MNM\n\nBeiträge in Fachzeitschriften\nISI:000521509800038\n31053513.0\n10.1016/j.clnu.2019.04.006\nNone\nAs vitamin D deficiency is associated with an increased risk of gestational diabetes mellitus (GDM), we aimed to test vitamin D supplementation as a strategy to reduce GDM risk (evaluated after fasting plasma glucose (FPG), insulin resistance and weight gain) in pregnant overweight/obese women.\n The DALI vitamin D multicenter study enrolled women with prepregnancy body mass index (BMI) ≥ 29 kg/m2, ≤19 + 6 weeks of gestation and without GDM. Participants were randomized to receive 1600 IU/day vitamin D3 or placebo (each with or without lifestyle intervention) on top of (multi)vitamins supplements. Women were assessed for vitamin D status (sufficiency defined as serum 25-hydroxyvitamin D (25(OH)D) ≥ 50 nmol/l), FPG, insulin resistance and weight at baseline, 24-28 and 35-37 weeks. Linear or logistic regression analyses were performed to assess intervention effects.\n Average baseline serum 25(OH)D was ≥50 nmol/l across all study sites. In the vitamin D intervention arm (n = 79), 97% of participants achieved target serum vitamin 25(OH)D (≥50 nmol/l) at 24-28 weeks and 98% at 35-37 weeks vs 74% and 78% respectively in the placebo arm (n = 75, p < 0.001). A small but significantly lower FPG (-0.14 mmol/l; CI95 -0.28, -0.00) was observed at 35-37 weeks with the vitamin D intervention without any additional difference in metabolic status, perinatal outcomes or adverse event rates.\n In the DALI vitamin D trial, supplementation with 1600 IU vitamin D3/day achieved vitamin D sufficiency in virtually all pregnant women and a small effect in FPG at 35-37 weeks. The potential of vitamin D supplementation for GDM prevention in vitamin D sufficient populations appears to be limited.\n ISRCTN70595832.\n Copyright © 2019 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.\n\nDesoye, Gernot\n\nKöfeler, Harald\n\nTrötzmüller, Martin\n\n\n"
},
{
"text": "\n2597\nThe prognostic significance of peritoneal seeding and size of postsurgical residual in patients with stage III epithelial ovarian cancer treated with surgery, chemotherapy, and high-dose radiotherapy.\n\nKapp, KS\n\nKapp, DS\n\nPoschauko, J\n\nStücklschweiger, GF\n\nHackl, A\n\nPickel, H\n\nPetru, E\n\nWinter, R\n\nBeiträge in Fachzeitschriften\nISI:000082708100013\n10479500.0\n10.1006/gyno.1999.5477\nNone\nThe aim of this study was to retrospectively analyze the prognostic importance of age, histologic type and grade, ascites, lymph node status, size and type of postoperative residual disease, and radiation dose on disease-specific (DSS) and progression-free survival (PFS) in stage III epithelial ovarian cancer patients who had been treated with radical surgery, postoperative chemotherapy, and high-dose radiotherapy.\n Consolidation radiotherapy including whole abdominal radiation, pelvic, and upper abdominal boosts was employed in 46 patients who showed no evidence of residual or progressive disease after completion of multiagent chemotherapy. The median follow-up for all patients was 36 months and 103 months for patients at risk. The prognostic impact of pretreatment and treatment parameters on DSS and PFS was tested in univariate and multivariate analyses.\n The 5-year DSS and PFS rates for all patients were 38 and 33%, and for patients with 0-< or =2 cm residual tumor 65 and 61%, respectively. In univariate analysis, initial peritoneal seeding (both: P = 0.02), ascites (P = 0.03; 0.01), size of residual (0-< or =2 cm vs >2 cm), and residual miliary subdiaphragmatic (MDS) and localized peritoneal seeding (LPS) in the upper abdomen (P = 0.0002; 0.0003) were significantly correlated with DSS and PFS. Dose of radiation (< or =30 vs >30 Gy) correlated with DSS only (P = 0.02). In multivariate analysis size of residual disease (0-< or =2 cm vs >2 cm and/or MDS or LPS) remained the only independent prognostic factor for DSS and PFS (both; P = 0. 001).\n Patients with localized peritoneal seeding who were rendered free of disease elsewhere had an outcome equally poor as that of patients with gross residuals (>2 cm) in the upper abdomen. If our findings can be confirmed, attempted resection of all localized seeding in patients who are otherwise cytoreducible to no or minimal residual disease may be considered in combination with Taxol-containing regimens as are now being utilized for patients with gross disease.\n Copyright 1999 Academic Press.\n\nPetru, Edgar\n\n\n"
},
{
"text": "\n80021\nCortical tibial bone volume in two strains of mice: effects of sciatic neurectomy and genetic regulation of bone response to mechanical loading.\n\nKodama, Y\n\nDimai, HP\n\nWergedal, J\n\nSheng, M\n\nMalpe, R\n\nKutilek, S\n\nBeamer, W\n\nDonahue, LR\n\nRosen, C\n\nBaylink, DJ\n\nFarley, J\n\nBeiträge in Fachzeitschriften\nISI:000081842100002\n10456383.0\n10.1016/S8756-3282(99)00155-6\nNone\nAlthough C3H/HeJ (C3H) and C57BL/6J (B6) mice are similar in body size (and adult weight), and have bones of similar external size, C3H mice have higher peak bone densities than B6 mice (e.g., 53% higher peak bone density in the femora). The current studies were intended to assess the role of mechanical loading/unloading as a possible determinant of the bone density difference between these inbred strains of mice and, specifically, to assess the effect of sciatic neurectomy on histomorphometric indices of bone formation and resorption in the tibiae of female C3H and B6 mice. Groups of 10 mice of each strain were subjected to left-side sciatic neurectomy (left hindlimb immobilization) or a sham procedure. The contralateral (right) legs of each mouse were used as controls. Four weeks of immobilization produced no systemic changes in bone formation indices in either strain of mice (i.e., no change in serum alkaline phosphatase or serum osteocalcin). However, histomorphometric assessments at the tibiofibular junction showed that 4 weeks of immobilization caused a time-dependent decrease in the length of the endosteal bone forming perimeter (e.g., 14% of control single-labeled, noneroded surface at 4 weeks, p < 0.005) with a concomitant increase in the length of the endosteal bone resorbing perimeter (i.e., 424% of control eroded surface at 4 weeks, p < 0.005), in the B6 mice. These effects were associated with an increase in medullary area (132% of control, p < 0.05) at this site, in the B6 mice. The pattern of response was different in the tibiae of the C3 mice-a much smaller decrease in bone forming perimeter (88% of control at 4 weeks, p < 0.05), with no associated increase in bone resorbing perimeter, and no change in medullary area. Similar effects were seen at a second cross-sectional sampling site, in the proximal tibia. Together, these findings indicate that B6 mice are more sensitive to endosteal bone loss from hindlimb immobilization than C3H mice.\n\nDimai, Hans\n\n\n"
},
{
"text": "\n84530\nOsteofibrous dysplasia and adamantinoma in children and adolescents: a clinicopathologic reappraisal.\n\nGleason, BC\n\nLiegl-Atzwanger, B\n\nKozakewich, HP\n\nConnolly, S\n\nGebhardt, MC\n\nFletcher, JA\n\nPerez-Atayde, AR\n\nBeiträge in Fachzeitschriften\nISI:000253742600003\n18300815.0\n10.1097/PAS.0b013e318150d53e\nNone\nOsteofibrous dysplasia (OFD) and adamantinoma are rare and most commonly arise in the tibia of young individuals. Although OFD has typical histopathologic features, areas resembling OFD have often been noted at the periphery of otherwise classic adamantinomas, and some have suggested that OFD may be either a precursor to or a regressive phase of adamantinoma. The so-called OFD-like adamantinoma encompasses some features of both OFD and adamantinoma. We studied the clinical, imaging, histopathologic, immunohistochemical, ultrastructural, and molecular features of 16 OFD and 8 adamantinomas (5 OFD-like and 3 classic) in an attempt to further define their morphology, clinical course, and relationship. Patients with OFD were generally younger than those with adamantinoma. Osteoblastic and osteoclastic activity was more prominent in OFD than in OFD-like adamantinoma. In addition to the inconspicuous small clusters of epithelial cells in OFD-like adamantinoma, isolated keratin-positive cells with a unique ultrastructural hybrid fibroblastic-epithelial phenotype were found in the stroma of all OFD and OFD-like adamantinomas. Fluorescence in situ hybridization analysis revealed trisomies 7, 8, and/or 12 in the spindle cell stroma of OFD, OFD-like, and classic adamantinoma, supporting a neoplastic origin of OFD and a common histogenesis for all 3 lesions. Trisomies were not observed in osteoblasts or osteoclasts suggesting that the osseous component is reactive and non-neoplastic. Of the 11 OFD patients with follow-up (median, 4.5 y), all 3 who underwent incisional biopsy had persistent, nonprogressive disease and 2 of 8 who underwent curettage or wide excision had recurrence; none developed adamantinoma. All 6 adamantinoma patients with follow-up (3 classic and 3 OFD-like) were treated with wide excision. One with classic adamantinoma died of pulmonary metastases 9 years after presentation; the other 5 were free of disease with a median follow-up of 12 years. None of the classic adamantinomas evolved into OFD-like adamantinoma or OFD. Although the histopathology, immunohistochemistry, ultrastructure, and cytogenetics indicate that these lesions are closely related, our data and the literature suggest that only classic adamantinoma has malignant potential. OFD, OFD-like adamantinoma, and classic adamantinoma appear to show a progressive complexity of cytogenetic aberrations, perhaps indicative of a multistep neoplastic transformation.\n\nLiegl-Atzwanger, Bernadette\n\n\n"
},
{
"text": "\n102986\nHIV-1 and HIV-2 isolates differ in their ability to activate the complement system on the surface of infected cells.\n\nMarschang, P\n\nGürtler, L\n\nTötsch, M\n\nThielens, NM\n\nArlaud, GJ\n\nHittmair, A\n\nKatinger, H\n\nDierich, MP\n\nBeiträge in Fachzeitschriften\nISI:A1993LL49200001\n7689323.0\n10.1097/00002030-199307000-00001\nNone\nOBJECTIVE: To analyse the ability of different HIV-1 and HIV-2 isolates to activate the complement system. DESIGN: H9 cells chronically infected with various HIV isolates and the corresponding purified viruses were tested for complement activation. To identify the molecules responsible for complement activation on the surface of infected cells, the expression of complement inhibitors/regulators and viral proteins on the cell surface was analysed. METHODS: C3 deposition on the cell surface and the expression of viral and cellular antigens were determined by flow cytometry analysis. Complement activation by purified viruses was measured using a complement consumption assay and a C1 activation assay. RESULTS: H9 cells infected with different HIV-1 and HIV-2 isolates showed varying degrees of complement activation on the cell surface, ranging from strong activation and deposition of large amounts of C3 to no increased C3 deposition compared to uninfected cells. The C3 deposition was eliminated by EDTA and reduced in the presence of EGTA. In contrast, all purified viral isolates tested activated the complement system in a comparable manner. While the expression of MCP, DAF and CD59 was not modified after infection with different viral isolates, the reaction of the infected cells with a monoclonal antibody (3D6) directed against a gp41 epitope (amino acids 601-620) was found to correlate with the complement activation on the cell surface. CONCLUSIONS: Some HIV-1 as well as HIV-2 isolates activate the complement system on the surface of infected cells independent of anti-HIV antibodies, while other isolates fail to do so. Complement activation on the cell surface is mediated by the alternative and, to a lesser extent, the classical pathway. The differences in complement activation on the cell surface are not caused by a modified expression of membrane-bound complement inhibitors/regulators. C3 deposition on the cell surface correlates with the expression of an epitope lying within the major complement activating domain of gp41 (amino acids 591-620). These results suggest a role of gp41 for complement activation on HIV-infected cells as has been described previously for purified HIV.\n\n\n"
},
{
"text": "\n103273\nMagnetic resonance images of 91 children with different causes of short stature: pituitary size reflects growth hormone secretion.\n\nNagel, BH\n\nPalmbach, M\n\nPetersen, D\n\nRanke, MB\n\nBeiträge in Fachzeitschriften\nISI:A1997YA31500005\n9365063.0\n10.1007/s004310050707\nNone\nIn order to validate an association between pituitary size and severity of growth hormone deficiency (GHD) we evaluated the magnetic resonance images (MRI) of 107 children with different causes of short stature. Ninety-one MRIs were evaluable (64 male, 27 female; age: 9.1 +/- 3.9 years). The levels of insulin-like growth factor-1 (IGF-1) and insulin-like growth factor binding protein-3 (IGFBP-3), and tests of GH stimulation and spontaneous secretion, led to the following subgroups: severe isolated GHD (SIGHD) (GH < 7 ng/ml) (n = 21); partial, isolated GHD (GH 7-10 ng/ml) (n = 22); multiple pituitary hormone deficiency (MPHD) (n = 13); neurosecretory dysfunction (n = 10); non-classifiable diagnosis (NC) (n = 13); idiopathic short stature (n = 9); and intra-uterine growth retardation (n = 3). Pituitary height (PHT) was measured and hypoplasia was assumed when PHT was < -2 SDS. An ectopic posterior pituitary with missing stalk and a hypoplastic anterior pituitary was present in 12 (57%) SIGHD cases, 12 (92%) MPHD cases and 1 patient from the NC group. An isolated hypoplastic anterior pituitary was observed in 15%-33% of the other groups. PHT (mm; mean, SD) in MPHD (1.7 +/- 0.5) was lower than in SIGHD (2.7 +/- 1.0, P < 0.05), with PHT of both groups being lower than in all the other groups (3.8 +/- 0.9, P < 0.0001). PHT SDS correlates with IGF-I SDS (r = 0.48, P < 0.0001), IGFBP-3 SDS (r = 0.46, P < 0.0001) and the highest peaks in tests of GH stimulation and GH spontaneous secretion (r = 0.36, P < 0.0001). In contrast to all the other groups, no correlation with age was observed in MPHD and SIGHD. Breech delivery was recorded in up to 26% of patients in all seven groups. Surprisingly, only 1 out of 23 patients with an ectopic posterior pituitary was born by breech delivery, suggesting that ectopia of the posterior lobe is not necessarily related to breech delivery. CONCLUSION: PHT is significantly correlated with GH secretion in several types of short stature. Patients with ectopic posterior pituitary, missing stalk and hypoplastic anterior pituitary either suffer from SIGHD or MPHD, and this anatomical defect is not necessarily related to breech delivery.\n\n\n"
},
{
"text": "\n115893\nMitral isthmus ablation with and without temporary spot occlusion of the coronary sinus: a randomized clinical comparison of acute outcomes.\n\nHocini, M\n\nShah, AJ\n\nNault, I\n\nRivard, L\n\nLinton, N\n\nNarayan, S\n\nMyiazaki, S\n\nJadidi, AS\n\nKnecht, S\n\nScherr, D\n\nWilton, SB\n\nRoten, L\n\nPascale, P\n\nPedersen, M\n\nDerval, N\n\nSacher, F\n\nJaïs, P\n\nClémenty, J\n\nHaïssaguerre, M\n\nBeiträge in Fachzeitschriften\nISI:000303662100007\n22229972.0\n10.1111/j.1540-8167.2011.02248.x\nPMC3390152\nTo evaluate the safety and outcomes of mitral isthmus (MI) linear ablation with temporary spot occlusion of the coronary sinus (CS).\n CS blood flow cools local tissue precluding transmurality and bidirectional block across MI lesion.\n In a randomized, controlled trial (CS-occlusion = 20, Control = 22), MI ablation was performed during continuous CS pacing to monitor the moment of block. CS was occluded at the ablation site using 1 cm spherical balloon, Swan-Ganz catheter with angiographic confirmation. Ablation was started at posterior mitral annulus and continued up to left inferior pulmonary vein (LIPV) ostium using an irrigated-tip catheter. If block was achieved, balloon was deflated and linear block confirmed. If not, additional ablation was performed epicardially (power ≤25 W). Ablation was abandoned after ∼30 minutes, if block was not achieved.\n CS occlusion (mean duration -27 ± 9 minutes) was achieved in all cases. Complete MI block was achieved in 13/20 (65%) and 15/22 (68%) patients in the CS-occlusion and control arms, respectively, P = 0.76. Block was achieved with significantly small number (0.5 ± 0.8 vs 1.9 ± 1.1, P = 0.0008) and duration (1.2 ± 1.7 vs 4.2 ± 3.5 minutes, P = 0.009) of epicardial radiofrequency (RF) applications and significantly lower amount of epicardial energy (1.3 ± 2.4 vs 6.3 ± 5.7 kJ, P = 0.006) in the CS-occlusion versus control arm, respectively. There was no difference in total RF (22 ± 9 vs 23 ± 11 minutes, P = 0.76), procedural (36 ± 16 vs 39 ± 20 minutes, P = 0.57), and fluoroscopic (13 ± 7 vs 15 ± 10 minutes, P = 0.46) durations for MI ablation between the 2 arms. Clinically uneventful CS dissection occurred in 1 patient\n Temporary spot occlusion of CS is safe and significantly reduces the requirement of epicardial ablation to achieve MI block. It does not improve overall procedural success rate and procedural duration. Tissue cooling by CS blood flow is just one of the several challenges in MI ablation.\n © 2012 Wiley Periodicals, Inc.\n\nScherr, Daniel\n\n\n"
},
{
"text": "\n128586\nEnoxaparin followed by once-weekly idrabiotaparinux versus enoxaparin plus warfarin for patients with acute symptomatic pulmonary embolism: a randomised, double-blind, double-dummy, non-inferiority trial.\n\nBüller, HR\n\nGallus, AS\n\nPillion, G\n\nPrins, MH\n\nRaskob, GE\n\nCassiopea Investigators\n\nBeiträge in Fachzeitschriften\nISI:000299317700033\n22130488.0\n10.1016/S0140-6736(11)61505-5\nNone\nBackground Treatment of pulmonary embolism with low-molecular-weight heparin and vitamin K antagonists, such as warfarin, is not ideal. We aimed to assess non-inferiority of idrabiotaparinux, a reversible longlasting indirect inhibitor of activated factor X, to warfarin in patients with acute symptomatic pulmonary embolism. Methods In our randomised, double-blind, double-dummy, non-inferiority trial, we enrolled adults with objectively documented acute symptomatic pulmonary embolism attending 291 centres in 37 countries. We excluded patients who were pregnant, had active bleeding, kidney failure, or malignant hypertension, or were at high risk of death, bleeding, or adverse reactions to study drugs. We randomly allocated patients to receive 5-10 days' enoxaparin 1.0 mg/kg twice daily followed by subcutaneous idrabiotaparinux (starting dose 3.0 mg) or adjusted-dose warfarin (target international normalised ratio 2.0-3.0); regimens lasted 3 months or 6 months dependent on clinical presentation. Block randomisation was done with a central interactive computerised system, stratified by study centre and intended treatment duration. The primary efficacy outcome was recurrent venous thromboembolism at 99 days after randomisation. We estimated the odds ratio and 95% CI with a Mantel-Haenzsel chi(2) analysis (non-inferiority margin 2.0) in the intention-to-treat population. The main safety outcome was clinically relevant bleeding (major or non-major) in all patients at day 99. This study is registered with ClinicalTrials.gov, number NCT00345618. Findings Between Aug 1, 2006, and Jan 31, 2010, we enrolled 3202 patients aged 18-96 years. 34 (2%) of 1599 patients randomly allocated to receive enoxaparin-idrabiotaparinux and 43 (3%) of 1603 patients randomly allocated to receive enoxaparin-warfarin had recurrent venous thromboembolism (odds ratio 0.79, 95% CI 0.50-1.25; p(non-inferiority)=0.0001). 72 (5%) of 1599 patients in the enoxaparin-idrabiotaparinux group and 106 (7%) of 1603 patients in the enoxaparin-warfarin group had clinically relevant bleeding (0.67, 0.49-0.91; p(superiority)=0.0098). We noted similar differences in outcomes in those patients treated to 6 months. Interpretation Idrabiotaparinux could provide an attractive alternative to warfarin for the long-term treatment of pulmonary embolism, and seems to be associated with reduced bleeding.\n\nPilger, Ernst\n\n\n"
},
{
"text": "\n139172\nReal-time sonoelastography of salivary glands for diagnosis and functional assessment of primary Sjögren's syndrome.\n\nDejaco, C\n\nDe Zordo, T\n\nHeber, D\n\nHartung, W\n\nLipp, R\n\nLutfi, A\n\nMagyar, M\n\nZauner, D\n\nLackner, A\n\nDuftner, C\n\nHorwath-Winter, J\n\nGraninger, WB\n\nHermann, J\n\nBeiträge in Fachzeitschriften\nISI:000345623400002\n25261905.0\n10.1016/j.ultrasmedbio.2014.06.023\nNone\nThe purpose of this study was to investigate the value of real-time sonoelastography (RTS) of salivary glands for the diagnosis and assessment of glandular damage in primary Sjögren's syndrome (pSS). After institutional review board approval, 45 pSS patients, 24 sicca patients and 11 healthy controls were investigated prospectively. Questionnaires were completed and Saxon and Schirmer tests and routine blood tests carried out in all patients. All patients underwent B-mode ultrasonography and RTS of parotid and submandibular glands. Abnormal findings were graded from 0 to 48 and from 0 to 16, respectively. Sialoscintigraphy was done according to a routine protocol; scoring ranged from 0 to 12. Statistical analysis comprised receiver operating characteristic curve and multivariate regression analysis. Patients with pSS had higher B-mode (median score = 25 [range: 2-44] vs. 9 [1-20], p < 0.001) and RTS (6.5 [2-13] versus 4 [1-9], p < 0.001) scores than controls with sicca syndrome, yielding areas under the curve of 0.83 and 0.85 (p < 0.05 each), respectively for pSS diagnosis. In cases with an inconclusive B-mode ultrasonography result, RTS (cutoff score: ≥ 6) led to a sensitive (66.7%) and specific (85.7%) classification of patients and sicca controls. In multivariate regression analysis, RTS (regression coefficient = -0.48, p = 0.005), but not B-mode ultrasonography, reflected impaired salivary gland function according to the Saxon test, whereas none of the subjective measures of dryness or discomfort were related to ultrasonography results. B-mode and RTS results were both associated with sialoscintigraphy scores (regression coefficient = 0.66, p < 0.001, and regression coefficient = 0.55, p = 0.001, respectively). Reproducibility of B-mode ultrasonography and RTS was good, with intra-class correlation coefficients of 0.93 (95% confidence interval: 0.57-0.98) and 0.93 (95% confidence interval: 0.79-0.98), respectively. In summary, RTS might be a useful adjunct to B-mode ultrasonography for diagnosis and assessment of salivary gland impairment in primary Sjögren's syndrome.\n Copyright © 2014 World Federation for Ultrasound in Medicine & Biology. Published by Elsevier Inc. All rights reserved.\n\nDejaco, Christian\n\nGraninger, Winfried\n\nHermann, Josef\n\nHorwath-Winter, Jutta\n\nLackner, Angelika\n\nLipp, Rainer\n\nMagyar, Marton\n\n\n"
},
{
"text": "\n142561\nInfluence of molecular subgroups on outcome of acute myeloid leukemia with normal karyotype in 141 patients undergoing salvage allogeneic stem cell transplantation in primary induction failure or beyond first relapse.\n\nPfeiffer, T\n\nSchleuning, M\n\nMayer, J\n\nHaude, KH\n\nTischer, J\n\nBuchholz, S\n\nBunjes, D\n\nBug, G\n\nHoller, E\n\nMeyer, RG\n\nGreinix, H\n\nScheid, C\n\nChristopeit, M\n\nSchnittger, S\n\nBraess, J\n\nSchlimok, G\n\nSpiekermann, K\n\nGanser, A\n\nKolb, HJ\n\nSchmid, C\n\nBeiträge in Fachzeitschriften\nISI:000319897700015\n22983588.0\n10.3324/haematol.2012.070235\nPMC3659981\nBased on molecular aberrations, in particular the NPM1 mutation (NPM1(mut)) and the FLT3 internal tandem duplication (Flt3-ITD), prognostic subgroups have been defined among patients with acute myeloid leukemia with normal karyotype. Whereas these subgroups are known to play an important role in outcome in first complete remission, and also in the indication for allogeneic stem cell transplantation, data are limited on their role after transplantation in advanced disease. To evaluate the role of molecular subgroups of acute myeloid leukemia with normal karyotype after allogeneic stem cell transplantation beyond first complete remission, we analyzed the data from 141 consecutive adults (median age: 51.0 years, range 18.4-69.3 years) who had received an allogeneic transplant either in primary induction failure or beyond first complete remission. A sequential regimen of cytoreductive chemotherapy (fludarabine, high-dose AraC, amsacrine) followed by reduced intensity conditioning (FLAMSA-RIC), was uniformly used for conditioning. After a median follow up of three years, overall survival from transplantation was 64 ± 4%, 53 ± 4% and 44 ± 5% at one, two and four years, respectively. Forty patients transplanted in primary induction failure achieved an encouraging 2-year survival of 69%. Among 101 patients transplanted beyond first complete remission, 2-year survival was 81% among patients with the NPM1(mut)/FLT3(wt) genotype in contrast to 43% in other genotypes. Higher numbers of transfused CD34(+) cells (hazard ratio 2.155, 95% confidence interval 0.263-0.964, P=0.039) and favorable genotype (hazard ratio 0.142, 95% confidence interval: 0.19-0.898, P=0.048) were associated with superior overall survival in multivariate analysis. In conclusion, patients with acute myeloid leukemia with normal karyotype can frequently be rescued after primary induction failure by allogeneic transplantation following FLAMSA-RIC. The prognostic role of NPM1(mut)/FLT3-ITD based subgroups was carried through after allogeneic stem cell transplantation beyond first complete remission.\n\nGreinix, Hildegard\n\n\n"
},
{
"text": "\n146871\nEarly detection of pulp necrosis and dental vitality after traumatic dental injuries in children and adolescents by 3-Tesla magnetic resonance imaging.\n\nAssaf, AT\n\nZrnc, TA\n\nRemus, CC\n\nKhokale, A\n\nHabermann, CR\n\nSchulze, D\n\nFiehler, J\n\nHeiland, M\n\nSedlacik, J\n\nFriedrich, RE\n\nBeiträge in Fachzeitschriften\nISI:000361078700018\n26165761.0\n10.1016/j.jcms.2015.06.010\nNone\nMore than 50% of all children suffer a traumatic dental injury (TDI) during childhood. In many cases, dentists apply root canal treatment (RCT), which is performed on an average of 7-10 days after replantation. Our aim was to evaluate whether RCT is necessary in many cases, and whether revitalization of affected teeth is possible and measurable by visualization using 3T magnetic resonance imaging (MRI).\n Seven healthy children with TDI were treated by repositioning of the affected teeth and reduction of alveolar process fractures followed by splinting. Two weeks after initial treatment, splints were removed. After 6 weeks, all children received 3-Tesla (3T), three-dimensional, high-resolution MRI with a 20-channel standard head and neck coil. The mean age of the children (male/female = 5:2) was 10.8 years (range, 8-17 years). In addition, all children received conventional dental examination for tooth vitality and dental sensitivity to cold and tenderness on percussion.\n 3T MRI provided excellent images that allowed fine discrimination between dental pulp and adjacent tooth. Using four in-house optimized, non-contrast-enhanced sequences, including panoramic reconstruction, the assessment and analysis of the dental pulp was sufficiently feasible. We could demonstrate reperfusion and thus vitality of the affected teeth in 11 sites. In one child, MRI was able to detect nonreperfusion after TDI of the affected tooth. MRI results were confirmed by clinical examination in all cases. As a consequence of this expectant management and proof of reperfusion and tooth vitality by 3T MRI, only one child had to be treated by RCT.\n 3T MRI is a very promising tool for visualization and detection in the field of dental and oromaxillofacial diseases. By using new 3T MRI sequences in children with TDI, we could demonstrate that RCT are not necessary in every case, and thus could prevent unnecessary treatment of children in the future. Larger studies should follow to confirm the potential benefit in clinical practice.\n Copyright © 2015 European Association for Cranio-Maxillo-Facial Surgery. Published by Elsevier Ltd. All rights reserved.\n\nZrnc, Tomislav\n\n\n"
},
{
"text": "\n146932\n[Pain care in Austrian health care centers: Questionnaire study on the current status of Austrian pain clinics].\n\nSzilagyi, IS\n\nBornemann-Cimenti, H\n\nMesserer, B\n\nVittinghoff, M\n\nSandner-Kiesling, A\n\nBeiträge in Fachzeitschriften\nISI:000365724400004\n26341376.0\n10.1007/s00482-015-0045-x\nNone\nPain clinics provide interdisciplinary therapy to treat chronic pain patients and to increase the return-to-work rate. In recent years and due to increased economic pressure in health care, a change in the management of pain in Austrian health care centers has been observed. For the analysis of the current situation, two surveys addressing all Austrian pain clinics were performed.\n In total, 133 heads of Austrian Anesthesia Departments were interviewed online and personally. The data from the first interview were confirmed by an additional telephone survey that was performed by one anesthetist per Austrian state (n = 9).\n Currently, 44 Austrian pain clinics are active. During the last 5 years, 9 pain clinics closed. Adding the current active pain clinics together, they represent a total of 17.5 full-time-operated clinics. The most common reasons for closing the pain clinics were lack of personnel (47%), lack of time resources (26%), lack of space resources (11%), and financial difficulties (11%). A reduction of >50% of operating hours during the last 3 years was reported by 9 hospitals. The reasons for not running a pain clinic were lack of personnel (36%), lack of time (25%) and department too small (16%). Estimates between actual and required clinics indicate that 49.5 full-time-operating pain clinics are lacking in Austria, resulting in 74% of the Austrian chronic pain patients not receiving interdisciplinary pain management.\n Our survey confirmed the closure of 9 pain clinics during the last 5 years due to lack of personnel and time. Pain clinics appear to provide the simplest economic saving potential. This development is a major concern. Although running a pain clinic seems to be expensive at the first sight, it reduces pain, sick leave, complications, and potential legal issues against health care centers, while simultaneously increasing the hospital's competitiveness. Our results show that 74% of Austrian chronic pain patients do not have access to an interdisciplinary pain clinic. Because of plans to further economize resources, Austria may lose its ability to provide state-of-the-art pain therapy and management.\n\nBornemann-Cimenti, Helmar\n\nMesserer, Brigitte\n\nSandner-Kiesling, Andreas\n\nSzilagyi, Istvan - Szilard\n\nVittinghoff, Maria\n\n\n"
},
{
"text": "\n167212\nRandomized clinical trial of the effect of a fibrin sealant patch on pancreatic fistula formation after pancreatoduodenectomy.\n\nSchindl, M\n\nFügger, R\n\nGötzinger, P\n\nLängle, F\n\nZitt, M\n\nStättner, S\n\nKornprat, P\n\nSahora, K\n\nHlauschek, D\n\nGnant, M\n\nAustrian Breast and Colorectal Cancer Study Group\n\nBeiträge in Fachzeitschriften\nISI:000431972200005\n29664999.0\n10.1002/bjs.10840\nPMC5989938\nThe potential for a fibrin sealant patch to reduce the risk of postoperative pancreatic fistula (POPF) remains uncertain. The aim of this study was to evaluate whether a fibrin sealant patch is able to reduce POPF in patients undergoing pancreatoduodenectomy with pancreatojejunostomy.\n In this multicentre trial, patients undergoing pancreatoduodenectomy were randomized to receive either a fibrin patch (patch group) or no patch (control group), and stratified by gland texture, pancreatic duct size and neoadjuvant treatment. The primary endpoint was POPF. Secondary endpoints included complications, drain-related factors and duration of hospital stay. Risk factors for POPF were identified by logistic regression analysis.\n A total of 142 patients were enrolled. Forty-five of 71 patients (63 per cent) in the patch group and 40 of 71 (56 per cent) in the control group developed biochemical leakage or POPF (P = 0·392). Fistulas were classified as grade B or C in 16 (23 per cent) and ten (14 per cent) patients respectively (P = 0·277). There were no differences in postoperative complications (54 patients in patch group and 50 in control group; P = 0·839), drain amylase concentration (P = 0·494), time until drain removal (mean(s.d.) 11·6(1·0) versus 13·3(1·3) days; P = 0·613), fistula closure (17·6(2·2) versus 16·5(2·1) days; P = 0·740) and duration of hospital stay (22·1(2·2) versus 18·2(0·9) days; P = 0·810) between the two groups. Multivariable logistic regression analysis confirmed that obesity (odds ratio (OR) 5·28, 95 per cent c.i. 1·20 to 23·18; P = 0·027), soft gland texture (OR 9·86, 3·41 to 28·54; P < 0·001) and a small duct (OR 5·50, 1·84 to 16·44; P = 0·002) were significant risk factors for POPF. A patch did not reduce the incidence of POPF in patients at higher risk.\n The use of a fibrin sealant patch did not reduce the occurrence of POPF and complications after pancreatoduodenectomy with pancreatojejunostomy. Registration number: 2013-000639-29 (EudraCT register).\n © 2018 The Authors. BJS published by John Wiley & Sons Ltd on behalf of BJS Society Ltd.\n\nKornprat, Peter\n\n\n"
},
{
"text": "\n168130\nRelation of placental alkaline phosphatase expression in human term placenta with maternal and offspring fat mass.\n\nHirschmugl, B\n\nCrozier, S\n\nMatthews, N\n\nKitzinger, E\n\nKlymiuk, I\n\nInskip, HM\n\nHarvey, NC\n\nCooper, C\n\nSibley, CP\n\nGlazier, J\n\nWadsack, C\n\nGodfrey, KM\n\nDesoye, G\n\nLewis, RM\n\nBeiträge in Fachzeitschriften\nISI:000437214200010\n29899523.0\n10.1038/s41366-018-0136-8\nPMC6173293\nAlkaline phosphatase is implicated in intestinal lipid transport and in the development of obesity. Placental alkaline phosphatase is localised to the microvillous plasma membrane of the placental syncytiotrophoblast at the maternal-fetal interface, but its role is unclear. We investigated the relations of placental alkaline phosphatase activity and mRNA expression with maternal body composition and offspring fat mass in humans.\n Term human placentas from the UK Birthright cohort (n = 52) and the Southampton Women's Survey (SWS) (n = 95) were studied. In the Birthright cohort, alkaline phosphatase activity was measured in placental microvillous plasma membrane vesicles. In the SWS, alkaline phosphatase mRNA was measured using Nanostring. Alkaline phosphatase gene expression was compared to other lipid-related genes.\n In Birthright samples placental microvillous plasma membrane alkaline phosphatase activity was positively associated with maternal triceps skinfold thickness and BMI (β = 0.04 (95% CI: 0.01-0.06) and β = 0.02 (0.00-0.03) µmol/mg protein/min per SD, P = 0.002 and P = 0.05, respectively) after adjusting for potential confounders. In SWS samples placental alkaline phosphatase mRNA expression in term placenta was positively associated with maternal triceps skinfold (β = 0.24 (0.04, 0.44) SD/SD, P = 0.02), had no association with neonatal %fat mass (β = 0.01 (-0.20 to 0.21) SD/SD, P = 0.93) and was negatively correlated with %fat mass at ages 4 (β = -0.28 (-0.52 to -0.04) SD/SD, P = 0.02), 6-7 (β = -0.25 (-0.49 to -0.02) SD/SD, P = 0.03) years. When compared with placental expression of other genes, alkaline phosphatase expression was positively related to genes including the lysophosphatidylcholine transporter MFSD2A (major facilitator superfamily domain containing 2A, P < 0.001) and negatively related to genes including the fatty acid transport proteins 2 and 3 (P = 0.001, P < 0.001).\n Our findings suggest relationships between placental alkaline phosphatase and both maternal and childhood adiposity. The inverse relationship between placental alkaline phosphatase gene expression and childhood %fat mass suggests that placental alkaline phosphatase may help to protect the foetus from the adverse effects of maternal obesity.\n\nDesoye, Gernot\n\nHirschmugl, Birgit\n\nKlymiuk, Ingeborg\n\nWadsack, Christian\n\n\n"
},
{
"text": "\n170576\nSurgical treatment of posterior cruciate ligament lesions does not cause growth disturbances in pediatric patients.\n\nWegmann, H\n\nJanout, S\n\nNovak, M\n\nKraus, T\n\nCastellani, C\n\nSinger, G\n\nTill, H\n\nBeiträge in Fachzeitschriften\nISI:000477030600041\n30465098.0\n10.1007/s00167-018-5308-5\nPMC6656898\nThe aim of the present study was to describe epidemiology, management and outcome of pediatric and adolescent patients with posterior cruciate ligament (PCL) injuries.\n Sixteen patients of less than 18 years of age with 7 PCL avulsion fractures and 9 PCL tears were included over a 10-year period. Trauma mechanism, additional injuries and treatment methods were analyzed. Follow-up examination included range of motion and ability to perform squats. Pedi-IKDC and Lysholm score were obtained and posterior shift was measured in kneeling view radiographs and compared to the contralateral side. Patients were grouped into pediatric patients with open physes at the time surgery and adolescent patients with closing or closed physes. In case of open physes, growth disturbances were assessed.\n Six of the treated patients (median age 12.5 years, range 10-13) had open physes at time of surgery. Five of those sustained avulsion fractures and treatment consisted of open reduction and screw fixation in four cases and graft reconstruction in one case. One patient sustained a PCL tear and underwent graft reconstruction. Follow-up at a median of 71.5 months (range 62-100) did not reveal any growth disturbances. Median Pedi-IKDC was 71.9 (range 51.7-92.1), median Lysholm score was 81.5 (range 66-88) and median posterior shift difference was 2.5 mm (range 0-11). The remaining 10 patients (median age 16 years, range 14-17) had closing/closed physis at the time of operation. Two patients presented with avulsion fractures treated with open reduction and screw fixation and 8 patients sustained PCL tears treated with graft reconstruction. At a median follow-up of 69.5 months (range 11-112), median Pedi-IKDC was 86.8 (range 36.8-97.7), median Lysholm score was 84.0 (range 45-95) and median posterior shift difference was 4 mm (range 0-15).\n In our small number of pediatric patients with PCL injuries, open reduction and epiphyseal screw fixation of displaced avulsed fractures and steep tunnel drilling in case of PCL reconstruction did not cause growth disturbances. Nevertheless, long-term functional impairment should be expected and close follow-up has to be recommended.\n Therapeutic, Level IV.\n\nCastellani, Christoph\n\nKraus, Tanja\n\nNovak, Michael Peter\n\nSinger, Georg\n\nTill, Holger\n\n\n"
},
{
"text": "\n173116\nA dual-targeting reconstituted high density lipoprotein leveraging the synergy of sorafenib and antimiRNA21 for enhanced hepatocellular carcinoma therapy.\n\nLi, M\n\nSu, Y\n\nZhang, F\n\nChen, K\n\nXu, X\n\nXu, L\n\nZhou, J\n\nWang, W\n\nBeiträge in Fachzeitschriften\nISI:000440125600034\n29859368.0\n10.1016/j.actbio.2018.05.049\nNone\nSorafenib (So) is a multi-target kinase inhibitor extensively used in clinic for hepatocellular carcinoma therapy. It demonstrated strong inhibition both in tumor proliferation and tumor angiogenesis, while hampered by associated cutaneous side-effect and drug resistance. The knockdown of miR-21 with antisense oligonucleotides (antimiRNA21) was regarded as an efficient strategy for increasing tumor sensibility to chemotherapy, which could be employed to appreciate the efficacy of So. Herein, we successfully formulated a dual-targeting delivery system for enhanced hepatocellular carcinoma therapy by encapsulating So and antimiRNA21 in RGD pentapeptide-modified reconstituted high-density lipoprotein (RGD-rHDL/So/antimiRNA21). The RGD and apolipoprotein A-I (ApoA-I) on nanoparticles (NPs) could drive the system simultaneously to tumor neovascular and parenchyma by binding to the overexpressed ανβ3-integrin and SR-B1 receptors, achieving precise delivery of therapeutics to maximize the efficacy. A series in vitro and in vivo experiments revealed that co-delivery of So and antimiRNA21 by RGD-rHDL significantly strengthened the anti-tumor and anti-angiogenic effect of So with negligible toxicity towards major organs, reversed drug-resistance and was capable of remodeling tumor environments. The constructed RGD-rHDL/So/antimiRNA21 with improved efficacy and excellent tumor targeting ability provided new idea for chemo-gene combined therapy in hepatocellular carcinoma.\n Sorafenib (So) is a multi-target kinase inhibitor which was approved by FDA as first-line drug for hepatocellular carcinoma (HCC) therapy. However, long term application of So in clinic was hampered by serious dermal toxicity and drug resistance. Although numerous researchers were devoted to finding alternatives or therapies as combination treatments with So to reach more desired therapeutic efficacy, the therapeutic options were still limited. The present study prepares RGD pentapeptide decorated biomimic reconstituted high-density lipoprotein (rHDL) loaded with So and antimiRNA21 (RGD-rHDL/So/antimiRNA21) for enhanced HCC therapy. The RGD-rHDL/So/antimiRNA21 NPs offer an effective platform for anti-tumor and anti-angiogenesis therapy in HCC and provide new approach to reverse drug-resistance of So for feasible clinical application.\n Copyright © 2018 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.\n\nZhang, Fangrong\n\n\n"
},
{
"text": "\n182357\nHuman Milk Oligosaccharides Modulate the Risk for Preterm Birth in a Microbiome-Dependent and -Independent Manner.\n\nPausan, MR\n\nKolovetsiou-Kreiner, V\n\nRichter, GL\n\nMadl, T\n\nGiselbrecht, E\n\nObermayer-Pietsch, B\n\nWeiss, EC\n\nJantscher-Krenn, E\n\nMoissl-Eichinger, C\n\nBeiträge in Fachzeitschriften\nISI:000576704900004\n32518196.0\n10.1128/mSystems.00334-20\nPMC7289590\nPreterm birth (PTB) is one of the leading causes of neonatal mortality. The causes for spontaneous PTB are multifactorial and often remain unknown. In this study, we tested the hypothesis that human milk oligosaccharides (HMOs) in blood and urine modulate the maternal urinary and vaginal microbiome and influence the risk for PTB. We analyzed the vaginal and urinary microbiome of a cross-sectional cohort of women with or without preterm labor and correlated our findings with measurements of metabolites and HMOs in urine and blood. We identified several microbial signatures, such as Lactobacillus jensenii, L. gasseri, Ureaplasma sp., and Gardnerella sp., associated with a short cervix, PTB, and/or preterm contractions. In addition, we observed associations between sialylated HMOs, in particular 3'-sialyllactose, with PTB, short cervix, and increased inflammation and confirmed an influence of HMOs on the microbiome profile. Since they identify serum and urinary HMOs and several key microorganisms associated with PTB, our findings point at two distinct processes modulating the risk for PTB. One process seems to be driven by sterile inflammation, characterized by increased concentrations of sialylated HMOs in serum. Another process might be microbiome mediated and potentially associated with specific HMO signatures in urine. Our results support current efforts to improve diagnostics and therapeutic strategies in PTB.IMPORTANCE The causes for preterm birth (PTB) often remain elusive. We investigated whether circulating human milk oligosaccharides (HMOs) might be involved in modulating urinary and vaginal microbiome promoting or preventing PTB. We identified here HMOs and key microbial taxa associated with indicators of PTB. Based on our results, we propose two models for how HMOs might modulate risk for PTB: (i) by changes in HMOs associated with sterile inflammation (microbiome-independent) and (ii) by HMO-driven shifts in microbiome (microbiome-dependent). Our findings will guide current efforts to better predict the risk for PTB in seemingly healthy pregnant women and also provide appropriate preventive strategies.\n Copyright © 2020 Pausan et al.\n\nJantscher-Krenn, Evelyn\n\nKolovetsiou-Kreiner, Vassiliki\n\nMadl, Tobias\n\nMoissl-Eichinger, Christine\n\nObermayer-Pietsch, Barbara\n\nRichter, Gesa Lucia\n\nWeiss, Eva-Christine\n\n\n"
},
{
"text": "\n184618\nPatterns of care and follow-up care of patients with uveal melanoma in German-speaking countries: a multinational survey of the German Dermatologic Cooperative Oncology Group (DeCOG).\n\nSteeb, T\n\nWessely, A\n\nAlter, M\n\nBayerl, C\n\nBender, A\n\nBruning, G\n\nDabrowski, E\n\nDebus, D\n\nDevereux, N\n\nDippel, E\n\nDrexler, K\n\nDücker, P\n\nDummer, R\n\nEmmert, S\n\nElsner, P\n\nEnk, A\n\nGebhardt, C\n\nGesierich, A\n\nGoebeler, M\n\nGoerdt, S\n\nGoetze, S\n\nGutzmer, R\n\nHaferkamp, S\n\nHansel, G\n\nHassel, JC\n\nHeinzerling, L\n\nKähler, KC\n\nKaume, KM\n\nKrapf, W\n\nKreuzberg, N\n\nLehmann, P\n\nLivingstone, E\n\nLöffler, H\n\nLoquai, C\n\nMauch, C\n\nMangana, J\n\nMeier, F\n\nMeissner, M\n\nMoritz, RKC\n\nMaul, LV\n\nMüller, V\n\nMohr, P\n\nNavarini, A\n\nVan Nguyen, A\n\nPfeiffer, C\n\nPföhler, C\n\nPosch, C\n\nRichtig, E\n\nRompel, R\n\nSachse, MM\n\nSauder, S\n\nSchadendorf, D\n\nSchatton, K\n\nSchulze, HJ\n\nSchultz, E\n\nSchilling, B\n\nSchmuth, M\n\nSimon, JC\n\nStreit, M\n\nTerheyden, P\n\nThiem, A\n\nTüting, T\n\nWelzel, J\n\nWeyandt, G\n\nWesselmann, U\n\nWollina, U\n\nZiemer, M\n\nZimmer, L\n\nZutt, M\n\nBerking, C\n\nSchlaak, M\n\nHeppt, MV\n\nGerman Dermatologic Cooperative Oncology Group (DeCOG, committee ocular melanoma)\n\nBeiträge in Fachzeitschriften\nISI:000591294500001\n33219855.0\n10.1007/s00432-020-03450-0\nPMC8076157\nUveal melanoma (UM) is an orphan cancer of high unmet medical need. Current patterns of care and surveillance remain unclear as they are situated in an interdisciplinary setting.\n A questionnaire addressing the patterns of care and surveillance in the management of patients with uveal melanoma was distributed to 70 skin cancer centers in Austria, Germany and Switzerland. Frequency distributions of responses for each item of the questionnaire were calculated.\n 44 of 70 (62.9%) skin cancer centers completed the questionnaire. Thirty-nine hospitals were located in Germany (88.6%), three in Switzerland (6.8%) and two in Austria (4.5%). The majority (68.2%) represented university hospitals. Most patients with metastatic disease were treated in certified skin cancer centers (70.7%, 29/41). Besides, the majority of patients with UM were referred to the respective skin cancer center by ophthalmologists (87.2%, 34/39). Treatment and organization of follow-up of patients varied across the different centers. 35.1% (14/37) of the centers stated to not perform any screening measures.\n Treatment patterns of patients with uveal melanoma in Germany, Austria and Switzerland remain extremely heterogeneous. A guideline for the treatment and surveillance is urgently needed.\n\nRichtig, Erika\n\n\n"
}
]
}