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"text": "\n145589\nThe syndrome of hemophagocytic lymphohistiocytosis in primary immunodeficiencies: implications for differential diagnosis and pathogenesis.\n\nBode, SF\n\nAmmann, S\n\nAl-Herz, W\n\nBataneant, M\n\nDvorak, CC\n\nGehring, S\n\nGennery, A\n\nGilmour, KC\n\nGonzalez-Granado, LI\n\nGroß-Wieltsch, U\n\nIfversen, M\n\nLingman-Framme, J\n\nMatthes-Martin, S\n\nMesters, R\n\nMeyts, I\n\nvan Montfrans, JM\n\nPachlopnik Schmid, J\n\nPai, SY\n\nSoler-Palacin, P\n\nSchuermann, U\n\nSchuster, V\n\nSeidel, MG\n\nSpeckmann, C\n\nStepensky, P\n\nSykora, KW\n\nTesi, B\n\nVraetz, T\n\nWaruiru, C\n\nBryceson, YT\n\nMoshous, D\n\nLehmberg, K\n\nJordan, MB\n\nEhl, S\n\nInborn Errors Working Party of the EBMT\n\nBeiträge in Fachzeitschriften\nISI:000361196400029\n26022711.0\n10.3324/haematol.2014.121608\nPMC4486233\nHemophagocytic lymphohistiocytosis is a hyperinflammatory syndrome defined by clinical and laboratory criteria. Current criteria were created to identify patients with familial hemophagocytic lmyphohistiocytosis in immediate need of immunosuppressive therapy. However, these criteria also identify patients with infection-associated hemophagocytic inflammatory states lacking genetic defects typically predisposing to hemophagocytic lymphohistiocytosis. These patients include those with primary immunodeficiencies, in whom the pathogenesis of the inflammatory syndrome may be distinctive and aggressive immunosuppression is contraindicated. To better characterize hemophagocytic inflammation associated with immunodeficiencies, we combined an international survey with a literature search and identified 63 patients with primary immunodeficiencies other than cytotoxicity defects or X-linked lymphoproliferative disorders, presenting with conditions fulfilling current criteria for hemophagocytic lymphohistiocytosis. Twelve patients had severe combined immunodeficiency with <100/μL T cells, 18 had partial T-cell deficiencies; episodes of hemophagocytic lymphohistiocytosis were mostly associated with viral infections. Twenty-two patients had chronic granulomatous disease with hemophagocytic episodes mainly associated with bacterial infections. Compared to patients with cytotoxicity defects, patients with T-cell deficiencies had lower levels of soluble CD25 and higher ferritin concentrations. Other criteria for hemophagocytoc lymphohistiocytosis were not discriminative. Thus: (i) a hemophagocytic inflammatory syndrome fulfilling criteria for hemophagocytic lymphohistiocytosis can be the initial manifestation of primary immunodeficiencies; (ii) this syndrome can develop despite severe deficiency of T and NK cells, implying that the pathophysiology is distinct and not appropriately described as "lympho"-histiocytosis in these patients; and (iii) current criteria for hemophagocytoc lymphohistiocytosis are insufficient to differentiate hemophagocytic inflammatory syndromes with different pathogeneses. This is important because of implications for therapy, in particular for protocols targeting T cells. \n Copyright© Ferrata Storti Foundation.\n\nSeidel, Markus\n\n\n"
},
{
"text": "\n153435\nDoes Platelet Reactivity Predict Bleeding in Patients Needing Urgent Coronary Artery Bypass Grafting During Dual Antiplatelet Therapy?\n\nMahla, E\n\nPrueller, F\n\nFarzi, S\n\nPregartner, G\n\nRaggam, RB\n\nBeran, E\n\nToller, W\n\nBerghold, A\n\nTantry, US\n\nGurbel, PA\n\nBeiträge in Fachzeitschriften\nISI:000389548100075\n27378554.0\n10.1016/j.athoracsur.2016.05.003\nNone\nUp to 15% of patients require coronary artery bypass grafting (CABG) during dual antiplatelet therapy. Available evidence suggests an association between platelet reactivity and CABG-related bleeding. However, platelet reactivity cutoffs for bleeding remain elusive. We sought to explore the association between platelet reactivity and bleeding.\n Patients on aspirin and a P2Y12 receptor inhibitor within 48 hours before isolated CABG (n = 149) were enrolled in this prospective study. Blood was drawn 2 to 4 hours preoperatively and platelet reactivity assessed by light transmittance aggregometry (LTA), vasodilator-stimulated phosphoprotein (VASP) assay, Multiplate analyzer and Innovance PFA2Y. The primary endpoint was calculated red blood cell loss computed as follows: (blood volume × preoperative hematocrit × 0.91) - (blood volume × hematocrit × 0.91 on postoperative day 5) + (mL of transfused red blood cells × 0.59).\n Preoperative platelet reactivity was low [median (interquartile range): LTA: 20 (9-28)%; VASP-PRI: 39 (15-73)%; Multiplate adenosine phosphate test: 16 (12-22) U∗min]. Innovance PFA2Y ≥300 seconds, 72%. Median (IQR) red blood cell loss in patients in first the LTA tertile was 1, 49 (1, 20 to 1, 54) mL compared with 1, 07 (858 to 1, 12) mL and 1, 75 (811 to 1, 69) mL in those in the second and third tertiles, respectively (p < 0.004). Bleeding Academic Research Consortium (BARC)-4 bleeding differed between tertiles (62% versus 46% versus 36%; p = 0.037). In a multivariable linear regression model, aspirin dose ≥300 mg, cardiopulmonary bypass time, EuroSCORE, and tertile distribution of platelet reactivity were significantly associated with red blood cell loss.\n A gradual decrease in red blood cell loss and BARC-4 bleeding occurs with increasing platelet reactivity in patients on antiplatelet therapy undergoing CABG. Our findings support current guidelines to determine time of surgery based on an objective measurement of platelet function (Platelet Inhibition and Bleeding in Patients Undergoing Emergent Cardiac Surgery; clinicaltrials.gov NCT01468597).\n Copyright © 2016 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.\n\nBeran, Elisabeth\n\nBerghold, Andrea\n\nMahla, Elisabeth\n\nPregartner, Gudrun\n\nPrüller, Florian\n\nRaggam, Reinhard Bernd\n\nToller, Wolfgang\n\n\n"
},
{
"text": "\n167470\nPhenotyping and Target Expression Profiling of CD34<sup>+</sup>/CD38<sup>-</sup> and CD34<sup>+</sup>/CD38<sup>+</sup> Stem- and Progenitor cells in Acute Lymphoblastic Leukemia.\n\nBlatt, K\n\nMenzl, I\n\nEisenwort, G\n\nCerny-Reiterer, S\n\nHerrmann, H\n\nHerndlhofer, S\n\nStefanzl, G\n\nSadovnik, I\n\nBerger, D\n\nKeller, A\n\nHauswirth, A\n\nHoermann, G\n\nWillmann, M\n\nRülicke, T\n\nSill, H\n\nSperr, WR\n\nMannhalter, C\n\nMelo, JV\n\nJäger, U\n\nSexl, V\n\nValent, P\n\nBeiträge in Fachzeitschriften\nISI:000433631900008\n29772458.0\n10.1016/j.neo.2018.04.004\nPMC5994777\nLeukemic stem cells (LSCs) are an emerging target of curative anti-leukemia therapy. In acute lymphoblastic leukemia (ALL), LSCs frequently express CD34 and often lack CD38. However, little is known about markers and targets expressed in ALL LSCs. We have examined marker- and target expression profiles in CD34+/CD38- LSCs in patients with Ph+ ALL (n = 22) and Ph- ALL (n = 27) by multi-color flow cytometry and qPCR. ALL LSCs expressed CD19 (B4), CD44 (Pgp-1), CD123 (IL-3RA), and CD184 (CXCR4) in all patients tested. Moreover, in various subgroups of patients, LSCs also displayed CD20 (MS4A1) (10/41 = 24%), CD22 (12/20 = 60%), CD33 (Siglec-3) (20/48 = 42%), CD52 (CAMPATH-1) (17/40 = 43%), IL-1RAP (13/29 = 45%), and/or CD135 (FLT3) (4/20 = 20%). CD25 (IL-2RA) and CD26 (DPPIV) were expressed on LSCs in Ph+ ALL exhibiting BCR/ABL1p210, whereas in Ph+ ALL with BCR/ABL1p190, LSCs variably expressed CD25 but did not express CD26. In Ph- ALL, CD34+/CD38- LSCs expressed IL-1RAP in 6/18 patients (33%), but did not express CD25 or CD26. Normal stem cells stained negative for CD25, CD26 and IL-1RAP, and expressed only low amounts of CD52. In xenotransplantation experiments, CD34+/CD38- and CD34+/CD38+ cells engrafted NSG mice after 12-20 weeks, and targeting with antibodies against CD33 and CD52 resulted in reduced engraftment. Together, LSCs in Ph+ and Ph- ALL display unique marker- and target expression profiles. In Ph+ ALL with BCR/ABL1p210, the LSC-phenotype closely resembles the marker-profile of CD34+/CD38- LSCs in chronic myeloid leukemia, confirming the close biologic relationship of these neoplasms. Targeting of LSCs with specific antibodies or related immunotherapies may facilitate LSC eradication in ALL.\n Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.\n\nSill, Heinz\n\n\n"
},
{
"text": "\n186146\nEUFOREA Rhinology Research Forum 2016: report of the brainstorming sessions on needs and priorities in rhinitis and rhinosinusitis.\n\nHellings, PW\n\nAkdis, CA\n\nBachert, C\n\nBousquet, J\n\nPugin, B\n\nAdriaensen, G\n\nAdvani, R\n\nAgache, I\n\nAnjo, C\n\nAnmolsingh, R\n\nAnnoni, E\n\nBieber, T\n\nBizaki, A\n\nBraverman, I\n\nCallebaut, I\n\nCastillo Vizuete, JA\n\nChalermwatanachai, T\n\nChmielewski, R\n\nCingi, C\n\nCools, L\n\nCoppije, C\n\nCornet, ME\n\nDe Boeck, I\n\nDe Corso, E\n\nDe Greve, G\n\nDoulaptsi, M\n\nEdmiston, R\n\nErskine, S\n\nGevaert, E\n\nGevaert, P\n\nGolebski, K\n\nHopkins, C\n\nHox, V\n\nJaeggi, C\n\nJoos, G\n\nKhwaja, S\n\nKjeldsen, A\n\nKlimek, L\n\nKoennecke, M\n\nKortekaas Krohn, I\n\nKrysko, O\n\nKumar, BN\n\nLangdon, C\n\nLange, B\n\nLekakis, G\n\nLevie, P\n\nLourijsen, E\n\nLund, VJ\n\nMartens, K\n\nMő Sges, R\n\nMullol, J\n\nNyembue, TD\n\nPalkonen, S\n\nPhilpott, C\n\nPimentel, J\n\nPoirrier, A\n\nPratas, AC\n\nProkopakis, E\n\nPujols, L\n\nRombaux, P\n\nSchmidt-Weber, C\n\nSegboer, C\n\nSpacova, I\n\nStaikuniene, J\n\nSteelant, B\n\nSteinsvik, EA\n\nTeufelberger, A\n\nVan Gerven, L\n\nVan Gool, K\n\nVerbrugge, R\n\nVerhaeghe, B\n\nVirkkula, P\n\nVlaminck, S\n\nVries-Uss, E\n\nWagenmann, M\n\nZuberbier, T\n\nSeys, SF\n\nFokkens, WJ\n\nBeiträge in Fachzeitschriften\nISI:000411920700003\n28501885.0\n10.4193/Rhin17.028\nNone\nThe first European Rhinology Research Forum organized by the European Forum for Research and Education in Allergy and Airway Diseases (EUFOREA) was held in the Royal Academy of Medicine in Brussels on 17th and 18th November 2016, in collaboration with the European Rhinologic Society (ERS) and the Global Allergy and Asthma European Network (GA2LEN). One hundred and thirty participants (medical doctors from different specialties, researchers, as well as patients and industry representatives) from 27 countries took part in the multiple perspective discussions including brainstorming sessions on care pathways and research needs in rhinitis and rhinosinusitis. The debates started with an overview of the current state of the art, including weaknesses and strengths of the current practices, followed by the identification of essential research needs, thoroughly integrated in the context of Precision Medicine (PM), with personalized care, prediction of success of treatment, participation of the patient and prevention of disease as key principles for improving current clinical practices. This report provides a concise summary of the outcomes of the brainstorming sessions of the European Rhinology Research Forum 2016.\n\nTeufelberger, Andrea Renate\n\n\n"
},
{
"text": "\n187077\nFrailty is associated with long-term outcome in patients with sepsis who are over 80 years old: results from an observational study in 241 European ICUs.\n\nHaas, LEM\n\nBoumendil, A\n\nFlaatten, H\n\nGuidet, B\n\nIbarz, M\n\nJung, C\n\nMoreno, R\n\nMorandi, A\n\nAndersen, FH\n\nZafeiridis, T\n\nWalther, S\n\nOeyen, S\n\nLeaver, S\n\nWatson, X\n\nBoulanger, C\n\nSzczeklik, W\n\nSchefold, JC\n\nCecconi, M\n\nMarsh, B\n\nJoannidis, M\n\nNalapko, Y\n\nElhadi, M\n\nFjølner, J\n\nArtigas, A\n\nde Lange, DW\n\nde Lange, DW\n\nBeiträge in Fachzeitschriften\nNone\n33744918.0\n10.1093/ageing/afab036\nNone\nSepsis is one of the most frequent reasons for acute intensive care unit (ICU) admission of very old patients and mortality rates are high. However, the impact of pre-existing physical and cognitive function on long-term outcome of ICU patients ≥ 80 years old (very old intensive care patients (VIPs)) with sepsis is unclear.\n To investigate both the short- and long-term mortality of VIPs admitted with sepsis and assess the relation of mortality with pre-existing physical and cognitive function.\n Prospective cohort study.\n 241 ICUs from 22 European countries in a six-month period between May 2018 and May 2019.\n Acutely admitted ICU patients aged ≥80 years with sequential organ failure assessment (SOFA) score ≥ 2.\n Sepsis was defined according to the sepsis 3.0 criteria. Patients with sepsis as an admission diagnosis were compared with other acutely admitted patients. In addition to patients' characteristics, disease severity, information about comorbidity and polypharmacy and pre-existing physical and cognitive function were collected.\n Out of 3, 96 acutely admitted VIPs with SOFA score ≥ 2, a group of 532 patients with sepsis were compared to other admissions. Predictors for 6-month mortality were age (per 5 years): Hazard ratio (HR, 1.16 (95% confidence interval (CI), 1.09-1.25, P < 0.0001), SOFA (per one-point): HR, 1.16 (95% CI, 1.14-1.17, P < 0.0001) and frailty (CFS > 4): HR, 1.34 (95% CI, 1.18-1.51, P < 0.0001).\n There is substantial long-term mortality in VIPs admitted with sepsis. Frailty, age and disease severity were identified as predictors of long-term mortality in VIPs admitted with sepsis.\n © The Author(s) 2021. Published by Oxford University Press on behalf of the British Geriatrics Society. All rights reserved. For permissions, please email: journals.permissions@oup.com.\n\nEller, Philipp\n\n\n"
},
{
"text": "\n187355\nComparison of the 7th and 8th version of the AJCC classification system for soft tissue sarcomas of extremities and trunk in patients with localised, intermediate or high-grade disease treated at European tertiary sarcoma centres.\n\nSmolle, MA\n\nvan de Sande, M\n\nHayes, A\n\nBergovec, M\n\nSmith, HG\n\nLiegl-Atzwanger, B\n\nTunn, PU\n\nNiethard, M\n\nWindhager, R\n\nSzkandera, J\n\nLeithner, A\n\nBeiträge in Fachzeitschriften\nNone\n33865657.0\n10.1016/j.ejso.2021.03.252\nNone\nThe updated 8th version of the AJCC-staging system for soft tissue sarcomas (STS) has been criticised for omitting tumour depth as category-defining variable and eventually not improving prognostic accuracy in comparison to the 7th version. This study aimed at investigating the prognostic accuracy of both AJCC-versions in STS-patients treated at European tertiary sarcoma centres.\n 1032 patients (mean age: 60.7 ± 16.3 years; 46.0% [n = 475] females; median follow-up: 38.6 months), treated at five tertiary sarcoma centres for localised, intermediate or high-grade STS of extremities and trunk were retrospectively included. Uni- and multivariate Cox-regression models and Harrell's C-indices were calculated to analyse prognostic factors for overall survival (OS) and assess prognostic accuracy.\n In univariate analysis, prognostic accuracy for OS was comparable for both AJCC-versions (C-index: 0.620 [8th] vs. 0.614 [7th]). By adding margins, age, gender, and histology to the multivariate models, prognostic accuracy of both versions could be likewise improved (C-index: 0.714 [8th] vs. 0.705 [7th]). Moreover, tumour depth did not significantly contribute to prognostic accuracy of the 8th version's multivariate model (C-index for both models: 0.714). Stratification into four main T-stages based on tumour size only, as implemented in the 8th version, significantly improved prognostic accuracy between each category. However, T-stages as defined in the 7th version had poorer discriminatory power (C-index: 0.625 [8th] vs. 0.582 [7th]).\n Both AJCC-versions perform equally well regarding prognostic accuracy. Yet, simplification of the 8 th version by omitting tumour depth as T-stage-defining parameter, whilst emphasizing the importance of tumour size, should be considered advantageous.\n Copyright © 2021 Elsevier Ltd, BASO ~ The Association for Cancer Surgery, and the European Society of Surgical Oncology. All rights reserved.\n\nBergovec, Marko\n\nLeithner, Andreas\n\nLiegl-Atzwanger, Bernadette\n\nSmolle, Maria Anna\n\nSzkandera, Joanna\n\n\n"
},
{
"text": "\n187684\nVitamin D levels in liver transplantation recipients and early postoperative outcomes: Prospective observational DLiverX study\n\nMartucci, G\n\nVolpes, R\n\nPanarello, G\n\nTuzzolino, F\n\nDi Carlo, D\n\nRicotta, C\n\nGruttadauria, S\n\nConaldi, PG\n\nLuca, A\n\nAmrein, K\n\nArcadipane, A\n\nBeiträge in Fachzeitschriften\nISI:000640358300010\n33158589.0\n10.1016/j.clnu.2020.10.027\nNone\nBackground & aims: In critically ill patients with liver disease, vitamin D deficiency is associated with higher disease severity, increased frequency of infections, and worse outcomes. This study sought to describe the trend of vitamin D in orthotopic liver transplantation (OLT) recipients and its association with outcomes. Methods: Prospective observational study of 67 consecutive OLT recipients enrolled between September, 2016 and August, 2017 at IRCCS-ISMETT, Palermo (Italy). Trend of vitamin D levels and potential factors influencing it levels were evaluated through a generalized linear mixed regression model. Results: Sixty-four (95.5%) recipients were vitamin D deficient (<20 ng/ml), with a median value of 8.8 ng/ml [6.2-12.9], and forty-seven of these (70.1%) showed severe deficiency (<12 ng/ml) at baseline, 7.9 ng/ml [5.4-8.9]. The baseline vitamin D showed an inverse correlation with liver disease severity: Child-Pugh, MELD score, bilirubin, INR, and organ failure (p < 0.01) at baseline. Vitamin D increased on postoperative day (POD) 28 compared with POD1: +4.5 ng/ml, C.I. 95% 3.6 -5.3 ng/ml, p < 0.01. Lower baseline vitamin D, donor age, transfusion of fresh frozen plasma (negative impact, all p < 0.05), and intra-operative bypass (positive impact at POD 28, p < 0.01) were associated with variation of vitamin D levels after transplantation. Incomplete graft recovery was associated with lower vitamin D on POD28: 8.2 ? 4.4 versus 13.8 ? 9.4 ng/ ml, p < 0.01; the odds ratio (OR) was 0.84; CI 95% 0.73-0.97, p = 0.014. The OR for infections within POD 28 was inversely associated with baseline vitamin D: 0.87; CI 95% 0.79-0.98, p = 0.02, and with vitamin D level at baseline <12 ng/ml: OR 6.44; CI 95% 1.66-24.94; p < 0.01. Conclusions: Preoperative Vitamin D is correlated with disease severity, and was highly associated with invasive infection in the first 28 PODs. After OLT, the value on POD 28 had a strong association with graft function. 0 2020 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.\n\nAmrein, Karin\n\n\n"
},
{
"text": "\n2305\nSelective decrease in serum immunoglobulin G1. A tissue nonspecific tumor marker detecting early stages of gynecologic malignant disease with high efficiency.\n\nSchauenstein, E\n\nLahousen, M\n\nWeblacher, M\n\nSteinschifter, W\n\nEstelberger, W\n\nSchauenstein, K\n\nBeiträge in Fachzeitschriften\nISI:A1996UY25400019\n8697398.0\n10.1002/(SICI)1097-0142(19960801)78:3<511::AID-CNCR19>3.0.CO;2-1\nNone\nBACKGROUND: Malignant diseases of various tissue origin have previously been found to be associated with a characteristic shift in the serum pattern of IgG subclasses, i.e., a highly significant reduction of the percent of IgG1 and an increase of the percentage of IgG2 relative to the total IgG. In the present study we examined the diagnostic performance of this indirect tumor marker in patients with carcinomas of various sites within the female reproductive tract. METHODS: Using quantitative affinity chromatography, the percents of IgG1 and IgG2 in the total IgG were determined for 207 patients with carcinoma of the ovary, cervix, or corpus uteri, prior to any treatment. The data were compared with those of 135 age matched healthy females and 52 patients with benign gynecologic diseases. RESULTS: It was found that (1) mean values for the percents of IgG1 and IgG2 of all of the cancer patients differed significantly from those of the patients with benign disease and healthy controls; (2) no differences were noted between carcinomas of the ovary, corpus or cervix uteri; (3) early stages of carcinoma exhibited the effect to the same extent as late stages; (4) the specificity of the percent of IgG1 to discriminate between controls and cancer patients ranged between 90 and 100%, regardless of localization and stage of tumor; and (5) whereas with ovarian cancer CA 125 showed a slightly greater sensitivity, the percent of IgG1 was by far more sensitive than the conventional markers CA 125, TPA, CEA, Ferritin, and SCC to diagnose carcinoma of the cervix and corpus uteri, notably at early stages. Combined analysis of the percent of IgG1 and CA 125 and/or TPA led to an increase in sensitivity with tumors of all three sites. CONCLUSIONS: Thus, the determination of the percent of IgG1 by itself and/or in combination with conventional markers may provide relevant information regarding the noninvasive detection of early stages of gynecologic carcinoma.\n\n\n"
},
{
"text": "\n2887\nEicosanoid release in the endotoxin-primed isolated perfused rat lung and its pharmacological modification.\n\nAmann, R\n\nSchuligoi, R\n\nPeskar, BA\n\nBeiträge in Fachzeitschriften\nISI:000084621300004\n10669114.0\n10.1007%2Fs000110050514\nNone\nOBJECTIVE: Recent observations have demonstrated a central role of the "inducible" isoform of the cyclooxygenase (COX), COX-2, in the rat lung. Therefore, the reported capacity of selective COX-2 inhibitors to potentiate the formation of leukotriene (LT) B4 may raise concern about pro-inflammatory side effects of such drugs in the respiratory system. The present study was aimed at determining the effects of the COX-2 inhibitor NS-398 on the release of COX and 5-lipoxygenase (LOX) metabolites of arachidonic acid in isolated perfused lungs obtained from endotoxin-treated rats before and after stimulation with the leukocyte secretagogue N-formyl-methionyl-leucyl-phenylalanine (FMLP). METHODS: Two hours after rats had received endotoxin i.v., the lung was dissected and perfused via the pulmonary artery with physiological salt solution. After an equilibration period of 20 min the outflow was collected (5-min fractions). In the respective treatment groups, indomethacin, NS-398, or the 5-LOX inhibitor MK886 were present throughout the experiment, while FMLP was added to the perfusate during a single 5-min period. The concentration of eicosanoids in the outflow was determined by radioimmunoassay. RESULTS: Endotoxin treatment of rats resulted in increased expression of COX-2 mRNA in lung tissue, and an elevated basal release of the prostaglandin (PG)I2 metabolite 6-keto PGF1alpha, without a detectable increase of leukotriene (LT) formation. In-vitro exposure to FMLP stimulated LT and prostanoid release, which was significantly enhanced in endotoxin-primed lungs, and was suppressed by the 5-LOX inhibitor MK-886 (3 microM) and the COX-inhibitor indomethacin (5 microM), respectively. Either compound showed selective inhibition of the respective pathway of arachidonic acid metabolism. In endotoxin-primed lungs, the COX-2 inhibitor NS-398 (0.3-1.0 microM) depressed basal as well as FMLP-stimulated release of 6-keto PGF1alpha, but did not cause a significant increase of LTB4 or cysteinyl-LT release. CONCLUSIONS: These results suggest that FMLP, presumably acting on inflammatory cells trapped in the pulmonary circulation of endotoxin treated rats, induced prostanoid formation mainly via the COX-2 pathway, and that its inhibition by NS-398 had no detectable potentiating effect on LTB4 or cysteinyl-LT biosynthesis.\n\nPeskar, Bernhard\n\nSchuligoi, Rufina\n\n\n"
},
{
"text": "\n3304\nAssociation of the vitamin D receptor genotype BB with low bone density in hyperthyroidism.\n\nObermayer-Pietsch, BM\n\nFrühauf, GE\n\nChararas, K\n\nMikhail-Reinisch, S\n\nRenner, W\n\nBerghold, A\n\nKenner, L\n\nLackner, C\n\nBeiträge in Fachzeitschriften\nISI:000089558700011\n11028447.0\n10.1359/jbmr.2000.15.10.1950\nNone\nBone mineral density (BMD) is modulated by genetic and environmental factors or certain diseases. In several conditions such as low calcium intake, an influence of vitamin D receptor (VDR) polymorphisms on BMD has been suggested. In the present study, we investigated the relationship of Bsm I and Fok I polymorphisms of the VDR gene and BMD in patients with hyperthyroidism, a disease that often results in low BMD. Bsm I and Fok I genotypes were determined in 76 postmenopausal hyperthyroid patients and 62 healthy postmenopausal women as controls. Patients and controls were matched for age, time since menopause, and lifestyle factors and were free of estrogen medication. BMD evaluation included axial dual X-ray absorptiometry (DXA) and peripheral quantitative computed tomography (PQCT). Low BMD was defined as -2.5 STD below the young adult mean value. Biochemical parameters investigated were thyroid hormones, osteocalcin, and 25-(OH)-vitamin D3 as well as routine laboratory data. Low BMD was found in 61% of hyperthyroid patients and in only 23% of euthyroid controls. In the group of hyperthyroid patients with low bone density, the BB genotype (VDR Bsm I polymorphisms) was significantly more frequent (39%) than in controls (13%; p = 0.003) and hyperthyroid patients with normal BMD (6%; p = 0.013). The odds ratio (OR) for low BMD in patients with BB genotype was 5.7 (95% CI, 1.7-19.1; p < 0.005) as compared with the Bb and bb genotypes and 5.5 (95% CI, 2.3-13.2; p < 0.0001) for hyperthyroidism alone. The cumulative risk for low BMD in patients with hyperthyroidism and BB genotype was 31.4 (95% CI, 3.9-256; p < 0.0003). VDR Fok I genotypes showed no significant relationship with BMD or other general or bone-specific parameters. Thus, hyperthyroidism and the genetic background of a BB genotype may promote synergistically the development of low BMD in hyperthyroid patients. Screening for the BB genotype in these patients therefore could help to identify those with particularly high risk for the development of low BMD and allow early treatment.\n\nBerghold, Andrea\n\nLackner, Karoline\n\nObermayer-Pietsch, Barbara\n\nRenner, Wilfried\n\n\n"
},
{
"text": "\n4539\nNitric oxide inhibits capacitative Ca2+ entry by suppression of mitochondrial Ca2+ handling.\n\nThyagarajan, B\n\nMalli, R\n\nSchmidt, K\n\nGraier, WF\n\nGroschner, K\n\nBeiträge in Fachzeitschriften\nISI:000179326300012\n12411413.0\n10.1038/sj.bjp.0704949\nPMC1573569\n1. Nitric oxide (NO) is a key modulator of cellular Ca(2+) signalling and a determinant of mitochondrial function. Here, we demonstrate that NO governs capacitative Ca(2+) entry (CCE) into HEK293 cells by impairment of mitochondrial Ca(2+) handling. 2. Authentic NO as well as the NO donors 1-[2-(carboxylato)pyrrolidin-1-yl]diazem-1-ium-1, -diolate (ProliNO) and 2-(N, -diethylamino)-diazenolate-2-oxide (DEANO) suppressed CCE activated by thapsigargin (TG)-induced store depletion. Threshold concentrations for inhibition of CCE by ProliNO and DEANO were 0.3 and 1 micro M, respectively. 3. NO-induced inhibition of CCE was not mimicked by peroxynitrite (100 micro M), the peroxynitrite donor 3-morpholino-sydnonimine (SIN-1, 100 micro M) or 8-bromoguanosine 3', '-cyclic monophosphate (8-BrcGMP, 1 mM). In addition, the guanylyl cyclase inhibitor 1H-[1, , ] oxadiazole[4, -a] quinoxalin-1-one (ODQ, 30 micro M) failed to antagonize the inhibitory action of NO on CCE. 4. DEANO (1-10 micro M) suppressed mitochondrial respiration as evident from inhibition of cellular oxygen consumption. Experiments using fluorescent dyes to monitor mitochondrial membrane potential and mitochondrial Ca(2+) levels, respectively, indicated that DEANO (10 micro M) depolarized mitochondria and suppressed mitochondrial Ca(2+) sequestration. The inhibitory effect of DEANO on Ca(2+) uptake into mitochondria was confirmed by recording mitochondrial Ca(2+) during agonist stimulation in HEK293 cells expressing ratiometric-pericam in mitochondria. 5. DEANO (10 micro M) failed to inhibit Ba(2+) entry into TG-stimulated cells when extracellular Ca(2+) was buffered below 1 micro M, while clear inhibition of Ba(2+) entry into store depleted cells was observed when extracellular Ca(2+) levels were above 10 micro M. Moreover, buffering of intracellular Ca(2+) by use of N, '-[1, -ethanediylbis(oxy-2, -phenylene)] bis [N-[25-[(acetyloxy) methoxy]-2-oxoethyl]]-, bis[(acetyloxy)methyl] ester (BAPTA/AM) eliminated inhibition of CCE by NO, indicating that the observed inhibitory effects are based on an intracellular, Ca(2+) dependent-regulatory process. 6. Our data demonstrate that NO effectively inhibits CCE cells by cGMP-independent suppression of mitochondrial function. We suggest disruption of local Ca(2+) handling by mitochondria as a key mechanism of NO induced suppression of CCE.\n\nGraier, Wolfgang\n\nGroschner, Klaus\n\nMalli, Roland\n\n\n"
},
{
"text": "\n4817\nAccuracy of whole-body 18F-FDP-PET for restaging malignant lymphoma.\n\nMikosch, P\n\nGallowitsch, HJ\n\nZinke-Cerwenka, W\n\nHeinisch, M\n\nPipam, W\n\nEibl, M\n\nKresnik, E\n\nUnterweger, O\n\nLinkesch, W\n\nLind, P\n\nBeiträge in Fachzeitschriften\nISI:000182539400003\n12752087.0\n10.1046%2Fj.1563-2571.2003.03003.x\nNone\nBACKGROUND: The aim of this retrospective study was to evaluate the accuracy of fluorine-18 fluorodeoxyglucose positron emission tomography (18F-FDG-PET) images, which were interpreted under daily routine conditions, in patients with Hodgkin's disease (HD) or non-Hodgkin lymphoma (NHL) for restaging after chemotherapy and/or radiotherapy. For this purpose, 18F-FDG-PET results were compared with morphological imaging methods and the patients' clinical background. METHODS: 121 PET images of 93 lymphoma patients (44 HD, 49 NHL) were investigated after chemotherapy/radiotherapy. For PET imaging, 160-200 MBq 18F-FDG was administered intravenously, followed by an infusion of 20 mg Furosemid in 250 mL saline. Whole-body 18F-FDG-PET images were obtained using a partial-ring PET scanner without attenuation correction. The morphological imaging consisted in computed tomography and ultrasound (CT/US) in all patients, additional MRI in some patients, and iliac crest biopsy in cases of suspicious bone marrow involvement. The standard of reference was composed of biopsy data, clinical status at the time of investigation, and follow-up of at least 12 months. The PET images were evaluated for their sensitivity, specificity and accuracy based on written reports, which were compiled from other imaging data and the clinical history of the patients. RESULTS: Sensitivity, specificity, and accuracy of 18F-FDG-PET was 91 %, 81 %, and 85 %; of CT/US, 88 %, 35 %, 56 %, respectively. Major sources of error in 18F-FDG-PET were due to asymmetric muscular hypermetabolism and inflammatory lesions misinterpreted as persistent viable lymphoma tissue. Furthermore, secondary malignancies other than lymphomas were another reason for misinterpretations of 18F-FDG-PET studies. CONCLUSIONS: 18F-FDG-PET showed a comparable sensitivity but a higher specificity and accuracy compared with CT/US. To achieve a high accuracy in 18F-FDG-PET, the nuclear medicine specialist needs imaging and clinical data as background information, which can only be acquired through close co-operation with the referring clinicians. Pharmacological muscular relaxation in the course of 18F-FDG-PET imaging may be advisable, as nonspecific muscular hypermetabolism was one of the problems at the image readings and a source of incorrect 18F-FDG-PET interpretations.\n\n\n"
},
{
"text": "\n20579\nEffect of sunscreens on UV radiation-induced enhancement of melanoma growth in mice.\n\nWolf, P\n\nDonawho, CK\n\nKripke, ML\n\nBeiträge in Fachzeitschriften\nISI:A1994MQ86400010\n8271307.0\n10.1093/jnci/86.2.99\nNone\nBACKGROUND: Epidemiologic evidence suggests that exposure to UV radiation plays a significant role in the development of melanoma skin cancers. As early surgical removal of the melanoma is the only effective therapy, current strategies for reducing mortality from melanoma focus on prevention of the disease. Chemical sunscreens protect mice from development of skin cancers that resemble sunlight-induced human squamous cell cancers, but there appears to be a complex relationship between UV radiation exposure and development of melanoma. PURPOSE: We asked whether common sunscreens would protect mice against UV radiation-induced enhancement of melanoma incidence. METHODS: C3H mice were exposed to 4.8 kJ/m2 UVB from FS40 sunlamps twice a week for 3 weeks. Sunscreens containing 7.5% 2-ethylhexyl-p-methoxycinnamate, 8% octyl-N-dimethyl-p-aminobenzoate, 6% benzophenone-3, or the oil-in-water vehicle alone were applied to the ears and tails of the mice 20 minutes before irradiation. At various times during and after exposure, we determined UV radiation-induced inflammation by measuring ear swelling. We also examined the ears histologically for UV radiation-induced alterations. One day after the final irradiation, 2.5 x 10(4) syngeneic K1735 melanoma cells were injected into the external ears. Mice were examined weekly for tumor growth for 5-8 weeks after tumor cell injection. Control mice were treated in the identical way except for exposure to UV radiation. RESULTS: The incidence of melanomas was significantly higher in the UV-irradiated mice. All three sunscreens protected against UV radiation-induced ear swelling and clearly diminished histopathologic alterations, including sunburn cell formation, epidermal hyperplasia, and mononuclear cell infiltrate in the dermis. However, the sunscreens failed to protect against UV radiation-induced increase in melanoma incidence. The sunscreens or vehicle alone did not significantly alter tumor growth. CONCLUSIONS: Protection against sunburn does not necessarily imply protection against other possible UV radiation effects, such as enhanced melanoma growth. IMPLICATIONS: Sunscreen protection against UV radiation-induced inflammation may encourage prolonged exposure to UV radiation and thus may actually increase the risk of melanoma development. These findings suggest that further research on the ability of sunscreens to prevent melanoma is urgently needed.\n\nWolf, Peter\n\n\n"
},
{
"text": "\n62070\nEfficacy and safety of topiramate in combination with metformin in the treatment of obese subjects with type 2 diabetes: a randomized, double-blind, placebo-controlled study.\n\nToplak, H\n\nHamann, A\n\nMoore, R\n\nMasson, E\n\nGorska, M\n\nVercruysse, F\n\nSun, X\n\nFitchet, M\n\nBeiträge in Fachzeitschriften\nISI:000242934100019\n16703004.0\n10.1038/sj.ijo.0803382\nNone\nOBJECTIVE: To investigate the efficacy and safety of topiramate in obese subjects with type 2 diabetes treated with metformin. DESIGN: This was a multicenter, double-blind, placebo-controlled trial. All subjects received a non-pharmacological program of diet, exercise and behavioral modification throughout the study; the assigned diet was 600 kcal/day less than the subject's individually calculated energy expenditure. After a 6-week single-blind placebo run-in, subjects were randomized to placebo, topiramate 96 mg/day or topiramate 192 mg/day. Following an 8-week titration period, subjects remained on their assigned dose for 52 weeks. However, the sponsor ended the study early in order to develop a new controlled-release formulation with the potential to enhance tolerability and simplify dosing in this patient population. A total of 646 obese men and women (age: 18-75 years, body mass index: 27-50 kg/m(2)) with an established history of type 2 diabetes mellitus controlled by metformin monotherapy were randomized. Efficacy was assessed in a pre-determined modified intent-to-treat (MITT) population of 307 subjects whose randomization date would have allowed them to complete 24 weeks on study medication before the announcement of study termination. MEASUREMENTS: Joint primary efficacy parameters were mean percent change in weight and change in glycosylated hemoglobin (HbA(1c)) from baseline to week 24. RESULTS: Subjects in the placebo, topiramate 96 mg/day and topiramate 192 mg/day groups lost 1.7%, 4.5% (P<0.001) and 6.5% (P<0.001), respectively, of their baseline body weight and had absolute decreases in HbA(1c) of 0.1%, 0.4% (P<0.001) and 0.6% (P<0.001) (MITT, last observation carried forward). Topiramate-treated subjects also experienced statistically significant decreases in systolic blood pressure. Most common adverse events were paresthesia and events related to the central nervous system. CONCLUSIONS: Topiramate was effective for weight reduction and improvement in glycemic control in obese subjects with type 2 diabetes treated with metformin monotherapy. Further study in obese diabetics is warranted.\n\nToplak, Hermann\n\n\n"
},
{
"text": "\n93409\nTreatment motivation and results of inpatient psychotherapy for women with depressive disorders: a prospective study\n\nNickel, C\n\nMuehlbacher, M\n\nKettler, C\n\nTritt, K\n\nEgger, C\n\nLahmann, C\n\nGil, FP\n\nLeiberich, P\n\nBachler, E\n\nBuschmann, W\n\nForthuber, P\n\nFartacek, R\n\nMitterlehner, F\n\nRother, W\n\nLoew, T\n\nNickel, M\n\nBeiträge in Fachzeitschriften\nISI:000235428200003\n16463240.0\n10.1055/s-2005-859011\nNone\nWhether the treatment results in inpatient psychotherapy are significantly influenced by the patient's motivation is a subject of discussion. The goal of this study was to assess whether the primary motivation for therapy in depressive women influences the results of psychotherapeutic treatment. In a prospective study, the monitored results from 64 female inpatients (32 who were highly motivated to enter therapy, and 32 who were minimally motivated) were compared to each other. The period of observation was six weeks. As instruments of assessment, the Fragebogen zur Therapiemotivation (FMP) (Questonnaire on Motivation for Entering Therapy) and the Beck Depression Inventory (BDI) were aministered upon admission; after the fourth and sixth weeks of therapy, the Veränderungsfragebogen des Erlebens und Verhaltens (VEV) (Questionnaire of Changes in Experience and Behavior) was administered as well. All patients who had applied for a pension were found in the group of less motivated patients and consolidated into a subgroup. The analysis was carried out according to the intent-to-treat principle. The variance analysis for the repeat measurements showed significant differences on all the FMP scales and on the BDI (all P< 0.001). The measurements with VEV likewise resulted in a significant difference (P< 0.01). The subgroup of "pension patients" showed significantly less change in all three of the above measurements. Patients with depressive symptomology who essentially are relatively highly motivated for therapy could profit significantly more from inpatient psychosomatic treatment than those who are less motivated. Establishing and developing motivation prior to inpatient hospitalization could possibly contribute to more efficient and cost-effective clinical treatment. Where legal proceedings pertaining to a pension are pending, relatively less motivated patients fare significantly worse not only in their motivational development for therapy, but also in their final treatment results. It should be noted, however, that the relatively small random sample, the restricted blinding, which was only partially possible, could have led to possible distortions.\n\nNickel, Marius\n\n\n"
},
{
"text": "\n106791\nCarbonyl proteins as a clinical marker in Alzheimer's disease and its relation to tryptophan degradation and immune activation.\n\nGreilberger, J\n\nFuchs, D\n\nLeblhuber, F\n\nGreilberger, M\n\nWintersteiger, R\n\nTafeit, E\n\nBeiträge in Fachzeitschriften\nISI:000284130500008\n21086789.0\nNone\nNone\nBackground: The question arises whether oxidative stress is connected with systemic immune activation in Alzheimer's disease (AD) and mild cognitive impairment (MCI). During immune response interferon-gamma stimulates the kynurenine (Kyn) pathway, a major route of L-tryptophan (Trp) degradation. Methods: Plasma Kyn, Trp and the Kyn to Trp ratio (Kyn/Trp), carbonyl proteins (CP) as oxidative stress parameter and homocysteine, neopterin, folate and vitamin B12 were measured from patients with AD and MCI (n = 16: 6 females and 4 males with AD, 3 females and 3 males with MCI; 63.3 +/- 13.7 years), and an age matched healthy control group (n = 15: 11 females and 4 males; 62.8 +/- 3.6 years). We correlated the oxidative stress parameter CP with the degradation of Trp creating a new quotient CP/Trp and calculated the sensitivity, specificity, and cut-off values for CP, Trp, CP/Trp, and Kyn/Trp using discriminate analysis. Results: CP was significantly higher in AD/MCI (930 +/- 265 pmol/mg; p < 0.001) compared to controls (300 +/- 120 pmol/mg), Trp was significantly lower in AD/MCI (48.9 +/- 9.0 mu mol/L; p < 0.001) than controls (65.2 +/- 10.7 mu mol/L). While Kyn showed no significant difference between AD/MCI (1.72 +/- 0.56 mu mol/L) and controls (1.53 +/- 0.29 mu mol/L), Kyn/Trp was significantly higher in AD/MCI (35.2 +/- 8.8 mu mol/mmol; p < 0.001) than in controls (23.7 +/- 4.2 mu mol/mmol). CP/Trp ratio was more than 4 fold higher in the AD/MCI group (19.8 +/- 7.76 [(pmol/mg)/(mu mol/L)]; p < 0.001) compared to controls (4.79 +/- 2.26 [(pmol/mg)/(mu mol/L)]). Homocysteine, folate, vitamin B12, and neopterin showed no significant difference. Discriminant analysis provided CP alone as the best clinical marker with highest sensitivity and highest specificity for AD/MCI followed by the ratio of CP/Trp. ROC curve analysis provided the best result for CP/Trp. Conclusions: These preliminary results support the hypothesis that oxidative damage to proteins is directly connected with Trp degradation and Kyn pathway in the systemic immune activation. (Clin. Lab. 2010;56:441-448)\n\nGreilberger, Joachim\n\nTafeit, Erwin\n\n\n"
},
{
"text": "\n148833\nThe relative effect of hospital and surgeon volume on failure to rescue among patients undergoing liver resection for cancer.\n\nBuettner, S\n\nGani, F\n\nAmini, N\n\nSpolverato, G\n\nKim, Y\n\nKilic, A\n\nWagner, D\n\nPawlik, TM\n\nBeiträge in Fachzeitschriften\nISI:000372388200002\n26652859.0\n10.1016/j.surg.2015.10.025\nNone\nAlthough previous reports have focused on factors at the hospital level to explain variations in postoperative outcomes, less is known regarding the effect of provider-specific factors on postoperative outcomes such as failure-to-rescue (FTR) and postoperative mortality. The current study aimed to quantify the relative contributions of surgeon and hospital volume on the volume-outcomes relationship among a cohort of patients undergoing liver resection.\n Patients undergoing liver surgery for cancer were identified using the Nationwide Inpatient Sample from 2001 and 2009. Multivariable logistic regression analysis was performed to identify factors associated with mortality and FTR. Point estimates were used to calculate the relative effects of hospital and surgeon volume on mortality and FTR.\n A total of 5, 75 patients underwent liver surgery and met inclusion criteria. Median patient age was 62 years (interquartile range, 52-70) and 55.2% of patients were male. Mortality was lowest among patients treated at high-volume hospitals and among patients treated by high-volume surgeons (both P < .001). Similar patterns in FTR were noted relative to hospital and surgeon volume (hospital volume: low vs intermediate vs high; 10.3 vs 9.0 vs 5.2%; surgeon volume: low vs intermediate vs high, 11.1 vs 9.1 vs 4.1%; both P < .05). On multivariable analysis, compared with high-volume surgeons, lower volume surgeons demonstrated greater odds for mortality (intermediate: odds ratio [OR], 2.27 [95% CI, 1.27-4.06; P = .006]; low, OR, 2.83 [95% CI, 1.52-5.27; P = .001]), and FTR (intermediate: OR, 2.86 [95% CI, 1.53-5.34, P = .001]; low, OR, 3.40 [95% CI, 1.75-6.63; P < .001]). While hospital volume accounted for 0.5% of the surgeon volume effect on increased FTR for low-volume surgeons, surgeon volume accounted for nearly all of the hospital volume effect on increased FTR in low-volume hospitals.\n The risk of complications, mortality, and FTR were less among both high-volume hospitals and high-volume surgeons, but the beneficial effect of volume on outcomes was attributable largely to surgeon volume.\n Copyright © 2016 Elsevier Inc. All rights reserved.\n\nWagner, Doris\n\n\n"
},
{
"text": "\n151300\nHuman biodistribution and radiation dosimetry of novel PET probes targeting the deoxyribonucleoside salvage pathway.\n\nSchwarzenberg, J\n\nRadu, CG\n\nBenz, M\n\nFueger, B\n\nTran, AQ\n\nPhelps, ME\n\nWitte, ON\n\nSatyamurthy, N\n\nCzernin, J\n\nSchiepers, C\n\nBeiträge in Fachzeitschriften\nISI:000288255500014\n21127859.0\n10.1007/s00259-010-1666-z\nPMC3053458\nDeoxycytidine kinase (dCK) is a rate-limiting enzyme in deoxyribonucleoside salvage, a metabolic pathway involved in the production and maintenance of a balanced pool of deoxyribonucleoside triphosphates (dNTPs) for DNA synthesis. dCK phosphorylates and therefore activates nucleoside analogs such as cytarabine, gemcitabine, decitabine, cladribine, and clofarabine that are used routinely in cancer therapy. Imaging probes that target dCK might allow stratifying patients into likely responders and nonresponders with dCK-dependent prodrugs. Here we present the biodistribution and radiation dosimetry of three fluorinated dCK substrates, (18)F-FAC, L: -(18)F-FAC, and L: -(18)F-FMAC, developed for positron emission tomography (PET) imaging of dCK activity in vivo.\n PET studies were performed in nine healthy human volunteers, three for each probe. After a transmission scan, the radiopharmaceutical was injected intravenously and three sequential emission scans acquired from the base of the skull to mid-thigh. Regions of interest encompassing visible organs were drawn on the first PET scan and copied to the subsequent scans. Activity in target organs was determined and absorbed dose estimated with OLINDA/EXM. The standardized uptake value was calculated for various organs at different times.\n Renal excretion was common to all three probes. Bone marrow had higher uptake for L: -(18)F-FAC and L: -(18)F-FMAC than (18)F-FAC. Prominent liver uptake was seen in L: -(18)F-FMAC and L: -(18)F-FAC, whereas splenic activity was highest for (18)F-FAC. Muscle uptake was also highest for (18)F-FAC. The critical organ was the bladder wall for all three probes. The effective dose was 0.00524, 0.00755, and 0.00910 mSv/MBq for (18)F-FAC, L: -(18)F-FAC, and L: -(18)F-FMAC, respectively.\n The biodistribution of (18)F-FAC, L: -(18)F-FAC, and L: -(18)F-FMAC in humans reveals similarities and differences. Differences may be explained by different probe affinities for nucleoside transporters, dCK, and catabolic enzymes such as cytidine deaminase (CDA). Dosimetry demonstrates that all three probes can be used safely to image the deoxyribonucleoside salvage pathway in humans.\n\nSchwarzenberg, Johannes\n\n\n"
},
{
"text": "\n161302\nThe role of tryptophan metabolism and food craving in the relationship between obesity and bipolar disorder.\n\nDalkner, N\n\nPlatzer, M\n\nBengesser, SA\n\nBirner, A\n\nFellendorf, FT\n\nQueissner, R\n\nPainold, A\n\nMangge, H\n\nFuchs, D\n\nReininghaus, B\n\nKapfhammer, HP\n\nHolasek, SJ\n\nReininghaus, EZ\n\nBeiträge in Fachzeitschriften\nISI:000447578700042\n28712531.0\n10.1016/j.clnu.2017.06.024\nNone\nIndividuals with bipolar disorder (BD) have a significantly increased risk of obesity-related conditions. The imbalance between food intake and energy expenditure is assumed to be a major risk factor for obesity in BD. This study analyzed food craving in relation to anthropometric, metabolic, and neurobiological parameters in a well-characterized cohort of euthymic individuals with BD.\n One-hundred-thirty-five patients completed the Food-Craving Inventory assessing four categories of food craving (fat, fast-food, sweets and carbohydrate craving). Additionally, clinical, metabolic and anthropometric parameters were assessed.\n Higher levels of fat craving were observed in males, versus females, with BD. High levels of carbohydrate craving positively correlated with kynurenine and the kynurenine-to-tryptophan ratio. Higher serum nitrite and neopterin levels were related to fat craving. Parameters of fat metabolism (triglycerides, high-density lipoprotein) were associated with fat and fast-food craving. Anthropometric measures of obesity (e.g. body mass index, waist-to-hip-ratio) were not related to food craving.\n Overweight/obese individuals with BD show an increased driving of tryptophan down the kynurenine pathways, as indicated by an increase in the serum kynurenine-to-tryptophan ratio. The driving of tryptophan down the kynurenine pathway is mediated by immune-inflammatory activity and stress. The correlation of increased kynurenine with food craving, especially carbohydrate craving, probably indicates a regulatory deficit in the maintenance of chronic inflammatory processes in obesity and BD. Food craving seems to be of clinical importance in the treatment of metabolic disturbances in BD, although not associated with anthropometric measures of obesity. Rather, food craving correlates with blood metabolic parameters and an increased activation of the kynurenine pathway, both of which are linked to higher affective symptomatology and the development of cardiovascular diseases.\n Copyright © 2017 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.\n\nBengesser, Susanne\n\nBirner, Armin\n\nDalkner, Nina\n\nFellendorf, Frederike\n\nHolasek, Sandra Johanna\n\nKapfhammer, Hans-Peter\n\nMangge, Harald\n\nPainold, Annamaria\n\nPlatzer, Martina\n\nQueissner, Robert\n\nReininghaus, Eva\n\n\n"
},
{
"text": "\n164455\nA multicenter prospective study on the diagnostic performance of a new liquid rapid urease test for the diagnosis of <i>Helicobacter pylori</i> infection.\n\nDolak, W\n\nBilgilier, C\n\nStadlmann, A\n\nLeiner, J\n\nPüspök, A\n\nPlieschnegger, W\n\nSiebert, F\n\nWewalka, F\n\nSchöfl, R\n\nHuber-Schönauer, U\n\nDatz, C\n\nBiowski-Frotz, S\n\nHögenauer, C\n\nSchrutka-Kölbl, C\n\nMakristathis, A\n\nSchöniger-Hekele, M\n\nSteininger, C\n\nAustrian Helicobacter Pylori Study Group\n\nBeiträge in Fachzeitschriften\nISI:000418875100001\n29299067.0\n10.1186/s13099-017-0226-5\nPMC5740919\nHelicobacter pylori (H. pylori) causes a diversity of gastric diseases. Rapid urease tests (RUT) are well established for the point-of-care, invasive diagnosis of H. pylori infection. The study aimed to evaluate the diagnostic performance of a new liquid RUT, the preOx-HUT, within a prospective cohort of treatment-naïve patients.\n The multicenter prospective clinical trial was conducted at nine Austrian centers for gastrointestinal endoscopy. Patients referred for a diagnostic upper gastrointestinal endoscopy underwent gastric biopsy sampling for routine histological evaluation, and in parallel, the preOx-HUT. Histology served as reference standard to evaluate the diagnostic performance of the preOx-HUT.\n From January 2015 to January 2016, a total of 183 consecutive patients (54 males and 129 females, median age 50 years) were included. Endoscopy revealed pathological findings in 149/183 cases (81%), which were mostly gastritis (59%) and gastro-esophageal reflux disease (27%). H. pylori infection was detected by histology in 41/183 (22%) cases. In relation to histology, the preOx-HUT had a sensitivity of 85%, a specificity of 94%, a positive predictive value of 80% and a negative predictive value of 96%. Performance of preOx-HUT was not affected significantly by concomitant PPI-use as present in 15% of cases (P = 0.73).\n This was the first study evaluating the preOx-HUT in a prospective, multicenter clinical setting. We found a high diagnostic accuracy for the point-of-care, invasive diagnostic test of H. pylori infection. Hence, this test may be a valuable diagnostic adjunct to the clinical presentation of patients with suspected H. pylori infection. Trial registration number EK 1548/2014, Name of registry: Register der Ethikkommission der Medizinischen Universität Wien, URL of registry: https://ekmeduniwien.at/core/catalog/2012/, Date of registration: 24.09.2014, Date of enrolment of the first participant to the trial: 15.01.2015.\n\nHoegenauer, Christoph\n\n\n"
}
]
}