976 resultados para 1-7


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This Letter presents a measurement of the W+ W- production cross section in sqrt(s) = 7  TeV pp collisions by the ATLAS experiment, using 34  pb(-1) of integrated luminosity produced by the Large Hadron Collider at CERN. Selecting events with two isolated leptons, each either an electron or a muon, 8 candidate events are observed with an expected background of 1.7 ± 0.6 events. The measured cross section is 41(-16)(+20)(stat) ± 5(syst)±1(lumi)  pb, which is consistent with the standard model prediction of 44 ± 3  pb calculated at next-to-leading order in QCD.

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Abstract Background and Aims: Data on the influence of calibration on accuracy of continuous glucose monitoring (CGM) are scarce. The aim of the present study was to investigate whether the time point of calibration has an influence on sensor accuracy and whether this effect differs according to glycemic level. Subjects and Methods: Two CGM sensors were inserted simultaneously in the abdomen on either side of 20 individuals with type 1 diabetes. One sensor was calibrated predominantly using preprandial glucose (calibration(PRE)). The other sensor was calibrated predominantly using postprandial glucose (calibration(POST)). At minimum three additional glucose values per day were obtained for analysis of accuracy. Sensor readings were divided into four categories according to the glycemic range of the reference values (low, ≤4 mmol/L; euglycemic, 4.1-7 mmol/L; hyperglycemic I, 7.1-14 mmol/L; and hyperglycemic II, >14 mmol/L). Results: The overall mean±SEM absolute relative difference (MARD) between capillary reference values and sensor readings was 18.3±0.8% for calibration(PRE) and 21.9±1.2% for calibration(POST) (P<0.001). MARD according to glycemic range was 47.4±6.5% (low), 17.4±1.3% (euglycemic), 15.0±0.8% (hyperglycemic I), and 17.7±1.9% (hyperglycemic II) for calibration(PRE) and 67.5±9.5% (low), 24.2±1.8% (euglycemic), 15.5±0.9% (hyperglycemic I), and 15.3±1.9% (hyperglycemic II) for calibration(POST). In the low and euglycemic ranges MARD was significantly lower in calibration(PRE) compared with calibration(POST) (P=0.007 and P<0.001, respectively). Conclusions: Sensor calibration predominantly based on preprandial glucose resulted in a significantly higher overall sensor accuracy compared with a predominantly postprandial calibration. The difference was most pronounced in the hypo- and euglycemic reference range, whereas both calibration patterns were comparable in the hyperglycemic range.

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PURPOSE: Previous analyses of adjuvant studies of aromatase inhibitors versus tamoxifen, including the Breast International Group (BIG) 1-98 study, have suggested a small numerical excess of cardiac adverse events (AEs) on aromatase inhibitors, a reduction in the incidence of hypercholesterolemia on tamoxifen, and significantly higher incidence of thromboembolic AEs on tamoxifen. The purpose of the present study is to provide detailed updated information on these AEs in BIG 1-98. PATIENTS AND METHODS: Eight thousand twenty-eight postmenopausal women with receptor-positive early breast cancer were randomly assigned (double-blind) between March 1998 and May 2003 to receive 5 years of adjuvant endocrine therapy with letrozole, tamoxifen, or a sequence of these agents. Seven thousand nine hundred sixty-three patients who actually received therapy are included in this safety analysis, which focuses on cardiovascular events. AE recording ceased 30 days after therapy completion (or after switch on the sequential arms). RESULTS: Baseline comorbidities were balanced. At a median follow-up time of 30.1 months, we observed similar overall incidence of cardiac AEs (letrozole, 4.8%; tamoxifen, 4.7%), more grade 3 to 5 cardiac AEs on letrozole (letrozole, 2.4%; tamoxifen, 1.4%; P = .001)--an excess only partially attributable to prior hypercholesterolemia--and more overall (tamoxifen, 3.9%; letrozole, 1.7%; P < .001) and grade 3 to 5 thromboembolic AEs on tamoxifen (tamoxifen, 2.3%; letrozole, 0.9%; P < .001). There was no significant difference between tamoxifen and letrozole in incidence of hypertension or cerebrovascular events. CONCLUSION: The present safety analysis, limited to cardiovascular AEs in BIG 1-98, documents a low overall incidence of cardiovascular AEs, which differed between treatment arms.

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Peptide hormone receptors overexpressed in human tumors, such as somatostatin receptors, can be used for in vivo targeting for diagnostic and therapeutic purposes. A novel promising candidate in this field is the GLP-1 receptor, which was recently shown to be massively overexpressed in gut and lung neuroendocrine tumors--in particular, in insulinomas. Anticipating a major development of GLP-1 receptor targeting in nuclear medicine, our aim was to evaluate in vitro the GLP-1 receptor expression in a large variety of other tumors and to compare it with that in nonneoplastic tissues. METHODS: The GLP-1 receptor protein expression was qualitatively and quantitatively investigated in a broad spectrum of human tumors (n=419) and nonneoplastic human tissues (n=209) with receptor autoradiography using (125)I-GLP-1(7-36)amide. Pharmacologic competition experiments were performed to provide proof of specificity of the procedure. RESULTS: GLP-1 receptors were expressed in various endocrine tumors, with particularly high amounts in pheochromocytomas, as well as in brain tumors and embryonic tumors but not in carcinomas or lymphomas. In nonneoplastic tissues, GLP-1 receptors were present in generally low amounts in specific tissue compartments of several organs--namely, pancreas, intestine, lung, kidney, breast, and brain; no receptors were identified in lymph nodes, spleen, liver, or the adrenal gland. The rank order of potencies for receptor binding--namely, GLP-1(7-36)amide = exendin-4 >> GLP-2 = glucagon(1-29)--provided proof of specific GLP-1 receptor identification. CONCLUSION: The GLP-1 receptors may represent a novel molecular target for in vivo scintigraphy and targeted radiotherapy for a variety of GLP-1 receptor-expressing tumors. For GLP-1 receptor scintigraphy, a low-background signal can be expected, on the basis of the low receptor expression in the normal tissues surrounding tumors.

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To investigate mechanisms by which angiotensin converting enzyme (ACE)-inhibition increases insulin sensitivity, spontaneously hypertensive (SH) rats were treated with or without ramipril (1 mg/kg per day) for 12 weeks. Insulin binding and protein levels of insulin receptor substrate-1 (IRS-1), p85-subunit of phosphatidylinositol 3'-kinase (p85) and Src homology 2 domain-containing phosphatase-2 (SHP2) were then determined in hindlimb muscle and liver. Additionally, protein tyrosine phosphatase (PTPase) activities towards immobilized phosphorylated insulin receptor or phosphorylated IRS-1 of membrane (MF) and cytosolic fractions (CF) of these tissues were measured. Ramipril treatment increased IRS-1-protein content in muscle by 31+/-9% (P<0.05). No effects were observed on IRS-1 content in liver or on insulin binding or protein expression of p85 or SHP2 in both tissues. Ramipril treatment also increased dephosphorylation of insulin receptor by muscle CF (22.0+/-1.0%/60 min compared to 16.8+/-1.5%/60 min; P<0.05), and of IRS-1 by liver MF (37.2+/-1.7%/7.5 min compared to 33.8+/-1.7%/7.5 min; P<0.05) and CF (36.8+/-1.0%/7.5 min compared to 33.2+/-1.0%/7.5 min; P<0.05). We conclude that the observed effects of ACE-inhibition by ramipril on the protein expression of IRS-1 and on PTPase activity might contribute to its effect on insulin sensitivity.

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BACKGROUND The long-term results after second generation everolimus eluting bioresorbable vascular scaffold (Absorb BVS) placement in small vessels are unknown. Therefore, we investigated the impact of vessel size on long-term outcomes, after Absorb BVS implantation. METHODS In ABSORB Cohort B Trial, out of the total study population (101 patients), 45 patients were assigned to undergo 6-month and 2-year angiographic follow-up (Cohort B1) and 56 patients to have angiographic follow-up at 1-year (Cohort B2). The pre-reference vessel diameter (RVD) was <2.5 mm (small-vessel group) in 41 patients (41 lesions) and ≥2.5 mm (large-vessel group) in 60 patients (61 lesions). Outcomes were compared according to pre-RVD. RESULTS At 2-year angiographic follow-up no differences in late lumen loss (0.29±0.16 mm vs 0.25±0.22 mm, p=0.4391), and in-segment binary restenosis (5.3% vs 5.3% p=1.0000) were demonstrated between groups. In the small-vessel group, intravascular ultrasound analysis showed a significant increase in vessel area (12.25±3.47 mm(2) vs 13.09±3.38 mm(2) p=0.0015), scaffold area (5.76±0.96 mm(2) vs 6.41±1.30 mm(2) p=0.0008) and lumen area (5.71±0.98 mm(2) vs 6.20±1.27 mm(2) p=0.0155) between 6-months and 2-year follow-up. No differences in plaque composition were reported between groups at either time point. At 2-year clinical follow-up, no differences in ischaemia-driven major adverse cardiac events (7.3% vs 10.2%, p=0.7335), myocardial infarction (4.9% vs 1.7%, p=0.5662) or ischaemia-driven target lesion revascularisation (2.4% vs 8.5%, p=0.3962) were reported between small and large vessels. No deaths or scaffold thrombosis were observed. CONCLUSIONS Similar clinical and angiographic outcomes at 2-year follow-up were reported in small and large vessel groups. A significant late lumen enlargement and positive vessel remodelling were observed in small vessels.

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BACKGROUND Management of persistent low-level viraemia (pLLV) in patients on combined antiretroviral therapy (cART) with previously undetectable HIV viral loads (VLs) is challenging. We examined virological outcome and management among patients enrolled in the Swiss HIV Cohort Study (SHCS). METHODS In this retrospective study (2000-2011), pLLV was defined as a VL of 21-400 copies/mL on ≥3 consecutive plasma samples with ≥8 weeks between first and last analyses, in patients undetectable for ≥24 weeks on cART. Control patients had ≥3 consecutive undetectable VLs over ≥32 weeks. Virological failure (VF), analysed in the pLLV patient group, was defined as a VL>400 copies/mL. RESULTS Among 9972 patients, 179 had pLLV and 5389 were controls. Compared to controls, pLLV patients were more often on unboosted PI-based (adjusted odds ratio, aOR, [95%CI] 3.2 [1.8-5.9]) and NRTI-only combinations (aOR 2.1 [1.1-4.2]) than on NNRTI and boosted PI-based regimens. At 48 weeks, 102/155 pLLV patients (66%) still had pLLV, 19/155 (12%) developed VF, and 34/155 (22%) had undetectable VLs. Predictors of VF were previous VF (aOR 35 [3.8-315]), unboosted PI-based (aOR 12.8 [1.7-96]) or NRTI-only combinations (aOR 115 [6.8-1952]), and VLs>200 during pLLV (aOR 3.7 [1.1-12]). No VF occurred in patients with persistent very LLV (pVLLV, 21-49 copies/mL; N=26). At 48 weeks, 29/39 patients (74%) who changed cART had undetectable VLs, compared to 19/74 (26%) without change (P<0.001). CONCLUSIONS Among patients with pLLV, VF was predicted by previous VF, cART regimen and VL ≥200. Most patients who changed cART had undetectable VLs 48 weeks later. These findings support cART modification for pLLV >200 copies/ml.

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Many observed time series of the global radiosonde or PILOT networks exist as fragments distributed over different archives. Identifying and merging these fragments can enhance their value for studies on the three-dimensional spatial structure of climate change. The Comprehensive Historical Upper-Air Network (CHUAN version 1.7), which was substantially extended in 2013, and the Integrated Global Radiosonde Archive (IGRA) are the most important collections of upper-air measurements taken before 1958. CHUAN (tracked) balloon data start in 1900, with higher numbers from the late 1920s onward, whereas IGRA data start in 1937. However, a substantial fraction of those measurements have not been taken at synoptic times (preferably 00:00 or 12:00 GMT) and on altitude levels instead of standard pressure levels. To make them comparable with more recent data, the records have been brought to synoptic times and standard pressure levels using state-of-the-art interpolation techniques, employing geopotential information from the National Oceanic and Atmospheric Administration (NOAA) 20th Century Reanalysis (NOAA 20CR). From 1958 onward the European Re-Analysis archives (ERA-40 and ERA-Interim) available at the European Centre for Medium-Range Weather Forecasts (ECMWF) are the main data sources. These are easier to use, but pilot data still have to be interpolated to standard pressure levels. Fractions of the same records distributed over different archives have been merged, if necessary, taking care that the data remain traceable back to their original sources. If possible, station IDs assigned by the World Meteorological Organization (WMO) have been allocated to the station records. For some records which have never been identified by a WMO ID, a local ID above 100 000 has been assigned. The merged data set contains 37 wind records longer than 70 years and 139 temperature records longer than 60 years. It can be seen as a useful basis for further data processing steps, most notably homogenization and gridding, after which it should be a valuable resource for climatological studies. Homogeneity adjustments for wind using the NOAA-20CR as a reference are described in Ramella Pralungo and Haimberger (2014). Reliable homogeneity adjustments for temperature beyond 1958 using a surface-data-only reanalysis such as NOAA-20CR as a reference have yet to be created. All the archives and metadata files are available in ASCII and netCDF format in the PANGAEA archive

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PURPOSE Radiolabelled glucagon-like peptide 1 (GLP-1) receptor agonists have recently been shown to successfully image benign insulinomas in patients. For the somatostatin receptor targeting of tumours, however, it was recently reported that antagonist tracers were superior to agonist tracers. The present study therefore evaluated various forms of the (125)iodinated-Bolton-Hunter (BH)-exendin(9-39) antagonist tracer for the in vitro visualization of GLP-1 receptor-expressing tissues in rats and humans and compared it with the agonist tracer (125)I-GLP-1(7-36)amide. METHODS Receptor autoradiography studies with (125)I-GLP-1(7-36)amide agonist or (125)I-BH-exendin(9-39) antagonist radioligands were performed in human and rat tissues. RESULTS The antagonist (125)I-BH-exendin(9-39) labelled at lysine 19 identifies all human and rat GLP-1 target tissues and GLP-1 receptor-expressing tumours. Binding is of high affinity and is comparable in all tested tissues in its binding properties with the agonist tracer (125)I-GLP-1(7-36)amide. For comparison, (125)I-BH-exendin(9-39) with the BH labelled at lysine 4 did identify the GLP-1 receptor in rat tissues but not in human tissues. CONCLUSION The GLP-1 receptor antagonist exendin(9-39) labelled with (125)I-BH at lysine 19 is an excellent GLP-1 radioligand that identifies human and rat GLP-1 receptors in normal and tumoural tissues. It may therefore be the molecular basis to develop suitable GLP-1 receptor antagonist radioligands for in vivo imaging of GLP-1 receptor-expressing tissues in patients.

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This paper presents a measurement of the cross-section for high transverse momentum W and Z bosons produced in pp collisions and decaying to allhadronic final states. The data used in the analysis were recorded by the ATLAS detector at the CERN Large Hadron Collider at a centre-of-mass energy of s = 7 TeV and correspond to an integrated luminosity of 4.6 fb−1. The measurement is performed by reconstructing the boosted W or Z bosons in single jets. The reconstructed jet mass is used to identify the W and Z bosons, and a jet substructure method based on energy cluster information in the jet centre-of mass frame is used to suppress the large multi-jet background. The cross-section for events with a hadronically decaying W or Z boson, with transverse momentum pT > 320 GeV and pseudorapidity |η| < 1.9, is measured to be σ + = ± W Z 8.5 1.7 pb and is compared to next-to-leading-order calculations. The selected events are further used to study jet grooming techniques.

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"Über Philosophie der Gesellschaft im 17. und 18. Jahrhundert", Vorlesung oder Seminar in Chicago (?), Datierung unklar, eigenhändige Notizen, 1 Heft, 95 Blätter, davon 76 leer; "Bemerkungen über Wissenschaft und Gesellschaft" (GS 3, S. 40-47), veröffentlicht unter dem Titel "Bemerkungen über Wissenschaft und Krise", in: Zeitschrift für Sozialforschung I, 1932, S. 1-7, Typoskript mit eigenhändiger Korrektur, 11 Blatt; Exzerpte zum Thema "Materialismus und Metaphysik", veröffentlicht in: Zeitschrift für Sozialforschung II, 1933, S.1-33.; Diskussionsbeiträge auf dem XI. Internationalen Soziologenkongress in Genf, Oktober 1933, 1. "Zum Problem der Voraussage in den Sozialwissenschaften" (GS 3, S. 150-157), veröffentlicht in: Zeitschrift für Sozialforschung II, 1933, S. 407-412, a) französische Fassung, Typoskript mit eigenhändiger Korrektur, 8 Blatt, b) französische Fassung, Typoskript mit eigenhändiger Korrektur, 9 Blatt; 2. "Über Funktion und Grenzen der Statistik in den Sozialwissenschaften", französische Fassung, Typoskript mit eigenhändiger Korrektur, 5 Blatt; Exzerpt zu: G.L. Duprat, Typoskript, 1 Blatt; "Auszug aus den dem Kongreß von verschiedenen Teilnehmern vorgelegten Thesen", Typoskript, 3 Blatt; Kongreß-Programme, Drucksachen, 3 Blatt;

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"American Jewish Committee. Progress Report of the Scientific Department" (22.6.1945), a) als Typoskript vervielfältigt, 27 Blatt, b) Typoskript, 28 Blatt; "Über Geschichte und Tätigkeiten des Instituts für Sozialforschung", Interview Leo Löwenthal - David Berger gesendet am 29.10.1947 (?) von Radio Newsreel, USA, deutsche Übersetzung, als Typoskript vervielfältigt, mit handschriftlichen Korrekturen, 19 Blatt; "Papers Regarding the Institute of Social Research" (August 1948), Abschriften aus verschiedenen Berichten und Briefen, Typoskript, 14 Blatt; P. Hübner: "Soziologie im Kampf gegen das Vorurteil. HICOG fördert Institut für Sozialforschung an Frankfurts Universität", veröffentlicht in: Neue Zeitung, Frankfurt (1950), Typoskript mit handschriftlichen Korrekturen von Max Horkheimer, 3 Blatt; Theodor W. Adorno: "Plans of New Research Projects of the 'Institut für Sozialforschung'" (November 1950), Typoskript, 7 Blatt; "Memorandum über das Institut für Sozialforschung an der Universität Frankfurt/Main" (November 1950), a)-d) deutsche Fassung, 41 Blatt (mit Anlagen); e)-f) englische Fassung, 25 Blatt (mit Anlagen); "The Institute for Social Research, Oslo, Norway" (1950), Drucksache, 2 Blatt; "Report for UNESCO, Paris", Über das Institut für Sozialforschung (5.4. 1951), a) englische Fassung, Typoskript, 3 Blatt, b) deutscher Entwurf, Typoskript, 3 Blatt; Institut zur Förderung öffentlicher Angelegenheiten e.V., Frankfurt am Main: "3 Rundschreiben. Betreff: Clearingstelle zur Meinungsforschung (empirische Sozialforschung), Materialien zur Meinungsforschung, Institut für Sozialforschung an der Johann-Wolfgang Goethe-Universität in Frankfurt am Main" (16.4.1951), als Typoskript vervielfältigt, 4 Blatt; "Progress Report on the Institute of Social Research's Work at Frankfurt University" (10.2.1951), als Typoskript vervielfältigt, 2 Blatt; "Bericht über Geschichte und Tätigkeit des Instituts für Sozialforschung an der Johann Wolfgang Goethe-Universität, Frankfurt am Main" (1.7.1951), a) Typoskript, 3 Blatt, b) als Entwurf für ein Rundschreiben von Friedrich Pollock, Typoskript, 4 Blatt; Angaben über das Institut für Sozialforschung, Frankfurt, Antworten für einen Fragebogen (September 1951), Typoskript, 2 Blatt; "Memorandum über Arbeiten und die Organisation des Instituts" (Mai 1953), Typoskript, 4 Blatt;

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"Institut für Sozialforschung: Research Projects", Tabellarische Zusammenstellung (Juni 1953), Typoskript, 2 Blatt; "Institut für Sozialforschung an der Johann Wolfgang Goethe-Universität Frankfurt, Germany: Memorandum" (1953), a) Typoskript, 12 Blatt, b) Typoskript, 13 Blatt; "Projects of the Institute for Social Research" (1.7.1954), Typoskript, 5 Blatt; "Institut für Soziaforschung: Mitteilungen an die Presse" (November 1955), als Typoskript vervielfältigt, 6 Blatt; Clark: "Institut für Sozialforschung an der Johann Wolfgang Goethe-Universität in Frankfurt am Main" (etwa 1955), Typoskript, englisch, mit handschriftlichen Korrekturen, unter anderem von Max Horkheimer, 2 Blatt; "Institut für Sozialforschung" (6.3.1958), a) als Typoskript vervielfältigt, 10 Blatt, b) Typoskript, 22 Blatt, c) Kurzfassung, Typoskript, 3 Blatt, d) Teilstück, Typoskript, 1 Blatt, e) Sonderdruck, 15 Seiten; Abgeschlossene und laufende Arbeiten des Instituts. Tabellarische Zusammenstellung (1958?), Typoskript, 1 Blatt; "Laufende Studien" Tabellarische Aufstellung (25.5.1961), Typoskript, 1 Blatt; Friedrich Pollock (?): Anmerkungen zu Paul Klukes Darstellung des Instituts für Sozialforschung in dessen "Geschichte der Frankfurter Universität" (8.9.1969), Typoskript mit handschriftlichen Korrekturen, 4 Blatt; Theodor W. Adorno: Über die Arbeiten des Instituts für Sozialforschung (Datierung unklar, etwa 1941-45), Teilstück eines Entwurfs, Typoskript mit eigenhändiger Korrektur, 2 Blatt; Über die wesentliche Aufgabe des Instituts: Vereinigung geisteswissenschaftlicher und empirischer Methoden (Datierung unklar), Typoskript, 1 Blatt; "Forschungsprojekte des Instituts" (Datierung unklar, etwa 1950), Typoskript mit handschriftlichen Ergänzungen von Friedrich Pollock, 5 Blatt; "Vorträge im Institut für Sozialforschung. Einladungen und tabellarische Aufstellungen" (1953 u.a.), 5 Blatt; "Vorlesungen und Übungen im Institut für Sozialforschung, Ankündigungen aus den Jahren 1952-64, 9 Blatt; "International Institute of Social Research: Research-Project on Anti-Semitism" (1939-42) (veröffentlicht in Studies in Philosophy and Social Science Bd. IX, 1941, S. 124-143): 1. "Research Project on Anti-Semitism", a) Typoskript, 45 Blatt;