89 research outputs found

    HCOOCH3 as a probe of temperature and structure of Orion-KL

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    We studied the O-bearing molecule HCOOCH3 to characterize the physical conditions of the different molecular source components in Orion-KL. We identify 28 methyl formate emission peaks throughout the 50" field of observations. The two strongest peaks are in the Compact Ridge (MF1) and in the SouthWest of the Hot Core (MF2). Spectral confusion is still prevailing as half of the expected transitions are blended over the region. Assuming that the transitions are thermalized, we derive the temperature at the five main emission peaks. At the MF1 position we find a temperature of 80K in a 1.8"x0.8" beam size and 120K on a larger scale (3.6" x2.2"), suggesting an external source of heating, whereas the temperature is about 130K at the MF2 position on both scales. Transitions of HCOOCH3 in vt=1 are detected as well and the good agreement of the positions on the rotational diagrams between the vt=0 and the vt=1 transitions suggests a similar temperature. The velocity of the gas is between 7.5 and 8.0km/s depending on the positions and column density peaks vary from 1.6x10^16 to 1.6x10^17cm^-2. A second velocity component is observed around 9-10 km/s in a North-South structure stretching from the Compact Ridge up to the BN object; this component is warmer at the MF1 peak. The two other C2H4O2 isomers are not detected and the derived upper limit for the column density is <3x10^14cm^-2 for glycolaldehyde and <2x10^15cm^-2 for acetic acid. From the 223GHz continuum map, we identify several dust clumps with associated gas masses in the range 0.8 to 5.8Msun. Assuming that the HCOOCH3 is spatially distributed as the dust, we find relative abundances of HCOOCH3 in the range <0.1x10^-8 to 5.2x10^-8. We suggest a relation between the methyl formate distribution and shocks as traced by 2.12 mum H2 emission.Comment: Accepted for publication in A&

    Acoustics and discourse function of two types of breathing signals

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    Cwiek A, Wlodarczak M, Heldner M, Wagner P. Acoustics and discourse function of two types of breathing signals. In: Abrahamsen JE, Koreman J, van Dommelen WA, eds. Nordic Prosody: Proceedings of the XIIth Conference, Trondheim 2016. Frankfurt a.M.: Peter Lang Publishing Group; 2017: 83-91.Breathing is fundamental for living and speech, and it has been a subject of linguistic research for years. Recently, there has been a renewed interest in tackling the question of possible communicative functions of breathing (e.g. Rochet-Capellan & Fuchs, 2014; Aare, Włodarczak & Heldner, 2014; Włodarczak & Heldner, 2015; Włodarczak, Heldner, & Edlund, 2015). The present study set out to determine acoustic markedness and communicative functions of pauses accompanied and non-accompanied by breathing. We hypothesised that an articulatory reset occurring in breathing pauses and an articulatory freeze in non-breathing pauses differentiates between the two types. A production experiment was conducted and some evidence in favour of such a phenomenon was found. Namely, in case of non-breathing pauses, we observed more coarticulation evidenced by a more frequent omission of plosive releases. Our findings thus give some evidence in favour of the communicative function of breathing

    Polymer-based or polymer-free stents in patients at high bleeding risk

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    Background: polymer-free drug-coated stents provide superior clinical outcomes to bare-metal stents in patients at high bleeding risk who undergo percutaneous coronary intervention (PCI) and are treated with 1 month of dual antiplatelet therapy. Data on the use of polymer-based drug-eluting stents, as compared with polymer-free drug-coated stents, in such patients are limited. Methods: in an international, randomized, single-blind trial, we compared polymer-based zotarolimus-eluting stents with polymer-free umirolimus-coated stents in patients at high bleeding risk. After PCI, patients were treated with 1 month of dual antiplatelet therapy, followed by single antiplatelet therapy. The primary outcome was a safety composite of death from cardiac causes, myocardial infarction, or stent thrombosis at 1 year. The principal secondary outcome was target-lesion failure, an effectiveness composite of death from cardiac causes, target-vessel myocardial infarction, or clinically indicated target-lesion revascularization. Both outcomes were powered for noninferiority. Results: a total of 1996 patients at high bleeding risk were randomly assigned in a 1:1 ratio to receive zotarolimus-eluting stents (1003 patients) or polymer-free drug-coated stents (993 patients). At 1 year, the primary outcome was observed in 169 of 988 patients (17.1%) in the zotarolimus-eluting stent group and in 164 of 969 (16.9%) in the polymer-free drug-coated stent group (risk difference, 0.2 percentage points; upper boundary of the one-sided 97.5% confidence interval [CI], 3.5; noninferiority margin, 4.1; P = 0.01 for noninferiority). The principal secondary outcome was observed in 174 patients (17.6%) in the zotarolimus-eluting stent group and in 169 (17.4%) in the polymer-free drug-coated stent group (risk difference, 0.2 percentage points; upper boundary of the one-sided 97.5% CI, 3.5; noninferiority margin, 4.4; P = 0.007 for noninferiority). Conclusions: among patients at high bleeding risk who received 1 month of dual antiplatelet therapy after PCI, use of polymer-based zotarolimus-eluting stents was noninferior to use of polymer-free drug-coated stents with regard to safety and effectiveness composite outcomes. (Funded by Medtronic; ONYX ONE ClinicalTrials.gov number, NCT03344653.)

    Effects of alirocumab on types of myocardial infarction: insights from the ODYSSEY OUTCOMES trial

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    Aims  The third Universal Definition of Myocardial Infarction (MI) Task Force classified MIs into five types: Type 1, spontaneous; Type 2, related to oxygen supply/demand imbalance; Type 3, fatal without ascertainment of cardiac biomarkers; Type 4, related to percutaneous coronary intervention; and Type 5, related to coronary artery bypass surgery. Low-density lipoprotein cholesterol (LDL-C) reduction with statins and proprotein convertase subtilisin–kexin Type 9 (PCSK9) inhibitors reduces risk of MI, but less is known about effects on types of MI. ODYSSEY OUTCOMES compared the PCSK9 inhibitor alirocumab with placebo in 18 924 patients with recent acute coronary syndrome (ACS) and elevated LDL-C (≥1.8 mmol/L) despite intensive statin therapy. In a pre-specified analysis, we assessed the effects of alirocumab on types of MI. Methods and results  Median follow-up was 2.8 years. Myocardial infarction types were prospectively adjudicated and classified. Of 1860 total MIs, 1223 (65.8%) were adjudicated as Type 1, 386 (20.8%) as Type 2, and 244 (13.1%) as Type 4. Few events were Type 3 (n = 2) or Type 5 (n = 5). Alirocumab reduced first MIs [hazard ratio (HR) 0.85, 95% confidence interval (CI) 0.77–0.95; P = 0.003], with reductions in both Type 1 (HR 0.87, 95% CI 0.77–0.99; P = 0.032) and Type 2 (0.77, 0.61–0.97; P = 0.025), but not Type 4 MI. Conclusion  After ACS, alirocumab added to intensive statin therapy favourably impacted on Type 1 and 2 MIs. The data indicate for the first time that a lipid-lowering therapy can attenuate the risk of Type 2 MI. Low-density lipoprotein cholesterol reduction below levels achievable with statins is an effective preventive strategy for both MI types.For complete list of authors see http://dx.doi.org/10.1093/eurheartj/ehz299</p

    Effect of alirocumab on mortality after acute coronary syndromes. An analysis of the ODYSSEY OUTCOMES randomized clinical trial

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    Background: Previous trials of PCSK9 (proprotein convertase subtilisin-kexin type 9) inhibitors demonstrated reductions in major adverse cardiovascular events, but not death. We assessed the effects of alirocumab on death after index acute coronary syndrome. Methods: ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) was a double-blind, randomized comparison of alirocumab or placebo in 18 924 patients who had an ACS 1 to 12 months previously and elevated atherogenic lipoproteins despite intensive statin therapy. Alirocumab dose was blindly titrated to target achieved low-density lipoprotein cholesterol (LDL-C) between 25 and 50 mg/dL. We examined the effects of treatment on all-cause death and its components, cardiovascular and noncardiovascular death, with log-rank testing. Joint semiparametric models tested associations between nonfatal cardiovascular events and cardiovascular or noncardiovascular death. Results: Median follow-up was 2.8 years. Death occurred in 334 (3.5%) and 392 (4.1%) patients, respectively, in the alirocumab and placebo groups (hazard ratio [HR], 0.85; 95% CI, 0.73 to 0.98; P=0.03, nominal P value). This resulted from nonsignificantly fewer cardiovascular (240 [2.5%] vs 271 [2.9%]; HR, 0.88; 95% CI, 0.74 to 1.05; P=0.15) and noncardiovascular (94 [1.0%] vs 121 [1.3%]; HR, 0.77; 95% CI, 0.59 to 1.01; P=0.06) deaths with alirocumab. In a prespecified analysis of 8242 patients eligible for ≥3 years follow-up, alirocumab reduced death (HR, 0.78; 95% CI, 0.65 to 0.94; P=0.01). Patients with nonfatal cardiovascular events were at increased risk for cardiovascular and noncardiovascular deaths (P<0.0001 for the associations). Alirocumab reduced total nonfatal cardiovascular events (P<0.001) and thereby may have attenuated the number of cardiovascular and noncardiovascular deaths. A post hoc analysis found that, compared to patients with lower LDL-C, patients with baseline LDL-C ≥100 mg/dL (2.59 mmol/L) had a greater absolute risk of death and a larger mortality benefit from alirocumab (HR, 0.71; 95% CI, 0.56 to 0.90; Pinteraction=0.007). In the alirocumab group, all-cause death declined wit h achieved LDL-C at 4 months of treatment, to a level of approximately 30 mg/dL (adjusted P=0.017 for linear trend). Conclusions: Alirocumab added to intensive statin therapy has the potential to reduce death after acute coronary syndrome, particularly if treatment is maintained for ≥3 years, if baseline LDL-C is ≥100 mg/dL, or if achieved LDL-C is low. Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01663402
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