Does direction of results of abstracts submitted to scientific conferences on drug addiction predict full publication?

<p>Abstract</p> <p>Background</p> <p>Data from scientific literature show that about 63% of abstracts presented at biomedical conferences will be published in full. Some studies have indicated that full publication is associated with the direction of results (publication bias). No study has looked into the occurrence of publication bias in the field of addiction.</p> <p>Objectives</p> <p>To investigate whether the significance or direction of results of abstracts presented at the major international scientific conference on addiction is associated with full publication</p> <p>Methods</p> <p>The conference proceedings of the US Annual Meeting of the College on Problems of Drug Dependence (CPDD), were handsearched for abstracts of randomized controlled trials and controlled clinical trials that evaluated interventions for prevention, rehabilitation and treatment of drug addiction in humans (years searched 1993–2002). Data regarding the study designs and outcomes reported were extracted. Subsequent publication in peer reviewed journals was searched in MEDLINE and EMBASE databases, as of March 2006.</p> <p>Results</p> <p>Out of 5919 abstracts presented, 581 met the inclusion criteria; 359 (62%) conference abstracts had been published in a broad variety of peer reviewed journals (average time of publication 2.6 years, SD +/- 1.78). The proportion of published studies was almost the same for randomized controlled trials (62.4%) and controlled clinical trials (59.5%) while studies that reported positive results were significantly more likely to be published (74.5%) than those that did not report statistical results (60.9%.), negative or null results (47.1%) and no results (38.6%), Abstracts reporting positive results had a significantly higher probability of being published in full, while abstracts reporting null or negative results were half as likely to be published compared with positive ones (HR = 0.48; 95%CI 0.30–0.74)</p> <p>Conclusion</p> <p>Clinical trials were the minority of abstracts presented at the CPDD; we found evidence of possible publication bias in the field of addiction, with negative or null results having half the likelihood of being published than positive ones.</p

Carrion Availability in Space and Time

Introduction Availability of carrion to scavengers is a central issue in carrion ecology and management, and is crucial for understanding the evolution of scavenging behaviour. Compared to live animals, their carcasses are relatively unpredictable in space and time in natural conditions, with a few exceptions (see below, especially Sect. “Carrion Exchange at the Terrestrial-Aquatic Interface”). Carrion is also an ephemeral food resource due to the action of a plethora of consumers, from microorganisms to large vertebrates, as well as to desiccation (i.e., loss of water content; DeVault et al. 2003; Beasley et al. 2012; Barton et al. 2013; Moleón et al. 2014). With a focus on vertebrate carcasses, here we give an overview of (a) the causes that produce carrion, (b) the rate of carrion production, (c) the factors affecting carrion quality, and (d) the distribution of carrion in space and time, both in terrestrial and aquatic environments (including their interface). In this chapter, we will focus on naturally produced carrion, whereas non-natural causes of animal mortality are described in chapter “Human-Mediated Carrion: Effects on Ecological Processes”. However, throughout this chapter we also refer to extensive livestock carrion, because in the absence of strong restrictions such as those imposed in the European Community after the bovine spongiform encephalopathy crisis (Donázar et al. 2009; Margalida et al. 2010), the spatiotemporal availability of carrion of extensive livestock and wild ungulates is similar

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

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

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