The Hunting of the SNaRC: A Snarky Solution to the Species Problem

We argue that the logical outcome of the cladistics revolution in biological systematics, and the move towards rankless phylogenetic classification of nested monophyletic groups as formalized in the PhyloCode, is to eliminate the species rank along with all the others and simply name clades. We propose that the lowest level of formally named clade be the SNaRC, the Smallest Named and Registered Clade. The SNaRC is an epistemic level in the classification, not an ontic one. Naming stops at that level because there is no currently acceptable evidence for clades within it, not because no smaller clades exist. Later, included clades may be named. They would then become the SNaRCs, while the original SNaRC would keep its original name. We argue that all theoretical tasks of biology, in evolution and ecology, as well as practical tasks such as conservation assessment, are better approached using this rankless phylogenetic approach

Gods Above: Naturalizing Religion in Terms of our Shared Ape Social Dominance Behavior

To naturalize religion, we must identify what religion is, and what aspects of it we are trying to explain. In this paper, religious social institutional behavior is the explanatory target, and an explanatory hypothesis based on shared primate social dominance psychology is given. The argument is that various religious features, including the high status afforded the religious, and the high status afforded to deities, are an expression of this social dominance psychology in a context for which it did not evolve: high-density populations made possible by agricultur

Što je u memu? Razmatranja iz perspektive povijesti i filozofije evolucijske biologije

Prevela: Petra Rodi

Genetic monogamy and biparental care in an externally fertilizing fish, the largemouth bass (Micropterus salmoides)

Breeding, male North American sunfish (Centrarchidae), are often brightly coloured and promiscuous. However, the largemouth bass (Micropterus salmoides) is sexually monomorphic in appearance and socially monogamous. Unlike some other nest-tending centrarchids in the genus Lepomis, largemouth bass have also been reported to provide biparental care to eggs and fry. Here we use microsatellite markers in order to test whether social monogamy predicts genetic monogamy in the largemouth bass. Offspring were collected from 26 nests each usually guarded by a pair of adults, many of which were also captured. Twenty-three of these progeny cohorts (88%) proved to be composed almost exclusively of full-sibs and were thus the product of monogamous matings. Cuckoldry by males was rare. The genetic data also revealed that some nests contain juveniles that were not the progeny of the guardian female, a finding that can be thought of as low-level 'female cuckoldry'. Overall, however, the data provide what may be the first genetic documentation of near-monogamy and biparental care in a vertebrate with external fertilization

PCSK9 monoclonal antibodies for the primary and secondary prevention of cardiovascular disease.

BACKGROUND: Despite the availability of effective drug therapies that reduce low-density lipoprotein (LDL)-cholesterol (LDL-C), cardiovascular disease (CVD) remains an important cause of mortality and morbidity. Therefore, additional LDL-C reduction may be warranted, especially for patients who are unresponsive to, or unable to take, existing LDL-C-reducing therapies. By inhibiting the proprotein convertase subtilisin/kexin type 9 (PCSK9) enzyme, monoclonal antibodies (PCSK9 inhibitors) may further reduce LDL-C, potentially reducing CVD risk as well. OBJECTIVES: Primary To quantify short-term (24 weeks), medium-term (one year), and long-term (five years) effects of PCSK9 inhibitors on lipid parameters and on the incidence of CVD. Secondary To quantify the safety of PCSK9 inhibitors, with specific focus on the incidence of type 2 diabetes, cognitive function, and cancer. Additionally, to determine if specific patient subgroups were more or less likely to benefit from the use of PCSK9 inhibitors. SEARCH METHODS: We identified studies by systematically searching the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, Embase, and Web of Science. We also searched Clinicaltrials.gov and the International Clinical Trials Registry Platform and screened the reference lists of included studies. We identified the studies included in this review through electronic literature searches conducted up to May 2016, and added three large trials published in March 2017. SELECTION CRITERIA: All parallel-group and factorial randomised controlled trials (RCTs) with a follow-up time of at least 24 weeks were eligible. DATA COLLECTION AND ANALYSIS: Two review authors independently reviewed and extracted data. When data were available, we calculated pooled effect estimates. MAIN RESULTS: We included 20 studies with data on 67,237 participants (median age 61 years; range 52 to 64 years). Twelve trials randomised participants to alirocumab, three trials to bococizumab, one to RG7652, and four to evolocumab. Owing to the small number of trials using agents other than alirocumab, we did not differentiate between types of PCSK9 inhibitors used. We compared PCSK9 inhibitors with placebo (thirteen RCTs), ezetimibe (two RCTs) or ezetimibe and statins (five RCTs).Compared with placebo, PCSK9 inhibitors decreased LDL-C by 53.86% (95% confidence interval (CI) 58.64 to 49.08; eight studies; 4782 participants; GRADE: moderate) at 24 weeks; compared with ezetimibe, PCSK9 inhibitors decreased LDL-C by 30.20% (95% CI 34.18 to 26.23; two studies; 823 participants; GRADE: moderate), and compared with ezetimibe and statins, PCSK9 inhibitors decreased LDL-C by 39.20% (95% CI 56.15 to 22.26; five studies; 5376 participants; GRADE: moderate).Compared with placebo, PCSK9 inhibitors decreased the risk of CVD events, with a risk difference (RD) of 0.91% (odds ratio (OR) of 0.86, 95% CI 0.80 to 0.92; eight studies; 59,294 participants; GRADE: moderate). Compared with ezetimibe and statins, PCSK9 inhibitors appeared to have a stronger protective effect on CVD risk, although with considerable uncertainty (RD 1.06%, OR 0.45, 95% CI 0.27 to 0.75; three studies; 4770 participants; GRADE: very low). No data were available for the ezetimibe only comparison. Compared with placebo, PCSK9 probably had little or no effect on mortality (RD 0.03%, OR 1.02, 95% CI 0.91 to 1.14; 12 studies; 60,684 participants; GRADE: moderate). Compared with placebo, PCSK9 inhibitors increased the risk of any adverse events (RD 1.54%, OR 1.08, 95% CI 1.04 to 1.12; 13 studies; 54,204 participants; GRADE: low). Similar effects were observed for the comparison of ezetimibe and statins: RD 3.70%, OR 1.18, 95% CI 1.05 to 1.34; four studies; 5376 participants; GRADE: low. Clinical event data were unavailable for the ezetimibe only comparison. AUTHORS' CONCLUSIONS: Over short-term to medium-term follow-up, PCSK9 inhibitors reduced LDL-C. Studies with medium-term follow-up time (longest median follow-up recorded was 26 months) reported that PCSK9 inhibitors (compared with placebo) decreased CVD risk but may have increased the risk of any adverse events (driven by SPIRE-1 and -2 trials). Available evidence suggests that PCSK9 inhibitor use probably leads to little or no difference in mortality. Evidence on relative efficacy and safety when PCSK9 inhibitors were compared with active treatments was of low to very low quality (GRADE); follow-up times were short and events were few. Large trials with longer follow-up are needed to evaluate PCSK9 inhibitors versus active treatments as well as placebo. Owing to the predominant inclusion of high-risk patients in these studies, applicability of results to primary prevention is limited. Finally, estimated risk differences indicate that PCSK9 inhibitors only modestly change absolute risks (often to less than 1%)