Is The Amphibian Tree of Life really fatally flawed?

Wiens (2007 , Q. Rev. Biol. 82, 55–56) recently published a severe critique of Frost et al.'s (2006, Bull. Am. Mus. Nat. Hist. 297, 1–370) monographic study of amphibian systematics, concluding that it is “a disaster” and recommending that readers “simply ignore this study”. Beyond the hyperbole, Wiens raised four general objections that he regarded as “fatal flaws”: (1) the sampling design was insufficient for the generic changes made and taxonomic changes were made without including all type species; (2) the nuclear gene most commonly used in amphibian phylogenetics, RAG-1, was not included, nor were the morphological characters that had justified the older taxonomy; (3) the analytical method employed is questionable because equally weighted parsimony “assumes that all characters are evolving at equal rates”; and (4) the results were at times “clearly erroneous”, as evidenced by the inferred non-monophyly of marsupial frogs. In this paper we respond to these criticisms. In brief: (1) the study of Frost et al. did not exist in a vacuum and we discussed our evidence and evidence previously obtained by others that documented the non-monophyletic taxa that we corrected. Beyond that, we agree that all type species should ideally be included, but inclusion of all potentially relevant type species is not feasible in a study of the magnitude of Frost et al. and we contend that this should not prevent progress in the formulation of phylogenetic hypotheses or their application outside of systematics. (2) Rhodopsin, a gene included by Frost et al. is the nuclear gene that is most commonly used in amphibian systematics, not RAG-1. Regardless, ignoring a study because of the absence of a single locus strikes us as unsound practice. With respect to previously hypothesized morphological synapomorphies, Frost et al. provided a lengthy review of the published evidence for all groups, and this was used to inform taxonomic decisions. We noted that confirming and reconciling all morphological transformation series published among previous studies needed to be done, and we included evidence from the only published data set at that time to explicitly code morphological characters (including a number of traditionally applied synapomorphies from adult morphology) across the bulk of the diversity of amphibians (Haas, 2003, Cladistics 19, 23–90). Moreover, the phylogenetic results of the Frost et al. study were largely consistent with previous morphological and molecular studies and where they differed, this was discussed with reference to the weight of evidence. (3) The claim that equally weighted parsimony assumes that all characters are evolving at equal rates has been shown to be false in both analytical and simulation studies. (4) The claimed “strong support” for marsupial frog monophyly is questionable. Several studies have also found marsupial frogs to be non-monophyletic. Wiens et al. (2005, Syst. Biol. 54, 719–748) recovered marsupial frogs as monophyletic, but that result was strongly supported only by Bayesian clade confidence values (which are known to overestimate support) and bootstrap support in his parsimony analysis was < 50%. Further, in a more recent parsimony analysis of an expanded data set that included RAG-1 and the three traditional morphological synapomorphies of marsupial frogs, Wiens et al. (2006, Am. Nat. 168, 579–596) also found them to be non-monophyletic. Although we attempted to apply the rule of monophyly to the naming of taxonomic groups, our phylogenetic results are largely consistent with conventional views even if not with the taxonomy current at the time of our writing. Most of our taxonomic changes addressed examples of non-monophyly that had previously been known or suspected (e.g., the non-monophyly of traditional Hyperoliidae, Microhylidae, Hemiphractinae, Leptodactylidae, Phrynobatrachus , Ranidae, Rana , Bufo ; and the placement of Brachycephalus within “ Eleutherodactylus ”, and Lineatriton within “ Pseudoeurycea ”), and it is troubling that Wiens and others, as evidenced by recent publications, continue to perpetuate recognition of non-monophyletic taxonomic groups that so profoundly misrepresent what is known about amphibian phylogeny. © The Willi Hennig Society 2007.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74688/1/j.1096-0031.2007.00181.x.pd

Time-integrated luminosity recorded by the BABAR detector at the PEP-II e+e- collider

This article is the Preprint version of the final published artcile which can be accessed at the link below.We describe a measurement of the time-integrated luminosity of the data collected by the BABAR experiment at the PEP-II asymmetric-energy e+e- collider at the ϒ(4S), ϒ(3S), and ϒ(2S) resonances and in a continuum region below each resonance. We measure the time-integrated luminosity by counting e+e-→e+e- and (for the ϒ(4S) only) e+e-→μ+μ- candidate events, allowing additional photons in the final state. We use data-corrected simulation to determine the cross-sections and reconstruction efficiencies for these processes, as well as the major backgrounds. Due to the large cross-sections of e+e-→e+e- and e+e-→μ+μ-, the statistical uncertainties of the measurement are substantially smaller than the systematic uncertainties. The dominant systematic uncertainties are due to observed differences between data and simulation, as well as uncertainties on the cross-sections. For data collected on the ϒ(3S) and ϒ(2S) resonances, an additional uncertainty arises due to ϒ→e+e-X background. For data collected off the ϒ resonances, we estimate an additional uncertainty due to time dependent efficiency variations, which can affect the short off-resonance runs. The relative uncertainties on the luminosities of the on-resonance (off-resonance) samples are 0.43% (0.43%) for the ϒ(4S), 0.58% (0.72%) for the ϒ(3S), and 0.68% (0.88%) for the ϒ(2S).This work is supported by the US Department of Energy and National Science Foundation, the Natural Sciences and Engineering Research Council (Canada), the Commissariat à l’Energie Atomique and Institut National de Physique Nucléaire et de Physiquedes Particules (France), the Bundesministerium für Bildung und Forschung and Deutsche Forschungsgemeinschaft (Germany), the Istituto Nazionale di Fisica Nucleare (Italy), the Foundation for Fundamental Research on Matter (The Netherlands), the Research Council of Norway, the Ministry of Education and Science of the Russian Federation, Ministerio de Ciencia e Innovación (Spain), and the Science and Technology Facilities Council (United Kingdom). Individuals have received support from the Marie-Curie IEF program (European Union) and the A.P. Sloan Foundation (USA)

Determination of the Form Factors for the Decay B0 --> D*-l+nu_l and of the CKM Matrix Element |Vcb|

We present a combined measurement of the Cabibbo-Kobayashi-Maskawa matrix element $|V_{cb}|$ and of the parameters $\rho^2$, $R_1$, and $R_2$, which fully characterize the form factors of the $B^0 \to D^{*-}\ell^{+}\nu_\ell$ decay in the framework of HQET, based on a sample of about 52,800 $B^0 \to D^{*-}\ell^{+}\nu_\ell$ decays recorded by the BABAR detector. The kinematical information of the fully reconstructed decay is used to extract the following values for the parameters (where the first errors are statistical and the second systematic): $\rho^2 = 1.156 \pm 0.094 \pm 0.028$, $R_1 = 1.329 \pm 0.131 \pm 0.044$, $R_2 = 0.859 \pm 0.077 \pm 0.022$, $\mathcal{F}(1)|V_{cb}| = (35.03 \pm 0.39 \pm 1.15) \times 10^{-3}$. By combining these measurements with the previous BABAR measurements of the form factors which employs a different technique on a partial sample of the data, we improve the statistical accuracy of the measurement, obtaining: $\rho^2 = 1.179 \pm 0.048 \pm 0.028, R_1 = 1.417 \pm 0.061 \pm 0.044, R_2 = 0.836 \pm 0.037 \pm 0.022,$ and $\mathcal{F}(1)|V_{cb}| = (34.68 \pm 0.32 \pm 1.15) \times 10^{-3}.$ Using the lattice calculations for the axial form factor $\mathcal{F}(1)$, we extract $|V_{cb}| =(37.74 \pm 0.35 \pm 1.25 \pm ^{1.23}_{1.44}) \times 10^{-3}$, where the third error is due to the uncertainty in $\mathcal{F}(1)$

Study of the Exclusive Initial-State Radiation Production of the DDˉD \bar D System

A study of exclusive production of the $D \bar D$ system through initial-state r adiation is performed in a search for charmonium states, where $D=D^0$ or $D^+$. The $D^0$ mesons are reconstructed in the $D^0 \to K^- \pi^+$, $D^0 \to K^- \pi^+ \pi^0$, and $D^0 \to K^- \pi^+ \pi^+ \pi^-$ decay modes. The $D^+$ is reconstructed through the $D^+ \to K^- \pi^+ \pi^+$ decay mode. The analysis makes use of an integrated luminosity of 288.5 fb$^{-1}$ collected by the BaBar experiment. The $D \bar D$ mass spectrum shows a clear $\psi(3770)$ signal. Further structures appear in the 3.9 and 4.1 GeV/$c^2$ regions. No evidence is found for Y(4260) decays to $D \bar D$, implying an up per limit \frac{\BR(Y(4260)\to D \bar D)}{\BR(Y(4260)\to J/\psi \pi^+ \pi^-)} < 7.6 (95 % confidence level)

Mineral deficiency and the presence of Pinus sylvestris on mires during the mid- to late Holocene: Palaeoecological data from Cadogan's Bog, Mizen Peninsula, Co. Cork, southwest Ireland

Pollen records across parts of Ireland, England and northern Scotland show a dramatic collapse in Pinus pollen percentages at approximately 4000 radiocarbon years BP. This phenomenon has attracted much palaeoecological interest and several hypotheses have been put forward to account for this often synchronous and rapid reduction in pine from mid-Holocene woodland. Explanations for the 'pine decline' include prehistoric human activity, climatic change, in particular a substantial increase in precipitation resulting in increased mire wetness, and airborne pollution associated with the deposition of tephra. Hitherto, one largely untested hypothesis is that mineral deficiency could adversely affect pine growth and regeneration on mire surfaces. The discovery of pine-tree remains (wood pieces, stumps and trunks) within a peat located at Cadogan's Bog on the Mizen Peninsula, southwest Ireland, provided an opportunity to investigate the history of Pinus sylvestris and also to assess the importance of mineral nutrition in maintaining pine growth on mires. Pollen, plant macrofossils, microscopic charcoal and geochemical data are presented from a radiocarbon dated monolith extracted from this peat together with tree ring-width data and radiocarbon dated age estimates from subfossil wood. Analyses of these data suggest that peat accumulation commenced at the site around 6000 years BP when pine was the dominant local tree. Thereafter Pinus pollen percentages diminish in two stages, with the second decline taking place around 4160 ± 50 years BP. Concomitant with this decline in Pinus pollen, there is a noticeable, short-lived increase in wet-loving mire taxa and a decrease in the concentration of phosphorus, potassium, magnesium, calcium, sodium, iron and zinc. These results suggest that increased mire surface wetness, possibly the result of a change in climate, created conditions unsuitable for pine growth c. 4000 years BP. Mire surface wetness, coupled with a period of associated nutrient deficiency, appears to be a possible explanation for a lack of subsequent pine-seedling establishment for most of the later Holocene

EuFe2_2As2_2 under high pressure: an antiferromagnetic bulk superconductor

We report the ac magnetic susceptibility $\chi_{ac}$ and resistivity $\rho$ measurements of EuFe$_2$As$_2$ under high pressure $P$. By observing nearly 100% superconducting shielding and zero resistivity at $P$ = 28 kbar, we establish that $P$-induced superconductivity occurs at $T_c \sim$~30 K in EuFe$_2$As$_2$. $\rho$ shows an anomalous nearly linear temperature dependence from room temperature down to $T_c$ at the same $P$. $\chi_{ac}$ indicates that an antiferromagnetic order of Eu$^{2+}$ moments with $T_N \sim$~20 K persists in the superconducting phase. The temperature dependence of the upper critical field is also determined.Comment: To appear in J. Phys. Soc. Jpn., Vol. 78 No.

Search for decays of B-0 -> e(+)e(-), B-0 -> mu(+)mu(-), B-0 -> e(+/-)mu(-/+)

We present a search for the decays B-0 -> e(+)e(-), B-0 ->mu(+)mu(-), and B-0 -> e(+/-)mu(-/+) in data collected at the Upsilon(4S) resonance with the BABAR detector at the SLAC B Factory. Using a data set of 111 fb(-1), we find no evidence for a signal in any of the three channels investigated and set the following branching fraction upper limits at the 90% confidence level: B(B-0 -> e(+)e(-))mu(+)mu(-)) e(+/-)mu(-/+))< 18x10(-8)

Measurements of Branching Fractions, Polarizations, and Direct CP-Violation Asymmetries in B→ρK∗ and B→f0(980)K∗ Decays

We report searches for B -meson decays to the charmless final states ρ K ∗ and f 0 ( 980 ) K ∗ with a sample of 232 × 10 6 B ¯¯¯ B pairs collected with the BABAR detector at the PEP-II e + e − collider. We measure in units of 10 − 6 the following branching fractions, where the first error quoted is statistical and the second systematic, or upper limits are given at the 90% confidence level : B ( B + → ρ 0 K * + ) < 6.1 , B ( B + → ρ + K * 0 ) = 9.6 ± 1.7 ± 1.5 , B ( B 0 → ρ − K * + ) < 12.0 , B ( B 0 → ρ 0 K * 0 ) = 5.6 ± 0.9 ± 1.3 , B ( B + → f 0 ( 980 ) K * + ) = 5.2 ± 1.2 ± 0.5 , and B ( B 0 → f 0 ( 980 ) K * 0 ) < 4.3 . For the significant modes, we also measure the fraction of longitudinal polarization and the charge asymmetry: f L ( B + → ρ + K * 0 ) = 0.52 ± 0.10 ± 0.04 , f L ( B 0 → ρ 0 K * 0 ) = 0.57 ± 0.09 ± 0.08 , A C P ( B + → ρ + K * 0 ) = − 0.01 ± 0.16 ± 0.02 , A C P ( B 0 → ρ 0 K * 0 ) = 0.09 ± 0.19 ± 0.02 , and A C P ( B + → f 0 ( 980 ) K * + ) = − 0.34 ± 0.21 ± 0.03

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Funding Information: GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska Läkaresällskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file : Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services. Publisher Copyright: © 2022, The Author(s).Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.Peer reviewe