Citações? Seus problemas acabaram: I4OC

Initiative for Open Citations

The Initiative for Open Citations I4OC is a collaboration between scholarly publishers, researchers, and other interested parties to promote the unrestricted availability of scholarly citation data.

About

Citations are the links that knit together our scientific and cultural knowledge. They are primary data that provide both provenance and an explanation for how we know facts. They allow us to attribute and credit scientific contributions, and they enable the evaluation of research and its impacts. In sum, citations are the most important vehicle for the discovery, dissemination, and evaluation of all scholarly knowledge.

As the number of scholarly publications is estimated to double every nine years, citations – and the computational systems that track them – enable researchers and the public to keep abreast of significant developments in any given field. For this to be possible, it is essential to have unrestricted access to bibliographic and citation data in machine-readable form.

The present scholarly communication system inadequately exposes the knowledge networks that already exist within our literature. Citation data are not usually freely available to access, they are often subject to inconsistent, hard-to-parse licenses, and they are usually not machine-readable.

An initiative to open up citation data

The aim of this initiative is to promote the availability of data on citations that are structured, separable, and open.

Structured means the data representing each publication and each citation instance are expressed in common, machine-readable formats, and that these data can be accessed programmatically. Separable means the citation instances can be accessed and analyzed without the need to access the source bibliographic products (such as journal articles and books) in which the citations are created. Open means the data are freely accessible and reusable.

Key benefits of achieving this aim include:

The establishment of a global public web of linked scholarly citation data to enhance the discoverability of published content, both subscription access and open access. This will particularly benefit individuals who are not members of academic institutions with subscriptions to commercial citation databases.

The ability to build new services over the open citation data, for the benefit of publishers, researchers, funding agencies, academic institutions and the general public, as well as enhancing existing services.

The creation of a public citation graph to explore connections between knowledge fields, and to follow the evolution of ideas and scholarly disciplines.

Reference distribution

Many publishers currently deposit reference lists from their journal articles to Crossref as part of their participation in Crossref’s Cited-by service. To open their references, along with the other bibliographic metadata that publishers send to Crossref, publishers need to turn on reference distribution for all of the Digital Object Identifier (DOI) prefixes they manage. This step allows references within the Crossref members’ articles to be distributed without restriction through all of Crossref's Metadata Delivery services, including the REST API and bulk metadata dumps, to any interested party. See below for additional information on reference distribution and on how to participate in Crossref’s Cited-by service.

Participating publishers

Before I4OC started, publishers releasing references in the open accounted for just 1% of citation metadata collected annually by Crossref. Following discussions over the past months, several subscription-access and open-access publishers have recently made the decision to release reference list metadata publicly. These include: American Geophysical Union, Association for Computing Machinery, BMJ, Cambridge University Press, Cold Spring Harbor Laboratory Press, EMBO Press, Royal Society of Chemistry, SAGE Publishing, Springer Nature, Taylor & Francis, and Wiley. These publishers join other publishers who have been opening their references through Crossref for some time.

The following list includes the names of all the publishers who have chosen to deposit and open up citation data as of March 30, 2017. I4OC will keep this list updated.

American Geophysical Union

Association for Computing Machinery

BMJ

Cambridge University Press

Co-Action Publishing

Cold Spring Harbor Laboratory Press

Copernicus GmbH

eLife

EMBO Press

Faculty of 1000, Ltd.

Frontiers Media SA

Geological Society of London

Hamad bin Khalifa University Press (HBKU Press)

Hindawi

International Union of Crystallography

Leibniz Institute for Psychology Information

MIT Press

PeerJ

Pensoft Publishers

Portland Press

Public Library of Science

Royal Society of Chemistry

SAGE Publishing

Springer Nature

Taylor & Francis Group

The Rockefeller University Press

The Royal Society

Ubiquity Press, Ltd.

Wiley

80% de contaminação de sequenciamento de amostras cruzadas!

Patterns of cross-contamination in a multispecies population genomic project: detection, quantification, impact, and solutions

Marion Ballenghien, Nicolas Faivre and Nicolas Galtier Email author

BMC Biology201715:25

DOI: 10.1186/s12915-017-0366-6 © Galtier et al. 2017 

 

Received: 6 December 2016 Accepted: 13 March 2017 Published: 29 March 2017

Source/Fonte: Sauri Nash - Flickr

Abstract

Background

Contamination is a well-known but often neglected problem in molecular biology. Here, we investigated the prevalence of cross-contamination among 446 samples from 116 distinct species of animals, which were processed in the same laboratory and subjected to subcontracted transcriptome sequencing.

Results

Using cytochrome oxidase 1 as a barcode, we identified a minimum of 782 events of between-species contamination, with approximately 80% of our samples being affected. An analysis of laboratory metadata revealed a strong effect of the sequencing center: nearly all the detected events of between-species contamination involved species that were sent the same day to the same company. We introduce new methods to address the amount of within-species, between-individual contamination, and to correct for this problem when calling genotypes from base read counts.

Conclusions

We report evidence for pervasive within-species contamination in this data set, and show that classical population genomic statistics, such as synonymous diversity, the ratio of non-synonymous to synonymous diversity, inbreeding coefficient FIT, and Tajima’s D, are sensitive to this problem to various extents. Control analyses suggest that our published results are probably robust to the problem of contamination. Recommendations on how to prevent or avoid contamination in large-scale population genomics/molecular ecology are provided based on this analysis.

Keywords RNAseq Transcriptome Animals SNP calling Genotyping Within-species

FREE PDF GRATIS: BMC Biology

O enigma da informação genética: a Academia não tem como responder via teoria da evolução de Darwin!!!

Ebook grátis: Molecular Mechanisms and Physiological Significance of Organelle Interactions and Cooperation

Molecular Mechanisms and Physiological Significance of Organelle Interactions and Cooperation

Edited by: Michael Schrader, Markus Islinger

Publisher: Frontiers Media SA

ISBN: 9782889451043

Product Name: Frontiers Research Topic Ebook

Source/Fonte: Front. Cell Dev. Biol.

Eukaryotic cells contain distinct membrane-bound organelles, which compartmentalise cellular proteins to fulfil a variety of vital functions. Many organelles have long been regarded as isolated and static entities (e.g., peroxisomes, mitochondria, lipid droplets), but it is now evident that they display dynamic changes, interact with each other, share certain proteins and show metabolic cooperation and cross-talk. Despite great advances in the identification and characterisation of essential components and molecular mechanisms associated with the biogenesis and function of organelles, information on how organelles interact and are incorporated into metabolic pathways and signaling networks is just beginning to emerge. Organelle cooperation requires sophisticated targeting systems which regulate the proper distribution of shared proteins to more than one organelle. Organelle motility and membrane remodeling support organelle interaction and contact. This contact can be mediated by membrane proteins residing on different organelles which can serve as molecular tethers to physically link different organelles together. They can also contribute to the exchange of metabolites and ions, or act in the assembly of signaling platforms. In this regard organelle communication events have been associated with important cellular functions such as apoptosis, antiviral defense, organelle division/biogenesis, ROS metabolism and signaling, and various metabolic pathways such as breakdown of fatty acids or cholesterol biosynthesis. 

In this research topic we will focus on recent novel findings on the underlying molecular mechanisms and physiological significance of organelle interaction and cooperation with a particular focus on mitochondria, peroxisomes, endoplasmic reticulum, lysosomes and lipid droplets and their impact on the regulation of cellular homeostasis. Our understanding of how organelles physically interact and use cellular signaling systems to coordinate functional networks between each other is still in its infancy. Nevertheless recent discoveries of defined membrane structures such as the mitochondria-ER associated membranes (MAM) are revealing how membrane domains enriched in specific proteins transmit signals across organelle boundaries, allowing one organelle to influence the function of another. In addition to its role as a mediator between mitochondria and the ER, contacts between the MAM and peroxisomes contribute to antiviral signaling, and specialised regions of the ER are supposed to initiate peroxisome biogenesis, whereas intimate contacts between peroxisomes, lipid droplets and the ER mediate lipid metabolism. In line with these observations it is tempting to speculate that further physical contact sites between other organelles exist. Alternatively, novel regulated vesicle trafficking pathways between organelles (e.g., mitochondria to peroxisomes or lysosomes) have been discovered implying another mode of organelle communication. Identifying the key molecular players of such specialised membrane structures will be a prerequisite to understand how organelle communication is physically accomplished and will lead to the identification of new regulatory networks. In addition to the direct transmission of interorganellar information, cytosolic messenger systems (e.g., kinase/phosphatase systems or redox signaling) may contribute to the coordination of organelle functions. This research topic will integrate new findings from both modes of communication and will provide new perspectives for the functional significance of cross-talk among organelles. 

We would like to thank all the researchers who contributed their valuable work to this research topic. Furthermore, we are grateful to the reviewers and Associate Editors who contributed valuable comments and positive criticism to improve the contributions.

Science > Cell and Developmental Biology > Mitochondrial Research

Science > Physiology > Mitochondrial Research

Keywords: membrane contact sites, organelle dynamics, Peroxisomes, Mitochondria, Endoplasmic Reticulum, Intracellular signaling, Organelle communication, lipid droplet

FREE EBOOK GRATIS: Frontiers 21.7 MBs

Pesquisas CRISPR tornam confusos os resultados de pesquisas genéticas mais antigas

CRISPR/Cas9 mutagenesis invalidates a putative cancer dependency targeted in on-going clinical trials

Ann Lin Christopher J Giuliano Nicole M Sayles Jason M Sheltzer 

Cold Spring Harbor Laboratory, United States; Stony Brook University, United States

DOI: http://dx.doi.org/10.7554/eLife.24179  

Published March 24, 2017 

Cite as eLife 2017;6:e24179

Source/Fonte: Advanced Analytical

Abstract

The Maternal Embryonic Leucine Zipper Kinase (MELK) has been reported to be a genetic dependency in several cancer types. MELK RNAi and small-molecule inhibitors of MELK block the proliferation of various cancer cell lines, and MELK knockdown has been described as particularly effective against the highly-aggressive basal/triple-negative subtype of breast cancer. Based on these preclinical results, the MELK inhibitor OTS167 is currently being tested as a novel chemotherapy agent in several clinical trials. Here, we report that mutagenizing MELK with CRISPR/Cas9 has no effect on the fitness of basal breast cancer cell lines or cell lines from six other cancer types. Cells that harbor null mutations in MELK exhibit wild-type doubling times, cytokinesis, and anchorage-independent growth. Furthermore, MELK-knockout lines remain sensitive to OTS167, suggesting that this drug blocks cell division through an off-target mechanism. In total, our results undermine the rationale for a series of current clinical trials and provide an experimental approach for the use of CRISPR/Cas9 in preclinical target validation that can be broadly applied.

DOI: http://dx.doi.org/10.7554/eLife.24179.001

eLife digest

Like a person who is dependent on coffee to be productive, cancer cells are dependent on the products of certain genes in order to dominate their environment and grow. Cancer cells will stop growing and die when the activity of these gene products is blocked. These genes are known as cancer dependencies or “addictions”. As a result, researchers are constantly looking for cancer dependencies and developing drugs to block their activity.

It was previously believed that a gene called MELK was an addiction in certain types of breast cancer. In fact, pharmaceutical companies had developed a drug to block the activity of MELK, and this drug is currently being tested in human patients. However, Lin, Giuliano et al. have now taken a second look at the role of MELK in breast cancer, and have come to a different conclusion.

Using a gene editing technology called CRISPR/Cas9, Lin, Giuliano et al. removed MELK activity from several cancer cell lines. This did not stop cancer cells from multiplying, suggesting that MELK is not actually a cancer addiction.

Additionally, when breast cancer cells that do not produce MELK were exposed to the drug that is supposed to block MELK activity, the drug still stopped cell growth. Since the drug works when MELK is not present in the cell, the drug must be binding to other proteins. This suggests that MELK is not the actual target of the drug.

Lin, Giuliano et al. suggest that, in the future, CRISPR/Cas9 technology could be used to better identify cancer dependencies and drug targets before cancer drugs are given to human patients.

DOI: http://dx.doi.org/10.7554/eLife.24179.002

FREE PDF GRATIS: eLIFE

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See article/Vide artigo: 

CRISPR studies muddy results of older gene research

Scientists face tough decisions when the latest gene-editing findings don’t match up with the results of other techniques.

Heidi Ledford

05 April 2017 Nature

Análise genômica de 63.220 tumores cancerígenos indica a inviabilidade de uma vacina universal contra o câncer.

Genomic analysis of 63,220 tumors reveals insights into tumor uniqueness and targeted cancer immunotherapy strategies

Ryan J. Hartmaier Email author, Jehad Charo, David Fabrizio, Michael E. Goldberg, Lee A. Albacker, William Pao and Juliann Chmielecki

Genome Medicine20179:16

DOI: 10.1186/s13073-017-0408-2 © The Author(s). 2017 

Received: 2 July 2016Accepted: 25 January 2017Published: 24 February 2017

Imagem © Wikimedia Commons/Dr. Cecil Fox

Abstract

Background

The integration of genomics with immunotherapy has potential value for cancer vaccine development. Given the clinical successes of immune checkpoint modulators, interest in cancer vaccines as therapeutic options has been revived. Current data suggest that each tumor contains a unique set of mutations (mutanome), thus requiring the creation of individualized cancer vaccines. However, rigorous analysis of non-individualized cancer immunotherapy approaches across multiple cancer types and in the context of known driver alterations has yet to be reported. We therefore set out to determine the feasibility of a generalizable cancer vaccine strategy based on targeting multiple neoantigens in an HLA-A/B subtype-directed manner.

Methods

A cancer gene-focused, hybrid capture-based genomic analysis was performed on 63,220 unique tumors. Neoantigens were predicted using a combined peptide processing and MHC-I binding prediction tool (IEDB) for all recurrent (>10 tumors) missense alterations and non-frameshift indels for the two most common HLA-A/B subtypes in North American/European populations.

Results

Despite being overwhelmingly unique overall, many mutanomes (~45%) contain at least one mutation from a set of ten mutations chosen to maximize the number of unique tumors. This held true for tumors driven by KRAS G12C (n = 1799), PIK3CA E545K (n = 1713), or EGFR L858R (n = 478) alterations, which define distinct sample subsets. We therefore hypothesized that sets of carefully selected mutations/neoantigens may allow the development of broadly applicable semi-universal cancer vaccines. To test the feasibility of such an approach, antigen processing and MHC-I binding prediction was applied for HLA subtypes A*01:01/B*08:01 and A*02:01/B*44:02. In tumors with a specific HLA type, 0.7 and 2.5% harbored at least one of a set of ten neoantigens predicted to bind to each subtype, respectively. In comparison, KRAS G12C-driven tumors produced similar results (0.8 and 2.6% for each HLA subtype, respectively), indicating that neoantigen targets still remain highly diverse even within the context of major driver mutations.

Conclusions

This “best case scenario” analysis of a large tumor set across multiple cancer types and in the context of driver alterations reveals that semi-universal, HLA-specific cancer vaccine strategies will be relevant to only a small subset of the general population. Similar analysis of whole exome/genome sequencing, although not currently feasible at scale in a clinical setting, will likely uncover further diversity.

Keywords: Neoantigens Cancer vaccines Genomic profiling Poly-epitope

Discovery Institute Brasil na Universidade Presbiteriana Mackenzie - São Paulo, SP

Núcleo de Pesquisa Mackenzie em Ciência, Fé e Sociedade – Discovery-Mackenzie

O Discovery-Mackenzie é um núcleo de pesquisa interdisciplinar da Universidade Presbiteriana Mackenzie que promove estudos científicos focados em complexidade e informação na busca de evidências que apontem para a ação de processos naturais ou design inteligente na natureza, explorando as implicações dessas descobertas para a relação entre ciência e sociedade, incluindo a fé. Para este fim, o Discovery-Mackenzie coordena ações que fomentem a pesquisa científica e sua divulgação, organiza encontros científicos e cursos de capacitação e produz materiais de divulgação científica e de cunho educacional, mantendo intercâmbio de conhecimento e pessoal com o Discovery Institute – USA e outros centros afiliados.

Evento de Inauguração

Press Release Discovery-Mackenzie 5-6 Maio 2017 | Inauguração do Discovery-Mackenzie

Na sexta a noite, 5 de Maio, as 18h, será inaugurada a sede do Discovery-Mackenzie, que acomodará uma biblioteca, sala de treinamento e workshops, e sala de leitura e escritórios. A inauguração da sede será seguida de uma cerimônia de inauguração (entrada franca para inscritos) iniciada as 19h30 no auditório da Escola Americana.

Nesses eventos, uma delegação de renomados nomes do DI-USA estará presente, entre eles o presidente do Discovery Institute-USA, Steven J. Buri e três de seus principais pesquisadores afiliados: Michel Behe, Douglas Axe e Brian Miller.

Michel Behe é famoso no mundo todo pelo seu Best Seller “A Caixa Preta de Darwin”, livro que lançou as teses do Design Inteligente moderno, mostrando ser a TDI referendada pela bioquímica moderna, catalisando assim uma ampla discussão sobre a viabilidade da Evolução Darwiniana. Douglas Axe se tornou hoje também um dos grandes defensores da TDI por intermédio de seu livro recentemente publicado, outro Best Seller intitulado “Undeniable: How Biology Confirms Our Intuition Life is Designed", sendo também diretor do "Biologic Institute”, um centro de pesquisas associado ao DI-USA. Em seu livro, Douglas Axe argumenta que o DI, à luz da Biologia moderna, é evidente e inquestionável, sendo ainda coincidente com a nossa intuição. Já Brian Miller é Ph.D em Física e dá palestras em todo o mundo sobre o DI e a suas implicações para a visão de mundo cristã.

Na cerimônia, que contará com a participação e palavras de várias autoridades e diretores da Universidade Presbiteriana Mackenzie, e da Sociedade Brasileira do Design Inteligente – TDI BRASIL, além de várias outras autoridades, serão apresentados os objetivos do Discovery-Mackenzie, suas metas e relevância no debate hoje reaquecido entre fé e ciência. Na noite de sexta, Michel Behe e Douglas Axe também proferirão palestras referentes ao tema fé e ciência.

No sábado, dia 6, um curso intensivo de treinamento em Design Inteligente será oferecido para convidados, e conjuntamente pelos pesquisadores do DI-USA e Discovery-Mackenzie, com o objetivo de treinar professores e palestrantes sobre os princípios gerais do Design Inteligente e sua viabilidade frente à evolução Darwiniana.

Convidados

Douglas Axe

É o autor do Livro Undeniable: How Biology Confirms Our Intuition Life is Designed e Diretor do "Biologic Institute", um centro de pesquisas patrocinado pelo Centro de Ciência e Cultura do Discovery Institute (DI-USA). Axe se formou doutor na Caltech e foi pós-doc e pesquisador na Inglaterra na Universidade de Cambridge, no Cambridge Medical Research Council Centre e no Instituto Babraham em Cambridge. Suas pesquisas se valem de experimentos e simulações computacionais para examinar os restrições funcionais e estruturais da Evolução de proteínas e sistemas proteicos.

Michael J. Behe

É Professor de Ciências Biológicas na Lehigh University, Pensilvânia - USA e um Membro Senior do DI-USA. Ele se formou doutor em Bioquímica pela Universidade da Pensilvânia. Seu livro "A Caixa Preta de Darwin: O Desafio Bioquímico para a Evolução" ajudou a inspirar o movimento moderno do Design Inteligente na Biologia e foi eleito pela National Review como um dos 100 mais importantes livros de não-ficção do século 20. Behe escreveu acerca de sua defesa do DI no The New York Times e tem dado palestras sobre DI ao redor do mundo em várias universidades.

Steven J. Buri

É o presidente do DI-USA, o elo intelectual do movimento moderno do Design Inteligente, sendo também um centro de pesquisas em áreas como a tecnologia, educação, bioética, e liberdade econômica. Buri foi também Diretor Executivo do Stewardship Partners, uma organização americana de livre mercado e fez parte também da equipe do senador americano Slade Gorton. Ele também foi prefeito da cidade de Newcastle perto de Seatle-USA. Em 2010, foi escolhido pelo American Council of Young Political Leaders para participar de uma delegação de políticos americanos ao Nepal.

Brian Miller

É coordenador de pesquisas do DI-USA. Ele tem doutorado em Física pela Duke University, e tem proferido palestras ao redor do mundo em universidades em tópicos como o DI e a visão de mundo cristã. Ele tem sido também consultor de igrejas, organizações e empresas em desenvolvimento estratégico e organizacional, e tem sido também consultor do Aslan Guild, um guia start-up para inventores, guia esse que se dedica a trazer inovação para o mercado de trabalho.

Programação

Local: Auditório da Escola Americana – Mackenzie São Paulo

Sexta 05 de Maio

18h - Inauguração do escritório Discovery-Mackenzie.

19h30 - Cerimônia de Abertura do Evento - Participação da Reitoria da UPM, Chancelaria, Presidência do IPM e Presidente do Discovery Institute – USA, Steven J. Buri, e demais autoridades convidadas.

20h15 - Apresentação do DI - Mackenzie. Planos e metas: Marcos N. Eberlin Presidente da TDI BRASIL.

20h30 - Palestra de Abertura 1- Michael Behe - "Celebrando os 20 anos da Complexidade Irredutível: O primeiro grande pilar da Teoria do Design Inteligente".

21h00 - Palestra de Abertura 2 - Douglas Axe - "Irrefutável: Como a bioquímica confirma a nossa intuição de que fomos planejados".

21h30 - Palavra de Encerramento.

Sábado 06 de Maio

9h – 17h - Curso para convidados sobre a Teoria do Design Inteligente:

O curso será ministrado pelos pioneiros e grandes nomes da TDI nos USA e no Brasil – entre eles Steven J. Buri (presidente do DI-USA), Michel Behe (autor do best-seller A Caixa preta de Darwin), Douglas Axe (autor do best-seller Undeniable) e Brian Miller (coordenador do Center for Science and Culture do DI-USA), Marcos N. Eberlin (presidente executivo da TDI-BRASIL) e Enézio Almeida Filho (presidente emérito da TDI-BRASIL). Terá como objetivo expor de forma correta e precisa os principais postulados da Teoria do Design Inteligente e assim treinar professores, palestrantes e líderes para se pronunciar, proferir palestras e aulas sobre a TDI.

Inscrever aqui

Núcleo de Pesquisa Mackenzie em Ciência, Fé e Sociedade

Auditório da Escola Americana – Mackenzie São Paulo

Rua da Consolação 930, São Paulo, SP 01302-907

Ceticismo sobre o ceticismo: a busca empenhada pela verdade e humildade

PHILOSOPHY

Skepticism About Skepticism

April 3, 20175:32 AM ET

Commentary

TANIA LOMBROZO

Getty Images - iStockphoto

Calling someone a "skeptic" can be a term of praise or condemnation.

Too often, it expresses approval when the target of skepticism is a claim we reject, and disapproval when the target is a claim we hold dear. I might praise skepticism towards homeopathic medicine, but disdain skepticism towards human evolution. Someone with a very different set of beliefs might praise skepticism regarding the moon landing, but disdain skepticism regarding the existence of God.

Sometimes, though, skepticism is taken to be a healthy attitude towards belief — a characteristic that we might praise regardless of its target. Skepticism is supposed to reflect a willingness to question and doubt — a key characteristic of scientific thinking. Skepticism encourages us to look at the evidence critically; it allows for the possibility that we are wrong. It seems like a win, then, to learn that courses in skepticism can decrease belief in the paranormal or — as reported in an article forthcoming in Science & Education — that teaching students to think critically about history can decrease belief in pseudoscience and other unwarranted claims.

But taken too far, skepticism misses its mark. It's important to avoid the error of believing something we ought not to believe, but it's also important to avoid the error of failing to believe that which we should. If the aim is to detect signal — and not merely to reject noise — then an educational win would require greater differentiation between warranted and unwarranted claims, not merely rejection of the unwarranted. This point is sometimes lost in praising skepticism and skeptical thinking, with its emphasis on what we reject rather than what we uphold.

It's important to say that this isn't intended as a criticism of the skeptical movement or of skeptical philosophy, both of which endorse more nuanced versions of what skepticism entails. It is, however, a criticism of the way skepticism (as used in casual conversation) is sometimes held up as a virtue in itself. The virtues we should really be upholding — and for which skepticism is only an oblique guide — are what I'll call truth-tracking and humility.

...

Read more here/Leia mais aqui: NPR

Um novo Tiranossauro com evidência para anagênese e sistema sensorial facial tipo crocodilo

A new tyrannosaur with evidence for anagenesis and crocodile-like facial sensory system

Thomas D. Carr, David J. Varricchio, Jayc C. Sedlmayr, Eric M. Roberts & Jason R. Moore

Scientific Reports 7, Article number: 44942 (2017)

doi:10.1038/srep44942  

Download Citation

Palaeontology Zoology

Received: 04 October 2016 Accepted: 14 February 2017 Published online: 30 March 2017

Figure 4: The craniofacial epidermis of Daspletosaurus horneri sp. nov., based on comparison with its closest living relatives, crocodylians and birds.

Abstract

A new species of tyrannosaurid from the upper Two Medicine Formation of Montana supports the presence of a Laramidian anagenetic (ancestor-descendant) lineage of Late Cretaceous tyrannosaurids. In concert with other anagenetic lineages of dinosaurs from the same time and place, this suggests that anagenesis could have been a widespread mechanism generating species diversity amongst dinosaurs, and perhaps beyond. We studied the excellent fossil record of the tyrannosaurid to test that hypothesis. Phylogenetic analysis places this new taxon as the sister species to Daspletosaurus torosus. However, given their close phylogenetic relationship, geographic proximity, and temporal succession, where D. torosus (~76.7–75.2 Ma) precedes the younger new species (~75.1–74.4 Ma), we argue that the two forms most likely represent a single anagenetic lineage. Daspletosaurus was an important apex predator in the late Campanian dinosaur faunas of Laramidia; its absence from later units indicates it was extinct before Tyrannosaurus rex dispersed into Laramidia from Asia. In addition to its evolutionary implications, the texture of the facial bones of the new taxon, and other derived tyrannosauroids, indicates a scaly integument with high tactile sensitivity. Most significantly, the lower jaw shows evidence for neurovasculature that is also seen in birds.

Source/Fonte: Thomas D. Carr

Acknowledgements

T.D.C. thanks the following people for access to specimens under their care: D. Brinkman, J. Horner, P. Makovicky, M. Norell, X. Wu, and S. Brusatte for assistance with obtaining the bootstrap values of the phylogenetic analysis. T.D.C. was supported by a Faculty Research & Development Grant from Carthage College. D.J.V. and J.R.M. thank the Bahamas crews of 2000 and 2001. D.J.V. thanks E. Metz, E. Przybyszewski, and A. Takekawa for help in the field and B. Harmon and J. Jette for preparation of specimens. J.C.S. thanks L. M. Witmer for guidance as his advisor during his dissertation work. J.C.S. was supported by a Dissertation Improvement Grant. E.M.R. thanks P. C. Owusu Agyemang and R. Holm for assistance with heavy mineral separations and U-Pb LA-ICPMS analysis. We thank D. A. Eberth for discussion on Belly River Group geochronology. J.R.M. thanks Channel 4 production company for contributing funding for fieldwork on MOR 1130. All authors thank D. Pulerà for rendering the life reconstruction of D. horneri, S. Williams for the photo of the quadratojugal of MOR 1130, S. Brusatte and an anonymous reviewer for their constructive comments, and R. McCrea for handling the manuscript.

Author information

Affiliations

Carthage College, 2001 Alford Park Drive, Kenosha, WI 53140, USA

Thomas D. Carr

Department of Earth Sciences, Montana State University, P.O. Box 173480, Bozeman, MT 59717-3480, USA

David J. Varricchio

Louisiana State University Health Sciences Centre - School of Medicine, 1901 Perdido Street, New Orleans, LA 70112, USA

Jayc C. Sedlmayr

Geosciences, College of Science and Engineering, James Cook University, Townsville, QLD 4811, Australia

Eric M. Roberts

Honors College, University of New Mexico, Albuquerque, NM 87131, USA.

Jason R. Moore

Contributions

T.D.C. wrote the description of the new taxon, collected and analyzed the phylogenetic and ontogenetic data, and wrote the corresponding parts of the manuscript. D.J.V. collected specimens MOR 553 and 1130 and analyzed the stratigraphic data in the field, and wrote the corresponding methods and results. T.D.C and J.C.S. collected and analyzed the data on epidermal soft tissue and associated neurovasculature; T.D.C. wrote the results. E.M.R. analyzed the geochronological data and wrote the corresponding methods and results. J.R.M. obtained funding for 2001 fieldwork on MOR 1130, helped excavate the specimen in 2000 and 2001, and helped write the manuscript.

Competing interests

The authors declare no competing financial interests.

Corresponding author

Correspondence to Thomas D. Carr.

FREE PDF GRATIS Scientific Reports Sup. Info. Excel Files 1, 2, 3.

Corrigindo o MITO de que a ciência se "autocorrige": NADA MAIS FALSO!!!

Correcting the “self-correcting” mythos of science

Douglas Allchin *

Source/Fonte: Boston University

Abstract: 

In standard characterizations, science is self-correcting. Scientists examine each other’s work skeptically, try to replicate important discoveries, and thereby expose latent errors. Thus, while science is tentative, it also seems to have a system for correcting whatever mistakes arise. It powerfully explains and justifies the authority of science. Self-correction thus often serves emblematically in promoting science as a superior form of knowledge. But errors can and do occur. Some errors remain uncorrected for long periods. I present five sets of historical observations that indicate a need to rethink the widespread mythos of self-correction. First, some errors persist for decades, wholly undetected. Second, many errors seem corrected by independent happenstance, not by any methodical appraisal. Third, some errors have been “corrected” in a cascade of successive errors that did not effectively remedy the ultimate source of the error. Fourth, some errors have fostered further serious errors without the first error being noticed. Finally, some corrections to erroneous theories have themselves been rejected when initially presented. In all these cases, scientists failed to identify and correct the errors in a timely manner, or according to any uniform self-correcting mechanism. These historical perspectives underscore that error correction in science requires epistemic work. We need deeper understanding of errors, through the emerging field of error analytics.

Keywords: scientific error; self-correction; error cascade; compounded error; error analytics

Corrigindo mitos “autocorrigíveis” da ciência

Resumo: 

Em caracterizações padrão, a ciência é autocorrigível. Os cientistas examinam o trabalho uns dos outros ceticamente, tentam repetir descobertas importantes e por isso expõem erros latentes. Assim, embora a ciência seja tentativa, parece também haver um sistema para corrigir quaisquer erros que apareçam. Isso explica poderosamente e justifica a autoridade da ciência. Autocorreção portanto serve em geral emblematicamente para promover a ciência como uma forma superior de conhecimento. Mas erros podem ocorrer e ocorrem. Alguns erros permanecem sem correção por longos períodos. Eu apresento aqui cinco casos de observações históricas que indicam uma necessidade de repensar o mito largamente difundido da autocorreção. Primeiro, alguns erros persistem por décadas, completamente despercebidos. Segundo, muitos erros parecem corrigidos por casualidade independente, não por alguma avaliação metodológica. Terceiro, alguns erros têm sido “corrigidos” em uma cascata de erros sucessivos que não remediam efetivamente a fonte final do erro. Quarto, alguns erros promoveram erros posteriores, mais graves, sem que o primeiro tenha sido notado. Finalmente, algumas correções a teorias erradas foram elas próprias rejeitadas quando inicialmente apresentadas. Em todos esses casos, os cientistas falharam em identificar e corrigir os erros em tempo hábil ou de acordo com algum mecanismo uniforme de autocorreção. Essas perspectivas históricas ressaltam que a correção do erro na ciência requer um trabalho epistêmico. Nós precisamos de uma compreensão mais aprofundada do erros, por meio do campo emergente da analítica do erro.

Palavras-chave: erros científicos; autocorreção; erro em cascata; erro composto; analítica do erro

* The Minnesota Center for the Philosophy of Science and STEM Education Center.

University of Minnesota, Minneapolis, MN, U.S.A, ZIP 55455. 

E-mail: allch001@umn.edu

FREE PDF GRATIS: Filosofia e História da Biologia

Quando a questão é Darwin não existe ceticismo saudável na maioria dos cientistas: pobre ciência!!!

Muito da vasta literatura neodarwinista é embaraçosamente acrítica. A possibilidade de que qualquer coisa esteja faltando seriamente com o relato da evolução de Darwin dificilmente é considerada... observadores ficam com a impressão de que há pouco ou nada sobre a teoria de Darwin que um naturalista científico pudesse objetar razoavelmente. O ceticismo metodológico que caracteriza a maior das áreas do discurso científico parece surpreendentemente ausente quando o Darwinismo é o tópico.

— Fodor e Piattelli-Palmarini, New Scientist 2/03/2010

Much of the vast neo-Darwinian literature is distressingly uncritical. The possibility that anything is seriously amiss with Darwin's account of evolution is hardly considered.... onlookers are left with the impression that there is little or nothing about Darwin's theory to which a scientific naturalist could reasonably object. The methodological scepticism that characterises most areas of scientific discourse seems strikingly absent when Darwinism is the topic.

— Fodor and Piattelli-Palmarini, New Scientist 2/03/2010

Abelhas melíferas navegam usando abdômens magnéticos: mero acaso, fortuita necessidade ou design inteligente?

Linking magnetite in the abdomen of honey bees to a magnetoreceptive function

Veronika Lambinet, Michael E. Hayden, Katharina Reigl, Surath Gomis, Gerhard Gries

Published 22 March 2017.DOI: 10.1098/rspb.2016.2873

Abstract

Previous studies of magnetoreception in honey bees, Apis mellifera, focused on the identification of magnetic material, its formation, the location of the receptor and potential underlying sensory mechanisms, but never directly linked magnetic material to a magnetoreceptive function. In our study, we demonstrate that ferromagnetic material consistent with magnetite plays an integral role in the bees' magnetoreceptor. Subjecting lyophilized and pelletized bee tagmata to analyses by a superconducting quantum interference device generated a distinct hysteresis loop for the abdomen but not for the thorax or the head of bees, indicating the presence of ferromagnetic material in the bee abdomen. Magnetic remanence of abdomen pellets produced from bees that were, or were not, exposed to the 2.2-kOe field of a magnet while alive differed, indicating that magnet exposure altered the magnetization of this magnetite in live bees. In behavioural two-choice field experiments, bees briefly exposed to the same magnet, but not sham-treated control bees, failed to sense a custom-generated magnetic anomaly, indicating that magnet exposure had rendered the bees' magnetoreceptor dysfunctional. Our data support the conclusion that honey bees possess a magnetite-based magnetoreceptor located in the abdomen.

FREE PDF GRATIS: Proc R Soc B

Mais complexidade - enzima "carpinteiro" dá recorte ao DNA: mero acaso, fortuita necessidade ou design inteligente?

Single-molecule FRET unveils induced-fit mechanism for substrate selectivity in flap endonuclease 1

Fahad Rashid Paul D Harris Manal S Zaher Mohamed A Sobhy Luay I Joudeh Chunli Yan Hubert Piwonski Susan E Tsutakawa Ivaylo Ivanov John A Tainer Satoshi Habuchi Samir M Hamdan 

King Abdullah University of Science and Technology, Saudi Arabia; Georgia State University, United States; Lawrence Berkeley National Laboratory, United States; University of Texas MD Anderson Cancer Center, United States

DOI: http://dx.doi.org/10.7554/eLife.21884  

Published February 23, 2017

Cite as eLife 2017;6:e21884

Abstract

Human flap endonuclease 1 (FEN1) and related structure-specific 5’nucleases precisely identify and incise aberrant DNA structures during replication, repair and recombination to avoid genomic instability. Yet, it is unclear how the 5’nuclease mechanisms of DNA distortion and protein ordering robustly mediate efficient and accurate substrate recognition and catalytic selectivity. Here, single-molecule sub-millisecond and millisecond analyses of FEN1 reveal a protein-DNA induced-fit mechanism that efficiently verifies substrate and suppresses off-target cleavage. FEN1 sculpts DNA with diffusion-limited kinetics to test DNA substrate. This DNA distortion mutually ‘locks’ protein and DNA conformation and enables substrate verification with extreme precision. Strikingly, FEN1 never misses cleavage of its cognate substrate while blocking probable formation of catalytically competent interactions with noncognate substrates and fostering their pre-incision dissociation. These findings establish FEN1 has practically perfect precision and that separate control of induced-fit substrate recognition sets up the catalytic selectivity of the nuclease active site for genome stability.

DOI: http://dx.doi.org/10.7554/eLife.21884.001

eLife digest

When a cell divides it must copy its genetic information, which is found in the form of strands of DNA. Damage to the DNA may lead to cancer or a number of genetic diseases. However, every time a cell divides more than 10 million toxic “flaps” of excess DNA are generated. A protein called flap endonuclease 1 (FEN1) keeps the DNA in good repair by cutting off the flaps in a highly specific and selective manner.

Many proteins that interact with DNA are attracted to specific genetic sequences within the DNA strands. However, this is not the case for FEN1 and several other “structure-specific” proteins that help to repair and replicate DNA strands. So how do these proteins select the correct regions of DNA to interact with?

Rashid et al. used single-molecule fluorescence measurements to examine how purified FEN1 proteins interact with DNA flaps. The results show that FEN1 can perfectly recognize and correctly remove flaps through a process called “mutual-induced fit”, where the DNA and FEN1 are shaped by each other to produce a highly specific structure.

Further work is now needed to examine whether other proteins that are related to FEN1 use a similar process to ensure that they always cut DNA in the same way. More detailed and direct examination of the structure of FEN1 through other experimental methods may also help to reveal how the mutual-induced fit process enables FEN1 to achieve such high levels of precision. This could increase our understanding of how problems with FEN1 and similar proteins lead to different genetic diseases.

DOI: http://dx.doi.org/10.7554/eLife.21884.002

FREE PDF GRATIS: eLIFE