A Revolta da Ciência - Episódio 3 - O DNA é um código: quem o codificou???

segunda-feira, junho 17, 2019



#ScienceUprising #RevoltaDaCiencia

Gases tóxicos em zona habitável podem dificultar o surgimento de vida extraterrestre

A Limited Habitable Zone for Complex Life

Edward W. Schwieterman1,2,3,4,5, Christopher T. Reinhard3,4,6, Stephanie L. Olson3,7, Chester E. Harman4,8,9, and Timothy W. Lyons1,3,4

Published 2019 June 10 • © 2019. The American Astronomical Society.

The Astrophysical Journal, Volume 878, Number 1

Trappist 1
No safe zone: do high carbon monoxide levels preclude the existence of life in the Trappist-1 system? (Courtesy: NASA/JPL-Caltech) Source/Fonte

Abstract

The habitable zone (HZ) is commonly defined as the range of distances from a host star within which liquid water, a key requirement for life, may exist on a planet's surface. Substantially more CO2 than present in Earth's modern atmosphere is required to maintain clement temperatures for most of the HZ, with several bars required at the outer edge. However, most complex aerobic life on Earth is limited by CO2 concentrations of just fractions of a bar. At the same time, most exoplanets in the traditional HZ reside in proximity to M dwarfs, which are more numerous than Sun-like G dwarfs but are predicted to promote greater abundances of gases that can be toxic in the atmospheres of orbiting planets, such as carbon monoxide (CO). Here we show that the HZ for complex aerobic life is likely limited relative to that for microbial life. We use a 1D radiative-convective climate and photochemical models to circumscribe a Habitable Zone for Complex Life (HZCL) based on known toxicity limits for a range of organisms as a proof of concept. We find that for CO2 tolerances of 0.01, 0.1, and 1 bar, the HZCL is only 21%, 32%, and 50% as wide as the conventional HZ for a Sun-like star, and that CO concentrations may limit some complex life throughout the entire HZ of the coolest M dwarfs. These results cast new light on the likely distribution of complex life in the universe and have important ramifications for the search for exoplanet biosignatures and technosignatures.

FREE PDF GRATIS: The Astrophysical Journal

The Fourth Paradigm: Data-Intensive Scientific Discovery

quinta-feira, junho 13, 2019

The Fourth Paradigm: Data-Intensive Scientific Discovery

Increasingly, scientific breakthroughs will be powered by advanced computing capabilities that help researchers manipulate and explore massive datasets.

The speed at which any given scientific discipline advances will depend on how well its researchers collaborate with one another, and with technologists, in areas of eScience such as databases, workflow management, visualization, and cloud computing technologies.

In The Fourth Paradigm: Data-Intensive Scientific Discovery, the collection of essays expands on the vision of pioneering computer scientist Jim Gray for a new, fourth paradigm of discovery based on data-intensive science and offers insights into how it can be fully realized.

Critical praise for The Fourth Paradigm

“The individual essays—and The Fourth Paradigm as a whole—give readers a glimpse of the horizon for 21st-century research and, at their best, a peek at what lies beyond. It’s a journey well worth taking.”

— James P. Collins
School of Life Sciences, Arizona State University

Um mapa topográfico microscópico de complexidade da função celular: mero acaso, fortuita necessidade ou design inteligente?

Direct visualization of the E. coli Sec translocase engaging precursor proteins in lipid bilayers

Raghavendar Reddy Sanganna Gari1,*, Kanokporn Chattrakun1, Brendan P. Marsh1,†, Chunfeng Mao2, Nagaraju Chada1,‡, Linda L. Randall2 and Gavin M. King1,2,§

1Department of Physics and Astronomy, University of Missouri, Columbia, MO 65211, USA.

2Department of Biochemistry, University of Missouri, Columbia, MO 65211, USA.

↵§Corresponding author. Email: kinggm@missouri.edu

↵* Present address: Department of Anesthesiology, Weill Cornell Medicine, New York, NY 10065, USA.

↵† Present address: Department of Applied Physics, Stanford University, Stanford, CA 94305, USA.

↵‡ Present address: Department of Biology, Johns Hopkins University, 3400 N. Charles Street, Baltimore, MD 21218, USA.

Science Advances 12 Jun 2019: Vol. 5, no. 6, eaav9404


Fig. 6 Precursor-dependent model of translocase activity.

Abstract

Escherichia coli exports proteins via a translocase comprising SecA and the translocon, SecYEG. Structural changes of active translocases underlie general secretory system function, yet directly visualizing dynamics has been challenging. We imaged active translocases in lipid bilayers as a function of precursor protein species, nucleotide species, and stage of translocation using atomic force microscopy (AFM). Starting from nearly identical initial states, SecA more readily dissociated from SecYEG when engaged with the precursor of outer membrane protein A as compared to the precursor of galactose-binding protein. For the SecA that remained bound to the translocon, the quaternary structure varied with nucleotide, populating SecA2 primarily with adenosine diphosphate (ADP) and adenosine triphosphate, and the SecA monomer with the transition state analog ADP-AlF3. Conformations of translocases exhibited precursor-dependent differences on the AFM imaging time scale. The data, acquired under near-native conditions, suggest that the translocation process varies with precursor species.

FREE PDF GRATIS: Science Advances

Como a célula se protege: mero acaso, fortuita necessidade ou design inteligente?

quarta-feira, junho 12, 2019

Nuclear Pre-snRNA Export Is an Essential Quality Assurance Mechanism for Functional Spliceosomes
 

Daniel Becker, Anna Greta Hirsch, Lysann Bender, Thomas Lingner, Gabriela Salinas, Heike Krebber

Open Access DOI: https://doi.org/10.1016/j.celrep.2019.05.031
Figure thumbnail fx1

Highlights

• All yeast snRNAs, including U6, shuttle into the cytoplasm

• Export is mediated by Mex67 and Xpo1, and re-import requires Mtr10 and Cse1

• snRNA export prevents an incorporation of immature snRNAs into spliceosomes

• Spliceosomal assembly with immature snRNAs results in genome-wide splicing defects
 
Summary

Removal of introns from pre-mRNAs is an essential step in eukaryotic gene expression, mediated by spliceosomes that contain snRNAs as key components. Although snRNAs are transcribed in the nucleus and function in the same compartment, all except U6 shuttle to the cytoplasm. Surprisingly, the physiological relevance for shuttling is unclear, in particular because the snRNAs in Saccharomyces cerevisiae were reported to remain nuclear. Here, we show that all yeast pre-snRNAs including U6 undergo a stepwise maturation process after nuclear export by Mex67 and Xpo1. Sm- and Lsm-ring attachment occurs in the cytoplasm and is important for the snRNA re-import, mediated by Cse1 and Mtr10. Finally, nuclear pre-snRNA cleavage and trimethylation of the 5′-cap finalizes shuttling. Importantly, preventing pre-snRNAs from being exported or processed results in faulty spliceosome assembly and subsequent genome-wide splicing defects. Thus, pre-snRNA export is obligatory for functional splicing and resembles an essential evolutionarily conserved quality assurance step.
 
FREE PDF GRATIS: Cell Reports

A Revolta da Ciência - Episódio 2 - A Mente: O Inescapável

segunda-feira, junho 10, 2019



#ScienceUprising #RevoltaDaCiencia

Como são regulados os ciclos de divisão celular: mero acaso, fortuita necessidade ou design inteligente?

sexta-feira, junho 07, 2019

Two Distinct E2F Transcriptional Modules Drive Cell Cycles and Differentiation

Maria C. Cuitiño, Thierry Pécot, Daokun Sun, Michael C. Ostrowski, Michele Pagano, Gustavo Leone


Open Access Published:May 23, 2019

Highlights

• E2F expression during cell division, differentiation, and quiescence is measured in vivo

• E2F3A, E2F8, and E2F4 accumulate sequentially in the nucleus of cycling cells

• E2F3A-4 nuclear accumulation controls gene expression during cell-cycle exit

• Deep learning tools are applied to nuclear segmentation of complex mammalian tissues


Summary


Orchestrating cell-cycle-dependent mRNA oscillations is critical to cell proliferation in multicellular organisms. Even though our understanding of cell-cycle-regulated transcription has improved significantly over the last three decades, the mechanisms remain untested in vivo. Unbiased transcriptomic profiling of G0, G1-S, and S-G2-M sorted cells from FUCCI mouse embryos suggested a central role for E2Fs in the control of cell-cycle-dependent gene expression. The analysis of gene expression and E2F-tagged knockin mice with tissue imaging and deep-learning tools suggested that post-transcriptional mechanisms universally coordinate the nuclear accumulation of E2F activators (E2F3A) and canonical (E2F4) and atypical (E2F8) repressors during the cell cycle in vivo. In summary, we mapped the spatiotemporal expression of sentinel E2F activators and canonical and atypical repressors at the single-cell level in vivo and propose that two distinct E2F modules relay the control of gene expression in cells actively cycling (E2F3A-8-4) and exiting the cycle (E2F3A-4) during mammalian development.


FREE PDF GRATIS: Cell Reports

Darwin, a tradução de genes é mais complexa do que esperada

Multi-Color Single-Molecule Imaging Uncovers Extensive Heterogeneity in mRNA Decoding

Sanne Boersma3 Deepak Khuperkar3 Bram M.P. Verhagen Jonathan B. Grimm Luke D. Lavis Marvin E. Tanenbaum4
Published:June 06, 2019 DOI: https://doi.org/10.1016/j.cell.2019.05.001
https://marlin-prod.literatumonline.com/cms/attachment/194e21d3-7287-455b-9c32-1e3162f66d66/fx1_lrg.jpg


Highlights

• Development of MoonTag, a fluorescence labeling system to visualize translation

• Combining MoonTag and SunTag enables visualization of translational heterogeneity

• mRNAs from a single gene vary in initiation frequency at different start sites

• Ribosomes take many different “paths” along the 5′ UTR of a single mRNA molecule



Summary

mRNA translation is a key step in decoding genetic information. Genetic decoding is surprisingly heterogeneous because multiple distinct polypeptides can be synthesized from a single mRNA sequence. To study translational heterogeneity, we developed the MoonTag, a fluorescence labeling system to visualize translation of single mRNAs. When combined with the orthogonal SunTag system, the MoonTag enables dual readouts of translation, greatly expanding the possibilities to interrogate complex translational heterogeneity. By placing MoonTag and SunTag sequences in different translation reading frames, each driven by distinct translation start sites, start site selection of individual ribosomes can be visualized in real time. We find that start site selection is largely stochastic but that the probability of using a particular start site differs among mRNA molecules and can be dynamically regulated over time. This study provides key insights into translation start site selection heterogeneity and provides a powerful toolbox to visualize complex translation dynamics.
FREE PDF GRATIS: Cell

A Revolta da Ciência contra a Ciência Fake e o Materialismo Entorpecente

terça-feira, junho 04, 2019



#ScienceUprising #RevoltaDaCiencia

Nullius in verba: a maioria dos artigos em química retraídos das publicações científicas por problemas sérios!

segunda-feira, junho 03, 2019

Correcting the Scientific Record: Retraction Practices in Chemistry and Materials Science

François-Xavier Coudert

Cite This: Chem. Mater.201931103593-3598

Publication Date:May 28, 2019

https://doi.org/10.1021/acs.chemmater.9b00897

Copyright © 2019 American Chemical Society




Peer-reviewed articles, published by scholarly journals, currently form the cornerstone of the modern scholarly publication system and guarantee the dissemination of research findings through the worldwide, ever-increasing community of researchers. Collectively these published works, stamped with the seal of approval of a review by the authors’ peers, form the scientific record—the record of knowledge accumulated by mankind. It is the duty of every scholar to add knowledge to this record by publishing but also to ensure the integrity of the existing works by critically assessing them: before publication, acting as a reviewer or editor, and post-publication, by building upon existing works, improving them, and checking their reproducibility.


The means of post-publication peer review of articles, which was once limited to formally published comments (“Comment on...”), journal clubs and conference coffee breaks, are rapidly expanding through the use of Internet and social media. Discussion of published papers regularly takes place on Twitter and through blog posts and preprints, as well as in structured discussions: comments on the webpage on published papers (e.g., PLOS Oneand Frontiers journals), indexing servers (PubMed Commons, now closed(1)), or dedicated websites (such as PubPeer(2)). Critique of published articles is a necessary and healthy part of the advancement of science. Sometimes, it can lead to the identification of serious flaws in the data or authors’ analysis, so that the findings or the conclusions published cannot be trusted anymore. In such cases, the paper may be corrected or retracted, i.e., expunged from the scientific record.


COPE, the Committee on Publication Ethics, publishes a series of guidelines (policies and practices) that are considered the industry standard in publishing ethics. The areas covered include the handling of allegations of misconduct, complaints and appeals, data issues and reproducibility, and standards of authorship, as well as post-publication corrections and the retraction of papers. COPE guidelines give clear insights into the difference in nature between corrections and retractions.(3) Articles should be corrected if “a small portion of an otherwise reliable publication proves to be misleading (especially because of honest error)”. On the other hand, “journal editors should consider retracting a publication if:

they have clear evidence that the findings are unreliable, either as a result of misconduct (e.g., data fabrication) or honest error (e.g. miscalculation or experimental error),

the findings have previously been published elsewhere without proper crossreferencing, permission or justification (i.e. cases of redundant publication),

it constitutes plagiarism,

it reports unethical research.”Retractions thus ensure that the literature is corrected, alerting readers to the fact that a publication contains erroneous or unreliable data, and give clear insight into the nature of the issues.

Despite the healthy role of retractions in preserving the scientific record, and while erroneous data can be the result of a good faith mistake, there is definitely a stigma associated with the retraction of a paper. COPE guidelines state that “The main purpose of retractions is to correct the literature and ensure its integrity rather than to punish authors who misbehave”,(3) but previous work has shown a notable resistance to admitting error in scientific papers.(4) The term retraction is too often associated with research misconduct, giving it a negative connotation for authors.(5) This is particularly true in a highly competitive environment, where academics are driven to publish often and produce high-impact papers: Jin et al. showed that retractions have a negative effect on citations for early career researchers.(6,7) The same argument can also be made for the publishers, who may fear a dent in the reputation of the journal. Thus, none of the actors involved have any direct incentive to retract a paper.

In this context, and while the number of retractions is rising,(8,9) there is relatively little information available about retractions and retracted papers, beyond the retraction notices infrequently published by journals. There is no central repository or authoritative database that can be easily queried—although the Retraction Watch website, which covers the topic of retractions and publication ethics in general, has been collating such a database.(10)Previous systematic studies have focused on retractions in specific fields, and in particular in medicine(11−13)—with the notable exception of a study by Grieneisen et al. that spanned several fields of research.(14) In order to better understand the existing practices for article retraction in the chemical sciences, I have performed a systematic survey of 331 papers retracted in 2017 and 2018 and their retraction notices, publicly available on the journals’ websites. This article looks at the statistics of retractions, their distribution per country, and the occurrence of multiple retractions. I also provide a classification of the reasons behind the retractions and the distribution of their occurrence.
...

FREE PDF GRATIS: ACS Chemistry Materials Sup. Info. 1, Sup. Info. 2.

A insurreição da ciência - 3 de junho-8 de julho de 2019

sábado, junho 01, 2019

Divisão celular requer nível equilibrado de RNA não codificante para estabilidade cromossômica: mero acaso, fortuita necessidade ou design inteligente?

sábado, maio 25, 2019

Point centromere activity requires an optimal level of centromeric noncoding RNA

Yick Hin Ling and Karen Wing Yee Yuen

PNAS March 26, 2019 116 (13) 6270-6279; first published March 8, 2019 https://doi.org/10.1073/pnas.1821384116

Edited by Douglas Koshland, University of California, Berkeley, CA, and approved February 5, 2019 (received for review December 21, 2018)

Fig. 5.
Fig. 5 Knockdown of total cenRNAs reduces mitotic stability of minichromosome.

Significance

Budding yeast harbors a simple point centromere, which is originally believed to be sequence dependent without much epigenetic regulation and is transcription incompatible, as inserting a strong promoter upstream inactivates the centromere completely. Here, we demonstrate that an optimal level centromeric noncoding RNA is required for budding yeast centromere activity. Centromeric transcription is induced in S phase, coinciding with the assembly of new centromeric proteins. Too much or too little centromeric noncoding RNA leads to centromere malfunction. Overexpression of centromeric noncoding RNA reduces the protein levels and chromatin localization of inner centromere and kinetochore proteins, such as CENP-A, CENP-C, and the chromosome passenger complex. This work shows that point centromere is epigenetically regulated by noncoding RNA.

Abstract

In budding yeast, which possesses simple point centromeres, we discovered that all of its centromeres express long noncoding RNAs (cenRNAs), especially in S phase. Induction of cenRNAs coincides with CENP-ACse4 loading time and is dependent on DNA replication. Centromeric transcription is repressed by centromere-binding factor Cbf1 and histone H2A variant H2A.ZHtz1. Deletion of CBF1 and H2A.ZHTZ1 results in an up-regulation of cenRNAs; an increased loss of a minichromosome; elevated aneuploidy; a down-regulation of the protein levels of centromeric proteins CENP-ACse4, CENP-A chaperone HJURPScm3, CENP-CMif2, SurvivinBir1, and INCENPSli15; and a reduced chromatin localization of CENP-ACse4, CENP-CMif2, and Aurora BIpl1. When the RNA interference system was introduced to knock down all cenRNAs from the endogenous chromosomes, but not the cenRNA from the circular minichromosome, an increase in minichromosome loss was still observed, suggesting that cenRNA functions in trans to regulate centromere activity. CenRNA knockdown partially alleviates minichromosome loss in cbf1Δ, htz1Δ, and cbf1Δ htz1Δ in a dose-dependent manner, demonstrating that cenRNA level is tightly regulated to epigenetically control point centromere function.

centromeric transcription long noncoding RNA centromere-binding factor Cbf1 histone H2A variant Htz1 chromosome instability

FREE PDF GRATIS: PNAS Sup. Info

Além de fabricar proteínas, ribossomos regulam a expressão de genes humanos

Translation affects mRNA stability in a codon-dependent manner in human cells


Qiushuang Wu, Santiago Gerardo Medina, Gopal Kushawah, Michelle Lynn DeVore, Luciana A Castellano, Jacqelyn M Hand, Matthew Wright, Ariel Alejandro Bazzini  

Stowers Institute for Medical Research, United States

RESEARCH ARTICLE Apr 23, 2019

Upstream regulator and downstream effect for codon optimality tRNA level, tRNA charged ratio, amino acid, and translational level might contribute to regulates the regulatory identity and/or strength of each codon to affect gene expression, by influencing the speed of translation elongation.

Abstract

mRNA translation decodes nucleotide into amino acid sequences. However, translation has also been shown to affect mRNA stability depending on codon composition in model organisms, although universality of this mechanism remains unclear. Here, using three independent approaches to measure exogenous and endogenous mRNA decay, we define which codons are associated with stable or unstable mRNAs in human cells. We demonstrate that the regulatory information affecting mRNA stability is encoded in codons and not in nucleotides. Stabilizing codons tend to be associated with higher tRNA levels and higher charged/total tRNA ratios. While mRNAs enriched in destabilizing codons tend to possess shorter poly(A)-tails, the poly(A)-tail is not required for the codon-mediated mRNA stability. This mechanism depends on translation; however, the number of ribosome loads into a mRNA modulates the codon-mediated effects on gene expression. This work provides definitive evidence that translation strongly affects mRNA stability in a codon-dependent manner in human cells.

https://doi.org/10.7554/eLife.45396.001

eLife digest

Proteins are made by joining together building blocks called amino acids into strings. The proteins are ‘translated’ from genetic sequences called mRNA molecules. These sequences can be thought of as series of ‘letters’, which are read in groups of three known as codons. Molecules called tRNAs recognize the codons and add the matching amino acids to the end of the protein. Each tRNA can recognize one or several codons, and the levels of different tRNAs inside the cell vary.

There are 61 codons that code for amino acids, but only 20 amino acids. This means that some codons produce the same amino acid. Despite this, there is evidence to suggest that not all of the codons that produce the same amino acid are exactly equivalent. In bacteria, yeast and zebrafish, some codons seem to make the mRNA molecule more stable, and others make it less stable. This might help the cell to control how many proteins it makes. It was not clear whether the same is true for humans.

To find out, Wu et al. used three separate methods to examine mRNA stability in four types of human cell. Overall, the results revealed that some codons help to stabilize the mRNA, while others make the mRNA molecule break down faster. The effect seems to depend on the supply of tRNAs that have a charged amino acid; mRNA molecules were more likely to self-destruct in cells that contained codons with low levels of the tRNA molecules.

Wu et al. also found that conditions in the cell can alter how strongly the codons affect mRNA stability. For example, a cell that has been infected by a virus reduces translation. Under these conditions, the identity of the codons in the mRNA has less effect on the stability of the mRNA molecule.

Changes to protein production happen in many diseases. Understanding what controls these changes could help to reveal more about our fundamental biology, and what happens when it goes wrong.

https://doi.org/10.7554/eLife.45396.002

FREE PDF GRATIS: eLIFE

Karl Popper, Ciência e Iluminação

terça-feira, maio 14, 2019





Karl Popper, Science and Enlightenment
Nicholas Maxwell 

ISBN: 9781787350397

Publication: September 26, 2017
 
Description
 
Here is an idea that just might save the world. It is that science, properly understood, provides us with the methodological key to the salvation of humanity. A version of this idea can be found in the works of Karl Popper. Famously, Popper argued that science cannot verify theories but can only refute them, and this is how science makes progress. Scientists are forced to think up something better, and it is this, according to Popper, that drives science forward.
But Nicholas Maxwell finds a flaw in this line of argument. Physicists only ever accept theories that are unified – theories that depict the same laws applying to the range of phenomena to which the theory applies – even though many other empirically more successful disunified theories are always available. This means that science makes a questionable assumption about the universe, namely that all disunified theories are false. Without some such presupposition as this, the whole empirical method of science breaks down.

By proposing a new conception of scientific methodology, which can be applied to all worthwhile human endeavours with problematic aims, Maxwell argues for a revolution in academic inquiry to help humanity make progress towards a better, more civilized and enlightened world. 

Praise for Karl Popper, Science and Enightenment
 ‘Maxwell has provided general philosophy of science with a book that is notably clear, earnestly written, passionate, and stunningly stimulating… a book with a panoply of exciting ideas and some relevance for almost anyone working in academia.'
Metapsychology Online Reviews 


Publication details

Format: Open Access PDF
390 Pages
ISBN: 9781787350397
Publication: September 26, 2017

About the Author

Nicholas Maxwell has devoted much of his working life to arguing that we need to bring about a revolution in academia so that it seeks and promotes wisdom and does not just acquire knowledge. He has published eight books on this theme, including How Universities Can Help Create a Wiser World (2014) and In Praise of Natural Philosophy (2017). For 30 years he taught philosophy of science at University College London, where he is now Emeritus Reader. For more about his work, see www.ucl.ac.uk/from-knowledge-to-wisdom.

Table of contents

Prologue: An idea to help save the world

Introduction

1. Karl Raimund Popper

2. Popper, Kuhn, Lakatos and aim-oriented empiricism

3. Einstein, aim-oriented empiricism, and the discovery of special and general relativity 

4. Non-empirical requirements scientific theories must satisfy: simplicity, unity, explanation, beauty

5. Scientific metaphysics

6. Comprehensibility rather than beauty

7. A mug’s game? Solving the problem of induction with metaphysical presuppositions

8. Does probabilism solve the great quantum mystery?

9. Science, reason, knowledge and wisdom: a critique of specialism

10. Karl Popper and the Enlightenment Programme 

FREE PDF GRATIS: UCL PRESS
 


O que é vida?

segunda-feira, maio 13, 2019

Journal of Biomolecular Structure and Dynamics 
Volume 29, 2011 - Issue 2

Vocabulary of Definitions of Life Suggests a Definition

Edward N. Trifonov

Pages 259-266 | Received 17 Mar 2011, Published online: 11 Jul 2012



Abstract

Analysis of the vocabulary of 123 tabulated definitions of life reveals nine groups of defining terms (definientia) of which the groups (self-)reproduction and evolution (variation) appear as the minimal set for a concise and inclusive definition: Life is self-reproduction with variations.

Key words: Consensus,  Definientia , Evolution, Origin of life, Self-reproduction, Variations, Vocabulary

Os evolucionistas sabem há muito tempo que Haeckel fraudou, mas o que vale é que prova a teoria da evolução!

Theory in Biosciences

May 2019, Volume 138, Issue 1, pp 9–29 

Ernst Haeckel’s contribution to Evo-Devo and scientific debate: a re-evaluation of Haeckel’s controversial illustrations in US textbooks in response to creationist accusations

Elizabeth Watts, Georgy S. Levit, Uwe Hossfeld

Original Article
First Online: 13 March 2019

Haeckel's fraud

True stages - Richardson et al, Science 1998
Abstract

As Blackwell (Am Biol Teach 69:135–136, 2007) pointed out, multiple authors have attempted to discredit Haeckel, stating that modern embryological studies have shown that Haeckel’s drawings are stylized or embellished. More importantly, though, it has been shown that the discussion within the scientific community concerning Haeckel’s drawings and the question of whether embryonic similarities are convergent or conserved have been extrapolated outside the science community in an attempt to discredit Darwin and evolutionary theory in general (Behe in Science 281:347–351, 1998; Blackwell in Am Biol Teach 69:135–136, 2007; Pickett et al. in Am Biol Teach 67:275, 2005; Wells in Am Biol Teach 61:345–349, 1999; Icons of evolution: science or myth? Why much of what we teach about evolution is wrong. Regnery Publishing, Washington, 2002). In this paper, we address the controversy surrounding Haeckel and his work in order to clarify the line between the shortcomings and the benefits of his research and illustrations. Specifically, we show that while his illustrations were not perfect anatomical representations, they were useful educational visualizations and did serve an important role in furthering studies in embryology.

Keywords Haeckel Visualization Creationism Evolution Science education Textbooks 

This article is a contribution to the Special Issue Ernst Haeckel (1834–1919): The German Darwin and his impact on modern biology—Guest Editors: U. Hossfeld, G. S. Levit, U. Kutschera.

FREE PDF GRATIS: Theory in Biosciences

Pesquisa Acadêmica no Século 21: Mantendo a Integridade Científica em um Clima de Incentivos Perversos e Hipercompetição

Academic Research in the 21st Century: Maintaining Scientific Integrity in a Climate of Perverse Incentives and Hypercompetition

Marc A. Edwards and Siddhartha Roy

Published Online:1 Jan 2017 https://doi.org/10.1089/ees.2016.0223



Abstract

Over the last 50 years, we argue that incentives for academic scientists have become increasingly perverse in terms of competition for research funding, development of quantitative metrics to measure performance, and a changing business model for higher education itself. Furthermore, decreased discretionary funding at the federal and state level is creating a hypercompetitive environment between government agencies (e.g., EPA, NIH, CDC), for scientists in these agencies, and for academics seeking funding from all sources—the combination of perverse incentives and decreased funding increases pressures that can lead to unethical behavior. If a critical mass of scientists become untrustworthy, a tipping point is possible in which the scientific enterprise itself becomes inherently corrupt and public trust is lost, risking a new dark age with devastating consequences to humanity. Academia and federal agencies should better support science as a public good, and incentivize altruistic and ethical outcomes, while de-emphasizing output.

Um guia sucinto para escrever uma boa revisão paritária

A quick guide to writing a solid peer review

Kimberly A. Nicholas  Wendy S. Gordon

First published: 12 July 2011 https://doi.org/10.1029/2011EO280001

Source/Fonte: Wiley


Abstract

[1] Scientific integrity and consensus rely on the peer review process, a defining feature of scientific discourse that subjects the literature forming the foundation of credible knowledge in a scientific field to rigorous scrutiny. However, there is surprisingly little training in graduate school on how to develop this essential skill [Zimmerman et al., 2011] or discussion of best practices to ensure that reviewers at all levels efficiently provide the most useful review. Even more challenging for the novice peer reviewer is that journals also vary widely in their review guidelines. Nonetheless, the goals of peer review are crystal clear: to ensure the accuracy and improve the quality of published literature through constructive criticism. To make the peer review process as efficient and productive as possible, you may want to consider a few useful approaches to tackling major steps throughout your review, from contemplating a review request and reading and assessing the manuscript to writing the review and interacting with the journal's editors (see Figure 1). These tips are particularly relevant for graduate students or other first‐time reviewers, but they may also be useful to experienced reviewers and to journal editors seeking to enhance their publication's processes.

FREE PDF GRATIS: EOS

David Gelernter (Yale University): desistindo de Darwin!

sexta-feira, maio 10, 2019

Giving up Darwin

By: David Gelernter

Posted: May 1, 2019

This article appeared in: Volume XIX, Number 2, Spring 2019



Darwinian evolution is a brilliant and beautiful scientific theory. Once it was a daring guess. Today it is basic to the credo that defines the modern worldview. Accepting the theory as settled truth—no more subject to debate than the earth being round or the sky blue or force being mass times acceleration—certifies that you are devoutly orthodox in your scientific views; which in turn is an essential first step towards being taken seriously in any part of modern intellectual life. But what if Darwin was wrong?

Like so many others, I grew up with Darwin’s theory, and had always believed it was true. I had heard doubts over the years from well-informed, sometimes brilliant people, but I had my hands full cultivating my garden, and it was easier to let biology take care of itself. But in recent years, reading and discussion have shut that road down for good.

This is sad. It is no victory of any sort for religion. It is a defeat for human ingenuity. It means one less beautiful idea in our world, and one more hugely difficult and important problem back on mankind’s to-do list. But we each need to make our peace with the facts, and not try to make life on earth simpler than it really is.

Charles Darwin explained monumental change by making one basic assumption—all life-forms descend from a common ancestor—and adding two simple processes anyone can understand: random, heritable variation and natural selection. Out of these simple ingredients, conceived to be operating blindly over hundreds of millions of years, he conjured up change that seems like the deliberate unfolding of a grand plan, designed and carried out with superhuman genius. Could nature really have pulled out of its hat the invention of life, of increasingly sophisticated life-forms and, ultimately, the unique-in-the-cosmos (so far as we know) human mind—given no strategy but trial and error? The mindless accumulation of small changes? It is an astounding idea. Yet Darwin’s brilliant and lovely theory explains how it could have happened.

Its beauty is important. Beauty is often a telltale sign of truth. Beauty is our guide to the intellectual universe—walking beside us through the uncharted wilderness, pointing us in the right direction, keeping us on track—most of the time.

Demolishing a Worldview

There’s no reason to doubt that Darwin successfully explained the small adjustments by which an organism adapts to local circumstances: changes to fur density or wing style or beak shape. Yet there are many reasons to doubt whether he can answer the hard questions and explain the big picture—not the fine-tuning of existing species but the emergence of new ones. The origin of species is exactly what Darwin cannot explain.

Stephen Meyer’s thoughtful and meticulous Darwin’s Doubt (2013) convinced me that Darwin has failed. He cannot answer the big question. Two other books are also essential: The Deniable Darwin and Other Essays (2009), by David Berlinski, and Debating Darwin’s Doubt (2015), an anthology edited by David Klinghoffer, which collects some of the arguments Meyer’s book stirred up. These three form a fateful battle group that most people would rather ignore. Bringing to bear the work of many dozen scientists over many decades, Meyer, who after a stint as a geophysicist in Dallas earned a Ph.D. in History and Philosophy of Science from Cambridge and now directs the Discovery Institute’s Center for Science and Culture, disassembles the theory of evolution piece by piece. Darwin’s Doubt is one of the most important books in a generation. Few open-minded people will finish it with their faith in Darwin intact.

Meyer doesn’t only demolish Darwin; he defends a replacement theory, intelligent design (I.D.). Although I can’t accept intelligent design as Meyer presents it, he does show that it is a plain case of the emperor’s new clothes: it says aloud what anyone who ponders biology must think, at some point, while sifting possible answers to hard questions. Intelligent design as Meyer explains it never uses religious arguments, draws religious conclusions, or refers to religion in any way. It does underline an obvious but important truth: Darwin’s mission was exactly to explain the flagrant appearance of design in nature.

The religion is all on the other side. Meyer and other proponents of I.D. are the dispassionate intellectuals making orderly scientific arguments. Some I.D.-haters have shown themselves willing to use any argument—fair or not, true or not, ad hominem or not—to keep this dangerous idea locked in a box forever. They remind us of the extent to which Darwinism is no longer just a scientific theory but the basis of a worldview, and an emergency replacement religion for the many troubled souls who need one.

As for Biblical religion, it forces its way into the discussion although Meyer didn’t invite it, and neither did Darwin. Some have always been bothered by the harm Darwin is said to have done religion. His theory has been thought by some naïfs (fundamentalists as well as intellectuals) to have shown or alleged that the Bible is wrong, and Judeo-Christian religion bunk. But this view assumes a childishly primitive reading of Scripture. Anyone can see that there are two different creation stories in Genesis, one based on seven days, the other on the Garden of Eden. When the Bible gives us two different versions of one story, it stands to reason that the facts on which they disagree are without basic religious significance. The facts on which they agree are the ones that matter: God created the universe, and put man there for a reason. Darwin has nothing to say on these or any other key religious issues.

Fundamentalists and intellectuals might go on arguing these things forever. But normal people will want to come to grips with Meyer and the downfall of a beautiful idea. I will mention several of his arguments, one of them in (just a bit of) detail. This is one of the most important intellectual issues of modern times, and every thinking person has the right and duty to judge for himself.

Looking for Evidence

Darwin himself had reservations about his theory, shared by some of the most important biologists of his time. And the problems that worried him have only grown more substantial over the decades. In the famous “Cambrian explosion” of around half a billion years ago, a striking variety of new organisms—including the first-ever animals—pop up suddenly in the fossil record over a mere 70-odd million years. This great outburst followed many hundreds of millions of years of slow growth and scanty fossils, mainly of single-celled organisms, dating back to the origins of life roughly three and half billion years ago.

Darwin’s theory predicts that new life forms evolve gradually from old ones in a constantly branching, spreading tree of life. Those brave new Cambrian creatures must therefore have had Precambrian predecessors, similar but not quite as fancy and sophisticated. They could not have all blown out suddenly, like a bunch of geysers. Each must have had a closely related predecessor, which must have had its own predecessors: Darwinian evolution is gradual, step-by-step. All those predecessors must have come together, further back, into a series of branches leading down to the (long ago) trunk.

But those predecessors of the Cambrian creatures are missing. Darwin himself was disturbed by their absence from the fossil record. He believed they would turn up eventually. Some of his contemporaries (such as the eminent Harvard biologist Louis Agassiz) held that the fossil record was clear enough already, and showed that Darwin’s theory was wrong. Perhaps only a few sites had been searched for fossils, but they had been searched straight down. The Cambrian explosion had been unearthed, and beneath those Cambrian creatures their Precambrian predecessors should have been waiting—and weren’t. In fact, the fossil record as a whole lacked the upward-branching structure Darwin predicted.

The trunk was supposed to branch into many different species, each species giving rise to many genera, and towards the top of the tree you would find so much diversity that you could distinguish separate phyla—the large divisions (sponges, mosses, mollusks, chordates, and so on) that comprise the kingdoms of animals, plants, and several others—take your pick. But, as Berlinski points out, the fossil record shows the opposite: “representatives of separate phyla appearing first followed by lower-level diversification on those basic themes.” In general, “most species enter the evolutionary order fully formed and then depart unchanged.” The incremental development of new species is largely not there. Those missing pre-Cambrian organisms have still not turned up. (Although fossils are subject to interpretation, and some biologists place pre-Cambrian life-forms closer than others to the new-fangled Cambrian creatures.)

Some researchers have guessed that those missing Precambrian precursors were too small or too soft-bodied to have made good fossils. Meyer notes that fossil traces of ancient bacteria and single-celled algae have been discovered: smallness per se doesn’t mean that an organism can’t leave fossil traces—although the existence of fossils depends on the surroundings in which the organism lived, and the history of the relevant rock during the ages since it died. The story is similar for soft-bodied organisms. Hard-bodied forms are more likely to be fossilized than soft-bodied ones, but many fossils of soft-bodied organisms and body parts do exist. Precambrian fossil deposits have been discovered in which tiny, soft-bodied embryo sponges are preserved—but no predecessors to the celebrity organisms of the Cambrian explosion.

This sort of negative evidence can’t ever be conclusive. But the ever-expanding fossil archives don’t look good for Darwin, who made clear and concrete predictions that have (so far) been falsified—according to many reputable paleontologists, anyway. When does the clock run out on those predictions? Never. But any thoughtful person must ask himself whether scientists today are looking for evidence that bears on Darwin, or looking to explain away evidence that contradicts him. There are some of each. Scientists are only human, and their thinking (like everyone else’s) is colored by emotion.
...


David Gelernter is professor of computer science at Yale University, chief scientist at Mirror Worlds Technologies, and member of the National Council of the Arts.


FREE PDF GRATIS: CRB

Mecânica Quântica Emergente - Perspectivas do Centenário de David Bohm

Emergent Quantum Mechanics - David Bohm Centennial Perspectives

Topics of the Special Issue:

Interpretations of Quantum Mechanics
Nonlocality and Violation of Bell Inequalities
Quantum Probabilities and Contextuality
Quantum Causality and Ontology
Information Measures in Quantum Theory
Quantum Observation and the Physics of the Experimenter Agent
Nonlinear Methods applied to Quantum Theory
Self-organization and Quantum Emergence
Hidden Variable Theories and Relativity
Emergent Space-time
ISBN 978-3-03897-616-5 (Pbk);
ISBN 978-3-03897-617-2 (PDF);
© 2019 by the authors; CC BY-NC-ND licence

Jan Walleczek, Gerhard Grössing, Paavo Pylkkänen and Basil Hiley (Eds.)
Pages: 544
Published: April 2019
  
Emergent quantum mechanics (EmQM) explores the possibility of an ontology for quantum mechanics. The resurgence of interest in realist approaches to quantum mechanics challenges the standard textbook view, which represents an operationalist approach. The possibility of an ontological, i.e., realist, quantum mechanics was first introduced with the original de Broglie–Bohm theory, which has also been developed in another context as Bohmian mechanics. This book features expert contributions which were invited as part of the David Bohm Centennial symposium of the EmQM conference series. Questions directing the EmQM research agenda are: Is reality intrinsically random or fundamentally interconnected? Is the universe local or nonlocal? Might a radically new conception of reality include a form of quantum causality or quantum ontology? What is the role of the experimenter agent in ontological quantum mechanics? The book features research examining ontological propositions also that are not based on the Bohm-type nonlocality. These include, for example, local, yet time-symmetric, ontologies, such as quantum models based upon retrocausality. The book offers thirty-two contributions which are organized into seven categories to provide orientation as is outlined in the Editorial contribution in the beginning of the book.

This book is a printed edition of the Special Issue Emergent Quantum Mechanics – David Bohm Centennial Perspectives that was published in Entropy.


FREE PDF GRATIS: Entropy

Pode o vírus gigante Medusa ajudar explicar a evolução da complexidade da vida?

quinta-feira, maio 09, 2019

Medusavirus, a Novel Large DNA Virus Discovered from Hot Spring Water

Genki Yoshikawa, Romain Blanc-Mathieu, Chihong Song, Yoko Kayama, Tomohiro Mochizuki, Kazuyoshi Murata, Hiroyuki Ogata, Masaharu Takemura
Joanna L. Shisler, Editor


Resultado de imagem para Medusavirus
A new giant virus may help scientists better understand the emergence of complex life.
Credit: © Tokyo University of Science

ABSTRACT

Recent discoveries of new large DNA viruses reveal high diversity in their morphologies, genetic repertoires, and replication strategies. Here, we report the novel features of medusavirus, a large DNA virus newly isolated from hot spring water in Japan. Medusavirus, with a diameter of 260 nm, shows a T=277 icosahedral capsid with unique spherical-headed spikes on its surface. It has a 381-kb genome encoding 461 putative proteins, 86 of which have their closest homologs in Acanthamoeba, whereas 279 (61%) are orphan genes. The virus lacks the genes encoding DNA topoisomerase II and RNA polymerase, showing that DNA replication takes place in the host nucleus, whereas the progeny virions are assembled in the cytoplasm. Furthermore, the medusavirus genome harbored genes for all five types of histones (H1, H2A, H2B, H3, and H4) and one DNA polymerase, which are phylogenetically placed at the root of the eukaryotic clades. In contrast, the host amoeba encoded many medusavirus homologs, including the major capsid protein. These facts strongly suggested that amoebae are indeed the most promising natural hosts of medusavirus, and that lateral gene transfers have taken place repeatedly and bidirectionally between the virus and its host since the early stage of their coevolution. Medusavirus reflects the traces of direct evolutionary interactions between the virus and eukaryotic hosts, which may be caused by sharing the DNA replication compartment and by evolutionarily long lasting virus-host relationships. Based on its unique morphological characteristics and phylogenomic relationships with other known large DNA viruses, we propose that medusavirus represents a new family, Medusaviridae.

IMPORTANCE 

We have isolated a new nucleocytoplasmic large DNA virus (NCLDV) from hot spring water in Japan, named medusavirus. This new NCLDV is phylogenetically placed at the root of the eukaryotic clades based on the phylogenies of several key genes, including that encoding DNA polymerase, and its genome surprisingly encodes the full set of histone homologs. Furthermore, its laboratory host, Acanthamoeba castellanii, encodes many medusavirus homologs in its genome, including the major capsid protein, suggesting that the amoeba is the genuine natural host from ancient times of this newly described virus and that lateral gene transfers have repeatedly occurred between the virus and amoeba. These results suggest that medusavirus is a unique NCLDV preserving ancient footprints of evolutionary interactions with its hosts, thus providing clues to elucidate the evolution of NCLDVs, eukaryotes, and virus-host interaction. Based on the dissimilarities with other known NCLDVs, we propose that medusavirus represents a new viral family, Medusaviridae.

FREE PDF GRATIS: Journal of Virology

Stuart Kauffman 'falou e disse': uma nova física é necessária para investigar as origens da vida

A World Beyond Physics: The Emergence and Evolution of Life Stuart A. Kauffman Oxford University Press (2019)

A protocell (artificial cell) dividing to produce two daughter cells.
An artist’s impression of early ‘protocells’ proliferating.Credit: Henning Dalhoff/Science Photo Library

Among the great scientific puzzles of our time is how life emerged from inorganic matter. Scientists have probed it since the 1920s, when biochemists Alexsandr Oparin and J. B. S. Haldane (separately) investigated the properties of droplets rich in organic molecules that existed in a ‘prebiotic soup’ on the primitive Earth (see T. Hyman and C. Brangwynne Nature 491, 524–525; 2012). Each hypothesized that organic compounds underwent reactions leading to more complex molecules, and eventually to the first life forms.

What was missing then, as now, is a concrete theory for the physics of what life is, testable against experiment — which is likely to be more universal than the chemistry of life on Earth. Decades after Oparin and Haldane, Erwin Schrödinger’s 1944 book What Is Life? (see P. Ball Nature 560, 548–550; 2018) attempted to lay conceptual foundations for such a theory. Yet, more than 70 years and two generations of physicists later, researchers still ponder whether the answers lie in unknown physics. No one has led the charge on these questions quite like Stuart Kauffman.

In the 1980s and 1990s, Kauffman — a complex-systems researcher — developed a highly influential theory for life’s origins, based on molecules that reproduce only collectively, called autocatalytic sets. He posited that if a chemical soup of polymers was sufficiently diverse, these sets would emerge spontaneously as a phase transition — that is, a significant change in state or function, akin to the shift from solid to liquid. The sets function holistically, mutually catalysing the formation of all their molecular members. (His inspiration was advances in the mathematics of networks by Paul Erdős and Alfréd Rényi, who had demonstrated how phase transitions occur in random networks as connectivity is increased.) Now, in A World Beyond Physics, Kauffman elaborates.

His key insight is motivated by what he calls “the nonergodic world” — that of objects more complex than atoms. Most atoms are simple, so all their possible states can exist over a reasonable period of time. Once they start interacting to form molecules, the number of possible states becomes mind-bogglingly massive. Only a tiny number of proteins that are modestly complex — say, 200 amino acids long — have emerged over the entire history of the Universe. Generating all 20020 of the possibilities would take aeons. Given such limitations, how does what does exist ever come into being?

This is where Kauffman expands on his autocatalytic-sets theory, introducing concepts such as closure, in which processes are linked so that each drives the next in a closed cycle. He posits that autocatalysing sets (of RNA, peptides or both) encapsulated in a sphere of lipid molecules could form self-reproducing protocells. And he speculates that these protocells could evolve. Thus, each new biological innovation begets a new functional niche fostering yet more innovation. You cannot predict what will exist, he argues, because the function of everything biology generates will depend on what came before, and what other things exist now, with an ever-expanding set of what is possible next.

Because of this, Kauffman provocatively concludes, there is no mathematical law that could describe the evolving diversity and abundance of life in the biosphere. He writes: “we do not know the relevant variables prior to their emergence in evolution.” At best, he argues, any ‘laws of life’ that do exist will describe statistical distributions of aspects of that evolution. For instance, they might predict the distribution of extinctions. Life’s emergence might rest on the foundations of physics, “but it is not derivable from them”, Kauffman argues.
...

FREE PDF GRATIS: Nature

Em meio a explosão de dados genômicos, cientistas descobrem proliferação de erros

Front. Microbiol., 28 February 2019 | https://doi.org/10.3389/fmicb.2019.00383

Whole Proteome Clustering of 2,307 Proteobacterial Genomes Reveals Conserved Proteins and Significant Annotation Issues

Svetlana Lockwood1, Kelly A. Brayton1,2,3, Jeff A. Daily4 and Shira L. Broschat1,2,3*

1 School of Electrical Engineering and Computer Science, Washington State University, Pullman, WA, United States

2 Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, WA, United States

3 Paul G. Allen School for Global Animal Health, Washington State University, Pullman, WA, United States

4 Pacific Northwest National Laboratory, Richland, WA, United States

NextCODE Reloads With $240M, Eyes IPO, As Genomic Data Demand Grows
Source/Fonte: Exome

Abstract

We clustered 8.76 M protein sequences deduced from 2,307 completely sequenced Proteobacterial genomes resulting in 707,311 clusters of one or more sequences of which 224,442 ranged in size from 2 to 2,894 sequences. To our knowledge this is the first study of this scale. We were surprised to find that no single cluster contained a representative sequence from all the organisms in the study. Given the minimal genome concept, we expected to find a shared set of proteins. To determine why the clusters did not have universal representation we chose four essential proteins, the chaperonin GroEL, DNA dependent RNA polymerase subunits beta and beta′ (RpoB/RpoB′), and DNA polymerase I (PolA), representing fundamental cellular functions, and examined their cluster distribution. We found these proteins to be remarkably conserved with certain caveats. Although the groEL gene was universally conserved in all the organisms in the study, the protein was not represented in all the deduced proteomes. The genes for RpoB and RpoB′ were missing from two genomes and merged in 88, and the sequences were sufficiently divergent that they formed separate clusters for 18 RpoB proteins (seven clusters) and 14 RpoB′ proteins (three clusters). For PolA, 52 organisms lacked an identifiable sequence, and seven sequences were sufficiently divergent that they formed five separate clusters. Interestingly, organisms lacking an identifiable PolA and those with divergent RpoB/RpoB′ were predominantly endosymbionts. Furthermore, we present a range of examples of annotation issues that caused the deduced proteins to be incorrectly represented in the proteome. These annotation issues made our task of determining protein conservation more difficult than expected and also represent a significant obstacle for high-throughput analyses.