In a chance discovery, researchers have for the first time observed the emergence of something akin to metabolism in molecules that also self-replicate. The replicator molecules catalyse a reaction that produces compounds that help to make the replicator's own building blocks. It might be one of the most lifelike chemical systems ever created, combining two of life's three essential features '" replication, metabolism and compartmentalisation.
'What it can teach us is that those functions that we see in living systems, they are not unique to life as we know it,' says origin of life scientist Kamila Muchowska from the University of Strasbourg, France, who wasn't involved in the work'
Systems that either replicate or perform metabolism-like reactions have existed before, and some can even switch from one function to the other upon addition of chemicals or environmental changes. But a team around Sijbren Otto from the University of Groningen in the Netherlands has now created molecules that do both at the same time.
Rob Stadler co-author with Change Laura Tan of The Stairway to Life: An Origin-Of-Life Reality Check, writes to puncture the balloon:
They use quite a generous definition of "self replicator". It has nothing to do with replication of biopolymers in life, yet they intend for the work to be encouraging to abiogenesis. Here are a few of the serious limitations for the application of this to abiogenesis:
1) The starting monomers are purified, concentrated, homochiral molecules purchased from a synthetic peptide lab. Certainly not prebiotically plausible.
2) the starting monomers have no relation to any biopolymer known in life - they are short polypeptides connected to a benzene dithiol.
3) the starting monomers do not covalently bond to create a polymer (as in life); they merely afinitize to form a macromolecular structure. Mechanical perturbation breaks the growing macromolecule to allow for an increased number of nucleation sites that subsequently grow. This is called "self-replication". It is closer to crystal growth than to replication of any biopolymer.
4) The system is not capable of molecular evolution because any "replication errors" that could convey a benefit would not be passed on to "daughter" molecules (i.e., no "information" could be "passed down" from "generation to generation").
The novelty in this paper is that they found catalytic abilities created by the macromolecular structure that could enhance the growth rate of this macromolecule.
So, it is entirely distinct from life, but intended to demonstrate one principle that is required for abiogenesis.
The fact that it is recognized as a meaningful contribution is a testimony to the desperation to show progress'-it stands out only because no meaningful progress can be made in any direction that is actually relevant to life.
The biggest abortion provider in the United States had to dump its founder, Margaret Sanger, on account of her advocacy of eugenics and social Darwinism. That wouldn't have been happening two decades ago. Back then, it was okay to just sneer at people who raised the issue.
Planned Parenthood, the biggest business in town, has had to eat humble pie and disown its patron saint, Margaret Sanger, a eugenicist who thought that black lives, among others, were multiplying too fast.
PPFA also has leadership issues, and staff in some clinics are fed up with bullying bosses and low wages. Indeed, one abortion activist blames Planned Parenthood for the fact that 'the pro-life movement has us on our heels.'
The left-liberal British daily, The Guardian, recently ran a piece by a US columnist under the heading, 'The pro-choice movement is in tatters. Planned Parenthood is part of the problem'. In it, feminist Jessa Crispin complains bitterly about the ineffectiveness of the organisation that is practically synonymous with the abortion industry in the US, and its political leadership.
Crispin herself worked for Planned Parenthood in Texas for five years. According to her, PPFA has become so invested in its political role that it is letting the industry itself go to pot, betraying the ranks of ordinary workers and the women whose access to abortion is reduced. It cannot simply blame Trump, she says, since the trend of conservative state governments passing restrictive abortion laws has been happening for decades.
While live baby dismemberment is an ultra-cool elite cause, fully in accord with Darwinian principles, it still horrifies many ordinary people. Time will tell if that still matters.
See also: Planned Parenthood Disavowed Margaret Sanger '- Finally(Barry Arrington)
There is no greater problem for materialists and physicalists that trying to explain how the brain could create consciousness. This video argues the hard problem implies the mind cannot reduce to matter.
' what may be 'junk' at one level may be of the utmost significance at another level. This happens I think by way of a top-down causal process that Paul Davies (2012) has alluded to, explainable in part by the augmentation of
'the normal terms referring to local forces contained in the Hamiltonian for chromatin with additional (presumably small) non-local terms representing functional (i.e. semantic or contextual) information. By coupling the mechanical and informational dynamics in this manner, the dynamical laws describing chromatin behaviour would become time-dependent and change according to the informational state of the system. Information would then possess direct, albeit subtle, traction over matter and permit epigenetic control to be exercised directly on the chromatin itself.'
Such would involve an 'explicit coupling between dynamical laws and information-rich states, thus endowing higher level entities, such as contextual information, with direct causal efficacy on matter alongside intermolecular forces.'
If we take such 'contextual information' to be resident at all tiers of the meiosis I network, from the spindle as whole to (say) each and every centromeric locus, then 'with direct causal efficacy' retroelement and satellite DNAs can be endowed with information-bearing states. Of course, 'such a proposal represents a decisive break with the normal formulation of the theory of dynamical systems,' as Davies notes, which means that 'theories of this sort remain largely unexplored.' But explore it we should'and especially where cytology meets 'junk' DNA.
It's not enough that DNA is a language but now it has proofreaders?:
On the DNA assembly line, two proofreading proteins work together as an emergency stop button to prevent replication errors. New research from North Carolina State University and the University of North Carolina at Chapel Hill shows how these proteins - MutL and MutS - prevent DNA replication errors by creating an immobile structure that calls more proteins to the site to repair the error. This structure could also prevent the mismatched region from being "packed" back into the cell during division.
When a cell prepares to divide, the DNA splits, with the double helix "unzipping" into two separate backbones. New nucleotides - adenine, cytosine, guanine or thymine - are filled into the gaps on the other side of the backbone, pairing with their counterparts (adenine with thymine and cytosine with guanine) and replicating the DNA to make a copy for both the old and the new cells. The nucleotides are a correct match most of the time, but occasionally - about one time in 10 million - there is a mismatch.
"Although mismatches are rare, the human genome contains approximately six billion nucleotides in every cell, resulting in approximately 600 errors per cell, and the human body consists of more than 37 trillion cells," says Dorothy Erie, chemistry professor at UNC-Chapel Hill, member of UNC's Lineberger Comprehensive Cancer Center and co-corresponding author of the work. "Consequently, if these errors go unchecked they can result in a vast array of mutations, which in turn can result in a variety of cancers, collectively known as Lynch Syndrome."
A pair of proteins known as MutS and MutL work together to initiate repair of these mismatches. MutS slides along the newly created side of the DNA strand after it's replicated, proofreading it. When it finds a mismatch, it locks into place at the site of the error and recruits MutL to come and join it. MutL marks the newly formed DNA strand as defective and signals a different protein to gobble up the portion of the DNA containing the error. Then the nucleotide matching starts over, filling the gap again. The entire process reduces replication errors around a thousand-fold, serving as one of our body's best defenses against genetic mutations that can lead to cancer.
It turns out that biological fine-tuning goes to the very extremes of physics. In this lecture, William Bialek shows that eyes can detect individual photons, and a number of other phenomena where biology operates on the very edge of what is possible in physics.
New York City's Bronx Zoo is apologizing for its racist past when the facility put Ota Benga, a central African man, on display in the Monkey House in 1906. 'In the name of equality, transparency, and accountability, we must confront our organization's historic role in promoting racial injustice as we advance our mission to save wildlife and wild places,' officials with the Wildlife Conservation Society said in a statement Wednesday.
The protests of Black ministers put an end to the show but Benga ended up committing suicide in 2016.
David Klinghoffer commends the Zoo for finally owning up to and repudiating this disgusting stuff but,he notes:
What's missing, and it's not fine, is any mention of where these evil ideas came from. What was the nature, the content, of the 'pseudoscientific racism' that motivated Ota Benga's treatment? To be accurate, the racism wasn't 'eugenics-based' it was 'evolution-based.' That is left out'
The truth is that placing a man in the Monkey House was intended as an education for the public in Darwinian evolution. As John West has said, Ota Benga was 'only one of thousands of indigenous peoples who were put on display in America in the name of Darwinian evolution.'
Though its article yesterday forgets to mention it ('Racist Incident from Bronx Zoo's Past Draws Apology'), the New York Times understood that clearly in 1906. Brushing aside protests from black clergymen that the African should be given an education not put in the cage, the newspaper explained:
'The suggestion that Benga should be placed in a school instead of a cage ignores the high probability that school would be a place of torture to him and one from which he could draw no advantage whatever. The idea that men are all much alike except as they have had or lacked opportunities for getting an education out of books is now far out of date.'
In other words, 'Listen to the science!' In fact, racial hierarchy was hailed as solid science at the time.
He recommends, again, John West's Human Zoos: America's Forgotten History of Scientific Racism (see it before YouTube finds another reason to restrict it or maybe pull it):
As an alternative to Canceling itself, the New York Times will likely just find someone else to blame.
Less than 2% of the human genome encodes proteins1. A grand challenge for genomic sciences has been mapping the functional elements '- the regions that determine the extent to which genes are expressed '- in the remaining 98% of our DNA. The Encyclopedia of DNA Elements (ENCODE) project, among other large collaborative efforts2'"4, was established in 2003 to create a catalogue of these functional elements and to outline their roles in regulating gene expression. In nine papers in Nature5'"13, the ENCODE consortium delivers the third phase of its valuable project'
This yet-to-be-completed encyclopedia has already become a quintessential tool for understanding gene regulation and genetic predisposition to disease. In the upcoming fourth phase of the ENCODE project, we would be excited to see a systematic assessment of whether the catalogued CREs actually performed the functions inferred on the basis of histone modifications and bound proteins; this could be achieved using high-throughput functional-genomic technologies. The continued expansion of ENCODE to wider biological contexts (such as disease samples and rare cell types) at single-cell resolution would help researchers to use genomic information to diagnose and prevent diseases.
Readers may also remember ENCODE from a flap a few years ago when Darwinian Dan Graur announced that the ENCODE team had to be wrong in saying that there wasn't nearly as much junk DNA as had been thought. After a while, Graur just wasn't doing politeness any more.
Now that ENCODE has so much information to offer, maybe Graur should do politeness again and try listening.
See also:
Junk DNA: Dan Graur (Junk!), ENCODE Team (Not Junk!), And the Science Media
It's called a 'refinement' to 12.6 billion years, down from 13.77 billion years:
Using known distances of 50 galaxies from Earth to refine calculations in Hubble's constant, a research team led by a University of Oregon astronomer estimates the age of the universe at 12.6 billion years'
A key calculation for dating is the Hubble's constant, named after Edwin Hubble who first calculated the universe's expansion rate in 1929. Another recent technique uses observations of leftover radiation from the Big Bang. It maps bumps and wiggles in spacetime - the cosmic microwave background, or CMB - and reflects conditions in the early universe as set by Hubble's constant.
However, the methods reach different conclusions, said James Schombert, a professor of physics at the UO. In a paper published July 17 in the Astronomical Journal, he and colleagues unveil a new approach that recalibrates a distance-measuring tool known as the baryonic Tully-Fisher relation independently of Hubble's constant'
Calculations drawn from observations of NASA's Wilkinson Microwave Anisotropy Probe in 2013 put the age of the universe at 13.77 billion years, which, for the moment, represents the standard model of Big Bang cosmology. The differing Hubble's constant values from the various techniques generally estimate the universe's age at between 12 billion and 14.5 billion years. The new study, based in part on observations made with the Spitzer Space Telescope, adds a new element to how calculations to reach Hubble's constant can be set, by introducing a purely empirical method, using direct observations, to determine the distance to galaxies, Schombert said.
Our physics color commentator Rob Sheldon writes to say,
The age of the universe is just the inverse of the Hubble constant, H0. This article relates a recent paper recalibrating galaxy distances, and recalculating H0 =75 km/s/Mpc. To recap, all methods that rely on measuring the cosmic microwave background (CMBR), get a value H0=67 +/- 1 km/s/Mpc. All methods that rely on the "distance ladder", measuring the distance to Cepheid variable stars, then using that to get galaxy distances, then using that to get supernovae distances, get a value H0=73-75 km/s/Mpc.
Initially, there was some hope that reanalysis might bring the two methods into alignment, but CMBR experiments such as COBE, WMAP, then Planck, then ACT all confirmed the 67 number, whereas recalibration of Cepheids stars by Riess and now recalibration of the Tully-Fisher galactic measure are all converging at 74.
So what are we to do? Here's the conclusion of the paper:
"Our resulting value is on the high side of the different schools of cosmology, signaling that our understanding of the physics of the universe is incomplete with the hope of new physics in the future," he said.
I have long advocated a rewrite of the Big Bang model that converts the cosmic microwave numbers into a Hubble constant. But strangely, like Darwin's model in biology, we see few cosmologists willing to kill the sacred cow. They would rather change the laws of physics ("new physics") than change their model. Models, creations of men, are held in more respect than laws of physics, creations of God.
