Why Warriors-Blazers series is banned on Turkish TV

first_imgTurkey isn’t a good place to be these days for NBA fans hoping to watch the Warriors and Trail Blazers in the Western Conference Finals, starting with Tuesday night’s Game 1.Because Portland’s Turkish center Enes Kanter is such a vocal opponent of Turkey’s president, the country’s sports broadcast channel S Sport has decided not to show any games involving him and the Blazers.“I can say clearly that we will not be broadcasting the Warriors-Blazers series,” S Sport announcer Omer Sarac told …last_img read more

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Natural Selection Demonstrated in European Heart-Disease Gene?

first_imgStephen Wooding (U. of Utah) is elated.  He sees an “exciting trend” in genetic research that might, finally, demonstrate positive natural selection acting on a gene with a clear phenotypic effect (measurable outward benefit).  Writing in the Sept. 7 Current Biology,1 he mentions a few recent papers suggesting this connection, but focuses particularly on one study by Rockman et al. in the same issue.2  This UK/American team claims to have identified a gene that has been positively selected to shape heart disease risk among Europeans.  The story was summarized by EurekAlert.    The gene under investigation is named MMP3, a regulator of a substance that builds coronary artery walls.  The amount of up- or down-regulation of this gene affects their elasticity and thickness.  The researchers compared this gene and its surrounding DNA between nine kinds of monkeys and apes, and between six human populations.  They claim to have found a trend among Europeans to possess a certain mutation that up-regulates the products of MMP3 (because it inhibits repressive factors).  This leads to less hardening of the arteries but more risk of blood clot induced heart attack or stroke (myocardial infarction).  The mutation changes one T to a C at a certain position on the gene.  Using molecular phylogenetic techniques, they estimated the mutation might have occurred in the European line anywhere from 36,600 to 2,200 years ago.  Maybe it came about in the Ice Age, they surmise, and natural selection acting on this mutation may have given Europeans dining on animal fat some protection from atherosclerosis.  Whatever, the selection probably did not act alone on that one gene, which only regulates other genes, but on a suite of genes due to pleiotropic effects (i.e., when one gene evolves, other unrelated phenotypic effects can result).    The authors seemed happy to be able to provide an example of natural selection acting positively on a gene for a beneficial physiological effect: “The evolutionary forces of mutation, natural selection, and genetic drift shape the pattern of phenotypic variation in nature, but the roles of these forces in defining the distributions of particular traits have been hard to disentangle.”  (Emphasis added in all quotes.) Natural selection is an important factor influencing variation in the human genome, but most genetic studies of natural selection have focused on variants with unknown phenotypic associations.  This trend is changing.  New studies are rapidly revealing the effects of natural selection on genetic variants of known or likely functional importance….These [studies on] variants [on genes with known phenotypic effects] are particularly interesting from an evolutionary standpoint because they are where the phenotypic rubber meets the road of natural selection – variants upon which natural selection could be having particularly direct effects.Those assuming this was old news since Darwin’s day might be surprised at this admission that studies have rarely connected a mutation to an actual physical benefit.  Analyses at the molecular level of the gene, to be fair, have only recently become possible.  Stephen Wooding is greatly encouraged by this study.  He thinks it represents not only an exciting trend, but a new means of paving “an unusually direct path between ancient human history and modern human health.”  Rockman’s team claims that British men would have 43% more heart attacks had this mutation not occurred among their distant ancestors.  But then, since hardening of the arteries seems to be a recent malady among humans, he admitted that maybe the natural selection at the time was for something else “and the heart disease effect was incidental.”    One other benefit Rockman claims for this study is that it shows natural selection can act not only on the genes the make proteins, but on the genes that regulate other genes– a factor he claims “traditional evolutionary biology has all but ignored.”  Considering the evolution of regulatory factors extends natural selection theory to the level of the “wiring diagram,” he says.  No longer should we just consider good genes and bad genes.  “Rather, there is a complex set of interactions” such that certain combinations might be best in one environment, others better in another.  “So we’re advocating a more nuanced view of how we view the genetic bases of disease,” he said in the press release from Duke University.1Stephen Wooding, “Natural Selection: Sign, Sign, Everywhere a Sign,” Current Biology, Volume 14, Issue 17, 7 September 2004, Pages R700-R701, doi:10.1016/j.cub.2004.08.041.2Rockman et al., “Positive Selection on MMP3 Regulation Has Shaped Heart Disease Risk,” Current Biology, Volume 14, Issue 17, 7 September 2004, Pages 1531-1539, doi:10.1016/j.cub.2004.08.051.Remember the old moron jokes?  “How do you keep a moron busy for an hour?  Put him in a round room and tell him there’s a penny in the corner.”  It doesn’t take much to amuse Darwinists.  Tell them there’s a hint of natural selection in the human genome, and it is incredible the amount of work they will do to find it.  You can bet any claims will be ambiguous, hazy, uncertain, questionable and open to different interpretations, but if they can be offered in homage to buddha Charlie, it’s worth it to them to run in logical circles and keep up the candles of hope burning.  (For another example, look at this story on EurekAlert, about Penn State scientists “hunting illusive signs of natural selection” between Europeans and Africans, and finding only ambiguous signs of differing susceptibility to disease or milk intolerance.)    What did these guys find, really?  One single-nucleotide polymorphism in just one gene out of hundreds that regulate heart health.  Sure, tweaking the regulation of this gene might put a person at risk for hardening of the arteries, but is Darwinian evolution the only explanation?  The Europeans could have descended from a clan whose grandpappy had the mutation at the Tower of Babel, for that matter; how could they prove otherwise?  The monkeys they studied had very different polymorphisms of these genes, and you don’t see them all keeling over from heart attacks.  If natural selection acted on this gene, why didn’t it act on Siberians or Eskimos or Australians or others at similar latitudes?  Did this mutation lead to a new organ or function or add to the genetic information?  No, it only tweaked the existing information.  And some evolution!  Pick your poison: increased risk of atherosclerosis, or increased risk of myocardial infarction.  Is this one of the finest examples they can find of the miracle-working mechanism of natural selection, the discovery that made Chairman Charlie famous, so powerful that during the same period of time it turned monkeys swinging from trees into humans writing books?    The line about Ice Age men benefiting from the mutation because of their mammal-fat diet is comical.  How could that help the population genetics, if the individuals most likely got their heart attacks after having children?  The error bars on their dates are huge, even if one were to swallow the highly questionable phylogenetic techniques they used, and the evolution-based assumptions about mutation rates.  A chain of reasoning is only as strong as its weakest link: e.g., “if there was water on Mars, there might have been life, therefore there might have been intelligent life, therefore there might have been lawyers.”  Evolutionists get away with stacked assumptions only because they have ruled out anything other than naturalistic explanations.  Since the only contender is something akin to Darwinism, it’s the best they can offer (see Best-in-Field Fallacy).    Why are we the only ones questioning the Darwinist spin on this paper, and asking the hard questions while the other science outlets mindlessly inherit the wind and parrot the spin with lines like “Heart gene yields insights into evolution”?  Why not consider the obvious, that a functioning circulatory system is a tremendous example of interrelated, functional design?  The diagnosis is simple.  It is that ancient human malady, hardness of heart.(Visited 133 times, 1 visits today)FacebookTwitterPinterestSave分享0last_img read more

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Mutations Accelerate Each Other’s Damage

first_imgAs reported in our 10/14/2004 entry, mutations do not work in isolation; even the good kind usually conspire against the host.  This fact has been largely ignored by neo-Darwinists.  Some researchers at the Weizmann Institute in Rehovot, Israel, writing in Nature,1 tested the interaction of mutations (epistasis) on proteins.  They found, in short, that harmful mutations usually accelerate the loss of fitness above what would occur in isolation.  Some organisms exhibit robustness against mutations, though, as in well-known cases of antibiotic resistance.  The team tested the robustness of E. coli while mutating a gene for a lactamase (TEM-1) that confers some resistance to ampicillin.  They found that, at best, the organisms could hold out at a threshold level of fitness only temporarily.  Beyond the threshold, death was speedy and inevitable.  This was even after they removed the bad mutations:Subjecting TEM-1 to random mutational drift and purifying selection (to purge deleterious mutations) produced changes in its fitness landscape indicative of negative epistasis; that is, the combined deleterious effects of mutations were, on average, larger than expected from the multiplication of their individual effects.  As observed in computational systems, negative epistasis was tightly associated with higher tolerance to mutations (robustness).  Thus, under a low selection pressure, a large fraction of mutations was initially tolerated (high robustness), but as mutations accumulated, their fitness toll increased, resulting in the observed negative epistasis.  These findings, supported by FoldX stability computations of the mutational effects, prompt a new model in which the mutational robustness (or neutrality) observed in proteins, and other biological systems, is due primarily to a stability margin, or threshold, that buffers the deleterious physico-chemical effects of mutations on fitness.  Threshold robustness is inherently epistatic—once the stability threshold is exhausted, the deleterious effects of mutations become fully pronounced, thereby making proteins far less robust than generally assumed.Their study also casts doubt on the ultimate survivability of so-called “neutral” mutations.  These initially have no obvious effect on the fitness of the organism.  This may be due to backup copies of a gene, suppressors of the mutated gene, and other mechanisms the cell uses to mask the damage.  Eventually, however, the threshold is exceeded and the system collapses just as rapidly as a cell toppled by interacting harmful mutations.    The authors of this study gave no indication that beneficial mutations can add up and help an organism.  In fact, they failed to say anything about evolution that would provide hope for progress.  By contrast, they offered a “new model” that sounds distinctly anti-evolutionary: cells are programmed to hold off the damage of mutations as long as they can, but will ultimately collapse under a mutational load.  They concluded that “proteins may not be as robust as is generally assumed.”  Their real-world experiment on bacteria showed robustness to mutations only to a certain point, then everything raced downhill:Thus, theory and simulations have predicted a tight correlation between robustness and epistasis.  Our work provides an experimental verification of this correlation and proposes a mechanism that accounts for it.  Our model implies that any biological system that exhibits threshold robustness, or redundancy robustness, is inevitably epistatic.  In such systems, mechanisms that purge potentially deleterious mutations, such as recombination (through sexual reproduction and other mechanisms) are of crucial importance, as they help to maintain this threshold.  In this way, recombination, threshold robustness and negative epistasis may be interlinked—each being an inevitable by-product of the other.They seem to be saying not only that mutations are not sources of positive fitness gains, but other proposed mechanisms like recombination are only stopgap measures to protect against the death spiral that would result when “randomly drifting proteins” gang up (negative epistasis) to cause a terror attack in the organism.1Bershtein et al, “Robustness-epistasis link shapes the fitness landscape of a randomly drifting protein,” Nature 444, 929-932 (14 December 2006) | doi:10.1038/nature05385.It is extremely important that followers of the creation-evolution debate understand this story and the earlier one (10/14/2004), because they cut to the heart of Darwinist claims that mutations and natural selection can create brains out of atoms given millions of years.  This is where the rubber meets the road: can mutations and recombination under selection act in concert to produce evolutionary progress, including wings and eyes and sonar and powered flight?  Complex systems need an explanation at the genetic level.  The modern synthesis of evolutionary theory (neo-Darwinism) maintains that mutations are the source of evolutionary novelty, and that natural selection preserves the rare beneficial mutations in a cumulative way.  This is the machine room from which “endless forms most beautiful” (06/29/2005) emerge without a Designer.  Two scientific papers reported here, that would likely be little noticed otherwise, have essentially falsified neo-Darwinism in the lab.  Theory and experiment both show it does not work.    In the previous entry (10/14/2004) we likened the situation to a victim held up by robbers but protected by guardian angels.  The bad news was that the robbers either shoot each other or shoot the victim simultaneously, and the guardian angels fight each other instead of helping the victim.  It’s like a Murphy’s “Non-Reciprocal Laws of Expectations” that state, (1) Positive expectations produce negative results, and (2) Negative expectations produce negative results.  The neo-Darwinists have put all their hope in positive expectations, but real-world experiments show that mutations do not and cannot add up for good.  They conspire for bad!  Only the built-in safety mechanisms in the cell hold off mutational catastrophe.  This same lesson should have been learned from the important 03/17/2003 entry almost four years ago; presumed benefits actually cause “slippage on the treadmill” to keep the organism, at best, just running in place.    Another analogy may illuminate what this new outwardly dry, boring, technical paper said.  Picture a large, well-run factory with numerous modern systems for safety, backup and security.  Along comes a motley gang with no plan other than to wreak havoc at random.  Some are blocked by the entrance controls.  Those that get inside start overturning tables, knocking out factory workers, setting off alarms and creating general mayhem.  The security systems each come into play as planned, trying to isolate the damage, restore backups, and start the redundant processes.  Workers scramble to copy off the important data to other sections of the factory where the work can continue.  Security guards manage to neutralize some of the attackers, but more keep coming in.  Some gangsters plug the real workers then steal their lab coats and badges, wandering around to do their harm by stealth.  To an outsider, it may not be apparent that anything is wrong – for awhile – because the factory continues to function; supplies come in, goods go out.  In time, however, the best-prepared factory may not be able to carry on.  Fires are set at random.  Automatic sprinklers respond as designed, but now they have damaged the computers.  Gangsters pull fire alarms here and there, confusing workers who don’t know whether to ignore them or run outside.  Security forces are eventually overwhelmed.  Backup systems are damaged as soon as they are brought online.  It’s too much; the factory implodes in a catastrophe, and everything shuts down.    If this is really the way mutations work in a cell, it should be obvious to everyone that trusting any random mechanism to produce order is a vain hope and supreme folly.  This, of course, is what anti-Darwinists have been maintaining since 1859.  That it would take two research teams with no ties to creationist organizations or the intelligent design movement, published in two of the most adamantly anticreationist scientific journals in the world (PNAS and Nature) to finally figure this out should be of great interest to historians and sociologists.  What is it about Darwinian faith that generates negative epistasis against common sense?    Evolutionary theory is coasting downhill on a dead-end track with no fuel in the engine, while the passengers are being served cheese and wine, not knowing anything is wrong.  Creation-Evolution Headlines is like the tattler running down the aisles warning everybody about bad news only the engine crew is aware of, despite the pleasant announcements on the intercom.  We think the customers who paid for the trip deserve to be told the truth: despite how smoothly things appear to be running, they just got sold a dead-end trip to destruction.(Visited 73 times, 1 visits today)FacebookTwitterPinterestSave分享0last_img read more

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