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DNA Backtracking

Posted on November 12, 2012 at 7:45 AM Comments comments (0)

Science Daily article says "Humans share over 90% of their DNA with their primate cousins." That's a bit of a reduction from the usual claims of 98% or more, so we have yet more backtracking from mainstream science and the gap between us and our, so called, nearest evolutionary relative gets wider.

Ther article reports that  Dr. Gilad (Ph.D., associate professor of human genetics at the University of Chicago) "reported that up to 40% of the differences in the expression or activity patterns of genes between humans, chimpanzees and rhesus monkeys can be explained by regulatory mechanisms that determine whether and how a gene's recipe for a protein is transcribed to the RNA molecule that carries the recipe instructions to the sites in cells where proteins are manufactured." .

So the RNA or Junk DNA has made a significance already

Read more at:

http://www.sciencedaily.com/releases/2012/11/121106201124.htm

Volcano Date Was 3,000% Wrong, Really!

Posted on November 2, 2012 at 2:20 PM Comments comments (0)

 

So much for scientific dating systems. Volcanoes near the south end of California’s Salton Sea last erupted less than 940 years ago, not 30,000 years ago, as previous dating has maintained.

Live Science reported the correction about theSalton Buttes

The buttes last erupted between 940 and0 B.C., not 30,000 years ago, as previously thought, a new study detailed online Oct. 15 in the journal Geology reports. The new age — which makes these some of California’s youngest volcanoes — pushes the volcanic quintuplets into active status. The California Volcano Observatory, launched in February by the U.S. Geological Survey (USGS), already lists the area as a high threat for future blasts.

New helium-zircon dating technique was used to arrive at the new date.  Scientists really should have known that the cones were young.  Native Americans worked the obsidian from the volcanoes between the fifth and sixth centuries BC, but probably not before that, because it wasn’t available before the last eruptions.

Ref November 1, 2012 in Dating Methods, Geology

 


Another Feathered Dinosaur

Posted on November 2, 2012 at 1:55 PM Comments comments (0)

 

The Telegraph Newspaper (UK - October 26th, 2012) isreporting the discovery of the first fossils of feathered dinosaurs in North America.  The report comes complete artist's impression and many assumptions.  Read the report at:

http://www.telegraph.co.uk/science/dinosaurs/9634930/Fossils-of-feathered-dinosaur-species-discovered-in-the-Americas.html

TheTelegraph says:

" The 75-million-year-old fossil specimens, uncovered in the badlands of Alberta, Canada, include remains of a juvenile and two adult ostrich-like creaturesknown as ornithomimids."

This might actually be a clue to the real origin of the fossil, not actually a dinosaur but a bird, a relative of the ostrich.

CreationEvolution Headlines website has a great article on this find and cuts throug hthe media hype, read the article at:

http://crev.info/2012/10/another-flap-over-dinosaur-feathers/

 


 


More Biased Interpretations on Turtle Bones

Posted on November 2, 2012 at 1:35 PM Comments comments (0)

Science Daily October 29th, 2012 reports the unearthing of 1800 turtle bones in China, even the fact that the boneswere in sedimentary stone, and China has a strong 'Flood' tradition, palaeontologistsmanaged to come up with an alternative explanation.

Extract from article below

Huge Depositof Jurassic Turtle Remains Found in China

ScienceDaily (Oct. 29, 2012) — “Bones upon bones, we couldn’tbelieve our eyes,” says Oliver Wings, paleontologist and guest researcher atthe Museum für Naturkunde in Berlin. He was describing thespectacular find of some 1800 fossilized mesa chelonia turtles from theJurassic era in China’s northwest province of Xinjiang. Wings and the University of Tübingen’s fossil turtlespecialist, Dr. Walter Joyce, were working with Chinese paleontologists there in2008.

Theresults of their further work in 2009 and 2011 have just been published in theGerman journal Naturwissenschaften.

“This site hasprobably more than doubled the known number of individual turtles from theJurassic,” says Walter Joyce. “Some of the shells were stacked up on top of oneanother in the rock.” It is what paleontologists call a “bone bed” – in thiscase consisting only of turtle remains.

Wings, Joyce and their team have made several expeditions to the arid regionsince 2007, finding fossil sharks, crocodiles, mammals and several dinosaurskeletons. Today one of the world’s driest regions, 160 million years agoXinjiang was a green place of lakes and rivers, bursting with life. Yet thescientists have shown that even then, conditions were not always ideal, withclimate change leading to seasonal drought – and this remarkable fossil find.

The turtles had gathered in one of the remaining waterholes during a very dryperiod, awaiting rain. Today’s turtles in Australia for instance do thesame thing. But for the Xinjiang turtles, the rain came too late. Many of theturtles were already dead and their bodies rotting. When the water arrived, itcame with a vengeance: a river of mud, washing the turtles and sediments alongwith it and dumping them in one place, as the paleontologists read the site andits layers of stone.

Could the explanation simply be that they were caught in Noah's flood?

 

Complex Insect Brains

Posted on October 19, 2012 at 7:45 AM Comments comments (0)

Scientific American reports that the discovery of the fossil of a supposedly "520 million-year-old" cockroach, which shows that complex brains evolved much earlier than science previously thought.

http://blogs.scientificamerican.com/observations/2012/10/10/complex-brains-existed-520-million-years-ago-in-cockroach-relative/?WT_mc_id=SA_WR_20121017

The report states that "within the first 20 million years of the group’s emergence, the arthropod brain had already become surprisingly advanced."  However this seems to be in contradiction with evolution, as a complex brain that already existed does not support evolution.

NicholasStrausfeld, a neurobiologist at the University of Arizona andco-author on the new paper, said “No one expected such an advancedbrain would have evolved so early in the history of multicellularanimals,' in a prepared statement."

 


 


 

Big Bang and religion mixed in Cern Conference

Posted on October 17, 2012 at 8:25 AM Comments comments (0)

Some of Europe's most prominent scientists have opened a debate with philosophers and theologians over the origins of everything. The event, in Geneva, Switzerland, is described as a search for "common ground" between religion and science over how the Universe began.

The conference was called by Cern, the European Organization for Nuclear Research, in the wake of its Higgs boson discovery

He added that he hoped, by the end of the conference, that delegates from very different backgrounds would be able to "start to discuss the origin of our Universe".

Co-organiser Canon Dr Gary Wilton, the Archbishop of Canterbury's representative in Brussels, said that the Higgs particle "raised lots of questions [about the origins of the Universe] that scientists alone can't answer".

More at:  http://www.bbc.co.uk/news/world-europe-19870036


 

John McKay Interview -

Posted on October 3, 2012 at 8:40 AM Comments comments (0)

Recommend people listen to this interview with John McKay (Creation Research) on Inspirational Breakfast with John Pantry.

http://www.premierradio.org.uk/listen/ondemand.aspx?mediaid={87D3C762-8083-442F-8EB8-D6D89414A99E}&dm_i=16DQ,ZI3P,619FOV,2ZJ0L,1,nkdkcf

 

Recommend copyand past the link in it's entirety.

 


Evolutionary 'U'-turns

Posted on September 27, 2012 at 9:15 AM Comments comments (0)

In a recent BBC interview/discussion between Britain's Lord Jonathan Sacks, the Chief Rabbi of the UK and the infamous the one-time Oxford professor, Richard Dawkins, the ENCODE (previously called 'Junk DNA' is discussed. Dawkins has previously stated [2009] that the, so called, Junk DNA was scientific proof of evolution and that a creator had no hand in the design of the creatures inhabiting this planet.

Back in 2009, in The Greatest Show on Earth (pp. 332-333), Dawkins states:

"pseudogenes," "useful for. . . embarrassing creationists."

"It stretches even their creative ingenuity to make a convincing reason why an intelligent designer should have created a pseudogene -- a gene that does absolutely nothing and gives every appearance of being a superannuated version of a gene that used to do something -- unless he was deliberately setting out to fool us."

" Leaving pseudogenes aside, it is a remarkable fact that the greater part (95 percent in the case of humans) of the genome might as well not be there, for all the difference it makes."

Clearly our professor did not expect the outcome of the ENCODE project, but now, in the above BBC programme he seems to have done a 'U'-turn in his opinion of Junk DNA, just as was predicted, he now says:

"I have noticed that there are some creationists who are jumping on [the ENCODE results] because they think that's awkward for Darwinism. Quite the contrary it's exactly what a Darwinist would hope for, to find usefulness in the living world.... "

"Whereas we thought that only a minority of the genome was doing something, namely that minority which actually codes for protein, and now we find that actually the majority of it is doing something. What it's doing is calling into action the protein-coding genes. So you can think of the protein-coding genes as being sort of the toolbox of subroutines which is pretty much common to all mammals -- mice and men have the same number, roughly speaking, of protein-coding genes and that's always been a bit of a blow to self-esteem of humanity. But the point is that that was just the subroutines that are called into being; the program that's calling them into action is the rest [of the genome] which had previously been written off as junk."

One by one the supporting pillars of evolution seem to be crumbling away beneath their feet, and evolutionists have built their house of straw are now grabbing at those straws.

Breakthrough study overturns theory of 'junk DNA' in genome

Posted on September 7, 2012 at 1:30 PM Comments comments (0)

This week is a landmark in evolutionary science, not however a landmark that many evolutionists will savour, however thirty papers have been published in various journals around the world, clearly stating that one of the cornerstones of evolution has crumbled.  The papers don't actually use that language of course but they all amount to the same thing.  The so called 'junk DNA' has been sited as evidence of the evolutionary path of all creatures, the DNA that is no longer needed, that we have grown out of.  The many believers in the Genesis account of creation have been scorned and derided for saying that this, until now seeming useless DNA, must be needed and must serve a function, because that is the way God desinged it.  Now at long last those believers have been vindicated, the 'jumk DNA' have a purpose. 

Below is reproduced the article from the British broadsheet newspaper, 'The Guardian' of Deptember 5th 2012.

Ref: http://www.guardian.co.uk/science/2012/sep/05/genes-genome-junk-dna-encode?INTCMP=SRCH

News Science Genetics Breakthrough study overturns theory of 'junk DNA' in genome

The international Encode project has found that about a fifth of the human genome regulates the 2% that makes proteins

Long stretches of DNA previously dismissed as "junk" are in fact crucial to the way our genome works, an international team of researchers said on Wednesday.

It is the most significant shift in scientists' understanding of the way our DNA operates since the sequencing of the human genome in 2000, when it was discovered that our bodies are built and controlled by far fewer genes than expected. Now the next generation of geneticists have updated that picture.

The results of the international Encode project will have a huge impact for geneticists trying to work out how genes operate. The findings will also provide new leads for scientists looking for treatments for conditions such as heart disease, diabetes and Crohn's disease that have their roots partly in glitches in the DNA. Until now, the focus had largely been on looking for errors within genes themselves, but the Encode research will help guide the hunt for problem areas that lie elsewhere in our DNA sequence.

Dr Ewan Birney, of the European Bioinformatics Institute near Cambridge, one of the principal investigators in the Encode project, said: "In 2000, we published the draft human genome and, in 2003, we published the finished human genome and we always knew that was going to be a starting point. We always knew that protein-coding genes were not the whole story."

For years, the vast stretches of DNA between our 20,000 or so protein-coding genes – more than 98% of the genetic sequence inside each of our cells – was written off as "junk" DNA. Already falling out of favour in recent years, this concept will now, with Encode's work, be consigned to the history books.

Encode is the largest single update to the data from the human genome since its final draft was published in 2003 and the first systematic attempt to work out what the DNA outside protein-coding genes does. The researchers found that it is far from useless: within these regions they have identified more than 10,000 new "genes" that code for components that control how the more familiar protein-coding genes work. Up to 18% of our DNA sequence is involved in regulating the less than 2% of the DNA that codes for proteins. In total, Encode scientists say, about 80% of the DNA sequence can be assigned some sort of biochemical function.

Scientists know that while most cells in our body contain our entire genetic code, not all of the protein-coding genes are active. A liver cell contains enzymes used to metabolise alcohol and other toxins, whereas hair cells make the protein keratin. Through some mechanism that regulates its genes, the hair cell knows it should make keratin rather than liver enzymes, and the liver cell knows it should make the liver enzymes and not the hair proteins.

"That control must have been somewhere in the genome, and we always knew that – for some individual genes – it was an element sometimes quite far away from the gene," said Birney. "But we didn't have a genome-wide view to this. So we set about working out how we could discover those elements."

The results of the five-year Encode project are published on Wednesday across 30 papers in the journals Nature, Science, Genome Biology and Genome Research. The researchers have mapped 4m switches in what was once thought to be junk DNA, many of which will help them better understand a range of common human diseases, from diabetes to heart disease, that depend on the complex interaction of hundreds of genes and their associated regulatory elements.

News Science Genetics Breakthrough study overturns theory of 'junk DNA' in genome The international Encode project has found that about a fifth of the human genome regulates the 2% that makes proteins

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Email Alok Jha, science correspondent guardian.co.uk, Wednesday 5 September 2012 20.03 BST Jump to comments (145) Science correspondent Ian Sample uses a visual aid to explain the implications of the new research. Video: Guardian Link to this video Long stretches of DNA previously dismissed as "junk" are in fact crucial to the way our genome works, an international team of researchers said on Wednesday.

It is the most significant shift in scientists' understanding of the way our DNA operates since the sequencing of the human genome in 2000, when it was discovered that our bodies are built and controlled by far fewer genes than expected. Now the next generation of geneticists have updated that picture.

The results of the international Encode project will have a huge impact for geneticists trying to work out how genes operate. The findings will also provide new leads for scientists looking for treatments for conditions such as heart disease, diabetes and Crohn's disease that have their roots partly in glitches in the DNA. Until now, the focus had largely been on looking for errors within genes themselves, but the Encode research will help guide the hunt for problem areas that lie elsewhere in our DNA sequence.

Dr Ewan Birney, of the European Bioinformatics Institute near Cambridge, one of the principal investigators in the Encode project, said: "In 2000, we published the draft human genome and, in 2003, we published the finished human genome and we always knew that was going to be a starting point. We always knew that protein-coding genes were not the whole story."

For years, the vast stretches of DNA between our 20,000 or so protein-coding genes – more than 98% of the genetic sequence inside each of our cells – was written off as "junk" DNA. Already falling out of favour in recent years, this concept will now, with Encode's work, be consigned to the history books.

Encode is the largest single update to the data from the human genome since its final draft was published in 2003 and the first systematic attempt to work out what the DNA outside protein-coding genes does. The researchers found that it is far from useless: within these regions they have identified more than 10,000 new "genes" that code for components that control how the more familiar protein-coding genes work. Up to 18% of our DNA sequence is involved in regulating the less than 2% of the DNA that codes for proteins. In total, Encode scientists say, about 80% of the DNA sequence can be assigned some sort of biochemical function.

Scientists know that while most cells in our body contain our entire genetic code, not all of the protein-coding genes are active. A liver cell contains enzymes used to metabolise alcohol and other toxins, whereas hair cells make the protein keratin. Through some mechanism that regulates its genes, the hair cell knows it should make keratin rather than liver enzymes, and the liver cell knows it should make the liver enzymes and not the hair proteins.

"That control must have been somewhere in the genome, and we always knew that – for some individual genes – it was an element sometimes quite far away from the gene," said Birney. "But we didn't have a genome-wide view to this. So we set about working out how we could discover those elements."

The results of the five-year Encode project are published on Wednesday across 30 papers in the journals Nature, Science, Genome Biology and Genome Research. The researchers have mapped 4m switches in what was once thought to be junk DNA, many of which will help them better understand a range of common human diseases, from diabetes to heart disease, that depend on the complex interaction of hundreds of genes and their associated regulatory elements.

Researchers at the forefront of the Encode project explain its findings. Video: Nature "Regulatory elements are the things that turn genes on and off," says Professor Mike Snyder of Stanford University, who was a principal investigator in the Encode consortium. "Much of the difference between people is due to the differences in the efficiency of these regulatory elements. There are more variants, we think, in the regulatory elements than in the genes themselves."

*Genes cannot function without these regulatory elements. If regulation goes wrong, malfunctioning genes can cause diseases including cancer, atherosclerosis, type 2 diabetes, psoriasis and Crohn's disease. Errors in the regulation of a gene known as Sonic Hedgehog, for example, are thought to underlie some cases of human polydactyly in which individuals have extra toes or fingers.

Prof Anne Ferguson-Smith, of Cambridge University, said: "They also have important implications for the growth and development of embryos and foetuses during pregnancy. These are the kinds of elements that make your tissues and organs grow properly, at the right time and place, and containing the right kinds of cells."

Encode scientists found that 9% of human DNA is involved in the coding for the regulatory switches, although Birney thinks the true figure may turn out to be about 20%. "One of the big surprises is that we see way more [regulatory] elements than I was expecting," he said.

The project has identified about 10,000 stretches of DNA, which the Encode scientists have called non-coding genes, that do not make proteins but, instead, a type of RNA – the single-stranded equivalent of DNA. There are many types of RNA molecule in cells, each with a specific role such as carrying messages or transcribing the DNA code in the first step of making a protein. However, the 10,000 non-coding genes carry instructions to build the large and small RNA molecules required to regulate the actions of the 20,000 protein-coding genes.

The results have already shed light on previous, massive studies of genetic data. In recent years, scientists have compared the genetic code of thousands of people with a specific disease (such as diabetes, bipolar disorder, Crohn's disease or heart disease) with the DNA code of thousands of healthy people, in an attempt to locate mutations that could account for some of the risk of developing that disease. These so-called genome-wide association studies (GWAS) have identified scores of locations in the DNA that seem to raise a person's risk of developing a disease – but the vast majority are nowhere near protein-coding genes. That makes sense if regions previously thought of as "junk" are actually vital for controlling the expression of protein-encoding genes.

Indeed, there is a big overlap between the locations identified by GWAS and the regulation switches identified in Encode. "When I first saw that result I thought it was too good to be true. We've done the analysis five different ways now and it still holds up," says Birney.

Understanding some of these regulatory elements could help explain some of the environmental triggers for different diseases.

Crohn's disease, for example, is a long-term condition that causes inflammation of the lining of the digestive system and affects up to 60,000 people in the UK, but scientists cannot fully explain why some people suffer from it and others do not, even when they all have the genetic mutations associated with an elevated risk. One hypothesis is that the disease could be triggered by a bacterial infection. "Maybe there's a place in the middle of nowhere [in the DNA], not close to a protein-coding gene, that if you have one variant you're more sensitive to this bacterium, if you have another variant you're less sensitive," says Birney. "So you get Crohn's disease probably because you have the more sensitive type and that particular bacterial infection occurred at a time when you were vulnerable."

The Encode consortium's 442 researchers, situated in 32 institutes around the world, used 300 years of computer time and five years in the lab to get their results. They examined a total of 147 types of tissue – including cancer cells, liver extracts, endothelial cells from umbilical cords, and stem cells derived from embryos – and subjected them to around a hundred different experiments, recording which parts of the DNA code were activated in which cells at which times.

The current and future phases of Encode will prove useful not only for scientists, but also for those who want a more personalised approach to medicine in the decades to come. "We're in an era where people are starting to get their genomes sequenced. With Encode data we could start mapping regulatory information," says Snyder.

This means that the individual differences in people's diseases can be more effectively targeted for treatment. "Diseases have been defined by the medical profession observing symptoms," says Dr Tim Hubbard of the Wellcome Trust Sanger Institute in Cambridge. "[But] we know, for example, that breast cancer is not one disease but there's multiple types of breast cancer with all sorts of different mechanistic processes going wrong.

"A given drug only works in about a third of the people you give it to, but you don't know which third. A lot of that is related to genomics, so if you knew the relationship between a person's genome and which drugs work for them and which ones they shouldn't take because it gives them side effects, that would improve medicine."

Understanding exactly how each type of cell in the body works – in other words which genes are switched on or off at different stages of its function – will also be useful in future stem cell therapies. If doctors want to grow replacement liver tissue, for example, they will be able to check that it is safe by comparing the DNA functions of their manufactured cells with data from normal liver cells.

Birney says that the decade since the publication of the first draft of the human genome has shown that genetics is much more complex than anyone could have predicted. "We felt that maybe life was easier beforehand and more comfortable because we were just more ignorant. The major thing that's happening is that we're losing some of our ignorance and, indeed, it's very complicated," he says. "You've got to remember that these genomes make one of the most complicated things we know, ourselves. The idea that the recipe book would be easy to understand is kind of hubris. I still think we're at the start of this journey, we're still in the warm-up, the first couple of miles of this marathon."

 *This line has been highlighted my me, because I see it as the key phrase in the article.  It is true that genes cannot function without these regulatory elements, this means that the DNA and the regulatory elements must 'evolve' at exactly the same time, any new gene wouldbe less than useless without a matched control gene/switch evolving at the same time.  As this is impossible because the two have a symbiotic relationship, it presents as a huge problem for evolution.

 



 



Day of Jesus' Crucifixion Believed Determined

Posted on August 28, 2012 at 8:40 AM Comments comments (0)

“And when Jesus had cried out again in a loud voice, he gave up his spirit. At that moment the curtain of the temple was torn in two from top to bottom. The earth shook, the rocks split and the tombs broke open.”

By Jennifer Viegas

Thu May 24, 2012 12:54 PM ET It's been debated for years, but researchers say they now have adefinitive date of the crucifixion. 

http://news.discovery.com/history/jesus-crucifixion-120524.html

The latest investigation, reported in the journal International Geology Review, focused on earthquake activity at the Dead Sea, located 13miles from Jerusalem. The Gospel of Matthew, Chapter 27, mentions that an earthquake coincided with the crucifixion:

To analyze earthquake activity in the region, geologist Jefferson Williams of Supersonic Geophysical and colleagues Markus Schwab and Achim Brauer of the German Research Center for Geosciences studied three cores from the beach of the Ein Gedi Spa adjacent to the Dead Sea.

Varves, which are annual layers of deposition in the sediments,reveal that at least two major earthquakes affected the core: a widespread earthquake in 31 B.C. and an early first century seismic event that happened sometime between 26 A.D. and 36 A.D.

The latter period occurred during “the years when Pontius Pilatewas procurator of Judea and when the earthquake of the Gospel of Matthew is historically constrained,” Williams said.

"The day and date of the crucifixion (Good Friday) are known with a fair degree of precision," he said. But the year has been in question.

In terms of textual clues to the date of the crucifixion, Williams quoted a Nature paper authored by Colin Humphreys and Graeme Waddington. Williams summarized their work as follows:

All four gospels and Tacitus in Annals (XV,44) agree that the crucifixion occurred when Pontius Pilate was procurator of Judea from 26-36 AD.

All four gospels say the crucifixion occurred on a Friday.

All four gospels agree that Jesus died a few hours before the beginning of the Jewish Sabbath (nightfall on a Friday).


The synoptic gospels (Matthew, Mark, and Luke) indicate that Jesus died before nightfall on the 15th day of Nisan; right before the start of the Passover meal.

John’s gospel differs from the synoptics; apparently indicating that Jesus died before nightfall on the 14th day of Nisan.

When data about the Jewish calendar and astronomical calculations are factored in, a handful of possible dates result, with Friday April 3, 33 A.D. being the best match, according to the researchers.

In terms of the earthquake data alone, Williams and his team acknowledge that the seismic activity associated with the crucifixion could refer to “an earthquake that occurred sometime before or after the crucifixion and was in effect ‘borrowed’ by the author of the Gospel of Matthew, and a local earthquake between 26 and 36A.D. that was sufficiently energetic to deform the sediments of EinGedi but not energetic enough to produce a still extant and extra-biblical historical record.”

“If the last possibility is true, this would mean that the report of an earthquake in the Gospel of Matthew is a type of allegory,” they write.

Williams is studying yet another possible natural happening associated with the crucifixion - darkness.

Three of the four canonical gospels report darkness from noon to 3PM after the crucifixion. Such darkness could have been caused by a dust storm, he believes.

Williams is investigating if there are dust storm deposits in thesediments coincident with the early first century Jerusalem regionearthquake.

 


 


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