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Category Archives: Transhuman News
Let’s Play Assassin’s Creed 3 – DNA vs. TFA english – Video
Posted: September 30, 2013 at 8:41 pm
Let #39;s Play Assassin #39;s Creed 3 - DNA vs. TFA english
Rheisen view:http://www.youtube.com/watch?v=1Ii9g6bWJ5Y These are 1 of the 3 friendly scrims we had against DNA. good games to DNA 🙂 hese matches were also ...
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Let's Play Assassin's Creed 3 - DNA vs. TFA english - Video
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Dan Winter – The Galactic History of DNA (HD) Part Eight – Video
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Dan Winter - The Galactic History of DNA (HD) Part Eight
Dan Winter - The Galactic History of DNA (HD) Part Eight ¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤¤ SUBSCRIBE THE NETWORK FOR THE BEST INFORMATION O...
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Dan Winter - The Galactic History of DNA (HD) Part Eight - Video
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DNA Funk – Qual é o Estilo Musical do Rio? – Video
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DNA Funk - Qual é o Estilo Musical do Rio?
Samba, Bossa Nova ou Funk? Qual o estilo musical que, atualmente, representa o Rio de Janeiro?
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DNA Funk - Qual é o Estilo Musical do Rio? - Video
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Kercher judge orders new DNA test
Posted: at 8:41 pm
30 September 2013 Last updated at 16:07 ET
The Italian judge hearing the retrial of Amanda Knox and and Raffaele Sollecito for the murder of Meredith Kercher has ordered a new DNA test on a knife allegedly used in the killing.
The two suspects spent four years in jail for the 2007 murder, but their convictions were overturned on appeal.
That ruling was itself overturned in March by Italy's highest court.
A separate trial convicted Rudy Guede from Ivory Coast of Miss Kercher's murder. He is serving 16 years in jail.
Neither the American Amanda Knox, nor her Italian former boyfriend Raffaele Sollecito, were in court for the start of the hearing in Florence.
Ms Knox was the housemate of Miss Kercher - a 21-year-old Briton who was found in their student lodgings in Perugia with her throat slashed.
Miss Kercher's sister Stephanie wrote to the court to express the family's feelings, nearly six years on from the brutal killing.
"We desperately want to discover the truth," she wrote, "and find justice for Meredith."
Miss Kercher, from Coulsdon in south London, was an undergraduate at the University of Leeds and was studying on an exchange programme at the University of Perugia at the time of her death.
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Kercher judge orders new DNA test
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Defence wants new DNA tests in Knox murder retrial
Posted: at 8:41 pm
Florence (Italy) (AFP) - Judges at the retrial of Amanda Knox for the murder of a British student on Monday ordered new DNA testing on the alleged murder weapon, a kitchen knife, on the first day of hearings.
The court in Florence also said it would re-hear the testimony of Luciano Aviello, a jailed mafia turncoat who at one point had accused his own brother of the grisly murder but then retracted.
Lawyers for the US student and her Italian former lover Raffaele Sollecito told the court the fresh tests were essential in clearing the defendants, as the victim's lawyer said the truth behind one of Italy's most notorious crimes was long overdue.
Knox and Sollecito spent four years behind bars for the murder of Meredith Kercher, who was found in a pool of blood in the house she shared with Knox in 2007, her body riddled with stab wounds.
An appeals court overturned their convictions in 2011 and Knox quickly returned to Seattle, but Italy's Supreme Court in March ordered a retrial following an appeal by prosecutors against what they slammed a "superficial ruling."
"We need a key step forward on the DNA evidence... We want the truth," Knox's lawyer Luciano Ghirga told the retrial's presiding judge Alessandro Nencini.
The knife, recovered from a kitchen drawer in Sollecito's house, bore tiny traces of Knox's DNA on the handle, and Meredith's DNA on the blade.
A third DNA trace had gone unexamined because it was seen as too low to produce conclusive results but the defence hopes it could help clear the pair.
I'm not coming back
Knox, 26, has insisted she will not return to Italy for any part of the retrial.
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Defence wants new DNA tests in Knox murder retrial
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New insights into DNA repair process may spur better cancer therapies
Posted: at 8:41 pm
Public release date: 30-Sep-2013 [ | E-mail | Share ]
Contact: Sarah Avery sarah.avery@duke.edu 919-660-1306 Duke University Medical Center
DURHAM, N.C. By detailing a process required for repairing DNA breakage, scientists at the Duke Cancer Institute have gained a better understanding of how cells deal with the barrage of damage that can contribute to cancer and other diseases.
The insights, reported online the week of Sept. 30, 2013, in the journal Proceedings of the National Academy of Sciences, build on earlier work by the research team and identify new prospects for developing cancer therapies.
The researchers have focused on a complex series of events that cells routinely undertake to repair DNA damaged by sun exposure, smoking and even normal metabolism. If not correctly repaired, DNA breakages can result in cellular damage leading to cancer.
"We never had good assays to measure how DNA breaks are repaired, and there were few good tools to study how that repair unfolds at the molecular level," said senior author Michael Kastan, M.D., PhD, executive director of the Duke Cancer Institute. "Our work for the first time enables us to both sensitively measure the repair of DNA breaks and study the molecular mechanisms by which they occur."
DNA inside the cell faces a challenge for repairing itself because it is so compacted in the cell nucleus. Tightly wrapped in a complex of proteins called chromatin, the DNA is spooled like thread around a protein structure called a nucleosome. DNA could suffer a breakage that would go unheeded if it remained deep within the reel.
The system developed by Kastan and colleagues induced DNA breakage at defined points on the DNA strands, enabling researchers to chronicle events as the cells launched the repair process.
What they described for the first time was a choreographed interaction in which the tightly wound DNA was temporarily loosened when a key protein, called nucleolin, was recruited to the breakage site, disrupting the nucleosome spool. The process was then reversed when the nucleosome was re-formed after repair was complete.
"Our study demonstrates for the first time the functional importance of nucleosome disruption in DNA repair," Kastan said. "This nucleosome disruption allows DNA repair proteins to access the DNA lesion and begin the process of mending the breakage."
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New insights into DNA repair process may spur better cancer therapies
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DNA link to sugar impact risk for heart disease and diabetes
Posted: at 8:41 pm
September 30, 2013 Sophie Langley
Genes in mitochondria, the powerhouses that turn sugar into energy in human cells, shape a persons risk for heart disease and diabetes, according to a study from researchers at the University of Alabama at Birmingham (UAB).
The findings may have implications for diet-planning and the ongoing debates surrounding added sugars in foods and beverages.
Researchers said the findings, published in the Biochemical Journal 8 August 2013, may explain why some people get sick and others do not despite having the same traditional risk factors like ageing, obesity and smoking.
Research in recent years has shown that miscues in mitochondrial energy production create too many particles called oxidants and free radicals that cause cells to self-destruct as part of heart disease, diabetes and cancer.
Having been in this field for decades, I remember when mitochondrial DNA variations were thought to play a role only in the rarest of genetic syndromes, said Scott Ballinger, PhD, Professor in the Division of Molecular and Cellular Pathology at the UAB School of Medicine and corresponding study author. Today there is a growing consensus that variation in mitochondrial DNA alone make a substantial contribution to each persons risk for heart disease, and ours is the first study to directly confirm it in a living mammal, he said.
Evolution of mitochondria in humans
The UAB study reflects the theory that humans ancient one-celled ancestors swallowed the bacterial forebears of what are now mitochondria. These gave their hosts the ability to convert sugar from food into about 15 times as much cellular energy as the hosts could by using oxygen. As the evolutionary process continued, the mitochondria became permanent sub-compartments of human cells.
Each human cell has two genomes, the long stretches of DNA that encode the blueprint for the human body: one set inherited from both parents in a central nucleus, and a separate, smaller set in each mitochondrion. The mitochondria genes are inherited from a childs mother.
Researchers have struggled to genetically engineer mice that would enable them to separate the impact of one gene set from the other, making the theory that mitochondria DNA shape disease risk difficult to prove. Additionally, the human nuclear genome contains more than 30,000 genes, compared to just 13 energy-related genes in the mitochondria.
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DNA link to sugar impact risk for heart disease and diabetes
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Photo Release — Complete Genomics Whole Genome Sequencing Enables Discovery of Point Mutation Responsible for Prader …
Posted: at 8:41 pm
MOUNTAIN VIEW, Calif., Sept. 30, 2013 (GLOBE NEWSWIRE) -- Complete Genomics, Inc. (formerly NASDAQ: GNOM) ("Complete"), a wholly-owned subsidiary of BGI-Shenzhen, a leading international genomics organization based in Shenzhen, China, today announced that its highly-accurate whole genome sequencing technology played a pivotal role in identifying a point mutation that causes Prader-Willi Syndrome (PWS). That discovery helped resolve a diagnostic conundrum for four young male patients. These data were published today in Nature Genetics.
A photo accompanying this release is available at http://www.globenewswire.com/newsroom/prs/?pkgid=21224
PWS is a rare genetic disorder that causes poor muscle tone, low levels of sex hormones, and a constant feeling of hunger, according to the Eunice Kennedy Shriver National Institute of Child Health and Human Development. As a result, people with this condition tend to overeat, leading to obesity.
The first patient in this study was tested for PWS when he was one year old, but the result was negative. Over the next 12 years, he began to manifest some, but not all, of the typical PWS symptoms.
Then the patient met with paper author Dr. C. Thomas Caskey, who was director and chief executive officer of the Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, part of the University of Texas Health Science Center at Houston. Dr. Caskey has since joined Baylor College of Medicine as professor of molecular and human genetics.
It was Dr.Caskey who referred the patient to Dr. Christian Schaaf, an assistant professor of molecular and human genetics at Baylor College of Medicine, and faculty member at the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, a co-lead author on the paper. Dr. Schaaf evaluated the patient and confirmed the earlier findings. Dr. Schaaf then used Complete's highly-accurate whole genome sequencing service to determine the genetic basis of his patient's symptoms.
Those sequencing results were reviewed by fellow co-lead author Dr. Manuel L. Gonzalez-Garay, an assistant professor and a bioinformatics expert at the University of Texas Health Science Center at Houston's Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases. Dr. Gonzalez-Garay identified a single mutation, a base deletion, on the protein-coding MAGEL2 gene in a section of chromosome 15 that had been previously linked to PWS. It proved to be a frame-shift deletion mutation in a difficult to sequence GC rich region, which disrupts the activity of the MAGEL2 protein product.
As MAGEL2 is only expressed on the paternal gene, it was important to determine whether the mutation was on the maternal or paternal version of chromosome 15. In this case, the MAGEL2 mutation was confirmed to be on the paternal gene using a modified version of Complete Genomics' Long Fragment Read technology.
To investigate MAGEL2's role in this disease further, the researchers reviewed more than 1,200 exome sequencing reports from the Baylor Whole Genome Sequencing Laboratory, searching for other patients with point mutations on that gene. They identified three additional patients -- one had classic PWS and the other two had PWS-like symptoms. However, they all had negative PWS tests as infants. All four patients were also diagnosed with autism spectrum disorder and intellectual disability.
"This is the first study to show that point mutations can cause Prader-Willi Syndrome," said Dr. Schaaf. "This is an important development that increases our understanding of this complex disorder, and also gives four boys a diagnosis, which they and their parents have sought for many years."
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Howard Jacob – Use of Whole Genome Sequencing in Clinical Practice – Video
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Howard Jacob - Use of Whole Genome Sequencing in Clinical Practice
Watch on LabRoots at: http://labroots.com/user/webinars/details/id/68 Learning Objectives: Know what personalized medicine is Understand how big data will im...
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Atopic eczema, children learning to apply the cream – La Roche-Posay (SST) – Video
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Atopic eczema, children learning to apply the cream - La Roche-Posay (SST)
Discover the video of children with eczema. Laetitia Coirier, educator at the chalet Lipi Kara, shows them how to apply the cream. First cheeks and forehea...
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Atopic eczema, children learning to apply the cream - La Roche-Posay (SST) - Video
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