Black Ops 2: Genetic Engineering
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By: Hacksaah

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World #39;s Greatest

By: PythagorasBeasley

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Synthetic biology has made such strides in recent years that the notion of reviving extinct species is no longer crazy talk. Researchers gathered recently in Washington, D.C. to discuss the prospects of bringing back a whole menagerie of fascinating creatures, including the passenger pigeon, once the most numerous bird in North America.

At least one scientist is busy devising a strategy to teach that genetic replica how to live like its flocking, migrating natural ancestors did. But other scientists arent convinced you could ever call this bird a true passenger pigeon.

Everything we know about species and individuals tells us that were a lot more than our genes, said David Blockstein of the National Council for Science and the Environment.

For one thing, an animals genes are influenced by its environment though chemical changes to DNA that affect how genes switch on and off. Those epigenetic changes may be a crucial part of what gives a species its unique characteristics, but the epigenetic profile of a bird created in a lab would never be the same as that of a bird raised in a flock by its natural parents, Blockstein says.

Conservation biologist David Ehrenfeld of Rutgers University is skeptical too.Lets say we could create a passenger pigeon with the same DNA and the same epigenetic marks, he said. That doesnt make it a passenger pigeon.

Ehrenfeld and others say passenger pigeons were perhaps the most social birds that have ever existed, living in flocks of hundreds of thousands. They needed enormous populations to nest properly and repel predators, Ehrenfeld said. Their behavior, as much as their DNA, defined the species.

This concept isnt lost on the people behind the plan to revive the passenger pigeon.

In my opinion you have to recreate the social structure, said Ben Novak, a young scientist who is heading the project, supported by a group called Revive & Restore. Novak outlined his plan at the meeting in Washington, and he described it in more detail in an interview with Wired last week.

The first passenger pigeons would be raised in captivity, with surrogate parents of a related species. Novak plans to cosmetically alter the surrogates with dyes to give them the reddish bellies and grey wings of passenger pigeons. These indoor aviaries would be adorned with tree branches and decorated to be as forest-like as possible. Ideally, birds would even have to forage for their own food, Novak says. After a few years of captive breeding to build up the population, the birds would gradually be transferred to outdoor aviaries.

As the captive flock continues to grow, Novak plans to train homing pigeons as guides to teach the passenger pigeons to migrate along the flyways of their extinct ancestors. The idea would be to dye the homing pigeons so they look like passenger pigeons, allow young passenger pigeons to imprint on them, and then release them all and hope that the passenger pigeons follow their homing-pigeon guides.

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Say We Really Do Bring the Passenger Pigeon Back From Extinction — Then What?

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Mar. 24, 2013 Research conducted in fruit flies at the University of North Carolina School of Medicine has pinpointed a specific DNA sequence that both triggers the formation of the "histone locus body" and turns on all the histone genes in the entire block.

Every time a cell divides it makes a carbon copy of crucial ingredients, including the histone proteins that are responsible for spooling yards of DNA into tight little coils. When these spool-like proteins aren't made correctly, it can result in the genomic instability characteristic of most birth defects and cancers.

Seven years ago, Dr. Joe Gall of the Carnegie Institute in Baltimore, Md. and coworkers noticed an aggregation of molecules along a a block of genome that codes for the critical histones, but they had no idea how this aggregate or "histone locus body" was formed.

Now, research conducted in fruit flies at the University of North Carolina School of Medicine has pinpointed a specific DNA sequence that both triggers the formation of this "histone locus body" and turns on all the histone genes in the entire block.

The finding, published March 25, 2013 in the journal Developmental Cell, provides a model for the coordinated synthesis of histones needed for assembly into chromatin, a process critical to keeping chromosomes intact and passing genetic information from generation to generation.

"Our study has uncovered a new relationship between nuclear architecture and gene activity," said senior study author Bob Duronio, PhD, professor of biology and genetics at UNC. "In order to make chromosomes properly, you need to make these histone building blocks at the right time and in the right amount. We found that the cell has evolved this complex architecture to do that properly, and that involves an interface between the assembly of various components and the turning on of a number of genes."

In the fruit fly, as in the human, the five different histone genes exist in one long chunk of the genome. The "histone locus" in flies contains 100 copies of each of the five genes, encompassing approximately 500,000 nucleotides of A's, C's, T's and G's. The proteins required for making the histone message -- a process that must happen every time a new strand of DNA is copied -- come together at this "histone locus" to form the "histone locus body."

Duronio and co-senior study author William Marzluff, PhD, Kenan Distinguished Professor of Biochemistry and Biophysics, wanted to figure out how these factors knew to meet at the histone locus.

They inserted different combinations of the five histone genes into another site of the genome, and looked to see which combinations recruited a new histone locus body. The researchers found that combinations that contained a specific 300 nucleotide sequence -- the region between the H3 and H4 histone genes -- formed a histone locus body. In contrast, combinations of genes that lacked this sequence did not form the body. They went on to show that this sequence turned on not only the H3 and H4 genes in its direct vicinity, but also other histone genes in the block.

Though the research was conducted entirely in fruit flies, it may lend insight into mechanisms that keep the genome from becoming unstable -- and causing early death or illness -- in higher organisms.

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Genetic sequence that helps to coordinate synthesis of DNA-packaging proteins identified

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Mar. 25, 2013 A new analysis has found that genetic alterations in a particular cellular pathway are linked with bladder cancer risk, recurrence, disease progression, and patient survival. Published early online in CANCER, a peer- reviewed journal of the American Cancer Society, the findings could help improve bladder cancer screening and treatment.

Alterations in the regulators of G-protein signaling (RGS) pathway, which is important for various cellular processes, have been implicated in several cancers. Eugene Lee, MD, of the MD Anderson Cancer Center in Houston, and his colleagues sought to determine the role of RGS alterations in bladder cancer risk, recurrence, disease progression, and patient survival. Dr. Lee is currently a fellow of Dr. Ashish M. Kamat. The researchers worked together with Dr. Xifeng Wu's Epidemiology Lab. They studied 803 patients with non-muscle invasive or muscle invasive bladder cancer and 803 healthy individuals.

After evaluating 95 single nucleotide alterations or variants in 17 RGS genes, the investigators identified several that were linked with overall risk of bladder cancer. The strongest association was seen with the rs10759 variant on the RGS4 gene: it was linked with a 0.77-fold reduced risk of overall bladder cancer. The researchers also found that with an increasing number of unfavorable variants, the risk of bladder cancer increased. "Screening for bladder cancer has proven to be difficult on a population level, and our work may be a first step in identifying molecular markers for potential genetic-based screening tests. This will help recognize specific groups at increased risk beyond the existing known risk factors such as smoking and chemical exposure," said Dr. Lee.

Dr. Lee and his team also revealed that in patients with non-muscle invasive bladder cancer, 11 variants were linked with recurrence and 13 variants were linked with progression. Ten were associated with earlier death in patients with muscle invasive bladder cancer; rs2344673 was the most significant, with an average survival of 13.3 months in patients with the variant compared with 81.9 months in patients without it.

In the current era of personalized medicine, an individual's genetic information can provide valuable information on screening, treatment, and surveillance. "Our study provides an initial step in how we can use a patient's genetic makeup to identify those at risk for bladder cancer. Furthermore, we can identify patients who already have a diagnosis of bladder cancer that are at increased risk of worsening of disease or dying from their cancer," said Dr. Lee. "The goal is to find as many genetic alterations that confer risk and create a panel of markers that would aid in diagnosis, treatment, and follow- up."

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Genetic alterations linked with bladder cancer risk, recurrence, progression, and patient survival

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Public release date: 26-Mar-2013 [ | E-mail | Share ]

Contact: Rosie Waldron r.waldron@ucl.ac.uk 020-767-99041 University College London

Previous research has shown that obesity runs in families, and twin studies suggest that this is largely due to genetic factors, with heritability estimates over 50%. 32 genes have been identified as risk factors for obesity but previous analyses suggest that these genes alone cannot fully explain the high level of heritability in childhood obesity, as together they explain only 2% of individual differences in childhood body weight. This has led to a problem of 'missing heritability'.

In this study, researchers used a new method called Genome-wide Complex Trait Analysis (GCTA), to investigate the molecular genetic heritability of body weight in children. GCTA takes advantage of the fact that some people are more genetically similar to one another than others, by chance; and looks to see whether individuals who just happen to be more genetically similar might also be more similar in weight. Using this approach, GCTA estimates the combined effects of all known common genes across the whole genome, associated with childhood body weight.

The study is based on data from a population-based cohort of 2,269 children aged between eight and eleven years old. Researchers looked at whether children who happen to be more genetically similar might also be more similar in body weight. Using the GCTA method, the researchers found that additive effects of multiple genes across the whole genome accounted for 30% of individual difference in childhood body weight.

Clare Llewellyn from UCL Health Behaviour Research Centre and lead author of the study, said: "These findings are important because they confirm that in children genes play a very important role in determining body weight. At present only a few genetic variants have been discovered, and these explain a very small amount of individual differences in body weight (~2%). These findings suggest there are hundreds of other genetic variants influencing body weight that are yet to be discovered".

This study underlines the importance of genetic effects in childhood obesity, supporting the current thinking that children of obese parents are most at risk of becoming obese.

###

Notes for Editors

1. For more information or to speak to Clare Llewellyn, please contact Rosie Waldron in the UCL Media Relations Office on tel: 44-020-7679-9041, out of hours 44-07917-271-364, e-mail: r.waldron@ucl.ac.uk

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Study finds strong genetic component to childhood obesity

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Genetics Mod Sneek Peek [Sonic Extractor Item]
Just a sneak peek of my new my Genetics Mod 😉 enjoy -------------------------------------------------------------------------------------------------------...

By: DocRedstone

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IMPROVEMENT IN THE HEALTH OF INDIVIDUALS WITH ADHD: WHAT IS THE ROLE OF THE ASSOCIATIONS IN EUROPE?
Speakers: Andrea Bilbow - ADDISS - UK.

By: Whaam Auth

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GNDU jashan 2013 giddha by social science dept.

By: shabaj khinda

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Richard McGee, M.D.
Dr. Richard McGee is a medical oncologist and hematologist at the Swedish Cancer Institute. His special interests are in cancer research, advances in cancer ...

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Runescape 2007 | B0aty - First PK Trip !
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Runescape 2007 | B0aty - First PK Trip ! - Video

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More Mobs Minecraft Ep 6- DNA!
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Dance Your Heart Away with Vehllia - Happiness Muscles

By: Kim Beasley

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Losing Fat on Lower Abs Stomach
Thanks for the support! Please LIKE and COMMENT if you enjoy! #9675; Top 5 Bodybuilding Snacks: http://youtu.be/s0CLtvWk3dc #9675; Six Pack Abs Workout: http://youtu.b...

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Losing Fat on Lower Abs

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Workout 1

By: Tara Nik-Khah

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YOU CAN #39;T BEAT ME! (The Hidden)
Enjoy the video? Subscribe! http://bit.ly/M0mU1V #9669; #9669; #9669; Want some gear? US Store: http://seananners.spreadshirt.com EU Store: http://seananners.spreadshirt....

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Can I Get Rid of "Gyno"?
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By: strengthcamp

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MIND GAMES (The Hidden)
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Carbing Up Before Bed?
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Outdoor Kettlebell Workout (while camping with my kids)
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How to Make Other Men Respect You
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Let #39;s Play Metal Walker (Part 19: Head Trauma for Metal Master Bow)
In this video we finally catch up to Metal Master Kurama but faster than we can quit talking gibberish Metal Master Bow steps in!

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Introduction to Viruses by David Baltimore
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Leukemia Cure Possibly Found in Potentially Major Medical Breakthrough
Memorial Sloan-Kettering researchers genetically alters patients #39; own immune cells to fight a deadly form of leukemia. For more GMA, click here: http://gma.y...

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Mathematics - Biology #39;s New Microscope
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