Ruth DeFries, chair of the department of ecology, evolution, and environmental biology at Columbia University, in New York, and author of The Big Ratchet: How Humanity Thrives in the Face of Natural Crisis, has spent much of her life looking down at Earth from a great height, using satellite images to track human development. But to understand how we went from being hunter-gatherers to a species that so completely dominates the planet, she had to go much further back in time.

Speaking from her home in New York, she guides us from the rain forest of Brazil to the latest developments in foods containing genetically modified organisms (GMOs). On the way she explains why food is at the heart of human civilization, what we need to do to feed the world in the coming decades, and why it's not just the quantity of the food we produce that matters, but also the quality.

My dictionary says a ratchet is either a tool or rap slang for a diva. What's the "Big Ratchet"?

A ratchet is a colloquial urban term, as you suggest. But it's also a mechanical tool. You turn the ratchet in one direction, and you can't go back. The ratchets in the book refer to the ways people have figured out how to manipulate nature to produce food.

Once we have these technologies, we produce more food, ratchet up the population, and that continues on. The Big Ratchet refers to the past 50 years, when we've had an explosive increase in food production. The amount of food produced has surpassed even the explosive growth in population.

So the story of the Big Ratchet is how we got to this point. How we figured out, through genetics, nutrients, irrigation, and pesticides, to lift the constraints that nature placed upon us.

You start your story in the Brazilian rain forest with the Kayapo Indians. Tell us how they feature in modern-day food production and why their story is part of our own evolutionary history.

I was doing work in the Brazilian rain forest using satellite data to track deforestation. That took me down to the ground to a very interesting part of the world, the state of Mato Grosso, in Brazil. At the time, in the early 2000s, it had the highest rate of deforestation in the world. Within that landscape there was a reserve for the Kayapo Indians, who were still living as hunter-gatherers.

So there was this amazing juxtaposition with modern agriculturegiant tractors, planes flying pesticides, everything you think of with modern agriculture for the cultivation of soy and other crops.

But before we started to domesticate plants and animals around ten or twelve thousand years ago, everyone lived like the Kayapo. Everyone hunted for wild animals, foraged for seeds and berries and fruits. That was the way we interacted with nature to get food.

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Humans' Amazing Evolution From Hunter-Gatherer to Safeway Shopper

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Big data in Personalized Medicine
80% of genomic data is unstructured. Mark Blatt and Joan Hankin outline how big data enables individual comparison to revolutionize diagnosis and treatment in the healthcare industry.

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The Expanding Role of the Genomic Counselor in Personalized Medicine - Rebecca Nagy, M.S., CGC
Ms. Nagy is a certified genetic counselor and clinical associate professor of internal medicine at The Ohio State University #39;s Wexner Medical Center in Colum...

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Spinal Cord Injury in a Car Accident Healed | Ravi Abraham Miracles 2014
Mr. Anup Kumar Mohapatro,whose Spinal Cord was severely damaged in a Car accident, was healed instantly healed after prayer. SUNDERGARH HIGHLIGHTS - 6.

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Epigenetics Stem Cells in Development Regenerative Medicine - Pier Lorenzo, Sanford-Burnham
Speaker: Pier Lorenzo Puri, M.D., Ph.D., Associate Professor, Development, Aging Regeneration Program, Sanford-Burnham Medical Research Institute.

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Epigenetics Stem Cells in Development Regenerative Medicine - Allen Wang, UC San Diego
Speaker: Allen Wang, Ph.D., Postdoctoral Fellow, Department of Pediatrics, UC San Diego.

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Blue Horizon Stem Cells and the Promise of Regenerative Medicine

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Adult stem cells: key to regenerative medicine - do you know?
Regenerative medicine is poised to dramatically alter conventional methods of treatment, shifting the focus away from symptoms and targeting the specific causes of different defects. Within...

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Last year, Maria Tun was in the audience at Hancock College's Bridges to the Baccalaureate Fall Symposium watching fellow students present their summer research projects. On Friday, she was explaining her participation in a Cal Poly gene research program.

The 20-year-old Tun worked Sandra Clement, an assistant professor in Cal Poly's Biological Sciences Department, on "post-transcriptional and post-translational regulation of gene expression by cell signaling pathways in mammalian cells." That is an accurate, but extensively technical description of research that scientists hope will one day eliminate diseases and birth defects.

"It was mainly focused on genetics. Basically they just want to regulate protein levels so that they create different functions of different genes at different times," said Tun, a 2012 graduate of Pioneer Valley High School, sounding very much like a seasoned research assistant. "The first step is to regulate a gene. Once youre able to regulate a gene, that goes back regulating protein levels that regulates a gene. Eventually through more research it'll lead to regulating any type of gene, so you could stop cancerous genes before they start."

The two-and-a-half month summer program allowed Tun to work with Clement's research team at Cal Poly. It not only opened her eyes to genetic research, it most likely was the first step in what she wants to be a career in genetics research.

"Obviously I wanted to do something in the science department, but after doing the genetics program with Bridges, thats where I'm focused," she said, adding her ultimate goal would be to join Clement's team at Cal Poly.

The University of California, Irvine is another possibility, she said.

The Bridges to the Baccalaureate program is a partnership between Cal Poly and Hancock College designed to give underrepresented minority students a chance to pursue careers in the biomedical or behavioral sciences.

This summer, Tun was one 13 Bridges students who had paid research internships at Cal Poly. Over the past five years, 65 Hancock students have been accepted into the program and 40 of them have transferred to four-year universities, including Cal Poly.

Len Miyahara, who wrote the grant that started the program and now serves as its director, said budget cuts have curtailed the program in recent years. When it started, Hancock College was one of eight such programs in the country. Miyahara said it is now one of three.

Last month, the National Institutes of Health Division of Minority Opportunities in Research awarded a five-year $966,000 grant to extend the program.

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Hancock College program spans education gap

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Genetics of Scleroderma: Towards Personalized Medicine in the Genomic Age
Presented by Benjamin Korman, MD at the Scleroderma Patient Education Conference on October 11, 2014. Hosted by the Scleroderma Foundation, Greater Chicago Chapter and the Northwestern ...

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Brust/Bizeps Workout + Posing - Iron-Genetics- Tolga Gn
Servus Leute, hier fr euch mein Brust/Bizeps Workout + Posing. Zum Schluss ein paar Kritikpunkte zum Thema, training im Fitnessstudio. Instagram: Iron_Gene...

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[1.09] How to use medical items
1) Pick up pills/gene therapy/bandages/med kit 2) Open your inventory wheel by pressing 1, and click on the item 3) Once you see a pair of hands, tap your left mouse button You can still shove...

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Stem Cell Therapy for Pets in Central Florida
http://www.NewmanVets.com Call your local Newman Veterinary Center for more information about stem cell therapy for pets. https://www.youtube.com/watch?v=7X23bmsy0Q8 feature=youtu.be.

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Stem Cell Therapy for Multiple Sclerosis: Ron McGill
Ron McGill suffers from relapsing-remitting multiple sclerosis. He was started experiencing symptoms in 2009 but was not diagnosed with MS until January of 2013. He received several infusion...

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WALES NEWS

The family of eight-year-old Hollie Clark broke the news yesterday on the Facebook page that they used to raise awareness of her battle with the bone marrow disorder MDS.

As part of a social media campaign to find a donor, celebrities including football player Gareth Bale posed with their underwear on their heads to rise awareness.

Hollie's father Stephen, of Penylan, Cardiff, wrote: "Sad news today I'm afraid. After a seven month battle with MDS Hollie passed away peacefully in her parents' arms.

"It is utterly heartbreaking and makes no sense.

"We have a million memories and take huge comfort in the number of Anthony Nolan registrations that the campaign made.

"We are sure that someday soon one of you will be asked to donate stem cells and give someone like Hollie a chance.

"Thank you all for your support. We would appreciate some time and space to try and pick ourselves up.

"Love from Hollie's Dad. The proudest Dad in the world."

WALES NEWS

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(Ivanhoe Newswire) CLEVELAND, Ohio -- In 1990 the Human Genome Project started. It was a massive scientific undertaking that aimed to identify and map out the body's complete set of DNA. This research has paved the way for new genetic discoveries; one of those has allowed scientists to study how to fix bad chromosomes.

Our bodies contain 23 pairs of them, 46 total. But if chromosomes are damaged, they can cause birth defects, disabilities, growth problems, even death.

Case Western scientist Anthony Wynshaw-Boris is studying how to repair damaged chromosomes with the help of a recent discovery. He's taking skin cells and reprogramming them to work like embryonic stem cells, which can grow into different cell types.

You're taking adult or a child's skin cells. You're not causing any loss of an embryo, and you're taking those skin cells to make a stem cell. Anthony Wynshaw-Boris, M.D., PhD, of Case Western Reserve University, School of Medicine told Ivanhoe.

Scientists studied patients with a specific defective chromosome that was shaped like a ring. They took the patients' skin cells and reprogrammed them into embryonic-like cells in the lab. They found this process caused the damaged ring chromosomes to be replaced by normal chromosomes.

It at least raises the possibility that ring chromosomes will be lost in stem cells, said Dr. Wynshaw-Boris.

While this research was only conducted in lab cultures on the rare ring-shaped chromosomes, scientists hope it will work in patients with common abnormalities like Down syndrome.

What we're hoping happens is we might be able to use, modify, what we did, to rescue cell lines from any patient that has any severe chromosome defect, Dr. Wynshaw-Boris explained.

It's research that could one day repair faulty chromosomes and stop genetic diseases in their tracks.

The reprogramming technique that transforms skin cells to stem cells was so ground-breaking that a Japanese physician won the Nobel Prize in medicine in 2012 for developing it.

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Stem cells to repair broken chromosomes

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Published November 07, 2014

A team of stem cell scientists has identified the biological mechanisms of Parkinsons disease and recreated a model of the disease in a dish.

Researchers at The New York Stem Cell Foundation (NYSCF) Research Institute studied a pair of identical twins one with Parkinsons and one without as well as another unrelated Parkinsons patient and four healthy control subjects to observe key characteristics of the disease. After comparing the individuals biological factors, they noticed differences in the patients neurons ability to produce dopamine. Dopamine production is deficient in Parkinsons disease.

"The unique scenario of identical twins, one with this disease and one without, allowed our scientists an unprecedented look into the mechanisms of Parkinson's disease," Susan L. Solomon, NYSCF chief executive officer, said in a news release. "Advanced stem cell research techniques allow us to push the boundaries of science and see what actually goes wrong at the cellular level, step by step during the disease process."

Parkinsons disease affects an estimated 500,000 people in the United States, according to the National Institutes of Health (NIH). The average age of onset is 60, and the risk of developing it increases with age. Symptoms of Parkinsons include tremor, shaking in the hands, arms, legs, jaw or head; impaired balance or postural instability; slowness of movement; and stiffness of the limbs and trunk.

There is currently no cure for Parkinsons.

While the disease is moderately hereditary, scientists have yet to fully understand the mechanisms of inheritance. The researchers note the DNA mutations that produce the enzyme glucocerebrosidase (GBA) have been linked to a five-fold increased risk of developing Parkinsons, but only 30 percent of people with this mutation have been shown to get the disease by age 80. This suggests that genetic and non-genetic factors cause Parkinsons. In studying the identical twins, scientists were able to analyze these mechanisms.

The scientists made induced pluripotent stem (iPS) cells from skin samples from both twins to generate a cellular model of Parkinsons in a dish, recreating the outstanding features of the disease specifically the dopamine and a-synuclein deficiency.

Scientists saw that the neurons from the twin affected by Parkinsons produced less dopamine and had higher levels of an enzyme called monomine oxidase B (MAO-B), as well as a poorer ability to connect with each other, compared to the twin that did not have the disease.

The findings suggest a possible therapy for Parkinsons: treating neurons with molecules that reduce the activity of MAO-B and GBA, while normalizing -synuclein and dopamine levels.

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David C P. Chen, MD., MHP - Stem Cell Therapy Q A3

By: advanced anti aging center

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A new study lends additional evidence to the likelihood that genes associated with high levels of the so-called good cholesterol appear to contribute to exceptionally long life expectancy and resistance to age-related disease.

Sofiya Milman , an assistant professor of medicine in geriatrics and endocrinology at Albert Einstein College of Medicine in New York, said her teams findings could open the way to finding drugs that target the gene and mimic its functions, thereby extending life.

These genotypes may explain the mechanisms responsible for the beneficial HDL, Milman said, saying further study of the genes could help unlock the secrets of what she called successful agers. One of the gene variants related to HDL cholesterol appeared to not only contribute to longer life, but to protect older people from age-related cognitive impairment, she said.

But Milman also cautioned that studies with larger sample sizes and more diverse populations should be conducted to validate the results.

Milmans research was one of several presentations on the science of aging offered Thursday at the annual meeting of the Gerontological Society of Americas annual scientific conference at the Walter E. Washington Convention Center. The conference, which opened Wednesday, draws about 4,000 researchers. More than 500 presentations of original research are scheduled before the conference ends Sunday.

The Einstein study focused on 300 women and 94 men who were at least 95 years old and living independently when the study began in 1998. All of the people were from the northeastern United States and all were Jews of European descent, a factor that was useful because of the relative homogeneity of their genetics.

Researchers then monitored the participants until the participants deaths, focused on their levels of HDL, which stands for high-density lipoprotein. HDL , helps the body regulate and maintain the level of cholesterol, an important component of health. Cholesterol, which is found in certain foods and created by the body itself, helps create hormones, synthesizes vitamin D, and builds and maintains cell membranes.

To transport and store cholesterol, the liver transforms it into lipoproteins. Low-density lipoproteins (LDL) carry cholesterol to the bodys cells; HDL moves through the bloodstream acting as a scavenger that returns cholesterol to the liver for excretion or recycling.

The Einstein team theorized that long life might be linked to high HDL levels and the presence of a gene variant of an enzyme known as CETP, or cholesterol ester transfer protein that transfers cholesterol between HDL particles and LDL particles circulating in the bloodstream.

The team also looked at a gene variant known as apolipoprotein 1 (APOA1), which codes for a protein that is a major component in HDL, to see whether that too might be a marker for exceptional longevity.

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Gene for HDL cholesterol linked to longer life, study finds

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PUBLIC RELEASE DATE:

7-Nov-2014

Contact: Raeka Aiyar press@genetics-gsa.org 202-412-1120 Genetics Society of America @GeneticsGSA

Bethesda, MD -- After many generations, rats bred for their bad attitude behave differently from those selected for a calm demeanor around humans. Research published November 7 in the journal GENETICS identifies gene regions that contribute to differences between nasty and nice rats in their behavior and the activity of genes in the brain. These results may provide important clues as to which genes make tame animals like dogs behave so differently from their wild ancestors.

"Tameness is one trait that all domestic animals share. Whether it's pigs or cats or horses, domestication changed species that used to fear humans into animals that now tolerate and even trust us. This research is an important step in uncovering the genetic basis of such remarkable transformations," said co-author Henrike Heyne, of the Max Planck Institute for Evolutionary Anthropology and the University of Leipzig in Germany.

The rats in the study are descendents of an experiment initiated more than forty years ago by Dmitry K. Belyaev, who is famous for his work on experimental domestication of foxes. Belyaev and his colleagues collected around 200 wild rats and divided them into two groups. In one group, the rats selected for breeding were the most aggressive of the bunch--those most likely to attack or show fear towards an approaching human hand. In the second group, only the tamest rats were bred. After repeating this process for more than sixty generations, rodents in the two groups reacted to humans very differently.

"Rats from the tame group allow you to pick them up and will sometimes even approach your hand on their own. In contrast, the aggressive rats immediately attack you or try to escape," said co-author Frank Albert of the Max Planck Institute for Evolutionary Anthropology and the University of California, Los Angeles.

To find gene variants responsible for these heritable behavior differences, the researchers crossed rats from each of the two groups to create a population of hybrids. These hybrid animals showed a wide range of behaviors and inherited a random mix of genetic variants from the original tame and aggressive parent rats. By combining information on the genes and the behavior of each hybrid, the team identified eight regions of the genome that contributed to the variation in tameness.

Within these broad regions, Heyne and colleagues looked for specific genes of interest by analyzing their activity in the brain. Eleven of the genes within these regions carried variants that made them more active in the brains of aggressive rats compared to tame rats, or vice versa. For five of these genes, the team found additional evidence that the variants regulating activity of the gene were the same variants that influenced behavior.

These five genes may play key roles in shaping behavior in the two populations. Several of the genes are involved in nervous system development and one, Slc17a7, has previously been implicated in fear and stress behavior in mice. Further experiments will be required to determine which genes contribute significantly to tameness or aggression.

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Genes contribute to behavior differences between fierce and friendly rats

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A team led by New York Stem Cell Foundation (NYSCF) Research Institute scientists conducted a study comparing induced pluripotent stem (iPS) cells and embryonic stem cells created using somatic cell nuclear transfer (SCNT). The scientists found that the cells derived from these two methods resulted in cells with highly similar gene expression and DNA methylation patterns. Both methods also resulted in stem cells with similar amounts of DNA mutations, showing that the process of turning an adult cell into a stem cell introduces mutations independent of the specific method used. This suggests that both methods of producing stem cells need to be further investigated before determining their suitability for the development of new therapies for chronic diseases.

The NYSCF Research Institute is one of the only laboratories in the world that currently pursues all forms of stem cell research including SCNT and iPS cell techniques for creating stem cells. The lack of laboratories attempting SCNT research was one of the reasons that the NYSCF Research Institute was established in 2006.

"We do not yet know which technique will allow scientists to create the best cells for new cellular therapies," said Susan L. Solomon, NYSCF CEO and co-founder. "It is critical to pursue both SCNT and iPS cell techniques in order to accelerate research and bring new treatments to patients."

While both techniques result in pluripotent stem cells, or cells that can become any type of cell in the body, the two processes are different. SCNT consists of replacing the nucleus of a human egg cell or oocyte with the nucleus of an adult cell, resulting in human embryonic stem cells with the genetic material of the adult cell. In contrast, scientists create iPS cells by expressing a few key genes in adult cells, like a skin or blood cell, causing the cells to revert to an embryonic-like state. These differences in methods could, in principle, result in cells with different properties. Advances made earlier this year by NYSCF Research Institute scientists that showed that human embryonic stem cells could be derived using SCNT revived that debate.

"Our work shows that we now have two methods for the generation of a patient's personal stem cells, both with great potential for the development of treatments of chronic diseases. Our work will also be welcome news for the many scientists performing basic research on iPS cells. It shows that they are likely working with cells that are very similar to human embryonic stem cells, at least with regard to gene expression and DNA methylation. How the finding of mutations might affect clinical use of stem cells generated from adult cells is the subject of an ongoing debate," said Dr. Dieter Egli, NYSCF Senior Research Fellow, NYSCF -- Robertson Investigator, Assistant Professor in Pediatrics & Molecular Genetics at Columbia University, and senior author on the paper.

The study, published today in Cell Stem Cell, compared cell lines derived from the same sources using the two differing techniques, specifically contrasting the frequency of genetic coding mutations seen and measuring how closely the stem cells matched the embryonic state through the analysis of DNA methylation and of gene expression patterns. The scientists showed that both methods resulted in cell types that were similar with regard to gene expression and DNA methylation patterns. This suggested that both methods were effective in turning a differentiated cell into a stem cell.

The scientists also showed that cells derived using both SCNT and iPS techniques showed similar numbers of genetic coding mutations, implying that neither technique is superior in that regard. A similar number of changes in DNA methylation at imprinted genes (genes that are methylated differentially at the maternal versus the paternal allele) were also found. It is important to note that both types of techniques led to cells that had more of these aberrations than embryonic stem cells derived from an unfertilized human oocyte, or than embryonic stem cells derived from leftover IVF embryos. These findings suggest that a small number of defects are inherent to the generation of stem cells from adult differentiated cells and occur regardless of the method used.

Story Source:

The above story is based on materials provided by New York Stem Cell Foundation. Note: Materials may be edited for content and length.

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SCNT derived cells, IPS cells are similar, study finds

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iOS android and windows phone Qvprep app Learn genetics and genetic engineering
This is our app title # 22 out of a total of 42 apps released till date. QVprep Genetic Engineering Covers * Introduction History of Genetic Engineering * ...

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iOS android and windows phone Qvprep app Learn genetics and genetic engineering - Video

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Free iOS, android, windows phone QVprep Lite Learn genetic engineering
This is our app title # 21 out of a total of 42 apps released till date. QVprep Lite Genetic Engineering is FREE and has limited content. The app gives you t...

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New laser scans of the dodo, perhaps the most famous animal to have gone extinct in human history, have unexpectedly exposed portions of its anatomy unknown to science, which are revealing secrets about how the bird once lived.

The dodo was a flightless bird about 3 feet (1 meter) tall that was native to the island of Mauritius in the Indian Ocean. It went extinct by 1693, less than a century after the Dutch discovered the island in 1598, killed off by creatures such as rats and pigs, which sailors introduced to Mauritius either accidentally or intentionally.

The giant bird was actually a type of pigeon. "The skull of the dodo is so large and its beak so robust that it is easy to understand that the earliest naturalists thought it was related to vultures and other birds of prey, rather than the pigeon family," said study co-author Hanneke Meijer at the Catalan Institute of Paleontology in Spain.

Surprisingly, despite the dodo's fame, and the fact the bird was alive during recorded human history, little is known about the anatomy and biology of this animal. "The dodo's extinction happened at a time when people didn't understand the concept of extinction science as we know it was still in its infancy,"lead study author Leon Claessens, a vertebrate paleontologist at the College of the Holy Cross in Worcester, Massachusetts, told Live Science. "This meant that nobody tried to make a collection of the bird or study it in detail." [Wipe Out! History's 7 Most Mysterious Extinctions]

To shed new light on the dodo, Claessens and his colleagues went to the Natural History Museum in Port Louis, Mauritius, to investigate the only known complete skeleton from a single dodo. All other dodo skeletons are composites of several birds.

Amateur naturalist and barber Etienne Thirioux found the specimen the researchers analyzed near Le Pouce Mountain on Mauritius in about 1903. It was unstudied by scientists until now.

The scientists used a laser scanner to create a 3D digital model of the specimen. In addition, they scanned a second dodo skeleton Thirioux also created, a composite of two or more skeletons that was housed at the Durban Museum of Natural Science in South Africa.

"We discovered that the anatomy of the dodo we were looking at was not previously described in detail," Claessens said. "There were bones of the dodo that were just unknown to science until now."

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Dodo Bird 3D Scan Reveals Previously Unknown Bones

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For entertainment giants such as Netflix and HBO, theres an oft-cited concept known as the last mile.

It refers to the performance bottleneck that can arise in the short, final stretch of cable that links their vast, sophisticated server farms to the humble jack on a subscribers wall.

More than a decade after the immense promise unleashed by the completion of Human Genome Project, precision medicine has struggled with its own last mile. Despite major leaps in the field as a whole, the technical work needed to integrate a patients genomic information into the day-to-day practice of medicine has lagged far behind.

This month, UCSF is unveiling its bridge across that persistent gap.

Kristen McCaleb, PhD, program manager for the UCSF Genomic Medicine Initiative, and Jonathan Hirsch, founder of Syapse. Photo by Elisabeth Fall

Robert Nussbaum, MD, leads the UCSF Genomic Medicine Initiative. Photo by Cindy Chew

Through its Genomic Medicine Initiative (GMI), UCSF has integrated data from a comprehensive cancer genetic testing program into the electronic medical records of patients at the UCSF Medical Center. Not only does it allow for continuity of care with all testing and treatment results tied to the same electronic record, but it also allows physicians and researchers to identify larger patterns in the data that can lead to the development of better treatments which is known as precision medicine.

Many major medical institutions, including UCSF, have long had the science and the technology to generate genomic test results, said Kristen McCaleb, PhD, program manager for the GMI who partnered with the Helen Diller Comprehensive Cancer Center on the project. The problem weve had is a lack of IT infrastructure to return those results to the clinicians who order the tests in a clearly actionable, doctor-friendly format.

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Bridging the Gap in Precision Medicine

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