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Viewing: Blog Posts Tagged with: genetics, Most Recent at Top [Help]
Results 1 - 25 of 30
1. The Cancer Moonshot

Announced on January 13th by President Obama in his eighth and final State of the Union Address, the multi-billion dollar project will be led by US Vice President, Joe Biden, who has a vested interest in seeing new cures for cancer. Using genomics to cure cancer is being held on par with JFK’s desire in 1961 to land men on the moon.

The post The Cancer Moonshot appeared first on OUPblog.

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2. A Q&A with the Editor of Environmental Epigenetics

Environmental Epigenetics is a new, international, peer-reviewed, fully open access journal, which publishes research in any area of science and medicine related to the field of epigenetics, with particular interest on environmental relevance. With the first issue scheduled to launch this summer, we found this to be the perfect time to speak with Dr. Michael K. […]

The post A Q&A with the Editor of Environmental Epigenetics appeared first on OUPblog.

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3. TED Talks and DNA

One of the most fun and exciting sources of information available for free on the Internet are the videos found on the Technology, Entertainment and Design (TED) website. TED is a hub of stories about innovation, achievement and change, each artfully packaged into a short, highly accessible talk by an outstanding speaker. As of April 2015, the TED website boasts 1900+ videos from some of the most imminent individuals in the world. Selected speakers range from Bill Clinton and Al Gore to Bono and other global celebrities to a range of academics experts.

The post TED Talks and DNA appeared first on OUPblog.

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4. Nature vs. nurture: genes strongly influence survival to the oldest ages

In our study analyzing data from the New England Centenarian Study, we found that for people who live to 90 years old, the chance of their siblings also reaching age 90 is relatively small – about 1.7 times greater than for the average person born around the same time.

The post Nature vs. nurture: genes strongly influence survival to the oldest ages appeared first on OUPblog.

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5. DNA Day 2015: celebrating advances in genetics and gene therapy [infographic]

Today, 25 April is a joint celebration for geneticists, commemorating the discovery of the helix nature of DNA by James Watson and Francis Crick in 1953 and the completion of the human genome project fifty years later in 2003. It may have taken half a century to map the human genome, but in the years since its completion the field of genetics has seen breakthroughs increase at an ever-accelerating rate.

The post DNA Day 2015: celebrating advances in genetics and gene therapy [infographic] appeared first on OUPblog.

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6. The third parent

The news that Britain is set to become the first country to authorize IVF using genetic material from three people—the so-called ‘three-parent baby’—has given rise to (very predictable) divisions of opinion. On the one hand are those who celebrate a national ‘first’, just as happened when Louise Brown, the first ever ‘test-tube baby’, was born in Oldham in 1978. Just as with IVF more broadly, the possibility for people who otherwise couldn’t to be come parents of healthy children is something to be welcomed.

The post The third parent appeared first on OUPblog.

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7. What makes you You? A Royal Society Young People’s Book Prize shortlistee

royalsocietyprizebuttonEach year the Royal Society awards a prize to the best book that communicates science to young people with the aim of inspiring young people to read about science. In the run up to the announcement of the winner of The Royal Society Young People’s Book Prize in the middle of November, I’ll be reviewing the books which have made the shortlist, and trying out science experiments and investigating the world with M and J in ways which stem from the books in question.

7277405-MFirst up is What makes you YOU? by Gill Arbuthnott , illustrated by Marc Mones.

Have you ever thought how your genes could get you out of prison?

Or what the consequences might be if a company owned and could make money out of one of your own genes?

How would you know if you were a clone?

Why might knowing something about junk DNA be important if you’re running an exclusive restaurant with slightly dodgy practices?

Answers to these and many other intriguing questions are to be found in this accessible introduction to genetics, pitched at the 9-11 crowd. Arbuthnott does a great job of showing how relevant a knowledge of genetics is, whether in helping us to understand issues in the news (e.g. ‘Cancer gene test ‘would save lives’‘) or understanding why we are partly but not entirely like our parents. What makes you YOU? covers key scientists in the past history of genetics and crucial stages in its development as a science, including the race to discover what DNA looked like, the Human Genome Project, and Dolly the Sheep.

wmyyinside

Arbuthnott portrays the excitement and potential in genetic research very well, leaving young readers feeling that this is far from a dry science; there are many ethical issues which make the discussion of the facts seem more relevant and real to young readers. Whilst on the whole I felt the author did a good job of balancing concerns with opportunities, I was sorry that in the discussion about genetically modified plants no mention was made of businesses ability to control supply to food stock, by creating plants which don’t reproduce, leaving farmers dependent on buying new seed from the business.

A timeline of discoveries, a very helpful list of resources for further study, a glossary and an index all make this a really useful book. Importantly, not only does the book contain interesting and exciting information, it also looks attractive and engaging. Lots of full bleed brightly coloured pages, and the use of cartoony characters make the book immediately approachable and funny – a world away from a dry dull school textbook.

What makes you YOU? provides a clear and enjoyable introduction to understanding DNA and many of the issues surrounding genetic research, perfect not only for learning about this branch of science, but also for generating discussion.

Extracting DNA is what the kids wanted to try after sharing What makes you YOU?. In the interest of scientific exploration we tried two different techniques to see which one we found easier and which gave the best results.

Method 1: Extracting your own DNA

What you’ll need:

dna1

  • A tablespoon
  • Salt
  • A measuring jug
  • Water
  • Washing-up liquid
  • A small bowl
  • A teaspoon
  • A small clean cup
  • A tall and narrow jar (or a test tube)
  • Clingfilm or a stopper/lid
  • A stirrer eg a plastic straw
  • Rubbing alcohol (surgical spirit – in the UK you can buy this easily in a chemists such as Boots)
  • dna4

  • 1. Dissolve 1 tablespoon of salt in 250ml of water to create a salt solution.
  • 2. Dilute the washing-up liquid by mixing 1 tbsp of washing-up liquid with 3 tbsp of water in your small bowl. We’ll call this the soap solution.
  • 3. Swish 1 teaspoon of tap water around in your mouth vigorously for at least 30 seconds. Spit this into the small cup. We’ll call this spit water.
  • 4. Put 1/4 teaspoon of your salt solution into your tall jar/test tube.
  • 5. Pour your spit water from the cub into the tall tar/test tube.
  • 6. Add 1/4 teaspoon of your soap solution to the test tube.
  • 7. Cover the top of your tall jar/test tube either with clingfilm/a stopper/a lid and gently turn the jar almost upside down several times to mix everything together. Avoid making any bubbles.
  • 8. Take the covering off the jar and dribble 1 teaspoon of surgical spirit down the side of the tall jar/test tube. Watch for the surgical spirit forming a layer on top of the spitwater/salt solution/soap solution mix.
  • 9. You should now see a white stringy layer forming between the two layers – this is your DNA (and a few proteins, but mostly it’s your DNA)
  • 10. You can use the stirrer to pull out the white goop to get a closer look at your DNA.
  • dna5.jpg

    We learned this method for extracting DNA from Exploratopia by Pat Murphy, Ellen Macaulay and the staff of the Exploratorium. Unfortunately it’s out of print now, but it is definitely worth tracking down a copy if you are interested in doing experiments at home.

    Method 2: Extracting strawberry DNA

    This second method is detailed in What makes you YOU? and involves strawberries, fresh pineapple, warm water and ice as well as washing-up liquid and salt. It also calls for methylated spirits but we swapped this for surgical spirit, as that’s what we had to hand.

    dna2

    This method is a little more involved than the first method but is a all round sensory experience: There are lots of strong smells (from crushed strawberries and puréed pineapple, as well as the surgical spirit), colours make it visually very appealing (perhaps this is why methylated spirits are called for in the original recipe as the purple of the meths adds another dimension) and there is also lots to feel, from the strange sensation of squishing the strawberries by hand, through to the different temperatures of the warm water in which the DNA-extracting-mix gently cooks followed by the ice water in which it cools down.

    squishingstrawbs

    strawberrydnaprocess

    strawberrydnaresult

    Look! Strawberry DNA!

    strawberrydnagoop

    Both methods were fun to try. We liked the first method because the result was seeing globs of our very own DNA, but the second method was a much more stimulating process, appealing to all the senses. Indeed this DNA extraction recipe alone makes it worthwhile seeking out a copy of What makes you YOU?.

    Whilst extracting DNA we listened to:

  • GENEticS, a rap by Oort Kuiper
  • The DNA song

  • The Galaxy DNA song By Eric Idle and John Du Prez (a re-worked Monty Python song)

  • Other activities which might go well with reading What makes you YOU? include:

  • Checking out this list of children’s books I previously compiled on genetics and DNA – with something for everyone no matter what their age.
  • Listening to an interview with Gill Arbuthnott
  • Watching this animation which helps explain how Mendel’s pea plants helped us understand genetics
  • What do you and your family look for in science books to really hook you in? Do share some examples of science books which you’ve especially enjoyed over the years.

    Disclosure: I received a free review copy of What makes you YOU? from the Royal Society.

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    8. Questioning the health of others and ourselves

    By Patricia Prijatel


    A little evergreen tree has died alongside our road and, as we walked by it yesterday, my husband wondered why. All the other trees around it are healthy and it did not look like it had been hit by lightning or damaged by wind or attacked by bugs. The tree is about six feet tall, so it lived several years. We are in the Rocky Mountains and this little guy took root on its own, growing precariously in that place by the road.

    Oak Tree. Photo by Glyn Baker. Creative Commons License.

    The trees all around it are scrub oak, so maybe the soil was not right for an evergreen. Maybe it just grew in the wrong place, in soil that could not sustain it. Still, there are evergreens nearby that soar to the sky, so maybe this little tree was just too weak to begin with.

    Could we have done something to save it? If we were in the city, would we have babied it and maybe kept it alive? Or would it have died sooner there?

    These are the same questions we ponder about why some people get sick, why one disease affects one person more than others, why people who live healthy lives still can’t beat some illnesses, yet people with deplorable habits keep going and going.

    It’s the old nature versus nurture argument. Bad genes or bad environment? Or both?

    I am sort of over being angry at people who have dodged major illnesses — largely because there aren’t that many of them. Seems like most people I know have something to contend with — debilitating arthritis, diabetes, heart disease, Alzheimer’s somewhere in their network of family and friends. But when I first got cancer I did look around at people who obviously were not living as healthy as I was and wondered: why me and not them? And then I realized that I had no idea what they were dealing with and I should just stop being so angry and judgmental and get over myself. It was not their fault I got sick.

    Still, you have to wonder about this poker game we all play with our health. Some seem to be dealt a good hand to begin with, some make the best of a poor hand, some try but can’t make a straight out of a pair of twos, and some look at their cards and just fold.

    I have one friend who never exercises and has a diet full of fat, yet she is in her mid-80s, hale, hearty, and youthful-looking. Another smoked all his life, drank, and never exercised, yet he is pushing 80 and has nothing seriously wrong physically, although I do think he looks back at his life with serious regret. But the big C didn’t get him, nor did any major illness. I wouldn’t swap places with him, though, even if I knew my cancer would return.

    I also know a wide variety of cancer patients who approach the disease like the individuals they are — fighters who refuse to let the disease get the upper hand; questioners who search for their own information rather than listening to the docs; accommodators who go along with whatever the doctor says; worriers who can’t get beyond the fact that they might die. Most of us are a mix of these traits, fighting one day, living in worry the next. But we are all built differently, both physically and mentally, so we all react to our disease differently. Nobody is right, nobody is wrong. We’re all just us, being our own little trees fighting our own little battles.

    We cannot escape our genes — they make us prone to certain diseases, give us the strength to fight others, and offer a blueprint for either a long or a short life. Still, we can change some of that; the science of epigenetics demonstrates that lifestyle and environmental factors can influence our genetic makeup so that, by improving things such as diet and physical activity and by avoiding unhealthy environmental pollutants including stress, bad air, and chemicals, we can eventually build a healthier DNA.

    I was born into a history of cancer. My grandmother and both of my parents had forms of cancer, although none of them had breast cancer. I was the pioneer there. But both parents lived into their 80s and remained in their home until they died, surrounded by their family. So, I might have a tendency toward cancer, but perhaps my genes also mean I will hang around for a couple more decades. And my particular mix of nature and nurture has given me an ability to love, to laugh, to process health information in a way that might make me proactive, and to keep going, assuming all will be well, at least at some level.

    Maybe I won’t end up as one of the stronger trees in the forest; maybe I will be the gnarled, crooked one. Maybe disease might slow me, but I feel I am rooted deeply in decent soil — family, friends, community — so I am going to push on, grow how I can, and, in the process, help shade and nurture the other trees around me.

    Patricia Prijatel is author of Surviving Triple-Negative Breast Cancer, published by Oxford University Press. She is the E.T. Meredith Distinguished Professor Emerita of Journalism at Drake University. She will do a webcast with the Triple Negative Breast Cancer Foundation on 16 October 2012. Read her previous blog posts on the OUPblog or read her own blog“Positives About Negative.”

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    9. “The Story of You: ENCODE And The Human Genome” By DC Turner

    The Story of You: ENCODE And The Human Genome is a primer about the latest developments in genetics research. Commissioned by Nature.com, the film was directed by DC Turner and narrated by Tim Minchin. Turner and Minchin previously collaborated on the animated short Storm.

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    10. SciWhys: a cure for Carys? Part Two

    Over the past year, the SciWhys column has explored a number of different topics, from our immune system to plants, from viruses to DNA. But why is an understanding of topics such as these so important? In short, using science to understand our world can help to improve our lives. In my last post and in this one, I want to illustrate this point with an example of how progress in science is providing hope for the future for one family, and many others like them.

    By Jonathan Crowe


    In my last post, I introduced you to Carys, a young girl living with the effects of Rett syndrome. Thanks to scientific research, we now understand quite a lot about why Rett syndrome occurs – what is happening among the molecules within our cells to mean that some cells don’t behave as they should. Simply knowing about something is one thing, though; making constructive use of this knowledge is another thing entirely. During this post I hope to show you how our understanding of what causes Rett syndrome is being translated into the potential for its treatment – a cure for Carys, and the other young girls like her.

    In my previous post I mentioned how Rett syndrome is caused by a faulty gene called MECP2 that affects the proper function of brain cells. However, the syndrome doesn’t actually kill the cells (unlike neurodegenerative diseases that do cause cells to die). Instead, the cells affected by Rett syndrome just function improperly. This leads us to an intriguing question: if the faulty gene that causes the syndrome could be ‘fixed’ somehow, would the cells start to behave properly? In other words, could the debilitating symptoms associated with Rett syndrome be relieved?

    Obviously, researchers can’t simply play around with humans and their genes to answer questions such as these. Instead, researchers have studied Rett syndrome by using “mouse models.” But what does this mean? In short, mice and humans have biological similarities that allow the mouse to act as a proxy – a model – for a human. How can this be? Well, even though the huge variety of creatures that populate the earth look very different to a casual observer, they’re not all that different when considered at the level of their genomes. In fact, around 85% of the human and mouse genomes are the same.

    Now, if the biological information – the information stored in these genomes – is similar, the outcome of using this information will also be similar. If we start out with two similar recipes, the foods we prepare from them will also be very similar. Likewise, if two creatures have similar genes, their bodies will work in broadly similar ways, using similar proteins and other molecules. (It is the bits of the mouse and human genomes that aren’t the same that make mice and humans different.)

    In essence, the mouse Mecp2 gene is to all intents and purposes the same as the human MECP2 gene, and has the same function in both mice and humans. Equally, if this gene malfunctions, the consequences are the same in both mouse and human: a mouse with a mutation in its Mecp2 gene exhibits symptoms that are very like a human with a mutation in the same gene – that is, someone with Rett syndrome. In short, mice with a Mecp2 gene mutation are a model for humans with the same mutation.

    With all this in mind, if we can learn how to overcome the effects of the Mecp2 mutation in the mouse, we might gain valuable insights into how we can overcome the equivalent effects in humans.

    And this is wh

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    11. SciWhys: a cure for Carys?

    Over the past year, the SciWhys column has explored a number of different topics, from our immune system to plants, from viruses to DNA. But why is an understanding of topics such as these so important? In short, using science to understand our world can help to improve our lives. In this post and the next, I want to illustrate this point with an example of how progress in science is providing hope for the future for one family, and many others like them.

    By Jonathan Crowe


    Carys is an angelic-looking two-year old, with a truly winning smile. At first sight, then, she seems no different from any other child her age. Yet Carys’ smile belies a heart-rending reality: Carys has Rett syndrome, a disorder of the nervous system that is as widespread in the population as cystic fibrosis, yet is recognised to only a fraction of the same extent. (I, for one, had never heard of it until just a few months ago.)

    Rett syndrome is a delayed onset disorder — something whose effects only become apparent with time. When Carys was born, she appeared perfectly healthy, and developed in much the same way as any other healthy infant. Just as she began to master her first few words, however, she lost the power of speech, and soon lost the use of her hands too. The effects of Rett syndrome were beginning to be felt.

    Over time, Rett syndrome robs young girls of their motor control: they lose the ability to walk, to hold or carry objects, and to speak. But there be other complications too: there may be digestive problems; difficulties eating, chewing, and swallowing; and seizures and tremors. It is a truly debilitating disorder.

    So what causes Rett syndrome? What’s happened inside the body of young girls like Carys? We know that the syndrome is caused by as little as a single error (a mutation) in a single gene. (As I mention in a previous post, it’s quite unsettling to realise that just one error in the tens of millions of letters that spell out the sequence of our genomes is sufficient to cause certain diseases. Sometimes there’s very little room for error.) The normal, healthy gene (called MECP2) contains the instructions for the cell to manufacture a particular protein; the mutated gene produces a broken form of this protein, which no longer functions as it should.

    But how can a single protein affect so many processes – from speech to the movement of limbs? The answer lies in the way the protein interacts with other genes, particularly in brain cells. Essentially, the protein acts like a cellular librarian by helping the cells in the brain to make use of the information stored in their genomes (their libraries of genes). If the protein is broken, the cells can no longer make use of all of the genetic information needed for them to work properly (a bit like trying to use an instruction manual with some of the pages blacked out), so normal processes begin to break down. The broken protein doesn’t just affect the ability of the brain cells to use one or two other genes, but a whole range of them – and that’s why the effects of Rett syndrome are so wide-ranging.

    But the story of Rett syndrome runs deeper than this. The mutation that causes Rett syndrome occurs in sperm; it happens after the sp

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    12. Fat, fate, and disease

    By Mark Hanson


    We are failing to deal with one of the most important issues of our time – in every country we are getting fatter. Although being fat is not automatically linked to illness, it does increase dramatically the risk of cardiovascular disease, diabetes, and other so-called non-communicable diseases. We are starting to see very high rates of these diseases in some places, sometimes affecting 50% of the population. Even in some of the poorest parts of the developing world, where such disease itself is not yet common, we nonetheless see warning signs of its arrival. There is great concern that it may soon outweigh the burden of communicable disease such as HIV/AIDS. The humanitarian and financial cost of this non-communicable disease in such parts of the world will be unbearable, and made even worse because the risk is passed across generations, so children born today and tomorrow will have a bleak future.

    It seems that we don’t know how to tackle this problem, because current attempts are obviously failing and obesity continues to increase. Governments, doctors, and even NGOs seem to have adopted the same strategy – to focus on our sins of “gluttony and sloth” and to transfer the responsibility for slimming down to each of us as individuals. Of course it’s true that we can’t get overweight unless we eat more than we need to, and the wrong types of foods, and get too little physical exercise. Our biology did not evolve to protect us from obesity and its consequences in today’s sedentary world with such easy access to food. But why is it that we find it so hard to lose weight and, if we do shed the kilos, it seems very hard not to put them back on again?

    What we are missing is a focus on our early development. We’re just not adopting the right approach to the problem. And it seems that the generals who are leading us in this global war on obesity and disease have adopted the wrong strategy, and they stick resolutely to it as if they were wearing blinkers. They blame us for the failure to win the war, for our greed and laziness; they blame parents for letting their children get fat; they blame the food industry for peddling unhealthy food, and so on. As if we choose to be fat. It’s important to realise just how limited this way of attacking the problem is on a global scale. Does the little girl force-fed before marriage in Mauritania have any choice in her life? Does the 12-year-old child bride in rural India have any choice when she becomes pregnant and drops out of school? Does the little toddler in Detroit have any choice when his mother feeds him French fries? Does the little boy from Tonga whose mother had diabetes in pregnancy have any choice about developing obesity? Does the little girl in Beijing have any choice in being an only child? And yet every one of these scenarios, and many more, sets that little child up to be at greater risk of becoming obese and to have non-communicable disease.

    But new research is uncovering many things that will give us new tactics and strategies for the war against obesity and non-communicable disease, and so we’re hopeful. We now know that we will have to give much greater focus to the mother and unborn child. We may well have to give emphasis to the lifestyle of the father as well. And most importantly of all, we’re starting to realise that behaviours such as propensity to exercise, or appetite and taste for certain foods, which we previously thought to be based on individual choice, have a large constitutional component – in part based on inherited genes, in part on epigenetic changes to gene function in response to the developmental environment, and

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    13. Ship Breaker - Review


    Ship Breaker (Ship Breaker #1) by Paolo Bacigalupi

    Publication Date: 1 May 2010 by Brilliance Audio
    ISBN 10/13: 1441883495 | 9781441883490

    Hardcover Date: 1 May 2010 by Little, Brown Books for Young Readers
    ISBN 10/13: 0316056219 | 9780316056212

    Category: Young Adult Science Fiction
    Keywords: Fantasy, dystopian, ships, pirates, genetic engineering, family
    Format: Hardcover, ebook, audiobook


    I was a little apprehensive about picking this one up. While I thought Bacigalupi's last book, The Windup Girl, was interesting, it wasn't a favorite. But a long road trip prompted me to pick up Ship Breaker in audio book at the library. Luckily, my fears were unfounded, and I am really glad I took a chance on it.

    The book takes place in a grim future where where global warming has caused a major shift in the ecological landscape. Rising water levels and "city killer" storms have left large metropolitan areas covered in water and refuse. Nailer, a young teenage boy, works a dangerous job on the light crew, stripping old tanker ships that have washed ashore for copper wire and other salvageable parts. Living a hand to mouth existence, with an abusive father at home, Nailer knows that any day might be his last. A lucky encounter with a downed clipper ship brings Nailer and his friend Pima to Nita, a "swank" rich girl and the only survivor of the ship. Nailer decides to risk it all to save Nita with the hope that she'll help him leave the ship yards for good.

    Ship Breaker is a tense roller coaster ride that keeps you on the edge of your seat. Well plotted and well paced, there's never a dull moment. With a male protagonist and an emphasis on peril and adventure, I can see this book appealing to boys. There's a bit of romance thrown in, though it's minor compared to everything else that happens in the book.

    Bacigalupi does a great job of creating a unique and believable dystopian future, one both familiar but also very different than our own. He tackles some heavy themes, including environmental responsibility, class disparity, and notions of family and loyalty. Though a bit heavy handed at times, Bacigalupi manages not to sound too preachy. Though their world is often cruel and heartless, there still exists kindness, friendship and love, as demonstrated by Nailer and others in the story.

    While the world is vast and rich, what impressed me the most about the book were the characters in it. They are diverse in breeding and background and are a complex lot, damaged and imperfect. No character is all good or all ba

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    14. Przewalski’s horses not ancestors of modern domestic horses

    By Danielle Venton


    For millions of years, the stout, muscular Przewalski’s horse freely roamed the high grasslands of Central Asia. By the mid-1960s, these, the last of the wild horses, were virtually extinct: a result of hunting, habitat loss, and cross breeding with domestic horses.

    Recovering from a tiny population of 12 individuals and only four purebred females, there are now nearly 2,000 Przewalski’s horses around the world. Once again, the light-colored horses, standing about 13 hands, or 1.3 meters, tall, are beginning to graze on the Asian steppe, thanks to captive breeding and reintroduction programs.

    Protecting Przewalski’s horses, listed as critically endangered by the International Union for Conservation of Nature, will require far more than protecting their habitat. Understanding and safeguarding their genetic diversity is key, said Kateryna Makova, an evolutionary genomicist at Pennsylvania State University. In a new study (Goto et al. 2011), Makova and her colleagues Hiroki Goto, Oliver Ryder, and others report on the most complete genetic analysis of Przewalski’s horses to date, clarifying previous genetic analyses that were inconclusive.

    Because Przewalksi’s horses are the only remaining wild horses, many people have hypothesized that they gave rise to modern domestic horses. The Australian Brumbies or the American Mustangs, sometimes referred to as wild horses, are actually feral domestic horses, adapted to life in the wild. Przewalski’s horses are not the direct progenitors of modern domestic horses, Makova and her colleagues conclude, but split approximately 0.12 Ma. Horses were likely domesticated several times on the Eurasian steppes. It is not known where and when the first event took place. Recent excavations in Kazakhstan indicate humans were using domestic horses as early as 5,500 years ago.

    Przewalski’s horse and offspring

    The team base their findings on a complete sequencing of the mitochondrial genome and a partial sequencing, between 1% and 2%, of the nuclear genome. They used one horse from each of the historical matrilineal lines. After processing the DNA samples with massively parallel sequencing technology, they compared the Przewalski’s horses to each other, to domestic Thoroughbred horses, and to an outgroup, the Somali wild ass.

    Their results carry several implications for breeding strategies. Przewalski’s horses and domestic horses come from different evolutionary gene pools, so breeders should avoid crosses with domestic horses, they advise. Przewalski’s horses and domestic horses have a different number of chromosomes (66 for the former, compared with 64); yet their offspring are fertile (with 65 chromosomes). The hybrids are viable because they differ only by a centric fusion translocation, also called a Robertsonian translocation. The process of pairing chromosomes during meiosis is not disrupted. Cross breeding should be a last resort, if too few Przewalski’s horses are available. Their analysis also suggests that, since diverging, Przewalski’s and domestic horses have both retained joint ancestral genes and swapped genes between populations. One of the two current major blood lines, the “Prague” line, is known to have a Mongol pony as one of its ancestors. The other primary line, the “Munich” line, is believed to be pure. However, because the two groups have historically mixed, keeping “pure” Przewalski’s horses from Przewalski’s horses with known domestic horse contributions might not be necessary, the authors write.

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    15. SciWhys: How does an organism evolve?

    This is the latest post in our regular OUPblog column SciWhys. Every month OUP editor and author Jonathan Crowe will be answering your science questions. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can. Today: how do organisms evolve?

    By Jonathan Crowe

    The world around us has been in a state of constant change for millions of years: mountains have been thrust skywards as the plates that make up the Earth’s surface crash against each other; huge glaciers have sculpted valleys into the landscape; arid deserts have replaced fertile grasslands as rain patterns have changed. But the living organisms that populate this world are just as dynamic: as environments have changed, so too has the plethora of creatures inhabiting them. But how do creatures change to keep step with the world in which they live? The answer lies in the process of evolution.

    Many organisms are uniquely suited to their environment: polar bears have layers of fur and fat to insulate them from the bitter Arctic cold; camels have hooves with broad leathery pads to enable them to walk on desert sand. These so-called adaptations – characteristics that tailor a creature to its environment – do not develop overnight: a giraffe that is moved to a savannah with unusually tall trees won’t suddenly grow a longer neck to be able to reach the far-away leaves. Instead, adaptations develop over many generations. This process of gradual change to make you better suited to your environment is called what’s called evolution.

    So how does this change actually happen? In previous posts I’ve explored how the information in our genomes acts as the recipe for the cells, tissues and organs from which we’re constructed. If we are somehow changing to suit our environment, then our genes must be changing too. But there isn’t some mysterious process through which our genes ‘know’ how to change: if an organism finds its environment turning cold, its genome won’t magically change so that it now includes a new recipe for the growth of extra fur to keep it warm. Instead, the raw ‘fuel’ for genetic change is an entirely random process: the process of gene mutation.

    In my last post, I considered how gene mutation alters the DNA sequence of a gene, and so alters the information stored by that gene. If you change a recipe when cooking, the end product will be different. And so it is with our genome: if the information stored in our genome – the recipe for our existence – changes, then we must change in some way too.

    I mentioned above how the process of mutation is random. A mutation may be introduced when an incorrect DNA ‘letter’ is inserted into a growing chain as a chromosome is being copied: instead of manufacturing a stretch of DNA with the sequence ATTGCCT, an error may occur at the second position, to give AATGCCT. But it’s just as likely that an error could have been introduced at the sixth position instead of the second, with ATTGCCT becoming ATTGCGT. Such mutations are entirely down to chance.

    And this is where we encounter something of a paradox. Though the mutations that occur in our genes to fuel the process of evolution do so at random, evolution itself is anything but random. So how can we reconcile this seeming conflict?

    To answer this question, let’s imagine a population of sheep, all of whom have a woolly coat of similar thickness. Quite by chance, a gene in one of the sheep in the population picks up a mutation so that offspring of that sheep develop a slightly thicker coat. However, the thick-coated sheep is in a minority: most of the population carry the normal, non-mutated gene, and so have coats of normal thickness. Now, the sheep population live in a fairly tempera

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    16. SciWhys: What is gene mutation?

    This is the latest post in our regular OUPblog column SciWhys. Every month OUP editor and author Jonathan Crowe will be answering your science questions. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can. Today: what is gene mutation?

    By Jonathan Crowe

    In my last three posts I’ve introduced you to the world of biological information, taking you from the storage of biological information in libraries called genomes, which house information in individual books called chromosomes (themselves divided into chapters called genes), to the way the cell makes use of that stored information to manufacture the molecular machines called proteins.

    But what happens when the storage of information goes wrong? If we’re reading a recipe and that recipe contains a mistake, chances are that the end-result of our culinary endeavour won’t end up as it should. And so it is at the level of cells. If the information the cell is using is somehow wrong, the end result will also be wrong – sometimes with catastrophic results.

    I’ve mentioned in previous posts how biological information is captured by the sequence of the building block ‘letters’ from which DNA is constructed. The sequence of letters is ultimately deciphered by a molecular machine called the ribosome, which reads the sequence of letters in sets of three, and uses each trio to determine which amino acid – the building block of proteins – should be used next in its mission to construct a particular protein. It should come as no surprise that, if the recipe for the protein is changed – if the sequence of DNA ‘letters’ is altered – the protein that is manufactured will probably contain errors as a result. And if a protein contains errors, it won’t be able to function correctly, just as flat-packed furniture will end up being decidedly wobbly if you construct it from the wrong parts.

    Imagine a snippet of DNA has the sequence GGTGCTAAG. The ribosome would ‘read’ this sequence, and would use it as the recipe for building a chain of three amino acids: Glycine-Alanine-Lysine. Now imagine that we alter just one letter in our original sequence so that it becomes GGTCCTAAG. All we’ve done is swap a G for a C at the fourth position in the DNA sequence. However, this change is sufficient to affect the composition of the protein that is produced when the sequence is deciphered: the ribosome will now build a chain with the composition Glycine-Proline-Lysine.

    Surely such a small change won’t actually cause significant problems in a cell, though. Right? Wrong. Amazingly (and perhaps unnervingly) the tiniest error can have really quite significant consequences.

    Let’s take just one example. Sickle cell anaemia is a condition that affects the red blood cells of humans.  Red blood cells fulfil the essential role of transporting oxygen from our lungs to all the living cells of our body: they continually circulate through our arteries and veins, shuttling oxygen from one place to another. A healthy red blood cell looks a bit like a ring doughnut (though it doesn’t actually have a hole right through the middle); by contrast, the red blood cells of individuals with sickle cell anaemia become warped into crescent-like shapes (like a sickle, the grass-cutting tool, after which the disease is named). These sickle cells no longer pass freely through our arteries and veins. Instead, they tend to get entangled with each other. As a result, the flow of oxygen round the body is impeded, and

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    17. So what do we think? “Solid” is a solid story!

    See our character education review at www.litland.com

    Workinger, Shelley. (2010). Solid. Published by CreateSpace. ISBN: 1-453-62482-1. Author recommended age Tweens & Teens: Litland.com recommends ages 14+ due to sexual references.

     Publisher’s description:   Eighteen years ago, a rogue Army doctor secretly experimented with a chromosomal drug on unknowing pregnant women. Almost two decades later, the newly self-proclaimed “open-book” military unearths the truth about the experiment, bringing Clio Kaid and the other affected teens to a state-of-the-art, isolated campus. While exploring her own special ability, forging new friendships and embarking on first love, Clio also stumbles onto information indicating that the military may not have been entirely forthcoming with them and that all may not be as it seems…

     Our thoughts:

     Showing rather than telling, the prologue opens to a high ranking military officer  engaged in some secret work. Invisibility. Glowing. But these are just lab rats…

     Fast forward to the present. Calliope Grace Kaid (Clio for short) starts at new schools frequently. While she may be an old hand at being the newbie, readers can still relate to how it feels. Worrying about making friends that move away, cliques excluding her, and just plain looking stupid, for the first time she is on a level playing field with her peers. They’ve all been invited to this high school summer camp, and at age 17 presumably have some maturity of social skills. Unlike Clio, whose military father died and her mother moved them around until becoming established in her own career, the other kids are military brats, military families that move from base to base as assigned. So for the first time, Clio is starting a camp where she at least has this in common with the other kids. Everyone’s a newbie here.

     The author has given Clio just enough sarcasm and cynicism to be a very realistic American teenager, while maintaining an inner nature of goodness which exemplifies the character traits we seek in good kid’s literature. Through her self-talk, we relate to her insecurities and self-criticisms, how she responds to a cute guy’s behaviour, hoping not to make too many social mistakes.

     It’s refreshing to have a female heroine who is solid in her own strengths, without a publisher seeking to make her a feminist vixen hoping to sell more books or make the story more attractive for a future movie. Through self-talk, we find this main character takes an inquisitive look at her world, particularly figuring out people, but in a manner that isn’t negatively judgmental of them. In doing so, she ponders how it is for adults to deal with issues like death, thus being able to almost empathize with them. An older teen should have achieved this level of maturity, thus rounding out her character well.

     For example, Clio isn’t desperate for friends even if she is used to moving a lot and losing them. Or as she puts it, just seeing them on Facebook. So she isn’t trying to endear herself to as many peers as possible in an attempt at securing popularity. Rather, she is using good discernment on who she intends to hang with, such as with Miranda:  “Abrasive was one thing, but if she turned out to be slutty too, our friendship would be short-lived.” 

     And how refreshing it is that the girls who might be

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    18. On queen honeybees and epigenetics

    By Jonathan Crowe


    What links a queen honeybee to a particular group of four atoms (one carbon and three hydrogen atoms, to be precise)? The answer lies in the burgeoning field of epigenetics, which has revolutionized our understanding of how biological information is transmitted from one generation to the next.

    The genetic information stored in our genome – the set of chromosomes that we inherit from our parents – directs the way in which we develop and behave. (We call the attributes and behaviours exhibited by an organism its ‘phenotype’.) Traditionally, the genetic information was thought to be encoded solely in the sequence of the four different chemical building blocks from which our DNA is constructed (that is, our genome sequence). If a DNA sequence changes, so the resulting phenotype changes too. (This is why identical twins, with genomes whose DNA sequences are identical, look the same, but other individuals, whose genomes comprise different DNA sequences, do not.) However, the field of epigenetics opens up a strong challenge to this traditional view of our DNA sequence being the sole dictator of phenotype.

    So what actually is epigenetics? In broad terms, epigenetics refers to the way that the information carried in our genome – and the phenotype that results when this information is ‘deciphered’– can be modified not by changes in DNA sequence, but by chemical modifications either to the DNA itself, or to the special group of proteins called histones that associate with DNA in the cell. (It’s a bit like taking a book, with a story told in the author’s words, and adding notes on the page that alter how the story is interpreted by the next person to read it.)

    But what has epigenetics to do with the group of four atoms, the one carbon and three hydrogen atoms mentioned at the start of this blog post? These four atoms can combine to form a methyl group – a central carbon atom, with three hydrogen atoms attached; the addition of methyl groups to both DNA and histone proteins in a process called methylation is a primary way in which epigenetic modification occurs. For example, the addition of a methyl group to one of the four chemical building blocks of DNA (called cytosine, C) either when it appears in the sequence CG (where G is the building block called guanine) or the sequence CNG (where N represents any of the four chemical building blocks of DNA) appears to result in that stretch of DNA being ‘switched off’. Consequently, the information stored in that stretch of DNA is not actively used by the cell; that stretch of DNA falls silent.

    But what of our queen honeybee? Where does she fit into our story? A queen honeybee has an identical DNA sequence to her workers. Yet she bears some striking differences to them in terms of physical appearance and behavior (amongst other attributes). These differences are more than just skin-deep, however: the pattern of methylation between queen and worker larvae differs. Their genomes may be the same at the level of DNA sequence, but their different patterns of methylation direct different fates: the queen honeybee and her workers develop into quite distinct organisms.

    Things take an interesting turn when we consider the cause of these different methylation patterns: the diets that the queen and workers experience during their development. The queen is fed on large quantities of royal jelly into adulthood, while worker larvae face a more meager feast, being switched to a diet of pollen and nectar early on. It is these diets that influence the way in which the queen and worker bees’ genes are switched on and off.

    It is not just the queen honeybee whose genome is affected by the environment (in her case, diet). Mice exposed to certain chemicals during pregnancy have be

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    19. Amazement In Small Doses

    I try to take amazement in small doses each day. Such a practice keeps the heart ticking without fear of an overdose of excitement. It also allows a body to stop long enough to appreciate those things which would otherwise be overlooked.

    Take this morning, for instance. The sun was shining as if it had just been let out of prison and had to rejoice for the world. I looked out the window to enjoy it because it’s been rather gloomy and gray around this part of the world for the last several days.

    That’s when it hit me. If I live to be a thousand years old, it will never cease to amaze me at how fast the sun’s position can shift from the northeast in the morning sky during high summer to the sky’s southeast during November.

    Think about it. For the solar system to work in such a way along with the rotation of the Earth, that the sun’s position can make such a marvelous change in it’s appearance is amazing. Of course, the Moon does much the same thing for much the same reasons, but we don’t pay much attention to how it hangs in the sky. The only time we really pay attention to it is if it’s hanging up there, full and glorious, during the daytime.

    Or, what about standing under a clear blue sky and have snowflakes falling gently to the ground. Where do they come from if there aren’t visible clouds over your location?

    How about the fact that a person can hear electricity running through power lines? What really makes them hum like that?

    I got to thinking about those sounds which make me cringe. For some it’s nails on a chalkboard. I hate that sound, too, but there are worse for me. An electric heater humming or a florescent light fixture’s hum. A motorcycle, especially the lesser beasts with smaller engines, make want to rip it to shreds. I think it’s the pitch that infuriates me so much.

    I do have a physical reaction to some sounds. Most people do.

    The question is, why do we have a physical response at all? Is it the pitch, the sound’s frequency, DB level, an unpleasant childhood experience?

    Or course, the same holds true for other stimuli. Why do some sights, sounds, or smells elicit pleasurable responses? I can understand kitchen odors such as fresh-baked bread or desserts and such. My mom was a great cook.

    Other smells, like that of hospitals, also bring some people to near tears. There are emotional ties for everyone to particular odors. That’s been proven. Yet, certain sights and sounds bring a sense of peace with them.

    Pictures and sounds of the sea have been used for decades to calm and refresh the mind and body. Some researchers profess that this response hails back to our primordial, genetic memory. Personally, I don’t buy that explanation. I think it comes from the susurration of the surf and it’s resemblance to a mother’s whispering shush when the baby wakes frightened and disoriented. That shush sound comes with warm comforting arms, many times.

    Watching the surf has much the same effect, I think. The hypnotic repetition of the waves making their way to shore and running up the sand calms the watcher because of the regularity of the movement as much as sound. Even breakers have their own regularity and effect.

    So, what does this have to do with amazement in small doses, you ask? Take the initiative to watch yourself today. If you hear someone laugh in pure delight/enjoyment, do you smile, too? If you see someone slip and fall, do you cringe from imagined pain? If there’s an incident o

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    20. Should Your Genetics Be Considered In the Workplace?

    By Lana Goldsmith, Intern

    Scott Shane is the A. Malachi Mixon III Professor of 9780195373424Entrepreneurial Studies at Case Western Reserve University.  In this post, Shane deliberates the pros and cons of genetic testing in the workplace.  This is an adaptation from his new book Born Entrepreneurs, Born Leaders: How Your Genes Affect Your Work Life which shows how a heightened awareness of your own – and your colleagues’ – genetic predispositions can make you a better employee or employer.

    Our genes impact numerous aspects of our work lives, from our tendency to start businesses to our job satisfaction to our leadership abilities to our decision-making styles. While we aren’t yet at the point where companies can use genetic information diagnostically, we might be in the near future.

    Some observers have pointed out that as knowledge of how our genes affect our behavior in the workplace grows, companies might benefit from using this information. That raises the question: Should companies be allowed to use genetic information in the workplace?

    Many, it seems, have come down against this prospect. In the United Kingdom, the Nuffield Council on Bioethics concluded in a 2002 report entitled Genetics and Human Behavior, “Employees should be selected and promoted on the basis of their ability to meet the requirements of the job. . . . Employers should not demand that an individual take a genetic test for a behavioral trait as a condition of employment.” (p. 183.) And, according to an April 24, 2004 article in the Wall Street Journal, Jane Zhang and Shirley Wang report that, in the recent genetic nondiscrimination bill, Congress made it illegal to use genetic information “to make hiring, firing, and other job placement decisions.” (p. A11).

    Like many things dealt with definitively, there is another part of the story, which makes the issue less simple than it appears at first glance. Congress in the United States and the Nuffield Council in the United Kingdom clearly addressed one side of the issue: companies should not be allowed to hire people on the basis of something that they have no control over and can’t really change, because doing so would be inherently unfair.

    On the other hand, how “fair” are other selection criteria relative to genetic testing? Numerous studies have shown the bias that people involved in the employment process have for physically attractive job candidates of the opposite sex. But appearance is, in large part, outside of one’s control, and is hard to change. So how is it fair to allow managers to make employment decisions on the basis of physical appearance, but bar them from using selection tools that incorporate genetic information?

    What about the issue of fairness that comes up if we do not allow companies to use genetic data to assign people to jobs or training? If employers aren’t permitted to use hereditary information in this way, and they subsequently punish people for poor performance on the job, then we are implicitly allowing the companies to engage in genetic discrimination.

    To see what I mean, take the example of a company which provides its employees with financial rewards if they take courses to develop their leadership skills, as Stephen Robbins and Tim Judge’s best selling textbook, Organizational Behavior (13th edition, Prentice Hall, 2009) reports a number of companies do. A sizeable portion of the difference between people in the ability to direct others comes from their DNA. This means that some people are genetically inclined to do better than others in leadership develop

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    21. Not a Chimp, Not Even Close

    Lauren, Publicity Assistant

    Not a Chimp: The Hunt to Find the Genes that Make Us Human is an exploration of why chimps and humans are far less similar than we have been led to believe. Genome mapping has revealed not-a-chimpthat the human and chimpanzee genetic codes differ by a mere 1.6%, but author Jeremy Taylor explains that the effects of seemingly small genetic difference are still vast. In the post below, he discusses how the discovery of “Ardi” deals a fatal blow to the chimpanzee ancestor myth.

    Jeremy Taylor has been a popular science television producer since 1973, and has made a number of programs informed by evolutionary theory, including two with Richard Dawkins.

    When discussing differences between chimpanzees and humans, I enjoy telling the hoary old joke about the traveler, lost in the midst of the Irish landscape, who approaches a farmer in a nearby field for directions. “Well,” says the farmer, on hearing his request, “If I were going to Kilkenny I wouldn’t start from here!”

    I share this to highlight the point that we have chosen the chimpanzee as the bench-mark comparison with humans to help us answer the big questions as to how we evolved into humans, and when, for the simple reason that it is our nearest relative in terms of living DNA and behavior. But that does not mean that chimpanzees are cheek by jowl with us or that chimpanzees represent the perfect starting point. Those myriad genome scientists need no reminding from me that necessity has forced comparison with a species that is actually separated from us by twelve million years of evolutionary time since the split from the common ancestor–six million years for the branch that led to us, plus six million for the branch that led to them. Although we know even less about chimpanzee evolution than the precious little we have learned about the genetic changes that led to modern humans, it is clearly reasonable to assume that chimpanzees have not remained evolutionarily inert these past six million years and may well have evolved as far and as fast as we have–though not in the same direction.

    Nevertheless, a number of primatologists who should know better, many great ape conservationists, large swathes of the science media, and therefore much of the lay audience, have become bewitched by incessant talk over the last few years about the extraordinary genetic proximity between apes and humans–what I call the 1.6% mantra–and the many cognitive and behavioral similarities that appear to have eroded the old idea of human uniqueness: tool manufacture and use, empathy, altruism, linguistic and mathematical skills, and an intuitive grasp of the way others’ minds work. All this has led to claims that chimps should be re-located, taxonomically, within the genus Homo, that they are more our brothers than our distant relatives, and that they should be therefore be accorded human rights. It has also led to the assumption that the common ancestor of chimps and humans must have looked and behaved very much like chimpanzees today and that our deep human ancestors must have clawed their way to us via a knuckle-walking chimpanzee-like stage before coming down from the trees, developing bipedality and bounding off into the savannas that were rapidly replacing dense forests due to climate change.

    This “chimps are us” cozy day-dream has been dealt a welcome (to me) wake-up call by the publication of the discovery and analysis of the fossilized remains of Ardipithecus ramidus–”Ardi.” At 4.4 million years of age, she is perilously close to the time of the split from the common ancestor–and, as one of the main researchers, Tim White, is repeatedly quoted, “Ardi is not a chimp. It’s not a human. It’s what we used to be.” Ardi was clearly bipedal–she had a pelvis with a low center of gravity and had a foot structure which acted like a plate, allowing her to launch herself forward as she walked. Her hands were more flexible than a chimp’s, would have allowed careful palmigrade movement when in the forest canopy which would have supported her weight, and, crucially, would have presented more recent human ancestors with less evolutionary distance to travel to achieve the highly dexterous human hand essential for sophisticated tool use. Plant and animal remains found with her point to an environment of mixed forest and grassland in which she foraged omnivorously for nuts, insects and small mammals.

    Was our common ancestor much more like Ardi than a chimp? Is the chimp we see today the result of six million years of specialized evolution away from this extraordinary biped with its mixture of primitive and derived features? Ardi seems fated to join two other odd-ball ancestors we have dug up in recent years: Sahelanthropus tchadensis (Toumai), who dates to approximately seven million years ago, around or before the split from the common ancestor–and Orrorin tugenensis, which dates between 5.8 and 6.1 million years. It is claimed that both were bipedal, though so little of the total skeleton in each case has been retrieved that these claims are open to dispute. Orrorin seems somewhat more similar to modern humans than the famous Lucy, Australopithecus afarensis, is three million years older, and appears to have inhabited a similar mixed forest/grassland environment as Ardi. These misfits may have been very similar, or identical to, the common ancestor, and represent a much better approximation of the deep roots of the human tree than do chimpanzees.

    Chimp-hugging conservationists have been over-playing their cards on chimpanzee-human proximity for years. Recent genomic research has unearthed a number of important structural and regulatory mechanisms at work in genomes that widen the gap between humans and chimps, and recent fascinating cognitive research with dogs and members of the corvid family of birds has shown that species that diverged hundreds of millions of years ago from both chimps and humans can out-perform chimpanzees on cognitive tests involving following human cues and in the making and use of tools, respectively.

    We are not “the third chimpanzee”–chimps with a tweak. The difference between human and chimp cognition, in the words of American psychologist Marc Hauser, is of the order of the difference in cognition between chimps and earthworms. Chimpanzees–and the other great apes–are the only species for which we erect the idea of near-identity as the motivating force for conservation. We don’t beseech the general public to save the white rhino because we share over 80% of our genes with it, or the tropical rain-forest because we share over 50% of our genes with the banana. Although I would be first into the firing line in the battle to save chimpanzees and their natural environments from extinction I believe this resort to chimp-human proximity is a distraction and the wrong way to go about it. As Ardi is showing us, it is high time we stopped ourselves falling prey to this narcissistic anthropomorphism that brands chimpanzees as the “nearly man.” Chimps are not us!

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    22. Book Review - The Peril of the Sinister Scientist



    THE PERIL OF THE SINISTER SCIENTIST
    Janet Ann Collins
    Guardian Angel Publishing Inc.
    ISBN 978-1-935137-79-5
    $7.95 US

    In a moment of panic Joshua’s Mom sets into motion a series of terrifying events that have Joshua on the run and questioning his real identity. As Joshua attempts to live up to what he believes is his genetic makeup he learns valuable lessons about life.

    This suspenseful book will have kids on the edge of their seats as Joshua runs from a sinister scientist and tries to figure out why he is being chased and who he can trust. What about Mom, has his pursuer controlled her mind? Joshua angers friends and enemies alike as he tries to avoid being captured.

    This is an imaginative tale kids are sure to love to the very end.

    Review 9/08/09 – Shari Soffe

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    23. Chimps are not us!

    Not a Chimp: The hunt to find the genes that make us human is an exploration of why chimps and humans are far less similar than we have been led to believe. Genome mapping has revealed that the human and chimpanzee genetic codes differ by a mere 1.6%, but author Jeremy Taylor explains that the effects of seemingly small genetic difference are still vast. In the post below, he looks at cases of domesticated chimps turning on their owners and argues that humans must learn to keep chimpanzees at arms’ length, literally and intellectually.

    Jeremy Taylor has been a popular science television producer since 1973, and has made a number of programmes informed by evolutionary theory, including two with Richard Dawkins. You can visit his blog here.


    In the first chapter of Not A Chimp I tell the blood-thirsty and cautionary tale of how two male chimpanzees attacked a middle-aged American couple and savaged the husband to within an inch of his life. I wanted to highlight the strangely ambivalent world of chimpanzee-human relations which can turn on a sixpence from anthropomorphic domestic bliss to berserk savagery. Sadly, but not surprisingly, attacks on humans by chimpanzee pets are not rare. Earlier this year, a young chimp called Travis, who had lived happily and docilely at home with a Connecticut woman, suddenly showed his dark side and mauled her friend, terrified the neighbourhood, attacked a posse of policemen who had rushed to the scene, and was dispatched, Dirty Harry style, by an officer’s fire-arm. One minute you can be sitting peacefully with your simian chum, both sipping Budweisers while watching a baseball game on TV, the next minute he’s biting a neighbour’s fingers off and causing havoc.

    There are over 200 chimpanzees kept as domestic pets - companions - in the United States, where their owners feel compelled to disregard the fact that chimps are immensely strong, emotionally labile, and potentially highly dangerous wild animals, in favour of the comfy tea-and-slippers notion that they are so like us humans in terms of genetics, behaviour and cognition, that they are, quite literally, one of the family. Not so long ago we were thought to have diverged from the line that led to chimps a massive 25 million years ago, and had since evolved unique cognitive powers that set us apart from them. Now we know that chimp and human ancestors diverged a mere 6 million years ago, and that, over many stretches of the DNA in our respective genomes, we appear to be almost 99% identical. Although hotly contested, a good number of cognitive psychologists contend that the mental lives of chimps and humans are also closer than we once thought, and that chimps can empathize, deceive and manipulate each other because, like us, they understand that other individuals have mental lives in which their actions are governed by beliefs, desires and knowledge - rather than acting like unconscious lumbering robots.

    Our lay persons’ ability to anthropomorphize our pets - in this case chimps - plays into the hands of what I call the “chimps are us” industry where scientists who should know better accentuate the similarities and trivialize the differences between chimps and humans such that humans, as Jared Diamond so memorably dubbed us, have become perceived as the “third chimpanzee”. But these scientists are simply behind the times, reading from a genetic script festooned with cobwebs. Over the last 10 years or so, thanks to increasingly powerful means to investigate the genetic structure and DNA sequence, we now know that chimpanzee and human genomes are nowhere near as similar as we have been told; that there are crucial differences between the timing and rate at which near-identical genes work in humans and chimps, particularly in the brain; and that there are a host of exotic structural differences between chimp and human genomes, caused by copy number variation of genes, multiple duplications of enormous sections of DNA, insertions, inversions and deletion of genetic code, and many more mechanisms, all of which serve to reduce the similarity of chimp and human DNA.

    I am not quite sure what the best explanation is for this persistent over-stressing of the similarity between us and chimpanzees, apart from a need to anchor us more firmly to the animal kingdom by abolishing the speciesism that has, in the past, held us apart, above, “better than” all the other great apes. Something unique. Perhaps this idea of cognitive uniqueness, an unbridgeable cognitive gap between us and chimps, sniffs too suspiciously, and dangerously, of religion - the perpetual assault on conventional evolutionary biology by creationists. We use science to close the ranks between us and the other great apes for fear that God will get a foot in between us and replace Darwinian origins with divine ones. Certainly, what similarity there is between us and chimps has been used to bolster our sense of affinity with them, the better to urge us to conserve them in a world in which their habitats are becoming rapidly decimated. Indeed, we are perilously close, in my opinion, to the philosophical insanity of widely using the concept of human rights to protect and conserve chimpanzees. Here the concepts of cognitive and genetic proximity are used to argue that chimps are “virtually human”, or even worse, that they are as human as little children or the feeble-minded. Though why we need to be persuaded to save chimps because they are nearly genetically identical to us, when we need no bidding through shared genetics to try to save the rainforest, the green-flowered Helleborine orchid or the Javan rhino, is beyond me.

    Even if, over parts of our respective genomes, chimps and humans are 99% identical this does not mean that chimps are 99% human or alternatively that we are 99% chimp. We must learn to keep chimpanzees at arms’ length - literally and intellectually - while still being capable of thrilling to their complex social intelligence and using them as an essential scientific tool to find out how we evolved from something that very probably looked and behaved quite like them. Chimps are NOT us!

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    24. This Gene is Not a Hedgehog

    from an article on nomenclature in New Scientist (via Bookforum):

    "We had particular problems with fruit-fly researchers," says Sue Povey of University College London, who chaired the committee approving names for human genes from 1996 to 2007. "They were always giving their genes names like hedgehog."

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    25. Paarlberg and Ronald: A Food FightPart Three

    Yesterday we posted part two in our dialogue between Robert Paarlberg (who recently published Starved For Science) and Pamela Ronald (author of Tomorrow’s Table). These two experts have been debating all week how to best ensure a safe food supply with the least amount of damage to the environment. This is the third and final part of the series, so be sure to read parts one and two first.

    Robert Paarlberg is the Betty F. Johnson Professor of Political Science at Wellesley College. His most recent book is Starved For Science: How Biotechnology is Being Kept Out of Africa(Harvard University Press), explains why poor African farmers are denied access to productive technologies, particularly genetically engineered seeds with improved resistance to insects and drought.

    Pamela C. Ronald is a Professor in the Department of Plant Pathology at the University of California, Davis. Her laboratory has genetically engineered rice for resistance to diseases and flooding. She is an elected Fellow of the American Association for the Advancement of Science. Her most recent book, written with Raoul W. Adamchak, is Tomorrow’s Table: Organic Farming, genetics, and the Future of Food, which argues that a judicious blend of two important strands of agriculture–genetic engineering and organic farming–is key to helping feed the world’s growing population in an ecologically balanced manner.

    Dear Pam,

    Thanks for your last note. I like your final observation:

    “So what I advocate is intensive farming using the most ecologically responsible approaches. In our view this would include many organic production practices and GE crops.”

    I am attracted, as you are, to a number of organic production practices. What I find less attractive are the strict prohibitions in organic farming against some practices, such as the prohibition against all synthetic fertilizer use, or against all synthetic pesticide use. In many cases it will make ecological sense to restore soil nutrients by using a combination of both compost and synthetic nitrogen, yet the rules of organic certification make this impossible. It makes ecological sense, in many cases, to adopt an integrated pest management strategy, eliminating the routine use of synthetic insecticides yet keeping the chemical option available for the occasional circumstance when pest damage crosses a certain threshold. Yet once again the rules of organic certification make this practice impossible, since no use of synthetics is permitted.

    I have another question about the rules of organic certification, which say it is perfectly all right to use “natural” poisons to kill insect pests. What is it that allows us to assume naturally occurring insecticidal substances are good, while those fabricated by people are always bad? This rule seems to derive, a bit too much, from the pre-scientific views held by the mystics and romantics who originated “biodynamic” and organic farming a century or more ago.

    But perhaps I am missing something here.

    Thanks,
    Rob


    Dear Rob

    The organic certification system provides guidelines for a biologically-based agricultural. One of the points of our book is that a truly sustainable agriculture will need to integrate many of these organic, scientifically-based principles. Yet it will also need to integrate new crop varieties, including those GE crops that satisfy principles of sustainable production. As you point out, different locations, crops and farmers will need to employ different approaches to achieve this vision. As Mike Madison, a fellow farmer, neighbor and writer says, “In dealing with nature, to be authoritarian is almost always a mistake. In the long run, things work out better if the farmer learns to tolerate complexity and ambiguity . . . Having the right tools helps”

    Unfortunately such a sustainable system, although increasingly used around the world, has not yet been clearly defined. We begin that dialog in our book and appreciate your valuable contributions.

    All the best
    Pam


    Dear Pam,

    Yes, I appreciate the dialog we have begun, and look forward to staying in touch. The point made by Mike Madison is solid. It was Rachel Carson who taught us best not to be either authoritarian or arrogant when working with biological systems, as we still know only a small amount about how they work, and especially how they work with each other. Whenever we introduce agricultural cropping systems into the natural environment we risk doing harm as well as good.

    I have just been asked by the Food and Agriculture Organization of the UN to prepare a background paper that tries to imagine how the world can double its food production by the year 2050 (as will be necessary, given projected population and income growth in the developing world between now and then) without doing unwanted harm to the natural environment. A tall order, I think you would agree. I will have your nice book, Tomorrow’s Table, open on my desk when I get started on this task. Your willingness to integrate multiple approaches - from organic to GMO - into the design of sustainable farming systems is a persuasive approach to me. Thank you for opening so many minds with this inclusive approach.

    Rob Paarlberg

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