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Balloon Trees, the new title from Sylvan Dell, written by Danna Smith and illustrated by Laurie Allen Klein, reveals that the rubber that makes up balloons, balls, tires, shoes and many more things actually comes from trees! What other surprising things do you think trees give us?

The house you live in may be made from wood from trees; that’s obvious, but did you know that that house is filled with gifts from trees also? Do you like that your parents are less grumpy in the morning when they have their coffee? You can thank the coffee arabica tree for that, a 20 foot evergreen that grows in warm climates of the world. A cup of hot cocoa has made a long journey from cocoa trees along the equator to reach your kitchen. Maple syrup, cinnamon, fruits, nuts, and many more delicious items also come from trees.

Ever wonder how jelly candies get so goopy and great? Check the ingredients and you’ll find “gum arabic” in the list. Gum arabic is hardened sap from an acacia tree, and it’s used in foods like desserts to lend its goopy texture to them. It is also a key ingredient in glues, paints, and many other products that manufacturers want to make ‘slimy,’ ‘goopy,’ or ‘jelly.’

“Cellulose” is part of the ‘skin’ of trees, and when manufactured it can become “Rayon” clothing to make our own skin warmer. Cellulose is even an ingredient in foods and beauty products, lending its texture to them to make them ‘thicker’ or ‘heavier.’ When fat is removed from some “diet” or “fat-free” products, cellulose is often added to try and make the food ‘feel’ the same in a person’s mouth as before. 

Trees also give us many kinds of medicine, such as aspirin, and even the first medicine for fighting malaria, “quinine.” If you’ve read our book, The Most Dangerous, you know how harmful the mosquito-spread disease malaria can be. Without the discovery of quinine from Peruvian trees, malaria would have harmed that many more people, and maybe even changed world history! Soldiers in WWII that fought in the Pacific jungles took quinine everyday, and it helped the building of the Panama Canal, and the Dutch and English to build their historical empires!

Of course, this is only the beginning of the gifts that trees give us. Say “thank you” back, by planting a tree, or at least reading a Sylvan Dell book under the shade of one!

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Like stratosphere, troposphere, and mesosphere, atmospheric regions with which it shares part of its name, the biosphere is a shell-shaped zone enveloping our planet. But where the others are made of nitrogen, oxygen, water vapor, and trace gases, the biosphere is made of life. It extends in two directions — up and down — farther [...]

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Here at Powells.com, in addition to exclusive interviews, original essays, and Q&As, we feature a wide selection of guest blogs from noteworthy authors. Each week, a new author contributes to our blog for five days straight, revealing everything from their thoughts on the writing process to details about their favorite neighborhood cat. We're constantly amazed [...]

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5 Stars Desert Baths Darcy Pattison Kathleen Rietz Syvan Dell Publishing 32 Pages      Ages 4 to 8 ………………….. Inside Jacket: As the sun and the moon travel across the sky, learn how twelve different desert animals face the difficulty of stay clean in a dray and parched land. Explore the desert habitat through its animals [...]

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Phytolacca americana

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By Dr Ivan R. Schwab

Well, yes, sort of. Dogs see colors, but their span of color vision closely resembles the array of colors seen by “color blind” males.

About 8%, or 1 out of 12 males (humans) and about 1 out of 200 females are “color blind.” We use that term to describe individuals that are color deficient, but they are not truly color blind. The eye has cells that perceive color and these are called cone photoreceptors or “cones.” We use another set of photoreceptors called “rods” for the black and white vision of dim light or nighttime. Our cones contain three visual pigments each of which responds to a different spectrum of wavelengths of light. It is these three visual pigments that combine their signals to permit us to have color vision by blending the signals, depending on the wavelengths received. Although it is an over-simplification, and misleading to some extent, we can describe our visual pigments as blue, green, and red. The brain receives the input from these three channels and then interprets the color we see. At least two different color channels are needed for color vision because the brain needs to “compare” these two different channels to determine color.

Color blindness in humans is caused by the genetic deficiency or loss of either the green or the red photopigment hence that input into the brain. So, the brain learns to see only those colors that can be interpreted or constructed by combining the input from the other two remaining visual pigments. The result is a less robust spectrum of colors, but colors are still seen. True color blindness in humans does exist when two of the three visual pigments are genetically unavailable, but it is exceedingly rare. If only one visual pigment channel is coming to the brain, say the blue cone input, it isn’t seen as blue but rather as on or off—hence that is “real” color blindness and would be a black and white world.

So, almost all color blindness in humans is not true color blindness but would be better described as color deficiency.

Now, let’s go back to your dog. Normal dogs have two different visual pigments in their cones, and much like humans afflicted with so-called “color blindness.” But they would see color. The color input would be weaker to some extent because dogs have fewer cones than we do because they are evolutionarily closer to their nocturnal ancestors. Cones are needed less, if at all, at night.

So, what about the other pets in the household? Your cat will have a similar color distribution as your dog although there are some subtle differences.

Birds, on the other hand, possess rich color vision, in many cases better than our own. Most birds have four cone visual pigments, although this varies. In general, birds have an additional ultraviolet pigment in their cones and many more cones than we have. Furthermore the visual pigments that would be similar to ours span different wavelengths. Their visual experience is richer than our own in ways impossible to describe or understand. Not o

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By Nina Schuyler, The Children’s Book Review
Published: January 27, 2012

Coral Reefs

By Jason Chin

Reading level: Ages 5 and up

Hardcover: 40 pages

Publisher: Flash Point (October 25, 2011)

Source: Publisher

What to expect: Science, Nature, Biology, Marine life, Water

Jason Chin does something pretty wonderful in his nonfiction book, Coral Reefs: He hasn’t forgotten the wild imagination of a kid.

What makes Coral Reefs unique is that along with loads of interesting information, he’s included colorful watercolor illustrations that tell their own story. In a sense he is blurring the boundary between fiction and nonfiction. The result is something completely engaging. And this hybrid form dishes out just enough facts without overwhelming. So you learn that though coral reefs may look like plants, they’re actually animals; and at the same time, the pictures, which often take up more than half the page, tell the story of a girl who goes to the library and picks up a book about coral reefs.

You learn coral reefs are the largest structures built by an animal on earth! The Belize barrier reef is over 180 miles long!; and at the same time, the illustrations show the girl’s world transforming, with the library slipping away and turning into coral, along with sea plants and fish. “There are so many species living in reefs that they are often called the cities of the sea,” writes Chin. And the water whooshes into the library, and the girl is swept up on a wave that carries with it octopus, sea turtles, fish and more coral. Very quickly, the girl is floating underwater, exploring and learning about the city of the sea. It’s a city, Chin tells us, with “a complex web of relationships, and each has its own place in the system.”

“There are so many species living in reefs that they are often called the cities of the sea,”

After you’ve fallen in love with coral reefs and the teeming life that calls it home—“More than four thousand kinds of fish and thousands of other species have been discovered in coral reefs—more than in any other part of the ocean”—after he’s completely hooked you, Chin has bad news. The reefs, just like so many other living things, are threatened by pollution and over-fishing. Thankfully, he gives a list of things you can do to help. You can—and you’ll want to—form a relationship with the reefs.

Add this book to your collection: Coral Reefs

Nina Schuyler‘s first novel, The Painting, (Algonquin Books of Chapel Hill/2004), was a finalist for the Northern California Book Awards. It was also selected by the San Francisco Chronicle as

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Every month OUP editor and author Jonathan Crowe answers your science questions in the monthly SciWhys column. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can. Today: Why do we eat food?

By Jonathan Crowe

You may well be thinking that the question posed in the title of this blog has an all-too-obvious answer. We all know that we eat food to keep ourselves alive. But why do we find ourselves slaves to our appetites and rumbling stomachs? What is actually happening inside each of us that couldn’t happen without another slice of toast, or piece of fruit, or that most vaunted of mid-afternoon pick-me-ups, the sneakily-consumed bar of chocolate?

We’re all familiar with the concept of something needing fuel to keep it going. Just as a power station requires gas or coal to power its turbines and generate energy, so we need fuel – in the form of food – to power our continued existence.

The foods we eat provide us with a range of nutrients: vitamins, minerals, water, fat, carbohydrates, fibre, and protein. These nutrients are put to different uses — as building materials to construct the tissues and organs from which our bodies are made; as the components of the molecular machinery that keeps our cells running as they should. All of these uses are unified by a common theme: a requirement for energy to make them happen. And this is where one particular type of nutrient comes into its own. Step forward the carbohydrates.

Carbohydrates are better known to us as sugars, but in fact the sweet crystals we know as sugar are only part of this group. Carbohydrates come in very different shapes and sizes. One of the smallest is glucose, which acts as a chemical building block — multiple copies of glucose can join together to form a range of much larger molecules. For example, starch – found in potatoes and flour – is a carbohydrate formed from many individual molecules of glucose joined together in long chains. (Based on taste alone, you wouldn’t think that starch was made of glucose. Even though individual molecules of glucose taste sweet to us, once they are linked together to form starch the sweetness is lost.)

To understand how the sugar in our food can power the processes occurring in our cells every minute of every day, let’s follow some starch on its journey through the body. Many of the foods we consume aren’t in a form with which our bodies can do anything useful. Instead, they need to be digested. And so it is with carbohydrates such as starch. This process of digestion starts as soon as the food enters our mouth; our saliva contains special substances (called enzymes) that start attacking the long chains of starch, breaking it into smaller fragments.

Digestion continues as our food is swallowed and slides down into our stomach, where an arsenal of other chemical weapons set to work on the mouthful we’ve just consumed. Before long, what were initially mouth-watering morsels are reduced to something rather less appetising and leave the stomach to enter the long, snaking tunnel of our intestines. By now, the long chains of starch have been broken down into glucose, which is small enough to pass through the lining of our intestine and into our bloodstream. Our bloodstream acts as a short- and long-distance transport network, carrying the newly-arrived sugar molecules to cells all over the body.

When glucose arrives at its destination and first enters the cell, it u

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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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On World Cancer Day 2012, we speak with Dr Lauren Pecorino, author of Why Millions Survive Cancer: the Successes of Science, to learn the latest in the field of cancer research. – Nicola

There are so many myths about cancer that it is sometimes difficult to understand exactly what it is. Can you briefly explain how cancer develops?

Cancer is a disease of the human genome. Many agents that cause cancer cause permanent changes to your genes. These permanent changes are called mutations. Cancer is usually caused by the accumulation of mutations over time. This is why cancer risk increases with age. The altered genes may produce faulty proteins that lead to abnormal cell growth and this appears as a tumour. Cancer is characterized by abnormal cell growth and the ability of tumour cells to spread throughout the body. It is this second characteristic, called metastasis that is the most difficult aspect to treat.

It is said that cancer now affects one in three people over a lifetime. What’s the latest progress in the field of cancer research?

There has been tremendous progress in the field of cancer management. The good news is that trends in death rates are decreasing for many cancers though that is not to say for all cancers. There are millions of cancer survivors who have had their diagnosis ten or more years ago. Many people are now living with cancer. Conventional treatments such as surgical procedures have been refined and new drugs that target tumour-specific molecules have proved efficient and promises less side effects.

In addition, we are learning to make lifestyle choices that science has shown reduces cancer risk — the most obvious being not smoking. We also have cancer screening programmes that can catch cancer early and even prevent cancer by treating pre-cancerous growths. The latest means for preventing a specific type of cancer is a cancer vaccine. Interestingly the vaccine designed to prevent cervical cancer vaccine also prevents several other cancers caused by the human papilloma virus such as some head and neck cancers.

What do you see as the priorities for future cancer research? Where will the next great advances be?

I see four main priorites for future cancer research.

1 –  To develop better and less invasive diagnostics so that we can detect cancer earlier. It is well-known that catching cancer earlier gives a better outcome or prognosis.

2 –  To expand our understanding of the individual molecular differences between tumors and to be able to fully practice personalized medicine which allows a better match between a patient and a drug. This understanding will need to be supported by technology that allows a patient’s tumour DNA to be sequenced (similar to the methods used for the Human Genome Project).

3 –  To understand if we can turn a cancer cell back into a normal cell. This may sound strange but lessons from stem cells and cloning tell us that changing one cell type into another is possible.

4 –  To better understand metastasis and how we can better treat it. The spreading of cancer cells throughout the body is the most difficult aspect of treating

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We don't have a staff member whose sole job is to keep up with what scientist, journalist, blogger, radio personality, and Press author Carl Zimmer is up to, but I'm beginning to suspect we should. This week, Carl's been all over the place: first, on The Loom, his Discover magazine blog

, he announced the launch of Download the Universe, a new collaborative venture from fifteen scientists and writers to cover science e-books. Carl explains:

We are fifteen writers and scientists who want to explore this new form. On a regular basis, we'll be delivering new reviews of ebooks about technology, medicine, natural history, neuroscience, astronomy, and anything else that fits under the comfortably large rubric of science. We also define ebooks generously—everything from a plain-vanilla pdf on an author's web site to a Kindle Single to an elaborate iPad app.

And since that apparently wasn't enough to keep Carl busy, he also had the cover story in this week's issue of Time: The Surprising Science of Animal Friendships.

Which is all the excuse we need to post cute photos of our cats!

So are these cats, all snuggled up together, really friends? To find out, you'll need to read the article, you have to be a Time subscriber, but Zimmer does say that

what may look like friendship may just be anthropomorphic projection. In the article, I explain that a lot of cross-species "friendships" may be nothing like the kind seen in, say, chimpanzees.

(So, no, the cats and the sock monkey most likely aren't friends.)

In the course of the article, Zimmer cites a number of Press authors, all of whom can shed light on new and different aspects of the eternally fascinating question of just how much we can know of animal minds.

First up, there's Dorothy Cheney and Robert Seyfarth, who have spent a career studying baboons, and in Baboon Metaphysics address the question of what sort of intelligence underlies the complex social organizations of baboons. In the field of primates, Zimmer also draws on the work of John Mitani, whose book The Evolution of Primate Societies we'll be publishing this fall.

We'd be remiss if we didn't also mention Marc Bekoff and Jessica Pierce's groundbreaking Wild Justice: The Moral Lives of Animals, which makes a strong case for the existence of a true sense of morality and ethics in animals.

All of which should provide you and your pets with plenty of reading. Once they finish reading and marking up Roberto BolaÃo's 2666, that is.

And now you'll have to excuse us, as we have an ap

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by Caroline Relton

Epidemiology, a well established cornerstone of medical research, is a group level discipline that aims to decipher the distribution and causes of diseases in populations. Epigenetics, perceived by many as the most fashionable research arena in which to be involved, is a mechanism of gene regulation. What brings these perhaps unlikely partners together?

Epigenetic processes are key features in gene regulation. Epigenetic patterns are laid down in early development and are moulded through in utero and early postnatal life and continue to show some degree of plasticity across the lifecourse. Many environmental, behavioural, nutritional and lifestyle factors are believed to influence epigenetic patterns and in some case the evidence base is substantial. What is less clear is the role of this environmentally modifiable ‘epigenome’ on disease risk in populations. This is where epidemiology can help. A good starting point for an epidemiological engagement with epigenetics is clearly identified by Nessa Carey, in her recent popular science book The Epigenetics Revolution:

“The majority of non-infectious diseases that afflict most people take a long time to develop, and then remain as a prob­lem for many years if there is no cure available. The stimuli from the environment could theoretically be acting on the genes all the time in the cells that are acting abnormally, leading to disease. But this seems unlikely, especially because most of the chronic diseases probably involve the interaction of multiple stimuli with multiple genes. It’s hard to imagine that all these stimuli would be present for decades at a time. The alternative is that there is a mechanism that keeps the disease-associated cells in an abnormal state, i.e. expressing genes inappropriately. In the absence of any substantial evidence for a role for somatic mutation, epigenetics seems like a strong candidate for this mech­anism”.

Recent literature points to a role for epigenetic variation in a range of diseases including neurological disease, cardiovascular disease, osteoarthritis and obesity but in most instances these are correlations without robust evidence of causality. Indeed, epigenetics is often proffered as the answer to many unresolved causes of disease. The enthusiasm for establishing whether epigenetic mechanisms link the environment with disease development must be tempered by the knowledge that the epigenome is dynamic and has as much  potential to  respond to disease as respond to the environment. Therefore it is very difficult to disentangle cause from consequence when studying epigenetic variation and disease.

This is just one of the many challenges that face researchers interested in understanding the role of epigenetics in common complex disease. Other challenges include the differences in interpretation of the term ‘epigenetics’ itself – in a field that attracts cell, developmental and evolutionary biologists, epidemiologists and bioinformaticians, amongst others, it is unsurprising that epigenetics means different things to different people and discussions of its relevance to disease can sometimes suffer misinterpretation.

The methods at our disposal to accurately measure epigenetic variation and in turn assess the impact this has upon disease risk are still being developed and there is much to do in this arena with respect to when, where and how to look at the epigenome. The complexity and interplay of multiple factors in determining d

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 5 Stars Rhyming text and illustrations explore some of the many things a leaf can be, from tree topper to rain stopper.  Includes facts about leafs and a glossary. A leaf is a leaf— A bit of a tree. But just try to guess What else it can be! This book, A Leaf Can Be [...]

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This post stems from the Thought Ripples over on Two Voices, One Song. Sometimes when you change a process for one thing, it sticks and bleeds over into other work, as well. That’s what happened here. I hope you enjoy it.

Once in a while, I take a trip through a zoo or sanctuary. While I gaze upon the residents within the confines of the area, taking note of mundane considerations, my mind focuses on the what-might-have-beens. Those are the natural landscapes and living conditions of whatever animal I’m viewing.

Take this guy, for instance. He was brought into man’s arena very early in his life. He worked for a living, hence his missing horn. And when his work was done, he was fortunate enough to find sanctuary on the Olympic Peninsula with other animal actors that had been retired.

He’s a sweetheart, who likes treats and people’s voices. He’s enclosed to keep him safe from those who would taunt and tease and stress him unduly. I think it’s sad that we have lock up the wild things to keep them safe from us, the civilized ones.

Because he’d not been allowed to be wild, he will never know his ancestors’ natural habitat. Then again, at least here he can live a peaceful existence without fear of someone taking his life, as well as his horn. And without his horn, he could have never survived in his natural habitat anyway.

Herds of elk and fallow deer have free run of many more acres of this wild animal park. The bison keep them company as they watch cars go by, occupants snapping and whirring with their cameras. Thankfully, no one can get out of their cars to aggravate the ones trying to eat or rest.

Peacocks keep order. Rabbits watch from the sidelines. Those in the petting zoo take little hands in stride. And everywhere are the sounds of human voices, rather than those of the residents.

Within the shadows cast by trees lurk yaks and zebras, not usual neighbors, though they seem to get along quite well.

The occasional small scene gives an idyllic glimpse of how life in the wild could be if allowed.

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This post stems from the Thought Ripples over on Two Voices, One Song. Sometimes when you change a process for one thing, it sticks and bleeds over into other work, as well. That’s what happened here. I hope you enjoy it.

Once in a while, I take a trip through a zoo or sanctuary. While I gaze upon the residents within the confines of the area, taking note of mundane considerations, my mind focuses on the what-might-have-beens. Those are the natural landscapes and living conditions of whatever animal I’m viewing.

Take this guy, for instance. He was brought into man’s arena very early in his life. He worked for a living, hence his missing horn. And when his work was done, he was fortunate enough to find sanctuary on the Olympic Peninsula with other animal actors that had been retired.

He’s a sweetheart, who likes treats and people’s voices. He’s enclosed to keep him safe from those who would taunt and tease and stress him unduly. I think it’s sad that we have lock up the wild things to keep them safe from us, the civilized ones.

Because he’d not been allowed to be wild, he will never know his ancestors’ natural habitat. Then again, at least here he can live a peaceful existence without fear of someone taking his life, as well as his horn. And without his horn, he could have never survived in his natural habitat anyway.

Herds of elk and fallow deer have free run of many more acres of this wild animal park. The bison keep them company as they watch cars go by, occupants snapping and whirring with their cameras. Thankfully, no one can get out of their cars to aggravate the ones trying to eat or rest.

Peacocks keep order. Rabbits watch from the sidelines. Those in the petting zoo take little hands in stride. And everywhere are the sounds of human voices, rather than those of the residents.

Within the shadows cast by trees lurk yaks and zebras, not usual neighbors, though they seem to get along quite well.

The occasional small scene gives an idyllic glimpse of how life in the wild could be if allowed.

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  12 days of sci-fi, day 8:

 Back on earth again, we switch gears to a story with a modern day setting that seems it could be straight out of today’s news…except the humanitarian aid workers aren’t quite what they seem to be. Parents should be advised that one of the themes to the plot is the abuse of very human-like female droids as sex slaves.

 Tin Servants by J. Sherer

 Patience

 Editor’s comment: “He’d (the author) read a lot of stories about robots trying to act human, but humans acting as robots?”

 This is a solid, fast-paced action drama set in Ghana nearly 50 years from now. The trauma and tragedy of a war-torn African nation, as well as risk to the protagonist, are realistically told almost as if we were watching an award-winning film. The beauty to reading stories instead of watching them in film is that the reader has the benefit of the character’s self-talk. We sense Paul’s, a/k/a TK-19’s, yearning to help the refugees with every cell in his body. Or at least the ones that are still human…

Don’t miss out. Pick up a copy of Infinite Space, Infinite God II at Amazon http://ow.ly/4F48e .

 (J Sherer lives in Southern California and works as a marketing supervisor for a large credit union. When he’s not writing, he enjoys playing sports, catching up on his favorite stories, and working with others on business strategies and tactics. His blog, Constructing Stories (www.jsherer.com), is a place where writers of all levels can engage in meaningful dialogue about the writing and storytelling process. He also partners with Nathan Scheck to present a free online science fiction adventure experience called Time Slingers (www.timeslingers.com). J Sherer’s past publication credits include Infinite Space, Infinite God; Dragons, Knights, and Angels Magazine; and the West Wind.)

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Today is Friday the 13th, so it makes me think of lucky and unlucky things. Personally, I like this date; but I know some people are uncomfortable with it. So, in keeping with the unlucky theme, I am reminded of a recent article about a very unlucky phenomenon in the marine environment. A level of ecological success that has been very lucky for one fish turns out to be extremely unfortunate for many other creatures in the Caribbean Sea.

The beautiful lionfish, with its red-striped face and body and long dorsal spines, is a native of the Indian and Pacific oceans. But in recent years it has gotten into the Caribbean Sea. How? It is thought that just a few lionfish escaped from a smashed aquarium tank during a hurricane in Florida. Usually an animal that gets loose in an alien environment is at a disadvantage. But the stealthy lionfish is a clever hunter and a successful breeder, producing thousands of eggs every four days. A few lionfish were first spotted in the waters around the Bahamas in 2005. Within three years, they had taken over the reefs, experiencing a population explosion by eating many of the native fish species, as well as shrimps and crabs. Scientists have found that the lionfish can reduce a reef’s native population by 75 to 80 percent in just a matter of weeks -- very unlucky for the local inhabitants. The same problem is now happening around the Grand Cayman Islands as well.

Just why are the lionfish so lucky in their new environment? It appears that, unlike the local reef fish, the lionfish are not infested by parasitic worms. Without parasites or any local predators, their mortality is quite low. And they are voracious predators, able to consume up to 30 times their stomach volume! This has caused a problem for local tourism, since people dive on the reefs to see all the beautiful native fishes--only to see an abundance of lionfish. In addition, their venomous dorsal spines can deliver a painful sting, making them a potential danger to divers who come too close. They are also a threat to the local commercial fisheries, since they are eating up native species.

So, what can be done about this fish invasion? Scientists catching a few here and there have not had an impact on their increasing population. But now, unfortunately for the lionfish, the tables have turned and there is one local predator it does have to worry about. Quite recently it has been determined that the lionfish makes a very tasty dish for humans when fried with nice seasonings. And this is turning out to be lucky for local residents and tourists in the Caribbean. Now the fishermen, not just the scientists, are turning their sights on the not-so-lucky lionfish!

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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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Every year I wait to see them. I saw my first one of 2011 on June 14, at dusk. It was just one lonely firefly, signaling its presence near a bunch of parked cars. For me it was an exciting moment. I am not even sure why. I just love the sight of these glowing insects; they mean summer is here. Their renewed presence means the species has survived yet another year and still exists to tell me it is June. But they are not really flies. So what are they?

Fireflies are actually winged beetles. The 2,000 species of fireflies that exist are found in temperate and tropical habitats around the world. They are also known as lightning bugs and even as glowworms (particularly in their larval phase) and they have these names because of their “conspicuous crepuscular use of bioluminescence to attract mates or prey” (per Wikipedia). In other words, they emit light at twilight to communicate with other insects. The light is produced by a chemical reaction that occurs within a special organ in their lower abdomen. Each species has its own pattern of light flashing to find mates.


Of course, I am not the only person who loves watching these bugs. There is a magic to watching children run through a field trying to capture fireflies. Professional institutions are also dedicated to the study of fireflies. The Museum of Science in Boston teams up with university researchers to study firefly sightings each year. Volunteers around the country help them count fireflies as a way of tracking their numbers. It seems that their population has been decreasing, and this could be due to environmental influences. There is even the Kumejima Firefly Museum in Okinawa, Japan, that is dedicated to this amazing insect. The museum celebrates the fact that there are seven species of firefly thriving on Kumejima because of the island’s clean ecosystem.

So, the next time you see some bug flying near you, please don’t reach out to swat it. Just keep an eye on it and you may be rewarded by the glow of a bioluminescent love signal.

Carol

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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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Danger!

I usually write about animal topics because they interest me the most. But quietly living alongside all the animals that catch our eyes are millions of plants, and they have exciting stories as well. Two surprising plant stories have recently made the news; while they do not quite range from the ridiculous to the sublime, they certainly do go from the bad to the good.

First, the bad plant news. I recently wrote a blog about an invasive fish species. There are many invasive animal species–both on land and in the water–that wreak havoc on native ecosystems. There are invasive plant species as well. Conservationists are already familiar with invasive plant species that can clog waterways or take over landscapes. But people usually do not think of invasive plants as personally threatening in the way that invasive animals can be. Think of the pythons that are now spreading through Florida. Now, however, there is an invasive giant weed that poses a threat to humans and it sounds like something from an Aliens movie. Called the Giant Hogweed, this plant is originally from the Caucasus region of Eurasia. In the 1900s, it was introduced to Europe, Britain, and North America as an ornamental species; it grows to over 15 feet in height and sprouts clusters of attractive white flowers. Now this plant is officially listed as a noxious weed; people are warned not to touch it because of the risk of skin irritation. It turns out that the sap of the Giant Hogweed can cause blisters and scarring in humans, and can even result in blindness if it comes into contact with the eyes. Giant Hogweed is called a phototoxic plant because its sap causes severe inflammations when the skin is exposed to sunlight. Blisters develop within 48 hours and form scars that can last several years. The plant should be removed by personnel from government environmental agencies, since cutting or mowing it can expose one to the dangerous sap. Be on the lookout for this giant plant and do not be tempted to touch it!

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