The Golden Goose Award celebrates federally funded research that is seemingly obscure but turns out to have an…

Posted on August 9, 2013 by madamescientist

The Golden Goose Award celebrates federally funded research that is seemingly obscure but turns out to have an unforeseen positive impact on society. This year, the prize goes to Dr. John Eng whose discovery of the peptide exendin-4 from the venom of the 2-foot long pink-and-black Gila Monster has provided relief to millions of diabetics. 

From Lizard to Laboratory: In 1990, Dr. Eng was intrigued by research at the NIH showing that venom from some snakes and lizards caused the pancreas to expand, as if they were overstimulated. He noted that the Gila Monster only eats about twice a year,  yet its blood sugar levels were strikingly constant.  The lizard deals with long periods of not eating by slowing its metabolism way down, and then turns it back on like the flick of a switch. He went on to discover exendin-4, a protein naturally found in the saliva and body of the Gila lizard that is remarkably similar to GLP-1, a hormone that triggers the release of insulin from the pancreas. Unlike GLP-1, which has a half-life of minutes, “lizard spit” is long lasting and effective for diabetics who cannot produce enough insulin to control blood sugar. 

A Case for Curiosity Driven Research: The Golden Goose award enjoys bipartisan support in Congress. Rep. Jim Cooper (D-TN) said, “Medicine from monsters and venom may sound like a science-fiction novel, but it’s a real-life breakthrough. Dr. Eng’s research shows that we can’t abandon science funding only because we don’t know where it might lead. Just ask millions of diabetics whose lives have been improved by his discovery.” Exendin’s secrets are still being revealed. More recently, it was found to reduce levels of amyloid beta protein (found in senile brain plaques), and a clinical trial to determine safety and efficacy in Alzheimer’s disease is underway (see http://goo.gl/wEy4bX).

Read more: http://goo.gl/UipSVe

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Nothing to Laugh About

Posted on August 8, 2013 by madamescientist

Nothing to Laugh About 

● Macabre Mask: The feeding cups of Naegleria fowleri, a single celled protist, may look comical but there is nothing funny about an infection of amebic meningitis: death within a week, with less than 1% survival rate. Fortunately, infections are very rare (“the medical equivalent of being struck by lightning”) although, paradoxically, the amoeba is abundant, living on bacteria in the sediments of warm lakes, ponds and hot springs, where lots of people swim. So relax, you’re not likely to be infected with the “brain eating ameoba”. But how would the amoeba get to your brain, anyway?

● Highway to Hell Or Stairway to Heaven? Water forced up the nose could carry a form of the amoeba (trophozoid) that can get past the lining to the olfactory nerves that detect smells. From there, its a short ride to the olfactory bulb, the only part of the brain with a direct link to the outside world. Once in the brain, the amoeba feeds off cells using its sucker like feeding cups. Research showed that N. fowleri can loosen the tight junctions between lining cells, whereas its non-pathogenic cousin cannot. Some infections have been linked to the use of neti pots to irrigate the nasal chamber. While this ancient practice helps clear symptoms of allergies and colds, it can inadvertently cause amoebic infection. So, always use sterile water. 

● Double Duty Drugs: Amebic meningitis is lethal because there are no effective drugs that target this microbe. Antibiotics don’t work. Recently, scientists at UCSF screened a chemical library of FDA-approved drugs and discovered that corifungin, an antifungal, kills Naegleria in a culture dish and in the mouse brain. Based on this, FDA has approved orphan drug status for corifungin to use against primary amebic meningoencephalitis. 

Pop Sci/Comic: http://sci-ence.org/the-mucosa-of-oz/

Image: The feeding structures of the amoeba Naegleria fowleri have a face-like appearance. Credit: D.T. John & T.B. Cole, Visuals Unlimited

Open Access Reference: http://goo.gl/Yek2Hu

#ScienceEveryday    #microbes  

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Ready, Set, Engage!

Posted on August 4, 2013 by madamescientist

Ready, Set, Engage!

Thanks to the initiative of Chris Robinson , I’ve been part of the effort to set up a public database of scientists on G+ (add your profile here http://goo.gl/yEg7M), and then on to moderate the Science on Google+ Community. It’s been a privilege to be part of this team. To celebrate, we offer you our Science Engager’s Circle as a promise to raise the bar on outreach via social networks. Thanks for your support, and I’ll be back with more science posts (after I’m done

engaging with baking my banana bread!) 🙂

#ScienceSunday

Originally shared by Science on Google+

Science Engager’s Circle

The Science on Google+ Community (http://goo.gl/uhJCN) is approaching 100,000 members!! To celebrate, we are making changes to the community categories to increase engagement and to highlight high quality posts (see http://goo.gl/EPPOAn for details). We are also starting a new Science Hangout On Air called “Posterside Hangouts”. The first Posterside Hangout will be announced soon! We also put together this really great circle of Science Engagers. Every profile and page in the circle can be found in the Science on Google+: A Public Database (see http://goo.gl/Yz8KR to access the database). Thanks to everyone who is following and contributing to the community and page! 

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Animal, mineral or vegetable?

Posted on July 30, 2013 by madamescientist

Animal, mineral or vegetable? If you can guess the identity of the object in this image, leave a hint or a cool fact in the comments (but try not to give the game away)! 

Story (and Hint): It was January, 1862 when Charles Darwin first laid eyes on a specimen of the Madagascar orchid Angraecum sesquipedale and exclaimed, “Good Heavens”. He went on to predict that an object like the one in this photo would be found. A few years later, Alfred Wallace agreed with Darwin’s hypothesis, saying of the orchid, “I maintain…that the laws of multiplication, variation, and survival of the fittest, already referred to, would under certain conditions necessarily lead to the production of this extraordinary XXX”. Wallace made a drawing of his prediction, and was proved correct a few decades later.  

Photo attribution: Steve Gschmeissner

#ScienceEveryday   #ISeeTheWorldWithScience  

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What do you see?

Posted on July 28, 2013 by madamescientist

What do you see? An alien sun rising over some distant desert landscape? Arid rivers marking the surface of Mars? Leave your guesses in the comments! #ISeeTheWorldWithScience  

● Forests in Flames: Actually, this photo was commissioned by the United Nations to bring attention to deforestation from coca cultivation. Three countries account for the global cocaine production: Peru, Columbia and Bolivia. A study led by SUNY professor Liliana Dávalos showed that in a 5 year period, coca cultivation led to the destruction of 890 square kilometers of rainforest. That accounts for ~6 percent of rainforest loss, totaling 14,000 square kilometers, or an area slightly larger than Jamaica. Spraying with herbicide proved to be an ineffective deterrent: for every 30 hectares sprayed, only one was eradicated. In contrast, government protection of land seemed to prevent illegal growth of coca plants. 

● Sunburned Eyes: Dilated pupils and red eyes are a visible sign of cocaine use. Curiously, cocaine was used to treat snow blindness, an extremely painful form of sunburn of the eye caused by UV radiation bouncing off snow cover. Did you know that British explorer Ernest Shackleton packed medicinal cocaine for his expedition to the South Pole in 1907 (see here for a fascinating pix http://goo.gl/W8Jo5). [Note: Shackleton came close, but did not make it to the South Pole. Later, his wife recounted : “The only comment he made to me about not reaching the Pole was “a live donkey is better than a dead lion, isn’t it?”] 

● Snow Blind Friend:The Urban Dictionary defines Snow Blindness as Cocaine addiction, as heard in this poignant song by Steppenwolf: SNOWBLIND FRIEND live John Kay & Steppenwolf 1989

He said he wanted Heaven but prayin’ was too slow

So he bought a one way ticket on an airline made of snow

John Kay, the charismatic frontsman of Steppenwolf, was legally blind with a congenital disorder of cone cells leaving him with complete color blindness and only black and white vision.  

Ref: Forests and Drugs: Coca-Driven Deforestation in Tropical Biodiversity Hotspots. Dávaloset al.,  http://goo.gl/B1NVbs

Photographer: Javier Crespo, Leo Burnett Colombia advertising agency.

#ScienceSunday 

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The Appendix: Don’t close the book on it yet!

Posted on July 25, 2013 by madamescientist

The Appendix: Don’t close the book on it yet!

● The vermiform appendix is the poster child of vestigial organs leading to the joke that, “Its major importance would appear to be financial support of the surgical profession.” Like the wings of an ostrich or the eyes of the blind cave-dwelling catfish, the appendix no longer supports the function that it was designed to do: digest tough cell walls of plants. In herbivores, this function resides in the caecum, an off shoot of the large intestine, that houses symbiotic bacteria, producing enzymes (cellulases) by fermentation. Did you know that in the koala, the caecum is longer than the animal itself?! But, as Darwin noted, in hominids -apes and humans, the switch from a leafy to predominantly fruit diet made the caecum redundant and eventually, it degenerated into the finger-like appendix. Although we still eat plants, our vestigial organ does not house enough cellulase-secreting bacteria to digest more than a few grams of cellulose per day. 

● So why do we still have an appendix? It is notoriously prone to infection, commonly in children 8-13 years old. Before modern surgical methods, acute appendicitis was often fatal. What a poor design! But there is evidence that the appendix has useful functions. Like the tonsils, the appendix houses lymphoid tissue, or white cells, important for immunity. It has been compared to a “safe house”, lodging beneficial bacteria that can repopulate our gut after an infection wipes out existing microbial flora. 

● A new study by a group at Duke University has concluded that the appendix has arisen independently more than 30 times in the evolution of mammals. By plotting diet on the evolutionary tree of mammals, researchers found that the appearance of the appendix did not correlate with a change away from herbivorous diets. Species with an appendix were scattered so widely on the evolutionary tree that they concluded that the appendix evolved separately along distinct branches. Also, they found that the larger the caecum, the larger the appendix: opposite to what one would expect for a vestigial remnant of the caecum. But naysayers argue, if it is so useful, why don’t all mammals have an appendix? We’ll have to wait until Science adds another Chapter to the Appendix! 

Ref: Multiple independent appearances of the cecal appendix in mammalian evolution and an investigation of related ecological and anatomical factors. Smith et al. (2013) http://goo.gl/zJyviw

Counterpoint: The vestigiality of the human vermiform appendix. A modern reappraisal. http://goo.gl/v9Qvm0

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Going Rogue : How does a cancer spread to become metastatic?

Posted on July 21, 2013 by madamescientist

Going Rogue : How does a cancer spread to become metastatic?  

Why do cells that are tightly packed or neatly arranged in rows (epithelia), come loose and become insidiously mobile? The answer lies in a basic developmental process known as EMT, short for epithelial to mesenchymal transition. 

❑ During EMT, cells no longer know which way is up (i.e., lose their polarity), break off their cell-cell junctions and extend pseudopodia or foot-like processes that help them move. In the image below, colon cancer cells were caught in the act of rearranging their junctional proteins (in red and green) to become amorphous, drug-resistant and invasive. Even more dangerous, these cells acquire stem cell properties, allowing them to seed new cancers. In short, cells lose their mature, differentiated form and recapitulate their origins. 

❑ But EMT, and its reverse process MET, are normal features of embryo development, leading to formation of the neural tube, heart valve and other organs. Also, during wound healing, skin cells at the edge of the wound undergo EMT, reverting back by MET after the wound is closed. Understanding what triggers these changes, and how they may be controlled, is key to cancer therapy. 

❑ This explanation is in response to the more sensationalistic title, New theory uncovers cancer’s deep evolutionary roots , shared on G+. The theory “promises to transform the approach to cancer therapy, and to link the origin of cancer to the origin of life and the developmental processes of embryos”. Choose between breathless science (http://goo.gl/yDsys) or the rational explanation here 🙂

Wiki entry for EMT: http://goo.gl/2U806

Reference (open access): Chronic oxaliplatin resistance induces epithelial-to-mesenchymal transition in colorectal cancer cell lines. Yang et al. http://www.ncbi.nlm.nih.gov/pubmed/16857785

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Artificial Chromosomes: Care for a Pair?

Posted on July 14, 2013 by madamescientist

Artificial Chromosomes: Care for a Pair?

⌘ How about a new pair of chromosomes to add to the 23 pairs you already own? They make a great vehicle to insert new genes to reprogram cells, to replace defective or damaged genes. Current forms of gene therapy use modified viruses to deliver a stripped down version of a gene into cells. But these minigenes are hard to control. They may insert randomly into the chromosome and disrupt some essential function (“insertional mutagenesis”), trigger undesired immune response to the viral carrier, or rarely, activate a cancer-causing gene. Artificial chromosomes offer an alternative system of gene delivery. 

⌘ Of YACs, BACs and Life HACs: Yeast artificial chromosomes (YACs) were first introduced 30 years ago, followed by bacterial versions (BACs) which are used in research as a convenient way to clone and sequence DNA from other genomes. More recently, human artificial chromosomes (HACs) have been successfully introduced into mice to cure Duchenne muscular dystrophy (http://goo.gl/xuvSS). 

⌘ How to Build a HAC: You probably know that DNA combines with proteins (called histones), like pearls on a string, which are then packaged and condensed into a chromosome.  Chromosomes have short repeating fragments of DNA sequence, known as alpha satellites that can stretch for millions of base pairs, to form a centromere (the central knot of the X-shaped chromosome in the image below). The tips of the chromosome are capped with other protective repeating units called telomeres. Then there are the origins of replication, which are designated start sites for copying. An artificial chromosome has all these features too. It can be made by a top down approach: small fragments of telomere sequence (TTAGGG)n are introduced into a cell where they insert into chromosomes, triggering the loss of all sequences distal to the point of insertion. This eventually whittles down a chromosome until only a functional stump, about a tenth the size of a normal chromosome, remains. Alternatively, they can be assembled by a bottom up approach starting with de novo assembly of blocks of alpha satellite DNA. Entire genes, such as the large dystrophin gene defective in muscular dystrophy, can now be inserted, using special targeting sites (loxP). 

⌘ Why are they better? Because the artificial chromosome has a centromere tethering it to the mitotic spindle during cell division, it can be partitioned into newly divided cells to survive stably in the long term. Second, there is no upper size limit to DNA cloned in a HAC: a gene with all its neighboring regulatory elements can be used so as to faithfully mimic the natural pattern of gene expression. In fact, groups of genes encoding complex pathways can be carried on a single HAC. Third, because of the lack of viral sequences, HAC vectors minimize harmful immune responses in the host and the risk of triggering cancers.

⌘ Scientist Gregory Stock thinks it may be another 20 years before we see artificial chromosomes put to use in humans. For now, artificial chromosomes are still difficult to introduce into cells, with efficiencies as low as 1 in 10,000.  “Bioengineers tend to underestimate the complexity of human biology,” he says. “These developments often come at a slower pace than we imagine. But they’re inexorable.”

▶ Image and Pop Sci story on the future of HACs: http://goo.gl/FfE5c

▶ Reference Paper on HAC (open access and easy to read introduction): http://goo.gl/cmkla

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A Frondly Challenge!  Banish the moth balls from your brain. Guess the biological identity of this macrophoto.

Posted on July 6, 2013 by madamescientist

A Frondly Challenge!  Banish the moth balls from your brain. Guess the biological identity of this macrophoto.

Clever Clue: The most sensitive chemical detector known in biology, the object in this image can selectively sniff one molecule in a cubic meter of air.

 

How to Play: If you’re sure you know what this is, don’t give the game away. Instead, contribute some scientific tidbit of information on the topic. Have fun, be creative, the loonier the better 😉

#ScienceEveryday  

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Cellular Fireworks : To celebrate #4thofjuly .

Posted on July 4, 2013 by madamescientist

Cellular Fireworks : To celebrate #4thofjuly .

When a cell embarks on mitosis, the envelope around the nucleus disappears and long rods known as microtubules assemble to form a spindle. Chromosomes line up at the equator of this spindle and are pulled to opposite poles in a carefully orchestrated event driven by chemical gradients of key proteins in the cell. Images of Mitosis From L to R:

⁂ A protein, known as RanGTP (yellow), brings cargo to the neighborhood of the mitotic spindle (red) so it can be assembled. A gradient of this protein, spreading out from the chromosomes, is key to the perfect alignment of chromosomes along the equator of the spindle. http://goo.gl/EgQzv

⁂ Chromosomes (blue) are being pulled to opposite poles of four dividing cells of an embryo by the fibers of the mitotic spindle (orange). http://goo.gl/eKl62

⁂ Chromosomes (red) line up at the equator of the mitotic spindle (green). http://goo.gl/D1G9u

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