Guest post on PLOS SciEd – Science Fairs: rewarding talent or privilege?

This week I have a guest post on the PLOS SciEd blog:

The room is crowded with row after row of trifold poster boards and judges squinting and taking notes. Among the posters illustrating the effects of soil character on worm health, or the effectiveness of hand sanitizer, I see a project on amino acid substitution due to missense mutations. I’m judging the middle school division, but this project is at the level of a high school or even college student. When it comes time to decide the winners, I battle the other judges who favor complex project topics over soundness of experimental design. The owner of the missense mutation project had access to resources and connections not shared by the students testing soil and hand-sanitizer. There are clearly two project tiers within the competition, and they aren’t separated by scientific understanding, but by access to the professional scientific world. If the mutation project wins over soil character, does it mean we are punishing students who don’t have pre-existing science connections?

Continue to SciEd to read more




Transforming Tasmanian Devils: Potential Uses for Synthetic Biology in Conservation

Can we use biotechnology to save Tasmanian devils from extinction? [image source]


Last post, I talked about the facial cancer that’s wiping our Tasmanian devils. We understand the problem fairly well – the facial cancer spreads unchecked among the devil population because devils have very similar MHCs, the cellular “flags” that allow your immune system to tell whether a cell is your own or a foreign invader. When the devils fight, cancer cells can get transferred from an infected devil to the face of an uninfected devil. Because of their similar MHCs, the immune system doesn’t recognize the invader and the cancer easily takes root. Since MHC similarity is the root of the problem, introducing MHC diversity might be the solution. What if scientists could create Tasmanian devils with different MHC complexes and introduce them back into the population? These different devils would be immune to the face cancer. In addition, devils born from a match between a Devil 2.0 and an original model would have a mix of their parent’s MHC complexes, creating even more variation. This is all assuming we could make a Tasmanian devil with new MHCs in the first place, something we may be able to do in the near future thanks to advances in genetic engineering and “cloning” technology.


Adding MHC Varaiation to the DNA

The first step is to code new MHC sequences into the devil genome. You could design new devil MHC sequences, or search for DNA samples from devils with different or less common MHC groups. Once you have these sequences, you have to insert them into the right place. Early genetic engineering suffered from the problem of poorly targeted gene insertion. Using viruses, scientists could handily integrate new genes into the genome; however, if the insertion site of these genes isn’t tightly controlled, they can disrupt essential native genes or turn on nearby a cancer-causing genes (aka oncogenes). In a gene therapy trial to treat severe combined immunodeficiency, gene insertion near an oncogene led to leukemia in some of the trial participants.

Viral gene therapy hijacks the ability of viruses to insert their genes into the genomes of their infected host. Scientists replace the viruses genes with the ones they want to insert instead [image source]


Genetic engineering today is a different story. Scientists have gotten very good at inserting DNA at specific locations in the genome. They use special proteins (or sometimes even RNA) that can target specific sequences in the genome, and then insert the new DNA between those sequences. Recently, these new genetic engineering techniques made headlines when scientists used them to create immune cells (T-cells) that can take out leukemia cancer cells. The therapy is currently in clinical trials. This same technology could be used to add new MHC sequences to a Tasmanian devil genome.

From new devil genome to new devil pups

Okay, so now we have a collection of altered devil cells. How do we turn these cells into an actual Tasmanian devil? The classic technique to turn an isolated cell into a whole organism is somatic cell nuclear transfer (SCNT), the cloning technique that was used to create Dolly the sheep. SCNT combines two cells by replacing the nucleus of a fertilized donor egg with the nucleus of a cell from the animal you want to clone. The word somatic refers to the fact that the non-egg nucleus comes from a non-reproductive body cell (e.g. skin, liver, fat), which are called somatic cells.   

The nucleus contains the genetic blueprints that tell the egg what animal it should become, and the cytoplasm of the egg (everything outside the nucleus) contains the cellular construction workers and machinery who will translate those blueprints into an animal. By taking out the donor egg nucleus and putting in a new one, you are swapping the egg blueprints for the blueprints of whatever your new nucleus came from. After implanting this altered egg in a surrogate mother, (if nothing goes wrong during gestation) you’ll get a new baby based off the inserted nucleus.

A schematic of SCNT, as used to create Dolly the sheep. [image source]


However, there are significant problems with SCNT. DNA is packaged differently in body cells compared to egg and sperm cells – it’s modified to make sure only the genes that relate to that cell’s function are activated. These modifications are what make a skin cell a skin cell and not a liver cell. In addition, DNA ages as you do. Mutations build up and protective “caps” on the end of the DNA molecule wear down with every cell replication. These modifications can cause improper fetal development or health problems later on.

One way to get around the problems of SCNT may be to create egg and sperm cells from body cells. Cells inside early embryos are blank slates, and can become any of the specialized cells in your body (e.g. bone, skin, and pancreas). Using genetic engineering, scientists can take these specialized cells and turn them back into embryonic-like blank slates called induced pluripotent stem cells (iPSCs). IPSCs can be theoretically reporgrammed into any specialized cell cell in the body – neurons, pancreatic beta cells, and white blood cells have all been produced from iPSCs in the lab.

To create iPSCs, scientist expose normal body cells to special factors that turn the body cells into blank-slate embryonic-like cells. These iPSCs can then be differentiated into your specialized cell of choice. [image source]

More importantly to reproductive biology, viable sperm and egg cells have already been made from mouse iPSCs. Fertilized eggs made with these lab-generated sperm or egg cells successfully became healthy baby mice. Although iPSC techniques are still in their nascent stages, it’s very possible that they could one day be used to turn MHC-altered Tasmanian devil cells into Tasmanian devil pups.

De-extinction and pre-extinction

The focus at TEDx DeExtinction was on how these technologies could be used to bring back extinct species. For example, Dr. Alberto Fernández-Arias semi-successfully used SCNT to create a baby Pyrinian Ibex: the ibex made it through pregnancy fine, but died several minutes after birth due to a lung defect.  Synthetic biology techniques have great potential for conservation (or “pre-extinction”) efforts as well. Before their population was culled by face cancer, Tasmanian devils were in no danger of extinction. If scientists could create a more varied devil population that wasn’t susceptible to the cancer, the devils could likely thrive again. However, careful breeding and monitoring would have to be used to prevent another genetic bottleneck. You don’t want to replace the original devil population with a similarly stunted genetic sampling. Synthetic biologists and conservationists would have to work together to create a varied and resilient devil population.

De-extinction and pre-extinction scientists could cooperate to create an overall healthier Tasmanian ecosystem, one that might prevent future facial cancer outbreaks among the devils. Dr. Michael Archer, who is trying to bring back the thylacine (or “Tasmanian tiger”) recently, discussed this possibility on NPR’s Science Friday. Archer talked about how losing the thylacine disrupted the ecosystem balance and allowed the devils to overpopulate:

“If we could get the Thylacine back, put that king of beasts back in the throne, which is still warm and waiting, it would suppress the number of devils, keep them at a manageable level and the disease would burn itself out wherever it started. So getting these ecosystems back by putting in key species can be critical to maintaining the stability of them.”

Even if the thylacine never returns, de-extinction advances could be used to keep Tasmanain devils from a similar fate. The World Wildlife Federation estimates that over 10,000 species go extinct every year, and many of these extinctions are caused by humans. In the wake of this devastation, we must save every species we can, and de-extinction driven synthetic biology can give us new means to preserve species like the devils.

After all, who would want to lose a face like this one?

Sympathy for the Devils

This work by Mike Lehmann is licensed under a Creative Commons Attribution 3.0 Unported License.

Tasmanian devil, a marsupial native to the Australian island of Tasmania
[This work by Mike Lehmann is licensed under a Creative Commons Attribution-Share Alike 3.0 Unported License.]

Last week, I was lucky enough to attend the TedX DeExtinction event in Washington, DC. The event, hosted by National Geographic and Revive & Restore, was a day long series of short talks about the science and ethics of “de-extinction.” De-extinction is the idea that you can use new reproductive and stem cell biology techniques to revive extinct species, from the recently disappeared (e.g. bucardos and gastric brooding frogs) to the long lost (e.g. wooly mammoths  and giant ground sloths). The event raised quite a few questions on the ramifications of bringing species back from the dead: would de-extinction take funding away from conservation efforts? Would a de-extinct mammoth really be a mammoth? Would there even be a place for these new old species in our changing world? Is de-extinction, like the moon landing, a vehicle to inspire scientific wonder and progress?

We can (and should) argue about the ethics and reasons for reviving lost species, but we should also explore how to use synthetic biology to save dwindling species from imminent extinction. Take for example, the Tasmanian devil. Though these large marsupials were once common across Tasmania, their population has been devastated by a strange form of contagious facial cancer.

In the late 1990’s, facial tumors were spotted on devils in northeastern Tasmania. The cancer was deadly, killing the animals it infected within six months. More importantly, the cancer jumped from devil to devil with ease by taking advantage of the species’ aggressive nature: when Tasmanian devils fight (which they often do), cancer cells can be transferred from the teeth of an infected devil to the face of their uninfected sparring partner. The facial cancer has caused a 90% drop in devil population since it appeared, and total extinction of the species within 30 years is a distinct possibility.

This work by Menna Jones is licensed under a Creative Commons Attribution 2.5 Generic License.

Tasmanian devil face tumors
[This work by Menna Jones is licensed under a Creative Commons Attribution 2.5 Generic License.]

Transmissible cancer isn’t unheard of. Dogs can pass on a form of venereal cancer, and there’s a contagious sarcoma that affects Syrian hamsters. Cancer transmission has also been known to happen in humans after organ transplants or by passing between mother and fetus. However, in most animals, the immune system recognizes and destroys foreign cells (cancerous or otherwise). In fact, this is one of the main hurdles with organ transplants. Recipients have to take immunosuppressive drugs and in some instances immune system reactivity leads to organ rejection. In the case of Tasmanian devils, however, this immune hurdle doesn’t exist.

Immune system recognition of “self” and “other” relies on molecules on the surface of the cell called major histocompatibility complexes (MHCs). MHCs act as signaling flags to the immune system, telling your immune cells whether a cell is normal, infected with a pathogen, cancerous, or an invader. There are two main classes of these molecules, and each one has regions that vary among members of the population. Variation in MHC molecules allow immune cell to differentiate your cells from other cells, kind of like knowing members of your sports team because you all wear the same jersey. Human MHC class I molecules have six sites where they can vary, and hundreds of variations available for most sites.

Tasmanian devils, on the other hand, have very little population diversity in MHCs. At some point in the past, the devils experienced what’s known a genetic bottleneck. A large portion of the population was killed (cause unknown), leaving only a small gene pool, and thus a small sampling of MHC variations.

Tasmanian devil MHC complexes are so similar that their bodies can’t  tell the difference between their own cells and those of other devils. Every team’s jersey is so similar that it’s hard to know who’s on the home team and who’s the visitor. So when cancer cells from an infected devil latch onto an uninfected devil, they go undetected by the immune system and spread unhindered. Genetic studies of the cancer have shown that the DNA of tumor cells is extraordinarily similar across the infected devil population. Furthermore, the tumor DNA is significantly different from the infected devil’s DNA. These facts point to a tumor that arose in one devil and spread as a tissue graft to other devils through bites. Because of their lack of immune diversity, the Tasmanian devil population is being wiped out by one giant tumor run amok.

What can we do to stop the eradication of Tasmanian devils? Synthetic biology may have the answers. Developing technology may allow scientists to create Tasmanian devils with more MHC diversity, devils with immune systems that would spot and destroy the invading cancer cells before they took root. In my next blog post, I’ll talk about the discoveries and technology that could save the Tasmanian devil, and other species that are near (or already) extinct.


How can we save these guys? Tune in next time to see!
[This work by KeresH is licensed under a Creative Commons Attribution-Share Alike 3.0 Unported License.]


O’Neill, Iain. “Tasmanian devil facial tumor disease: Insights into reduced tumor surveillance from an unusual malignancy.” International Journal of Cancer. 127.7 (2010): 1637-1642.

 Siddle, Hannah et al. “Transmission of a fatal clonal tumor by biting occurs due to depleted MHC diversity in a threatened carnivorous marsupial.” PNAS. 104.41 (2007): 16221-16226.

Siddle, Hannah et al. “MHC gene copy number variation in Tasmanian devils: implications for the spread of a contagious cancer.” Proceedings of the Royal Society: Biology. 277.1690 (2010): 2001-2006.

Woods, Gregory et al. “The Immune Response of the Tasmanian Devil & Devil Facial Tumour Disease.” EcoHealth. 4.3 (2007): 338-345.

Sequestration: Much Better in Nature Than in Congress

“You are what you eat” has become a cliché spouted by parents and diet gurus alike. Of course, while most of us might feel a bit sick after eating all the leftover Halloween candy, we’re not going to turn the yellow of Lemon Heads or start oozing chocolate out of our skin glands. For some members the animal world, however, diet is important for more than nutrients and energy. In fact, many species depend on their food to give them the colors, poison, and unearthly glow for which we know them best. Here are four animals for which “you are what you eat” is a fact of life:


The golden poison dart frog. The size of a paper-clip but toxic enough that one frog has enough poison to kill 2 elephants. [image source]

The golden poison dart frog is only as big as a jumbo paper-clip, but so deadly that one frog contains enough poison to kill two elephants. [image source]

1.  The golden poison dart frog goes by the scientific name P. terriblis with good reason. It may be the most poisonous animal in the world – terrible indeed for would-be predators. Despite their diminutive size (up to 55 millimeters long, about two US quarters placed side by side), golden poison dart frogs pack quite a punch. One frog carries enough poison to kill ten to twenty humans. However, unlike many other poisonous animals, golden poison dart frogs outsource their poison production. The frogs isolate and concentrate alkaloid batrachotoxins from the bugs that they eat, a process called sequestration. During digestion, batrachotoxin is shuttled from the frogs’ gut to special skin glands, where it becomes a key ingredient in the deadly slime that coats their skin. Concentrating the poisonous chemicals in their food is a common thread with all poison dart frogs, but P. terriblis’s use of batrachotoxin in particular is what makes it especially deadly. Frogs kept in captivity will lose their toxicity, since their new diet doesn’t usually include the alkaloid-rich bugs crucial to toxin production.

Frogs aren’t the only animal that uses the capture-and-concentrate tactic for making poisons. For example, the monarch caterpillar is also poisonous because of an alkaloid-rich diet (in this case, the leaves of the milkweed plant). Some of this toxin carries over to the adult butterfly, making it an unpleasant meal for predators.  There are even several species of birds in Papua New Guinea that use the same strategy, appropriating insect alkaloid toxin and storing it in their skin and feathers.



Flamingos and many other birds get bright colors by sequestering pigments from their food [image source]


2. Sometimes an animal’s signature color comes from what it eats – flamingos owe their lovely pink-red hue to a class of pigments called carotenoids. Carotenoids are first produced by plants (beta-carotene is what gives carrots their orange color). Flamingos get their carotenoids from the plankton, algae, and brine shrimp they eat. In fact, a lot of the color variation across flamingo species comes from their food source. Flamingos that feed on carotenoid-producing algae directly are a darker hue than those that get their carotenoids through a second-hand source (like eating shrimp that eat algae). Without this dietary infusion of color, flamingos would be a dull gray or white. Flamingo coloring is a big concern in zoos and aquaria, where the birds don’t get all the carotenoids they would in the wild. To keep their animals more naturally colored (and attractive to visitors), zookeepers may feed them extra prawns or sprinkle their food with a concentrated carotenoid additive.

Scarlet tanager males and females are both colored by carotenoids [image source: male female]


Carotenoid-derived coloring is not uncommon, especially among birds. The red plumage of scarlet ibises and cardinals and the pink bellies of salmon all owe their distinctive color to a diet high in the pigment. Scarlet tanager males are turned (you guessed it) scarlet by a high-carotenoid diet, while the females are an olive-green from the interaction of carotene and another pigment, melanin.



Nudibranch sea slugs steal both color and poison from their food [image source]


3. Members of the nudibranch sea slug family scavenge both color and toxins from their prey. Among the family are some of the most brightly colored denizens of the ocean – and that’s saying a lot for since nudibranchs make their home in the kaleidoscopic world of coral reefs. These slugs dine on other invertebrates like baby jellyfish, coral polyps, anenomes, and even other sea slugs. Nudibranchs can sequester pigments from their prey and then display them on their own skin, creating a colorful pattern well matched to their environment. Among the brilliant background of a coral reef, the nudibranchs’ rainbow hues are the perfect camouflage.

Considering the fact that many nudibranchs can also recycle more active defense mechanisms, their bright skin is also warning to predators. Nudibranchs that feed on jellyfish can steal their prey’s special stinging cells (nematocysts). The nematocysts travel harmlessly through the slug’s digestive tract and are transported to their back, where the nematocysts begin their new life as a slug defense mechanism. And like poisonous dart frogs, certain nudibranchs concentrate toxins from the sponges they eat to make their own poisonous brew. 



Aequorea Victoria jellies need to eat fluorescent food to flow [image source]


4. Aequorea victoria jellyfish, like many other bioluminescent animals, glow a soft fluorescent blue and green thanks to a chemical cascade taking place inside their clear flesh. This species of jellyfish holds a special place in the hearts of many biologists, who use the jelly’s green fluorescent protein (GFP) in everything from imaging to genetic engineering. In fact, the discovery and development of GFP as a tool won several scientists a Nobel Prize in 2008.

For all the glory given to GFP, it’s not actually the piece of the cascade that supplies the jellyfish their glow. GFP simply takes the light from another molecule, coelenterazine, and shifts it from blue to green. Coelenterazine is a type of luciferin, a light-emitting molecule. During the light-producing chemical cascade, coelenterazine is energized to an excited state by the enzyme luciferase. Coelenterazine then returns to an unexcited state by releasing energy in the form of light.


A simplified version of the light-producing cascade in A. victoria jellies

Scientists in the lab have to externally supply coelenterazine to their specimens for them to glow; as it turns out, the A. victoria jellies have to import coelenterazine as well. A. victoria at the Monterey Bay aquarium slowly lost their ability to glow, but when the jellies were fed a diet of bioluminescent plankton, they lit right back up. The luciferase enzyme part of the bioluminescence cascade is coded into the jellyfishes’ DNA. However, they need to scavenge the actual light source from already glowing prey – like having to steal a bulb from a neighbor every time you wanted to turn on your lamp.

The Whistling Ducks of Pointe-a-Pierre

Black-Bellied Whistling Tree Ducks at the Point-a-Pierre Wildfowl Trust


My family hails from the Trinidad, the southernmost island in the Caribbean.  We still go back every few years to visit, and I always look forward to good food and time with my extended family. I also try to squeeze in as much jungle and beach visiting as I can. When my family planned a trip for this past Christmas, I vowed to myself that I would drag them on some eco-adventures by whatever means necessary. The means turned out to be whining (and a lot of it). But, on our second to last day on the island, we made it out to the Pointe-a-Pierre Wildfowl Trust.

Pointe-a-Pierre Wildfowl Trust is a bird sanctuary and breeding center tucked away inside the grounds of the Petrotrin Oil Refinery. The friendly guards at the refinery gates waved us in once we’d explained why we were there (they don’t want people to just come wander around the refinery for no good reason). We followed their directions down winding roads through the refinery grounds. When we finally made it to the Wildfowl Trust, we were greeted by a different sort of guard – a curious but wary Indian Peacock, who was seemingly unaware that his bedraggled tail was more sympathy-inducing than impressive. He strutted around our car, fanning that molting tail if we got too close and letting out some extraordinarily strident cries. He eventually seemed satisfied that we weren’t a threat (or he’d figured out that we weren’t going to feed him) and left us alone after we started down the gravel path to the visitor center of the Trust.

Indian Peacock that greeted us

The Indian Peacock that greeted us in the parking lot

Pointe-a-Pierre’s main visitor building, the Learning Centre, serves as a staging area for tourists and students, souvenir shop, and tiny museum. It’s filled with preserved animal and insect specimens in varying states of disrepair and yellowing educational posters. You don’t come to the Trust for the Leaning Centre, however – you come for the gardens and birds surrounding it.

On the porch outside the building, Frankie the Blue-and-Gold Macaw gives guests a much friendlier greeting than the peacocks in the parking lot. A victim of the illegal pet trade, Frankie was confined at a young age, disrupting proper wing growth. He’ll never be able to fly and is kept separate from the other macaws at the Trust (a small breeding population) due to his special needs. He is now used to educate visitors and students about conservation and animal treatment. In a scratchy voice, Frankie tells visitors “Hello” as they pass by.

Frankie, the Blue-and-Gold Macaw, having a snack.

Frankie, the Blue-and-Gold Macaw

The Learning Centre is also surrounded by a tropical garden, filled with bright flowering trees and plants. More peacocks, including alabaster White Peacocks, strut through the garden, occasionally followed by a group of peahens (female peafowl, peacocks are the male of the species); the ladies seemed much less interested in the humans wandering around their home.

A White Peacock and some peahens enjoying food that Frankie dropped out of his cage. A Muscovy Duck joined in the feast.

A White Peacock and some peahens enjoying food that Frankie dropped out of his cage. A Muscovy Duck (left) joined in the feast.

Our official tour starts with one of Pointe-a-Pierre’s lakes. The Trust serves two main purposes – to educate the public about environmental issues and to breed and release several species of endangered or threatened birds.

The commitment of the Trust to breeding native wildfowl is evident as soon as we reach the lake. The shore is covered in ducks. Many of them rest standing on one leg on a nearby tree and nesting boxes. The vast majority of the birds are small waterfowl with bright coral-orange beaks and feet. Their bodies are mostly a soft brown fading to grey on their heads, with black-edged white wings, black bellies, and black tails. And though these are definitely ducks, they don’t quack. When we first approached the lake, I thought we were hearing the cries of native songbirds, but the whistling “pichichi” sound that filled the air was coming from the collection of ducks on the lake shore. These are the Black-Bellied Whistling Tree Ducks for which the Trust was founded.

Black-Bellied Whistling Tree Ducks resting on one of their nesting boxes. In the wild, they nest in hollow trees.


It was actually a hunter who took the first steps to preserve the Black-Bellied Ducks. He noticed that there were fewer ducks around each year, and decided that something had to be done to preserve the island population. Black-Bellied Whistling Tree Ducks weigh only 1.5-2 pounds; each duck provides very little meat, so hunters must kill more of them to get the same amount of meat that fewer larger ducks would provide. The Black-Bellied Ducks are also docile and easy to catch. While the bird isn’t endangered worldwide, they are threatened by over-hunting in Trinidad. Since 1962, the Wildfowl Trust has released over 1300 Black-Bellied Whistling Tree ducks alone and over 1400 other ducks of various species.

Black-Bellied Whistling Tree Duck in flight. Source:

Black-Bellied Whistling Tree Duck in flight.   (Source)

The wild Trinidadian population of Black-Bellied Ducks lived in the island swamps, feeding at night. They can also be found along the coast of Mexico and northern South America. Whistling tree ducks live in family groups, which they protect aggressively against outsiders (including other Black-Bellied Ducks). They huddle in groups on the shore and swim in neat rows among the lily pads, like something out of a children’s book.

Black-Bellied Whistling Tree Ducks swimming in a row

Black-Bellied Whistling Tree Ducks swimming in a row

Duck mating pairs are monogamous and will stay together for years raising and taking care of their young. Some of the ducks at the Trust are still young enough to have a grey beak instead of the orange beak of an adult (placing them at under 8 months old). 

Juvenile Black-Bellied Duck. In addition to a grey instead of orange beak, their plumage is also less bright than adults. Source:


Birds like the whistling tree duck aren’t as flashy as macaws or peacocks, but they’re an important part of the ecosystem all the same. The ducks eat mosquito larva, keeping down the insect population. They also disperse plant seeds in their scat; water lilies in particular rely on species like ducks to spread their seeds. The Trust aims to educate school kids and visitors alike on links between humans and the environment, by immersing visitors in the natural world around them and through educational signs posted around the Trust grounds.

Our tour takes us past several signs detailing the rain cycle, feeding chain, and climate change. We also pass breeding cages of Blue-and-Gold Macaws (like Frankie), who had been driven to extinction on the island by the illegal pet trade. These birds had been imported from Venezuela in an effort to re-establish a native population. There are more ducks too – White-Faced Whistling Ducks, Fulvous Whistling Ducks, White Cheeked Pintails, and Muscovy Ducks (easy to pick out by the red patches on their faces).

A Muscovy Duck (with some Black-Bellies in the background). Muscovy's are much larger than the Black-Bellied ducks. Females like the one pictured here can weigh up to 7 pounds, and males  can weigh up to 15

Muscovy Ducks like the one in the foreground are much larger than Black-Bellied Ducks. Females (like the one pictured here) can weigh up to 7 pounds, and males can weigh up to 15

The trust even breeds Scarlet Ibis, a bright pinkish-red bird with a long curving bill that lives in the same swampy habitat as the Black-Bellied Whistling Tree Ducks. Ibises are hard to breed and require a very particular diet of shrimp and insects to maintain their vibrant color. The Scarlet Ibises in the Trust are the brightest I’ve ever seen, and the Trust has successfully released almost 100 specimens into the wild.


Scarlet Ibis breeding enclosure. Juvenile ibises are grey and their scarlet feathers come in as they mature

It’s fitting that we leave the Trust the same way we came in, escorted by a curious (and probably hungry) group of peacocks. They’re still swaggering around like we humans are but lowly peasants in their kingdom. From the loving treatment and reverence I’ve seen given to the birds here, I think they’re right.


Further reading:
Pointe-a-Pierre WildFowl Trust webiste
Listen to the calls of the Whistling Tree Duck 

Waste(water) Not, Want Not

Did you ever wonder what happens to the water that swirls down the drain when you take a shower or flows into the sewer after a heavy thunderstorm?

Twelve billion gallons of wastewater are dumped in oceans and estuaries every day in the United States alone. With that much water you could take a 3,000-year-long shower or fill more than half a million swimming pools!

A better (and much more practical) option is recycling that water for anything from watering crops to reclaiming wetlands to flushing the toilet. We hear about recycling cans, bottles, and paper all the time – but water recycling is just as important. The world is filled with over 7 billion people who need a fresh supply of water, but this year drought gripped 80 percent of the world’s (and 60 percent of the U.S.’s) agricultural lands. Water recycling plays a growing role in making sure people get enough water to drink, clean, grow crops, and run factories. It means cities in drought don’t have to bring in as much water from outside or take the salt out of seawater (desalination) for their water supply.

Luggage Point Wastewater Treatment Plant Luggage Point Wastewater Treatment Plant in Brisbane, Australia sewage river,tanks,ponds

Wastewater treatment plant in Brisbane, Australia

The big question is, how can you take sewage and transform it back into usable water? Let’s follow rain runoff as an example. When it rains, water is funneled down storm drains into the sewer, where it flows along until it reaches a water treatment plant for recycling. First, large debris like dirt, leaves, trash, and rocks are taken out. The water can filter through screens (like the ones on your windows) or sit in large tanks where heavy debris settles to the bottom as sludge and grease and oil float to the top where they can be skimmed off.

The water is then sent to secondary cleaning to remove smaller leftover waste and pollutants – stuff like soap, food, and chemicals. Most water recycling centers use microscopic organisms like bacteria to break down and eat any sugars, fats, or other waste left in the water. Bacteria in your local wastewater treatment plant could be enjoying the fruits of your dishwashing labor right now. In some plants, water is trickled through a special filter that’s coated with a thin film of bacteria. The bacteria digest waste as it passes by, and cleaner water comes out the other side. In other plants, the water is put into pools, where special floating mixers keep the bacteria well supplied with oxygen and fresh debris to break down.

This step in water cleaning can even be used for environmental conservation. Marshes and swamps clean dirty water in nature through bacterial breakdown, like the pools used in wastewater plants. Artificial wetlands can not only help clean our sewer water, they provide a habitat for wildlife.

Artificial wetlands in Stockton, CA provide clean water and an animal habitat

After the bacteria have done their job, the water gets filtered and disinfected with special chemicals or UV light to remove anything living that’s left over. Water that’s been through secondary treatment is clean enough to be used where it won’t come in extensive contact with people (or human food and homes). For example, it’s used for the irrigation of nonfood crops, refilling dangerously low lakes or wetlands, or cooling and heating at factories.

Even after all that work, the water’s not quite ready for general human use. For this, wastewater plants use several final rounds of cleaning (sometimes this is called “polishing”). The water goes through more microorganism treatment (often with special chemical-eating bacteria), filtration, and chemical treatment to remove leftover particles, or chemicals like nitrogen and phosphorous. The water is disinfected one more time and is now ready for many new uses. This water that’s been cleaned (at least) three can be used to water golf courses, lawns, and food crops. It can also supply fire-safety sprinkler systems, toilets, car washes, and artificial snow machines.

As you can imagine, recycling water has its hurdles. It’s a long and complex process, and a special system of pipelines is needed to make sure water that’s not clean enough doesn’t make it into the drinking or food-crop water supply. In addition, water from farm runoff is often filled with fertilizer chemicals even after cleaning – bad for the human use, but great for watering crops – so it needs to be directed back to farms.

However, one of the biggest hurdles is the word “wastewater” itself. Who wants to ski in snow or eat lettuce that’s been watered with “waste” water filled with chemicals, dirt, and decomposing food? Of course, that’s not the case – you now know that wastewater goes through a rigorous cleaning process before it’s sent back out into the world. In fact, recycled wastewater is often cleaner than well water, and recycling water prevents the flow of waste into oceans and rivers, making the rest of the water around us cleaner as well. Many water treatment advocates are coming up with new names to make wastewater reuse sound more pleasant, like reclaimed water (you could even call recycled water “vintage”).

Recycling water, whatever name you call it by, is the opposite of waste – it’s a vital part of making sure humans have the reliable supply of fresh water we need to survive.


Getting Hot and Heavy with Hydrogen

Deep within the cores of stars and the atmosphere of giant gas planets, intense pressure converts atoms into an unusual state physicists call degenerate matter. A normal atom is made up of a nucleus of protons and neutrons surrounded by a cloud of electrons. In degenerate matter, atoms become so squished that the tidy collections of nuclei and electrons break down into a slurry of sub-atomic particles. Hundreds of miles within Jupiter and Saturn lies a thick layer of a type of degenerate matter known as metallic hydrogen.

A sea of liquid hydrogen sloshes around below Jupiter’s surface.

Hydrogen on Earth exists as a gas, unless super-cooled into a liquid. You may have seen science class demonstrations with a different super-cooled gas, liquid nitrogen. The liquid would have evaporated continuously into a dense fog, like a b-movie special effect, and frozen anything that came into contact with it. Your teacher might have used liquid nitrogen to freeze bananas into such a brittle state that they could be shattered them with a hammer. Nitrogen atom are tiny, and like all elements that are gases at room temperature, it takes very little energy to make the atoms so agitated that they bounce around as a gas (instead of the relative stillness of liquid or solid matter). Liquid nitrogen requires temperatures below -300°F, and smaller atoms like helium and hydrogen need to be cooled even further (lower than -400°F) to become liquids.  For reference, the coldest (naturally occurring) temperature ever recorded on Earth was about -129°F.

When you add in the intense pressure of gas planets, though, the rules change. And I mean INTENSE pressure. At sea level on Earth, you’d feel a pressure of one atmosphere, or atm. At the bottom of the Mariana trench, six and a half miles under the sea, the pressure reaches over 1000 atm. About 6000 miles deep inside Jupiter (still over 30,000 miles from the core), the pressure reaches two million atmospheres. At this pressure, hydrogen atoms are crammed close together into a liquid state (even though they’ve been heated to a temperature of 17,000°F). The pressure is so high that atoms are forced to stick together and they can’t move apart the way they would if you heated them that high on Earth.

Normally, there’s a limit to how dense you can pack atoms – they can’t get any closer than the distance between the nuclei and electrons. Imagine a group of people each spinning a ball on a string above their head.  The people can’t get any closer than the length of the strings or the balls will collide – and nuclei can’t get any closer than their buzzing electron shells will allow. However, if you squish a bunch of ball-spinning people or atoms into a small space, they are forced into each other. Balls go bouncing off, and so do electrons.

Larger atoms, like iron, give up electrons all the time under normal temperature and pressure. They have plenty of electrons to spare, and the outermost electrons are far away (relatively speaking) from the charged protons in the nucleus. Positively charged protons in the nucleus attract the negatively charged electrons and hold them in the atom, but the distance between nucleus and electrons in larger atoms makes it easier for the electrons to go flying off to greet their neighbors. In fact, this is what makes an element conductive. The computer you’re reading this on right now depends on the fact that some elements’ atoms have no problem releasing electrons in a river of current. Insulators, on the other hand, hold tight to all of their electrons and prevent the flow of current. Hydrogen atoms only have one electron, and they are loath to give it up under normal conditions.

Iron’s outer electrons are shielded from the positive charge of the nucleus by all the electrons below them. Hydrogen only has one electron.

However, when smushed together by the crushing pressure of a gas giant’s atmosphere, hydrogen atoms are forced to release it into a big soupy mess of protons and electrons (hydrogen doesn’t have any neutrons). This hydrogen soup is called metallic hydrogen because it’s highly conductive, a key property of metals.

Click for a video overview of how metallic hydrogen is made inside gas giants

The currents that swirl around the metallic hydrogen seas in Jupiter and Saturn are what give these planets their magnetic fields (which on Earth is produced by a molten iron core). The magnetic field of Jupiter is so strong that it’s likely that hundreds of Earths could fit just in the metallic hydrogen layer of the planet.

Metallic hydrogen has only survived creation in the lab briefly and in tiny amounts, but physicists theorize that it could be used as a clean fuel or a superconductor if they could just get it to stick around. Liquid hydrogen is already used as a rocket propellant, and converting from liquid hydrogen to metallic hydrogen fuel would allow us to pack 30-40 times the amount of fuel in the same space. Years from now a metallic hydrogen engine could drive spacecraft out to Jupiter where they stop by for a quick refuel before heading out into the galaxy.

Further reading:
WiseGeek – What is Metallic Hydrogen?
Metallic Hydrogen college lecture notes – 1 & 2

What goes munch in the night?

A historical reenactment of a night eating rampage. Ice cream, chips, and granola bars are my typical fodder.

Food goes mysteriously missing in my house all the time. Cookies and cupcakes don’t last more than a few days, and forget keeping anything chocolate around. The latest casualty was a Costco-sized bag of tortilla chips. The evidence of their demise is scattered around the kitchen in the morning, and on more than one occasion, I have woken surrounded by granola bar wrappers and with chocolate on my face. Despite my best intentions and strictest diet plans, I am undone by the monster that emerges while I sleep. Sleep-me devoured my husband’s birthday cake – by the time I realized what I was doing only one scant piece remained. Sleep eating beleaguers a fair number of people, ranging from total wakefulness and recall (that late night cookie binge I berate myself over even as it’s happening) to waking up in the morning surrounded by chocolate wrappers with no idea what happened. Two different disorders flank each end of the spectrum: sleep related eating disorder and night eating syndrome. Both are chronic, lasting months to years, and often coincide with weight gain obesity.

On the unaware while eating side of the spectrum, you have sleep-related eating disorder (SRED). Patients generally can’t remember their episodes of night bingeing and, like sleepwalkers, are mostly unconscious during the event (my husband calls these episodes “werewolfing”). Other sleep disorders, like sleepwalking, obstructive sleep apnea, and restless leg syndrome, are often present alongside SRED. SRED patients consume food normally during the day, but are driven from their beds at night by an involuntary urge to eat. They make their way to the kitchen where, all while mostly unconscious, they binge on high calorie, high carbohydrate food like peanut butter, bread, and ice cream. They may even prepare an entire meal while asleep – obviously not the safest task with clumsy, sleepy fingers. SRED patients have also been known to eat inedible, toxic, or just plain weird things like soap, raw pasta, coffee grounds, or cat food.

Night eating syndrome (NES) patients, in contrast, are mostly awake during their episodes and can remember them come morning. NES was first brought to light in 1955, in patients with treatment-resistant obesity. It’s is characterized by eating a significant number of calories between dinner and sleeping (at least 25%), waking in the night to eat compulsively, and decreased hunger in the morning. Interestingly, one of the theories explaining NES is a disconnect in sleeping/waking and eating patterns. One study found NES patients had the same caloric intake and bedtime as controls, but their meal times were delayed. Animal studies that disconnected genes controlling sleeping/waking and eating found similar symptoms to NES.

Your sleep/wake and eating cycle are circadian rhythms – physical, mental, and behavioral changes that follow a 24 hour cycle. A short quiz from shows my circadian rhythms are slightly delayed from the norm 

Sleep eating behavior rarely falls neatly into one of these two disorders. It’s a spectrum – patients can have episodes ranging anywhere between full consciousness and sleep – making studying and treating the problem complicated. Night eating disorders do have a lot in common, though. SRED and NES are both found more often in obese populations. Whether sleep eating causes obesity or not is still up for debate, but it certainly make it harder to lose weight (as I can attest). NES also associates strongly with depression or anxiety. Both disorders have a genetic component and can be passed down in families.

Doctors treating a suspected sleep eater (wherever they lie on the spectrum) start by giving the patient a special questionnaire addressing hunger, caloric intake, familial history, sleep habits, and how long the problem has been going on. The doctor can confirm the diagnosis by performing a sleep study. Patients bring in foods they’d normally consume at night to a sleep lab, and their wakefulness and eating habits are monitored overnight. Both disorders can be treated with serotonin modulation, like taking SSRIs (commonly prescribed for anxiety and depression). Serotonin acts on the hypothalamus, which controls sleeping/waking cycles and feeding behavior. The effectiveness of serotonin modulating drugs also ties back to the high carb intake of sleep eaters – high carb food items increase the availability of tryptophan, which the body converts into serotonin. Sleep eaters might eat high carb foods because their serotonin levels are low. Topiramate, an anti-seizure medication that causes appetite reduction, can also be used to treat NES and SRED. However, topiramate comes with its share of unpleasant side effects, including dizziness, headache, nausea, and skin numbness or tingling. SRED is often successfully treated by addressing any other sleep disorders the patient may have (excluding sleepwalking) or discontinuing any drugs that induce night eating as a side effect. Sedatives, unfortunately, can often exacerbate night eating, especially in NES cases.

My most successful treatment strategy is a combination of avoidance and food stashing. I’m (mostly) vegan during my waking hours, but if there’s ice cream in the house when I go to sleep it will be gone by the morning. When I buy snacks for my friends, I have to make them take home the leftovers or buy things I won’t be tempted by. Luckily, my sleep eating self is vegetarian and hates yogurt cluster cereal. The food I can’t live without, I have my husband hide. Somewhere in my house is a host of gourmet dark chocolate bars, safe from my nocturnal rampages. Life’s a little more boring without being able to keep cinnamon toast crunch and gelato in the house, but at least I can wake up in the morning to minimal food casualties.

Sources/further reading:
Howell, Shenk, and Crow – “A review of nightime eating disorders”
Sleep Medicine Reviews (2009) 13, 23e34

Winkelman, Johnson and Richards – “Sleep related eating disorder”
Handbook of Clinical Neurology (2011), Vol. 98 (3rd series)

Circadian Rhythms Quiz