Science-- there's something for everyone

Friday, February 28, 2014

When did animals arrive on Earth?

One explanation for why multicellular animal life (metazoan) arose when it did is that the oxygen levels in the oceans and atmosphere had finally reached levels that allowed those life forms to thrive. It was estimated that until the oxygen, which was generated by simple plants, reached between 1-10% of what we have on Earth today, there could have been no complex animal life.

Since the oceans did not reach this level of oxygenation until 635 million years ago, this sets a limit for how early metazoans could have evolved on Earth. However, researchers from the University of Southern Denmark, the University of British Columbia and Caltech are challenging that notion. They claim that the arrival of animal life didn’t necessarily require as much oxygen as was thought.

The scientists, led by Daniel Mills of the University of South Denmark, used sponges as their model organisms. Since the last common ancestor of all living animals most likely did resemble a sponge, this was an appropriate choice. The cells that make up a sponge are each in direct contact with the sea water, so that oxygen need not be carried to them through any kind of circulatory system. This means that sponges can live at much lower oxygen levels than other animals. And indeed, the researchers found that modern sponges are able to live in water with oxygen levels as low as 0.5% of today's levels.

Sea sponge Halichondria panicea was used in the experiment at the University of Southern Denmark.
Credit: Daniel Mills/SDU


This corresponds well with the molecular clock estimate for when sponges first evolved on Earth. This method takes into account how long it took for cumulative mutations in DNA to have occurred. Those estimates place the arrival of sponges on Earth around 800 million years ago, well before oxygen could have reached the 1% of current levels previously thought to be required for multicellular life.

We don’t actually know exactly when animal life first appeared on Earth, but this new data may push that arrival back a few hundred million years. Of course, more complex life forms probably did require higher levels of oxygen. Thi
s could mean that the earliest animal life persisted on Earth for much longer than we thought.

Mills DB, Ward LM, Jones C, Sweeten B, Forth M, Treusch AH, & Canfield DE (2014). Oxygen requirements of the earliest animals. Proceedings of the National Academy of Sciences of the United States of America PMID: 24550467.

Thursday, February 27, 2014

How old is your heart? disease (CVD) is the leading cause of death in the world, yet most people are sure that they won’t be felled by CVD. This is unfortunate because, according to the World Health Organization (WHO), about 80% of premature CVD deaths could have been avoided if the victims had been better informed and had made better health choices.

Doctors actually have a pretty good idea of who is at greatest risk for CVD. If your cholesterol is high and you smoke, you’re looking at big trouble down the road. However, it’s hard to impart that information in a way that people can understand it and, more importantly, use it to change harmful behaviors.

Therefore, Balearic Island researchers led by Angel Lopez-Gonzalez tested a new ‘Heart Age’ calculator to see whether it encouraged people to adopt healthier lifestyles.

Close to 3000 participants were divided into three groups. The control group was given typical heart health advice like you might receive at a check-up. The second group were evaluated for their ten-year CVD risk using the Framingham Heart Study risk score, the standard way to evaluate cardiovascular health. They were then given individualized advice based on the results.

The third group used the Heart Age calculator to find their ‘heart age value’. The significance of this measure was explained to them, along with advice on what to do about it.

Twelve months later, the subjects were reevaluated. The metabolic profile of the control group had gotten worse, but the profiles of the other two groups got better. The same was true for smoking, more people quit smoking in the Framingham and Heart Age groups than in the control group. The biggest gains were seen in the Heart Age group.  Apparently, being confronted with a prematurely aging heart is a great motivator.

If you're interested (and who isn't?), you can find out your own heart age. I found out that my heart is fourteen years younger than I am. Nice to know. 

Angel A Lopez-Gonzalez, Antoni Aguilo, Margalida Frontera, Miquel Bennasar-Veny, Irene Campos, Teofila Vicente-Herrero, Matias Tomas-Salva, Joan De Pedro-Gomez, & Pedro Tauler (2014). Effectiveness of the Heart Age tool for improving modifiable cardiovascular risk factors in a Southern European population: a randomized trial European Journal of Preventive Cardiology DOI: 10.1177/2047487313518479.

Wednesday, February 26, 2014

Just for fun: The inner life of toys

Jason Freeny doesn't look at toys the same way the rest of us do, and lucky for us. Otherwise, we'd never know what was going on beneath the surface.

Here are some examples:

These sculptures reveal the muscles, bones, and organs inside toys

These sculptures reveal the muscles, bones, and organs inside toys

Tuesday, February 25, 2014

Will your child become obese?

Your child is perfect right now. But will he end up suffering from obesity later in life? Researchers from the University of Amsterdam, University of Vermont, Cornell University and the VTT Technical Research Centre of Finland found a novel way to answer that problem. Rather than asking experts in nutrition and metabolism, they used crowdsourcing.

Adults recruited on social media were asked to provide their current height and weight. They were then asked a question about their own childhood environment or behavior that could have led to them to have their current body mass index (BMI). For example, “When you were a child, did you drink juice or soda more often than water?” They were then given the opportunity to suggest new questions, such as “When you were a child, did you have many friends?” The new questions were included in the ones asked of subsequent participants and each person’s predicted BMI was continuously updated based on his or her answers.

All together, 532 people participated over a two week period. Thirty-seven of them generated 56 new questions that they thought could help predict whether children grow into slim or obese adults. Interestingly, the question most highly correlated to future BMI was “When you were a child, did someone consistently pack a lunch for you to take to school?”

You can see the top nineteen questions below.

Table 2 Questions with highest correlations with BMI. 
Interestingly, some of the questions with the most predictive power were not ones typically considered by health care professionals.

To be clear, the data does not show that if you pack your child’s school lunch everyday, he’ll never become obese. For one thing, it’s just a correlation. There could and probably are underlying factors that go along with bag lunches, like how nutritious that lunch is likely to be, or even whether that child has a caretaker with the time to pack a lunch. This is true for all the questions. Also, the adults participating in the study were relying on their memories of their childhoods to generate and answer questions.

The bigger point is that crowdsourcing can be a way of finding correlations that experts might miss. By asking people what life was like for them as children, health care professionals can gather new insights into how to keep the next generation of kids from becoming obese.  

Bevelander KE, Kaipainen K, Swain R, Dohle S, Bongard JC, Hines PD, & Wansink B (2014). Crowdsourcing novel childhood predictors of adult obesity. PloS one, 9 (2) PMID: 24505310.

Monday, February 24, 2014

Unclumping a killer

Staphylococcus aureus is an extremely common bacteria that about one third of people routinely have on their skin with no ill effects. Unfortunately, S. aureus can turn deadly, especially if it takes a hold in someone’s bloodstream.

One of the steps in going from benign hitchhiker to pathogenic killer is for the S. aureus to combine into masses of cells. Like other types of bacteria, S. aureus can form a nearly indestructible biofilm layer across a surface. However, unlike many other microbes, S. aureus can also form free-floating balls of cells by attaching to each other and to proteins within blood. This means that understanding exactly how and why the cells clump together might give us a way to defeat this increasingly antibiotic-resistant bug.

The good news is that Alexander Horswill and his colleagues from the University of Iowa have discovered a type of S. aureus mutant that is unable to stick together. Unlike normal bacteria, the surfaces of these mutants are coated with ‘Giant Staphylococcus Surface Protein (GSSP)’. These are spiky proteins that protrude from the outer membrane of the microbe. The more of them that are present, the less that cell can clump together with other cells.

Caption: Images taken with a scanning electron microscope show wild-type bacteria (left) forming tight aggregates or clumps in the presence of blood proteins. In contrast, cells of the mutant strain (right) over produce a giant surface protein, have a spiky appearance, and do not clump tightly together. This clumping defect makes the mutant strain less deadly in an experimental model of the serious staph infection, endocarditis.
Credit: Alexander Horswill, University of Iowa

This is particularly significant because when S. aureus is unable to combine in these clumps, it's also non-pathogenic. Thus, finding a way to increase production of GSSP may keep this microbe from becoming a killer.

Walker JN, Crosby HA, Spaulding AR, Salgado-Pabón W, Malone CL, Rosenthal CB, Schlievert PM, Boyd JM, & Horswill AR (2013). The Staphylococcus aureus ArlRS Two-Component System Is a Novel Regulator of Agglutination and Pathogenesis. PLoS pathogens, 9 (12) PMID: 24367264.

Friday, February 21, 2014

Why has the crime rate gone down?

By the end of the 1990s, the crime rate in the U.S. had plummeted by more than 40%. There were a lot of hypotheses as to why this occurred, ranging from increased patrolling by police officers, to beautification of neighborhoods, to the legalization of abortion (the theory being that there were fewer unwanted, and hence poorly cared for, children being born). However, it’s likely that none of those factors holds the lion’s share of responsibility for the decline in crime. No, that distinction almost certainly goes to the banning of lead in gasoline and paint in the ‘70s. Lauren Wolf, associate editor of Chemical and Engineering News gives us the evidence.

The Environmental Protection Agency (EPA) currently states that the highest acceptable level of lead in a child’s bloodstream is 5 micrograms per deciliter (µg/dL). Above that limit, people begin to show impaired cognition. Before the ban on leaded gas and paint, the average U.S. resident had blood lead levels of 16 µg/dL. Yes, that’s over three times the safe limit. By 1991, most people had only 3 µg/dL of lead in their blood.

As you can see from the follow
ing chart, the crime rate tracks quite closely with the amount of lead exposure.

The double line graph shows correlation between blood-lead levels in children and violent crime statistic 18-23 years later. The timeline shows how lead limits were reduced over the past four decades.
Economists hypothesize that regulation of leaded gasoline and lead paint in the 1970s caused crime rates to drop in the U.S. about 20 years later.CPSC = Consumer Product Safety Commission.
SOURCES: Rick Nevin, FBI Uniform Crime Reporting Statistics

Remember, there were lead-using cars on the road for many years after leaded gasoline was banned, and lots of people still live in older houses that contain lead paint today. This means that some regions of the country had high amounts of lead exposure for much longer than other areas. Sure enough those areas had higher crime rates. In fact, you can correlate lead exposure with crime not just in the U.S. as a whole, but by neighborhood.

Don't think this is where the evidence for the lead/violence connection ends though. There is good reason to accept that relationship. Studies confirm that lab animals that are exposed to higher amounts of lead do in fact become more aggressive. 

So how exactly does lead wreak all this havoc?

In the brain, lead interferes with communication between brain cells. In particular, lead can mess with the dopamine system (responsible for reward and impulse behavior) and the glutamate system (which is involved in learning and memory). So, too much lead gives you someone with diminished impulse control and limited ability to learn from mistakes. If ever I've heard a recipe for baking up criminals, this is it.

Lead is especially problematic for young children because it also interferes with brain development. Children with higher blood lead levels have less gray matter and lower IQs.

I’d like to point out that the acceptable level of lead has been dropping steadily. We may very well find out that 5 µg/dL is still far too high. If you add the fact that many neighborhoods still contain large amounts of lead dust, it’s clear that we cannot relax our standards or our desire to clean the air of all lead contamination.

Thursday, February 20, 2014

Using music to replace vision

Sensory substitution devices (SSDs) do exactly what their name implies, they substitute one type of sensory input for another. Why would anyone wish to do this? Well, if you were blind and could substitute sound for visual information, you might have an easier time navigating your world.

Researchers from The Hebrew University of Jerusalem developed a new SSD, dubbed EyeMusic, which can translate screen images into musical sounds. The height of a pixel is indicated by pitch (pixels at the top of the image are represented by higher pitched notes) and the horizontal position of the pixel is indicated by the timing of that note. Meanwhile, the color of the pixel is indicated by the type of musical instrument playing the note (for example, piano for white and marimba for blue).

When the system was tested on blindfolded, sighted volunteers, they were able to track the location of squares on a screen just by using EyeMusic. They used the auditory information from EyeMusic to make a visual map.

Of course, the goal isn’t to help blind people play pong. It’s to provide a portable device that blind people can use in place of the visual sense they’re missing.


 Image credit: Maxim Dupily, Amir Amedi, Shelly Levy Tzedek.

You can try your hand at EyeMusic here.

Levy-Tzedek S, Hanassy S, Abboud S, Maidenbaum S, & Amedi A (2012). Fast, accurate reaching movements with a visual-to-auditory sensory substitution device. Restorative neurology and neuroscience, 30 (4), 313-23 PMID: 22596353.

Wednesday, February 19, 2014

Just for fun: Olympic style!

I'm not a big sports fan, but I love the Olympics. It's like a sampler platter of sports. Perhaps you'd like a bit of short track speed skating? Ooh, snowboard cross looks fun! 

That doesn't mean there isn't a lot of science involved. Take figure skating, for example. Jim Richards of the University of Delaware and his team use motion capture and computer simulations to help skaters learn how to do those amazing jumps.

Four of this year's crop of U.S. Olympic skaters (Jeremy Abbott, Jason Brown, Gracie Gold, and Ashley Wagner) have used Richards' system.

Tuesday, February 18, 2014

Not all canines learn from other canines

We all know that dogs evolved from wolves. Along with domestication came a much greater sensitivity to humans, but a lesser ability to learn from members of their own species. At least, that’s the hypothesis that Friederike Range and Zsófia Virányi of the University of Vienna wished to test. In particular, they wondered whether wolves could learn from other wolves. Because dogs don’t seem to learn much from watching each other.

Sixteen six-month old wolves and fifteen six-month old mixed breed dogs were the test subjects for these experiments. All the animals were housed and raised under the same conditions in similar sized groups so that they were equally socialized to other canines and to humans.

For the experiment, the pups were allowed to watch a trained dog (unfortunately, the researchers did not have an adult wolf that could serve as demonstrator) open a box with either its paw or its mouth. Inside was a treat that the pup was permitted to take once the box was opened. After the wolf or dog puppy had observed the box being opened at least six times, it was allowed to try to get at the treat by itself.

A) two experimental apparatuses for different sized puppies
B) a paw demonstration
C) a mouth demonstration.
All the wolf pups were successful in opening the box by themselves. In contrast, only four dogs got the box open. Three quarters of the wolves used the same method they had observed to open the box, whereas none of the four successful dogs used the method they had seen the demonstrator dog using. The wolves also continued to be successful at opening the box in subsequent trials. Only two dogs managed to open the box more than once. 

The success of the animals did seem to hinge on whether they had paid attention during the demonstration. Among wolf pups who had not seen a demonstration of how to open the box, only one in five were able to get the treat out.

Just to make sure there wasn’t a maturity difference between six-month old dogs and wolves, the dogs were retested at nine-months of age, with similar results. This time a different set of four dogs managed to get the box open, but still without using the method they had observed.

While the dogs did look at the humans for help, by the time they did so, the wolves had already opened the box. In other words, the dogs spent just as long as the wolves trying to open the boxes on their own, they just weren’t able to figure them out.

These data suggest that wolf pups are much better at copying the behavior of other canines than dogs are. Domestication may have altered how canines relate to each other as much as how they relate to us.

Friederike Range, & Zsófia Virányi (2014). Wolves Are Better Imitators of Conspecifics than Dogs PLOS ONE DOI: 10.1371/journal.pone.0086559.

Friday, February 14, 2014

Children who are born blind can develop sight years later

Being born with cataracts in both eyes (bilateral cataracts) is a common cause of blindness in newborns. Ideally, children with this condition are operated on very soon after birth, restoring normal vision. However, in poor regions of the world, families can’t afford the treatment until much later, if ever. This is especially problematic because it had been thought that after a few short years, blind children would lose the ability of ever being able to process sight. Even if their vision were corrected, they would never be able to interpret the visual inputs.

However, the conventional wisdom on curing blindness in children is changing. In some cases, children who were as old as fifteen years when they underwent treatment were able to learn how to see at least to some extent.

Five out of eleven children who had been born with cataracts and not treated until they were at least eight years old showed remarkable improvement in seeing contrast six months after their surgery. While, this may sound like a modest improvement, discriminating between shades of gray is critical for many visual activities, like reading.

Some of the shapes used for testing sensitivity to contrast.
Image courtesy of Luis Lesmes and Michael Dorr
Nature doi:10.1038/nature.2014.14592

Perhaps more significant, some children even learned to recognize objects by sight, though it didn’t happen immediately. When they first gained the ability to see, the kids couldn’t recognize an object without feeling it.

These results show doctors that it is worthwhile to restore sight to children, even if they are fifteen years old when they are first given the opportunity to undergo treatment. Contrary to prior thought, the window on developing normal vision does not close very early in childhood.

Kalia A, Lesmes LA, Dorr M, Gandhi T, Chatterjee G, Ganesh S, Bex PJ, & Sinha P (2014). Development of pattern vision following early and extended blindness. Proceedings of the National Academy of Sciences of the United States of America PMID: 24449865.  

Sinha P, Chatterjee G, Gandhi T, & Kalia A (2013). Restoring vision through "Project Prakash": the opportunities for merging science and service. PLoS biology, 11 (12) PMID: 24358024.


Thursday, February 13, 2014

Will a fast reaction time save your life?

Researchers led by Gareth Hagger-Johnson from University College London examined the relationship between reaction time and mortality. According to their results, you’d better hope you’re quick at the draw.

Over five thousand people aged 20-59 participated in a set of simple reaction tests. They were asked to press a button as soon as they saw a ‘0’ appear on the screen in front of them. Each person performed fifty trials. Educational level reached, smoking, drinking and physical activity were all self-reported. Body mass index, blood pressure and metabolic factors were assessed during clinical exams.

People with longer reaction times were significantly more likely to die during the fifteen year follow-up period.

Now for the caveats.

From the paper itself:

Adjusted for age, participants who died were more likely to be male, have lower socio-economic position, were physically inactive, and smoked cigarettes and drank alcohol more heavily.
You don’t say.

The authors claim that there was still a noticeable effect even after accounting for health and behavioral variables. However, they also point out that reaction time and cognition tends to be inversely related. That is, people who have a lower cognitive ability also have slower, more variable reaction times. It also turns out that lower cognitive ability by itself is associated with higher mortality.

Given that the authors lump all causes of death together, I don’t think this study says all that much. I wouldn’t rush to test my own reaction time as a harbinger of my coming demise.

Gareth Hagger-Johnson, Ian J. Deary, Carolyn A. Davies, Alexander Weiss, & G. David Batty (2014). Reaction Time and Mortality from the Major Causes of Death: The NHANES-III Study PLOS ONE DOI: 10.1371/journal.pone.0082959

Wednesday, February 12, 2014

Just for fun: ISS fly by

David Peterson took footage from the International Space Station and created the following time-lapse montage.

Or, for those who prefer gifs:

This ISS Timelapse Compilation Is Fantastic

Tuesday, February 11, 2014

Bad news for astronauts—microgravity can affect your immune system

Being in space can affect you in ways you may not have considered. Retired Canadian astronaut and total rock star Chris Hadfield has scores of videos explaining exactly what life was like on board the International Space Station. Among those effects are problems with the immune system.

As far as gravity is concerned, spaceflight can be divided into two components. You’re exposed to hypergravity during launch and landing. Most of the time in between those events, there is microgravity. Researchers led by Katherine Taylor of the University of California Davis and her colleagues used some space-faring flies (Drosophila) to figure out how our immune systems might be compromised by those changes in gravity.

Flies have two major responses to infection, one (Toll) that is used primarily to fight off fungi, and the other (Imd) for bacteria. Mammals have similar immune pathways, which is why flies are a good model organism.

The researchers infected flies with a fungus and then simulated hypergravity by putting the flies in a centrifuge, essentially fast-spinning wheel like the kind used to train astronauts. Interestingly, the spinning flies were more able to fight off the fungi than their sedentary neighbors. For some reason, their Toll systems seemed to be improved over flies not exposed to hypergravity.

Testing the effects of microgravity was less simple. For that, the researchers used a population of flies that had been reared entirely on board the shuttle Discovery (now resting at the Smithsonian National Air and Space Museum) during one of its missions. Upon arriving on Earth, the space flies had severely compromised Toll systems. In contrast the flies’ Imd pathway seemed to be intact. They were just as capable of dealing with bacterial infection as their Earth-reared cohorts, but terrible at fighting off fungi.

Many genes involved in all sorts of processes from metabolism to metamorphosis were over-expressed in the Space flies and a few others were under-expressed. In particular, the production of proteins associated with the stress response was altered. Some of these changes could have resulted in the immune effects.

It’s not clear why hypergravity would have one effect and microgravity the opposite effect on the flies. Human space missions spend a tiny percentage of their time exposed to hypergravity compared to the time at microgravity. Hopefully, the problems of microgravity will be solved for the next generation of astronauts.

By the way, if you're worried about Chris Hadfield, he's adjusting to life back on Earth just fine. 

Taylor K, Kleinhesselink K, George MD, Morgan R, Smallwood T, Hammonds AS, Fuller PM, Saelao P, Alley J, Gibbs AG, Hoshizaki DK, von Kalm L, Fuller CA, Beckingham KM, & Kimbrell DA (2014). Toll mediated infection response is altered by gravity and spaceflight in Drosophila. PloS one, 9 (1) PMID: 24475130.

Monday, February 10, 2014

Just when you thought you were safe from smokers

You know smoking is bad for you. You’ve also heard about the dangers of secondhand smoke (SHS), the kind you’re exposed to when a smoker exhales in your face. However, you’re not out of the woods just because no one around you is actively smoking. If you’re in a room where people have smoked, you could be exposed to thirdhand smoke (THS), and that might be even worse.

When people smoke indoors, the surfaces and dust in that room become contaminated with the residue of those cigarettes. Not only is nicotine released from that dust, and in levels similar to what you’d get by smoking yourself, but new toxins are created as the cigarette byproducts age.

OK, that sounds terrible, but just how bad is it? I’m glad you asked. University of California, Riverside researchers led by Manuela Martins-Green studied the effect that THS had on mice. It was not good news.

The researchers exposed household items to SHS from a smoking machine until the particulate matter on them corresponded to that typically seen in a smoker’s house. Mice were housed in well-ventilated cages containing those items. Urine tests indicated that the mice were indeed picking up chemicals from the THS, though not as much as young children typically do by living with a smoker.

After six months, the mice had the metabolic markers of non-alchoholic fatty liver disease. This is troubling because nonalcoholic fatty liver disease is aggravated by acetaminophen, which is of course, an extremely common drug, particularly for young children.

The unfortunate THS-exposed mice also had lung damage, showed signs of being pre-diabetic, and took longer to heal from skin wounds than unexposed mice. Finally, THS-exposed mice showed signs of hyperactivity compared to controls.

All of this indicates that just because a person doesn’t smoke in front of his family doesn’t mean that they aren’t being exposed to toxins. Just living in a house where someone smokes can have a whole host of detrimental health effects. Yet another reason to quit if you possibly can.

Manuela Martins-Green, Neema Adhami, Michael Frankos, Mathew Valdez, & et al (2014). Cigarette Smoke Toxins Deposited on Surfaces: Implications for Human Health PLOS ONE DOI: 10.1371/journal.pone.0086391.

Friday, February 7, 2014

Should you disable comments?


A few months ago, the aptly named science magazine Popular Science decided to shut off comments on their new articles. Their rationale for doing so was to prevent a ‘fractious minority’ from altering the focus or perceived validity of accepted scientific topics. The folks at Popular Science may have been on to something. It turns out that  even positive comments can do more harm than good.
University of Pennsylvania researchers Rui Shi, Paul Messaris and Joseph Cappella tested the effect comments have on anti-smoking public service announcements (PSAs). The researchers selected eight PSAs, four of which had previously been rated as highly effective (strong) and four of which had proven to be ineffective (weak). They then combined each PSA with comments that were positive (pro-PSA and anti-smoking), or negative (anti-ad, anti-quitting) and civil (no insults or profanity) or uncivil. Thus, a PSA could be strong, with positive but uncivil comments, or any other combination of the three variables. There were also control PSAs with no comments.
The authors then recruited close to 600 current smokers to watch the anti-smoking PSAs. Before and after watching the ads, the participants were asked about their readiness to quit smoking. 
As expected, strong ads were more effective than weak ads. People who were more highly motivated to quit smoking found the positive comments more convincing than the negative comments, but people who were not ready to quit were not swayed by either set of comments. 
What was more interesting was that the PSAs that lacked comments of any kind were more effective than PSAs with positive comments. And if comments were present, the fewer of them people read the more effective they found the PSA.
One reason for this may be that comments, even ones that agree with the message of the PSA, are distracting. This was confirmed by testing participants’ memories of details of the PSA they had watched. People didn’t remember a PSA as well when it was followed by comments.
This suggests that if you really want to get your message out, you should make everyone else shut up. 

Rui Shi, Paul Messaris, & Joseph N. Cappella (2014). Effects of Online Comments on Smokers' Perception of Antismoking Public Service Announcements Journal of Computer-Mediated Communication DOI: 10.1111/jcc4.12057.

Thursday, February 6, 2014

Irradiating the cancer-free breast

Today, about three quarters of the women who have been diagnosed with breast cancer will live at least another fifteen years. Considering that up to one in every eight women will eventually develop breast cancer, that’s an outstanding achievement, and a real credit to the hard-working doctors and researchers studying the disease.
Unfortunately, about one in six women who live twenty years past their original diagnosis will develop cancer in the second, initially unaffected breast. For this reason, some women choose to have both breasts removed as a prophylactic measure. There are also drug therapies (tamoxifen or aromatase inhibitors for estrogen-receptor positive tumors) that can reduce the risk of secondary cancer, but they can have severe side affects are not effective for all types of cancer.
Columbia University Medical Center researchers led by Igor Shuryak decided to see if they could improve the odds by irradiating the noncancerous breast. This could be particularly important for women with estrogen-receptor negative tumors, and could be used in conjunction with drug therapies for other women.
Of course, as the following graphic shows, finding the right dose of radiation is critical, especially since any amount of radiation can trigger the development of new tumors. Too little or too much radiation will create more new tumors than it kills. The idea is to hit the sweet spot where the radiation kills all the pre-malignant cells that are already hiding in the non-symptomatic breast without inducing new tumors to form. 

Figure 1 Schematic of radiation dose-effects on breast-cancer risk in the contralateral breast of breast cancer patients.
The overall cancer risk is determined by a balance between killing of pre-existing pre-malignant cell clones vs. induction of new pre-malignant cell clones by radiation. The hypothesis underlying the present work is that there is a dose “window” at intermediate doses where killing of pre-existing pre-malignant clones dominates, thus reducing overall cancer risks.
The scientists tested their radiation idea on mice, and found that it worked as expected. At the right dosage of radiation, there were three times fewer new breast tumors in the originally unaffected breast tissue, a significant improvement.
These results are extremely preliminary, but promising enough to start clinical trials on women. As noted above, it will be essential to find the right dose of radiation, and that may well depend on a number of factors, including the age of the woman and the type of cancer she had in her first breast. If this therapy proves to be effective, it may become standard to irradiate the second breast at the time the initial cancer is treated.
I have to say that I love the fact that we’re now thinking, ‘we’d better deal with this problem some of these long term breast cancer survivors are having.’ That says a lot about the state of cancer treatment.

Igor Shuryak, Lubomir B. Smilenov, Norman J. Kleiman, & David J. Brenner (2013). Potential Reduction of Contralateral Second Breast-Cancer Risks by Prophylactic Mammary Irradiation: Validation in a Breast-Cancer-Prone Mouse Model PLoS ONE DOI: 10.1371/journal.pone.0085795.

Wednesday, February 5, 2014

Just for fun: Brains

Ever wonder what a fresh brain looks like? Here's a fascinating look. 

I mean a graphic, revolting look. 

No, no, fascinating. I'm sticking with that. 

Good thing our brains are encased in hard skulls, that's all I'm saying.

Tuesday, February 4, 2014

Good news for giant seaweeds

Just as trees form the backbone of many a terrestrial ecosystem, so too do macroalgae (seaweeds) play a critical role in providing food and shelter for marine organisms. Unfortunately, large canopy-forming seaweeds are in decline. I don’t want to point fingers, but ocean warming, overfishing and coastal urbanization are definitely implicated in those declines. 

These declines are bad news for the many creatures that make their homes or livings in or on the seaweeds. One species of seaweed, Phyllospora comosa, used to be abundant around Sydney, Australia providing resources for many of the local fisheries, including abalone. Unfortunately, the seaweed died off in the 1970s. Coincidentally, there was an excess of sewage discharged into the area at that time. 

Although the water  in the area has since been cleaned, P. comosa has not come back. Alexandra Campbell and her colleagues from the University of New South Wales set about remedying that problem. They attempted to transplant mature P. comosa seaweeds back to Sydney. 

Researcher tying P. comosa plants to the sea floor.

Giant seaweeds like P. comosa attach to the sea floor with their aptly named holdfasts. They don’t have a root system that you can bury in soil like you would if you were planting a tree. Therefore, to reestablish the P. comosa colony, the plants had to be tied to mesh matts with cable ties. In order to determine whether that procedure itself was overly traumatic, some of the plants were removed and then tied down in their original habitats. Other plants were left completely undisturbed.

Survival of algae that were translocated to Sydney was about 70%. This is about the same survival rate as that of totally undisturbed plants, suggesting that moving P. comosa to a new habitat is not harmful. Even more promising, the transplanted algae were able to successfully reproduce at their new site.

It is possible to clean a marine environment so that it’s once again suitable for its original inhabitants. The question is only whether we have the will to do so.

Campbell AH, Marzinelli EM, Vergés A, Coleman MA, & Steinberg PD (2014). Towards restoration of missing underwater forests. PloS one, 9 (1) PMID: 24416198.

Monday, February 3, 2014

Who has the largest genome?

When you think of the largest genomes in the animal kingdom, what comes to mind? Humans? Not even close. Some other type of mammal? Nope. At least it must be a vertebrate, right? Sorry. The largest genome found to date belongs to Locusta migratoria, aka the locust.

A team of dozens of scientists from the Chinese Academy of Sciences and other institutions have managed to sequence the locust’s genome, which weighs in at a whopping 6.5 gigabytes. To put that in perspective, the human genome, with which we’ve managed to be fairly successful, contains a little less than half as much DNA. Why on Earth does a lowly insect need that much DNA?

Many of the genes discovered by the authors may be required for the insects’ Jekyll to Hyde transformation from relatively benign grasshoppers into swarming locusts. As grasshoppers, the insects live solitary lives close to home. However, when their numbers reach a certain threshold where they start bumping into one another, they transmogrify into ravenous swarms that travel up to 100 miles per day. Locusts need whole classes of genes to cope with the energy requirements for long distance flight and to allow them to digest everything they encounter.

However, the main reason that the locust genome is so enormous is that it contains a massive number of repetitive elements. These are fragments of DNA that, due to a replication error, have become duplicated over and over again. This kind of thing can happen in any genome, but locusts seems to be particularly lazy about trimming away the excess DNA.

Wang X, Fang X, Yang P, Jiang X, Jiang F, Zhao D, Li B, Cui F, Wei J, Ma C, Wang Y, He J, Luo Y, Wang Z, Guo X, Guo W, Wang X, Zhang Y, Yang M, Hao S, Chen B, Ma Z, Yu D, Xiong Z, Zhu Y, Fan D, Han L, Wang B, Chen Y, Wang J, Yang L, Zhao W, Feng Y, Chen G, Lian J, Li Q, Huang Z, Yao X, Lv N, Zhang G, Li Y, Wang J, Wang J, Zhu B, & Kang L (2014). The locust genome provides insight into swarm formation and long-distance flight. Nature communications, 5 PMID: 24423660.