Science This Week (June 23-29, 2014)

A new computer program can select the best embryos, raising in vitro fertilization success rates to 76%

What did Neanderthals eat?  A 50 000 year old poop tells us. (Open Access)

Down Syndrome and Alzheimers have something in common.

The first-ever sighting of fashion fads in Chimpanzee societies.  More here.

Neuroscientists report being able to inhibit muscle contraction by shining a light on spinal cord neurons. (Open Access)

A low-cost non-toxic chemical extracted from sea water can be substituted into the production of solar cells.

Why you can't remember being a baby.

Live oceanography here.  The vampire squid caught on camera:

No chemicals were used in the making of this paper (by my dear friend Alex Goldberg).

The marine microbial transcriptome sheds light on the diversity of life in the oceans. (Open Access).

Pattern recognition software shows how birds are able to differentiate between their own eggs and cuckoo eggs.

Insects are the food of the future? (with video)

The Evolution of Language is Based on the Ability to Learn by Trial and Error

Identifying the evolutionary root of language and speech is a complex area of study.  The development of language skills is often considered as a form of "operant conditioning", in which toddlers babble using trial and error until what they are saying is eventually rewarded.  Finding the molecular basis for language and speech has relied on the study of language impairment disorders with a genetic link.  Scientists find it helpful to study language impairment in other species as well, since the genes involved in human language are often similar to those involved in singing, calling, and other forms of communication among animals.  One group of researchers has been using fruit flies in their search for the evolution of language.

Cancer Pre-Dates Vertebrates: new evidence shows the disease is as old as mutli-cellular life

Members of the genus Hydra

Will we ever live to see the day when cancer is eradicated?  Apparently not, according to German scientist Thomas Bosch.  As it turns out, cancer pre-dates vertebrates, it is as old as multi-cellular life.  We have a fairly good understanding of the nature of tumor development in vertebrates, but until now, we had no knowledge of the incidence and development of tumors in invertebrates, and definitely not outside of the bilateral clade.  A new study, published in Nature Communications, is the first ever to find evidence of naturally occurring tumors in two species of Hydra.  These results indicate that the molecular basis for cancer development came about very early in evolutionary history.

Members of the genus Hydra are small, simple fresh-water animals.  They are predatory, eating primarily small invertebrates like Daphnia and Cyclops.  They are typically sedentary, but they can move around, especially when hunting, using a somersaulting motion (there are lots of videos of this on youtube).

GMOs Take 4: What Are Our Options?

Pesticides are being dragged through the mud, with two major announcements this week: that pesticide exposure during pregnancy may cause autism, and that they are responsible for declining bee populations.  And rightfully so, many common pesticides are neurotoxins.  Banning pesticides leaves us with only two solutions in agriculture: no pesticide use, or the growth of genetically modified crops that are resistant to pests - like Bt crops.

BEES!
The current buzz around pesticides like neonicotinoids is due to the findings that these chemicals are causing the same kind of environmental degradation that DDT was causing in the 1960s.  Neonicotinoids are neuro-active insecticides that are similar in structure to nicotine, and bind to nicotinic acetylcholine receptors (NAR). 

Science This Week (June 16-22, 2014)

Who knew spiders have personalities?  A female spider's personality determines her position in the colony.

And speaking of spiders who will haunt your dreams: fish-eating spiders found on six continents.

Urine can be used as an energy source. (Open Access)

There's a scientific reason your headphones are always tangled.

New technology makes decayed teeth repair themselves. 

Methane hunting could boost the search for extraterrestrial life. (Open Access)

Dr. Oz admits to lying and pseudoscience:

Bionic pancreas system created to help people with Type I diabetes. (Open Access)

New Tardigrade species discovered!

Making an origami-based paper microscope - amazing!

How does stress cause heart attacks?  By disrupting the good bacteria trying to save you. (Open Access)

Brown bears in captivity engage in oral sex. 

A new approach to fighting antibiotic resistant superbugs?

Physics bonus: researching time travel.

Molecular Time Travel Experiment Speculates on the Likelihood of Different Evolutionary Paths

History is made up of a number of chance events - a wrong turn here, a miscarriage there - and historians can only speculate on what might have been had these chance events not occurred.  Evolution works the same way, and understanding how chance historical events shape evolutionary processes is a hot topic in evolutionary biology.  Recently, a team of evolutionary biologists turned the "what if" speculation into an experiment by reconstructing an ancient protein and using directed evolution to look at alternate evolutionary trajectories.

The authors had previously found that the evolution of cortisol specificity in the ancestral glucocorticoid receptor (GR) protein was made possible through a series of amino acid mutations at residues that had no apparent effect on receptor function.  The researchers speculate that these substitutions were necessary for GR to tolerate the larger mutations needed to shift specificity.  These are referred to as "permissive mutations", and have been found in the evolution of a number of other ancestral proteins.  Since these mutations are neutral, they are not selected against, and they are allowed to accumulate in the protein.  But, these mutations are needed to stabilize function-altering mutations.

The catch here is that we currently don't know how many of these permissive mutations are needed to enable evolutionary transitions.  If a lot of these mutations are needed, then there are many evolutionary paths that could facilitate alteration in function, and thus the outcome of protein evolution would only be weakly contingent on a specific historical event (in evolutionary biology, a historical event is a mutation).  But, if only a few permissive mutations are needed, then that narrows the potential evolutionary paths, and the outcome of protein evolution would be more strongly contingent on a specific mutation event.

Using directed evolution, the authors introduced random mutations into every new copy of GR, mimicking the variation that evolution could have produced over a longer time scale.  The idea was to create a number of potential "might-have-been" scenarios.  To identify mutations, the library of mutated GR was introduced into a yeast strain only able to grow through a cortisol-dependent interaction, meaning that yeast growth required GR to specifically bind with cortisol.  The researchers found 10 unique mutations that either completely or partially improved the yeast strain's cortisol sensitivity.  Of these 10 mutations, one pair of mutations affected cortisol sensitivity similar to the historical set.

The form of GR that existed 450
million years ago is labeled here as
AncGR1

The mutations were introduced into the resurrected ancestral GR, as it existed 450 million years ago, to determine if they could have existed and enabled the evolutionary transition.  But these mutations actually disrupted the ancestral GR's regulation, leading the authors to conclude that no other permissive mutations could have opened an evolutionary path to modern-day GR.  They found that permissive mutations must satisfy three criteria:

1. they must stabilize specific local elements of the protein structure,
2. maintain the correct energetic balance between functional conformations, and
3. be compatible with the ancestral and derived structures.

Meeting these three criteria is challenging, and indicates why permissive mutations are rare.  As the authors have shown, very few mutations can satisfy these narrow constraints.  If evolutionary history were replayed from its ancestral starting point, it would be unlikely that the same mutations that allowed the shift in GR function would re-occur.  On a larger scale, that means that the evolution of many other proteins could also be different, and we would end up with a radically different biology from the one we have now. 

These results are a highly significant contribution to our understanding of how proteins can evolve new functions.  While large-scale historical events, like mass extinctions and climate change, are generally the focus of evolutionary biology, smaller-scale, equally low-probability events like permissive mutations are also a factor in evolution and in the diversity of life.

Microbes Shoulder the Blame for Melting Glaciers

No one ever really thinks of glaciers as a really happenin' place; in fact, the recognition of glaciers (and other portions of the cryosphere) as a biome emerged only recently.  Although glacial surfaces are lower in cell number than more temperate environments, the microbes found on glaciers have a significant impact on the rate of glacier melting.

Illustration only.

Productivity among glacier-inhabiting microbes is limited, often because of light and nutrient availability.  But algae, which are equipped with pigments (like chlorophyll) allowing them to photosynthesize, are able to thrive in frozen, apparently barren environments.  Ice algae differ from snow algae, with a less complex life cycle as immotile cells that rarely form spores.  Snow algae may be green or red, while ice algae has a brownish pigment, making the ice look gray-brown.  Meanwhile, water-filled holes in glaciers tend to be dominated by cyanobacteria.  Most studies to-date have looked at the microbiome in individual cryosphere habitats.

A Ph.D. candidate out of the University of Leeds spent three weeks studying the Mittivakkat glacier, in the southeast of Greenland, during the high-melt season in July 2012.  Her work integrated the three types of glacier environments discussed above, and the effects of the various microbes on the physical characteristics of the Mittivakkat glacier.

What the researchers found was that over the course of the three week study, as ice and snow began melting under the higher-than-average temperatures, algae began creeping up the glacier:

When the ice started melting, a number of small water pools began to form, and became rich in a brownish biofilm.  This biofilm was characterized by high microbial content and photosynthetic activity, and also by an accumulation of cryconite - dust, black carbon, soot, and microbes.  Cryconite is composed of residues from natural occurrences (fires and volcanic eruptions) and from human activities (burning of fossil fuels).  Normally, snow is able to reflect most sunlight, but the accumulation of black cryconite on snow and ice absorbs sunlight and speeds up melting.  At the end of three weeks, the researchers observed that 70-90% of the glacier was snow-free, and was dominated by a grey-looking ice interspersed with cryconite holes (as shown in the diagram above).

The level of light being reflected (technical term: albedo) changed from one habitat to another, with clean white snow reflecting 75% of light, red snow (covered by red algae) reflecting 49% of light, and biofilm reflecting 20% of light, similar to the cryconite holes.  This is attributed to the pigmentation and mineral content of each habitat.  Like the melanin in your skin, pigments like chlorophyll and carotenoids also absorb light.  The increasing levels of pigments in each habitat of the glacier, along with cryconite, contributes to faster warming and melting of the glacier.

Dr. Liane Benning, the principal investigator of the study, proposes that future climate change scenarios need to take the microbiome into consideration, as well as cryconite, when predicting cryosphere melting.

Science This Week (June 9-15, 2014)

Were dinosaurs warm- or cold-blooded?  Turns out, they were lukewarm-blooded (technical term mesothermy).

Microbeads in your face scrub are filling up the Great Lakes, and have the potential to really screw up the ecosystem.

Researchers have modified stem cells to express a mutation conferring resistance to HIV.  If the cells can be safely transferred to people, this could be a functional cure for HIV!

Megalodon lives?  Speculation over what ate this 9-foot Great White Shark made the internet rounds this week.  Spoiler: it was neither Megalodon nor Giant Octopus.

A species of snakes in North Carolina may need to up their mimicry game - they have been mimicking coral snakes, which have been extinct from the region for over 50 years.

Retinal tissue was developed from stem cells.  Good news for people with vision impairment.

The herpes virus pre-dates humans!

Scientists have tricked fat into burning more calories.

Honeybee death rates are too high for species survival.

Check out this cool infographic: how your brain evolved from bacteria

And in non-biology news:

Scientists created a supernova explosion in the lab!

A huge underground ocean was discovered.

And why it's better to not be a "cool kid" in middle school.

How to Make a Genetically Modified Mosquito

By now the news of GM mosquitoes has made the internet rounds, receiving a mixed reception.  The idea behind these genetically modified mosquitoes was the reduce the spread of mosquito-borne diseases, like malaria, by creating a fully fertile strain of mosquitoes that produced 95% male offspring.  The females of the species are the blood-feeding pests, gathering proteins from human blood to produce eggs, and acting as a major summertime pet peeve.

The authors of the recently published study (which is Open Access!), led by Andrea Crisanti and Nikolai Windbichler out of Imperial College London, generated a method for skewing the mosquito sex ratio, producing lots of males and few females - known as an extreme male-biased reproduction sex ratio.  The lack of females led to the decline of four out of five of the mosquito populations in which the genetically modified males were introduced.

So how do you make a genetically modified mosquito?  The authors exploited a highly specific endonuclease (an enzyme that cuts nucleotide bonds), called I-PpoI, which cuts a very specific portion of ribosomal RNA (rRNA) repeats on the X-chromosome of mosquitoes.  Since males contain both an X and a Y chromosome, each sperm contains one of either.  On the other hand, females possess two X chromosomes, and so all eggs have an X chromosome.  The expression of I-PpoI during the production of sperm cuts up the X-chromosomes, resulting in only Y-chromosome-carrying sperm - that means all male offspring.  But I-PpoI is a persistent protein with a long half-life, so when eggs are fertilized, it also cleaves the resulting embryo's X-chromosome.  This causes something like a miscarriage, and this makes the I-PpoI-expressing males essentially sterile.

Proposed mechanism of I-PpoI skewing the sex-ratio of mosquito offspring

The authors designed I-PpoI to decrease its stability, so that males expressing it produce only Y-carrying sperm, but the enzyme is unable to affect the X-chromosome of the resulting embryo.  They created site-directed mutants, making individual amino acid changes within the protein sequence, in order to decrease the thermal stability of the protein.  Residues that were selected were located in the catalytic core, the dimer interface, or that interacted with zinc molecules in the protein fold.

Percent male progeny based on mutation
of I-PpoI at various residues

Each of the 11 mutants showed a significant reduction in half-life, from 73.5 hours for the wild-type protein down to 4 mins to 30 hours for the mutant proteins.  The genetically modified mosquitoes were created by injecting mosquito embryos with mutated proteins.  When these mosquitoes were mated with wild-type (normal) male mosquitoes, the result was a dramatically skewed sex-ratio (right).  Since the unstable I-PpoI does not result in sterile males, these males are able to reproduce, producing more male offspring, and eventually leading to the demise of the population due to lack of females.

The researchers then exposed these GM mosquitoes to cages containing populations of wild-type mosquitoes.  The collapse of the populations after a few generations has led the authors to hypothesize that, if released in the wild, the accumulation of X-chromosome damage caused by I-PpoI could significantly reduce mosquito populations.  According to Dr. Windbichler, one of the more promising aspects of these results is that this would be a sustainable system, freeing us of our pesticide-dependence, at least when it comes to mosquito control.

Now, I've always been told that the world would whither and die if we suddenly lost all our mosquitoes - they do a lot of our pollination, after all.  But a 2010 Nature news feature has a different take on it.  Can you imagine a world free from mosquitoes?

Turtle Gets a C-Section to Save Her Life (video)

In 2013, a suddenly listless turtle was brought to the vet by her owners.  X-rays found 14 eggs stuck inside her cloaca that she was unable to pass - called egg binding.  The poor turtle would have died if not for the decision to perform a C-section to remove the eggs.  The turtle survived!

Underlying Cause of a New Type of Cancer Discovered!

In 2012, a new type of cancer - causing facial tumors and primarily affecting women - was described.  This cancer, known as biphenotypic sinonasal sarcoma (SNS), affects the nasal and paranasal pathway of middle-aged patients, and is quite rare.  The tumor begins in the nose and can infiltrate the rest of the face, requiring disfiguring surgery to save the affected patient.  The researchers who discovered this cancer, led by Drs. André Oliveira and Jean Lewis of the Mayo Clinic, have now identified the genetic makeup of this cancer.

chromosomal fusion of PAX3 and MAML3

Cytogenetic analysis has found that SNS is caused by a fusion, or chimera, of PAX3 and MAML3, genes that are harmless on their own.  When combined during an abnormal but recurrent chromosomal mismatch, they result in a chimera - a new gene containing half of the two original genes.  The PAX3-MAML3 fusion encodes a protein that is a potent transcriptional activator of PAX3 response elements.  PAX3 is involved in ear, eye, and facial development; PAX3 mutations are associated with a number of human disorders, including Waardenburg syndrome and craniofacial-deafness-hand syndrome.  MAML3 is a transcription activator for the NOTCH family of proteins, which are involved in cell proliferation, differentiation, and death.

The PAX3-MAML3 chimera altered the expression of several genes involved in neural crest, skeletal, and general embryonic development, particularly neurogenic genes like NTRK3, which is important in oncogenesis (the creation of cancer).  The PAX3-MAML3 fusion closely resembles the activity of another PAX3 chimeric, PAX3-FOXO1, associated with Alveolar Rhabdomysarcoma, a common cancer in children.  

The Mayo Clinic has released a video of the authors discussing SNS:

The authors are confident that this finding will help in the diagnosis and treatment of this rare cancer, and that it could also help researchers find better treatments for alveolar rhabdomysarcoma, for which there is currently no treatment.  

A Single Mutation Responsible for Blonde Hair

Blonde hair is caused by low levels of melanin - the same dark pigment that protects your skin from the sun.  Researchers have now found that a specific gene that encodes KIT ligand, known as KITLG, is significantly associated with blond hair in Northern Europeans.  This finding sheds light on the evolution of blonde hair. 

KIT ligand protein structure

KITLG is also known as a stem cell factor, playing an important role in the formation of blood cells (hematopoiesis), sperm cells, and melanin production.  In mice, mutations in the coding region of KITLG are lethal at worst, or they cause white fur color, anemia, and sterility.  Interestingly, a non-coding mutation at a single nucleotide upstream of the start site of KITLG is responsible for blonde hair in Iceland and the Netherlands.  This guanine substitution in place of the normal adenine nucleotide is prevalent in northern European populations, but virtually absent in African and Asian populations.  This mutation alters the binding site for the LEF1 transcription factor, reducing transcription of KITLG, and thus reducing its ability to make melanin in hair follicles.  That single substitution means that in this position, the guanine codes for light hair, and the adenine codes for dark hair.

consensus sequence showing
A/G substitution

The authors, led by Dr. Catherine Guenther out of Stanford University, used human DNA spanning the blonde-associated region, fused it to a minimal promoter, and injected it into mouse embryos.  Mice containing even one copy of a non-coding mutation upstream of KITLG (shown below -SI^pan) had lighter coat colors than those without a mutation (shown below - +/+).  Mouse fur color patterns were similar in LEF1 knock-out mice - that is, mice that do not express the LEF1 transcription factor.

Fur color in mice expressing non-coding mutation upstream
of KITLG.

The regulatory region of KITLG also effects the activity of a hair follicle enhancer.  The A/G mutation in this region significantly alters the activity of this follicle enhancer.  This may explain why (natural) blondes have significantly more hair on their heads: on average 30 000 more hairs than brunettes, and 60 000 more hairs than redheads. 

So how did blonde hair evolve from this mutation?  There are two explanations for the evolution of blondes: vitamin D requirements and rare-mate advantage.  In the vitamin D hypothesis, it is proposed that increasing migration to northern latitudes required an increase in sun exposure to ensure adequate vitamin D formation - hence lighter skin and hair color in Northern European populations.  On the other hand, darker skin and hair colors among native northern populations, such as Inuit populations, opposes this idea.  It has also been proposed that blonde hair evolved after the last ice age as a form of sexual selection, when males were hard to find and blonde hair helped females stand out against their competition.  However, it is more likely that blonde hair evolved more than once in human history.

Science this week (June 2-8, 2014)

The difference between resilience and depression is in the neural connections of the prefrontal cortex.

Bacterial flora plays a major role in malnutrition, and they're persistent.

Rats can sniff out landmines with 100% accuracy:

Humans are to blame for Ice Age animal extinction, not climate change.

Bromine is essential for human and animal life.

Fake sugar makes a pretty good insecticide.

Researchers have discovered brain cells able to tell stem cells to develop more neurons.

Why you need to let your kids get dirty.

Transplanted neurons flourished over ten years in the brains of people with Parkinson's.

Drinking tea reduces breast cancer risk.

And for my sister - knitting is good for your brain, blood pressure, and overall well-being:

And some non-biology science news:

Researchers find that solar energy can rival fossil fuels.

A planet that shouldn't exist has been discovered.

And in gross news: humans have now created a new type of rock.

Looking Through the Human Genome to Find Intellectual Disability

Almost 1 in 200 children has a severe intellectual disability, marked by delayed development of language, memory, problem-solving, and social skills.  While intellectual disabilities are largely assumed to be genetic in origin, often caused by gene copy number variations (CNV) and single nucleotide polymorphisms (SNPs, pronounced "snip"), the exact cause can be difficult to detect.  

Molecular diagnosis of intellectual disability is complicated because it is difficult to find the exact location of these DNA variations, and the smaller-scale diagnostic tools, like microarray detection of CNV or exome sequencing, are not as effective as we would like.  A joint Dutch-American study, recently published in Nature, found that the diagnosis of severe intellectual disability is greatly improved with the use of whole genome sequencing.  According to researcher Han Brunner, whole genome sequencing produces 100 times more data than exome sequencing, making it a huge step forward as a diagnostic tool.

The authors, led by Christian Gilissen, used whole genome sequencing on 50 patients with severe intellectual disabilities, who had not received a positive molecular diagnosis after extensive screening using conventional methods.  They found 84 new SNPs causing loss-of-function mutations in certain genes and enhancement of other genes previously implicated with intellectual disability.  The substitution rate of these SNPs detected using whole genome sequencing was significantly higher than any previously reported using other diagnostic tools.  The authors also found 8 new CNVs, which included single-exon and intra-exonic deletions, and duplications of sections of DNA within chromosomes, all of which significantly affected genes implicated with intellectual disability.

Ultimately, the authors were able to give a molecular diagnosis to 42% of their patients using whole genome sequencing, while microarray and exome sequencing diagnosed 12% and 27% of patients, respectively.  They also found that spontaneous mutation is responsible for up to 60% of cases of intellectual disability, and heritability accounts for only 2% of cases.  With the decreasing cost of whole genome sequencing (see right), $100 000 000 to a few thousand dollars in 10 years, the authors are confident that this tool will continue to be useful in diagnosing not only intellectual disability, but other disorders with a genetic origin (i.e. cancer) as well.

The Politicization of Science – and what that means for climate change.

Science is frequently used as a pawn, manipulated for political gain, using pressure to influence scientific findings, their dissemination, and use.  This is referred to as the politicization of science, which has become increasingly common in industrialized nations.  In Canada, for example, this has been accomplished through changes in the allocation of funding, the muzzling of scientists, and the blatant disregard of scientific evidence in policy-making.  (For a really great book on this subject, click here) 

Science has always been political: specifically, it has historically been used to inform policies and to direct tax-payer money into the funding of scientific research.  During the cold war, the U.S. government held science in high esteem, because it was used to stay ahead of the Soviet Union.  Environmental science and climate change policies were seen as an issue of national security, since it was believed that melting polar ice would benefit Russia with a longer agricultural season.[1]  Only recently has science become a dirty word in politics, and political orientations have shaped a public distrust of science, thus influencing how science is funded and organized.

(Gauchet, 2012)

The modern politicization of science involves the treatment of scientific claims – for example, those related to anthropogenic climate change – as political arguments to be debated.  This phenomenon traces back to the 1970s, with the emergence of the New Right (NR) social movement in the U.S.  This group, which included Ronald Reagan, Phyllis Schlafly, and Terry Dolan, among others, believed in the protection of traditional values against the increasingly permissive and chaotic modern society, and were thus skeptical of scientific advancements and intellectual establishment.[2]  The fast-paced nature of scientific findings and technological innovations is often at odds with traditional viewpoints, and is often associated with a push-back from social conservatives.  Corporations that are subject to governmental regulations often challenge science to undermine the evidence-based policies and regulations placed on them, and to protect their profit margins.  Political conservatives tend to dislike the idea of governmental regulation, and so this shift in science toward risk assessment and regulation has made the right distrustful of science.  Further, religious groups, who tend to be socially conservative, clash with science over moral, ontological, and epistemological issues, such as evolution and medical research, particularly stem cell and AIDS research.[3] 

The last decade has seen a shift in the presentation of politicians as well.Increasingly, people running for public office (particularly with Leftist platforms) are accused of being “elites”: out-of-touch with the public, and therefore unfit to represent them in public office.  These tactics were recently used by Rob Ford in the 2010 Toronto mayoral election, Stephen Harper to undermine Michael Ignatieff’s 2011 bid for Prime Minister, and Sarah Palin in the 2008 U.S. presidential election.  In the latter case, anyone opposing Ms. Palin became a member of this elusive “elite”, and this polarized people against intellectuals, including scientists.  The Harper government has admitted to having steered away from expert-approved policy making, and boasted in the 2008 federal election campaign that the party’s platform was not grounded in evidence-based policy.[4]  Further, modifying policies based on new evidence is attacked as inconsistency in political platforms, and so politicians are encouraged and conditioned by voters to entrench themselves in their original views.  

What is particularly interesting is that it is primarily life sciences that have been politicized.  Generally, physics, chemistry, and mathematics are not debated to the same extent as environmentalism, evolution, and medicine.[5]  Politicians, as guardians of tax-payer money, are bound by public perceptions; the more the public believes there is doubt or debate on a given issue, the more difficult it becomes for a government to take a strong position.  On a topic like climate change, there is a consensus among the scientific community that climate change is a real problem, but there is doubt over the details.[6]  These include the extent to which human activities cause climate change, when and by how much sea levels will rise, and the rate of desertification, for example.  With no clear consensus over these details, or with dispute over the rates of change, the public is less likely to believe the issue or support policy response.[7]  This type of ambiguity has been associated with fearful, emotional, and illogical responses in the brain, decreasing an individual’s ability to make informed, rational decisions.[8]

 
Psychologically, uncertainty and evidence that opposes our own viewpoints makes us uncomfortable.  The subconscious brain negatively responds to the information, and attempts to find arguments that allow us to maintain our current views.  In other words, our subconscious brains act like lawyers, attempting to win our “case”, either by placing higher emphasis on evidence that agrees with our beliefs (confirmation bias), or by spending large amounts of energy working to disprove opposing evidence (disconfirmation bias).[9]  Ultimately, if we do not want to believe something, we can go to great lengths to explain it away.

So what does that mean for climate change policies?  Well, in countries like Canada and the U.S., business interests, backed by petrochemical companies with deep pockets, are very powerful lobby groups.  Between 2002-2010, anonymous conservative billionaires donated almost $120 million (USD) to over 100 groups aimed at casting doubt about climate change science.[10]  So while it may be in the global best interest to create sound, evidence-based environmental conservation policies, the economics of climate change policies are still the largest barrier to any real change.  And many will use anything at their disposal, including the denial of evidence and distrust of scientists, to protect their interests. 

Note: please forgive the formatting, I transferred this from a word document, and apparently Blogger CANNOT handle this.

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[1] Baker B. Politicization of Science. BioScience, 2014; 63(3): 171-7. 
[2] Gauchet G. Politicization of Science in the Public Sphere: a study of public trust in the United States, 1974-2010. American Sociological Review, 2012; 77(2): 167-87. 
[3] Ibid. 
[4] Geddes J. Why Stephen Harper thinks he’s smarter than the experts. MacLean’s 2010, Aug 9. 
[5] Baker B. Politicization of Science. BioScience, 2014; 63(3): 171-7. 
[6] Ibid. 
[7] Aklin M., Urpelainen J. Perceptions of scientific dissent undermine public support for environmental policy. Environmental Science and Policy, 2014; 38: 173-7. 
[8] Hsu M., Bhatt M., Adolphs R., Tranel D., Carmerer CF. Neural systems responding to degrees of uncertainty in human decision-making. Science, 2005; 310(5754): 1680-3. 
[9] Mooney C. The Science of Why We Don’t Believe Science. Mother Jones. 2011 May/June. 
[10] Goldenburg, S. Secret Funding Helped Build Vast Network of Climate Change Denial Thinktanks. The Guardian. 2013, Feb. 14.

A Burger With a Side of Sadness: fast-food negatively affects people's well-being and happiness

In our modern society, convenience and speed are key to consumers, and has remarkably influenced how we choose to spend our time.  We see time as linear and nonrecoverable, and therefore as a valuable resource, and so the less time we spend on a product, service, or activity, the better we feel about it.  But is it our impatience that has made these qualities so prevalent, or has the availability of technology, fast food, and time-efficient consumer products made us crave them more?

A recent open access study, published in Social Psychological and Personality Science, tackled this question.  The researchers, out of the University of Toronto, studied the effect of fast food on people's patience and happiness.  Fast food is everywhere in Western culture, and increasingly in developing countries and their cultures, as a means of quickly filling our bellies and moving on.  In this statement though, I think the authors ignore the convenience of price and time-efficiency for individuals with lower socioeconomic status, and just look at fast food and society as a whole.  

It turns out though, the the more we are exposed to time-saving technologies, the more impatient we become, and the more we want them.  This is also true when exposed to logos of time-saving technologies.  For example, individuals exposed to fast-food logos exhibited faster reading speeds than those who were not, even though they were not under any time constraint.  The authors of this study, led by Julian House, took these findings one step further by measuring how this increased impatience can undermine people's happiness and enjoyment.

They completed three studies, the first involved looking at the presence of various fast-food restaurants (or exposure to fast-food logos) in different neighborhoods, and the savoring of pleasant experiences among people in those neighborhoods.  The second study examined fast-food packaging - or a person's ability to take the food elsewhere vs. having to eat in the restaurant - interfered with enjoyment of photos of a natural scenery.  The third study looked at perceived passage of time after exposure to fast-food - the researchers primed some participants with fast-food, then showed them a video clip of an opera.  

What they found was that people exposed to more fast-food logos were less likely to savor pleasant experiences.  The second study found that individuals exposed to fast-food rated themselves as less happy than the control group.  That means that fast-food in this case did not make people unhappier, but it made them less likely to savor a pleasant experience.  Finally the third study found that people who had been primed with a fast-food meal were more likely to find that the video was very long, and to feel more impatient.  

A reduction in a person's ability to enjoy pleasant experiences, to "stop and smell the roses", affects their well-being and overall happiness.  Although the authors found that fast-food consumption itself did not make people unhappy, it made them less patient, undermined their ability to enjoy a pleasant experience.  That means that, ultimately, eating fast-food has a negative effect on people's well-being and experienced happiness, on top of the well-known effect on people's health.  It also means that the more we are exposed to time-saving technologies like fast-food, the more likely we are to be impatient and to crave them more.  These findings may be useful in creating policies to minimize the exposure of people to fast-food (including vending machines) in schools and in the workplace, as they have strong psychological impacts.

Science this week (May 26 - June 1, 2014)

How did dinosaurs evolve into the diversity of birds we see today? (Open Access)

A tiny marine animal, thought to be extinct for the past 4 million years, has been found alive and well in New Zealand!

Birdwatching?  There's an app for that.

Global malnutrition could decrease by 84% in 2050, if certain conditions are met.

Researchers have found a way to coax stem cells into specialization, for the first time!

Parasitism of plant-eating insects uses some pretty sneaky tactics. (Open Access)

An artificial lung the size of a sugar cube may replace animal testing.

Ancient volcanic eruptions in Australia found responsible for the first mass extinction.

Melting Arctic ice provides opportunities for invasive species.

Are we one step closer to a breath test for lung cancer?

Eradicating invasive species may further damage endangered species.

Why does bacon smell so good?  Well:

And a physics bonus: the quantum teleportation of data!