This week in biology/medicine (April 21-27, 2014)

Hey folks,
Tomorrow is the big day, and then I'll be back writing my regular posts.  There was a lot of really cool developments in science this week, here are the highlights:

While the bacterial and fungal life in the Chernobyl area hasn't quite bounced back, it seems the birds are doing quite well in adapting to the radiation.

The Y chromosome isn't so unimportant after all.

Your smartphone could soon become a microscope.

Ravens have a pecking order, and they keep track of it.

Monkeys can do math, there go all of our excuses... (Open Access)

Researchers have discovered a new genetic brain disorder, and Cell has made the papers freely available for two months! (Open Access)

Microbes provide insight into human language development (Open Access)

A new antiviral particle may be useful in protecting against ebola.

Lab-grown skin has the potential to replace animal testing!

National Geographic has created a ranking of the exoplanets most able to support life as we know it.

Scientists are making mantis shrimp inspired superstrong materials that could be used in making armor, cars, and space ships!

And interestingly, the humpback whale is no longer considered threatened in Canada.  The debate on whether this decision is based in scientific evidence or in economical policy rages on.

Happy DNA Day!

On this day 61 years ago, the structure of DNA was published in Nature.

All of the papers that were published by Watson and Crick, Rosalind Franklin, and Maurice Wilkins are now openly available!

While we often credit Watson and Crick for this amazing and important discovery, their work would not have been possible without Franklin's (and her grad student's) x-ray diffraction images (shown right).  Wilkins took the images and showed them to Watson and Crick without her knowledge.  The two then used characteristics and features of the images to make their model of the structure of DNA.  

While Crick was quick to give credit to Franklin's work in this important discovery, Watson has repeatedly painted her in a negative way, even referring to her patronizingly as "Rosy" in his memoirs (a name by which she never actually went).  But no one ever accused Watson of being a nice guy.

All four scientists were nominated for a Nobel prize in 1962, though Franklin was not alive to receive it - she died in 1958.  Rosalind Franklin's lesser-known contributions to science include the structure of RNA and viruses.

(anyone remember this awesome google doodle?)

Anyone interested in reading about other women in science who were snubbed, feel free to start here.

This week in biology/medicine (April 14-20, 2014)

Hey science lovers!
As I'm starting to ramp up my preparation for my upcoming PhD defense, I will most likely not be writing my usual posts.  But since science never stops, I'll continue with my normal Sunday summary.  So, this week in science:

Stress and trauma affect sperm RNA in mice.  This has implications for the heritability of depressive mood disorders.

Thanks to rare male advantage - a type of sexual selection where females of a species prefer a male with an uncommon trait - beards may be on their way out!

Coupling role reversals: insects have been found where the females have penises and the males have vaginas.

Babies may be crying at night so that mom and dad can't get it on.  No sex, no siblings.

In astrobiology news: new insights were outlined on the origins of life (Open Access)

Fearing the cuckoo mafia: birds know they're raising cuckoo offspring, but they're afraid of retaliation if they do something about it.

A new technique has been designed for facilitating the genetic characterization of the genes involved in photosynthesis. (Open Access)

Lifestyle determines gut flora, which directly influences health. (Open Access)

Nano-particle combinations used to deliver multiple cancer treatments.

Researchers have discovered when flesh eating bacteria developed their flesh eating capability (Open Access)

New insights into shark evolution: a skeletal gill-supporting structure from Paleozoic Arkansas shows a connection with bony fishes.

Vitamin B3 may have come from meteors striking the Earth.

Five anthropogenic factors that will drastically change North American forests in 50 years. (Open Access)

This week in biology/medicine (April 7-13, 2014)

An insect-transmitted pathogen that hijacks the plant's ability to reproduce. (Open Access)

Would you use a jelly fish as a diaper?  A group in Israel is developing a technology to turn jelly fish into useful household products.

Apparently, science is running out of juice.

The true meaning of zombie plants.

Coral reefs around the world are in danger of this newly identified flatworm.

Have scientists found a cure for Hepatitis C?

Want to get over jet lag?  There's an app for that.

Scientists have grown cartilage and successfully reconstructed a nose. (Open Access)

And in other lab-grown organ news, vaginal organs have been successfully grown and implanted into patients. (Open Access)

Flies use fighter jet moves to evade swatting.

And a bonus (not biology): the Large Hadron Collider found a new form or matter!

Predicting the Severity of Infection with Antibiotic-Resistant Bacteria

Antibiotic resistance is an adaptation through natural selection in which populations of micro-organisms, like bacteria, become resistant to the drugs that we use to treat them.  This is becoming a big problem in public health due to the widespread, overprescribed, and incorrect use of antibiotics.  Hospital acquired infections from antibiotic resistant bacteria are especially common.  The WHO keeps track of antibiotic resistant bacterial infections worldwide, and it also keeps a list of antibiotics that are considered to be most important for human medicine.

One "super bug" in particular that's problematic in hospitals and other health care facilities is methicillin-resistant Staphylococcus aureus (MRSA).  S. aureus is a sphere-shaped (coccus), gram-positive species of bacteria (pictured) naturally found in the respiratory tract and skin of humans that, when pathogenic, causes skin conditions and respiratory problems like sinusitis.  In the pre-antibiotic era, S. aureus was usually fatal.  S. aureus contains a number of surface proteins, called microbial surface components recognizing adhesive matrix molecules (MSCRAMM) that recognize and bind to molecules like collagen, fibrinogen, and fibronectin.  Once bound to these molecules, S. aureus cells can survive, grow, and persist.  During infection, S. aureus produces enzymes, like proteases, lipases, and elastases, that allow the bacteria to invade and destroy host tissues by interfering with the coagulation pathway.  The virulent factors of S. aureus are typically categorized as toxins (causing damage to host tissue) or adhesins (facilitate adherence and invasion of host tissue).  The treatment of choice for S. aureus is through the use of a beta-lactam family antibiotic, which includes penicillins (like methicillin, dicloxacillin, nafcillin, etc) and cephalosporins.  MRSA is a strain of S. aureus that is resistant to beta-lactams.  That means that infections are harder to treat, and people die from these infections.

A new European (open access) study that was made available online yesterday, published in Genome Research, has reported a method for predicting the severity of MRSA infection based on its genome sequence.  Prior to this study, genome sequencing of bacterial isolates from infected patients could determine factors like antibiotic resistance, but more complex phenotypes that involve contributions from a number of genes or epigenetic processes, like virulence, just wasn't possible.  Using a genome-wide association study (GWAS), the authors, led by co-contributors Laabei and Recker, determined the feasibility of predicting virulence through genetic signatures associated with specific phenotypes.

A GWAS is an examination of a number of common genetic variants to see if any variants are associated with any specific trait.  They typically focus on single nucleotide polymorphisms (SNPs, discussed previously here).  They took 90 MRSA isolates, and found that toxicity varies across isolates more than adhesiveness does, and that this toxicity correlates with disease severity.  Out of the 3060 SNPs found in the genome, 100 were identified as being associated with toxicity.  A further 22 specific indels (mutations involving insertions or deletions of DNA bases) were also identified as toxicity-related.  These polymorphisms and indels were located in genes that were involved in metabolism and regulation.

Since the GWAS approach is likely to produce a high number of false positives, the authors looked at the functional effect of these polymorphisms.  Each of the 13 SNPs they focused on was involved in virulence.  Furthermore, looking at epistatic interactions (in which a mutation in one gene masks the phenotypic effect of a mutation at another locus) found that a small number of genetic loci containing SNPs are interacting with numerous other loci.  For example, the authors identified 5 genes that interact with 20 other loci, involved in everything from tRNA synthesis to cell wall synthesis to carotenoid synthesis.  From all of this, the authors were able to identify SNPs/indels that can be used to predict the virulence of a particular strain of MRSA.

This study is a first step in the creation of a predictive model for identifying the most virulent strains of MRSA in a clinical setting, which can influence the approach taken to treat the infection.

   

                                                                                   

(I love Giant Microbes)

Let's call a spade a spade: gluten-free is the newest fad diet

Hello science lovers!

I have received my first commission to address the pseudoscience behind the gluten-free craze, but I've decided to expand it a bit to include fad diets.  After all, unless it's for an actual gluten intolerance, a gluten-free diet is actually a fad diet.

Gluten is a protein found in grains, particularly in wheat, barley, rye, spelt, etc.  It makes dough elastic and helps it rise - when yeast is added to bread dough, it produces carbon dioxide, which becomes trapped in the network of gluten proteins.  It is what makes bread so lovely; I had a colleague who with coeliac disease, and she always said she missed the gooey fluffiness of regular bread most of all.

Anyway, the people who are intolerant to gluten typically have some kind of allergy to it, or they suffer from coeliac disease.  Coeliac disease is an autoimmune disorder of the small intestine in which exposure to gliadin (a gluten protein) causes an inflammatory response in the small intestine, compromising nutrient absorption.  The only cure for coeliac disease is sticking to a gluten-free diet.  Gluten-free products like bread and beer are often made using non-grain based foods like rice.  The symptoms of coeliac disease include bloating, diarrhea, cramps, abdominal pain, weight loss, and a long-term increased risk of gastrointestinal disease.  Untreated or undiagnosed coeliac disease can led to a number of health problems, including neurological complications, heart disease, diabetes, and cancers.

But somewhere along the line, people started thinking that all of these health problems were associated with gluten consumption, not coeliac disease.  Lots of people on the low-carb diet bandwagon are the ones crying foul over gluten.  Lots of people think that they have some kind of gluten intolerance, or that gluten is evil, because they feel better on a gluten-free diet.  But there is little scientific evidence to support this, and it typically comes down to the types of foods that are being consumed.  Foods that contain gluten, like bread, pasta, crackers, etc. are often processed and contain sugars.  By avoiding such foods and replacing them with nutrient-dense whole foods, it makes sense that you would feel better.  It doesn't mean that gluten will kill you.  While coeliac disease is generally underdiagnosed, gluten intolerance and wheat allergy are generally overdiagnosed.  Unnecessary elimination of foods through adherence to fad diets has been found responsible for cases of acute protein energy malnutrition (PEM) in North American children.  Considering that this is a problem that typically occurs in areas of famine, that's kind of a big deal!  And remember when Atkins was popular?  Turns out that a high protein, high fat, low carb diet can actually be rough on your heart. 

(source)

Then there's the assumption that going gluten-free helps you lose weight, but in reality it can cause weight gain.  If you're not switching to whole foods, but instead simply switching to gluten-free flours, which are higher in in carbs and calories, then you may not find yourself losing weight.  Gluten-free baking generally has more fat in it to compensate for no gluten.  Gluten-free diets based on packaged foods are often low in fiber and don't have the folic acid, calcium, and vitamin fortifications that we generally get from consuming wheat products.  That's why as a fad, the gluten-free craze is potentially harmful, because quick-fix weight loss schemes typically involve the consumption of a fad product (in this case gluten-free products) rather than adherence to a basic, healthier diet.

 

(source)

Gluten is being blamed for a huge amount of health problems, from obesity to diabetes, even cancer.  This has led the mainstream public to believe gluten is this "silent killer", and media outlets are capitalizing on this and sensationalizing the stories to get traffic or sell newspapers.  That link I just gave you?  It's for an article written by a doctor talking about how eating gluten can kill you from some big scientific studies.  Oh no, gluten!  What I don't know might kill me! (not meant to be snarky, this is the actual title of the article).  But each of those studies was conducted on participants with coeliac disease.  Here's the main point (in bold, just so you don't miss it): all of these health risks from eating gluten are associated with eating gluten if you are actually medically gluten-intolerant!  So yes, people who suffer from coeliac disease can develop diabetes or heart problems or IBS or cancer or what have you, if they eat gluten, and these risks are increased in people who don't know they have coeliac disease or are not being treated for it.  But average not-gluten-intolerant Joe?  You're fine!  

I found this quote from an article in the National Post, sent to me by my friend and colleague over at The Rhizome journal of permaculture design, and I think it genuinely sums up what it is about fad diets that I find so annoying:

This post was not intended to shame anyone for their food choices.  If you genuinely feel better on a gluten-free diet, that's fantastic!  But that doesn't mean that there's any science behind your claims or that any scientific evidence supports gluten-free diets and weight loss of overall health.  I have to say that the one good thing that has come out of the gluten-free craze is that now gluten-free foods are easier to find for my gluten-intolerant friends. 

Cancer cells can recover from chemotherapy treatment by eating themselves

Programmed cell death (apoptosis) is a beneficial process by which biochemical processes signal the cell to alter its characteristics (morphology) and die.  Apoptosis is what allows fingers and toes to separate, because the cells between the digits die.  It is unlike necrosis, which is a form of traumatic cell death resulting from an injury.  Apoptosis is a huge area of study in biology and medicine, because the inhibition of the apoptotic pathway can lead to a number of cancers, autoimmune diseases, inflammatory diseases, and viral infections.  

The way it works is, cells release an intracellular apoptotic signal in response to a stress.  There are two ways in which this signal is received: either by affecting mitochondrial function (intrinsic), or through directly passing the signal to the apoptotic mechanisms (extrinsic).  The mitochondrion is the part of the cell that is responsible for aerobic respiration and for essentially making all the energy that your cells require to survive.  If signals are received that alter its function, this tells the cell that it is essentially committing suicide and triggers the apoptotic mechanism.  On the other hand, passing the signal directly onto the apoptotic mechanisms, in a process called signal transduction - which is basically like a relay race through the cell passing on a signal from one protein to another - by-passes the mitochondrial step.  Either way, the end-result is the same, and each way can be reversed if cells no longer need to die.

(source)

Apoptosis and autophagy are closely linked.  Autophagy comes from the Greek "self" and "to eat", so that's pretty self-explanatory.  The process of autophagy is when a cell begins to degrade unnecessary or dysfunctional cellular components, which can ensure survival by maintaining cellular energy levels during starvation stress.  Sometimes (and this is gross), animals use autophagy to avoid starvation by eating their own limbs.

On the cellular level, autophagy and apoptosis are thought to be opposite pathways, and there are distinct mechanisms through which apoptosis can inhibit autophagy.  But the process through which autophagy protects cells against apoptosis is not well understood.  Well, a group out of the U.S. recently found a way in which autophagy can control apoptosis and determine cell-fate decisions.  This study is being published in Cell in the next few days, but is already available online and is open access which makes me unbelievably happy!

Typically, the point-of-no-return in apoptosis is the point in which mitochondria are broken down, called Mitochondiral Outer Membrane Permeabilization, or MOMP (those cell biologists love their acronyms, so sometimes it's hard to keep up).  This group, led by Jacqueline Thorburn, found that autophagy can control apoptosis by regulating the timing of MOMP.  They treated HeLa cells with a tumor necrosis factor-related apoptosis inducing ligand (TRAIL), and monitored MOMP using time lapse microscopy, and cells died within 5 minutes.  But when autophagy was induced, MOMP still happened, but it was delayed.  That's because autophagy regulates the levels of a protein called PUMA (p53 upregulated modulator of apoptosis), which is key in MOMP.

Once apoptosis gets started, cells contract and die fairly quickly.  But when autophagy was induced in the cells, cell contraction after MOMP was delayed.  When this happened, some of the cells were able to recover after MOMP and display a normal morphology, which is surprising.  The more autophagy and PUMA degradation present in the cells, the better the cells were able to recover from MOMP.  The use of time lapse microscopy also means that there are videos of this, which the authors included in their supplemental information - and isolated frames are included in the text of the article as figures.

This is time lapse microscopy showing inefficient MOMP and eventual cell recovery and division in cells that were not expressing PUMA.  I've also included the relevant part of the in-text figure, so that you can have an idea of what you're looking at.  These all come from the paper, so as usual, if you're going to be using any of this, please cite properly.

So what's happening here is that in the first few frames, the mitochondria are undergoing MOMP, but then high autophagy allows the cell to engulf the released mitochondrial proteins, which keeps the rest of apoptosis from occuring, thus allowing the cells to recover and ultimately divide.  The authors speculate that this may be the process that allows cancer cells to recover and rescue themselves under stress from chemotherapy, with the implication being that if we can find a way to inhibit autophagy, then maybe we can increase the chance of cancer cell death during treatment.  

This week in biology/medicine (March 31st-April 6th, 2014)

Strange animal defense mechanisms.

Chemists have developed small peptides of 7 amino acids that have enzymatic activity.  This could revolutionize the study of modern-day enzymes and of neurological diseases that are characterized by aggregates of small proteins.

Large-scale fences undermine the ecosystem functioning and can damage biodiversity.

Researchers have genetically engineered poplar trees with lignin that is more easily broken down for the purpose of paper production and biofuel.  The idea is that production of these compounds will require fewer chemicals, less energy, and be overall less damaging to the environment.

A dynamic genome database of the Chinese population has been created using genome sequencing data of 194 individuals.  The previously available human reference genome was made using the genetic data of 13 Caucasian individuals. (Open Access)

Starvation affects wing size/shape and color in monarch butterflies. (Open Access)

A new method for detecting changes in GM crops. (Open Access)

Researchers have generated a blueprint for how to build a human brain.

A comprehensive map of the hummingbirds' 22-million year family tree from a decade-long study shows rapid and on-going diversification.

Erectile dysfunction can be treated without medication.

Cute animal conservation: one step forward, two steps back

I have a friend who hates pandas with a passion.  At first I thought he was completely nuts, but it ultimately makes sense.  It's about the conservation efforts and all the money people are giving, but only to specific animals.  Actually, only to the cute ones.  What we're doing now is we're overriding natural diversity and selecting for what we consider to be cute animals, and in doing so, we're contributing to the loss of biodiversity across the planet.  This is not necessarily a new issue in biology, but just one that I happen to feel strongly about.  Most people don't really think much about conservation efforts for plant biodiversity either.  I find our myopic approach to wild-life conservation upsetting and potentially disastrous.

Because many people are more concerned about tigers or pandas than they are about, say, the Proboscis monkey (pictured right), these so-called "ugly" animals are seriously endangered, and their plight is largely ignored.  The proboscis monkey is critically endangered and is facing a very high risk of extinction.  Its habitat in Borneo is being gradually destroyed, which has led to a 50% decrease in the population of the primate in the last 40 years.

The danger with selectively conserving only the cute animals is that it can disturb whole ecosystems.  A recent Open Access study examined human attitudes toward cute animals (technical term: human aesthetic appreciation) and their conservation efforts.  The scientists, split between the U.S. and Portugal, interviewed farmers (both livestock and crop) in three locations at varying distances from Kenya's Amboseli National Park.  Participants were asked to rank animals in order of "cuteness" - specifically being aesthetically pleasing, not necessarily based on harmlessness/danger.  Animals chosen as beautiful included giraffes, elands, gazelles, zebras, and lions, while animals chosen as ugly included hyenas, elephants, buffaloes, warthogs, hippos, and rhinos.  The hyena was considered by-far the ugliest animal, the poor little guys.

So what does that mean?  Well, the respondents were given the option of saving only one animal.  Almost 80% of participants chose animals they considered beautiful, and when asked why, the reason was aesthetic: because they are nice to watch.  When the respondents were asked which species, if it went extinct, they would not be upset about, they answered with the animals they had listed as ugly, primarily elephants and hyenas.  This time, when prompted, the responses were about the threats these animals pose to their livelihood, although those who would not be sad to see the hyenas disappear also admitted to being relieved to not have to look at them.  Through general linear mixed methods (GLMM) analysis, the authors found that perceived ugliness was the most important.

This figure shows the variables most selected as reasons in support of conserving or removing species.  I took it from the paper, so please reference properly if you are planning to use it.

Lets say, hypothetically, that hyenas and elephants were removed from this ecosystem based on a lack of conservation efforts.  Hyenas are high up on the food chain.  Once considered to be scavengers, it has been found that they kill 95% of what they eat.  The removal of top predators, as well as top herbivores, is having substantial effects on all of Earth's ecosystems.  Maybe it's time that conservation organizations begin looking at conservation at the whole-ecosystem level, rather than focusing on one animal at a time.

In closing, I'll leave you with some ugly animal appreciation:

 
(the blob fish)

 
(the aye-aye)


(the angler fish)