WSU scientist Craig Parks along with Asako Stone set out to figure out exactly how much loutish behavior a group will tolerate before throwing the selfish out. What they discovered is far more interesting:

…we also observed a completely unanticipated and, we argue, more interesting result: Those who give much to the group effort yet take little of its subsequent reward are not applauded but rather targeted for expulsion. The effect was replicated across three subsequent studies. Two of these studies ruled out some rather mundane explanations for the finding (lack of understanding of the task by the benevolent other, the other behaving unpredictably), and a third suggested that people are motivated to expel the benevolent other either for self-image reasons or because the other is not adhering to common rules of behavior. In this article, we report on this series of studies.

What the hell. The authors go on to attempt to explain why:

These data, then, provide potential explanations for why people want to remove a benevolent individual from the group. In some cases, the individual makes others feel they look bad in comparison, and, in other cases, the person is seen as violating rules of social interaction for mixed-motive situations. As we solicited these explanations after the expulsion preference had been stated, it is certainly possible that they represent not motivations for removing a benevolent other but rather rationalizations for why subjects want the benevolent person removed.

If you were looking for an empiric basis for the “Keep the government’s hands off my Medicare” red state, federal subsidy dependent elderly white teapartier, this is a good place to start.

New research reveals there is hope for Mars yet. The first definitive detection of methane in the atmosphere of Mars indicates the planet is still alive, in either a biologic or geologic sense, according to a team of NASA and university scientists.

“Methane is quickly destroyed in the Martian atmosphere in a variety of ways, so our discovery of substantial plumes of methane in the northern hemisphere of Mars in 2003 indicates some ongoing process is releasing the gas,” said Dr. Michael Mumma of NASA’s Goddard Space Flight Center in Greenbelt, Md.
…
“Right now, we don’t have enough information to tell if biology or geology — or both — is producing the methane on Mars,” said Mumma. “But it does tell us that the planet is still alive, at least in a geologic sense. It’s as if Mars is challenging us, saying, hey, find out what this means.” Mumma is lead author of a paper on this research appearing in Science Express Jan. 15.

Back when I was a fresh and new graduate student, I took a course co-chaired by him and fellow Hutch professor Dan Gottschling—on the chromosome—that propelled me forward to my thesis project. At the time, he was working on a truly funky pair of problems: Why don’t we spontaneously combust? How do some animals hibernate?

In a strange way, these unknowns are related.

Inside each of our cells are mitochondria. These are the reactors powering our bodies. At the core of mitochondria is something called the electron transport chain–in which the energy contained in electrons gleaned by breaking down fats and sugars is first used to pump hydrogen, and later these pumped hydrogen are converted into useful energy stores called ATP. High energy electrons go in, tired electrons come out at the end.

The used up electrons need to go somewhere. The mitochondria stuff them onto a passing oxygen molecule, creating carbon dioxide. Basically, it’s just like when a candle burns; in a living system, it’s called respiration. And like any combustion, it generates heat.

If left unchecked, if nothing slowed down the electron transport chain in this process, we’d probably light on fire. Something has to be putting on the breaks. In other words, if an individual was mutant for this slowing down mechanism, they might burst into flames.

Well, what could it be?

Dr. Roth has a guess: Hydrogen Sulfide. While about one in five molecules in air today–once you’ve stripped out the water–are oxygen, back when life started there was almost no free oxygen in the atmosphere. It took green living things and photosynthesis to produce all of this free oxygen gas. Before our present cycle of photosynthesis and respiring–most living things lived off of chemical sources of energy, things like volcanic vents. Chief among the fuel sources? Sulfur containing compounds.

Where we live–where most creatures live–on the planet, there isn’t much sulfide gas. Yet, our cells all make a small amount of it. What if this gas was the mystery regulator of the electron transport chain?

Mark discovered that when you add hydrogen sulfide to mitochondria, the gas reversibly slows down the electron transport chain. His prediction was right!

Next he considered, if you slow down the chain, and thus the need for oxygen, perhaps you could make an entire animal hibernate just by giving it this gas. In came the mice, and what followed was a groundbreaking paper in the Journal Science, H2S Induces a Suspended Animation–Like State in Mice.

Clinical trials, on humans are ongoing. The implications are staggering–for space travel, for management of traumatic injury, for war and even for immortality.

The startling case of an AIDS patient who underwent a bone marrow transplant to treat leukemia is stirring new hope that gene-therapy strategies on the far edges of AIDS research might someday cure the disease.

The patient, a 42-year-old American living in Berlin, is still recovering from his leukemia therapy, but he appears to have won his battle with AIDS. Doctors have not been able to detect the virus in his blood for more than 600 days, despite his having ceased all conventional AIDS medication. Normally when a patient stops taking AIDS drugs, the virus stampedes through the body within weeks, or days….

The breakthrough appears to be that Dr. Hütter, a soft-spoken hematologist who isn’t an AIDS specialist, deliberately replaced the patient’s bone marrow cells with those from a donor who has a naturally occurring genetic mutation that renders his cells immune to almost all strains of HIV, the virus that causes AIDS.

This story has received much media attention.

Here’s the big concept. The cells in your immune system that voraciously gobble up invaders, macrophages, have a protein on their surface called CCR5. CCR stands for chemokine receptor. Chemokines and chemokine receptors are how your immune cells talk to one another when fending off an invasion–a cellular game
of Marco-Polo.

Macrophages are constantly crawling all over your body, including just below the skin. When you have sex with an HIV positive individual, some of their virus can enter your body–through mucous membranes or small cuts in the skin. Your macrophages dutifully chase after the invading virus. When they meet, the virus turns tables on the macrophage–using the viral gp120 protein as a key to open up the CCR5 protein, using it as a door into the cell. Once safely inside the macrophage, the HIV virus can produce billions of copies of itself, per day per cell. Macrophages are hardy cells. They easily survive, even while pumping out virus.

In other words, the HIV gp120 protein in Rick Moranis, the macrophage’s CCR5 protein in Sigourney Weaver. Putting the two of them together? Extremely dangerous.

Eventually, the virus gp120 protein mutates until it can open the CXCR5 protein on the surface of CD4+ helper T cells (the generals of your immune system) like it opened the CCR5 protein on the macrophages. When this happens, the virus can efficiently enter into the T cells. These cells are much weaker than the macrophages, and die off when stressed by being forced to produce new virus copies. When enough T cells die off, you have AIDS.

About 1% of the population, thanks to having two mutant copies of the gene, completely lack the CCR5 protein. With no CCR5 protein, there is no way for the HIV virus to enter macrophages. Thus, these people are immune to HIV infection. Somewhere around 10-15% of the population has one bad copy of the CCR5 gene, and therefore have delayed progression to AIDS, as their macrophages are more resistant to infection than those with two good copies of the gene.

Whew.

The bone marrow makes all the cells in the blood. If you have a blood cancer, the last ditch treatment is to kill off your (cancerous) bone marrow, and replace it with bone marrow from a healthy donor. The patient described in the article had leukemia (blood cancer) and was HIV positive. To treat his leukemia, his bone marrow was killed off. His donor marrow was mutant for CCR5. Now six hundred days after receiving the CCR5-lacking bone marrow, his doctors cannot detect HIV virus in his blood–even though the patient is no longer on drug treatment for HIV.

As much as I respect the awesome power of Rupert Murdoch and the Wall Street Journal, I’d like to see some of the claims here undergo a bit of scrutiny, as they would if published in a proper medical journal.

This is a case report, of an experience in a single patient. I’m loathe to declare that since “[d]octors have not been able to detect the virus in his blood for more than 600 days” this patient is cured from AIDS, let alone consider this as proof that transplantation of CCR5 mutant bone marrow will cure everyone with HIV of the infection.

If this is generally true–transplantation with CCR5 lacking bone marrow can “cure” you of HIV infection–big, but solvable, problems remain.

First, donors lacking CCR5 are rare–about 1% of the population. And it’s already difficult to find CCR5 normal bone marrow that is a close enough match to transplant. This could potentially be solved by using gene knockdown, to turn off the normal CCR5 genes most donor bone marrow contains.

The bigger problem is, undergoing a bone marrow transplant is both dangerous an unpleasant. The first step? A lethal dose of irradiation. If the bone marrow transplant doesn’t work, you die. Horribly. If the bone marrow takes, but then starts attacking your body, you die even more horribly. If it works perfectly, you’re still at a heightened risk of a whole slew of cancers, thanks to all the irradiation.

I’d stick with drug therapy, if given the choice.

Scientists say an understanding of how the Twin Towers collapsed will help them develop the materials needed to build fusion reactors.

New research shows how steel will fail at high temperatures because of the magnetic properties of the metal…

The key advance is the understanding that, at high temperatures, tiny irregularities in a steel’s structure can disrupt its internal magnetic fields, making the rigid metal soft.

“Steels melt at about 1,150C (2,102F), but lose strength at much lower temperatures,” explained Dr Sergei Dudarev, principal scientist at the United Kingdom Atomic Energy Authority (UKAEA).

At room temperature, the magnetic fields between iron atoms remain regular, but when heated, these fields are altered allowing the atoms to slide past each other, weakening the steel….

The peak in this pliability is at 911.5C, but begins at much lower temperatures, at around 500C (932F) – a temperature often reached during building fires.

The steel backbone of the Twin Towers was probably exposed to temperatures close to this, when insulating panels – meant to protect the buildings’ structural frame – were dislodged by the impacts of the hijacked planes.

Part of the mysteries of the falling towers has to do with the extremity of the situation. Steel really hadn’t been placed into such a situation–with both intense heat and enormous stress and strain–before the towers fell. We learned something about our world that we can now apply to the future.

These alleles should drop out of the population.

Huh.

Well, what is known about gay men and their family members?

i. Gay men are everywhere, persisting in every culture and in every human population at more-or-less the same frequency–regardless of how much a culture loves gay men.

ii. The sisters, mothers and aunts of gay men have more babies than those without a gay brother, son or nephew–but only if the relation is through the gay man’s mother.

iii. A gay man’s male relatives are more likely to be gay–but only if related again through the gay man’s mother.

Well, we can come up with a few possible explanations, and see what best fits these observations.
1. Kin Selection.

The idea? A gay man in the family can only help make the heterosexual relatives pop out more kids and have the kids do better after birth. Babysitting, sexual counseling, consoling, food preparation, hunting…. it’s all gotta be good for making kids, right? Even if the gay uncle, brother or son doesn’t have babies himself, all those related babies are so much better off, the gay alleles survive to make future gay men!

Sadly, this appears to not be the explanation.

2. Overdominance.

This is the gay-is-like-sickle-cell-anemia argument. If having two gay alleles makes you gay, and therefore less prone to baby-making, perhaps having one gay allele makes you such a better straight man. Therefore, straight men carrying one gay and one straight allele do better than their all straight allele counterparts. So, the gay alleles survive.

3. Maternal effects

In other words, the ever popular mom-made-you-gay theory. Genetically this time. For almost all genes, we get one copy from mom and one copy from dad. For a few of these genes, one of these copies is always turned off from the mom or dad, called genetic imprinting. For example, while dad tend to want the biggest babies possible, mothers tend to prefer surviving childbirth–genetically speaking here. So, the mother’s copies of the genes for growing big tend to be turned off in the baby. Perhaps the same thing is going on for genes that make boys straight.

4. Sexually antagonistic selection.

This is the general blame-women theory. Perhaps the gene for making a gay man (not so good for future reproductive prospects) is super good for straight women (making baby making more likely and easier).

Ok, well which is it? Andrea Camperio Ciani, Paolo Cermelli, Giovanni Zanzotto recently published a possible answer in PlosONE.

Running the available empiric data about gay men through a whole bunch of models of these possibilities, they discovered one combination that best fit reality and a few aren’t really possible at all.

Overdominance seems really unlikely. None of the models including this idea fit the data all that well. Nor did the models based on maternal effects. It appears that mom cannot make you gay. Sorry.

The best fits neededtwo genetic loci (two genes), with at least one of these loci on the X chromosome. Recall, while women get two X-chromosomes, men only get one. Additionally, at least one of these alleles must be sexually antagonistic–in favor of women reproducing if they have it, even if it makes you gay as a boy.

Or, as the authors of the study stated:

Our analysis allows us to draw several conclusions that clarify the basic evolutionary dynamics of the genetic factors influencing human male homosexuality and the related female fecundity increase, resolving a number of open questions. As a main point, we can exclude the GFMH propagation mechanisms based on overdominance (male heterozygote advantage), because none of the models (1b), (5a), (5b) account satisfactorily for the sexual-orientation asymmetries of requirement (B1). At this level of genetic analysis, we can also exclude maternal effects, including maternal genomic imprinting, as they lead too easily to GFMH extinction or fixation, against requirement (A). Only the hypothesis that the GFMH are characterized by sexually antagonistic selection (i.e. the GFMH favor one sex and disfavor the other) produces viable population genetic models (see the case (4) above) leading to the persistence of the trait at low frequencies and capable of accounting for the related pedigree asymmetries. For this reason, predictions of possible widespread diffusion of male homo- or bisexuality in human populations are not warranted, as stable low levels of this character are actually compatible with a broad range of parameters in population genetic models.

For what could this allele be? Well, an obvious choice is digging dudes. If a woman has an allele that really makes her like guys, she’s more likely to have babies than a woman who has a less guy-loving allele for this gene. If she passes on this dude loving allele to her son, via the X-chromosome, perhaps he’ll be gay. But since she’s having more babies, it’s a wash.

Neat.

(Updated for clarity and some more details.)

Thanks to our continuing success in Iraq, you might have noticed distinctly fewer limbs in today’s America. Hence this recent work published in the journal Nature is quite encouraging:

Here we describe a system that permits embodied prosthetic control; we show how monkeys (Macaca mulatta) use their motor cortical activity to control a mechanized arm replica in a self-feeding task. In addition to the three dimensions of movement, the subjects’ cortical signals also proportionally controlled a gripper on the end of the arm. Owing to the physical interaction between the monkey, the robotic arm and objects in the workspace, this new task presented a higher level of difficulty than previous virtual (cursor-control) experiments. Apart from an example of simple one-dimensional control, previous experiments have lacked physical interaction even in cases where a robotic arm or hand was included in the control loop, because the subjects did not use it to interact with physical objects—an interaction that cannot be fully simulated. This demonstration of multi-degree-of-freedom embodied prosthetic control paves the way towards the development of dexterous prosthetic devices that could ultimately achieve arm and hand function at a near-natural level.

The big plan here? Brain cells make electrical currents when doing their jobs. By listening for these electrical spikes with electrodes, we can eavesdrop. Using a map of the brain, giving us a clue which part of the brain controls (or controlled) the limb, we can put the electrodes over the right spot. When we detect a change in the brain cells in this spot, we can move a robot arm. Enjoy your new cyborg limb!
Well, Meel Velliste et al got a monkey to move a robotic arm just by thinking. Nifty. Many groups, including my buddy Kai Miller right here in Seattle, have gotten people to play video games just by thinking. This brings us one step closer to replacing all those lost limbs.
Still, we really don’t have the best idea of exactly what these brain cells must say to one another when they want to move a limb or a finger. The better we understand this language, the better we can program the computer sitting between the electrodes on the brain and the robotic limb. Back to my friend’s thesis defense this week.
Listening to the brain with these electrodes, that read millions of brain cells at a time, is a bit like listening to the crowd at a stadium. You can hear large groups chanting in unison, horns or general roar; trying to pick out an individual conversation in all of this is next to impossible.

Still, we can figure a lot out at this level. When parts of the brain are at rest, they’re subject to regular gonging. The idea is somewhat like the best scene in Blazing Saddles (“Dag namit. The sheriff is a n{GONG}…”) Every time the part of the brain starts getting an idea to activate out of turn, the gonging from deeper levels interrupts the planning. So, the absence of this gonging is one way to detect when a part of the brain is activated. The problem is, this happens over a huge area of the brain. We need to figure a way to listen in on the planning among the brain cells that can now proceed uninhibited. A good old-fashioned scientific knife fight emerged in the field. One camp figured this planning would be synchronized–like a section in the stadium starting to chant, “Wave! Wave! Wave!” The other camp figured it’s hard to plan anything by only chanting in unison. Any meaningful planning would be the brain cells taking to one another, out of sync, and thus just sound like a bit louder roar from a small section. Screw listening for chants, listen for an increase in crowd noise and you’ll figure out when the brain is trying to, say, wiggle a finger.

My friend, sifting through recordings from human brains and using complex mathematical earplugs to separate the raw data from the electrodes into manageable pieces, figured out the second camp is probably right. Listen for the roar!
Two fun advances in science at a timely moment.

Broiler (meat) chickens have been subjected to intense genetic selection. In the past 50 years, broiler growth rates have increased by over 300% (from 25 g per day to 100 g per day). There is growing societal concern that many broiler chickens have impaired locomotion or are even unable to walk. Here we present the results of a comprehensive survey of commercial flocks which quantifies the risk factors for poor locomotion in broiler chickens. We assessed the walking ability of 51,000 birds, representing 4.8 million birds within 176 flocks. We also obtained information on approximately 150 different management factors associated with each flock. At a mean age of 40 days, over 27.6% of birds in our study showed poor locomotion and 3.3% were almost unable to walk. The high prevalence of poor locomotion occurred despite culling policies designed to remove severely lame birds from flocks. We show that the primary risk factors associated with impaired locomotion and poor leg health are those specifically associated with rate of growth. Factors significantly associated with high gait score included the age of the bird (older birds), visit (second visit to same flock), bird genotype, not feeding whole wheat, a shorter dark period during the day, higher stocking density at the time of assessment, no use of antibiotic, and the use of intact feed pellets. The welfare implications are profound. Worldwide approximately 2×10¹⁰ broilers are reared within similar husbandry systems. We identify a range of management factors that could be altered to reduce leg health problems, but implementation of these changes would be likely to reduce growth rate and production. A debate on the sustainability of current practice in the production of this important food source is required.

Or eat at Juliano’s:

Gluten sensitivity is widespread among humans. For example, in celiac disease patients, an inflammatory response to dietary gluten leads to enteropathy, malabsorption, circulating antibodies against gluten and transglutaminase 2, and clinical symptoms such as diarrhea. There is a growing need in fundamental and translational research for animal models that exhibit aspects of human gluten sensitivity…

When fed with a gluten-containing diet, gluten-sensitive macaques showed signs and symptoms of celiac disease including chronic diarrhea, malabsorptive steatorrhea, intestinal lesions and anti-gliadin antibodies. A gluten-free diet reversed these clinical, histological and serological features, while reintroduction of dietary gluten caused rapid relapse….

Gluten-sensitive rhesus macaques may be an attractive resource for investigating both the pathogenesis and the treatment of celiac disease.

Dogs still don’t belong in restaurants, but for one less reason:

In many countries in the world, livestock and humans are affected with hydatid disease, which is caused by the development, in the viscera, of the larval stage of the cestode Echinococcus granulosus. They become infected by ingesting the eggs of this parasite, which are passed in the feces of the dog—the host of the adult worm. Domestic dogs are key in the transmission to livestock and humans….
…we propose that a recombinant oral vaccine given to the small number of dogs keeping the herd would decrease the number of Echinococcus granulosus adult worms and, consequently, the number of infective eggs. This measure would help reduce the contamination risk factors for humans and livestock, and would be cost-effective for the owners of the dogs.

A video of Echinococcus Hydatid cysts being removed from a patient’s brain:

(Not safe for anyone to view. Ever.)

Attention fellow nerds worldwide–eat better, work out and clean up:

Basic daily healthy practices including nutritious diet, hygiene and physical activity are common approaches in comprehensive health promotion programs in school settings, however their relationship to these aggressive behaviours is vague. We attempted to show the advantages of these healthy lifestyle behaviours in 9 developing countries by examining the association with being frequently bullied, violence and injury…

Healthy lifestyle showed an association to decreased relative risk of being frequently bullied and violence/injury in developing countries. A comprehensive approach to risk and health promoting behaviours reducing bullying and violence is encouraged at school settings.