It's all about osmosis. According to the researchers, who published their study last week in PLoS One:

[Fungi] with the longest ranges are powered by hydrostatic pressure and include “squirt guns” that are most common in the Ascomycota and Zygomycota. In these fungi, fluid-filled stalks that support single spores or spore-filled sporangia, or cells called asci that contain multiple spores, are pressurized by osmosis.

Basically, the fungus contains, as the scientists put it, "squirt guns" that are under such tremendous pressure that when they burst open they push the spores out at the speed of a car on a U.S. highway.

Fastest Flights in Nature [via PLoS One]

The new study, conducted by a team of researchers from the UK, France, and China, used genomic analysis to determine at whether married couples were more likely to be "MHC-dissimilar." The results showed that European couples were overwhelmingly MHC-dissimilar, while African couples were neither similar nor dissimilar (in other words, they were just as likely to be similar as dissimilar). The researchers concluded that in the European population, mate selection may be driven more by biology than in other populations.

Conclude the researchers in their paper:

At the molecular level, we found that the European American couples we studied are significantly more MHC-dissimilar than random pairs of individuals, and that this pattern of dissimilarity is extreme when compared to the rest of the genome, both globally and when broken into windows having the same length and recombination rate as the MHC . . . Such dissimilarity, observed from both molecular and serological data, cannot be explained by demographic processes, since such effects would affect the whole genome.

They're saying that the MHC-dissimilarity is not just caused by demographic factors like geographical location.

Even more interesting was that the offspring of the MHC-dissimilar couples "were not more MHC-diverse than expected by random selection." So the marry-by-smell method may not actually be creating more robust offspring. More research is needed to discover why Europeans are more likely to marry for biological reasons than other populations are.

Is Mate Choice in Humans MHC-Dependent? [via PLoS Genetics]

It turns out that Ebola exploits a vulnerability in something called the "PI3 kinase pathway," a biochemical mechanism that is responsible for cell longevity and movement, as well for causing the cell to pull things from outside into the cell via a little bubble called an "endosome." Ebola tricks the cell into wrapping it in the endosome bubble and pulling it inside — sort of like a trojan horse. Once inside the cell, the virus breaks out of the endosome and starts replicating.

What the researchers discovered was that if they used a drug that shut down the PI3 kinase pathway, the Ebola remained trapped inside that endosome. Essentially, they used a drug to patch the cell's vulnerable system and keep the virus out.

University of Texas Medical Branch at Galveston immunology professor Robert Davey, an author on the paper, said in a statement:

The nice part about identifying entry mechanisms is you can prevent the virus from infecting the cell. You can stop the whole show before it even gets started. Up to that point, it's really a bus ride for these viruses, and PI3 kinase is the bus driver. Whether you're talking about Ebola or Ebola virus-like particles, they've all got the virus envelope proteins that trigger the PI3 kinase pathway, which is the first step of getting the virus onto that bus.

He also noted that there are other viruses that exploit the PI3 kinase vulnerability, though Ebola is the first that has been observed in the act of doing it. That means the team's breakthrough might affect how other viruses are treated too. And how cells are manipulated, since once you start mucking around with PI3 kinase pathways, you are playing with cellular movement and longevity. Maybe Ebola will actually prove to be the key to unlocking the secret of longevity at a cellular level.

PI3 Kinase-Akt Pathway Controls Cellular Entry of Ebola Virus [PLoS Pathogens via Eurekalert]

A group of researchers the U.S. and the Netherlands peered into people's brains using fMRI machines while those people were doing a series of three tasks: reading about something disgusting, watching images of something disgusting, and actually tasting something disgusting. Turns out the same regions in their brains activated consistently regardless of whether they were imagining, watching, or tasting disgusting things. (For the curious: the "disgusting" story apparently had to do with swallowing somebody else's vomit).

In an article published last night in PLoS One, the researchers write:

[This experiment] provides insights into the neural basis of the captivating experience of reading a book: While previous studies on social perception used movies of other people's experiences or arbitrarily colored symbolic cues, our combination of movies and written material in the present experiment demonstrates that reading (mental imagery) as well as watching other people experience what is imagined recruits brain regions involved in experiencing an emotion.

In other words, your emotions are toyed with in exactly the same way, regardless of whether you are reading or watching TV. Maybe that's why social critics of the nineteenth century were always going about the way the masses were having their minds ruined by books, while today's worry about ruination from videogames. Regardless of the medium, the brainwashing remains the same.

A Common Anterior Insula Representation of Disgust Observation, Experience and Imagination Shows Divergent Functional Connectivity Pathways [via PLoS One]

Published this weekend in PLoS Genetics, the study is extraordinary not just because of its futuristic implications, but because of the cool new super-rapid system the researchers used to identify which genes are active during brain development. The technique is called RNA interference, or RNAi:

Dr. Katharine Sepp and her fellow researchers took fresh neuronal cells extracted from embryos of the fruit fly genus Drosophila and screened them using RNA interference techniques. The team tested all genes, one by one in a rapid manner, for their potential role in neuronal development. The team then validated the method in mice.

A combination of live-cell imaging and quantitative analysis allowed Sepp et al to characterize neurons’ morphological phenotypes in response to RNAi-mediated gene knockdown. The researchers focused on 104 evolutionary conserved genes that, when downregulated by RNAi, have morphological defects. The team developed algorithms to help streamline the analysis of the thousands of images created in the process.

The analysis revealed unexpected, essential roles in neurite outgrowth for genes representing a wide range of functional categories including signalling molecules, enzymes, channels, receptors, and cytoskeletal proteins. Results also determined that genes known to be involved in protein and vesicle trafficking show similar RNAi phenotypes.

The researchers believe that this study provides an effective method for future studies of a large variety of genes, including those with important functions in the nervous system.

This research will open up new ways to tinker with brain development, but right now the genes have only been identified in flies and mice. Humans share a lot of genes with both creatures. Still, don't expect to order your supergenius baby next week. Or your army of slave drones.

Identification of Neural Outgrowth Genes Using Genome-Wide RNAi [PLoS Genetics]

According to the authors of the study, diabetes and lung disease were the biggest life-shorteners. In an introductory note to their study, PLoS editors write:

The researchers looked at differences in death rates between all counties in US states plus the District of Columbia over four decades, from 1961 to 1999. They obtained the data on number of deaths from the National Center for Health Statistics, and they obtained data on the number of people living in each county from the US Census. The NCHS did not provide death data after 2001. They broke the death rates down by sex and by disease to assess trends over time for women and men, and for different causes of death.

Over these four decades, the researchers found that the overall US life expectancy increased from 67 to 74 years of age for men and from 74 to 80 years for women. Between 1961 and 1983 the death rate fell in both men and women, largely due to reductions in deaths from cardiovascular disease (heart disease and stroke). During this same period, 1961-1983, the differences in death rates among/across different counties fell. However, beginning in the early 1980s the differences in death rates among/across different counties began to increase. The worst-off counties no longer experienced a fall in death rates, and in a substantial number of counties, mortality actually increased, especially for women, a shift that the researchers call "the reversal of fortunes." This stagnation in the worst-off counties was primarily caused by a slowdown or halt in the reduction of deaths from cardiovascular disease coupled with a moderate rise in a number of other diseases, such as lung cancer, chronic lung disease, and diabetes, in both men and women, and a rise in HIV/AIDS and homicide in men. The researchers' key finding, therefore, was that the differences in life expectancy across different counties initially narrowed and then widened.

For people who aren't in the soldiering life, the study offers a different insight: Being depressed makes you likely to seek out situations that will depress you more. Because you've become less risk-averse, you're more likely to go down a dark alley that people with higher levels of serotonin would avoid. And if you got beaten up in that dark alley, the resulting compounded depression might make you do something even riskier next time.

Taking a serotonin reuptake inhibitor like Prozac, which keeps more serotonin circulating in your brain, actually causes you to avoid bad situations as well as evening out your mood.

Seratonin, Inhibition, and Negative Mood [PLoS Computational Biology]

According to an announcement from PLoS Genetics:

Researchers have created baker's yeast capable of living to 800 in yeast years without apparent side effects. The basic but important discovery, achieved through a combination of dietary and genetic changes, brings scientists closer to controlling the survival and health of the unit of all living systems: the cell. "We're setting the foundation for reprogramming healthy life," says study leader Valter Longo of the University of Southern California.

Longo's group put baker's yeast on a calorie-restricted diet and knocked out two genes - RAS2 and SCH9 - that promote aging in yeast and cancer in humans.

"We got a 10-fold life span extension that is, I think, the longest one that has ever been achieved in any organism," Longo says. Normal yeast organisms live about a week.

"I would say 10-fold is pretty significant," says Anna McCormick, chief of the genetics and cell biology branch at the National Institute on Aging (NIA) and Longo's program officer. The NIA funds such research in the hope of extending healthy life span in humans through the development of drugs that mimic the life-prolonging techniques used by Longo and others, McCormick adds.

Baker's yeast is one of the most studied and best understood organisms at the molecular and genetic level. Remarkably, in light of its simplicity, yeast has led to the discovery of some of the most important genes and pathways regulating aging and disease in mice and other mammals.

Longo's group next plans to further investigate life span extension in mice. The group is already studying a human population in Ecuador with mutations analogous to those described in yeast.

"People with two copies of the mutations have very small stature and other defects," Longo says. "We are now identifying the relatives with only one copy of the mutation, who are apparently normal. We hope that they will show a reduced incidence of diseases and an extended life span."

Longo cautions that, as in the Ecuador case, longevity mutations tend to come with severe growth deficits and other health problems. Finding drugs to extend the human life span without side effects will not be easy.

I've always been a skeptic when it comes to life-extending research, but this has me rethinking my position.

Lifespan Extension [PLoS Genetics]

The researchers also assumed that we'd be using the same disease-fighting methods we used in the SARS outbreak. This map doesn't mean that huge chunks of the world will soon be wiped out by a pandemic. It's actually, according to the researchers, a warning. They want national health organizations to be aware which areas of the world need better systems for handling viral outbreaks. That way, flu doesn't reach epidemic proportions and shoot all over the world. Of course, if governments handle the next epidemic it the way they did in 28 Weeks Later and Resident Evil: Extinction, this "help" might come in the form of nukes.

Predicting Outbreaks [BMC Medicine]