VANCOUVER--Last fall, the Tevatron accelerator at Fermilab in Illinois shut down for good. The long-running accelerator had been eclipsed by the vastly more powerful Large Hadron Collider outside of Geneva, Switzerland, which since 2010 has been generating data at an impressive rate. The move appeared to quash any hopes that Fermilab had of discovering the Higgs boson, the last great known unknown of modern particle physics.

Yet according to Rob Roser, the leader of the CDF experiment at the Tevatron, we shouldn't count Fermilab out quite yet. Though the machine is no longer generating data, physicists have not had time to properly analyze all the data that has been collected thus far.  Today at the annual meeting of the American Association for the Advancement of Science, Roser announced that Fermilab will reveal its final Higgs results in March. "We will be able to say something interesting," he said, "though whether it is that we don't see it or we do see it remains to be seen."

Asked to clarify, Roser said that if the Higgs has a mass of around 125 gigaelectron volts--the mass that recent LHC results seem to indicate is most likely--the Tevatron would be able to identify the Higgs with "three-sigma" certainty. This is a statistical term that indicates the finding only has a tenth of a percent chance of being due to a random statistical fluctuation. Such a result would still fall short of being considered a "discovery," however, as the field of particle physics has adopted the more stringent five-sigma standard--a one-in-a-million chance.

The early signs of autism are visible in the brains of 6-month-old infants, a new study finds, suggesting that future treatments could be given at this time, to lessen the impact of the disorder on children.

Researchers looked at how the brain develops in early life, and found that tracts of white matter that connect different regions of the brain didn't form as quickly in children who later developed autism, compared with kids who didn't develop the disorder.

"The way the wiring was changing was dampened" in the children with autism, said study researcher Jason Wolff, who studies developmental disabilities at the University of North Carolina, Chapel Hill. "It was a more blunted change over time, in how the brain was being wired,"

In contrast, in the brains of infants who did not later develop autism, white matter tracts were swiftly forming, Wolff said. "Their brains were organizing themselves in a pretty rapid fashion."

A killer cancer that is threatening to wipe Tasmanian devils off the map for good has been spreading--from an original infected female 15 years ago--via live cancer cells, according to evidence from genome sequences of the cancer and the animal, published online Thursday in Cell. Finding out how this happened could help save this species from extinction--and it could also prepare researchers for the unlikely event that a contagious cancer ever appeared in humans.

The facial cancer, which is spread through bites, has plagued this animal's precarious population for more than a decade. Tasmanian devils (Sarcophilus harrisii) are the largest surviving carnivorous marsupials and live on Australia's island state Tasmania. [Read more about this scourge in "The Devil's Cancer," from Scientific American's June 2011 issue.] All of the tumors afflicting the animals today contain cells from one original devil, genetic sequences show. "I call her the immortal devil," Elizabeth Murchison, a researcher at the Wellcome Trust Sanger Institute and co-author of the new paper, said in a prepared statement. "Her cells are living on long after she died."

An earlier version of the Tasmanian devil genome was published last year in Proceedings of the National Academy of Sciences and revealed some secrets about why the cancer hasn't killed off the species already. One of the two devils sequenced, named Cedric, showed resistance to at least two strains of the cancer, although he later succumbed to a third.

ScienceDaily (Feb. 17, 2012) -- A University of Arkansas biologist has created a sketch of what the first common ancestor of plants and algae may have looked like. He explains that primitive organisms are not always simple.

The image appears as part of a "Perspective" article in the Feb. 17 issue of Science.

Fred Spiegel, professor of biological sciences in the J. William Fulbright College of Arts and Sciences, suggests what microscopic parts would have been present in this common ancestor based on findings by Dana Price of Rutgers University and his colleagues, who examined the genome of a freshwater microscopic algae and determined that it showed that algae and plants are derived from one common ancestor. This ancestor formed from a merger between some protozoan-like host and cyanobacterium, a kind of bacteria that use photosynthesis to make energy, that "moved in" and became the chloroplast of this first alga. Price and his colleagues show that today's algae and plants have to be descended from this first alga, but they give no idea what it looked like.

"The work that Price and his group did nailed down what the relationships are" between this organism, the algae and plants, and all other eukaryotes, organisms that have a true nucleus in their cells, Spiegel said. "Once you know that, you can compare the structure of cells and characteristics you see in algae and plants with other eukaryotes and get a reasonable idea of what the original critter must have looked like."

The study, funded by the Medical Research Council and to be published online in Nature Genetics, not only demonstrates a mechanism which is likely to be widely relevant in vertebrate development, but also provides confidence that chemicals called morphogens, which control these patterns, can be used in regenerative medicine to differentiate stem cells into tissue.

The findings provide evidence to support a theory first suggested in the 1950s by famous code-breaker and mathematician Alan Turing, whose centenary falls this year. He put forward the idea that regular repeating patterns in biological systems are generated by a pair of morphogens that work together as an 'activator' and 'inhibitor'.