Many of you have probably already heard about Ardi, the 4.4 million year old fossil from the family Ardipithecus ramidus recently discovered in Aramis, Ethiopia. Ardi is 1.2 million years older than Lucy, the skeleton fossil that revolutionized our understanding of human evolution in 1974.

A huge turning point in the evolution of humans involved the ability to walk upright. Our closest primate relatives, gorillas and chimpanzees walk on their knuckles. Understanding this development has been a goal of both evolutionary biologists and anthropologistrs for decades. The discovery of Lucy, a 3.2 million year old fossil, allowed researchers to determine that the evolutionary ancestor to humans could walk upright before it developed the large brains that are a hallmark of modern humans.

Ardi has also provided a wealth of information. As researchers dug further and further into the past many expected to find a common ancestor to modern primates that looked similar to a chimpanzee or gorilla in its movement, but Ardi actually looks like neither todays great apes or today's humans.

47 scientists have contributed to 11 papers which appear in Science this month detailing what can be learned from Ardi and the bits and pieces of her brothers and sisters. In addition, the Discovery Channel will be airing "Discovering Ardi" Sunday, October 11th at 9 pm.

Catch the Fossil Fever going around and get to know Ardi for yourself!

To link to Science's Ardipithecus ramidus page, click here.

To find out more about the Discovery Channel special, click here.

It turns out that animals have already figured out a lot of the conundrums that stump us humans, and scientists are really beginning to see the value in looking to our feathered, furred, shelled and slimy friends for hints.

For example, take the toucan bill. As any fan of fruit loops can tell you toucans carry quite a beak. Yet these incredibly strong beaks are very light. Modern engineers, such as Marc Meyers, Professor of Engineering at UCSD are beginning to take a closer look at the material that makes up the toucan beak to see how this is accomplished. A recent paper by Meyers published in Acta Biomaterial described the structure and material of the toucan bill in detail and how this construction could be used to make lighter, safer car door panels.

Researchers in San Diego aren't the only ones looking to animals for inspiration. Many ideas, from velcro to better tools for the blind have been ispired by animals.

To get the most in depth information possible on how aimals can inspire genius sign up for the up-coming symposium "Biomimicry: Designs Inspired by Nature" being held October 1-2 by the San Diego Zoo, the Biomimicry Institute and Mirasol by Qualcomm. To register, click here.

To read the Toucan Bill paper by Marc Meyers, click here.

To read more about other technologies and ideas lifted from nature, click here.

A recent study out of Ohio State University found that people who performed 20 minutes of yoga and meditation at work experienced lowered stress levels. Participants attended weekly 1-hour "mindfulness" training where they learned to spot and handle stress differently. They also performed 20 minutes of meditation or modified yoga (yoga that can be done in business attire-I would pay to see this) in their office every day.

It may sound silly, but the participants did show lower self-reported stress levels and better sleep than the control group. Cortisol (a hormone produced in response to stress) was the same in both groups.

What do you think? Did yoga really lower stress or just the perception of stress? And does it really matter as long as the participants thought they were less stressed?

To read more about the study click here.

DNA polymerase V is a DNA repair enzyme that's activated in times of high DNA damage, but it's extremely error prone compared to other DNA polymerase enzymes. So why would cells evolve such an error-prone repair engine?

A recent study by researchers at the University of Southern California suggests that this enzyme is economic in its motions and fast to engage problem DNA that it is an asset to the cell despite its tendency to create random mutation.

What do you think?

To read the study, click here

Malaria is a hot button issue for many human rights activists. It is the most deadly communicable disease on earth, killing over 1 million people every year. Yet it is one of the least studied diseases. Many claim this paradox is due to the fact that virtually all deaths from malaria occur in undeveloped countries and decimate populations with no financial resources.

There are some drugs that can be used in the treatment of malaria, but over time the parasites evolve immunity to the drug, renderring them ineffective. Every ten years or so a new malaria drug must be developed. Resaerchers have attempted to develop vaccines to malaria before, but haven't been able to produce enough proteins specific to Plasmodium (the malaria causing parasite) to initiate a host reaction, until now.

Researchers at Johns Hopkins have expressed enough Pfs48/45 (a Plasmodium protein) to develop a vaccine that initiates antibody production in mice and non-human primates. Protection against malaria may be on the horizon.

To read more about this research, click here

A recent study performed at the Research Institute of Wildlife Ecology in Austria suggests that the right kind of fat can make mammals faster.

Mice fed on sunflower oil, with high levels of n-6 fatty acids, sprinted 6.3% faster than mice fed on linseed oil, which contains high levels of n-3 fatty acids. In a previous study the researchers found that a range of mammals with high n-6 fatty acid diets had higher maximum running speeds.

Improvements in running speed offer obvious advantages in eluding predators and catching prey, suggesting that animals with higher poly-unsaturated fat diets might have had an evolutionary advantage.

This research was presented at the Society for Experimental Biology Annual Meeting on June 29th. To visit the website for the Society for Experimental Biology click here.

It's difficult to imagine a single-celled miroorganism planning for the future, but according to a paper by two research teams in Isreal that's exactly what some bacteria are doing.

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The paper, which appears in the June issue of Nature, describes E. coli who are conditioned to pre-respond to their environment. E. coli in the gut are exposed to the same sugars, in the same order, over and over agian. When the bacteria are exposed to lactose they know they will see maltose next. In preparation for this they kick on maltose digestion genes. They are conditioned to associate one the presence of one sugar with the expectation of another. it's a little reminiscent of Pavlov's dogs salivating in response to a bell.

If the cells are removed from this conditioning environment and grown under circumstances where the presence of lactose is not followed by maltose the cells will eventually lose their conditioning. Eventually they will not turn on maltose digestion genes in response to maltose. Pavlov saw the same effect when he stopped feeding his dogs every time he rang the bell.

While a conditioned response may not be the same as planning ahead it seems pretty stunning that it can occur in a single cell.

To read the paper, click here.

In December of 2008 an Iraqi reporter threw his shoes at George W. Bush during a news conference in Baghdad. The American public had a mixed reaction. Some people were offended, while others found it hilarious. Leffrey Lin and fellow researchers at the University of Washington, may have been the only people who felt encouraged.

Lin and colleagues were studying the visual system. They hypothesized that humans operate on a dual vision system. One controls action and the other controls perception. The action vision system can allow a person to react to an object that is coming at them befre the eyes have time to percieve the object. The authors believe that Bush and the Iraqi Prime Minister Nouri al-Maliki provide a perfect example of this in the youtube video in which Bush dodges the flying shoe.

The action system kicks in and Bush dodges the shoe. Next to him, and safely out of the line of contact, Nouri al-Maliki doesn't even process the show until much later.

Does this suggest two systems for processing what we see? Does it explain action before reaction?

Is the youtube footage convincing evidence for the dual system hypothesis?

To read the paper from the June issue of Current Biology, click here

To watch the youtube video of the shoe sailing news conference, click here.

Are you optimized for peak performance?

Does biology play a role in "clutch" performance? Protein interactions in the brain could help predict who will rise up when the pressure is on and who will fold. A review recently written by Martin Paulus and colleagues takes a deeper look at the studies that have investigated high pressure performance in order to see what can be taken away from the data collected.

The authors posit that optimized stress response in the brain may contribute to high performance in intense situations and environments.

What do you think? Is performance in intense situations biological? Does training, motivation or personality play a role?

As many of you are probably already aware, during his inaugural speech Obama said he wanted to "restore science to its rightful place". This has sparked many people, including scientists and science enthusiasts, to post their views about where science belongs. I thought it might be worthwhile to start a similar discussion on mySDscience.com.

I'm curious about your ideas on what the rightful place of science is. But I'm even more curious about ideas on how we get science to that rightful place and how it got pushed out in the first place.

As sceintists I think one of the keys to addressing this is re-engaging the public. Getting people informed about science is starting to become an important goal in science, as evidenced by the San Diego Science Festival help last April. What other efforts will get people involved in science? Any ideas?

Let me know what you think on any of these issues.

While I was writing my last article on predictive tools and their emerging role in drug development some one posed the question of whether or not these approaches will ever really save money. They found it unlikely that a drug candidate would ever really be shut down just because some model suggests it might have possible side effects. Instead this prediction would just lead to more testing and more spending. Is this true?

More and more predictive tools and computer modeling are becoming a common part of science. Protein structure, pathway interactions and molecule interactions are all being modeled these days. Whole careers are focused on finding ways to make the modeling systems more accurate.

What is the real role of modeling in science? Will we ever be able to wholly replace bench work with computer simulation? Are these tools real value as sign posts-telling us which direction is the best to follow? Or will they forever be relegated to telling us things we already know? Are there any drawbacks to computer modeling?

Let me know what you think.

To read my article on the drug interaction modeling approach of Chemical Systems Biology click here.

Image provided by addiandcassie.com/rethink/

At a routine check-up recently the nurse asked me if I drink and I said yes. When she asked me how much I said it probably evened out to about one a day. She told me that was nothing, but what if I was one of those people who crammed a week's worth of drinks into a single night? Would that still be nothing? 

Not a lot is known about the effects of binge drinking aside from the splitting headaches and nauseau people experience the next morning. But what do those symptoms mean for your body? After all, isn't this a mild kind of alcohol poisoning? Researchers at UC San Diego are starting to look into the effects of binge drinking and what it does to a person's brain.

To find out more read my article under "Local Sci-News" above or click here

A paper in the April issue of Genes and Development describes two new mouse models for aculte myeloid leukemia (AML). These models show promise for elucidating the mechanisms of specific cancers and for predicting how patients will respond to treatment.

One of the most confounding aspects of cancer is the genetic instability that is a hallmark of the uncontrolled cells. Because of this genetic instability the same cancer can have completely different genetic mutations in two different patients and it is the specific mutations that will determine whether or not a treatment is effective. A good example of this is AML, which can be the end result of different mutations in white blood cells. Most patients with AML recieve the same standard treatment of chemotherapy followed by either bone marrow transplant or additional rounds of chemotherapy, but this treatment is only effective in one fourth of patients. Most patients with AML die within months of diagnosis.

To understand this phenomenon researchers at the Lowe lab in Cold Spring Harbor engineered two mouse models of AML. One which combined mutations in the genes N-Ras and  AML1/ETO and another that combined N-Ras and the gene MLL. These are common combinations seen in populations of patients with AML.

Just like in human cases, mice expressing the AML1/ETO containing combination responded to treatment. Mice expressing MLL/N-ras did not respond to chemotherapy and succumbed to the leukemia. The MLL expressing version of the cancer is similarly associateed with a dismal prognosis in humans. The researchers found that mice expressing the MLL oncogene were unable to activate the p53 pathway. When they knocked down p53 in AML/ETO mice the leukemia became unresponsive to treatment and the mice died.

Not only did the model correctly mimic what is seen in real cases but it also allowed investigation into the mechanism responsible. Use of specifically tailored mouse models may provide the key to bridging the gap between what scientists have learned about cancer and how that knowledge is used.

To read the paper click here