Very cool animation, by Cold Spring Harbor Laboratory and Interactive Knowledge, of the working of the inner workings of our bodies as they react to a cut. If you want to get right to the science, skip the first minute. Providing these types of educational animations is a great way for educational institutions to take advantage of technology to achieve their mission in ways not possible before.
It is annoying how many of those “educational” institutions don’t provide such educational material online (and even take material offline that was online). Have they become more focused on thinking and operating the way they did in 1970 than promoting science education? It is a shame some “educational” institutions have instead become focused on looking backward. I will try to promote those organizations that are providing online science education.
For the new study, researchers first collected DNA samples collected in 1991 and again between 2002 and 2006 from 600 participants already enrolled in the AGES Reykjavik Study. The AGES study is renowned for its value to genetics research because of the historic isolation and reduced number of genetic “variables” among Iceland’s population, making certain patterns of genetic information easier to identify.
Among the 600, the research team measured the total amount of DNA methylation in each of 111 samples and compared total methylation from DNA collected in 2002 to 2005 to that person’s DNA collected in 1991.
They discovered that in almost one-third of the subjects, methylation changed over that 11-year span, with some gaining DNA methylation and others losing it.
“The key thing this part of the study told us is that levels changed over time, proof of principle that an individual’s epigenetic profile does change with age,” said M. Daniele Fallin, Ph.D., an associate professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health.
Still a puzzle, though, was why or how, Fallin said, “so we wondered whether the tendency to those changes was also inherited, right along with our DNA sequences. That would explain why certain families are more susceptible to certain diseases.”
In Uganda, meanwhile, the disease has become so widespread that yields on banana farms have reached dangerously low levels. Acres and acres of crops have been lost, creating a cascade of economic losses in a trading system that spreads from the tiniest villages to Uganda’s cities, all based on the transport and trade of bananas.
The urgency of this cannot be overstated. Uganda and the nations surrounding it absolutely depend on bananas as a staple foodstuff. Millions rely on bananas for survival. And the spread of BXW into Kenya is yet another indicator that this deadly disease is on the march. As with Panama Disease – the wilting fungus that threatens our banana, the Cavendish – BXW (a bacterial malady) is incurable. The difference between the two is that BXW moves faster and threatens, right now, food supplies in nations with fragile governments.
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First, banana diversity. In order to mitigate the spread of disease, the number of kinds of bananas being grown needs to be increased.
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Second, genetic engineering: It is time for the general public to recognize that working at the DNA level is not always a corporate trojan horse into destroying local agriculture and contaminating the environment. This isn’t all about Monsanto. While consumers in the suburbs and Whole Foods stores protest against all GMO foods – while barely knowing what GMO is – they bluntly prevent out legitimate public research that might stop hunger. Time learn that everything has nuance, the disease that are killing the bananas: they work in just two modes: off – and on.
Foldit is a revolutionary new computer game enabling you to contribute to important scientific research. This is another awesome combination of technology, distributed problem solving, science education…
Essentially the game works by allowing the person to make some decisions then the computer runs through some processes to determine the result of those decisions. It seems the human insight of what might work provides an advantage to computers trying to calculate solutions on their own. Then the results are compared to the other individuals working on the same protein folding problem and the efforts are ranked.
This level of interaction is very cool. SETI@home, Rosetta@home and the like are useful tools to tap the computing resources of millions on the internet. But the use of human expertise really makes fold.it special. And you can’t help but learn by playing. In addition, if you are successful you can gain some scientific credit for your participation in new discoveries.
Proteins are the workhorses in every cell of every living thing. Your body is made up of trillions of cells, of all different kinds: muscle cells, brain cells, blood cells, and more. Inside those cells, proteins are allowing your body to do what it does: break down food to power your muscles, send signals through your brain that control the body, and transport nutrients through your blood. Proteins come in thousands of different varieties, but they all have a lot in common. For instance, they’re made of the same stuff: every protein consists of a long chain of joined-together amino acids.
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structure specifies the function of the protein. For example, a protein that breaks down glucose so the cell can use the energy stored in the sugar will have a shape that recognizes the glucose and binds to it (like a lock and key) and chemically reactive amino acids that will react with the glucose and break it down to release the energy.
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Proteins are involved in almost all of the processes going on inside your body: they break down food to power your muscles, send signals through your brain that control the body, and transport nutrients through your blood. Many proteins act as enzymes, meaning they catalyze (speed up) chemical reactions that wouldn’t take place otherwise. But other proteins power muscle contractions, or act as chemical messages inside the body, or hundreds of other things.
But we were very lucky 🙂 We managed to see 5 desert tortoises (Gopherus agassizii) on that particular day, and one of them was spotted on the dirt road (not in the burrow)!
Desert tortoises are thought to live 40 – 60 years. They grow relatively slowly and adult females are larger than adult males (for obvious reasons). They typically breed from April to June and the female tortoises lay between 1 and 11 eggs. Incubation period for eggs varies from 80 to more than 100 days.
Pelf is experiencing a turtle conservation training and tour of the USA (see Turtle Camps in Malaysia). Her blog is doing a great job showing they made a good selection in choosing her for the scholarship.
“If you compare the 23 chromosomes of humans with the 19 chromosomes of amphioxus, you find that both genomes can be expressed in terms of 17 ancestral pieces. So, we can say with some confidence that 550 million years ago, the common ancestor of amphioxus and humans had 17 chromosomal elements.”
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Each of those 17 ancestral segments was duplicated twice in the evolution of vertebrates, after which most of the routine “housekeeping” genes lost the extra copies. Those left, totaling a couple thousand genes, found new functions that, Putnam said, make us different from all other creatures.
“These few thousand genes have been retooled to make humans more elaborate than their simpler ancestors. They are involved in setting up the body plan of an animal and differentiating different parts of the animal,” he said. “The hypothesis, pretty strongly supported by this data, is that the multiplication of this particular kind of gene and differentiation into different functions was important in the formation of vertebrates as we know them.”
“The most exciting thing that the amphioxus genome does is provide excellent evidence for the idea that Ono proposed in 1970, that the human genome had undergone two rounds of whole-genome duplication with subsequent losses,”
A great example of the scientific method in action. It often isn’t a matter of developing a theory one day, testing it the next and learning the outcome the next. The process can take decades for complex matters.
The chicken molecule, an antibody called IgY, looks remarkably similar to the human antibody IgE. IgE is known to be involved in allergic reactions and humans also have a counterpart antibody called IgG that helps to destroy invading viruses and bacteria. Scientists know that both IgE and IgG were present in mammals around 160 million years ago because the corresponding genes are found in the recently published platypus genome. However, in chickens there is no equivalent to IgG and so IgY performs both functions.
Lead researcher, Dr. Rosy Calvert said: “Although these antibodies all started from a common ancestor, for some reason humans have ended up with two rather specialised antibodies, whereas chickens only have one that has a much more general function.
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Professor Brian Sutton, head of the laboratory where the work was done said: “It might be that there was a nasty bug or parasite around at the time that meant that humans needed a really dramatic immune response and so there was pressure to evolve a tight binding antibody like IgE. The problem is that now we’ve ended up with an antibody that can tend to be a little over enthusiastic and causes us problems with apparently innocuous substances like pollen and peanuts, which can cause life-threatening allergic conditions.”
So far, the signs are good. The bill commits $500 million for research facilities, infrastructure improvements, and other capital projects; $250 million for tax credits; and $250 million for research grants. The plan is flexible enough to support research at private institutions while making major investments at public universities. Patrick and legislators fended off the most flagrant attempts to divert money into political pet projects with little direct relevance to the biotech industry, such as $49.5 million for a science building at a state college with no graduate science programs.
As I have mentioned many times the centers of scientific excellence are important for economic success. Massachusetts has some great advantages with MIT, Harvard, many biotech companies… but still must continue to focus on staying a center of excellence.
The study authors, from McNeese State University and Louisiana State University, said their research is the first to take an in-depth look at alligator blood’s prospects as an antibiotic source. According to the researchers, alligators can automatically fight germs such as bacteria and viruses without having been exposed to them before launching a defense.
For the study, the researchers extracted proteins known as peptides from white cells in alligator blood. As in humans, white cells are part of the alligator’s immune system. The researchers then exposed various types of bacteria to the protein extracts and watched to see what happened.
In laboratory tests, tiny amounts of these protein extracts killed a so-called “superbug” called methicillin-resistant Staphylococcus aureus, or MRSA. The bacteria has made headlines in recent years because of its killing power in hospitals and its spread among athletes and others outside of hospitals.
The extracts also killed six of eight strains of a fungus known as Candida albicans, which causes a condition known as thrush, and other diseases that can kill people with weakened immune systems.
A major evolutionary innovation has unfurled right in front of researchers’ eyes. It’s the first time evolution has been caught in the act of making such a rare and complex new trait. And because the species in question is a bacterium, scientists have been able to replay history to show how this evolutionary novelty grew from the accumulation of unpredictable, chance events.
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sometime around the 31,500th generation, something dramatic happened in just one of the populations – the bacteria suddenly acquired the ability to metabolise citrate, a second nutrient in their culture medium that E. coli normally cannot use. Indeed, the inability to use citrate is one of the traits by which bacteriologists distinguish E. coli from other species.
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The replays showed that even when he looked at trillions of cells, only the original population re-evolved Cit+ – and only when he started the replay from generation 20,000 or greater. Something, he concluded, must have happened around generation 20,000 that laid the groundwork for Cit+ to later evolve.
Lenski and his colleagues are now working to identify just what that earlier change was, and how it made the Cit+ mutation possible more than 10,000 generations later.
