Science leads the way: cloning is used to create embryonic stem cells!
Ants: when should ants just wait out bad weather and when should they forage? Evolution works out an answer.
Brinicles: yes, super cold “icicles of brine” can reach below the surface of water and become a finger of death for the things that it touches:
I can see how an ancient person might see this as a “finger of god”.
Via Jerry Coyne’s site: Why Evolution is True, where there are more cool photos.
Here a Frog fights off a grass snake:
In this longer video, it appears as if the frog is a goner (at 4-4:30 into it). The frog keeps fighting, gets in the water and works its way almost out; then at 8:30 another frog appears (slow it down) and appears to attack the snake; a biologist told me that the second frog was probably either attacking the first frog or trying to mate with it. In either event, the snake gets chased off and swims away, still hungry and completely humiliated.
I had heavy legs this morning; this worried me a bit. It turns out that my legs were heavy from doing three sets of 5 squats with…45 pounds. OMG, my legs are weak.
So I ran outside in perfect weather; 1:01:10 for 6.4 hilly miles; 9:45 out, 8:49 back: 35:40, 12:33, 4:07, 8:49. (9:33 mpm pace) and then did some light leg exercises afterward. I’ll probably start this program and do these after my runs. My legs are too weak.
Note: last night, I did 2 miles of walking with the group and another 2 (harder) with Vickie.
Yes, the hotness is being bred out of the jalapeno pepper; it isn’t just your imagination. This is what happens when you aim for the mean.
Genes and cancer:
Via the New York Times:
Scientists have discovered that the most dangerous cancer of the uterine lining closely resembles the worst ovarian and breast cancers, providing the most telling evidence yet that cancer will increasingly be seen as a disease defined primarily by its genetic fingerprint rather than just by the organ where it originated. [...]
Over the past year, as part of this project, researchers have reported striking genetic changes in breast, colon and lung cancers that link them to other cancers. One kind of breast cancer was closely related to ovarian cancer. Colon cancers often had a genetic change found in breast cancer. And about half of squamous cell lung cancers might be attacked by drugs being developed for other cancers.
The endometrial cancer and leukemia efforts alone involved more than 100 researchers who studied close to 400 endometrial tumors and 200 leukemias. Endometrial cancer is the most common gynecological cancer in American women and strikes nearly 50,000 of them a year, killing about 8,000. Acute myeloid leukemia, the most prevalent acute adult leukemia, is diagnosed in about 14,000 Americans a year and kills about 10,000.
“This is exploring the landscape of cancer genomics,” said Dr. David P. Steensma, a leukemia researcher at the Dana-Farber Cancer Institute who was not involved with the studies. “Many developments in medicine are about treatments or tests that are only useful for a certain period of time until something better comes by. But this is something that will be useful 200 years from now. This is a landmark that will stand the test of time.”
Dr. Douglas Levine of Memorial Sloan Kettering Cancer Center, the principal investigator on the endometrial cancer study, said the group scoured the country for samples of this cancer.
The cancer has long been evaluated by pathologists who examine thin slices of endometrial tumors under a microscope and put them in one of two broad categories. But the method is not ideal. In general, one category predicts a good prognosis and tumors that could be treated with surgery and radiation, while the other holds a poorer prognosis and requires chemotherapy after surgery. But pathologists often disagree about how to classify the tumors and can find it difficult to distinguish between the two types, Dr. Levine said.
The new genetic analysis of hundreds of tumors found patterns of genetic aberrations that more precisely classify the tumors, dividing them into four distinct groups. About 10 percent of tumors that had seemed easily treated with the old type of exam now appear to be more deadly according to the genetic analysis and would require chemotherapy.
Another finding was that many endometrial cancers had a mutation in a gene that had been seen before only in colon cancers. The mutation disables a system for repairing DNA damage, resulting in 100 times more mutations than typically occur in cancer cells.
“That was a complete surprise,” Dr. Levine said.
It turned out to be good news. Endometrial cancers with the mutation had better outcomes, perhaps because the accumulating DNA damage is devastating to cancer cells.
Another surprise was that the worst endometrial tumors were so similar to the most lethal ovarian and breast cancers, raising the tantalizing possibility that the three deadly cancers might respond to the same drugs.
The bottom line: cancers shouldn’t really be classified by what organ they attack but rather by their genomes; it is this classification which should determine which treatment to use.
Why are some drugs so effective at treating cancer cells? It might depend on how the drug causes proteins to be polarized in the cell: (via University of Manchester):
Professor Daniel Davis and his team used high quality video imaging to investigate why the drug rituximab is so effective at killing cancerous B cells. It is widely used in the treatment of B cell malignancies, such as lymphoma and leukaemia – as well as in autoimmune diseases like rheumatoid arthritis.
Using high-powered laser-based microscopes, researchers made videos of the process by which rituximab binds to a diseased cell and then attracts white blood cells known as natural killer (NK) cells to attack. They discovered that rituximab tended to stick to one side of the cancer cell, forming a cap and drawing a number of proteins over to that side. It effectively created a front and back to the cell – with a cluster of protein molecules massed on one side.
But what surprised the scientists most was how this changed the effectiveness of natural killer cells in destroying these diseased cells. When the NK cell latched onto the rituximab cap on the B cell, it had an 80% success rate at killing the cell. In contrast, when the B cell lacked this cluster of proteins on one side, it was killed only 40% of the time.
Professor Davis says: “These results were really unexpected. It was only possible for us to unravel the mystery of why this drug was so effective, through the use of video microscopy. By watching what happened within the cells we could clearly identify just why rituximab is such an effective drug – because it tended to reorganise the cancerous cell and make it especially prone to being killed.”
He continues: “What our findings demonstrate is that this ability to polarise a cell by moving proteins within it should be taken into consideration when new antibodies are being tested as potential treatments for cancer cells. It appears that they can be up to twice as effective if they bind to a cell and reorganise it.”
Hurray for Science!
Woo and yoga
Someone asked me how I could like yoga and be down on “alternative (quack) medicine”. Well, there have been some rigorous studies done on yoga and it CAN be recommended for physical therapy purposes (e. g. back aches). Via our National Institute of Health.
This Tiger Frog from Ghana is a cutie:
Movies: I want to see this one:
Note: my beef with religion, at least as practiced in the west, is that too many of them require people to accept “miracles” (resurrections, parting seas, virgin births, etc.) on “faith” (sans evidence). So once you “accept” that the laws of science (naturalism) can be suspended at set times, then, well, why trust science with anything? Seriously: if there is, say, water on your basement floor and a pipe joint above that with green on the joint…well…if you didn’t SEE it drip, then maybe the water and the green just appeared because of the work of some devil or pixie? Why not…if suspensions of naturalism are allowed?
My beef is NOT with religions that don’t require acceptance of miracles.
It is my opinion that a deity/spirit/whatever that is interested in humans and human affairs makes no sense, but that is the realm of opinion.
The eye of a super-hurricane at Saturn’s north pole looks like a peaceful red rose in a fresh bouquet of pictures from NASA’s Cassini orbiter. But don’t be fooled: That rosy appearance is merely due to the false colors ascribed to infrared wavelengths.
This storm’s eye measures 1,250 miles (2,000 kilometers) in diameter, about 20 times wider than the average hurricane’s eye on Earth. The outer clouds at the hurricane’s edge are traveling at 330 mph (530 kilometers per hour), which would be off the scale on our planet. The vortex whirls inside Saturn’s mysterious hexagonal cloud pattern, and it’s not going anywhere.
How do you like this image of the moon taking from space near the earth?
Here is a picture of a solar eclipse via Scientific American:
Miloslav Druckmüller, a mathematician at the Brno University of Technology in the Czech Republic, and his colleagues were on Enewetak as the eclipse’s shadow raced toward them from the northwest at more than twice the speed of sound. This composite of 31 images from the eclipse shows the solar corona, the wispy “atmosphere” of the sun peeking out from behind the moon as well as the cratered, rayed surface of the moon itself.
Back on Earth Again
This species of fish, commonly found in China, Russia and Korea, has been found in New York. It is an invasive species.
Even more interestingly, it can actually breathe outside of water for a short period of time (days) and even hunt.
Baby octopi hatching.
Evolution About that fish to land animal transition:
In the hope of reconstructing a pivotal step in evolution — the colonization of land by fish that learned to walk and breathe air — researchers have decoded the genome of the coelacanth, a prehistoric-looking fish whose form closely resembles those seen in the fossils of 400 million years ago.
Often called a living fossil, the coelacanth (pronounced SEE-luh-canth) was long believed to have fallen extinct 70 million years ago, until a specimen was recognized in a fish market in South Africa in 1938. The coelacanth has fleshy, lobed fins that look somewhat like limbs, as does the lungfish, an air-breathing freshwater fish. The coelacanth and the lungfish have long been battling for the honor of which is closer to the ancestral fish that first used fins to walk on land and give rise to the tetrapods, meaning all the original vertebrates and their descendants, from reptiles and birds to mammals.
The decoding of the coelacanth genome, reported online Wednesday in the journal Nature, is a victory for the lungfish as the closer relative to the first tetrapod. But the coelacanth may have the last laugh because its genome — which, at 2.8 billion units of DNA, is about the same size as a human genome — is decodable, whereas the lungfish genome, a remarkable 100 billion DNA units in length, cannot be cracked with present methods. The coelacanth genome is therefore more likely to shed light on the central evolutionary question of what genetic alterations were needed to change a lobe-finned fish into the first land-dwelling tetrapod.
Another helpful preadaptation is a snippet of DNA that enhances the activity of the genes that drive the formation of limbs in the embryo. The Amemiya team focused on the enhancer DNA sequence because it occurred in the coelacanth and animals but not in ordinary fish. They then inserted the coelacanth enhancer DNA into mice.
“It lit up right away and made an almost normal limb,” said Neil Shubin, meaning that the coelacanth gene enhancer successfully encouraged the mouse genes to make a limb. Dr. Shubin, a member of the team, is a paleontologist at the University of Chicago.
Surf to the New York Times article to read more. Note: Neil Shubin wrote a couple of good books on evolution: Your Inner Fish and The Universe Within. I highly recommend both.
The not so good
See a GIF that shows, in graphic form, how each individual state’s obesity rates went up with the passing years. Read the accompanying article at Slate.
Pesticides: it is no secret that bees are dying. Part of the reason is the weather. It sure appears that part of the reason is new pesticides:
In the last half century, the domesticated honeybee population has declined by about 50 percent. In the United States, this year marks the highest losses of honeybee populations, with some of the biggest beekeepers losing more than 60 percent of their insects. But identifying the culprit has proved daunting. Pathogens, parasites, pesticides, and habitat loss are likely involved. Recently, the potential role of neonicotinoid pesticides has taken center stage, as a flurry of studies has yielded conflicting findings—and the controversy is getting political.[...]
Neonicotinoids—“neonics”—are systemic pesticides broadly used in Europe and the United States. Absorbed by plants from the soil, they eventually reach the pollen and nectar, which is ingested by bees and other insects. Last year, research demonstrated that even low levels of neonics can strongly affect bee behavior. In one study, bumblebees that were exposed to the neonic imidacloprid in the lab, then allowed to forage in the field, had sharply reduced colony growth rates and produced 85 percent fewer queens to found new colonies in the spring. In another study, more than 30 percent of free-ranging honeybees exposed to the neonic thiamethoxam got lost, failing to return to the hive.
The papers were “the straw that broke the camel’s back,” said David Goulson of the University of Stirling in the U.K., a coauthor of the bumblebee study. Previous research implicating neonics in bee decline had been done entirely in the lab. “We wanted to see what happens when the bees have to navigate over realistic distances, find patches of flowers, and bring the food back to the hive,” he said. “We found really striking results.”
So striking that the U.K.’s Department for Environment, Food and Rural Affairs (DEFRA) decided to reevaluate existing publications. But the agency concluded last month that “the risk to bee populations from neonics, as they are currently used, is low.” Moreover, DEFRA’s own research, also released last month, stated that “laboratory-based studies demonstrating sub-lethal effects on bees from neonics did not replicate realistic conditions, but extreme scenarios.”
But many researchers disagree. “We used exactly the levels found in a treated crop in the field,” said Goulson. Suggesting that the experiments linking neonics to bee decline use doses that are unrealistically high is “part of the smoke screen of lies and confusion that have been thrown up by the agrochemical industry” to defend the use of neonics, he added.
Independently, the European Commission asked the European Food Safety Authority (EFSA) to also review the existing literature on neonics, specifically Syngenta’s thiamethoxam and Bayer’s clothianidin and imidacloprid. EFSA’s report, released this January, concluded that neonics pose an unacceptable risk to bees and that they should not be used on flowering crops. This prompted the E.U.’s ban proposal and fevered campaigning from both sides of the debate.
Now I know some GMO “activists” are concerned about this. The problem here is that the GMO crop isn’t the culprit but rather the pesticides used on those crops. There really is a distinction.
Of course, this area of science is beyond my professional expertise (way beyond it) so I’ll be following this dust up closely.
Human endurance: this New York Times story talks about an incredible endurance athlete. The whole story is good; here is one bit:
Born into a Catalan family, Jornet grew up in the Spanish Pyrenees at 6,500 feet, and his gifts are literally in his blood. “When you are born and bred at altitude, you tend to have a higher blood volume and red-cell count for oxygen-carrying capacity,” which translates to better endurance, says Stacy Sims, a researcher at Stanford who holds a doctorate in exercise physiology and nutrition science. Years of daily running and skiing up mountains have further bolstered this advantage. This helps explain why Jornet sweats so little. During exercise, the bodies of very fit people quickly act to disperse heat by, among other things, vasodilation — expanding blood vessels at the skin’s surface where the air can cool the body. A body that sweats less loses less precious liquid from its circulatory system, a major factor in fatigue. In moderate temperatures, Jornet says, he can run easily for eight hours without drinking water.
For me: running at a moderate pace, I usually don’t drink during runs 2 hours or less. Walking: it is about 3 hours. No, I am not that fit and I do need to drink more when I am going very hard.
Physics Mano Singham has an interesting piece on particle physics. It requires a bit of effort to read, but it isn’t technical (though you have to know that subatomic particles are made of quarks and realize that mass of these particles isn’t just the mass of the quarks that make up the particle; the energy adds to the mass.
When we try to date human genetic lineages, the mutation rates are important:
Recent measurements of the rate at which children show DNA changes not seen in their parents — the “mutation rate” — have challenged views about major dates in human evolution.
The researchers show that pre-ice age hunter-gatherers from Europe carry mtDNA that is related to that seen in post-ice age modern humans such as the Oberkassel fossils. This suggests that there was population continuity throughout the last major glaciation event in Europe around 20,000 years ago. Two of the Dolni Vestonice hunter-gatherers also carry identical mtDNAs, suggesting a close maternal relationship among these individuals who were buried together.
The researchers also used the radiocarbon age of the fossils to estimate human mutation rates over tens of thousands of year back in time. This was done by calculating the number of mutations in modern groups that are absent in the ancient groups, since they had not yet existed in the ancient population. The mutation rate was estimated by counting the number of mutations accumulated along descendent lineages since the radiocarbon dated fossils.
Using those novel mutation rates — capitalizing on information from ancient DNA — the authors cal-culate the last common ancestor for human mitochondrial lineages to around 160,000 years ago. In other words, all present-day humans have as one of their ancestors a single woman who lived around that time.
There is more there; right now there is a disparity between modern family mutation rates and the observed mutation rates of ancient humans (as derived from fossils.
Both the hunters and the prey benefit from camouflage. There is a gecko that resembles a leaf; below is an insect that also resembles a leaf.
Does excessive salt in your diet harm your autoimmune system? There is some evidence that it might;
Salt may play an important role in autoimmune diseases, according to two new papers published today (March 6) in Nature. Exposure to high levels of salt was found to make both cultured mouse and human T cells more pathogenic, and high-salt diets worsened autoimmune disease in mice.
“I thought the papers were very exciting and provocative,” said John O’Shea, a doctor at the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), who wrote a Nature commentary accompanying the new findings and was not involved in the study.
Meanwhile, David Hafler’s lab at Yale University was coming to similar conclusions from the opposite direction. The group had completed a study where they measured TH17 cells in the blood of healthy human subjects, sequenced the people’s microbiomes, and had them fill out questionnaires about their diets. While the study was supposed to be focused on the influence of the microbiome, the researchers noticed that participants who frequently ate in fast food restaurants had elevated levels of pathogenic TH17 cells. They hypothesized that the saltiness of the food could be part of the explanation.
“That led to a whole series of experiments trying to figure out the role of salt,” Hafler said. Unlike Regev and Kuchroo’s labs, which looked at TH17 differentiation in mouse cells, Hafler’s lab added salt to human cell cultures. They also found that it was associated with more pathogenic TH17 cells. “Salt just seems to trigger all the genes associated with bad autoimmune T cells,” Hafler said.
But the effect hasn’t been proven in humans. There is proof for mice, and some correlation in humans.
The Brain: help for us oldies:
The flip of a single molecular switch helps create the mature neuronal connections that allow the brain to bridge the gap between adolescent impressionability and adult stability. Now Yale School of Medicine researchers have reversed the process, recreating a youthful brain that facilitated both learning and healing in the adult mouse.
Scientists have long known that the young and old brains are very different. Adolescent brains are more malleable or plastic, which allows them to learn languages more quickly than adults and speeds recovery from brain injuries. The comparative rigidity of the adult brain results in part from the function of a single gene that slows the rapid change in synaptic connections between neurons.
By monitoring the synapses in living mice over weeks and months, Yale researchers have identified the key genetic switch for brain maturation a study released March 6 in the journal Neuron. The Nogo Receptor 1 gene is required to suppress high levels of plasticity in the adolescent brain and create the relatively quiescent levels of plasticity in adulthood. In mice without this gene, juvenile levels of brain plasticity persist throughout adulthood. When researchers blocked the function of this gene in old mice, they reset the old brain to adolescent levels of plasticity.
That would be nice; I’ve found it is harder for me to absorb brand new material, though I have more context for other material.
Nature Cicadas have interesting wings: they have a structure that enables them to kill bacteria by an interesting mechanism:
The veined wing of the clanger cicada kills bacteria solely through its physical structure — one of the first natural surfaces found to do so. An international team of biophysicists has now come up with a detailed model of how this defence works on the nanoscale. The results are published in the latest issue of the Biophysical Journal1.
The clanger cicada (Psaltoda claripennis) is a locust-like insect whose wings are covered by a vast hexagonal array of ‘nanopillars’ — blunted spikes on a similar size scale to bacteria (see video, bottom). When a bacterium settles on the wing surface, its cellular membrane sticks to the surface of the nanopillars and stretches into the crevices between them, where it experiences the most strain. If the membrane is soft enough, it ruptures
Note: this is “rupture by stretching” rather than by puncturing.
Austerity during a recession does NOT drive down the deficit; remember that stimulus puts money into the economy.
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