1. bpod-mrc:

    14 September 2014

    Blood Cleaner

    Microbial pathogens in the bloodstream can lead to sepsis, when the immune system goes wild in response to the infection, often causing organ failure and death. It usually takes days to identify the culprit, so doctors use broad-spectrum antibiotics, which are not very effective. Now, though, researchers have debuted a potential solution: an external device that removes pathogens and toxins from blood. As infected blood passes through the device, it’s mixed with magnetic nanobeads coated with engineered proteins that bind to a range of nasties. Pictured is a protein-coated magnetic bead (blue) binding to Escherichia coli. The bead-bound invaders are then pulled from the flowing blood by a magnet, before the cleansed blood is returned to the patient. When tested in infected rats, the device worked well: the cleansed blood brought down the number of inflammatory proteins and reduced the impact on the rats’ vital organs.

    Written by Daniel Cossins

    Image by Donald Ingber and colleagues
    Wyss Institute at Harvard, USA
    Copyright held by Nature Publishing Group
    Research published in Nature Medicine, September 2014

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  2. scienceisbeauty:

    Everything in this 1991 RadioShack ad exists in a single smartphone. This one and some other unexpected facts at Thinking Humanity: Unbelievable…These 23 Mind Blowing Facts Will DESTROY Your Understanding Of Time.  I’m pretty sure more than one surprises you.

  4. compoundchem:

    Ever wondered how much water/caffeine/alcohol you’d need to drink to reach a lethal dose? This graphic shows the median lethal dose for all three!

    Read more detail about LD50 tests in the accompanying post: http://wp.me/p4aPLT-ol

    (via we-are-star-stuff)


  5. For decades, health-conscious people around the globe have taken antioxidant supplements and eaten foods rich in antioxidants, figuring this was one of the paths to good health and a long life.
    Yet clinical trials of antioxidant supplements have repeatedly dashed the hopes of consumers who take them hoping to reduce their cancer risk. Virtually all such trials have failed to show any protective effect against cancer. In fact, in several trials antioxidant supplementation has been linked with increased rates of certain cancers. In one trial, smokers taking extra beta carotene had higher, not lower, rates of lung cancer.
    In a brief paper appearing today in The New England Journal of Medicine, David Tuveson, M.D. Ph.D., Cold Spring Harbor Laboratory Professor and Director of Research for the Lustgarten Foundation, and Navdeep S. Chandel, Ph.D., of the Feinberg School of Medicine at Northwestern University, propose why antioxidant supplements might not be working to reduce cancer development, and why they may actually do more harm than good.
    Their insights are based on recent advances in the understanding of the system in our cells that establishes a natural balance between oxidizing and anti-oxidizing compounds. These compounds are involved in so-called redox (reduction and oxidation) reactions essential to cellular chemistry.
    Oxidants like hydrogen peroxide are essential in small quantities and are manufactured within cells. There is no dispute that oxidants are toxic in large amounts, and cells naturally generate their own anti-oxidants to neutralize them. It has seemed logical to many, therefore, to boost intake of antioxidants to counter the effects of hydrogen peroxide and other similarly toxic “reactive oxygen species,” or ROS, as they are called by scientists. All the more because it is known that cancer cells generate higher levels of ROS to help feed their abnormal growth.
    Drs. Tuveson and Chandel propose that taking antioxidant pills or eating vast quantities of foods rich in antioxidants may be failing to show a beneficial effect against cancer because they do not act at the critical site in cells where tumor-promoting ROS are produced – at cellular energy factories called mitochondria. Rather, supplements and dietary antioxidants tend to accumulate at scattered distant sites in the cell, “leaving tumor-promoting ROS relatively unperturbed,” the researchers say.
    Quantities of both ROS and natural antioxidants are higher in cancer cells – the paradoxically higher levels of antioxidants being a natural defense by cancer cells to keep their higher levels of oxidants in check, so growth can continue. In fact, say Tuveson and Chandel, therapies that raise the levels of oxidants in cells may be beneficial, whereas those that act as antioxidants may further stimulate the cancer cells. Interestingly, radiation therapy kills cancer cells by dramatically raising levels of oxidants. The same is true of chemotherapeutic drugs – they kill tumor cells via oxidation.
    Paradoxically, then, the authors suggest that “genetic or pharmacologic inhibition of antioxidant proteins” – a concept tested successfully in rodent models of lung and pancreatic cancers—may be a useful therapeutic approach in humans. The key challenge, they say, is to identify antioxidant proteins and pathways in cells that are used only by cancer cells and not by healthy cells. Impeding antioxidant production in healthy cells will upset the delicate redox balance upon which normal cellular function depends.
    The authors propose new research to profile antioxidant pathways in tumor and adjacent normal cells, to identify possible therapeutic targets.
    Explore further: Blocking antioxidants in cancer cells reduces tumor growth in mice
    More information: “The Promise and Perils of Antioxidants for Cancer Patients” appears in The New England Journal of Medicine on July 10, 2014.
    Journal reference: New England Journal of Medicine
    Provided by Cold Spring Harbor Laboratory

  7. jtotheizzoe:

    The oldest living thing in the world: These actinobacteria, recovered from the subterranean brrrrr-osphere that is Siberian permafrost, are estimated to be 500,000 years old. While many ancient microbes have been revived from ancient dormant states, these bacterial cells have been continuously living for half a million years. It’s known that the bacteria aren’t mobile in the frozen Earth, so by radioactively dating the layers of soil around the microbes, scientists were able to estimate their age.

    Unable to divide and reproduce, these microbes were shown to be actively repairing their DNA despite the frigid temperatures, their enzymes uniquely adapted to an environment that would mean certain death for perhaps every other creature on Earth. While not growing, moving, or reproducing, this sort of cryostasis counts as living if you ask me (and the scientists who study them).

    What do you think this means for the possibility of life on other planets?

    (via Rachel Sussman and Brain Pickings. Check out the original 2007 research paper here)

  8. nevver:

    Papercraft, Varga Natália

    (via jtotheizzoe)

  9. bpod-mrc:

    12 July 2014

    Silver Bullet

    It’s long been the ambition of cancer researchers to find the ‘silver bullet’ to treat tumours. Now the dream may have come true, although so far only in the lab. Researchers have developed tiny silver nanoparticles that directly target tumour cells, smuggling in a deadly payload of cancer-killing drugs. They’ve found a way of coating the particles with different molecules that get taken up by specific types of cells, as well as fluorescent dyes that reveal their location. For example, the top two cells in this image have taken up particles that glow red, while the lower cell prefers the green ones. What’s more, the particles break down quickly if they’re not gobbled up by cells, potentially reducing side effects in the body. It’s still early days and there’s more work to do, but this technique could help to pull the trigger on cancer.

    Written by Kat Arney

    Image by Gary Braun and colleagues
    Sanford-Burnham Medical Research Institute, USA
    Originally published under a Creative Commons Licence (BY 4.0)
    Research published in Nature Materials, June 2014

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  10. Cholesterol Controlled for Good by Gene Therapy in Mice
    By Angela Zimm Jun 10, 2014 11:01 PM CT 0 Comments Email Print
    By altering how a liver gene works, scientists say they’ve developed a way to cut cholesterol permanently with a single injection, eliminating the need for daily pills to reduce the risk of heart attack.

    In a test in mice, scientists at the Harvard Stem Cell Institute and the University of Pennsylvania disrupted the activity of a gene, called PCSK9, that regulates cholesterol, the fatty material that builds up in veins, hindering blood flow. The process permanently dropped levels of the lipid by 35 to 40 percent, said Kiran Musunuru, the lead researcher.

    “That’s the same amount of cholesterol you’ll get with a cholesterol drug,” said Musunuru, who is a cardiologist and assistant professor at Harvard. “The kicker is we were able to do that with a single injection, permanently changing the genome. Once that changes, it’s there forever.”

    Pfizer Inc. (PFE)’s Lipitor and AstraZeneca Plc (AZN)’s Crestor, both of which target so-called bad cholesterol, are pills that are designed to be taken daily. The prospect of replacing them with the newly tested procedure may be 5 to 10 years away, Musunuru said in a telephone interview.

    The PCSK9 gene is the same one now being targeted by Amgen Inc., Sanofi (SAN) and Regeneron Pharmaceuticals Inc. (REGN) with experimental compounds designed to suppress the protein the gene produces. Certain rare PCSK9 mutations are found to cause high cholesterol and heart attacks. Good mutations also exist, and people with them have a heart attack risk that ranges from 47 to 88 percent below average, the researchers said.

    ‘Good Mutations’

    “It’s not too much of a leap to think that if it works as well in mice, it will work as well in humans,” said Musunuru, who works in the Cambridge, Massachusetts school’s Department of Stem Cell and Regenerative Biology. With one shot, a patient “would be like those people born with the good mutations.”

    The research was published yesterday in Circulation Research, a journal of the American Heart Association.

    The approach used a two-part genome-engineering technique that first targets the DNA sequence where the gene sits, and then creates a break in the system. The therapy was carried to the liver using an injected adenovirus.

    The genome-editing technique used in the experiment has only been around for about a year and a half, Musunuru said.

    The next step is to see how effective the therapy is in human cells, by using mice whose liver cells are replaced with human-derived liver cells, he said. Assessing safety will be the primary concern.

    To contact the reporter on this story: Angela Zimm in Boston at azimm@bloomberg.net

    To contact the editors responsible for this story: Reg Gale at rgale5@bloomberg.net Andrew Pollack