A virus that creates electricity
A virus called simply M13 has the power (literally) to change the world. A team of scientists at the Berkeley Lab have genetically engineered M13 viruses to emit enough electricity to power a small LED screen. M13 poses no threat to humans — it can only infect bacteria — but it could one day serve humanity by powering your laptop, or even your city.
Illustration by Iaroslav Neliubov via Shutterstock
UCLA researchers say they’ve shown that genetically engineered stem cells can attack HIV-infected cells in a living organism.
The ‘warrior’ cells have been shown to seek out and destroy HIV in mice.
“We believe that this study lays the groundwork for the potential use of this type of an approach in combating HIV infection in infected individuals, in hopes of eradicating the virus from the body,” says UCLA assistant professor of medicine Scott Kitchen.
The scientists had already identified the molecule known as the T cell receptor - which guides the T cell in recognizing and killing HIV-infected cells - cloned it and used it to genetically engineer human blood stem cells.
When these cells were placed in human thymus tissue that had been implanted in mice, they blossomed into a large population that could specifically target cells containing HIV proteins.
Now, the researchers have engineered human blood stem cells in much the same way and found that they can form mature T cells that can attack HIV in tissues where the virus resides and replicates.
In a series of tests on the mice’s peripheral blood, plasma and organs, they found that the number of CD4 ‘helper’ T cells — which die off as a result of HIV infection — increased, while levels of HIV in the blood decreased.
This shows that the engineered cells were able to develop and migrate to the organs to fight infection there.
“We believe that this is the first step in developing a more aggressive approach in correcting the defects in the human T cell responses that allow HIV to persist in infected people,” says Kitchen.
The researchers will now begin making T cell receptors that target different parts of HIV and that could be used in more genetically matched individuals, he says.
Bioluminescent bacteria!
Lol lol! hope you guys understand this!
(Source: kaylamayeux)
I hope this doesn’t happen to me.
ScienceDaily (Mar. 2, 2012) — St. Jude Children’s Research Hospital scientists have discovered a key enzyme structure in bacteria, a finding that lays the foundation for a new generation of antibiotics that are safer and less prone to drug resistance.
More than 70 years after the first sulfa drugs helped to revolutionize medical care and save millions of lives, St. Jude Children’s Research Hospital scientists have determined at an atomic level the mechanism these medications use to kill bacteria. The discovery provides the basis for a new generation of antibiotics that would likely be harder for bacteria to resist and cause fewer side effects.
The work focused on sulfa drugs and their target enzyme, dihydropteroate synthase (DHPS). Most disease-causing microorganisms need DHPS to help make the molecule folate, which is required for the production of DNA and some amino acids. Working with enzymes from gram-negative and gram-positive bacteria, researchers used a variety of techniques to determine for the first time the key intermediate structure DHPS forms during the chemical reaction to advance folate production. The structure also explains at a molecular level how sulfa drugs function and how resistance causing mutations help bacteria withstand them.
The findings mark a major advance in both microbial biochemistry and anti-microbial drug discovery. The study is published in the March 2 issue of the journal Science.
“The structure we found was totally unexpected and really opens the door for us and others to design a new class of inhibitors targeting DHPS that will help us avoid side effects and other problems associated with sulfa drugs,” said Stephen White, Ph.D., chair of the St. Jude Department of Structural Biology and the paper’s corresponding author.
Co-author Richard Lee, Ph.D., a member of the St. Jude Department of Chemical Biology and Therapeutics, added: “Now we want to leverage this information to develop drugs against the opportunistic infections that threaten so many St. Jude patients.”
Sulfa drugs were discovered in the 1930s and became the first antibiotic in widespread use. Although the drugs were early victims of antibiotic resistance, they are still widely used against emerging infectious diseases and to prevent infections in patients with weakened immune systems, including St. Jude patients undergoing cancer chemotherapy. The growing problem of antibiotic resistance has prompted renewed interest in sulfa drugs as a possible source of new therapeutic targets, Lee said.
Previous work had shown that sulfa drugs target DHPS and work by mimicking a molecule called pABA. DHPS advances folate production by accelerating the fusion of pABA and another molecule called dihydropteridine pyrophosphate (DHPP). Until now, however, scientists did not know exactly how the DHPS reaction occurred or how sulfa drugs disrupted the process.
Working on enzymes from gram-positive Bacillus anthracis and gram-negative Yersinia pestis, the bacteria that cause anthrax and plague, researchers first used computational methods to predict the enzyme’s activity. Next they used a technique called X-ray crystallography to capture the unfolding chemical reaction and confirm the prediction. X-ray crystallography involves bombarding proteins trapped in crystals with X-rays to determine the protein structure.
Researchers showed that DHPP binds to a specific pocket in DHPS. Aided by magnesium, the binding promotes the break-up of DHPP and release of pyrophosphate. Two long flexible loops then create an intermediate structure that sets the stage for pABA to enter and bind in a second short-lived pocket, allowing pABA to fuse with the cleaved DHPP. Investigators captured all four actors in the drama in a single crystal structure, including the intermediate cleaved DHPP molecule whose existence was previously unknown.
The results showed that the mechanism involves a chemical reaction known as an Sn1 reaction rather than the anticipated Sn2 reaction. “This is a key finding for drug discovery because it reveals chemical features of the DHPS enzyme’s active site that we can exploit in developing new drugs,” said study co-author Donald Bashford, Ph.D., an associate member of the St. Jude Department of Structural Biology.
The study also provided insights into sulfa drug resistance. Investigators showed that the binding sites of pABA and the sulfa drugs overlap, but that sulfa drugs extend beyond the pocket in which pABA binds. Mutations associated with drug resistance cluster around this extended region of the pABA pocket, which explains how mutations can prevent the drugs from binding without seriously affecting the binding of pABA. The work also highlights the transitory structure made by the two DHPS loops as a target for a new class of drugs that would be difficult for bacteria to develop resistance against.
“When we set out on this project eight years ago, a goal was to truly understand the catalytic mechanism of the DHPS protein and how the inhibitors targeting it work. I am ecstatic we’ve succeeded,” Lee said. The success grew out of an interdisciplinary effort and some luck, White said. The plague enzyme turned out to be well suited to this project. Unlike the DHPS enzymes from other bacteria, the two extended loops are free to form the short-lived structure and the pABA pocket when the enzyme is immobilized in the crystal.
(Source: donnesdistractions)
The debate around stem cell research has revolved around some of the very same issues that the abortion debate hinges on, namely, where the line between potential for human life and actual human life lies, and what to do when potentiality is weighed against problems and pressures that affect current, non-potential human beings. So, in some ways this new development in the field of stem cell research is tinged with irony.
Stem Cells: they don’t just have the potential to cure numerous degenerative diseases and neurological injuries, they also might also make it easier to make more babies.
If you remember your Sex Ed class (if you had one that was any good, or if you had one at all, not a guarantee in many places, including all over the U.S.) you’ll remember that men make tons and tons of their gametes, or cells that merge to make embryos. The male gamete is sperm and after hitting puberty men start to produce it, and do so for the rest of their lives. Women, however, are born with all the gametes they’ll ever have already sitting in their ovaries. When we hit puberty, we start dispensing those ova until we run out. Then, it’s Menopause City. This is the oft-quoted-sitcom-phrase Biological Clock: if a lady wants to have children, she’s got to make time in her life, career, and relationships to do it before then.
Research done in mice in the last decade indicates that there may be a surprising caveat to all this, however. Scientists have found cells in female mice that might be persuaded to create new eggs, and now we’ve found similar cells in the tissue of human women as well. Discovery is on the case, however, with some sobering words:
We feel compelled to point out that this paper doesn’t mean that we will be able to grow fresh new eggs in Petri dishes, and it doesn’t prove that in real, live women these cells actually mature into eggs that can develop into offspring. It does, however, provide an interesting chance to see whether egg production by these cells can be jump-started using drugs…
This research is pretty exciting, but not for the reasons that some media outlets have been citing. It is unlikely that this finding will result in Petri dishes thronging with lab-grown eggs that women can then use to replenish their dwindling stores. Cells grown in the artificial environment of the lab for long periods of time tend to get a little strange: they accumulate mutations at a fast clip, which wouldn’t bode well for pregnancies resulting from such eggs.
What it might be useful for, however, is fertility treatments on pre-menopausal women. For example, those whose ability to reproduce has been damaged by chemotherapy. The right chemicals might induce these stem cells to make more eggs, so that a simple pill or series of treatments could get them started and provide some fresh ova. The next step is for researchers to, under the UK’s stem cell regulatory laws, see if they can get any of the proto-ova they’ve grown to make it to full blown egg stage, and then see if they can be fertilized. Injecting lab grown cells into an actual woman is probably beyond what would be considered good ethics, but Discover says that enough indirect evidence for the technique’s success might drive other venues of research.
Bacteria-Killing Viruses Wield an Iron Spike
Tiny warfare involves tiny weapons. Now a group of biologists has finally described the tiny spike that a bacteriophage uses to invade its bacterial victims.
Bacteriophage are likely the most abundant biological entity on Earth. We know that any scoop of sea water or soil will have billions of bacteria in it. But just like the abundance of viruses that surround humans every day, these bacteria are vastly outnumbered and warding off phages, bacterial viruses.
At the bottom of their angular heads is a long protein shaft that they use to deliver their DNA into their victim. A new structure has been determined showing an iron-tipped spike at the tip of the shaft, almost like a nail to pierce the bacterial membrane.
(via ScienceNOW, images from Cell Press)
(via hemija)
Happy Valentines Day <3
Cancer Found in Ancient Mummy Caused by Genetics
A professor from American Univ. in Cairo says the discovery of prostate cancer in a 2,200-year-old mummy indicates the disease was caused by genetics, not environment. The genetics-environment question is key to understanding cancer.
Read more: http://www.laboratoryequipment.com/news-cancer-found-in-ancient-mummy-caused-by-genetics-013012.aspx
