ORIGINAL: OBR Review
by: Roundtable Review News
by: Roundtable Review News
Friday, 2nd August 2013
BAY AREA
New app puts smartphones to work for science If you have ever wondered what it might be like to walk on an asteroid or wished you could improve the lives of people around the world, you can now get a little closer to these dreams by simply charging your smartphone. A new Android app developed at Berkeley through the Berkeley Open Infrastructure for Network Computing (BOINC) aims to use your smartphone to advance computationally intensive research. The app, also called BOINC, allows users to donate idle computing power to projects that would otherwise require cost-prohibitive supercomputers. BOINC was available as of July 22 from the Google Play Store for Android versions 2.3 and later and by default only runs when the phone is plugged in, has greater than 95% charge, and is connected to WiFi. The projects currently available through BOINC include
BAY AREA
New app puts smartphones to work for science If you have ever wondered what it might be like to walk on an asteroid or wished you could improve the lives of people around the world, you can now get a little closer to these dreams by simply charging your smartphone. A new Android app developed at Berkeley through the Berkeley Open Infrastructure for Network Computing (BOINC) aims to use your smartphone to advance computationally intensive research. The app, also called BOINC, allows users to donate idle computing power to projects that would otherwise require cost-prohibitive supercomputers. BOINC was available as of July 22 from the Google Play Store for Android versions 2.3 and later and by default only runs when the phone is plugged in, has greater than 95% charge, and is connected to WiFi. The projects currently available through BOINC include
- Asteroids@Home, which aims to better define the physical properties of asteroids;
- FightAIDS@Home, which searches for more effective AIDS treatments;
- Einstein@Home, which searches radio telescope data to identify pulsars; and
- other math and natural science projects that deal with the analysis of complex algorithms surrounding large quantities of data.
SAN DIEGO
UC San Diego receives grant to promote science at the intersection of biology and physics A professor of biology and physics at UCSD, Suckjoon Jun, has received a $1.15 million grant from the National Science Foundation (NSF) to create “boot camps” designed to introduce local high school and college students to quantitative biology. Jun describes quantitative biology as the application of “quantitative rigor” traditionally found in the physical sciences to biological questions. For example, this approach can be used to model complex processes such as drug interactions in human patients before the drugs are actually tested in clinical trials. In Jun’s lab, he utilizes a device he developed to analyze cell growth at the single cell level. Dubbed the “mother machine”, the instrument allows Jun’s lab to probe how cells sense their size and when to divide, and has potential to shed light on a variety of basic biological problems, such as the aberrant cell division that occurs in cancer. The NSF grant pairs Jun with a biology professor at San Diego State University, Anca Segall, who will help establish and run the boot camps. The goal of the boot camps, Jun says, is to first “spread the culture of quantitative biology” among young scientists in the San Diego area, and then to implement quantitative biology curriculum and undergraduate research opportunities at local universities.
LOS ANGELES
New amyloid-targeting compound for Alzheimer’s discovered Researchers at the University of California, Los Angeles have identified compounds that target amyloid beta fibrils, the protein aggregates found in abundance in the brains of Alzheimer’s patients. The research team, led by UCLA professor David Eisenberg, employed a structure-based approach to identify promising compounds – a technique that has been used for drug design in infectious and metabolic diseases, but had not yet been applied to neurodegenerative diseases like Alzheimer’s. To identify their candidate compounds,
- the team used their detailed knowledge of the atomic structure of the amyloid beta protein to find compounds that would interact with that structure. They first computationally screened 18,000 compounds, and
- then tested those with a strong potential for binding amyloid beta in a cell culture model. Of the tested compounds, they identified 8 compounds and 3 compound derivatives that significantly protected cells from amyloid beta’s toxic effects. Interestingly, these compounds did not reduce protein aggregation in culture, but they did increase amyloid fibril stability and reduce cell toxicity.
Happiness may aid proper gene expression in immune cells If you’re happy and you know it, your genes will surely show it according to a new study from UCLA and the University of North Carolina. What you may not know is that what type of happiness yours is will also affect your genes. Previous research has established that during periods of stress, threat, or uncertainty, the genes related to the inflammatory immune response are turned on, whereas the activity of those related to antiviral responses significantly decreases. The question is then does happiness and well-being have a similar effect? Barbara Fredrickson of the University of North Carolina and Steven Cole of UCLA’s Cousins Center for Psychoneuroimmunology sought to answer this by assessing the happiness of 80 healthy adults while accounting for potentially problematic psychological and behavioral factors. The study, published in the current online edition of PNAS, further divides the happiness measurements into two different categories:
- eudaimonic well-being and
- hedonic well-being.
LONDON
Aggressive form of leukemia puts stem cells to sleep Scientists from Queen Mary, University of London have found that malignant cells comprising Acute Myeloid Leukemia (AML), an aggressive blood cancer, actually put their stem cell counterparts in the bone marrow to sleep, rather than outcompeting them as originally believed. Conducted with support from the London Research Institute, this discovery could open the door to new treatment strategies where these ‘sleeping’ stem cells are reawakened. While healthy bone marrow generates the hematopoietic stem cells that become our various blood cell types, including red blood cells and platelets, the bone marrow of AML patients is instead colonized by leukemic myeloid cells incapable of any further development. Dr. David Taussig, who led the research project, said, “The widely accepted explanation has held that AML causes bone marrow failure by depleting the bone marrow of normal hematopoietic stem cells by killing or displacing them. However, we have found that samples of bone marrow in both mice models and patients with AML contain the same, or more, of these normal stem cells than usual. So the cancer isn’t getting rid of them, instead it appears to be turning them off so they aren’t going on to form healthy blood cells. If we can find out how the cancer cells are doing this, we can look at exploiting it to find ways to wake these stem cells up.”
Monogamy as a mating strategy evolved due to infanticide Social monogamy arose relatively late in primate evolution – only about 16 million years ago. The scientific community have proposed three major hypotheses:
- Monogamy provides more effective parental care for infants;
- it prevents females from mating with rival males; or
- it protects against the risk of infanticide, which is very high among some primate species, including chimpanzees and gorillas, and is often explained by the desire of a rival male to quickly return a mother to a fertile state.
CAMBRIDGE
Second study finds an alternative explanation for the evolution of monogamy A comparative study carried out by researchers at the University of Cambridge has revealed that social monogamy, where one female and one breeding male are closely associated with each other over several breeding seasons, appears to have evolved as a mating strategy. This contrasts with previous theories that explained monogamy as a means to elicit extra parental care from the father. Instead, it has been suggested that paternal involvement evolved after the onset of monogamy. The research, published in Science, shows that monogamy in mammals evolved where males were unable to monopolise and defend multiple females. This generally corresponds to habitats with low densities of females. Furthermore, it was found that species with diets that rely on high quality but patchily distributed food sources are more likely to become monogamous. Although these findings were based on investigation of 2500 mammalian species, the human species was not included in the analysis, and the researchers are sceptical that the results tell us much about human breeding systems.
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