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Behavioral economics show that women tend to make better investments than men - Washington Post

Behavioral economics show that women tend to make better investments than men - Washington Post | Personal Statement ideas | Scoop.it
Washington Post Behavioral economics show that women tend to make better investments than men Washington Post It's happy hour at Hanaro in Bethesda, and I'm with my wife.
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Top stories in health and medicine, October 9, 2013 - KevinMD.com

Top stories in health and medicine, October 9, 2013 - KevinMD.com | Personal Statement ideas | Scoop.it
Top stories in health and medicine, October 9, 2013.
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Dual Action Virolytic Entry Inhibitor ("DAVEI") neutralizes HIV virus by making it think it's attached to a cell

Dual Action Virolytic Entry Inhibitor ("DAVEI") neutralizes HIV virus by making it think it's attached to a cell | Personal Statement ideas | Scoop.it

Pinning down an effective way to combat the spread of the human immunodeficiency virus, the viral precursor to AIDS, has long been a challenge for scientists and physicians, because the virus is an elusive one that mutates frequently and, as a result, quickly becomes immune to medication. A team of Drexel University researchers is trying to get one step ahead of the virus with a microbicide they’ve created that can trick HIV into “popping” itself into oblivion.

 

Its name is DAVEI - which stands for “Dual Action Virolytic Entry Inhibitor”- and it can pull a fast one on HIV. DAVEI was invented and tested by scientists from Drexel’s College of Engineering; School of Biomedical Engineering, Science and Health Systems; and College of Medicine, and is the latest in a new generation of HIV treatments that function by specifically destroying the virus without harming healthy cells.

 

“While several molecules that destroy HIV have recently been announced, DAVEI is unique among them by virtue of its design, specificity and high potency,” said Dr. Cameron Abrams, a professor in Drexel’s College of Engineering and a primary investigator of the project.

 

A team co-led by Abrams and Dr. Irwin Chaiken in the Department of Biochemistry and Molecular Biology in Drexel’s College of Medicine, and including Dr. Mark Contarino and doctoral students Arangassery Rosemary Bastian and R. V. Kalyana Sundaram, developed the chimeric recombinantly engineered protein – that is, a molecule assembled from pieces of other molecules and engineered for a specific purpose, in this case to fight HIV. Their research will be published in the October edition of the American Society for Microbiology’s Antimicrobial Agents and Chemotherapy.

 

The idea behind DAVEI was to design a molecule that hijacks the virus’s fusion machinery, the tools it uses to attach to and attack a healthy cell, and tricks the virus into destroying itself. HIV invades a healthy cell by first attaching via protein “spikes” that then collapse to pull viral and cell membranes together, fusing them and allowing the genetic contents of the virus to enter the healthy cell. The cell is rewired by the viral genetic material into producing more viruses instead of performing its normal function, which, in the case of cells infected by HIV, involves normal immunity. AIDS is the result.

 

“We hypothesized that an important role of the fusion machinery is to open the viral membrane when triggered, and it follows that a trigger didn't necessarily have to be a doomed cell,” Abrams said. “So we envisioned particular ways the components of the viral fusion machinery work and designed a molecule that would trigger it prematurely,” Abrams said.

 

The team designed DAVEI from two main ingredients. One piece, called the Membrane Proximal External Region (MPER), is itself a small piece of the fusion machinery and interacts strongly with viral membranes. The other piece, called cyanovirin, binds to the sugar coating of the protein spike.

 

Working together, the MPER and cyanovirin in DAVEI “tweak” the fusion machinery in a way that mimics the forces it feels when attached to a cell.    

“For lack of a better term, DAVEI 'tricks' the virus into 'thinking' it is about to infect a healthy cell, when, in fact, there is nothing there for it to infect,” Abrams said. “Instead, it releases its genetic payload harmlessly and dies.”


Via Dr. Stefan Gruenwald
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Why Laughter May Be the Best Pain Medicine: Scientific American

Why Laughter May Be the Best Pain Medicine: Scientific American | Personal Statement ideas | Scoop.it
Laughter with friends releases endorphins, the brain's "feel-good" chemicals (http://t.co/pkeo3tnPOv http://t.co/MIbAgu6pLJ)...
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3-D-printed bacteria in any number of shapes may unlock secrets of antibiotic resistance and disease

3-D-printed bacteria in any number of shapes may unlock secrets of antibiotic resistance and disease | Personal Statement ideas | Scoop.it

Bacteria are often social creatures. Suspended in colonies of varying shapes and sizes, these microbes communicate with their brethren and even other bacterial species — interactions that can sometimes make them more deadly or more resistant to antibiotics.

 

Now, bacterial colonies sculpted into custom shapes by a 3-D printer could be a key to understanding how some antibiotic-resistant infections develop. The new technique uses methods similar to those employed by commercial 3-D printers, which extrude plastic, to create gelatin-based bacterial breeding grounds. These microbial condos can be carved into almost any three-dimensional shape, including pyramids and nested spheres. This 3-D-printing technique could be used to investigate questions like "how many bacteria have to be clustered together, and in what size and what shape, in order for that microcolony to start acting differently than the cells do on their own," said study researcher Jason Shear, a professor of chemistry and biochemistry at the University of Texas at Austin. 

 

Bacterial clustering is important precisely because bacteria bunched together often act differently than a single cell on its own. In some cases, bacteria even cement themselves together and onto surfaces with a gluelike substance, creating biofilms that are stubbornly resistant to antibiotics or the immune system. The plaque dentists scrape off your teeth is a biofilm that can contain dozens of interacting bacterial types, Shear told LiveScience.

 

More deadly are the biofilms that gather in the lungs of patients with the respiratory disease cystic fibrosis. Antibiotics can halt scattered bacteria that cause lung infections in these patients, but persistent biofilms on the lung tissue lurk, waiting to spit out new bacterial vagabonds. The result, Shear said, is a cycle of infection and treatment that is often fatal for the patient. On average, people with cystic fibrosis live to just their mid-30s, according to the Cystic Fibrosis Foundation.

 

Understanding biofilms and other bacterial communities is crucial for learning how to breach bacterial defenses, but "really, technologies just haven't been there," Shear said.


Via Dr. Stefan Gruenwald
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Wide range of differences, mostly unseen, among humans: Silent mutations more significant than expected

Wide range of differences, mostly unseen, among humans: Silent mutations more significant than expected | Personal Statement ideas | Scoop.it

No two human beings are the same. Although we all possess the same genes, our genetic code varies in many places. And since genes provide the blueprint for all proteins, these variants usually result in numerous differences in protein function. But what impact does this diversity have? Bioinformatics researchers at Rutgers University and the Technische Universitaet Muenchen (TUM) have investigated how protein function is affected by changes at the DNA level. Their findings bring new clarity to the wide range of variants, many of which disturb protein function but have no discernible health effect, and highlight especially the role of rare variants in differentiating individuals from their neighbors.

 

The slightest changes in human DNA can result in an incorrect amino acid being incorporated into a protein. In some cases, all it takes is for a single base to be substituted in a person's DNA, a variant known as a single nucleotide polymorphism (SNP). "Many of these pointmutations have no impact on human health. However, of the roughly 10,000 'missense' SNPs in the human genome – that is, SNPs affecting the protein sequence – at least a fifth can change the function of the protein," explains Prof. Yana Bromberg of the Department of Biochemistry and Microbiology at Rutgers University. "And in some cases, the affected protein is so important and the change so large that we have to wonder why the person with this mutation is still healthy."

 

Furthermore, two unrelated individuals have thousands of different mutations that affect proteins. Previously, scientists did not fully understand how this large number of mutations affects the coding sequences of DNA. To investigate these "silent" mutations, Bromberg joined forces with Rutgers colleague Prof. Peter Kahn and Prof. Burkhard Rost at TUM.

 

"We found that many of the mutations are anything but silent," declares Rost, head of the TUM Chair for Bioinformatics and a fellow of the TUM Institute for Advanced Study. The research indicates an extremely wide range of mutations. Many SNPs, for example, are neutral and do not affect protein function. Some, however, cause pathogenic disruption to protein functionality. "There is a gray area between these extremes," Rost explains. "Some proteins have a reduced biological function but are tolerated by the organism and therefore do not directly trigger any disease."

 

The research team analyzed over one million SNPs from a number of DNA databases. They used artificial learning methods to simulate the impact of DNA mutations on the function of proteins. This approach enabled them to investigate the impact of a large number of SNPs quickly and efficiently.

 

The study's findings suggest that, with respect to diversity in protein function, the individual differences between two people are greater than previously assumed. "It seems that humans can live with many small changes in protein function," says Rost. One conclusion the researchers draw is that the wide functional spectrum of proteins must play a key role in evolution. In addition, Bromberg says, "Protein functional diversity may also hold the key to developing personalized medicine."

 

http://www.pnas.org/cgi/doi/10.1073/pnas.1216613110


Via Dr. Stefan Gruenwald
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