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Comment by Dr. Krishna Kumari Challa on March 17, 2015 at 8:22am

BIOENGINEERING
A synthetic fibrin cross-linking polymer for modulating clot properties and inducing hemostasis

New gel can stop wounds from bleeding

And could find applications on the battlefield, or in the toolkits of emergency response teams.
Traumatic injuries resulting from gunshot wounds or traffic accidents, can often be fatal if the injured person doesn’t receive prompt medical care.

Now, an injectable polymer material that encourages faster, more durable blood clotting at wound sites, could stop bleeding following these life-threatening injuries.
The material, known as PolySTAT, was developed by engineers at the University of Washington in the US, and mimics a natural protein in our body that helps strengthen blood clots.

The team says that following injection, their wound healing polymer “circulates innocuously in the blood, identifies sites of vascular injury, and promotes clot formation to stop bleeding”.

So far they have only tested their polymer on rats, but report in the press release that 100 percent of the animals injected survived “a typically-lethal injury to the femoral artery”.
The results have been published in the journal Science Translational Medicine
http://stm.sciencemag.org/content/7/277/277ra29

Comment by Dr. Krishna Kumari Challa on March 17, 2015 at 8:08am

A small success for scientists in antibiotic search: European biologists have discovered a bacteria-killing compound in common mushrooms that grow in horse dung. Unusually for an antibiotic, copsin is a protein; but laboratory trials showed it to have the same effect on bacteria as traditional antibiotics.

Chemists around the world are involved in a race against time to find a solution to the growing problem of bacteria becoming resistant to antibiotics. It's a major threat to the health of the global population, which had long assumed that antibiotics would always be available to cure bacterial illness.
copsin in the common inky cap mushroom Coprinopsis cinerea that grows on manure, while researching how the fungus and various bacteria affected each other's growth. According to lead researcher, post-doc Andreas Essig, horse manure's rich substrate is key.

"Horse dung is a very rich substrate that harbours a diversity of micro-organisms, including fungi and bacteria," said Essig. "Now these micro-organisms are in a constant competition for nutrients and space and it's therefore very likely to find potent antibiotics in such an environment, which are used by the different organisms to inhibit the growth of the competitors."
"Horse dung is a very rich substrate that harbours a diversity of micro-organisms, including fungi and bacteria," said Essig. "Now these micro-organisms are in a constant competition for nutrients and space and it's therefore very likely to find potent antibiotics in such an environment, which are used by the different organisms to inhibit the growth of the competitors."
Essig and his colleagues from ETH Zurich and the University of Bonn cultivated the fungus in a laboratory, along with several different types of bacteria, and found that C. cinerea killed certain bacteria. Further research demonstrated that the copsin produced by the mushroom was responsible for this antibiotic effect.

"Now copsin kills bacteria by binding to an essential cell wall building block".
When you disrupt the cell wall synthesis bacteria usually dies rapidly. The binding pattern of copsin on this building block is very unique and therefore copsin is active against bacteria resistant to conventional antibiotics."
Copsin is a protein, whereas traditional antibiotics are often non-protein organic compounds. It belongs to the group of defensins, a class of small proteins produced by numerous to counter disease-causing micro-organisms. In fact, the human body produces defensins in the skin and mucous membranes to protect itself against infections.

http://www.jbc.org/content/early/2014/10/23/jbc.M114.599878

Comment by Dr. Krishna Kumari Challa on March 15, 2015 at 1:34pm

How wounds are healed....
In recent years, researchers have gained a better understanding of the molecular machinery of cell migration, but not what directs it to happen in the first place. What, exactly, is orchestrating this system common to all living organisms?

The answer, it turns out, involves delicate interactions between biomechanical stress, or force, which living cells exert on one another, and biochemical signaling.
The University of Arizona researchers discovered that when mechanical force disappears -- for example at a wound site where cells have been destroyed, leaving empty, cell-free space -- a protein molecule, known as DII4, coordinates nearby cells to migrate to a wound site and collectively cover it with new tissue. What's more, they found, this process causes identical cells to specialize into leader and follower cells. Researchers had previously assumed leader cells formed randomly.
The team observed that when cells collectively migrate toward a wound, leader cells expressing a form of messenger RNA, or mRNA, genetic code specific to the DII4 protein emerge at the front of the pack, or migrating tip. The leader cells, in turn, send signals to follower cells, which do not express the genetic messenger. This elaborate autoregulatory system remains activated until new tissue has covered a wound.

The same migration processes for wound healing and tissue development also apply to cancer spreading, the researchers noted. The combination of mechanical force and genetic signaling stimulates cancer cells to collectively migrate and invade healthy tissue.
With this new knowledge, researchers can re-create, at the cellular and molecular levels, the chain of events that brings about the formation of human tissue. Bioengineers now have the information they need to direct normal cells to heal damaged tissue, or prevent cancer cells from invading healthy tissue.
http://www.nature.com/ncomms/2015/150313/ncomms7556/full/ncomms7556...

Comment by Dr. Krishna Kumari Challa on March 15, 2015 at 12:34pm

Comment by Dr. Krishna Kumari Challa on March 15, 2015 at 12:29pm

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Comment by Dr. Krishna Kumari Challa on March 15, 2015 at 12:25pm

According to science, practice doesn't make you perfect!

So forget what you've been told, 10,000 hours of practice isn't guaranteed to turn you into an expert. Here is why:

There's a long-standing myth that, in order to master a skill, all it takes is roughly 10,000 hours of practice. Scientists have debunked the myth once and for all, and shown that, while some people can become an expert with 10,000 hours of practice - or less - many can't, and there's a whole lot more involved than just hard work. In fact, an international team of psychologists found that deliberate practice can only explain around one-third of the difference in skill levels in chess players and musicians.

This leaves "the majority of the reliable variance unexplained and potentially explainable by other factors". Those factors, we're assuming, are natural talent and genetic ability.

-Journal "Intelligence"

http://www.sciencedirect.com/science/article/pii/S0160289614000087

The researchers came to this conclusion after analysing data taken across six previous studies of chess competitions (1,082 subjects in total) and eight studies of musicians (628 subjects), and looking for any kind of correlation between practice and success. What they found was that, well, there kinda wasn't one, and there were huge variations in how much of a role practice seemed to have played in success.

One chess player, for example, had taken 26 years to reach a level that another reached in a mere two years. Clearly, there's more at work than just the sheer volume of hours practiced, the study (and a similar one by the same authors published in May [2014]) argues.

http://www.sciencedirect.com/science/article/pii/S0160289613000421

"The evidence is quite clear," wrote lead author David Hambrick from Michigan State University in the US in a press release in 2013, "that some people do reach an elite level of performance without copious practice, while other people fail to do so despite copious practice."

Comment by Dr. Krishna Kumari Challa on March 14, 2015 at 9:18am

Stem cells lurking in tumors can resist treatment​​​​
Till now we have heard about the good side of stem cells. Now time for some not-so-good news about these angels:
Scientists are eager to make use of stem cells’ extraordinary power to transform into nearly any kind of cell, but that ability also is cause for concern in cancer treatment. Malignant tumors contain stem cells, prompting worries among medical experts that the cells’ transformative powers help cancers escape treatment.
New research proves that the threat posed by cancer stem cells is more prevalent than previously thought. Until now, stem cells had been identified only in aggressive, fast-growing tumors. But a mouse study at Washington University School of Medicine in St. Louis shows that slow-growing tumors also have treatment-resistant stem cells. The low-grade brain cancer stem cells identified by the scientists also were less sensitive to anticancer drugs. By comparing healthy stem cells with stem cells from these brain tumors, the researchers discovered the reasons behind treatment resistance, pointing to new therapeutic strategies.
The research results appear online March 12 in Cell Reports.
http://www.cell.com/cell-reports/abstract/S2211-1247%2815%2900199-0...

Comment by Dr. Krishna Kumari Challa on March 13, 2015 at 9:40am

Research reported today by Tufts University biologists shows for the first time that bioelectrical signals among cells control and instruct embryonic brain development and manipulating these signals can repair genetic defects and induce development of healthy brain tissue in locations where it would not ordinarily grow.

The research reveals that bioelectric signaling regulates the activity of two cell reprogramming factors (proteins that can turn adult cells into stem cells), which for the first time were analyzed in Xenopus laevis embryos, which share many evolutionary traits with humans. Results appear in the March 11, 2015, edition of the Journal of Neuroscience.

http://www.jneurosci.org/content/35/10/4366.short

Comment by Dr. Krishna Kumari Challa on March 12, 2015 at 8:44am

Comment by Dr. Krishna Kumari Challa on March 11, 2015 at 9:55am

Irisin – a myth rather than an exercise-inducible myokine

The myth of Irisin - the exercise hormone:

The discovery of the "exercise hormone" irisin three years ago and more than 170 related papers about it since have been called into question by recent research showing they were based on flawed testing kits.

Previous studies suggested that the hormone irisin -- named for the Greek messenger goddess Iris -- travels from muscle to fat tissue after exercise to tell fat cells to start burning energy instead of storing it. The finding ignited hope and press coverage that irisin could hold the key to fighting diabetes and obesity, perhaps one day taking the form of a pill that could melt away the pounds without the hassle of a workout.

But new research from an international team of scientists has found that the antibodies used to measure levels of irisin in blood were poorly vetted and nonspecific. These researchers argue that the irisin levels reported by commercial kits were actually due to unknown blood proteins, misconstruing the role of the hormone in human metabolism.

The study, appearing March 9 in the journal Scientific Reports, directly tested the antibodies used in previous analyses and showed that they cross-reacted with proteins other than irisin, yielding a false positive result. Furthermore, none of the proteins detected by these test kits in any human or animal blood samples were the correct size to be irisin.

http://www.nature.com/srep/2015/150309/srep08889/full/srep08889.html

"From the start, the study of irisin has been complicated by unvalidated reagents and contradictory data that have raised flags about the existence of irisin and its role in humans and other species," said Harold P. Erickson, Ph.D., an author of the study and professor of cell biology and biochemistry at Duke University School of Medicine. "We provide compelling evidence that the signals reported by previous studies were due to non-specific blood proteins, not irisin. Hopefully, our findings will finally convince other researchers to stop chasing a myth."

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