Novel Bicycle Saddle Prevents Chafing, Pain and Other Damage Associated With the Genital Area

Researchers at the University of Alicante have developed a novel bicycle saddle that prevents chafing, pain and other damage associated with the genital area as impotence and prostatitis.

It is a hinged articulated saddle whose coccyx-support narrow front and wide back have been articulately joined. The front part is mobile while the back is fixed, and both may change their positions at the user's will.
This new concept of bicycle saddle is designed and patented by researchers from the University of Alicante's Institute of Physics Applied to Science and Technology and the Department of Physics at the Polytechnic Higher School.
The UA researcher, Alfonso Panchón Ruiz, head of the research work, explained that "the main advantage of this new design compared to traditional saddles, is that it allows -at the user's will- to rest and recover from fatigue the perineal area suffering lasting intense compression for which they are not designed anatomically."
"The classic bicycle saddle has a unitary structure formed by a rigid body in anteroposterior direction which makes that, permanently, the perineal tissues, which are soft and not ready to withstand these forces, are being compressed, independent of the position taken by the user. For this reason, soon after starting the exercise, nerves and arteries reach high levels of compression, which causes problems associated with lack of blood supply, such as numbness and affection of the genitals in both men and women, and in the long run, significant pathologies requiring medical treatment may appear," Alfonso Panchón says.
Up to date, only two solutions have been found, either to go up on the pedals, on a typical pedalling, visible both in professional races and gyms, or dismounting the bike and standing up, abandoning thus, the exercise started.
In this sense, Alfonso Panchón explains that "with this new design, it is not the user who must be separated and rising from the seat, but it is the saddle which separates spinning or scrolling down to the perineal area of the user. Thus, it radically prevents pressure on that area, immediately improving the blood supply to the affected areas, resulting in functional recovery of the tissues concerned.
Another advantage is that the user does not lose balance control ability in driving, regardless of the conditions of use, race, walk, gym, mountain, etc.., and this allows users to make new lateral movements on the anterior mobile part as well as immediately recover -at their will- the traditional full seat with a slight initial reverse movement.
Also, with this model of saddle, more than ten centimetres can be released between the seat and handlebars, which can be availed with competitive advantage in declines as it allows an aerodynamic position on very steep slopes.
The research team has a prototype that allows them to check the health and medical benefits of this innovative aerodynamic concept of saddle. Currently, there is nothing similar on the market, so it is a technology with great potential for international marketing.
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Where Do Muscles Get Their Power? Fifty-Year-Old Assumptions About Strength Muscled Aside

Doctors have a new way of thinking about how to treat heart and skeletal muscle diseases. Body builders have a new way of thinking about how they maximize their power. Both owe their new insight to high-energy X-rays, a moth and cloud computing.

The understanding of how muscles get their power has been greatly expanded with new results published online July 10 in the Royal Society journal Proceedings of the Royal Society B. The Royal Society is the U.K.'s national academy of sciences.
The basics of how a muscle generates power remain the same: Filaments of myosin tugging on filaments of actin shorten, or contract, the muscle -- but the power doesn't just come from what's happening straight up and down the length of the muscle, as has been assumed for 50 years.
Instead, University of Washington-led research shows that as muscles bulge, the filaments are drawn apart from each other, the myosin tugs at sharper angles over greater distances, and it's that action that deserves credit for half the change in muscle force scientists have been measuring.
Researchers made this discovery when using computer modeling to test the geometry and physics of the 50-year-old understanding of how muscles work. The computer results of the force trends were validated through X-ray diffraction experiments on moth flight muscle, which is very similar to human cardiac muscle. The X-ray work was led by co-author Thomas Irving, an Illinois Institute of Technology professor and director of the Biophysics Collaborative Access Team (Bio-CAT) beamline at the Advanced Photon Source, which is housed at the U.S. Department of Energy's Argonne National Laboratory.
A previous lack of readily available access to computational power and X-ray diffraction facilities are two reasons that this is the first time these findings have been documented, speculated lead-author C. David Williams, who earned his doctorate at the UW while conducting the research, and now is a postdoctoral researcher at Harvard University. Currently, X-ray lightsources have a waiting list of about three researchers for every one active experiment. The APS is undergoing an upgrade that will greatly increase access and research power and expedite data collection.
The new understanding of muscle dynamics derived from this study has implications for the research and use of all muscles, including organs.
"In the heart especially, because the muscle surrounds the chambers that fill with blood, being able to account for forces that are generated in several directions during muscle contraction allows for much more accurate and realistic study of how pressure is generated to eject blood from the heart," said co-author Michael Regnier, a UW bioengineering professor. "The radial and long axis forces that are generated may be differentially compromised in cardiac diseases and these new, detailed models allow this to be studied at a molecular level for the first time. They also take us to a new level in testing therapeutic treatments targeted to contractile proteins for both cardiac and skeletal muscle diseases. "
This study gives scientists and doctors a new basis for interpreting experiments and understanding the mechanisms that regulate muscle contraction. Researchers have known for sometime that the muscle filament lattice spacing changes over the length-tension curve, but its importance in generating the steep length dependence of force has not been previously demonstrated.
"The predominant thinking of the last 50 years is that 100 percent of the muscle force comes from changes as muscles shorten and myosin and actin filaments overlap. But when we isolated the effects of filament overlap we only got about half the change in force that physiologists know muscles are capable of producing," Williams said.

The rest of the force, he said, should be credited to the lattice work of filaments as it expands outward in bulging muscle -- whether in a body builder's buff biceps or the calves of a sinewy marathon runner.
"One of the major discoveries that David Williams brought to light is that force is generated in multiple directions, not just along the long axis of muscle as everyone thinks, but also in the radial direction," said Thomas Daniel, UW professor of biology and co-author on the paper.
"This aspect of muscle force generation has flown under the radar for decades and is now becoming a critical feature of our understanding of normal and pathological aspects of muscle," Daniel added.
Since the 1950s scientists have had a formula -- the so-called length-tension curve -- that accurately describes the force a muscle exerts at all points from fully outstretched, when every weight lifter knows there is little strength, to the middle points that display the greatest force, to the completely shortened muscle when, again, strength is minimized.
Williams developed computer models to consider the geometry and physics at work on the filaments at all those points.
"The ability to model in three dimensions and separate the effects of changes in lattice spacing from changes in muscle length wouldn't even have been possible without the advent of cloud computing in the last 10 years, because it takes ridiculous amounts of computational resources," Williams said Story source

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Marital Status Reduces Risk of Death from HIV/AIDS for Men

At the height of the AIDS epidemic in the 1980s men who were married were significantly less likely to die of HIV/AIDS than their divorced or otherwise single counterparts, according to a University of California, Riverside analysis of new mortality data for that era.

For women, marital status had little impact on who was more likely to die of the disease. But race proved to be a significant risk factor, with African-American women nine times more likely to die of HIV/AIDS and Latinas seven times more likely to die of the disease than white women. Those mortality rates were considerably higher than those for men of color compared to white men.
The study by UCR sociology professor Augustine Kposowa -- "Marital status and HIV/AIDS mortality: evidence from the U.S. National Longitudinal Mortality Study" -- is the first to examine the effects of marital status on deaths of individuals with HIV/AIDS. It appears in the International Journal of Infectious Diseases, the official publication of the International Society for Infectious Diseases.
Using data from a recent release of the U.S. National Longitudinal Mortality Study and the National Death Index, Kposowa tracked nearly 763,000 individuals age 15 and older between 1983 and 1994. A total of 410 of those individuals died of HIV/AIDS in that period of time.
"These data capture when HIV/AIDS was approaching pandemic level," Kposowa explained. "People were very afraid. The perception was that only men who had sex with men were getting infected, so no one was looking at risk factors for people who were married, widowed or separated."
Kposowa's analysis of 11 years of mortality data found that marital status was a significant risk factor for men, but not women. Divorced and separated men were more than six times more likely to die of AIDS than married men, and those who had never married were 13.5 times more likely to die of the disease than those who were married. African-American men were 2.7 times as likely to die of HIV/AIDS as white men, and Hispanic men were more than twice as likely to die of the disease as white men.
"It turns out that the big story for women is race, particularly for African-Americans and Latinos," Kposowa said. "The question is, why would Latino and African-American women have been more at risk of HIV?"
The most logical explanation, Kposowa believes, relates to how little was known in the 1980s about how the HIV virus was transmitted, and a health care system that historically disadvantages the poor.
"Those without care are more likely to be minority women," he said. "It's really a function of the health care system, who has access, and how soon people seek care. So in the 1980s, poor people and minorities, who often lack information about health care, were at greater risk of death from HIV/AIDS. By the time they presented themselves for health care, the disease would have progressed."
Kposowa said his assertion is supported by other studies showing that women of color typically receive less aggressive treatment for diseases such as cancer, and that African-Americans and Hispanics are less likely to be prescribed narcotic pain medications for back pain than whites even when one takes into account pain severity. He noted that in the US, post diagnosis cancer survival rates are much lower for people of color than whites.
"The elephant in the room is the health care system and the value we put on different people because of their color and background," the sociologist added. "We don't say that consciously, but it is why the Obama administration has put so much emphasis on reducing health disparities in this country."
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Cells in the Early Embryo Battle Each Other to Death for Becoming Part of the Organism

Spanish researchers at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) have found that during the early stages of mammalian development, embryonic cells embark on a battle for survival. Through this battle, the less active of these cells are eliminated by their stronger sisters.

The work is published today in the journal Nature.
This phenomenon, termed cell competition, occurs in a defined time window, between days 3 and 7 of mouse development. During this period all embryonic cells compete with each other, as explained by Dr. Cristina Claveria, first author of the study, and Dr. Miguel Torres, director of this work and Head of the Department of Cardiovascular Development and Repair at CNIC.
"Thanks to cell competition the developing organism optimizes itself by selecting the cells theoretically more capable of supporting vital functions throughout the life of the new individual," says Dr. Claveria. According to the authors, this would be particularly important in long-lived organisms, like humans, where the functionality of their tissues must be maintained throughout a long life.
Dr. Miguel Torres also explains that when cell competition is prevented, cells that normally would have lost the battle now become able to contribute to the new organism: "We think, however, that this organism will probably be less capable than the one which would have been formed under normal circumstances. In what sense will it be less adequate is a matter of great interest that we will address in the coming years."
Indeed, the researchers are able to determine in advance which cells will win this battle: those with higher levels of the Myc protein, an important controller of cell metabolic capacity. Moreover, using a new technique that they have developed for the production of genetic mosaics, they are able to manipulate the levels of Myc protein in cells, thus changing the outcome of the fight.
According to Claveria and Torres, the study shows that the early embryo is a mosaic of cells with very different levels of Myc ,in which cells with higher levels of Myc eliminate those with lower levels. However, it is important to understand that those who die are viable cells. "Their removal occurs only because the embryo has more suitable cells able to replace them, and therefore this is an optimization mechanism, not a repair one," the researchers point out.
A fascinating aspect of the work is the illustration that this battle does not waste cellular resources; dying loser cells are engulfed and digested by their winning neighbours, who then recycle and use all the nutrients for the benefit of the embryo. This research provides answers to some of the questions raised nearly forty years ago by Spanish scientists Ginés Morata and Pedro Ripoll, who in 1975 discovered cell competition in the fruit fly. On that occasion, by experimental manipulation, they described the phenomenon in the fly's wing. Since then cell competition has been suggested to be involved in multiple processes, including tumour progression and tissue regeneration; but never, until this study, had a natural function been described.

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Researchers Perform DNA Computation in Living Cells

Chemists from North Carolina State University have performed a DNA-based logic-gate operation within a human cell. The research may pave the way to more complicated computations in live cells, as well as new methods of disease detection and treatment.

Logic gates are the means by which computers "compute," as sets of them are combined in different ways to enable computers to ultimately perform tasks like addition or subtraction. In DNA computing, these gates are created by combining different strands of DNA, rather than a series of transistors. However, thus far DNA computation events have typically taken place in a test tube, rather than in living cells.
NC State chemist Alex Deiters and graduate student James Hemphill wanted to see if a DNA-based logic gate could detect the presence of specific microRNAs in human cells. The researchers utilized a DNA-based logic gate known as an "AND" gate that was engineered to respond to the presence of two specific microRNAs -- known as miRNA-21 and miRNA-122.
Just as computer operations utilize different inputs to create a particular output, the researchers' DNA-based Boolean logic gate was activated only when both miRNA-21 and miRNA-122 "inputs" were present in cells. If they were present, the gate generated an "output" by releasing a fluorescent molecule.
Deiters believes that use of these logic gates could lead to more accurate tests and treatments for human disease, especially cancer.
"The fluorescent molecule we used in this logic-gate design could be useful as a marker that identifies a cancer cell," he says. "Or, instead of directing the gate to release a fluorescent molecule in the presence of particular microRNAs, we could attach therapeutic agents that are released to treat the disease itself."
Their results appear in the Journal of the American Chemical Society. The research was funded in part by grants from the American Chemical Society and the American Cancer Society.

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