Friday, April 5, 2013

New Anti-Rape Underwear Claims to Send Electric Shock Through ...

Engineering Students From SRM University Create Anti Rape Underwear

(Photo: Manisha Mohan, Niladri Basu Bal, Rimpi Tripathi via Techpedia)

Engineering students from India claim to have made underwear that could thwart would-be rapists by jolting them with an electric shock as they try to attack a woman.

The students from?SRM University in?Chennai call the prototype of the anti-rape underwear ?Society Harnessing Equipment? (SHE) and hope to someday introduce commercial versions of it.

?The lingerie with global positioning system (GPS), global system for mobile communications (GSM) and also pressure sensors, is capable of sending shock waves of 3,800 kV as well as alerts to parents and police,? Manisha Mohan, one of the developers, said according to Times of India.

Mohan continued that the underwear can shock up to 82 times.

?A person trying to molest a girl will get the shock of his life the moment pressure sensors get activated, and the GPS and GSM modules would send an SMS on emergency number 100, as well as to parents of the girl,? she told the Times.

According to a paper about the underwear, a camisole-like garmet is what has been developed so far with the shock technology placed in the chest.

?The circuit is placed near the bosom because in the attempt of rape or road?side eve?teasing, as per survey, women are attacked first on their bosom,? the paper stated.

Currently, the students are working with the?National Institute of Fashion Technology to find the best fabric for the product that would allow it to be washed without foiling the electronics.

Watch WPIX?s report about the anti-rape underwear:

?Studying in a convent girls school, we were always taught to be good to everyone around and bear a cheerful smile,? the engineering students stated in the paper about the underwear. ?After stepping into the real, cruel world we realized that our smile could not last for long as the threat to our purity and integrity always lingered on. Since the law makers take ages to come up with just laws and even after that, women are unsafe. Hence, we have initiated the idea of self?defense which protects the women from domestic, social and workplace harassment.?

Read more about the underwear in the paper posted on Techpedia here.

Source: http://www.theblaze.com/stories/2013/04/04/new-anti-rape-underwear-claims-to-send-electric-shock-through-would-be-assailants/

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Wednesday, April 3, 2013

Waist-deep in mud, Cameron rescues distressed sheep

LONDON (Reuters) - Bogged down by a stagnating economy and sinking poll ratings, British Prime Minister David Cameron ventured into a new swamp when he waded waist-deep into mud to rescue a drowning sheep.

Cameron was on his way back from visiting a farmer near his weekend home in the Oxfordshire countryside last month when he heard bleating and spotted a ewe that had got stuck in the mud after following her two lambs.

In jeans and rubber boots, Cameron waded into the swamp, followed by his two bodyguards, wrestled the sodden sheep and hoisted it onto safe ground, the Sun newspaper reported.

"When I got there, David (Cameron) was in the swamp, waist-deep in mud, along with the two police, who had all gone in there to help drag this sheep out," farmer Julian Tustian told the Daily Telegraph.

"He was brilliant, pulling, pushing and shoving. He was covered in mud, he looked a mess."

The ewe, which has since been nicknamed Swampy, has fully recovered from the ordeal, which unfolded on the evening of March 1, Tustian said. The lambs drowned.

The story of the lost sheep's messy rescue could have passed for an April fool joke but a Downing Street spokeswoman confirmed it had taken place.

Twitter users mocked what they labelled Cameron's "ewe turn", describing it as an unusual show of compassion from a prime minister imposing harsh welfare cuts and talking tough on immigration.

"Are you sure it was not the over way round? The ewe saved #Cameron from the swamp he's in?" wrote one user calling himself @Brianma68.

(Reporting by Natalie Huet; editing by Estelle Shirbon and Guy Faulconbridge)

Source: http://news.yahoo.com/waist-deep-mud-cameron-rescues-distressed-sheep-150906581.html

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New instrument will quickly detect botulinum, ricin, other biothreat agents

Apr. 2, 2013 ? Researchers at Sandia National Laboratories are developing a medical instrument that will be able to quickly detect a suite of biothreat agents, including anthrax, ricin, botulinum, shiga and SEB toxin.

The device, once developed, approved by the Food and Drug Administration and commercialized, would most likely be used in emergency rooms in the event of a bioterrorism incident.

"This is an unmet need for the nation's biodefense program," said Anup Singh, senior manager for Sandia's biological science and technology group. "A point-of-care device does not exist."

Sandia's work is funded by a recent grant -- nearly $4 million over four years -- from the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health. NIH has funded a number of recent projects at Sandia.

Sandia's biosciences and microfluidics program areas have continued to evolve with a string of notable projects, including:

  • MicroChemLab, a trailblazer in lab-on-a-chip technology, developed in the early 1990s
  • The "saliva device" and a follow-up technology, RapiDx, developed in the early-to-mid 2000s
  • SpinDx, the latest medical diagnostic tool developed at Sandia

"This will take things to the next level," said Singh. In addition to the broader suite of toxins and bacterial agents that the device would test for, the project includes comprehensive testing with animal (mouse) samples.

This is an important step, Singh said, since toxins may behave differently in live animals and humans than in laboratory blood samples. "We are getting closer and closer to translational elements of research, which involves testing in animal and clinical facilities. This is part of the maturation of our bioresearch activities at Sandia."

The project also will increase what SpinDx can do, he added.

"When you look for bacterial agents, you don't want to rely solely on proteins because you won't get the detection sensitivity you need," explained Singh. "So we are also using other methods that may lead to better detection limits and additional confirmation."

The new NIH project includes collaborators with expertise in animal modeling as well as device manufacturing.

The University of Texas Medical Branch, with whom Sandia enjoys a years-long partnership, together with the U.S. Department of Agriculture's Western Regional Research Center in Albany, Calif., are providing Sandia with expert insight into toxins and diseases at animal lab facilities. Bio-Rad, a manufacturer and distributor of a variety of devices and laboratory technologies, is serving as a consultant on the project to evaluate plans for product development, assist with manufacturers' criteria on the device that is developed, and provide important feedback when a prototype is built.

Although the latest NIH award represents a continuing success story for Sandia's microfluidics/bioresearch work, Singh stresses that it was part of a thoughtful multi-year strategy.

"You've got to keep innovating and coming up with the next thing," he said. "Every technology has its lifecycle. As good as SpinDx is, we know there will be other technologies, better technologies that come along in the next few years. We have to continue to innovate to meet the needs of our customers, understand what other competing technologies are being designed to solve the problems and develop technologies that provide an improvement."

The need for diagnostic devices for biodefense is not going away, Singh said, since there are always new diseases springing up that lack good diagnostic assays.

"Plus, we want dual-use devices that combat both man-made and nature-made problems," he added. "We're not just going to wait for the next anthrax letter incident to happen for our devices to be used and tested; we want them to be useful for other things as well, like infectious diseases."

Expanding into those areas, he said, will keep Sandia's bioresearch efforts engaged for years to come.

"That's where the value of the national labs really comes in," Singh said. "Our capabilities and culture are a very good fit for tackling long-term problems that require a sustained effort."

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Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_technology/~3/-XrvjLPE6GY/130402101146.htm

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NRA Study Backs Teacher, Staff Guns (ABC News)

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Targeting cholesterol buildup in eye may slow age-related vision loss

Targeting cholesterol buildup in eye may slow age-related vision loss [ Back to EurekAlert! ] Public release date: 2-Apr-2013
[ | E-mail | Share Share ]

Contact: Daniel Stimson
neinews@nei.nih.gov
301-496-5248
NIH/National Eye Institute

Targeting cholesterol metabolism in the eye might help prevent a severe form of age-related macular degeneration (AMD), one of the most common causes of blindness in older Americans, according to indications in a study in mice, which was supported by the National Institutes of Health.

Cholesterol build-up in arteries and veins, or atherosclerosis, occurs as a natural consequence of aging. Likewise, in AMD, cholesterol is known to accumulate in the eye, within deposits called drusen.

The study, published in Cell Metabolism, shows that large cells called macrophages appear to play a key role in clearing cholesterol from the eye, and that with aging, these cells become less efficient at this task. Eye drops containing a type of drug known to promote cholesterol release from macrophages, called a liver X receptor (LXR) agonist, helped restore macrophage function and prevent AMD progression in a mouse model. The study was led by Rajendra Apte, M.D., Ph.D., a professor of ophthalmology and vision sciences at Washington University in St. Louis.

An estimated 2 million Americans have AMD. The disorder causes damage to the macula, a region of the retina responsible for central, high-resolution vision. The macula is dense with light-sensing cells called photoreceptors, and is what humans rely on for tasks that require sharp vision, such as reading, driving, and recognizing faces. This sharp vision deteriorates in AMD, which can take two forms. In one, sometimes referred to as dry AMD, vision loss is due to a gradual loss of photoreceptors in the macula. In the other, referred to as wet or neovascular AMD, abnormal blood vessels grow under the macula, leaking blood and causing rapid damage to the photoreceptors.

"This study points to a novel strategy for early intervention to prevent the progression of AMD to the severe neovascular form of the disease," said Grace Shen, Ph.D., a program director at NIH's National Eye Institute, which funded the research.

An eye doctor can detect AMD prior to vision loss by looking for drusen, which are yellow deposits under the retina that contain cholesterol and other debris. Although small drusen are a normal part of aging, larger drusen typically indicate AMD.

What triggers neovascular AMD is unclear. Drusen, and the cholesterol within them, have been prime suspects. And based on genetic studies, including a recent genome-wide association analysis (http://www.nei.nih.gov/news/pressreleases/030313.asp), the immune system appears to play a role, too. (Also see http://www.nei.nih.gov/news/pressreleases/112712.asp.) But researchers have had few details to connect these two pathways.

Dr. Apte theorizes that macrophages, a type of immune cell, may provide a crucial link. Macrophages, literally "big eaters" in Greek, act like garbage collectors. They scavenge for debris, engulf it, and process it. In previous studies, Dr. Apte found that macrophages normally help limit the growth of new blood vessels in the eye, but with age, the cells lose this ability. The new study suggests that prior to these changes, old macrophages become less efficient at processing cholesterol.

"Ideally, macrophages should take up cholesterol, process it, and spit it out into the bloodstream. In AMD, we think the cells are ingesting cholesterol but not able to spit it out. So you get these inflamed macrophages that promote blood vessel growth," he said.

A protein called ABCA1 is needed for macrophages to release cholesterol into the bloodstream. In these experiments on mice, Dr. Apte and his team found that in old macrophages, there is a decrease in the level of ABCA1 protein. The researchers found a similar drop in ABCA1 levels in blood cellsthe source of macrophagesin samples donated by older people (ages 67-87) vs. younger ones (ages 25-34). The ABCA1 gene has been identified as a risk factor for AMD (http://www.nei.nih.gov/news/pressreleases/041210.asp).

To investigate the link between these changes and blood vessel growth, the researchers first performed tests in cell culture. When grown in a dish with blood vessel cells, young macrophages efficiently stopped the cells from multiplying, but old macrophages did not. Deleting the ABCA1 gene in young macrophages caused them to behave like old macrophages. Next, the researchers tried treating old macrophages with an LXR agonist; these drugs are known to enhance cholesterol transport from macrophages by turning on the ABCA1 gene. Exposure to the drug rejuvenated the old macrophages and enabled them to inhibit blood vessel cell growth.

The researchers also tested the LXR agonist in mice with an eye injury that produces abnormal blood vessel growth, similar to that seen in neovascular AMD. Eye drops of the drug significantly reduced this blood vessel growth when given several days before the injury.

Although there is no cure for AMD, a number of treatments are available. A combination of antioxidants and zinc known as the AREDS formulation can help slow vision loss in people with intermediate (but not early) stages of AMD. There are several treatments for advanced neovascular AMD; the most common choice involves injecting the eye with drugs that block the effects of a secreted protein involved in new blood vessel formation. However, such drugs must be given frequentlyup to once a monthand the repeated injections carry a risk of infection.

"If we could prevent the blood vessels from growing, it would be better than trying to eliminate them after the fact," Dr. Apte said. LXR agonists or other drugs to help macrophages clear away cholesterol might help, he said.

Having high blood cholesterol is not strongly related to AMD, and it remains to be determined whether statins and other cholesterol-modifying drugs on the market can reduce the risk of AMD. LXR agonists and other agents that modify cellular release of cholesterol are at various stages of investigation for many disorders. Some studies have found that when the drugs are given orally to mice, they appear to reduce atherosclerosis, but there have been concerns about potential toxic effects on the liver. Dr. Apte theorizes that therapy limited to the eye would not raise the same safety issues.

###

For more information about AMD, visit: http://www.nei.nih.gov/health/maculardegen/index.asp.

This research was supported in part by NEI grants EY016139, EY019287, and EY002687. Additional support was provided by NIH's National Heart, Lung, and Blood Institute (grants HL049373, HL094525, HL067773, HL107794, and HL30568) and National Institute of Diabetes and Digestive and Kidney Diseases (grant DK020579).

Reference: Sene A, and Khan A. et al. "Impaired cholesterol efflux in senescent macrophages promotes age-related macular degeneration." Cell Metabolism, published online April 2, 2013. DOI: http://dx.doi.org/10.1016/j.cmet.2013.03.009

The National Eye Institute, part of the National Institutes of Health, leads the federal government's research on the visual system and eye diseases. NEI supports basic and clinical science programs that result in the development of sight-saving treatments. For more information, visit http://www.nei.nih.gov.

About the National Institutes of Health (NIH):

NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.


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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.


Targeting cholesterol buildup in eye may slow age-related vision loss [ Back to EurekAlert! ] Public release date: 2-Apr-2013
[ | E-mail | Share Share ]

Contact: Daniel Stimson
neinews@nei.nih.gov
301-496-5248
NIH/National Eye Institute

Targeting cholesterol metabolism in the eye might help prevent a severe form of age-related macular degeneration (AMD), one of the most common causes of blindness in older Americans, according to indications in a study in mice, which was supported by the National Institutes of Health.

Cholesterol build-up in arteries and veins, or atherosclerosis, occurs as a natural consequence of aging. Likewise, in AMD, cholesterol is known to accumulate in the eye, within deposits called drusen.

The study, published in Cell Metabolism, shows that large cells called macrophages appear to play a key role in clearing cholesterol from the eye, and that with aging, these cells become less efficient at this task. Eye drops containing a type of drug known to promote cholesterol release from macrophages, called a liver X receptor (LXR) agonist, helped restore macrophage function and prevent AMD progression in a mouse model. The study was led by Rajendra Apte, M.D., Ph.D., a professor of ophthalmology and vision sciences at Washington University in St. Louis.

An estimated 2 million Americans have AMD. The disorder causes damage to the macula, a region of the retina responsible for central, high-resolution vision. The macula is dense with light-sensing cells called photoreceptors, and is what humans rely on for tasks that require sharp vision, such as reading, driving, and recognizing faces. This sharp vision deteriorates in AMD, which can take two forms. In one, sometimes referred to as dry AMD, vision loss is due to a gradual loss of photoreceptors in the macula. In the other, referred to as wet or neovascular AMD, abnormal blood vessels grow under the macula, leaking blood and causing rapid damage to the photoreceptors.

"This study points to a novel strategy for early intervention to prevent the progression of AMD to the severe neovascular form of the disease," said Grace Shen, Ph.D., a program director at NIH's National Eye Institute, which funded the research.

An eye doctor can detect AMD prior to vision loss by looking for drusen, which are yellow deposits under the retina that contain cholesterol and other debris. Although small drusen are a normal part of aging, larger drusen typically indicate AMD.

What triggers neovascular AMD is unclear. Drusen, and the cholesterol within them, have been prime suspects. And based on genetic studies, including a recent genome-wide association analysis (http://www.nei.nih.gov/news/pressreleases/030313.asp), the immune system appears to play a role, too. (Also see http://www.nei.nih.gov/news/pressreleases/112712.asp.) But researchers have had few details to connect these two pathways.

Dr. Apte theorizes that macrophages, a type of immune cell, may provide a crucial link. Macrophages, literally "big eaters" in Greek, act like garbage collectors. They scavenge for debris, engulf it, and process it. In previous studies, Dr. Apte found that macrophages normally help limit the growth of new blood vessels in the eye, but with age, the cells lose this ability. The new study suggests that prior to these changes, old macrophages become less efficient at processing cholesterol.

"Ideally, macrophages should take up cholesterol, process it, and spit it out into the bloodstream. In AMD, we think the cells are ingesting cholesterol but not able to spit it out. So you get these inflamed macrophages that promote blood vessel growth," he said.

A protein called ABCA1 is needed for macrophages to release cholesterol into the bloodstream. In these experiments on mice, Dr. Apte and his team found that in old macrophages, there is a decrease in the level of ABCA1 protein. The researchers found a similar drop in ABCA1 levels in blood cellsthe source of macrophagesin samples donated by older people (ages 67-87) vs. younger ones (ages 25-34). The ABCA1 gene has been identified as a risk factor for AMD (http://www.nei.nih.gov/news/pressreleases/041210.asp).

To investigate the link between these changes and blood vessel growth, the researchers first performed tests in cell culture. When grown in a dish with blood vessel cells, young macrophages efficiently stopped the cells from multiplying, but old macrophages did not. Deleting the ABCA1 gene in young macrophages caused them to behave like old macrophages. Next, the researchers tried treating old macrophages with an LXR agonist; these drugs are known to enhance cholesterol transport from macrophages by turning on the ABCA1 gene. Exposure to the drug rejuvenated the old macrophages and enabled them to inhibit blood vessel cell growth.

The researchers also tested the LXR agonist in mice with an eye injury that produces abnormal blood vessel growth, similar to that seen in neovascular AMD. Eye drops of the drug significantly reduced this blood vessel growth when given several days before the injury.

Although there is no cure for AMD, a number of treatments are available. A combination of antioxidants and zinc known as the AREDS formulation can help slow vision loss in people with intermediate (but not early) stages of AMD. There are several treatments for advanced neovascular AMD; the most common choice involves injecting the eye with drugs that block the effects of a secreted protein involved in new blood vessel formation. However, such drugs must be given frequentlyup to once a monthand the repeated injections carry a risk of infection.

"If we could prevent the blood vessels from growing, it would be better than trying to eliminate them after the fact," Dr. Apte said. LXR agonists or other drugs to help macrophages clear away cholesterol might help, he said.

Having high blood cholesterol is not strongly related to AMD, and it remains to be determined whether statins and other cholesterol-modifying drugs on the market can reduce the risk of AMD. LXR agonists and other agents that modify cellular release of cholesterol are at various stages of investigation for many disorders. Some studies have found that when the drugs are given orally to mice, they appear to reduce atherosclerosis, but there have been concerns about potential toxic effects on the liver. Dr. Apte theorizes that therapy limited to the eye would not raise the same safety issues.

###

For more information about AMD, visit: http://www.nei.nih.gov/health/maculardegen/index.asp.

This research was supported in part by NEI grants EY016139, EY019287, and EY002687. Additional support was provided by NIH's National Heart, Lung, and Blood Institute (grants HL049373, HL094525, HL067773, HL107794, and HL30568) and National Institute of Diabetes and Digestive and Kidney Diseases (grant DK020579).

Reference: Sene A, and Khan A. et al. "Impaired cholesterol efflux in senescent macrophages promotes age-related macular degeneration." Cell Metabolism, published online April 2, 2013. DOI: http://dx.doi.org/10.1016/j.cmet.2013.03.009

The National Eye Institute, part of the National Institutes of Health, leads the federal government's research on the visual system and eye diseases. NEI supports basic and clinical science programs that result in the development of sight-saving treatments. For more information, visit http://www.nei.nih.gov.

About the National Institutes of Health (NIH):

NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.


[ Back to EurekAlert! ] [ | E-mail | Share Share ]

?


AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.


Source: http://www.eurekalert.org/pub_releases/2013-04/nei-tcb040213.php

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'G.I. Joe: Retaliation' Offers Easter Eggs For Die-Hard Fans

The franchise's latest installment managed to work in a few nods to the classic Joe cartoons and comics between explosions.
By Brett White


Dwayne Johnson in "G.I. Joe: Retaliation"
Photo: Paramount

Source: http://www.mtv.com/news/articles/1704645/gi-joe-retaliation-easter-eggs.jhtml

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Teachers' gestures boost math learning

Monday, April 1, 2013

Students perform better when their instructors use hand gestures ? a simple teaching tool that could yield benefits in higher-level math such as algebra.

A study published in Child Development, the top-ranked educational psychology journal, provides some of the strongest evidence yet that gesturing may have a unique effect on learning. Teachers in the United States tend to use gestures less than teachers in other countries.

"Gesturing can be a very beneficial tool that is completely free and easily employed in classrooms," said Kimberly Fenn, study co-author and assistant professor of psychology at Michigan State University. "And I think it can have long-lasting effects."

Fenn and Ryan Duffy of MSU and Susan Cook of the University of Iowa conducted an experiment with 184 second-, third- and fourth-graders in Michigan elementary classrooms.

Half of the students were shown videos of an instructor teaching math problems using only speech. The others were shown videos of the instructor teaching the same problems using both speech and gestures.

The problem involved mathematical equivalence (i.e., 4+5+7=__+7), which is known to be critical to later algebraic learning. In the speech-only videos, the instructor simply explains the problem. In the other videos, the instructor uses two hand gestures while speaking, using different hands to refer to the two sides of the equation.

Students who learned from the gesture videos performed better on a test given immediately afterward than those who learned from the speech-only video.

Another test was given 24 hours later, and the gesture students actually showed improvement in their performance while the speech-only students did not.

While previous research has shown the benefits of gestures in a one-on-one tutoring-style environment, the new study is the first to test the role of gestures in equivalence learning in a regular classroom.

The study also is the first to show that gestures can help students transfer learning to new contexts ? such as transferring the knowledge learned in an addition-based equation to a multiplication-based equation.

Fenn noted that U.S. students lag behind those in many other Western countries in math and have a particularly hard time mastering equivalence problems in early grades.

"So if we can help them grasp this foundational knowledge earlier," she said, "it will help them as they learn algebra and higher levels of mathematics."

###

Michigan State University: http://www.newsroom.msu.edu

Thanks to Michigan State University for this article.

This press release was posted to serve as a topic for discussion. Please comment below. We try our best to only post press releases that are associated with peer reviewed scientific literature. Critical discussions of the research are appreciated. If you need help finding a link to the original article, please contact us on twitter or via e-mail.

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Source: http://www.labspaces.net/127534/Teachers__gestures_boost_math_learning

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