Climate ups risk of toxic harm

CRC CARE

A leading scientist has warned that climate change could expose Australians to greater risks from toxic contamination. Increased flooding could release contaminants previously regarded as secure into groundwater, rivers, oceans, the food supply and the atmosphere, the director of the CRC for Contamination Assessment and Remediation of the Environment, Professor Ravi Naidu, said. “Most of our urban landfills contain highly toxic substances from past decades – and were designed for the climatic conditions at the time. These have now changed, with the risk of bigger and more frequent floods, droughts, heat and acidity releasing substances we thought were gone for good,” he says. Professor Naidu is inviting Federal, state, and Environmental Protection Agencies to rethink nationwide contamination and cleanup policy in light of the risk that yesterday’s poisons could be remobilised in our environment. “The floods in Queensland and northern NSW illustrate how things are changing – and how we can no longer count on toxic disposal systems designed half a century or more ago to work as well in future under changed climate conditions,” he says. “From now on all landfills and contaminated sites will need better flood protection upstream and high-tech contamination barriers downstream to filter the groundwater that leaches out of them, and remove the heavy metals, pesticides, hydrocarbons and organic toxins it contains.”  Other contaminated land containment systems such as cover systems, stabilisation, etc could also be adversely impacted by climate change via factors such as wet-dry and freeze-thaw cycles. Professor Naidu says that climate change also brings increased urgency to the task of rehabilitating contaminated lands. “Where you have a large area of contaminated land, it is often very hard for plants or soil microbes to regrow, leading to reduced carbon sequestration, which adds to climate change. Researchers are currently working on specially-adapted trees, grasses and soil microbes, which can be used to recover these sites, devastated by historic industrial and mining activities – but there is a need to speed up national efforts to adopt such solutions, he adds. Another form of contamination likely to accelerate under climate change is acidification. “Acid rain produced by the industrial release of sulphur dioxide from coal-fired power stations into the atmosphere is poisoning lakes, forests, and soils in the northern hemisphere. When soils become more acidic, they can release toxic heavy metals as well as carbon. “At the same time, the carbon dioxide we release when we use vehicles or fossil-fuelled electricity is increasing acidity in the world’s oceans and endangering their food chains,” Prof. Naidu explains. “There are engineering solutions to these problems, which involve trapping the gases before they enter the atmosphere and disposing of them safely – but they are costly and must be adopted universally.” These issues illustrate how climate change can affect the total toxic load delivered to society in its food, water and environment and the importance of acting in a timely fashion to prevent this from happening. “People often regard contamination as a local issue, and contaminants as things which tend to stay in one place or where they are put. “This is no longer the case. Man-made contamination by toxic organic chemicals and metals is already swirling around the planet in air, water and wildlife – and there is a risk that the changes unleashed by climate change will mobilise even more,” Prof. Naidu warns. “Containment of contaminants is critical in the sustainable management of legacy contaminants. It is not yet time to be alarmed – but we should be concerned. And we should certainly begin to think about the solutions.” He says Australian industries, including the mining, energy, and agriculture sectors, are world leaders in developing and implementing environmentally friendly and cost-effective solutions to contamination issues. “If Australia makes an early start in overcoming these unforseen impacts of climate change it will also position us as a world leader and exporter of clean, green solutions for a changing world. It will not only be healthy – it will also be profitable and create jobs.” Editor's Note: Original news release can be found here.

Why the middle finger has such a slow connection

Each part of the body has its own nerve cell area in the brain -- we therefore have a map of our bodies in our heads. The functional significance of these maps is largely unclear. What effects they can have is now shown by Ruhr-University Bochum (Germany) neuroscientists through reaction time measurements combined with learning experiments and "computational modeling." They have been able to demonstrate that inhibitory influences of neighboring "finger nerve cells" affect the reaction time of a finger.

The fingers on the outside – i.e. the thumb and little finger - therefore react faster than the middle finger, which is exposed to the "cross fire" of two neighbours on each side. Through targeted learning, this speed handicap can be compensated. The working group led by PD Dr. Hubert Dinse (Neural Plasticity Lab at the Institute for Neuroral Computation) report in the current issue of PNAS.

The researchers set subjects a simple task to measure the speed of decision: they showed them an image on a monitor that represented all ten fingers. If one of the fingers was marked, the subjects were to press a corresponding key as quickly as possible with that finger. The thumb and little finger were the fastest. The middle finger brought up the rear. "You might think that this has anatomical reasons or depends on the exercise" said Dr Dinse, "but we were able to rule that out through further tests. In principle, each finger is able to react equally quickly. Only in the selection task, the middle finger is at a distinct disadvantage."

To explain their observations, the researchers used computer simulations based on a so-called mean-field model. It is especially suited for modelling large neuronal networks in the brain. For these simulations, each individual finger is represented by a group of nerve cells, which are arranged in the form of a topographic map of the fingers based on the actual conditions in the somatosensory cortex of the brain. "Adjacent fingers are adjacent in the brain too, and thus also in the simulation", explained Dr. Dinse. The communication of the nerve cells amongst themselves is organised so that the nerve cells interact through mutual excitation and inhibition.

The computer simulations showed that the longer reaction time of the middle finger in a multiple choice task is a consequence of the fact that the middle finger is within the inhibition range of the two adjacent fingers. The thumb and little finger on the other hand only receive an inhibitory effect of comparable strength from one adjacent finger each. "In other words, the high level of inhibition received by the nerve cells of the middle fingers mean that it takes longer for the excitement to build up – they therefore react more slowly" said Dr. Dinse.

From the results of the computer simulation it can be concluded that weaker inhibition from the neighbouring fingers would shorten the reaction time of the middle finger. This would require a so-termed plastic change in the brain – a specialty of the Neural Plasticity Lab, which has been studying the development of learning protocols that induce such changes for years. One such protocol is the repeated stimulation of certain nerve cell groups, which the laboratory has already used in many experiments. "If, for example, you stimulate one finger electrically or by means of vibration for two to three hours, then its representation in the brain changes" explained Dr. Dinse. The result is an improvement in the sense of touch and a measurable reduction of the inhibitory processes in this brain area. This also results in the enlargement of the representation of the finger stimulated.

The Bochum researchers then conducted a second experiment in which the middle finger of the right hand was subjected to such stimulation. The result was a significant shortening of the reaction time of this finger in the selection task. "This finding confirms our prediction" Dr. Dinse summed up. Thus, for the first time, Bochum's researchers have established a direct link between the so-called lateral inhibitory processes and decision making processes. They have shown that learning processes that change the cortical maps can have far-reaching implications not only for simple discrimination tasks, but also for decision processes that were previously attributed to the so-called "higher" cortical areas.

More information: Claudia Wilimzig, Patrick Ragert, and Hubert R. Dinse. Cortical topography of intracortical inhibition influences the speed of decision making, PNAS (2012), doi/10.1073/pnas.1114250109

Provided by Ruhr-University Bochum

"Why the middle finger has such a slow connection." February 7th, 2012. http://medicalxpress.com/news/2012-02-middle-finger.html

 

Posted by
Robert Karl Stonjek

Parkinson's disease: Study of live human neurons reveals the disease's genetic origins

Parkinson's disease researchers at the University at Buffalo have discovered how mutations in the parkin gene cause the disease, which afflicts at least 500,000 Americans and for which there is no cure.

The results are published in the current issue of Nature Communications.

The UB findings reveal potential new drug targets for the disease as well as a screening platform for discovering new treatments that might mimic the protective functions of parkin. UB has applied for patent protection on the screening platform.

"This is the first time that human dopamine neurons have ever been generated from Parkinson's disease patients with parkin mutations," says Jian Feng, PhD, professor of physiology and biophysics in the UB School of Medicine and Biomedical Sciences and the study's lead author.

As the first study of human neurons affected by parkin, the UB research overcomes a major roadblock in research on Parkinson's disease and on neurological diseases in general.

The problem has been that human neurons live in a complex network in the brain and thus are off-limits to invasive studies, Feng explains.

"Before this, we didn't even think about being able to study the disease in human neurons," he says. "The brain is so fully integrated. It's impossible to obtain live human neurons to study."

But studying human neurons is critical in Parkinson's disease, Feng explains, because animal models that lack the parkin gene do not develop the disease; thus, human neurons are thought to have "unique vulnerabilities."

"Our large brains may use more dopamine to support the neural computation needed for bipedal movement, compared to quadrupedal movement of almost all other animals," he says.

Since in 2007, when Japanese researchers announced they had converted human cells to induced pluripotent stem cells (iPSCs) that could then be converted to nearly any cells in the body, mimicking embryonic stem cells, Feng and his UB colleagues saw their enormous potential. They have been working on it ever since.

"This new technology was a game-changer for Parkinson's disease and for other neurological diseases," says Feng. "It finally allowed us to obtain the material we needed to study this disease."

The current paper is the fruition of the UB team's ability to "reverse engineer" human neurons from human skin cells taken from four subjects: two with a rare type of Parkinson's disease in which the parkin mutation is the cause of their disease and two healthy subjects who served as controls.

"Once parkin is mutated, it can no longer precisely control the action of dopamine, which supports the neural computation required for our movement," says Feng.

The UB team also found that parkin mutations prevent it from tightly controlling the production of monoamine oxidase (MAO), which catalyzes dopamine oxidation.

"Normally, parkin makes sure that MAO, which can be toxic, is expressed at a very low level so that dopamine oxidation is under control," Feng explains. "But we found that when parkin is mutated, that regulation is gone, so MAO is expressed at a much higher level. The nerve cells from our Parkinson's patients had much higher levels of MAO expression than those from our controls. We suggest in our study that it might be possible to design a new class of drugs that would dial down the expression level of MAO."

He notes that one of the drugs currently used to treat Parkinson's disease inhibits the enzymatic activity of MAO and has been shown in clinical trials to slow down the progression of the disease.

Parkinson's disease is caused by the death of dopamine neurons. In the vast majority of cases, the reason for this is unknown, Feng explains. But in 10 percent of Parkinson's cases, the disease is caused by mutations of genes, such as parkin: the subjects with Parkinson's in the UB study had this rare form of the disease.

"We found that a key reason for the death of dopamine neurons is oxidative stress due to the overproduction of MAO," explains Feng. "But before the death of the neurons, the precise action of dopamine in supporting neural computation is disrupted by parkin mutations. This paper provides the first clues about what the parkin gene is doing in healthy controls and what it fails to achieve in Parkinson's patients."

He noted in this study that these defects are reversed by delivering the normal parkin gene into the patients' neurons, thus offering hope that these neurons may be used as a screening platform for discovering new drug candidates that could mimic the protective functions of parkin and potentially even lead to a cure for Parkinson's.

While the parkin mutations are only responsible for a small percentage of Parkinson's cases, Feng notes that understanding how parkin works is relevant to all Parkinson's patients. His ongoing research on sporadic Parkinson's disease, in which the cause is unknown, also points to the same direction.

Provided by University at Buffalo

"Parkinson's disease: Study of live human neurons reveals the disease's genetic origins." February 7th, 2012. http://medicalxpress.com/news/2012-02-parkinson-disease-human-neurons-reveals.html

 

Posted by
Robert Karl Stonjek

Shri Sai Baba Ji - Sangkat Haran Shri Sai Baba (Real Stories)

s

Brains of addicts are inherently abnormal: study

Drug addicts have inherited abnormalities in some parts of the brain which interfere with impulse control, said a British study published on Thursday.

Previous research has pointed to these differences, but it was unclear if they resulted from the ravages of addiction or if they were there beforehand to predispose a person to drug abuse.

Scientists at the University of Cambridge compared the brains of addicts to their non-addicted siblings as well as to healthy, unrelated volunteers and found that the siblings shared many of the same weaknesses in their brains.

That indicates that the brain vulnerabilities had a family origin, though somehow the siblings of addicts -- either due to environmental factors or other differences in brain structure -- were able to resist addiction.

"Presumably, the siblings must have some other resilience factors that counteract the familial vulnerability to drug dependence," said the study led by Karen Ersche of the University of Cambridge, published in the journal Science.

"An individual's predisposition to become addicted to stimulant drugs may be mediated by brain abnormalities linked to impaired self-control."

Researchers tested 50 biological sibling pairs, in which one was addicted to drugs and the other one had no history of chronic drug abuse. They also tested 50 healthy, unrelated pairs of people as a control group.

The tests involved measuring how well they could control their impulses in a stop-signal reaction time test that assesses how quickly a person can switch from following one set of instructions to another.

Addicts are known to have poor impulse control.

The researchers found that the sibling pairs -- even the non-addicts -- fared significantly worse on the test than the healthy volunteers.

Brain scans showed that the siblings shared some of the same weaknesses in the frontal lobe and its connections to the basal ganglia, which mediates motor, cognition and behavior.

In an accompanying Perspective article, Nora Volkow and Ruben Baler of the US National Institute on Drug Abuse said that knowing more about brain circuitry could help understand and treat other "impaired control" disorders, like obesity, pathological gambling, attention deficit hyperactivity disorder, and obsessive-compulsive disorders.

"Several childhood and adolescent interventions can improve executive function and self-control," though more study is needed to see how such work may or may not impact the brain, they wrote.

More information: http://www.science … 601.abstract

(c) 2012 AFP

"Brains of addicts are inherently abnormal: study." February 2nd, 2012. http://medicalxpress.com/news/2012-02-brains-addicts-inherently-abnormal.html

Posted by
Robert Karl Stonjek

Mental gyms reap younger minds

(Medical Xpress) -- A daily mental ‘work-out' has given a group of over 50s the brain performance of people several years younger, a Swinburne University of Technology clinical trial has shown.

The independent study is one of the first to examine brain training and shed light on its effects on mental processing speed.

The 34 Australians aged 53 to 75 achieved significant increases in mental processing speed - which underpins efficient daily decision-making and learning - after completing a popular US online brain-training program, Swinburne Professor of Cognitive Neuroscience Con Stough said.

"We found an improvement in simple reaction time of about 10 per cent compared to the control group, which is quite a lot. The intervention improved speed of processing which translates to younger brain performance," he said.

While the initial results were promising, Professor Stough cautioned that the study size was small and the findings needed to be replicated by other researchers on a larger scale.

"However if the research can be replicated it could suggest that speed of processing is improved so much that the training group might have ameliorated several years of cognitive ageing," Professor Stough said.

The results stand in contrast to the normal age-related deficits in cognitive abilities that have been consistently reported across a range of cognitive areas including processing speed, attention, episodic memory, spatial ability and executive function.

Professor Stough said if the results can be replicated, they could have important implications for both the longevity of older workers and enjoyment by retirees.

"A major societal health issue for an ageing population is not only the greater incidence of neurodegenerative disorders such as Alzheimer's disease, but also the impact of normal age-related cognitive decline. Up to 50 per cent of adults aged 64 and over have reported difficulties with their memory," he said.

Economic pressures meant people were staying in the workforce longer, and it made no sense for them to be leaving the workplace because of cognitive impairment unless it was necessary.

"We want them to be as active as possible as they get older and continue to enjoy the world and continue to engage in our community. So people are looking at these brain training programs - which are growing in number - but which have been subject to little research."

In the current independent study, the 34 individuals played www.mybraintrainer.com - which describes itself as the world's first and best mental gymnasium - for a minimum of 20 minutes a day over 21 days, and were compared to a control group that played Solitaire.

The computerised training consisted of reaction time, inspection time, short term memory for words, executive function, visual spatial acuity, arithmetic, visual spatial memory, visual scanning/discrimination and working memory, with tasks becoming increasingly more challenging.

Participants were tested at baseline, post-training and at a three-week follow-up using a battery of neuropsychological outcome measures. The results of the study have been accepted for publication in the journal Educational Gerontology.

Provided by Swinburne University of Technology

"Mental gyms reap younger minds." February 2nd, 2012. http://medicalxpress.com/news/2012-02-mental-gyms-reap-younger-minds.html

 

Posted by
Robert Karl Stonjek

What the Brain Hears

By recording nerve impulses in sound-processing regions of the brain, researchers can recreate the words people think.

By Edyta Zielinska | 

Flickr, Travis Isaacs

 

Researchers were able to reverse engineer the sounds of human speech using only patterns of neuron firing measured in subjects listening to such sounds.

They measured nerve impulses in one of the auditory regions of patients’ brains while playing them a recording of words and sentences.  After feeding the electrical impulses through an algorithm that interpreted certain characteristics of the sounds, such as volume changes between syllables in a word, the computer could recreate the words or sentences.  The research, published in PLoS Biology

 

 on Monday (January 31), could help improve treatment for people with aphasia, or locked-in syndrome.

“A major goal is to figure out how the human brain allows us to understand speech despite all the variability, such as a male or female voice, or fast or slow talkers,” first author Brian Pasley told Nature

 

. While the sounds made on the computer are still somewhat crude in comparison to actual speech, they are recognizable when heard following their natural counterpart. (Listen to a recording of the computer generated words

 

.)

True speech recognition from neuronal recordings may still be a ways off. But “this approach may enable [the authors] to start determining the kinds of transformations and representations underlying normal speech perception,” University College London neuroscientist Sophie Scott, who was not involved in the research, told Nature.

Source: TheScientist
http://the-scientist.com/2012/02/01/what-the-brain-hears/

 

Posted by
Robert Karl Stonjek

Peacock Dance at Thiruketheeswaram Temple

   Video by R.Kaliyugavarathan                                      

Nature and Flowers

Photography by R.Kaliyugavarathan 

New RNA-based therapeutic strategies for controlling gene expression

Nucleic Acid Therapeutics is an authoritative, peer-reviewed journal published bimonthly in print and online that focuses on cutting-edge basic research, therapeutic applications, and drug development using nucleic acids or related compounds to alter gene expression. ©2012, Mary Ann Liebert Inc., publishers

Small RNA-based nucleic acid drugs represent a promising new class of therapeutic agents for silencing abnormal or overactive disease-causing genes, and researchers have discovered new mechanisms by which RNA drugs can control gene activity. A comprehensive review article inNucleic Acid Therapeutics

 

, a peer-reviewed journal published by Mary Ann Liebert, Inc., details these advances.

Short strands of nucleic acids, called small RNAs, can be used for targeted gene silencing, making them attractive drug candidates. These small RNAs block gene expression through multiple RNA interference (RNAi) pathways, including two newly discovered pathways in which small RNAs bind to Argonaute proteins or other forms of RNA present in the cell nucleus, such as long non-coding RNAs and pre-mRNA.

Keith T. Gagnon, PhD, and David R. Corey, PhD, University of Texas Southwestern Medical Center, in Dallas, review common features shared by RNAi pathways for controlling gene expression and focus in detail on the potential for Argonaute-RNA complexes in gene regulation and other exciting new options for targeting emerging forms of non-coding RNAs and pre-mRNAs in the article "Argonaute and the Nuclear RNAs: New Pathways for RNA Mediated Control of Gene Expression

 

."

"The field of RNA-mediated control of gene expression is rapidly evolving and the article by Gagnon and Corey provides a highly informative and up-to-date review of this exciting and often surprising area of biomedical research. We are delighted to publish this important review for the field," says Co-Editor-in-Chief Bruce A. Sullenger, PhD, Duke Translational Research Institute, Duke University Medical Center, Durham, NC.

Provided by Mary Ann Liebert, Inc.

"New RNA-based therapeutic strategies for controlling gene expression." February 2nd, 2012. http://www.physorg.com/news/2012-02-rna-based-therapeutic-strategies-gene.html

 

Posted by

Robert Karl Stonjek

Emotional grief could lead to heart attack

In the past, suffering from a broken heart was simply a way to describe the emotional pain one felt when dealing with a personal misfortune—a breakup or even the death of a loved one.  

There is a physiological condition, known as broken heart syndrome or stress-induced cardiomyopathy, that does exist, says Imran Arif, MD, UC Health interventional cardiologist, but a new study shows that an actual heart attack can result from life tragedy.

"Stress-induced cardiomyopathy is a known temporary heart condition that causes sudden chest pain and feels like a heart attack,” Arif says, adding that stress and depression have been linked to heart disease and that sudden emotional stress or bad news has been linked to sudden cardiac death as well.

Arif says the symptoms of broken-heart syndrome may be brought on by the heart’s reaction to a surge of stress hormones, and as a result, part of the heart muscle suffers damage.

The newest study by researchers at Beth Israel Deaconess Medical Center and the Harvard School of Public Health in Boston shows that the day following the loss of a loved one, a person is 21 times more likely to suffer a heart attack, and the spike occurs even in people at a low risk for heart attack. The study was published in the journal Circulation on Jan. 9.

These researchers reviewed charts or interviewed nearly 2,000 adult heart attack survivors who suffered heart attacks between 1989 and 1994 and determined that 270 people experienced a heart attack within six months of losing someone important to them; 19 people lost a loved one the day before having a heart attack.

Arif says the same reaction to a surge of stress hormones in the body, leading to changes in the way blood clots, could be the reason that this occurs.

"Stress changes coagulation in the body, which increases the risk of heart attack,” Arif says, adding that stress also increases heart rate and blood pressure, which also raise risk for heart attack.

But regardless of whether it’s just emotional hurting, broken heart syndrome or a real heart attack, Arif warns to not ignore symptoms of an impending heart complication.

"Scientists in this study were not sure about how the grief and stress of losing a loved one leads to heart attack,” he says. "The same goes for the true mechanisms behind broken heart syndrome, but everyone should know that if you feel like you are having a heart attack—experiencing symptoms like chest discomfort, nausea, shortness of breath, cold sweats, dizziness or stomach pain—regardless of the cause, call 911 immediately.

"We have no control over tragedy around us, but knowing your risk for certain complications and realizing that you may not just be dealing with grief could save your life.”

Provided by University of Cincinnati

"Emotional grief could lead to heart attack." February 2nd, 2012. http://medicalxpress.com/news/2012-02-emotional-grief-heart.html

 

Posted by
Robert Karl Stonjek

Man mandir mein...Shirdi Sai Baba

Societal Control of Sugar Essential to Ease Public Health Burden, Experts Urge

A group of researchers argues that sugar -- which they say is fueling a global obesity pandemic -- should be controlled like alcohol and tobacco to protect public health. (Credit: © Alexey Bragin / Fotolia)

ScienceDaily — Sugar should be controlled like alcohol and tobacco to protect public health, according to a team of UCSF researchers, who maintain in a new report that sugar is fueling a global obesity pandemic, contributing to 35 million deaths annually worldwide from non-communicable diseases like diabetes, heart disease and cancer.

---

Non-communicable diseases now pose a greater health burden worldwide than infectious diseases, according to the United Nations. In the United States, 75 percent of health care dollars are spent treating these diseases and their associated disabilities.
In the Feb. 2 issue of Nature, Robert Lustig MD, Laura Schmidt PhD, MSW, MPH, and Claire Brindis, DPH, colleagues at the University of California, San Francisco (UCSF), argue that sugar's potential for abuse, coupled with its toxicity and pervasiveness in the Western diet make it a primary culprit of this worldwide health crisis.
This partnership of scientists trained in endocrinology, sociology and public health took a new look at the accumulating scientific evidence on sugar. Such interdisciplinary liaisons underscore the power of academic health sciences institutions like UCSF.
Sugar, they argue, is far from just "empty calories" that make people fat. At the levels consumed by most Americans, sugar changes metabolism, raises blood pressure, critically alters the signaling of hormones and causes significant damage to the liver -- the least understood of sugar's damages. These health hazards largely mirror the effects of drinking too much alcohol, which they point out in their commentary is the distillation of sugar.
Worldwide consumption of sugar has tripled during the past 50 years and is viewed as a key cause of the obesity epidemic. But obesity, Lustig, Schmidt and Brindis argue, may just be a marker for the damage caused by the toxic effects of too much sugar. This would help explain why 40 percent of people with metabolic syndrome -- the key metabolic changes that lead to diabetes, heart disease and cancer -- are not clinically obese.
"As long as the public thinks that sugar is just 'empty calories,' we have no chance in solving this," said Lustig, a professor of pediatrics, in the division of endocrinology at the UCSF Benioff Children's Hospital and director of the Weight Assessment for Teen and Child Health (WATCH) Program at UCSF.
"There are good calories and bad calories, just as there are good fats and bad fats, good amino acids and bad amino acids, good carbohydrates and bad carbohydrates," Lustig said. "But sugar is toxic beyond its calories."
Limiting the consumption of sugar has challenges beyond educating people about its potential toxicity. "We recognize that there are cultural and celebratory aspects of sugar," said Brindis, director of UCSF's Philip R. Lee Institute for Health Policy Studies. "Changing these patterns is very complicated"
According to Brindis, effective interventions can't rely solely on individual change, but instead on environmental and community-wide solutions, similar to what has occurred with alcohol and tobacco, that increase the likelihood of success.
The authors argue for society to shift away from high sugar consumption, the public must be better informed about the emerging science on sugar.
"There is an enormous gap between what we know from science and what we practice in reality," said Schmidt, professor of health policy at UCSF's Philip R. Lee Institute for Health Policy Studies (IHPS) and co-chair of UCSF's Clinical and Translational Science Institute's (CTSI) Community Engagement and Health Policy Program, which focuses on alcohol and addiction research.
"In order to move the health needle, this issue needs to be recognized as a fundamental concern at the global level," she said.
The paper was made possible with funding from UCSF's Clinical and Translational Science Institute, UCSF's National Institutes of Health-funded program that helps accelerate clinical and translational research through interdisciplinary, interprofessional and transdisciplinary work.
Many of the interventions that have reduced alcohol and tobacco consumption can be models for addressing the sugar problem, such as levying special sales taxes, controlling access, and tightening licensing requirements on vending machines and snack bars that sell high sugar products in schools and workplaces.
"We're not talking prohibition," Schmidt said. "We're not advocating a major imposition of the government into people's lives. We're talking about gentle ways to make sugar consumption slightly less convenient, thereby moving people away from the concentrated dose. What we want is to actually increase people's choices by making foods that aren't loaded with sugar comparatively easier and cheaper to get."

Skin Augmented With Spider-Silk Stops a Speeding Bullet

By Clay Dillow 

Skin Augmented With Spider-Silk Stops a Bullet via New Scientist

Extolling the many virtues of spider silk is something of a trend these days, as the fine yet remarkably hardy material continues to best even the strongest synthetic materials (a good spider silk weave is supposedly four times stronger than Kevlar). But this latest application makes transgenic, spider silk-producing goats seem simple by comparison: A bioengineered skin so tough that it stops a speeding bullet from penetrating.
To be perfectly fair up front, the bullet in the first clip in the video below is moving at half speed. Repeated with a round moving at a full 1,080 feet per second, the skin gives way. But both half-speed and full-speed tests were also conducted with real human skin and human skin augmented with regular silkworm silk, as well as with piglet skin. In all cases, the bullet won out. The only exception was the bioengineered spider silk tissue.
Which begs the question: Is it possible to someday augment human skin to make it tougher--possibly even bulletproof? Probably not, and even if so that certainly wouldn’t make the human body impervious to the other factors involved in being struck by a bullet (like the sheer bone-breaking, potentially heart-stopping impact).
Regardless, chalk it up as another potential application for nature’s toughest fiber, one that’s getting closer and closer to mass-production and integration into a range of materials that need strengthening.


[New Scientist]

Handheld Pathogen Sensor Could Diagnose HIV in 30 Minutes

Two techs are better than one

By Clay Dillow 

Chaining Synthetic DNA to Detect Pathogens Two Y-shaped structures of synthetic DNA attach themselves to the target molecule in different places. From there, the other two arms of the "Y" can link with other similar DNA structures, causing pathogens to chain together into easily detectable clumps. Cornell

Working with support of the Bill & Medlinda Gates Foundation’s Grand Challenge to develop field-worthy point-of-care diagnostics for the developing world, a couple of Cornell researchers are mashing up their individual inventions to create a handheld pathogen detector that can quickly diagnose pathogens ranging from chlamydia and tuberculosis to HIV.
The portable device is a blend of a synthetic DNA tagging technology developed by Cornell biological and environmental engineering prof Dan Luo and a CMOS chip developed by Edwin Kan, an electrical and computer engineering professor. Luo’s technology does the actual detecting, while Kan’s chip is able to identify and respond to the amplified signals generated by the sensor. The result: a handheld disease targeting machine that can diagnose pathogens in half an hour rather than days.

The sensor works via Y-shaped segments of synthetic DNA that Luo’s research group devised. At the bottom of the Y the team installed antibody designed to target and lock onto a certain pathogen. On one of the upper arms it placed a molecule that will link up with other similar molecules in the presence of UV light. In practice, two slightly different Y-structures are introduced to a sample, where they attach themselves to opposite sides of any target pathogen molecule they come in contact with. But tiny strands of Y-shaped DNA attaching themselves to a single molecule doesn’t send a very strong signal--the entire combined structure is still so small that only highly tuned and very precise sensors or microscopes could detect that the DNA had attached itself to the pathogen at all. But if you have a bunch of DNA structures attached to a bunch of pathogen molecules, the signal is clearly amplified. As such, the handheld sensor will bathe samples in UV light causing the DNA structures to begin binding together in a chain that is far easier to detect than a single pathogen molecule or a single DNA structure. Kan’s sensor chip can then measure both the mass and charge of molecules that come in contact with it. From those measurements, the chip can tell whether the synthetic DNA chain is towing pathogen particles along with it--and thus if they are present in the sample or not.
Add some nanofluidics and a power source to the mix, and you basically have an inexpensive handheld diagnostic device ready to go to work far from the convenience of hospitals and well-stocked medical labs. Further tests will ensure that the system is durable enough to take a beating out in the field and still return valid diagnostic results. More via Cornell.