BUMBLEBEES SENSES AND INTERPRETATION OF SIGNALS TRANSMITTED BY FLOWERS

Dancing hairs alert bees to floral electric fields

Tiny, vibrating hairs may explain how bumblebees sense and interpret the signals transmitted by flowers, according to a study by researchers at the University of Bristol.

Although it's known that flowers communicate with pollinators by sending out electric signals, just how bees detects these fields has been a mystery -- until now.

Using a laser to measure vibrations, researchers found that both the bees' antenna and hairs deflect in response to an electric field, but the hairs move more rapidly and with overall greater displacements.

Researchers then looked at the bees' nervous system, finding that only the hairs alerted the bee's nervous system to this signal.

The findings, published in the international journal Proceedings of the National Academy of Sciences (PNAS) today, suggest that electroreception in insects may be widespread.

Electroreception may arise from the bees' hairs being lightweight and stiff, properties that confer a rigid, lever-like motion similar to acoustically sensitive spider hairs and mosquito antennae.

Dr Gregory Sutton, a Research Fellow in the University of Bristol's School of Biological Sciences, led the research. He said: "We were excited to discover that bees' tiny hairs dance in response to electric fields, like when humans hold a balloon to their hair. A lot of insects have similar body hairs, which leads to the possibility that many members the insect world may be equally sensitive to small electric fields."

Scientists are particularly interested in understanding how floral signals are perceived, received and acted upon by bees as they are critical pollinators of our crops.

Research into these relationships has revealed the co-evolution of flowers and their pollinators, and has led to the unravelling of this important network which keeps our planet green.

Electroreception is common in aquatic mammals. For example, sharks are equipped with sensitive, jelly-filled receptors that detect fluctuations in electric fields in seawater which helps them to home in on their prey.

The research was funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and The Royal Society.

TOXIN HEME, ESSENTIAL FOR LIFE

Heme, a poisonous nutrient, tracked by 'Green Lantern' sensor

Labile heme's movements illuminated for the first known time thanks to ratiometric sensor.

A pinch of poison is good for a body, at least if it's heme.

In minuscule amounts, it works in cells as an essential catalyst called a cofactor and as a signaling molecule to trigger other processes. Now, for the first known time, researchers have tracked those activities inside of cells.

"Poor heme management can cause things like Alzheimer's, heart disease, and some types of cancers, so cells have to do a good job of managing how much heme is available," said Amit Reddi, a biochemist and assistant professor at the Georgia Institute of Technology. "By having biosensors that can monitor heme in cells, we have this new window into how cells make this essential toxin available in carefully sparse concentrations," he said.

'Heme' as in 'hemoglobin'

People may recognize heme from its role at the core of hemoglobin, the component of red blood cells responsible for transporting oxygen. The ionic iron in the heme molecule is what the oxygen molecule sticks to.

In hemoglobin, the heme is embedded tightly in protein, rendering it non-toxic. Many scientists have long assumed that heme, even in other cells, is basically always static, held tight by the proteins it works with.

But the researchers' results shatter that assumption.

They published their findings in the Proceedings of the National Academy of Sciences, on Monday, May, 30, 2016. Their research is funded by the National Science Foundation and the National Institutes of Health.

Potentially hazardous nutrient

The labile heme serves as a nutrient instead of a poison. But to make sure things stay that way, heme needs to be carefully trafficked through the cell, Reddi said.

The research team, led by Reddi and Hanna, designed a fluorescent sensor molecule to keep tabs on that. With heme at very low baseline levels, the sensor lit up bright green then as heme concentration increased, it caused the light to fade out.

Using the heme sensors, Georgia Tech graduate student Osiris Martinez-Guzman found an enzyme, GAPDH, known for its involvement in breaking down sugar, that the team observed helping buffer cellular labile heme (iron protoporphyrin IX), which got tied up in proteins, leaving only a limited amount free for biochemical reactions.

When more labile heme is needed, nitric oxide, a signaling molecule, rapidly released heme from entangling proteins, so it could do jobs such as regulating gene expression.

'Green Lantern' glow

"If you increase nitric oxide, you see the green glowing sensor dim as the heme becomes labile then the glow brightens back up over time as heme gets bound up again," Reddi said.

Not having a sensor was one reason labile heme has not been previously observed, so the Georgia Tech researchers used a ratiometric fluorescence approach to design one that could be described a little like the comic book superhero "Green Lantern."

As hemes are attracted to him like, say, fans, they become clutter, said Reddi, the paper's principal investigator. "He holds them in front of his green light, and they block it, making it appear dimmer."

"Ratiometric fluorescent techniques have been around for a while, but our technique is new, because it specifically senses heme," Reddi said. "We took a heme binding protein from bacteria and clipped it onto to green fluorescent protein."

The researchers used a blue laser to charge up the lamp part of the sensor protein pair like a glow-in-the-dark sticker, then it re-emitted the green light. "You see this green image disappearing and reappearing depending on how much heme is available," Reddi said. "You can see what's happening in real time."

PROSTRATE CANCER : Mindful meditation helps men deal with uncertainty surrounding their cancer

Men with prostate cancer who are under close medical surveillance reported significantly greater resilience and less anxiety over time after receiving an intervention of mindfulness meditation, according to a recently published pilot study from the Northwestern University Feinberg School of Medicine.

The anxiety and uncertainty that men who choose active surveillance experience when diagnosed with prostate cancer causes one in four to receive definitive therapies within one to three years, even when there is no sign of tumor progression.

Health psychologist David Victorson, the principal investigator of the study and an associate professor of medical social sciences at Northwestern University Feinberg School of Medicine, researches the emotional stress of active surveillance and how mindfulness training helps alleviate the anxiety.

Mindfulness meditation is a well-known contemplative awareness practice dating back some 2,500 years. It is a form of meditation designed to develop the skill of paying attention to our inner and outer experiences with acceptance, patience and compassion.

"It's very understandable that some men will feel concerned with the knowledge that they indeed have prostate cancer but are asked to NOT do anything to remove it," Victorson said. "For many men this can create a great deal of inner turmoil. This turmoil can build up over time and eventually lead to men seeking surgical intervention when it may not ultimately be necessary."

Victorson and his Northwestern team now are partnering with other academic medical institutions to conduct a five-year multi-site controlled trial where men and their spouses will be randomized to eight weeks of intensive mindfulness meditation training or an eight-week control group.

"I believe we have an opportunity to investigate and equip men with additional tools above and beyond surgical intervention that can help them manage cancer-related uncertainty intolerance," Victorson said.

SKIN CANCER : NEW DRUG FOR TREATMENT

Finding new, more effective and personalised treatments for cancer is the challenge of many researchers. A challenge that has been successfully met by a team from Inserm led by Stéphane Rocchi (Inserm Unit 1065, "Mediterranean Center for Molecular Medicine"), which has just synthesised and developed new drugs for melanoma. One of them, known as HA15, reduces the viability of melanoma cells without being toxic for normal cells. This work has just been published in the journal Cancer Cell.

Melanoma is a highly aggressive form of skin cancer. It affects melanocytes, the cells responsible for the synthesis of melanin, which gives the skin its colour. There are 3 stages of tumour progression: radial growth, in which the cells proliferate in a disordered manner in the epidermis, the vertical growth phase, which involves invasion of the dermis, and finally the metastatic phase, corresponding to the dissemination of the cancer cells in the peripheral tissues.

Although encouraging results have been obtained for treating the metastatic phase (using targeted therapies or immunotherapies), most patients will need additional treatments to prevent the tumour from coming back, and to prevent more metastases from developing. The identification of new drug candidates is therefore an unavoidable element for the establishment of effective biotherapies against this cancer, the incidence of which is doubling every ten years.

In this context, researchers from Nice discovered a new family of drugs, the Thiazole Benzensulfonamides (TZB), which have useful anticancer properties. "Initially this family of drugs was identified in type 2 diabetes, as it increased the sensitivity of cells to insulin. If we wanted to use it against cancer, we had to be able to eliminate this proinsulin activity," explains Stéphane Rocchi. "Thus we started to modify its structure."

After many attempts, the initial TZD structure was extensively modified thanks to a fruitful collaboration with Dr Benhida's team from the Nice Institute of Chemistry, to obtain a formulation in which the "lead compound" was called HA15.

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The above post is reprinted from materials provided by INSERM (Institut national de la santé et de la recherche médicale). Note: Materials may be edited for content and length.

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Journal Reference:

1. Michaël Cerezo, Abdelali Lehraiki, Antoine Millet, Florian Rouaud, Magali Plaisant, Emilie Jaune, Thomas Botton, Cyril Ronco, Patricia Abbe, Hella Amdouni, Thierry Passeron, Veronique Hofman, Baharia Mograbi, Anne-Sophie Dabert-Gay, Delphine Debayle, Damien Alcor, Nabil Rabhi, Jean-Sébastien Annicotte, Laurent Héliot, Mariano Gonzalez-Pisfil, Caroline Robert, Solange Moréra, Armelle Virougoux, Philippe Gual, Maruf M.U. Ali, Corine Bertolotto, Paul Hofman, Robert Ballotti, Rachid Benhida, Stéphane Rocchi. Compounds Triggering ER Stress Exert Anti-Melanoma Effects and Overcome BRAF Inhibitor Resistance.Cancer Cell, 2016; DOI: 10.1016/j.ccell.2016.04.013

CANCER ECONOMIC CRISES

The researchers found that increases in unemployment were associated with increased mortality from all the cancer types included in the study. The association was strongest for treatable cancers, suggesting that lack of access to care may have been a factor in these excess deaths.

Credit: © enterlinedesign / Fotolia

The economic crisis of 2008-10, and the rise in unemployment that accompanied it, was associated with more than 260,000 excess cancer-related deaths--including many considered treatable--within the Organization for Economic Development (OECD), according to a study from Harvard T.H. Chan School of Public Health, Imperial College London, and Oxford University. The researchers found that excess cancer burden was mitigated in countries that had universal health coverage (UHC) and in those that increased public spending on health care during the study period.

The study will be published May 25, 2016 in The Lancet.

"Higher unemployment due to economic crisis and austerity measures is associated with higher number of cancer deaths. Universal health coverage protects against these deaths. That there are needless deaths is a major societal concern," said Rifat Atun, professor of global health systems at Harvard Chan School and senior author of the study. He added that increased joblessness during the economic crisis may have limited people's access to health care, leading to late-stage diagnoses and poor or delayed treatment.

"Cancer is a leading cause of death worldwide so understanding how economic changes affect cancer survival is crucial," says lead author Mahiben Maruthappu from Imperial College London, UK. "We also found that public healthcare spending was tightly associated with cancer mortality--suggesting healthcare cuts could cost lives."

Although previous studies have shown connections between economic changes and rates of suicides, cardiovascular disease, and overall mortality, only a few had examined the relationship between economic downturns and cancer outcomes, especially in countries with underdeveloped social security and health care systems.

The researchers analyzed the link between unemployment, public health care spending, and cancer mortality using data from 1990-2010 from more than 70 high- and middle-income countries around the world, representing roughly 2 billion people. The researchers looked at deaths from several "treatable" cancers, for which survival rates exceed 50%--including breast cancer in women, prostate cancer in men, and colorectal cancers in both men and women--and from a few "untreatable" cancers (with five-year survival rates less than 5%), including lung and pancreatic cancers in men and women.

The researchers found that increases in unemployment were associated with increased mortality from all the cancer types included in the study. The association was strongest for treatable cancers, suggesting that lack of access to care may have been a factor in these excess deaths. Also, comparing estimates of expected cancer deaths with actual deaths from 2008-10, they found that the recent global economic crisis was linked with more than 260,000 excess cancer deaths among the 35 member states of the OECD alone.

Adverse health effects persisted for several years after initial increases in unemployment, the study found. In addition, excess cancer deaths were a more significant problem in middle-income countries than in high-income countries.

In countries with UHC--defined in the study as countries that have legislation mandating UHC, more than 90% health care coverage, and more than 90% skilled birth attendance--the link between unemployment and excess cancer deaths disappeared, suggesting that greater access to health care played a key role in mitigating the problem. Twenty-six OECD countries were listed in the study as having UHC, while nine--Barbados, Latvia, Lithuania, Malta, Mexico, Poland, Russia, the U.S., and Uruguay--did not have it.

Researchers also found that increases in public sector health spending helped blunt the negative health impact of unemployment increases.

One limitation of the study was that it was not a truly global analysis, given scarcity of data from China, India, and low-income countries. The study was also unable to draw any firm conclusions about causality, although the authors did note that changes in unemployment were followed by changes in cancer mortality, which does suggest a causal link.

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The above post is reprinted from materials provided by Harvard T.H. Chan School of Public Health. Note: Materials may be edited for content and length.

PEANUT INTRODUCTION AT INFANT REDUCES ALLERGY EVEN WITH LATER ABSTINENCE

The early introduction of peanut to the diets of infants at high-risk of developing peanut allergy significantly reduces the risk of peanut allergy until 6 years of age, even if they stop eating peanut around the age of five, according to a new study led by King's College London.

Published today in the New England Journal of Medicine, the LEAP-On study followed on from the LEAP (Learning Early About Peanut Allergy) study, both led by Professor Gideon Lack at King's, which found that the majority of infants at high-risk of developing peanut allergy are protected from peanut allergy at age 5 years if they eat peanut frequently, starting within the first 11 months of life.

LEAP-On asked whether those infants who had consumed peanut in the LEAP study would remain protected against peanut allergy if they then stopped eating peanut for 12 months. The study findings conclude that the early introduction of peanut protects against the development of peanut allergy, and such protection is sustained even when peanut is no longer consumed for 12 months.

The LEAP-On study was undertaken at Evelina London Children's Hospital, and enrolled 556 participants from LEAP (out of a total of 628), of whom 550 had a complete primary outcome. All participants were instructed to avoid peanut for 12 months after they had completed the LEAP study, regardless of whether they had been randomized to avoid or eat peanut in the LEAP study. At the completion of LEAP-On, a rigorous clinical assessment of peanut allergy was made by oral peanut challenge. Additional peanut allergy assessments were made by questionnaire, skin prick test (SPT), and peanut-specific immune markers IgE and IgG4 were also measured in participants' blood.

Of the 550 LEAP-On participants, 280 had been randomized to peanut avoidance and 270 to peanut consumption on the LEAP Study; adherence to these interventions was high at 92%. All participants were asked to avoid peanut during LEAP-On and adherence during this study was also high: 90.4% for previous LEAP avoiders and 69.3% for previous LEAP consumers.

The study found that at 6 years of age, there was no statistically significant increase in allergy after 12 months of avoidance, in those who had consumed peanut during the LEAP trial (3.6% (10/274) at 60 months versus 4.8% (13/270) at 72 months). The study also found that peanut allergy was significantly more prevalent in those who had avoided eating peanuts in LEAP, than those who consumed (18.6% vs 4.8%). There were only 3 subjects from the consumer group who developed new peanut allergy during the 12 months of peanut avoidance, but there were also 3 subjects from the avoidance group who developed new peanut allergy.

The authors therefore concluded that in infants at high-risk for allergy in whom peanut was introduced in the first year of life, and continued until age 5, a 12-month period of peanut avoidance was not associated with a significant increase in peanut allergy. Overall, the study saw a 74% relative reduction in the prevalence of peanut allergy in those who consumed peanut compared to those who avoided.

The authors caution that the LEAP study design did not allow a determination of the minimum frequency or amount of peanut consumption required in early childhood to prevent an allergic response to peanut. Further studies are planned to establish whether the effects of early-life peanut consumption followed by ad-lib consumption of peanut over many years maintains this protection against allergy.

Professor Gideon Lack, Head of Department of Paediatric Allergy, King's College London and Head of the Children's Allergy Service at Guy's and St Thomas' NHS Foundation Trust, who led the study, presented the findings at the American Academy of Allergy, Asthma and Immunology meeting (AAAAI). "The aim of our study was to find out whether infants who had consumed peanut in the LEAP study would remain protected against peanut allergy after they stopped eating peanut for 12 months. LEAP-On clearly demonstrates that the majority of infants did in fact remain protected and that the protection was long-lasting," he said.

Professor Lack further noted that: "The longer term effects of stopping eating peanut following introduction early in life are not known, and further studies are needed. Parents of infants and young children with eczema and/or egg allergy, and so considered high-risk to peanut allergy, should consult with an Allergist, Paediatrician, or their General Practitioner prior to feeding them peanut products."

Dr George Du Toit, consultant in Paediatric Allergy at Guy's and St Thomas' NHS Foundation Trust and Honorary Reader in Paediatric Allergy, King's College London, co-investigator of the study, said: "We need more research to better understand the mechanisms behind the development and prevention of allergic responses to peanut, and how this might translate to other food allergies. However, it is reassuring that the highly protective intervention demonstrated in LEAP was not only safe, nutritionally favorable and acceptable to participant families but also sustained even with cessation of peanut consumption for 12 months."

The incidence of food allergy has risen in recent decades, and peanut allergy now affects up to 1 in 50 school age children in the UK; the occurrence of peanut allergy has more than doubled in the last 10 years in the UK and North America. It affects between 1-3% of children in Western Europe, the USA, and Australia and in recent years has become an important cause of food allergies in African and Asian countries. Peanut allergy develops early in life, is rarely out-grown and there is currently no cure. It imposes a considerable burden, impacting negatively on quality of life for patients and their families.

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The above post is reprinted from materials provided by King's College London. Note: Materials may be edited for content and length.

BENZYL BUTYL PHTHALATE (BBP) can Increase fat store in body

BBP is not used in food preparation, but it is used in the conveyor belts and plastic fittings on machines used to process many prepared foods. Food becomes contaminated when BBP leeches into it from the plastic.

Credit: Texas A&M Health Science Center

Benzyl butyl phthalate (BBP), a chemical commonly used in the food manufacturing process, can increase fat stores in the body even before we're born, according to a new study published in the Journal of Molecular and Cellular Endocrinology.

The study, led by Mahua Choudhury, Ph.D., assistant professor at the Texas A&M Health Science Center Irma Lerma Rangel College of Pharmacy, used animal stem cells to identify changes to the epigenome of the stem cell line when exposed to the chemical BBP when compared to a control. The cell lines exposed to increasingly higher levels of BBP also showed higher levels of adipogenesis -- the process by which fat cells develop -- as much as five times higher, depending on the dose.

"We were quite surprised by the results," Choudhury said. "We had thought we would see some increase, but nothing this dramatic." Stem cells are undifferentiated cells, capable of becoming different specialized cells. Because of this, the epigenetic changes observed in the animal stem cells could affect not just an adult exposed to BBP, but also a growing fetus.

The study involved exposing animal stem cells to varying concentrations of BBP. While the results were striking, researchers were quick to note they could not yet be applied to a human population. "These results are important, but they are just the first step in further study," Choudhury cautioned.

Phthalates & human exposure

BBP is part of a chemical family called phthalates, which are typically used to make plastics soft and malleable. While BBP is used in many consumer products such as carpet and vinyl flooring, the primary human exposure comes from food consumption. BBP is not used in food preparation, but it is used in the conveyor belts and plastic fittings on machines used to process many prepared foods. Food becomes contaminated when BBP leeches into it from the plastic.

Choudhury noted that BBP is banned in all toys and childcare articles both manufactured in, and imported into, the European Union (EU). The EU has also banned BBP's use in nail polish, as it is considered to be carcinogenic, mutagenic or toxic to reproduction (CMR-substance). While the United States has set limits on the amount of BBP permissible in certain consumer products, it has yet to take the same steps as the EU. "I don't think there is enough evidence yet for government to step in," Choudhury said. "The issue is very complex."

Obesity epidemic & epigenetics

More than one-third of adult Americans are obese, and obesity-related illnesses, including type 2 diabetes, stroke and heart disease, have risen exponentially along with climbing obesity rates. This epidemic costs the United States health care system $190 billion annually, according to one estimate.

"For many years, we viewed obesity as a very simple problem, one that had to do with diet and inactivity only," says investigator Ravi Sonkar, Ph.D. also of the Texas A&M Rangel College of Pharmacy.

"Researchers have investigated the role that genetics plays in obesity," said co-author Catherine A. Powell, Ph.D., also of the Texas A&M Rangel College of Pharmacy, "but we have not paid much attention to the impact the environment can have on how our genes are expressed."

Epigenetics is the study of how the environment, including environmental chemicals, can alter gene expression without changing the genetic code. Previous research has associated epigenetic changes with increasing rates of obesity and obesity-related illnesses.

"Phthalates have recently been associated with obesity, but this was the first time we were able to show the mechanism by which BBP may cause fat accumulation and program the stem cell to become obese via an epigenetic balance," Choudhury said.

Choudhury's lab at Texas A&M has several additional studies planned to study the effect of BBP on fat accumulation and the development of diabetes and obesity (diabesity), one of which includes an epidemiological study tracking exposure and diabesity in humans.

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ASPIRIN REDUCES RISK OF MAJOR STROKE

After a mini-stroke, almost all of the benefit of aspirin in reducing the risk of another stroke was found to be in the first few weeks, and researchers also found that aspirin also likely reduced the severity of these early strokes.

Credit: © Veniamin Kraskov / Fotolia

Using aspirin urgently could substantially reduce the risk of major strokes in patients who have minor 'warning' events, a group of European researchers has found. Writing in theLancet, the team say that immediate self-treatment when patients experience stroke-like symptoms would considerably reduce the risk of major stroke over the next few days.

Aspirin is already given to people who have had a stroke or transient ischaemic attack (TIA -- often called a 'mini-stroke') to prevent further strokes after they have been assessed in hospital and in the longer-term, reducing the subsequent stroke risk by about 15%. However, based on a previous study in Oxford (the EXPRESS Study) the team suspected that the benefits of more immediate treatment with aspirin could be much greater.

Lead researcher Professor Peter Rothwell, a stroke expert from the University of Oxford, explained: 'The risk of a major stroke is very high immediately after a TIA or a minor stroke (about 1000 times higher than the background rate), but only for a few days. We showed previously in the 'EXPRESS Study' that urgent medical treatment with a 'cocktail' of different drugs could reduce the one-week risk of stroke from about 10% to about 2%, but we didn't know which component of the 'cocktail' was most important.'

'One of the treatments that we used was aspirin, but we know from other trials that the long-term benefit of aspirin in preventing stroke is relatively modest. We suspected that the early benefit might be much greater. If so, taking aspirin as soon as possible after 'warning symptoms' event could be very worthwhile.'

The team -- from Oxford (UK), University Medical Center Utrecht (Netherlands), University Duisburg-Essen (Germany), and Lund University (Sweden) -- therefore revisited the individual patient data from twelve trials (about 16,000 people) of aspirin for long-term secondary prevention -- that is, to prevent a further stroke -- and data on about 40,000 people from three trials of aspirin in treatment of acute stroke.

They found that almost all of the benefit of aspirin in reducing the risk of another stroke was in the first few weeks, and that aspirin also reduced the severity of these early strokes. Rather than the 15% overall reduction in longer-term risk reported previously in these trials, aspirin reduced the early risk of a fatal or disabling stroke by about 70-80% over the first few days and weeks.

Professor Rothwell said: 'Our findings confirm the effectiveness of urgent treatment after TIA and minor stroke -- and show that aspirin is the most important component. Immediate treatment with aspirin can substantially reduce the risk and severity of early recurrent stroke. This finding has implications for doctors, who should give aspirin immediately if a TIA or minor stroke is suspected, rather than waiting for specialist assessment and investigations.'

'The findings also have implications for public education. Public information campaigns have worked in getting more people to seek help sooner after a major stroke, but have been less effective in people who have had minor strokes or TIAs. Many patients don't seek medical attention at all and many delay for a few days. Half of recurrent strokes in people who have a TIA happen before they seek medical attention for the TIA. Encouraging people to take aspirin if they think they may have had a TIA or minor stroke -- experiencing sudden-onset unfamiliar neurological symptoms -- could help to address this situation, particularly if urgent medical help is unavailable.'

Dr Dale Webb, Director of Research and Information at the Stroke Association, said: 'A TIA is a medical emergency and urgent neurological assessment must always be sought. We welcome this research which shows that taking aspirin after TIA can dramatically reduce the risk and severity of further stroke. The findings suggest that anyone who has stroke symptoms, which are improving while they are awaiting urgent medical attention can, if they are able, take one dose of 300 mg aspirin.

'The research findings are also timely, as the stroke community is currently working to develop a new set of national clinical guidelines on stroke.'

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The above post is reprinted from materials provided by University of Oxford. Note: Materials may be edited for content and length.

THE NET CASTING SPIDER

Evolving the largest eyes among all known arachnids may have helped the net-casting spider add walking prey to its airborne menu of midnight snacks, says new research from University of Nebraska-Lincoln biologists.

Doctoral student Jay Stafstrom reached the conclusion after two months living out of a tent in a Florida state park, where he observed how the nocturnal species Deinopis spinosa hunted with and without the aid of secondary eyes roughly 2,000 times more light-sensitive than human eyes.

The net-casting spider earns its name by spinning a rectangular band of woolly silk to capture prey while rappelling upside-down from a single thread. When the time comes, the spider lunges forth and stretches the net to engulf prey in one fell swoop that lasts about one-thousandth of a second.

Stafstrom discovered that the spider snared prey about 3 1/2 times more often when relying on its massive secondary eyes than when those eyes were covered by vision-impairing dental silicone. But the effect seemed to depend on whether that prey traveled by leg or by wing.

While the silicone had no discernible effect on the species' ability to snag flying prey, it greatly reduced the odds of the spider capturing a crawling critter. Though one of every four specimens without the silicone blindfold would capture prey that walked their way -- roughly the same proportion that caught prey flying through their attack radius -- none managed to snare a walking meal while their vision was impaired.

Stafstrom collected the data by reviewing infrared video footage from four closed-circuit cameras that he set up in Paynes Prairie Preserve State Park. The footage further revealed that the average ground-bound prey was nearly twice as long as the flying variety, suggesting the former may provide greater nutritional value, Stafstrom said.

The findings may also help explain why D. spinosa is one of the few web-building spiders to have evolved large secondary eyes, which are more common among species that hunt along the ground and rely less on vibrational cues to find prey.

"Vision is really expensive," said Stafstrom, who co-authored a new study with faculty adviser Eileen Hebets. "Simply keeping photoreceptors healthy and functional requires a lot of energy. Now if you wanted to grow the size of the eye to gain more visual information, it would become disproportionately more expensive as the mass of the eye increases. It's a really good example of the Law of Diminishing Returns, where you're spending way too much to get just a little bit more information.

"(The spiders) can still catch things out of the air (without those eyes). Why are they, presumably, investing so much in these large eyes? One of our hypotheses is that it's because there's a lot of prey on the ground, and by having vision in these enlarged eyes, not only are they getting things off the ground, but those things are bigger and probably more nutritious."

Stafstrom and Hebets ran a similar experiment in the lab, placing each net-casting spider in a cylindrical arena with a cricket. Though some blindfolded spiders eventually captured the crickets, they did so only when their prey bumped into the silken support beams of the spiders' A-shaped webs. On average, the successful blindfolded hunters still took 10 times longer to catch a cricket than when aided by their secondary sight.

The researchers also suspect that the spider's enlarged secondary eyes -- just two of their eight total -- enabled it to become a solely nocturnal hunter. The species literally lies low during the day, pulling together its legs while stretching out to resemble the tips of the palm fronds it often inhabits. This nocturnal nature likely helps the spiders avoid predators that rely on sight to track their prey, Hebets said.

Stafstrom said he never saw the spiders move before sunset. In fact, he struggled to even find them.

"Not only are they really looking like a stick and (lying) completely motionless, but on their first pair of legs, they actually have some hairs that puff out a bit and cover their eyes somewhat," he said.

Technical difficulties

Locating the spiders represented just one of the challenges that Stafstrom faced during his two-month field experiment amid the humidity and frequent downpours of a Florida summer.

His first tent was too small, so he had to purchase another. His closed-circuit cameras, which he powered with car batteries, recorded in analogue rather than digital format. Though he had purchased laptops to digitize the signals and allow him to review the video on site, his initial approach failed.

"The first two weeks were really bad," he said. "I thought everything would be peachy, (but) it was not peachy. I actually went to RadioShack a couple of times and made a friend there. We soldered some stuff together and found a way to make it work."

Catching and restraining the spiders required the assistance of garbage bags. Applying the dental silicone demanded many wooden toothpicks and more patience. Stafstrom even improvised to ensure his cameras would have the proper vantage points.

"I MacGyver-ed it," he said. "I had a bunch of palm fronds that were dead, so I shaved them so that I could make tripods out of them."

Hebets said the toil paid off in the form of insights that Stafstrom could not have gained in the lab alone.

"The fact that such a large component of this was done in the field, in pretty harsh conditions, is amazing," said Hebets, professor of biological sciences. "It was a ton of work and physical hardship and technical hardship. The data came out beautifully, but the effort behind it was monumental."

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The above post is reprinted from materials provided by University of Nebraska-Lincoln. The original item was written by Scott Schrage. Note: Materials may be edited for content and length.

How to Get Treatment for Hepatitis C

Three Parts:Getting Medical Treatment for HCVTrying Alternative Therapies for HCVPreventing Hepatitis CQuestions and Answers

Hepatitis C is a viral infection that attacks the liver and triggers chronic inflammation.^[1] Most people who have hepatitis C don't notice any symptoms until it damages their liver — typically after many years. Due to its destructive nature over time, hepatitis C is often considered more serious than hepatitis A or B infections. The hepatitis C virus (HCV) is usually passed between people via contaminated blood, commonly from sharing needles during illegal drug use. Antiviral drugs are the main treatment for HCV, although prevention and lifestyle changes are also important.

1

Consult with your doctor. Symptoms of hepatitis C infection don't often show up for about 3 months or later, and typically include: fatigue, mild fever, nausea, muscle and joints aches, reduced appetite, abdominal pain, dark-colored urine and yellowish discoloration of the skin and eyes.^[2] If you notice any of these symptoms, especially if you're an illicit drug user or have received blood products in the past, then make an appointment with your doctor for an examination and testing.

• More advanced symptoms of HCV infection include: fluid accumulation in your abdomen (called ascites), swelling on your legs (called edema), itchy skin, spider veins on skin, bruising, reduced clotting ability of blood, unexplained weight loss, drowsiness, confusion and slurred speech.
• Your doctor will order urine and blood tests that look for HCV and high levels of liver enzymes, which indicate liver damage.
• In more advanced cases, your doctor may recommend a liver biopsy — taking a small sample of liver tissue (via a long, thin needle) and looking at it under a microscope for evidence of injury.
• 
  
• 2 Be honest about your drug use. When consulting with your doctor, it's important to be honest about a past or current history of injecting illicit drugs, such as heroin, because it's the biggest risk factor for catching hepatitis C and many other types of infections.^[3] Doctor-patient confidentiality will typically prevent you from getting in trouble with the law, unless you're putting your child or other people in direct harm from using or selling.
• • Depending on your family situation and history of drug use, social services may be informed and have to get involved.
  • If you're pregnant and using illicit drugs, your doctor may feel compelled ethically or forced by law (depending on the state) to force addiction treatment on you so your baby is not harmed any further.^[4]
  • Getting treatment for your drug addiction is just as important, if not more so, than dealing with hepatitis C infection. Seek addiction treatment immediately.
  
• 1. 3
     Talk to your doctor about antiviral drugs. Once it's established that you have hepatitis C, the primary (and only) medical treatment is with antiviral medications that are meant to clear the HCV from your body.^[5] Commonly used older antivirals for hepatitis include: pegylated interferon (Roferon-A, Intron-A, Rebetron, Alferon-N, Peg-Intron), ribavirin (Rebetol), lamivudine (Epivir-HBV), adefovir dipivoxil (Hepsera) and entecavir (Baraclude).^[6]
     

     • Newer types of antivirals tailored specifically for HCV are classified as either protease inhibitors or polymerase inhibitors and include: boceprevir (VictrelisI), telaprevir (Incivek), simeprevir (Olysio), sofosbuvir (Sovaldi) and daclatasvir (Daklinza).^[7]
     • The goal of antiviral treatment is to have no HCV detected in your body at least 3 months after you finish the medication(s).
     • Although drugs to treat hepatitis C have gradually improved over the decades, they still have serious side effects, such as flu-like symptoms, debilitating fatigue, hair loss, depression and destruction of healthy red and/or white blood cells.^[8]
  2. 4
     Take the antivirals as directed. Older antiviral medications were typically taken daily and for up to 72 weeks to be able to rid the body of HCV, but side effects were a common concern due to toxicity. Newer antiviral drugs tend to be more effective at killing HCV, so they can be taken for shorter periods of time (daily for between 12-24 weeks) and consequently lead to less serious side effects.^[9] As such, follow your doctor's instructions very closely to avoid unwanted side effects.
     

     • Sometimes combining newer anti-viral medications with existing ones (ribavirin with interferon, for example) can be more effective than solo drug therapy.
     • Interferon therapy is given by injection by your doctor, but most other antivirals are taken orally as pills at home. It's best to always take antivirals pills with food or after meals.
     • Regimens and dosages of antivirals vary depending on the hepatitis C genotype, extent of liver damage and other medical conditions.
  3. 5
     Consider a liver transplant as a last resort. If your liver is severely damaged and it's not functioning properly, then a liver transplant becomes a possible option.^[10] During a transplant, the surgeon removes as much of your damaged liver as possible and replaces it with a healthier liver from a deceased donor or a portion of healthy liver tissue from a living donor. Liver tissue actually grows relatively quickly and can regenerate itself better than other organs.
     

     • Realize that a liver transplant is often not a cure for hepatitis C, as treatment with antiviral drugs typically must continue.
     • In approximately 50% of the patients with chronic hepatitis who get a liver transplant, the HCV infection recurs and causes liver injury again.^[11]
     • The 5-year survival rate after a liver transplant is between 60-80%, depending on the surgical expertise, health of the new liver tissue and lifestyle of the patient.

  Part2

  Trying Alternative Therapies for HCV

  1. 1
     Talk to a herbalist or naturopath. Taking herbal remedies and/or supplements for infections and other diseases is often confusing and difficult to understand their potential effectiveness. Your doctor is not likely to know much about herbs / supplements and medical websites don't often mention them, so you need to seek out a knowledgeable health professional. Licensed herbalists, naturopaths or even chiropractors might be a great way to start.
     

     • Spend quality time online researching various herbs / supplements that can positively impact hepatitis C. Unfortunately, specific dosage information is rare to come by because so many variables are involved.
     • Always tell your medical doctor if you're taking or thinking of taking herbs / supplements because some may interact dangerously with medications.^[12] In most cases, herbs and medications can be taken concurrently.
     • As a general guideline, you can use herbs as dried extracts (capsules, powders, teas) or tinctures (alcohol extracts).^[13]
       • Unless otherwise indicated, make herbal teas with 1 tsp. of dried plant material per cup of very warm water.
       • Steep covered for up to 20 minutes, especially if you're using the roots of a plant.
       • Drink between 2-4 cups of the herbal tea per day.
  2. 2
     Take milk thistle supplements. Milk thistle extract has been used to treat liver problems for many centuries. The most helpful compound in milk thistle is called silymarin, which has been shown to protect the liver from various viruses, toxins, alcohol and many drugs. The studies are mixed, but milk thistle (silymarin) seems to have the potential to reduce the symptoms of chronic hepatitis and improve quality of life, although it may not always improve liver function tests or reduce HCV levels in the blood.^[14]
     

     • Look for standard silymarin extracts that contain 70% silybin for best results, as they seem to be the most effective.
     • Silybin is a strong antioxidant and anti-inflammatory that can stimulate the immune system, which is why it's helpful for all causes of hepatitis and cirrhosis.
     • People with ragweed allergies should be cautious with milk thistle products. Milk thistle can also have estrogen-like effects, so people with hormone-sensitive conditions (breast cancer, for example) should be careful too.
     • The effective dose to help with hepatitis C is not known, so some experimentation is needed.
  3. 3
     Consider taking SNMC (Stronger Neominophagen C). SNMC is a liquid supplement that contains glycine, glycyrrhizin and cysteine in a 20:2:1 ratio all mixed in a saline solution.^[15] SNMC is helpful for reducing hepatitis symptoms, improving liver function (based on enzymes in the blood) and healing liver tissue, but it doesn't directly kill HCV.^[16]
     

     • SNMC solution is often administered via daily intravenous (IV) injections, although some recent studies suggest that oral forms (drinking it) may be just as effective for chronic hepatitis.
     • Typical formulations of SNMC are 2,000mg of glycine, 200mg of glycyrrhizin and 100mg of cysteine all mixed in a 100cc IV bag of saline solution.
     • Glycyrrhizin is the main active compound in licorice root, which has also been used to treat liver disease for centuries.
  4. 4
     Try Cordyceps mushrooms. Cordyceps are types of mushrooms commonly used in traditional Chinese medicine to treat liver diseases. Some studies show Cordyceps mushroom can stimulate immune function and improve liver function in patients with hepatitis B, so it may be worth a try also for hepatitis C.^[17] Cordyceps mushroom supplements typically come in capsules, but also liquid extracts. An ideal dosage for hepatitis C is not known, so some experimentation is needed.
     

     • Cordyceps may slow down blood's ability to clot, so be cautious if you're on blood-thinning medications. Always tell your doctor about all supplements you're taking so there's less risk of a negative reactions with drugs.
     • Another type of mushroom that helps with chronic hepatitis B infection and may also be helpful for hepatitis C is Reishi mushroom.^[18]
  5. 5
     Experiment with high doses of vitamin C. Vitamin C (ascorbic acid) isn't a direct treatment for hepatitis C infection, but high doses can help stimulate the immune response to eliminate viruses from the bloodstream.^[19] Vitamin C is also a strong antioxidant that has some antiviral abilities, so it might be worth experimenting with for HCV due to its relative safety and lack of expense.
     

     • High dosages of vitamin C range from 3,000mg to 10,000mg daily, spread out over the day. The vitamin can be taken as capsules, muscle injections or IV bags.
     • The effective dose to help with hepatitis C is not known, so some experimentation is needed.
     • It's best to build up to higher daily doses and not take more than 1,000mg at a time because it can trigger loose bowels and short-term diarrhea.
     • High doses of vitamin C has not actually been proven to increase the risk of kidney stones, despite its reputation for doing so.
  6. 6
     Learn about SBEL1. A newly discovered and tested Chinese herbal compound called SBEL1 seems to have the ability to inhibit and kill HCV by about 90%, at least in lab studies on human liver cells.^[20] Research on patients with HCV is next, so learn more about SBEL1 and remember it for potential future use against hepatitis.
     

     • SBEL1 is extracted from a medicinal herb found in Taiwan and Southern China normally used by local populations to treat sore throats and inflammation.
     • Scientists are excited that SBEL1 can make a big impact on hepatitis C worldwide, as it's estimated to affect 150-200 million people and cause more than 350,000 deaths each year.^[21]

  
  

  1. 1
     Don't share needles. Hepatitis C (and B) are transmitted through contact with infected blood, so illicit drug users who share needles to inject are at greatest risk.^[22] As such, either stop the drug use altogether (ideally) or always use clean, unused needles for injecting.
     

     • In addition to needles, don't share any drug paraphernalia, such as syringes, containers or any preparation equipment — they can all be contaminated with infected blood.
     • Heroin users are particularly at risk due to the greater likelihood of using needles and syringes to deliver the drug directly into the bloodstream.
  2. 2
     Practice safe sex. Having unprotected sex with someone who is infected can also pass on hepatitis causing viruses, although it's much more common with the hepatitis B virus (HBV) than HCV for reasons that are not entirely understood.^[23] Regardless, always use condoms for sexual activities, even with people you think you know well.
     

     • Unprotected anal sex has the highest risk of transmitting STDs and other blood-born viruses such as HCV.
     • Up to 40% of HCV infections are of unknown cause, although a good percentage of those cases are due to secretive drug behavior from spouses and significant others.
  3. 3
     Be cautious with tattoos and piercing. Although they are not common methods of spreading viral infections, there still is risk with piercing and tattooing because they use needles to puncture the skin. As such, be cautious about body piercing and tattooing and always choose a reputable shop that's been there for a while.^[24] Ask the service provider how they go about cleaning their equipment and preventing the transfer of contaminated blood.
     

     • If the shop or beauty parlor seem evasive or hostile to your polite questioning, go somewhere else.
     • Make sure the service providers always use sterile or new needles. Consider buying your own sterile tools and giving them to the employee to use on you..
  4. 4
     Cut back on alcohol. Reducing your alcohol consumption (or stopping completely) is not a method for directly preventing hepatitis C infection, but alcohol (ethanol) is toxic to the liver and speeds up the progression of every liver disease.^[25] As such, limit your consumption to no more than 1-2 drinks daily if you're healthy, but stop immediately if you have any infection that impacts your liver.
     

     • Binge drinking (more than 3 or 4 drinks in an evening) is especially damaging to your liver, particularly if you have any type of hepatitis.
     • Grain-based alcohol (vodka, whiskey) is much worse for your liver than red wine, which contains some health benefits due to the antioxidant content. Beer is between the two in terms being damaging.