NEW ANALYSIS LINKS TREE HEIGHT TO CLIMATE

From the FMS Global News Desk of Jeanne Hambleton Released: 14-Aug-2014   Citations Ecology Source Newsroom: University of Wisconsin-Madison

Newswise — MADISON, Wis. — What limits the height of trees? Is it the fraction of their photosynthetic energy they devote to productive new leaves? Or is it their ability to hoist water hundreds of feet into the air, supplying the green, solar-powered sugar factories in those leaves?

Both factors — resource allocation and hydraulic limitation — might play a role, and a scientific debate has arisen as to which factor (or what combination) actually sets maximum tree height, and how their relative importance varies in different parts of the world.

In research to be published in the journal Ecology — and currently posted online as a preprint — Thomas Givnish, a professor of botany at the University of Wisconsin-Madison, attempts to resolve this debate by studying how tree height, resource allocation and physiology vary with climate in Victoria state, located in southeastern Australia. There, Eucalyptus species exhibit almost the entire global range in height among flowering trees, from 4 feet to more than 300 feet.

“Since Galileo’s time,” Givnish says, “people have wondered what determines maximum tree height: ‘Where are the tallest trees, and why are they so tall?’ Our study talks about the kind of constraints that could limit maximum tree height, and how those constraints and maximum height vary with climate.”

One of the species under study, Eucalyptus regnans — called mountain ash in Australia, but distinct from the smaller and unrelated mountain ash found in the U.S. — is the tallest flowering tree in the world. In Tasmania, an especially rainy part of southern Australia, the tallest living E. regnans is 330 feet tall. (The tallest tree in the world is a coastal redwood in northern California that soars 380 feet above the ground.)

Southern Victoria, Tasmania and northern California all share high rainfall, high humidity and low evaporation rates, underlining the importance of moisture supply to ultra-tall trees. But the new study by Givnish, Graham Farquhar of the Australian National University and others shows that rainfall alone cannot explain maximum tree height.

A second factor, evaporative demand, helps determine how far a given amount of rainfall will go toward meeting a tree’s demands. Warm, dry and sunny conditions cause faster evaporation from leaves, and Givnish and his colleagues found a tight relationship between maximum tree height in old stands in Australia and the ratio of annual rainfall to evaporation. As that ratio increased, so did maximum tree height.

Other factors — like soil fertility, the frequency of wildfires and length of the growing season — also affect tree height. Tall, fast-growing trees access more sunlight and can capture more energy through photosynthesis. They are more obvious to pollinators, and have potential to outcompete other species.

“Infrastructure” — things like wood and roots that are essential to growth but do not contribute to the production of energy through photosynthesis — affect resource allocation, and can explain the importance of the ratio of moisture supply to evaporative demand.

“In moist areas, trees can allocate less to building roots,” Givnish says. “Other things being equal, having lower overhead should allow them to achieve greater height.

“And plants in moist areas can achieve higher rates of photosynthesis, because they can open the stomata on their leaves that exchange gases with the atmosphere. When these trees intake more carbon dioxide, they can achieve greater height before their overhead exceeds their photosynthetic income.”

The constraints on tree height imposed by resource allocation and hydraulics should both increase in drier areas. But Givnish and his team wanted to know the importance of each constraint.

The scientists examined the issue by measuring the isotopic composition of carbon in the wood along the intense rainfall gradient in their study zone. If hydraulic limitation alone were to set maximum tree height, the carbon isotope composition should not vary because all trees should grow up to the point at which hydraulics retards photosynthesis. The isotopic composition should also remain stable if resource allocation alone sets maximum height, because resource allocation does not directly affect the stomata.

But if both factors limit tree height, the heavier carbon isotopes should accumulate in moister areas where faster photosynthesis (enhanced by wide-open stomata) can balance the costs of building more wood in taller trees. Givnish, Farquhar and their colleagues found exactly that, implying that hydraulic limitation more strongly constrains maximum tree height under drier conditions, while resource allocation more strongly constrains height under moist conditions.

Most studies of tree height have focused on finding the tallest trees and explaining why they live where they do, Givnish says.

“This study was the first to ask, ‘How does the maximum tree height vary with the environment, and why?’”

WIRELESS SENSORS AND FLYING ROBOTS: A WAY TO MONITOR DETERIORATING BRIDGES

From the FMS Global News Desk of Jeanne Hambleton  Released: 15-Aug-2014
Source Newsroom:
Tufts University

Newswise — MEDFORD/SOMERVILLE, Mass. – As a recent report from the Obama administration warns that one in four bridges in the United States needs significant repair or cannot handle automobile traffic, Tufts University engineers are employing wireless sensors and flying robots that could have the potential to help authorities monitor the condition of bridges in real time.

Today, bridges are inspected visually by teams of engineers who dangle beneath the bridge on cables or look up at the bridge from an elevated work platform. It is a slow, dangerous, expensive process and even the most experienced engineers can overlook cracks in the structure or other critical deficiencies.

A New Monitoring System for Bridges

In the detection system being developed by Babak Moaveni, an assistant professor of civil and environmental engineering at Tufts School of Engineering, smart sensors are attached permanently to bridge beams and joints. Each sensor can continuously record vibrations and process the recorded signal. Changes in the vibration response can signify damage, he says.

Moaveni, who received a grant from the National Science Foundation (NSF) for his research, is collaborating with Tufts Assistant Professor of Electrical and Computer Engineering Usman Khan to develop a wireless system that would use autonomous flying robots (quad-copters) to hover near the sensors and collect data while taking visual images of bridge conditions. The drone-like robots would transmit data to a central collection point for analysis. Khan received a $400,000 Early Career Award from the NSF earlier this year to explore this technology, which requires addressing significant navigational and communications challenges before it could be a reliable inspection tool.

The recent Obama administration report that analyzed the condition of the transportation infrastructure, points across the country out that 25 percent of the approximately 600,000 bridges are in such a poor state that they are incapable of handling daily automobile traffic. In Massachusetts, more than 50 percent of the 5,136 bridges in use are deficient, the report says.

Moaveni and Khan’s work could help monitor bridges and identify those that are at risk more accurately than current methods. Once installed, the sensors would provide information about the condition of bridges that cannot be obtained by visual inspection alone and would allow authorities to identify and focus on bridges that need immediate attention.

Moaveni installed a network of 10 wired sensors in 2009 on a 145-foot long footbridge on Tufts’ Medford/Somerville campus. In 2011, Moaveni added nearly 5,000 pounds of concrete weights on the bridge deck to simulate the effects of damage on the bridge—a load well within the bridge’s limits. Connected by cables, the sensors recorded readings on vibration levels as pedestrians walked across the span before and after installation of the concrete blocks. From the changes in vibration measurements, Moaveni and his research team could successfully identify the simulated damage on the bridge, validating his vibration-based monitoring framework.

A major goal of his research, Moaveni says, is to develop computer algorithms that can automatically detect damage in a bridge from the changes in its vibration measurements. His work is ongoing.

“Right now, if a bridge has severe damage, we are pretty confident we can detect that accurately. The challenge is building the system so it picks up small, less obvious anomalies.”

Tufts University School of Engineering Located on Tufts’ Medford/Somerville campus, the School of Engineering offers a rigorous engineering education in a unique environment that blends the intellectual and technological resources of a world-class research university with the strengths of a top-ranked liberal arts college.

Close partnerships with Tufts’ excellent undergraduate, graduate and professional schools, coupled with a long tradition of collaboration, provide a strong platform for interdisciplinary education and scholarship.

The School of Engineering’s mission is to educate engineers committed to the innovative and ethical application of science and technology in addressing the most pressing societal needs, to develop and nurture twenty-first century leadership qualities in its students, faculty, and alumni, and to create and disseminate transformational new knowledge and technologies that further the well-being and sustainability of society in such cross-cutting areas as human health, environmental sustainability, alternative energy, and the human-technology interface.

SALT CONTRIBUTES TO 1,650,000 DEATHS GLOBALLY EACH YEAR

From the FMS Global News Desk of Jeanne Hambleton  Posted on August 13, 2014                              By Stone Hearth News Eureka Alert

BOSTON — More than 1.6 million cardiovascular-related deaths per year can be attributed to sodium consumption above the World Health Organization’s recommendation of 2.0g (2,000mg) per day, researchers have found in a new analysis evaluating populations across 187 countries. The findings were published in the August 14 issue of The New England Journal of Medicine.

“High sodium intake is known to increase blood pressure, a major risk factor for cardiovascular diseases including heart disease and stroke,” said first and corresponding author Dariush Mozaffarian, M.D.,

Dr.P.H., dean of the Friedman School of Nutrition Science and Policy at Tufts University, who led the research while at the Harvard School of Public Health. “However, the effects of excess sodium intake on cardiovascular diseases globally by age, sex, and nation had not been well established.”

The researchers collected and analyzed existing data from 205 surveys of sodium intake in countries representing nearly three-quarters of the world’s adult population, in combination with other global nutrition data, to calculate sodium intakes worldwide by country, age, and sex. Effects of sodium on blood pressure and of blood pressure on cardiovascular diseases were determined separately in new pooled meta-analyses, including differences by age and race. These findings were combined with current rates of cardiovascular diseases around the world to estimate the numbers of cardiovascular deaths attributable to sodium consumption above 2.0g per day.

The researchers found the average level of global sodium consumption in 2010 to be 3.95g per day, nearly double the 2.0g recommended by the World Health Organization. All regions of the world were above recommended levels, with regional averages ranging from 2.18g per day in sub-Saharan Africa to 5.51g per day in Central Asia. In their meta-analysis of controlled intervention studies, the researchers found that reduced sodium intake lowered blood pressure in all adults, with the largest effects identified among older individuals, blacks, and those with pre-existing high blood pressure.

“These 1.65 million deaths represent nearly one in 10 of all deaths from cardiovascular causes worldwide. No world region and few countries were spared,” added Mozaffarian, who chairs the Global Burden of Diseases, Nutrition, and Chronic Disease Expert Group, an international team of more than 100 scientists studying the effects of nutrition on health and who contributed to this effort.

“These new findings inform the need for strong policies to reduce dietary sodium in the United States and across the world.”

In the United States, average daily sodium intake was 3.6g, 80 percent higher than the amount recommended by the World Health Organization. [The federal government's Dietary Guidelines for Americans recommend limiting intake of sodium to no more than 2,300mg (2.3g) per day.] The researchers found that nearly 58,000 cardiovascular deaths each year in the United States could be attributed to daily sodium consumption greater than 2.0g. Sodium intake and corresponding health burdens were even higher in many developing countries.

“We found that four out of five global deaths attributable to higher than recommended sodium intakes occurred in middle- and low-income countries,” added John Powles, M.B., B.S., last author and honorary senior visiting fellow in the department of public health and primary care at the University of Cambridge.

“Programs to reduce sodium intake could provide a practical and cost effective means for reducing premature deaths in adults around the world.”

The authors acknowledge that their results utilize estimates based on urine samples, which may underestimate true sodium intakes. Additionally, some countries lacked data on sodium consumption, which was estimated based on other nutritional information; and, because the study focuses on cardiovascular deaths, the findings may not reflect the full health impact of sodium intake, which is also linked to higher risk of nonfatal cardiovascular diseases, kidney disease and stomach cancer, the second most-deadly cancer worldwide.

This research was supported by a grant from the Bill and Melinda Gates Foundation.

Mozaffarian, D; Fahimi, S; Singh, G; Micha, R; Khatibzadeh, S; Engell, R; Lim, S; Goodarz, D; Ezzati, M; and Powles, J. “Global sodium consumption and death from cardiovascular causes.” N Engl J Med 2014. 371:7, 624-634. DOI: 10.1056/NEJMoa130412

About the Friedman School of Nutrition Science and Policy

The Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy at Tufts University is the only independent school of nutrition in the United States. The school’s eight degree programs – which focus on questions relating to nutrition and chronic diseases, molecular nutrition, agriculture and sustainability, food security, humanitarian assistance, public health nutrition, and food policy and economics – are renowned for the application of scientific research to national and international policy.

Back tomorrow – Jeanne

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PATIENTS SELF-PRESCRIBE ‘CANCER-PREVENTING’ ASPIRIN AS PHARMACY SALES SOAR

PATIENTS SELF-PRESCRIBE ‘CANCER-PREVENTING’ ASPIRIN AS PHARMACY SALES SOAR

From the FMS Global News Desk of Jeanne Hambleton      3 August  2014  By Caroline Price Pulse Today

BREAKING NEWS

 

Exclusive Pharmacies have reported big hikes in aspirin sales in the past week after UK academics called for people in late-middle age to start taking daily doses of the drug to prevent stomach and bowel cancer, Pulse has learnt.

Health retailer Superdrug reported a doubling in the amount of low-dose aspirin sold last week in its stores, recording a 229% increase in sales on the preceding week.

The figures came as UK experts claimed the benefits of taking a low dose of aspirin daily to prevent stomach and bowel cancer outweigh any risks for most people aged 50-65.

The researchers had warned there were still some doubts regarding the evidence – in particular over what dose should be taken and for how long – and advised people to consult their GP before choosing to self-prescribe aspirin.

But one Superdrug store in Bolton last week reported a massive 500% increase in sales after the announcement, a finding reflected by a big jump in national sales of 75 mg aspirin across Superdrug stores nationally compared with the previous week – and a 400% increase in the London region.

A spokesperson for Superdrug told Pulse: ‘Aspirin sales were up 229% nationally week on week, on aspirin 75mg last week in comparison to the week before. In London sales were up 400% week-on-week.’

Elsewhere independent chain LloydsPharmacy told Pulse they had noticed a smaller but still marked increase in sales nationally, with a 27% increase in the volume of sales compared with the same week last year, and a 36% increase in volume compared with the preceding week.

Boots declined to share information on its aspirin sales while Day Lewis, Morrisons and Whitworth said they had not seen a big change in the overall pattern of sales.

GP leaders stressed there is still not enough evidence to recommend anyone takes aspirin routinely for cancer prevention – but said it was more appropriate for the public to consult their local pharmacist about the pros and cons, rather than visiting over-stretched GPs.

Dr Andrew Green, chair of the GPC clinical and prescribing subcommittee, said: ‘I would be encouraging people to have a chat with their pharmacist about it rather than their GP. Whether someone should be taking aspirin or not is well within the pharmacists’ competence.’

He added: ‘The advice from a GP I would suggest is at the moment is we don’t have enough evidence to recommend it for everybody. If a patient wants to disregard that and take it then they should still get some advice – but the pharmacist can advise them if there is anything in their past medical history or their current prescriptions that means they shouldn’t take aspirin.’

Dr Richard West agreed that while people should get advice before deciding to take aspirin, consulting a GP may not be necessary.

Dr West said: ‘It’s a difficult balance – there are undoubtedly some risks from taking it and therefore it is worth discussing it with an appropriate healthcare professional beforehand.

‘However, as we know general practice is under a lot of pressure at the moment and therefore if a pharmacist felt capable of giving that advice then I think that would be perfectly appropriate.’

A spokesperson for the Royal Pharmaceutical Society said: ‘Pharmacists are well practiced in dealing with requests for treatments following a big media story. The links between cancer prevention and aspirin are not new but as yet haven’t lead to a change in indication or licence of aspirin.

‘Although aspirin is often portrayed as a wonder drug, it can cause serious harms, especially in people with pre-existing conditions such as stomach ulcers.’

 

ASPIRIN FOR PRIMARY PREVENTION IN DIABETES ‘SHOULD BE RESTRICTED’

From the FMS Global News Desk of Jeanne Hambleton 9 May 2013             By Caroline Price Pulse Today

 

Daily low-dose aspirin treatment does not prevent cardiovascular events or death in people with type 2 diabetes and no previous cardiovascular disease (CVD), and may even increase the risk of coronary heart disease (CHD) in female patients, shows a large cohort study.

The study

Researchers analysed the outcomes of 18,646 men and women with type 2 diabetes and no CVD history, aged between 30 and 80 years, over an average of four years beginning in 2006, using data from the Swedish National Diabetes Registry. In all, 4,608 patients received low-dose (75 mg/day) aspirin treatment while 14,038 patients received no aspirin treatment, giving 69,743 aspirin person-years and 102,754 non-aspirin person-years of follow-up.

The findings

Aspirin treatment was not associated with any benefit in terms of cardiovascular outcomes or mortality, after propensity score and multivariable adjustment. Aspirin-treated and non-aspirin-treated groups had equivocal risks of the outcomes non-fatal or fatal CVD, fatal CVD, fatal CHD, non-fatal or fatal stroke, fatal stroke and total mortality.

Patients who received aspirin had a significant 19% increased risk of non-fatal or fatal CHD; further analysis stratifying the group by gender showed this was driven by a significant 41% increased risk in women, while there was no increased risk in men. Women also had a 28% increased risk of fatal or non-fatal CVD.

There was also a borderline significant 41% increase in risk of non-fatal or fatal total haemorrhage with aspirin, but this association became weaker when broken down by gender.

Risks of cerebral or ventricular bleeding did not differ between groups, but aspirin use was associated with a significant 64% increased risk of ventricular ulcer, driven by a 2.3-fold increased in women, while no increased risk was found in men.

Furthermore, the effects of aspirin on these endpoints were similar in patients with high estimated CV risk (five-year risk 15% or higher) and those with low estimated CV risk (five-year risk below 15%).

What this means for GPs.

The results support current guidance from the European Society of Cardiology and the European Association for the Study of Diabetes that do not recommend primary prevention with aspirin in patients with diabetes, but conflict with the NICE type 2 diabetes guidelines, which recommend primary prevention with 75 mg/day aspirin in patients aged 50 years or older if their blood pressure is below 145/90 mm/Hg and in patients younger than 50 who have another significant cardiovascular risk factor.

The authors conclude: ‘The present study shows no association between aspirin use and beneficial effects on risks of CVD or mortality in patients with diabetes and no previous CVD and supports the trend towards a more restrictive use of aspirin in these patients, also underlined by the increased risk of ventricular ulcer associated with aspirin.’

 

GPS TOLD TO REVIEW ASPIRIN USE IN PATIENTS WITH ATRIAL FIBRILLATION

From the FMS Global News Desk of Jeanne Hambleton 18 June 2014        By Caroline Price Pulse Today

 

GPs are to be tasked with reviewing all their patients with atrial fibrillation who are taking aspirin, under final NICE guidance published today that recommends anticoagulant therapy as the only option for stroke prevention in these patients.

The new guidance means GPs will need to start advising patients with atrial fibrillation who are on aspirin to stop taking it, and encourage them to take warfarin or one of the newer oral anticoagulants.

NICE said just over a fifth of the UK population with atrial fibrillation – around 200,000 patients – are currently on aspirin, many of whom should be able to be switched onto anticoagulation therapy of some sort.

GP leaders have warned that practices do not have the capacity to proactively call in patients, and suggested that changing management of this number of patients could only be achieved through incentive schemes such as enhanced services or the QOF.

But NICE advisors and CCG cardiology leads have claimed that GPs can do the reviews opportunistically over the coming year.

The final publication comes after it emerged the GPC had raised serious concerns over the complexity of the draft guidance – and warned CCGs would need to consider developing enhanced services to support GPs in delivering it.

Dr Andrew Green, chair of the GPC’s clinical and prescribing subcommittee, told Pulse GPs should feel they can refer patients on if they are not able to deal with all the changes as part of annual reviews.

Dr Green said: ‘I would expect GPs as part of their normal work to consider whether [atrial fibrillation] patients not on anticoagulation should be, in the light of the new guidance. If they should be, then the choice is between anticoagulation with warfarin or one of the newer agents, and if GPs do not feel they have the expertise or resources to do this properly, they have a duty to refer to someone who can.’

He added: ‘Commissioners need to predict this activity and may want to commission a service specifically for this which is more cost-effective than a traditional out-patient referral.’

Local GP leaders told Pulse practices would not take a systematic approach to reviewing and updating patients’ medications unless the work was specifically funded.

Dr Peter Scott, a GP in Solihull and chair of the GPC in West Midlands, said: ‘It’s not going to happen unless it’s resourced and incentivised as part of a DES or LES, or through the QOF – until then I don’t think a systematic approach to this will happen.’

But Dr Matthew Fay, a GP in Shipley, Yorkshire, and member of the NICE guidelines development group, acknowledged the workload concerns and said GPs should be advised to review patients opportunistically.

Dr Fay said: ‘I think it’s perfectly acceptable [to review patients opportunistically]. A lot of these patients who are at risk in this situation we will be reviewing because of their hypertension and other comorbidities, and those patients on aspirin should have that discussed at the next presentation.’

He added: ‘I think anticoagulation is an intimidating topic for clinicians – both in primary and secondary care. I would suggest one person in each practice one clinician is involved with the management of the anticoagulated patients – whether that’s keeping a check on them during the warfarin clinic or being the person who initiates the novel oral anticoagulants.

‘If GPs feel uncomfortable with [managing anticoagulation] then they should be approaching the CCG executive to say, “we need a service to provide expert support for this”. The CCG may choose to come up with an enhanced service – but then whoever is providing the service needs to make sure they are well versed in use of the latest anticoagulants.’

The new guidance says GPs must use the CHA2DS2-VASc score to assess patients’ stroke risk and advise any patients with a score of at least one (men) or two (women) to go onto anticoagulation therapy with warfarin, or another vitamin K antagonist, or with one of the novel oral anticoagulants (NOACs) dabigatran, apixaban or rivaroxaban.

It adds that aspirin should no longer be prescribed solely for stroke prevention to patients with atrial fibrillation.

The HAS-BLED score should be used to assess patients’ risk of bleeding as part of the decision over which anticoagulant to choose.

In the only major revision to the draft guidance, aspirin is no longer to be considered even as part of dual antiplatelet therapy for patients at particularly high bleeding risk, as this combination has now also been ruled out.

 

BENEFITS OF ASPIRIN A DAY FOR CANCER PREVENTION IN MIDDLE-AGED PEOPLE ‘OUTWEIGH HARMS

This story was published a few days ago

 

 

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POTENTIAL THERAPY FOR THE SUDAN STRAIN OF EBOLA COULD HELP CONTAIN SOME FUTURE OUTBREAK

From the FMS Global News Desk of Jeanne Hambleton August 27 2014   American Chemical Society ACS Chemical Biology

Scientists report a new potential weapon in the fight against a strain of ebola (above) that is just as deadly as the one currently devastating West Africa.

Ebola is a rare, but deadly disease that exists as five strains, none of which have approved therapies. One of the most lethal strains is the Sudan ebolavirus (SUDV). Although not the strain currently devastating West Africa, SUDV has caused widespread illness, even as recently as 2012.

In a new study appearing in the journal ACS Chemical Biology, researchers now report a possible therapy that could someday help treat patients infected with SUDV.

John Dye, Sachdev Sidhu, Jonathan Lai and colleagues explain that about 50-90 percent of ebola patients die after experiencing the typical symptoms of the disease, which include fever, muscle aches, vomiting and bleeding. Of the five known ebolaviruses, the Zaire (EBOV) and SUDV strains are the most deadly and cause the most recurring outbreaks.

Many studies have focused on EBOV, the culprit of the current epidemic, but much less attention has been placed on SUDV until now. To develop a therapy for SUDV, this research team turned to an antibody that Dye’s group previously reported.

The team’s antibody was directed against SUDV and was made in mice. But the human immune system could potentially recognize that antibody as foreign and ultimately get rid of it, preventing the antibody from treating the disease. To avoid this situation, they wanted to make a “humanized” version of the antibody.

In the newly published work, the team put the ebola-specific part of the mouse antibody onto a human antibody scaffold and made some changes to this molecule. They identified two versions that were able to fend off SUDV in laboratory tests on cells and in specially bred mice.

“These antibodies represent strong immunotherapeutic candidates for the treatment of SUDV infection,” say the researchers.

This research, however, is not expected to help with the current ebola outbreak that, as of mid-August, has killed at least 1,200 people. That is because antibodies that kill off one strain of the virus have not worked against other strains.

The U.S. Food and Drug Administration — which has not yet approved any ebola therapies — did allow two U.S. aid workers infected during the current outbreak to be treated with an experimental drug, which is a cocktail of antibodies specifically targeting EBOV.

NEW STUDY THROWS INTO QUESTION LONG-HELD BELIEF ABOUT DEPRESSION

From the FMS Global News Desk of Jeanne Hambleton 27 August 2014                                                  ACS Chemical Neuroscience American Chemical Society

New evidence puts into doubt the long-standing belief that a deficiency in serotonin — a chemical messenger in the brain — plays a central role in depression. In the journal ACS Chemical Neuroscience, scientists report that mice lacking the ability to make serotonin in their brains (and thus should have been “depressed” by conventional wisdom) did not show depression-like symptoms.

Donald Kuhn and colleagues at the John D. Dingell VA Medical Center and Wayne State University School of Medicine note that depression poses a major public health problem. More than 350 million people suffer from it, according to the World Health Organization, and it is the leading cause of disability across the globe.

In the late 1980s, the now well-known antidepressant Prozac was introduced. The drug works mainly by increasing the amounts of one substance in the brain — serotonin. So scientists came to believe that boosting levels of the signaling molecule was the key to solving depression. Based on this idea, many other drugs to treat the condition entered the picture. But now researchers know that 60 to 70 percent of these patients continue to feel depressed, even while taking the drugs. Kuhn’s team set out to study what role, if any, serotonin played in the condition.

To do this, they developed “knockout” mice that lacked the ability to produce serotonin in their brains. The scientists ran a battery of behavioral tests. Interestingly, the mice were compulsive and extremely aggressive, but did not show signs of depression-like symptoms. Another surprising finding is that when put under stress, the knockout mice behaved in the same way most of the normal mice did. Also, a subset of the knockout mice responded therapeutically to antidepressant medications in a similar manner to the normal mice. These findings further suggest that serotonin is not a major player in the condition, and different factors must be involved. These results could dramatically alter how the search for new antidepressants moves forward in the future, the researchers conclude.

The authors acknowledge funding from the Department of Veterans Affairs and the Department of Psychiatry and Behavioral Neurosciences at Wayne State University.

 

WHEN WILL I DIE? HOW I DECIDED WHETHER TO TEST FOR EARLY-ONSET ALZHEIMER’S

From the FMS Global News Desk of Jeanne Hambleton Aug. 19, 2014                                                     Stone Hearth Newsletter – Time Magazine By Matthew Thomas

 

People ask me all the time if I want to find out how and when I am going to die. But that is not exactly how they ask it. What they ask is whether I am going to get tested for the gene associated with early-onset Alzheimer’s disease. It is hard, though, to miss the subtext in the question: How morbidly curious are you? How much terror can you withstand?

I do not blame them. These friends know I am 39 and that my father started showing symptoms of Alzheimer’s in his early fifties (and possibly earlier). They know that after a handful of difficult years my father was diagnosed when I was a freshman in college and that he died less than a decade later. They wonder if I am going to take advantage of the remarkable opportunity science affords us to uncover our genetic destinies and plan accordingly.

Modern life is all about making us forget we are capable of dying. We love to feel in control of our mortality, even if we understand that that control is only an illusion. Alzheimer’s disease is the opposite of modern life. It is the ascendancy of entropy and chaos.

My father’s disease had a devastating effect on our family. It did not just take away our time with him and his with us. It also took away his time with the not yet conceived children who would populate the family in his absence. He would have been in his 70s now, surrounded by three grandchildren through my sister and two through my wife and me. It is painful to know what a resource he would have been for them and how much they have lost. He will live, faintly grasped, if at all, only in stories.

When he was still living, we tried to make the best of the situation. When my sister got married, my mother brought my father’s tux to the nursing home and had the staff dress him in it. After the ceremony, while everyone else headed to the reception, two limos carrying my immediate family took a detour to the nursing home for photos.

When I look at the framed shot of us huddled around my father in his wheelchair, I see how hard my sister is trying to keep her emotions in. She is smiling big, but tears are streaming down her face. We are all smiling hard, though there is no driving off the pain and awkwardness of the moment. Everyone’s looking at the camera except my father, who is gazing vacantly the other way, his mouth hanging open. Moments later we drove to the reception, leaving him behind, feeling terrible for doing so. I wanted him not to understand a thing that was happening in that scene, but you never knew what he knew.

For most of my youth, my father seemed to know everything. A universe of information swirled around in his brain. I could hardly put a question to him that he could not answer. The rare times he came up short, he pulled me into his study, took a book off the shelf, lay it on the desk and stood flipping through it with me. I think sometimes he pretended not to know things just so that we could look them up together.

Once, when I was about 10 and my sister about 14, we were walking with my father on the outskirts of his old neighborhood. He stopped in front of a town house and told us Winston Churchill’s mother was born there.

“The iconic English statesman of the century!” he said. “A mother from Brooklyn!” He gave us a look almost wild with the significance of what he was about to say. “The wit!” he said. “The chutzpah! That was the Brooklyn in him!”

Three decades later, I can still remember the moment, bathed in that ethereal light that we reserve for our happiest memories. Why do I remember it, though? How did such a quotidian moment burrow its way into my consciousness and survive? Was it the juxtaposition of incongruous worlds, England and Brooklyn? I don’t think so. I think it was the joy my father took in sharing his knowledge with us.

My father would have loved my twin children. They are 3 years old and full of vitality and personality. My son is unusually strong for such a skinny kid, and remarkably agile. He climbs whatever is available, with a monkey’s speed. When he sits at the piano and pounds the keys, it sounds as if he is playing a real song. My daughter is a sensitive cuddler who remembers everything.

“Daddy, is this from the hotel we stayed at?” she asked the other day, handing me a pad from a Marriott where we stayed six months ago.

Recently my daughter came into our bed in the early morning, lying between my wife and me, and started in on iguanas.

“Iguanas are baby alligators,” she said, and I chuckled at the powers of observation of a developing mind. “Can iguanas learn to open doors?” she asked, and after I offered the opinion that they could not, I pulled her close, gave her kisses and began to choke up.

Maybe when my twins are older, science will have caught up to this disease. We have the best scientific minds working on the problem of Alzheimer’s.

Much like the search for the cure for cancer, there is a massive payout at the end of the rainbow for anyone who comes up with a solution. If there is anything to put one’s faith in in the health care system, it is that the confluence of genius and capital will, in this case, produce the outcome if the outcome is producible. And I do believe it is producible. But if it is not produced in time, no amount of awareness of my fate, if it is to be my fate, is going to forestall its unfolding on me.

My wife and I have little battles over my forgetfulness. She asked me to fix the kink in the hose that runs from the humidifier in our basement to the French drain. A few days later, she gave up and fixed it herself. We had a grill delivered for our backyard, and the flame kept going out on it as soon as we lit it. I was supposed to call about it the next morning, but I would more or less forgotten that we had bought a grill in the first place when I heard my wife on the phone with the store. These are not terrifying signs in themselves — everyone is a little forgetful occasionally — but they make me pause enough to wonder if the worst is coming.

I am built like my father, I sound like him, and if I have a genetic mutation in one of three genes that are all variations of the apolipoprotein E gene, then I will likely develop early-onset Alzheimer’s like him. These genes are rare, accounting for only 1% to 5% of all Alzheimer’s cases. But if I inherited the mutation from my father, then I will probably get the disease.

My grandfather — my father’s father — died relatively young of other causes, so there’s no saying whether he would have gotten early-onset Alzheimer’s. No one else in the family had it that we know of. I have as good a chance of getting familial Alzheimer’s as I have of avoiding it. Genetic testing would settle the question for good.

But what would I gain by knowing I was getting Alzheimer’s? I would not gain another day with my family. I would not gain a leg up on planning. My wife and I have taken care of practical considerations. We have wills. My wife has a durable power of attorney that enables her to make decisions on my behalf. Every policy, every asset, is in both our names. We opened college savings accounts for the kids. I am working hard on my next book. How much more could I prepare?

After some deliberation, I have decided not to get genetic testing done. Instead, I am going to try to live every day as if I know that I am dying. The fact is, we are all dying. If I try to wring the most I can out of every moment, if I set aside time every day that my wife and I keep as inviolate as possible, if I give my wife and children quality interactions whenever we are in the same room, if I leave the smartphone on the counter and realize there is no information more important than the information I get in my interactions with my loved ones, then how different is any of that from what I would do if I knew I was getting Alzheimer’s?

Scientific studies suggest that my children are at just the age when they can begin to form lasting memories of their experiences. If I am aware that I am going to be gone someday and I consider it possible that that day will come far sooner than I would like, then I want them to grow up not only knowing their father well but also knowing that they are well loved. I want to get in better shape for them, because I would like them to see what a truly vital father looks like. And I have decided to read to them whenever they ask, if I possibly can. I do not have any memory of my father telling me, “No more books” at bedtime. I will forever picture him with an arm around me, holding a book out before me, showing me the world.

Thomas is the author of the debut novel,’We Are Not Ourselves’, out now.

 

Back tomorrow Jeanne

 

 

 

 

 

 

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BEYOND DNA: EPIGENETICS PLAYS LARGE ROLE IN BLOOD FORMATION

From FMS Global News Desk of Jeanne Hambleton Released: 11-Aug-2014
Source: Weizmann Institute of ScienceScience, August 7, 2014

Newswise — Blood stem cells have the potential to turn into any type of blood cell, whether it be the oxygen-carrying red blood cells, or the immune system’s many types of white blood cells that help fight infection. How exactly is the fate of these stem cells regulated? Preliminary findings from research conducted by scientists from the Weizmann Institute of Science and the Hebrew University are starting to reshape the conventional understanding of the way blood stem cell fate decisions are controlled, thanks to a new technique for epigenetic analysis they have developed. Understanding epigenetic mechanisms (environmental influences other than genetics) of cell fate could lead to the deciphering of the molecular mechanisms of many diseases, including immunological disorders, anemia, leukemia, and many more. It also lends strong support to findings that environmental factors and lifestyle play a more prominent role in shaping our destiny than previously realized.

The process of differentiation – in which a stem cell becomes a specialized mature cell – is controlled by a cascade of events in which specific genes are turned “on” and “off” in a highly regulated and accurate order. The instructions for this process are contained within the DNA itself in short regulatory sequences. These regulatory regions are normally in a “closed” state, masked by special proteins called histones to ensure against unwarranted activation. Therefore, to access and “activate” the instructions, this DNA mask needs to be “opened” by epigenetic modifications of the histones so it can be read by the necessary machinery.

In a paper published in Science, Dr. Ido Amit and David Lara-Astiaso of the Weizmann Institute’s Department of Immunology, along with Prof. Nir Friedman and Assaf Weiner of the Hebrew University of Jerusalem, charted – for the first time – histone dynamics during blood development. Thanks to the new technique for epigenetic profiling they developed, in which just a handful of cells – as few as 500 – can be sampled and analyzed accurately, they have identified the exact DNA sequences, as well as the various regulatory proteins, that are involved in regulating the process of blood stem cell fate.

Their research has also yielded unexpected results: As many as 50% of these regulatory sequences are established and opened during intermediate stages of cell development. This means that epigenetics is active at stages in which it had been thought that cell destiny was already set. “This changes our whole understanding of the process of blood stem cell fate decisions,” says Lara-Astiaso, “suggesting that the process is more dynamic and flexible than previously thought.”

Although this research was conducted on mouse blood stem cells, the scientists believe that the mechanism may hold true for other types of cells. “This research creates a lot of excitement in the field, as it sets the groundwork to study these regulatory elements in humans,” says Weiner.

Discovering the exact regulatory DNA sequence controlling stem cell fate, as well as understanding its mechanism, holds promise for the future development of diagnostic tools, personalized medicine, potential therapeutic and nutritional interventions, and perhaps even regenerative medicine, in which committed cells could be reprogrammed to their full stem cell potential.

Dr. Ido Amit’s research is supported by the M.D. Moross Institute for Cancer Research; the J&R Center for Scientific Research; the Jeanne and Joseph Nissim Foundation for Life Sciences Research; the Abramson Family Center for Young Scientists; the Wolfson Family Charitable Trust; the Abisch Frenkel Foundation for the Promotion of Life Sciences; the Leona M. and Harry B. Helmsley Charitable Trust; Sam Revusky, Canada; the Florence Blau, Morris Blau and Rose Peterson Fund; the estate of Ernst and Anni Deutsch; the estate of Irwin Mandel; and the estate of David Levinson. Dr. Amit is the incumbent of the Alan and Laraine Fischer Career Development Chair.

The Weizmann Institute of Science in Rehovot, Israel, is one of the world’s top-ranking multidisciplinary research institutions. Noted for its wide-ranging exploration of the natural and exact sciences, the Institute is home to scientists, students, technicians, and supporting staff. Institute research efforts include the search for new ways of fighting disease and hunger, examining leading questions in mathematics and computer science, probing the physics of matter and the universe, creating novel materials, and developing new strategies for protecting the environment.

 

RESEARCHERS IDENTIFY A BRAIN “SWITCHBOARD” IMPORTANT IN ATTENTION AND SLEEP

From the FMS Global News Desk of Jeanne Hambleton  Embargoed: 14-Aug-2014
Source : NYU Langone Medical Center Citations Cell

Newswise — New York City, August 14, 2014 – Researchers at NYU Langone Medical Center and elsewhere, using a mouse model, have recorded the activity of individual nerve cells in a small part of the brain that works as a “switchboard,” directing signals coming from the outside world or internal memories. Because human brain disorders such as schizophrenia, autism, and post-traumatic stress disorder typically show disturbances in that switchboard, the investigators say the work suggests new strategies in understanding and treating them.

In a study to be published in the journal Cell online Aug. 14, a team led by Michael Halassa, MD, PhD, assistant professor of psychiatry, neuroscience and physiology, and a member of the NYU Neuroscience Institute, showed how neurons in the thalamic reticular nucleus (TRN) — the so-called switchboard — direct sensory signals such as vision from the outside world, and internal information such as memories, to their appropriate destinations.

“We have never been able to observe as precisely how this structure worked before,” says Dr. Halassa. “This study shows us how information can be routed in the brain, giving us tremendous insight into how it might be broken in psychiatric disorders.”

For the study, researchers used a multi-electrode technique to record the activity of individual neurons in the TRN, a thin layer of nerve cells that covers the thalamus, a structure in the forebrain that relays information to the cerebral cortex, the seat of higher-level functions such as learning and language. TRN cells are known to send inhibitory signals to the thalamus, determining which information is blocked.

The activity of TRN cells, the researchers found, depended on whether the mouse was asleep or awake and alert. TRN cells that controlled sensory input were far more active during sleep, particularly during the periods of sleep when brief bursts of fast-cycling brain waves, called spindles, occur. Sleep spindles, which are associated with blocking sensory input during sleep, are known to be diminished among people with autism and schizophrenia.

Dr. Halassa says the new findings suggest that faulty TRN cells may be disrupting the appropriate filtering of information in these conditions. His group is now exploring this filtering process in animal models of schizophrenia and autism.

In experiments with alert mice, Dr. Halassa’s group found that sensory TRN cells fired very little. This suggested that while these neurons block the flow of external information during sleep, they facilitate the flow of information when an animal is awake and alert.

By contrast, TRN cells that control the flow of internal signals behaved in an opposite fashion, firing very little in sleep. This lowered level of activity, Dr. Halassa suspects, may allow memories to form, which is known to occur during sleep. The thalamus has nerve connections to the hippocampus, which plays an important role in learning and memory.

In a second part of the study, Dr. Halassa’s group employed a technique called optogenetics, which uses light to turn nerve cells on and off, to test whether altering TRN nerve cell firing affected attention behavior in the mice.

In one experiment, mice learned to associate a visual stimulus with food. Well-rested mice took just a second or two to find food when a stimulus was presented, while sleep-deprived mice took much longer. By turning on TRN cells that specifically controlled the visual part of the thalamus, as would happen normally in sleep, the rested mice behaved like they were sleep deprived. On the other hand, when the researchers turned off these TRN cells, sleep-deprived mice quickly found the food.

“With a flick of a light switch, we seemed able to alter the mental status of the mice, changing the speed at which information can travel in the brain,” says Dr. Halassa. Mapping brain circuits and disrupting their pathways will hopefully lead to new treatment targets for a range of neuropsychiatric disorders, he adds.

In addition to Halassa, other NYU Langone researchers involved in this study were Zhe Chen, PhD, and Ralf Wimmer, PhD. Additional research support was provided by Philip Brunetti and Matthew Wilson, PhD, at the Picower Institute for Learning and Memory at the Massachusetts Institute of Technology in Cambridge, Mass.; Shengli Zhao, PhD, and Fan Wang, PhD, at Duke University in Durham, NC; Basilis Zukopoulos, PhD, at Boston University; and Emery Brown, MD, PhD, at Harvard University and the Massachusetts Institute of Technology.

About NYU Langone Medical Center:
NYU Langone Medical Center, a world-class, patient-centered, integrated academic medical center, is one of the nation’s premier centers for excellence in clinical care, biomedical research, and medical education. Located in the heart of Manhattan, NYU Langone is composed of four hospitals — Tisch Hospital, its flagship acute care facility; Rusk Rehabilitation; the Hospital for Joint Diseases, the Medical Center’s dedicated inpatient orthopaedic hospital; and Hassenfeld Children’s Hospital, a comprehensive pediatric hospital supporting a full array of children’s health services across the Medical Center — plus the NYU School of Medicine, which since 1841 has trained thousands of physicians and scientists who have helped to shape the course of medical history. The Medical Center’s tri-fold mission to serve, teach, and discover is achieved 365 days a year through the seamless integration of a culture devoted to excellence in patient care, education, and research.

 

COOL TEMPERATURE ALTERS HUMAN FAT AND METABOLISM

From the FMS Global News Desk of Jeanne Hambleton July 28, 2014                                                                       NIH Research Matters National Institute of Health

 

Men exposed to a cool environment overnight for a month had an increase in brown fat with corresponding changes in metabolism.

The finding hints at new ways to alter the body’s energy balance to treat conditions such as obesity and diabetes.

Humans have several types of fat. White fat stores extra energy. Too much white fat, a characteristic of obesity, increases the risk of type 2 diabetes and other diseases.

Brown fat, in contrast, burns chemical energy to create heat and help maintain body temperature. Researchers have previously shown that, in response to cold, white fat cells in both animals and humans take on characteristics of brown fat cells.

A team led by Dr. Francesco S. Celi of Virginia Commonwealth University and Dr. Paul Lee, now at the Garvan Institute of Medical Research in Australia, explored the effects of ambient temperature on brown fat and metabolism. The study was supported in part by NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and the NIH Clinical Center. Results appeared online on June 22, 2014, in Diabetes.

The researchers had 5 healthy men, average age 21 years, reside for 4 months in a clinical research unit in the NIH Clinical Center in Bethesda, Maryland. The men engaged in regular activities during the day and then returned to their private room each evening. The temperature of the room was set to 24 °C (75 °F) during the first month, 19 °C (66 °F) the second month, 24 °C again for the third month, and 27 °C (81 °F) the remaining month.

The participants were exposed to the temperature for at least 10 hours each night. They wore standard hospital clothing and had bed sheets only. All meals were provided, with calorie and nutrient content carefully controlled and all consumption monitored. At the end of each month, the men underwent extensive evaluations, including energy expenditure testing, muscle and fat biopsies, and PET/CT scanning of an area of the neck and upper back region to measure brown fat volume and activity.

After a month of exposure to mild cold, the participants had a 42% increase in brown fat volume and a 10% increase in fat metabolic activity. These alterations returned to near baseline during the following month of neutral temperature, and then were completely reversed during the final month of warm exposure. All the changes occurred independently of seasonal changes.

The increase in brown fat following a month of cold exposure was accompanied by improved insulin sensitivity after a meal during which volunteers were exposed to mild cold. Prolonged exposure to mild cold also resulted in significant changes in metabolic hormones such as leptin and adiponectin. There were no changes in body composition or calorie intake.

The findings suggest that humans may acclimate to cool temperature by increasing brown fat, which in turn may lead to improvements in glucose metabolism. These changes can be dampened or reversed following exposure to warmer temperatures.

“The big unknown until this study was whether or not we could actually manipulate brown fat to grow and shrink in a human being,” Lee says. “The improvement in insulin sensitivity accompanying brown fat gain may open new avenues in the treatment of impaired glucose metabolism.”

—by Carol Torgan, Ph.D.

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HOW EBOLA IS TRANSMITTED

From the FMS Global News Desk of Jeanne Hambleton Posted on August 23, 2014               By Stone Hearth News

Boston, MA – Although the Centers for Disease and Prevention (CDC) reports no known cases of Ebola transmission in the United States, a Harvard School of Public Health (HSPH)/SSRS poll released today (August 21, 2014) shows that four in ten (39%) adults in the U.S. are concerned that there will be a large outbreak in the U.S., and a quarter (26%) are concerned that they or someone in their immediate family may get sick with Ebola over the next year.

The nationally representative poll of 1,025 adults was conducted August 13-17, 2014 by researchers at HSPH and SSRS, an independent research company. The margin of error for total respondents is +/-3.6 percentage points at the 95% confidence level.

Ebola: a brief insight into what it is all about

Ebola hemorrhagic fever is a severe, often fatal disease in humans and nonhuman primates, such as monkeys, gorillas and chimpanzees. Four countries have reported infections: Guinea, Liberia, Nigeria, and Sierra Leone. Officials report 1,350 have died as of August 21, 2014 and over 2,473 people have been infected since March 2014. For an update on the outbreak, see this CDC link: http://www.cdc.gov/vhf/ebola/outbreaks/guinea/index.html

The HSPH/SSRS poll found people with less education are more likely to be concerned about an outbreak in the U.S. (less than high school 50% vs. some college 36% vs. college grad or more 24%). People with less education are also more concerned they or their family will get sick with Ebola (less than high school 37% vs. some college 22% vs. college grad or more 14%). Perhaps related, those with less education are also less likely to be following the news about the Ebola outbreak in West Africa closely (total 63%; less than high school 57% and some college 62% vs. college grad or more 73%).

Two-thirds of people (68%) surveyed believe Ebola spreads “easily” (“very easily” or “somewhat easily”) from those who are sick with it. This perception may contrast with CDC, World Health Organization (WHO), and other health experts who note that Ebola is not an airborne illness, and is transmitted through direct contact with infected bodily fluids, infected objects, or infected animals. For more on how Ebola is transmitted: http://www.cdc.gov/vhf/ebola/transmission/index.html

A third of those polled (33%) believe there is “an effective medicine to treat people who have gotten sick with Ebola.” According to the CDC and WHO, there is no proven anti-viral medicine, however, treating symptoms – such as maintaining fluids, oxygen levels, and blood pressure – can increase the odds of survival. To date, the media reports two people infected with Ebola overseas have been treated in the U.S.

“Many people are concerned about a large scale outbreak of Ebola occurring in the U.S.,” said Gillian SteelFisher, PhD, deputy director of the Harvard Opinion Research Program and research scientist in the HSPH Department of Health Policy and Management. “As they report on events related to Ebola, the media and public health officials need to better inform Americans of Ebola and how it is spread.”

For more information about the disease, see the CDC’s Questions and Answers about Ebola: http://www.cdc.gov/vhf/ebola/outbreaks/guinea/qa.html

WHO information: http://www.who.int/csr/disease/ebola/en/

Harvard School of Public Health brings together dedicated experts from many disciplines to educate new generations of global health leaders and produce powerful ideas that improve the lives and health of people everywhere. As a community of leading scientists, educators, and students, we work together to take innovative ideas from the laboratory to people’s lives—not only making scientific breakthroughs, but also working to change individual behaviors, public policies, and health care practices. Each year, more than 400 faculty members at HSPH teach 1,000-plus full-time students from around the world and train thousands more through online and executive education courses. Founded in 1913 as the Harvard-MIT School of Health Officers, the School is recognized as America’s oldest professional training program in public health.

SSRS is a full-service survey and market research firm managed by a core of dedicated professionals with advanced degrees in the social sciences. SSRS designs and implements solutions to complex strategic, tactical, public opinion, and policy issues in the U.S. and in more than 40 countries worldwide. SSRS partners with clients interested in conducting high-quality research. SSRS is renowned for its sophisticated sample designs and its experience with all modes of data collection, including those involving multimodal formats. SSRS provides the complete set of analytical, administrative and management capabilities needed for successful project execution.

 

IBUPROFEN POSING POTENTIAL THREAT TO FISH

From FMS Global News Desk of Jeanne HambletonPosted on August 22, 2014    By Stone Hearth News – Source University of York – Environmental International

Research led by the University of York UK suggests that many rivers contain levels of ibuprofen that could be adversely affecting fish health.

Using a new modelling approach, the researchers estimated the levels of 12 pharmaceutical compounds in rivers across the UK. They found that while most of the compounds were likely to cause only a low risk to aquatic life, ibuprofen might be having an adverse effect in nearly 50 per cent of the stretches of river studied.

The results of the study, which involved York’s Environment Department, the Centre for Ecology and Hydrology, F. Hoffmann-La Roche Ltd (Switzerland) and the Food and Environment Research Agency (Fera), are reported in the journal Environment International.

In what is believed to be the first study to establish the level of risk posed by ibuprofen at the country scale, the researchers examined 3,112 stretches of river which together receive inputs from 21 million people.

Professor Alistair Boxall, from the University of York’s Environment Department, said: “The results of our research show that we should be paying much closer attention to the environmental impacts of drugs such as ibuprofen which are freely available in supermarkets, chemists and elsewhere.”

The researchers have developed a combined monitoring and modelling approach that takes into account factors such as the non-use of prescribed drugs by patients, and addresses differences in metabolism in individuals who are using a drug. The new approach also accounts for removal processes in the local sewerage network and for differences in the effectiveness of different wastewater treatment technologies. In this way, it provides more accurate estimates of the concentrations of compounds entering rivers than previous modelling approaches.

Richard Williams, from the Centre for Ecology & Hydrology (CEH) – a public-sector research centre which is part of the Natural Environment Research Council (NERC), said: “When we compared the results of our modelling with available monitoring data for pharmaceuticals in the UK, we were delighted at the close agreement between the modelled and measured data.”

Professor Boxall added: “While our study focused on pharmaceuticals, the approach we have developed could also be valuable in assessing the risks of other ‘down the drain’ chemicals and could help inform our understanding of the important dissipation processes for pharmaceuticals in the pathway from the patient to the environment.”

 

CITIES ARE MAKING SPIDERS GROW BIGGER AND MULTIPLY FASTER

From FMS Global News Desk of Jeanne Hambleton Posted on August 20, 2014    Stone Hearth News  By Nick Stockton   Permalink WIRED

Something about city life appears to be causing spiders to grow larger than their rural counterparts. And if that is not enough to give you nightmares, these bigger urban spiders are also multiplying faster.

A new study published today in PLOS One shows that golden orb weaver spiders living near heavily urbanized areas in Sydney, Australia tend to be bigger, better fed, and have more babies than those living in places less touched by human hands.

The study’s authors collected 222 of the creatures from parks and bushland throughout Sydney, and correlated their sizes to features of the built and natural landscape.

They dissected each specimen back at the lab, and determined its size, health, and fecundity by measuring four attributes: the length of the spider’s longest leg segment, the ratio of that leg segment to overall body weight, the amount of fat on the spider, and its ovary size.

To measure urbanization, the authors looked primarily at ground cover throughout the city, at several scales, where they collected each spider: Are surfaces mostly paved? Is there a lack of natural vegetation? Lawns as opposed to leaf litter?

“The landscape characteristics most associated with larger size of spiders were hard surfaces (concrete, roads etc) and lack of vegetation,” said Elizabeth Lowe, a Ph.D student studying arachnids at the University of Sydney.

Humped golden orb weavers are a common arachnid along Australia’s east coast. They get their name from their large, bulging thorax, and the gold silk they use to spin their spherical webs. They typically spend their lives in one place, constantly fixing the same web (which can be a meter in diameter). Each web is dominated by a single female, though 4 or 5 much smaller males usually hang around the edges of the web, waiting for an opportunity to mate (only occasionally does the female eat them afterwards).

Paved surfaces and lack of vegetation mean cities are typically warmer than the surrounding countryside. Orb weavers are adapted to warm weather, and tend to grow bigger in hotter temperatures. The correlation between size and urban-ness manifested at every scale. Citywide, larger spiders were found closer to the central business district. And, their immediate surroundings were more likely to be heavily paved and less shady.

More food also leads to bigger spiders, and the scientists believe that human activity attracts a smorgasbord of orb weavers’ favorite prey. Although the study was not designed to determine exactly how the spiders were getting bigger, the researchers speculate that things like street lights, garbage, and fragmented clumps of plant life might attract insects. They also believe that the heat island effect might let urban spiders mate earlier in the year, and might even give them time to hatch multiple broods.

The orb weavers could also be keeping more of what they catch. Because they are such prolific hunters, orb weavers’ webs are usually home to several other species of spiders that steal food. The researchers found that these little kleptos were less common in webs surrounded by pavement and little vegetation.

Lowe says quite a few species of spider are successful in urban areas, and she would not be surprised if some of these other species were also getting bigger. Despite how terrifying this sounds, she assures me that this is actually a good thing.

“They control fly and pest species populations and are food for birds,” she said.

 (I do not like spiders  and the idea of them getting bigger does not make me happy. Glad I do not live in Sydney with those beasties.)  Back tomorrow,  Jeanne
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HOW LIZARDS REGENERATE THEIR TAILS: RESEARCHERS DISCOVER GENETIC ‘RECIPE’

Finding may impact future therapies for spinal cord injuries -regeneration of limbs in humans

From FMS Global News Desk of Jeanne Hambleton Released: 20-Aug-2014
Source : Arizona State University College of Liberal Arts and Sciences          Citations PLOS ONE

 

Newswise — TEMPE, Ariz. – By understanding the secret of how lizards regenerate their tails, researchers may be able to develop ways to stimulate the regeneration of limbs in humans. Now, a team of researchers from Arizona State University is one step closer to solving that mystery. The scientists have discovered the genetic “recipe” for lizard tail regeneration, which may come down to using genetic ingredients in just the right mixture and amounts.

An interdisciplinary team of scientists used next-generation molecular and computer analysis tools to examine the genes turned on in tail regeneration. The team studied the regenerating tail of the green anole lizard (Anolis carolinensis), which when caught by a predator, can lose its tail and then grow it back.

The findings are published today in the journal PLOS ONE.

“Lizards basically share the same toolbox of genes as humans,” said lead author Kenro Kusumi, professor in ASU’s School of Life Sciences and associate dean in the College of Liberal Arts and Sciences.

“Lizards are the most closely-related animals to humans that can regenerate entire appendages. We discovered that they turn on at least 326 genes in specific regions of the regenerating tail, including genes involved in embryonic development, response to hormonal signals and wound healing.”

Other animals, such as salamanders, frog tadpoles and fish, can also regenerate their tails, with growth mostly at the tip. During tail regeneration, they all turn on genes in what is called the ‘Wnt pathway’ — a process that is required to control stem cells in many organs such as the brain, hair follicles and blood vessels. However, lizards have a unique pattern of tissue growth that is distributed throughout the tail.

“Regeneration is not an instant process,” said Elizabeth Hutchins, a graduate student in ASU’s molecular and cellular biology program and co-author of the paper.

“In fact, it takes lizards more than 60 days to regenerate a functional tail. Lizards form a complex regenerating structure with cells growing into tissues at a number of sites along the tail.”

“We have identified one type of cell that is important for tissue regeneration,” said Jeanne Wilson-Rawls, co-author and associate professor with ASU’s School of Life Sciences.

“Just like in mice and humans, lizards have satellite cells that can grow and develop into skeletal muscle and other tissues.”

“Using next-generation technologies to sequence all the genes expressed during regeneration, we have unlocked the mystery of what genes are needed to regrow the lizard tail,” said Kusumi.

“By following the genetic recipe for regeneration that is found in lizards, and then harnessing those same genes in human cells, it may be possible to regrow new cartilage, muscle or even spinal cord in the future.”

The researchers hope their findings will help lead to discoveries of new therapeutic approaches to spinal cord injuries, repairing birth defects, and treating diseases such as arthritis.

The research team included Kusumi, Hutchins, Wilson-Rawls, Alan Rawls, and Dale DeNardo from ASU School of Life Sciences, Rebecca Fisher from ASU School of Life Sciences and the University of Arizona College of Medicine Phoenix, Matthew Huentelman from the Translational Genomic Research Institute, and Juli Wade from Michigan State University. This research was funded by grants from the National Institutes of Health and Arizona Biomedical Research Commission.

ASU’s School of Life Sciences is an academic unit of the College of Liberal Arts and Sciences.

Arizona State University is the largest public research university in the United States under a single administration, with total student enrollment of more than 70,000 in metropolitan Phoenix, the nation’s sixth-largest city. ASU is creating a new model for American higher education, an unprecedented combination of academic excellence, entrepreneurial energy and broad access. This New American University is a single, unified institution comprising four differentiated campuses positively impacting the economic, social, cultural and environmental health of the communities it serves. Its research is inspired by real-world application, blurring the boundaries that traditionally separate academic disciplines. ASU champions intellectual and cultural diversity, and welcomes students from all 50 states and more than 120 nations.

 (WOW what an exciting development for soldiers who lost limbs in war and those born less fortunate than ourselves. What great excitement there must have been in that laboratory! Well done to those involved.)

SINGLE GENE CONTROLS JET LAG

Salk researchers discover a master gene responsible for sleep and wake cycles, offering hope for a drug that could help reset sleep

From the FMS Global News Desk of Jeanne Hambleton Released: 13-Aug-2014
Source: Salk Institute for Biological Studies Citations eLife

 

Newswise — LA JOLLA–Scientists at the Salk Institute for Biological Studies have identified a gene that regulates sleep and wake rhythms.

The discovery of the role of this gene, called Lhx1, provides scientists with a potential therapeutic target to help night-shift workers or jet lagged travelers adjust to time differences more quickly. The results, published in eLife, can point to treatment strategies for sleep problems caused by a variety of disorders.

“It’s possible that the severity of many dementias comes from sleep disturbances,” says Satchidananda Panda, a Salk associate professor who led the research team. “If we can restore normal sleep, we can address half of the problem.”

Every cell in the body has a “clock” – an abundance of proteins that dip or rise rhythmically over approximately 24 hours. The master clock responsible for establishing these cyclic circadian rhythms and keeping all the body’s cells in sync is the suprachiasmatic nucleus (SCN), a small, densely packed region of about 20,000 neurons housed in the brain’s hypothalamus.

More so than in other areas of the brain, the SCN’s neurons are in close and constant communication with one another. This close interaction, combined with exposure to light and darkness through vision circuits, keeps this master clock in sync and allows people to stay on essentially the same schedule every day. The tight coupling of these cells also helps make them collectively resistant to change. Exposure to light resets less than half of the SCN cells, resulting in long periods of jet lag.

In the new study, researchers disrupted the light-dark cycles in mice and compared changes in the expression of thousands of genes in the SCN with other mouse tissues. They identified 213 gene expression changes that were unique to the SCN and narrowed in on 13 of these that coded for molecules that turn on and off other genes. Of those, only one was suppressed in response to light: Lhx1.

“No one had ever imagined that Lhx1 might be so intricately involved in SCN function,” says Shubhroz Gill, a postdoctoral researcher and co-first author of the paper. Lhx1 is known for its role in neural development: it’s so important, that mice without the gene do not survive. But this is the first time it has been identified as a master regulator of light-dark cycle genes.

By recording electrical activity in the SCN of animals with reduced amounts of the Lhx1 protein, the researchers saw that the SCN neurons weren’t in sync with one another, despite appearing rhythmic individually.

“It was all about communication–the neurons were not talking to each other without this molecule,” says Ludovic Mure, a postdoctoral researcher and an author on the paper. A next step in the work will be to understand exactly how Lhx1 affects the expression of genes that creates this synchronicity.

Studying a mouse version of jet lag–an 8-hour shift in their day-night cycle–the scientists found that those with little or no Lhx1 readjusted much faster to the shift than normal mice. This suggests that because these neurons are less in sync with one another, they are more easily able to shift to a new schedule, though it is difficult for them to maintain that schedule, Panda says.

These mice also exhibited reduced activity of certain genes, including one that creates vasoactive intestinal peptide or Vip, a molecule that has important roles in development and as a hormone in the intestine and blood. In the brain, Vip affects cell communication, but nobody had known that Lhx1 regulated it until now, Panda says. Interestingly, the team also found that adding Vip restored cell synchrony in the SCN.

“This approach helped us to close that knowledge gap and show that Vip is a very important protein, at least for SCN,” Panda says. “It can compensate for the loss of Lhx1.”

On the other hand, cutting back on Vip could be another way to treat jet lag. Vip could be an even easier drug target compared with Lhx1 because Vip is secreted from cells rather than inside cells, Panda says. “If we find a drug that will block the Vip receptor or somehow break down Vip, then maybe that will help us reset the clock much faster,” he adds.

The new results take the group a step closer to their goal of creating cell regenerative therapies that restore the SCN and ameliorate sleep problems. The scientists have made their gene expression data available through a searchable web interface at http://scn.salk.edu, giving other researchers a handy way to explore the effect of light and dark in genes in the SCN and other tissues.

Other researchers on the study were Megumi Hatori, now at Keio University School of Medicine in Tokyo, and Martyn Goulding and Dennis D.M. O’Leary of Salk.

The work was supported by fellowships from The Japan Society for the Promotion of Science, Messinger Healthy Living, the Fyssen and Catharina Foundation, the Mary K. Chapman Foundation, The Leona M. and Harry B. Helmsley Charitable Trust, the National Institutes of Health, the Hearst Foundation and the Glenn Foundation.

About the Salk Institute for Biological Studies:
The Salk Institute for Biological Studies is one of the world’s preeminent basic research institutions, where internationally renowned faculty probe fundamental life science questions in a unique, collaborative and creative environment. Focused both on discovery and on mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer’s, diabetes and infectious diseases by studying neuroscience, genetics, cell and plant biology, and related disciplines.

Faculty achievements have been recognized with numerous honors, including Nobel Prizes and memberships in the National Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas Salk, MD, the Institute is an independent nonprofit organization and architectural landmark.

 (ANOTHER FANTASTIC DEVELOPMENT for fibromites who have problems sleeping and the elderly who we were learn have increasing sleep problems with age.)

TO CONTROL DRINKING, USE A RULE OF THUMB

From the FMS Global News Desk of Jeanne Hambleton      Posted on August 22, 2014 by Stone Hearth News

Newswise — AMES, Iowa – Sticking to a general rule of pouring just a half glass of wine limits the likelihood of over consumption, even for men with a higher body mass index. That is the finding of a new Iowa State and Cornell University study to be published in a forthcoming issue of the International Journal of Drug Policy.

Laura Smarandescu, lead author and an assistant professor of marketing at Iowa State, says the research team looked at a variety of factors to understand and control over pouring. Researchers found BMI affected how much men poured, but had no influence on women. However, people who used a “rule of thumb,” such as a half-glass rule or a two-fingers-from-the-top rule when pouring wine, poured less regardless of BMI or gender.

“About 70 percent of the people in the sample used the half-glass rule, and they poured significantly less by about 20 percent,” Smarandescu said.

“It is a big difference. We would suggest using a rule of thumb with pouring because it makes a big difference in how much people pour and prevents them from over drinking.”

Men with a higher BMI, who did not use a rule of thumb, poured more – 31 percent more for men considered overweight or obese and 26 percent more for men at the midpoint of the normal BMI range. While BMI did not affect how much women poured, those at the midpoint of the normal BMI poured 27 percent less when using the half-glass rule than those who did not.

Researchers were not surprised to find men poured more than women, which is consistent with other studies of alcohol consumption. However, they did not expect the half glass rule would be an exception to men pouring more.

“In this study, we had every expectation that men would always pour more than women, no matter what. But what we found is that the rule of thumb effect is so strong that men using a rule of thumb at all levels of BMI actually poured less than women who were not using a rule of thumb,” said Doug Walker, an assistant professor of marketing at Iowa State.

Researchers asked 74 college students and staff to pour wine in a variety of settings so that they could control for the size, shape and color of the glass, as well as if wine is poured with a meal. They poured both red and white wine from bottles with different levels of fullness. Participants were told to pour as much as wine as they normally would in one setting.

Impact of social norms

Drinking is more socially acceptable for men than women, which is one explanation for why BMI did not have the same effect on women, researchers said. Women are often more conscious of how much they are pouring and will pour less.

“Women are more likely to socially compare with other women. They are aware that drinking is not as socially acceptable for women as it is for men, although it is becoming more acceptable than it has been in the past. But for men there is still more of a culture of drinking and pouring more,” Smarandescu said.

The study looked only at pours, not consumption. However, researchers point to previous studies that show serving size is linked with overeating. Free pouring wine increases the tendency to over consume because it is not as easily measured as other types of beer or spirits.

“It is essential for all drinkers, especially men of higher BMIs, to have a rule of thumb for self-serving, because eye-balling a serving size is a difficult task and will often lead people to pour too much,” said Brian Wansink, a professor of marketing at Cornell.

“Next time you open a bottle, serve yourself a half glass – regardless of the size of your glass—and you will be less likely to accidentally drink too much.”

(Let us hope these folks pouring all these half glasses of wine are not drink driving to get home.) Back tomorrow Jeanne

 

 

 

 

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GPs FEEL UNDER PRESSURE TO PRESCRIBE ANTIBIOTICS

From the FMS Global News Desk of Jeanne Hambleton                                       PULSE 19 August 2014 | By Caroline Price

GPs feel pressure to prescribe antibiotics and sometimes prescribe them even when they do not feel it is necessary, a survey has revealed.

The survey of 1,000 GPs found 90% of respondents felt pressure from patients to prescribe them antibiotics, while over a quarter – 28% – said they prescribe them several times a week when they are unsure they are medically necessary.

The survey was commissioned by charity Nesta for the £10 million Longitude Prize – after the public voted for the prize to be focused on antibiotic use and the growing problem of antibiotic resistance.

Nearly half – 45% – of the GPs surveyed said they had prescribed antibiotics for a viral infection, knowing it would not be effective. But 70% of GPs also said they sometimes prescribed them because of doubts about whether an infection was viral or bacterial, with 24% citing a lack of easy-to-use diagnostic tools.

Dr Rosemary Leonard, a GP in London, said: ‘These results show the pressure GPs face to prescribe antibiotics when they are not necessary, something I understand very well.’ 

‘The more antibiotics taken, the more resistant bacteria come to them. Antibiotic resistance is a real issue and more needs to be done conserve antibiotics for the future. Diagnostics play a valuable role in making this happen. Not only can diagnostics help determine the type of infection someone has, they could gather valuable data and aid the global surveillance efforts.’

 

RESEARCHERS OBTAIN KEY INSIGHTS INTO HOW THE INTERNAL BODY CLOCK IS TUNED

From FMS Global News Desk of Jeanne Hambleton Released: 18-Aug-2014
Source : UT Southwestern Medical Center

Newswise — DALLAS – August 18, 2014 – Researchers at UT Southwestern Medical Center have found a new way that internal body clocks are regulated by a type of molecule known as long non-coding RNA.

The internal body clocks, called circadian clocks, regulate the daily “rhythms” of many bodily functions, from waking and sleeping to body temperature and hunger. They are largely “tuned” to a 24-hour cycle that is influenced by external cues such as light and temperature.

“Although we know that long non-coding RNAs are abundant in many organisms, what they do in the body, and how they do it, has not been clear so far,” said Dr. Yi Liu, Professor of Physiology.

“Our work establishes a role for long non-coding RNAs in ‘tuning’ the circadian clock, but also shows how they control gene expression.”

Determining how circadian clocks work is crucial to understanding several human diseases, including sleep disorders and depression in which the clock malfunctions. The influence of a functional clock is evident in the reduced performance of shift workers and the jet lag felt by long-distance travellers.

Dr. Liu and his team were able to learn more about the circadian rhythms by studying model systems involving the bread mold, Neurospora crassa. The researchers found that the expression of a clock gene named frequency (frq) is controlled by a long non-coding RNA named qrf (frq backwards) − an RNA molecule that is complementary, or antisense, to frq. Unlike normal RNA molecules, qrf does not encode a protein, but it can control whether and how much frq protein is produced.

Specifically, qrf RNA is produced in response to light, and can then interfere with the production of the frq protein. In this way, qrf can “re-set” the circadian clock in a light-dependent way. This regulation works both ways: frq can also block the production of qrf. This mutual inhibition ensures that the frq and qrf RNA molecules are present in opposite “phases” of the clock and allows each RNA to oscillate robustly. Without qrf, normal circadian rhythms are not sustained, indicating that the long non-coding RNA is required for clock functions.

The findings are published online in the journal Nature.

“We anticipate a similar mode of action may operate in other organisms because similar RNAs have been found for clock genes in mice. In addition, such RNAs may also function in other biological processes because of their wide presence in genomes,” said Dr. Liu, who is the Louise W. Kahn Scholar in Biomedical Research.

UT Southwestern investigators are leaders in unraveling the gene networks underlying circadian clocks and have shown that most body organs, such as the pancreas and liver, have their own internal clocks, and that virtually every cell in the human body contains a clock. It now appears that the clocks and clock-related genes – some 20 such genes have been identified – affect virtually all of the cells’ metabolic pathways, from blood sugar regulation to cholesterol production.

Other UT Southwestern researchers involved in the latest findings include Dr. Zhihong Xue, Qiaohong Ye, Dr. Juchen Yang and Dr. Guanghua Xiao. Support for this research included grants from the National Institutes of Health, the Welch Foundation, the Cancer Prevention Research Institute of Texas, and the Biotechnology and Biological Sciences Research Council.

“This study adds to an important body of work that has shown the ubiquity of a circadian clock across species, including humans, and its role in metabolic regulation in cells, organs, and organisms,” said Dr. Michael Sesma, Program Director in the Division of Genetics and Developmental Biology at the of the National Institutes of Health’s National Institute of General Medical Sciences, which partially funded the research.

“These new results from Dr. Liu and his colleagues also extend beyond understanding the function of an anti-sense RNA in the fine tuning of a cell’s daily rhythm; they provide an example of the means by which anti-sense transcription likely regulates other key molecular and physiological processes in cells and organisms.”

About UT Southwestern Medical Center

UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty includes many distinguished members, including six who have been awarded Nobel Prizes since 1985.

Numbering more than 2,700, the faculty is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in 40 specialties to nearly 91,000 hospitalized patients and oversee more than 2 million outpatient visits a year.

 

OPIOID USERS BREATHE EASIER WITH NOVEL DRUG TO TREAT RESPIRATORY DEPRESSION

From the FMS Global News Desk of Jeanne Hambleton   Embargoed: 19-Aug-2014       Source : American Society of Anesthesiologists (ASA) Citations Anesthesiology

Newswise — Chicago – August 19, 2014 – People taking prescription opioids to treat moderate to severe pain may be able to breathe a little easier, literally. A study published in the September issue of Anesthesiology, the official medical journal of the American Society of Anesthesiologists® (ASA®), found that a new therapeutic drug, GAL-021, may reverse or prevent respiratory depression, or inadequate breathing, in patients taking opioid medication without compromising pain relief or increasing sedation.

“Although opioids such as oxycodone, methadone and fentanyl are commonly used to manage perioperative and postoperative pain, opioids are associated with an increased risk of adverse effects, the most serious being respiratory depression,” said Albert Dahan, M.D., lead author and professor of anesthesiology at Leiden University Medical Center in the Netherlands. “Opioid-induced respiratory depression can lead to brain damage, cardiac arrest or death.”

Current drug treatments for opioid-induced respiratory depression (OIRD) include administering a drug such as naloxone that counteracts the effect of the opioid and/or decreasing opioid doses; however, both compromise pain relief. Conversely, GAL-021 is an intravenous respiratory stimulant that works by blocking certain potassium channels in the brain that regulate breathing. It has been previously reported that GAL-021 reverses respiratory depression in animals without diminishing opioid-related pain relief.

In the study, GAL-021 stimulated breathing in 12 healthy male volunteers who underwent opioid-induced respiratory depression, at which time their breathing capacity was decreased by 25 to 30 percent. All patients experienced an increase in respiratory rate and tidal volume, which is the amount of air that is expelled during a normal breath. Researchers also found that GAL-021 had no adverse affect on non-respiratory variables such as sedation, pain relief, blood flow or safety parameters.

“The development of potent painkillers that do not increase the risk of respiratory depression seems still far away,” said Dr. Dahan. “Using an add-on drug that reverses or prevents respiratory depression caused by opioid use, without affecting pain relief, is currently our best option to treat this condition. While our data suggest that GAL-021 is an attractive alternative to other respiratory stimulants, additional studies are needed to further confirm these findings.”

The Leiden University Medical Center respiratory laboratory is currently funded by some other parties involved in opioid-induced respiratory depression and reversal of respiratory depression: Mundipharma (Cambridge, United Kingdom) and Revive Therapeutics (Vaughan, Ontario, Canada).

THE AMERICAN SOCIETY OF ANESTHESIOLOGISTS
Founded in 1905, the American Society of Anesthesiologists (ASA) is an educational, research and scientific society with more than 52,000 members organized to raise and maintain the standards of the medical practice of anesthesiology. ASA is committed to ensuring that physician anesthesiologists evaluate and supervise the medical care of patients before, during, and after surgery to provide the highest quality and safest care that every patient deserves.

For more information on the field of anesthesiology, visit the American Society of Anesthesiologists online at asahq.org. To learn more about the role physician anesthesiologists play in ensuring patient safety, visit asahq.org/WhenSecondsCount.

Back tomorrow. Jeanne

 

 

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THE OLDEST METAL OBJECT FOUND TO DATE IN THE MIDDLE EAST

According to Dr. Danny Rosenberg of the University of Haifa’s Zinman Institute of Archeology, the copper awl is a unique and very rare artifact, whose discovery, along with other items during the excavations at Tel Tsaf in the Jordan Valley, indicates that the site was an ancient international commercial center
From the FMS Global News Desk of Jeanne Hambleton   Released: 21-Aug-2014      Citations PLOS One    Source Newsroom: University of Haifa

Newswise — A copper awl, the oldest metal object found to date in the Middle East, was discovered during the excavations at Tel Tsaf, according to a recent study published by researchers from the Zinman Institute of Archaeology and the Department of archaeology at the University of Haifa , in conjunction with researchers from the Hebrew University of Jerusalem and the German Archaeological Institute of Berlin.

According to the study, which appeared in the prestigious journal PLOS One, the awl dates back to the late 6th millennium or the early 5th millennium BCE, moving back by several hundred years the date it was previously thought that the peoples of the region began to use metals.

Tel Tsaf, a Middle Chalcolithic village dated to about 5200-4600 BCE, is located near the Jordan River and the international border with Jordan. The site was first documented in the 1950s and excavations there began at the end of the 1970s.

From the earliest digs nearly 40 years ago, this area, the most important archeological site in the region dated to this period, has been supplying researchers with a great deal of valuable data, and continues to do so during this latest research project led by Dr. Danny Rosenberg of the University of Haifa in conjunction with Dr. Florian Klimscha of the Eurasia Department of the German Archaeological Institute in Berlin.

For example, the researchers learned of the community’s great wealth and the long-distance commercial ties it maintained from the large buildings made of mud-bricks and the large number of silos in which wheat and barley were stored on an unprecedented scale.

There were many roasting ovens in the courtyards, all filled with burnt animal bones testifying to the holding of large events and many other findings, among them items made of obsidian (a volcanic glass with origins in Anatolia or Armenia), shells from the Nile River in Egypt and other areas around the Mediterranean, figurines of people and animals, and pottery unlike that found in almost any other location in the region.

But the most important finding to date is only 4 centimeters long. This unique item, a copper awl, which is 1 millimeter thick at the tip that was set in a wooden handle, was actually found during a previous excavation at the site by Prof. Yosef Garfinkel of the Hebrew University.

The cone-shaped awl was found in a sealed grave of a woman about 40 years old that was dug inside a silo, and around her waist was a belt made of 1,668 ostrich-egg shell beads. The grave was covered with several large stones, and according to Dr. Rosenberg, its location within a silo testifies to both the importance of the deceased and the importance the community ascribed to the facility in which she was buried.

But while the grave, the woman’s skeleton, and the beaded belt were all previously reported in scientific journals, the little awl was only reported on recently, after its chemical components were analyzed by Prof. Sariel Shalev of the Department of Archaeology at the University of Haifa’s.

As noted, the awl was found to made of copper, and according to Dr. Rosenberg, the fact that it was found just above the skeleton ad in a sealed grave, meant that it was buried with the woman, apparently as a burial offering, and may have belonged to her.

This artifact is important because until now, researchers believed that area residents began to use metals only in the Late Chalcolithic period (during the second half of the 5th millennium BCE, so that this finding moves back the appearance of metal in our region by several hundred years. This has significant impact on our understanding of the developing use of complex technologies and the related social contexts.

But this is not the only reason the awl is significant. The chemical examination of the metal shows it may have come from the Caucasus, some 1,000 kilometers from Tel Tsaf.

According to Dr. Rosenberg, while the long-distance commercial ties maintained by village communities in our region were already known from even earlier periods, the import of a new technology combined with the processing of a new raw material coming from such a distant location is unique to Tel Tsaf and provides additional evidence of the importance of this site in the ancient world.

The researchers are still not sure what the awl was used for, but the early use of a metal object, as well as its distant source, also testify to the high social status of the woman and the importance of the building she was buried in.

“The appearance of the item in a woman’s grave, which represents one of the most elaborate burials we have seen in our region from that era, testifies to both the importance of the awl and the importance of the woman, and it is possible that we are seeing here the first indications of social hierarchy and complexity,” said Dr. Rosenberg.

“However, in this area far more is unknown than is known, and although the discovery of the awl at Tel Tsaf constitutes evidence of a peak of technological development among the peoples of the region and is a discovery of global importance, there is a lot of progress still to be made and many parts of the wider picture are still unknown to us.

“It seems that at least some of the questions raised by this unique item will be answered by an interdisciplinary research project we have been conducting at the site since last year,” Dr. Rosenberg continued.

“This project integrates multi-national archeologists and researchers from a variety of other scientific disciplines, who will address the even more complex questions that will undoubtedly arise.”

 

8,000-YEAR-OLD MUTATION KEY TO HUMAN LIFE AT HIGH ALTITUDES

University of Utah-led study identifies genetic basis for Tibetan adaptation

From the FMS Global News Desk of Jeanne Hambleton Embargo expired: 17-Aug-2014 Citations Nature Genetics  Newsroom: University of Utah Health Sciences

 

SALT LAKE CITY – In an environment where others struggle to survive, Tibetans thrive in the thin air on the Tibetan Plateau, with an average elevation of 14,800 feet.

A University of Utah led discovery that hinged as much on strides in cultural diplomacy as on scientific advancements, is the first to identify a genetic variation, or mutation, that contributes to the adaptation, and to reveal how it works. The research appears online in the journal Nature Genetics on Aug. 17, 2014.

“These findings help us understand the unique aspects of Tibetan adaptation to high altitudes, and to better understand human evolution,” said Josef Prchal, M.D., senior author and University of Utah professor of internal medicine.

For his research, Prchal needed Tibetans to donate blood, from which he could extract their DNA, a task that turned out to be more difficult than he ever imagined. It took several trips to Asia, meeting with Chinese officials and representatives of exiled Tibetans in India, to get the necessary permissions to recruit subjects for the study. But he quickly learned that official documents would not be enough. Wary of foreigners, the Tibetans refused to participate.

To earn the Tibetans’ trust, Prchal obtained a letter of support from the Tibetan spiritual leader, the Dalai Lama.

“The Dalai Lama felt that a better understanding of the adaptation would be helpful not only to the Tibetan community but also to humanity at large,” said Prchal.

He also enlisted the help of native Tibetan Tsewang Tashi, M.D., an author and clinical fellow at the Huntsman Cancer Institute at the University of Utah. More than 90 Tibetans, both from the U.S. and abroad, volunteered for the study.

Published in Science in 2010, Prchal’s group was the first to establish that there was a genetic basis to Tibetan high altitude adaptation. In the intervening years, first author Felipe Lorenzo, M.D., Ph.D., pioneered new techniques to tease out the secret to one of the adaptations from a “GC-rich” region of the Tibetans’ DNA that was particularly difficult to penetrate.

Their efforts were worth it; the DNA had a fascinating story to tell. About 8,000 years ago, the gene EGLN1 changed by a single DNA base pair. Today, a relatively short time later on the scale of human history, the vast majority of Tibetans – 88 percent – have the genetic variation, and it is virtually absent from closely related lowland Asians. The findings indicate the tiny genetic change endows its carriers with a selective advantage.

Prchal collaborated with experts throughout the world, including co-senior author Peppi Koivunen, Ph.D., from Biocenter Oulu in Finland, to determine that the newly identified genetic variation protects Tibetans by decreasing an aversive over-response to low oxygen. In those without the adaptation, the thin air causes their blood to become thick with oxygen-carrying red blood cells, often causing long-term complications such as heart failure. The EGLN1 variation, together with other unidentified genetic changes, collectively support life at high altitudes.

Prchal says the research also has broader implications. Because oxygen plays a central role in human physiology and disease, a deep understanding of how high altitude adaptations work may lead to novel treatments for various conditions, including cancer.

“There is much more that needs to be done, and this is just the beginning,” he said.

When traveling with Tashi in Asia, Prchal was surprised at how he got Tibetans to grasp the research they were being asked to take part in. Tashi simply helped them realize that their ability to adapt to life at high altitude was unique.

“They usually responded by a little initial surprise quickly followed by agreement,” said Tashi.

“It was as if I made them realize something new, which only then became obvious.”

The research, “A genetic mechanism for Tibetan high-altitude adaptation” is published in Nature Genetics.

 

ANTIBACTERIAL SOAP EXPOSES HEALTH WORKERS TO HIGH TRICLOSAN LEVELS

UCSF-led study finds exposure to hormone disruptor from soap exceeds that from toothpaste

From FMS Global News Desk of Jeanne Hambleton Released: 19-Aug-2014
Source Newsroom: University of California, San Francisco (UCSF)                Citations Journal of Occupational and Environmental Medicine, Aug-2014

 

Newswise — Handwashing with antibacterial soap exposes hospital workers to significant and potentially unsafe levels of triclosan, a widely-used chemical currently under review by the U.S. Food and Drug Administration, according to a study led by researchers from UC San Francisco.

Triclosan, a synthetic antibacterial agent, is found in thousands of consumer products, including soaps, cosmetics, acne creams and some brands of toothpaste. The FDA is reviewing its safety based on a growing body of research indicating that it can interfere with the action of hormones, potentially causing developmental problems in fetuses and newborns, among other health concerns.

In the current study, published in the August issue of the Journal of Occupational and Environmental Medicine, researchers analyzed urine samples from two groups of 38 doctors and nurses – three fourths of them women – at two hospitals, identified as Hospital 1 and Hospital 2. Hospital 1 used an antibacterial soap containing 0.3 percent triclosan, while Hospital 2 used plain soap and water.

Workers at Hospital 1 had significantly higher levels of triclosan in their urine than workers at Hospital 2.

The scientists also asked the study participants if they used a popular commercial toothpaste containing triclosan. While those who did had higher triclosan levels than those who did not, the researchers found that washing with antibacterial soap accounted for even higher triclosan levels than did brushing with the toothpaste.

“Antimicrobial soaps can carry unknown risks, and triclosan is of particular concern,” said co-investigator Paul Blanc, MD, a professor of medicine at UCSF who holds the Endowed Chair in Occupational and Environmental Medicine.

“Our study shows that people absorb this chemical at work and at home, depending on the products that they use.”

Blanc recommended that “if non-triclosan-containing soaps are available, use the alternative. This is based on the precautionary principle – that is, if you do not know for certain that something is unsafe, it is better to err on the side of caution.”

The same principle “could be applied more generally in this case,” said Blanc. “It should not be up to the individual to inspect every product for triclosan. Instead, it is the duty of the FDA to carry out a review of this chemical and, if indicated, get it off the market.”

Co-authors of the study are Julia K. MacIsaac, MD, MPH, of UCSF and the Natural Resources Defense Council (NRDC); Roy G. Gerona, PhD, of UCSF; Latifat Apatira, MD, MPH, of Kaiser Permanente Medical Center, San Francisco; Matthew W. Friesen, of UCSF; Michael Coppolino, MD, of UCSF and Kaiser Permanente; and Sarah Janssen, MD, PhD, MPH, of UCSF, Kaiser Permanente, and NRDC.

The study was funded in part by the Passport Foundation, Science Innovation Fund, NRDC, the National Center for Advancing Translational Sciences and the National Institutes of Health through a UCSF Clinical and Translational Science Institute grant.

UCSF is the nation’s leading university exclusively focused on health. Now celebrating the 150th anniversary of its founding as a medical college, UCSF is dedicated to transforming health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy; a graduate division with world-renowned programs in the biological sciences, a pre-eminent biomedical research enterprise and two top-tier hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco.

 You learn something every day….Back tomorrow Jeanne

 

 

 

 

 

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SCARCITY OF ELEMENTS IN PRODUCTS LIKE SMARTPHONES NEEDS ADDRESSING, SAY SCIENTISTS

From the FMS Global News Desk of Jeanne Hambleton Released: 10-Aug-2014 Citations ACS’ 248th National Meeting & Exposition    Source Newsroom: American Chemical Society (ACS) American Chemical Society (ACS)

Newswise — SAN FRANCISCO, Aug. 10, 2014 — Many of today’s technological innovations from the iPhone to electric motors for hybrid cars require the use of materials — elements — that are scarce or difficult to obtain. As demand for these devices grows, the problem of dwindling critical element supplies must be addressed. That is the conclusion of a white paper written by eminent scientists. The product of the 5th Chemical Sciences and Society Summit (CS3), the white paper recommends focusing research on finding alternative materials and new approaches to technology development in order to prevent these elements from disappearing.

The white paper, “The Efficient Use of Elements,” is a topic of discussion at this year’s the 248th National Meeting & Exposition of the American Chemical Society (ACS), the world’s largest scientific society. The meeting features nearly 12,000 reports on new advances in science and other topics. It is being held here through Thursday.

Technology advances made in the past few decades are resulting in unprecedented levels of comfort and convenience, improved medical diagnostics and treatment, more efficient transportation and rapid access to quantities of information that, a generation ago, were unimaginable. Much of this new technology, however, is heavily dependent on the excavation and use of scarce elements. For example, smartphones contain a mix of these rare materials such as indium, platinum and copper. And the manufacturing of pharmaceuticals uses elements such as palladium and rhodium.

The scarcity of these elements makes it difficult to manufacture innovative devices responsibly. One of the agreements reached in the white paper is the need for the development of materials that can be used to substitute for these rare elements. Research on alternatives, the white paper states, must be a priority area. If a solution is not found, technology advances may be limited, creating social, political and economic challenges across the world.

The white paper discusses several approaches to resolving problems of material scarcity, and suggests that a multi-faceted, global strategy will be necessary to avoid serious disruptions. A key part of any strategy will be recovery and recycling, because elements are a strictly limited resource. It is also essential that these critical resources be used with consideration of the entire use cycle, from mining and manufacturing to recovery and reuse.

The annual Chemical Sciences and Society Summit (CS3) brings together some of the most accomplished chemists and chemical engineers from around the globe and challenges them to propose meaningful approaches to solving society’s most pressing needs in the areas of health, food, energy and the environment. The CS3 initiative is a collaboration between the American Chemical Society, the Chemical Society of Japan, the Chinese Chemical Society, the German Chemical Society, and the Royal Society of Chemistry. The symposia are supported by the German Research Foundation, the Japan Society for the Promotion of Science, the National Science Foundation of China, the U.K. Engineering and Physical Sciences Research Council and the U.S. National Science Foundation.

“The Efficient Use of Elements” is the product of the fifth CS3 meeting, held in Narita, Japan in September 2013. Over 30 chemists representing the five participating countries worked together to identify and clarify problems associated with the rapid increase in demand for scarce elements and proposed rational, meaningful approaches to resolving this challenge we all face.

The American Chemical Society is a nonprofit organization chartered by the U.S. Congress. With more than 161,000 members, ACS is the world’s largest scientific society and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.

 

ALL IVORY MARKETS MUST CLOSE

From the FMS Global News Desk of Jeanne Hambleton       Released: 7-Aug-2014 Citations Conservation Biology
Source Newsroom: Wildlife Conservation Society Willey on Line

Peer-reviewed paper says any legal trade in ivory will contribute to elephant’s demise.  Corruption, organized crime, and lack of enforcement make legal trade an impossibility if elephants are to survive, says Wildlife Conservation Society. Paper appears in August 7 edition of the online version of Conservation Biology. For abstract see below.

Newswise — NEW YORK (August 7, 2014) – The message is simple: to save elephants, all ivory markets must close and all ivory stockpiles must be destroyed, according to a new peer-reviewed paper by the Wildlife Conservation Society. The paper says that corruption, organized crime, and a lack of enforcement make any legal trade of ivory a major factor contributing to the demise of Africa’s elephants.

Appearing in the August 7th online edition of the journal Conservation Biology, the paper says that if we are to conserve significant wild populations of elephants across all regions of Africa, all domestic and international ivory markets need to be closed. In addition, government stockpiles of ivory, currently scattered around the world, need to be destroyed since they are known to be significant sources of ivory leaking into the illegal trade. According to the paper’s author, corruption undermines all aspects of controls as long as a legal market remains.

“If we are to conserve remaining wild populations of elephants, we must close all markets because, under current levels of corruption, they cannot be controlled in a way that does not provide opportunities for illegal ivory being laundered into legal markets,” said the paper’s author, Elizabeth Bennett, WCS Vice President for Species Conservation.

The paper looked at the corruption index of 177 assessed countries, noting that half of the 12 countries in Africa that contain elephants are in the bottom 40 percent. Six of the eight countries identified by the Convention on International Trade in Endangered Species of Wild Fauna and Flora (CITES) as most implicated in ivory trafficking globally are in the bottom half of the most corrupt countries in the world.

The paper comes at a time of growing opposition to ivory bans by some groups claiming that carefully regulated ivory sales would help protect elephants and contribute to conservation through sales of ivory stockpiles and other legal sources.

Bennett refutes this saying that saying that financial incentives to break the law and reap profits far outweigh those of abiding by it, as poachers and traffickers can rapidly pay their way out of trouble. Once illegal ivory has entered into the legal trade, it is difficult or impossible for enforcement officers to know what is legal and what is not.

Bennett says that with good enforcement on the ground, the tide of poaching can be slowed. For example, forest elephants in Central Africa occur in densities seven times higher in sites with ecoguards than without them. However, the costs of such site-based protection in terms of funds and human lives will continue to increase and be unsustainable as long as ivory profits continue to escalate giving ever-increasing incentives to kill elephants illegally and traffic in their ivory.

Says Bennett: “In the long term, the only sustainable solution is for the demand for ivory – the ultimate driver of the system – to be reduced. Until that happens, if elephants are to survive, we need to close existing legal markets.”

Wildlife Conservation Society (WCS)
MISSION: WCS saves wildlife and wild places worldwide through science, conservation action, education, and inspiring people to value nature. VISION: WCS envisions a world where wildlife thrives in healthy lands and seas, valued by societies that embrace and benefit from the diversity and integrity of life on earth. To achieve our mission, WCS, based at the Bronx Zoo, harnesses the power of its Global Conservation Program in more than 60 nations and in all the world’s oceans and its five wildlife parks in New York City, visited by 4 million people annually. WCS combines its expertise in the field, zoos, and aquarium to achieve its conservation mission.

Legal Ivory Trade in a Corrupt World and its Impact on African Elephant Populations         By Elizabeth L. Bennett

Abstract

Illegal hunting of African elephants (Loxodonta africana) for ivory is causing rapid declines in their populations.

Since 2007, illegal ivory trade has more than doubled. African elephants are facing the most serious conservation crisis since 1989, when international trade was banned.

One solution proposed is establishment of a controlled legal trade in ivory. High prices for ivory mean that the incentives to obtain large quantities are high, but the quantity of tusks available for trade are biologically constrained.

Within that context, effective management of a legal ivory trade would require robust systems to be in place to ensure that ivory from illegally killed elephants cannot be laundered into a legal market. At present, that is not feasible due to corruption among government officials charged with implementing wildlife-related legislation.

With organized criminal enterprises involved along the whole commodity chain, corruption enables the laundering of illegal ivory into legal or potentially legal markets. Poachers and traffickers can rapidly pay their way out of trouble, so the financial incentives to break the law heavily outweigh those of abiding by it.

Maintaining reliable permitting systems and leak-proof chains of custody in this context is challenging, and effective management breaks down. Once illegal ivory has entered the legal trade, it is difficult or impossible for enforcement officers to know what is legal and illegal.

Addressing corruption throughout a trade network that permeates countries across the globe will take decades, if it can ever be achieved.

That will be too late for wild African elephants at current rates of loss. If we are to conserve remaining wild populations, we must close all markets because, under current levels of corruption, they cannot be controlled in a way that does not provide opportunities for illegal ivory being laundered into legal markets.

 

ASPIRIN, TAKE TWO

From  FMS Global News Desk of Jeanne Hambleton18-Aug-2014  Source: University of California, San Diego Health Sciences Citations PNA

Newswise — Hugely popular non-steroidal anti-inflammation drugs like aspirin, naproxen (marketed as Aleve) and ibuprofen (Advil, Motrin) all work by inhibiting or killing an enzyme called cyclooxygenase – a key catalyst in production of hormone-like lipid compounds called prostaglandins that are linked to a variety of ailments, from headaches and arthritis to menstrual cramps and wound sepsis.

In a new paper, published this week in the online early edition of PNAS, researchers at the University of California, San Diego School of Medicine conclude that aspirin has a second effect: Not only does it kill cyclooxygenase, thus preventing production of the prostaglandins that cause inflammation and pain, it also prompts the enzyme to generate another compound that hastens the end of inflammation, returning the affected cells to homeostatic health.

“Aspirin causes the cyclooxygenase to make a small amount of a related product called 15-HETE,” said senior author Edward A. Dennis, PhD, Distinguished Professor of Pharmacology, Chemistry and Biochemistry.

“During infection and inflammation, the 15-HETE can be converted by a second enzyme into lipoxin, which is known to help reverse inflammation and cause its resolution – a good thing.”

Specifically, Dennis and colleagues looked at the function of a type of white blood cells called macrophages, a major player in the body’s immune response to injury and infection. They found that macrophages contain the biochemical tools to not just initiate inflammation, a natural part of the immune response, but also to promote recovery from inflammation by releasing 15-HETE and converting it into lipoxin as the inflammation progresses.

Dennis said the findings may open new possibilities for anti-inflammatory therapies by developing new drugs based on analogues of lipoxin and other related molecules that promote resolution of inflammation.

“If we can find ways to promote more resolution of inflammation, we can promote health,” he said.

Co-authors include Paul C. Norris, David Gosselin, Donna Reichart and Christopher K. Glass, all at UC San Diego.

WORDPRESS HITCH

Back tomorrow if we finally get on the page rather than the  Archives.  We are published there  NOT ON THE DAILY PAGE but need to check the Archives  to see where we are  as the usual  page is still on August 14.  Back soon  WordPress permitting. Jeanne

 

 

 

 

 

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