Monthly Archives: September 2012

From ‘Angry Birds’ to multi-player video games, NASA ramps up investment in educational technology

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Forty-three years after putting a man on the moon, NASA sent the Angry Birds video game to space. A few months later, the birds traveled to the moon and later to Mars.

NASAs recent collaboration with gamemaker Rovio to create Angry Birds Space, in which players use slingshots to launch birds at pigs, is part of a series of computer game projects spearheaded by government agencies to encourage science, technology and math education.

Today, NASA has loftier goals: An upcoming $10 million massively multi-player video game would simulate life on Mars and eventually provide 100 hours of playing time on the iPad, Sony Playstation and Microsoft Xbox. When a beta version of Starlite is released later this year, it will be NASAs biggest foray into gaming, and one that Laughlin hopes will set the stage for future collaborations with commercial game developers.

There are more higher-end gaming projects going on at NASA than ever before, Laughlin said. Very few people are looking to textbooks to get students inspired anymore.

In the past few years, NASA has released an air traffic control simulator for the iPhone, a trivia game called Space Race Blastoff for Facebook and MoonBase Alpha, a multi-player game that cost $300,000 to develop and resulted in 20 minutes of playing time.

But as the agency grapples with persistent education budget cuts, NASA is experimenting with new business models to fund upcoming projects.

The agency had originally planned to pour $5 million to $7 million into Starlite over three or four years. But budget cuts took their toll, Laughlin said.

Gradually, NASA nibbled down the budget until it turned out we could only afford to fund the educational side of the game, he said.

The agency will now invest about $1.5 million in NASA content and expertise in the Starlite, while Project Whitecard, a Winnipeg-based firm that has already created two games for the Canadian Space Agency, will finance the rest.

The premise of Starlite is quite simple, said Khal Shariff, chief executive of Project Whitecard: Its the year 2035. You are a first-time explorer who has to leave the Earths orbit and travel to Mars. Once you reach the Red Planet, there are a series of challenges, such as orchestrating an emergency rescue mission to find a stranded astronaut.

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From ‘Angry Birds’ to multi-player video games, NASA ramps up investment in educational technology

A move to show ownership, Tokyo officials survey disputed islands

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Tokyo city officials surveyed five tiny uninhabited islands in the East China Sea, which are controlled by Japan, but also claimed by China and Taiwan. Tokyo plans to buy the islands, a sale China calls 'invalid.'

Tokyo city officials planning to buy tiny islands at the center of a longtime territorial dispute with China surveyed the area Sunday on a visit meant to send a message of ownership.

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The boat, carrying 25 experts and officials as well as journalists from news organizations including The Associated Press, circled the five uninhabited islands in the East China Sea which are controlled by Japan but also claimed by China and Taiwan.

China responded quickly to the survey, saying any unilateral action by Japan on the islands is "illegal" and "invalid."

Tokyo city officials say the survey is crucial and includes measuring the water depth to build a dock at the islands, known as Senkaku in Japan and Diaoyu in China. Japan's central government did not grant permission to land on the islands.

Tokyo Gov. Shintaro Ishihara, a strong nationalist, has raised 1.45 billion yen ($19 million) in private donations over the last several months to buy the islands from the Japanese family that owns them. Supporters think having the government own the islands will strengthen Japan's control over them and send a tougher message to China.

"It is an undeniable fact that the islands are Japanese territory, so our task is to see how we can best maintain that," Yoshihiko Yamada, a special adviser to the city's team, said aboard the boat.

The team was scheduled to study the islands for about 10 hours Sunday before heading back to Okinawa in southwestern Japan.

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A move to show ownership, Tokyo officials survey disputed islands

Ex-Obama advisers seek health care cost control – Sun, 02 Sep 2012 PST

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September 2, 2012 in Health

Ricardo Alonso-Zaldivar Associated Press

WASHINGTON (AP) Some of President Barack Obamas former advisers are proposing major changes aimed at controlling health care costs as political uncertainty hovers over his healthlaw.

Call it Health Care Overhaul, Version 2.0. Their biggest idea is a first-ever budget for the nations $2.8-trillion health care system, through negotiated limits on public and private spending in eachstate.

The approach broadly resembles a Massachusetts law signed this summer by Democratic Gov. Deval Patrick that puts pressure on hospitals, insurers, and other major players to keep rising costs within manageable limits. It could become the Democratic counterpoint to private market strategies favored by Republican presidential nominee Mitt Romney and running mate PaulRyan.

Health costs lie at the heart of budget problems confronting the next president. Health care accounts for 18 percent of the economy and about one-fourth of the federal budget, and many experts believe it cant grow unchecked without harming other priorities. Because the United States spends much more than other advanced countries, theres a consensus that savings from cutting waste and duplication wont harmquality.

We think of these as the next generation of ideas, said Neera Tanden, who was a senior member of the White House team that helped pass the health law. Tanden is now president of the Center for American Progress, a Washington think tank close to theadministration.

Under the proposal, the major public and private players in each state would negotiate payment rates with service providers such as hospitals. The idea is to get away from paying for each individual test and procedure. Negotiated rates could be based on an entire course of treatment. Payments would have to fit within an overall budget that could grow no faster than the average rise inwages.

The spending limits would be enforced by an independent council, but crucial details need to be spelled out. In Massachusetts, for example, budget-busting providers will be required to file plans with the state laying out how theyll amend their spendthriftways.

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Ex-Obama advisers seek health care cost control - Sun, 02 Sep 2012 PST

Cooper Green Mercy Hospital changes could draw on indigent care report

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BIRMINGHAM, Alabama -- OK, let's clear the air about Cooper Green Mercy Hospital.

First, it's not going to close.

Come Dec. 1, the target date for changes ordered last week by the Jefferson County Commission, the venerated health care institution for the county's indigent residents will still occupy its building on Sixth Avenue South. Its outpatient clinics will still see and treat the sick. And walk-in care still will be provided 24 hours a day, seven days a week, said County Manager Tony Petelos.

"Our patients will continue to be served, and none will be left on the street," he said.

But at least three major changes are coming, Petelos said:

That 24/7 walk-in service at Cooper Green will be urgent care, not an emergency room, meaning it will handle problems that require immediate attention but are not life-threatening.

Cooper Green patients who need to be admitted to a hospital will go to some other hospital -- sites still to be determined through agreements between the hospitals and the county -- and Cooper Green will shutter its inpatient hospital care.

Many of Cooper Green's staff will lose their jobs. In addition to about 100 who have been cut since March, Petelos said he expects more than 200 layoffs. The hospital employs 528 people.

"The staff of Cooper Green is very upset," he said. "There is a lot of uncertainty."

[Cooper Green Mercy Hospital discretionary fund audit raises questions.]

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Cooper Green Mercy Hospital changes could draw on indigent care report

National Democrats Eye Mass. Health Care Cost Containment Law

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WASHINGTON (AP) Some of President Barack Obamas former advisers are proposing major changes aimed at controlling health care costs as political uncertainty hovers over his health law.

Call it Health Care Overhaul, Version 2.0. Their biggest idea is a first-ever budget for the nations $2.8-trillion health care system, through negotiated limits on public and private spending in each state.

The approach broadly resembles a Massachusetts law signed this summer by Democratic Gov. Deval Patrick that puts pressure on hospitals, insurers, and other major players to keep rising costs within manageable limits. It could become the Democratic counterpoint to private market strategies favored by Republican presidential nominee Mitt Romney and running mate Paul Ryan.

Health costs lie at the heart of budget problems confronting the next president. Health care accounts for 18 percent of the economy and about one-fourth of the federal budget, and many experts believe it cant grow unchecked without harming other priorities. Because the United States spends much more than other advanced countries, theres a consensus that savings from cutting waste and duplication wont harm quality.

We think of these as the next generation of ideas, said Neera Tanden, who was a senior member of the White House team that helped pass the health law. Tanden is now president of the Center for American Progress, a Washington think tank close to the administration.

Under the proposal, the major public and private players in each state would negotiate payment rates with service providers such as hospitals. The idea is to get away from paying for each individual test and procedure. Negotiated rates could be based on an entire course of treatment. Payments would have to fit within an overall budget that could grow no faster than the average rise in wages.

The spending limits would be enforced by an independent council, but crucial details need to be spelled out. In Massachusetts, for example, budget-busting providers will be required to file plans with the state laying out how theyll amend their spendthrift ways.

The federal government would provide grants to states interested in developing their plans.

Tanden joined a brain trust of former administration officials floating the proposal recently in the New England Journal of Medicine. The group included Peter Orszag (former budget director), John Podesta (transition director), Donald Berwick (first Medicare chief), Ezekiel Emanuel (Orszags health policy guru), and Joshua Sharfstein (former No. 2 at the Food and Drug Administration). Also on board was former Senate Majority Leader Tom Daschle, D-S.D., Obamas first pick to shepherd his health care overhaul.

Their proposal includes other ideas, such as a malpractice liability shield for doctors who follow best clinical practices, and competitive bidding for all Medicare supplies and lab tests, not just home health equipment. All of the signers support Obamas health care law, but see cost control as unfinished business.

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National Democrats Eye Mass. Health Care Cost Containment Law

NIH-funded researchers restore sense of smell in mice using genetic technique

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Public release date: 2-Sep-2012 [ | E-mail | Share ]

Contact: Robin Latham lathamr@nidcd.nih.gov 301-496-7243 NIH/National Institute on Deafness and Other Communication Disorders

Scientists funded by the National Institutes of Health have restored the ability to smell in a mouse model of a human genetic disorder that causes congenital anosmiathe inability to smell from birth. The approach uses gene therapy to regrow cilia, cell structures that are essential for olfactory function. The study was funded by four parts of NIH: the National Institute on Deafness and Other Communications Disorders (NIDCD), the National Institute on Diabetes and Digestive and Kidney Diseases (NIDDK), the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), and the National Eye Institute (NEI). It was published online in the September 2, 2012, issue of the journal Nature Medicine.

"These results could lead to one of the first therapeutic options for treating people with congenital anosmia," said James F. Battey, Jr., M.D., Ph.D., director of NIDCD. "They also set the stage for therapeutic approaches to treating diseases that involve cilia dysfunction in other organ systems, many of which can be fatal if left untreated."

Olfactory dysfunction can be a symptom of a newly recognized class of genetic disorders, known as ciliopathies, which include diseases as diverse as polycystic kidney disease and retinitis pigmentosa, an inherited, degenerative eye disease that causes severe vision impairment and blindness. The disorders are caused by defects in cilia, antenna-like projections on cells that help them sense their environment. Scientists believe that nearly every cell in the body has the capacity to grow one or more cilia. In the olfactory system, multiple cilia project from olfactory sensory neurons, sensory cells that are found in the olfactory epithelium, tissue high up in the nasal cavity. Receptors that bind odorants are localized on the cilia, which is why a loss of cilia results in a loss in the ability to smell.

The team of researchers, led by Jeffrey R. Martens, Ph.D., at the University of Michigan, Ann Arbor, and Jeremy C. McIntyre, Ph.D., a post-doctoral fellow in Martens' laboratory, worked with a mouse model carrying a mutation in the IFT88 gene. The mutation causes a decrease in the IFT88 protein, which leads to a dramatic reduction in cilia function in several different organ systems, including the olfactory system.

The researchers used an adenovirus to introduce a healthy copy of the gene as a way to restore IFT88 protein levels in the mice. They wanted to see if the reintroduction of the lost protein could restore cilia to the olfactory sensory neurons and return the ability to smell. For three consecutive days, the mice received intranasal gene delivery therapy and then were allowed 10 days for the infected sensory neurons to express the viral-encoded IFT88 protein. After that time, the mice were tested with increasing concentrations of an odorant (amyl acetate). Their responses were measured at the cellular, tissue, and synaptic levels, which all indicated that the mice had regained olfactory function.

"By restoring the protein back into the olfactory neurons, we could give the cell the ability to regrow and extend cilia off the dendrite knob, which is what the olfactory neuron needs to detect odorants," said McIntyre.

The change in olfactory function also has implications in the feeding behavior of the mice. The mouse model the scientists used is born underweight and its anosmia interferes with the motivation to eat, which in many mammals, including humans, is driven by smell. Treatment with adenovirus therapy increased bodyweight by 60 percent in treated compared to untreated mice, indicating that the restored olfactory function was motivating feeding.

The researchers plan to continue their work by developing another mouse model to look at the impact on olfactory function and the potential for restoring function when the IFT88 gene is completely missing, rather than just mutated. Future studies could begin to plot a way to bring this therapeutic tactic to human study volunteers, which could eventually restore the sense of smell, and a better quality of life, to people who are born with anosmia. Further research could also advance the treatments for other ciliopathies, as these findings show that gene therapy is a viable option for the functional rescue of cilia in established, already differentiated cells.

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NIH-funded researchers restore sense of smell in mice using genetic technique

Can’t smell anything? Discovery may give you hope

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ScienceDaily (Sep. 2, 2012) Scientists have restored the sense of smell in mice through gene therapy for the first time -- a hopeful sign for people who can't smell anything from birth or lose it due to disease.

The achievement in curing congenital anosmia -- the medical term for lifelong inability to detect odors -- may also aid research on other conditions that also stem from problems with the cilia. Those tiny hair-shaped structures on the surfaces of cells throughout the body are involved in many diseases, from the kidneys to the eyes.

The new findings, published online in Nature Medicine, come from a team at the University of Michigan Medical School and their colleagues at several other institutions.

The researchers caution that it will take time for their work to affect human treatment, and that it will be most important for people who have lost their sense of smell due to a genetic disorder, rather than those who lose it due to aging, head trauma, or chronic sinus problems. But their work paves the way for a better understanding of anosmia at the cellular level.

"Using gene therapy in a mouse model of cilia dysfunction, we were able to rescue and restore olfactory function, or sense of smell," says senior author Jeffrey Martens, Ph.D., an associate professor of pharmacology at U-M. "Essentially, we induced the neurons that transmit the sense of smell to regrow the cilia they'd lost."

The mice in the study all had a severe genetic defect that affected a protein called IFT88, causing a lack of cilia throughout their bodies. Such mice are prone to poor feeding and to early death as a result. In humans, the same genetic defect is fatal.

The researchers were able to insert normal IFT88 genes into the cells of the mice by giving them a common cold virus loaded with the normal DNA sequence, and allowing the virus to infect them and insert the DNA into the mouse's own cells. They then monitored cilia growth, feeding habits, and well as signals within and between the nerve cells, called neurons, that are involved in the sense of smell.

Only 14 days after the three-day treatment, the mice had a 60 percent increase in their body weight, an indication they were likely eating more. Cell-level indicators showed that neurons involved in smelling were firing correctly when the mice were exposed to amyl acetate, a strong-smelling chemical also called banana oil.

"At the molecular level, function that had been absent was restored," says Martens.

"By restoring the protein back into the olfactory neurons, we could give the cell the ability to regrow and extend cilia off the dendrite knob, which is what the olfactory neuron needs to detect odorants," says postdoctoral fellow and first author Jeremy McIntyre, Ph.D.

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Can’t smell anything? Discovery may give you hope

Can't smell anything? This discovery may give you hope

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Public release date: 2-Sep-2012 [ | E-mail | Share ]

Contact: Kara Gavin kegavin@umich.edu 734-764-2220 University of Michigan Health System

ANN ARBOR, Mich. Scientists have restored the sense of smell in mice through gene therapy for the first time -- a hopeful sign for people who can't smell anything from birth or lose it due to disease.

The achievement in curing congenital anosmia -- the medical term for lifelong inability to detect odors -- may also aid research on other conditions that also stem from problems with the cilia. Those tiny hair-shaped structures on the surfaces of cells throughout the body are involved in many diseases, from the kidneys to the eyes.

The new findings, published online in Nature Medicine, come from a team at the University of Michigan Medical School and their colleagues at several other institutions.

The researchers caution that it will take time for their work to affect human treatment, and that it will be most important for people who have lost their sense of smell due to a genetic disorder, rather than those who lose it due to aging, head trauma, or chronic sinus problems. But their work paves the way for a better understanding of anosmia at the cellular level.

"Using gene therapy in a mouse model of cilia dysfunction, we were able to rescue and restore olfactory function, or sense of smell," says senior author Jeffrey Martens, Ph.D., an associate professor of pharmacology at U-M. "Essentially, we induced the neurons that transmit the sense of smell to regrow the cilia they'd lost."

The mice in the study all had a severe genetic defect that affected a protein called IFT88, causing a lack of cilia throughout their bodies. Such mice are prone to poor feeding and to early death as a result. In humans, the same genetic defect is fatal.

The researchers were able to insert normal IFT88 genes into the cells of the mice by giving them a common cold virus loaded with the normal DNA sequence, and allowing the virus to infect them and insert the DNA into the mouse's own cells. They then monitored cilia growth, feeding habits, and well as signals within and between the nerve cells, called neurons, that are involved in the sense of smell.

Only 14 days after the three-day treatment, the mice had a 60 percent increase in their body weight, an indication they were likely eating more. Cell-level indicators showed that neurons involved in smelling were firing correctly when the mice were exposed to amyl acetate, a strong-smelling chemical also called banana oil.

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Can't smell anything? This discovery may give you hope

Low bacteria levels kept Missouri beaches open during hot summer

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JEFFERSON CITY A hot summer gave Missouri residents plenty of reasons to want to cool off at state park swimming beaches, and a drought seems to have helped offer more opportunities to do so.

Tests from water samples at state swimming beaches showed that bacteria levels were low enough to keep beaches open more often than during the past two years.

Results from the past three years were provided to The Associated Press by the Missouri Department of Natural Resources. They showed bacteria were high a dozen times at beaches this spring and summer, with half coming in April or May. That is less than half the frequency of 2011 and just a fraction of the nearly four dozen times that high bacteria were recorded at beaches in 2010.

High bacteria levels did not force any state park beaches to be closed this year from late May through the last week of July as summer heat was setting records. Since the end of July, the beach at the Cuivre River in northeastern Missouri was closed for one week and Watkins Woolen Mill near Kansas City has been closed in August.

This past week, park officials closed one beach at the Lake of the Ozarks in central Missouri. The area around the popular tourist lake received some rain last weekend. Water samples are collected near the state park beaches at the beginning of the week.

Ken Midkiff, director of the Missouri Clean Water Campaign, said the lack of summer rainfall has contributed to fewer tests showing high bacteria levels and more open swimming beaches. Pollutants can be washed into lakes and rivers.

"A lot of the high readings were attributable to runoff. We've had no or very little rain," Midkiff said.

Precipitation figures collected by the National Weather Service from local airports and observers showed how little rain has fallen in Missouri. The figures are from May 1 to Aug. 29, which was just before the start of Missouri's drenching from remnants of what once was Hurricane Isaac. Those statistics showed that St. Louis was short by nearly 9 inches of rain, and Farmington was behind by 10 inches. Columbia has reported its driest summer ever and was short by 13 inches.

The U.S. Drought Monitor map reported that through Aug. 28, more than 97 percent of Missouri fell in the two worst categories of drought.

Missouri closes state park beaches when the bacteria level from a single water sample or a rolling average of sample data exceed the levels recommended by the Environmental Protection Agency. Officials say the tests provide important information but are a small snapshot from a single moment and do not reflect the overall water quality in a lake or river.

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Low bacteria levels kept Missouri beaches open during hot summer

Little Compton beaches back open

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LITTLE COMPTON, R.I. (WPRI) -- Beaches are back open to swimmers in Little Compton a day after a great white shark washed up on shore.

PHOTO GALLERY: 13-Foot Great White Washes Ashore in Westport

A man out for a morning fishing trip on South Shore Beach found the 13-foot shark Saturday morning, a few hundred feet over the state line into Westport, Massachusetts.

Researchers say the shark weighed in at about 1,700 pounds and after dissecting it to marine biologists were unable to determine what killed it.

Officials plan to leave the shark where it is and let the tide take it out to sea.

Little Compton Police say Goosewing and South Shore Beaches are back open to swimmers Sunday morning, but there will be boat patrols just offshore keeping watch for sharks.

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Little Compton beaches back open

Beaches to be cleaned September 15

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GARBAGE will be removed from several beaches across the island on September 15, as Jamaica joins the rest of the world in observing International Coastal Cleanup Day.

Programme Director at the Jamaica Environment Trust (JET), which is organising the days activity, Suzanne Stanley, said a number of sites have been confirmed for cleaning.

She said that a list of sites will be posted on the JET website at http://www.jamentrust.org, where persons can register as volunteers

She said already, several schools, youth and community groups, non-government organisations and service clubs, have indicated that they will participate, and we have support from several corporate entities that will send teams and will also assist us with refreshments for the volunteers."

She is imploring Jamaicans to come out on the day and support the coastal cleanup effort.

Its the largest volunteer event in the world so come out and support the event, become familiar with the solid waste management issues that are (affecting the beaches) and play your part and try to contribute to reducing the amount of waste that we have on our beaches, she urged.

JET has organised beach cleanups in Jamaica since 1994. On International Coastal Cleanup Day 2011, observed on September 17, JET, with the support of the Tourism Enhancement Fund (TEF) and the business community, mobilised more than 4,000 volunteers for the cleaning of 55 beaches.

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Beaches to be cleaned September 15

Beaches Reopen Day After Great White Shark Washes Up In Westport

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(Photo Credit: Matt Gill)

LITTLE COMPTON, R.I. (AP) Beaches in southeastern Rhode Island have reopened to swimmers after a dead great white shark washed ashore just over the Massachusetts line.

Officials reopened Goosewing and South Shore Beaches in Little Compton, R.I., on Sunday morning. Little Compton police say the sharks carcass remains on the beach just over the state line in Westport, Mass.

Police say a boat patrol will monitor the beach area for other sharks.

MORE PHOTOS:Shark Washes Ashore In Westport

A Little Compton fisherman found the 13-foot shark on Saturday morning a few hundred feet over the line in Westport, forcing officials to close the Little Compton beaches.

Its not clear what officials plan to do with the carcass.

A marine biologist dissected the shark on Saturday. His findings havent been released.

Copyright 2012 The Associated Press.

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Beaches Reopen Day After Great White Shark Washes Up In Westport

RI beaches reopen after dead shark washes ashore

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LITTLE COMPTON, R.I.Beaches in southeastern Rhode Island have reopened to swimmers after a dead great white shark washed ashore just over the Massachusetts line.

Officials reopened Goosewing and South Shore Beaches in Little Compton, R.I., on Sunday morning. Little Compton police say the shark's carcass remains on the beach just over the state line in Westport, Mass.

Police say a boat patrol will monitor the beach area for other sharks.

A Little Compton fisherman found the 13-foot shark on Saturday morning a few hundred feet over the line in Westport, forcing officials to close the Little Compton beaches.

It's not clear what officials plan to do with the carcass.

A marine biologist dissected the shark on Saturday. His findings haven't been released.

Copyright 2012 Associated Press. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed.

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RI beaches reopen after dead shark washes ashore

OAD Shoots for the Stars

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The International Astronomical Union's (IAU) Office of Astronomy for Development (OAD) programme is announcing a number of exciting new partnerships that will assist with the IAU's decadal strategic plan, aimed at realising the societal benefits of astronomy. These landmark decisions involve establishing two new coordinating centres that use astronomy as a tool for development in the East and South East Asian regions, as well as launching an array of exciting programmes and events with different institutions across the world.

The first of these pioneering agreements, concerning a coordinating centre to be established in the East Asian region (in China), was signed on Tuesday 21 August 2012 by a consortium of institutes: the Kavli Institute for Astronomy and Astrophysics (KIAA, Peking University), Beijing Planetarium and Yunnan Astronomical Observatory.

The consortium is supported in their efforts by various important partners including the National Astronomical Observatories of the Chinese Academy of Sciences (NAOC), the East Asian Core Observatories Association (EACOA), and Pyongyang Astronomical Observatory (PAO).

The centre will cover two important functions: a regional node, which will coordinate astronomy for development activities in countries within the general geographical region of East Asia, and a Language Expertise Centre, which will deal with all aspects relating to (mainly) Chinese language and culture.

A second regional node will be established in the South East Asian region (in Thailand) and coordinated by the National Astronomical Research Institute of Thailand (NARIT).

These agreements are the first of their kind to be signed anywhere in the world. They follow the IAU's Announcement of Opportunity that went out in January 2012, and which has attracted 31 letters of intent and 15 full proposals (received from every populated continent) to establish coordinating nodes.

In addition to these exciting announcements, the OAD, in partnership with The Abdus Salam International Centre for Theoretical Physics (ICTP) has launched a call for proposals for a number of global activities aimed at using astronomy to stimulate high quality education and research at university level.

One of these activities is the Associate Scientists programme, where scientists and lecturers from developing regions, who are interested in using astronomy to develop university-level education in their home countries, will be provided with the means to travel to the ICTP in Italy and stay for a period of up to six weeks per year. Individual travel grants, funds for meetings and workshops as well as regional schools for young scientists are also included in this programme.

An additional agreement with the Inter-University Centre for Astronomy and Astrophysics (IUCAA, based in Pune, India) will provide training for potential leaders in the development of astronomy education at university, school and public levels, as well as facilitate visits from skilled experts.

A separate agreement with the University of Central Lancashire will award 12 scholarships for their distance learning astronomy programme to African students.

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OAD Shoots for the Stars

What's Really Delaying the Defeat of Aging?

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By way of following on from yesterday's thoughts on progress in longevity science, I'll point out that the August 2012 issue of Rejuvenation Research is available online. The leading editorial by Aubrey de Grey of the SENS Foundation covers much the same set of topics and is presently open access - so head on over and read it while that lasts.

What's Really Delaying the Defeat of Aging?

In the mid-1990s, when I decided to switch from computer science to gerontology, I recognized that the creation of a credible assault on aging would require solving three basic problems: (1) Creating a credible plan; (2) getting the people best placed to implement it to be interested in doing so; and (3) giving them the financial resources to get on with the job.

I broke the back of the first problem in mid-2000, when I realized that regenerative medicine - repairing the accumulating damage of aging - will probably be far simpler and easier to implement than the alternative followed by most biogerontologists, namely slowing the creation of that damage. By that time, I had also done most of the heavy lifting of item 2 (as I continued to do thereafter), by connecting with leading researchers worldwide, mostly face to face at conferences, and improving their understanding of how their expertise could be productively applied to aging. By way of illustration, quite a few of the most prestigious such people are named on the front cover of this journal as associate editors, and they accepted such a position for that reason. But what about item 3?

Unfortunately, I cannot tell so positive a story with respect to financial resources. Nearly a decade ago, I began to make public predictions of how soon we would achieve success in our crusade. I did so, as I still do, in the manner that (for better or worse) preoccupies the general public, namely in terms of longevity, but I have always been careful to incorporate two key caveats: (1) The level of uncertainty of the time frames, even if only scientific uncertainty is considered, and (2) the reliance of such estimates on adequate funding.

The first of these caveats is often elided, but it is simple: I estimate that we have a 50% chance of achieving the milestone of "robust human rejuvenation" (essentially, the rejuvenation of 60 year olds comprehensively enough that they won't be biologically 60 again until they're chronologically 90) within 25 years, but I also estimate that we have at least a 10% chance of not getting there in 100 years. But...that is all subject to the second caveat, namely funding.

Tragically, the level of funding that has been forthcoming during the past decade is only a few percent (at most) of what is necessary. The rate of progress in research to defeat aging has been quite amazing in view of that, but nonetheless, I estimate that it has been only about one-third of what could have been achieved with 10-20 times more money.

Which is much as I said yesterday: there are now plenty of researchers and research groups who would work on building real rejuvenation biotechnology as described in the SENS vision if they were given a budget to do so. That budget is, however, sadly lacking at this time. Millions of dollars are going to SENS and SENS-like research programs these days (which is a big improvement over their non-existence ten years ago) - but a hundred times that flow of resources would be needed to achieve earnest progress at the best possible rate.

One of the logical conclusions emerging from this point of view is that longevity science remains in that stage of growth wherein advocacy and education are the primary drivers of progress. There is sufficient buy-in from the scientific community to make institutional investment in research the bottleneck to progress, and obtaining that funding is a matter of persuasion.

In one sense this is encouraging: it is a characteristic state of affairs during a rapid shift in priorities for any field of human endeavor. Organizations with large sums to place into research tend to be the most conservative portions of their community, and thus among the last to heed the changing winds of knowledge and priority. This present stage, in which researchers are now interested and supportive but lacking in sources of funding that will allow them to actually work on the problem at hand, is a natural, albeit frustrating, part of the process. It is a considerable step up from the previous era in which few researchers had any interest in working on the biotechnologies of engineered human longevity, and even talking about it in public was discouraged.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

What’s Really Delaying the Defeat of Aging?

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By way of following on from yesterday's thoughts on progress in longevity science, I'll point out that the August 2012 issue of Rejuvenation Research is available online. The leading editorial by Aubrey de Grey of the SENS Foundation covers much the same set of topics and is presently open access - so head on over and read it while that lasts.

What's Really Delaying the Defeat of Aging?

In the mid-1990s, when I decided to switch from computer science to gerontology, I recognized that the creation of a credible assault on aging would require solving three basic problems: (1) Creating a credible plan; (2) getting the people best placed to implement it to be interested in doing so; and (3) giving them the financial resources to get on with the job.

I broke the back of the first problem in mid-2000, when I realized that regenerative medicine - repairing the accumulating damage of aging - will probably be far simpler and easier to implement than the alternative followed by most biogerontologists, namely slowing the creation of that damage. By that time, I had also done most of the heavy lifting of item 2 (as I continued to do thereafter), by connecting with leading researchers worldwide, mostly face to face at conferences, and improving their understanding of how their expertise could be productively applied to aging. By way of illustration, quite a few of the most prestigious such people are named on the front cover of this journal as associate editors, and they accepted such a position for that reason. But what about item 3?

Unfortunately, I cannot tell so positive a story with respect to financial resources. Nearly a decade ago, I began to make public predictions of how soon we would achieve success in our crusade. I did so, as I still do, in the manner that (for better or worse) preoccupies the general public, namely in terms of longevity, but I have always been careful to incorporate two key caveats: (1) The level of uncertainty of the time frames, even if only scientific uncertainty is considered, and (2) the reliance of such estimates on adequate funding.

The first of these caveats is often elided, but it is simple: I estimate that we have a 50% chance of achieving the milestone of "robust human rejuvenation" (essentially, the rejuvenation of 60 year olds comprehensively enough that they won't be biologically 60 again until they're chronologically 90) within 25 years, but I also estimate that we have at least a 10% chance of not getting there in 100 years. But...that is all subject to the second caveat, namely funding.

Tragically, the level of funding that has been forthcoming during the past decade is only a few percent (at most) of what is necessary. The rate of progress in research to defeat aging has been quite amazing in view of that, but nonetheless, I estimate that it has been only about one-third of what could have been achieved with 10-20 times more money.

Which is much as I said yesterday: there are now plenty of researchers and research groups who would work on building real rejuvenation biotechnology as described in the SENS vision if they were given a budget to do so. That budget is, however, sadly lacking at this time. Millions of dollars are going to SENS and SENS-like research programs these days (which is a big improvement over their non-existence ten years ago) - but a hundred times that flow of resources would be needed to achieve earnest progress at the best possible rate.

One of the logical conclusions emerging from this point of view is that longevity science remains in that stage of growth wherein advocacy and education are the primary drivers of progress. There is sufficient buy-in from the scientific community to make institutional investment in research the bottleneck to progress, and obtaining that funding is a matter of persuasion.

In one sense this is encouraging: it is a characteristic state of affairs during a rapid shift in priorities for any field of human endeavor. Organizations with large sums to place into research tend to be the most conservative portions of their community, and thus among the last to heed the changing winds of knowledge and priority. This present stage, in which researchers are now interested and supportive but lacking in sources of funding that will allow them to actually work on the problem at hand, is a natural, albeit frustrating, part of the process. It is a considerable step up from the previous era in which few researchers had any interest in working on the biotechnologies of engineered human longevity, and even talking about it in public was discouraged.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

SIRT6 Overexpression Reverses DNA Repair Decline in Aging Mice

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This interesting research result adds a little more to the debate over whether nuclear DNA damage is relevant to aging beyond its effects on cancer risk - though I think it's still a bit early to point to differences in DNA repair as the definitive cause of SIRT6-related longevity in mice: researchers "found that the decline in a cell's ability to repair DNA during aging coincided with a global reduction in the levels of proteins involved in the repair process. [They] tried to reverse the age-related decline in DNA repair efficiency by restoring the proteins to their original levels and found only one protein, SIRT6, did the trick. ... [Other research results have shown] that overexpressing the SIRT6 protein extended the lifespans of mice. Our research looked at DNA repair and found a reason for the increased longevity, and that is SIRT6's role in promoting more efficient DNA repair. ... The next step [is] to study the factors that regulate SIRT6, in an effort to learn more about the early stages of the DNA repair process. ... multiple groups are trying to develop drugs that activate SIRT6, and [researchers hope] that this research will one day lead to therapies that help extend a person's lifespan and treat cancer. ... SIRT6 plays a critical role in repairing the most dangerous type of DNA damage: double-strand breaks. DNA is a two-stranded molecule, and breaks can occur to one strand of the molecule or to both. In the case of single-strand breaks, the unbroken strand guides the repair process and the DNA molecule is typically restored to its original state. However, double-strand breaks, in which both strands are severed, are particularly hazardous because they are more difficult to repair and can lead to a rearrangement of the cell's genetic material."

Link: http://phys.org/news/2012-08-protein-dna-aging-cells.html

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm