terça-feira, 14 de outubro de 2014

A long-touted health-care revolution may at last be about to arrive

 

Oct 11th 2014 | | From the print edition

THE idea of telemedicine—health care provided using telecommunications equipment—has a lengthy history. Radio News, an American magazine, devoted its cover to a patient at home consulting a doctor in his surgery via a television link as long ago as 1924. When NASA began monitoring astronauts in space in the 1960s, fantasy became reality. It has been touted as health care’s future ever since.

But even smartphones and tablets have failed to usher in the telemedicine revolution: most health care still happens face to face. Now, enthusiasts think the wait is nearly over. Governments have been slow to embrace an approach that could improve coverage and outcomes, as well as saving money. But they are under increasing pressure from ageing populations and a surge in chronic diseases, just as public budgets are being squeezed.

At an industry conference in Rome on October 7-8th, participants discussed the problems that must be solved if telemedicine’s day is to come. They include redesigning laws and payment systems set up for face-to-face care, and finding ways to keep patients’ data secure and private.

In America, the world’s largest health-care market, states license doctors. Jurisdiction depends on the patient’s location, not the doctor’s—so doctors must be licensed in all states where they have patients, and meet care standards that René Quashie, a health-care lawyer, says are “complicated, incoherent and sometimes contradictory”.

The situation in the European Union is simpler: countries may not pass laws that would stop doctors practising telemedicine, and doctors need only be licensed in one country to practise in all. But member states do not agree on whether to pay for care that is administered remotely; some, including Germany, rarely pay for it at all.

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In America only 21 states mandate that telemedicine be compensated at the same rate as face-to-face care. At the federal level, the Veterans Administration has embraced telemedicine whereas Medicare, the public-health programme for the elderly, largely ignores it. But private employers and insurers are increasingly paying for telemedicine, encouraged by a shift to paying doctors for packages of care rather than per service. This has “opened the door” to remote care, says Jonathan Linkous of the American Telemedicine Association.

Telemedicine is more than a Skype chat between doctor and patient, says Michael Young, who works on remote care for the University of North Carolina. The technology can look similar but the need for security and privacy is greater. Earlier this year the FBI warned American health-care providers that their cyber-security systems were not up to snuff. Electronic versions of sensitive documents such as X-rays or doctors’ notes must be as secure as paper ones. That is hard when they are flying through the ether. In August one of America’s biggest hospital groups said Chinese hackers had stolen data on 4.5m patients.

Some small countries are in the vanguard. Israel’s health-care system is fully digitised: all doctors use electronic medical records, and patients have access to their data. Doctors can write repeat prescriptions and refer patients to specialists over the internet. The health ministry noticed an uptick in telemedicine in 2010 and introduced relatively lax guidelines in 2012.

China is spending billions on health-care reform, with a focus on telemedicine. But keen interest is no guarantee of success in any country. “If you have a chaotic system and add technology, you get a chaotic system with technology,” says Peteris Zilgalvis, a health official at the European Commission. Telemedicine may even increase costs if it is added to old routines rather than replacing them. There is little evidence of its cost-effectiveness, says Marc Lange of the European Health Telematics Association, because studies simply lump it on top of standard care.

Lights, camera, interaction

Some doctors have been reluctant to embrace telemedicine, says Nils Kolstrup, a Norwegian doctor, fearing it may lessen their authority by making it easier for patients to seek advice elsewhere. Patients, too, may feel they are being fobbed off with second-best, and governments worry that it could stimulate frivolous demand.

So countries where provision is currently limited or non-existent may be quickest to move. Rwanda, for example, is short of oncologists, so American specialists consult on difficult cases. Doctors at the Cleveland Clinic look at tumours from several African countries. But if telemedicine is to take off, big, rich countries must embrace it—not least because that is where the money is.

From the print edition: International

Snap 2014-10-14 at 08.54.13

Revving up fluorescence for superfast LEDs

 


This is an artist's representation of light trapped between a silver nanocube and a thin sheet of gold. When fluorescent molecules -- shown in red -- are trapped between the two, they emit photons up to 1,000 times faster than normal.

Duke University researchers have made fluorescent molecules emit photons of light 1,000 times faster than normal -- setting a speed record and making an important step toward realizing superfast light emitting diodes (LEDs) and quantum cryptography.

This year's Nobel Prize in physics was awarded for the discovery of how to make blue LEDs, allowing everything from more efficient light bulbs to video screens. While the discovery has had an enormous impact on lighting and displays, the slow speed with which LEDs can be turned on and off has limited their use as a light source in light-based telecommunications.

In an LED, atoms can be forced to emit roughly 10 million photons in the blink of an eye. Modern telecommunications systems, however, operate nearly a thousand times faster. To make future light-based communications using LEDs practical, researchers must get photon-emitting materials up to speed.

In a new study, engineers from Duke increased the photon emission rate of fluorescent molecules to record levels by sandwiching them between metal nanocubes and a gold film.

The results appear online October 12 in Nature Photonics.

"One of the applications we're targeting with this research is ultrafast LEDs," said Maiken Mikkelsen, an assistant professor of electrical and computer engineering and physics at Duke. "While future devices might not use this exact approach, the underlying physics will be crucial."

Mikkelsen specializes in plasmonics, which studies the interaction between electromagnetic fields and free electrons in metal. In the experiment, her group manufactured 75-nanometer silver nanocubes and trapped light between them, greatly increasing the light's intensity.

When fluorescent molecules are placed near intensified light, the molecules emit photons at a faster rate through an effect called Purcell enhancement. The researchers found they could achieve a significant speed improvement by placing fluorescent molecules in a gap between the nanocubes and a thin film of gold.

To attain the greatest effect, Mikkelsen's team needed to tune the gap's resonant frequency to match the color of light that the molecules respond to. With the help of co-author David R. Smith, the James B. Duke Professor and Chair of Electrical and Computer Engineering at Duke, they used computer simulations to determine the exact size of the gap needed between the nanocubes and gold film to optimize the setup.

That gap turned out to be just 20 atoms wide. But that wasn't a problem for the researchers.

"We can select cubes with just the right size and make the gaps literally with nanometer precision," said Gleb Akselrod, a postdoc in Mikkelsen's lab and first author on the study. "When we have the cube size and gap perfectly calibrated to the molecule, that's when we see the record 1,000-fold increase in fluorescence speed."

Because the experiment used many randomly aligned molecules, the researchers believe they can do even better. They plan to design a system with individual fluorescent molecule placed precisely underneath a single nanocube. According to Akselrod, they can achieve even higher fluorescence rates by standing the molecules up on edge at the corners of the cube.

"If we can precisely place molecules like this, it could be used in many more applications than just fast LEDs," said Akselrod. "We could also make fast sources of single photons that could be used for quantum cryptography. This technology would allow secure communication that could not be hacked -- at least not without breaking the laws of physics."

This work was supported by the Lord Foundation of North Carolina and the Air Force Office of Scientific Research (Contract No. FA9550-12-1-0491).


Story Source:

The above story is based on materials provided by Duke University. Note: Materials may be edited for content and length.


Journal Reference:

  1. Gleb M. Akselrod, Christos Argyropoulos, Thang B. Hoang, Cristian Ciracì, Chao Fang, Jiani Huang, David R. Smith, Maiken H. Mikkelsen. Probing the mechanisms of large Purcell enhancement in plasmonic nanoantennas. Nature Photonics, 2014; DOI: 10.1038/nphoton.2014.228

 

Duke University. "Revving up fluorescence for superfast LEDs." ScienceDaily. ScienceDaily, 12 October 2014. <www.sciencedaily.com/releases/2014/10/141012134843.htm>.

Hands-on: Is Samsung's bold Gear S ahead of the smartwatch curve?

 

Gizmag goes hands-on with Samsung's boldest smartwatch to date, the Gear S

Gizmag goes hands-on with Samsung's boldest smartwatch to date, the Gear S

Image Gallery (59 images)

Last week we told you about Samsung's latest smartwatch, the Gear S. With a curved display and built-in 3G wireless, it's certainly a bold step forward. But what's it like to actually use? Read on, as Gizmag goes wrists-on with the Samsung Gear S.

The Gear S is unmistakably bold, but it's also walking a fine line. On one hand, it has a gorgeous and spacious 2-in curved screen. The Super AMOLED display looks terrific and the curved aesthetic is a pleasure to swipe and tap. It gives you much more real estate than any mainstream smartwatch to date – and that alone could open some interesting doors.

On the other hand, this sucker takes the tech producty look that has been so common in smartwatches, and pushes it to a new extreme. Wear this thing in public, and you're sure to get some looks. I personally think it looks pretty cool, but it's also a huge departure from classic timekeeping watches. Dick Tracy? More like George Jetson.

Samsung Gear S (Photo: Will Shanklin/Gizmag.com)

It's quite possible that most customers aren't ready for a watch that looks like this. Or, on the other hand, maybe customers just need to know that it packs in enough cool features to justify its sci-fi appearance. That's where the Gear S has more potential than previous smartwatches.

Nike+ app on the Samsung Gear S (Photo: Will Shanklin/Gizmag.com)

Though it runs a newer version of the same Tizen software, using the Gear S is very different from using any of the older Samsung watches. And it all goes back to that display. It's going to raise the bar for what's possible on a smartwatch.

Samsung Gear S (Photo: Will Shanklin/Gizmag.com)

From where I stand now, I'd say the Gear S' killer feature is its virtual keyboard. It's a bit strange rapping out texts or emails on a curved 2-in screen, but Samsung's auto-correct seems to be quite good. In my testing during the hands-on session, it almost always corrected my gibberish into exactly what I was trying to type.

A Samsung rep also tells me that the watch will support third-party keyboards. So, though the stock Samsung one doesn't have a Swype-like trace feature, we'll surely see alternatives that will (perhaps from companies like SwiftKey or Swype itself).

Samsung Gear S with the Gear 2 Neo (Photo: Will Shanklin/Gizmag.com)

Back to that curved screen. Yes, it's huge for a watch. And yes, this design is going to be way too radical for some people. But it's also a joy to use. It's a lot like the Gear Fit's screen, only much bigger, more curved and attached to a more powerful device.

We'll need to spend more time with the Gear S before jumping to conclusions. But, from where I stand now, I think Samsung has hit a pretty nice balance of packing in smartphone-like space and power – but without going too ridiculously crazy with the design (though opinions will undoubtedly vary on that point).

Samsung Gear S (Photo: Will Shanklin/Gizmag.com)

The Tizen UI is similar to what we've seen on older Gear watches, but it's more mature on the Gear S. From the main clock face, you'll find widgets lined up to your right. Notifications live permanently on the left. Below the main screen is an app drawer. This latest version of the Tizen software is inching closer to being like a smartphone OS.

Samsung Gear S (Photo: Will Shanklin/Gizmag.com)

So what about the 3G wireless and that SIM card slot that you see above? Well, I couldn't get a cut-and-dry answer from Samsung about what features will be available without a paired smartphone, and which will require the phone. The impression I get is that, right now, there is no answer. Apparently the point hasn't yet been decided (I suspect carrier demands and politics are at play). But we do know that at least some key features will work without having your phone around.

The gist that I got from Samsung's reps is that, despite its 3G radio, the Gear S isn't designed to replace your phone. It's still a companion device. But, in a pinch, it can work without one ... at least partially.

A lot is still fuzzy there, so we should consider the standalone wireless factor a question mark at this point. We'll be keeping an eye on this when the watch launches.

Samsung Gear S (Photo: Will Shanklin/Gizmag.com)

In poking through the watch's settings, I noticed that there were options for calling or sending texts from either your paired phone's number or from the Gear's own number (above). There were also options for forwarding calls from your phone to the Gear. When I asked a Samsung rep about this, I was told that the software isn't final, so these options may or may not be in the final shipping version. Perhaps it will also vary from carrier to carrier.

Samsung also hasn't revealed anything about pricing, but a company rep hinted to me that it may cost more than previous Gear watches. With 3G, built-in GPS and that large curved screen, I guess that shouldn't be too surprising. My guess is that the Gear S will land in the US$350-550 range. In the US, maybe we'll even see carriers sell it subsidized with a contract or installment plan (that's completely speculation on my part, by the way).

Samsung Gear S (Photo: Will Shanklin/Gizmag.com)

As for that built-in GPS, we could only test it so much in an indoor hands-on area. But it looks like exactly what you'd expect out of any navigation app. It's Nokia's Here, it's on the Gear and it's designed for pedestrian travel. Until we get our hands on a review unit, that's the long and short of it.

Samsung Gear S (Photo: Will Shanklin/Gizmag.com)

Of the four products Samsung revealed today, the Gear S was the one I gravitated towards the most. It's going to make a very interesting alternative to Android Wear (and perhaps the iWatch). And while I still think most people will prefer watches that look a bit less ... futuristic, I've always appreciated Samsung's full-throttle approach to this space. Once we get a review unit in house, this is going to be, at the very least, one hell of a fun device to play with.

For more on today's announcements, you can hit up our hands-ons with the Galaxy Note 4 and Galaxy Note Edge. And for more on the Gear S, you can see how it compares to Samsung's five previous smartwatches.

Snap 2014-09-11 at 19.35.16

 

Green tea nanocarrier delivers cancer-killing drugs more effectively

 

Green tea has been used for the first time to deliver cancer-killing drugs (Photo: Shutter...

Green tea has been used for the first time to deliver cancer-killing drugs (Photo: Shutterstock)

Many of us drink green tea for its wonderful health benefits, including proven antioxidant, antimicrobial, anti-aging and anti-cancer properties. Now, researchers in Singapore have taken its cancer-fighting properties to the next level, developing a green tea-based nanocarrier that encapsulates cancer-killing drugs. It is the first time green tea has been used to deliver drugs to cancer cells, with promising results. Animal studies show far more effective tumor reduction than use of the drug alone while significantly reducing the accumulation of drugs in other organs.

The new drug delivery system, developed at the Institute of Bioengineering and Nanotechnology (IBN) of A*STAR, uses epigallocatechin gallate (EGCG), a powerful antioxidant and catechin found in green tea and used therapeutically to treat cancer and other disorders.

"We have developed a green tea-based carrier in which the carrier itself displayed anti-cancer effect and can boost cancer treatment when used together with the protein drug," says Dr Motoichi Kurisawa, IBN Principal Research Scientist and Team Leader.

One of the main drawbacks of chemotherapy is that it also kills healthy cells in surrounding tissues and organs. Carriers allow more accurate treatment, acting like homing missiles that target diseased cells and release cancer-destroying drugs. However, the amount of the drug they can deliver is limited so more carriers need to be administered for treatment to be effective. Current carriers are made of materials that at best offer no therapeutic value and at worst may have adverse effects when used in large quantities, so the green tea-based carrier is an exciting development.

Green tea nanocarrier delivers cancer-killing drugs more effectively

The carrier uses a core made of an oligomer of EGCG to enclose cancer-destroying drugs. The shell of the carrier is made of PEG, a molecule which camouflages the carrier and prevents the immune system from destroying it before it reaches its target.

Animal studies using the green tea-based nanocarrier loaded with Herceptin, a drug used to treat breast cancer, delivered promising results. Twice as much Herceptin accumulated in cancer cells than if the drug had been used alone, enabling more effective tumor targeting and reduced tumor growth. On the other hand, the level of Herceptin in surrounding organs was significantly lower, with a 70 percent reduction in the liver and kidneys and a 40 percent reduction in the lungs.

The IBN team is developing the technology for clinical applications.

The research has been published in nature nanotechnology.

Source: IBN (PDF)

 

9 Awesome Infographics for Graphic Designers

 

We just released our biggest post so far. Read all about Mattia's 'No flying for a year' experience in this post!

Published by Brian Morris on January 28, 2013 in Infographic 10 images

As a graphic designer, you’ve probably designed at least a few infographics for your clients – or even for fun.  You can create (and sell) infographics for any topic or industry, which means infographics can be a lucrative source of income.  Some designers make a full-time living designing infographics alone.  And while infographics always require the talents of a graphic designer, how many infographics have you seen that feature graphic designers?  The following 10 awesome infographics were made by graphic designers, for graphic designers.  Follow the links to view the full infographics.  Enjoy!

1. Psychology of Color

Learn what different colors represent and what emotions they stir, and when and how to use them in your own designs.

Psychology of Color

2. Elements of Design

This infographic serves as a quick reference for the basic elements of design, complete with tips for how and why each should be considered when creating any design.

Elements of Design

 

3. Graphic Designer’s Roadmap

Want to be a better, more successful, more inspired graphic designer?  This infographic serves as a roadmap to all of these things.

Graphic Designer’s Roadmap

4. What Your Web Design Says About You

Your favorite fonts, colors, and other design elements reveal a lot about your personality, goals and dreams. 

5. Freelance to Freedom.

How do you get out from under your bosses’ thumb, grow your freelance business and eventually life on a good income with minimal effort? 

6. Facts About Graphic Design Careers

How much do other graphic designers make?  Where are the best jobs located?  Learn the answers to these questions and more from this graphic design infographic.

Facts About Graphic Design Careers

7. State of Graphic Design

This infographic reveals the results of polling the world’s most successful graphic designers to determine what, in fact, is necessary to be a truly successful graphic designer

State of Graphic Design

8. Creative Salaries

What to know what graphic designers make?  How about creative directors?  Learn more about income differences and gaps revealed in a 2012 survey among creative professionals with this infographic.

Creative Salaries

9. Anatomy of a Graphic Designer

A humorous look at what makes a graphic designer, a graphic designer.

Anatomy of a Graphic Designer

by Glantz Design

 

Snap 2014-10-14 at 05.00.33

Construction of Royal Navy's new River class OPVs gets underway

 

Artist's concept of HMS Forth, which is now under construction

Artist's concept of HMS Forth, which is now under construction

Image Gallery (9 images)

BAE Systems has begun construction of the first of the Royal Navy’s three new River class Batch 3 Offshore Patrol Vessels (OPV). During a ceremony at BAE Systems Surface Ships’ Govan facility in Glasgow, Bernard Gray, the Ministry of Defence’s (MoD) Chief of Defence Material, activated a plasma cutting machine, which sliced through first plate of steel for HMS Forth. The ship will be the first in the Royal Navy to incorporate the state-of-the-art Shared Infrastructure operating system in its construction.

HMS Forth and her two sister ships are based on a design already used in ships built by BAE for the Brazilian Navy and the Royal Thai Navy, but which has now been upgraded and adapted for Britain’s requirements. One key element to the new River class is the Shared Infrastructure system, which is already being retrofitted to the helicopter carrier HMS Ocean. It’s designed to integrate the hardware of the ship’s combat and management systems, so they can all be accessed from a single console instead of from a series of dedicated consoles.

According the BAE, Shared Infrastructure is scheduled to be deployed across the Royal Navy’s entire surface fleet over the next decade. It is expected to significantly reduce operating costs while freeing up more space below decks and in the stores thanks to fewer spare parts being needed at sea to repair multiple console types.

Artist's concept of the Royal Navy's new OPVs

When construction is completed, HMS Forth and the other two planned OPVs will join the previous five River class ships that will replace the Island and Castle-class patrol vessels. Larger and longer than previous ships in their class, the Batch 3s and the rest of the River class will be used mainly for Fishery Protection Squadron and Economic Exclusion Zone (EEZ) patrol, though they are designed for global deployment, with one in the class having been assigned to protect the Falkland Islands.

The new River class ships displace 2,000 tonnes (2,204 tons), are 90.5 m (297 ft) long and have a draft of 3.8 m (12.4 ft). They’re powered by two Ruston 12RK 270 diesel engines that give them a cruising speed of 24 knots (27 mph, 44 km/h), a range of 5,500 nmi (6,300 mi, 10,200 km), and an endurance of 35 days at sea. In addition to their complement of 36, they can also carry 20 troops, and their longer length allows them to accommodate a Merlin helicopter on the flight deck, as well as a 30mm DS30B gun forward.

"We've kept many of the engineering qualities that have made the [previous batch] River class OPVs so successful and reliable, and enhanced them with a design that is larger, more efficient, and more capable,” says Iain Stevenson, Head of the Offshore Patrol Vessel Programme BAE Systems Naval Ships. “This design is tried and tested and already in service with the Brazilian Navy and Royal Thai Navy, who are operating similar versions of these ships. For the Royal Navy, our engineering teams have modified this proven design, ensuring that it meets the demanding UK requirements, demonstrating just how flexible the design of the ship is.”

HMS Forth is scheduled for delivery to the Royal Navy in 2017.

 

Source: BAE Systems

 

segunda-feira, 13 de outubro de 2014

Research findings could pave way for a fructose tolerance test

 

October 13, 2014

Beth Israel Deaconess Medical Center

The FGF21 hormone may be a reliable predictor of altered fructose metabolism and provide the basis for a "fructose tolerance test," researchers report. Determining the body’s metabolic response to fructose has been a difficult task, researchers say and consequently, there is no equivalent test to warn of impaired or altered fructose metabolism. That may soon change, thanks to new research.


Increased consumption of table sugar and high-fructose corn syrup has been linked to rising rates of obesity and type 2 diabetes in the United States and throughout the world. Both sweeteners are commonly found in processed foods and sugar-sweetened beverages, and both are made up of nearly equal amounts of two basic sugars, glucose and fructose.

The effects of glucose ingestion in humans are well understood, in part, because they are easily assessed by performing a Glucose Tolerance Test, which measures serum glucose levels after glucose ingestion and has become the diagnostic cornerstone for modern diabetes care. Furthermore, the hormone insulin can also be easily measured to assess the acute metabolic effects of glucose ingestion and evaluate a person's risk for developing diabetes and cardiovascular disease.

But determining the body's metabolic response to fructose has been much more difficult, and consequently, there is no equivalent test to warn of impaired or altered fructose metabolism.

That may soon change. A new study led by investigators at Beth Israel Deaconess Medical Center (BIDMC) now finds that blood levels of the hormone Fibroblast Growth Factor 21 (FGF21) increases rapidly acutely and robustly after fructose ingestion. Reported online in Molecular Metabolism, the new findings suggest that FGF21 is a reliable predictor of altered fructose metabolism and, in essence, provides the basis for a "fructose tolerance test."

"Accumulating evidence suggests that the fructose component of sugar may have a particularly deleterious effect on health," explains co-senior author Mark Herman, MD, of the Division of Endocrinology, Diabetes and Metabolism at BIDMC and Assistant Professor of Medicine at Harvard Medical School (HMS). "If you feed animals or people higher-than-normal amounts of fructose, they become obese, less responsive to the key actions of insulin, and develop fatty liver disease and abnormal blood lipid levels. All of these increase the risk of developing diabetes and cardiovascular disease." Fructose is a pervasive presence throughout our foods: high fructose corn syrup, for example, can be found in everything from processed cookies and sweets to seemingly healthy foods, such as yogurt.

"Fructose is taken up by the liver as soon as it's ingested and very little of it makes it to peripheral blood where it might be sampled and measured," adds co-senior author Eleftheria Maratos-Flier, MD, HMS Professor of Medicine in the Division of Endocrinology, Diabetes and Metabolism at BIDMC. "This makes it very hard to determine how an individual responds to fructose ingestion. Furthermore, there has, to date, been no known hormonal response to fructose in the way that the hormone insulin responds to glucose."

Maratos-Flier has been studying the FGF21 hormone for almost a decade and previously found that in both humans and animals, FGF21 levels are elevated in association with obesity, insulin resistance, and non-alcoholic fatty liver disease. Herman's work, meanwhile, had focused on a cellular factor, Carbohydrate Responsive-Element Binding Protein (ChREBP), which senses simple sugars and responds by activating cellular gene expression programs. Observations that fructose potently activates ChREBP in rodent livers and that ChREBP can regulate FGF21 expression suggested to Maratos-Flier and Herman the intriguing hypothesis that fructose ingestion might stimulate production of circulating FGF21 in people.

To test this hypothesis, the researchers, led by first author Jody Dushay, MD, HMS Instructor in Medicine, recruited 10 lean, healthy study subjects. They first tested the effect of glucose on FGF21 by giving volunteers a drink of 75 grams of glucose and measuring blood levels over the course of five hours. There was no immediate effect on FGF21 levels although modest changes in FGF21 were seen three to four hours later. In contrast, after ingesting 75 grams of fructose, FGF21 levels dramatically increased by an average of 400 percent -- within only two hours.

"This tells us that fructose actively regulates FGF21 in humans," says Maratos-Flier. "The hormone-like response of FGF21 to fructose ingestion suggests that FGF21 might play an unanticipated role in regulating fructose metabolism. We were totally surprised by this dramatic effect becausej, to date, there has been no way of assessing the body's acute metabolic response to fructose ingestion. We haven't had a simple quick test like we have for glucose."

Furthermore, she adds, the findings demonstrated that the FGF21 response was exaggerated in subjects with metabolic disease, suggesting that either some aspect of fructose metabolism changes during the development of metabolic syndrome and/or there are innate differences in fructose metabolism among individuals and those with an exaggerated FGF21 response to fructose are predisposed to developing disease.

"For the first time, this provides an avenue for labs everywhere to easily study fructose metabolism in people," adds Herman. "This study provides a foundational observation for further investigation into the genetic and environmental determinants of an individual's metabolic response to fructose and this type of knowledge will be essential to develop personalized dietary recommendations as well as pharmacological strategies to prevent and treat cardiometabolic disease."


Story Source:

The above story is based on materials provided by Beth Israel Deaconess Medical Center. Note: Materials may be edited for content and length.


 

Beth Israel Deaconess Medical Center. "Research findings could pave way for a fructose tolerance test." ScienceDaily. ScienceDaily, 13 October 2014. <www.sciencedaily.com/releases/2014/10/141013123018.htm>.

 

New cancer drug to begin trials in multiple myeloma patients

 

October 13, 2014

Imperial College London

A new cancer drug has been developed, which researchers plan to trial in multiple myeloma patients by the end of next year. The researchers report how the drug, known as DTP3, kills myeloma cells in laboratory tests in human cells and mice, without causing any toxic side effects, which is the main problem with most other cancer drugs. The new drug works by stopping a key process that allows cancer cells to multiply.


Scientists at Imperial College London have developed a new cancer drug which they plan to trial in multiple myeloma patients by the end of next year.

In a paper published today in the journal Cancer Cell, the researchers report how the drug, known as DTP3, kills myeloma cells in laboratory tests in human cells and mice, without causing any toxic side effects, which is the main problem with most other cancer drugs. The new drug works by stopping a key process that allows cancer cells to multiply.

The team have been awarded Biomedical Catalyst funding from the Medical Research Council (MRC) to take the drug into a clinical trial in multiple myeloma patients, scheduled to begin in late 2015.

Multiple myeloma is an incurable cancer of the bone marrow, which accounts for nearly two per cent of all cancer deaths.

Professor Guido Franzoso, from the Department of Medicine at Imperial College London, who led the research, said: "Lab studies suggest that DTP3 could have therapeutic benefit for patients with multiple myeloma and potentially several other types of cancer, but we will need to confirm this in our clinical trials, the first of which will start next year."

The new drug was developed by studying the mechanisms that enable cancer cells to outlive their normal lifespan and carry on multiplying. In the 1990s, a protein called nuclear factor kappa B (NF-kB), which plays an important role in inflammation, and the immune and stress response systems, was discovered to be overactive in many types of cancer, and responsible for switching off the normal cellular mechanisms that naturally lead to cell death. This enables the cancer cells to survive.

The pharmaceutical industry and scientists around the world have invested heavily in research into NF-kB inhibitors, but such compounds have not been successfully developed as therapies because they also block the many important processes controlled by NF-kB in healthy cells, causing serious toxic side effects.

The Imperial researchers took a different approach, looking for target genes downstream of NF-kB that might be responsible for its role in cancer specifically.

By studying cells from multiple myeloma patients, they identified a protein complex, named GADD45β/MKK7, that appeared to play a critical role in allowing the cancer cells to survive.

Searching for a safe way to target the NF-kB pathway, they screened over 20,000 molecules and found two that disrupted the protein complex. Further refinements led to the experimental drug, DTP3, which tests showed kills cancer cells very effectively but appears to have no toxicity to normal cells at the doses that eradicate the tumours in mice.

"We had known for many years that NF-kB is very important for cancer cells, but because it is also needed by healthy cells, we did not know how to block it specifically. The discovery that blocking the GADD45β/MKK7 segment of the NF-κB pathway with our DTP3 peptide therapeutic selectively kills myeloma cells could offer a completely new approach to treating patients with certain cancers, such as multiple myeloma," Professor Franzoso said.

A spinout company, Kesios Therapeutics, was formed to commercialise DTP3 and other drug candidates based on Professor Franzoso's research, with support from Imperial Innovations, a technology commercialisation company focused on developing the most promising UK academic research.

"The significant progress made by Professor Franzoso in multiple myeloma is one of the many cancers we believe his signal transduction research could be applied to. To help develop this ground-breaking research further, Imperial Innovations created the spin out Kesios Therapeutics," explained Dayle Hogg from the Healthcare Ventures team at Imperial Innovations.


Story Source:

The above story is based on materials provided by Imperial College London. Note: Materials may be edited for content and length.


Journal Reference:

  1. Laura Tornatore, Annamaria Sandomenico, Domenico Raimondo, Caroline Low, Alberto Rocci, Cathy Tralau-Stewart, Daria Capece, Daniel D’Andrea, Marco Bua, Eileen Boyle, Mark van Duin, Pietro Zoppoli, Albert Jaxa-Chamiec, Anil K. Thotakura, Julian Dyson, Brian A. Walker, Antonio Leonardi, Angela Chambery, Christoph Driessen, Pieter Sonneveld, Gareth Morgan, Antonio Palumbo, Anna Tramontano, Amin Rahemtulla, Menotti Ruvo, Guido Franzoso. Cancer-Selective Targeting of the NF-κB Survival Pathway with GADD45β/MKK7 Inhibitors. Cancer Cell, 2014; 26 (4): 495 DOI: 10.1016/j.ccr.2014.07.027

Imperial College London. "New cancer drug to begin trials in multiple myeloma patients." ScienceDaily. ScienceDaily, 13 October 2014. <www.sciencedaily.com/releases/2014/10/141013123034.htm>.

 

Chemical derived from broccoli sprouts shows promise in treating autism

 


Broccoli sprouts are shown.

Results of a small clinical trial suggest that a chemical derived from broccoli sprouts -- and best known for claims that it can help prevent certain cancers -- may ease classic behavioral symptoms in those with autism spectrum disorders (ASDs).

The study, a joint effort by scientists at MassGeneral Hospital for Children and the Johns Hopkins University School of Medicine, involved 40 teenage boys and young men, ages 13 to 27, with moderate to severe autism.

In a report published online in the journal Proceedings of the National Academy of Sciences during the week of Oct. 13, the researchers say that many of those who received a daily dose of the chemical sulforaphane experienced substantial improvements in their social interaction and verbal communication, along with decreases in repetitive, ritualistic behaviors, compared to those who received a placebo.

"We believe that this may be preliminary evidence for the first treatment for autism that improves symptoms by apparently correcting some of the underlying cellular problems," says Paul Talalay, M.D., professor of pharmacology and molecular sciences, who has researched these vegetable compounds for the past 25 years.

"We are far from being able to declare a victory over autism, but this gives us important insights into what might help," says co-investigator Andrew Zimmerman, M.D., now a professor of pediatric neurology at UMass Memorial Medical Center.

ASD experts estimate that the group of disorders affects 1 to 2 percent of the world's population, with a much higher incidence in boys than girls. Its behavioral symptoms, such as poor social interaction and verbal communication, are well known and were first described 70 years ago by Leo Kanner, M.D., the founder of pediatric psychiatry at The Johns Hopkins University.

Unfortunately, its root causes remain elusive, though progress has been made, Talalay says, in describing some of the biochemical and molecular abnormalities that tend to accompany ASD.

Many of these are related to the efficiency of energy generation in cells. He says that studies show that the cells of those with ASD often have high levels of oxidative stress, the buildup of harmful, unintended byproducts from the cell's use of oxygen that can cause inflammation, damage DNA, and lead to cancer and other chronic diseases.

In 1992, Talalay's research group discovered that sulforaphane has some ability to bolster the body's natural defenses against oxidative stress, inflammation and DNA damage. In addition, the chemical later turned out to improve the body's heat-shock response -- a cascade of events used to protect cells from the stress caused by high temperatures, including those experienced when people have fever.

Intriguingly, he says, about one-half of parents report that their children's autistic behavior improves noticeably when they have a fever, then reverts back when the fever is gone. In 2007, Zimmerman, a principal collaborator in the current study, tested this anecdotal trend clinically and found it to be true, though a mechanism for the fever effect was not identified.

Because fevers, like sulforaphane, initiate the body's heat-shock response, Zimmerman and Talalay wondered if sulforaphane could cause the same temporary improvement in autism that fevers do. The current study was designed to find out.

Before the start of the trial, the patients' caregivers and physicians filled out three standard behavioral assessments: the Aberrant Behavior Checklist (ABC), the Social Responsiveness Scale (SRS) and the Clinical Global Impressions-Improvement scale (CGI-I). The assessments measure sensory sensitivities, ability to relate to others, verbal communication skills, social interactions and other behaviors related to autism.

Twenty-six of the subjects were randomly selected to receive, based on their weight, 9 to 27 milligrams of sulforaphane daily, and 14 received placebos. Behavioral assessments were again completed at four, 10 and 18 weeks while treatment continued. A final assessment was completed for most of the participants four weeks after the treatment had stopped.

Most of those who responded to sulforaphane showed significant improvements by the first measurement at four weeks and continued to improve during the rest of the treatment. After 18 weeks of treatment, the average ABC and SRS scores of those who received sulforaphane had decreased 34 and 17 percent, respectively, with improvements in bouts of irritability, lethargy, repetitive movements, hyperactivity, awareness, communication, motivation and mannerisms.

After 18 weeks of treatment, according to the CGI-I scale, 46, 54 and 42 percent of sulforaphane recipients experienced noticeable improvements in social interaction, aberrant behaviors and verbal communication, respectively.

Talalay notes that the scores of those who took sulforaphane trended back toward their original values after they stopped taking the chemical, just like what happens to those who experience improvements during a fever. "It seems like sulforaphane is temporarily helping cells to cope with their handicaps," he says.

Zimmerman adds that before they learned which subjects got the sulforaphane or placebo, the impressions of the clinical team -- including parents -- were that 13 of the participants noticeably improved. For example, some treated subjects looked them in the eye and shook their hands, which they had not done before. They found out later that all 13 had been taking sulforaphane, which is half of the treatment group.

Talalay cautions that the levels of sulforaphane precursors present in different varieties of broccoli are highly variable. Furthermore, the capacity of individuals to convert these precursors to active sulforaphane also varies greatly. It would be very difficult to achieve the levels of sulforaphane used in this study by eating large amounts of broccoli or other cruciferous vegetables.

 

Story Source:

The above story is based on materials provided by Johns Hopkins Medicine. Note: Materials may be edited for content and length.


Journal Reference:

  1. Kanwaljit Singh, Susan L. Connors, Eric A. Macklin, Kirby D. Smith, Jed W. Fahey, Paul Talalay, and Andrew W. Zimmerman. Sulforaphane treatment of autism spectrum disorder (ASD). PNAS, October 13, 2014 DOI: 10.1073/pnas.1416940111

Johns Hopkins Medicine. "Chemical derived from broccoli sprouts shows promise in treating autism." ScienceDaily. ScienceDaily, 13 October 2014. <www.sciencedaily.com/releases/2014/10/141013152608.htm>.

 

 

Greater rates of mitochondrial mutations discovered in children born to older mothers

 


The inner membrane of each mitochondrion contains distinctive folds known as cristae. In a normal mitochondrion (left) these folds fill the interior, but these folds are lost in damaged or dysfunctional mitochondria (right). Dozens of rare diseases have been shown to result from this type of mitochondrial dysfunction. Several others -- including Alzheimer disease, autism, cancer, cardiovascular disease, Parkinson disease, and type 2 diabetes -- are suspected to involve the mitochondria.

The discovery of a "maternal age effect" by a team of Penn State scientists that could be used to predict the accumulation of mitochondrial DNA mutations in maternal egg cells -- and the transmission of these mutations to children -- could provide valuable insights for genetic counseling. These mutations cause more than 200 diseases and contribute to others such as diabetes, cancer, Parkinson's disease, and Alzheimer's disease. The study found greater rates of the mitochondrial DNA variants in children born to older mothers, as well as in the mothers themselves. The research will be published in the early online edition of the Proceedings of the National Academy of Sciences on October 13, 2014.

Mitochondria are structures within cells that produce energy and that contain their own DNA. "Many mitochondrial diseases affect more than one system in the human body," said Kateryna Makova, professor of biology and one of the study's primary investigators. "They affect organs that require a lot of energy, including the heart, skeletal muscle, and brain. They are devastating diseases and there is no cure, so our findings about their transmission are very important."

The multidisciplinary research team set out to learn whether maternal age is important in the accumulation of mitochondrial DNA (mtDNA) mutations, both in the mother and in the child as a result of transmission. Collaborating with Ian Paul, a pediatrician at the Penn State Milton S. Hershey Medical Center, they took samples of blood and of cells inside the cheek from 39 healthy mother-child pairs. Because mtDNA is inherited only maternally, paternal mtDNA was not a factor in the study. Studying healthy individuals gave the researchers a baseline for future studies of disease-causing mutations.

Through DNA sequencing, they found more mutations in blood and cheek cells in the older mothers in the study. Maternal age of study participants ranged from 25 to 59. "This finding is not surprising," Makova said, "because as we age, cells keep dividing, and therefore we will have more mutant genes." But finding greater rates of mutations in children born to the older mothers did come as a surprise. The researchers believe a similar mutation process is occurring both in the cells of the mothers' bodies and in their germ lines.

The study led to another important discovery about egg-cell development. Although it was known that developing egg cells go through a "bottleneck" period that decreases the number of mtDNA molecules, scientists didn't know how small or large this bottleneck is. "If the bottleneck is large, the genetic makeup of the mother's mitochondria will be passed to her children," Makova explained. "However, if it is tiny -- if there is a severe decrease in mitochondrial molecules during the egg-cell development -- then the genetic makeup of the child might differ dramatically from that of the mother. What we discovered is that this bottleneck is indeed very small."

This finding is especially important for mothers who have a mitochondrial disease. For many mitochondrial diseases, 70 to 80 percent of molecules need to have the disease-causing variant for the disease to manifest itself. But for others, only 10 percent of the mtDNA molecules with the variant are needed to cause disease. "If the bottleneck is very small, as we've found in our study, these percentages can change dramatically," Makova said. "Knowing the size of the bottleneck allows us to predict, within a range, the percentage of disease-carrying molecules that will be passed on to the child."

Knowledge about both the maternal age effect and the bottleneck size is useful in family planning. "We have some predictive power now and can assist genetic counselors in advising couples about the chances of mitochondrial diseases being passed to the next generation," Makova said. "Everyone is concerned about Down syndrome because that is a common genetic problem. We have now added another set of genetic disorders that also might be affected by the age of the mother. It is good for couples to have this knowledge as they make family-planning decisions."


Story Source:

The above story is based on materials provided by Penn State. The original article was written by Krista Weidner. Note: Materials may be edited for content and length.


Journal Reference:

  1. Boris Rebolledo-Jaramillo, Marcia Shu-Wei Su, Nicholas Stoler, Jennifer A. Mcelhoe, Benjamin Dickins, Daniel Blankenberg, Thorfinn S. Korneliussen, Francesca Chiaromonte, Rasmus Nielsen, Mitchell M. Holland, Ian M. Paul, Anton Nekrutenko, and Kateryna D. Makova. Maternal age effect and severe germ-line bottleneck in the inheritance of human mitochondrial DNA. PNAS, October 2014 DOI: 10.1073/pnas.1409328111