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Tim Parker, Benzinga Staff Writer

Before scientists create something that has mainstream uses, it often starts as science fiction.

A new technology deep within IBM’s (NYSE: IBM [FREE Stock Trend Analysis]) Singapore research facility isn’t quite ready for the mainstream but when it is, the implications for those who suffer from fungal infections and later, other infections, could have a new ally in their fight but this ally is completely different than current treatments.

If you’re a fan of Star Trek, you’ve seen nanotechnology. These are microscopic machines that get inside machines or in this case, the body, to identify and fix problems.

Scientists have developed a nanomedicine 1,000 times small than a grain of sand that fights fungal infections. Here’s how it works: By creating an electrical charge on each of these tiny particles, they can be programmed to attack only fungal cells while leaving healthy cells alone.

The particles attach themselves to the fungi and rip their cellular membranes apart killing the cell.

This is different than conventional treatments in that it’s a physical attack where the cell is torn apart instead of a drug-like attack where the cell is put to sleep. By killing the cell, there is no opportunity for it to develop a resistance to the nanoparticle. This eliminates the growing problem plaguing doctors: Infections that are increasingly becoming resistant to current therapies.

“It rips the membrane out in a physical attack,” said IBM scientist, James Hedric. “It’s kind of like popping a balloon. We don’t put them to sleep like most drugs do. We kill them. That is why it is so effective. And they can’t adapt to a physical attack. They can adapt to drugs.”

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Bebionic3

Simple tasks, like plucking the stem off a cherry, are still monumental challenges for artificial hands. With a bill of materials perhaps a few hundred components long, it is not surprising that their functionality is low compared with one assembled from trillions of components. A new prosthetic bionic hand, designed and built by researchers at Case Western University is now capable of using measurements from 20 sensor points to control the grip force of its digits. Incredibly, the sensor data is linked directly to the sensory nerves in the patient’s forearm. The control for the grip closure is then extracted myoelectrically from the normal biological return loop to the muscles in the forearm.

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surgery

Hands-free devices like Google Glass can be really transformative when the hands they free are those of a surgeon. And leading hospitals, including Stanford and the University of California at San Francisco, are beginning to use Glass in the operating room.

In October, UCSF’s Pierre Theodore, a cardiothoracic surgeon, became the first doctor in the United States to obtain Institutional Review Board approval to use the device to assist him during surgery. Theodore pre-loads onto Glass the scans of images of the patient taken just before surgery and consults them during the operation.

“To be able to have those X-rays directly in your field without having to leave the operating room or to log on to another system elsewhere, or to turn yourself away from the patient in order to divert your attention, is very helpful in terms of maintaining your attention where it should be, which is on the patient 100 percent of the time,” said Theodore.

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Kelsey Campbell-Dollaghan on Gizmodo

How 3D Printers Are Cranking Out Eyes, Bones, and Blood Vessels

At the dawn of rapid prototyping, a common predication was that 3D printing would transform manufacturing, spurring a consumer revolution that would put a printer in every home. That hasn’t quite happened—-and like so many emerging technologies, rapid prototyping has found its foothold in a surprisingly different field: Medicine.

The following studies and projects represent some of the most fascinating examples of “bioprinting,” or using a computer-controlled machine to assemble biological matter using organic inks and super-tough thermoplastics. They range from reconstructing major sections of skull to printing scaffolding upon which stem cells can grow into new bones. More below—and look out for more 3D printing week content over the next few days.

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Tongue piercing

Body piercings have been used to control wheelchairs and computers in a move scientists believe could transform the way people interact with the world after paralysis.

The movement of a tiny magnet in a tongue piercing is detected by sensors and converted into commands, which can control a range of devices.

The US team said it was harnessing the tongue’s “amazing” deftness.

The development is reported in the journal Science Translational Medicine.

The team at the Georgia Institute of Technology made the unlikely leap from body art to wheelchairs because the tongue is so spectacularly supple.

A large section of the brain is dedicated to controlling the tongue because of its role in speech. It is also unaffected by spinal cord injuries that can render the rest of the body paralysed, tetraplegic, as it has its own hotline to the brain.

“We are tapping in to the inherent capabilities of the tongue, it is such an amazing part of the body,” Dr Maysam Ghovanloo told the BBC.

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November 11, 2013

Anyone who has left youth behind them knows that bumps and scrapes don’t heal as fast as they used to. But that could change with researchers at the Stem Cell Program at Boston Children’s Hospital finding a way to regrow hair, cartilage, bone, skin and other soft tissues in a mouse by reactivating a dormant gene called Lin28a. The discovery could lead to new treatments that provide adults with the regenerative powers they possessed when very young.

Lin28 is a gene that is abundant in embryonic stem cells and which functions in all organisms. It is thought to regulate the self-renewal of stem cells with the researchers finding that by promoting the production of certain enzymes in mitochondria, it enhances the metabolism of these cellular power plants that found in most of the cells of living organisms. In this way, Lin28 helps generate the energy needed to stimulate the growth of new tissues.

“We already know that accumulated defects in mitochondrial metabolism can lead to aging in many cells and tissues,” says Shyh-Chang Ng. “We are showing the converse – that enhancement of mitochondrial metabolism can boost tissue repair and regeneration, recapturing the remarkable repair capacity of juvenile animals.”

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A University of Alabama at Birmingham (UAB) surgical team has performed one of the first surgeries using a telepresence augmented reality technology from VIPAAR in conjunction with Google Glass.

The combination of the two technologies could be an important step toward the development of useful, practical telemedicine.

VIPAAR (Virtual Interactive Presence in Augmented Reality) is commercializing a UAB-developed technology that provides real-time, two-way, interactive video conferencing.

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In is now quite clear that aging is not a simple phenomenon and it will not be overcome by using simple approaches. We need to increase the complexity and sophistication of our efforts in order to be in a better position to develop strategies against it. For this reason, I set up the ELPIS Foundation for Indefinite Lifespans (www.elpisfil.org) which is a scientific research organisation aiming to study aging from a complex evolutionary perspective.

The foundation’s research methodology is based mainly upon the ELPIS hypothesis (www.elpistheory.info). The initials stand for ‘Extreme Lifespans through Perpetual –equalising Interventions’. I developed this hypothesis in 2010 whilst trying to examine the reason behind the presence of aging. It was clear that aging is not an essential component of our evolutionary development, and if we find ways to study why nature has developed it, we may then be able to eradicate it. Currently, the chances of us dying from aging are heavily against us. By developing suitable interventions, we may be able to equalise the odds against us dying (i.e. remove aging as a cause of death).

Our method is different from most existing approaches aiming to eliminate aging. We are mainly interested in the ‘connection-approach’ and not so much in the ‘component-approach’. We believe that it is important to study how the different components of the organism are interconnected and regulated, rather than just repair the individual components. It is the ‘why aging happens’ rather than the ‘how it happens’ that interests us most. In order to make this clear let me mention an analogy with poliomyelitis.

Polio
*How it happens? There is inflammation and necrosis leading to damage of motor neurons and, ultimately, muscle weakness and paralysis
* Why it happens? Because the poliovirus causes it

Aging
* How it happens? There is cellular and molecular damage through oxidation and glycation, as well as damage to mitochondria, DNA etc.
* Why it happens? Because evolution has selected reproduction (and thus aging) as a mechanism for maximising the use of thermodynamical resources, and so ensure the survival of the species.

In this analogy, the obvious cure for polio is to somehow eradicate the poliovirus itself, and not just keep repairing the already damaged motor neurons. And in the case of aging, the best tactic is to somehow change the reason why aging happens, instead of just keep repairing already existing damage.

Attempts such as SENS and similar, aim to repairing existing damage, were as we aim primarily to eliminate the evolutionary reasons behind aging in the first place. This is not to say that we are not at all interested in damage repair. In fact, one of our main projects deals with the repair problem. But, overall we want to explore the evolution of aging and not its secondary effects.

We see aging as a specific and well-defined process. Our aim is unambiguous: we seek to eliminate this particular process. By eliminating aging we will have a life without age-related disease and degeneration, and a lifespan without a predetermined end. We do not seek immortality. In order to be immortal, one has to totally and permanently eliminate all causes of death (not just reduce their incidence). We seek to eliminate aging as one of the causes of death. People will still die from any other cause. In this case, our lifespan would be ‘indefinite’ because the current absolute limit of around 110–120 years will be lifted. There would not be a pre-defined limit; therefore the lifespan would be indefinite. It will not be infinite. This distinction is crucial because it clarifies any ambiguity and vagueness in the terminology. We do not seek eternal youth. We merely concentrate on the process of aging as one of the many other causes of death, the same as other researchers concentrate on the cure for cancer or the cure for HIV infection.

Within ELPIs Foundation we have scientific advisors from a wide range of disciplines, including biomedicine, transhumanism, social sciences, neurosciences, complex systems, and systems biology. Our affiliate researchers are scientists who conduct research in their own facilities and share information and ideas with each other. We are always looking for visionary, ‘out-of the box’ scientific thinkers, those who ‘zoom out’ of reductionist views, and see aging in a wider perspective without being uncritically blinkered by existing dogma.

We ask questions such as: If aging happens because nature withholds resources from the soma and diverts these to the germ-line, how can we reverse this process and divert resources back to the soma in order to maximise biological repair? What is the role of digital hyperconnectivity of billions of humans (the Global Brain) in facilitating such a transition? Where does aging and the elimination of aging fit within an ever-evolving technological tendency of nature? Some ideas we currently explore are:
* Induced Whole-Body Somatic Cell Turnover, for regenerative repair
* Aging and evolutionary changes as applied to human sexual patterns, reproduction, ecosystems, society and the planet
* The role of energy, entropy and thermodynamics in metasystem transitions with regards to human longevity
*Theoretical aspects of Germ-line penetration

May symposium

In May 2014 we will be organising the second symposium on ‘Pathways to Indefinite Lifespans’ in Larnaca, Cyprus. This is a small, very select, highly focused meeting exploring the most cutting-edge research and ideas with regards to the total abolition of aging. We aim to discuss new insights and hypotheses in the fields of biomedical technology, evolutionary anthropology, complex systems, a hyperconnected society, and digital communications technology. The meeting will be accessible live online and will include both local and remote presentations. Those interested in coming need to contact me at: [email protected]. We are also exploring the possibility of offering PhD positions to exceptional candidates, in order to facilitate research in this area.

This article was originally published here: http://hplusmagazine.com/2013/11/05/defying-aging-the-elpis-…lifespans/

By Avi Roy, University of Buckingham and Anders Sandberg, University of Oxford

Men who are unemployed for more than two years show signs of faster ageing in their DNA, according to a study published today in the journal PLOS ONE.

Researchers at the University of Oulu, Finland and Imperial College, London arrived at this conclusion by studying blood samples collected from 5,620 men and women born in Northern Finland in 1966. The researchers measured the lengths of telomeres in their white blood cells, and compared them with the participants’ employment history for the prior three years, and found that extended unemployment (more than 500 days in three years) was associated with shorter telomere length.

Telomeres are repetitive DNA sequences at the ends of chromosomes, which protect the chromosomes from degrading. With every cell division, it appears that these telomeres get shorter. And the result of each shortening is that these cells degrade and age.

When cells are grown in a lab, their telomeres do indeed shorten each time the cells divide. This process can be used to find a cell’s “expiry date”, a prediction of when that cell will run out of telomeres and stop dividing. However, this does not seem to relate to the actual health of the cells.

In the new study, the researchers found that that on average, men who had been unemployed for more than two of the preceding three years were more than twice as likely to have short telomeres compared to men who were continuously employed. In women, there was no association between unemployment status and telomere length.

The researchers accounted for telomere length differences resulting from medical conditions, obesity, socio-economic status and early childhood environment.

Previous studies, noted by the study authors, have found a correlation between shorter telomeres and higher rates of age-related diseases like Type 2 diabetes and heart disease. The authors conclude that the reduction in these men’s telomeres may have been the result from the stress of long-term unemployment, adding to evidence of a direct connection between prolonged unemployment and poor health.

An abstract concept

Employment is something very abstract; an employed and unemployed body are apparently more or less the same. So it might seem surprising that such an abstract thing as employment can affect a body on the cellular level. But the same is true for how stimuli affect our brains: remote objects trigger electrochemical cascades in our visual system – and when we learn new things, gene expression in the brain changes. We are interactive creatures, with innumerable stimuli that are constantly shaping multiple processes in our bodies. In this sense, the hypothesis that employment experience has cellular effects is not surprising.

This was an association study, which means than under certain set of circumstances two variables are statistically linked. This study is therefore incapable of genuinely predicting whether unemployment is the cause, and short telomeres the effect. Perhaps the opposite is true: maybe people whose cells lose their telomeres also lose their jobs. More likely, an outside factor that shortens telomeres could have a limiting effect on success in the labour market. For example, such a factor might somehow contribute towards illness or pessimism.

Additionally, because the study was conducted in an isolated and genetically quite homogeneous population, the results of the study may be due to their genetic make-up as well as (or instead of) environmental effects.

In the end, we do not need a genetic study to know long-term unemployment is bad for people socially, medically and psychologically; there is plenty of evidence for that. Additionally, the bio-gerontology community (those who study the biological processes of ageing) recognises telomere attrition as one of the nine causes of the disease of ageing, including Type 2 diabetes and cardiovascular diseases.

Where this study does make a significant contribution is in recognising long-term, low-level stress as a major problem. In momentarily stressful situations, the instant fight-or-flight response stimulates us; but being under pressure for a long time with no relief wears us down. Prolonged stress is bad for memory and health, and could quite conceivably shorten telomeres – making an unemployed person significantly more unhealthy, with the effects persisting even after they get a job.

In the long run, what we really need to learn to slow or stop the ageing process is how to reduce or repair the damage done by stress.

The authors do not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article. They also have no relevant affiliations.

This article was originally published at The Conversation.
Read the original article.

Grindhouse Wetware is a collective of makers and engineers founded on a basic principle – human augmentation should be accessible and open. All of our devices are built off of open source platforms. This allows our users to peer into the hardware and code of their implanted device and truly control their augmented experience. Grindhouse Wetware’s devices are tailored to Makers and DIY Transhumanists that want to build a specific, unique augmentation. What do you want to be?

After three years of development, our flagship project – Circadia, is in its final stages. Grindhouse Wetware is seeking financial support from individuals or organizations to facilitate the production of this device.

The Circadia implant records bio-medical data and transmits it to the user’s phone via bluetooth. Instead of a snapshot of the user’s state of health, the Circadia records the up-to-date status of the their well being. Grindhouse Wetware firmly believes that once an implant has been installed in an individual, it becomes a part of their person. As such, the data generated by the Circadia belongs to the user.

If you are interested in supporting Grindhouse Wetware and the Circadia implant, please contact me at [email protected] or 631−715−9209

Below are pictures of our prototypes.

HELEDD Printed 2 DSCF1998 DSCF1996