After showcasing its bendible technology for the last few years, Samsung’s first foldable smartphone could finally launch in January 2016.
Facebook FB is working on a stand-alone app that would support 360-degree—or “spherical”—video, allowing users to alter their viewing perspective with the mere tilt of their phones.
The app is still in early development, and would be available for both Apple AAPL and Android operating systems if it proves to be a go, sources close to the project told The Wall Street Journal.
Typically compiled from multiple cameras, the video format allows users to change their viewing perspective by tilting their phones, the Journal reported.
If there’s one thing R2-D2 knows, it’s flying. The astromech droid has provided air support for both Anakin and Luke Skywalker who know a few things about piloting.
However, the blue and white robot’s next flight will be on Earth thanks to the newly themed Boeing 787 Dreamliner made to look like the lovable Star Wars staple. Here’s hoping that the flights are more comfortable than some of R2’s space dog fights or dodgy landings on Dagobah.
Starting on October 18, Japanese carrier ANA will fly the newly minted plane between Tokyo and Vancouver before extending the service to include Munich, Paris, Seattle, Sydney and beyond. The 215-seater plane isn’t just Star Wars-y on the outside, though. In addition to featuring all six Star Wars films on the seat back screens, the cups, headsets, and napkins will also carry the theme on inside.
The Campaign Against Sex Robots
Companies should be stopped from developing sex robots with artificial intelligence for fear of harming humanity, according to campaigners.
Many engineers are looking to add artificial intelligence to sex toys and dolls in an attempt to make them more like humans, and therefore more attractive to customers. But such moves are unethical and will harm humanity, according to a new campaign.
The Campaign Against Sex Robots, launched this week, says that the “increasing effort” that has gone into producing sex robots — “machines in the form of women or children for use as sex objects, substitutes for human partners or prostitutes” — is harmful and makes society more unequal.
Our gut and the microbiome play a crucial role in our health, but could better understanding of that role help us avoid disease and live longer?
The microbiome weighs 2–3 pounds and contains 10 times more cells than our own, but we’ve neglected our microbial tenants for a long time. These little denizens help us break down food, provide key nutrients and even play a role in inflammation and the integrity of our intestinal tract. It’s no surprise then that fermented foods and probiotics are gaining popularity as we become more aware of how important our gut is. Recent evidence even links poor digestive health to chronic inflammation and Parkinson’s disease.
New research suggests that both gut integrity, and the amount and type of bacteria that reside within it, can actually predict an individual’s health. They may even quicken or slow the pace of aging.
This short post is not about Bitcoin. It’s about a new method of organizing and arbitrating communications that is at the heart of Bitcoin
We hear a lot about the blockchain. We also hear a lot of misconceptions about its purpose and benefits. Some have said that it represents a threat to banks or to governments. Nonsense! It is time to form a simple, non-political, and non-economic explanation…
What is a Blockchain?
The blockchain is a distributed approach to bookkeeping. It offers an empowering, efficient and trusted way for disparate parties to reach consensus. It is “empowering”, because conclusions built on a blockchain can be constructed in a way that is inherently fair, transparent, and resistant to manipulation.
This is why blockchain-backed systems are generating excitement. Implemented as distributed and permissionless, they take uncertainty out of accounting, voting, legislation or research, and replace it with trust and security. Benefits are bestowed without the need for central authority or arbitration. The blockchain not only solves a fundamental transaction challenge, it addresses communication and arbitration problems that have bedeviled thinkers since the ancient Egyptians.
Related:
- Can a blockchain accomplish things that were previously impossible?
- Why do we not see many blockchain services entering the market?
—Philip Raymond, CRYPSA Co-chair
Cryptocurrency Standards Association
Progress always seems to ride a slippery slope. Innovations generally bring a plethora of potential benefits and just as many dangers, the obvious and the hidden. Technologies that tamper with our biological constructs is well underway in the neuro- and biotech industries. Historically, innovations in medicine have usually been beneficial on the aggregate.
But these new breakthroughs go beyond preventing and healing pre-existing causes. Transhuman technologies hold the promise of enhancing who we are as individuals and potentially as an entire species, and the decisions surrounding these technologies are far from simple. Dr. Nayef Al-Rodhan, a philosopher, neuroscientist, and director of the Geneva Center for Security Policy, believes we should be acting now to prepare for the inevitable and the unpredictable ramifications.
Framing Human Motivation
Considering our mixed track record as a species in rolling out groundbreaking innovations, discussing and finding potential solutions to many of the hidden dangers, and obvious ones, seems more than reasonable. One of the more puzzling questions is, where do we begin to have a pragmatic conversation on the ethics of these technologies?
There are plenty of theories about what drive human decisions, not least because human morality is infinitely complex and our minds crave frames through which to make sense of chaos. Dr. Al-Rodhan has his own conception of what drives human motivations. He makes meaning using the lens of “5 P’s” – Power, Pride, Profit, Pleasure, and Permanence – which he posits drive human motivations. “This is my view, the foundation of my outlook…this perceived emotion of self interest drives our moral compass.”
Al-Rodhan’s view of human nature seems to make a lot of sense, bridging the rational with the emotional. Such a frame is particularly helpful when considering technology that undoubtedly taps into our deepest fears and hopes, and invokes rational (and irrational) debate. During a recent TechEmergence interview with Nayef, I asked for his thoughts on the concerns and considerations of this brand of technology in the coming decade.
The Near Business of Enhancement
Al-Rodhan believes that we will see cognitive enhancement primarily through neuropharmacology, or neuro- and psychostimulants. This concept of this technology is nothing new — the military and many other organization have used their stimulants of choice in the past, one of the most pervasive being alcohol. But this new wave of neuro- and psychostimulants will methodically target specific areas in the brain, giving way to the possibility for innovations like increased mood modulation and more cognitive ability within the confines of the brain’s neuronal population.
Neuromodulation has been used in the military, with some efforts to make soldiers less emotional and to require less sleep. The difficulties with side effects are often more pronounced when soldiers return from combat. “They are all messed up due to severe brutality, fear, and some of these agents they are given make them addicts to certain things,” says Nayef, acknowledging that this happens in most all militaries. “The point is that psychostimulants and neuromodulators will make us feel very good, but they are very dangerous because they require addictive behavior…and we need strict oversight mechanisms.”
Nayef says that technologies such as brain machine interface (BMI) are likely beyond the span of a decade, but that implantable microchips (whether bio or biotechnological) are as much of an immediate concern as the introduction of neurostimulants. “The FDA in the United States is entrusted with keeping us on the right path,” says Al-Rodhan.
Finding Common Regulatory Ground
Is it possible to put in place national or international structures for managing these new and emerging technologies? Al-Rodhan believes it is more than possible; however, the primary issue is that our regulation is way behind innovation. Regulatory frameworks are lacking for a number of reasons. The unpopularity in politics is a major obstacle to overcome. In elections, these types of contradictory frameworks are not politically on the front burner for most candidates, and the long-term outlook is limited.
Another area for concern is corporate pharmaceutical entities, which Nayef says are not as well regulated as some might think. Businesses are concerned about the bottom line above all else, which at times yields unfortunate outcomes for the whole of society. “This is part of their role as executive, they’re not too concerned about moral regulation,” says Nayef. As unappealing as it might sound to free market capitalists, the institution that traditionally steps into these frontiers to regulate is government.
A relevant and current example is the science and business of moderating genomes in China, which is already investing a lot of money in this industry. Some effects of this technology may not be so obvious at first, and it is possible that negative ramifications could occur without the correct bioethical oversight. Al-Rodhan asks “what happens if you get a piece of DNA that preludes the biosphere? Who knows what kind of mutation that may produce spontaneously or by merging with other DNA in an organism.” These are the types of questions that governments, academic institutions, corporations, and individual citizens need to be asking, considering the multiple perspectives that emerge from a framework like Al-Rodhan’s that applies across cultural boundaries.
Al-Rodhan describes the process of implementing such regulatory frameworks as a transnational effort, but says that such efforts start with countries like the U.S., Japan, and Europe, where accountable mechanisms already exist. Taking the lead doesn’t guarantee the same priorities will be given elsewhere, but it can provide an example — and ideally a positive one. “We have about a decade to get our act together,” says Al-Rodhan.
Dr Michael Fossel is a PhD and MD heading up telomerase research and therapy and has kindly written a blog article for Bioviva detailing the work both they and his company Telocyte are doing to fight back against Alzheimer’s.
How Alzheimer’s Can Be Prevented and Cured…
Michael Fossel, MD, PhD
As I said in my medical textbook on aging, “If age is a thief, then the greatest treasure we lose is ourselves.” We fear Alzheimer’s not simply because it takes away our health, but because it steals our souls.
Once, we thought it was simply “old age” that gradually killed the cells that carry information and memory. These are brain cells that make us who we are and define our consciousness.
Only in the past two decades, have we gradually come to realize that it’s not the neurons, which are merely the innocent bystanders in the tragedy,
but the microglial cells that cause the disease. It’s our microglia, not our neurons that steal our very souls.
Alzheimer’s disease begins in our glial cells. These cells together form.
90% of our brains, while neurons are only a small minority in the nervous system.
One set of these glial cells, the microglia, have the critical job of protecting the neurons and supporting them metabolically. These are the cells that, among dozens of other functions, are responsible for clearing metabolic waste products and recycling the extracellular proteins that surround the neurons.
Unfortunately, as we age, the microglial cells not only fail to divide, but gradually lose telomere length. By itself, telomere loss is unimportant,
but this loss begins a cascade of crucial changes in our cells.
As these telomeres shorten, they trigger a gradual shift in gene expression throughout the entire microglial cell. While the genes remain unchanged,
the “tune they play” i.e. the epigenetic pattern of gene expression becomes a sinister song. Proteins that are critical to DNA repair, to making our mitochondria work, to holding free radical damage to a minimum, begin to become scant. Where once, a young microglial cell would recycle proteins quickly and efficiently– including beta amyloid proteins — as the cell ages, the rate of turnover slows to a crawl.
The problem is much like many other things in life. If cell phones were replaced not every two years, but every twenty years, few of them would work. If a garden is weeded not every week, but once every two years, it would be engulfed in weeds. If we showered not once a day, but once every year, few of us would have friends.
Cells are no different: if we recycle proteins quickly, there is little damage, but if we recycle proteins slowly, then the damage begins to become obvious. Our cells don’t age because they are damaged; rather our cells permit damage to accumulate because they age. Shorter telomeres cause changes in gene expression, slower cell recycling, with the end results being old, damaged cells.
In Alzheimer’s disease, the microglia is the earliest change, the key change that begins the entire cascade of pathology to dementia. As our microglial cells slow down, they no longer keep up with the damage around them and the result is a gradual accumulation of damaged and denatured proteins.
The disaster begins.
At first, only trivial amounts of beta amyloid begin to accumulate in small aggregates, but then they grow larger, gathering into huge amyloid plaques.
Where once they could barely be seen, they now become visible under a microscope. But the problem is not simply these plaques themselves, but their effect on the neurons. Beta amyloid protein is critical to cell function, but only in small amounts, not in the vast plaques that now surround the besieged neuron. These growing plaques are toxic to neurons,
making it harder and harder for these cells to survive, let alone function normally.
Tau proteins likewise begin to form tangles and the neurons can no longer maintain themselves. At first, they begin to lose the ability to transmit nerve impulses, then they become more and more damaged internally, until the neurons die, first only a few, then in larger populations, leaving only scars, inflammation, and empty space. One-by-one our neurons are snuffed out, submerged under the rising effects of beta amyloid and tau proteins,
and all of this, the plaques, the tangles, and the dying neurons characteristic of Alzheimer’s can be traced back to the failing microglial cells.
As I write this, there have been more than 1,300 clinical Alzheimer’s trials looking at potential interventions. Many deal only with nursing care, but of those that try to intervene in the actual pathology, most have amyloid as their target, and a few target tau proteins. Small wonder then,
that none of these trials has ever been able to slow, let alone stop, or even reverse the disease. Every one of them is aimed at the wrong target.
Instead of trying to reverse the primary problem — the changes within the aging microglial cell — they aim at what are merely symptoms and results rather than causes. Imagine what would happen if we tried to cure bacterial infections by aiming merely at fevers, rather than aiming at the bacterial themselves. Current clinical trials are much the same: instead of aiming at the cause, they aim at the result.
Can we do better?
Almost certainly, we can. We know that the changes in gene expression that define aging in our cells are controlled by the changing telomere lengths as these cells divide.
We also know that if we reset the telomere to the original length, we not only reset gene expression, but end up with a cell that looks and acts like a young cell.
We have even done this not only in human tissues, in the lab, but in animals such as mice and rats. When we reset telomere lengths in the aging rodent brain, the animals begin to act normally again and we see the brains returning toward normal volume and function.
Can we do the same for human patients? Can we cure Alzheimer’s disease? We almost certainly can. We now not only understand how the disease works, and we not only have been able to show we can manage to intervene in animals,
but we already have the tools we need to cure Alzheimer’s disease in those we love.
Telomeres can be reset using telomerase, and enzymes comprising hTERT and hTERC. hTERT stands for human telomerase reverse transcriptase. hTERC
stands for human telomerase RNA component. Both of these telomere length extending enzymes can be delivered into the human brain, using either liposomes or viral vectors, much as has already been done in animal trials.
Once we can reverse the disease, once we can cure Alzheimer’s, it will change from the most frightening of illnesses to one we can deal with:
easily prevented, easily cured, and (much as it once erased our personal memories) a forgotten thing of the past.
There are at least two biotech projects currently aimed at human trials,
one via standard FDA-sponsored research (Telocyte), the other using a faster and less formal, “offshore” approach (BioViva). We support both approaches, wanting an effective therapy for Alzheimer’s that is both safe and rapidly available to all.
BioViva is seeking funding to initiate the use of these kinds of microglial telomere lengthening therapies in human test subjects immediately. If successful, we might not just eradicate Alzheimer’s disease, but also the cognitive impairment that strikes all people as they age past 30.
Maximum Life Foundation is raising $250,000 to give a grant to BioViva to test these therapies on human volunteers. 100% of donations earmarked for this study will be sent to BioViva with nothing subtracted for overhead.
The grant would cover this initial phase of the study and more.
To make your tax-deductible donation to this special fund aimed at quickly testing these telomere lengthening approaches in aging humans, go to www. MaxLife.org, or send your check to:
Maximum Life Foundation (BioViva)
2324 Colony Plaza Newport Beach,
CA 92660
Tele: (800) 881‑5346.