Friday, March 16, 2012

March Contest: Abundance Giveaway Redux!

Because I believe this book is so powerful in its message I am going to give away 3 copies of Abundance: The Future Is Better Than You Think. The rules are much simpler this time (mainly given that I did not receive a single entry into last months contest). To get 1 of 3 copies of Abundance all that is required is that you like the fan page on face book for this blog. I will select three people at random from the fan page and they will win.
Its that simple. The message of this book is one that should be spread to as many people as possible.

Rules Recap:
1.Like Event Horizon - Approaching Singularity on Facebook via the fan page box to the left.
2.Three winners will be selected on March 30th, those winners will receive a copy of Abundance!

Wednesday, March 14, 2012

The Age Of Abundance Is Coming.

Today I am posting a video and a response. The topic is the coming age of abundance and the impact that it may have.

The rate at which technology increases is exponential. Emerging technologies are not only going to make many of the worlds problems vanish but enhance our lives on a socioeconomic level that is unheard of. Advances in nanotechnology will solve shortages for water, food, and energy. Nano fabrication eventually is going to be able to produce almost anything. Nano assemblers will be able to fabricate material by constructing things atom by atom. This would include food products. The major shortages in the world are food and water, and with in decades these will be cured. The news is filled with doom and gloom about the condition of the planet. However, the rise in technology is going to find a way to solve these problems.

A question to ask is when we reach the end of a scarcity based economy will there be need for socioeconomic classes? When everyone has access to everything they need then money will become obsolete. The end of money and shortage of resources will elevate humanity like never before.
I highly recommend that you read Abundance: The Future Is Better Than You Think. I am still in the process of reading this book but I have already learned so much as far as the state of the world that we are approaching. Plentiful food, clean water, and limitless energy are on the horizon. Abundance is our future. Imagine what we could do as a species if we no longer needed to fight over resources. I know this view is very Utopian but there is nothing wrong in wanting the best for everyone. That is why I am going to school for Bio-engineering and Anthropology. I want to be on the front of developing technologies to aide and elevate.

Tuesday, March 13, 2012

The Pursuit Of Immortality: Gilgamesh

Immortality has been a goal that has been sought since the beginning of time. From the Epic of Gilgamesh to the search for the fountain of youth, ever generation of man has had those that seek to beat the reaper. Today I want to share an interesting essay that I found. It is a summery about Gilgamesh and his search for immortality.


The Epic of Gilgamesh: A Summary

The Epic of Gilgamesh is a moving tale of the friendship between Gilgamesh, the demigod king of Uruk, and the wild man Enkidu. Accepting ones own mortality is the overarching theme of the epic as Gilgamesh and Enkidu find their highest purpose in the pursuit of eternal life.

The epic begins with Gilgamesh terrorizing the people of Uruk. They call out to the sky god Anu for help. In response Anu tells the goddess of creation, Aruru, to make an equal for Gilgamesh. Thus Aruru created Enkidu, a brute with the strength of dozens of wild animals. After being seduced by a harlot from the temple of love in Uruk, Enkidu loses his strength and wildness yet gains wisdom and understanding. The harlot offers to take him into Uruk where Gilgamesh lives, the only man worthy of Enkidu's friendship. After a brief brawl the two become devoted friends.

The newfound friends gradually weaken and grow lazy living in the city, so Gilgamesh proposes a great adventure that entails cutting down a great cedar forest to build a great monument to the gods. However to accomplish this they must kill the Guardian of the Cedar Forest, the great demon, Humbaba the Terrible. Enkidu, along with theelders of the city, have serious reservations about such an undertaking but in the end Gilgamesh and Enkidu kill the terrible demon.

As Gilgamesh cleans himself and his blood stained weapons, Ishtar, the goddess of love and beauty, takes notice of his beauty and offers to become his wife. Gilgamesh refuses with insults, listing all her mortal lovers and recounting the dire fates they all met with at her hands. Ishtar is enraged at the rebuff. She returns to heaven and begs her father, Anu, to let her have the Bull of Heaven to wreak vengeance on Gilgamesh and his city. Anu reluctantly gives in, and the Bull of Heaven is sent down to terrorize the people of Uruk. Gilgamesh and Enkidu, work together to slay the mighty bull. That following night Enkidu dreams that the chief gods met in a council and had decided that someone should be punished for the killing of Humbaba and the Bull of the Heavens. That someone is he. Enkidu commends himself to Gilgamesh, and after suffering terribly for twelve days, he finally dies.

After Enkidu's death, Gilgamesh comes to the realization that one day he too will succumb to the same fate as his friend. He sets out to find Utnapishtim the only mortal that the gods have granted eternal life in attempt to find the secret of immortality. After a long perilous journey through the land of darkness, through the garden of the gods, and across the waters of death, Gilgamesh arrives a shore where Utnapishtim lives. Gilgamesh recounts the story of Enkidu's death to Utnapishtim and how he came to his shore. He asks Utnapishtim to tell him the secret of eternal life. Utnapishtim advises Gilgamesh that death is a necessary fact because it is the will of the gods. Gilgamesh pursues the issue further until Utnapishtim recounts how he received immortality and reveals the greatest secret hidden from humans. At the end of his story, which is famously similar to Noah's flood in the book of Genesis, Utnapishtim offers Gilgamesh a chance at immortality. If Gilgamesh can stay awake for six days and seven nights, he, too, will become immortal. Gilgamesh accepts these conditions and sits down on the shore; the instant he sits down he falls asleep. When Gilgamesh awakes, he deigns that he had fallen asleep. Utnapishtim points to the loaves of bread that his wife laid at his side to count the number of days he slept. Utnapishtim's wife convinces the old man to have mercy on him; he offers Gilgamesh in place of immortality a secret plant that will make Gilgamesh young again. The plant is at the bottom of the ocean surrounding the shore. Gilgamesh ties stones to his feet, sinks to the bottom, and plucks the magic plant. But he doesn't use it because he does not trust it. He decides to take it back to Uruk and test it out on an old man first to make sure it work. On his way back, Gilgamesh stops at a well of cool water to drink. There hiding deep in the pool was a snake. When the snake sensed the sweetness of the flower, it rose up out of the water and snatched the plant away causing the snake to slough its skin.

There are a lot of similar themes to this epic as to some of the other mythological stories I have read in the past. I found this particular observation oddly strange because this tale was written thousands of years before many other similar tales. I think this is why this story of Gilgamesh has endured for so long. All in all it was a good read. However, it can be a little confusing at times. I especially like the part where Gilgamesh refuses Istar's advances. The imagery was quite amusing! 

How to Cite this Page

MLA Citation:
"A Summary of the Epic of Gilgamesh." 13 Mar 2012

Despite how powerful of a godking Gilgamesh became, he eventually dies. Gilgamesh becomes content with his life and accepts death. What about those of us that do not wish to accept death. Are we modern day Gilgameshes? However, this generation I am confident will succeed. Immortality is inevitable for humanity. However, the question becomes. Do we want it? If we are to live forever are we capable of doing so? The technology may exist but the human spirit may not endure to enjoy it. Will life loose its meaning if we no longer need to die?

Personally I believe that Humanity will change as the technology changes. Recently I transported a patient at work. This patient was born in the year 1910, they were over 100 years old. Think about the type of technology that was around when this patient was born. Here is a link that shows some information about what life was like during the 1910's: .
In 100 years our technological advances have increased astronomically. We are on the cusp of grasping something that Gilgamesh could not. Immortality. Imagine what the world will be like in another 100 years or even just 50 years. It is a good chance that most of us will be alive and well to see and in young bodies to enjoy it.

Sunday, March 11, 2012

Genetic Manipulation Boosts Growth of Brain Cells Linked to Learning, Enhances Effects of Antidepressants

Life has been hectic. School, work picking up, and the release of Mass Effect 3 have kept me from making any new posts. Today I want to get back into the process of my daily posts. Today I am featuring an article from science daily. Scientists are experimenting with genetic manipulation as a means to boost the brain. It is interesting to think about how giving the brain an “upgrade” will impact society. What will life be like if people can be made to think faster and solve problems quicker. All that would be missing would be matrix style learning. Downloading skills directly into the brain may also be closer then we think. With the rate at which technology doubles, about every 18 months, we can expect to see more amazing advancements in the coming years. 

Story Source:
Web address:

Genetic Manipulation Boosts Growth of Brain Cells Linked to Learning, Enhances Effects of Antidepressants

UT Southwestern Medical Center investigators have identified a genetic manipulation that increases the development of neurons in the brain during aging and enhances the effect of antidepressant drugs. (Credit: © rolffimages / Fotolia)
ScienceDaily (Mar. 8, 2012) — UT Southwestern Medical Center investigators have identified a genetic manipulation that increases the development of neurons in the brain during aging and enhances the effect of antidepressant drugs.

The research finds that deleting the Nf1 gene in mice results in long-lasting improvements in neurogenesis, which in turn makes those in the test group more sensitive to the effects of antidepressants.
"The significant implication of this work is that enhancing neurogenesis sensitizes mice to antidepressants -- meaning they needed lower doses of the drugs to affect 'mood' -- and also appears to have anti-depressive and anti-anxiety effects of its own that continue over time," said Dr. Luis Parada, director of the Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration and senior author of the study published in The Journal of Neuroscience.
Just as in people, mice produce new neurons throughout adulthood, although the rate declines with age and stress, said Dr. Parada, chairman of developmental biology at UT Southwestern. Studies have shown that learning, exercise, electroconvulsive therapy and some antidepressants can increase neurogenesis. The steps in the process are well known but the cellular mechanisms behind those steps are not.
"In neurogenesis, stem cells in the brain's hippocampus give rise to neuronal precursor cells that eventually become young neurons, which continue on to become full-fledged neurons that integrate into the brain's synapses," said Dr. Parada, an elected member of the National Academy of Sciences, its Institute of Medicine, and the American Academy of Arts and Sciences.
The researchers used a sophisticated process to delete the gene that codes for the Nf1 protein only in the brains of mice, while production in other tissues continued normally. After showing that mice lacking Nf1 protein in the brain had greater neurogenesis than controls, the researchers administered behavioral tests designed to mimic situations that would spark a subdued mood or anxiety, such as observing grooming behavior in response to a small splash of sugar water.
The researchers found that the test group mice formed more neurons over time compared to controls, and that young mice lacking the Nf1 protein required much lower amounts of anti-depressants to counteract the effects of stress. Behavioral differences between the groups persisted at three months, six months and nine months. "Older mice lacking the protein responded as if they had been taking antidepressants all their lives," said Dr. Parada.
"In summary, this work suggests that activating neural precursor cells could directly improve depression- and anxiety-like behaviors, and it provides a proof-of-principle regarding the feasibility of regulating behavior via direct manipulation of adult neurogenesis," Dr. Parada said.
Dr. Parada's laboratory has published a series of studies that link the Nf1 gene -- best known for mutations that cause tumors to grow around nerves -- to wide-ranging effects in several major tissues. For instance, in one study researchers identified ways that the body's immune system promotes the growth of tumors, and in another study, they described how loss of the Nf1 protein in the circulatory system leads to hypertension and congenital heart disease.
The current study's lead author is former graduate student Dr. Yun Li, now a postdoctoral researcher at the Massachusetts Institute of Technology. Other co-authors include Yanjiao Li, a research associate of developmental biology, Dr. Renée McKay, assistant professor of developmental biology, both of UT Southwestern, and Dr. Dieter Riethmacher of the University of Southampton in the United Kingdom.
The study was supported by the National Institutes of Health's National Institute of Neurological Disorders and Stroke, and National Institute of Mental Health. Dr. Parada is an American Cancer Society Research Professor.

Journal Reference:
Y. Li, Y. Li, R. M. McKay, D. Riethmacher, L. F. Parada. Neurofibromin Modulates Adult Hippocampal Neurogenesis and Behavioral Effects of AntidepressantsJournal of Neuroscience, 2012; 32 (10): 3529 DOI:10.1523/JNEUROSCI.3469-11.2012

Monday, February 20, 2012

Physicists Create a Working Transistor From a Single Atom | Nanorobotic Technology Is On The Horizon.

It has been a few days since my last post. This has been due to a busy weekend and a busy EMS shift. Today I am posting about an article where physicists have successfully constructed a working transistor from a single atom. This is perhaps some of the biggest news I have read about to date. A working transistor means that soon atomic sized integrated circuitry will be able to be built. With atomic integrated circuitry comes molecular sized robots. True nanomachines. As computers become smaller and smaller soon nanobots will be programmable.
Nanotechnology represents the keystone in helping humanity transcend its biology. A symbiotic merger of biology and machine is inevitable. And the article below describes another step, be it one of many, to reaching the transhuman. This news story gives me hope that one day my current job will, being an EMT, will become obsolete to a degree. I would welcome a future free of the disease of aging and put nursing homes out of business.
As technology, such as nanotech, emerges there will be social opposition. Neo-Luddites that are trapped by the romance of death will see the enhancement of humanity as unethical instead of the clear choice for controlled and accelerated evolution. The political climate over the next 2 decades will be interesting to say the least.
This article was taken from the New York Times website.
February 19, 2012

Physicists Create a Working Transistor From a Single Atom

Australian and American physicists have built a working transistor from a single phosphorus atom embedded in a silicon crystal.
The group of physicists, based at the University of New South Wales and Purdue University, said they had laid the groundwork for a futuristic quantum computer that might one day function in a nanoscale world and would be orders of magnitude smaller and quicker than today’s silicon-based machines.
In contrast to conventional computers that are based on transistors with distinct “on” and “off” or “1” and “0” states, quantum computers are built from devices called qubits that exploit the quirky properties of quantum mechanics. Unlike a transistor, a qubit can represent a multiplicity of values simultaneously.
That might make it possible to factor large numbers more quickly than with conventional machines, thereby undermining modern data-scrambling systems that are the basis of electronic commerce and data privacy. Quantum computers might also make it possible to simulate molecular structures with great speed, an advance that holds promise for designing new drugs and other materials.
“Their approach is extremely powerful,” said Andreas Heinrich, a physicist at I.B.M. “This is at least a 10-year effort to make very tiny electrical wires and combine them with the placement of a phosphorus atom exactly where they want them.”
Dr. Heinrich said the research was a significant step toward making a functioning quantum computing system. However, whether quantum computing will ever be harnessed for useful tasks remains uncertain, and the researchers noted that their work demonstrated the fundamental limits that today’s computers would be able to shrink to.
“It shows that Moore’s Law can be scaled toward atomic scales in silicon,” said Gerhard Klimeck, a professor of electrical and computer engineering at Purdue and leader of the project there. Moore’s Law refers to technology improvements by the semiconductor industry that have doubled the number of transistors on a silicon chip roughly every 18 months for the past half-century. That has led to accelerating increases in performance and declining prices. “The technologies for classical computing can survive to the atomic scale,” Dr. Klimeck said.
Demonstrations of single-atom transistors date from 2002, but the researchers from Purdue and New South Wales said they had made advances on two fronts: in the precision with which they placed the Lilliputian switch; and in the use of industry-standard techniques to build the circuitry, making it possible to read and write information from the tiniest conceivable switch.
The results were reported on Sunday in the journal Nature Nanotechnology.
Until now, single-atom transistors have been created on a hit-or-miss basis, the scientists said.
“But this device is perfect,” Michelle Simmons, a group leader and director of the ARC Centre for Quantum Computation and Communication at the University of New South Wales, said in a statement. “This is the first time anyone has shown control of a single atom in a substrate with this level of precise accuracy.”
In the 1950s, the physicist Richard P. Feynman predicted a world where there would be “plenty of room at the bottom,” opening new vistas into engineering disciplines that would use individual atoms as bricks and mortar in fields as diverse as computing and biology.
Since then, computer designers have moved ever closer to the smallest components that are possible to fabricate. Now, with the publication of the New South Wales and Purdue research, the scientists said they had shown the fundamental limits to which the components of silicon-based computers would be able to shrink in the future. Currently, the smallest dimension in state-of-the-art computers made by Intel is 22 nanometers — less than 100 atoms in diameter.
If the semiconductor industry remains on its current pace, it might be possible to reach that limit within two decades, Dr. Klimeck noted.
The scientists placed the single phosphorus atom using a device known as a scanning tunneling microscope. They used it to essentially scrape trenches and a small cavity on a surface of silicon covered with a layer of hydrogen atoms. Phosphine gas was then used to deposit a phosphorus atom at a precise location, which was then encased in further layers of silicon atoms.
While offering astounding precision for research, these microscopes are not currently applicable as manufacturing tools to make chips that contain billions or even trillions of transistors. Moreover, the devices now operate at very low temperatures.
Despite these limits, the semiconductor industry has made great progress in finding ways to build circuits that are far smaller than the wavelength of visible light. And recently, equipment makers have begun making it possible to assemble layers in silicon chips a single atom at a time.
The low temperatures at which the experiment was performed led Intel scientists to express caution about the results. “It’s good science, but it’s complicated,” said Mike Mayberry, an Intel vice president who is the director of the company’s components research group. “By cooling it to very low temperatures, they’ve frozen out a lot of effects that might otherwise be there.”
Shrinking conventional computer circuitry offers radical increases in the speed at which computers can solve problems, lowers the power they require and drastically increases the amount of data they can store.
Yet some scientists and engineers believe that even when conventional computers stop improving in performance, quantum computing will offer a way to continue to offer vast improvements, making it possible to solve problems beyond the reach of today’s machines.
There have been a series of recent technical advances that suggest that engineers will not hit a wall ending the advance in computer performance any time soon. In January, the Purdue and New South Wales researchers reported in the journal Science that they were able to create silicon nanowires that were just a single atom thick and four atoms wide by assembling thin strands of phosphorus atoms.
Combining the two advances indicates that they have made progress at assembling the basic building blocks of a new ultra-small generation of nanoelectronics that would be assembled from the bottom up.
Also in January, scientists at I.B.M.’s Almaden Research Center used similar techniques to store and retrieve digital 1’s and 0’s from an array of just 12 atoms in an advance that demonstrated the fundamental limits of the magnetic storage of digital information.

Wednesday, February 15, 2012

How to Build the Perfect Human

Building the perfect human. What an interesting question. published a small story in its mad science section that addresses this topic. In its article is discusses using animal DNA to give humanity enhancements that are on par with the animal kingdom, One example that stood out was birds being able to see more colors then we can. However, I think the splicing of animal DNA into the human genome should be approached cautiously.

Splicing animal DNA into human DNA could have some unforeseen consequences. Some examples would prove to be fatal. On a more humorous note we could see a live action version of "The Fly". Animals have advantages over our natural senses. That specialization came at a price evolutionary speaking. Our ancestors became smart and made the environment adapt to them. Animals are animals, and subject to the whims of nature. Evolution is a process that takes place over  along period of time. Physiological specializations take time to develop and is based on environmental stresses. Humanities specialization is symbolic thought. The inclusion of animal DNA into our genetic structure may mess with what makes a human a human and more then likely in a grotesque way.

Building the perfect human should involve tweaking our current genetic structure. sequencing out the bad genetics that lead to disease and other disorders. Once a healthier genome is sequences, the next phase of building the perfect human would be in the inclusion of GNR technologies. First and foremost the perfect human should think faster. 

With computer technology effectively doubling in power every 18-24 months, the human brain will be obsolete before the 2040s. Using GNR technologies the human mind would e enhanced to compete with computer technology. Another enhancement that would contribute to a perfect human would be nano enhancement to reflexes, muscle structures, and audiovisual senses.

The article below was written most likely to be non serious but it does beg the question. Will it be possible to build the perfect human. The answer is yes, and sooner then you think.
Taken From:
How to Build the Perfect Human
What if you could improve the human race by splicing in some animal parts? Would we be better off with cats' eyes? What if you added the lungs of a goose, the muscles of a chimp, and the circulatory system of a penguin? Let's discover which animal parts could enhance our feeble human bodies.

Let's face it. Compared to most animals, humans are the sensory equivalent of those creepy eyeless cave fish (only we don't have the whiskers to guide us). We're just a sad bunch — not smelling, seeing, tasting, or hearing nearly as much as any of the creatures around us. It's time to fix that.

First, we need to start with the eyes. Our eyes have rods and cones, which allow us to see black, white, and three colors, the combination of which give us the "visible spectrum." Birds eyes have special double cones, plus cones that contain a droplet of oil that filters light and allows them to see more specific wavelengths.

Birds can see five colors, which would not only enhance our appreciation of the world, but give us a way to see ultraviolet light-reflections in flowers, off reflective surfaces, and off certain fluids. Wouldn't it be nice to know if a patch of grass you're about to sit on was recently peed on by a dog?

The double-cone structure also lets birds see motion faster than humans can — this gives them a head start when it comes to reaction time. And just to top things off, birds' right eyes have cryptochromes, or special proteins that let them see magnetic fields. And finally, for eye protection, we have to turn to the stately crocodile. They have an extra lid that they can shut over their eyes, letting them see in saltwater without ocular damage.

But what good are eyes if they barely function at night? Other creatures possess a layer of cells called the tapetum lucidum. It's a simple reflective layer at the back of the eye that shoots incoming light out across all the light receptors again, doubling the incoming amount of light. This is why cats' eyes shine in the dark.

But why rely on eyes (which can only see the present) when we can rely on smell (which can see the past)? Dogs' sense of smell allows them to understand what happened in a place days, weeks, months, or years ago. And it doesn't even take a giant tweak. They just have 230 million olfactory cells, or about forty times as many as we do. There has to be a way of making our nasal cavities bigger or more efficient.

Fractals have shown us that it's possible to make pits in tissue, and pits in those pits, and pits in those pits, until the entire tissue becomes like a sponge with a massive amount of surface area. True, that would make the nose more delicate, but it's already a delicate area.
And lastly, there's taste. To be honest, I don't think we need to improve taste, but there are a few things we could do to make it more fun. If we want to taste things right now, we have to put them in our mouth. This is both unsanitary, and triggers the instinct to chew, which then pulls the thing down into our stomach, and brings up the calorie count.

Catfish have taste buds all over their bodies — if we had one section of our outer body that could just taste things for us — say a patch of skin on one forearm — we could just tape a piece of chocolate to our arms and have dessert all morning.

But sense just isn't enough. Compared to the paragons of the animal kingdom, we're not fast — and although our size gives us an advantage over many animals — we're not very strong. Something needs to be done about this.

Because muscles are complicated, it's best to turn to our near-relatives for improvements. The fastest land animal is still the cheetah, but its speed lies mostly in its shape and in its oversized heart. We need something that will make the actual muscles fast. A bat's muscles move around a hundred times as fast a human muscles do (and the muscles in a bat's larynx move faster than that).

Scientists believe the source of this speed is the sarcoplasmic reticulum, a store of calcium in the bat's muscle cells that spring into action and make the muscles contract extremely quickly. We'd have to increase our calcium intake, but this is worth choking down some yogurt.

Next we need strength, and for that we need to go a little closer to home. Chimpanzee muscle fibers are approximately five times as strong as human muscle fibers. This has a specific fix. There are genes, in humans, that limit muscle development. These same genes are in chimpanzees, but they've been deactivated. Deactivate them in humans as well, and they'll have more muscle development. Chimpanzee muscle fibers are also longer than human being's muscle fibers. The fibers contract to contract a muscle, so a chimp's muscle contraction will naturally do more work than a human's.

So far we've looked at the superficial stuff — let's take a look at the interior, starting at the bottom of the world. Down in Antarctica, penguins spent entire winters huddled around together to survive the elements. Although their bodies are layered with insulation, their feet are exposed.

It seems like either the feet would freeze off, or the incoming rush of cold blood would freeze the rest of the penguin. They've gotten around this like many cold-weather animals do: excellent plumbing. Outgoing blood, about to be exposed to the cold and lose a lot of its heat, is routed right near incoming blood from the feet. What happens is a heat-exchange. The cool incoming blood is given rush of heat before it comes back into the body. The outgoing blood cools down, still delivering heat to the extremities, but losing some of its extreme heat, which would have been sucked away by the ice and snow anyway. It's a much more efficient system, made with only a few changes to blood vessel placement, and we should have it.

While we're making adjustments to how the blood flows, let's tweak the blood itself Why bother adding that clear eyelid that we get from crocodiles if we can't go in the water? There are a few problems with aquatic life - the primary one being that we need air.

The secondary problem is that, when we have air but we go too far down, it dissolves into the blood and then bubbles up again during the release of pressure when we surface. These bubbles can kill us. Seals don't seem to have this problem. They dive deep, and they do it without bubbles in the blood. But these bubbles are a result of pressurized gas. And when you bring gas (such as the gas in the lungs) underwater, it will always be under pressure. That's physics, not biology. The seals can't overcome that, but they can circumvent it.

Seals simply empty their lungs of oxygen before they dive. No gas, no pressure difference, no bubbly blood. They manage to do this by transferring all the oxygen in their lungs to the massive quantities of hemoglobin and myoglobin, two proteins that grab oxygen and ferry it around the body, in their blood. We have these proteins as well. We just need more. Then we'd be able to dive like seals, and stay underwater.

But what's the good of having a lot of oxygen underwater if we can't even oxygenate ourselves on land? Put a human too far up in the world and they'll just flat-out drop over from lack of oxygen. The increase in hemoglobin and myoglobin will help that, but how to get oxygen in there in the first place? Once again birds need to be our inspiration.

The Himalayan goose is the perfect oxygenator. It literally lifts itself over Everest twice a year when its migrating, and for that to work its muscles need to be oxygenated with as little effort as possible. It does this by having little balloons at the bottom of its lungs. When oxygen floods into human lungs, it fills the little sacs called alveoli inside each lung. Blood passes along the alveolus wall, picks up oxygen, drops off carbon dioxide, and then the lungs exhale, pushing the gas out again.

During this exhalation period, humans don't pull in any more oxygen. But these geese do. The small balloon-like sacks at the bottom of their lungs fill up with extra air during the inhalation. When humans exhale, the sacks squeeze out that air, which again fills the tiny alveoli with oxygen. The goose literally gets air twice with each breath. If we were to engineer ourselves right, even breathing would be easier.

And so we have the ultimate human. No messing around in the brain. No cat-like face or giant teeth. No paws, no claws, no gaping maws. Just a few internal tweaks that could let us swing through the trees like chimps, dive like seals, run races with cheetahs, breath easier underwater and above the clouds, and see and smell everything. It's enough to make you think that scientists need to get a little madder.

Tuesday, February 14, 2012

First-Of-Its-Kind Stem Cell Study Re-Grows Healthy Heart Muscle in Heart Attack Patients

Having a heart attack can lead to serious life long complications. The heart can become damaged and un able to pump correctly. This condition called CHF or congestive heart failure can rob a person of their lifestyle. Over do it and it can lead to tiredness and shortness of breath. This exasperation promotes a sedentary lifestyle which further complicates the heart condition because of lack of exercise. Your health becomes a downward spiral. There are other conditions that come as a result of having a heart attack. A heart attack can damage the electrical circuitry in your heart leading to arrhythmias and increased chances of further heart conditions.

Stem cells are cells that can become any cell in the body, like cardiac muscle. The Article below, from Science Daily, shows a first of a kind procedure that is being used to replace dead cardiac muscle with stem cells and the stem cells actually regrow and repair the damaged heart. Having a heart attack while scary, has become treatable. Hopefully recipients of this treatment will take a look at their second chance and live a healthy lifestyle.

Web address:

First-Of-Its-Kind Stem Cell Study Re-Grows Healthy Heart Muscle in Heart Attack Patients

Heart surgery. A new clinical trial show that treating heart attack patients with an infusion of their own heart-derived cells helps damaged hearts re-grow healthy muscle. (Credit: © muratolmez / Fotolia)
ScienceDaily (Feb. 13, 2012) — Results from a Cedars-Sinai Heart Institute clinical trial show that treating heart attack patients with an infusion of their own heart-derived cells helps damaged hearts re-grow healthy muscle.
Patients who underwent the stem cell procedure demonstrated a significant reduction in the size of the scar left on the heart muscle by a heart attack. Patients also experienced a sizable increase in healthy heart muscle following the experimental stem cell treatments.
One year after receiving the stem cell treatment, scar size was reduced from 24 percent to 12 percent of the heart in patients treated with cells (an average drop of about 50 percent). Patients in the control group, who did not receive stem cells, did not experience a reduction in their heart attack scars.
"While the primary goal of our study was to verify safety, we also looked for evidence that the treatment might dissolve scar and regrow lost heart muscle," said Eduardo Marbán, MD, PhD, the director of the Cedars-Sinai Heart Institute who invented the procedures and technology involved in the study. "This has never been accomplished before, despite a decade of cell therapy trials for patients with heart attacks. Now we have done it. The effects are substantial, and surprisingly larger in humans than they were in animal tests."
"These results signal an approaching paradigm shift in the care of heart attack patients," said Shlomo Melmed, MD, dean of the Cedars-Sinai medical faculty and the Helene A. and Philip E. Hixon Chair in Investigative Medicine. "In the past, all we could do was to try to minimize heart damage by promptly opening up an occluded artery. Now, this study shows there is a regenerative therapy that may actually reverse the damage caused by a heart attack."
The clinical trial, named CADUCEUS (CArdiosphere-Derived aUtologous stem CElls to Reverse ventricUlar dySfunction), was part of a Phase I investigative study approved by the U.S. Food and Drug Administration and supported by the National Heart, Lung, and Blood Institute.
As an initial part of the study, in 2009, Marbán and his team completed the world's first procedure in which a patient's own heart tissue was used to grow specialized heart stem cells. The specialized cells were then injected back into the patient's heart in an effort to repair and re-grow healthy muscle in a heart that had been injured by a heart attack.
The 25 patients -- average age of 53 -- who participated in this completed study experienced heart attacks that left them with damaged heart muscle. Each patient underwent extensive imaging scans so doctors could pinpoint the exact location and severity of the scars wrought by the heart attack. Patients were treated at Cedars-Sinai Heart Institute and at Johns Hopkins Hospital in Baltimore.
Eight patients served as controls in the study, receiving conventional medical care for heart attack survivors, including prescription medicine, exercise recommendations and dietary advice.
The other 17 patients who were randomized to receive the stem cells underwent a minimally invasive biopsy, under local anesthesia. Using a catheter inserted through a vein in the patient's neck, doctors removed small pieces of heart tissue, about half the size of a raisin. The biopsied heart tissue was then taken to Marbán's specialized lab at Cedars-Sinai, using methods he invented to culture and multiply the cells.
In the third and final step, the now-multiplied heart-derived cells -- approximately 12 million to 25 million -- were reintroduced into the patient's coronary arteries during a second, minimally invasive [catheter] procedure.
Patients who received stem cell treatment experienced an average of 50 percent reduction in their heart attack scars 12 months after infusion while patients who received standard medical management did not experience shrinkage in the damaged tissue.
"This discovery challenges the conventional wisdom that, once established, scar is permanent and that, once lost, healthy heart muscle cannot be restored," said Marbán, The Mark S. Siegel Family Professor.
The process to grow cardiac-derived stem cells involved in the study was developed earlier by Marbán when he was on the faculty of Johns Hopkins University. The university has filed for a patent on that intellectual property and has licensed it to a company in which Dr. Marbán has a financial interest. No funds from that company were used to support the clinical study. All funding was derived from the National Institutes of Health and Cedars-Sinai Medical Center.

Story Source:
The above story is reprinted from materials provided by Cedars-Sinai Medical Center.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:
  1. Raj R Makkar et al. Intracoronary cardiosphere-derived cells for heart regeneration after myocardial infarction (CADUCEUS): a prospective, randomised phase 1 trialThe Lancet, 2012 DOI: 10.1016/S0140-6736(12)60195-0

Sunday, February 12, 2012

Gene Therapy For Inherited Blindness And The Allegory of the Cave

Another victory for genetic therapy, restoring sight to the blind. Certain genetic disorders rob individuals of sight. Imagine trying to navigate the world without being able to see. This article describes how genetic therapy is being used to reverse a type of genetic blindness.

I wonder what the impact technology like this would have on a person who has spent their entire life in darkness. I am reminded of the Allegory Of The Cave.

The Allegory of the Cave

  1. Plato realizes that the general run of humankind can think, and speak, etc., without (so far as they acknowledge) any awareness of his realm of Forms.
  2. The allegory of the cave is supposed to explain this.
  3. In the allegory, Plato likens people untutored in the Theory of Forms to prisoners chained in a cave, unable to turn their heads. All they can see is the wall of the cave. Behind them burns a fire.  Between the fire and the prisoners there is a parapet, along which puppeteers can walk. The puppeteers, who are behind the prisoners, hold up puppets that cast shadows on the wall of the cave. The prisoners are unable to see these puppets, the real objects, that pass behind them. What the prisoners see and hear are shadows and echoes cast by objects that they do not see. Here is an illustration of Plato’s Cave:

    From Great Dialogues of Plato (Warmington and Rouse, eds.) New York, Signet Classics: 1999. p. 316.
  4. Such prisoners would mistake appearance for reality. They would think the things they see on the wall (the shadows) were real; they would know nothing of the real causes of the shadows.
  5. So when the prisoners talk, what are they talking about? If an object (a book, let us say) is carried past behind them, and it casts a shadow on the wall, and a prisoner says “I see a book,” what is he talking about?He thinks he is talking about a book, but he is really talking about a shadow. But he uses the word “book.” What does that refer to?
  6. Plato gives his answer at line (515b2). The text here has puzzled many editors, and it has been frequently emended. The translation in Grube/Reeve gets the point correctly:
    And if they could talk to one another, don’t you think they’d suppose that the names they used applied to the things they see passing before them?”
  7. Plato’s point is that the prisoners would be mistaken. For they would be taking the terms in their language to refer to the shadows that pass before their eyes, rather than (as is correct, in Plato’s view) to the real things that cast the shadows.If a prisoner says “That’s a book” he thinks that the word “book” refers to the very thing he is looking at. But he would be wrong. He’s only looking at a shadow. The real referent of the word “book” he cannot see. To see it, he would have to turn his head around.
  8. Plato’s point: the general terms of our language are not “names” of the physical objects that we can see. They are actually names of things that we cannot see, things that we can only grasp with the mind.
  9. When the prisoners are released, they can turn their heads and see the real objects. Then they realize their error. What can we do that is analogous to turning our heads and seeing the causes of the shadows? We can come to grasp the Forms with our minds.
  10. Plato’s aim in the Republic is to describe what is necessary for us to achieve this reflective understanding. But even without it, it remains true that our very ability to think and to speak depends on the Forms. For the terms of the language we use get their meaning by “naming” the Forms that the objects we perceive participate in.
  11. The prisoners may learn what a book is by their experience with shadows of books. But they would be mistaken if they thought that the word “book” refers to something that any of them has ever seen.
  12. Likewise, we may acquire concepts by our perceptual experience of physical objects. But we would be mistaken if we thought that the concepts that we grasp were on the same level as the things we perceive.

People in darkness their entire lives would not be unlike the prisoners from Plato's cave. They grew up hearing things described to them. And now are granted sight for the first time their entire perceptions of reality would be changed. When humanity crosses the threshold into singularity will it be similar to these patients?

Humanity itself could be seen as blind and the concepts of what will come post singularity are earth shattering. Reality changes around us all the time. These patients that are going to be able to see for the first time have a unique chance to look at the world through innocent eyes. Will they like what they see?


Article Taken From


Gene therapy for inherited blindness succeeds in patients’ other eye

February 12, 2012

Retina photo of a patient with Leber congenital amaurosis (credit: National Eye Institute, NIH)
Retinal gene therapy for congenital blindness has taken another step forward, as research further improved vision in three adult patients previously treated in one eye.
After receiving the same treatment in their other eye, the patients became better able to see in dim light, and two were able to navigate obstacles in low-light situations, according to researchers at The Children’s Hospital of Philadelphia and the University of Pennsylvania . No adverse effects occurred.
Neither the first treatment nor the readministered treatment triggered an immune reaction that cancelled the benefits of the inserted genes, as has occurred in human trials of gene therapy for other diseases. The current research targeted Leber congenital amaurosis (LCA), a retinal disease that progresses to total blindness by adulthood.
“Patients have told us how their lives have changed since receiving gene therapy,” said study co-leader Jean Bennett, M.D., Ph.D., F.M. Kirby professor of Ophthalmology at Penn. “They are able to walk around at night, go shopping for groceries and recognize people’s faces — all things they couldn’t do before. At the same time, we were able to objectively measure improvements in light sensitivity, side vision and other visual functions.”
Other objective results came from brain signals seen in neuroimaging. When a dimly flickering checkerboard pattern flashed in front of a patient’s recently treated eye, an area in the brain responsible for vision lit up during functional magnetic resonance imaging (fMRI).“This finding is telling us that the brain is responding to the eye’s sensitivity to dim light,” said radiology researcher Manzar Ashtari, Ph.D., of The Children’s Hospital of Philadelphia, the study’s co-leader.
LCA is a group of hereditary retinal diseases in which a gene mutation impairs production of an enzyme essential to light receptors in the retina. The study team injected patients with a vector, a genetically engineered adeno-associated virus, which carried a normal version of a gene called RPE65 that is mutated in one form of LCA.
Previous clinical trial with one eye
The researchers in the current study previously carried out a clinical trial of this gene therapy in 12 patients with LCA, four of them children aged 11 and younger when they were treated. Exercising caution, the researchers treated only one eye — the one with worse vision. This trial, reported in October of 2009, achieved sustained and notable results, with six subjects improving enough to no longer be classified as legally blind.
The Center for Cellular and Molecular Therapeutics (CCMT) at The Children’s Hospital of Philadelphia sponsored both the initial clinical trial and the current study, and manufactured the vector used to carry the corrective gene. Katherine A. High, M.D., a co-author of both studies, is the director of the CCMT, and a pioneering gene therapy researcher.
The research team’s experiments in animals had showed that readministering treatment in a second eye was safe and effective. While these results were encouraging, the researchers were concerned that readministering the vector in the untreated eye of the patients might stimulate an inflammatory response that could reduce the initial benefits in the untreated eye.
“Our concern was that the first treatment might cause a vaccine-like immune response that could prime the individual’s immune system to react against a repeat exposure,” said Bennett. Because the eye is “immune-privileged” — relatively isolated from the body’s immune system — such a response was considered less likely than in other parts of the body, but the idea needed to be tested in practice.
As in the first study, retina specialist Albert M. Maguire, M.D., a study co-author, injected the vector into the untreated eyes of the three subjects at The Children’s Hospital of Philadelphia. The patients had been treated one and a half to three years previously.
The researchers continued to follow the three patients for six months after readministration. They found the most significant improvements were in light sensitivity, such as the pupil’s response to light over a range of intensities. Two of the three subjects were able to navigate an obstacle course in dim light, as captured in videos that accompanied the published study.
No safety problems found
There were no safety problems and no significant immune responses. There was even an unexpected benefit — the fMRI results showed improved brain responses not just in the newly injected eye, but in the first one as well, possibly because the eyes were better able to coordinate with each other in fixating on objects.
The researchers caution that follow-up studies must be done over a longer period and with additional subjects before they can definitively state that readministering gene therapy for retinal disease is safe in humans. However, said Bennett, the findings bode well for treating the second eye in the remaining patients from the first trial, including children, who may have better results because their retinas have not degenerated as much as those of the adults.
Furthermore, Bennett added, the research holds promise for using a similar gene therapy approach for other retinal diseases. Ashtari said that fMRI may play a future role in helping to predict patients more likely to benefit from gene therapy for retinal disease.
Ref.: Jean Bennett and Manzar Ashtari et al. AAV2 Gene Therapy Readministration in Three Adults with Congenital BlindnessScience Translational Medicine, Feb. 8, 2012 DOI: 10.1126/scitranslmed.3002865.
Ref.: Gene Therapy for Leber Congenital Amaurosis, National Eye Institute

Deus Ex:Human Revolution and Transhumanism (Extended Eyeborg Documentary)

This morning I am posting a video. This short documentary has been out for a while but it is important to be reminded of the future that is coming. The video is shot by a man who lost his eye in a gun accident and chose to have a camera prosthetic. He meets other real life augmented people and correlates how todays cybernetics compare to the ones in the game Deus Ex: Human Revolution. The rate of prosthetic technology doubles every 18 months in regards to how close a prosthetic limb is functionally top a natural limb. It will not belong till they surpass us and we have arms and legs 2.0.

Don't forget about this months book contest! Two winners will receive a copy of the up coming book "Abundance: The Future is Better Than You Think".

Saturday, February 11, 2012

Bypassing The “Chrome Age” Robocop to Nanocop

A favorite form of science fiction growing up was the cyberpunk genre. It featured rebellious and shady individuals that fought against “The Man” using his own technologies. A common motif in these stories was the enhancement of humans with robotic parts such as being able to plug a brain into a computer and experience a full sensory immersion of virtual reality. A future like that would be pretty cool. However, with the advances of technology and the coming singularity it is more likely that the “chrome age” will be almost completely bypassed.

Many cyberpunk role-playing games, books, movies and TV shows, displayed a future that had a linear view. Sure Robocop was advanced but the surrounding technology was boxy and styled after the time frame the movies were made in. Lets look at Robocop. The basic story is that a police officer was killed in the line of duty and his brain and CNS (central nervous system) were harvested and plugged into a robot body. The Robot was jerky and movements not fluid. Robocop was a walking tank with a targeting system. While cool, this is not the direction science will go.

Don't forget about this months book contest! Two winners will receive a copy of the up coming book "Abundance: The Future is Better Than You Think".

The same scenario with more modern technology that represents a exponential view. A cop falls in the line of duty. He is rushed to a medical center and expires. The corporation running the police department requires a subject to test a new form of supercop so they extract the brain. With either medical scanners or physically cutting the brain into nano-slides, the brain is mapped and a exact digital copy is constructed. The digital copy is then up loaded into a computer that directs nanites to reconstruct the brain inside a new body. The cop wakes up not even realising he died except for perhaps a missing chunk of time.

This new body is genetically modified to be faster, stronger, and smarter. A majority of the body is biological, the skin is bullet proof thanks to the splicing in of spider genes that make the skin as strong as steel while as flexible as natural skin. The new cop has eyes that contain nano systems that display an AR overlay and other headware that allow Nanocop direct access to internet via brain machine interfacing. He can pull up what ever he needs to know at a moments notice through an AR overlay he can actually see. No need for typing or interfacing because everything is wireless he thinks and it happens. His vision is enhanced so that he has multi-spectrum vision including ultrasonic like a bat.

He has become a transhuman cop for a transhuman age. With regular updates to a central computer housing his brain profile, if the officer falls in duty again he can simply be resurrected into a new body. When his current body is obsolete he can leave it and upgrade to a new body. Essentially the mind becomes software and the body is hardware. 

This scenario does beg the question: If the person dies and a his consciousness is transferred into another body, is it still him? At what point is he no longer human and is posthuman? Does the corporation now own his consciousnesses? Can it be reprogrammed like software? Can it be Hacked? Please comment with your views.

Gene Therapy Boosts Brain Repair for Demyelinating Diseases

Multiple Sclerosis is a horrible genetic disorder where the myelin sheaths around neurons become destroyed. Without these sheaths, neurons are prone to damage and are unable to communicate properly. It would be akin to taking the insulation off of a power line and expect it to work. The below article taken from science daily talks about gene therapy and the use of stem and other progenitor cells as a way to rebuild damages to neurons from MS. Applications of gene therapy are starting to become more commonplace as a way to fight afflictions once thought untreatable. Perhaps gene therapies like this can be applied to more diseases such as ALS.
Don't forget about this months book contest! Two winners will receive a copy of the up coming book "Abundance: The Future is Better Than You Think".

Taken From:

Gene Therapy Boosts Brain Repair for Demyelinating Diseases

Caltech researchers promote repair in a mouse model of MS by enhancing the production of myelin producing cells (shown in green). (Credit: Image courtesy of California Institute of Technology)
ScienceDaily (Feb. 9, 2012) — Our bodies are full of tiny superheroes -- antibodies that fight foreign invaders, cells that regenerate, and structures that ensure our systems run smoothly. One such structure is myelin -- a material that forms a protective, insulating cape around the axons of our nerve cells so that they can send signals quickly and efficiently. But myelin, and the specialized cells called oligodendrocytes that make it, become damaged in demyelinating diseases like multiple sclerosis (MS), leaving neurons without their myelin sheaths. As a consequence, the affected neurons can no longer communicate correctly and are prone to damage. Researchers from the California Institute of Technology (Caltech) now believe they have found a way to help the brain replace damaged oligodendrocytes and myelin.

The therapy, which has been successful in promoting remyelination in a mouse model of MS, is outlined in a paper published February 8 in The Journal of Neuroscience.

"We've developed a gene therapy to stimulate production of new oligodendrocytes from stem and progenitor cells -- both of which can become more specialized cell types -- that are resident in the adult central nervous system," says Benjamin Deverman, a postdoctoral fellow in biology at Caltech and lead author of the paper. "In other words, we're using the brain's own progenitor cells as a way to boost repair."
The therapy uses leukemia inhibitory factor (LIF), a naturally occurring protein that was known to promote the self-renewal of neural stem cells and to reduce immune-cell attacks to myelin in other MS mouse models.
"What hadn't been done before our study was to use gene therapy in the brain to stimulate these cells to remyelinate," says Paul Patterson, the Biaggini Professor of Biological Sciences at Caltech and senior author of the study.

According to the researchers, LIF enables remyelination by stimulating oligodendrocyte progenitor cells to proliferate and make new oligodendrocytes. The brain has the capacity to produce oligodendrocytes, but often fails to prompt a high enough repair response after demyelination.

"Researchers had been skeptical that a single factor could lead to remyelination of damaged cells," says Deverman. "It was thought that you could use factors to stimulate the division and expansion of the progenitor population, and then add additional factors to direct those progenitors to turn into the mature myelin-forming cells. But in our mouse model, when we give our LIF therapy, it both stimulates the proliferation of the progenitor cells and allows them to differentiate into mature oligodendrocytes."
In other words, once the researchers stimulated the proliferation of the progenitor cells, it appeared that the progenitors knew just what was needed -- the team did not have to instruct the cells at each stage of development. And they found that LIF elicited such a strong response that the treated brain's levels of myelin-producing oligodendrocytes were restored to those found in healthy populations.

The researchers note, too, that by placing LIF directly in the brain, one avoids potential side effects of the treatment that may arise when the therapy is infused into the bloodstream.

"This new application of LIF is an avenue of therapy that has not been explored in human patients with MS," says Deverman, who points out that LIF's benefits might also be good for spinal-cord injury patients since the demyelination of spared neurons may contribute to disability in that disorder.

To move the research closer to human clinical trials, the team will work to build better viral vectors for the delivery of LIF. "The way this gene therapy works is to use a virus that can deliver the genetic material -- LIF -- into cells," explains Patterson. "This kind of delivery has been used before in humans, but the worry is that you can't control the virus. You can't necessarily target the right place, and you can't control how much of the protein is being made."

Which is why he and Deverman are developing viruses that can target LIF production to specific cell types and can turn it on and off externally, providing a means to regulate LIF levels. They also plan to test the therapy in additional MS mouse models.

"For MS, the current therapies all work by modulating or suppressing the immune system, because it's thought to be a disease in which inflammation leads to immune-associated loss of oligodendrocytes and damage to the neurons," says Deverman. "Those therapies can reduce the relapse rate in patients, but they haven't shown much of an effect on the long-term progression of the disease. What are needed are therapies that promote repair. We hope this may one day be such a therapy."
The work done in this study, "Exogenous Leukemia Inhibitory Factor Stimulates Oligodendrocyte Progenitor Cell Proliferation and Enhances Hippocampal Remyelination," was funded by the California Institute for Regenerative Medicine, the National Institutes of Neurological Disorders and Stroke, and the McGrath Foundation.

Story Source:
The above story is reprinted from materials provided by California Institute of Technology. The original article was written by Katie Neith.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:
  1. B. E. Deverman, P. H. Patterson. Exogenous Leukemia Inhibitory Factor Stimulates Oligodendrocyte Progenitor Cell Proliferation and Enhances Hippocampal Remyelination.Journal of Neuroscience, 2012; 32 (6): 2100 DOI: 10.1523/JNEUROSCI.3803-11.2012