Humans Played Role in Neanderthal Extinction

neanderthal-human-skulls

neanderthal-human-skulls

Ancient teeth from Italy suggest that the arrival of modern humans in Western Europe coincided with the demise of Neanderthals there, researchers said.

This finding suggests that modern humans may have caused Neanderthals to go extinct, either directly or indirectly, scientists added.

Neanderthals are the closest extinct relatives of modern humans. Recent findings suggest that Neanderthals, who once lived in Europe and Asia, were closely enough related to humans to interbreed with the ancestors of modern humans — about 1.5 to 2.1 percent of the DNA of anyone outside Africa is Neanderthal in origin. Recent findings suggest that Neanderthals disappeared from Europe between about 41,000 and 39,000 years ago.

Scientists have hotly debated whether Neanderthals were driven into extinction because of modern humans. To solve this mystery, researchers have tried pinpointing when modern humans entered Western Europe. [Image Gallery: Our Closest Human Ancestor]

Modern human or Neanderthal?

The Protoaurignacians, who first appeared in southern Europe about 42,000 years ago, could shed light on the entrance of modern humans into the region. This culture was known for its miniature blades and for simple ornaments made of shells and bones.

Scientists had long viewed the Protoaurignacians as the precursors of the Aurignacians — modern humans named after the site of Aurignac in southern France who spread across Europe between about 35,000 and 45,000 years ago. Researchers had thought the Protoaurignacians reflected the westward spread of modern humans from the Near East — the part of Asia between the Mediterranean Sea and India that includes the Middle East.

However, the classification of the Protoaurignacians as modern human or Neanderthal has long been uncertain. Fossils recovered from Protoaurignacian sites were not conclusively identified as either.

Now scientists analyzing two 41,000-year-old teeth from two Protoaurignacian sites in Italy find that the fossils belonged to modern humans.

“We finally have proof for the argument that says that modern humans were there when the Neanderthals went extinct in Europe,” study lead author Stefano Benazzi, a paleoanthropologist at the University of Bologna in Ravenna, Italy.

A fossil tooth found at an Italian site called Grotta di Fumane (shown here) came from a modern human, scientists say.

The researchers investigated a lower incisor tooth from Riparo Bombrini, an excavation site in Italy, and found it had relatively thick enamel. Prior research suggested modern human teeth had thicker enamel than those of Neanderthals, perhaps because modern humans were healthier or developed more slowly. They also compared DNA from an upper incisor tooth found in another site in Italy — Grotta di Fumane — with that of 52 present-day modern humans, 10 ancient modern humans, a chimpanzee, 10 Neanderthals, two members of a recently discovered human lineage known as the Denisovans, and one member of an unknown kind of human lineage from Spain, and found that the Protoaurignacian DNA was modern human.

“This research really could not have been done without the collaboration of researchers in many different scientific research fields — paleoanthropologists, molecular anthropologists, physical anthropologists, paleontologists and physicists working on dating the fossils,” Benazzi said.

Killing off Neanderthals

Since the Protoaurignacians first appeared in Europe about 42,000 years ago and the Neanderthals disappeared from Europe between about 41,000 and 39,000 years ago, these new findings suggest that Protoaurignacians “caused, directly or indirectly, the demise of Neanderthals,” Benazzi said.

These 3D models show an incisor tooth from two Italian sites, Riparo Bombrini (left) and Grotta di Fumane (right).
Credit: Daniele Panetta, CNR Institute of Clinical Physiology, Pisa, Italy

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It remains unclear just how modern humans might have driven Neanderthals into extinction, Benazzi cautioned. Modern humans might have competed with Neanderthals, or they might simply have assimilated Neanderthals into their populations.

Moreover, prior research suggests that Neanderthals in Europe might have been headed toward extinction before modern humans even arrived on the continent. Neanderthals apparently experienced a decline in genetic diversity about the time when modern humans began turning up in Europe.

“The only way we might have proof of how modern humans caused the decline of Neanderthals is if we ever find a modern human burying a knife into the head of a Neanderthal,” Benazzi joked.

The researchers now hope to find more Protoaurignacian human remains. “Hopefully, we can find DNA that may say something about whether these modern humans and Neanderthals interbred,” Benazzi said.

 

Source:   livescience.com

Humans evolution rapidly evolving

Evolution Human

Evolution Human

 

Humans are evolving more rapidly than previously thought, according to the largest ever genetics study of a single population.

Scientists reached the conclusion after showing that almost every man alive can trace his origins to one common male ancestor who lived about 250,000 years ago. The discovery that so-called “genetic Adam”, lived about 100,000 years more recently than previously understood suggests that humans must have been genetically diverging at a more rapid rate than thought.

Kári Stefánsson, of the company deCODE Genetics and senior author of the study, said: “It means we have evolved faster than we thought.”

The study also shows that the most recent common male ancestor was alive at around the same time as “mitochondrial Eve” – the last woman to whom all females alive today can trace their mitochondrial DNA.

Unlike their biblical counterparts, genetic Adam and Eve were by no means the only humans alive, and although they almost certainly never met, the latest estimate which gives a closer match between their dates makes more sense, according to the researchers.

When the overall population size is stable – as it has been for long periods in the past – men have, on average, just one son, and women, just one daughter. This means that for any given man, there is a high chance that his paternal line will eventually come to an end. This means any male descendants, for instance his daughter’s son, would have Y-chromosomes inherited from other men. If you travelled back far enough in time, the theory goes, there would be only one man whose paternal line extends unbroken to the present day: this man is Y-chromosome Adam.

The researchers dated the existence of this man by comparing the Y-chromsomes of 753 Icelandic men, who were also grouped into 274 paternal lines. The researchers used a “molecular clock”, based on the number of DNA mutations that arise with each generation, to estimate Adam’s age.

The study, published in Nature Genetics, put the new age for genetic Adam at between 174,000 and 321,000 years ago. Genetic Eve is thought to have walked the Earth around 200,000 years ago: well within the new error margin for Adam.

“It gives us enormous confidence to have a timeline that is similar,” said Stefánsson.

Previous dates for ancestral Adam ranged from far more recent, just 50,000 years ago, right back to around 500,000 years ago, with some estimates showing major mismatches with the dating of ancestral Eve. Some researchers had suggested that polygamy could explain the gap, in the cases where Adam was more recent, by reducing the number of men who would pass on their Y-chromosome. Stefánsson describes this argument as a “crock of shit”. “The two sexes are inseparable,” he said. “It doesn’t matter how many women a man has children with – half of them will be boys and half girls.”

Agnar Helgason, also of deCODE, said the latest findings could help refine dates for major events during human evolution, such as when humans first migrated out of Africa and arrived in Europe. “We’re curious about where we came from and when,” he said. “This gives us a bit more solid information about when.”

Previous research also suggested that humans are evolving more quickly now than at any time since the split with the ancestors of modern chimpanzees 6m years ago. The study, by the University of Wisconsin, found that at least 7% of human genes have undergone recent evolution. Some of the changes included the emergence of fair skin and blue eyes in northern Europe, greater resistance to malaria in some African populations and the appearance of a gene that allows lactose to be digested.

 

Source:  theguardian.com

Head transplants could be a reality by 2017

Head Transplant

Head Transplant

 

 

Transplanting a human head onto a donor body may sound like the stuff of science fiction comics, but not to Italian doctor Sergio Canavero. He has not only published a paper describing the operation in detail, but also believes that the surgery could be a reality as early as 2017.

Canavero, Director of the Turin Advanced Neuromodulation Group, initially highlighted the idea in 2013, stating his belief that the technology to successfully join two severed spinal cords existed. Since then he’s worked out the details, describing the operation in his recent paper, as the Gemini spinal cord fusion protocol (GEMINI GCF).

To carry out the transplant, a state of hypothermia is first induced in both the head to be transplanted and the donor body, to help the cells stay alive without oxygen. Surgeons would then cut into the neck tissue of both bodies and connect the blood vessels with tubes. The next step is to cut the spinal cords as neatly as possible with minimal trauma.

The severed head would then be placed on the donor body and the two spinal cords encouraged to fuse together with a sealant called polyethylene glycol, which Canavero notes in his paper, has “the power to literally fuse together severed axons or seal injured leaky neurons.”

After suturing the blood vessels and the skin, the patient is kept in a comatose state for three to four weeks to discourage movement and give both spinal stumps time to fuse. The fusion point will also be electrically stimulated to encourage neural connections and accelerate the growth of a functional neural bridge. The patient will additionally be put on a regime of anti-rejection medications.

According to Canavero, with rehabilitation the patient should be able to speak in their own voice and walk within a year’s time. The goal is to help people who are paralyzed, or whose bodies are otherwise riddled with degenerative diseases and other complications. While the procedure sounds extremely complex and disturbing on multiple levels, Canvero tells us he’s already conducting interviews with volunteers who’ve stepped forward.

“Many are dystrophic,” Canavero says “These people are in horrible pain.”

The most well-known example of a head transplant was when Dr. Robert White, a neurosurgeon, transplanted the head of one rhesus monkey onto another in 1970. The spinal cords, however, were not connected to each other, leaving the monkey unable to control its body. It subsequently died after the donor body rejected the head.

Current technology and recent advances hold out more promise. Canavero plans to garner support for the project, when he presents it at the American Academy of neurological and Orthopaedic Surgeons conference in Annapolis, Maryland, later this year. Understandably his proposal has generated incredible controversy, with experts questioning the specifics and ethics of the procedure, even going as far as calling it bad science.

 

Source:   gizmag.com

Brains communicate from thousands of miles away

Brain study

Brain study

 

Brain-to-brain communication study conducted in coordination with Harvard Medical School has proven that extrasensory mind-to mind interaction can happen over great distances by leveraging different pathways in the mind. (Technological telepathy)

The study, coauthored by Alvaro Pascual-Leone, Director of the Berenson-Allen Center for Noninvasive Brain Stimulation at Beth Israel Deaconess Medical Center (BIDMC) and a Professor of Neurology at Harvard Medical School, found that information can be successfully transmitted between two intact human brains from distances over 5000 miles apart.

The following is excerpt from an article featured on Smithsonian Mag:

An international research team develops a way to say “hello” with your mind

In a recent experiment, a person in India said “hola” and “ciao” to three other people in France. Today, the Web, smartphones and international calling might make that not seem like an impressive feat, but it was. The greetings were not spoken, typed or texted. The communication in question happened between the brains of a set of study subjects, marking one of the first instances of brain-to-brain communication on record.

The team, whose members come from Barcelona-based research institute Starlab, French firm Axilum Robotics and Harvard Medical School, published its findings earlier this month in the journal PLOS One. Study co-author Alvaro Pascual-Leone, director of the Berenson-Allen Center for Noninvasive Brain Stimulation at Beth Israel Deaconess Medical Center and a neurology professor at Harvard Medical School, hopes this and forthcoming research in the field will one day provide a new communication pathway for patients who might not be able to speak.

“We want to improve the ways people can communicate in the face of limitations—those who might not be able to speak or have sensory impairments,” he says. “Can we work around those limitations and communicate with another person or a computer?”

Pascual-Leone’s experiment was successful—the correspondents neither spoke, nor typed, nor even looked at one another. But he freely concedes that the test was more a proof of concept than anything else, and the technique still has a long way to go. “It’s still very, very early,” he says, “[but] we can show that this is even possible with technology that’s available. It’s the difference between talking on the phone and sending Morse code. To get where we’re going, you need certain steps to be taken first.”

Indeed, the process was drawn out, if not downright inelegant. First, the team had to establish binary-code equivalents of letters; for example “h” is “0-0-1-1-1.” Then, with EEG (electroencephalography) sensors attached to the scalp, the sender moved either his hands or feet to indicate a 1 or a 0. The code then passed to the recipient over email. On the other end, the receiver was blindfolded with a transcranial magnetic stimulation (TMS) system on his head. (TMS is a non-invasive method of stimulating neurons in the brain; it’s most commonly used to treat depression.) The TMS headset stimulated the recipient’s brain, causing him to see quick flashes of light. A flash was equivalent to a “1” and a blank was a “0.” From there, the code was translated back into text.

 

Source:   earthweareone.com

Nanomotors Placed Inside Live Human Cells

Tiny Nanomotors Successfully Placed Inside Live Human Cells For The First Time:

Tiny Nanomotors Successfully Placed Inside Live Human Cells For The First Time

Tiny Nanomotors Successfully Placed Inside Live Human Cells For The First Time

Scientists have successfully placed tiny synthetic motors in live human cells through nanotechnology. Using ultrasonic waves as the power source and magnets to steer, the nanomotors can zip around the cell and perform tasks.

The main obstacle for placing nanomotors in cells is the power source. Previous nanomotors needed toxic fuels to propel them. It wouldn’t move in a biological environment.

The researchers at Penn State University and at Weinberg Medical Physics found that ultrasonic waves can be used to power these motors and that magnetic fields can be used to steer them.

The image above is that of a HeLa cell with some gold-ruthenium nanomotors inside it. The arrows indicate the trajectories of the nanomotors, and the solid white line shows its propulsion. There are several nanomotors is spinning at the center. HeLa cells are a line of human cervical cancer cells that are used in research studies. Image credit: Mallouk lab, Penn State University.

Bionanotechnology is fast becoming popular in medical and scientific research. Implants and devices hundreds of times smaller than the width of a human hair, can be integrated into cells. This technology can open up various medical applications such as surgery, deliver medication, and even eradicate cancer cells. Because of its microscopic size, bionanotech devices are non-invasive and results in fewer complications normal open surgery would have.

For the first time, a team of chemists and engineers at Penn State University have placed tiny synthetic motors inside live human cells, propelled them with ultrasonic waves and steered them magnetically. It’s not exactly “Fantastic Voyage,” but it’s close. The nanomotors, which are rocket-shaped metal particles, move around inside the cells, spinning and battering against the cell membrane.

“As these nanomotors move around and bump into structures inside the cells, the live cells show internal mechanical responses that no one has seen before,” said Tom Mallouk, Evan Pugh Professor of Materials Chemistry and Physics at Penn State. “This research is a vivid demonstration that it may be possible to use synthetic nanomotors to study cell biology in new ways. We might be able to use nanomotors to treat cancer and other diseases by mechanically manipulating cells from the inside. Nanomotors could perform intracellular surgery and deliver drugs noninvasively to living tissues.”

The researchers’ findings will be published in Angewandte Chemie International Edition on 10 February 2014. In addition to Mallouk, co-authors include Penn State researchers Wei Wang, Sixing Li, Suzanne Ahmed, and Tony Jun Huang, as well as Lamar Mair of Weinberg Medical Physics in Maryland U.S.A.

Up until now, Mallouk said, nanomotors have been studied only “in vitro” in a laboratory apparatus, not in living human cells. Chemically powered nanomotors first were developed ten years ago at Penn State by a team that included chemist Ayusman Sen and physicist Vincent Crespi, in addition to Mallouk. “Our first-generation motors required toxic fuels and they would not move in biological fluid, so we couldn’t study them in human cells,” Mallouk said. “That limitation was a serious problem.” When Mallouk and French physicist Mauricio Hoyos discovered that nanomotors could be powered by ultrasonic waves, the door was open to studying the motors in living systems.

For their experiments, the team uses HeLa cells, an immortal line of human cervical cancer cells that typically is used in research studies. These cells ingest the nanomotors, which then move around within the cell tissue, powered by ultrasonic waves. At low ultrasonic power, Mallouk explained, the nanomotors have little effect on the cells. But when the power is increased, the nanomotors spring into action, moving around and bumping into organelles — structures within a cell that perform specific functions. The nanomotors can act as egg beaters to essentially homogenize the cell’s contents, or they can act as battering rams to actually puncture the cell membrane.

While ultrasound pulses control whether the nanomotors spin around or whether they move forward, the researchers can control the motors even further by steering them, using magnetic forces. Mallouk and his colleagues also found that the nanomotors can move autonomously — independently of one another — an ability that is important for future applications. “Autonomous motion might help nanomotors selectively destroy the cells that engulf them,” Mallouk said. “If you want these motors to seek out and destroy cancer cells, for example, it’s better to have them move independently. You don’t want a whole mass of them going in one direction.”

The ability of nanomotors to affect living cells holds promise for medicine, Mallouk said. “One dream application of ours is Fantastic Voyage-style medicine, where nanomotors would cruise around inside the body, communicating with each other and performing various kinds of diagnoses and therapy. There are lots of applications for controlling particles on this small scale, and understanding how it works is what’s driving us.”

quantumday.com

Source:

Human cartilage grown in lab

Engineers grow functional human cartilage in lab:

Engineers grow functional human cartilage in lab

Engineers grow functional human cartilage in lab

 

 

Researchers at Columbia Engineering announced that they have successfully grown fully functional human cartilage in vitro from human stem cells derived from bone marrow tissue. Their study, which demonstrates new ways to better mimic the enormous complexity of tissue development, regeneration, and disease.
“We’ve been able — for the first time — to generate fully functional human cartilage from mesenchymal stem cells by mimicking in vitro the developmental process of mesenchymal condensation,” says Gordana Vunjak-Novakovic, who led the study and is the Mikati Foundation Professor of Biomedical Engineering at Columbia Engineering and professor of medical sciences. “This could have clinical impact, as this cartilage can be used to repair a cartilage defect, or in combination with bone in a composite graft grown in lab for more complex tissue reconstruction.”

 

For more than 20 years, researchers have unofficially called cartilage the “official tissue of tissue engineering,” Vunjak-Novakovic observes. Many groups studied cartilage as an apparently simple tissue: one single cell type, no blood vessels or nerves, a tissue built for bearing loads while protecting bone ends in the joints. While there has been great success in engineering pieces of cartilage using young animal cells, no one has, until now, been able to reproduce these results using adult human stem cells from bone marrow or fat, the most practical stem cell source.
Vunjak-Novakovic’s team succeeded in growing cartilage with physiologic architecture and strength by radically changing the tissue-engineering approach.
The general approach to cartilage tissue engineering has been to place cells into a hydrogel and culture them in the presence of nutrients and growth factors and sometimes also mechanical loading. But using this technique with adult human stem cells has invariably produced mechanically weak cartilage. So Vunjak-Novakovic and her team, who have had a longstanding interest in skeletal tissue engineering, wondered if a method resembling the normal development of the skeleton could lead to a higher quality of cartilage.

 

Sarindr Bhumiratana, postdoctoral fellow in Vunjak-Novakovic’s Laboratory for Stem Cells and Tissue Engineering, came up with a new approach: inducing the mesenchymal stem cells to undergo a condensation stage as they do in the body before starting to make cartilage. He discovered that this simple but major departure from how things were usually? being done resulted in a quality of human cartilage not seen before.

 

Gerard Ateshian, Andrew Walz Professor of Mechanical Engineering, professor of biomedical engineering, and chair of the Department of Mechanical Engineering, and his PhD student, Sevan Oungoulian, helped perform measurements showing that the lubricative property and compressive strength — the two important functional properties — of the tissue-engineered cartilage approached those of native cartilage.
The researchers then used their method to regenerate large pieces of anatomically shaped and mechanically strong cartilage over the bone, and to repair defects in cartilage.

 

“Our whole approach to tissue engineering is biomimetic in nature, which means that our engineering designs are defined by biological principles,” Vunjak-Novakovic notes. “This approach has been effective in improving the quality of many engineered tissues — from bone to heart. Still, we were really surprised to see that our cartilage, grown by mimicking some aspects of biological development, was as strong as ‘normal’ human cartilage.”

 

The team plans next to test whether the engineered cartilage tissue maintains its structure and long-term function when implanted into a defect.

 

“This is a very exciting time for tissue engineers,” says Vunjak-Novakovic. “Stem cells are transforming the future of medicine, offering ways to overcome some of the human body’s fundamental limitations. We bioengineers are now working with stem cell scientists and clinicians to develop technologies that will make this dream possible. This project is a wonderful example that we need to ‘think as a cell’ to find out how exactly to coax the cells into making a functional human tissue of a specific kind. It’s emblematic of the progress being driven by the exceptional young talent we have among our postdocs and students at Columbia Engineering.”

 

Source:  sciencedaily.com

Bacteria exploit proteins to trigger potentially lethal infections

New research by scientists at the University of York sheds light on how bacteria exploit human proteins during infections:

bacteria exploit proteins

bacteria exploit proteins

 

 

A research team led by Professor Jennifer Potts, a British Heart Foundation Senior Research Fellow in York’s Department of Biology, studied how Staphylococcus aureus, which can cause life-threatening human infections, attach to two proteins fibronectin and fibrinogen found in human blood.

The human proteins play important roles in clot formation and wound healing and the bacteria appear to exploit them during the process of infection. Scientists had earlier shown that the binding sites for fibrinogen and fibronectin on the S. aureus protein FnBPA appear to “co-operate” in causing the dangerous heart infection infective endocarditis and the latest research suggest how the process occurs. The researchers, who included Vaclav Stemberk and Dr Richard Jones at York and Dr Ruth Massey, a microbiologist at the University of Bath, used X-ray crystallography, biophysical techniques and bacterial assays to investigate the process.

In research published in the Journal of Biological Chemistry, they solved the three dimensional structure of the bacterial protein FnBPA in complex with a small part of the human protein fibrinogen. This work showed that the fibrinogen binding site on FnBPA is close to, but not overlapping with, the binding site for fibronectin.

They then studied the binding of the two human proteins simultaneously to FnBPA and found that binding of fibronectin appears to block binding of fibrinogen to the bacterial protein. It appears that regulation of binding arises due to the close proximity of the fibrinogen and fibronectin binding sites on the bacterial protein and the large size of the human proteins. While the research provides the first biophysical evidence in support of the co-operation previously observed in the infection studies, it is still not clear how these two observations are linked. The scientists are planning further studies.

Professor Potts said: “Bacteria have evolved various mechanisms to exploit human proteins to cause infection. Understanding these mechanisms might not only lead to the development of new therapeutics but can also provide important information regarding the normal role of these human proteins in the body.”

Dr Sanjay Thakrar, Research Advisor at the British Heart Foundation, which co-funded the study, said: “The bacteria studied can cause a wide range of infections including the potentially fatal heart infection known as infective endocarditis.

“This study showed how this bacterium interacts with proteins found in our blood, which may give us an insight into how these deadly heart infections occur. This is an important step towards developing new treatments, but more research is needed to fully understand this interaction.”

 

Source:   eurekalert.org

Hominin DNA suggests link to mystery population

A dig at the Sima de los Huesos cave in Spain, the site of ancient hominin fossils.

Hominin DNA baffles experts  Analysis of oldest sequence from a human ancestor suggests link to mystery population.

Hominin DNA baffles experts
Analysis of oldest sequence from a human ancestor suggests link to mystery population.

 

Another ancient genome, another mystery. DNA gleaned from a 400,000-year-old femur from Spain has revealed an unexpected link between Europe’s hominin inhabitants of the time and a cryptic population, the Denisovans, who are known to have lived much more recently in southwestern Siberia.

The DNA, which represents the oldest hominin sequence yet published, has left researchers baffled because most of them believed that the bones would be more closely linked to Neanderthals than to Denisovans. “That’s not what I would have expected; that’s not what anyone would have expected,” says Chris Stringer, a palaeoanthropologist at London’s Natural History Museum who was not involved in sequencing the femur DNA.

The fossil was excavated in the 1990s from a deep cave in a well-studied site in northern Spain called Sima de los Huesos (‘pit of bones’). This femur and the remains of more than two dozen other hominins found at the site have previously been attributed either to early forms of Neanderthals, who lived in Europe until about 30,000 years ago, or to Homo heidelbergensis, a loosely defined hominin population that gave rise to Neanderthals in Europe and possibly humans in Africa.

But a closer link to Neanderthals than to Denisovans was not what was discovered by the team led by Svante Pääbo, a molecular geneticist at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany.

The team sequenced most of the femur’s mitochondrial genome, which is made up of DNA from the cell’s energy-producing structures and passed down the maternal line. The resulting phylogenetic analysis ­— which shows branches in evolutionary history — placed the DNA closer to that of Denisovans than to Neanderthals or modern humans. “This really raises more questions than it answers,” Pääbo says.

The team’s finding, published online in Nature this week, does not necessarily mean that the Sima de los Huesos hominins are more closely related to the Denisovans, a population that lived thousands of kilometres away and hundreds of thousands of years later, than to nearby Neanderthals. This is because the mitochondrial genome tells the history of just an individual’s mother, and her mother, and so on.

 

Nuclear DNA, by contrast, contains material from both parents (and all of their ancestors) and typically provides a more accurate overview of a population’s history. But this was not available from the femur.

With that caveat in mind, researchers interested in human evolution are scrambling to explain the surprising link, and everyone seems to have their own ideas.

Pääbo notes that previously published full nuclear genomes of Neanderthals and Denisovans suggest that the two had a common ancestor that lived up to 700,000 years ago. He suggests that the Sima de los Huesos hominins could represent a founder population that once lived all over Eurasia and gave rise to the two groups. Both may have then carried the mitochondrial sequence seen in the caves. But these mitochondrial lineages go extinct whenever a female does not give birth to a daughter, so the Neanderthals could have simply lost that sequence while it lived on in Denisovan women.

“I’ve got my own twist on it,” says Stringer, who has previously argued that the Sima de los Huesos hominins are indeed early Neanderthals. He thinks that the newly decoded mitochondrial genome may have come from another distinct group of hominins. Not far from the caves, researchers have discovered hominin bones from about 800,000 years ago that have been attributed to an archaic hominin called Homo antecessor, thought to be a European descendant of Homo erectus. Stringer proposes that this species interbred with a population that was ancestral to both Denisovans and Sima de los Huesos hominins, introducing the newly decoded mitochondrial lineage to both populations .

This scenario, Stringer says, explains another oddity thrown up by the sequencing of ancient hominin DNA. As part of a widely discussed and soon-to-be-released analysis of high-quality Denisovan and Neanderthal nuclear genomes, Pääbo’s team suggests that Denisovans seem to have interbred with a mysterious hominin group.

The situation will become clearer if Pääbo’s team can eke nuclear DNA out of the bones from the Sima de los Huesos hominins, which his team hopes to achieve within a year or so.

Obtaining such sequences will not be simple, because nuclear DNA is present in bone at much lower levels than mitochondrial DNA. And even obtaining the partial mitochondrial genome was not easy: the team had to grind up almost two grams of bone and relied on various technical and computational methods to sequence the contaminated and damaged DNA and to arrange it into a genome. To make sure that they had identified genuine ancient sequences, they analysed only very short DNA strands that contained chemical modifications characteristic of ancient DNA.

Clive Finlayson, an archaeologist at the Gibraltar Museum, calls the latest paper “sobering and refreshing”, and says that too many ideas about human evolution have been derived from limited samples and preconceived ideas. “The genetics, to me, don’t lie,” he adds.

Even Pääbo admits that he was befuddled by his team’s latest discovery. “My hope is, of course, eventually we will not bring turmoil but clarity to this world,” he says.

Scientists Grow Human Brain

Scientists Grow Human Brain From Stem Cells:

Scientists Grow Human Brain From Stem Cells

Scientists Grow Human Brain From Stem Cells

Ear, eye, liver, windpipe, bladder and even a heart. The list of body parts grown from stem cells is getting longer and longer. Now add to it one of the most complex organs: the brain.

A team of European scientists has grown parts of a human brain in tissue culture from stem cells. Their work could help scientists understand the origins of schizophrenia or autism and lead to drugs to treat them, said Juergen Knoblich, deputy scientific director at the Institute of Molecular Biotechnology of the Austrian Academy of Sciences and one of the paper’s co-authors.

The advance could also eliminate the need for conducting experiments on animals, whose brains are not a perfect model for humans.

To grow the brain structures, called organoids, the scientists used stem cells, which can develop into any other kind of cell in the body. They put the stem cells into a special solution designed to promote the growth of neural cells. Bits of gel interspersed throughout the solution gave the cells a three-dimensional structure to grow upon. In eight to 10 days, the stem cells turned into brain cells. After 20 days to a month, the cells matured into a size between three and four millimeters, representing specific brain regions such as the cortex and the hindbrain.

Growing brain tissue this way marks a major advancement because the lab-grown brain cells self-organized and took on growth patterns seen in a developing, fetal brain.

Currently, the organoids are limited on how big they can get because they do not have a circulatory system to move around nutrients.

Knoblich’s team didn’t stop at growing the brain organoids, though. They went a step further and used the developing tissue to study microcephaly, a condition in which the brain stops growing. Microcephalic patients are born with smaller brains and impaired cognitive development. Studying microcephaly in mice doesn’t help because human and mouse brains are too different.

For this part of the study, the researchers used stem cells from a microcephalic patient and grew neurons in a culture. They found that normal brains have progenitor stem cells that make neurons and can do so repeatedly. In microcephalic brains, the progenitor cells differentiate into neurons earlier, said Madeline A. Lancaster, the study’s lead author. The brain doesn’t make as many neurons and a child is born with a much smaller brain volume.

Yoshiki Sasai, a stem-cell biologist at the Riken Center for Developmental Biology in Kobe, Japan, garnered headlines last year by growing the precursors to a human eye.

“The most important advancement is that they combined this self-organization culture with disease-specific cells to model a genetic disease of human brain malformation,” he said.

“Everything we have done with other organs starts with this stage,” said Dr. Anthony Atala, the director of the Wake Forest Institute for Regenerative Medicine, who has done years of research on using 3D printers to build organs. Atala was not involved in this study, but he noted that before he could build organs, he needed to grow the pieces in order to get the cells to differentiate in just the right way. So though it’s unlikely anyone will print brains the way he did a kidney, this kind of experiment is where organ regeneration starts.

Knoblich said the next step is studying other brain disorders, but it will take some time to grow enough brain tissue. One factor is maximum size and how far the brain can develop in the culture. Brain cells develop in layers, and there are several by the time a baby is born. The cortical cells Knoblich’s team grew only had one such layer. Another factor is getting blood vessels inside the tissue. That problem could be solved some time in the future, though he said he couldn’t predict when.

It is tempting to think one day there will be whole brains in vats, but that isn’t likely to happen.

“Aside from the severe ethical problem, I do not think this will be possible,” Knoblich said. To form actual functioning neural circuits, a brain needs sensory input. “Without any sensory input, the proper organization may not happen.”

What makes human muscle age

Scientists discover clues on why human muscle ages:

 Scientists discover clues to what makes human muscle age


Scientists discover clues to what makes human muscle age

A study led by researchers at the University of California, Berkeley, has identified critical biochemical pathways linked to the aging of human muscle. By manipulating these pathways, the researchers were able to turn back the clock on old human muscle, restoring its ability to repair and rebuild itself.

Young, healthy muscle (top row) appears pink and red. In contrast, old muscle is marked by scarring and inflammation, as evidenced by the yellow and dark areas. This difference between old and young tissue occurs both in the muscle's normal state and after immobilization in a cast.
Young, healthy muscle (top row) appears pink and red. In contrast, old muscle is marked by scarring and inflammation, as evidenced by the yellow and dark areas. This difference between old and young tissue occurs both in the muscle’s normal state and after immobilization in a cast.  “Our study shows that the ability of old human muscle to be maintained and repaired by muscle stem cells can be restored to youthful vigor given the right mix of biochemical signals,” said Professor Irina Conboy, a faculty member in the graduate bioengineering program that is run jointly by UC Berkeley and UC San Francisco, and head of the research team conducting the study. “This provides promising new targets for forestalling the debilitating muscle atrophy that accompanies aging, and perhaps other tissue degenerative disorders as well.” Previous research in animal models led by Conboy, who is also an investigator at the Berkeley Stem Cell Center and at the California Institute for Quantitative Biosciences (QB3), revealed that the ability of adult stem cells to do their job of repairing and replacing damaged tissue is governed by the molecular signals they get from surrounding muscle tissue, and that those signals change with age in ways that preclude productive tissue repair. Those studies have also shown that the regenerative function in old stem cells can be revived given the appropriate biochemical signals. What was not clear until this new study was whether similar rules applied for humans. Unlike humans, laboratory animals are bred to have identical genes and are raised in similar environments, noted Conboy, who received a New Faculty Award from the California Institute of Regenerative Medicine (CIRM) that helped fund this research. Moreover, the typical human lifespan lasts seven to eight decades, while lab mice are reaching the end of their lives by age 2. Working in collaboration with Dr. Michael Kjaer and his research group at the Institute of Sports Medicine and Centre of Healthy Aging at the University of Copenhagen in Denmark, the UC Berkeley researchers compared samples of muscle tissue from nearly 30 healthy men who participated in an exercise physiology study. The young subjects ranged from age 21 to 24 and averaged 22.6 years of age, while the old study participants averaged 71.3 years, with a span of 68 to 74 years of age. In experiments conducted by Dr. Charlotte Suetta, a post-doctoral researcher in Kjaer’s lab, muscle biopsies were taken from the quadriceps of all the subjects at the beginning of the study. The men then had the leg from which the muscle tissue was taken immobilized in a cast for two weeks to simulate muscle atrophy. After the cast was removed, the study participants exercised with weights to regain muscle mass in their newly freed legs. Additional samples of muscle tissue for each subject were taken at three days and again at four weeks after cast removal, and then sent to UC Berkeley for analysis.
Human muscle stem cell regenerative activity is depicted in green and red. Stem cell responses were incapacitated when researchers inhibited the activation of key biochemical pathways, making the young muscle behave like old muscle. Old cells exhibited regenerative responses when properly triggered by experimental activation of biochemical signals.
Human muscle stem cell regenerative activity is depicted in green and red. Stem cell responses were incapacitated when researchers inhibited the activation of key biochemical pathways, making the young muscle behave like old muscle. Old cells exhibited regenerative responses when properly triggered by experimental activation of biochemical signals. Morgan Carlson and Michael Conboy, researchers at UC Berkeley, found that before the legs were immobilized, the adult stem cells responsible for muscle repair and regeneration were only half as numerous in the old muscle as they were in young tissue. That difference increased even more during the exercise phase, with younger tissue having four times more regenerative cells that were actively repairing worn tissue compared with the old muscle, in which muscle stem cells remained inactive. The researchers also observed that old muscle showed signs of inflammatory response and scar formation during immobility and again four weeks after the cast was removed. “Two weeks of immobilization only mildly affected young muscle, in terms of tissue maintenance and functionality, whereas old muscle began to atrophy and manifest signs of rapid tissue deterioration,” said Carlson, the study’s first author and a UC Berkeley post-doctoral scholar funded in part by CIRM. “The old muscle also didn’t recover as well with exercise. This emphasizes the importance of older populations staying active because the evidence is that for their muscle, long periods of disuse may irrevocably worsen the stem cells’ regenerative environment.” At the same time, the researchers warned that in the elderly, too rigorous an exercise program after immobility may also cause replacement of functional muscle by scarring and inflammation. “It’s like a Catch-22,” said Conboy. The researchers further examined the response of the human muscle to biochemical signals. They learned from previous studies that adult muscle stem cells have a receptor called Notch, which triggers growth when activated. Those stem cells also have a receptor for the protein TGF-beta that, when excessively activated, sets off a chain reaction that ultimately inhibits a cell’s ability to divide. The researchers said that aging in mice is associated in part with the progressive decline of Notch and increased levels of TGF-beta, ultimately blocking the stem cells’ capacity to effectively rebuild the body. This study revealed that the same pathways are at play in human muscle, but also showed for the first time that mitogen-activated protein (MAP) kinase was an important positive regulator of Notch activity essential for human muscle repair, and that it was rendered inactive in old tissue. MAP kinase (MAPK) is familiar to developmental biologists since it is an important enzyme for organ formation in such diverse species as nematodes, fruit flies and mice. For old human muscle, MAPK levels are low, so the Notch pathway is not activated and the stem cells no longer perform their muscle regeneration jobs properly, the researchers said. When levels of MAPK were experimentally inhibited, young human muscle was no longer able to regenerate. The reverse was true when the researchers cultured old human muscle in a solution where activation of MAPK had been forced. In that case, the regenerative ability of the old muscle was significantly enhanced. “The fact that this MAPK pathway has been conserved throughout evolution, from worms to flies to humans, shows that it is important,” said Conboy. “Now we know that it plays a key role in regulation and aging of human tissue regeneration. In practical terms, we now know that to enhance regeneration of old human muscle and restore tissue health, we can either target the MAPK or the Notch pathways. The ultimate goal, of course, is to move this research toward clinical trials.”

 

 

Drugs Create Super-Soldier

5 Drugs Used to Create a Super-Soldier:

 

5 Drugs Used to Create a Super-Soldier

5 Drugs Used to Create a Super-Soldier

Even though Super-Soldiers might sound like a bad narrative from a sci-fi film, they are more real than ever in a world obsessed with technological and biological advancement. Forget about crazy scientists in abandoned castlesthese drugs are real and they really work too. These drugs aren’t locked away in Area 51 type secret government bases either, a lot of these drugs are actually available right now for anyone to buy.

 

1. XBD173 : Anxiety Killer

Shell shock, post traumatic stress, different names but the same meaning. XBD173 is a drug that can not only eradicate anxiety and fear but it can do it instantly without any side effects or withdrawal symptoms. In total 1 in 8 soldiers, who’ve fought in the Iraq war, suffer from post traumatic stress disorder which is over 10% of the armed forces. Removing anxiety would create fearless and unstoppable soldiers who wouldn’t be affected by any of war’s brutalities or cruelties.

2. Provigil : No More Sleep

Imagine a soldier that didn’t need to sleep or rest half as much as a ‘normal’ soldier did? Completely possible with Provigil (AKA Modafinil) which was initially created to deal with narcolepsy, shift work sleep disorder and excessive daytime sleepiness. The drug radically improves work rate and alertness which means even with less sleep or rest, a soldier can work harder and more effectively.

3. D-IX : Nazi Cocaine

D-IX is a cocaine based drug originally created by the Nazis under Hitler’s evil reign. Criminologist and expert Wolf Kemper said “It was Hitler’s last secret weapon to win a war he had already lost long ago”. The drug was initially tested on prisoners at the Sachsenhausen concentration camp, they were given 20kg packs to carry and which marched with for 90km without rest.

4. Valproic Acid : Super Survivors

When a soldier suffers an injury that causes rapid blood loss, the body’s reaction is to go into shock which will sustain life for a short time however, if the body stays in shock for more than a short time, it can lead to organ failure, and death can soon follow. Valproic acid causes 87% of blood loss victims to survive (well in cows at least) which means that it could be possible to survive for prolonged hours after a bad injury.

5. Select Androgen Receptor Modulators : Instant Muscle Mass

Anabolic steroids are simply concentrated amounts of testosterone that rapidly build muscle mass but scientists have never been able to completely rid undesired side effects, until now. SARMs are a new and improved version of anabolic steroids that allows huge muscle growth without any side effects, whilst a potential super soldier wouldn’t be the size of the Incredible Hulk or nearly as green, this almost overnight treatment could turn a scrawny bunch of boys into a bulky troop of men.

Anti-CD47 eliminates all cancer cells

One Drug to Shrink All Tumors:

 anti-CD47 in addition to chemotherapy

anti-CD47 in addition to chemotherapy

A single drug can shrink or cure human breast, ovary, colon, bladder, brain, liver, and prostate tumors that have been transplanted into mice, researchers have found. The treatment, an antibody that blocks a “do not eat” signal normally displayed on tumor cells, coaxes the immune system to destroy the cancer cells. A decade ago, biologist Irving Weissman of the Stanford University School of Medicine in Palo Alto, California, discovered that leukemia cells produce higher levels of a protein called CD47 than do healthy cells. CD47, he and other scientists found, is also displayed on healthy blood cells; it’s a marker that blocks the immune system from destroying them as they circulate. Cancers take advantage of this flag to trick the immune system into ignoring them. In the past few years, Weissman’s lab showed that blocking CD47 with an antibody cured some cases of lymphomas and leukemias in mice by stimulating the immune system to recognize the cancer cells as invaders. Now, he and colleagues have shown that the CD47-blocking antibody may have a far wider impact than just blood cancers. “What we’ve shown is that CD47 isn’t just important on leukemias and lymphomas,” says Weissman. “It’s on every single human primary tumor that we tested.” Moreover, Weissman’s lab found that cancer cells always had higher levels of CD47 than did healthy cells. How much CD47 a tumor made could predict the survival odds of a patient. To determine whether blocking CD47 was beneficial, the scientists exposed tumor cells to macrophages, a type of immune cell, and anti-CD47 molecules in petri dishes. Without the drug, the macrophages ignored the cancerous cells. But when the CD47 was present, the macrophages engulfed and destroyed cancer cells from all tumor types. Next, the team transplanted human tumors into the feet of mice, where tumors can be easily monitored. When they treated the rodents with anti-CD47, the tumors shrank and did not spread to the rest of the body. In mice given human bladder cancer tumors, for example, 10 of 10 untreated mice had cancer that spread to their lymph nodes. Only one of 10 mice treated with anti-CD47 had a lymph node with signs of cancer. Moreover, the implanted tumor often got smaller after treatment — colon cancers transplanted into the mice shrank to less than one-third of their original size, on average. And in five mice with breast cancer tumors, anti-CD47 eliminated all signs of the cancer cells, and the animals remained cancer-free 4 months after the treatment stopped. “We showed that even after the tumor has taken hold, the antibody can either cure the tumor or slow its growth and prevent metastasis,” says Weissman. Although macrophages also attacked blood cells expressing CD47 when mice were given the antibody, the researchers found that the decrease in blood cells was short-lived; the animals turned up production of new blood cells to replace those they lost from the treatment, the team reports online today in the Proceedings of the National Academy of Sciences. Cancer researcher Tyler Jacks of the Massachusetts Institute of Technology in Cambridge says that although the new study is promising, more research is needed to see whether the results hold true in humans. “The microenvironment of a real tumor is quite a bit more complicated than the microenvironment of a transplanted tumor,” he notes, “and it’s possible that a real tumor has additional immune suppressing effects.” Another important question, Jacks says, is how CD47 antibodies would complement existing treatments. “In what ways might they work together and in what ways might they be antagonistic?” Using anti-CD47 in addition to chemotherapy, for example, could be counterproductive if the stress from chemotherapy causes normal cells to produce more CD47 than usual. Weissman’s team has received a $20 million grant from the California Institute for Regenerative Medicine to move the findings from mouse studies to human safety tests. “We have enough data already,” says Weissman, “that I can say I’m confident that this will move to phase I human trials.”

 

U.S. Waterboarding Evidence Shows Widespread Torture

 

U.S. Waterboarding Evidence Shows More Widespread Torture, Says Human Rights Watch:

 U.S. Waterboarding Evidence Shows More Widespread Torture, Says Human Rights Watch


U.S. Waterboarding Evidence Shows More Widespread Torture, Says Human Rights Watch

Human Rights Watch said it has uncovered evidence of a wider use of waterboarding than previously acknowledged by the CIA, in a report Thursday detailing brutal treatment of detainees at U.S.-run lockups abroad after the 9/11 attacks. The accounts by two former Libyan detainees who said they underwent simulated drowning emerge only days after the Justice Department closed its investigation of the CIA’s use of severe interrogation methods. Investigators said they could not prove any agents crossed the lines authorized by the Bush administration in the “war on terror” program of detention and rendition. Any new instances of waterboarding, however, would go beyond the three that the CIA has said were authorized. The 154-page report features interviews by the New York-based group with 14 Libyan dissident exiles. They describe systematic abuses while they were held in U.S.-led detention centers in Afghanistan – some as long as two years – or in U.S.-led interrogations in Pakistan, Morocco, Thailand, Sudan and elsewhere before the Americans handed them over to Libya. The report also paints a more complete picture of Washington’s close cooperation with the regime of Libya’s former dictator Moammar Gadhafi. Islamist opponents of Gadhafi detained by the U.S. were handed over to Libya with only thin “diplomatic assurances” they would be properly treated, and several of them were subsequently tortured, Human Rights Watch said. “Not only did the U.S. deliver (Gadhafi) his enemies on a silver platter, but it seems the CIA tortured many of them first, said Laura Pitter, counterterrorism adviser at Human Rights Watch and author of the report. “The scope of the Bush administration abuse appears far broader than previously acknowledged,” she said.  Asked about the new waterboarding claim, CIA spokeswoman Jennifer Youngblood said the agency “has been on the record that there are three substantiated cases” of its use. She said she could not comment on the specific allegations but noted the Justice Department’s decision not to prosecute after it “exhaustively reviewed the treatment of more than 100 detainees in the post-9/11 period – including allegations involving unauthorized interrogation techniques.” Former President George W. Bush, his Vice President Dick Cheney and the CIA have said that waterboarding was used only on three senior al-Qaida suspects at secret CIA black sites in Thailand and Poland – Khaled Sheikh Mohammed, Aby Zubayda and Abd al-Rahman al-Nashiri, all currently being held at Guantanamo Bay, Cuba. The technique involves pouring water on a hooded detainee’s nose and mouth until he feels he is drowning. Rights groups and some Obama administration officials say waterboarding and other severe techniques authorized by the CIA constitute torture, while Bush administration officials argue they do not. The Obama administration has ordered a halt to waterboarding and many of the harsh techniques. The 14 Libyans interviewed by Human Rights Watch were swept up in the American hunt for Islamic militants and al-Qaida figures around the world after the Sept. 11, 2001 attacks. They were mostly members of the anti-Gadhafi Libyan Islamic Fighting Group who fled in the 1980s and 1990s to Pakistan, Afghanistan and African countries. The group ran training camps in Afghanistan at the same time al-Qaida was based there but it largely shunned Osama bin Laden and his campaign against the United States, focusing instead on fighting Gadhafi. Ironically, the U.S. turned around and helped the Libyan opposition overthrow Gadhafi in 2011. Now several of the 14 former detainees hold positions in the new Libyan government. The accounts of simulated drowning came from Mohammed al-Shoroeiya and Khaled al-Sharif, who also described a gamut of abuses they went through – all reflecting the methods known to have been authorized by the CIA. The two were seized in Pakistan in April 2003 and taken to U.S.-run prisons in Afghanistan, where al-Shoroeiya was held for 16 months and al-Sharif for two years before they were handed over to Libya. In Afghanistan, they were shackled in cells for months in variety of positions, often naked in almost total darkness with music blaring continuously, left to defecate and urinate on themselves. For example, al-Sharif spent three weeks seated on the ground with his ankles and wrists chained to a ring in the cell’s wall, forcing him to keep his arms and legs elevated. He said he was taken out of his shackles once a day for a half-hour to eat. For the first three months, they were not allowed to bathe. “We looked like monsters,” al-Shoroeiya said. Al-Shoroeiya described being locked naked for a day and a half in a tall, tight, half-meter-wide (1 1/2-foot-wide) chamber with his hands chained above his head, with no food as Western music blasted loudly from speakers next to his ears the entire time. At another point, he was stuffed into a box resembling a footlocker, about 1 meter by 1 meter (3 feet by 3 feet), and kept there for more than an hour as interrogators prodded him with long, thin objects through holes in the side of the box. Both he and Sharif said they were repeatedly taken to a room where they were slammed against a wooden wall and punched in the abdomen. Al-Shoroeiya said one female American interrogator told him, “Now you are under the custody of the United States of America. In this place there will be no human rights. Since September 11, we have forgotten about something called human rights,” according to the report. Al-Shoroeiya described being waterboarded, though he did not use the term. He said he was put in a hood and strapped upside down on a wooden board. Freezing water was poured over his nose and mouth until he felt he was suffocating. During several half-hour interrogation sessions, they would waterboard him multiple times, asking him questions in between while a doctor monitored his body temperature. “They wouldn’t stop until they got some sort of answer from me,” he told HRW. Al-Sharif described a similar technique. Instead of being strapped to a board, he was put on a plastic sheet with guards holding up the edges, while freezing water was poured over him, including onto his hooded face directly over his mouth and nose. “I felt as if I were suffocating,” he told HRW. “I spent three months getting interrogated heavily … and they gave me a different kind of torture every day. Sometimes they used water, sometimes not.” Others of the 14 former detainees, including three held in the same U.S.-led prisons in Afghanistan, described similar treatment as al-Shoroeiya and al-Sharif, though not simulated drowning. One of them, Majid Mokhtar Sasy al-Maghrebi, said he nearly went insane in isolation after months being shackled naked in dark, freezing cells with music blaring, pounding his head against the wall and screaming, “I want to die, why don’t you just kill me?” Another, detained in Mauritania, said that during interrogations by a foreigner he believed was American, his wife was brought to the detention center; his captors showed him his wife through a peephole and threatened to rape her if he did not cooperate. Human Rights Watch said the U.S. failed in its post-9/11 campaign to distinguish between Islamists targeting the United States and those who “may simply have been engaged in armed opposition against their own repressive regimes. “This failure risked aligning the United States with brutal dictators,” the report said. Eight of those interviewed were handed over to Libya in 2004 – the same year then-British Prime Minister Tony Blair made a public rapprochement with Gadhafi and Anglo-Dutch oil giant Shell signed a major exploration deal off the Libyan coast, the HRW report noted. The remaining six were transferred to Libya over the two following years. All were jailed by Gadhafi’s regime, most freed only after his fall. Most said they were not physically tortured – perhaps a result of Gadhafi’s attempts to mend fences with the West – but were kept in solitary confinement for long periods. Several, however, told HRW they were beaten and tortured, including being given electrical shocks. The report also calls into question Libyan claims that one figure handed over by the Americans, Ibn el-Sheikh al-Libi, committed suicide in a Libyan prison. Al-Libi was held in U.S. secret prisons for years and gave information under torture by the Egyptians that the Bush administration used to justify the 2003 invasion of Iraq but was later discredited. After his handover, Libyan authorities said he hanged himself in his cell. But HRW researchers said they were shown photos of his body that showed signs of torture. Messages to Libya from the CIA and British intelligence among the Tripoli Documents published by HRW indicated the United States and Britain were eager to help Libya obtain several senior LIFG figures, including its co-founders, Abdel-Hakim Belhaj and Sami al-Saadi. Belhaj and his then-pregnant wife were detained by Malaysia in 2004 with the help of British intelligence and then handed over to the CIA in Thailand, where he told HRW he was stripped and beaten. They were then taken to Libya, where Belhaj was imprisoned. After Belhaj arrived in Libya, a message believed to be from the then-head of counterterrorism at British intelligence congratulates the Libyan intelligence chief. Britain’s help “was the least we could do for you and for Libya to demonstrate the remarkable relationship we have built,” he wrote.

Human Cells Powerful as Lighting Bolts

Human Cells have Electric Fields as Powerful as Lighting Bolts:

Human Cells have Electric Fields as Powerful as Lighting Bolts

Human Cells have Electric Fields as Powerful as Lighting Bolts

Using newly developed voltage-sensitive nanoparticles, researchers have found that the previously unknown electric fields inside of cells are as strong, or stronger, as those produced in lightning bolts. Previously, it has only been possible to measure electric fields across cell membranes, not within the main bulk of cells, so scientists didn’t even know cells had an internal electric field. This discovery is a surprising twist for cell researchers. Scientists don’t know what causes these incredibly strong fields or why they’ are there. But now using new nanotools, such as voltage-sensitive dyes, they can start to measure them at least. Researchers believe they may be able to learn more about disease states, such as cancer, by studying these minute, but powerful electric fields. University of Michigan researchers led by chemistry professor Raoul Kopelman encapsulated voltage-sensitive dyes in polymer spheres just 30 nanometers in diameter. Testing these nanoparticles in the internal fluid of brain-cancer cells, Kopelman found electric fields as strong as 15 million volts per meter, up to five times stronger than the field found in a lightning bolt. However, this discovery goes beyond being incredibly interesting; the finding will likely change the way researchers look at disease. “They have developed a tool that allows you to look at cellular changes on a very local level,” said Piotr Grodzinski, director of the National Cancer Institute Alliance for Nanotechnology in Cancer in Technology Review. Grodzinski believes many developments in cancer research, for example, over the past few years have been “reactive” rather than proactive. Despite how far cancer treatments have come, the way that cancer, and other diseases, progresses at the cellular level in the first place is still not well understood. With a better understanding, researchers could improve diagnostics and care. “This development represents an attempt to start using nanoscale tools to understand how disease develops,” said Grodzinski. Kopelman has developed encapsulated voltage-sensitive dyes that aren’t hydrophobic and can operate anywhere in the cell, rather than just in membranes. Because it’s possible to place his encapsulated dyes in a cell with a greater degree of control, Kopelman likens them to voltmeters. “Nano voltmeters do not perturb [the cellular] environment, and you can control where you put them,” he says. The existence of strong electric fields across cellular membranes is accepted as a basic fact of cell biology. The fact that cells have internal electric fields as well, however, is a whole new revelation. Scientists previously did not know of the existence of internal cellular energy fields, and are just in the earliest stages of understand the phenomenon. Kopelman presented his results at the annual meeting of the American Society for Cell Biology this month. “There has been no skepticism as to the measurements,” says Kopelman. “But we don’t have an interpretation.” Daniel Chu of the University of Washington in Seattle agrees that Kopelman’s work provides proof of concept that cells have internal electric fields. “It’s bound to be important, but nobody has looked at it yet,” Chu says.

Scan contents of human brain for Immortality

Will scientists ever discover the secret of immortality?:

Will scientists ever discover the secret of immortality?

Will scientists ever discover the secret of immortality?

As Western science still has not found the immortality gene, it is perhaps not surprising that in Silicon Valley and on the outskirts of Moscow the eccentric wealthy (and it always is the eccentric wealthy) are now turning their attention – and their money – to projects that are promising to deliver a new version of the age-old fantasy (or folly) of everlasting life: digital immortality. And this time it may actually work.  For writer Stephen Cave, author of the new book Immortality, digital immortality does not refer to the “legacy” we have left on our Facebook pages. Cave’s book explores the quest to live for ever and how – he believes – it has been the driving force behind civilisations, coming to a climax in modern science. “Digital immortality,” he says, “is about there being a silicon you for when the physical you dies” as a kind of “Plan B if bioscience fails to deliver an actual biological immortality”.  And of course, he adds, biological immortality would not stop you being run over by a bus.  “So your brain is scanned and your essence uploaded into a digital form of bits and bytes, and this whole brain emulation can be saved in a computer’s memory banks ready to be brought back to life as an avatar in a virtual world like Second Life, or even in the body of an artificially intelligent robot that is a replica of who we were.”  For Cave, though, this “is not true immortality” as “you physically die” and this new you, “even though its behaviour could fool your mum”, is then just a copy. A copy that, he admits, could carry on growing, marrying and even having children.  Currently, however, this is still “almost science fiction”, as there are “three big challenges” that stand between us and digital immortality – challenges that projects such as Carbon Copies and Russia 2045 already believe they can overcome within 40 years.  “The first is that we have to be able to read all the information that makes up who you are, and this is likely to be achieved destructively by removing the human brain from the body and then preserving, slicing and scanning in the data it contains. Then there is the challenge to store an amount of information many millions of orders of magnitude bigger than the current computer systems. And finally we need to find a way to animate it.”  In the end, Cave argues, “theoretically the problems of digital immortality seem solvable, but whether the solutions are practical is another story… Although when it does happen it is simply inevitable that the rich will get there as they have the most power among us.”  Others are more positive about the prospect of true digital immortality within a generation.  For Dr Stuart Armstrong, the rise of the idea of digital immortality is due to the realisation that this time – perhaps – we actually have the key to immortality in our hands. Dr Armstrong is research fellow at the Future of Humanity Institute, University of Oxford.  “Technology is now advancing faster and faster and we understand it a lot better because we built it ourselves. So the problems that digital immortality is facing are merely engineering problems – albeit complicated and difficult ones – that could be solved within the decade if we decided to set up a scheme on the scale of the Manhattan Project.”  In particular, he feels that “scanning is the critical problem” and that if you “spent stupid amounts of cash then within a decade many of the limitations of scanning, such as its resolution, could be solved”.  If computer power continues to double every two years, as described by “Moore’s law”, then in the end that will not be an issue either.  “Or it may be that at first we just have to accept a trade-off between what we can do and not do,” he suggests. And for Armstrong this represents true immortality, since, rather pragmatically, “if this avatar or robot is to all intents and purposes you, then it is you.”  Dr Randal A. Koene, though, is determined to take digital immortality from the pages of books like Cave’s and turn it into reality. Koene is founder of the non-profit Carbon Copies Project in California, which is tasked with creating a networking community of scientists to advance digital immortality – “although I prefer to talk about substrate-independent minds, as digital immortality is too much about how long you live, not what you can do with it”.  And for Koene it is very much “you”, there being a “continuity of self” in the same way that “the person you are today is still the same person you were when you were age five”.  “This isn’t science fiction, either, this is closer to science fact,” he argues. Carbon Copies “is working to create a road map to substrate independence by pulling together all the research that is going on, identify where the gaps are and then what we need to do to plug it.  “A Manhattan Project can easily have its funding removed by government, whereas in this network there are usually multiple projects going on in the same area, and only one needs to succeed.”  Furthermore, he feels, the tide of science is moving his way, with India expecting to have built by 2017 a supercomputer big enough to handle the one exaflop of memory required for one brain upload, and such institutions as the Allen Institute for Brain Science spending $300 million to try to crack problems he also needs to solve, such as how the brain encodes, stores and processes information. “Ultimately we won’t even be aware that we are being scanned, uploaded and replaced,” he believes.  In the end, in Stephen Cave’s opinion, digital immortality may well turn out to be a curse, as it always does in mythology.  “If my child died and I replaced her with a digital avatar to help me overcome the grieving, would I let her grow up or even have children of her own? Would I tell her she was a copy? I can imagine just how easy it would be to tell her in a row.”  The complications have more serious and wide-ranging implications if humans cannot resist the temptation to “tweak their digital avatars”, which may – as Stuart Armstrong argues – lead us closer to a world of “super-upgraded copies” and “the real game changer, multiple copies or clones”.  “You could copy the best five programmers in the world a million times or the best call centre worker and these copies would simply replace the humans, who would no longer have any economic value,” Armstrong says. “Humans would be left to die, face a life on welfare or live under coercive regulation to control the technology.”  For Koene, human societies have faced these kinds of problems many times before. What matters more, he believes, is that digital immortality is the next stage of human evolution as it will “allow us as a species to have the flexibility to survive the process of natural selection that every species has to face”, whether on this planet or another.  This time it won’t just be the rich who benefit, either, as the technology will be made “open source” for everyone to have the choice whether to be digitally immortal or not. And that would be a curse.