IMPORTANT OLD ARTICLE : Immortal Jellyfish , the ONLY creature so far that can live for ever !

Well who wouldn't love to live forever ? A species of jellyfish does :

While the humans have been looking for the elixir of life throughout every period of history, it appears that there is one species of jellyfish that are actually immortal. Turritopsis nutricula, or sometimes – Turritopsis dohrnii, is able to transform its cells from mature state back to immaturity, in other words – back to youth. The medusa leads a regular cycle of life, but after maturing and mating, it reverts back to its initial state – a polyp colony. The process is referred to as “transdifferentiation”, and it basically makes the jellyfish unable to die.

The bell-shaped immortal jellyfish measures up to a maximum of bout 4.5 millimeters (0.18 in) and is about the same in its length and width. Originating in the Caribbean, it has now spread worldwide, and the discovery of its unique ability has heated up many discussions among the scientists. Some claim that their mystery is soon to be solved and applied to humans, while others only expect it to improve the quality of life at our final stages. Either way, knowing that something out there goes back and forth from being young to old to young again, blows your mind!

IMPORTANT: LSD and Other Psychedelics Not Linked With Mental Health Problems

The use of LSD, magic mushrooms, or peyote does not increase a person's risk of developing mental health problems, according to an analysis of information from more than 130,000 randomly chosen people, including 22,000 people who had used psychedelics at least once.

Researcher Teri Krebs and clinical psychologist Pål-Ørjan Johansen, from the Norwegian University of Science and Technology's (NTNU) Department of Neuroscience, used data from a US national health survey to see what association there was, if any, between psychedelic drug use and mental health problems. The authors found no link between the use of psychedelic drugs and a range of mental health problems. Instead they found some significant associations between the use of psychedelic drugs and fewer mental health problems. The results are published in the journal PLOS ONE and are freely available online after 19 August.

Symptoms and mental health treatment considered

The researchers relied on data from the 2001-2004 National Survey on Drug Use and Health, in which participants were asked about mental health treatment and symptoms of a variety of mental health conditions over the past year. The specific symptoms examined were general psychological distress, anxiety disorders, mood disorders, and psychosis. Armed with this information, Krebs and Johansen were able to examine if there were any associations between psychedelic use and general or specific mental health problems. They found none. "After adjusting for other risk factors, lifetime use of LSD, psilocybin, mescaline or peyote, or past year use of LSD was not associated with a higher rate of mental health problems or receiving mental health treatment," says Johansen.

Could psychedelics be healthy for you?

The researchers found that lifetime use of psilocybin or mescaline and past year use of LSD were associated with lower rates of serious psychological distress. Lifetime use of LSD was also significantly associated with a lower rate of outpatient mental health treatment and psychiatric medicine prescription. The design of the study makes it impossible to determine exactly why the researchers found what they found. "We cannot exclude the possibility that use of psychedelics might have a negative effect on mental health for some individuals or groups, perhaps counterbalanced at a population level by a positive effect on mental health in others," they wrote. Nevertheless, "recent clinical trials have also failed to find any evidence of any lasting harmful effects of psychedelics," the researchers said, which supports the robustness of the PLOS ONE findings. In fact, says Krebs, "many people report deeply meaningful experiences and lasting beneficial effects from using psychedelics." "Other studies have found no evidence of health or social problems among people who had used psychedelics hundreds of times in legally-protected religious ceremonies," adds Johansen.

What's the bottom line on psychedelic use?

Psychedelics are different than most other recreational drugs. Experts agree that psychedelics do not cause addiction or compulsive use, and they are not known to harm the brain. When evaluating psychedelics, as with any activity, it is important to take an objective view of all the evidence and avoid being biased by anecdotal stories either of harm or benefit, the researchers say. "Everything has some potential for negative effects, but psychedelic use is overall considered to pose a very low risk to the individual and to society," Johansen says, "Psychedelics can elicit temporary feelings of anxiety and confusion, but accidents leading to serious injury are extremely rare."

"Early speculation that psychedelics might lead to mental health problems was based on a small number of case reports and did not take into account either the widespread use of psychedelics or the not infrequent rate of mental health problems in the general population," Krebs explains. "Over the past 50 years tens of millions of people have used psychedelics and there just is not much evidence of long-term problems," she concludes. Both researchers were supported by the Research Council of Norway.

How Information from Different Senses are Integrated by Brain Microcircuits

A new publication in the top-ranked journal Neuron sheds new light onto the unknown processes on how the brain integrates the inputs from the different senses in the complex circuits formed by molecularly distinct types of nerve cells. The work was led by new Umeå University associate professor Paolo Medini. Share This:

One of the biggest challenges in neuroscience is to understand how the cerebral cortex of the brain processes and integrates the inputs from the different senses (like vision, hearing and touch) to control for example, that we can respond to an event in the environment with precise movement of our body.

The brain cortex is composed by morphologically and functionally different types of nerve cells, e.g. excitatory, inhibitory, that connect in very precise ways. Paolo Medini and co-workers show that the integration of inputs from different senses in the brain occurs differently in excitatory and inhibitory cells, as well as in superficial and in the deep layers of the cortex, the latter ones being those that send electrical signals out from the cortex to other brain structures.

"The relevance and the innovation of this work is that by combining advanced techniques to visualize the functional activity of many nerve cells in the brain and new molecular genetic techniques that allows us to change the electrical activity of different cell types, we can for the first time understand how the different nerve cells composing brain circuits communicate with each other," says Paolo Medini. The new knowledge is essential to design much needed future strategies to stimulate brain repair. It is not enough to transplant nerve cells in the lesion site, as the biggest challenge is to re-create or re-activate these precise circuits made by nerve cells.

SOCKING NEWS : Plans to make H7N9 bird flu virus more virulent in high-security tests

Scientists say genetically modifying the H7N9 virus in the lab will help drive efforts to develop pandemic drugs and vaccines Scientists have unveiled plans to genetically engineer a lethal strain of bird flu to understand how it could mutate in nature and trigger a catastrophic pandemic. The H7N9 bird flu virus has infected more than 130 people and killed 43 since it emerged in China in March. The first strong evidence that the virus can spread from person to person appeared in the British Medical Journal this week.

While the closure of poultry markets has brought the outbreak under control, researchers fear infections may rise again in the winter. As long as the virus is in circulation, it can transform into a strain that is more dangerous, through natural mutations or by mixing with other strains of bird flu in animals such as cattle and pigs. Scientists outlined their plans to work with the virus in joint letters to the journals Nature and Science on Wednesday. The 22 signatories include Ron Fouchier at Erasmus Medical Centre in Rotterdam and Yoshihiro Kawaoka at the University of Wisconsin-Madison. Work by the scientists on another strain of bird flu sparked security fears last year.

The controversial experiments are expected to make the H7N9 virus more virulent and increase its ability to spread between people. But researchers argue the work is crucial for public health because it will drive research into drugs and vaccines, and help identify dangerous mutations to watch out for in the wild. "The pandemic risk rises exponentially should these viruses acquire the ability to transmit readily among humans," the authors write. They go on to describe a raft of experiments that should reveal how the virus might adapt to humans, spread more rapidly, become more virulent and develop resistance to frontline drugs. Scientists already track mutations in bird flu viruses found in patients, but this kind of surveillance does not give health authorities time to respond if they find a pandemic strain. The proposed experiments should give scientists early warning of the kinds of mutations that could spark a pandemic.

The work will be done in high-security laboratories to minimise the risk of the modified viruses escaping and causing precisely the kind of devastation the research aims to prevent. Last year, the US government's biosecurity watchdog raised the alarm over similar work on another bird flu virus called H5N1. The panel feared that details of the experiments by Fouchier and Kawaoka could help terrorists create lethal viruses as bioweapons. Their papers were eventually published, but tougher review procedures have since been brought in by US authorities on "dual use research", along with updated guidelines to ensure the work is done under tight security. Fouchier told the Guardian that he and the other scientists announced their plans to be as open as possible about their research. Much of the work can continue under European funding without further scrutiny. Wendy Barclay, a virologist at Imperial College London, said it would be "ludicrous" not to do the experiments. "They allow us to see how the virus might evolve and what we can expect from nature," she said. "This type of work is like fitting glasses for someone who can't see well – without the glasses the vision is blurred and uncertain, with them you can focus on the world and deal with it a lot more easily."

Oxitocin : Is it finally that pure ?

It turns out the love hormone oxytocin is two-faced. Oxytocin has long been known as the warm, fuzzy hormone that promotes feelings of love, social bonding and well-being. It's even being tested as an anti-anxiety drug. But new Northwestern Medicine® research shows oxytocin also can cause emotional pain, an entirely new, darker identity for the hormone.

Oxytocin appears to be the reason stressful social situations, perhaps being bullied at school or tormented by a boss, reverberate long past the event and can trigger fear and anxiety in the future. That's because the hormone actually strengthens social memory in one specific region of the brain, Northwestern scientists discovered.

If a social experience is negative or stressful, the hormone activates a part of the brain that intensifies the memory. Oxytocin also increases the susceptibility to feeling fearful and anxious during stressful events going forward. (Presumably, oxytocin also intensifies positive social memories and, thereby, increases feelings of well being, but that research is ongoing.) The findings are important because chronic social stress is one of the leading causes of anxiety and depression, while positive social interactions enhance emotional health. The research, which was done in mice, is particularly relevant because oxytocin currently is being tested as an anti-anxiety drug in several clinical trials. "By understanding the oxytocin system's dual role in triggering or reducing anxiety, depending on the social context, we can optimize oxytocin treatments that improve well-being instead of triggering negative reactions," said Jelena Radulovic, the senior author of the study and the Dunbar Professsor of Bipolar Disease at Northwestern University Feinberg School of Medicine. The paper was published July 21 in Nature Neuroscience.

This is the first study to link oxytocin to social stress and its ability to increase anxiety and fear in response to future stress. Northwestern scientists also discovered the brain region responsible for these effects -- the lateral septum – and the pathway or route oxytocin uses in this area to amplify fear and anxiety. The scientists discovered that oxytocin strengthens negative social memory and future anxiety by triggering an important signaling molecule -- ERK (extracellular signal regulated kinases) -- that becomes activated for six hours after a negative social experience. ERK causes enhanced fear, Radulovic believes, by stimulating the brain's fear pathways, many of which pass through the lateral septum. The region is involved in emotional and stress responses.

The findings surprised the researchers, who were expecting oxytocin to modulate positive emotions in memory, based on its long association with love and social bonding. "Oxytocin is usually considered a stress-reducing agent based on decades of research," said Yomayra Guzman, a doctoral student in Radulovic's lab and the study's lead author. "With this novel animal model, we showed how it enhances fear rather than reducing it and where the molecular changes are occurring in our central nervous system.' The new research follows three recent human studies with oxytocin, all of which are beginning to offer a more complicated view of the hormone's role in emotions. All the new experiments were done in the lateral septum. This region has the highest oxytocin levels in the brain and has high levels of oxytocin receptors across all species from mice to humans. "This is important because the variability of oxytocin receptors in different species is huge," Radulovic said. "We wanted the research to be relevant for humans, too." Experiments with mice in the study established that 1) oxytocin is essential for strengthening the memory of negative social interactions and 2) oxytocin increases fear and anxiety in future stressful situations.

Experiment 1: Oxytocin Strengthens Bad Memories

Three groups of mice were individually placed in cages with aggressive mice and experienced social defeat, a stressful experience for them. One group was missing its oxytocin receptors, essentially the plug by which the hormone accesses brain cells. The lack of receptors means oxytocin couldn't enter the mice's brain cells. The second group had an increased number of receptors so their brain cells were flooded with the hormone. The third control group had a normal number of receptors. Six hours later, the mice were returned to cages with the aggressive mice. The mice that were missing their oxytocin receptors didn't appear to remember the aggressive mice and show any fear. Conversely, when mice with increased numbers of oxytocin receptors were reintroduced to the aggressive mice, they showed an intense fear reaction and avoided the aggressive mice.

Experiment 2: Oxytocin Increases Fear and Anxiety in Future Stress

Again, the three groups of mice were exposed to the stressful experience of social defeat in the cages of other more aggressive mice. This time, six hours after the social stress, the mice were put in a box in which they received a brief electric shock, which startles them but is not painful. Then 24 hours later, the mice were returned to the same box but did not receive a shock. The mice missing their oxytocin receptors did not show any enhanced fear when they re-entered the box in which they received the shock. The second group, which had extra oxytocin receptors showed much greater fear in the box. The third control group exhibited an average fear response.

Biological computer can decrypt images stored in DNA

Californian and Israeli researchers have created a biological computer — a machine made from biological molecules — that has successfully decoded two images stored and encrypted within DNA.

Storing data in DNA isn’t all that hard — its primary purpose is to store genetic data, after all — but creating a biological computer to decode those long strings of nucleotides is impressive. We’re not talking about a molecular computer that’s comparable to the CPU in your PC, though; rather, the scientists created a simple Turing machine-like finite state automaton. “Our biological computing device is based on the 75-year-old design by the English mathematician, cryptanalyst, and computer scientist Alan Turing,” says Ehud Keinan who led the research.

In the original Turing machine, a long strip of paper contains data and instructions. The data is fed into the machine, and rules (software) decide what kind of computation is done to the data. Basically, Keinan and co created a mixture of molecules in a test tube that were capable of performing the same, repeatable set of instructions on a helix of DNA. Encoded DNA goes into the biological computer and decoded DNA comes out the other. To track the progress of the machine, the DNA was tagged with fluorescent markers.For example its like having this encrypted code :

CODE HERE

and you want to decrypt this! The end result is a biological computer that can take an encoded image (left) and decode it into fluorescent images (right). The power source, in case you’re wondering, is ATP — the same adenosine triphosphate that powers the metabolism of every cell in your body.

Decoding DNA with biological molecules As far as the applications of biological computers go, the jury’s still out. Molecular computers are nothing like digital computers: Where a CPU generally processes data in a linear fashion, biological systems are basically a huge mess of chemical reactions that occur autonomously and without much in the way of timing. As such, biological computers are massively parallel. Molecular computers are also incredibly specialized: You can’t make a molecular CPU (at least not yet!); you have to carefully craft a mixture of molecules that perform a very specific task. It’s unlikely, at least for the time being, that biological computers will ever replace general purpose digital computers.

Still, it’s impossible to ignore that these systems are completely biological. There’s no electricity, no silicon, no external display; we’re storing usable data in DNA and processing it using molecules. Who’s to say that, one day, we won’t have a biotech implant that reads (or rewrites!) our DNA when needed? Imagine a future where you can store data in your bloodstream…

Advance in regenerative medicine could make reprogrammed cells safer while improving their function

The enormous promise of regenerative medicine is matched by equally enormous challenges. But a new finding by a team of researchers led by Weill Cornell Medical College has the potential to improve both the safety and performance of reprogrammed cells.

The researchers' study, published in today's issue of the journal Nature, found that an enzyme, activation-induced cytidine deaminase (AID), helps in the process that changes an adult human cell into an induced pluripotent stem cell (iPS cell). These iPS cells can then be developed into any kind of cell needed to therapeutically restore tissues and organs. The finding settles an ongoing controversy regarding use of AID to reprogram cells, says the study's senior investigator, Dr. Todd Evans, vice chair for research and professor of cell and developmental biology in the Department of Surgery at Weill Cornell Medical College. "The dispute was whether AID is required to make iPS cells, and we found that the enzyme does make reprogramming very efficient, although it is not absolutely necessary," says Dr. Evans, an internationally-recognized authority on regenerative medicine. "In fact, we plan to test if reprogramming iPS cells without AID may even be helpful." One reason is that AID can cause genetic mutations that can lead to cancer. AID is best known as a master regulator of antibody diversity in B cells, and in order to create varied types of beneficial antibodies, it routinely mutates antibody genes. But sometimes the process goes awry, resulting in development of B cell lymphoma, Dr. Evans says. "That leads us to believe that if you can reprogram cells without AID, it could reduce risk of potential mutations, and thus be safer."

iPS Cells Without AID Remember What They Once Were In order to push a cell, such as a fibroblast, to revert to an iPS cell, the epigenetic "markers" that define an adult cell must be removed. "All cells of the body have the same genes, but they are used differently in different tissues," Dr. Evans explains. "If an undifferentiated cell becomes a heart cell, somehow it has to lock in and stabilize that particular adult phenotype and not forget what it is."

One way that function is accomplished is by placing a methylation group on top of certain genes that activate other cell destinations -- such as to become a liver cell -- usually switching those genes off. "We have known how these marks are put on genes, but we didn't know how they were taken off in the process of pushing an adult cell to revert back to a stem-cell-like state," Dr. Evans says. Dr. Evans and his colleagues found that the AID enzyme removed those epigenetic markers. They then created a mouse that did not produce AID to see if the animal's adult fibroblast cells could be pushed back to iPS cells. "If you need AID to reprogram the cells, you shouldn't be able to do it, or do it well." Surprisingly, they found that the cells at first seemed to want to reprogram even faster than normal cells, but most never fully reverted to a stem-cell-like state. "They eventually crashed and differentiated back into a fibroblast," Dr. Evans says. "What that meant is that they never cleared their memory of being a fibroblast cell. AID efficiently removes that epigenetic memory, smoothing the way for a cell to morph into an undifferentiated state." But some of the mouse adult fibroblasts lacking AID -- those that Dr. Evans says they "babysat" -- did become iPS cells. Despite the fact that reprogramming adult cells without AID is inefficient, the researchers say that the method may offer another advantage besides increased safety.

"It might be useful to allow epigenetic memory to be retained," Dr. Evans says. "If you want to make new cardiac cells to repair a patient's heart, it might be better to start with a cardiac cell and push it to become an iPS cell, from which other cardiac cells could be made. If these cells remember they were cardiac cells, they might make a better heart cell than if they came from reprogrammed fibroblasts." The study was supported by National Institutes of Health grants (HL056182 and AI072194) and a National Science Foundation CAREER grant (1054964). Other study co-authors include Ritu Kumar, Ting-Chun Liu, Philipp Franck and Olivier Elemento from Weill Cornell Medical College; Lauren DiMenna, Nadine Schrode, Silvia Muñoz-Descalzo, Anna-Katerina Hadjantonakis and Jayanta Chaudhuri from Memorial Sloan-Kettering Cancer Institute; and Ali A. Zarrin from Genentech.