Day: 09/14/2015

Researchers identify the longevity genes that may keep some life-long smokers healthy

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The golden ticket.

Smoking is bad for us. We know that. We also know that it’s one of the leading causes of death for people around the world. Not smoking, all told, is a pretty clever thing for you to do.

But for a small minority of very lucky people, smoking doesn’t seem to cause all the life-shortening illnesses that threaten most other smokers. Indeed, some of the world’s oldest people reach extreme ages while being smokers. The world’s documented longest-living person, Jeanne Calment, was a smoker for most of her life, and another claimant to the title is said to smoke a pack a day. What’s their secret?

According to new research, the lifespans of such long-living smokers aren’t a coincidence. A study published in The Journals of Gerontology, Series A: Biological Sciences & Medical Sciences this month has found that SNP (single nucleotide polymorphism) sequences of DNA in some people appears to help them better withstand and mitigate the environmental damage caused by long-term smoking.

“We identified a set of genetic markers that together seem to promote longevity,” said Morgan E. Levine, corresponding author of the study, in a press release. “What’s more, many of these markers are in pathways that were discovered to be important for ageing and lifespan in animal models.”

The researchers sequenced the genomes of 90 long-lived smokers who lived past 80 years of age – “a group whose survival may signify innate resilience” – and contrasted them with the genomes of 730 smokers who died before they reached 70.

They identified a network of SNPs in genes that conferred significant anti-ageing benefits, offering those with the longevity genes effectively a 22 percent increase in the likelihood of reaching 90–99 years of age, and a threefold increase in the likelihood of becoming a centenarian. And those same genes are associated with an almost 11 percent lower cancer prevalence.

“There is evidence that these genes may facilitate lifespan extension by increasing cellular maintenance and repair,” said Levine. “Therefore, even though some individuals are exposed to high levels of biological stressors, like those found in cigarette smoke, their bodies may be better set up to cope with and repair the damage.”

The researchers conclude that long-lived smokers may represent a “biologically distinct group, endowed with genetic variants allowing them to respond differentially to environmental stressors”.

As Levine told Ariana Eunjung Cha of The Washington Post, in the future it’s quite possible that individualised testing will be available to consumers to help them determine whether they carry the genetic markers that could help them resist the effects of ageing and stave off illnesses.

But there’s a limit to how much the knowledge will do for them.

“[The proportion] of people who have a ‘genetic signature’ that would help them cope with the biological stresses of smoking is extremely small, and therefore, nobody should use this paper as an excuse to continue smoking,” he said.

Physicists figure out how to make ‘molecules’ of pure light.

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But no lightsabers yet, sorry.

Physicists have just gotten us a little closer to the dream of building objects out of pure light – hello, lightsabers – by figuring out how to join weightless light particles together to form a kind of ‘two-atom molecule’ with its own, strange type of force.

“It’s not a molecule per se, but you can imagine it as having a similar kind of structure,” one of the researchers, Alexey Gorshkov from the University of Maryland in the US said in a press release. “We’re learning how to build complex states of light that, in turn, can be built into more complex objects. This is the first time anyone has shown how to bind two photons a finite distance apart.”

Before you get too excited, the technique is purely theoretical at this stage, but it shows how two light particles – or photons – can travel in waves towards each other before being locked together at just a short distance apart. This would allow them to travel together at all times, with a set distance between them.

The idea is based on previous research that showed how two photons could be joined – one superimposed on top of the other – as they travelled through a gas. By adjusting certain aspects of the binding process, Gorshkov and his colleagues have now repositioned the photons to be side-by-side as they travel, just like how two hydrogen atoms sit next to each other in a hydrogen molecule.

So when can we build things out of it? The challenge in actually putting this technique into practice is creating the conditions needed to bind the photos together.

For example, when scientists first achieved photon-binding back in 2013, they had to fire pairs of photons – blue laser light with the specific wavelength of 479 nm – through an ultracold gas made from rubidium atoms. This slowed them down and facilitated an attraction between the two and caused the photons to stick together and become quantum-mechanically entangled. And figuring out how to arrange all of this in the handle of a lightsaber isn’t exactly feasible… yet.

Hamish Johnston from Physics World explains:

“Getting photons to stick together is not easy because they normally pass through each other without interacting. However, a photon has an associated electromagnetic field that can modify its surrounding medium. These changes can affect nearby photons and create an effective interaction between them. Although this effect is usually tiny, the interactions can be significant if the medium is chosen carefully.”

A more likely application, says Gorshkov, is in computing, as scientists around the world race to develop computer chips that can deliver information at light-speed. “Light is the fastest thing you can use to transmit information,” says Rajesh Menonfrom the University of Utah in the US, who has been working on a new type of silicon chip for light-based computers. “But that information has to be converted to electrons when it comes into your laptop. In that conversion, you’re slowing things down. The vision is to do everything in light.”

By binding and entangling photons, scientists could turn them into information processors, which means that final, time- and energy-sapping step of converting the light beams that carry our phone messages and other data into electrons can be completely bypassed. “They’re massless and fly at the speed of light,” Gorshkov says of photons. “Slowing them down and binding them may show us other things we didn’t know about them before.”

Releasing the Brakes on Cancer Immunotherapy

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After mapping out the molecular mechanisms of T-cell antigen recognition, regulation, and function in the 1980s and 1990s, immunologist James P. Allison hypothesized that blocking negative immune regulators (checkpoints) would give the human immune system the power to fight cancer. His testing of this hypothesis in preclinical models led to the clinical development of a new generation of active agents for cancer treatment. In some subgroups of patients, unleashing native immune-system cells to fight cancer now provides a realistic chance of long-term remission. For this seminal work, Allison, a professor at the M.D. Anderson Cancer Center in Houston, has won the 2015 Lasker–DeBakey Clinical Medical Research Award, announced on September 8.

It had been known for more than a century that occasionally when there was evidence that a patient’s immune system had attacked a metastatic cancer, a long-lasting remission occurred. But for a long time, although scientists were aware of the immune system’s role, they had no mechanistic understanding of why the immune system worked in a particular patient and why the immune responses could not reliably be repeated. Recognizing the great success of vaccines in preventing infectious diseases, cancer researchers tested multiple vaccines made up of inactivated cancer cells and tried injecting infectious agents into tumors, with the hope of activating the immune system against the cancer. But evidence of clinical responses to these approaches was mostly anecdotal.

Knowledge of immune-system regulation improved over time and led to the testing of recombinant cytokines, such as interferons and interleukin-2, for activating the immune system against cancer. With these agents, tumor responses became more reproducible and sometimes durable, but they were infrequent (achieved in 5 to 10% of patients) and occurred in very few types of cancers, such as melanoma and renal-cell carcinoma.

Nevertheless, these initial clinical experiences showed that immunotherapy had potential in cancer treatment. Further progress would hinge on an understanding of how immune-system cells recognize cancer cells and are regulated to kill them. In his early scientific career, Allison made important contributions to elucidating the rules of T-cell activation, including defining the structure of the T-cell receptor (TCR) that specifically recognizes antigens1 and demonstrating that the T-cell molecule CD28 provides costimulatory signals necessary for full T-cell activation.2 The TCR and the CD28 molecule are the molecular basis of what we know as immunologic signal 1 (TCR recognition of antigens) and immunologic signal 2 (costimulation), respectively. Both are required to license T cells to specifically kill their target cells T-cell Activation in the Lymph Node.).

But solving the puzzle of how an immune response can lead to the eradication of cancer also required understanding how the immune system is specifically activated by certain antigens mostly foreign to the body, rather than by endogenous antigens. Allison then described the inhibitory function of the checkpoint molecule cytotoxic T-lymphocyte–associated protein 4 (CTLA-4), which blocks immunologic signal 2 and thereby prevents T cells from becoming fully activated. In a series of studies in preclinical models, he demonstrated that blocking CTLA-4 with therapeutic antibodies could unleash an immune response against cancer (Figure 1B).3 With these studies, Allison shifted the paradigm from attempting to activate the immune system (i.e., vaccinating) to releasing the checkpoints that keep it in a negative regulatory mode.

Checkpoint-blockade immunotherapy has arguably been the most exciting advance made in cancer treatment in recent years. High on the list of scientific achievements in the fight against cancer, it has joined the ranks of radical surgery, radiation therapy, chemotherapy, endocrine therapy, and targeted oncogene therapies. Blockade of CTLA-4 with the monoclonal antibody ipilimumab was the first treatment to improve overall survival in patients with metastatic melanoma and has gained worldwide approval for the treatment of that cancer. Further insights into the release of immune inhibitory checkpoints led to the strategy of “releasing” the programmed cell death 1 (PD-1) receptor on T lymphocytes, from which cancer cells protect themselves by expressing the PD-1 ligand 1 (PD-L1).

T-cell Activation in Tumor Milieu.).4 Antibodies blocking PD-1 or PD-L1 are in clinical development for the treatment of more than 30 types of cancer, and pembrolizumab and nivolumab, two antibodies blocking PD-1, have gained approval for the treatment of metastatic melanoma and lung carcinoma. Combining CTLA-4 and PD-1 blockade provides even higher response rates than either approach alone in patients with advanced melanoma,5highlighting the potential of combination immunotherapy based on blocking immune checkpoints to push the limits of what the immune system can achieve.

In the history of cancer treatment, there will be a full chapter dedicated to unleashing the immune system by releasing its negative regulatory checkpoints. That chapter will start with the seminal studies by Allison involving blocking CTLA-4 in mouse models. As the successful clinical development of ipilimumab and PD-1 and PD-L1 blocking antibodies has shown, Allison’s early insight was correct: “What we needed to do was to release the brakes of the immune system to fight cancer.” The obvious risk as we push the limits of this approach to cancer treatment is the appearance of autoimmune side effects, which can be serious. But by learning how to safely utilize combinations of immune activators and checkpoint inhibitors, we should be able to expand the potential of immunotherapy for cancer.

Indian scientists decode Tulsi plant genome

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The plant synthesises a wide range of bioactive compounds, known for their anti-bacterial, anti-fungal, anti-pyretic and anti-cancer properties. Image courtesy: Facebook

 

Indian scientists have deciphered the entire genetic make-up of Tulsi, a herb widely used for therapeutic purposes. The genome map will help in making new medicines using the plant.

A multi-institutional team led by Sowdhamini Ramanathan from the National Centre of Biological Science, Bengaluru revisited the age-old knowledge of the plant and its medicinal effects in their laboratories.

The plant synthesises a wide range of bioactive compounds, known for their anti-bacterial, anti-fungal, anti-pyretic and anti-cancer properties.

These compounds are metabolites, compounds that are a by-product of plant metabolism, typically used for plant self-defence. These metabolites are very poorly understood because of lack of genomic information.

Sowdhamini and team have produced the first draft genome of O. tenuiflorum Krishna subtype, which is an important step in understanding and identifying the genes responsible for production of metabolites with medicinal properties.

“The sequence reveals the interesting pathways used by Tulsi to make ursolic acid a medically important compound.AIf one could now use modern synthetic biology techniques to synthesise ursolic acid, it would be of great benefit,” said S. Ramaswamy, one of the researchers.

Sowdhamini said, “This is the first report of draft genome sequencing of a plant species from NCBS and we hope to do more”. – See more at: http://m.deccanherald.com/content/500915/indian-scientists-decode-tulsi-plant.html/#sthash.u8qpJr05.dpuf

Marine Life Needs Protection from Noise

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An international group of scientists is calling for stricter regulations to protect marine wildlife from noise pollution. In a study published last week in the journal Frontiers in Ecology and the Environment, researchers argue that action is needed to tackle excessive ocean noise from industrial activities such as shipping and seismic surveys, which use loud sound pulses fired from compressed air guns to explore the sea floor and find natural resources.

Nature asked two authors of the study, conservation ecologists Douglas Nowacek at the Duke University Marine Laboratory in Beaufort, North Carolina, and Howard Rosenbaum at the Wildlife Conservation Society in New York City, why this is such an urgent problem. This interview has been edited for length and clarity.

How does noise pollution harm marine life?

Douglas Nowacek (DN): One concern is hearing damage in animals. That can happen either with very loud sounds or over longer periods of exposure to lower levels of noise. Also, with air guns, the reverberations raise the background noise level and so risk masking animals’ communication and navigation signals. A final concern is stress. Short-term stress is not that big a deal, but long-term stress is really detrimental. It causes physiological and reproductive problems; and we don’t know a lot about how sensitive marine animals are to it.

Howard Rosenbaum (HR): Effects have been documented across a range of species, from bowhead whales in the Arctic and sperm whales in the Gulf of Mexico, to herring in the North Sea. There are still questions out there about what these impacts mean in the long term for individual animals or populations, but there’s an increasing body of evidence.

Don’t industries already have to take measures to limit possible damage to marine life?

HR: The requirements vary from region to region. In many places around the world, surveyors must slowly ramp up the air-gun strength at the beginning of a survey, to warn off animals in the area, but we really don’t know how effective this practice is. Surveyors might be required to limit their operations in areas where endangered animals are present or have been previously observed, and shut down if animals enter a certain zone. The overall benefits from many of these measures are still really unknown. We feel that more needs to be done to safeguard marine species and their most important habitats.

What do you suggest?

DN: First, we are calling for restrictions on activities in biologically sensitive habitats, based on data. In an ideal world, you would want to have a good inventory of data on the marine animals present in a region and when these animals breed, spawn and feed. Then you would use that information to decide when to survey, and check afterwards whether there had been any unforeseen outcomes. Second, we want overall noise limits based on monitoring that counts cumulative contributions to noise. The Australian Ocean Data Network Portal is a good example of this kind of data collection. The European Union has proposed putting limits on overall noise, but the United States doesn’t consider the cumulative impact of all activities when giving out survey permits.

HR: Third, there are already new techniques that use steady streams of energy at lower levels than air guns and which might help to reduce risks to marine species. Fourth, we think that intergovernmental science coordination is critical because it’s a transboundary problem. Finally, we want to see the effects of cumulative noise incorporated into environmental-impact assessments.

Should some seismic surveying be banned?

DN: No. For the foreseeable future, seismic is a tool being used to find oil and gas at sea and, at lower amplitudes, to site wind farms, but you need to use it wisely. In the United States, the issue of redundant surveys is ridiculous. I can tell you from my experience of being out on the water in the Gulf of Mexico—on any given day, there may be 6, 8, 10 or 12 surveys going on nearby.

For the Atlantic, the US authorities are considering whether to permit multiple companies to carry out exploratory seismic surveys off the coast. One of the affected regions near Cape Hatteras happens to be the most diverse and richest area for cetaceans in the northwest Atlantic. To go out there and survey the same piece of water over and over again is ridiculous. Norway has instituted multi-client surveys, in which companies that are interested in seismic data from a particular area get together so that only one survey is done.

How will you persuade the international community to agree on regulations?

DN: The EU’s Marine Strategy Framework Directive is trying to limit overall noise to a certain level, taking into account all sources. They are currently taking an inventory of shipping noise in many areas, with plans to then seek methods to reduce the noise, particularly in biologically sensitive areas. We are earnestly looking for a forum, or a way to start talking about this and to create some standards internationally. One possible way of creating a legally binding instrument to restrict noise pollution to an acceptable level is to add an annex for noise pollution to MARPOL [the International Convention for the Prevention of Pollution from Ships], similar to the newly added annex on air pollution.

Do you think industry and regulatory authorities will agree with your recommendations?

HR: We are presenting peer-reviewed science that shows the extent of the issue. Industry or governments may not fully agree with what we suggest is a responsible way forward, but it’s something that we feel could be very beneficial for industry and regulators as well—especially a standard set of ‘best practices’ for mitigating impacts on marine species and their habitats.

Scientists have developed a shark-repelling device for your surfboard

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Scientists have developed a shark-repelling device for your surfboard

Thank you, science.

 

Researchers have developed an electronic device that you can attach to your surfboard or wear while swimming to help deter sharks. The aim is to harmlessly mess with the animals’ electroreceptive system, and studies so far have shown that they can prevent more than 90 percent of shark encounters.

Before you all rush off to buy one, let’s get one thing straight: shark attacks are incredibly rare, with on average just 75 being reported worldwide every year. That means you have on average a roughly one in 11.5 million chance of being attacked by a shark (and if you rarely swim more than 25 metres out from the beach, it’s even lower than that) – which is far less than your risk of dying from home repairs or, say, a bicycle-related injury.

But despite all of us very sensible people knowing that we’re probably not going to be attacked by a shark in our lifetimes, we can’t help but be terrified by the idea of it. Which is why scientists have been working for decades on humane ways to repel the animals.

Several countries, including Australia, have experimented with culling sharks in the past to see if that would help to reduce shark attacks. But not only is the practice inhumane and bad for the environment – we already wipe out around 100 million of these crucial apex predators every year for their fins – it actually doesn’t do anything to reduce attacks.

So researchers have been looking for ways we can use the animals’ biology to keep them away without having to harm them. What’s unique about sharks is that they have two extra senses that we don’t have that allow them to hunt underwater – the ability to sense both vibrations and electrical fields through a network of sensors in their heads.

It’s this second sense that the shark repelling devices target, by sending out electromagnetic pulses that aim to make a shark uncomfortable and confused so it moves away from the area.

There are a couple of these devices on the market at the moment, but the one that’s been the most widely and independently tested is the Shark Shield, which was developed in Western Australia. The device is made up of two electrodes that emit a 3D electronic field once they’re submerged in water.

The electronic field causes sharks to experience muscle spasms in their snouts the closer they get to the device. Researchers have tested this on reef and great white sharks in the wild using bait, and found that 100 percent of sharks ate bait that was left unprotected, while only 10 percent took it if it was protected by the Shark Shield.

Scientists at the University of Western Australia are now fine-tuning the frequency of the device in the lab, using embryonic bamboo sharks, which mature in an egg case outside their mother’s body. This allows scientists to test which frequencies affect the sharks the most – they’ve even managed to find one that makes sharks play dead.

There are a few different models of Shark Shield – all of which retail upwards of A$600 – including one that attaches to the bottom of a surfboard and one that can be worn around a swimmer’s ankle. But despite the promising results so far, it’s hard to know how effective these types of devices will be in the long run.

“The natural reaction of sharks, when they first detect something they aren’t familiar with – such as one of these electrical pulses – is to turn away,” shark researcher Ryan Kempster from the University of Western Australia’s Ocean Institute told Simon White from The Sydney Morning Herald back in 2012. “But we don’t know yet whether that reaction stays the same for the fourth time or the fifth time.”

The other issue is that sharks can only detect electric fields from around 50 cm away, which means that sharks can still get pretty close before being repelled by the device.

Still, it’s promising research that will hopefully help people feel safe in the water again – without having to kill or harm a crucial part of our ocean ecosystems.

Watch the video. URL:https://youtu.be/ZlI-e2NA1Ic