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Genetically Engineered Pigs Could Be The Organ Donors Of The Future

Genetically Engineered Pigs Could Be The Organ Donors Of The Future | Amazing Science | Scoop.it

According to the US Department of Health and Human Services more and more people are waiting for a lifesaving organ transplant each year. At this time 122,407 people need a new organ for survival. The statistics look pretty grim because on average 22 people die each day while waiting for a transplant and every 10 minutes a new person is added to the national transplant waiting list.


Scientists are looking to find an alternative tissue source and it seems that they are close to finding one. The research is called xenotransplantation research and it is making good progress. Xenografts (tissue or organs that are transplanted into or grafted from an organism of one species into an organism of another species) are not new because a very common example of this is the use of pig heart valves in humans. But the new research takes it a step further and tries to get more pig organs available for humans.


A peer reviewed paper has just recently been published in the Journal of the International Xenotransplantation Association where the researchers show that they were able to keep a pig kidney alive in a baboon for 136 days which is a record for a life-supporting organ graft survival to date. The researchers also claim that they were able to keep a pig heart alive in a baboon for 945 days, but that research hasn’t been published yet.


The researchers have reported that they were able to achieve this by humanizing the pigs with adding as many as five human genes to them. This is being done to diminish and even stop organ rejection in the organism that is accepting the new organ. Organ rejection is one of the biggest problems with animal organ transplants because it sets of a very strong immune response and the scientists hope to prevent such a response with the use of genetically modified animals. Bruno Reichart, a professor at the University of Munich, called the survival of these pig hearts “a major breakthrough.”

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Technology demonstrated for first time: Device delivers drugs to brain via remote control​​

Technology demonstrated for first time: Device delivers drugs to brain via remote control​​ | Amazing Science | Scoop.it

A team of researchers has developed a wireless device the width of a human hair that can be implanted in the brain and activated by remote control to deliver drugs.


The technology, demonstrated for the first time in mice, one day may be used to treat pain, depression, epilepsy and other neurological disorders in people by targeting therapies to specific brain circuits, according to the researchers atWashington University School of Medicine in St. Louis and the University of Illinois at Urbana-Champaign.


The research is a major step forward in pharmacology and builds on earlier work in optogenetics, a technology that makes individual brain cells sensitive to light and then activates those targeted populations of cells with flashes of light. Because it’s not yet practical to re-engineer human neurons, the researchers made the tiny wireless devices capable of delivering drugs directly into the brain, with the remote push of a button.


“In the future, it should be possible to manufacture therapeutic drugs that could be activated with light,” said co-principal investigator Michael R. Bruchas, PhD, associate professor of anesthesiology and neurobiology at Washington University. “With one of these tiny devices implanted, we could theoretically deliver a drug to a specific brain region and activate that drug with light as needed. This approach potentially could deliver therapies that are much more targeted but have fewer side effects.”


Previous attempts to deliver drugs or other agents, such as enzymes or other compounds, to experimental animals have required the animals to be tethered to pumps and tubes that restricted their movement. But the new devices were built with four chambers to carry drugs directly into the brain. By activating brain cells with drugs and with light, the scientists are getting an unprecedented look at the inner workings of the brain.


“This is the kind of revolutionary tool development that neuroscientists need to map out brain circuit activity,” said James Gnadt, PhD, program director at the National Institute of Neurological Disorders and Stroke at the National Institutes of Health (NIH). “It’s very much in line with the goals of the NIH’s BRAIN Initiative.”

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HIV spreads like computer worms, say scientists

HIV spreads like computer worms, say scientists | Amazing Science | Scoop.it

HIV spreads throughout the body in a similar way to some computer worms, according to a new model, which also suggests that early treatment is key to finding a cure to the disease.


HIV specialists and network security experts at University College London (UCL) have found that HIV progresses both via the bloodstream and directly between cells – akin to computer worms spreading themselves through two routes to infect as many computers as possible.


Prof Benny Chain, from UCL’s infection and immunity division, the co-senior author of the research, said: “I was involved in a study looking in general at spreading of worms across the internet and then I realised the parallel. They have to consistently find another computer to infect outside. They can either look locally in their own networks, their own computers, or you could remotely transmit out a worm to every computer on the internet. HIV also uses two ways of spreading within the body.”


The model was inspired by similarities between HIV and computer worms such as the highly damaging “Conficker” worm, first detected in 2008, which has infected military and police networks across Europe and is still active today.


The researchers’ findings, published on Thursday, told them that just as computer worms spread most efficiently by a combination of two routes, so must HIV – enabling the researchers to create a model for this “hybrid spreading”, which accurately predicted patients’ progression from HIV to Aids.


Detailed sample data from 17 HIV patients from London were used to verify the model, suggesting that hybrid spreading provides the best explanation for HIV progression and highlighting the benefits of very prompt treatment.


Chain said the model provided strong evidence of cell-to-cell spread, which he said some HIV scientists remained sceptical about, as it is difficult to observe in human beingsbecause it occurs in tissue.

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Scientists hope computer modelling can help predict flu outbreaks

Scientists hope computer modelling can help predict flu outbreaks | Amazing Science | Scoop.it

There’s no shortage of experts monitoring influenza outbreaks around the globe. The Centers for Disease Control and Prevention tracks flu activity in the United States year-round and produces weekly flu activity reports between the peak months of October to May. Likewise, the World Health Organisation constantly gathers epidemiological surveillance data, and releases updates on outbreaks taking place anywhere, anytime.


Still, despite the monitoring and the annual push to administer flu vaccines, influenza sickens millions of people around the world each year, leading to as many as 500,000 deaths annually. Young children and the elderly in particular are at risk. But what if we were better at predicting – and preparing for – seasonal outbreaks.That’s the impetus driving a team of researchers trying to show that it is possible to predict the timing and intensity of flu outbreaks in subtropical climates, such as Hong Kong, where flu seasons occur at irregular intervals throughout the year. The group, which includes scientists from Columbia University and the University of Hong Kong, has created a computer model to run various simulations of an outbreak and predict its magnitude and peak, according to a study published in the journal PLOS Computational Biology.


As a test case, the researchers gathering flu data from dozens of outpatient clinics and lab reports in Hong Kong between 1998 and 2013, then explored whether their system could accurately predict how outbreaks played out during those years. They said the program did remarkably well at predicting the peak of an outbreak several weeks in advance.


That’s not to say it was perfect. Researchers said the accuracy of the predictions varied, depending on the strength of an outbreak and how far in advance they tried to make a prediction. In addition, forecasts for specific strains of influenza proved more reliable than those for overall epidemics, and it was easier to predict the peak and magnitude of an outbreak than exactly when it would begin or how long it might last.

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New Nanotech Device Will Be Able To Target And Destroy Blood Clots

New Nanotech Device Will Be Able To Target And Destroy Blood Clots | Amazing Science | Scoop.it

One problem following a heart attack incident or a stroke is the presence of blood clots. These can make the severity of the condition worse or can trigger a recurrence. Medical procedures to address these life-threatening events need to be carried out in specialist hospital units and, in some cases due to the risk of internal bleeding, they cannot be performed. A blood clot is technically known as a venous thromboembolism (VTE). It is a serious medical condition and some groups of people are more at risk than others.


A research group have come up with a novel method based on nanotechnology to deal with blood clots. The method is easy to administer and it could be potentially given by medical staff on arriving to deal with a medical issue.


The developed device is a nanoparticle packed with a clot destroying compound. The outer shell of the nanoparticle is equipped with an antibody that is designed to target activated platelets (the cells that form blood clots.) The nanoparticles are given the lengthy name “poly(2-oxazoline) (POx)-based multifunctional polymer capsules.”


Once the nanoparticle reaches the blood clot, thrombin (a molecule at the center of the clotting process) breaks the shell of the nanocapsule. This releases the drug that wipes out the blood clots and prevents blockage to a blood vessel.


Speaking with International Business Times, lead researcher Professor Hagemeyer said of the nanoparticle method: “This can be given in the ambulance straight away so you really save a lot of time and restore the blood flow to the critical organs much faster than currently possible.” The nanotech device is at the early design stage. However, trials on animals have been successful and the objective is to move to human trials in the near future.


The research was carried out between Baker IDI Heart and the University of Melbourne. The study was funded by the National Heart Foundation of Australia. The findings have been published in the journal Advanced Materials, in a paper headed “Multifunctional Thrombin-Activatable Polymer Capsules for Specific Targeting to Activated Platelets.”

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Control of signaling-mediated clearance of apoptotic cells by the tumor suppressor p53

Control of signaling-mediated clearance of apoptotic cells by the tumor suppressor p53 | Amazing Science | Scoop.it

Programmed cell death occurs throughout life in all tissues of the body, and more than a billion cells die every day as part of normal processes. Thus, rapid and efficient clearance of cell corpses is a vital prerequisite for homeostatic maintenance of tissue health. Failure to clear dying cells can lead to the accumulation of auto-antigens in tissues that foster diseases, such as chronic inflammation, autoimmunity, and developmental abnormalities. In the normal immune system, phagocytic engulfment of apoptotic cells is accompanied by induction of a certain degree of immune tolerance in order to prevent self-antigen recognition. Over the past few decades, enormous efforts have been made toward understanding various mechanisms of tumor suppressor p53–mediated apoptosis. However, the involvement of p53 in post-apoptosis has yet to be addressed.


One of the most intriguing, yet enigmatic, questions in studying homeostatic control of efficient dead cell clearance and proper immune tolerance is how these two essential activities are interrelated: The complexity of these processes is demonstrated by the many receptors and signaling pathways involved in the engulfment of apoptotic cells and stringent discrimination of self antigens from non-self antigens. Thus, there must be key connection(s) linking the balance between immune homeostasis and inflammation. In addition to the anti-tumor functions of p53, p53 has been implicated in immune responses and inflammatory diseases, with various roles in the immune system becoming apparent. We identified a post-apoptotic target gene of p53, Death Domain1α(DD1α), that is responsive to genotoxic stresses and expressed in immune cells. DD1α appears to function as an immunoregulator of T cell tolerance. p53 controls signaling-mediated phagocytosis of apoptotic cells through its target, DD1α. A group of scientists now determined that DD1α functions as an engulfment ligand or receptor that is involved in homophilic intermolecular interaction at intercellular junctions of apoptotic cells and macrophages. They also investigated whether DD1α deficiency caused any defects in dead cell clearance in vivo.


The researchers found that DD1α has similarity with several members of the immunoglobulin superfamily with the extracellular immunoglobulin V (IgV) domain, such as TIM family proteins and an immune checkpoint regulator, PD-L1. They also found that the p53 induction and maintenance of DD1α expression in apoptotic cells and its subsequent functional intercellular homophilic interaction between apoptotic cells and macrophages are required for engulfment of apoptotic cells. DD1α-deficient mice showed less reduction in organ size and cell number after ionizing radiation (IR), owing to defective dead cell clearance. DD1α-null mice are viable and indistinguishable in appearance from wild-type littermates at an early age. However, at a later age, DD1α deficiency resulted in the development of autoimmune phenotypes and prominent formation of immune infiltrates in the skin, lung, and kidney, which indicated an immune dysregulation and breakdown of self-tolerance in DD1α-null mice. The team demonstrated that DD1α also plays an important role as an intercellular homophilic receptor on T cells, which suggests that DD1α is a key-connecting molecule linking postapoptotic processes to immune surveillance. DD1α deficiency in T cells impaired DD1α-mediated inhibitory activity of T cell proliferation. These data indicate that potential homophilic DD1α interactions are important for the DD1α-mediated T cell inhibitory role. Therefore, the results indicate a role for p53 in regulating expression of immune checkpoint regulators, including PD-1, PD-L1, and DD1α.

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Tiny laser cells reveal cancer mechanisms

Tiny laser cells reveal cancer mechanisms | Amazing Science | Scoop.it

Researchers at the University of St Andrews, Scotland, UK, are claiming a photonics-based breakthrough in biomedicine; having successfully tracked a day-in-the-life of a number of white blood cells by feeding them microlasers, according to a research report published in Nano Letters The technique is expected to allow new insights into how cancers spread in the human body.


The Soft Matter Photonics Group led by Professor Malte Gather of the School of Physics and Astronomy, in collaboration with immunologists in the University’s School of Medicine, found that by “swallowing” an optical micro-resonator, cells gain the ability to produce green laser light.


Research groups around the world have worked on lasers based on single cells for several years now. However, all previously reported cell lasers required optical resonators that were much larger than the cell itself, meaning that the cell had to be inserted into these resonators. By drastically shrinking resonator size and exploiting the capability of cells to spontaneously take up foreign objects, the latest work now allows generation of laser light within a single living cell.


Dr Gather said, “This miniaturization paves the way to applying cell lasers as a new tool in biophotonics. In the future, these new lasers can help us understand important processes in biomedicine. For instance, we may be able to track—one by one—a large number of cancer cells as they invade tissue or follow each immune cell migrating to a site of inflammation.”


He continued, “The ability to track the movement of large number of cells will widen our understanding of a number of important processes in biology. For instance being able to see where and when circulating tumor cells invade healthy tissue can provide insight into how cancers spread in the body which would allow scientists to develop more targeted therapies in the future.”


The investigators put different types of cells onto a diet of optical "whispering gallery" micro-resonators. Some types of cells were particularly quick to ‘swallow’ the resonators; macrophages—immune cells responsible amongst other things for ‘garbage collection’ in our body—internalized the resonators within less than five minutes. However, even cells without particularly pronounced capacity for endocytosis readily internalized the micro-resonators, showing that laser barcodes are applicable to many different cell types.


What are future objectives?

Dr Gather believes these self-contained cell lasers have great potential to become a widely used tool in biology. Conventional fluorescent tags have rather broad emission spectra which means that one can only distinguish a limited number of different tags. The narrow spectrum of the cell laser facilitates distinguishing hundreds of thousands of different tags. The availability of such a tool will lead to new insights in cancer research as it would allow one to monitor how the cells from a tumor form metastasis, providing single cell resolution; i.e. one could see exactly which cells and how many cells from a primary tumor invade healthy tissue and form a new tumor site. The objectives are to develop the technology further, by confirming accuracy, improving speed, and reducing the size of the micro-resonators required to guarantee that their presence does not influence the behavior of the cell.

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Mirror-Touch Synesthesia: This Doctor Knows Exactly How You Feel

Mirror-Touch Synesthesia: This Doctor Knows Exactly How You Feel | Amazing Science | Scoop.it

Dr. Salinas himself has a rare medical condition, one that stands in marked contrast to his patients’: While Josh appeared unresponsive even to his own sensations, Salinas is peculiarly attuned to the sensations of others. If he sees someone slapped across the cheek, Salinas feels a hint of the slap against his own cheek. A pinch on a stranger’s right arm might become a tickle on his own. “If a person is touched, I feel it, and then I recognize that it’s touch,” Salinas says.

The condition is called mirror-touch synesthesia, and it has aroused significant interest among neuroscientists in recent years because it appears to be an extreme form of a basic human trait. In all of us, mirror neurons in the premotor cortex and other areas of the brain activate when we watch someone else’s behaviors and actions. Our brains map the regions of the body where we see someone else caressed, jabbed, or whacked, and they mimic just a shade of that feeling on the same spots on our own bodies. For mirror-touch synesthetes like Salinas, that mental simulacrum is so strong that it crosses a threshold into near-tactile sensation, sometimes indistinguishable from one’s own. Neuroscientists regard the condition as a state of “heightened empathic ability.”

This might sound like a superpower of sorts, a mystical connection between one person’s subjective experience and another’s. But to be clear, Salinas cannot read minds. He doesn’t know whether Josh felt the impact of the reflex hammer, and the tingling in his kneecap says more about his own extraordinary nervous system than it does about that of his patient. What’s more, for those who experience mirror-touch synesthesia—an estimated 1.6 percent of the general population—the condition is often more debilitating than it is empowering.

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Are 'Stem Cell Factories' The Future Of Regenerative Medicine? Scientists Eye Possible Breakthrough

Are 'Stem Cell Factories' The Future Of Regenerative Medicine? Scientists Eye Possible Breakthrough | Amazing Science | Scoop.it

Scientists have found a synthetic substrate that has ability to produce billions of stem cells, a new study showed. The findings could potentially pave way for creation of "stem cell factories," which can be used in treatment of the heart, liver, and brain.


Researchers at the University of Nottingham in the U.K. developed the cost-effective substrate that allows the growth of stem cells, and can also survive long-term storage.  Findings of the study were published in the June issue of Advanced Materials journal.


Chris Denning, study co-author and a professor of stem cell biology at the University of Nottingham, explained that a person loses about 5 billion cells during a heart attack and in order to replace those cells, doctors need about 10 to 15 billion stem cells as some of the cells do not survive or differentiate into heart cells. 


Researchers also said that patients with eye disorders in some countries have already receive stem cell-derived treatments.


"The field of regenerative medicine has snowballed in the last five years and over the coming five years a lot more patients will be receiving stem cell treatments," Denning said. "Clinical trials are still in the very early stages. However, with this kind of product, if we can get it commercialized and validated by the regulators, it could be helping patients in two to three years."


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Researchers uncover that abnormal C9orf72 is linked to ALS and frontotemporal dementia

Researchers uncover that abnormal C9orf72 is linked to ALS and frontotemporal dementia | Amazing Science | Scoop.it

A University of Toronto research team has discovered new details about a key gene involved in ALS, perhaps humanity’s most puzzling, intractable disease.


In this fatal disorder with no effective treatment options, scientists (including members of U of T) achieved a major breakthrough in 2011 when they discovered mutations in the gene C9orf72, as the most frequent genetic cause of ALS and frontotemporal dementia. But little was known about how this gene and its related protein worked in the cell.


To solve this problem, Professor Janice Robertson and her team at the Tanz Centre for Research in Neurodegenerative Diseases developed novel antibodies that not only specifically detected C9orf72 in human tissues, but could also distinguish between both the long and short isoforms.  


“Using these antibodies we have made the remarkable discovery that C9orf72 is localized to the nuclear membrane in healthy neurons, but is mislocalized to the plasma (outer membrane) in diseased neurons,” says Robertson, whose research was published July 14 online in the journal Annals of Neurology. 


Robertson and her team also showed that C9orf72 directly interacts with components of the nuclear shuttling complex, which is responsible for the movement of proteins across the nuclear membrane. One such protein is TDP-43, which normally resides in the nucleus but is wrongly localized to the cytoplasm in diseased neurons in ALS. TDP-43 accumulation and aggregation in the cytoplasm diagnoses most ALS cases – but the link with C9orf72 was absent. Now through the use of the C9orf72 antibodies the Robertson lab has found that loss of C9orf72 from the nuclear membrane correlates with TDP-43 pathology. These results suggest that defects in C9orf72 affect the proper functioning of the nuclear shuttling complex, resulting in TDP-43 build up in the cytoplasm.


“We’ve discovered a link between the genetic cause of ALS and its pathology that appears to be important for all cases, not just familial ones,” says Robertson, a Canada Research Chair in ALS. “The possible involvement of C9orf72 in the shuttling between nucleus and cytoplasm opens intriguing new avenues of research into the causes of ALS – and hopefully, one day an effective treatment or cure.”

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Rapid Ebola diagnostic successful in field trial

Rapid Ebola diagnostic successful in field trial | Amazing Science | Scoop.it
A new test can accurately diagnose Ebola virus disease within minutes, providing clinicians with crucial information for treating patients and containing outbreaks.


Researchers from Harvard Medical School, Partners In Health and Boston Children's Hospital have shown that a new commercially developed rapid diagnostic test performed at bedside was as sensitive as the conventional laboratory-based method used for clinical testing during the recent outbreak in Sierra Leone. The results are published in The Lancet.


While the West African Ebola epidemic has slowed since its peak last fall, the crisis simmers on; there were still 24 confirmed cases of Ebola reported in Guinea and Sierra Leone in the week ending June 14, 2015.


To fight Ebola, the first step is to determine which patients are sick with the disease and which with other illnesses with a similar presentation. To use the currently recommended molecular approach, laboratories must be built and samples of highly infectious blood must be drawn, often with unsafe needles and syringes, and then shipped over potentially great distances at substantial risk to the health care workers involved in the process. Then, clinicians and patients must wait for results—sometimes for several days.


These obstacles and delays prevent timely diagnosis and treatment, and also result in individuals without Ebola being admitted to holding units where they may become infected with the virus, the researchers said.

"Simplifying the process and speeding up diagnosis could have a major impact," said Nira Pollock, senior author of the paper and HMS assistant professor of medicine and associate medical director of the Infectious Diseases Diagnostic Laboratory at Boston Children's Hospital.


As the Ebola outbreak in West Africa began to surge in 2014, Pollock and Partners In Health researcher Jana Broadhurst worked with the research core of the HMS Department of Global Health and Social Medicine to reach out to teams around the world who were developing diagnostic tools that would enable clinicians to diagnose Ebola patients quickly.


One candidate, the ReEBOV Antigen Rapid Test, developed by Corgenix, seemed like a promising tool. Working with colleagues at Partners In Health and the Ministry of Health and Sanitation in Sierra Leone, the HMS team was able to plug into an environment that allowed it to train local technicians to perform the test and help collect data for the study. The team at the Public Health England lab at Port Loko, where clinical samples were routinely sent for standard molecular diagnostic testing, were also key collaborators. Corgenix donated test kits to the HMS team.


The field trial took place at two treatment centers operated by the Ministry of Health and Sanitation of Sierra Leone and supported by PIH, where 106 patients suspected of having Ebola were tested during February 2015 using the rapid diagnostic test (performed on a fingerstick blood sample at the point of care). The patients were also tested using the standard RT-PCR (performed on plasma in the laboratory). Both rapid diagnostic tests, on whole blood, and RT-PCR, on plasma, were also performed on 284 samples in the laboratory.


The rapid diagnostic test detected all confirmed cases of Ebola that were positive by the benchmark test in both point-of-care and laboratory testing with sensitivity of 100 percent (identifying all patients with Ebola found by the benchmark method), and a specificity of 92 percent (few false positives).

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Can ‘jumping genes’ cause cancer?

Can ‘jumping genes’ cause cancer? | Amazing Science | Scoop.it

Statistically speaking, your genome contains a lot of junkLess than two per cent of it is made up of actual genes – stretches of DNA carrying instructions that tell cells to make protein molecules. A larger (and hotly debated) proportion is given over to regulatory ‘control switches’, responsible for turning genes on and off at the right time and in the right place. There are also lots of sequences that are used to produce what’s known as ‘non-coding RNA’. And then there’s a whole lot that is just boring and repetitive. As an example, the human genome is peppered with more than half a million copies of a repeated virus-like sequence called Line-1 (also known as L1). Usually these L1 repeats just sit there, passively padding out our DNA. But a new study from our researchers in Cambridge suggests that they can start jumping around within the genome, potentially contributing to the genetic chaos underpinning esophageal cancer.


Let’s take a closer look at these so-called ‘jumping genes’, and how they might be implicated in cancer.  The secret of L1’s success is that it’s a transposon – the more formal name for a jumping gene. These wandering elements were first discovered in plants by the remarkable Nobel prize-winning scientist Barbara McClintockback in 1950They’re only a few thousands DNA ‘letters’ long, and many of them are damaged. But intact L1 transposons contain all the instructions they need to hijack the cell’s molecular machinery and start moving. Firstly, their genetic code is ‘read’ (through a process called transcription) to produce a molecule of RNA, containing instructions for both a set of molecular ‘scissors’ that can cut DNA, together with an unusual enzyme called reverse transcriptase, which can turn RNA back into DNA.


Together these molecules act as genetic vandals. The scissors pick a random place in the genome and start cutting, while the L1 RNA settles itself into the resulting gap. Then the reverse transcriptase gets to work, converting the RNA into DNA and weaving the invader permanently into the fabric of the genome. This cutting and pasting is a risky business. Although many transposons will land safely in a stretch of unimportant genomic junk without causing any problems, there’s a chance that one may hopscotch its way into an important gene or control region, affecting its function.


So given that cancers are driven by faulty genes, could hopping L1 elements be responsible for some of this genetic chaos? In fact, this idea isn’t new. More than two decades ago, scientists in Japan and the US published a paper looking at DNA from 150 bowel tumor samples. In one of them they discovered that an L1 transposon had jumped into a gene called APC, which normally acts as a ‘brake’ on tumor growth. This presumably caused so much damage that APC could no longer work properly, leading to cancer.


Because every L1 ‘hop’ is a unique event, it’s very difficult to detect them in normal cells in the body. But tumours grow from individual cells or small groups of cells, known as clones. So if a transposon jump happens early on during cancer development, it will probably be detectable in the DNA of most – if not all – of the cells in a tumor.


Thanks to advances in DNA sequencing technology, it’s now possible to detect these events – something that researchers are starting to do in a range of cancer types.

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Picture This? Some Just Can’t: Congenital aphantasia

Picture This? Some Just Can’t: Congenital aphantasia | Amazing Science | Scoop.it
Aphantasia, the inability to summon up mental images, is a little-known condition on the verge of wider study.


Certain people, researchers have discovered, can’t summon up mental images — it’s as if their mind’s eye is blind. In June 2015, in the journal Cortex, the condition received a name: aphantasia, based on the Greek word phantasia, which Aristotle used to describe the power that presents visual imagery to our minds.


In 2005, a 65-year-old retired building inspector paid a visit to the neurologist Adam Zeman at the University of Exeter Medical School. After a minor surgical procedure, the man — whom Dr. Zeman and his colleagues refer to as MX — suddenly realized he could no longer conjure images in his mind.


Dr. Zeman couldn’t find any description of such a condition in medical literature. But he found MX’s case intriguing. For decades, scientists had debated how the mind’s eye works, and how much we rely on it to store memories and to make plans for the future.


MX agreed to a series of examinations. He proved to have a good memory for a man of his age, and he performed well on problem-solving tests. His only unusual mental feature was an inability to see mental images.


Dr. Zeman and his colleagues then scanned MX’s brain as he performed certain tasks. First, MX looked at faces of famous people and named them. The scientists found that certain regions of his brain became active, the same ones that become active in other people who look at faces.


Then the scientists showed names to MX and asked him to picture their faces. In normal brains, some of those face-recognition regions again become active. In MX’s brain, none of them did.


Paradoxically, though, MX could answer questions that would seem to require a working mind’s eye. He could tell the scientists the color of Tony Blair’s eyes, for example, and name the letters of the alphabet that have low-hanging tails, like g and j. These tests suggested his brain used some alternate strategy to solve visual problems.


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New Molecule That Mimics Exercise May Help Diabetics

New Molecule That Mimics Exercise May Help Diabetics | Amazing Science | Scoop.it

Diabetes mellitus is a disease that affects an estimated 390 million people worldwide, with that figure expected to rise by over 50% by 2035. This potentially deadly ailment results in the failure of glucose to reach the interior of cells to be processed for energy, and is most commonly found in two closely linked forms. In type 1 diabetes (DM1), the pancreas ceases to produce insulin, the hormone responsible for triggering cellular glucose uptake. In type 2 diabetes (DM2), the issue is that the cells become insensitive to the presence of insulin. While DM1 is most commonly caused by an autoimmune response, DM2 is generally, but not always, caused by poor diet and obesity.


Exogenous insulin is required for the control of DM1, whereas medication for DM2 centres on drugs that serve to lower blood sugar, and increase cellular uptake. Roughly two-thirds of DM2 sufferers are put on at least one drug, with the most common being metformin. One job that metformin does well is to reduce glucose production in the liver, which is up-regulated in diabetes, primarily as a response to low intracellular glucose levels. Metformin’s other mechanism, the increased cellular uptake of blood sugars, is not fully understood. However, the mechanism most favoured by theorists is the increased activation of AMP-activated protein kinase (AMPK), and there is some evidence to support this.


The formation of adenosine triphosphate (ATP) is the end goal of all energy systems, and it is the breakdown of this molecule that allows the body to function. ATP is eventually cleaved to ADP, and then AMP (Adenosine diphosphate and monophosphate, respectively) before being re-phosphorylated back to ATP. AMPK is a heterotrimeric enzyme that plays a key role in the regulation of many catabolic (energy producing) processes, including cellular glucose uptake. Activation of AMPK is primarily triggered by an increase in the AMP:ATP ratio, which is essentially an indicator of cellular starvation. It is believed that mysterious metformin activates AMPK by increasing the concentration of cytosolic AMP.


Now, new research at the University of Southampton, England, has uncovered another potential pathway to AMPK activation. For now, they are simply calling this molecule ‘compound 14’. This compound acts by inhibiting a cellular enzyme known as ATIC; the effect of this is the build up of a molecule called ZMP (an analogue of AMP). It would seem that this increase in ZMP initiates the same reaction as an increase in AMP; activation of AMPK. So, it appears that compound 14 causes a very similar response to metformin, but possibly via a slightly different mechanism. In this new study, two groups of mice, one normal weight and one obese, were given compound 14, daily for one week. While the weight and blood sugar of the standard mice remained stable, as it was before drug administration, the obese mice lost approximately 5% body weight, matched by a coinciding drop in blood sugar levels. This shows great promise for compound 14, which will now enter the next stage of its trials, a study of long term effects.

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Trans fats, but not saturated fats, linked to greater risk of death and heart disease

Trans fats, but not saturated fats, linked to greater risk of death and heart disease | Amazing Science | Scoop.it

A study led by researchers at McMaster University has found that that trans fats are associated with greater risk of death and coronary heart disease, unlike saturated fats, which are also not associated with an increased risk of stroke or Type 2 diabetes. These findings were recently published in an open-access paper August 12 by the British Medical Journal (BMJ).


“For years everyone has been advised to cut out fats,” said lead author Russell de Souza, an assistant professor in the Department of Clinical Epidemiology and Biostatistics with the Michael G. DeGroote School of Medicine. But there are different “fats.”


Saturated fats come mainly from animal products, such as butter, cows’ milk, meat, salmon, and egg yolks, and some plant products such as chocolate and palm oils. Trans unsaturated fats (trans fats) are mainly produced industrially from plant oils (a process known as hydrogenation) for use in margarine, snack foods and packaged baked goods.


Trans fats have no health benefits and pose a significant risk for heart disease, but the case for saturated fat is less clear,” said de Souza. “That said, we aren’t advocating an increase of the allowance for saturated fats in dietary guidelines, as we don’t see evidence that higher limits would be specifically beneficial to health.”


Saturated fats are limited to less than 10 per cent of energy, and trans fats to less than one per cent of energy, to reduce risk of heart disease and stroke, guidelines cited in the BMJ paper (citations 14 to 19) currently recommend.


Contrary to prevailing dietary advice, a recent evidence review found no excess cardiovascular risk associated with intake of saturated fat. In contrast, research suggests that industrial trans fats may increase the risk of coronary heart disease.


To help clarify these controversies, de Souza and colleagues analyzed the results of 50 observational studies assessing the association between saturated and/or trans fats and health outcomes in adults. Study design and quality were taken into account to minimize bias, and the certainty of associations were assessed using a recognized scoring method developed at McMaster.


The team found no clear association between higher intake of saturated fats and death for any reason, coronary heart disease (CHD), cardiovascular disease (CVD), ischemic stroke or type 2 diabetes.

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New Urine Test Could Tell if a Person is Suffering from MDD or Bipolar Disorder

New Urine Test Could Tell if a Person is Suffering from MDD or Bipolar Disorder | Amazing Science | Scoop.it

Patients suffering from bipolar disorder (manic-depressive illness), which is a mental condition, causing instant mood, activity and energy changes, making the afflicted persons daily tasks much harder to do could soon be more accurately diagnosed. The ones having bipolar disorder are often misdiagnosed with another serious mental condition MDD (Major Depressive Disorder) and for a good reason as the condition first becomes more noticeable when the person is in a depressive state which is one of the major symptoms of the MDD.


Around 2.6%of the US population is suffering from bipolar disorder as opposed to almost 7%of the adult population with MDD in the US so making an accurate diagnosis is much more crucial to quickly get the patients the correct treatment.


Current diagnostics relies on interviewing patients and the final diagnosis is determined on these observations, which isn’t the best way as this tests are of subjective nature and can be misleading. The new method developed by the Peng Xie and his team from Chongqing Medical University relies on objective testing to differentiate between the two.


The new method is a combination of nuclear magnetic resonance and gas chromatography-mass spectrometry and with this novelty method the team analysed urine metabolites in samples from patients who either had bipolar disorder or MDD and the end results identified a panel of 6 biomarkers with an 89 to 91 percent chance of predicting each disorder.

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Antibody found that fights MERS coronavirus

Antibody found that fights MERS coronavirus | Amazing Science | Scoop.it

An international team of researchers has found a MERS neutralizing antibody—a discovery that could perhaps lead to a treatment for people infected with the virus. In their paper published in Proceedings of the National Academy of Sciences, the team describes the study they undertook that led to the discovery and why they believe what they found might lead to both prevention and treatment for the oftentimes deadly disease.


Middle East Respiratory Syndrome coronavirus (MERS-CoV) is an ailment that causes severe respiratory problems for those infected and has a high mortality rate. It is believed to have got its start in humans after jumping from camels (who got it from bats) somewhere in the Middle East but has subsequently been found in patients in many other places. The virus does not transmit from person to person very easily, thus the source of most infections is still not clear. To date MERS has killed more than 500 people in 26 countries since it was first identified back in 2012. The most recent outbreak has been taking place in South Korea.


Efforts to find a means of preventing people from falling prey to the virus or combating it in those afflicted have thus far failed. In this new effort, the researchers studied the immune response of a 49 year old male patient suffering from the condition, but whose immune system finally won out. In so doing, they were able to locate the specific antibody that they believe was instrumental in saving the man's life—known as LCA60, it binds to the virus when it encounters it, preventing the virus from binding to CD26 receptor cells.


The researchers tested the antibody in mice (by both injection and inhalation) and found that doing so caused a steep reduction in the number of virus cells in the lungs. Notably, they found that they got nearly the same results whether the mice were given the antibody before or after they were infected. This suggests it might be possible to inject the antibody into people at risk to help them fight off the disease and also to use it as a treatment for those that already have it.

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New Treatment for Rett Syndrome Suggests the Disorder is Reversible

New Treatment for Rett Syndrome Suggests the Disorder is Reversible | Amazing Science | Scoop.it

Rett syndrome is a very rare autistic-like disorder that is not detectable at birth (in most cases signs of it develop at 6 to 18 months of age) and occurs in about 1 in 10,000 to 1 in 15,000 females, as 90% of the children who have Rett syndrome are girls. Most boys diagnosed with this disorder die within the first 2 years due to a severe encephalopathy. Mostly girls are affected because they have two X chromosomes, and the disorder is caused by mutations in a gene on the X chromosome called MECP2.


Rett syndrome is considered as one of the most devastating and deadliest neurological disorders and current therapy relies only on treatment of the symptoms. Children diagnosed with this disease typically have no communicating skills, most of the affected individuals can’t walk, and some of the other very common problems that occur are growth problems, scoliosis, constipation, and brain decline.


Professor Nicholas Tonks at the Cold Spring Harbor Laboratory and his team developed the first drug, codenamed CPT157633, that shows promise at reversing Rett syndrome symptoms. First studies have been done on mice and X-ray crystallography at atomic level shows that the drug binds to its target, the enzyme PTP1B that was discovered after 25 years of research, which helps in regulating key metabolic and signaling pathways.


The PTP1B group of enzymes is responsible for growth and development and Tonks team found 105 different PTP1B enzymes. One of these PTP1B enzymes was found to be elevated in mice that had the chromosome defect causing Rett syndrome, and Tonks’ team developed a few drugs that inhibit the function of this PTP1B enzyme that is associated with the MECP2 chromosome.


These drugs extended lifespan in male mice by as much as 90 days; female mice showed reversal of symptoms with at least 25% efficiency making this the first drug therapy that has the potential to reverse Rett syndrome at atomic-level, showing a lot of promise to further test it’s effects and hopefully in a very near future help the children coping with this disorder to get the best possible treatment.


The findings have been published in The Journal of Clinical Investigation titled “PTP1B inhibition suggests a therapeutic strategy for Rett syndrome”.


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Brain's ability to dispose of key Alzheimer's protein drops dramatically with age

Brain's ability to dispose of key Alzheimer's protein drops dramatically with age | Amazing Science | Scoop.it
The greatest risk factor for Alzheimer's disease is advancing age. After 65, the risk doubles every five years, and 40 percent or more of people 85 and older are estimated to be living with the devastating condition.


Researchers at Washington University School of Medicine in St. Louis have identified some of the key changes in the aging brain that lead to the increased risk. The changes center on amyloid beta 42, a main ingredient of Alzheimer'sbrain plaques. The protein, a natural byproduct of brain activity, normally is cleared from the brain before it can clump together into plaques. Scientists long have suspected it is a primary driver of the disease.


"We found that people in their 30s typically take about four hours to clear half the amyloid beta 42 from the brain," said senior author Randall J. Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology. "In this new study, we show that at over 80 years old, it takes more than 10 hours."


The slowdown in clearance results in rising levels of amyloid beta 42 in the brain. Higher levels of the protein increase the chances that it will clump together to form Alzheimer's plaques. The results will appear in the Annals of Neurology.


For the study, the researchers tested 100 volunteers ages 60 to 87. Half had clinical signs of Alzheimer's disease, such as memory problems. Plaques had begun to form in the brains of 62 participants. The subjects were given detailed mental and physical evaluations, including brain scans to check for the presence of plaques.


The researchers also studied participants' cerebrospinal fluids using a technology developed by Bateman and co-author David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology at Washington University. The technology—known as stable isotope-linked kinetics (SILK)— allowed the researchers to monitor the body's production and clearance of amyloid beta 42 and other proteins.


In patients with evidence of plaques, the researchers observed that amyloid beta 42 appears to be more likely to drop out of the fluid that bathes the brain and clump together into plaques. Reduced clearance rates of amyloid beta 42, such as those seen in older participants, were associated with clinical symptoms of Alzheimer's disease, such as memory loss, dementia and personality changes.


Scientists believe the brain disposes of amyloid beta in four ways: by moving it into the spine, pushing it across the blood-brain barrier, breaking it down or absorbing it with other proteins, or depositing it into plaques. "Through additional studies like this, we're hoping to identify which of the first three channels for amyloid betadisposal are slowing down as the brain ages," Bateman said. "That may help us in our efforts to develop new treatments."

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Ebola vaccine trial proves 100% successful in Guinea

Ebola vaccine trial proves 100% successful in Guinea | Amazing Science | Scoop.it

A vaccine against Ebola has been shown to be 100% successful in trials conducted during the outbreak in Guinea and is likely to bring the west African epidemic to an end, experts say. The results of the trials involving 4,000 people are remarkable because of the unprecedented speed with which the development of the vaccine and the testing were carried out.


Scientists, doctors, donors and drug companies collaborated to race the vaccine through a process that usually takes more than a decade in just 12 months.


“Having seen the devastating effects of Ebola on communities and even whole countries with my own eyes, I am very encouraged by today’s news,” said Børge Brende, the foreign minister of Norway, which helped fund the trial.

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Zebrafish reveal drugs that may improve bone marrow transplant

Zebrafish reveal drugs that may improve bone marrow transplant | Amazing Science | Scoop.it

sing large-scale zebrafish drug-screening models, Harvard Stem Cell Institute (HSCI) researchers at Boston Children’s Hospital have identified a potent group of chemicals that helps bone marrow transplants engraft or “take.” The findings, featured on the cover of the today’s issue of Nature, could lead to human trials in patients with cancer and blood disorders within a year or two, says senior investigator Leonard Zon, a member of the HSCI executive committee and a professor in Harvard’s Department of Stem Cell and Regenerative Biology.


The compounds, known as epoxyeicosatrienoic acids, or EETs, boosted stem cell engraftment in both zebrafish and mice and could make human bone marrow transplants more efficient. Better engraftment could also allow umbilical cord blood to be used as an alternative to marrow as a source of blood stem cells, greatly increasing a patient’s chances of finding a matched donor and enhancing safety.


“Ninety percent of cord blood units can’t be used because they’re too small,” explains Zon, who directs the Stem Cell Program at Boston Children’s. “If you add these chemicals, you might be able to use more units. Being able to get engraftment allows you to pick a smaller cord blood sample that might be a better match.”


EETs are fats that appear to work by stimulating cell migration. They were among the top hits in a screen of 500 known compounds conducted in Boston Children’s newly upgraded Karp Aquatics Facility. While zebrafish have previously led Zon’s team to compounds that boost blood stem cell numbers, such as prostaglandin (currently in several clinical trials under the name ProHema), the new drug screen specifically tested the stem cells’ transplantability and engraftment.

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Next Generation Genomic Sequencing Technologies Speed Pathogen Detection

Next Generation Genomic Sequencing Technologies Speed Pathogen Detection | Amazing Science | Scoop.it

Earlier this year, researchers reported details of 2 curious medical cases that left clinicians stumped. In one, after sustaining numerous tick bites, a Kansas man began experiencing fever, fatigue, anorexia, nausea, and vomiting. Doxycycline, prescribed because some tickborne illnesses respond to this drug, brought no improvement. His condition rapidly deteriorated, and despite hospitalization and additional treatment with antimicrobials, he experienced multiorgan failure and shock, dying about a week later.


In the second case, 3 men in Germany were hospitalized for and later died of encephalitis of unknown cause. An intriguing clue to a possible cause was an unusual activity the men had in common: they all bred variegated squirrels, an animal native to Central America. In both cases, diagnostic testing for a range of known infections failed to reveal the causes. Instead, answers emerged only when researchers applied powerful genomics tools to their investigations, which ultimately identified 2 novel viruses.


In the US case, the Centers for Disease Control and Prevention (CDC) sent a blood sample to its virology laboratory in Fort Collins, Colorado, to determine if the Kansas man had been infected with tickborne Heartland virus, identified in 2012 in the Midwest. The laboratory found no signs of this pathogen, but cultures showed evidence of an unknown virus (Kosoy OI et al. Emerg Infect Dis. 2015;21[5]:760-764). The team then turned to next-generation sequencing (NGS), which allows for high-throughput sequencing of millions of snippets of DNA in parallel, to sequence the mystery virus and to bioinformatic analysis to compare the data with reference sequences cataloged in genomic databases, explained J. Erin Staples, MD, PhD, one of the report’s coauthors. The results revealed the novel virus, named the Bourbon virus after the county in which the patient lived, to be most closely related to 2 tickborne Thogotoviruses never before found in the Americas.


To search for the pathogen that killed the 3 squirrel breeders, researchers in Germany turned to metagenomics, which uses NGS to sequence genetic material from uncultured samples that might contain many species of microbes. This approach led to the discovery of a novel Bornavirus in brain tissue samples from the deceased patients and from the carcass of a squirrel owned by one of them (http://bit.ly/1LQh0Qe).


  • Next-generation sequencing (NGS): High-throughput DNA sequencing that allows rapid parallel sequencing of millions of DNA fragments in a sample; multiple rounds of sequencing improve accuracy and completeness of a reconstructed genome sequence. Bioinformatics tools are then needed to map the sequence data to a reference genome or to reconstruct the genome of a novel microbe.

  • Whole-genome sequencing: Sequencing an organism’s entire genetic sequence, including protein coding, noncoding, and regulatory sequences. Next-generation sequencing has greatly reduced the time necessary for whole-genome sequencing.

  • Metagenomic sequencing: High-throughput simultaneous sequencing of random fragments of genetic material (eg, whole genome, transcriptome, or 16S ribosomal RNA) recovered directly from an uncultured environmental sample that makes it possible to profile microbial communities. In contrast to PCR-based approaches, metagenomic sequencing relies on NGS technology and is “unbiased” in that it does not target any specific microbe.



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Comprehensive genomic profiles of small cell lung cancer : Virtually all had Rb and p53 inactivation

Comprehensive genomic profiles of small cell lung cancer :  Virtually all had Rb and p53 inactivation | Amazing Science | Scoop.it
We have sequenced the genomes of 110 small cell lung cancers (SCLC), one of the deadliest human cancers. In nearly all the tumours analysed we found bi-allelic inactivation of TP53 and RB1, sometimes by complex genomic rearrangements. Two tumours with wild-type RB1 had evidence of chromothripsis leading to overexpression of cyclin D1 (encoded by the CCND1 gene), revealing an alternative mechanism of Rb1 deregulation. Thus, loss of the tumour suppressors TP53 and RB1 is obligatory in SCLC. We discovered somatic genomic rearrangements of TP73 that create an oncogenic version of this gene, TP73Δex2/3. In rare cases, SCLC tumours exhibited kinase gene mutations, providing a possible therapeutic opportunity for individual patients. Finally, we observed inactivating mutations in NOTCH family genes in 25% of human SCLC. Accordingly, activation of Notch signalling in a pre-clinical SCLC mouse model strikingly reduced the number of tumours and extended the survival of the mutant mice. Furthermore, neuroendocrine gene expression was abrogated by Notch activity in SCLC cells. This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer.
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First ever large-scale human study validates multiple biomarkers for Alzheimer's disease

First ever large-scale human study validates multiple biomarkers for Alzheimer's disease | Amazing Science | Scoop.it

Studying brain scans and cerebrospinal fluid of healthy adults, scientists have shown that changes in key biomarkers of Alzheimer’s disease during midlife may help identify those who will develop dementia years later, according to new research. 


The study, at Washington University School of Medicine in St. Louis, is published July 6 in JAMA Neurology. “It’s too early to use these biomarkers to definitively predict whether individual patients will develop Alzheimer’s disease, but we’re working toward that goal,” said senior author Anne Fagan, PhD, a professor of neurology. “One day, we hope to use such measures to identify and treat people years before memory loss and other cognitive problems become apparent.”


The study focused on data gathered over 10 years and involved 169 cognitively normal research participants ages 45 to 75 when they entered the study. Each participant received a complete clinical, cognitive imaging and cerebrospinal fluid biomarker analysis every three years, with a minimum of two evaluations.


At the participants’ initial assessments, researchers divided them into three age groups: early-middle age (45-54); mid-middle age (55- 64); and late-middle age (65-74).  Among the biomarkers evaluated in the new study were:

  • Amyloid beta 42, a protein that is the principal ingredient of Alzheimer’s plaques;
  • Tau, a structural component of brain cells that increases in the cerebrospinal fluid as Alzheimer’s disease damages brain cells;
  • YKL-40, a newly recognized protein that is indicative of inflammation and is produced by brain cells; and
  • The presence of amyloid plaques in the brain, as seen via amyloid PET scans.


The scientists found that drops in amyloid beta 42 levels in the cerebrospinal fluid among cognitively normal participants ages 45-54 are linked to the appearance of plaques in brain scans years later. The researchers also found that tau and other biomarkers of brain-cell injury increase sharply in some individuals as they reach their mid-50s to mid-70s, and YKL-40 rises throughout the age groups focused on in the study.


Previous research has shown that all of these biomarkers may be affected by Alzheimer’s disease, but this is the first large data set to show that the biomarkers change over time in middle-aged individuals. 

All of these changes were more pronounced in participants who carried a form of a gene that significantly increases the risk of Alzheimer’s disease.


The gene is known as APOE, and scientists have known that people with two copies of a particular version of this gene have up to 10 times the risk of developing Alzheimer’s as those with other versions of the gene. 


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Atomic force microscope advance leads to new breast cancer research

Atomic force microscope advance leads to new breast cancer research | Amazing Science | Scoop.it

Researchers who developed a high-speed form of atomic force microscopy have shown how to image the physical properties of live breast cancer cells, for the first time revealing details about how deactivation of a key protein may lead to metastasis. The new findings also are providing evidence for the mechanisms involved in a cell's response to anti-cancer drugs, said Arvind Raman, Purdue University's Robert V. Adams Professor of Mechanical Engineering.


In atomic force microscopy (AFM), a tiny vibrating probe called a cantilever passes over a material, precisely characterizing its topography and physical properties. However, before now the procedure has been too slow to record some quickly changing biological processes in action.


“Before this advance you could see only the before and after, but not what happened in between, the dynamics of the event,” Raman said. “There is evidence based on this work and our previous findings that there might be a mechanical signature to drug resistance.”


Advanced models allow researchers to convert AFM data into properties about the cell’s internal scaffolding, called the cortical actin cytoskeleton, including the motion of fibers called actin. Findings are detailed in a paper appearing Monday (June 29) in the research journal Scientific Reports,the open access journal of the Nature Publishing Group. The researchers used the technique to study breast cancer cells, probing a key enzyme called spleen tyrosine kinase, or Syk.


Kinases cause phosphorylation of proteins, a biochemical process that can alter enzymes and plays a significant role in a wide range of cellular processes. “So if you turn the kinase off, proteins will get dephosphorylated and then changes could occur,” said Robert L. Geahlen, Distinguished Professor of Medicinal Chemistry at Purdue. “We were able to show the turn off of this kinase very rapidly alters the physical properties of the cell. So it’s undoubtedly due to the phosphorylation events that are having immediate effects on cytoskeletal proteins.”


The paper was authored by former doctoral student Alexander X. Cartagena-Rivera, now a postdoctoral fellow at the National Institutes of Health's National Institute on Deafness and Other Communication Disorders (NIDCD); Purdue postdoctoral research associate Wen-Horng Wang; Geahlen; and Raman.


The researchers studied breast cancer cells exposed to a chemical “inhibitor” that blocks the functioning of Syk, leaving the cells free to metastasize. Because of the new higher-speed AFM, the researchers for the first time have been able to observe what happens when the inhibitor is added. After adding the inhibitor, actin bands propagate across the cell, causing the cell to change shape. "This takes about 10 minutes, which is quite fast compared to many biological processes," Raman said.


The images can be taken at a speed of about 50 seconds per frame.

“Before we did this it would take roughly 15 to 20 minutes to take one frame, which is too slow to observe this transition process,” he said.

Bands of actin were shown to move in a sweeping motion across the cell. “You think of actin as a scaffolding, but it’s a dynamic scaffolding,” Raman said. “We can see bands of actin that are going around and changing the physical properties during the transition, which was not understood before.”


When Syk is missing or deactivated, breast cancer cells undergo a process called EMT, or epithelial-mesenchymal transition, causing them to become highly motile and to undergo metastasis. “If this kinase is in the cells, the cells cannot metastasize, so we’ve been trying to figure out what the mechanisms are by which you have to get rid of this kinase in order to become highly motile and metastatic,” said Geahlen, who is affiliated with the Purdue Center for Cancer Research. “And that’s one of the reasons we were looking at this particular type of cancer cell with this particular form of Syk in it.”


One goal of the research is to correlate physical properties of cells with tumor suppression and the action of the kinase on the cell.

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