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First laboratory-grown vaginas successfully implanted

First laboratory-grown vaginas successfully implanted | Amazing Science | Scoop.it

Four teenage girls have received vaginas grown from their own cells in a lab. And they work. These girls were born with underdeveloped or missing vaginas because of a rare condition called Mayer-Rokitansky-Küster-Hauser Syndrome that affects about 1 in 5,000 women. While their labia looked like those of other girls, their vaginas, cervixes and wombs, which are necessary for menstruation and childbirth, never fully formed.


Medical researchers took a vaginal tissue sample from each patient, who were between 13 and 18 at the time, and used them to grow cells in the lab. After four weeks, the researchers had enough cells to layer them on to degradable scaffolding — “like the layers of a cake,” lead researcher Anthony Atala of the Wake Forest School of Medicine explained. Then they were implanted.


The surgeries were done between 2005 and 2008. Atala and the team monitored the women for long-term complications before publishing the results in the medical journal The Lancet this week. The achievement was the work of a large team listed here.


The technique is a potentially important alternative to reconstructing tissue using grafts from other parts of the body, which medical researchers say produces too many complications. The trick was growing cells until they were mature enough to “recruit” other cells once implanted in the body and form tissue that includes blood vessels and nerves.

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The challenge of cancer genomics: Embarking on CLARITY 2

The challenge of cancer genomics: Embarking on CLARITY 2 | Amazing Science | Scoop.it

There is tremendous potential for genome sequencing to improve clinical diagnosis and care once it becomes routinely accessible, but this will require formalizing research methods into clinical best practices in the areas of sequence data generation, analysis, interpretation and reporting. The CLARITY Challenge was designed to spur convergence in methods for diagnosing genetic disease starting from clinical case history and genome sequencing data.


DNA samples were obtained from three families with heritable genetic disorders and genomic sequence data was donated by sequencing platform vendors. The challenge was to analyze and interpret these data with the goals of identifying disease causing variants and reporting the findings in a clinically useful format. Participating contestant groups were solicited broadly, and an independent panel of judges evaluated their performance.


Results: A total of 30 international groups were engaged. The entries reveal a general convergence of practices on most elements of the analysis and interpretation process. However, even given this commonality of approach, only two groups identified the consensus candidate variants in all disease cases, demonstrating a need for consistent fine-tuning of the generally accepted methods. There was greater diversity of the final clinical report content and in the patient consenting process, demonstrating that these areas require additional exploration and standardization.


http://genomebiology.com/content/pdf/gb-2014-15-3-r53.pdf

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Columbia Scientists Identify Key Cells in Touch Sensation

Columbia Scientists Identify Key Cells in Touch Sensation | Amazing Science | Scoop.it

In a study published online today in the journal Nature, a team of Columbia University Medical Center researchers led by Ellen Lumpkin, PhD, associate professor of somatosensory biology, solve an age-old mystery of touch: how cells just beneath the skin surface enable us to feel fine details and textures.


Touch is the last frontier of sensory neuroscience. The cells and molecules that initiate vision—rod and cone cells and light-sensitive receptors—have been known since the early 20th century, and the senses of smell, taste, and hearing are increasingly understood. But almost nothing is known about the cells and molecules responsible for initiating our sense of touch.


This study is the first to use optogenetics—a new method that uses light as a signaling system to turn neurons on and off on demand—on skin cells to determine how they function and communicate.

The team showed that skin cells called Merkel cells can sense touch and that they work virtually hand in glove with the skin’s neurons to create what we perceive as fine details and textures.


“These experiments are the first direct proof that Merkel cells can encode touch into neural signals that transmit information to the brain about the objects in the world around us,” Dr. Lumpkin said.


Several conditions—including diabetes and some cancer chemotherapy treatments, as well as normal aging—are known to reduce sensitive touch. Merkel cells begin to disappear in one’s early 20s, at the same time that tactile acuity starts to decline. “No one has tested whether the loss of Merkel cells causes loss of function with aging—it could be a coincidence—but it’s a question we’re interested in pursuing,” Dr. Lumpkin said.


In the future, these findings could inform the design of new “smart” prosthetics that restore touch sensation to limb amputees, as well as introduce new targets for treating skin diseases such as chronic itch.

The study was published in conjunction with a second study by the team done in collaboration with the Scripps Research Institute. The companion study identifies a touch-activated molecule in skin cells, a gene called Piezo2, whose discovery has the potential to significantly advance the field of touch perception.


“The new findings should open up the field of skin biology and reveal how sensations are initiated,” Dr. Lumpkin said. Other types of skin cells may also play a role in sensations of touch, as well as less pleasurable skin sensations, such as itch. The same optogenetics techniques that Dr. Lumpkin’s team applied to Merkel cells can now be applied to other skin cells to answer these questions.

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PCAF gives new hope to patients with spinal cord injury

PCAF gives new hope to patients with spinal cord injury | Amazing Science | Scoop.it

Curious as to why nerves of the peripheral nervous system (PNS) show some capacity for regrowth and repair, whereas nerves of the central nervous system (CNS) do not, scientists undertook a study of the PNS’ regenerative mechanisms, the chemical and genetic events that help peripheral nerves recover from injury. These scientists were already aware that damaged peripheral nerves emit “retrograde” signals, which activate an epigenetic program, which in turn initiates nerve growth. But the scientists were dissatisfied with how little was known about how, exactly, retrograde signaling could trigger the epigenetic mechanism.


The scientists hoped that if more were understood about the trigger, which works in the PNS, they might learn how it could be made to work in the CNS. Then CNS damage, which is currently irreparable, might become amenable to treatment, and people suffering spinal cord injury, stroke, or brain trauma might avoid loss of sensation or permanent paralysis.


Scientists representing Imperial College London and the Hertie Institute, University of Tuebingen compared the responses to PNS damage and CNS damage in a type of neuron called a dorsal root ganglion, which connects to both the PNS and the CNS. (The researchers considered cells in culture as well as mouse models.) Then, through systematic epigenetic studies, they discovered a protein that appears to be essential for a series of chemical and genetic events that allow nerves to regenerate.


The details of this work appeared April 1, 2014 in Nature Communications, in an article entitled “PCAF-dependent epigenetic changes promote axonal regeneration in the central nervous system.” As the title indicates, the crucial protein is called PCAF, for the histone acetyltransferase p300/CBP-associated factor. PCAF, the researchers found, “promotes acetylation of histone 3 Lys 9 at the promoters of established key regeneration-associated genes following a peripheral but not a central axonal injury.”


When researchers injected PCAF into mice with damage to their central nervous system, this significantly increased the number of nerve fibers that grew back, indicating that it may be possible to chemically control the regeneration of nerves in the CNS.


The researchers also found that extracellular signal-regulated kinase (ERK)-mediated retrograde signaling is required for PCAF-dependent regenerative gene reprogramming. “PCAF,” the authors wrote, “is necessary for conditioning-dependent axonal regeneration and also singularly promotes regeneration after spinal cord injury.”


One of the study’s authors, Radhika Puttagunta, Ph.D., from the University of Tuebingen, said, “With this work we add another level of understanding into the specific mechanisms of how the body is able to regenerate in the PNS and have used this knowledge to drive regeneration where it is lacking in the CNS. We believe this will help further our understanding of mechanisms that could enhance regeneration and physical recovery after CNS injury.”


“The results suggest that we may be able to target specific chemical changes to enhance the growth of nerves after injury to the central nervous system,” said lead study author Simone Di Giovanni, M.D., Ph.D., from Imperial College London’s Department of Medicine. "The ultimate goal could be to develop a pharmaceutical method to trigger the nerves to grow and repair and to see some level of recovery in patients.”

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Experimental Cancer Drug FRAX486 Reverses Schizophrenia Symptoms in Mice

Experimental Cancer Drug FRAX486 Reverses Schizophrenia Symptoms in Mice | Amazing Science | Scoop.it

Johns Hopkins researchers discover anticancer compound reverses schizophrenic behaviors in mice.



The team say an experimental anticancer compound - FRAX486 – can reverse behaviours associated with schizophrenia in adolescent mice with the rodent version of the disease. They also discovered some of the lost brain cell function was restored in mice being administered the cancer drug.


Published in the Proceedings of the National Academy of Sciences, the researchers discovered the compound FRAX486 appears to halt a pruning process in the schizophrenic brain in which vital neural connections are destroyed.


The drug is one of a class of compounds called PAK inhibitors which provide some protection from brain damage caused through inherited disease. There is also evidence to show the drug could be used to treat Alzheimer's, while previous studies have found the PAK protein can initiate cancer and cell growth, meaning inhibitors could be developed to fight cancers.


The team said they were able to restore disabled neurons in adolescent and young adult mice with schizophrenia through FRAX486.


Study leader Akira Sawa said: "By using this compound to block excess pruning in adolescent mice, we also normalised the behaviour deficit. That we could intervene in adolescence and still make a difference in restoring brain function in these mice is intriguing."


In their experiments, the researchers reduced the expression of a gene called Disrupted-in-Schizophrenia 1 (DISC1), which appears to regulate the fate of neurons involved in higher order functions like information processing.


The deficit in DISC1 caused deterioration of parts of the brain that help neurons to communicate with one another. It also means the regulation of another protein, Rac1, cannot be controlled. Excess Rac1 leads to excess PAK in mice.


By reducing the activity of PAK, the team was able to protect the mice against the effects of having too little DISC1. It is not yet known if PAK is elevated in the brains of humans with schizophrenia, meaning further research is needed before the drug is considered for use in humans.

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CRISPR-CAS9 Reverses Disease Symptoms in Living Animals for First Time

CRISPR-CAS9 Reverses Disease Symptoms in Living Animals for First Time | Amazing Science | Scoop.it

MIT scientists report the use of a CRISPR methodology to cure mice of a rare liver disorder caused by a single genetic mutation. They say their study (“Genome editing with Cas9 in adult mice corrects a disease mutation and phenotype”), published in Nature Biotechnology, offers the first evidence that this gene-editing technique can reverse disease symptoms in living animals. CRISPR, which provides a way to snip out mutated DNA and replace it with the correct sequence, holds potential for treating many genetic disorders, according to the research team.


“What's exciting about this approach is that we can actually correct a defective gene in a living adult animal,” says Daniel Anderson, Ph.D., the Samuel A. Goldblith associate professor of chemical engineering at MIT, a member of the Koch Institute for Integrative Cancer Research, and the senior author of the paper.


The recently developed CRISPR system relies on cellular machinery that bacteria use to defend themselves from viral infection. Researchers have copied this cellular system to create gene-editing complexes that include a DNA-cutting enzyme called Cas9 bound to a short RNA guide strand that is programmed to bind to a specific genome sequence, telling Cas9 where to make its cut.


At the same time, the researchers also deliver a DNA template strand. When the cell repairs the damage produced by Cas9, it copies from the template, introducing new genetic material into the genome. Scientists envision that this kind of genome editing could one day help treat diseases such as hemophilia, and others that are caused by single mutations.


For this study, the researchers designed three guide RNA strands that target different DNA sequences near the mutation that causes type I tyrosinemia, in a gene that codes for an enzyme called FAH. Patients with this disease, which affects about 1 in 100,000 people, cannot break down the amino acid tyrosine, which accumulates and can lead to liver failure. Current treatments include a low-protein diet and a drug called NTCB, which disrupts tyrosine production.


In experiments with adult mice carrying the mutated form of the FAH enzyme, the researchers delivered RNA guide strands along with the gene for Cas9 and a 199-nucleotide DNA template that includes the correct sequence of the mutated FAH gene.

“Delivery of components of the CRISPR-Cas9 system by hydrodynamic injection resulted in initial expression of the wild-type Fah protein in ~1/250 liver cells,” wrote the investigators. “Expansion of Fah-positive hepatocytes rescued the body weight loss phenotype.”


While the team used a high pressure injection to deliver the CRISPR components, Dr. Anderson envisions that better delivery approaches are possible. His lab is now working on methods that may be safer and more efficient, including targeted nanoparticles. 

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Cancer vaccine a step closer as natural killer cells are correctly activated

Cancer vaccine a step closer as natural killer cells are correctly activated | Amazing Science | Scoop.it

The E3 ligase Cbl-b and TAM receptors regulate cancer metastasis via natural killer cells.


Vaccines work. Their widespread use has saved millions of lives. With an ageing population that is increasingly becoming a victim to cancer, a vaccine to treat it would do wonders. In a study published in Nature, scientists have taken a step in that direction.


Few attempts to develop a cancer vaccine have been made, but the side effects have been overwhelming, such as the immune system turning against not just diseased but also healthy cells. Researchers need to understand how to activate our immune system such that it kills only cancer cells, and does not have any side effects.


In a new study, Josef Penninger at the Institute of Molecular Biotechnology of the Austrian Academy of Sciences and his colleagues have identified the molecular mechanism underlying this strategy.


The immune system protects human beings from diseases caused by viruses or parasites, and it even tries to fight cancer. It has the ability to distinguish external agents from our own healthy tissue, and kill them.


Natural killer (NK) cells in our immune system are like the soldiers of an army, they mediate a rapid response to an infection or a growing tumor. They constitute the first line of body’s defence mechanism. These cells can also inhibit the spread of cancer to different parts of the body, which is not only beyond the scope of current treatments such as chemotherapy and radiotherapy, but also accounts for more than 90% of deaths due to cancer.


Penninger has now shown, using mice that act as proxy for humans, that natural killer cells can be activated to inhibit the spread of cancer, and thus the survival of cancer patients can be prolonged, without any side effects.


First they showed that natural killer cells where a specific enzyme was not active killed target tumor cells more efficiently than natural killer cells that had normal enzyme activity. They also showed that cancer-bearing mice in which the enzyme, known as Cbl-b, had been deleted had fewer sites to which the cancer had spread, and a longer survival rate.


What’s more is that the loss of Clb-b did not lead to any side effects as seen with previous attempts to boost the immune system against cancer. The usual function of the enzyme is to help inhibit the immune response by preventing many lines of defence becoming active, including natural killer cells.


As an aside, understanding this mechanism helped Penninger answer how warfarin, a drug widely used to stop blood from clotting, also reduces cancer spread in mice. He showed warfarin adopts a similar strategy to activate natural killer cells by having a similar effect as that of the loss of Cbl-b. Thus, the hope is now that we can develop a vaccine that wakes up our immune system to stop the spread of cancer.

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Cologuard stool-based DNA test for colon cancer demonstrates 93.3% sensitivty

Cologuard stool-based DNA test for colon cancer demonstrates 93.3% sensitivty | Amazing Science | Scoop.it

Colon cancer screening is crucial because it can prevent colon-related cancer deaths by as much as 60 percent if adults who are at least 50-years old get screened routinely. What stops many people from getting screened though is the discomfort associated with traditional screening methods.


The number of adults getting screened for colon cancer, however, may soon increase as the U.S Food and Drug Administration (FDA) is likely to give its approval to a less invasive stool-based DNA test for detecting colon cancer.


On Thursday, a panel of FDA advisers unanimously recommended the approval of Cologuard, a colon cancer screening test that analyzes DNA found in the stool. The FDA may not follow the panel's recommendation but it usually does. Cologuard was developed by Madison-based Exact Sciences which specializes in colon cancer.

"Exact Sciences Corp. (Nasdaq: EXAS) today announced that the U.S. Food and Drug Administration's (FDA) Molecular and Clinical Genetics Panel of the Medical Devices Advisory .


Committee determined by a unanimous vote of 10 to zero that Exact Sciences has demonstrated safety, effectiveness and a favorable risk benefit profile of Cologuard, the company's stool-based DNA (sDNA), non-invasive colorectal cancer screening test," Exact Sciences announced on its website.


Findings of a study published in the New England Journal of Medicine last week suggest that Cologuard is more efficient in detecting early-stage cancer than the Fecal Immunochemical Test (FIT), another non-invasive colon cancer screening test. The study, which was participated by 12,776 individuals, found that Exact Science's stool-based DNA test could detect 92.3 percent of colon cancers. Cologuard was also found to be 94 percent efficient in detecting early stage cancers.


Colonoscopy remains to be the most accurate way of detecting colon cancer but many avoid it because of its invasive approach of inserting a tube into the patient's anus. Cologuard will be used as a screening test if it gets FDA's approval but patients found positive of cancer will still be asked to undergo colonoscopy.

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Holographic imaging for rapidly sorting stem cells and cancer cells

Holographic imaging for rapidly sorting stem cells and cancer cells | Amazing Science | Scoop.it

MIT scientists have developed a way to image cells (without fluorescent markers or other labels) as they flow through a tiny microfluidic channel for sorting. This is an important step toward cell-sorting systems that could help scientists separate stem cells at varying stages of development, or to distinguish healthy cells from cancerous cells, the scientists say.


Other cell-sorting methods require adding a fluorescent molecule that highlights the cells of interest, but those tags can damage the cells and make them unsuitable for therapeutic uses. The new method is based on a 2007 microscopy development that allowed the scientists to detail the interior of a living cell in three dimensions, without adding any fluorescent markers or other labels. This technique also revealed key properties, such as the cells’ density.


“Many stem cell applications require sorting of cells at different stages of differentiation. This can be done with fluorescent staining, but once you stain the cells they cannot be used,” says Yongjin Sung, a former postdoc in MIT’sLaser Biomedical Research Center and lead author of a paper describing the technique in the inaugural issue of the journal PRApplied.


“With our approach, you can utilize a vast amount of information about the 3-D distribution of the cells’ mass to sort them.” Instead of using fluorescent tags, the MIT method analyzes the cells’ index of refraction — a measurement of how much the speed of light is reduced as it passes through a material. Every material has a distinctive index of refraction, and this property can be used, along with cells’ volume, to calculate their mass and density.


Different parts of a cell, including individual organelles, have different indices of refraction, so the information generated by this approach can also be used to identify some of these internal cell structures, such as the nucleus and nucleolus, a structure located within the nucleus.


In the original 2007 version of this technology, known as tomographic phase microscopy, researchers led by the late MIT professor Michael Feld created 3-D images by combining a series of 2-D images taken as laser beams passed through cells from hundreds of different angles. This is the same concept behind CT scanning, which combines X-ray images taken from many different angles to create a 3-D rendering.


A key feature of the new MIT system is the use of a focused laser beam that can illuminate cells from many different angles, allowing the researchers to analyze the scattered light from the cells as they flow across the beam. Using a technique known as off-axis digital holography, the researchers can instantaneously record both the amplitude and phase of scattered light at each location of the cells. “As the cell flows across, we can effectively illuminate the entire sample from all angles without having to rotate a light source or the cell,” says former MIT graduate student Niyom Lue, a coauthor of the new paper.


The current system can image about 10 cells per second, but the researchers hope to speed it up to thousands of cells per second, which would make it useful for applications such as sorting stem cells. The researchers also hope to use the system to learn more about how cancer cells grow and respond to different drug treatments.

“This label-free method can look at different states of the cell, whether they are healthy or whether they maybe have cancer or viral or bacterial infections,” says Peter So, an MIT professor of mechanical engineering and biological engineering who is senior author of the new paper. “We can use this technique to look at the pathological state of the cell, or cells under treatment of some drug, and follow the population over a period of time.”


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Gene Expression Signature Reveals New Way to Classify Gum Disease

Gene Expression Signature Reveals New Way to Classify Gum Disease | Amazing Science | Scoop.it

Researchers at Columbia University Medical Center (CUMC) have devised a new system for classifying periodontal disease based on the genetic signature of affected tissue, rather than on clinical signs and symptoms. The new classification system, the first of its kind, may allow for earlier detection and more individualized treatment of severe periodontitis, before loss of teeth and supportive bone occurs. The findings were published recently in the online edition of the Journal of Dental Research.


Currently, periodontal disease is classified as either “chronic” or “aggressive,” based on clinical signs and symptoms, such as severity of gum swelling and extent of bone loss. “However, there is much overlap between the two classes,” said study leader Panos N. Papapanou, DDS, PhD, professor and chair of oral and diagnostic sciences at the College of Dental Medicine at CUMC. “Many patients with severe symptoms can be effectively treated, while others with seemingly less severe infection may continue to lose support around their teeth even after therapy. Basically, we don’t know whether a periodontal infection is truly aggressive until severe, irreversible damage has occurred.”


Looking for a better way to classify periodontitis, Dr. Papapanou turned to cancer as a model. In recent years, cancer biologists have found that, in some cancers, clues to a tumor’s aggressiveness and responsiveness to treatment can be found in its genetic signature. To determine if similar patterns could be found in periodontal disease, the CUMC team performed genome-wide expression analyses of diseased gingival (gum) tissue taken from 120 patients with either chronic or aggressive periodontitis. The test group included both males and females ranging in age from 11 to 76 years.


The researchers found that, based on their gene expression signatures, the patients fell into two distinct clusters. “The clusters did not align with the currently accepted periodontitis classification,” said Dr. Papapanou. However, the two clusters did differ with respect to the extent and severity of periodontitis, with significantly more serious disease in Cluster 2. The study also found higher levels of infection by known oral pathogens, as well as a higher percentage of males, in Cluster 2 than in Cluster 1, in keeping with the well-established observation that severe periodontitis is more common in men than in women.


“Our data suggest that molecular profiling of gingival tissues can indeed form the basis for the development of an alternative, pathobiology-based classification of periodontitis that correlates well with the clinical presentation of the disease,” said Dr. Papapanou.

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Anesthesia may have lingering side effects on the brain, even years after an operation

Anesthesia may have lingering side effects on the brain, even years after an operation | Amazing Science | Scoop.it

Two and a half years ago Susan Baker spent three hours under general anesthesia as surgeons fused several vertebrae in her spine. Everything went smoothly, and for the first six hours after her operation, Baker, then an 81-year-old professor at the Johns Hopkins Bloomberg School of Public Health, was recovering well. That night, however, she hallucinated a fire raging through the hospital toward her room. Petrified, she repeatedly buzzed the nurses' station, pleading for help. The next day she was back to her usual self. “It was the most terrifying experience I have ever had,” she says.


Baker's waking nightmare was a symptom of postoperative delirium, a state of serious confusion and memory loss that sometimes follows anesthesia.


Anesthesia comes in three main types. Local anesthesia, the mildest form, merely numbs a very small area, such as a single tooth. Regional anesthesia desensitizes a large section of someone's body by injecting drugs into the spine that block nerve signals to the brain. Often a patient getting regional anesthesia also takes a relatively small dose of a powerful sedative drug, such as propofol—not enough to put them under but enough to alter brain activity in a way that makes the person less aware and responsive.


General anesthesia relies on a cocktail of drugs that renders patients completely unconscious, prevents them from moving and blocks any memories of the surgery. Although anesthetic drugs have been around since 1846, many questions remain as to how exactly they work. To date, the strongest evidence suggests that the drugs are effective in part because they bind to and incapacitate several different proteins on the surface of neurons that are essential for regulating sleep, attention, learning and memory. In addition, it seems that interrupting the usual activity of neurons may disrupt communication between far-flung regions of the brain, which somehow triggers unconsciousness.


When postoperative delirium was first recognized, researchers wondered whether certain anesthetic drugs—but not others—deserved the blame. Yet studies comparing specific drugs and rates of delirium in patients after surgery have always been scant and inconclusive. “No particular anesthetic has been exonerated in patients,” says Roderic G. Eckenhoff, a professor of anesthesiology at the University of Pennsylvania. But “we can't say yet that there is an anesthetic that patients should not get.”

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Medical microrobots to deliver drugs on demand

Medical microrobots to deliver drugs on demand | Amazing Science | Scoop.it

Advances in micro- and nanoscale engineering in the medical field have led to the development of various robotic designs that one day will allow a new level of minimally invasive medicine. These micro- and nanorobots will be able to reach a targeted area, provide treatments and therapies for a desired duration, measure the effects and, at the conclusion of the treatment, be removed or degrade without causing adverse effects. Ideally, all these tasks would be automated but they could also be performed under the direct supervision and control of an external user.Several approaches have been explored for the wireless actuation of microrobots. Among these, magnetic fields have been the most widely employed strategy for propulsion because they do not require special environmental properties such as conductivity or transparency (for instance: "Artificial nano swimmers", with a video that shows the controlled motions of particles in a magnetic field).


This approach allows for the precise manipulation of magnetic objects toward specific locations, and magnetic fields are biocompatible even at relatively high field strengths (MRI).In a new work, a team of researchers from ETH Zurich and Harvard University (David Mooney's lab) demonstrate that additional intelligence – including sensing and actuation – can be instantiated in these microrobots by selecting appropriate materials and methods for the fabrication process.


"Our work combines the design and fabrication of near infrared light (NIR) responsive hydrogel capsules and biocompatible magnetic microgels with a magnetic manipulation system to perform targeted drug and cell delivery tasks, Dr." Mahmut Selman Sakar, a research scientist in Bradley Nelson's Institute of Robotics and Intelligent Systems at ETH Zurich, tells Nanowerk.Reporting their results in the November 4, 2013 online edition of Advanced Materials ("An Integrated Microrobotic Platform for On-Demand, Targeted Therapeutic Interventions"), first-authored by Sakar's co-researcher Stefano Fusco, the team fabricated an untethered, self-folding, soft microrobotic platform, in which different functionalities are integrated to achieve targeted, on-demand delivery of biological agents.

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Jose Mejia R's comment, March 30, 2014 11:40 AM
TRADUCCION:<br>Los avances en la ingeniería de micro-y nanoescala en el campo de la medicina han conducido al desarrollo de diversos diseños robóticos que un día permitirá un nuevo nivel de la medicina mínimamente invasiva. Estos micro-y nano-robots serán capaces de llegar a un área objetiva, proporcionar tratamientos y terapias para una duración deseada, medir los efectos y, a la conclusión del tratamiento, deberá ser eliminado o degradado sin causar efectos adversos. Lo ideal sería que todas estas tareas se pueden automatizar, pero también pueden ser realizados bajo la supervisión y el control directos de un usuario externo. Varios enfoques se han explorado para el accionamiento inalámbrico de microrobots. Entre éstos, los campos magnéticos han sido la estrategia más ampliamente empleada para la propulsión, ya que no requieren propiedades especiales del medio ambiente tales como la conductividad o la transparencia (por ejemplo: "nadadores nano artificial", con un vídeo que muestra los movimientos controlados de partículas en una magnética campo).<br> <br>Este enfoque permite la manipulación precisa de objetos magnéticos hacia lugares específicos, y los campos magnéticos son biocompatibles, incluso a intensidades de campo relativamente altas (MRI). En un nuevo trabajo, un equipo de investigadores de ETH Zurich y la Universidad de Harvard (el laboratorio de David Mooney) demuestran que con inteligencia adicional - incluyendo detección y actuación - se puede crear instancias de estos microrobots seleccionando materiales y procedimientos para el proceso de fabricación adecuadas.<br><br>"Nuestro trabajo combina el diseño y la fabricación de la luz en el infrarrojo cercano (NIR) cápsulas de hidrogel sensible y microgeles magnéticas biocompatibles con un sistema de manipulación magnética para realizar tareas de administración de drogas y de suministro de células específicas, nos diece el Dr. Mahmut Sakar Selman, un científico de investigación en el Instituto de Bradley Nelson de Robótica y Sistemas Inteligentes en la ETH Zurich. Sus resultados indicados el 04 de noviembre 2013 en la edición en línea de Materiales Avanzados ...
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Musical Anhedonia - the inability to enjoy music - is recognized as a brain condition

Musical Anhedonia - the inability to enjoy music - is recognized as a brain condition | Amazing Science | Scoop.it

For most people, music is one of life's great pleasures. But the inability to enjoy it is a real condition that has just been recognized and described by science. The new condition, known as specific musical anhedonia, is described in a new paper published this week in the journal Current Biology.


People with the condition have no trouble perceiving or identifying music, or even describing the mood the music is supposed to convey, said Robert Zatorre, a McGill University neuroscientist who co-authored the paper. The condition affects about two per cent of the population. Many of those who have it said they have tried to mask their dislike of music from others.


Zatorre had previously done studies that showed music activates the pleasure and reward centres of the brain, just as food and sex do. Scientists are interested in studying the brain's reward system because problems with it are implicated in a lot of problems such as eating disorders and drug and gambling addictions.


Zatorre and colleagues in Spain, including Josep Marco-Pallares of the University of Barcelona, began to wonder if music activated the pleasure centre of the brain in everyone, or if there were some people who didn't respond the same way.


To figure that out, they surveyed around 500 students at the University of Barcelona about their music habits and response to music  — for example, did they often have music playing and did they like to share music with their friends?


Groups of students who scored high, average, and low on the questionnaire were tested in the lab for their body's response to music — changes in heart rate and skin conductance, which indicate emotional or nervous system arousal.


While those who scored average or high on the questionnaire had a strong physiological response to the music, those who scored low "more or less flatlined," Zatorre recalled, confirming that they did not derive pleasure from music.


The students were given additional questionnaires to make sure they weren't depressed and were able to experience pleasure from other things.


Then they were tested in another experiment – a slot-machine-like gambling video game in which they would sometimes receive a big payout.


"People who didn't respond to music nonetheless showed a perfectly normal response to the monetary reward," Zatorre said.

That's interesting because previously, researchers had thought the brain's reward centre was an "all or none" system that was functioning normally, hyperactive, or underactive as a whole.

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Australian Study Confirms Homeopathy Doesn't Work

Australian Study Confirms Homeopathy Doesn't Work | Amazing Science | Scoop.it
The Australian National Heath and Medical Research Council (NHMRC) has released a paper concluding “there is no reliable evidence that homeopathy is effective". The paper is still in draft; if homeopathy advocates are going to get it changed they have until May 26 to come up with something better than what they have been turning out for the last two centuries.
 
The NHMRC's primary role is funding medical research, providing most of the grants for Australian medical scientists. However, it also sometimes conducts inquiries into issues such as the effectiveness of certain treatments or the health implications of particular practices. These do not do primary research, but summarise and examine existing studies to a standard seldom achieved elsewhere.
 
The NHMRC initiated the study to answer the question “Is homeopathy an effective treatment for health conditions, compared with no homeopathy, or compared to other treatments?”
 
In response to outrage from homeopaths, the NHMRC established the Homeopathy Working Committee to provide guidance on the best methods for conducting the study. In addition to figures such as Professor Frederick Mendelsohn, one of Australia’s leading neuroscientists, the committee included two specialists in Complimentary and Alternative Medicine, Professor Peter Brooks and Dr Evelin Tiralongo, whose history clearly refutes any notion that they are biased against ideas outside the medical mainstream.
 
The review looked at 68 conditions for which homeopathic products are marketed, ranging from asthma and flu to cholera and heroin addiction. Strangely it did not include traumatic injuries resulting from being struck by large moving vehicles.
 
“No good-quality, well-designed studies with enough participants for a meaningful result reported either that homeopathy caused greater health improvements than a substance with no effect on the health condition (placebo), or that homeopathy caused health improvements equal to those of another treatment,” the report's summary states.
 
However, showing true scientific caution the report distinguishes between conditions where research is extensive and high quality, and therefore they can definitively rule out homeopathy's effectiveness, and those where the evidence is more sparse. In the latter case it merely concludes there is no evidence homeopathy works better than placebos.
 
The report has been welcomed by the Australian Medical Association and the group Friends of Science in Medicine (FSM), which campaigns against the use of unsubstantiated products. So far homeopathy lobby groups do not appear to have responded, but no doubt will produce something similar to the allegations of bias and bullying they trotted out when the study was commissioned.
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Janet Bedwell's comment, April 12, 2014 3:07 AM
It does work and very well indeed
Janet Bedwell's comment, April 12, 2014 3:07 AM
very sad to read this
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Liquid biopsy blood test could provide rapid, accurate method of detecting solid cancers, study finds

Liquid biopsy blood test could provide rapid, accurate method of detecting solid cancers, study finds | Amazing Science | Scoop.it

A blood sample could one day be enough to diagnose many types of solid cancers, or to monitor the amount of cancer in a patient’s body and responses to treatment. Previous versions of the approach, which relies on monitoring levels of tumor DNA circulating in the blood, have required cumbersome and time-consuming steps to customize it to each patient or have not been sufficiently sensitive.


Now, researchers at the Stanford University School of Medicine have devised a way to quickly bring the technique to the clinic. Their approach, which should be broadly applicable to many types of cancers, is highly sensitive and specific. With it they were able to accurately identify about 50 percent of people in the study with stage-1 lung cancer and all patients whose cancers were more advanced.


“We set out to develop a method that overcomes two major hurdles in the circulating tumor DNA field,” said Maximilian Diehn, MD, PhD, assistant professor of radiation oncology. “First, the technique needs to be very sensitive to detect the very small amounts of tumor DNA present in the blood. Second, to be clinically useful it’s necessary to have a test that works off the shelf for the majority of patients with a given cancer.”


Even in the absence of treatment, cancer cells are continuously dividing and dying. As they die, they release DNA into the bloodstream, like tiny genetic messages in a bottle. Learning to read these messages — and to pick out the one in 1,000 or 10,000 that come from a cancer cell — can allow clinicians to quickly and noninvasively monitor the volume of tumor, a patient’s response to therapy and even how the tumor mutations evolve over time in the face of treatment or other selective pressures.


“The vast majority of circulating DNA is from normal, non-cancerous cells, even in patients with advanced cancer,” Bratman said. “We needed a comprehensive strategy for isolating the circulating DNA from blood and detecting the rare, cancer-associated mutations. To boost the sensitivity of the technique, we optimized methods for extracting, processing and analyzing the DNA.


The researchers’ technique, which they have dubbed CAPP-Seq, for Cancer Personalized Profiling by deep Sequencing, is sensitive enough to detect just one molecule of tumor DNA in a sea of 10,000 healthy DNA molecules in the blood. Although the researchers focused on patients with non-small-cell lung cancer (which includes most lung cancers, including adenocarcinomas, squamous cell carcinoma and large cell carcinoma), the approach should be widely applicable to many different solid tumors throughout the body. It’s also possible that it could one day be used not just to track the progress of a previously diagnosed patient, but also to screen healthy or at-risk populations for signs of trouble.


Tumor DNA differs from normal DNA by virtue of mutations in the nucleotide sequence. Some of the mutations are thought to be cancer drivers, responsible for initiating the uncontrolled cell growth that is the hallmark of the disease. Others accumulate randomly during repeated cell division. These secondary mutations can sometimes confer resistance to therapy; even a few tumor cells with these types of mutations can expand rapidly in the face of seemingly successful treatment.

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FDA OKs Naloxone Pen to Rapidly Reverse an Opioid Overdose

FDA OKs Naloxone Pen to Rapidly Reverse an Opioid Overdose | Amazing Science | Scoop.it

 The FDA has okayed anauto-injector formulation of naloxone (Evzio), intended to expand the use of an agent that can rapidly reverse an opioid overdose. In a call with stakeholders Thursday, Health and Human Services Secretary Kathleen Sebelius called the auto-injector a "more user-friendly version" of naloxone, which is only currently available in syringe form, although an off-label nasal version has been used in first-responder programs in several cities.


Anyone at risk for overdose can obtain a prescription for the drug, as can family members or caregivers of those at risk, Douglas Throckmorton, MD, deputy directory for regulatory programs at the FDA's Center for Drug Evaluation and Research, said during a separate telephone briefing with reporters.


The device itself gives verbal instructions on how to use it, similar to instructions relayed by automated external defibrillators found in public facilities, FDA Commissioner Margaret Hamburg, MD, said during that call.


Officials emphasized that the final direction is to seek medical care: "We don't want people to have the sense that this is the last thing they need to do," Throckmorton said. "They need to get help."


Since many prescription opioids on the market are long-acting drugs, the naloxone may not work as long as those opioids, so repeat doses may be needed, the agency said.

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Stem Cell-Derived Beta Cells Under Skin Secret Insulin Only When Needed

Stem Cell-Derived Beta Cells Under Skin Secret Insulin Only When Needed | Amazing Science | Scoop.it

Scientists at University of California, San Diego School of Medicine and Sanford-Burnham Medical Research Institute have shown that by encapsulating immature pancreatic cells derived from human embryonic stem cells (hESC), and implanting them under the skin of diabetic mouse models, sufficient insulin is produced to maintain glucose levels without unwanted potential trade-offs of the technology.


The research, published online in Stem Cell Research, suggests that encapsulated hESC-derived insulin-producing cells may be an effective and safe cell replacement therapy for insulin dependent-diabetes.


“Our study critically evaluates some of the potential pitfalls of using stem cells to treat insulin dependent-diabetes,” said Pamela Itkin-Ansari, PhD, assistant project scientist in the UC San Diego Department of Pediatrics and adjunct assistant professor in Development, Aging and Regenerative program at Sanford-Burnham.


“We have shown that encapsulated hESC-derived insulin-producing cells are able to produce insulin in response to elevated glucose without an increase in the mass or their escape from the capsule,” said Itkin-Ansari. “These results are important because it means that the encapsulated cells are both fully functional and retrievable.”


Previous attempts to replace insulin producing cells, called beta cells, have met with significant challenges. For example, researchers have tried treating diabetics with mature beta cells, but because these cells are fragile and scarce, the method is fraught with problems. Moreover, since the cells come from organ donors, they may be recognized as foreign by the recipient’s immune system – requiring patients to take immunosuppressive drugs to prevent their immune system from attacking the donor’s cells, ultimately leaving patients vulnerable to infections, tumors and other adverse events.


Encapsulation technology was developed to protect donor cells from exposure to the immune system – and has proven extremely successful in preclinical studies.


Itkin-Ansari and her research team previously made an important contribution to the encapsulation approach by showing that pancreatic islet progenitor cells are an optimal cell type for encapsulation. They found that progenitor cells were more robust than mature beta cells to encapsulate, and while encapsulated, they matured into insulin-producing cells that secreted insulin only when needed.

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New evidence that Autism 'begins long before birth'

New evidence that Autism 'begins long before birth' | Amazing Science | Scoop.it

Patchy changes in the developing brain long before birth may cause symptoms of autism spectrum disorder (ASD), research suggests.

The study, in the New England Journal of Medicine, raises hopes that better understanding of the brain may improve the lives of children with autism. It reinforces the need for early identification and treatment, says a University of California team.


US scientists analysed post-mortem brain tissue of 22 children with and without autism, all between two and 15 years of age. This reinforces the importance of early identification and intervention”, said Dr. Thomas Insel from the National Institute of Mental Health.


They used genetic markers to look at how the outermost part of the brain, the cortex, wired up and formed layers. Abnormalities were found in 90% of the children with autism compared with only about 10% of children without.


The changes were dotted about in brain regions involved in social and emotional communication, and language, long before birth, they say.

The researchers, from the University of California, San Diego and theAllen Institute for Brain Science in Seattle, say their patchy nature may explain why some toddlers with autism show signs of improvement if treated early enough.


They think the plastic infant brain may have a chance of rewiring itself to compensate. "The finding that these defects occur in patches rather than across the entirety of cortex gives hope as well as insight about the nature of autism," said Prof Eric Courchesne, a neuroscientist at the University of California San Diego.


Dr Thomas Insel, director of the National Institute of Mental Health, said: "If this new report of disorganised architecture in the brains of some children with autism is replicated, we can presume this reflects a process occurring long before birth.

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CD47-signal regulatory protein alpha (SIRPa) interaction is a therapeutic target for human solid tumors

CD47-signal regulatory protein alpha (SIRPa) interaction is a therapeutic target for human solid tumors | Amazing Science | Scoop.it

CD47, a “don't eat me” signal for phagocytic cells, is expressed on the surface of all human solid tumor cells. Analysis of patient tumor and matched adjacent normal (nontumor) tissue revealed that CD47 is overexpressed on cancer cells. CD47 mRNA expression levels correlated with a decreased probability of survival for multiple types of cancer. CD47 is a ligand for SIRPα, a protein expressed on macrophages and dendritic cells. In vitro, blockade of CD47 signaling using targeted monoclonal antibodies enabled macrophage phagocytosis of tumor cells that were otherwise protected. Administration of anti-CD47 antibodies inhibited tumor growth in orthotopic immunodeficient mouse xenotransplantation models established with patient tumor cells and increased the survival of the mice over time. Anti-CD47 antibody therapy initiated on larger tumors inhibited tumor growth and prevented or treated metastasis, but initiation of the therapy on smaller tumors was potentially curative. The safety and efficacy of targeting CD47 was further tested and validated in immune competent hosts using an orthotopic mouse breast cancer model. These results suggest all human solid tumor cells require CD47 expression to suppress phagocytic innate immune surveillance and elimination. These data, taken together with similar findings with other human neoplasms, show that CD47 is a commonly expressed molecule on all cancers, its function to block phagocytosis is known, and blockade of its function leads to tumor cell phagocytosis and elimination. CD47 is therefore a validated target for cancer therapies.


Avoiding phagocytosis by tumor-associated macrophages is required for the growth and metastasis of solid tumors (1). Accumulating evidence suggests that cell-surface expression of CD47 is a common mechanism by which cells protect themselves from phagocytosis (1). CD47 expression is required to protect transfused red blood cells, platelets, and lymphocytes from rapid elimination by splenic macrophages (24). Mobilized hematopoietic stem cells protect themselves from phagocytosis by increasing CD47 expression as they pass through phagocyte-lined sinusoids and decrease it after relocating to marrow niches (5). Moreover, CD47 expression levels predicted the probability that hematopoietic stem cells would be phagocytosed while circulating (5).


CD47 is a widely expressed transmembrane protein with numerous functions (6). CD47 functions as a ligand for signal regulatory protein-α (SIRPα), a protein expressed on macrophages and dendritic cells (7). Upon binding CD47, SIRPα initiates a signaling cascade that results in the inhibition of phagocytosis (6). This “don't eat me” signal is transmitted by phosphorylation of the immunoreceptor tyrosine-based inhibition motifs present on the cytoplasmic tail of SIRPα (8). Subsequent binding and activation of SHP-1 and SHP-2 [src homology-2 (SH2)-domain containing protein tyrosine phosphatases] blocks phagocytosis, potentially by preventing the accumulation of myosin-IIA at the phagocytic synapse (912).


Scientists now show that CD47 is expressed on all human patient cancer cells tested. It appears that CD47 is a unique non-housekeeping cell-surface marker expressed by all human cancers. Increased CD47 mRNA expression levels in some solid tumors correlated with a decreased probability of patient survival. Monoclonal antibodies targeted to CD47 enabled the phagocytosis of patient solid tumor cells in vitro, inhibited the growth of orthotopically xenotransplanted human patient tumors, and prevented the metastasis of human patient tumor cells. These results establish CD47 as a critical regulator of innate immune surveillance.

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First comprehensive atlas of human gene activity released

First comprehensive atlas of human gene activity released | Amazing Science | Scoop.it

A large international consortium of researchers has produced the first comprehensive, detailed map of the way genes work across the major cells and tissues of the human body. The findings describe the complex networks that govern gene activity, and the new information could play a crucial role in identifying the genes involved with disease.


“Now, for the first time, we are able to pinpoint the regions of the genome that can be active in a disease and in normal activity, whether it’s in a brain cell, the skin, in blood stem cells or in hair follicles,” said Winston Hide, associate professor of bioinformatics and computational biology at Harvard School of Public Health (HSPH) and one of the core authors of the main paper in Nature.


“This is a major advance that will greatly increase our ability to understand the causes of disease across the body.”


The research is outlined in a series of papers published March 27, 2014, two in the journal Nature and 16 in other scholarly journals. The work is the result of years of concerted effort among 250 experts from more than 20 countries as part of FANTOM 5 (Functional Annotation of the Mammalian Genome). The FANTOM project, led by the Japanese institution RIKEN, is aimed at building a complete library of human genes.


Researchers studied human and mouse cells using a new technology called Cap Analysis of Gene Expression (CAGE), developed at RIKEN, to discover how 95% of all human genes are switched on and off. These “switches” — called “promoters” and “enhancers” — are the regions of DNA that manage gene activity. The researchers mapped the activity of 180,000 promoters and 44,000 enhancers across a wide range of human cell types and tissues and, in most cases, found they were linked with specific cell types.


“We now have the ability to narrow down the genes involved in particular diseases based on the tissue cell or organ in which they work,” said Hide. “This new atlas points us to the exact locations to look for the key genetic variants that might map to a disease.”

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Eli Levine's curator insight, March 28, 2014 7:27 PM
There it is. As it is in our genes, so too is it in our individual psyches and societies. Check it out!
Martin Daumiller's curator insight, March 29, 2014 12:27 PM

original article: http://www.nature.com/nature/journal/v507/n7493/full/nature13182.html

 

 

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A small pressure sensor can make the difference between life and death

A small pressure sensor can make the difference between life and death | Amazing Science | Scoop.it

When people have nerve problems such as those caused by spinal injuries, they can lose the ability to feel when their bladder is full. This means that they don't know when it needs to be emptied, resulting in a build-up of pressure that can damage both the bladder and their kidneys. Now, a tiny sensor may offer a better way of assessing their condition, to see if surgery is required or if medication will suffice.


Presently, in order to observe how well the bladder is functioning, a catheter is inserted into the patient's urethra and used to fill their bladder with saline solution. This is understandably uncomfortable for the patient, plus it's claimed to provide an inaccurate picture of what's going on, as the bladder fills up much more quickly than would normally be the case.


That's why scientists at Norwegian research group SINTEF are proposing replacing the catheters with tiny pressure sensors. The current prototypes can be injected into the bladder directly through the skin, and could conceivably stay in place for months or even years, providing readings without any discomfort, and without requiring the bladder to be filled mechanically.


Patients would be able to move around normally, plus the risk of infection would reportedly be reduced. Currently readings are transmitted from the prototypes via a thin wire that extents from the senor out through the skin, although it is hoped that subsequent versions could transmit wirelessly – perhaps even to the patient's smartphone.


Next month, a clinical trial involving three spinal injury patients is scheduled to begin at Norway's Sunnaas Hospital. Down the road, plans call for trials involving 20 to 30 test subjects.


Although they're currently about to be tested in the bladder, the sensors could conceivably be used to measure pressure almost anywhere in the body.

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Germline EGFR T790M mutation results in a rare and unique lung cancer hereditary syndrome associated with a 31% risk

Germline EGFR T790M mutation results in a rare and unique lung cancer hereditary syndrome associated with a 31% risk | Amazing Science | Scoop.it

Two studies found that germline EGFR T790M mutation results in a rare and unique lung cancer hereditary syndrome associated with an estimated 31% risk for the disease in never-smokers. Lead author Adi Gazdar, MD, of the Department of Pathology, UT Southwestern Medical Center, Dallas, TX, and colleagues studied a family with germline EGFR T790M mutations over five generations (14 individuals) and combined their observations with data obtained from a literature search (15 individuals). They found that the mutation occurred in approximately 1% of NSCLCs and in less than one in 7,500 subjects without lung cancer.


Female never-smokers were overrepresented in the family cohort. Among 13 patients for whom gender and smoking status were known, nine were female never-smokers, two were male never-smokers, and two were ever-smokers (one male and one female).


“The risk of lung cancer development in never-smoking carriers is greater than the risk of heavy smokers with or without the mutation,” says Dr. Gazdar, who is an IASLC member. “Unaffected carriers with this mutation are at increased risk for the development of lung cancer irrespective of their smoking status and should be followed by increased surveillance, including low-dose computed tomography,” he adds.


The cancers associated with germline EGFR T790M mutations share several similar features with lung cancers containing sporadic EGFR mutations, such as a predominance for adenocarcinoma histology, female gender, and never-smoking status. However, a difference with lung cancers having sporadic EGFR mutations is a predominance for white ethnicity (compared with East Asian). 


“Germline EGFR T790M mutations are present in approximately 50% of all patients with baseline EGFR T790M identified in their tumor specimens before treatment,” says Dr. Yu, also an IASLC member. “In our practice, we recommend that all patients with baseline  EGFR T790M identified in their lung tumor tissue be referred to clinical genetics to discuss EGFR T790M germline testing. Carriers of this mutation need to be prospectively studied to better understand the clinical implications of this germline mutation.


The presence of a germline EGFR T790M mutation also predicts for resistance to standard tyrosine kinase inhibitors (TKIs), which adds complexity to treatment. Until newer third- and fourth-generation TKIs designed to overcome T790M-mediated resistance become available, standard chemotherapy may be the preferred first-line therapy option in the absence of another known or suspected molecular target.

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By screening over 1,000 different compounds, scientists have identified one that "vacuolizes" glioblastoma cells

By screening over 1,000 different compounds, scientists have identified one that "vacuolizes" glioblastoma cells | Amazing Science | Scoop.it

Currently, only 5 percent of patients with GBM survive longer than three years, and the average life expectancy of a patient is 15 months. Even when aggressive therapies are implemented, "GBM is essentially incurable," the researchers wrote in the study. So identifying vulnerabilities in this cancer's cells is an essential step in the development of new drug therapies.

The compound that eventually caught researchers' attention is called "Vacquinol-1," and although it certainly did kill cancer cells, it did so in a way that was unlike anything else they'd seen.

The molecule works by shutting off the cells' ability to control what gets in and out of their walls. This causes bag-like vessels filled with water and other materials, called vacuoles, to accumulate in the cells. Under these conditions, the cells eventually reach capacity and explode. But what's truly remarkable is that the noncancerous cell types that surround the cancer cells remain intact, so the treatment is actually GBM-specific.


Treatments that work in a petri dish, however, don't always work in the living. So the scientists set up a second test involving mice, and fed the compound to a group of mice with brain tumors for five days. The treatment did not cause any severe side effects. Instead, the tumors stopped growing and eventually disappeared. Moreover, six of the eight mice who received the treatment survived for 80 days following the feeding period — about 50 days longer than the mice who weren't given the drug.


Ravi Bellamkonda, a neuroscientist at the Georgia Institute of Technology who did not participate in the study, wrote in an email to The Verge that he was intrigued by the idea of being able to induce death in glioma cells specifically. "They have shown very exciting results."


But Bellamkonda also expressed some reservations about the approach, because the study's researchers had to administer what he calls "relatively high levels of the drug" to make it work. Furthermore, it's unclear if the concentrations of the drug need to be higher elsewhere in the body to reach the cancer cells — which might induce side-effects that would have been difficult to identify in the study. "This said, enhancing survival by several fold in aggressive tumor models is encouraging," he wrote. "I'd love to see more studies."


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Three-Fourths of Flu-Infected People Won’t Know It: Study Shows

Three-Fourths of Flu-Infected People Won’t Know It: Study Shows | Amazing Science | Scoop.it
Nearly three fourths of all influenza infections each season are asymptomatic, according to a recent study, indicating officials know less about the influenza virus than once thought.


Influenza causes roughly 250 000—500 000 deaths worldwide each year.[1] In the 20th century there were three influenza pandemics for which there are varying mortality estimates: 1918 A/H1N1 at least 20—40 million excess deaths, 1957 A/H2N2 about 4 million excess deaths, and 1968 A/H3N2 about 2 million excess deaths.[2—4] In 2009 a new pandemic virus,[5] influenza A(H1N1) pdm09, emerged in Mexico[6] and spread globally over 2009—10, causing an estimated 200 000 respiratory deaths and 83 000 cardiovascular deaths during the first 12 months of circulation.[7] WHO declared an end to the pandemic on Aug 10, 2010.[8] However, a further pandemic wave occurred in some European and other countries outside North America[9] in 2010—11 with reports of excess deaths in, for example, England.[10]

Internationally, influenza activity surveillance provides real-time information to inform prevention and control policy.[11] Surveillance focuses on cases seeking medical attention: the so-called tip of the iceberg of infection. Underestimation of the number of community cases leads to overestimates of severity.[12, 13] Heightened concern during a pandemic can change patient consultation thresholds and clinician recording and investigation behavior, thus distorting surveillance information.[14] Information on the community burden of influenza is key to informing control,[15] but is not routinely collected. For example, influenza transmission models, which are widely used to consider the efficacy and cost-effectiveness of vaccines, antivirals, and non-pharmaceutical countermeasures, depend on valid epidemiological estimates of the community occurrence of disease.

Testing the blood of the participants at the end of each season allowed researchers to conclude that while a great many participants proved to have been infected each year, approximately 77 percent of them never displayed any symptoms of infection, proving to be asymptomatic. Whether or not the flu infections cause unusual adverse symptoms in any of these infected participants remained unclear.


What does this mean? The study concluded that the human body might be more capable at fighting off or at least quelling the influenza virus than what is commonly thought. Health organization in North America and Europe both push for vaccination for the seasonal influenza virus in order to help stifle the virus's spread, but it has been revealed by past studies of these same organizations that the influenza virus only proves effective at preventing an infection 50 to 60 percent of the time.


The study was funded by the Medical Research Council and Wellcome Trust and published by The Lancet on March 17, 2014.


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Internet surveillance predicts disease outbreak before WHO

Internet surveillance predicts disease outbreak before WHO | Amazing Science | Scoop.it

Have you ever Googled for an online diagnosis before visiting a doctor? If so, you may have helped provide early warning of an infectious disease epidemic.


In a new study published in Lancet Infectious Diseases, Internet-based surveillance has been found to detect infectious diseases such as Dengue Fever and Influenza up to two weeks earlier than traditional surveillance methods, according to Queensland University of Technology (QUT) research fellow and senior author of the paper Wenbiao Hu.


Hu, based at the Institute for Health and Biomedical Innovation, said there was often a lag time of two weeks before traditional surveillance methods could detect an emerging infectious disease.


“This is because traditional surveillance relies on the patient recognizing the symptoms and seeking treatment before diagnosis, along with the time taken for health professionals to alert authorities through their health networks. In contrast, digital surveillance can provide real-time detection of epidemics.”


Hu said the study used search engine algorithms such as Google Trends and Google Insights. It found that detecting the 2005–06 avian influenza outbreak “Bird Flu” would have been possible between one and two weeks earlier than official surveillance reports.


“In another example, a digital data collection network was found to be able to detect the SARS outbreak more than two months before the first publications by the World Health Organization (WHO),” Hu said.

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