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Screening technology used for humans a success for Sherbert the horse – Cornwall Live

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In July 2016, dressage competitor Sherbert the horse was having subtle and occasional lameness issues which owner Libby Gill said was "frustrating" because "one day, or literally one minute he would be fine, the next he would feel lame".

Lameness is an abnormal stance of an animal, usually caused by pain or a mechanical dysfunction. Sherbert suffered from it so badly during a competition at the Badminton Championships last year, that Libby and him were unable to continue despite the lameness being random.

Vets were unable to diagnose Sherbert because, when taken to the vet, he was not appearing lame. Libby was told she had to make Sherbert lame before the vet was able to help, but this was impossible as the lameness would occur on a random basis.

After a chance conversation with a friend Libby heard about Sync Thermology. A type of physiological screening that has been successful for humans for ten years and developed into a service that is accessible for use in veterinary medicine.

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Libby, from Truro, contacted Louisa Jenkins, from Camborne, the Cornwall technician for Sync Thermology.

"Thermography is essentially a test of physiology," Louisa said. "It measures the sympathetic nervous response and detects physiological abnormalities and inflammatory responses."

After consulting the vet Libby took Sherbert to Louisa, who has screening facilities in her yard with medically graded cameras also used on humans.

Louisa Jenkin, Cornwall technician for Sync Thermology.

"I took Sherbert to Louisa's yard as she has the proper facilities there to do it, and it only took about an hour and a half in total from start to finish," Libby said.

"I got the report back really quickly and it identified a few things for us to investigate. I am really pleased my friend mentioned this service to me as without it I might still be going around in circled trying to get to the bottom of it all."

Louisa said she screened Sherbert before and after letting him move around so the screen would show the physiological differences before and after work.

"You see the images and then send them through to our team of vets who interpret the images," Louisa added. "They are also trained in thermography and have interpretation software."

Read more: Man takes Cornish holiday park to court over 'filthy' chalet

The interpretation software allows the vets to pinpoint areas of distress or increased blood flow to certain areas of the animals.

She said pinpointing certain areas has helped vets in the past discover hairline stress fractures related to the area of increased blood flow in the animal.

Sync Thermology has been used on dogs, giraffes and other animals in the zoo. "There are technicians all over the country," Louisa said. "So it's pretty much a national coverage."

Louisa said this service was popular because of the little harm it brings to animals and the fact it is the only form of physiological screening which assists vets in pinpointing a problem.

After taking Sherbert to Louisa and having his issues resolved through the screening, the pair have since had a very successful Winter Dressage Championship in Hartpury in April this year. They were placed fourth in the Preliminary Area Festival Final.

"It was such a great weekend and fantastic experience," Libby said. "Sherbert was really on form and pulled it out of the bag just at the right time, I'm delighted."

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Baum named chair of APS Nutrition Physiology Research Interest Group – Newton County Times (subscription)

FAYETTEVILLE Jamie I. Baum, assistant professor of nutrition for the University of Arkansas System Division of Agriculture, has been named chair of the of the Nutrition Physiology Research Interest Group for the American Physiological Society.

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Baum named chair of APS Nutrition Physiology Research Interest Group - Newton County Times (subscription)

Cornell Postdoc Found Dead in Adirondack Mountain River – Cornell University The Cornell Daily Sun

11 hours ago Weill institute By Anne Snabes | 11 hours ago

Matthew Miller, a postdoc in the Weill Institute for Cell and Molecular Biology, died Monday in the Ausable river in the Adirondack Mountains.

Police are looking into the death as a drowning. The river had been experiencing tall water levels, according to the Adirondack Daily Enterprise.

Miller earned his Ph.D. from SUNY Upstate Medical University. Miller then worked in the lab of Prof. Anthony Bretscher, molecular biology and genetics, for the past two years where he was doing a cell biology project, trying to understand how cells are polarized, Bretscher said.

He just actually last week made a big breakthrough, which he told us about at group meeting, which we had last Wednesday, Bretscher said. He knocked out two genes out of cultured cells and saw a strong phenotype, which will tell us what those genes do.

Outside the lab, Miller was someone who lived life to the full[est], Bretscher said, known for his passion for hiking.

You never saw him in a sad mood, he said. He was always happy, and he spread happiness to everybody he met.

Miller was also a 46er, meaning that he climbed all 46 peaks in the Adirondacks that are taller than 4,000 feet, Bretscher said.

He had climbed most of them for a second time with his fianc for her to also become a 46er, he added.

Photo Courtesy of Anthony Bretscher

Photo Courtesy of Anthony Bretscher

He had lots of plants at home, he had pets at home, Bretscher said. He chose to live in a rural area as he loved nature and the outdoors.

Rob Gingras, a graduate student in the Bretscher lab and friend of Miller, echoed Bretschers sentiments, characterizing Miller as a fun guy.

Matt was an avid concert-goer, a professional fun-haver and an absolute destroyer of silence, Gingras said. He was great at the work he did, but more importantly he was a great friend to me and all who knew him.

Ccile Sauvanet, a postdoc in the Bretscher lab, also spoke to Millers presence both in and out of the lab, describing that he was talkative, joyful and always joking around.

[The lab is] kind of empty, Sauvanet said. He was kind of a presence. You couldnt miss him.

He was someone who was filling the lab and the space, the whole floor, even the whole institute, Sauvanet said.

Anne Snabes is a sophomore in the College of Arts and Sciences. She is a staff writer for the news department and can be reached at asnabes@cornellsun.com.

We are an independent, student newspaper. Help keep us reporting with a tax-deductible donation to the Cornell Sun Alumni Association, a non-profit dedicated to aiding The Sun.

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Cornell Postdoc Found Dead in Adirondack Mountain River - Cornell University The Cornell Daily Sun

The trickiest family tree in biology – Nature.com

Illustration by Jasiek Krzysztofiak/Nature

For 18 months in the early 1980s, John Sulston spent his days watching worms grow. Working in twin 4-hour shifts each day, Sulston would train a light microscope on a single Caenorhabditis elegans embryo and sketch what he saw at 5-minute intervals, as a fertilized egg morphed into two cells, then four, eight and so on. He worked alone and in silence in a tiny room at the Medical Research Council Laboratory of Molecular Biology in Cambridge, UK, solving a Rubik's cube between turns at the microscope. I did find myself little distractions, the retired Nobel prize-winning biologist once recalled.

His hundreds of drawings revealed the rigid choreography of early worm development, encompassing the births of precisely 671 cells, and the deaths of 111 (or 113, depending on the worms sex). Every cell could be traced to its immediate forebear and then to the one before that in a series of invariant steps. From these maps and others, Sulston and his collaborators were able to draw up the first, and so far the only, complete cell-lineage tree of a multicellular organism1.

Although the desire to record an organisms development in such exquisite detail preceded Sulston by at least a century, the ability to do so in more-complex animals has been limited. No one could ever track the fates of billions of cells in a mouse or a human with just a microscope and a Rubiks cube to pass the time. But there are other ways. Revolutions in biologists ability to edit genomes and sequence them at the level of a single cell have sparked a renaissance in cell-lineage tracing.

The effort is attracting not just developmental biologists, but also geneticists and technology developers, who are convinced that understanding a cells history where it came from and even what has happened to it is one of biologys next great frontiers. The results so far serve up some tantalizing clues to how humans are put together. Individual cells from an organ such as the brain could be related more closely to cells in other organs than to their surrounding tissue, for example. And unlike the undeviating developmental dance of C. elegans, more-complex organisms invoke quite a bit of improvisation and chance, which will undoubtedly complicate efforts to unpick the choreography.

But even incomplete cellular ancestries could be informative. Sulstons maps paved the way for discoveries surrounding programmed cell death and small, regulatory RNA molecules. New maps could elucidate the role of stem cells in tissue regeneration or help combat cancer a disease of unharnessed lineage expansion. Theres a real feeling of a new era, says Alexander Schier, a developmental biologist at Harvard University in Cambridge, Massachusetts, who is using genome editing to trace the cell-lineage history of zebrafish and other animals.

A cells history is written in its genome: every mutation acquired that gets passed on to daughter cells serves as a record. In 2005, the computer scientist Ehud Shapiro at the Weizmann Institute of Science in Rehovot, Israel, calculated that researchers could use the natural mutations in individual human cells to piece together how they are related2. He conceived of a corollary (in concept at least) to the C. elegans cell map, which he called the Human Cell Lineage Project. But the field, he says, wasnt ready. When we offered this vision, neither the field nor the name of single-cell genomics existed.

Fast forward a decade, and researchers have developed a suite of powerful tools to probe the biology of lone cells, from their RNA molecules and proteins to their individual and unique genomes. Now, he envisions a way of capturing the developmental course of a human, frame by frame, from fertilized egg to adult. You want the whole movie with 3D frames from beginning to end, he says. To make such a film, its not even necessary to look at the entire genome. Shapiros team is focusing on repetitive stretches of DNA peppered across the genome called microsatellites. These sequences tend to mutate more frequently than other bits of the genome, and his team is working on sequencing tens of thousands of them across the genomes of hundreds of individual human cells to determine how they relate.

Were beginning to see the rules of development in normal human beings.

Christopher Walsh, a neuroscientist and developmental biologist at Boston Childrens Hospital and Harvard Medical School, doubts that researchers will ever reconstruct a complete human cell-lineage map to match that of C. elegans, but even a less than complete tree will pay dividends, he says. Ive been studying cell lineage in the cortex for 25 years, and the idea of studying it directly in the human brain was an inconceivable dream. Now its a reality.

In experiments described in 2015, Walshs team sequenced the complete genomes of 36 cortical neurons from 3 healthy people who had died and donated their brains to research3. Reconstructing the relationship between the brain cells in an individual revealed that closely related cells can be spread across the cortex, whereas local areas can contain multiple distinct lineages. Successive generations of cells seem to venture far from their ancestral homes. One cortical neuron, for instance, was more closely related to a heart cell from the same person than to three-quarters of the surrounding neurons. We were not expecting to find that, Walsh says.

Walshs team is trying to understand how mosaicism in the brain in which some cells harbour different gene variants affects health. They have identified, for example, forms of epilepsy that occur even when just a small percentage of cells in a tiny brain region carry a disease-causing mutation. And they have found that individual neurons from healthy individuals can bear mutations that would cause seizures and schizophrenia if present more widely. It seems from this work that it matters which cells end up with a mutation. The lineage basically determines what diseases are possible, Walsh says.

Reporter Shamini Bundell finds out what can be learned from studying cells one by one.

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Other scientists are uncovering records of lifes earliest events in the genomes of adult cells. In experiments published this year4, Michael Stratton, a geneticist at the Wellcome Trust Sanger Institute in Hinxton, UK, and his team sequenced white blood cells from 241 women with breast cancer and looked for mutations found in only a subset of their blood cells. The study revealed mutations that occurred very early in development, perhaps as far back as the two-cell embryo. And they noted that the descendants of these cells do not contribute equally to the blood system of adults. This could be because one cell multiplies more efficiently than the other; or it could, as Stratton suspects, be that by chance one ends up contributing more to a developing fetus than to a placenta or other supporting tissues.

Future studies, Stratton says, will look for bottlenecks in development that limit the contribution of some cell lineages. Were beginning to see the rules of development in normal human beings, he says.

Jay Shendure, a geneticist at the University of Washington in Seattle, still remembers the day he became fascinated with cellular histories. As a 14-year-old with an interest in biology and computers, he wrote a program that modelled a mass of multiplying cells to impress his uncle, a reconstructive surgeon visiting from India. He said, This is amazing. One day youll do the same thing, and instead of a blob it will be a whole baby, Shendure recalls.

Nearly a decade later, Shendure was a first-year graduate student working for the Harvard geneticist George Church. Church presented a list of ideas (all of which, at the time, seemed totally absurd, Shendure says); one of them was to reconstruct the lineages of many cells at once, in a single experiment. Shendure toiled for six months trying to use DNA-flipping enzymes called recombinases to create a readable record in the genomes of bacteria as they divide. Rather than relying on naturally acquired mutations in the genome, the system would essentially create variants to keep track of.

Shendure eventually switched projects, but he revived the idea a few years ago when graduate students Aaron McKenna and Greg Findlay joined his laboratory in Seattle. They realized that the popular genome-editing tool CRISPRCas9 would be ideal for introducing traceable mutations to whatever part of the genome they wanted (see The lines of succession). Teaming up with Schiers lab, they unleashed CRISPRCas9 in two single-cell zebrafish embryos and instructed it to edit DNA barcode sequences that had been engineered into their genomes. They then sequenced these barcodes in cells of an adult animal and used the mutations in them to piece together their lineage5.

The trees they produced show that a small number of early-forming embryonic lineages give rise to the majority of cells in a given organ. More than 98% of one fishs blood cells, for instance, came from just 5 of the more than 1,000 cell lineages that the team traced. And although these five contributed to other tissues, they did so in much lower proportions. They were almost entirely absent from the muscle cells in the heart, for example, which was mostly built from its own small number of precursors. It was profoundly surprising to me, says Shendure. His colleague Schier says he is still trying to make sense of the data.

Jan Philipp Junker, a quantitative developmental biologist at the Max Delbrck Center for Molecular Medicine in Berlin, says that the cell-lineage trees of early embryos probably vary greatly between individuals, and that the dominance of particular lineages observed by Shendure and Schiers team could be the result of chance events. The cells of an early embryo move around, and only a fraction of them contribute to the final organism, for example. It would be more revealing, he adds, to track later developmental events, such as the formation of the three germ layers that give rise to different organs, because these events are less governed by luck.

Junker and others have developed a bevy of other CRISPR-based techniques for piecing together developmental histories. He and Alexander van Oudenaarden, a systems biologist at Utrecht University in the Netherlands, applied such an approach to track the regeneration of a damaged fin in zebrafish. Regeneration, they discovered, occurred in the same kind of way as development: few of the cell lineages that gave rise to the original fin were lost when it was remade from stem cells. The finding confirmed previous studies, but the CRISPR-based methods allowed the team to trace lineages of thousands of cells in a single experiment6.

Church says his team has used CRISPR to study mouse development and has managed to record the embryonic cell divisions that give rise to the three major germ layers, which form all the bodys organs7. I dont think were that far away from doing a complete lineage, he says.

Some researchers strive to know not just how an organisms cells relate to one another, but what happened to them along the way. Michael Elowitz and Long Cai, both at the California Institute of Technology in Pasadena, have developed a lineage tracer that creates fluorescent probes to help them observe the histories of cells as they develop8. Their method can track whether certain developmental genes have been turned on in the past for a given lineage. On 5 July, Elowitz, along with Shendure and Schier, were awarded a 4-year, US$10 million grant from the Paul G. Allen Frontiers Group to combine their technologies. The trio plan to develop synthetic chromosomes that act as tape recorders for cell-lineage history and molecular events.

Such recordings might allow scientists to tinker with a cells development in more delicate ways than current cell-reprogramming techniques allow, says Tim Liu, a synthetic biologist at the Massachusetts Institute of Technology in Cambridge who is also working on a technology to record a cells history9. You might see some version of these recorders being inserted into the cell therapies of the future, although it wont be for a while, he cautions. Im not going to go and inject my CRISPR recorder into a patient.

Cancer is where new lineage-tracing methods are likely to make waves first. Cancer is a disease of lineage its a disease of stem cells, says Walsh. One question that researchers are starting to tackle is the origin of metastatic cells, which emerge from the primary tumour and invade sometimes distant organs. They tend to be the hardest tumour cells to vanquish and the ones most likely to kill patients.

A team led by cancer geneticist Nick Navin at the University of Texas MD Anderson Cancer Center in Houston published lineage maps of two colon cancers in May10. The results showed that liver-invading metastatic cells shared many DNA mutations with the primary tumours they came from, suggesting that the metastasis had emerged at a late stage and hadnt needed a bunch of new mutations to spread. Lineage mapping could also show whether tumours really develop from single cells, as geneticists have argued, or whether they originate from multiple cells, as some imaging studies have suggested. Navin suspects that similar work could be used to direct treatment. His team and others are tracing cancer-cell lineages in patients as they begin taking drugs. They hope these studies can spot resistant lineages, allowing doctors to pick better treatments and switch medicines in time to make a difference.

Cancer is a disease of lineage its a disease of stem cells.

At the moment, however, promise in the field far exceeds the reality. And Sulstons lineage maps of C. elegans still loom large over current efforts. Stephen Quake, a bioengineer at Stanford University in California, devised his own method for tracking cellular ancestry through CRISPR and decided to test it in the worm11. Its nice to have a gold standard, Quake says. He and his team sequenced the cells of a mature animal after CRISPR had mutated its genome during development. The efforts took much less time than the year and a half that Sulston spent with his microscope. But Quake says that the picture they developed was also less than complete. Yes, it captured a key transition in roundworm development the segregation of cells bound for the intestine and those that give rise to the rest of the body but it lacked the exquisite detail Sulston observed with his eyes. Ill be perfectly blunt. Im not very impressed with my results, says Quake, who hadnt even planned to publish the work until he saw the rush of other papers using similar techniques. No one has really got it licked yet, he says.

There is an argument to be made that Sulston set the bar too high with C. elegans. This whole concept of a lineage tree is very much influenced by this classic work, says Junker. And that may deserve a rethink.

In fish, mice and humans, no two individuals cell lineage trees are likely to look exactly the same, and each probably changes throughout the individuals lifetime, as tissues repair and regenerate themselves. Junker and others hope that the new techniques will allow biologists to ask questions about the variability in lineage trees between individuals, between their organs and as they age. As Schier puts it: We dont know how many ways there are to make a heart.

It is that vast unknown that could make such work transformative, says Elowitz: It would change the kinds of questions you could ask. Sulstons map led biologists into uncharted territory, says Schier, and this could do the same. We cant tell you what exactly were going to find, but there is a sense that were going to find some new continents out there.

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The trickiest family tree in biology - Nature.com

Most Relationships Survive Infertility Challenges – WebMD – WebMD

By Robert Preidt

HealthDay Reporter

FRIDAY, July 7, 2017 (HealthDay News) -- There's good news for couples who are struggling to conceive.

Those who are undergo fertility treatment are no more likely to break up, according to a new study. It's been suggested that the disappointment of infertility and the stress of treatment can push relationships to the breaking point.

But a study of more than 40,000 women in Denmark who had fertility treatment between 1994 and 2009 found no link between it and separation or divorce. Researchers said 20 percent split up within 16 years, compared to 22 percent of women who were not treated.

The study was presented this week at the annual meeting of the European Society of Human Reproduction and Embryology in Geneva, Switzerland.

Researcher Mariana Martins said the findings should reassure couples who have had or are considering in vitro fertilization.

"Findings on the security of relationships and parenthood can be particularly helpful in supporting patients' commitment to treatment," said Martins, a psychology faculty member at the University of Porto in Portugal.

"We have previously found that subjects who divorce, re-partner and come back to treatment are the ones that five years before had the most stress," she said in a meeting news release. "We also know that despite all the strain that this infertility can bring, going through [assisted reproduction treatment] can actually bring benefit to a couple's relationship, because it forces them to improve communication and coping strategies."

Studies presented at meetings should be considered preliminary until published in a peer-reviewed journal.

WebMD News from HealthDay

SOURCE: European Society of Human Reproduction and Embryology, news release, July 5, 2017

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Most Relationships Survive Infertility Challenges - WebMD - WebMD

Constitutive resistance to viral infection in human CD141 – Science (subscription)

Research ArticleDENDRITIC CELLS

* These authors contributed equally to this work.

Present address: INSERM U955, IMRB Equipe-16, VRI, F-94010, Creteil, France.

Present address: Drukier Institute for Childrens Health, Weill Cornell Medical College, New York, NY 10021, USA.

+ See all authors and affiliations

Science Immunology 07 Jul 2017: Vol. 2, Issue 13, eaai8071 DOI: 10.1126/sciimmunol.aai8071

Aymeric Silvin

Immunity and Cancer Department, Institut Curie, PSL Research University, INSERM U932, 75005 Paris, France.

Chun I Yu

Baylor Institute for Immunology Research, Dallas, TX 75204, USA.The Jackson Laboratory for Genomic Medicine, Farmington, CT 06032, USA.The Jackson Laboratory, Bar Harbor, ME 04609, USA.

Xavier Lahaye

Immunity and Cancer Department, Institut Curie, PSL Research University, INSERM U932, 75005 Paris, France.

Francesco Imperatore

Centre dImmunologie de Marseille-Luminy, Aix Marseille University, UM2, INSERM U1104, CNRS UMR7280, France.

Jean-Baptiste Brault

Institut Curie, PSL Research University, CNRS, UMR144, Molecular Mechanisms of Intracellular Transport, 75005 Paris, France.

Sylvain Cardinaud

Centre dImmunologie et des Maladies Infectieuses-Paris, Pierre and Marie Curie University UMRS C7, INSERM U1135, CNRS ERL 8255, Paris, France.INSERM U955, IMRB Equipe-16, Vaccine Research Institute (VRI), F-94010, Creteil, France.

Christian Becker

Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine; and Immunology Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.

Wing-Hong Kwan

Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.

Ccile Conrad

Immunity and Cancer Department, Institut Curie, PSL Research University, INSERM U932, 75005 Paris, France.

Mathieu Maurin

Immunity and Cancer Department, Institut Curie, PSL Research University, INSERM U932, 75005 Paris, France.

Christel Goudot

Immunity and Cancer Department, Institut Curie, PSL Research University, INSERM U932, 75005 Paris, France.

Santy Marques-Ladeira

Immunity and Cancer Department, Institut Curie, PSL Research University, INSERM U932, 75005 Paris, France.

Yuanyuan Wang

Baylor Institute for Immunology Research, Dallas, TX 75204, USA.

Virginia Pascual

Baylor Institute for Immunology Research, Dallas, TX 75204, USA.

Esperanza Anguiano

Baylor Institute for Immunology Research, Dallas, TX 75204, USA.

Randy A. Albrecht

Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.

Matteo Iannacone

Division of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy.

Adolfo Garca-Sastre

Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.

Bruno Goud

Institut Curie, PSL Research University, CNRS, UMR144, Molecular Mechanisms of Intracellular Transport, 75005 Paris, France.

Marc Dalod

Centre dImmunologie de Marseille-Luminy, Aix Marseille University, UM2, INSERM U1104, CNRS UMR7280, France.

Arnaud Moris

Centre dImmunologie et des Maladies Infectieuses-Paris, Pierre and Marie Curie University UMRS C7, INSERM U1135, CNRS ERL 8255, Paris, France.

Miriam Merad

Precision Immunology Institute, Human Immune Monitoring Center, Tisch Cancer institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.

A. Karolina Palucka

Baylor Institute for Immunology Research, Dallas, TX 75204, USA.The Jackson Laboratory for Genomic Medicine, Farmington, CT 06032, USA.The Jackson Laboratory, Bar Harbor, ME 04609, USA.

Nicolas Manel

Immunity and Cancer Department, Institut Curie, PSL Research University, INSERM U932, 75005 Paris, France.

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Constitutive resistance to viral infection in human CD141 - Science (subscription)

How a Few Drops of Blood Led to An Immunology Breakthrough – Drug Discovery & Development

Scientists from the Research Institute of the McGill University Health Centre (RI-MUHC) may have cracked the code to understanding the function of special cells called regulatory T Cells. Treg cells, as they are often known, control and regulate our immune system to prevent excessive reactions. The findings, published in Science Immunology, could have a major impact in our understanding and treatment of all autoimmune diseases and most chronic inflammatory diseases such as arthritis, Crohns disease as well as broader conditions such as asthma, allergies and cancer.

Researchers made this discovery by investigating a rare human mutation in a gene called FOXP3. Although the importance of the FOXP3 gene in the proper function of Treg cells has been well documented, its mechanisms were still not fully understood by scientists.

We discovered that this mutation in the FOXP3 gene affects the Treg cells ability to dampen the immune response, which results in the immune system overreacting and causing inflammation, explains the studys lead author, Dr. Ciriaco Piccirillo, immunologist and senior scientist in the Infectious Diseases and Immunity in the Global Health Program at the RI-MUHC, and a professor of Immunology at McGill University. This discovery gives us key insights on how Treg cells are born and how they can be regulated.

Thanks to an international collaboration and cutting-edge technology from the Immunophenotyping Platform at the RI-MUHC, the team was able to make their discovery using only a few drops of blood from a five-week-old newborn boy who died in 2009 from a rare and often fatal inherited genetic immune disorder called IPEX. In the past 40 years, fewer than 200 cases of IPEX have been identified worldwide. Over 60 different mutations of the FOXP3 gene are known to cause IPEX and believed to result in non-functional Treg Cells.

What was unique about this case of IPEX was that the patients Treg cells were fully functional apart from one crucial element: its ability to shut down the inflammatory response, says Dr. Piccirillo.

Understanding this specific mutation has allowed us to shed light on how many milder forms of chronic inflammatory diseases or autoimmune diseases could be linked to alterations in FOXP3 functions, adds the studys first author, Khalid Bin Dhuban, a postdoctoral fellow in Dr. Piccirillos laboratory.

From fundamental biology to clinical treatment

Dr. Piccirillo and his colleagues have already developed a molecule that could restore the Treg cells' ability to control the immune system for patients with the same rare mutation. The drug has been tested in animal models and the researchers are hopeful they can also develop similar drugs that will apply for other conditions where Treg cells are known to be slightly defective such as arthritis, type I diabetes, multiple sclerosis and lupus.

"Currently, we have to shut down the whole immune system with aggressive suppressive therapies in various autoimmune and inflammatory diseases," explains Dr. Piccirillo. Our goal is to increase the activity of these Treg cells in certain settings, such as autoimmune diseases, but we want to turn it down in other settings, such as cancer. With this discovery, we are taking a big step in the right direction.

Dr. CiriacoPiccirillo is also the director of theCentre of Excellence in Translational Immunology (CETI), a newly established research coalition based at the Research Institute of the MUHC that fosters linkages among biomedical investigators and clinicians for interdisciplinary immunology research focused on the understanding and treatment of immune-based diseases.

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How a Few Drops of Blood Led to An Immunology Breakthrough - Drug Discovery & Development

The ‘Rick And Morty: Anatomy Park’ Board Game Is Almost Here – Konbini US

Can't stand to wait another two weeks for the release of Rick and Morty season 3? In that case, create your own wacky adventure by getting the Rick and Morty: Anatomy Park board game.

That's right, of all the disgusting, crazy and bonkers adventures the mad scientist and his grandson have gone through, you can now relive the season 1 episode that sees the duo venture into a microscopic theme park built inside Ruben, the homeless Santa.

(Image: Konbini)

As you've probably guessed, the goal of the game is to successfully build a theme park inside the human body. Just like the characters in the series, you'll have to face many diseases and bodily reactions to win.

However, since it's a Rick and Morty-themed game, there's a catch! If someone pulls a "Bodily Reaction" card, the holder will actually have to act out its actions. Each player will get to choose between Rick, Morty, Annie, Poncho, Roger and park operator Dr. Xenon Bloomone, all of which featured in the episode.

The game itself will feature all you need to spend a gruesome, yet hilarious evening:

46 park tiles;Nine focus group tiles;14 bodily reactions cards;Three dice;Six oversized character cards;Six character standees;Six disease standees;Six Master Plan cards;30 control cubes;Lots of Victory Points tokens;Rulebook.

Lead designer Matty Hyra announced the game will also include exclusive attractions that did not feature in the original episode. As long as "Pirates of the Pancreas" and the friendly Hepatitis C are there, it'll be a hit for sure.

Rick and Morty: Anatomy Park comes out on July 12 and is expected to cost $30.

ReadMore ->Microsoft Put The Entire First Season Of 'Dragon Ball Z' Online For Free

I like watching films and going to music festivals. Get in touch at aurelien.huet@konbini.com

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The 'Rick And Morty: Anatomy Park' Board Game Is Almost Here - Konbini US

Trump vs Putin: anatomy of an underhanded handshake – Telegraph.co.uk

Today is an historic day, as world leaders from each oftheG20 nations have gathered in Hamburg to watchDonald Trump and Vladamir Putin shake hands (and also discuss geopolitics and climate change and other such secondary stuff).

Trump's unorthodox handshakingmethodhas been the subject of much scrutiny. His typical technique has been the 'clasp, yank, release':a powerplay that sees him draw his interlocutor close, whether they like it or not.

Given Putin's similarly elaborate taste in alpha male posturing (remember his shirtless horseback riding phase?), speculation has been rife: will Trump try his usual tactics again?

Let's dissect exactly how it went down when these two titans clashed.

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Trump vs Putin: anatomy of an underhanded handshake - Telegraph.co.uk

‘Grey’s Anatomy’ season 14 spoilers: Have we seen the last of Eliza … – Hidden Remote

Photo Credit: Grey's Anatomy/ABC Image Acquired from Disney ABC Media MARIKA DOMINCZYK, JESSICA CAPSHAW

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Photo Credit: Greys Anatomy/ABC Image Acquired from Disney ABC Media

From the minute Dr. Eliza Minnick waltzed into the hallways of Grey Sloan Memorial in the seventh episode ofGreys Anatomythirteenth season as the doctor brought in to take Richards place as the hospitals Residency Director, she was fighting an uphill battle. Unfortunately for Dr. Minnick, her actions only made things worse and she quickly became one of the most hated characters in the history of the show.

When the Season 13 finale rolled around, Dr. Minnicks robotic approach to medicine and inability to see beyond a patients charts finally caught up with her. After the dust settled from the explosion thatturned the hospital upside down, Bailey finally decided to take a stand for Richard by firing Dr. Minnick from her position due to her actions during the hospital crisis. But have we truly seen the last of Dr. Minnick or will she somehow manage to find a way to stay on staff at the hospital come Season 14?

While ABC has not yet commented on her portrayer Marika Dominczyks status on the show,Dominczyk is currently not credited beyond the Season 13 finale. Add that to the fact that Dr. Minnick was fired in the finale and it seems highly likely that Dr. Minnick has left the building for good!

Greys Anatomyreturns for its fourteenth seasonThursdays this fall on ABC. Be sure to tune in!

OkayGreysfans, time to join the conversation! Do you hope that weve seen the last of Dr. Eliza Minnick after the way in which her character was introduced in Season 13 or would you like to see Dr. Minnick get a shot a redemption? Keep the conversation going in the comments section below!

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'Grey's Anatomy' season 14 spoilers: Have we seen the last of Eliza ... - Hidden Remote