SANTA CLARA, Calif.--(BUSINESS WIRE)--Agilent Technologies Inc. (NYSE: A) announced today that it has received two Life Science Industry Awards (LSIA) for Most Innovative New Products in 2019 fromBioInformatics Inc. Since 2002, the LSIA have recognized manufacturers of the tools of science that help advance biological research and drug discovery.

It is a great honor for our xCELLigence RTCA eSight, the latest addition to Agilents cell analysis portfolio, to receive one of the Most Innovative New Product in 2019 Award - Cell Biology from Bioinformatics

The Agilent products were theMagnis NGS Prep System, which received a Silver Award in the genomics category, and thexCELLigence RTCA eSight, which received a Bronze Award in the cell analysis category. Agilent was the only life sciences company nominated twice.

Id like to congratulate Agilent for winning not one, but two, Life Science Industry Awards in the categories of cell biology and genomics," said Craig Overpeck, CEO of BioInformatics Inc. xCELLigence RTCA eSight and the Magnis NGS Prep System are examples of Agilents innovative thinking and commitment to driving life science research forward.

The fully automated Magnis NGS Prep System includes reagents and protocols that make it easy to assay multiple genes and complex genetic aberrations from genomic DNA, including degraded samples such as formalin-fixed paraffin-embedded (FFPE).

With complex NGS library preparation, customers often struggle with retaining skilled lab personnel who can routinely produce high-quality results, said Kevin Corcoran, Agilent VP, and general manager for biomolecular analysis. The Magnis was designed as a turn-key automation solution to enable any lab to adopt NGS. Magnis has innovated library prep processing, ensuring optimized, reproducible results that work seamlessly with Agilents SureSelect platform.

The xCELLigence RTCA eSight provides label-free, real-time biosensor measurements, as well as kinetic imaging of the same live cell populations, independently, or simultaneously. It enables scientists to obtain unprecedented information and deep insight into cell health and their responses to a variety of chemical or biological manipulations across a wide spectrum of basic research and therapeutics fields, including cell biology, immunology, immuno-oncology, and immunotherapy.

"It is a great honor for our xCELLigence RTCA eSight, the latest addition to Agilents cell analysis portfolio, to receive one of the Most Innovative New Product in 2019 Award - Cell Biology from Bioinformatics," said Xiaobo Wang, Ph.D., who joined Agilent from ACEA, as general manager of the Flow Cytometry and Real-Time Cell Analysis Business. "The launch of xCELLigence RTCA eSight, with its highly multiplexing capabilities including real-time electronic biosensor measurements and live cell imaging with up to four independent, bright field and fluorescent channels, represents the frontier in live cell analysis. Now researchers can observe cell health and behavior in the greatest mechanistic details to analyze and more fully understand complex cellular environments and interactions through the entire course of the cell-based assay.

About Agilent Technologies

Agilent Technologies Inc. (NYSE: A) is a global leader in life sciences, diagnostics and applied chemical markets. Now in its 20thyear as an independent company delivering insight and innovation toward improving the quality of life, Agilent instruments, software, services, solutions, and people provide trusted answers to customers' most challenging questions. The company generated revenue of $5.16 billion in fiscal 2019 and employs 16,300 people worldwide. Information about Agilent is available atwww.agilent.com. To receive the latest Agilent news, subscribe to the AgilentNewsroom. Follow Agilent onLinkedIn,Twitter, andFacebook.

Naomi GoumilloutAgilent Technologies+1.781.266.2819naomi.goumillout@agilent.com

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Agilent Receives Multiple Life Science Industry Awards for Innovation - BioSpace

The buildup of scar tissue makes recovery from torn rotator cuffs, jumpers knee, and other tendon injuries a painful, challenging process, often leading to secondary tendon ruptures. New research led by Carnegies Chen-Ming Fan and published in Nature Cell Biology reveals the existence of tendon stem cells that could potentially be harnessed to improve tendon healing and even to avoid surgery.

Tendons are connective tissue that tether our muscles to our bones, Fan explained. They improve our stability and facilitate the transfer of force that allows us to move. But they are also particularly susceptible to injury and damage.

Unfortunately, once tendons are injured, they rarely fully recover, which can result in limited mobility and require long-term pain management or even surgery. The culprit is fibrous scars, which disrupt the tissue structure of the tendon.

Working with Carnegies Tyler Harvey and Sara Flamenco, Fan revealed all of the cell types present in the Patellar tendon, found below the kneecap, including previously undefined tendon stem cells.

Because tendon injuries rarely heal completely, it was thought that tendon stem cells might not exist, said lead author Harvey. Many searched for them to no avail, but our work defined them for the first time.

Stem cells are blank cells associated with nearly every type of tissue, which have not fully differentiated into a specific functionality. They can also self-renew, creating a pool from which newly differentiated cell types can form to support a specific tissues function. For example, muscle stem cells can differentiate into muscle cells. But until now, stem cells for the tendon were unknown.

Surprisingly, the teams research showed that both fibrous scar tissue cells and tendon stem cells originate in the same space the protective cells that surround a tendon. Whats more, these tendon stem cells are part of a competitive system with precursors of fibrous scars, which explains why tendon healing is such a challenge.

The team demonstrated that both tendon stem cells and scar tissue precursor cells are stimulated into action by a protein called platelet-derived growth factor-A. When tendon stem cells are altered so that they dont respond to this growth factor, then only scar tissue and no new tendon cells form after an injury.

Tendon stem cells exist, but they must outcompete the scar tissue precursors in order to prevent the formation of difficult, fibrous scars, Fan explained. Finding a therapeutic way to block the scar-forming cells and enhance the tendon stem cells could be a game-changer when it comes to treating tendon injuries.

This work was supported by the U.S. National Institutes of Health.

Source:

Carnegie Institution for Science. .

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Research: Discovery of tendon stem cells could be a game-changer when it comes to treating tendon injuries, avoiding surgery - Tdnews

DURHAM, N.C. Seven members of the Duke University faculty have been named Fellows of the American Association for the Advancement of Science (AAAS). Election as a AAAS Fellow is an honor bestowed upon AAAS members by their peers.

Dukes 2020 inductees are among 443 new fellows this year who are being recognized for scientifically or socially distinguished efforts to advance science or its applications. They are:

Ravi Bellamkonda, Ph.D., Vinik Dean of Engineering and Professor of Biomedical Engineering. For contributions to neural engineering through the use of materials for nerve and spinal cord repair and brain tumor therapies, and for innovations in engineering education.

Ashutosh Chilkoti, Ph.D., Alan L. Kaganov Professor and Chair of Biomedical Engineering. For distinguished contributions to field of biomedical engineering, particularly in the development of novel methods to deliver biotherapeutics and develop surfaces that resist protein interactions.

Tony Huang, Ph.D., William Bevan Professor of Mechanical Engineering and Mechanical Science. For distinguished contributions to the field of acoustofluidics, particularly for developing acoustic tweezers that are capable of precisely manipulating bioparticles in complex fluids.

Kevin LaBar, Ph.D., Professor of Psychology and Neuroscience in Trinity College of Arts & Sciences and associate director of the Center for Cognitive Neuroscience. For distinguished contributions to the study of the neuroscience of how emotional events modulate cognitive processes in the human brain.

Donald W. Loveland, Ph.D., Professor Emeritus of Computer Science in Trinity College of Arts & Sciences. For distinguished contributions to the field of automated deduction and development of the model elimination theorem-proving procedure. He is best known for the Davis-Putnam-Logemann-Loveland algorithm, a backtracking-based search algorithm.

Kenneth D. Poss, Ph.D., James B. Duke Professor of Cell Biology in the Medical School and Director of the Regeneration Next Initiative. For distinguished contributions to the field of organ regeneration, particularly using zebrafish as a model to study mechanisms underlying heart regeneration.

David M. Tobin, Ph.D., Associate Professor of Molecular Genetics and Microbiology in the Medical School. For distinguished contributions to the field of mycobacterial pathogenesis and host response, particularly using a zebrafish model to understand both bacterial and host contributions.

The new fellows will be presented with an official certificate and a gold and blue (representing science and engineering, respectively) rosette pin on February 15 during the 2020 AAAS Annual Meeting in Seattle.

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Seven From Duke Named Fellows of American Association for the Advancement of Science - Duke Today

The American Association for the Advancement of Science, which is the worlds largest scientific society, has named six UCLA faculty members as 2019 fellows. Since 1874, the AAAS, which publishes the journal Science, has chosen members for their distinguished efforts to advance science or its applications.

UCLAs new fellows are:

Paula Diaconescu, professor of chemistry and biochemistry. Diaconescus research focuses on the design of reactive metal complexes with applications to small molecule activation, organic synthesis and polymer formation. She is being honored for seminal contributions to the field of catalysis, particularly for applications of switchable catalytic systems to block copolymer synthesis.

David Glanzman, professor of integrative biology and physiology and of neurobiology. Glanzman studies the cell biology of learning and memory in marine snails and the zebrafish. He transferred a memory from one marine snail to another in 2018, thereby creating an artificial memory. Glanzman is being honored for his groundbreaking research on learning and memory, particularly on memory consolidation and erasure.

Margaret Jacob,distinguished professor emeritus of history. Jacobs expertise includes the history of science and intellectual history. She has played a critical role in shedding light on how the scientific and theoretical advancements of the Enlightenment worked their way into the mainstream of 17th- and 18th-century life. Jacob is being honored for distinguished and groundbreaking contributions to the cultural history of the Scientific Revolution, Newtonianism, and the Enlightenment, and effective communication of these to wider audiences.

Thomas Mason, professor ofphysical chemistry and professor of physics. Masons experimental research focuses on designing and studying new forms of soft matter that have innovative multi-scale dynamic micro- and nano-architectures and morphologies. He is being honored for distinguished contributions to the field of soft matter, particularly for creating and developing thermal-entropic passive microrheology, and for advances in emulsification and nanoemulsions.

Dr. Stephen Smale, vice dean for research at the at the David Geffen School of Medicine at UCLA and distinguished professor in the department of microbiology, immunology and molecular genetics. Smales research addresses the molecular mechanisms of gene regulation in cells of the immune system. He is being honored for distinguished contributions to the field of transcriptional regulation of eukaryotic gene expression, particularly in the immune system.

Yang Yang, professor of materials science and engineering, and the Carol and Lawrence E. Tannas, Jr. Professor of Engineering at the UCLA Samueli School of Engineering. Yangs research involves advanced technologies in thin film solar cells, transparent conductors, metal oxide transistors and other electronic devices, and has large potential for future applications at extremely low cost. He is being honored for extraordinary contributions to organic and hybrid electronic materials and interface processing, leading to highly efficient solar cells, digital memory, and organic displays.

A total of 443 scholars were selected as fellows this year. They will be honored Feb. 15, 2020, at the associations annual meeting in Seattle.

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Six professors named 2019 fellows of the American Association for the Advancement of Science - UCLA Newsroom

An intrinsically photosensitive retinal ganglion cell (ipRGC) as it would appear if you looked at a mouses retina through the pupil. The white arrows point to the many different types of cells with which it networks: other subtypes of ipRGCs (red, blue and green) and retinal cells that are not ipRGCs (red). The white bar is 50 micrometers long, approximately the diameter of a human hair. Credit: Franklin Caval-Holme, UC Berkeley

By the second trimester, long before a babys eyes can see images, they can detect light.

But the light-sensitive cells in the developing retina the thin sheet of brain-like tissue at the back of the eye were thought to be simple on-off switches, presumably there to set up the 24-hour, day-night rhythms parents hope their baby will follow.

University of California, Berkeley, scientists have now found evidence that these simple cells actually talk to one another as part of an interconnected network that gives the retina more light sensitivity than once thought, and that may enhance the influence of light on behavior and brain development in unsuspected ways.

In the developing eye, perhaps 3% of ganglion cells the cells in the retina that send messages through the optic nerve into the brain are sensitive to light and, to date, researchers have found about six different subtypes that communicate with various places in the brain. Some talk to the suprachiasmatic nucleus to tune our internal clock to the day-night cycle. Others send signals to the area that makes our pupils constrict in bright light.

But others connect to surprising areas: the perihabenula, which regulates mood, and the amygdala, which deals with emotions.

In mice and monkeys, recent evidence suggests that these ganglion cells also talk with one another through electrical connections called gap junctions, implying much more complexity in immature rodent and primate eyes than imagined.

Given the variety of these ganglion cells and that they project to many different parts of the brain, it makes me wonder whether they play a role in how the retina connects up to the brain, said Marla Feller, a UC Berkeley professor of molecular and cell biology and senior author of a paper that appeared this month in the journal Current Biology. Maybe not for visual circuits, but for non-vision behaviors. Not only the pupillary light reflex and circadian rhythms, but possibly explaining problems like light-induced migraines, or why light therapy works for depression.

The cells, called intrinsically photosensitive retinal ganglion cells (ipRGCs), were discovered only 10 years ago, surprising those like Feller who had been studying the developing retina for nearly 20 years. She played a major role, along with her mentor, Carla Shatz of Stanford University, in showing that spontaneous electrical activity in the eye during development so-called retinal waves is critical for setting up the correct brain networks to process images later on.

Hence her interest in the ipRGCs that seemed to function in parallel with spontaneous retinal waves in the developing retina.

We thought they (mouse pups and the human fetus) were blind at this point in development, said Feller, the Paul Licht Distinguished Professor in Biological Sciences and a member of UC Berkeleys Helen Wills Neuroscience Institute. We thought that the ganglion cells were there in the developing eye, that they are connected to the brain, but that they were not really connected to much of the rest of the retina, at that point. Now, it turns out they are connected to each other, which was a surprising thing.

UC Berkeley graduate student Franklin Caval-Holme combined two-photon calcium imaging, whole-cell electrical recording, pharmacology and anatomical techniques to show that the six types of ipRGCs in the newborn mouse retina link up electrically, via gap junctions, to form a retinal network that the researchers found not only detects light, but responds to the intensity of the light, which can vary nearly a billionfold.

Gap junction circuits were critical for light sensitivity in some ipRGC subtypes, but not others, providing a potential avenue to determine which ipRGC subtypes provide the signal for specific non-visual behaviors that light evokes.

Aversion to light, which pups develop very early, is intensity-dependent, suggesting that these neural circuits could be involved in light-aversion behavior, Caval-Holme said. We dont know which of these ipRGC subtypes in the neonatal retina actually contributes to the behavior, so it will be very interesting to see what role all these different subtypes have.

The researchers also found evidence that the circuit tunes itself in a way that could adapt to the intensity of light, which probably has an important role in development, Feller said.

In the past, people demonstrated that these light-sensitive cells are important for things like the development of the blood vessels in the retina and light entrainment of circadian rhythms, but those were kind of a light on/light off response, where you need some light or no light, she said. This seems to argue that they are actually trying to code for many different intensities of light, encoding much more information than people had previously thought.

###

Reference: Gap Junction Coupling Shapes the Encoding of Light in the Developing Retina by Franklin Caval-Holme and Marla B. Feller, 7 November 2019, Current Biology.DOI: 10.1016/j.cub.2019.10.025

The research was supported by the National Institutes of Health (NIH F31EY028022-03, RO1EY019498, RO1EY013528, P30EY003176).

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Scientists Shocking Discovery That Babies in the Womb May See Much More Than We Thought - SciTechDaily

Applications are invited for the post of Research Associate at Prof. Kinya Otsus research group in the School of Cardiovascular Medicine and Sciences at King's College London. The postholder will focus on mechanisms of development of heart failure. We are utilizing integrated research approach including genetically engineered disease models, miniaturized physiological technology and a range of molecular and cell biological techniques and investigating the relationship among cell death including autophagy, inflammation and mitochondrial dynamics. Minimum qualifications are PhD and/or MD with strong expertise in molecular, cellular, biochemical biology and imaging. Excellent publication history is required. Candidates should be highly motivated individuals with excellent communication skills and have the ability to work independently. A contribution to undergraduate/postgraduate education will be part of the job, at an appropriate level as determined by the Head of Division.

This post will be offered on a fixed-term contract for 3 years.

This is a full-time role - 100% FTE.

For an informal discussion to find out more about the role please contact: Professor Kinya Otsu; kinya.otsu@kcl.ac.uk

To apply, please register with the Kings College London application portal and complete your application online.

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Research Associate in the School of Cardiovascular Medicine & Sciences job with KINGS COLLEGE LONDON | 187528 - Times Higher Education (THE)

Hypoxia is a key factor that accompanies most brain pathologies, including ischemia and neurodegenerative diseases. Reduced oxygen concentration results in irreversible changes in nerve cell metabolism that entails cell death and destruction of intercellular interactions. Since neural networks are responsible for the processing, storage and transmission of information in the brain, the loss of network elements can lead to dysfunction of the central nervous system and, consequently, the development of neurological deficiency and the patient's severe disability.

This is the reason why the world's neurobiological community is currently involved in an active search for compounds that can prevent the death of nerve cells and support their functional activity under stress.

According to Maria Vedunova, Director of the Institute of Biology and Biomedicine at Lobachevsky University (UNN), the Institute's researchers propose to use the body's own potential to combat hypoxia and its consequences.

Our particular interest is in the glial cell line-derived neurotrophic factor (GDNF). These signal molecules take an active part in the growth and development of nerve cells in the embryonic period, and they are also involved in the implementation of protective mechanisms and adaptation of brain cells when exposed to various stressors in adulthood,"

Maria Vedunova, Director of the Institute of Biology and Biomedicine, Lobachevsky University

By applying advanced techniques for the study of the structure and functional activity of brain neural networks, a team of researchers from the Lobachevsky State University of Nizhny Novgorod and from the Institute of Cell Biology and Neurobiology at the Charit University Hospital in Berlin have shown that activation of the neurotrophic factor GDNF prevents the death of nerve cells and helps to maintain neural network activity after hypoxic injury. Of particular significance are the data that identify key players in the molecular cascades responsible for the implementation of the GDNF protective effect, namely, the RET, AKT1, Jak1 and Jak2t enzyme kinases.

"Thanks to the results already obtained, Lobachevsky University scientists have significantly advanced in developing the theoretical basis for a new method for correcting the hypoxic conditions of the central nervous system. The next stage of the work will be focused on studying the possibility of neurotrophic factor GDNF activation in experimental animals in a simulated hypoxic damage," continues Maria Vedunova.

It was shown by the researchers that activation of the glial cell line-derived neurotrophic factor helps protect brain cells from death during hypoxic damage and maintain the function of neural networks in the long term after the damaging effects.

A thorough understanding of the principles of work of neural networks subjected to hypoxic damage and of the protective action mechanisms of biologically active molecules of the body (the neurotrophic factor GDNF) can provide the basis for developing an effective method for correcting various CNS pathologies developing under oxygen deficiency.

The obtained results are of a fundamental nature, but they can be an important element in the comprehensive research aimed at developing new methods of diagnosis and treatment of CNS hypoxic conditions, which undoubtedly has great commercial potential.

Source:

Journal reference:

Mitroshina, E.V., et al. (2019) Intracellular Neuroprotective Mechanisms in Neuron-Glial Networks Mediated by Glial Cell Line-Derived Neurotrophic Factor. Oxidative Medicine and Cellular Longevity. doi.org/10.1155/2019/1036907.

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New method for correcting hypoxic conditions of the central nervous system - News-Medical.net

Soft tissue sarcoma cells stop a key metabolic process which allows them to multiply and spread, and so restarting that process could leave these cancers vulnerable to a variety of treatments. The enzyme that controls the process is called FBP2, and researchers from the Abramson Cancer Center of the University of Pennsylvania, who detailed their findings in Cell Metabolism, also showed that manipulating sarcoma cells to ramp up FBP2 expression slows or even stops their growth entirely. This ultimately leaves them susceptible to targeted therapies and potentially takes away their ability to develop treatment resistance.

Soft tissue sarcoma is actually a collection of distinct, rare cancer types affecting tissues that connect and surround other parts of the body, including muscle, fat, tendons, nerves, and blood vessels. While they can grow anywhere, the arms, legs, chest, and stomach are the most common sites. Because these cancers appear in so many different places in the body, their biology is incredibly diverse, making it difficult to develop one targeted treatment that can be broadly effective for all patients. Currently, the best options for treatment are surgery - which may involve amputation - chemotherapy, and radiation.

"While other cancer types associated with high mutational burden have benefitted from the development of immunotherapies, the diversity and low frequency of genetic mutations in soft tissue sarcomas have made them more difficult to treat, which is why our identification of a broadly expressed metabolic approach is potentially so exciting," said the study's senior author M. Celeste Simon, PhD, the Arthur H. Rubenstein, MBBCh Professor of Cell and Developmental Biology in Penn's Perelman School of Medicine and scientific director of the Abramson Family Cancer Research Institute. The study's lead author is Peiwei Huangyang, who performed the work while obtaining her PhD in Simon's lab.

While FBP2 is broadly expressed in normal cells, soft tissue sarcomas have a way of dramatically suppressing it. Building on their previous work - published in Nature - showing a related pathway controlled by FBP1 serves a similar function in renal and liver cancer, Simon and her team used mouse models to show that causing soft tissue sarcoma cells to re-express FBP2 the way healthy cells do stops the cancer from growing, potentially making it more vulnerable to both targeted and immune-based therapies.

Essentially, once they start acting like normal cells, they don't hide and grow the way cancer normally does."

M. Celeste Simon, PhD, study's senior author

The team also found that the enzymes involved in this process are located in the cell's nucleus, meaning this pathway could stop cancer cells from adapting to their natural environment and becoming resistant to cytotoxic drugs. It's tied to the understanding of how cells respond to environmental stresses to alter their metabolism and survive, which is the work that received the 2019 Nobel Prize in Physiology or Medicine.

While this study shows the importance of FBP2, further research is needed to show that using drugs to manipulate cells to re-express FB2 will have the expected effect. Simon points out that these drugs already exist in other cancer treatments - specifically blood cancers - meaning the pipeline to translate this approach to patients should be relatively rapid if research proves it is effective.

Source:

Journal reference:

Huangyang, P., et al. (2019) Fructose-1,6-Bisphosphatase 2 Inhibits Sarcoma Progression by Restraining Mitochondrial Biogenesis. Cell Metabolism. doi.org/10.1016/j.cmet.2019.10.012.

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Broadly expressed metabolic approach could make sarcoma susceptible to targeted therapies - News-Medical.net