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 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

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

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)

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