May 4, 2017

10x Genomics, a company focused on enabling the mastery of biology by accelerating genomic discovery, today announced publication of an article in the journal Nature of a collaborative research study with researchers at the Stanford University School of Medicine. The article entitled, "Non-equivalence of Wnt and R-spondin ligands during Lgr5+ intestinal stem-cell self-renewal," utilizes the 10x Genomics' Single Cell 3' Solution for single-cell RNA-seq (scRNA-seq) to unravel the priming and self-renewal mechanisms of intestinal stem cells (ISCs).

The renewal and differentiation of Lgr5+ ISCs is critical to the continuous regeneration of the epithelial lining of the gut, which enables us to absorb nutrients and provides a barrier to protect us from the external environment. Disruptions in this process can lead to or worsen human intestinal disorders such as inflammatory bowel disease (IBD), gastrointestinal cancer and Celiac disease.

This carefully regulated process occurs within a stem-cell niche called the intestinal crypt, and depends on Wnt signaling, which can be turned up by Wnt and R-spondin (RSPO) ligands. The authors sought to identify the unique functional roles of Wnt and RSPO ligands for regulating Lgr5+ ISCs and the relative contributions of both ligands to in vivo Wnt signaling and stem-cell biology.

The authors were able to show using in vivo experiments that Wnt and RSPO are not redundant signals. RSPO was shown to expand stem cell number. Although Wnt was needed to maintain Lgr5+ ISCs in the presence of RSPO, Wnt was not sufficient to induce additional numbers of Lgr5+ ISCs above a certain threshold, demonstrating that RSPO, and not Wnt, establishes the set point for Lgr5+ ISC number. The authors performed single-cell RNA-seq to definitively show that the signaling contributions of Wnt and RSPO elicited distinct effects on ISCs, by fully characterizing the expression profile for each unique cellular subtype on a cell-by-cell basis upon perturbation of those signals in vivo.

By characterizing gene expression from 13,102 single cells, Yan and colleagues were able to show that Lgr5- control cells represented differentiated cell types of the small intestinal lineages, including Paneth, goblet, enteroendocrine, enterocyte, pre-enterocyte, and tuft cells. The Lgr5+ cells consisted of three cellular sub-populations, corresponding to cycling stem cells, non-cycling stem cells, and transit amplifying cells. The authors were able to further show that these three distinct sub-populations of Lgr5+ cells were each uniquely affected by perturbations in Wnt and RSPO signaling, conclusively demonstrating that Wnts are priming factors that enable stem cells to be competent by expressing RSPO receptors on their cell surface, whereas RSPOs are actual self-renewal factors that expand stem cell number.

"Single-cell analysis provided conclusive evidence for the unique roles of Wnt and RSPO signaling to their respective function, either co-operatively priming Lgr5+ cells for competency, or for RSPO-mediated self-renewal," said Grace Zheng, Ph.D., research scientist at 10x Genomics. "This powerfully illustrates the utility of single-cell RNA-seq to monitor discrete stem-cell states and their dynamic perturbation. To do this with any other technology would have been extremely cumbersome, if not impossible."

"We are very excited about this result, and it opens up the possibility that analogous multi-tiered regulation by priming and self-renewal factors may be a generalized property of stem cells across other organ systems, either through Wnt and RSPO or functionally equivalent stem-cell niche components," said Ben Hindson, Ph.D., president, co-founder, and chief scientific officer of 10x Genomics. "This could have wide-reaching implications for stem-cell research and potentially yield new insight towards therapeutic applications in the future."

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New study uses 10x Genomics' Single Cell 3' Solution to unravel stem cell self-renewal mechanism - News-Medical.net

May 3, 2017 The cover image of the MCB journal. Credit: IDIBELL

Researchers from the Cell death group of the Bellvitge Biomedical Research Institute (IDIBELL), led by Dr. Cristina Muoz-Pinedo, have characterized the cell death process due to starvation, in which the endoplasmic reticulum plays a leading role. Their work, chosen as the cover of the latest Molecular and Cellular Biology journal, was carried out within TRAIN-ERs, a European collaborative action that studies diseases associated with this cellular organelle.

"Usually, programmed cell deathalso called apoptosisfollows a biochemical pathway related to the permeabilization of mitochondria; However, we observed that in cases of cell death due to lack of glucose, cells die in an unexpected way, following a process similar to what we would expect from an immune response", explains Dr. Cristina Muoz-Pinedo, last author of the study.

In cell-death-related treatments such as chemotherapy, the mitochondrial pathway is activated. Instead, when starved, cells activate the so-called "death receptors" on their membrane, which are normally used by the lymphocytes of the immune system to attack and destroy infected cells.

IDIBELL researchers have been able to relate the activation of these membrane receptors to the endoplasmic reticulum, a cellular organelle involved in protein synthesis and lipid metabolism, as well as intracellular transport. "Feeling the stress produced by the lack of nutrients, the reticulum send an alarm signal that triggers the appearance of death receptors in the membrane", says Dr. Muoz-Pinedo.

"According to our in vitro results, we assume that this is how the tumor cells located in the center of a tumorthe so-called necrotic coredie, because there are never enough nutrients in those areas", adds the IDIBELL researcher. "On the other hand, in ischemia, besides the lack of oxygen there is also cell death due to lack of glucose, so this process could also be related to the activity of the endoplasmic reticulum at a biochemical level".

Explore further: Scientists reveal alternative route for cell death

More information: Raffaella Iurlaro et al, Glucose Deprivation Induces ATF4-Mediated Apoptosis through TRAIL Death Receptors, Molecular and Cellular Biology (2017). DOI: 10.1128/MCB.00479-16

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Starvation causes atypical cell death - Phys.Org

Yale deans Kyle Vanderlick and Lynn Cooley, faculty member Dr. Arthur Horwich, alumnus Jonathan Ayers, and outstanding undergraduates were honored at the 103rd annual meeting and awards dinner of the Yale Science & Engineering Association (YSEA), held on April 28 in the Presidents Room at the Quinnipiack Club.

At the event, YSEA officials announced that the organization had created the Dean Kyle Vanderlick Research Grantin recognition of the deans legacy in establishing the Yale School of Engineering and Applied Science as a bridge between the sciences and the humanities on the Yale campus and beyond. YSEA President John Siemon credited Vanderlick with greatly expanding the scope of the School of Engineering and Applied Science (SEAS) since she was appointed dean in 2008. Through this transformation, he said, interest and enrollment in Yales engineering programs and student groups have flourished.

He also cited the numerous cross-disciplinary collaborations between SEAS and other fields of research at Yale. The grant will be available annually to Yale science and engineering undergraduates who demonstrate the values that Dean Vanderlick has exemplified throughout her tenure at SEAS.

YSEA officials also announced the awardees for three honors:

Lynn Cooley, dean of the Graduate School of Arts and Sciences, theC.N.H. Long Professor of Genetics, and professor of cell biology and of molecular, cellular, and developmental biology, received the YSEA Award for Meritorious Service.

Cooley has focused her research on the mechanisms and regulation of oogenesis inthe fruit fly (drosophila). In her work, she has elucidated numerous aspects of Drosophila biology, utilizing techniques for genetic analysis in Drosophila that she has pioneered in her career.

At Yale, she has served as a member of the Biological Sciences Advisory Committee (20052007), director of the Combined Program in the Biological and Biomedical Sciences (20012014), director of the Medical Research Scholars Program (20062014), and director of the China Scholarship CouncilYale World Scholars Program (20062014).

Dr. Arthur Horwich, Sterling Professor of Genetics and Pediatrics at the Yale School of Medicine and an investigator at Howard Hughes Medical Institute, received the YSEA Award for Advancement of Basic & Applied Science

His research into protein foldingestablished the existence of a large class of proteins termed chaperonins, which help proteins fold correctly in various cellular locales. Previously, researchers believed that proteins folded into shape by themselves

In addition to their significance in fundamental biology, chaperonins have been recognized as being of great medical significance: Derangement of protein folding has been connected with numerous disorders, including neurodegenerative diseases. Most recently Horwichs laboratory has been studying the role of misfolding of the enzyme known as superoxide dismutatse I (SOD1), which leads to a specific type of amyotrophic laterals sclerosis (ALS).

Jonathan Ayers 78, chair, president and CEO of IDEXX Laboratories, Inc. received the YSEA Award for Distinguished Service to Industry, Commerce or Education

IDEXX is a leading innovator in veterinary medicine, producing test protocols, novel chemistry, diagnostic equipment, and software to deliver rapid and accurate results. IDEXX also protects water supplies for millions of people worldwide through their drinking water and wastewater quality tests. In addition, IDEXX tests help to protect dairy, poultry and livestock around the world.

IDEXXs growing global workforce of 7,000 includes over 700 veterinariansand Ph.D.s who bring a consistent stream of diagnostic and software innovations to the veterinary industry.

Siemon cited the companys sponsorship of STEM activities in local schools and universities, adding that IDEXX expands this culture of innovation far beyond its walls, both retaining and attracting top talent.

The YSEA Awards for Outstanding Academic Achievement were presented to the science and engineering undergraduates with the highest GPAs in their classes after five and seven terms, respectively. The winners are

Malini Gandhi 17 Molecular, cellular & developmental biology, GPA of 4.0

Anna Russo 17 Applied mathematics, GPA of 4.0

Christopher Chute 17 Mathematics, GPA of 3.99

Yumi Koga 17 Chemistry, GPA of 3.99

Stan Swidwinski 17 Electrical engineering/computer science, GPA of 3.99

Christopher Chute 17 Mathematics/computer science, GPA of 3.99

Julia Borowski 18 Chemistry, GPA of 4.00

Martin Lim 18 Economics/chemistry, GPA of 4.00

Adam Lowet 18 Cognitive science/molecular, cellular & developmental biology, GPA of 4.00

Scott Stankey 18 Mathematics, GPA of 4.00

Sara Meyers 18 Molecular, cellular & developmental biology, GPA of 3.99

Lionel Jin 18 Molecular, cellular & developmental biology, GPA of 3.99

Ilana Kaufman 18 Physics, GPA of 3.99

James Diao 18 Molecular biophysics & biochemistry, GPA of 3.99

Alexander Epstein 18 Molecular, cellular & developmental biology, GPA of 3.99

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Deans Vanderlick and Cooley among those honored by YSEA - Yale News

CAMBRIDGE, Mass., May 1, 2017 /PRNewswire/ --Dragonfly Therapeutics, Inc. ("Dragonfly"), today announced the addition of Dr. Asya Grinberg to its senior team. Dr. Grinberg joins Dragonfly from Acceleron Pharma (Nasdaq: XLRN), where she led a multidisciplinary team in cell biology and protein chemistry. As Dragonfly's Head of Biologics, Dr. Grinberg leads its protein engineering, purification, characterization and structural biology team.

Dr. Grinberg brings to Dragonfly an extensive track record of scientific accomplishments and creativity in protein-based drug development. "Asya's experience developing multiple drug candidates from concept deep into the clinic represents a great addition to our company," stated Dragonfly co-founder and head of the Koch Institute for Integrative Cancer Research at MIT, Dr. Tyler Jacks.

Prior to joining Dragonfly, Dr. Grinberg spent 12 years at Acceleron Pharma discovering and developing novel protein therapeutics for treatment of hematopoietic diseases and cancer. She most recently served as Senior Director of Cell Biology and Protein Chemistry and has been a strong scientific and strategic driver of internal innovation. Dr. Grinberg's efforts were instrumental to the development of five clinical candidates, including Luspatercept (currently in Phase III testing) for treatment of beta-thalassemia and MDS. Dr. Grinberg is the key inventor of the IntelliTrap drug discovery platform targeting the TGF-beta superfamily. Dr. Grinberg received her M.Sc. in Bioorganic Chemistry from Moscow State University and did her Ph.D. studies at Max Delbrck Centre for Molecular Medicine in Germany. She completed her post-doctoral fellowship at the University of Michigan supported by the at Howard Hughes Medical Institute. Dr. Grinberg is a co-author of more than 40 scientific publications, and co-inventor on a number of patents.

"We are thrilled to welcome Dr. Grinberg to Dragonfly," said Dragonfly co-founder and CEO Bill Haney. "Her depth of understanding of protein therapeutics, coupled with her talent for innovation, will accelerate our development of novel cancer therapies, which use Natural Killer cells to both enhance the effectiveness of T cell performance and attack cancer directly."

About Dragonfly

Dragonfly Therapeutics is a discovery-stage company developing drugs to stimulate immune responses against cancer.

Our scientific founders are major figures in cancer biology and immunology and launched Dragonfly to harness the power of the innate immune system to provide breakthrough cancer treatments for patients.

For more information visit: http://www.dragonflytx.com, https://www.facebook.com/dragonflytherapeutics/, https://twitter.com/dragonflytx

Media Contact: Maura McCarthy 617-588-0086 x702 rel="nofollow">maura@dragonflytx.com

To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/leading-protein-scientist-dr-asya-grinberg-joins-dragonfly-therapeutics-as-head-of-biologics-300448535.html

SOURCE Dragonfly Therapeutics, Inc.

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Leading Protein Scientist Dr. Asya Grinberg Joins Dragonfly ... - Markets Insider

PLEASANTON, Calif.--(BUSINESS WIRE)--10x Genomics, a company focused on enabling the mastery of biology by accelerating genomic discovery, today announced publication of an article in the journal Nature of a collaborative research study with researchers at the Stanford University School of Medicine. The article entitled, Non-equivalence of Wnt and R-spondin ligands during Lgr5+ intestinal stem-cell self-renewal, utilizes the 10x Genomics Single Cell 3 Solution for single-cell RNA-seq (scRNA-seq) to unravel the priming and self-renewal mechanisms of intestinal stem cells (ISCs).

The renewal and differentiation of Lgr5+ ISCs is critical to the continuous regeneration of the epithelial lining of the gut, which enables us to absorb nutrients and provides a barrier to protect us from the external environment. Disruptions in this process can lead to or worsen human intestinal disorders such as inflammatory bowel disease (IBD), gastrointestinal cancer and Celiac disease.

This carefully regulated process occurs within a stem-cell niche called the intestinal crypt, and depends on Wnt signaling, which can be turned up by Wnt and R-spondin (RSPO) ligands. The authors sought to identify the unique functional roles of Wnt and RSPO ligands for regulating Lgr5+ ISCs and the relative contributions of both ligands to in vivo Wnt signaling and stem-cell biology.

The authors were able to show using in vivo experiments that Wnt and RSPO are not redundant signals. RSPO was shown to expand stem cell number. Although Wnt was needed to maintain Lgr5+ ISCs in the presence of RSPO, Wnt was not sufficient to induce additional numbers of Lgr5+ ISCs above a certain threshold, demonstrating that RSPO, and not Wnt, establishes the set point for Lgr5+ ISC number. The authors performed single-cell RNA-seq to definitively show that the signaling contributions of Wnt and RSPO elicited distinct effects on ISCs, by fully characterizing the expression profile for each unique cellular subtype on a cell-by-cell basis upon perturbation of those signals in vivo.

By characterizing gene expression from 13,102 single cells, Yan and colleagues were able to show that Lgr5- control cells represented differentiated cell types of the small intestinal lineages, including Paneth, goblet, enteroendocrine, enterocyte, pre-enterocyte, and tuft cells. The Lgr5+ cells consisted of three cellular sub-populations, corresponding to cycling stem cells, non-cycling stem cells, and transit amplifying cells. The authors were able to further show that these three distinct sub-populations of Lgr5+ cells were each uniquely affected by perturbations in Wnt and RSPO signaling, conclusively demonstrating that Wnts are priming factors that enable stem cells to be competent by expressing RSPO receptors on their cell surface, whereas RSPOs are actual self-renewal factors that expand stem cell number.

Single-cell analysis provided conclusive evidence for the unique roles of Wnt and RSPO signaling to their respective function, either co-operatively priming Lgr5+ cells for competency, or for RSPO-mediated self-renewal. said Grace Zheng, Ph.D., research scientist at 10x Genomics. This powerfully illustrates the utility of single-cell RNA-seq to monitor discrete stem-cell states and their dynamic perturbation. To do this with any other technology would have been extremely cumbersome, if not impossible.

We are very excited about this result, and it opens up the possibility that analogous multi-tiered regulation by priming and self-renewal factors may be a generalized property of stem cells across other organ systems, either through Wnt and RSPO or functionally equivalent stem-cell niche components, said Ben Hindson, Ph.D., president, co-founder, and chief scientific officer of 10x Genomics. This could have wide reaching implications for stem-cell research and potentially yield new insight towards therapeutic applications in the future.

The lead author of the study is Kelley Yan, M.D. Ph.D., lead author of the study, formerly a postdoctoral fellow at Stanford and now an Assistant Professor of Medicine and of Genetics and Development in the Columbia Center for Human Development at Columbia University Medical Center. The senior author is Calvin Kuo, M.D. Ph.D., Professor of Medicine at Stanford.

The article entitled, Non-equivalence of Wnt and R-spondin ligands during Lgr5+ intestinal stem-cell self-renewal, can be accessed from Nature online: http://dx.doi.org/10.1038/nature22313

For more information about this research, visit the Kuo Lab at Stanford: http://kuolab.stanford.edu/index.html

About 10x Genomics

10x Genomics is changing the definition of sequencing by providing an innovative genomics platform that dramatically upgrades the capabilities of existing sequencing technologies. This is achieved through a combination of new microfluidic science, chemistry and bioinformatics. By implementing GemCode Technology within the Chromium System, researchers can now, for the first time, find new structural variants, haplotypes and other valuable genomic information with comprehensive workflows for Single Cell, V(D)J, Genome, Exome and de novo Assembly applications that incorporate their pre-existing sequencing technologies. http://www.10xGenomics.com.

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Recent Study Published in Nature Unravels a Novel Pathway for ... - Business Wire (press release)

For USC Stem Cell researcher Leonardo Morsut, the word set refers to a collection of scientific data. Set is also the prelude to spiking a volleyball over the net something he used to do for a living as a professional athlete in Italy.

Morsut in action on the volleyball court (Photo/Courtesy of Leonardo Morsut)

In my mind, professional volleyball was always a side project, said Morsut, who played for seven years for the professional teams in his hometown of Padova and in Trentino. It was science that was the main thing.

True to his words, Morsut has always put research first. Even while playing pro volleyball for seven hours a day, he found the time and energy to attend the University of Padova, where Galileo was once a lecturer. Morsut earned bachelors and masters degrees in medical biotechnologies before pursuing a second bachelors in mathematics.

Then, at age 25, at the peak of his volleyball career, he quit. He walked away from fame and a handsome salary to lead the humble life of a PhD student at the University of Padova. His decision made national headlines in Italy.

People ask me if I regretted it, he said. I dont even think about leaving that way. There wasnt really a turning point. There was just one path.

As a PhD student, he pursued research in bioscience, genetics and the molecular biology of development. He spent years focused on mouse gastrulation, the early embryonic phase during which a ball of cells organizes itself into distinct layers as a prelude to organ formation.

In the midst of this research, he picked up an unrelated side project: how stem cells behave differently depending upon whether theyre on a hard or a soft surface. Specifically, he and his colleagues found that when stem cells are on a hard surface, they react by producing two signals called YAP and TAZ that encourage them to become bone cells. The side project quickly became his main project, and Morsut and his team published their discovery in the journal Nature.

It was really a rush and a blast, Morsut said. And it was what launched my career because then it was easier to get a postdoc in a bigger lab.

After receiving his PhD and spending an additional postdoctoral year at the University of Padova, he became increasingly fascinated by the emerging field known as synthetic biology.

Synthetic biology is pretty much trying to bring the engineering approach of building things into biology.

Leonardo Morsut

Synthetic biology is pretty much trying to bring the engineering approach of building things into biology, Morsut said. You think about the biological system not as something that you want to learn about, but as something that you want to use to achieve a goal.

Inspired by this approach, he accepted a postdoctoral fellowship in the lab of one of the founders of synthetic biology: Wendell Lim at the University of California, San Francisco.

Wendell and I didnt even know what I was going to work on, but we liked each other, Morsut said.

After some early experimentation, Morsut settled on his main project: building a synthetic cellular communication system known as synNotch, which enables scientists to direct the behavior of cells in useful ways.

Morsut created synNotch by co-opting a relatively simple natural communication system, called Notch, in which a cell uses a sensor on its surface to recognize and trigger a particular response to a specific signal. In Morsuts synthetic version of Notch, he swapped in a new sensor, allowing him to control which signal the sensor recognizes, as well as what the cell does in response.

SynNotch or a similar system could have many potential medical applications. For example, scientists could swap in a sensor that enables an immune cell to recognize a signal from a tumor and then respond with an attack. Alternatively, researchers could use this technology to prompt cells to differentiate and organize into tissues with special properties, such as enhanced injury resistance or regenerative capacity.

The breakthrough earned Morsut a position as the newest assistant professor of stem cell biology and regenerative medicine at USC. At the same time, his wife Sabina accepted a postdoctoral fellowship in art history at the university. Other big changes are on the horizon: The couple, who originally met when they were 12 years old in their hometown of Padova, will expand their family with the arrival of their second child in June.

When hes not enjoying his family or building tissues in the lab, Morsut can be found on the yoga mat, developing his meditation and hatha yoga practice under Yogarupa Rod Stryker.

As he starts his own lab at USC, Morsut plans to use synNotch to direct the differentiation of stem cells into blood vessels, which can supply oxygen and nutrients to engineered tissues and organs in the future. He is also working to develop additional synthetic biology tools and looks forward to collaborating with researchers from across the university, especially at the USC Viterbi School of Engineering and the USC Michelson Center for Convergent Bioscience, slated to open this fall.

The stem cell department is very exciting, and it has a lot of potential and a lot of forward thinking, Morsut said. Engineering is also a strength of USC, and there is interest on both sides to grow more at that interface. That is definitely something that will benefit my research program and vice versa. I have high expectations.

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The gift will support early-stage research projects at three California university stem cell centers, including USCs.

Middle and high school students visit labs and tour USCs stem cell research center,cancer center and Keck Hospital of USC.

Adnan Chowdhury ventures into uncharted scientific territory.

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From pro volleyball to biology: USC scientist is at the top of his game - USC News

Humanity has come a long way in understanding human biology and the applications of this knowledge to the reduction of human suffering by disease; however, we still have a long way to go. Some of the most basic processes of the cell are still not completely understood, and this lack of understanding leaves humanity in a particularly precarious position.

There are some 20,000 gene-coding proteins in the human cell, and some of the most devastating diseases arise from the dysfunction of just a single gene-product. Niemann-Pick Type C (NPC) represents one of these diseases, and arises when one of two critical NPC genes is mutated in both parents and passed onto their offspring.

When the NPC proteins are mutated, the recycling center of the cell, the lysosome, is unable to recycle certain moleculesmost notably, cholesterol. As a result of this inability to recycle certain molecules, they accumulate inside the cell and ultimately lead to the symptoms associated with NPC disease. Some of the more prominent symptoms associated with this devastating disease include an enlarged liver and spleen, balance problems, seizures, and many other neurological symptoms that usually develop during childhood or early adolescence. The prognosis is very poor, and this disease always results in death.

Though NPC disease is not yet completely understood, there are passionate researchers who have dedicated their careers to understanding how this disease develops and how it might be treated. Understanding NPC disease requires scientists to better understand basic processes of cell metabolism and NPC proteins.

These researchers are committed to unlocking these secrets of the cell and using their findings to develop treatments for NPC. One particularly relevant area of NPC research is focused on understanding why neurons are so disproportionately affected by the disease.

Dr. Steven Walkley, a leading researcher in the field of NPC research, is a Neuroscientist at the Albert Einstein College of Medicine. Walkley has a strong interest in genetic brain diseases and strives to understand not only how NPC disease affects neurons, but is also committed to investigating and developing therapies to treat the disease. Unlike most other cells in the body, the neurons that you are born with do not replicate, and must be maintained for a lifetime.

Walkley stresses that this static nature of brain cells contributes to their keen sensitivity of even the slightest changes in homeostasis. As a result, these cells are disproportionately damaged by the accumulation of cholesterol and other molecules as a result of NPC, and Walkley is determined to understand why this happens and how it can be mitigated.

To better understand how neurons are affected by NPC disease, Walkleys lab studies mice with a naturally occurring NPC disease to understand the disease pathology and potential treatments. In fact, he discovered one of the first treatments for NPC diseasemiglustat, a drug that was originally developed as a potential therapy for Tay-Sachs and Gaucher diseases.

Furthermore, his labs discovery of the amazing therapeutic effects of a compound called cyclodextrin was one of his most significant contributions to the field. Cyclodextrin has been shown to significantly increase the lifespan of mice and cats with naturally occurring models of NPC disease.

Another leading researcher in this field is Dr. Charles Vite, a veterinary Neurologist at the University of Pennsylvania. Vite uses a cat as a model to study NPC disease in the brainstriving to understand why neurons are disproportionately affected and how therapies might mitigate this. He explained that sometimes larger models of the disease better mirror what is seen in the human diseaseand he often works in close collaboration with Walkley to understand how findings in the mouse model compare to the larger cat model. A prominent and vital component of Vites contributions to the field are his investigations on how cyclodextrin treats NPC in his cat model; the results have been extremely uplifting. Upon treatment with cyclodextrin, cats with the disease live about three years longer, on average, than they do when left untreated!

I had the great honor of speaking with both of these leading researchers. During our conversations, I came to realize how truly committed these researchers are to their fields. Their love for neuroscience, deep curiosity and passion to better the lives of individuals afflicted with this disease left me in awe. Thanks to dedicated researchers like Walkley and Vite, scientists are understanding more about NPC and basic cell biology every day. Things are finally starting to look brighter for those who are afflicted with NPC and their families.

Walkley and Vite both agree that cyclodextrin is one of the most promising therapies out there for NPC today, and it is currently in clinical trials. Vite believes that one of the greatest difficulties in working with this disease is that too often, individuals do not receive these developing treatments until the disease has already progressed significantly. To avoid this problem, researchers are looking into the development of newborn screening for NPC, and this is something that will likely be established as a concrete treatment for NPC is developed.

As current students, it is critical to realize the importance of the scientific pursuit of knowledge for humanity. With a better understanding of biology comes an ever- increasing freedom from human disease and suffering. With this in mind, we should dive into our coursework with vigor, and look for opportunities to get involved with current research. Walkley stressed the importance for college students to reach out to local scientists to get involved.

The fight for knowledge is by no means finishedwe will continue this trek into the unknown where scientists of today leave off. With every increase in knowledge, we will bring humanity one step closer to a freedom from human suffering by disease.

Denston Carey is a student majoring in cell and molecular biology. He can be reachedat [emailprotected]

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Unlocking the secrets of the cell to heal humanity - Quad (subscription)

3D printers have been causing revolutions in many different fields, with materials as different as food, mud, plastic, and plants. The game-changer is that you can create very precise, complex shapes that werent able to be created before. Another use of 3D printing is a potentially life-saving one. 3D bioprinters are being developed that can print out tissues and organs. Some that are being tested now areskin cells, bone, heart tissue, and now cartilage. A team of researchers at Sahlgrenska Academy has created cartilage tissue by printing stem cells with a 3D-bioprinter. It appears to be just like human cartilage and could be used to replace damaged cartilage.

In nature, the differentiation of stem cells into cartilage is a simple process, but its much more complicated to accomplish in a test tube. Were the first to succeed with it, and we did so without any animal testing whatsoever, says Stina Simonsson, Associate Professor of Cell Biology, who led the research.

The lead researcher, Stina Simonsson, holding some 3D-printer cartilage. Image credits: Elin Lindstrm Claessen.

The researchers took cartilage cells from patients who had recently had knee surgery and their cells were manipulated to become pluriplotent, so they can develop into many different types of cells. Next, they created a scaffold to print the cells on. The stem cells were coated withnanocellulose to survive the printing process. Once printed, the stem cells multiplied and were given growth factors so they differentiated into cartilage tissues. The cells formed cartilage cells on the printed structure. After a few weeks, the cells lost their ability to change into other cells. This change is good because pluripotency increases the risk of tumour formation.

We investigated various methods and combined different growth factors. Each individual stem cell is encased in nanocellulose, which allows it to survive the process of being printed into a 3D structure. We also harvested mediums from other cells that contain the signals that stem cells use to communicate with each other so called conditioned medium. In laymans terms, our theory is that we managed to trick the cells into thinking that they arent alone, says Stina Simonsson.

Cartilage can be 3D-printed. Image credits: United States NIH National Institute of Arthritis and Musculoskeletal and Skin Diseases.

The 3D bio-printed structure is very similar to human cartilage. Experienced surgeons did not see a difference between natural and bio-printed cartilage. The cells appear well-formed under the microscope and similar to the patients own cartilage.

When this method is perfected, cartilage could be 3D printed from a patients own stem cells to repair damaged cartilage or heal osteoarthiritis(cartilage decay in the joints). The method can create a lot of cartilage, making it very useful for cartilage replacement. Right now, it isnt known how compatible it is in the human body. The structural material needs to be ableto break down and be absorbed safely by the body so only cartilage is left. Further development and testing needto be conducted. Bioprinting has a lotof potential;in the near future, tissues and organ could be printed on demand.

Journal reference: Nguyen, D. et al. 2017. Cartilage Tissue Engineering by the 3D Bioprinting of iPS Cells in a Nanocellulose/Alginate Bioink. Scientific Reports.

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It is a well-known fat that sedentary living and the consumption of calorie dense and nutritionally deplete foods is implicated in the global epidemic of Globesity. As part and parcel of this trend is the precipitous rise of obesity related diseases such as type 2 diabetes, heart disease, insulin resistance, high blood pressure and various types of cancer.

Brown adipose (fat) tissue is a key site of thermogenesis (heat production) in mammals and for many decades has been considered by researchers as a possible option to promote weight loss.

The biomedical interest in brown and beige (fat that is on its way in the conversion from white to brown) fat cells is centered mostly on the ability of these cells to counteract metabolic diseases including type 2 diabetes and obesity.

Increasing the activity of brown and beige fat holds tremendous promise for the treatment of these diseases as well as for weight loss.

An interesting article published in Nature Medicine in 2013 entitled Brown and Beige Fat Development, Function, and Therapeutic Potential, noted that many genes and pathways that regulate brown and beige cell biology are now identified, and the authors suggested that mature white fat cells can differentiate into beige fat calls under certain conditions.

Recent findings suggest that exercise doesnt just shrink the size of your fat and possibly increase your muscle mass, and build stronger bones, but also stimulates the beiging of white adipose tissue.

The white fat accumulates more mitochondria within the cells and therefore become more metabolically active as it beiges.

The mitochondria is the sub-cellular organelle responsible for generating energy.

An article published in Diabetes in 2015 (Exercise Effects on White Adipose tissue: Beiging and Metabolic Adaptations) reported that the newly formed beige fat releases adipokines a protein which function as hormonal messengers to improve the metabolism of skeletal muscle and the liver.

As well, it is noted that the adipokines induce cells to be more sensitive to insulin and glucose signaling. Of course, the opposite is true of a sedentary lifestyle which is correlated to obesity, insulin resistance, and high blood glucose leading to type 2 diabetes.

In another very interesting article published in the Journal of Physiology in December of 2013, researchers demonstrated that exercise could counteract some of the metabolic consequences of short-term overeating.

In the study, active young men were randomly assigned to either consume 50 percent more calories than normal while strictly limiting their physical activity or to consume 50 percent more calories than normal but add 45 minutes of daily treadmill running.

In the group who did not exercise, the insulin responses of the participants indicated that they developed insulin resistance (a condition which leads to type 2 diabetes) whereas the participants in the exercise group did not develop insulin resistance.

In the group who did not exercise, 7 of the 17 genes related to fat storage were increased while in the exercising group, no significant changes were noted. The researchers concluded that vigorous exercise counteracted most of the harmful effects of short-term overeating with respect to fat.

Clearly, the value of exercise goes far beyond just looking good and feeling well. It surpasses the increase in bone density, the balance, the flexibility, the strength, the endurance, the power, and the lithe lean body that is possible at any age. Your very cells respond, even your fat cells change for the better.

Dr. Jane Riley, EdD., is a certified personal fitness trainer, nutritional adviser and bhavior change specialist. She can be reached at janerileyfitness@gmail.com, 212-8119 cell/text and http://www.janerileyfitness.com.

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Beige and brown fat making your body healthier - Thegardenisland.com

Minerva Baumann, For the Sun-News 4:00 p.m. MT April 29, 2017

NMSU alumnus Don W. Cleveland, professor and chair of the Department of Cellular and Molecular Medicine at the University of California at San Diego and member of the Ludwig Institute for Cancer Research, will visit with students and give a lecture about his research into treatment for neurodegenerative disease at NMSU on Monday, May 1.(Photo: Courtesy photo)

LAS CRUCES A Las Cruces native and field-leading researcher in the areas of cancer genetics and neurosciences will give a talk at New Mexico State University about breakthrough discoveries that could impact future treatment of diseases such as Lou Gehrigs disease, Huntingtons disease and Alzheimers disease.

Don W. Cleveland, a professor and chair of the Department of Cellular and Molecular Medicine at the University of California at San Diego as well as a member of the Ludwig Institute of Cancer Research, will return to NMSU on Monday, May 1, to share insights about his research with students and the community. Cleveland will spend the day meeting with different groups, touring the campus, talking with NMSU students in biology, chemistry and physics and giving a public lecture about his research titled Gene silencing therapy for human neurodegenerative disease, which will begin at 3:30 p.m. May 1 in the Domenici Hall Yates Auditorium, Room 109.

Its a real pleasure to visit NMSU and Las Cruces again, said Cleveland, who graduated from Las Cruces High School and earned a bachelors degree from NMSU in physics in 1972. They gave me a great start in my scientific career and made me into a lifelong New Mexican (no matter where I live).

After NMSU, Cleveland earned a doctorate at Princeton and moved to California to continue his groundbreaking research into neurodegenerative disorders. Cleveland has uncovered the mechanisms underlying the major genetic forms of amyotrophic lateral sclerosis (ALS), commonly known as Lou Gehrigs disease, and developed gene silencing therapies using designer DNA drugs that have entered clinical trials for four neurodegenerative diseases, including ALS and Huntingtons diseases.

Cleveland initially identified tau, the protein that accumulates abnormally in Alzheimers disease. It is also the protein whose misfolding underlies chronic traumatic brain injury, which is now receiving nationwide attention from the National Football League.

We are proud to welcome Dr. Cleveland back to NMSU, said Enrico Pontelli, interim dean of the College of Arts and Sciences. This is part of our Alumni Connections series, which seeks to connect our Arts and Sciences alumni with our students. One of the keys to students long-term success is the connections they build, not only with their professors and fellow students but also with alumni like Dr. Cleveland, who are leaders in their field of study.

Cleveland has earned numerous awards for his work. Among them, three National Institutes of Health Merit Awards, the Wings Over Wall Street MDA Outstanding Scientist award and The Sheila Essey Prize from the ALS Association and American Academy of Neurology as well as the Judd award from Memorial Sloan-Kettering Cancer Center.

NMSU biology professor Brad Shuster remembers Cleveland as a mentor when Shuster was a graduate student. He also invited Cleveland to NMSU for a seminar several years ago.

Don has made enormous contributions to our understanding of the basic structure and function of cells, and has lent profound insights into pathologies such as cancer and neurodegenerative diseases, said Shuster. His leadership has extended well beyond the bench, serving as president of the American Society for Cell Biology and an editor of our disciplines top journal. Plus, hes a great guy and one of the most successful scientists NMSU has ever produced.

Pontelli believes Clevelands engagement with NMSU students one-on-one will be just as valuable for them as the knowledge of his cutting-edge research.

This is an amazing opportunity for our faculty and students, Pontelli said. We are fortunate Dr. Cleveland is making the time to share his research and insights.

Clevelands lecture is free and open to the public. Campus parking passes for visitors are available at http://auxadminforms.nmsu.edu/ParkingForms/ePermit.aspx.

Minerva Baumannwrites for University Communications and can be reached atmbauma46@nmsu.edu

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Leading cancer researcher, NMSU alum to lecture May 1 - Las Cruces Sun-News