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NEW YORK (TheStreet) -- Newlink Genetics (NLNK - Get Report) has been upgraded by TheStreet Ratings from Sell to Hold with a ratings score of C. TheStreet Ratings Team has this to say about their recommendation:

TheStreet Ratings team rates NEWLINK GENETICS CORP as a Hold with a ratings score of C. TheStreet Ratings Team has this to say about their recommendation:

"We rate NEWLINK GENETICS CORP (NLNK) a HOLD. The primary factors that have impacted our rating are mixed some indicating strength, some showing weaknesses, with little evidence to justify the expectation of either a positive or negative performance for this stock relative to most other stocks. The company's strengths can be seen in multiple areas, such as its robust revenue growth, largely solid financial position with reasonable debt levels by most measures and notable return on equity. However, as a counter to these strengths, we find that the stock has had a generally disappointing performance in the past year."

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Newswise The genes that increase the risk of Type 1 diabetes have lost their hiding place.

A research group that includes a University of Florida genetics expert has located and narrowed down the number of genes that play a role in the disease, according to a study published Monday in the journal Nature Genetics. Knowing the identities and location of causative genes is a crucial development: Other researchers can use this information to better predict who might develop Type 1 diabetes and how to prevent it.

Its a game-changer for Type 1 diabetes, said Patrick Concannon, director of the University of Florida Genetics Institute.

Researchers gathered information about the genetic makeup of 27,000 people, including those who had Type 1 diabetes and others who did not. They then began looking for individual differences in DNA that raise the risk of Type 1 diabetes. Starting with 200,000 possible locations in the genome, researchers used a technique known as fine mapping to pinpoint DNA sequence variations that can lead to diabetes. In some genomic regions, they narrowed the number of disease-causing DNA variations -- known as single nucleotide polymorphisms or SNPs -- from the thousands down to five or less.

That will make diabetes researchers work more effective and efficient by giving them the most detailed directions yet about where to look for the genetic variations that cause Type 1 diabetes and perhaps other autoimmune diseases such as arthritis, Concannon said. Now that the group of geneticists has identified the important genes and SNPs, diabetes researchers will reap the benefits, according to Concannon.

Weve taken this genetic data which was interesting but hard to work with, and weve condensed it down into something that people can actually use to begin to explore the mechanism of the disease. It moves it out of the realm of genetics to being broadly applicable to Type 1 diabetes research, he said.

Type 1 diabetes occurs when the bodys immune system kills off insulin-producing cells in the pancreas. Some 3 million people in the United States have the disease, according to the JDRF, a group that funds Type 1 diabetes research and education. Experts dont know exactly what causes the disease but suspect that genetics and environmental factors may play a role.

The researchers findings are the most comprehensive yet in the effort to locate and identify the genetic risk variants for Type 1 diabetes and other autoimmune diseases, said Todd Brusko, a member of the UF Diabetes Institute and an assistant professor in the UF College of Medicines department of pathology, immunology and laboratory medicine, part of UF Health.

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Genetics Breakthrough by Group That Includes University of Florida Expert Will Boost Diabetes Research

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(Boston)--Today's physicians require an increasingly comprehensive understanding of the principles of genetics and genomics in order to make informed clinical decisions. Scientific discoveries are bringing genomic technology directly to consumers at an increasingly rapid pace. The availability of genomic information necessitates that educators provide adequate training in genetics and genomics for future health-care providers.

In a new study in the journal Genetics in Medicine, researchers have shown that genetics curricula are evolving to include current topics in genomics however the majority of the content is taught in the first two years of medical school, with minimal and declining formal instruction in genetics during years three and four.

This study was the result of a survey of course directors in the U.S. and Canada who teach genetics to medical students. The survey collected information on what topics are currently being taught, how they are taught, who the instructors are, how student learning is evaluated, what strategies are used when students do not pass the subject at their schools.

Medical schools that participated in the survey used a variety of innovative teaching strategies to bring genetics into medical training including using integrated curricular models, as well as diverse and innovative teaching and assessment strategies. "We found the curriculum has evolved to include topics of particular relevance to the practice of genomic medicine, including personalized medicine, direct-to-consumer genetic testing, genome wide association studies, pharmacogenetics and bioinformatics," explained corresponding author Shoumita Dasgupta, PhD, associate professor of medicine at Boston University School of Medicine (BUSM). "However, while important topics emerging in genomic medicine are frequently being added to the curricula, more than 40 percent of the responding medical schools in the U.S. and Canada still don't teach them," said Dasgupta.

According to Dasgupta and her colleagues, in order to produce genomically literate physicians, it is critical to improve the coverage of topics relating to genomic medicine. One way they recommend is to increase exposure to these topics by promoting more integration of genetics across the four-year curriculum and highlight existing genetics topics in core clerkships. "These results point to an opportunity to extend formal training in genetics across the entire medical school continuum," she added.

The researchers suggest concrete steps are needed to ensure the readiness of future physicians to practice genomic medicine, including increasing clinical exposure to genetic topics both locally and through curricula developed by national organizations such as the Association of Professors of Human and Medical Genetics, tracking student performance in the subject even when taught alongside other topics, and involving genetics experts in curriculum development and student mentoring.

"This is a pivotal moment in clinical genetics, and as educators, it is our responsibility to ensure our graduates are prepared to practice in the era of genomic medicine. While powerful technologies that allow whole genome analysis gain traction, it becomes increasingly critical to train the next generation of future physicians to translate genomic technologies and discoveries into their clinical practice across a range of specialties and practices," said Dasgupta.

###

Funding for this multi-institution study was provided by the Association of Professors and Medical Genetics.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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Study finds positive trends in medical genetics education

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BETHESDA, MD - Over 1,500 scientists from 30 countries and 46 states will attend next week's 56th Annual Drosophila Research Conference organized by the Genetics Society of America (GSA), March 4-8 in Chicago, IL. The conference will feature close to 1,000 presentations (including 170 talks) describing cutting-edge research on genetics, developmental biology, cancer, stem cells, neurology, epigenetics, genetic disease, aging, immunity, behavior, drug discovery, and technology. It is the largest meeting in the world that brings together researchers who use the fruit fly Drosophila melanogaster to study biology.

Of special note are scientists whose achievements in genetics are being honored through awards and special lectures:

The fruit fly Drosophila melanogaster is one of the most versatile and widely used model organisms applied to the study of genetics, physiology, and evolution. Drosophila research has led to some of the most significant breakthroughs in our understanding of biology, including five Nobel prizes. It is an effective system for studying a range of human genetic diseases, ranging from cancer to diabetes to neurodegenerative disorders. Fruit flies are a valuable resource for biomedical research because of the efficiency and cost-effectiveness with which comprehensive, sensitive, and accurate biological data can be generated. Research presented at the Drosophila conference, like that at other GSA conferences, helps advance our fundamental understanding of living systems and provides crucial insight into human biology, health and disease.

The conference will take place at the Sheraton Chicago Hotel & Towers at 301 East North Water Street. The organizers include Gregory J. Beitel, PhD (Northwestern University), Michael Eisen (University of California, Berkeley; Howard Hughes Medical Institute), Marc Freeman (University of Massachusetts Medical School; Howard Hughes Medical Institute), and Ilaria Rebay (University of Chicago). For additional information, please see the conference website at http://www.genetics-gsa.org/drosophila/2015/.

###

More information on the importance of Drosophila research:

Fruit Flies in Biomedical Research. Michael F. Wangler, Shinya Yamamoto, and Hugo J. Bellen. Genetics; Early online January 26, 2015

Media Eligibility: The 2015 Drosophila Research Conference is open to media representatives, including those from bona fide print, broadcast, radio, and online venues, and freelance writers on a verifiable assignment from an established news source. Please contact press@genetics-gsa.org">press@genetics-gsa.org for information about complimentary press registration.

About the Genetics Society of America (GSA)

Founded in 1931, the Genetics Society of America (GSA) is the professional scientific society for genetics researchers and educators. The Society's more than 5,000 members worldwide work to deepen our understanding of the living world by advancing the field of genetics, from the molecular to the population level. GSA promotes research and fosters communication through a number of GSA-sponsored conferences including regular meetings that focus on particular model organisms. GSA publishes two peer-reviewed, peer-edited scholarly journals: GENETICS, which has published high quality original research across the breadth of the field since 1916, and G3: Genes|Genomes|Genetics, an open-access journal launched in 2011 to disseminate high quality foundational research in genetics and genomics. The Society also has a deep commitment to education and fostering the next generation of scholars in the field. For more information about GSA, please visit http://www.genetics-gsa.org.

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Disease, evolution, drugs: Fruit fly research continues to teach us about human biology

Recommendation and review posted by Bethany Smith

IMAGE:This is a maritime pine forest in the Castilian Plateau, central Spain. Maritime pine forests support a great diversity of associated fauna and flora, in particular in the Mediterranean region... view more

Data from only a small number of gene variants can predict which maritime pine trees are most vulnerable to climate change, scientists report in the March issue of GENETICS. The results will improve computer models designed to forecast where forests will grow as the climate changes, and promises to help forestry managers decide where to focus reforestation efforts. The results will also guide the choice of tree stocks.

The maritime pine (Pinus pinaster) grows widely in southwestern Europe and parts of northern Africa. But the tree's important economic value and ecological roles in the region may be at risk as the changing climate threatens the more vulnerable forests and the productivity of commercial plantations.

To predict which regions will sustain pine forests in the future, researchers and managers rely on computer models. But these forecasts don't take into account two major factors that influence a forest's fate: genetics and evolution. Genetic differences between tree populations mean that forests vary in how well they cope with warmer, drier conditions. Ongoing evolution of trees also influences the prevalence of these genetic differences; for example, trees with gene variants allowing them to withstand higher temperatures will become increasingly common as the climate changes.

"These genetic effects are not included in forest range shift models, but we know they can completely change the resulting predictions. Our goal was to identify such effects in a way that can be readily incorporated into the forecasts," said study leader Santiago Gonzlez-Martnez, from the Forest Research Centre of Spain's Institute for Agricultural Research (CIFOR-INIA).

To find genetic variants that affect the species' fitness in different climate conditions, maritime pine researchers from around the world pooled their expertise and the results of previous research, yielding a list of more than 300 variants in 200 candidate genes. Creating a shortlist of targets is considerably faster and more economical than searching the entire genome of the maritime pine, which is about nine times larger than the human genome.

From this list, the team tested whether any of the candidates were more common in regions that shared similar climates. Such geographic patterns can be the result of natural selection and point to gene variants that influence tree survival and reproduction according to climate. By testing the frequency of each variant at 36 locations in Portugal, Spain, France, Morocco, and Tunisia, the researchers found 18 variants that showed correlations with the local climate. These variants affected genes involved in many different biological processes, including growth and response to heat stress.

The researchers then looked for evidence that these variants are important for the trees' fitness by planting seedlings from 19 of the locations together in a dry part of Spain, at the extreme end of the species' climatic range. This allowed the team to compare how well genetically different trees would survive under similar conditions. After five years, the seedlings carrying gene variants predicted to be beneficial in the local climate indeed tended to have higher survival rates.

These results demonstrate the feasibility of this relatively fast approach of finding and confirming genetic variants associated with climate. "Now that we have shown that the method works well, we are planning similar experiments on a bigger scale, with more test sites, looking at more genes, and different traits. For example, the single biggest climate change threat to pine forests is the increased frequency of wildfires, so we're searching for variants that affect fire tolerance," said Gonzlez-Martnez.

"Good decisions require good data, and this collaborative work shows how crucial genetic data can be for managing biodiversity and commercial forestry amid a changing climate," said GENETICS Editor-in-Chief Mark Johnston.

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Genetic data can help predict how pine forests will cope with climate change

Recommendation and review posted by Bethany Smith

'Genetically Speaking' series showcases research findings, technological advances, and applications of human genetics in the evaluation, diagnosis, and treatment of health conditions

BETHESDA, MD and Fort Washington, PA - The American Society of Human Genetics (ASHG) and ReachMD announced today the launch of 'Genetically Speaking', a series of audio interviews designed to educate healthcare professionals on the application of human genetics in disease prevention and management.

The series features peer-to-peer interviews conducted during the ASHG 2014 Annual Meeting and includes topics such as:

"One of our primary goals at ASHG is to develop a healthcare workforce that is genetics-literate and capable of interpreting and applying information in clinical practice," said Joseph D. McInerney, MA, MS, Executive Vice President of ASHG. "We are excited to team up with ReachMD to produce and deliver peer-to-peer programming to healthcare professionals nationwide."

'Genetically Speaking' is co-produced by ASHG and ReachMD and broadcast on ReachMD's integrated online, mobile, and on air content distribution network. Content is accessible both on demand and through 24/7 radio streaming on ReachMD, iHeartRadio, TuneIn, and iTunes digital platforms.

"This series is an excellent addition to the ReachMD lineup," said Matt Birnholz, MD, Vice President and Medical Director of ReachMD. "Our users love cutting-edge programming, and the scientific and medical experts on this series really showcase the latest research and the applications of genetics in disease prevention and management."

###

Link to 'Genetically Speaking': https://reachmd.com/programs/genetically-speaking/

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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ASHG and ReachMD launch educational series on genetics and genomics

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An effective vaccine for HIV has eluded researchers for several decades, due to the pathogen's infamous shape-shifting abilities.

Even though researchers have identified certain broadly neutralizing antibodies that can conquer multiple strains of the human immunodeficiency virus, many strains of rapidly mutating HIV remain resistant to the these super antibodies.

In recent years however,researches have proposed a new method of battling the virus that involves gene therapy.

Instead of using a vaccine to stimulate the body's own immune system, so that it produces HIV antibodies, scientists are bypassing the immune system entirely.

In experiments involving rats and monkeys, the researchers have used non-life-threatening viruses to alter the animals' genome so that its cells produce designer molecules capable of neutralizing HIV.

In a paper published Wednesday in the journal Nature, a team of researchers said they had used the technique to protect rhesus macaques from repeated intravenous injections of a SHIV, a combination of simian immunodeficiency virus and humanimmunodeficiency virus.

The technique, researchers said, "can function like an effective HIV-1 vaccine." (HIV-1 is the main family of the virus, and accounts for most infections worldwide.)

When HIV enters the body, it attacks specific immune cells. As the virus copies itself over and over, and kills more and more host cells, the immune system grows progressively weaker. If left untreated, this progressive weakening will give rise to AIDS.

In most cases, the HIV virus begins its attack by latching onto two separate protein structures on the surface of its target white blood cells. One of these structures is called CD4, and the other is called CCR5.

In the Nature study, researchers set out to engineer an antibody-like molecule that would mimic both of these proteins, so that it would act as decoy of sorts for the virus. Instead of latching onto a host cell, HIV would latch onto a specially enhanced protein molecule, or eCD4-Ig, that was released by the cell.

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With genetic engineering, scientists use decoy molecule to trick HIV

Recommendation and review posted by Bethany Smith

An effective vaccine for HIV has eluded researchers for several decades, due to the pathogen's infamous shape-shifting abilities.

Even though researchers have identified certain broadly neutralizing antibodies that can conquer multiple strains of the human immunodeficiency virus, many strains of rapidly mutating HIV remain resistant to the these super antibodies.

In recent years however,researches have proposed a new method of battling the virus that involves gene therapy.

Instead of using a vaccine to stimulate the body's own immune system, so that it produces HIV antibodies, scientists are bypassing the immune system entirely.

In experiments involving rats and monkeys, the researchers have used non-life-threatening viruses to alter the animals' genome so that its cells produce designer molecules capable of neutralizing HIV.

In a paper published Wednesday in the journal Nature, a team of researchers said they had used the technique to protect rhesus macaques from repeated intravenous injections of a SHIV, a combination of simian immunodeficiency virus and humanimmunodeficiency virus.

The technique, researchers said, "can function like an effective HIV-1 vaccine." (HIV-1 is the main family of the virus, and accounts for most infections worldwide.)

When HIV enters the body, it attacks specific immune cells. As the virus copies itself over and over, and kills more and more host cells, the immune system grows progressively weaker. If left untreated, this progressive weakening will give rise to AIDS.

In most cases, the HIV virus begins its attack by latching onto two separate protein structures on the surface of its target white blood cells. One of these structures is called CD4, and the other is called CCR5.

In the Nature study, researchers set out to engineer an antibody-like molecule that would mimic both of these proteins, so that it would act as decoy of sorts for the virus. Instead of latching onto a host cell, HIV would latch onto a specially enhanced protein molecule, or eCD4-Ig, that was released by the cell.

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A new twist on HIV vaccines shows results in monkeys, study says

Recommendation and review posted by Bethany Smith

Carrollton Spinal Cord Injury

By: ZindaDavis

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Carrollton Spinal Cord Injury - Video

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Waco Spinal Cord Injuries: Overview
For more information: http://www.zdfirm.com/waco/spinal-cord-injury/ Zinda Davis, PLLC discusses spinal cord injuries in Waco, Texas. Contact Us 7215 Bosque Blvd. Waco, Texas 76710 Phone:...

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Waco Spinal Cord Injuries: Overview - Video

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Stiles family Ugly Tie Video
Step up to the plate, get your ugly ties on and support Spinal Cord Injury BC with a small donation here http://bitly.com/uglytiesNorth This is the deal if you can watch this without smiling...

By: Rob Stiles

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A mast cell (also known as a mastocyte or a labrocyte[1]) is derived from the myeloid stem cell and a part of the immune system that contains many granules rich in histamine and heparin. Although best known for their role in allergy and anaphylaxis, mast cells play an important protective role as well, being intimately involved in wound healing and defense against pathogens.[2]

The mast cell is very similar in both appearance and function to the basophil, another type of white blood cell. They differ in that mast cells are tissue resident, e.g., in mucosal tissues, while basophils are found in the blood.[3]

Mast cells were first described by Paul Ehrlich in his 1878 doctoral thesis on the basis of their unique staining characteristics and large granules. These granules also led him to the incorrect belief that they existed to nourish the surrounding tissue, so he named them Mastzellen (from German Mast, meaning "fattening", as of animals).[4][5] They are now considered to be part of the immune system.

Mast cells are very similar to basophil granulocytes (a class of white blood cells) in blood. Both are granulated cells that contain histamine and heparin, an anticoagulant. Both cells also release histamine upon binding to immunoglobulin E.[6] These similarities have led many to speculate that mast cells are basophils that have "homed in" on tissues. Furthermore they share a common precursor in bone marrow expressing the CD34 molecule. Basophils leave the bone marrow already mature, whereas the mast cell circulates in an immature form, only maturing once in a tissue site. The site an immature mast cell settles in probably determines its precise characteristics.[2] The first in vitro differentiation and growth of a pure population of mouse mast cells has been carried out using conditioned medium derived from concanavalin A-stimulated splenocytes.[7] Later, it was discovered that T cell-derived interleukin 3 was the component present in the conditioned media that was required for mast cell differentiation and growth.[8]

Mast cells in rodents are classically divided into two subtypes: connective tissue-type mast cells and mucosal mast cells. The activities of the latter are dependent on T-cells.[9]

Mast cells are present in most tissues characteristically surrounding blood vessels and nerves, and are especially prominent near the boundaries between the outside world and the internal milieu, such as the skin, mucosa of the lungs, and digestive tract, as well as the mouth, conjunctiva, and nose.[2]

Mast cells play a key role in the inflammatory process. When activated, a mast cell rapidly releases its characteristic granules and various hormonal mediators into the interstitium. Mast cells can be stimulated to degranulate by direct injury (e.g., physical or chemical [such as opioids, alcohols, and certain antibiotics such as polymyxins]), cross-linking of immunoglobulin E (IgE) receptors, or complement proteins.[2]

Mast cells express a high-affinity receptor (FcRI) for the Fc region of IgE, the least-abundant member of the antibodies. This receptor is of such high affinity that binding of IgE molecules is in essence irreversible. As a result, mast cells are coated with IgE, which is produced by plasma cells (the antibody-producing cells of the immune system). IgE molecules, like all antibodies, are specific to one particular antigen.

In allergic reactions, mast cells remain inactive until an allergen binds to IgE already in association with the cell (see above). Other membrane activation events can either prime mast cells for subsequent degranulation or act in synergy with FcRI signal transduction.[10] In general, allergens are proteins or polysaccharides. The allergen binds to the antigen-binding sites, which are situated on the variable regions of the IgE molecules bound to the mast cell surface. It appears that binding of two or more IgE molecules (cross-linking) is required to activate the mast cell. The clustering of the intracellular domains of the cell-bound Fc receptors, which are associated with the cross-linked IgE molecules, causes a complex sequence of reactions inside the mast cell that lead to its activation. Although this reaction is most well-understood in terms of allergy, it appears to have evolved as a defense system against intestinal worm infestations (tapeworms, etc.)[citation needed].

The molecules released into the extracellular environment include:[2]

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Mast cell - Wikipedia, the free encyclopedia

Recommendation and review posted by simmons

(March 5, 2015) - Gender equality has not yet been achieved in science, medicine, and engineering, but The New York Stem Cell Foundation (NYSCF), through its Initiative on Women in Science and Engineering, is committed to making sure progress is made. NYSCF convened the Inaugural Meeting of its Initiative on Women in Science and Engineering (IWISE) Working Group in February 2014, where the group put forward seven actionable strategies for advancing women in science, medicine, and engineering, and reconvened in February 2015 to further develop the strategies.

NYSCF began this initiative after an analysis of its own programs. "We found that the ratio of men and women in our own programs was OK but it could certainly be improved," said Susan L. Solomon, CEO and Co-Founder, of NYSCF. "We wanted to take action and actually make tangible progress, so we brought together many of the leading men and women who have already committed time, energy, and resources towards this problem."

Today, the recommendations were published in Cell Stem Cell. They were divided into three categories: direct financial support strategies, psychological and cultural strategies, and major collaborative and international initiatives. The group chose to highlight the most high-impact and implementable strategies from a larger list developed during the meeting. They also sought to promote promising, long-term initiatives that will require significant collaboration among multiple stakeholders with the aim of connecting potential partners.

"Advancing women in science and medicine is of critical importance to the academic and research enterprise in our country," said Dr. Marc Tessier-Lavigne, President of Rockefeller University. "This paper is important as it not only brings attention to this key issue but also outlines creative strategies that can help break down barriers to gender equality in science."

Changing financing structures, embedded cultural norms, and tying funding to gender balance to enact real change are the pillars underlying the seven strategies recommended by the Working Group.

"The brain power provided by women in science is essential to sustaining a thriving US society and economy. It is time to move beyond just lamenting its loss and embrace the actions called for in this timely report," Dr. Claire Pomeroy, President, the Lasker Foundation and a member of the IWISE Working Group.

The seven strategies include:

1) Implement flexible family care spending 2) Provide "extra hands" awards 3) Recruit gender-balanced external review committees and speaker selection committees 4) Incorporate implicit bias statements 5) Focus on education as a tool 6) Create an institutional report card for gender equality 7) Partner to expand upon existing searchable databases of women in science, medicine, and engineering

The IWISE Working Group reconvened in February 2015 to continue to work on the Institutional Report Card for Gender Equality. The paper published today includes the proposed Phase 1 Institutional Report Card, and the group plans to release the Phase 2 report card once finalized.

###

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Achieving gender equality in science, engineering and medicine

Recommendation and review posted by simmons

Despite the progress made by women in science, engineering, and medicine, a glance at most university directories or pharmaceutical executive committees tells the more complex story. Women in science can succeed, but they are succeeding in fields that may not even be conscious of the gender imbalances. These imbalances manifest themselves in the number of women that are invited to speak at conferences, the percentage of grants awarded to women scientists, and the higher rates of attrition of women at every stage of the career ladder compared to those of men.

In the March 5 issue of the journal Cell Stem Cell, the Initiative on Women in Science and Engineering Working Group, a collection of more than 30 academic and business leaders organized by the New York Stem Cell Foundation, present seven strategies to advance women in science, engineering, and medicine in this modern landscape.

"We wanted to think about broad ways to elevate the entire field, because when we looked at diversity programs across our organizations we thought that the results were okay, but they really could be better," said Susan L. Solomon, co-founder and CEO of the New York Stem Cell Foundation and a member of the working group. "We've identified some very straightforward things to do that are inexpensive and could be implemented pretty much immediately."

The working group's seven strategies are broken into three categories: the first two are direct financial support strategies, the next three are psychological and cultural strategies, and the final two are major collaborative and international initiatives.

1. Implement flexible family care spending

Make grants gender neutral by permitting grantees to use a certain percentage of grant award funds to pay for childcare, eldercare, or family-related expenses. This provides more freedom for grantees to focus on professional development and participate in the scientific community.

2. Provide "extra hands" awards

Dedicate funds for newly independent young investigators who are also primary caregivers to hire technicians, administrative assistants, or postdoctoral fellows.

3. Recruit gender-balanced review and speaker selection committees

Adopt policies that ensure that peer review committees are conscious of gender and are made up of a sufficient number of women.

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Seven strategies to advance women in science

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Published February 10, 2015

A British biotech company founded by a Nobel prize winner has raised what it says is a record 691,000 pounds ($1 million) via crowdfunding to help launch a stem cell-based regenerative medicine for use following heart trauma.

Cell Therapy, based in the Welsh capital Cardiff, says the medicine has the potential to reduce scarring of the heart muscle caused by a heart attack or failure.

Chief Executive Ajan Reginald, previously at Roche, said crowd funding was a quick way to raise money for final stage trials or commercial launches.

"It was very fast and very efficient," he told Reuters on Monday. "We have spent 5 percent of our time on fundraising, which enables me to spend 95 percent of my time on the business."

The company, whose founder Martin Evans shared the 2007 Nobel Prize for medicine for groundbreaking stem cell research, used website Crowdcube to raise nearly three times its original target from more than 300 investors.

Reginald said the backers included investment bankers, hedge fund employees and scientists.

"Crowd funding allows investors to look in detail at a company in their own time," he said, adding that some 10,000 investors had seen the pitch.

The company would publish data from clinical trials of the drug, called Heartcel, next month, before final stage trials with a view to a launch in 2016.

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British biotech firm sets crowdfunding record with heart drug

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Under normal conditions, many of the different types of tissue-specific adult stem cells, including hematopoietic stem cells, exist in a state or dormancy where they rarely divide and have very low energy demands. "Our theory was that this state of dormancy protected hematopoietic stem cells from DNA damage and therefore protects them from premature aging," says Dr. Michael Milsom, leader of the study.

However, under conditions of stress, such as during chronic blood loss or infection, hematopoietic stem cells are driven into a state of rapid cell division in order to produce new blood cells and repair the damaged tissue. "It's like forcing you out of your bed in the middle of the night and then putting you into a sports car and asking you to drive as fast as you can around a race circuit while you are still half asleep," explains Milsom. "The stem cells go from a state of rest to very high activity within a short space of time, requiring them to rapidly increase their metabolic rate, synthesize new DNA and coordinate cell division. Suddenly having to simultaneously execute these complicated functions dramatically increases the likelihood that something will go wrong."

Indeed, experiments described in the study show that the increased energy demands of the stem cells during stress result in elevated production of reactive metabolites that can directly damage DNA. If this happens at the same time that the cell is trying to replicate its DNA, then this can cause either the death of the stem cell, or potentially the acquisition of mutations that may cause cancer.

Normal stem cells can repair the majority of this stress-induced DNA damage, but the more times you are exposed to stress, the more likely it is that a given stem cell will inefficiently repair the damage and then die or become mutated and act as a seed in the development of leukemia. "We believe that this model perfectly explains the gradual accumulation of DNA damage in stem cells with age and the associated reduction in the ability of a tissue to maintain and repair itself as you get older," Milsom adds.

In addition, the study goes on to examine how this stress response impacts on a mouse model of a rare inherited premature aging disorder that is caused by a defect in DNA repair. Patients with Fanconi anemia suffer a collapse of their blood system and have an extremely high risk of developing cancer. Mouse models of Fanconi anemia have exactly the same DNA repair defect as found in human patients but the mice never spontaneously develop the bone marrow failure observed in nearly all patients.

"We felt that stress induced DNA damage was the missing ingredient that was required to cause hematopoietic stem cell depletion in these mice," says Milsom. When Fanconi anemia mice were exposed to stimulation mimicking a prolonged viral infection, they were unable to efficiently repair the resulting DNA damage and their stem cells failed. In the same space of time that normal mice showed a gradual decline in hematopoietic stem cell numbers, the stem cells in Fanconi anemia mice were almost completely depleted, resulting in bone marrow failure and an inadequate production of blood cells to sustain life.

"This perfectly recapitulates what happens to Fanconi anemia patients and now gives us an opportunity to understand how this disease works and how we might better treat it," commented Milsom.

Prof. Dr. Andreas Trumpp, director of HI-STEM and head of the Division of Stem Cells and Cancer at the DKFZ believes that this work is a big step towards understanding a range of age-related diseases. "The novel link between physiologic stress, mutations in stem cells and aging is very exciting," says Trumpp, a co-author of the study. "By understanding the mechanism via which stem cells age, we can start to think about strategies to prevent or at least reduce the risk of damaged stem cells which are the cause of aging and the seed of cancer."

###

Dagmar Walter, Amelie Lier, Anja Geiselhart, Frederic B. Thalheimer, Sina Huntscha, Mirko C. Sobotta, Bettina Moehrle, David Brocks, Irem Bayindir, Paul Kaschutnig, Katja Muedder, Corinna Klein, Anna Jauch, Timm Schroeder, Hartmut Geiger, Tobias P. Dick, Tim Holland-Letz, Peter Schmezer, Steven W. Lane, Michael A. Rieger, Marieke A. G. Essers, David A. Williams, Andreas Trumpp und Michael D. Milsom: Exit from dormancy provokes DNA damage-induced attrition in haematopoietic stem cells. Nature 2015, DOI: 10.1038/nature14131

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A good night's sleep keeps your stem cells young

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Stem Cell Therapy Cream
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WATERTOWN, Conn. (AP) A year ago, Nancy Demers, 71, was diagnosed with myelodysplastic syndrome, a deficiency in the bone marrow. The disease can eventually become leukemia.

Its treated as if it were cancer but there is no cure for it, said her son, Scott Demers.

Now Nancy Demers has a new chance at life, thanks to advances in bone marrow stem cell transplants.

If I didnt do this, once I went out of remission its not if, its when I would go into acute leukemia and there will be nothing there to help me, Nancy Demers said. This will save my life and give me time.

Demers is one of a rapidly growing number of people looking to depend on strangers to donate marrow since she doesnt have a match within her family.

The rising number of patients seeking bone marrow has created new demands on registries that seek to match patient needs with willing donors.

Each sibling has a 25 percent chance of being a transplant match, according to Dr. Joseph Antin, chief and program director of the adult stem cell transplantation program at Dana Farber Brigham and Womens Hospital in Boston.

In the United States, about 30 percent of patients find a donor within their family, according to Be the Match. Those who dont must turn to international registries to find an unrelated donor.

Around 15 years ago, doctors couldnt do a transplant on anyone over the age of 50, according to Dr. Leslie Lehmann, clinical director of the Stem Cell Transplant Center at Dana Farber.

Its a big stress on the body, Lehmann said.

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Registries seek to match donors with rising marrow demand

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http://www.InnovationsStemCellCenter.com.

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Snow day lesson on GE.

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My very first animation and video-- Created using PowToon -- Free sign up at http://www.powtoon.com/join -- Create animated videos and animated presentations...

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Rheumatiod Arthritis and Genetics
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1. Introduction

This chapter provides an overview of the main current applications of gene therapy for chronic pain in what concerns animal studies and putative clinical applications. The value of gene therapy in unravelling neuronal brain circuits involved in pain modulation is also analysed. After alerting to the huge socioeconomic impact of chronic pain in modern societies and justifying the need to develop new avenues in pain management, we review the most common animal studies using gene therapy, which consisted on deliveries of replication-defective viral vectors at the periphery with the aim to block nociceptive transmission at the spinal cord. Departing from the data of these animal studies, we present the latest results of clinical trials using gene therapy for pain management in cancer patients. The animal studies dealing with gene delivery in pain control centres of the brain are analysed in what concerns their complexity and interest in unravelling the neurobiological mechanisms of descending pain modulation. The chapter will finish by analysing possible futures of gene therapy for chronic pain management based on the development of vectors which are safer and more specific for the different types of chronic pain.

Pain is not easy to define since it is a highly subjective experience. The more consensual definition of pain was provided by the International Association for the Study of Pain (IASP) and states that Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage [1]. Acute pain is important as an alert signal to potentially threaten situations (internal or external to the organism) and it is important for survival. Acute pain may progress to chronic pain which, according to IASP, is the pain that lasts more than 3 months and persists beyond the normal tissue healing time [2].

Chronic pain may be divided into "nociceptive" and "neuropathic" [3]. Nociceptive pain is caused by activation of nociceptors, the thin nerve fibers which convey nociceptive input from the periphery to the spinal cord. Neuropathic pain is caused by malfunction or damage of the nervous system. Neuropathic pain is frequently difficult to treat being associated to spontaneous pain, exaggerated responses to nociceptive stimuli (hyperalgesia) and nociceptive responses to stimuli which are usually non-nociceptive (allodynia).

The number of people affected by chronic pain is increasing due to multifactorial causes such as increasing aging of the population. In Europe, about 20% of people suffer from moderate to severe chronic pain [4]. In the United States the prevalence of chronic pain ranges from 2% to 40%, with a median of 15% [5], which cost the country 560 to 635 million dollars [6]. People suffering from chronic pain are less able to walk, sleep normally, perform social activities, exercise or have sexual relations. Chronic pain strongly affects the productivity. About 60% of chronic pain patients are unable or less able to work, 19% lost their jobs and 13% change jobs due to their pain [6]. Chronic pain is associated to several co-morbidities, namely depression and anxiety [6]. Besides all of these indirect costs, chronic pain is a burden due to direct costs of pain management. Despite major investments in basic and clinical pain research, the available analgesics remain considerably unchanged during the last decades. Opioids are useful to manage several pain types but they have a modest efficacy in several pain conditions (e.g. neuropathic pain). Furthermore, long term treatments with opioids frequently induce severe off-target effects, like nausea, constipation and addiction [7]. Intractable pain remains a clinical problem and a drama for the patients and their families [8]. During the last decade, pain clinicians and pain researchers were challenged to search for alternatives to conventional pain treatment, which should be more specific and sustained than conventional analgesics. Gene therapy outstands as a powerful technique to overcome some current problems of chronic pain treatments.

Neurobiological research in the pain field provided solid information regarding the transmission and modulation of nociceptive information from the periphery to the brain, where a pain sensation is produced (Fig. 1). Nociceptive signals are conveyed by primary afferent fibers from peripheral organs, like the bladder or muscles, to the spinal cord. This is the first relay station involved in the modulation of nociceptive information namely by local inhibitory interneurons that use opioid peptides or aminoacids (-amminobutiric acid-GABA- and glycine). Nociceptive information is then transmitted supraspinally, namely to the thalamus, and to several brainstem areas, where additional modulation of the nociceptive signal occurs. The thalamo-cortical pathway ensures that the nociceptive information reaches the somatosensory and prefrontal cortices, where the nociceptive signal is finally perceived as a pain sensation [9, 10]. Some brain areas which directly or indirectly receive nociceptive information from the spinal cord are also involved in descending pain modulation. Both inhibition and facilitation may occur and chronic pain may derive from a reduction of the former and enhancement of the latter [9, 11]. This neurobiological knowledge has been used to design gene therapy studies for chronic pain, namely to choose the somatosensory system areas and neurotransmitters/receptors to be targeted in order to block nociceptive transmission.

Schematic diagram of pain pathways involved in pain transmission and modulation. Nociceptive information is transmitted from the periphery to the spinal dorsal horn by primary sensory neurons. At the spinal level, these neurons transmit nociceptive information to second order neurons (Ascending pathways) through the release of neurotransmitters like the excitatory amino acids (EAA) glutamate and aspartate, calcitonin gene-related peptide (CGRP), substance P (SP) galanin (Gal) and neuropeptide Y (NPY). In the brain, the nociceptive information is then perceived as a pain sensation. The transmission of nociceptive information at the spinal level is modulated by interneurons (mainly inhibitory) through the release of opioid pepides and GABA and also by supraspinal descending neurons (Descending pathways) through the release of serotonin (5-HT) and noradrenaline (NA). Descending pathways may inhibit or enhance nociceptive transmission from the spinal cord.

Gene therapy is an especially versatile tool for chronic pain management since it is based in a triad of controllable parameters: the vector, the transgene and the promoter. By knowing the neurobiological features of each chronic pain type, namely the neurotransmitters and receptors affected, it is possible to design gene therapy strategies based on the best combination of vectors, transgenes and promoters. As to vectors, gene therapy for pain uses mainly vehicles which have a certified experience in infecting neurons, namely replication-defective forms of viruses. Non-viral vectors have seldom been used in gene therapy studies for pain but their transduction efficiency and specificity are much lower than those of viral vectors. Some of these vectors have the ability to migrate retrogradely (i.e., contrary to the direction of nerve impulse) which is very useful to target neurons that are located in structures of difficult surgical access. A good example is the application of replication-defective forms of Herpes Simplex Virus type 1 (HSV-1) at the periphery (e.g. the skin) to transduce neurons at the spinal ganglia (dorsal root ganglia-DRGs), which are difficult to access due to their bone protection. Regarding the transgenes to include in the vectors for gene therapy of pain, it is possible to increase the expression of neurotransmitters and receptors involved in nociceptive inhibition (e.g. opioids), neurotrophic factors or substances with anti-inflammatory properties. Finally, and in what concerns the promoters, it is possible to choose those that restrict transgene expression to a cell type, such as a neuron or a glial cell, or even target selective neurochemical neuronal populations. Examples of neuron-specific promoters are synapsin I, calcium/calmodulin-dependent protein kinase II, tubulin alpha I and neuron-specific enolase [12]. Some possibilities of controlling the vectors, transgenes and promoters will be discussed in the next two sections using gene therapy in animal models.

One of the main advantages of experimental gene therapy studies is that they can be performed using several pain models. This is important since each pain type may induce specific changes in neuronal circuits devoted to the transmission and modulation of nociceptive transmission [13]. Studies of gene therapy for pain have used clinically relevant models of inflammatory [14-22] and neuropathic pain [23-34]. In a much lower incidence, models of acute [35-38], post-operative pain [39] and cancer [40] pain have been used in experimental gene therapy studies. The large majority of studies were performed in pain models affecting the limbs or the trunk, in the latter case being of visceral origin [22, 37]. Two studies used gene therapy to block nociceptive transmission coming from the head/face in pain models that reproduces some types of craniofacial pain, like trigeminal neuralgia [41] or temporomandibular joint disorders [42].

Gene therapy studies for pain in animal models may be divided in studies targeting the spinal cord (Table 1) and studies directed to pain control centres located in the brain (Table 2). Studies directed to the spinal cord mainly aim to manipulate the expression of transgenes in order to block the transmission of nociceptive input at the spinal dorsal horn (Table 1). Most of the spinal cord studies using gene therapy for pain elected HSV-1 as the most suitable vector, due to its natural affinity to the neuron and its ability for retrograde transport [43]. HSV-1 has the additional advantage over other vectors of carrying multiple transgenes or large transgenes and not integrating in the host genome, which reduces the possibility of mutagenic events [44, 45]. After application of replication-defective forms of HSV-1 at the periphery in order to transduce DRG neurons (or trigeminal ganglion neurons), delivery of the transgene product by the spinal branch of transduced neurons at the spinal dorsal horn induced analgesia in several rodent models of pain (Table 1). Gene therapy in animal models of craniofacial pain [41, 42] aimed to release the transgene products at the level of the spinal trigeminal nucleus and this structure is homolog of the spinal cord, which prompted to include these studies in the section devoted to spinal cord studies.

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