Short video on Stem Cell Therapy Treatment for Muscular Dystrophy by Dr Alok Sharma
Stem Cell Therapy Treatment for Muscular Dystrophy by Dr Alok Sharma. He is a known case of MD with history of gradual onset of progressive lower extremities...

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Short video on Stem Cell Therapy Treatment for Muscular Dystrophy by Dr Alok Sharma - Video

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Symmetry (ASSR) - Cell Therapy (Lemon Water) prod. Tha Professa
Almighty Shing Shing Regime 2013© Cell Therapy (Lemon Water) Symm and Tha Professa return with another vibe from "Cell Therapy", this time bringing an awaren...

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Symmetry (ASSR) - Cell Therapy (Lemon Water) prod. Tha Professa - Video

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Lemon Water (Cell Therapy) - Symmetry
Symm and Tha Professa return with another vibe from "Cell Theryrapy", this time bringing an awareness of supreme health in hip-hop form. On Cell Therapy (Lem...

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Lemon Water (Cell Therapy) - Symmetry - Video

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Dr. Mayo Friedlis - Introduction to Stem Cell Therapy
Dr. Mayo Friedlis of Stemcell ARTS (an affiliate of National Spine and Pain Centers) in Fairfax, Virginia introduces stem cell therapy, an innovative solution that can deliver non-surgical...

By: StemCell ARTS

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Dr. Mayo Friedlis - Introduction to Stem Cell Therapy - Video

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Dr. Mayo Friedlis - Stem Cell Therapy for Athletes and Sports-Related Injuries
Dr. Mayo Friedlis of Stemcell ARTS (an affiliate of National Spine and Pain Centers) in Fairfax, Virginia introduces stem cell therapy for athletes, an innovative solution that can deliver...

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Dr. Mayo Friedlis - Stem Cell Therapy for Athletes and Sports-Related Injuries - Video

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Dr. Mayo Friedlis - Stem Cell Therapy for Common Injuries?
Dr. Mayo Friedlis of Stemcell ARTS (an affiliate of National Spine and Pain Centers) in Fairfax, Virginia introduces stem cell therapy, an innovative solution that can deliver non-surgical...

By: StemCell ARTS

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Dr. Mayo Friedlis - Stem Cell Therapy for Common Injuries? - Video

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Dr. Mayo Friedlis - When Should You Use Stem Cell Therapy?
Dr. Mayo Friedlis of Stemcell ARTS (an affiliate of National Spine and Pain Centers) in Fairfax, Virginia introduces stem cell therapy, an innovative solution that can deliver non-surgical...

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Dr. Mayo Friedlis - When Should You Use Stem Cell Therapy? - Video

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Dr. Mayo Friedlis - Stem Cell Therapy for Hip Problems
Dr. Mayo Friedlis of Stemcell ARTS (an affiliate of National Spine and Pain Centers) in Fairfax, Virginia introduces stem cell therapy, an innovative solution that can deliver non-surgical...

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Dr. Mayo Friedlis - Stem Cell Therapy for Hip Problems - Video

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The bad news: "Stem cells by themselves do not work."

The good news: "Stem cells by themselves do not work."

Take it from the doctor who has treated 5,000 patients with stem cell therapy, a doctor who is himself a cancer survivor. Thirteen years ago, Dr. Sam Bernal - oncologist, chemist, molecular biologist, lawyer, professor and lecturer, among other things - was a cancer patient who thought he was at death's door. Using stem cells sourced from his bone marrow and peripheral blood, he overcame the disease and has since become an advocate of living fit, living well in order to look good.

Dr. Bernal, who divides his time between Los Angeles, Prague, Makati, and Germany, was a pioneer in stem cell research in the Philippines early on in his career, for which he was cited when he received the Presidential Award for Outstanding Filipinos Overseas from President Benigno S, Aquino III in 2012.

At a recent meeting with journalists, Dr. Bernal hurled the challenge: "What do you need stem cell therapy for if you eat well, sleep soundly, exercise regularly, don't smoke, have a positive attitude, and know how to live in the moment as you gaze at a painting and get a thrill out of small things like that?"

Not only is the doctor a passionate advocate of living the good life, the simple life, and, yes, Argentine tango - "It's better than boring exercises at the gym!" - he believes in healthy eating. "I brought a group of European friends to Manila and they were flabbergasted at our vegetable dishes - laing, gising-gising, buko juice - our simplest food was gourmet cuisine to them!"

No, he's not a vegetarian, but a "flexitarian."

But if stem cells - the body's own master and repair cells - aren't the key to staying young, what is? The holistic approach works best, according to the doctor, stating that the procedure should be recommended by doctors "on a case by case basis." In effect, the doctor prescribes "customizing your stem cell therapy."

In his book, molecular biology provides the battleground from which to attack the afflictions of aging that signal a desire or need to repair or replace one's stem cells. Speaking of books, Dr. Bernal continues to teach at Harvard, Ateneo, UST, and Medical City as a component of his mission to spread the benefits of technology transfer, which is the vision of his company, GlobeTek Science Foundation (based in Makati).

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‘Customize’ your stem cell therapy

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Researchers create first ever map showing distribution of red head genes In south-east Scotland 40 per cent carry one of the common variants Results show Yorkshire and Humberside are as redheaded as Ireland

By Damien Gayle

PUBLISHED: 07:30 EST, 24 August 2013 | UPDATED: 11:00 EST, 24 August 2013

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Former Dr Who assistant Karen Gillan: Redheads still face prejudice despite prominence of stars with red hair and numbers of women who dye their hair red

They suffer a lot of stick for their unusual hair colouring, with hurtful taunts of 'Ginger!' resonating around playgrounds across the country.

Despite the prominence of stars Karen Gillan, Prince Harry and Damien Lewis, redheads still complain that they fall victim to prejudice and discrimination.

But new research shows that, far from being rare, Britain and Ireland are in fact host to a secret army of red hair gene carriers.

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Who you calling ginger? Research reveals that far from being rare nearly 20MILLION red hair gene carriers in Britain ...

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Researchers create first ever map showing distribution of red head genes In south-east Scotland 40 per cent carry one of the common variants Results show Yorkshire and Humberside are as redheaded as Ireland

By Damien Gayle

PUBLISHED: 07:30 EST, 24 August 2013 | UPDATED: 11:00 EST, 24 August 2013

1,298 shares

99

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Former Dr Who assistant Karen Gillan: Redheads still face prejudice despite prominence of stars with red hair and numbers of women who dye their hair red

They suffer a lot of stick for their unusual hair colouring, with hurtful taunts of 'Ginger!' resonating around playgrounds across the country.

Despite the prominence of stars Karen Gillan, Prince Harry and Damien Lewis, redheads still complain that they fall victim to prejudice and discrimination.

But new research shows that, far from being rare, Britain and Ireland are in fact host to a secret army of red hair gene carriers.

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Ginger genes: Research reveals that 20MILLION red hair gene carriers in Britain and Ireland

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Can GMO cure us?: Peter Celec at TEDxBratislava 2013
Peter Celec is the Head of the Institute of Molecular Biomedicine of Faculty of Medicine, Comenius University. In the area of science he deals with the impac...

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Gene Therapy Dr. Cary Harding, MD - 2012 Conference
Liver-directed gene therapy is a promising novel treatment approach for PKU. Dr. Harding expands on overcoming limitations, alternative approaches, and the o...

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By Susan E. Matthews

Those lucky enough to have survived a heart attack often face an uphill battle the trauma associated with the attack can often kill enough heart cells to leave survivors much weaker than before. But with a new personalized genetic approach, researchers may have found a way to reinvigorate the damaged cells, and even get them beating again./p>

Researchers from the Gladstone Institutes in San Francisco found that injecting a therapy of genes into dead heart cells has promising implications for restarting the cells, based on studies done in mice and human cells in a lab. After receiving this therapy, most cells showed some signs of transformation, and 20 percent of them were up and working again, according to the study, published in Stem Cell Reports.

More from Everyday Health: Not Broken, Just Different: Explaining ADHD to a Young Child ADHD and College Success: Nicolas' Story Fiery Facts About Redheads

The research builds on the Gladstone teams previous work that successfully reinvigorated dead heart cells in mice through an injection of three genes, called GMT. In the latest study, the researchers used a new cocktail of five genes GMT with MYOCD and ZFPM2 and successfully reprogrammed damaged human cells.

The concept behind the approach is sound, but the current efficiency levels are low, warranting more research, said Konstantinos Malliaras, MD, assistant professor at the Cedars-Sinai Heart Institute.

The researchers are targeting the hearts fibroblasts, a specific type of scar-forming cell that makes up 50 percent of the human heart. The results are preliminary, and researchers noted that they still have some work to do to perfect the cocktail and test the process in larger animals.

Success rates might be improved by transforming the fibroblasts within living hearts rather than in a dish something we also observed during our initial experiments in mice, said Deepak Srivastava, MD, director of Gladstone cardiovascular and stem cell research. However, the researchers also noted that it takes longer to reprogram human cells than mouse cells, and the process remains inefficient.

Unlike some organs, such as the liver, the heart cannot regenerate quickly. The study out today represents one of three approaches currently explored as possible ways to regenerate the heart.

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New Gene Therapy May Help Heart Attack Survivors

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Quality Is the Key, Says Veteran of Personalized Medicine
0:40 Building one of the first molecular diagnostics labs at UCSF 6:47 Where are we at with personalized medicine today? 11:27 What can we do to better quali...

By: mendelspod

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Quality Is the Key, Says Veteran of Personalized Medicine - Video

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Study found that stress triggers a 'master switch' gene called ATF3 This corrupts the immune system, giving cancer an fast-track around body Discovery could help develop drugs to dampen the 'stress gene'

By Emma Robertson

PUBLISHED: 08:56 EST, 23 August 2013 | UPDATED: 10:46 EST, 23 August 2013

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Stress fuels cancer by triggering a 'master switch' gene which allows the disease to spread, according to new research.

The 'unexpected' discovery could lead to the development of drugs that target the protein and stop tumours spreading to other organs and causing death.

Stress has long been linked to many forms of the disease including breast and prostate cancer, but the reason has remained a mystery.

Doctors have discovered the 'stress gene' ATF3 can make immune cells behave erratically, giving cancer an 'escape route' to other areas of the body

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Stress DOES have an impact on cancer: Anxiety switches on a gene that speeds up the spread of the disease

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Aug. 22, 2013 In an unexpected finding, scientists have linked the activation of a stress gene in immune-system cells to the spread of breast cancer to other parts of the body.

Researchers say the study suggests this gene, called ATF3, may be the crucial link between stress and cancer, including the major cause of cancer death -- its spread, or metastasis. Previous public health studies have shown that stress is a risk factor for cancer.

Researchers already know that ATF3 is activated, or expressed, in response to stressful conditions in all types of cells. Under typical circumstances, turning on ATF3 can actually cause normal and benign cells to commit suicide if the cells decide that the stressors, such as irradiation and a lack of oxygen, have irrevocably damaged the cells.

This research suggests, however, that cancer cells somehow coax immune-system cells that have been recruited to the site of a tumor to express ATF3. Though it's still unclear how, ATF3 promotes the immune cells to act erratically and give cancer an escape route from a tumor to other areas of the body.

"It's like what Pogo said: 'We have met the enemy, and he is us,'" said Tsonwin Hai, professor of molecular and cellular biochemistry at The Ohio State University and senior author of the study. "If your body does not help cancer cells, they cannot spread as far. So really, the rest of the cells in the body help cancer cells to move, to set up shop at distant sites. And one of the unifying themes here is stress."

Hai and colleagues first linked the expression of the ATF3 gene in immune-system cells to worse outcomes among a sample of almost 300 breast-cancer patients. They followed with animal studies and found that mice lacking the ATF3 gene had less extensive metastasis of breast cancer to their lungs than did normal mice that could activate ATF3.

This stress gene could one day function as a drug target to combat cancer metastasis if additional studies bear out these results, Hai said. In the meantime, she said the results provide important insights into how cells in a tumor use their signaling power to coopt the rest of the body into aiding cancer's survival and movement to distant organs.

The research is published in a recent issue of the Journal of Clinical Investigation.

Hai, a member in the Ohio State University Comprehensive Cancer Center, has studied ATF3 in cancer cells for years. When she had a chance to examine human samples from about 300 breast-cancer patients, she was stunned to find that the expression of ATF3 gene in certain immune-system cells was associated with worse cancer outcomes in this group of patients. ATF3 in cancer cells showed no such association.

To test that clinical data, she and colleagues conducted two rounds of studies in mice. The researchers first injected breast cancer cells into two groups: normal mice and mice that cannot express ATF3 in any cells. The cancer in normal mice metastasized to the lungs far more rapidly and extensively than did cancer in the mice lacking ATF3. In the second round of experiments, they used genetically altered mice that could not express ATF3 in a group of immune system cells called myeloid cells, and the results were similar.

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The stress and cancer link: 'Master-switch’ stress gene enables cancer's spread

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Washington, August 23 (ANI): Researchers have associated the activation of a stress gene in immune-system cells to the spread of breast cancer to other parts of the body.

According to the researchers, the study suggests this gene, called ATF3, may be the crucial link between stress and cancer, including the major cause of cancer death - its spread, or metastasis.

Researchers already know that ATF3 is activated, or expressed, in response to stressful conditions in all types of cells.

Under typical circumstances, turning on ATF3 can actually cause normal and benign cells to commit suicide if the cells decide that the stressors, such as irradiation and a lack of oxygen, have irrevocably damaged the cells.

This research suggests, however, that cancer cells somehow coax immune-system cells that have been recruited to the site of a tumor to express ATF3.

Though it's still unclear how, ATF3 promotes the immune cells to act erratically and give cancer an escape route from a tumor to other areas of the body.

Tsonwin Hai, professor of molecular and cellular biochemistry at The Ohio State University and senior author of the study, said that if your body does not help cancer cells, they cannot spread as far. So really, the rest of the cells in the body help cancer cells to move, to set up shop at distant sites. And one of the unifying themes here is stress.

Hai and colleagues first linked the expression of the ATF3 gene in immune-system cells to worse outcomes among a sample of almost 300 breast-cancer patients.

They followed with animal studies and found that mice lacking the ATF3 gene had less extensive metastasis of breast cancer to their lungs than did normal mice that could activate ATF3.

ATF3 is a master switch type of gene: Its gene product, the ATF3 protein, turns on and off other genes. Knowing this, the researchers analyzed the genes that are controlled by ATF3 using a genome-wide global approach. Combining this set of data with another set of data from human samples, Hai and colleagues were able to identify an ATF3 gene signature that can predict whether cancer patients had a low or high risk of dying.

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Stress gene implicated in cancer spread

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York University biology Professor Samuel Benchimol has been awarded the Progeria Research Foundations Established Investigator award, a three-year grant worth $300,000 US.

Dr. Benchimol

Benchimol, who ischair of the Department of Biology at York University and Canada Research Chair in Biomedical Health, is internationally recognized for studies focusing on the p53 gene. Specifically, his research focuses on theinactivating mutations in the p53 gene that contribute to cancer development. He was among a group of researchers that discovered new genes affecting p53 function.

Progeria or Hutchinson-Gilford Progeria Syndrome (HGPS), is a rare, fatal genetic condition characterized by an appearance of accelerated aging in children, with average life expectancy being 13 years. It is caused by a mutation in the gene called LMNA (pronounced lamin-a). The LMNA gene produces the lamin A protein which is the structural scaffolding that holds the nucleus of a cell together. The abnormal lamin A protein that causes Progeria is called progerin. Researchers now believe that progerin makes the nucleus unstable. That cellular instability leads to the process of premature aging and disease in progeria.

Were very pleased to hear that Dr. Benchimol received this grant, says Robert Tsushima, associate dean, research & partnerships, in York Universitys Faculty of Science. His research is critical, both in terms of finding a cure for progeria and furthering our understanding of cancer. The p53 gene is the most commonly mutated gene in human cancers.

Benchimols research will build upon preliminary data and test novel hypotheses regarding the role of p53 in mediating the premature aging shown by cells from Hutchinson-Gilford Progeria syndrome (HGPS) patients.

His work, in collaboration with Keith Wheaton, a postdoctoral fellow in his laboratory,will test the hypothesis that progerin causes replication stress, which in turn elicits a growth arrest, and that p53 acts downstream of the progerin-induced replication stress. The hope is that researchers can determine how progerin and p53 collaborate to elicit this cell-aging response.

Prior to joining York University, Benchimol conducted research at the Ontario Cancer Institute and the University of Toronto.

The Progeria Research Foundation (PRF) funds medical research aimed at developing treatments and a cure for progeria. The foundation also has its own cell and tissue bank that provides the biological materials researchers need to conduct their experiments. Additionally, PRF has established a medical and research database to supply physicians and families with medical recommendations for cardiac care, nutrition and other medical issues to help children and adults with progeria have a better quality of life. PRF is also involved in progeria clinical drug trials testing potential treatments.

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Prof receives prestigious award from Progeria Research Foundation

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Public release date: 23-Aug-2013 [ | E-mail | Share ]

Contact: Alison Barbuti alison.barbuti@manchester.ac.uk 44-016-127-58383 University of Manchester

A University of Manchester professor and his wife have had their own DNA analysed for compatibility as part of the research for a new book out on 1 October in the US and next week in the UK.

Professor Daniel Davis and his wife Katie's experience is documented in The Compatibility Gene, published by Oxford University Press in the US and Penguin in the UK, which discusses how our crucial compatibility genes may influence finding a life partner as well as our health and individuality.

Professor Davis said: "We each possess a similar set of around 25,000 human genes. Some of our genes vary from person to person, like those that give us a particular eye or hair colour. But my book is about the few genes our compatibility genes that vary the most between each of us. First and foremost these are immune system genes; they control how we combat disease. But recent research shows that they may be even more important than we once thought there is evidence that they can influence how our brains are wired, how attractive we are, even how likely we are to reproduce.''

"I'm used to writing academic papers looking at particular cells and genes but I had to write this book to highlight the wonder of this new research take stock of the big picture - and make this fascinating new science accessible to everyone."

The book explains how research has radically transformed knowledge of the way our bodies work - with profound consequences for medical research and ethics. The story begins with a small band of scientific pioneers who, during the Second World War, struggled to understand the mysteries of transplants and grafts. And continues to the Swiss zoologist who had people rank the sexiness of smells from worn T-shirts - and found the results related to our compatibility genes. Very recent experiments discussed in the book show that these same genes may also influence the likelihood of problems in pregnancy.

Professor Davis, Director of Research at the University of Manchester's Collaborative Centre for Inflammation Research, said finding out more about his and his wife's genetic make-up had been a surprisingly nerve-wracking experience. The couple had their saliva sent to the Anthony Nolan Trust a UK charity that helps match transplantation donors and recipients.

"The tubes were bar- coded and shuffled down a series of robotic instruments that first isolated the DNA and then made copies of our compatibility genes," Professor Davis said. "Small beads, each having a different short piece of DNA attached, were added to a solution containing our genes. Beads with DNA just right to bind to one of our compatibility genes are picked out by a sensor, revealing which versions of these genes we have."

Professor Davis discovered his compatibility genes were quite rare, while his wife's were more common. One group of his genes were frequently found in Europe, particularly Eastern Europe, while the other set were common in India or Australia. His wife found she had a gene which would be helpful if she ever suffered an infection with HIV but which also increased her susceptibility to the auto-immune disease ankylosing spondylitis.

Read more from the original source:
Nice genes! What makes you genetically compatible with your partner?

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In an unexpected finding, scientists have linked the activation of a stress gene in immune-system cells to the spread of breast cancer to other parts of the body.

Researchers say the study suggests this gene, called ATF3, may be the crucial link between stress and cancer, including the major cause of cancer death its spread, or metastasis. Previous public health studies have shown that stress is a risk factor for cancer.

Researchers already know that ATF3 is activated, or expressed, in response to stressful conditions in all types of cells. Under typical circumstances, turning on ATF3 can actually cause normal and benign cells to commit suicide if the cells decide that the stressors, such as irradiation and a lack of oxygen, have irrevocably damaged the cells.

This research suggests, however, that cancer cells somehow coax immune-system cells that have been recruited to the site of a tumor to express ATF3. Though it's still unclear how, ATF3 promotes the immune cells to act erratically and give cancer an escape route from a tumor to other areas of the body.

"It's like what Pogo said: 'We have met the enemy, and he is us,'" said Tsonwin Hai, professor of molecular and cellular biochemistry at The Ohio State University and senior author of the study. "If your body does not help cancer cells, they cannot spread as far. So really, the rest of the cells in the body help cancer cells to move, to set up shop at distant sites. And one of the unifying themes here is stress."

Hai and colleagues first linked the expression of the ATF3 gene in immune-system cells to worse outcomes among a sample of almost 300 breast-cancer patients. They followed with animal studies and found that mice lacking the ATF3 gene had less extensive metastasis of breast cancer to their lungs than did normal mice that could activate ATF3.

This stress gene could one day function as a drug target to combat cancer metastasis if additional studies bear out these results, Hai said. In the meantime, she said the results provide important insights into how cells in a tumor use their signaling power to coopt the rest of the body into aiding cancer's survival and movement to distant organs.

The research is published in the Journal of Clinical Investigation.

Hai, a member in the Ohio State University Comprehensive Cancer Center, has studied ATF3 in cancer cells for years. When she had a chance to examine human samples from about 300 breast-cancer patients, she was stunned to find that the expression of ATF3 gene in certain immune-system cells was associated with worse cancer outcomes in this group of patients. ATF3 in cancer cells showed no such association.

To test that clinical data, she and colleagues conducted two rounds of studies in mice. The researchers first injected breast cancer cells into two groups: normal mice and mice that cannot express ATF3 in any cells. The cancer in normal mice metastasized to the lungs far more rapidly and extensively than did cancer in the mice lacking ATF3. In the second round of experiments, they used genetically altered mice that could not express ATF3 in a group of immune system cells called myeloid cells, and the results were similar.

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Stress gene enables breast cancer's spread

Recommendation and review posted by Bethany Smith

Artificial 47th Chromosome - Genetic Engineering in Humans
Jeff Rense and Texe Marrs, August 19, 2013.

By: TheRapeOfJustice

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Artificial 47th Chromosome - Genetic Engineering in Humans - Video

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Public release date: 23-Aug-2013 [ | E-mail | Share ]

Contact: Cathia Falvey cfalvey@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, August 19, 2013 Mary Ann Liebert, Inc., publishers is pleased to announce the launch of its new Chinese version website.

The Chinese version has been developed in collaboration with The Charlesworth Group, extending easy access to Mary Ann Liebert, Inc.'s more than 80 industry-leading journals. This customized platform provides a direct portal for Chinese researchers, policy makers, and industry experts to all of the publisher's cutting-edge publications.

In addition to all of the peer-reviewed content, the website includes information for authors with guidance about manuscript submission and Mary Ann Liebert, Inc.'s Open Access policies. The Chinese website provides access to Liebert Connect enabling users to personalize their email alerts while keeping up-to-date with Tables of Content, featured articles, press releases, and journal announcements. Chinese librarians can access library-specific resources and support. Furthermore, readers can share and recommend articles through the social platform Weibo Connect.

The launch of this customized website underscores Mary Ann Liebert, Inc.'s commitment to providing access to readers in China.

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About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 80 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website.

Mary Ann Liebert, Inc. 140 Huguenot St., New Rochelle, NY 10801-5215 Phone: (914) 740-2100 (800) M-LIEBERT Fax: (914) 740-2101 http://www.liebertpub.com

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Mary Ann Liebert, Inc. and The Charlesworth Group launch customized web platform

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Aug. 23, 2013 In an era of widespread genetic sequencing, the ability to edit and alter an organism's DNA is a powerful way to explore the information within and how it guides biological function.

A paper from the University of Wisconsin-Madison in the August issue of the journal Genetics takes genome editing to a new level in fruit flies, demonstrating a remarkable level of fine control and, importantly, the transmission of those engineered genetic changes across generations.

Both features are key for driving the utility and spread of an approach that promises to give researchers new insights into the basic workings of biological systems, including embryonic development, nervous system function, and the understanding of human disease.

"Genome engineering allows you to change gene function in a very targeted way, so you can probe function at a level of detail" that wasn't previously possible, says Melissa Harrison, an assistant professor of biomolecular chemistry in the UW-Madison School of Medicine and Public Health and one of the three senior authors of the new study.

Disrupting individual genes has long been used as a way to study their roles in biological function and disease. The new approach, based on molecules that drive a type of bacterial immune response, provides a technical advance that allows scientists to readily engineer genetic sequences in very detailed ways, including adding or removing short bits of DNA in chosen locations, introducing specific mutations, adding trackable tags, or changing the sequences that regulate when or where a gene is active.

The approach used in the new study, called the CRISPR RNA/Cas9 system, has developed unusually fast. First reported just one year ago by scientists at the Howard Hughes Medical Institute and University of California, Berkeley, it has already been applied to most traditional biological model systems, including yeast, zebrafish, mice, the nematode C. elegans, and human cells. The Wisconsin paper was the first to describe it in fruit flies and to show that the resulting genetic changes could be passed from one generation to the next.

"There was a need in the community to have a technique that you could use to generate targeted mutations," says Jill Wildonger, a UW-Madison assistant professor of biochemistry and another senior author of the paper. "The need was there and this was the technical advance that everyone had been waiting for."

"The reason this has progressed so quickly is that many researchers -- us included -- were working on other, more complicated, approaches to do exactly the same thing when this came out," adds genetics assistant professor Kate O'Connor-Giles, the third senior author. "This is invaluable for anyone wanting to study gene function in any organism and it is also likely to be transferable to the clinical realm and gene therapy."

The CRISPR RNA/Cas9 system directs a DNA-clipping enzyme called Cas9 to snip the DNA at a targeted sequence. This cut then stimulates the cell's existing DNA repair machinery to fill in the break while integrating the desired genetic tweaks. The process can be tailored to edit down to the level of a single base pair -- the rough equivalent of changing a single letter in a document with a word processor.

The broad applicability of the system is aided by a relatively simple design that can be customized through creation of a short RNA sequence to target a specific sequence in the genome to generate the desired changes. Previous genome editing methods have relied on making custom proteins, which is costly and slow.

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Unprecedented control of genome editing in flies promises insight into human development, disease

Recommendation and review posted by Bethany Smith

Public release date: 23-Aug-2013 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, August 15, 2013Existing urban water systems are at the end of their design lifetimes. New, innovative solutions are needed, and these must combine technology and engineering with an understanding of social systems and institutions. The current issue of Environmental Engineering Science, the Official Journal of the Association of Environmental Engineering and Science Professors, focuses on Re-inventing Urban Water Systems. Of particular note is an insightful article that presents the challenges and opportunities facing urban water system innovation, available free on the Environmental Engineering Science website.

The article, entitled "The Innovation Deficit in Urban Water: The Need for an Integrated Perspective on Institutions, Organizations, and Technology," contends that for new innovations to be implemented successfully, engineers must understand the social, economic, institutional, and political mechanisms that underlie the human-technology interface. Coauthors Michael Kiparsky, David Sedlak, Barton Thompson, and Bernhard Truffer (University of California at Berkeley School of Law; University of California at Berkeley School of Engineering; Stanford Law School and Woods Institute for the Environment, Stanford, CA; and Swiss Federal Institute of Aquatic Science and Technology, Dbendorf, Switzerland, respectively) are all members of a U.S. National Science Foundation Engineering Research Center focused on developing new approaches to urban water infrastructure - ReNUWIt (Reinventing the Nation's Urban Water Infrastructure).

"The Kiparsky paper and the EES special issue are timely and are destined to be among the most influential and important contributions to the field of environmental engineering in recent times," says Domenico Grasso, PhD, Editor-in-Chief and Provost, University of Delaware. "The holistic approaches outlined are not only well suited for addressing the complex problems of the urban infrastructure but may serve as a template for addressing many other sociotechnological challenges of the 21st century."

Guest Editors of this special issue of Environmental Engineering Science on Re-inventing Urban Water Systems, David Sedlak, Jrg Drewes, Colorado School of Mines, Golden, and Richard Luthy, Stanford University, compiled a series of articles that focus on topics including innovation in complex systems; active management of natural systems to enhance the performance of urban water infrastructure; and management of concentrates from water treatment processes.

"Our modern urban water infrastructure is one of the greatest engineering achievements of the 20th century," says Jennifer Becker, President of the Association of Environmental Engineering and Science Professors. "This important issue of EES highlights a paradigm shift in our urban water systems and that technological innovations are urgently needed if the growing demands for water and other resources are to be sustainably met."

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About the Journal

Environmental Engineering Science is an authoritative monthly, online peer-reviewed journal from Mary Ann Liebert, Inc., publishers. Publishing state-of-the-art studies of innovative solutions to problems in air, water, and land contamination and waste disposal, the Journal features applications of environmental engineering and scientific discoveries, policy issues, environmental economics, and sustainable development including climate change, complex and adaptive systems, contaminant fate and transport, environmental risk assessment and management, green technologies, industrial ecology, environmental policy, and energy and the environment.

See the article here:
Can we save our urban water systems?

Recommendation and review posted by Bethany Smith