CHICAGO, April 2, 2015 /PRNewswire-USNewswire/ --After surgery failed to relieve extreme pain caused by peripheral artery disease in her right leg, Denise Hopkins-Glover was facing a bleak outlook she might never walk again.

"They said they had done everything they could and the only option was amputation of the right leg from the knee down," she said.

Undeterred, Hopkins-Glover chose to participate in an investigational trial at Northwestern Medicine called the MOBILE Study, which makes use of a device called the MarrowStim PAD Kit. In the trial, a randomized group of patients receive injections of their own stem cells retrieved through a bone marrow extraction to try to restore blood flow to the leg.

"MarrowStim offers a new approach for patients with a grim prognosis," said principal investigator Melina Kibbe, MD, a vascular surgeon at Northwestern Memorial Hospital and Edward G. Elcock Professor of Surgical Research at Northwestern University Feinberg School of Medicine. "We're pleased to be part of this national trial to see if there might be a significant chance of improving treatment for patients with few choices left for treatment."

Hopkins-Glover, a 55-year-old grandmother of two, suffers from peripheral artery disease (PAD), a condition affecting 20 percent of Americans where cholesterol and fatty plaque pool in blood vessels, restricting blood flow to the limbs. In its most severe form, PAD causes critical limb ischemia (CLI), which can cause pain in resting legs, sores or ulcers that don't heal, thickening of the toenails and gangrene, which can eventually lead to amputation.

The Chicago resident worked as a phlebotomist before her PAD worsened, and had to stop working because she could no longer walk or stand for extended stretches of time.

"I can walk only a certain distance before the circulation stops getting to certain parts of the body," she said. "It feels like a terrible leg cramp, like a jabbing, stabbing pain."

During the procedure, patients are put under general anesthesia as bone marrow is harvested through a needle from the hip. The bone marrow is loaded into the MarrowStim PAD Kit, an investigational device, where it is processed in a centrifuge. This spinning separates the marrow into different layers, with one of the layers containing the stem cells. Immediately following the separation, the stem cells are injected in 40 different spots on the affected limb, delivering concentrated bone marrow in each one. The entire procedure takes about 90 minutes. Patients follow up with investigators at different intervals in the year following the injections.

Karen Ho, MD, a Northwestern Medicine vascular surgeon who is also an investigator on the trial, said the exact reason the bone marrow injections might help chronic limb ischemia is still a mystery.

"Nobody really knows the exact mechanism," said Dr. Ho, who is also an assistant professor in vascular surgery at Feinberg. "The idea is that it might improve or enhance new blood vessels in the calf."

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Cancer Research UK scientists have discovered that a vital self-destruct switch in cells is hijacked -- making some pancreatic and non small cell lung cancers more aggressive, according to research published in Cancer Cell.

The team, from the Cancer Research UK Centre at the UCL (University College London) Cancer Institute, found that mutations in the KRAS gene interferes with protective self-destruct switches, known as TRAIL receptors, which usually help to kill potentially cancerous cells.

The research, carried out in cancer cells and mice, shows that in cancers with faulty versions of the KRAS gene these TRAIL receptors actually help the cancer cells to grow and spread to new areas in the body.

These KRAS faults occur in 95 per cent of pancreatic cancers and 30 per cent of non small cell lung cancers.

Professor Henning Walczak, lead researcher of the study and scientific director of the Cancer Research UK-UCL Centre, said: "Our research has unveiled a new strategy used by some pancreatic and non small cell lung cancers to overcome our body's natural defences against cancer. By understanding the faults in these cancers we think we can develop more tailored treatments, which could one day provide urgently-needed options for patients with these types of pancreatic and non small cell lung cancers."

Each year in Great Britain 32,500 people are diagnosed with non small cell lung cancer and around 8,600 people are diagnosed with pancreatic cancer. Survival for these cancers has not shown much improvement for 40 years.

Nell Barrie, senior science information manager at Cancer Research UK, said: "Sadly survival from pancreatic and lung cancers remains far too low, partly because these cancers are very difficult to treat once they have spread.

"We urgently need better treatments, so it's vital to delve deeper into the molecular workings of these cancers to find ways to combat them. This research may one day help us find a way to block cancer spread, which would be a vital step to save more lives."

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The above story is based on materials provided by Cancer Research UK. Note: Materials may be edited for content and length.

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Body's cancer defenses hijacked to make pancreatic, lung cancers more aggressive

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CANCER RESEARCH UK scientists have discovered that a vital self-destruct switch in cells is hijacked - making some pancreatic and non small cell lung cancers more aggressive, according to research published in Cancer Cell today (Thursday)*.

The team, from the Cancer Research UK Centre at the UCL (University College London) Cancer Institute, found that mutations in the KRAS gene interferes with protective self-destruct switches, known as TRAIL receptors, which usually help to kill potentially cancerous cells.

The research, carried out in cancer cells and mice, shows that in cancers with faulty versions of the KRAS gene these TRAIL receptors actually help the cancer cells to grow and spread to new areas in the body.

These KRAS faults occur in 95 per cent of pancreatic cancers** and 30 per cent of non small cell lung cancers.

Professor Henning Walczak, lead researcher of the study and scientific director of the Cancer Research UK-UCL Centre, said: "Our research has unveiled a new strategy used by some pancreatic and non small cell lung cancers to overcome our body's natural defences against cancer. By understanding the faults in these cancers we think we can develop more tailored treatments, which could one day provide urgently-needed options for patients with these types of pancreatic and non small cell lung cancers."

Each year in Great Britain 32,500 people are diagnosed with non small cell lung cancer and around 8,600 people are diagnosed with pancreatic cancer. Survival for these cancers has not shown much improvement for 40 years.

Nell Barrie, senior science information manager at Cancer Research UK, said: "Sadly survival from pancreatic and lung cancers remains far too low, partly because these cancers are very difficult to treat once they have spread.

"We urgently need better treatments, so it's vital to delve deeper into the molecular workings of these cancers to find ways to combat them. This research may one day help us find a way to block cancer spread, which would be a vital step to save more lives."

###

For media enquiries contact Emily Head in the Cancer Research UK press office on 020 3469 6189 or, out of hours, on 07050 264 059.

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Body's cancer defences hijacked to make pancreatic and lung cancers more aggressive

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(Boston)--Using patient-derived stem cells known as induced pluripotent stem cells (iPSC) to study the genetic lung/liver disease called alpha-1 antitrypsin (AAT) deficiency, researchers have for the first time created a disease signature that may help explain how abnormal protein leads to liver disease.

The study, which appears in Stem Cell Reports, also found that liver cells derived from AAT deficient iPSCs are more sensitive to drugs that cause liver toxicity than liver cells derived from normal iPSCs. This finding may ultimately lead to new treatments for the condition.

IPSC's are derived from the donated skin or blood cells of adults and, with the reactivation of four genes, are reprogrammed back to an embryonic stem cell-like state. Like embryonic stem cells, iPSC can be differentiated toward any cell type in the body, but they do not require the use of embryos. Alpha-1 antitrypsin deficiency is a common genetic cause of both liver and lung disease affecting an estimated 3.4 million people worldwide.

Researchers from the Center for Regenerative Medicine (CReM) at Boston University and Boston Medical Center (BMC) worked for several years in collaboration with Dr. Paul Gadue and his group from Children's Hospital of Philadelphia to create iPSC from patients with and without AAT deficiency. They then exposed these cells to certain growth factors in-vitro to cause them to turn into liver-like cells, in a process that mimics embryonic development. Then the researchers studied these "iPSC-hepatic cells" and found the diseased cells secrete AAT protein more slowly than normal cells. This finding demonstrated that the iPSC model recapitulates a critical aspect of the disease as it occurs in patients. AAT deficiency is caused by a mutation of a single DNA base. Correcting this single base back to the normal sequence fixed the abnormal secretion.

"We found that these corrected cells had a normal secretion kinetic when compared with their diseased, parental cells that are otherwise genetically identical except for this single DNA base," explained lead author Andrew A. Wilson, MD, assistant professor of medicine at Boston University School of Medicine and Director of the Alpha-1 Center at Bu and BMC.

They also found the diseased (AAT deficient) iPSC-liver cells were more sensitive to certain drugs (experience increased toxicity) than those from normal individuals. "This is important because it suggests that the livers of actual patients with this disease might be more sensitive in the same way," said Wilson, who is also a physician in pulmonary, critical care and allergy medicine at BMC.

According to Wilson, while some patients are often advised by their physicians to avoid these types of drugs, these recommendations are not based on solid scientific evidence. "This approach might now be used to generate that sort of evidence to guide clinical decisions," he added.

The researchers believe that studies using patient-derived stem cells will allow them to better understand how patients with AAT deficiency develop liver disease. "We hope that the insights we gain from these studies will result in the discovery of new potential treatments for affected patients in the near future," said Wilson.

###

Funding was provided by an ARRA stimulus grant (1RC2HL101535-01) awarded by the National Institutes of Health (NIH) to Boston University School of Medicine, Boston Medical Center and the Children's Hospital of Philadelphia. Additional funding was provided by K08 HL103771, FAMRI 062572_YCSA, an Alpha-1 Foundation Research Grant and a Boston University Department of Medicine Career Investment Award. Additional grants from NIH 1R01HL095993 and 1R01HL108678 and an ARC award from the Evans Center for Interdisciplinary Research at Boston University supported this work.

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Researchers produce iPSC model to better understand genetic lung/liver disease

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All living things--from dandelions to reindeer--evolve over time. Cancer cells are no exception, and are subject to the two overarching mechanisms described by Charles Darwin: chance mutation and natural selection.

In new research, Carlo Maley, PhD., and his colleagues describe compulsive evolution and dramatic genetic diversity in cells belonging to one of the most treatment-resistant and lethal forms of blood cancer: acute myeloid leukemia (AML). The authors suggest the research may point to new paradigms in both the diagnosis and treatment of aggressive cancers, like AML.

Maley is a researcher at Arizona State University's Biodesign Institute and an assistant professor in ASU's School of Life Sciences. His work focuses on applying principles of evolutionary biology and ecology to the study of cancer.

The group's findings appear in this week's issue of the journal Science Translational Medicine.

The cells, they are a changin'

A tumor is a laboratory for evolutionary processes in which nature experiments with an immense repertoire of variants. Mutations that improve a cell's odds of survival are "selected for," while non-adaptive cells are weeded out in the evolutionary lottery.

Genetic diversity therefore provides cancer cells with a library of possibilities, with some mutations conferring heightened resistance to attack by the body's immune system and others helping malignant cells foil treatments like chemotherapy. Generally speaking, the seriousness of a given cancer diagnosis may be linked with genetic diversity in cancerous cells. High diversity means the cancer has many pathways for outsmarting treatment efforts.

The diagnosis of cancer and study of disease progression is often accomplished by examining a tumor sample containing many billions or even trillions of cells. These are subjected to so-called next generation sequencing, a technique that sifts the vast genetic composite, ferreting out sequence variants (or alleles) caused by mutations in genes. The process then evaluates the frequency of these alleles, using the results to chart disease progression and assess the effectiveness of treatment.

According to Maley, such methods may obscure the true degree of genetic diversity, as well as the manner in which mutations arise. "One issue here is that if a mutation occurs in less than 20 percent of the cells, it's hard to detect by modern methods," he says. For example, because individual cells in the tumor probably carry unique mutations, they would be virtually impossible to observe with standard sequencing methods.

A further issue is that tracking mutations through bulk analysis of cells is typically based on certain assumptions as to how mutations arise and what their frequencies mean.

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Cancer's relentless evolution

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Using patient-derived stem cells known as induced pluripotent stem cells (iPSC) to study the genetic lung/liver disease called alpha-1 antitrypsin (AAT) deficiency, researchers have for the first time created a disease signature that may help explain how abnormal protein leads to liver disease.

The study, which appears in Stem Cell Reports, also found that liver cells derived from AAT deficient iPSCs are more sensitive to drugs that cause liver toxicity than liver cells derived from normal iPSCs. This finding may ultimately lead to new treatments for the condition.

IPSC's are derived from the donated skin or blood cells of adults and, with the reactivation of four genes, are reprogrammed back to an embryonic stem cell-like state. Like embryonic stem cells, iPSC can be differentiated toward any cell type in the body, but they do not require the use of embryos. Alpha-1 antitrypsin deficiency is a common genetic cause of both liver and lung disease affecting an estimated 3.4 million people worldwide.

Researchers from the Center for Regenerative Medicine (CReM) at Boston University and Boston Medical Center (BMC) worked for several years in collaboration with Dr. Paul Gadue and his group from Children's Hospital of Philadelphia to create iPSC from patients with and without AAT deficiency. They then exposed these cells to certain growth factors in-vitro to cause them to turn into liver-like cells, in a process that mimics embryonic development. Then the researchers studied these "iPSC-hepatic cells" and found the diseased cells secrete AAT protein more slowly than normal cells. This finding demonstrated that the iPSC model recapitulates a critical aspect of the disease as it occurs in patients. AAT deficiency is caused by a mutation of a single DNA base. Correcting this single base back to the normal sequence fixed the abnormal secretion.

"We found that these corrected cells had a normal secretion kinetic when compared with their diseased, parental cells that are otherwise genetically identical except for this single DNA base," explained lead author Andrew A. Wilson, MD, assistant professor of medicine at Boston University School of Medicine and Director of the Alpha-1 Center at Bu and BMC.

They also found the diseased (AAT deficient) iPSC-liver cells were more sensitive to certain drugs (experience increased toxicity) than those from normal individuals. "This is important because it suggests that the livers of actual patients with this disease might be more sensitive in the same way," said Wilson, who is also a physician in pulmonary, critical care and allergy medicine at BMC.

According to Wilson, while some patients are often advised by their physicians to avoid these types of drugs, these recommendations are not based on solid scientific evidence. "This approach might now be used to generate that sort of evidence to guide clinical decisions," he added.

The researchers believe that studies using patient-derived stem cells will allow them to better understand how patients with AAT deficiency develop liver disease. "We hope that the insights we gain from these studies will result in the discovery of new potential treatments for affected patients in the near future," said Wilson.

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The above story is based on materials provided by Boston University Medical Center. Note: Materials may be edited for content and length.

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iPSC model helps to better understand genetic lung/liver disease

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People differ in the size and composition of their chromosomes, which can affect the test results

IMAGE:This is conceptual art of maternal blood screening of fetal DNA. view more

Credit: Alice C Gray

Prenatal blood screening for extra or missing chromosomes in the fetus might give false-positive results if the mother's genome contains more than the usual number of certain DNA segments. This finding is reported April 1 in the New England Journal of Medicine. The article is part of a collection of papers examining screening tests now available to patients due to recent advances in genome sciences.

Researchers at the University of Washington, Fred Hutchinson Cancer Research Institute, and the Howard Hughes Medical Institute worked together to analyze false-positive results from the newer prenatal genetic screens.

Dr. Hilary Gammill, UW assistant professor of obstetrics and gynecology and research associate at Fred Hutchinson Cancer Research Institute, and Dr. Jay Shendure, UW professor of genome sciences, are the senior authors of the study. The lead authors are Matthew W. Snyder, UW genome sciences graduate student, and Dr. Lavone Simmons, former UW fellow in maternal-fetal medicine.

The newer prenatal genetic screens analyze cell-free DNA circulating in the mother's blood during pregnancy. The tests are safer and less invasive than sampling the fluid surrounding the fetus in the uterus.

The blood tests are now routinely offered to pregnant women whose offspring might face greater odds of certain genetic conditions, such as the chromosome trisomies that are more common in children born to older mothers. In a trisomy, there three, instead of the usual two, copies of a particular chromosome. Some trisomies, such as Edwards and Patau syndromes, cause life-threatening medical problems and have high stillbirth and newborn mortality rates.

Based on previous investigations, the new screening tests reportedly have a high accuracy in pregnancies that are at high risk for aneuploidy (extra or missing chromosomes), as well as in pregnancies that are at low risk.

The overall reduced incidence of uneven chromosome counts in low-risk pregnancies, however, limits the positive predictive value of these non-invasive prenatal screening tests. Researchers want to understand why false positive results occur so they could be minimized.

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Some false postive prenatal genetic screens due to mother's extra DNA segments

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Spring Fling Genetics Seminar, Dr. George Wiggans Speaking
Spring Fling Genetics Seminar, Dr. George Wiggans Speaking.

By: HolsteinWorld MOOTUBE

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Spring Fling Genetics Seminar, Dr. George Wiggans Speaking - Video

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The gene editing method called CRISPR is already used in the lab to insert and remove genome defects in animal embryos

Genome editing has generated controversy, with unconfirmed reports of its use in human embryos. Credit: NIAID/Flickr

A tweak to a technique that edits DNA with pinpoint precision has boosted its ability to correct defective genes in people. Called CRISPR, the method is already used in the lab to insert and remove genome defects in animal embryos. But the genetic instructions for the machinery on which CRISPR reliesa gene-editing enzyme called Cas9 and RNA molecules that guide it to its targetare simply too large to be efficiently ferried into most of the human bodys cells.

This week, researchers report a possible way around that obstacle: a Cas9 enzyme that is encoded by a gene about three-quarters the size of the one currently used. The finding, published on 1April inNature, could open the door to new treatments for a host of genetic maladies (F. A. Ranetal. Naturehttp://dx.doi.org/10.1038/nature14299; 2015).

There are thousands of diseases in humans associated with specific genetic changes, says David Liu, a chemical biologist at Harvard University in Cambridge, Massachusetts, who was not involved in the latest study. A fairly large fraction of those have the potential to be addressed using genome editing.

Genome editing has generated controversy, with unconfirmed reports of its use in human embryos. Some scientists have expressed concern that the technique might be used by fertility doctors to edit the genes of human embryos before its safety is established (see alsoE.Lanphieret al. Nature519,410411; 2015). That concern is exacerbated by the fact that changes made by the procedure in embryos would be passed to all subsequent generations without giving anyone affected the opportunity to consent (seeNature519,272; 2015). But in the non-reproductive cells of children and adults, where intergenerational issues are not a concern, researchers and companies are already racing to develop CRISPR as a clinical tool.

The ethics of that pursuit may be more straightforward, but its execution can be harder than using CRISPR in embryos. An embryo consists of a small number of cells that give rise to a human. To edit the genome at that stage is simply a matter of injecting the necessary CRISPR components into a few cells. An adult human, however, is a mix of trillions of cells assembled into many different tissues. Researchers fret over how to target the CRISPR machinery to the specific cells where defective genes are disrupting physiological processes.

You can have the most optimal gene-editing system in the world, but if you cant deliver it to the proper cell type, its irrelevant, says Nessan Bermingham, chief executive of Intellia Therapeutics in Cambridge, Massachusetts, which aims to bring genome editing to the clinic. Were spending a tremendous amount of time working on it.

Snug fit Gene-therapy researchers often harness a virus called AAV to shuttle foreign genes into mature human cells. However, most laboratories use a gene encoding the Cas9 protein that is too large to fit in the snug confines of the AAV genome alongside the extra sequences necessary for Cas9 function.

Feng Zhang of the Broad Institute of MIT and Harvard in Cambridge, Massachusetts, and his colleagues decided to raid bacterial genomes for a solution, because the CRISPR system is derived from a process that bacteria use to snip unwanted DNA sequences out of their genomes. Zhangs team analysed genes encoding more than 600 Cas9 enzymes from hundreds of bacteria in search of a smaller version that could be packaged in AAV and delivered to mature cells.

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New Discovery Moves Gene Editing Closer to Use in Humans

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CEN4GEN Institute for Genomics and Molecular Diagnostics
CEN4GEN Institute for Genomics and Molecular Diagnostics is a provider of quality, vital, comprehensive and important Genetic testing, Personalized medicine and Biomedical research services....

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No. 907 - Pharmakustik - Regenerative Medicine
No. 907 - Pharmakustik - Tissue Engineering Track 3 - Regenerative Medicine Released March 2015 https://no-ware.bandcamp.com/album/tissue-engineering http://no-wa.re.

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When do you see results from this therapy?
Dr. Trevor Bullock of Regen Orthopedics describes regenerative medicine in orthopedics. This non-surgical therapy has been shown to repair injured tissues with new, functioning tissues ...

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CardioCel has been initially well received with surgeons in Australia and overseas. Photo: Geoff Fisher

For 10 years researchers at Admedus worked day and night trying to work out how to improve soft tissue repair in the human body.

And with the vital help of CSIRO they have been to develop CardioCel, a life-saving heart patch for the repair and reconstruction of cardiovascular defects.

According to the Children's Heart Foundation, congenital heart disease occurs in one out of 100 births and in at least half of those cases surgery is required and a patch is needed. They state it is the leading cause of birth defect related deaths.

Research undertaken with CSIRO investigated new, potentially ground-breaking applications for CardioCel. The research focused on using stem cells. It found the heart patch has the potential to deliver stem cells and help tissue heal better than other existing products, when used for cardiac repair.

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Derived from animal tissue, the CardioCel patch is engineered over 14 days.

"The first unique feature of this product is that it doesn't calcify in young patients," Professor Leon Neethling, Admedus technical director and heart researcher says.

The flexible patch works like human tissue to cover holes in the heart thereby eliminating the need for repeat surgery.

"In the cardiac repair field it has long been recognised that strong, flexible, biocompatible and calcification-resistant tissue scaffolds would be ideal tissues for repair of heart defects," Admedus' chief operating officer Dr Julian Chick, says.

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Local innovation repairs holes in the heart

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Low doses of the anti-cancer drug imatinib can spur the bone marrow to produce more innate immune cells to fight against bacterial infections, Emory researchers have found.

The results were published March 30, 2015 in the journal PLOS Pathogens.

The findings suggest imatinib, known commercially as Gleevec , or related drugs could help doctors treat a wide variety of infections, including those that are resistant to antibiotics, or in patients who have weakened immune systems. The research was performed in mice and on human bone marrow cells in vitro, but provides information on how to dose imatinib for new clinical applications.

"We think that low doses of imatinib are mimicking 'emergency hematopoiesis,' a normal early response to infection," says senior author Daniel Kalman, PhD, professor of pathology and laboratory medicine at Emory University School of Medicine.

Imatinib, is an example of a "targeted therapy" against certain types of cancer. It,blocks tyrosine kinase enzymes, which are dysregulated in cancers such as chronic myelogenous leukemia and gastrointestinal stromal tumors.

Imatinib also inhibits normal forms of these enzymes that are found in healthy cells. Several pathogens - both bacteria and viruses - exploit these enzymes as they transit into, through, or out of human cells. Researchers have previously found that imatinib or related drugs can inhibit infection of cells by pathogens that are very different from each other, including tuberculosis bacteria and Ebola virus.

In the new PLOS Pathogens paper, Emory investigators show that imatinib can push the immune system to combat a variety of bacteria, even those that do not exploit Abl enzymes. The drug does so by stimulating the bone marrow to make more neutrophils and macrophages, immune cells that are important for resisting bacterial infection.

"This was surprising because there are reports that imatinib can be immunosuppressive in some patients," Kalman says. "Our data suggest that at sub-clinical doses, imatinib can stimulate bone marrow stem cells to produce several types of myeloid cells, such as neutrophils and macrophages, and trigger their exodus from the bone marrow. However, higher doses appear to inhibit this process."

The authors note that imatinib appears to stimulate several types of white blood cells, which may provide a limit on inflammation, rather than increasing neutrophils only, which can be harmful. The authors go on to suggest that imatinib or related drugs may be useful in treating a variety of infections in patients whose immune system is compromised, such as those receiving chemotherapy for cancer.

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Anticancer drug can spur immune system to fight infection

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Scott Logdon is a die-hard University of Kentucky basketball fan, but he can't deny he's got some Wisconsin blood in him -- literally.

When the father of four was being treated for high-risk leukemia at UK in 2013, 20-year-old University of Wisconsin student Chris Wirz anonymously donated bone marrow stem cells to him. The two men first spoke just after the Wildcats bested the Badgers during last year's NCAA Final Four, and basketball was a frequent topic of conversation as their friendship grew.

While each will be rooting for his own team during this Saturday's Final Four rematch, both say they have a soft spot for the other team.

"I've stayed true to UK," said Logdon, 44, of Salvisa, Ky. "But when I talked to Chris for the first time I told him, 'That's why I felt so bad when we beat you: I've got Badger blood in me!"'

Wirz, who lives three blocks from where the Badgers play, hopes Wisconsin wins this year, and has even predicted an upset in his basketball bracket. "Who doesn't want to root for the underdog?" he said.

But he plans to send a text of congratulations if Logdon's team wins -- since their connection is much deeper than basketball rivalry.

"We're literally working off the same immune system," said Wirz, now 22 and a University of Wisconsin senior. "This has been one of the most emotionally overwhelming experiences of my life, realizing how important he is to his family and his community and seeing the hole that would've been left by him."

A dire diagnosis

Logdon, chief deputy at Woodford County Detention Center in Versailles, Ky., and a youth minister in his church, recalled playing basketball with teenagers just a few nights before going to the doctor for what his wife, Angela, initially thought was strep.

But tests showed he had acute myeloid leukemia, a blood cancer estimated by the American Cancer Society to have stricken 18,860 Americans last year and killed about 10,460, mostly adults.

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Blood ties: Ky. basketball fan gets Wisconsin assist

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That's the promise of a high-end new facial treatment.

In a tiny room inside an Upper East Side dermatologist's office, I'm attempting to regain my youth. Or, at the very least, look better. I've come to try the HydraFacial, a multistep treatment that promises to erase wrinkles, reverse sun damage, lighten dark spots, and prevent acne. All of these transformations come from one key innovation using stem cells from an infant's foreskin to trick skin into behaving young again.

Why foreskin? Dr. Gail Naughton, a leader in regenerative science she developed technology to growhuman tissues and organs outside the body explains it this way: When we're born, our skin is in its best shape. Our cells naturally secrete proteins known as growth factors "that keep the cells healthy and stimulate them to divide," Naughton says. As we age, our cells divide at a slower rate, which contribute to the telltale signs of aging, like wrinkles and loss of firmness and luminosity. Growth factors captured from the donated foreskin of a baby (just one can generate over a million treatments) are at their peak ability in promoting rapid cell turnover. Applied topically, they spur adult skin cells to regenerate. This is said to have a smoothing effect on the skin.

I'm here to see if the process actually works specifically, on my nasolabial folds, the hereditary creases that stretch from my nose to my mouth. I'm told that three HydraFacial treatments will smooth the creases into near invisibility.

There are five parts to the HydraFacial. My skin is first wiped clean with a cleanser and then treated with a salicylic-and-glycolic-acid peel using a giant machine that looks like a cousin of R2D2. This is the HydraFacial machine, a fully equipped device with tiny suction tubes as arms and bottles of facial-treatment mixtures attached at the belly.

The salicylicand glycolic acids, like micro sandblasters, sweep away dead cells lingering on the surface of skin. The chemicals are a lightweight goop that feels cool on my face. Zahra, my esthetician, keeps asking me if I feel any tingling on my skin. I don't but she tells me that most people feel a slight burning sensation at this point. Must be my thick skin.

Next up is the extraction step. The tube that deposited the peel now works in reverse and becomes a micro vacuum cleaner. Blackheads and flaky skin are swept up in what feel (and looks) like the suction tube from a dentist's chair. It's an odd but not unpleasant feeling. I can actually see tiny deposits of my skin now swirling around in the extraction cup. Gross, but also kind of cool.

After my pores are cleared, a blend of skin-nourishing antioxidants and hydrating hyaluronic acid is smeared over my face. Here's where the foreskin extracts come in they're smeared on, too. The growth factors from the foreskin stem cells don't feel different than any other serum as the esthetician applies them to my face.

The final step of the facial is a quick, light therapy session, where a blue and red LED light targets oily skin, fine lines, and hyperpigmentation. In all, the entire facial lasts 30 minutes and induces not the faintest trace of redness or irritation.

Of course when it comes to facials, the proof is in the mirror. My skin glows in a way that I thought only Jennifer Lopez could glow. Fresh from the facial, I saunter into a photo shoot wearing no makeup because my confidence is at Beyonc levels. My nasolabial folds are still visible, although a bit less pronounced now. (Presumably, two more treatments would help even more.) And a part of me feels like a Disney evil queen, draining youth from a newborn for a few weeks of a restored complexion. Is this the future of facials? And if so, is it wrong that I want more?

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Can Cells From a Babys Foreskin Give You Youthful Skin?

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Orthopedic Stem Cell Therapy for Arthritic Joint Pain
Dr. Sergio Viroslav, board certified orthopedic surgeon and joint replacement specialist with The San Antonio Orthopaedic Group, appeared on Great Day SA on March 30th, 2015 to discuss the...

By: The San Antonio Orthopaedic Group

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Orthopedic Stem Cell Therapy for Arthritic Joint Pain - Video

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When billions of dollars are at stake in scientific research, researchers quickly learn that optimism sells.

A new study published inScience Translational Medicineoffersa window into how hype arises in the interaction between the media and scientific researchers, and how resistant the hype machine is to hard, cold reality. The report'sfocus is on overly optimisticreporting on potentialstem cell therapies. Its findings are discouraging.

The study by Timothy Caulfield and Kalina Kamenova of the University of Alberta law school (Caulfieldis also on the faculty at the school of public health) found that stem cell researchers often ply journalists with "unrealistic timelines" for the development of stem cell therapies, and journalists oftenswallow these claims uncritically.

The authorsmostly blame the scientists, who need to be more aware of "the importance of conveying realistic ... timelines to the popular press." We wouldn't give journalists this much of a pass; writers on scientific topics should understand that the development of drugs and therapies can take years and involve myriad dry holes and dead ends. They should be vigilant againstgaudypromises.

That's especially true instem cell research, whichis slathered with so much money that immoderate predictions of success are common. The best illustration of that comes from California's stem cell program -- CIRM, or the California Institute for Regenerative Medicine -- a $6-billion public investment that was born in hype.

The promoters of Proposition 71, the 2004 ballot initiative that created CIRM, filled the airwaves with adsimplyingthat the only thing standing between Michael J. Fox being cured of Parkinson's or Christopher Reeve walking again was Prop. 71's money. Theycommissioned a studyassertingthat California might reap a windfall in taxes,royalties and healthcare savings up to seven times the size ofits $6-billion investment. One wouldn't build a storage shed on foundations this soft, much less a $6-billion mansion.

As we've observed before, "big science" programs create incentivesto exaggerateresults to meet the public's inflated expectations. The phenomenon was recognized as long ago as the 1960s, when the distinguished physicist Alvin Weinberg warnedthat big science "thrives on publicity," resulting in "the injection of a journalistic flavor into Big Science which is fundamentally in conflict with the scientific method.... The spectacular rather than the perceptive becomes the scientific standard."

Interestingly, the event used by the Alberta researchers as the fulcrum of their study has a strong connection to CIRM. It's the abrupt 2011 decision by Geron Corp.to terminate its pioneering stem cell development program. This was a big blow to the stem cell research community and to CIRM, which had endowed Geron with a $25-million loan for its stem cell-basedspinal cord therapy development. Then-CIRM Chairman Robert Klein II had called the loan a "landmark step."

There had been evidence, however, that CIRM, eager to show progress toward bringing stem cell therapies to market, had downplayed legitimate questions about the state of Geron's science and the design of the clinical trial. AndGeron had been criticized in the past for over-promising results.

In their study, Caulfield and Kamenova examined more than 300 articles appearing in 14 general-interest newspapers in the United States, Canada and Britain from 2010 to2013. They scrutinizedthe articles' reporting oftimelines for the "realization of the clinical promise of stem cell research" and their perspective on the future of the field generally. The U.S. newspapers were the New York Times, the Wall Street Journal, the Washington Post and USA Today.

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New study: Stem cell field is infected with hype

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By Gary McCallister Tuesday, March 31, 2015

Scientists from Colorado Mesa University have made a major breakthrough in genetic research. Dr. Margot Bechtel and Dr. Denise McKenney have teamed up to insert a gene for Luciferase, a bioluminescent protein from fireflies (Photinus pyralis), into sunflowers (Helianthus annuus). While this is not the first gene transfer between multicellular organisms, the difference in this procedure is that the gene can be made to express bioluminescence from the actual flower when the plant is watered with a special solution.

This is a fantastic breakthrough. We have the potential to replace electric lamps with indoor houseplants, reducing electric demand, and providing sources of light using simple chemicals to activate the protein, Bechtel said.

With further development, we might be able to light streets at night using trees and thereby not only save electricity but reduce greenhouse gases, added McKenney.

Scientists made the first transgenic gene transfer between multicellular organisms back in 1986. David W. Ow, Keith V. Wood, Marlene DeLuca, Jeffrey R. de Wet, Donald R. Helinski and Stephen H. Howell were able to transfer the gene for luciferase into a tobacco plant. They were working with the extensive support of the Promega Corporation and used the cauliflower mosaic virus 35S RNA promoter to insert the gene into the tobacco plant.

However, their success was limited in that the bioluminescence was extremely weak. It required as much as eight to 10 hours on a photographic film to be seen. Further, it was only expressed in the early stages of plant growth called the callus. At the time, their stated goal was to create either a self-lighting tobacco for a new cigarette market or to create a plant that could make its own light for photosynthesis, thereby enhancing productivity. This initial attempt falls far short of the current breakthrough that was accomplished with limited resources but new insight and ingenuity.

Local scientists chose the sunflower for their research as a bit of whimsy. According to Bechtel, they thought if they were going to try to create a glowing plant they might as well do one that would be symbolic.

Besides, Helianthus lends itself to growth in our local climate, she said.

With their current procedure, bioluminescence is expressed in the adult stem, leaf and flower at an intensity that is readily visible to the naked eye. It has the added advantage of being able to switch on the luminescence using common chemicals. Previous work has required that the plant be watered with luciferin, the actual luminescent protein, to react with the enzyme luciferase.

We did several things differently from previous researchers. Instead of using a mosaic virus to carry the gene, we utilized Psuedomonas syringae, a common plant pathogen. But our big breakthrough came when we discovered we could turn the production of luciferase on with common, relatively inexpensive chemicals, a mixture of bleach, phosphorus, and hydrogen peroxide, McKenney said.

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Research breakthrough burns bright at CMU

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Unidentifiable shopping trolley - Source: Breakfast

Cancer-fighting pink pineapples, heart-healthy purple tomatoes and less fatty vegetable oils may someday be on grocery shelves alongside more traditional products.

These genetically engineered foods could receive government approval in the coming years, following the OK given recently in the US to apples that don't brown and potatoes that don't bruise.

The companies and scientists that have created these foods are hoping that customers will be attracted to the health benefits and convenience and overlook any concerns about genetic engineering.

"I think once people see more of the benefits they will become more accepting of the technology," says Michael Firko, who oversees the US Agriculture Department's regulation of genetically modified organisms, or GMOs.

Critics aren't so sure. They say there should be more thorough regulation of modified foods, which are grown from seeds engineered in labs, and have called for mandatory labeling of those foods. The Agriculture Department only has the authority to oversee plant health of GMOs, and seeking Food and Drug Administration's safety approval is generally voluntary.

"Many of these things can be done through traditional breeding," says Doug Gurian-Sherman of the advocacy group Center for Food Safety. "There needs to be skepticism."

What could be coming next? Del Monte has engineered a pink pineapple that includes lycopene, an antioxidant compound that gives tomatoes their red color and may have a role in preventing cancer. USDA has approved importation of the pineapple, which would be grown only outside of the United States; it is pending FDA approval.

A small British company is planning to apply for US permission to produce and sell purple tomatoes that have high levels of anthocyanins, compounds found in blueberries that some studies show lower the risk of cardiovascular disease and cancer. FDA would have to approve any health claims used to sell the products.

Seed giants Monsanto and Dow AgroSciences are separately developing modified soybean, canola and sunflower oils with fewer saturated fats and more Omega-3 fatty acids. The Florida citrus company Southern Gardens is using a spinach gene to develop genetically engineered orange trees that could potentially resist citrus greening disease, which is devastating the Florida orange crop. Okanagan Specialty Fruits Inc., the company that created the non-browning apples, is also looking at genetically engineering peaches, cherries and apples to resist disease and improve quality.

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Cancer-fighting pink pineapples? Genetic engineering looms

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IMAGE:This infographic shows how prostate cancer spreads. view more

Credit: Cancer Research UK

Scientists have revealed the root of prostate cancers in individual men, discovering that despite huge genetic variety between tumours they also share common gene faults - insight that could offer new treatment hopes, according to research published in Nature today (Wednesday).

In a landmark paper, Cancer Research UK funded scientists alongside an international team of researchers read all of the DNA in tumour samples from 10 men with prostate cancer. This allowed them to map a 'family tree' of the changes happening at a genetic level as the disease spreads, forms new tumours, and becomes resistant to treatment.

They also revealed more detail about how prostate cancer spreads, showing that the group of cells that first spread from the prostate carry on travelling around the body, forming more secondary tumours.

The research is part of the International Cancer Genome Consortium (ICGC) - a global project using the latest gene-sequencing technology to reveal the genetic changes driving the disease.

The ICGC Prostate Cancer UK group - funded by Cancer Research UK, the Dallaglio Foundation, the Wellcome Trust, the Academy of Finland and others - is examining how the disease evolves in patients to help develop approaches for personalised medicine, tailored to the genetic makeup of each person's cancer.

The team has already revealed a huge amount of genetic diversity between cancer cells taken from different sites within each man's prostate.

And this new study shows that, despite the diversity, prostate cancer cells that break free from the tumour and spread share common genetic faults unique to the individual patient.

Study author Ros Eeles, professor of oncogenetics at The Institute of Cancer Research, London, and honorary consultant at The Royal Marsden NHS Foundation Trust, said: "We gained a much broader view of prostate cancer by studying both the original cancer and the cells that had spread to other parts of the body in these men. And we found that all of the cells that had broken free shared a common ancestor cell in the prostate.

More here:
Scientists drill down to genetic root of prostate tumor development

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Let #39;s Play The Sims 3 - Perfect Genetics Challenge - Episode 64
Make sure to leave baby names in the comments!. #VampireClan #VampireClan4Life.

By: vampiregirl101101101

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Let's Play The Sims 3 - Perfect Genetics Challenge - Episode 64 - Video

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Transmission Genetics Mendelism
This Lecture talks about Transmission Genetics Mendelism.

By: Cec Ugc

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Transmission Genetics Mendelism - Video

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THG TV - Episode 5
Treehouse Genetics Television - Episode 5 --- In this episode Proto demonstrates the Cannabis Rosin Extraction Technique, gives a solid review on Roots Organics: Oregonism XL, reveals our M-42b...

By: Treehouse Genetics TV

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THG TV - Episode 5 - Video

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Gene therapy slows vision loss in mouse models
Harvard Medical School genetics professor Connie Cepko and postdoctoral researcher Wenjun Xiong talk about developing a gene therapy to stave off blindness. Read the full story at http://hms.harva.

By: Harvard Medical School

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Gene therapy slows vision loss in mouse models - Video

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