Archive for March, 2015

Mayo Clinic Sports Medicine Center, Mayo Clinic Square Profile
Jonathan Finnoff, D.O., Medical Director for Mayo Clinic Square, Sports Medicine Center, Minneapolis, Minnesota discusses the services they provide in their program. Sports performance training,...

By: Mayo Clinic

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Mayo Clinic Sports Medicine Center, Mayo Clinic Square Profile - Video

Fox Morning Blend - The Prolotherapist March 17, 2015
In this segment, Ross Hauser, MD (The Prolotherapist) discusses how computer usage and smart phones/tablet devices can cause neck and thumb pain. If you would like more information about how...

By: Caring Medical Regenerative Medicine Clinics

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Fox Morning Blend - The Prolotherapist March 17, 2015 - Video

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Newswise A bone marrow transplant can mean the difference between life and death for people with blood cancers and related disorders. But many patients in India cant afford the high treatment costs, and for them a transplant is not an option. This is changing thanks to a newly launched bone marrow transplant unit at M.S. Ramaiah Medical College in Bangalore.

The five-bed unit, which opened last month, was established by local physicians and hospital administrators working with Dr. Damiano Rondelli, director of the blood and marrow transplant program at the University of Illinois Hospital & Health Sciences System.

Bone marrow transplants in India are done mainly at nonacademic institutions and can be prohibitively expensive. Clinical standards, including infection control, can vary at these unaccredited transplant programs.

Ramaiah aims to become the first internationally accredited bone marrow transplant program in India. It will provide transplantation under high standards of care and at a significantly lower cost. The service will be subsidized by revenues from the for-profit hospital associated with the medical college.

Its a very nice model -- sustainable, and every patient gets the same treatment, regardless of what they can pay, said Rondelli.

Rondelli first visited Ramaiah in October at the invitation of his colleague Bellur S. Prabhakar, professor and head of microbiology and immunology and associate dean for technological innovation and training at the University of Illinois at Chicago College of Medicine. Prabhakar had been meeting with leaders at Ramaiah to discuss working together through UICs Center for Global Health.

One of the things they wanted to do was to establish a world-class bone marrow transplantation unit, said Prabhakar.

The need for bone marrow transplantation is high in India, a country of more than a billion people. Southeast Asians have a higher genetic risk for thalassemia, a disorder of hemoglobin, the molecule in red blood cells that carries oxygen and carbon dioxide to and from the tissues. Bone marrow transplantation is the only cure.

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Chicago Physician Helps Launch Bone Marrow Unit in Bangalore

Written by Lidia Dinkova on March 18, 2015

University of Miami stem cell research on generating healthy heart tissue in heart attack survivors is on track to be tested across the US.

The National Heart, Lung and Blood Institute, part of federal medical research arm the National Institutes of Health, is to fund the $8 million cost if the trial wins necessary approvals.

The trial, the first of this research in humans, is a step toward restoring full heart function in heart attack survivors.

The research developed at the UM Miller School of Medicines Interdisciplinary Stem Cell Institute is on combining two types of stem cells to generate healthy heart tissue in heart attack survivors. Scientists have in the past studied using one type of stem cell at a time, a method thats worked OK, said Dr. Joshua Hare, founding director of the UM stem cell institute.

But UM research shows that combining two types of stem cells expedites healing and regeneration of healthy heart muscle.

We could remove twice the scar tissue than with either cell alone, Dr. Hare said. We had some scientific information that they actually interacted and worked together, so we tested that. It worked.

Researchers combined mesenchymal stem cells, usually generated from human bone marrow, and cardiac stem cells, isolated from a mammals heart.

Stem cells are cells that havent matured to specialize to work in a particular part of the body, such as the heart. Because these cells are in a way nascent, they have the potential to become specialized for a particular body function.

Doctors have been using stem cells to regenerate lost tissue from bones to heart muscle. The mesenchymal and cardiac stem cells each work well in generating healthy heart tissue in heart attack survivors, Dr. Hare said. Combining them expedites the process, according to the UM research.

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UM stem cell research on heart may go national

Scientists at the University of Cambridge have successfully created 'mini-lungs' using stem cells derived from skin cells of patients with cystic fibrosis, and have shown that these can be used to test potential new drugs for this debilitating lung disease.

The research is one of a number of studies that have used stem cells -- the body's master cells -- to grow 'organoids', 3D clusters of cells that mimic the behaviour and function of specific organs within the body. Other recent examples have been 'mini-brains' to study Alzheimer's disease and 'mini-livers' to model liver disease. Scientists use the technique to model how diseases occur and to screen for potential drugs; they are an alternative to the use of animals in research.

Cystic fibrosis is a monogenic condition -- in other words, it is caused by a single genetic mutation in patients, though in some cases the mutation responsible may differ between patients. One of the main features of cystic fibrosis is the lungs become overwhelmed with thickened mucus causing difficulty breathing and increasing the incidence of respiratory infection. Although patients have a shorter than average lifespan, advances in treatment mean the outlook has improved significantly in recent years.

Researchers at the Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute used skin cells from patients with the most common form of cystic fibrosis caused by a mutation in the CFTR gene referred to as the delta-F508 mutation. Approximately three in four cystic fibrosis patients in the UK have this particular mutation. They then reprogrammed the skin cells to an induced pluripotent state, the state at which the cells can develop into any type of cell within the body.

Using these cells -- known as induced pluripotent stem cells, or iPS cells -- the researchers were able to recreate embryonic lung development in the lab by activating a process known as gastrulation, in which the cells form distinct layers including the endoderm and then the foregut, from which the lung 'grows', and then pushed these cells further to develop into distal airway tissue. The distal airway is the part of the lung responsible for gas exchange and is often implicated in disease, such as cystic fibrosis, some forms of lung cancer and emphysema.

The results of the study are published in the journal Stem Cells and Development.

"In a sense, what we've created are 'mini-lungs'," explains Dr Nick Hannan, who led the study. "While they only represent the distal part of lung tissue, they are grown from human cells and so can be more reliable than using traditional animal models, such as mice. We can use them to learn more about key aspects of serious diseases -- in our case, cystic fibrosis."

The genetic mutation delta-F508 causes the CFTR protein found in distal airway tissue to misfold and malfunction, meaning it is not appropriately expressed on the surface of the cell, where its purpose is to facilitate the movement of chloride in and out of the cells. This in turn reduces the movement of water to the inside of the lung; as a consequence, the mucus becomes particular thick and prone to bacterial infection, which over time leads to scarring -- the 'fibrosis' in the disease's name.

Using a fluorescent dye that is sensitive to the presence of chloride, the researchers were able to see whether the 'mini-lungs' were functioning correctly. If they were, they would allow passage of the chloride and hence changes in fluorescence; malfunctioning cells from cystic fibrosis patients would not allow such passage and the fluorescence would not change. This technique allowed the researchers to show that the 'mini-lungs' could be used in principle to test potential new drugs: when a small molecule currently the subject of clinical trials was added to the cystic fibrosis 'mini lungs', the fluorescence changed -- a sign that the cells were now functioning when compared to the same cells not treated with the small molecule.

"We're confident this process could be scaled up to enable us to screen tens of thousands of compounds and develop mini-lungs with other diseases such as lung cancer and idiopathic pulmonary fibrosis," adds Dr Hannan. "This is far more practical, should provide more reliable data and is also more ethical than using large numbers of mice for such research."

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Scientists grow 'mini-lungs' to aid study of cystic fibrosis

Scientists at the University of Cambridge have successfully created 'mini-lungs' using stem cells derived from skin cells of patients with cystic fibrosis, and have shown that these can be used to test potential new drugs for this debilitating lung disease.

The research is one of a number of studies that have used stem cells - the body's master cells - to grow 'organoids', 3D clusters of cells that mimic the behaviour and function of specific organs within the body. Other recent examples have been 'mini-brains' to study Alzheimer's disease and 'mini-livers' to model liver disease. Scientists use the technique to model how diseases occur and to screen for potential drugs; they are an alternative to the use of animals in research.

Cystic fibrosis is a monogenic condition - in other words, it is caused by a single genetic mutation in patients, though in some cases the mutation responsible may differ between patients. One of the main features of cystic fibrosis is the lungs become overwhelmed with thickened mucus causing difficulty breathing and increasing the incidence of respiratory infection. Although patients have a shorter than average lifespan, advances in treatment mean the outlook has improved significantly in recent years.

Researchers at the Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute used skin cells from patients with the most common form of cystic fibrosis caused by a mutation in the CFTR gene referred to as the delta-F508 mutation. Approximately three in four cystic fibrosis patients in the UK have this particular mutation. They then reprogrammed the skin cells to an induced pluripotent state, the state at which the cells can develop into any type of cell within the body.

Using these cells - known as induced pluripotent stem cells, or iPS cells - the researchers were able to recreate embryonic lung development in the lab by activating a process known as gastrulation, in which the cells form distinct layers including the endoderm and then the foregut, from which the lung 'grows', and then pushed these cells further to develop into distal airway tissue. The distal airway is the part of the lung responsible for gas exchange and is often implicated in disease, such as cystic fibrosis, some forms of lung cancer and emphysema.

The results of the study are published in the journal Stem Cells and Development.

"In a sense, what we've created are 'mini-lungs'," explains Dr Nick Hannan, who led the study. "While they only represent the distal part of lung tissue, they are grown from human cells and so can be more reliable than using traditional animal models, such as mice. We can use them to learn more about key aspects of serious diseases - in our case, cystic fibrosis."

The genetic mutation delta-F508 causes the CFTR protein found in distal airway tissue to misfold and malfunction, meaning it is not appropriately expressed on the surface of the cell, where its purpose is to facilitate the movement of chloride in and out of the cells. This in turn reduces the movement of water to the inside of the lung; as a consequence, the mucus becomes particular thick and prone to bacterial infection, which over time leads to scarring - the 'fibrosis' in the disease's name.

Using a fluorescent dye that is sensitive to the presence of chloride, the researchers were able to see whether the 'mini-lungs' were functioning correctly. If they were, they would allow passage of the chloride and hence changes in fluorescence; malfunctioning cells from cystic fibrosis patients would not allow such passage and the fluorescence would not change. This technique allowed the researchers to show that the 'mini-lungs' could be used in principle to test potential new drugs: when a small molecule currently the subject of clinical trials was added to the cystic fibrosis 'mini lungs', the fluorescence changed - a sign that the cells were now functioning when compared to the same cells not treated with the small molecule.

"We're confident this process could be scaled up to enable us to screen tens of thousands of compounds and develop mini-lungs with other diseases such as lung cancer and idiopathic pulmonary fibrosis," adds Dr Hannan. "This is far more practical, should provide more reliable data and is also more ethical than using large numbers of mice for such research."

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Scientists grow 'mini-lungs' to aid the study of cystic fibrosis

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Newswise Stem cells can have a strong sense of identity. Taken out of their home in the hair follicle, for example, and grown in culture, these cells remain true to themselves. After waiting in limbo, these cultured cells become capable of regenerating follicles and other skin structures once transplanted back into skin. Its not clear just how these stem cells and others elsewhere in the body retain their ability to produce new tissue and heal wounds, even under extraordinary conditions.

New research at Rockefeller University has identified a protein, Sox9, that takes the lead in controlling stem cell plasticity. In a paper published Wednesday (March 18) in Nature, the team describes Sox9 as a pioneer factor that breaks ground for the activation of genes associated with stem cell identity in the hair follicle.

We found that in the hair follicle, Sox9 lays the foundation for stem cell plasticity. First, Sox9 makes the genes needed by stem cells accessible, so they can become active. Then, Sox9 recruits other proteins that work together to give these stemness genes a boost, amplifying their expression, says study author Elaine Fuchs, Rebecca C. Lancefield Professor, Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development. Without Sox9, this process never happens, and hair follicle stem cells cannot survive.

Sox9 is a type of protein called a transcription factor, which can act like a volume dial for genes. When a transcription factor binds to a segment of DNA known as an enhancer, it cranks up the activity of the associated gene. Recently, scientists identified a less common, but more powerful version: the super-enhancer. Super-enhancers are much longer pieces of DNA, and host large numbers of cell type-specific transcription factors that bind cooperatively. Super-enhancers also contain histones, DNA-packaging proteins, that harbor specific chemical groups epigenetic marks that make genes they are associated with accessible so they can be expressed.

Using an epigenetic mark associated specifically with the histones of enhancers, first author Rene Adam, a graduate student in the lab, and colleagues, identified 377 of these high-powered gene-amplifying regions in hair follicle stem cells. The majority of these super-enhancers were bound by at least five transcription factors, often including Sox9. Then, they compared the stem cell super-enhancers to those of short-lived stem cell progeny, which have begun to choose a fate, and so lost the plasticity of stem cells. These two types of cells shared only 32 percent of their super-enhancers, suggesting these regions played an important role in skin cell identity. By switching off super-enhancers associated with stem cell genes, these genes were silenced while new super-enhancers were being activated to turn on hair genes.

To better understand these dynamics, the researchers took a piece of a super-enhancer, called an epicenter, where all the stem cell transcription factors bind, and they linked it to a gene that glowed green whenever the transcription factors were present. In living mice, all the hair follicle stem cells glowed green, but surprisingly, the green gene turned off when the stem cells were taken from the follicle and placed in culture. When they put the cells back into living skin, the green glow returned.

Another clue came from experiments performed by Hanseul Yang, another student in the lab. By examining the new super-enhancers that were gained when the stem cells were cultured, they learned that these new super-enhancers bound transcription factors that were known to be activated during wound-repair. When they used one of these epicenters to drive the green gene, the green glow appeared in culture, but not in skin. When they wounded the skin, then the green glow switched on.

We were learning that some super-enhancers are specifically activated in the stem cells within their native niche, while other super-enhancers specifically switch on during injury, explained Adam. By shifting epicenters, you can shift from one cohort of transcription factors to another to adapt to different environments. But we still needed to determine what was controlling these shifts.

Originally posted here:
Scientists Pinpoint Molecule That Controls Stem Cell Plasticity by Boosting Gene Expression

(Source: Thinkstock; art by Tanya Leigh Washington)

We're no strangerswhen it comes to wild beauty products. Snail venom, check. Probiotic bacteria, of course. Charcoal, yes, please. But when we started noticing stem cells popping up as ingredients in beauty products, we raised an eye brow.

First off, these aren't the stem cells that have caused a lot of controversy in recent years. These are (typically) stem cells extracts from plants andfruits and are believed by some to encourage cell regeneration, restoration and repair. However, some products are using human stem cell derived proteins as active ingredients. The basic idea is this:stem cell extracts uppotential growth for collagen and elastinyou know, those tissues that keep us looking youthful.

Althoughthe jury is still out on the effectiveness of stem cell-based products, one thing's for surethispossible fountain of youth comes at a steep price tag. Due to the extraction and cultivation process of stem cell extracts, products tend to be on the higher end side.

If stem cell technology sounds like something you're ready to invest in, take a peek at a view of the products on the market that caught our eyes.

Rodial Stemcell Super-Food Cleanser, $40, atus.spacenk.com

Stem cell technology from thePhytoCellTec Alp Rose mixed with Coconut Oil, Rose Hip Oil, Rose Wax and Cocoa Butter hydrate and cleanses.

Juice Beauty Stem Cellular Lifting Neck Cream, $55, atjuicebeauty.com

This blend of fruit stem cells are infused into a Vitamin C, resveratrol rich grapeseed formula to provide antioxidant protection and firm up skin.

StemologyCell Revive Smoothing Serum, $99, at stemologyskincare.com

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Why Stem Cell Beauty Products are Causing a Buzz in Anti-Aging

Experiments placed Sox9 at the crux of a shift in gene expression associated with hair follicle stem cell identity

IMAGE:Researchers made stem cells fluoresce green (at the base of hair follicles above) by labeling their super-enhancers, regions of the genome bound by gene-amplifying proteins. It appears one such protein,... view more

Credit: Laboratory of Mammalian Cell Biology and Development at The Rockefeller University/Nature

Stem cells can have a strong sense of identity. Taken out of their home in the hair follicle, for example, and grown in culture, these cells remain true to themselves. After waiting in limbo, these cultured cells become capable of regenerating follicles and other skin structures once transplanted back into skin. It's not clear just how these stem cells -- and others elsewhere in the body -- retain their ability to produce new tissue and heal wounds, even under extraordinary conditions.

New research at Rockefeller University has identified a protein, Sox9, that takes the lead in controlling stem cell plasticity. In a paper published Wednesday (March 18) in Nature, the team describes Sox9 as a "pioneer factor" that breaks ground for the activation of genes associated with stem cell identity in the hair follicle.

"We found that in the hair follicle, Sox9 lays the foundation for stem cell plasticity. First, Sox9 makes the genes needed by stem cells accessible, so they can become active. Then, Sox9 recruits other proteins that work together to give these "stemness" genes a boost, amplifying their expression," says study author Elaine Fuchs, Rebecca C. Lancefield Professor, Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development. "Without Sox9, this process never happens, and hair follicle stem cells cannot survive."

Sox9 is a type of protein called a transcription factor, which can act like a volume dial for genes. When a transcription factor binds to a segment of DNA known as an enhancer, it cranks up the activity of the associated gene. Recently, scientists identified a less common, but more powerful version: the super-enhancer. Super-enhancers are much longer pieces of DNA, and host large numbers of cell type-specific transcription factors that bind cooperatively. Super-enhancers also contain histones, DNA-packaging proteins, that harbor specific chemical groups -- epigenetic marks -- that make genes they are associated with accessible so they can be expressed.

Using an epigenetic mark associated specifically with the histones of enhancers, first author Rene Adam, a graduate student in the lab, and colleagues, identified 377 of these high-powered gene-amplifying regions in hair follicle stem cells. The majority of these super-enhancers were bound by at least five transcription factors, often including Sox9. Then, they compared the stem cell super-enhancers to those of short-lived stem cell progeny, which have begun to choose a fate, and so lost the plasticity of stem cells. These two types of cells shared only 32 percent of their super-enhancers, suggesting these regions played an important role in skin cell identity. By switching off super-enhancers associated with stem cell genes, these genes were silenced while new super-enhancers were being activated to turn on hair genes.

To better understand these dynamics, the researchers took a piece of a super-enhancer, called an epicenter, where all the stem cell transcription factors bind, and they linked it to a gene that glowed green whenever the transcription factors were present. In living mice, all the hair follicle stem cells glowed green, but surprisingly, the green gene turned off when the stem cells were taken from the follicle and placed in culture. When they put the cells back into living skin, the green glow returned.

Another clue came from experiments performed by Hanseul Yang, another student in the lab. By examining the new super-enhancers that were gained when the stem cells were cultured, they learned that these new super-enhancers bound transcription factors that were known to be activated during wound-repair. When they used one of these epicenters to drive the green gene, the green glow appeared in culture, but not in skin. When they wounded the skin, then the green glow switched on.

The rest is here:
Scientists pinpoint molecule that switches on stem cell genes

Mar 18, 2015 by Marla Vacek Broadfoot A jelly fish-green fluorescent gene marks stem cells and other proliferating primitive cells of an intestine-like structure. The central lumen hollow space is stained red. Credit: Magness Lab

The human gut is a remarkable thing. Every week the intestines regenerate a new lining, sloughing off the equivalent surface area of a studio apartment and refurbishing it with new cells. For decades, researchers have known that the party responsible for this extreme makeover were intestinal stem cells, but it wasn't until this year that Scott Magness, PhD, associate professor of medicine, cell biology and physiology, and biomedical engineering, figured out a way to isolate and grow thousands of these elusive cells in the laboratory at one time. This high throughput technological advance now promises to give scientists the ability to study stem cell biology and explore the origins of inflammatory bowel disease, intestinal cancers, and other gastrointestinal disorders.

But it didn't come easy.

One step forward

When Magness and his team first began working with intestinal stem cells some years ago, they quickly found themselves behind the eight ball. Their first technique involved using a specific molecule or marker on the surface of stem cells to make sure they could distinguish stem cells from other intestinal cells.

Then Magness's team would fish out only the stem cells from intestinal tissues and grow the cells in Petri dishes. But there was a problem. Even though all of the isolated cells had the same stem cell marker, only one out of every 100 could "self-renew" and differentiate into specialized cells like a typical stem cell should. (Stem cells spawn cells that have specialized functions necessary for any organ to work properly.)

"The question was: why didn't the 99 others behave like stem cells?" Magness said. "We thought it was probably because they're not all the same, just like everybody named Judy doesn't look the same. There are all kinds of differences, and we've been presuming that these cells are all the same based on this one name, this one molecular marker. That's been a problem. But the only way to solve it so we could study these cells was to look at intestinal stem cells at the single cell level, which had never been done before."

Magness is among a growing contingent of researchers who recognize that many of the biological processes underlying health and disease are driven by a tiny fraction of the 37 trillion cells that make up the human body. Individual cells can replenish aging tissues, develop drug resistance, and become vehicles for viral infections. And yet the effects of these singular actors are often missed in biological studies that focus on pooled populations of thousands of seemingly "identical" cells.

Distinguishing between the true intestinal stem cells and their cellular look-a-likes would require isolating tens of thousands of stem cells and tracking the behavior of each individual cell over time. But Magness had no idea how to accomplish that feat. Enter Nancy Allbritton, PhD, chair of the UNC/NCSU Joint Department of Biomedical Engineering. The two professors met one day to discuss Magness joining the biomedical engineering department as an adjunct faculty member. And they did discuss it. And Magness did join. But the meeting quickly turned into collaboration.

One of Allbritton's areas of expertise is microfabrication the ability to squeeze large devices into very small footprints. During their meeting, Allbritton showed Magness her latest creation, a device smaller than a credit card dotted with 15,000 tiny wells for culturing cells.

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A single-cell breakthrough

Arthritis of low back, knees, and shoulder 2 years after stem cell therapy by Harry Adelson ND
Jim describes his results two years after bone marrow stem cell therapy by Harry Adelson ND for treatment of his arthritic low back, knees, and shoulder http://www.docereclinics.com.

By: Harry Adelson, N.D.

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Arthritis of low back, knees, and shoulder 2 years after stem cell therapy by Harry Adelson ND - Video

Biologists at the University of California, San Diego have developed a new method for generating mutations in both copies of a gene in a single generation that could rapidly accelerate genetic research on diverse species and provide scientists with a powerful new tool to control insect borne diseases such as malaria as well as animal and plant pests.

Their achievement was published today in an advance online paper in the journal Science. It was accomplished by two biologists at UC San Diego working on the fruit fly Drosophila melanogaster who employed a new genomic technology to change how mutations could spread through a population--a concept long established in plants by the father of modern genetics, Gregor Mendel.

"Mendel conducted classic genetic experiments with peas that revealed the fundamental of inheritance in many organisms including humans," explains Ethan Bier, a professor of biology at UC San Diego whose graduate student, Valentino Gantz, developed the method. "According to these simple rules of inheritance, the fertilized egg receives one copy of most genes from our mothers and one from our fathers so that the resulting individual has two copies of each gene."

One advantage of having two copies of a gene is that if one copy carries a non-functional mutation, then the other "good" copy typically can provide sufficient activity to sustain normal function. Thus, most mutations resulting in loss of gene function are known as recessive, meaning that an organism must inherit two mutant copies of the gene from its parents before an overt defect is observed, as is the case in humans with muscular dystrophy, cystic fibrosis or Tay Sachs disease.

"Because individuals carrying a single mutant copy of a gene often mate with an individual with two normal copies of gene, defects can be hidden for a generation and then show up in the grandchildren," Bier adds. "This is how genetics has been understood for over a century in diverse organisms including humans, most animals we are familiar with, and many plants."

But in the past two years, Bier and other molecular biologists have witnessed a veritable revolution in genome manipulation. "It is now routine to generate virtually any change in the genome of an organism of choice at will," he notes. "The technology is based on a bacterial anti-viral defense mechanism known as the Cas9/CRISPR system."

By employing this development in their experiments with laboratory fruit flies, Gantz and Bier demonstrated that by arranging the standard components of this anti-viral defense system in a novel configuration, a mutation generated on one copy of a chromosome in fruit flies spreads automatically to the other chromosome. The end result, Bier says, is that both copies of a gene could be inactivated "in a single shot."

The two biologists call their new genetic method the "mutagenic chain reaction," or MCR.

"MCR is remarkably active in all cells of the body with one result being that such mutations are transmitted to offspring via the germline with 95 percent efficiency," says Gantz, the first author of the paper. "Thus, nearly all gametes of an MCR individual carry the mutation in contrast to a typical mutant carrier in which only half of the reproductive cells are mutant."

Bier says "there are several profound consequences of MCR. First, the ability to mutate both copies of a gene in a single generation should greatly accelerate genetic research in diverse species. For example, to generate mutations in two genes at once in an organism is typically time consuming, because it requires two generations, and involved, because it requires genetic testing to identify rare progeny carrying both mutations. Now, one should simply be able to cross individuals harboring two different MCR mutants to each other and all their direct progeny should be mutant for both genes."

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New genetic method promises to advance gene research and control insect pests

IMAGE:Dr. Ivan Barrero Farfan, a Texas A&M University student working with Dr. Seth Murray during the study, pollinates corn to make hybrids for testing. view more

Credit: (Texas A&M AgriLife Research photo by Dr. Seth Murray)

COLLEGE STATION - A ground-breaking Texas A&M AgriLife Research-led study on corn has identified useful gene variations for yield increases, drought tolerance and aflatoxin resistance that could make a real difference to Texas producers in the years to come, according to researchers.

The study, titled "Genome Wide Association Study for Drought, Aflatoxin Resistance, and Important Agronomic Traits of Maize Hybrids in the Sub-Tropics" was recently published in PLOS ONE, an international, peer-reviewed, open-access, online publication.

The study included the growing years of 2011, a drought year, and 2012, and was conducted on dryland and irrigated corn in College Station and in Mississippi, all with similar results, said Dr. Seth Murray, an AgriLife Research corn breeder in the soil and crop science department of Texas A&M University at College Station.

Murray said at this time all corn seed available to growers in Texas comes from commercial breeding conducted in the Midwest. As a result, there's been no significant increase in corn yields in Texas for many years, as reflected in their previous publications.

Murray designed this recently published study to see if there was a genetic reason, possibly the use of Midwest-temperate rather than sub-tropical genetics, limiting production.

He was joined in his research by Dr. Mike Kolomiets, an AgriLife Research plant pathologist, and Dr. Tom Isakeit, a Texas A&M AgriLife Extension Service plant pathologist, both in College Station, along with students Dr. Ivan Barrero Farfan, Gerald De La Fuente and Pei-Cheng Huang.

Other researchers who also grew the test plots and contributed to the analysis were Dr. Marilyn Warburton, Dr. Paul Williams and Dr. Gary Windham, all U.S. Department of Agriculture-Agricultural Research Service researchers at Mississippi State University.

The study was funded by a USDA National Institute of Food and Agriculture, Agriculture and Food Research Initiative for Plant Breeding and Education grant. Additional support was given by the Texas Corn Producers and Texas A&M AgriLife.

Originally posted here:
AgriLife Research study opens doors for increases in Texas corn yields, aflatoxin resistance

A pioneering class of drugs that target cancers with mutations in the BRCA breast cancer genes could also work against tumours with another type of genetic fault, a new study suggests.

Scientists at The Institute of Cancer Research, London, found that errors in a gene called CLBC leave cancer cells vulnerable to PARP inhibitor drugs. Around 2 per cent of all tumours have defects in CLBC.

The study, which was carried out in collaboration with colleagues in Denmark and the Czech Republic, was funded in the UK by the European Union, and was published today (Thursday) in the journal Oncotarget.

Olaparib, a PARP inhibitor, became the first cancer drug targeted at an inherited genetic fault to reach the market when it was approved in December for use in ovarian cancer patients with BRCA1 or BRCA2 mutations. Its development was underpinned by research at The Institute of Cancer Research (ICR).

Using an approach known as RNA interference screening - which 'silences' genes to analyse their function - researchers systematically tested which of the 25,000 genes in the human genome affected the response of cancer cells to olaparib.

The ICR team found that cancer cells with a defect in the CBLC gene were as sensitive to the drug as those with a faulty BRCA2 gene.

By analysing the molecular processes that the CBLC gene controls, researchers found that it normally allows cells to repair damaged DNA by fixing broken DNA strands back together.

This finding indicates that a flaw in DNA repair mechanisms explains the sensitivity of CBLC-defective cancer cells to PARP inhibitors - which knock out the action of another DNA repair mechanism.

DNA repair is often disrupted in cancer cells, which sacrifice genetic stability as they gain mutations that allow them to divide uncontrollably. These cancer cells may be particularly vulnerable to drugs to block DNA repair proteins, since they may lack any alternative functioning repair systems to fall back on.

Study co-leader Dr Chris Lord, Team Leader in Gene Function at The Institute of Cancer Research, London, said:

Continued here:
World-first cancer drugs could work in larger group of patients

IMAGE:Cyberpsychology, Behavior, and Social Networking is an authoritative peer-reviewed journal published monthly online with Open Access options and in print that explores the psychological and social issues surrounding... view more

Credit: Mary Ann Liebert, Inc., publishers

New Rochelle, NY, March 18, 2015--Job recruiters may review hundreds of online resumes for a position, often screening them quickly and discarding those that are not appropriate. An applicant's email address can greatly impact first impressions and affect one's chances of getting hired according to a new study published in Cyberpsychology, Behavior, and Social Networking, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers . The article is available free on the Cyberpsychology, Behavior, and Social Networking website until April 18, 2015.

Marlies van Toorenburg, Janneke Oostrom, and Thomas Pollet, VU University, Amsterdam, designed a study to determine whether the use of an informal rather than a more formal email address by a job applicant when sending an online resume affects how hirable the person would seem to a professional recruiter. An informal email address includes slang, cute, or made-up names instead of the applicant's real name.

In the article "What a Difference Your Email Makes: Effects of Informal Email Addresses in Online Rsum Screening," the authors describe how the formal or informal nature of an applicant's email address impacts a recruiter's hirability perceptions. The researchers also compare the importance of the email address to spelling errors and the typeface used in the email in passing judgment on an online resume.

"We all have unconscious biases, and first impressions, as we know, are often difficult to change," says Editor-in-Chief Brenda K. Wiederhold, PhD, MBA, BCB, BCN, Interactive Media Institute, San Diego, California and Virtual Reality Medical Institute, Brussels, Belgium. "This study may assist recruiters in becoming more conscious of their biases, as well as aiding job applicants in understanding the importance of their electronic identities."

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About the Journal

Cyberpsychology, Behavior, and Social Networking is an authoritative peer-reviewed journal published monthly online with Open Access options and in print that explores the psychological and social issues surrounding the Internet and interactive technologies, plus cybertherapy and rehabilitation. Complete tables of content and a sample issue may be viewed on the Cyberpsychology, Behavior, and Social Networking website.

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Could your email address keep job recruiters from reading your online resume?

While it holds promise for eradicating genetic diseases, the technology also has big implications for the human genome: A person whose DNA is edited would pass the altered genes on to his or her children.

There's also a fear the technology could be used in unethical ways, such as "engineering" a baby to look a certain way, or to be athletic or intelligent.

"One of the concerns is that some people may want to use the technology to make trivial or cosmetic changes, rather than using it to prevent devastating diseases," said Carroll, distinguished professor of biochemistry at the University of Utah School of Medicine.

The paper Carroll co-signed is expected to amplify discussion in the scientific community, which last week heard from another group of researchers who recommend that the new technology never be used on human embryos.

Changing the genome could have unpredictable effects on future humans, and that's unacceptable, the group says.

Instead, that group, led by Edward Lanphier, chief executive of the biotechnology company Sangamo Biosciences, suggests research focus on somatic, or non-reproductive cells.

CRISPR-Cas9, was developed in the lab of Jennifer Doudna, the University of California-Berkeley scientist who organized the Napa meeting.

Hundreds of papers in the past two years have proven the usefulness of the new tool in research involving mammals.

"The applications to humans are potentially just around the corner," Carroll said.

CRISPR-Cas9 allows more subtle, precise changes in DNA than was possible with technologies used in genetically modified organisms (GMOs), he added. Such genetic engineering typically involves introducing new genes into an organism.

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Engineering humans: Utah professor joins group urging caution

BERKELEY

A group of 18 scientists and ethicists today warned that a revolutionary new tool to cut and splice DNA should be used cautiously when attempting to fix human genetic disease, and strongly discouraged any attempts at making changes to the human genome that could be passed on to offspring.

Among the authors of this warning is Jennifer Doudna, the co-inventor of the technology, called CRISPR-Cas9, which is driving a new interest in gene therapy, or genome engineering. She and colleagues co-authored a perspective piece that appears in the March 20 issue of Science, based on discussions at a meeting that took place in Napa on Jan. 24. The same issue ofSciencefeatures a collection of recent research papers, commentary and news articles on CRISPR and its implications.

Given the speed with which the genome engineering field is evolving, our group concluded that there is an urgent need for open discussion of the merits and risks of human genome modification by a broad cohort of scientists, clinicians, social scientists, the general public and relevant public entities and interest groups, the authors wrote.

Doudna, director of UC Berkeleys Innovative Genomics Initiative, was joined by five current and two former UC Berkeley scientists, plus David Baltimore, a Nobel laureate and president emeritus of the California Institute of Technology, Stanford Nobelist Paul Berg and eminent scientists from UC San Francisco, Stanford, Harvard and the universities of Wisconsin and Utah. Several of these scientists are currently involved in gene therapy to cure inherited diseases.

Such warnings have been issued numerous times since the dawn of genetic engineering in 1975, but until now the technology to actually fix genetic defects was hard to use.

However, this limitation has been upended recently by the rapid development and widespread adoption of a simple, inexpensive and remarkably effective genome engineering method known as CRISPR-Cas9, the scientists wrote. The simplicity of the CRISPR-Cas9 system enables any researcher with knowledge of molecular biology to modify genomes, making feasible many experiments that were previously difficult or impossible to conduct.

Correcting genetic defects

Scientists today are changing DNA sequences to correct genetic defects in animals as well as cultured tissues generated from stem cells, strategies that could eventually be used to treat human disease. The technology can also be used to engineer animals with genetic diseases mimicking human disease, which could lead to new insights into previously enigmatic disorders.

The CRISPR-Cas9 tool is still being refined to ensure that genetic changes are precisely targeted, Doudna said. Nevertheless, the authors met to initiate an informed discussion of the uses of genome engineering technology, and to identify proactively those areas where current action is essential to prepare for future developments. We recommend taking immediate steps toward ensuring that the application of genome engineering technology is performed safely and ethically.

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Scientists urge caution in using new CRISPR technology to treat human genetic disease

IMAGE:Violence and Gender is the only peer-reviewed journal focusing on the understanding, prediction, and prevention of acts of violence. Through research papers, roundtable discussions, case studies, and other... view more

Credit: Mary Ann Liebert, Inc., publishers

New Rochelle, NY, March 18, 2015-Who intentionally seeks to kill a policeman and why? In 2014 the rate of policemen purposely killed in the line of duty in the U.S. was nearly 1.5 times greater than in 2013. These incidents and what may have motivated the killers is the focus of an in-depth article in the peer-reviewed journal Violence and Gender, from Mary Ann Liebert, Inc., publishers. The article is available free on the Violence and Gender website until April 18, 2015.

In the article "Men Who Kill Policemen," Michael Stone, MD, Columbia College of Physicians and Surgeons (New York, NY) and Mid-Hudson Forensic Psychiatric Hospital (Goshen, NY), reviews details of the intentional killings of police in the line of duty in 2013-2014. All the killers were male, and most used a gun. Dr. Stone describes whether the perpetrators were killed or committed suicide during the incidents, or were actively involved in a crime at the time of the killing. He examines a variety of possible motivations for intentional killing of a policeman, including belonging to a "cop-hating" group, mental illness, or intoxication. He also discusses societal factors that may lead to higher or lower rates of policemen killing in different social or minority groups.

"This unique study by Dr. Michael Stone, an Associate Editor of Violence and Gender, could not be more timely and relevant," says Editor-in-Chief Mary Ellen O'Toole, PhD, Director, Forensic Science Program, George Mason University; Forensic Behavioral Consultant; and Senior FBI Profiler/Criminal Investigative Analyst (ret.).

"Dr. Stone looked at all the police officers intentionally killed in the line of duty in the United States between 2013 and 2014," Dr. O'Toole continues. "He found that all of the 66 cop-killers were males, and their choice of weapon was a firearm. Dr. Stone identifies factors that led up to and contributed to these murders, and based on his experience and expertise as a world-renowned psychiatrist he offers the opinion that only a minority of these men likely suffered from a mental illness at the time of these murders. In the study of violence it is quite rare that research is so quickly available on contemporary issues, and this study exemplifies Dr. Stone's and the Journal's commitment to bring headline topics to our readers in scholarly and insightful ways."

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About the Journal

Violence and Gender is the only peer-reviewed journal focusing on the understanding, prediction, and prevention of acts of violence. Through research papers, roundtable discussions, case studies, and other original content, the Journal critically examines biological, genetic, behavioral, psychological, racial, ethnic, and cultural factors as they relate to the gender of perpetrators of violence. Led by Editor-in-Chief Mary Ellen O'Toole, PhD, Forensic Behavioral Consultant and Senior FBI Profiler/Criminal Investigative Analyst (ret.), Violence and Gender explores the difficult issues that are vital to threat assessment and prevention of the epidemic of violence. Violence and Gender is published quarterly online with Open Access options and in print, and is the official journal of The Avielle Foundation. Tables of content and a sample issue may be viewed on the Violence and Gender website.

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What motivates men who kill police?

If wine tends to give you a hangover, science may have a solution, and it starts with a "genome knife." The phrase refers to an enzyme called RNA-guided Cas9 nuclease that's able to knock down a longstanding hurdle to genetic engineering in fermented foods, a researcher at the University of Illinois explains in a press release.

It's a little complicated, but the strains of yeast that ferment wine (along with beer and bread) are "polyploid" strains. Those strains "contain multiple copies of genes in the genome," says Yong-Su Jin, whose study was published in Applied and Environmental Microbiology.

The difficulty comes into play when you try to alter a gene in one copy of the genome. Essentially, you can't: "An unaltered copy would correct the one that had been changed." The enzyme fixes that problem.

It allows the genetic engineering of polyploid strains, specifically Saccharomyces cerevisiaewhich you're more likely to know as baker's yeast, Jove notes. Researchers are calling the engineered result a "jailbreaking" yeast.

Engineered yeast could make wine healthier by boosting the amount of a nutrient called resveratrol "by 10 times or more," Jin notes. As for post-booze headaches, the "genome knife" could act on what's known as malolactic fermentation, which can result in hangover-inducing toxic substances.

That's good news, though Medical Daily reports that the variety of factors leading to hangovers likely means such a product wouldn't get rid of them completely.

(It's not just the genetics involved in winemaking that affect your hangover risk: Your own genes do, too, according to research last year.)

This article originally appeared on Newser: Scientists Find a Way to Cut Wine Hangovers

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Researchers find a way to cut wine hangovers

Mutants Genetics Gladiators Ultimas Luchas Del Evento Nu Roma
Gracias por todo Lindo Dia Y Espero este contentos con mi trabajo.

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Lot 700 - McCabe Genetics Bred Heifers
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The Sim 3 | Perfect Genetics Challenge #2
The hunt for a man begins! Poorly! There are mullets...and mooches...and some more getting to know Azkadellia! Founder Sim: Azkadellia Ideal Challenge Rules: --------- Perfect Genetics Challenge...

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The following is an interview with Victor A. McKusick, University Professor of Medical Genetics, Johns Hopkins University School of Medicine, Baltimore. The interview was conducted by his student,...

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LA CONFIDENTIAL DNA Genetics weed grow report Trichome World
A quick review what you can see in our full cannabis grow report (+300 pics) Review for medical users weed plant lovers http://trichome-world.com/category/strains-test/dna-genetics/la-confident...

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Minecraft ARTIFACTS SMP #39;LEARNING HOW TO FLY (Advanced Genetics) #39; Ep 10
Enjoy this video? Help me out and share it with your friends on twitter, facebook and any other social media site! Friends - https://www.youtube.com/user/joyceANDcarlo https://www.youtube.com/use...

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