Archive for the ‘Gene Therapy Research’ Category

How genetics and environment work together to shape our destiny: Milena Georgieva at TEDxAUBG
A young scientist in Bulgaria with lots of prestigious awards for best scientific excellence practices I put my all energy in revealing the secrets of the wa...

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How genetics and environment work together to shape our destiny: Milena Georgieva at TEDxAUBG - Video

Add productivity and profitability with Balancer genetics
Scott Hamilton, a cow-calf producer in South Dakota, uses Balancer bulls to add productivity and profitability in his calves as well as his cow herd. For more information, visit http://www.gelbvieh.org.

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Macular Degeneration And Acupuncture: Gene Therapy and Stem Cell for AMD Safe?
http://www.MacularDegenerationSupport.com or (908) 264-5484 Download the FULL webinar for free by clicking the link. Dr. Andy Rosenfarb conducted an hour lon...

By: Dr. Andy Rosenfarb

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Macular Degeneration And Acupuncture: Gene Therapy and Stem Cell for AMD Safe? - Video

OMICS Group Gene Therapy 2012 Opening Ceremony

By: Srinu Babu Gedela

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OMICS Group Gene Therapy 2012 Opening Ceremony - Video

Gene Therapy for the Eyes is Coming of Age
Dr. Joe talks more about gene therapy. http://online.liebertpub.com/doi/full/10.1089/hum.2013.050.

By: Joe Prendergast

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Gene Therapy for the Eyes is Coming of Age - Video

Mac Stem Cell Therapy 2012
Before and After Mac #39;s Stem Cell Therapy. Surgery done by Dr. Mark McCloskey, DVM, Columbus, OH.

By: Mary Hammond

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Mac Stem Cell Therapy 2012 - Video

Cardiac Reconstruction: The Latest in Cell Therapy - kchrs2011
Cardiac Reconstruction: The Latest in Cell Therapy - kchrs2011.

By: Dhanunjaya Lakkireddy

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Cardiac Reconstruction: The Latest in Cell Therapy - kchrs2011 - Video

Aug. 2, 2013 Specific mutations (N676K) in the FLT3 receptor can contribute to the development of acute myeloid leukemia. The FLT3 receptor regulates cell growth, while activating gene mutations promote the uncontrolled proliferation of white blood cells. These findings were reported in the specialist journal Blood by a group of scientists from the Helmholtz Zentrum Mnchen and the Hospital of the Ludwig Maximilians University (LMU) in Munich as part of a clinical research collaboration with the German Cancer Consortium (DKTK). The results provide the basis for the development of new leukemia treatments using specific inhibitors, which block growth signals.

Gene mutations often trigger cancer. These changes in the DNA mostly affect the regulators of cellular metabolism or cell growth, which cause cells to degenerate and proliferate rapidly. Many such gene mutations that cause leukemia have been identified.

In about one third of patients with acute myeloid leukemia (AML) the malignant cells have a mutation in the growth-regulating FLT3 receptor. As the team of scientists headed by Dr. Philipp Greif and Professor Karsten Spiekermann have now discovered, blood cancer cells from a substantial number of patients in a subgroup of AML (so-called core-binding factor leukemias) also carry mutations in this receptor. Mutations affecting amino-acid position N676 have not been previously detected and may allow a new classification of this form of leukemia, which is characterized by extremely high white blood cell counts. "The FLT3 receptor mutations we have found in these leukemia patients provide a new basis for treating the disease," says Dr. Philipp Greif. "We already have FLT3 receptor inhibitors at hand, which we can now use to treat the affected patients."

The study was conducted by the clinical cooperative group "Pathogenesis of acute myeloid leukemia," a collaboration between the Helmholtz Zentrum Mnchen (HMGU) and the Department of Internal Medicine 3 at the Hospital of the Ludwig Maximilians University (LMU). The project leader and last author, Dr. Philipp Greif, heads a team of young scientists funded by the German Cancer Consortium (DKTK) within the clinical cooperative group. Professor Wolfgang Hiddemann, who heads the group, stresses the importance of this interdisciplinary collaboration: "Our results show in an exemplary way how innovative research methods, such as high-throughput DNA sequencing, allow discoveries, even in structures that have already been thoroughly examined. These insights into the molecular basis of the disease open up new treatment options for patients."

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The above story is based on materials provided by Helmholtz Zentrum Muenchen - German Research Centre for Environmental Health.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

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Discovery of novel gene mutations in leukemia patients opens up personalized therapy options

Aug. 2, 2013 A study of gene expression led by scientists at the EMBL-European Bioinformatics Institute (EMBL-EBI) and the University of Cambridge has revealed the first steps of evolution in gene regulation in mice. Published in the journal Cell, the research has implications for the study of differences in gene regulation between people.

"We found an impressive amount of variation between these apparently very similar mice in terms of transcription-factor binding, which is an important indicator of gene-regulation activity," says Paul Flicek of EMBL-EBI. "Often you'll see a specific combination of these transcription factors acting in concert -- and it was fascinating for us to see just how important these combinations are. They're much more likely to be conserved over the course of evolution than whatever DNA sequence they might be binding to."

The team studied gene expression in five very closely related mouse species in order to pinpoint changes at the very earliest stages of evolution. To do this, they compared the way that three transcription factors (TFs) bind to genes to control if they're turned on or off in liver cells in the different mouse species.

"By looking at mice that are very closely related to each other, we were able to capture a snapshot of what regulatory evolution is happening," explains Duncan Odom of the University of Cambridge. "That's important because it's much harder to see how something has evolved when you don't have a clear picture of the starting point."

Say you wanted to know how an orange tree evolved, but you could only compare it to an elm or oak. You'd have greater insight into how an orange tree evolved if you could compare it to much more closely related plants like grapefruit and lemons, which could give insight into how each came from an ancestral citrus plant. In this study, instead of comparing leaf and fruit shapes, the team looked at gene regulation in mice that had only recently diverged from one another. They demonstrated that TFs work in clusters that are conserved in order to ensure genetic and evolutionary stability.

The researchers contrasted their findings with gene-regulation data from another model organism, Drosophila, to see where the similarities lay. They found that there were a lot more differences between closely related mouse strains than there are between distantly related fruit-fly strains.

"Mammals have lots of DNA kicking around that doesn't code for proteins, while fruit flies have relatively little. So a mouse's regulatory wiring will just have a lot more wiggle room than a fruit fly's," says Paul. "That gives us a clearer picture of what we can expect to learn about mammalian genetic regulation from fruit flies."

The study could help scientists understand how gene regulation differs from one person to the next, explaining why genes that cause disease in some people don't have that effect in others.

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Study of gene expression has revealed first steps of evolution in gene regulation in mice

Charli (8, left) and sister Meg (4), with Daisy at home in Kaitangata this week. Photo by Helena de Reus.

Charli (8) and Meg (4) Owen, of Kaitangata, have undiagnosed cerebellar ataxia, which affects their co-ordination and balance and makes them tire easily.

The sisters' geneticist, Cure Kids chairman Prof Stephen Robertson, has been working on some revolutionary research in conjunction with Prof Russell Snell, of the Centre for Brain Research in Auckland.

The research aimed to deliver methods for diagnosing such disorders in the future.

''The nub of this family's issue is a neurological disorder, which affects the girls' gait and balance. Their ataxia is not associated with any intellectual disability; it's all about balance,'' he said this week.

"A lot of people have ataxia, but in this instance we've exhausted all the tests in conventional medicine to diagnose what form they have and we're now looking in the research arena for an answer for them,'' he said.

''It's clearly genetic, but the precise cause is proving hard to pinpoint.

''What has caused it in the family and what is the prognosis? That's the big question.

"We might find something that's brand new knowledge here, but in the end I hope it provides new and useful information for the family,'' Prof Robertson said.

The human genetic constitution has about 21,000 genes accounting for about 1% of a human's DNA.

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Gene tech research may aid diagnosis

Brainstorm #39;s Applied Human Genetic Engineering Speech
A persuasive speech advocating that we should create Neosapiens. I had requested a three day conference at a stadium with teleprompters. Denied.

By: brainsturm6

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Brainstorm's Applied Human Genetic Engineering Speech - Video

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Key points in the genetically modified food debate

GeneticS-TenZ - Black Ops II Game Clip
Game Clip.

By: Genetics Gaming

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Genetics, Epigenetics, Biology and the Emotions. Chris Astill-Smith - Chapter 8 of 9

By: Clive Bingham

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Genetics, Epigenetics, Biology and the Emotions. Chris Astill-Smith - Chapter 8 of 9 - Video

Aug. 1, 2013 If two women have the same genetic mutation that puts them at higher-than-average risk for a disease such as breast cancer, why does only one develop the disease?

In the current issue of PLoS Genetics, Michigan State University genetic scientists have begun to understand how the rest of the genome interacts with such mutations to cause the differences we see among individuals.

"It's been known for a while that genetic mutations can modify each other's effects," said Ian Dworkin, MSU associate professor of zoology and co-author of the paper. "And we also know that the subtle differences in an individual's genome -- what scientists call wild type genetic background -- also affects how mutations are manifested."

Dworkin and Sudarshan Chari, zoology doctoral student and the paper's lead author, wanted to know how common it was for wild type genetic background to alter the way genetic mutations interact with each other. This is the first time that it's been examined in a systematic manner, Dworkin added.

Using the fruit fly genome, the researchers found that wild type genetic background affected the outcomes of interactions between genetic mutations about 75 percent of the time. This could have huge implications in how scientists construct genetic networks -- maps of how genes interact with each other.

"It may be that some crucial portions of genetic networks are missing," he said. "It also seems that network descriptions are more fluid than we thought."

Fruit flies have been called humans with wings, genetically speaking, due to their similarities. By focusing on wings and a genetic mutation that alters them, the researchers demonstrated the influence of wild type genetic background was actually quite common.

The broader implication for humans is that even for diseases with a simple genetic basis, variation in the genome may matter for both understanding and treatment, Dworkin said.

This new insight explains how, in an example like breast cancer, every woman's genetic background is likely influencing how the mutation is expressed, causing different disease outcomes. The research also may help explain why some people benefit from a specific treatment for a disease, while others get no benefits or become resistant to a drug after a short time.

It's likely that most diseases with a suspected genetic component, such as cancer, asthma or Parkinson's, involve reactions between more than one set of genes. For Dworkin and Chari, the next step is to tease apart the intricacies of what's happening.

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Genetics: More than merely a mutated gene

Public release date: 1-Aug-2013 [ | E-mail | Share ]

Contact: Tamzin Byrne tamzin@scienceinpublic.com.au 043-297-4400 Centenary Institute

Researchers from the Gene and Stem Cell Therapy Program at Sydney's Centenary Institute have confirmed that, far from being "junk", the 97 per cent of human DNA that does not encode instructions for making proteins can play a significant role in controlling cell development.

And in doing so, the researchers have unravelled a previously unknown mechanism for regulating the activity of genes, increasing our understanding of the way cells develop and opening the way to new possibilities for therapy.

Using the latest gene sequencing techniques and sophisticated computer analysis, a research group led by Professor John Rasko AO and including Centenary's Head of Bioinformatics, Dr William Ritchie, has shown how particular white blood cells use non-coding DNA to regulate the activity of a group of genes that determines their shape and function. The work is published today in the scientific journal Cell.

"This discovery, involving what was previously referred to as "junk", opens up a new level of gene expression control that could also play a role in the development of many other tissue types," Rasko says. "Our observations were quite surprising and they open entirely new avenues for potential treatments in diverse diseases including cancers and leukaemias."

The researchers reached their conclusions through studying intronsnon-coding sequences which are located inside genes.

As part of the normal process of generating proteins from DNA, the code for constructing a particular protein is printed off as a strip of genetic material known as messenger RNA (mRNA). It is this strip of mRNA which carries the instructions for making the protein from the gene in the nucleus to the protein factories or ribosomes in the body of the cell.

But these mRNA strips need to be processed before they can be used as protein blueprints. Typically, any non-coding introns must be cut out to produce the final sequence for a functional protein. Many of the introns also include a short sequenceknown as the stop codonwhich, if left in, stops protein construction altogether. Retention of the intron can also stimulate a cellular mechanism which breaks up the mRNA containing it.

Dr Ritchie was able to develop a computer program to sort out mRNA strips retaining introns from those which did not. Using this technique the lead molecular biologist of the team, Dr Justin Wong, found that mRNA strips from many dozens of genes involved in white blood cell function were prone to intron retention and consequent break down. This was related to the levels of the enzymes needed to chop out the intron. Unless the intron is excised, functional protein products are never produced from these genes. Dr Jeff Holst in the team went a step further to show how this mechanism works in living bone marrow.

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How 'junk DNA' can control cell development

Aug. 1, 2013 Researchers at UCLA's Jonsson Comprehensive Cancer Center (JCCC) have successfully combined cellular therapy and gene therapy in a mouse model system to develop a viable treatment strategy for breast cancer that has metastasized, or spread, to the patient's brain. The laboratory study was led by Carol Kruse, professor of neurosurgery and member of JCCC and the UCLA Brain Research Institute. The study was published in the journal Clinical Cancer Research on August 1, 2013.

Breast cancer is the most common form of cancer in women, and metastasis is a major cause of health deterioration and death from the disease. Management of metastasis is difficult for several reasons. The circulatory network known as the blood-brain barrier prevents many anti-cancer drugs from reaching the areas of the brain to which cancer has spread. Also, the tendency of metastasis to spring up in multiple places in the brain simultaneously makes current treatments such as radiation challenging.

Cellular therapy is a type of immunotherapy (treatment that involves the immune system) that uses T cells, the foot soldiers of the immune system, which have been sensitized in the laboratory to kill breast cancer cells. Those T cells are injected into the part of the brain to which the cancer has spread. The research shows the T cells move through tissue and can recognize and then directly kill the tumor cells. With the gene therapy, cancer cells are killed by a drug called 5-flurocytosine (5-FC) because they have been gene-modified. To get the gene into the cancer cells, the researchers first insert the gene into a virus that can infect (penetrate and spread among) the tumor cells. After the virus has infected the cells, nontoxic 5-FC is given to the patient. Tumor cells infected by the virus convert the nontoxic drug to a toxic form that kills the cancer cells. Dr. Noriyuki Kasahara, a professor in the department of medicine, developed the gene therapy method in his laboratory.

While the two methods alone each show efficacy in mouse models, the greatest reduction in metastatic brain tumor size happened when the cellular and gene therapies were combined.

"There is a significant lack of Federally funded research addressing translational studies on brain metastases of systemic cancers," Dr. Kruse said, "even though metastatic brain tumors occur ten times more frequently than primary brain tumors in humans. These patients have a dismal prognosis because the brain represents a 'sanctuary site' where appropriate access by many chemotherapeutics is ineffective. Our research addresses this unmet need."

Both experimental therapies are being tested individually in ongoing clinical trials for primary malignant brain tumors, which presents a unique opportunity for rapid translation of this technology from the laboratory to the clinic for breast and other types of cancer that metastasize to the brain.

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The above story is based on materials provided by University of California, Los Angeles (UCLA), Health Sciences, via Newswise.

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New treatment strategy for breast cancer spread to brain

Stem Cell Therapy - Amazing Breakthrough in Skin wrinkles treatment
Stem Cell Therapy is the newest bio-active topical cream that actually stimulates your own existing skin stem cells to grow smooth, supple, firm new skin. Fo...

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Newswise Researchers at the University of California, San Diego School of Medicine have identified the gene mutation responsible for a particularly severe form of pontocerebellar hypoplasia, a currently incurable neurodegenerative disease affecting children. Based on results in cultured cells, they are hopeful that a nutritional supplement may one day be able to prevent or reverse the condition.

The study, from a team of international collaborators led by Joseph G. Gleeson, MD Howard Hughes Medical Institute investigator and professor in the UCSD Departments of Neurosciences and Pediatrics and at Rady Childrens Hospital-San Diego, a research affiliate of UC San Diego will be published in the August 1 issue of the journal Cell.

Pontocerebellar hypoplasia is a group of rare, related genetic neurological disorders characterized by abnormal development of the brain, resulting in disabilities in movement and cognitive function. Most patients do not survive to adulthood.

Gleeson and colleagues identified a specific gene mutation that causes pontocerebellar hypoplasia and linked it to an inability of brain cells to generate a form of energy required to synthesize proteins. Without this ability, neurons die, but the researchers also found that bypassing this block with a nutritional supplement restored neuronal survival.

The goal is to one day use this supplement to prevent or reverse the course of neurodegeneration in humans, and thus cure this disease, said Gleeson.

Nucleotides are the main energy source of cells. They exist in two forms: ATP and GTP. While ATP fuels most energy requirements, GTP is the source for protein synthesis. Mutations in the gene AMPD2 lead to the accumulation of ATP, and the subsequent depletion of GTP. The result, said Gleeson, is an imbalance in the cells energy source, which prevents protein synthesis and causes neurodegeneration.

These patients have what is described in medical textbooks as an untreatable disease, yet show mutations in a neuronal pathway that should be amenable to medication, said study co-author Naiara Akizu, PhD, a member of Gleesons lab. We chose to bypass this block using AICAR, a substance known to improve exercise endurance.

The researchers tested their AICAR-based treatment in genetic models of the disease and in human cells. The next step, said Gleeson, will be to test AICAR in a mouse model of pontocerebellar hypoplasia that his lab has created, followed by human trials.

We dont know if AICAR will work in mice or humans yet, but our work in cells definitely points in that direction, said co-author Vincent Cantagrel, PhD. This rare disorder might be one of the first treatable neurodegenerative diseases in humans.

Other co-authors include Jana Schroth, Na Cai, Keith Vaux, Ali G. Fenstermaker, Jennifer L. Silhavy, Emily Spencer, Rasim Ozgur Rosti, Eric Scott, Douglas McCloskey, Robert K. Naviaux, Jeremy Van Vleet, UCSD Departments of Neurosiences, Bioengineering, Medicine, Pediatrics, Pathology and Glycotechnology Core Resource; Edward W. Holmes, Sanford Consortium for Regenerative Medicine; Judith S. Scheliga Sanford-Burnham Medical Research Institute; Keiko Toyama, Hiroko Morisaki and Takayuki Morisaki, Osaka University; Fatma Mujgan Sonmez and Figen Celep, Turgut Ozal University and Karadeniz Technical University, Turkey; Azza Oraby and Maha S. Zaki, Cairo University Childrens Hospital, and National Research Center, Egypt; Raidah Al-Baradie, Eissa Faqeih and Mohammed Saleh, King Fahd Specialist Hospital and Childrens Hospital, Kingdom of Saudi Arabia; Elizabeth Nickerson and Stacey Gabriel, The Broad Institute of MIT and Harvard University.

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Potential Nutritional Therapy for Childhood Neurodegenerative Disease

Childhood neurodegenerative diseases, while rare, can be devastating. Characterized by a progressive loss of neural function and the eventual death of the brains neurons, these disorders tend to lack treatment options and are often fatal.

Now, researchers from the University of California, San Diego School of Medicine are providing hope for some families with neurodegenerative conditions, after discovering a gene mutation responsible for a very severe childhood disorder called pontocerebellar hypoplasia.

Based on their experiments, the research team believes a nutritional supplement could be used to treat and reverse the condition, which is currently thought to be incurable.

Its very poorly defined in the textbooks; medical doctors have probably heard about it, but wouldnt recognize it in the clinic, lead study author Dr. Joseph Gleeson, Howard Hughes Medical Institute investigator and professor in the department of neurosciences and pediatrics at UCSD, told FoxNews.com. By doing this genetic evaluation, I think itll help raise the idea in doctors minds that this is a unique condition and needs to be recognized and treated.

Pontocerebellar hypoplasia is a group of rare, genetic neurological disorders characterized by the shrinkage of the cerebellum and brain stem over time. Children with the condition initially have problems with balance, breathing and swallowing, and the disease eventually elevates to include disabilities in movement and cognitive function. The average lifespan for patients is five to 10 years.

Gleeson and his colleagues have been conducting genome sequencing the mapping of genetic information of children with brain conditions, such as cerebral palsy and mental retardation. It was through this work that the stumbled upon children with pontocerebellar hypoplasia, pinpointing the mutated gene they all had in common: AMPD2.

This gene is involved in metabolism in some of the most basic building blocks of cells. Gleeson said of AMPD2. Its how cells meet their energy requirements.

Nucleotides provide the main sources of energy for cells, existing in two forms: ATP and GTP. ATP is responsible for most of the energy requirements, while GTP is the source of protein synthesis. However, the two forms must be balanced in order for cells to function properly. According to Gleeson, the mutation of AMPD2 results in the accumulation of ATP and the depletion of GTP, an imbalance that ultimately leads to neurodegeneration.

Upon this discovery, the researchers theorized they could bypass this GTP block by giving patients a nutritional supplement. They found that a non-toxic performance enhancing drug known as AICAR, a purified form of GTP, could restore balance to the cells. The supplement was tested in genetic models of the disease, as well as human cells in vitro, and the treatment successfully rescued the cells from degeneration and death.

Gleeson cautions families against buying this drug and testing it on their children independently, as researchers are still unaware of any potential side effects the supplements could have in humans with pontocerebellar hypoplasia. However, he is hopeful that AICAR will soon be developed into a drug by pharmaceutical companies, providing a model of treatment for other neurodegenerative disorders.

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Nutritional therapy could potentially treat childhood neurodegenerative disease

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/32zzzl/stem_cell) has announced the addition of the "Stem Cell Research: Opportunities, Tools & Technologies" report to their offering.

To facilitate research resulting from interest in the far-ranging applications of stem cells, a large and growing stem cells research products market has emerged. Large companies selling stem cell research products include Life Technologies, BD Biosciences, Thermo Fisher Scientific, and Millipore, although dozens of other suppliers exist as well. Products offered by these companies include: antibodies to stem cell antigens, bead-based stem cell separation systems, stem cell protein purification and analysis tools, tools for DNA and RNA-based characterization of stem cells, stem cell culture and media reagents, stem cell specific growth factors and cytokines, tools for stem cell gene regulation, a range of stem cell services, tools for in vivo and in vitro stem cell tracking, and stem cell lines.

Currently, the federal government is an important, although not dominant, source of funding for stem cell research. The reason is that states are spending almost as much as the federal government on stem cell research and are actually spending more than the federal government on human embryonic stem cell (hESC) research. Private sources also contribute a huge about of funding, with analysis of recent large gifts summing to over $1.7 billion.

Furthermore, growth in research into stem cells has exploded in the past decade. And so the market to supply stem cell research products has grown to meet this huge demand.

This report identifies, defines, and quantifies each market segment within the stem cell product industry, including Stem Cell Research Products, Stem Cell Antibodies, and Stem Cell Therapies.

Because of the massive size of this market, developing either niche products or a diverse stem cell product line represents a significant opportunity for research supply companies. This report explores current market conditions and provides guidance for companies interested in developing strategically positioned stem cell product lines.

Featured elements of this report include:

- What are novel stem cells research products that can be developed?

- What stem cells types are most frequently used by research scientists?

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Research and Markets: The Stem Cell Research Market: A Comprehensive Guide on Market Conditions for Companies ...

Public release date: 31-Jul-2013 [ | E-mail | Share ]

Contact: Yivsam Azgad news@weizmann.ac.il 972-893-43856 Weizmann Institute of Science

One of life's most basic processes -- transcription of the genetic code -- resembles road traffic, including traffic jams, accidents and a police force that controls the flow of vehicles. This surprising finding, reported recently by Weizmann Institute researchers in Nature Communications, might facilitate the development of a new generation of drugs for a variety of disorders.

Transcription indeed involves a step resembling the motion of a vehicle: Enzymes "ride" along gene "tracks," creating molecules that will later be translated into the various proteins involved in the life of the cell. In the new study, a research team headed by Prof. Rivka Dikstein of the Biological Chemistry Department has found that just as on the road, maintaining a reasonable distance between the vehicles -- that is, the transcribing enzymes -- is the surest way to reach a destination safely. In addition to Dikstein, the team included Dr. Nadav Marbach-Bar, Amitai Ben-Noon, Shaked Ashkenazi, Ana Tamarkin-Ben Harush, Dr. Tali Avnit-Sagi and Prof. Michael Walker.

The scientists tracked the transcription of genes coding for tiny regulatory molecules called microRNAs. Working with human cells, they experimented with different rates of transcription: a high rate, in which the enzymes are launched in bursts, and a low one, in which the enzymes are launched individually, at greater intervals. The experiments yielded a paradoxical finding: When the transcription enzymes were launched in bursts, the amount of the resultant microRNA dropped; conversely, when the enzymes were launched at greater intervals, production of microRNA was more efficient.

It turned out that when the enzymes were launched in bursts, one rapidly following the next, they ended up in a traffic jam: When the first enzyme paused at a "road bump" -- a molecular signal that creates a pause in transcription -- the enzymes that followed crashed into it, falling off the gene. Naturally, such "traffic accidents" reduced the amount of resultant microRNA. In contrast, when the enzymes were launched one by one, they maintained a safe distance: Each had sufficient time to slow down at the "bump" and to succeed at creating a microRNA molecule. In other words, the lower rate of release of individual enzymes proved to be a more efficient method for creating microRNAs.

Because these findings shed new light on the manufacture of microRNAs, they might help in the design of drugs based on these molecules. Discovered as recently as in the 1990s, microRNAs hold great promise for serving as future therapeutics because they can help control gene expression -- for example, blocking the activity of cancer-causing genes. This ability is particularly valuable when a molecular process needs to be manipulated at the deepest possible level, inside the cell nucleus.

In a more fundamental sense, the new study helps reveal how transcription is regulated. For example, the study has shown that in inflammation, when the body is threatened with invasion by a virus or bacterium, the release of anti-inflammatory microRNAs is temporarily suspended. The suspension occurs because inflammation increases the launch rate of transcription enzymes, creating traffic jams that reduce the production of the microRNA. This reduction, in turn, "buys time" for the inflammation, giving it a chance to perform its healing function before it is terminated by the microRNA.

Finally, this study helps explain an earlier finding in Dikstein's lab: In longer genes, transcription enzymes tend to be launched at a low rate, that is, at great intervals. The longer the gene, the greater the risk that it has molecular "bumps" that can create traffic jams, derailing transcription. Therefore, transcription enzymes riding along such genes at a lower rate can do their job more efficiently than the enzymes launched in rapid bursts.

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Gene decoding obeys road traffic rules

July 31, 2013

By the time the purple flowers of witchweed have bloomed, the crops have already been lost. John Yoder hopes his gene research can stop the weed. (John Yoder/UC Davis photo)

An international research team, including a University of California, Davis, plant scientist, is using the molecular magic of gene sequencing and transfer to break the stranglehold of witchweed and other parasitic plants that annually cause billions of dollars in crop losses around the world.

Joining forces through the Parasitic Plant Genome Project, funded by the National Science Foundation, UC Davis Professor John Yoder and colleagues are identifying the genome-wide changes that have evolved to equip this intriguing but often devastating group of wild plants to develop their parasitic lifestyle.

We know that parasitic plants evolved from non-parasitic plants, so we take an evolutionary approach and ask, What are the genetic changes that make a plant parasitic, and what are the genetic consequences once a plant becomes a parasite? said Yoder, whose lab in the UC Davis Department of Plant Sciences is contributing to the Parasitic Plant Genome Project. The next stage is to identify critical parasite genes and pathways and use this information to develop parasite-resistant crops, he said.

In a May cover article for the journal Molecular Plant-Microbe Interactions, Yoder and co-author Pradeepa C.G. Bandaranayake of the University of Peradeniya, Sri Lanka, demonstrated a new strategy for engineering within host plants a killer DNA molecule that is toxic to at least one species of Orobanchaceae. This family of almost 2,000 parasitic plant species includes some of the worlds worst agricultural pests, notably Striga or witchweed and Orobanche, also known as broomrape.

Striga, for example, has a reputation for covertly destroying crop fields. By the time the purple flowers of this parasitic weed have bloomed, the field is already ruined. Removed from the soil, Striga can return decades later through dormant seeds. The infestations are particularly devastating to staple crops like rice, maize, millet and sorghum in sub-Saharan Africa and the Middle East.

Because Striga and Orobanche can be so invasive, researchers in the Yoder lab instead use in their studies the closely related parasitic plant Triphysaria, or dwarf owls clover, which is native to California.

The recently published study showed that an inhibitory RNA gene-transfer technique could reduce by 80 percent the viability of Triphysaria roots after the parasite has attached to the genetically modified host.

A $3.4 million grant, recently awarded by the National Science Foundation to the Parasitic Plant Genome Project, will enable Yoder and his research colleagues to conduct controlled laboratory experiments that will be followed by field testing in Israel, Kenya or Morocco.

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Gene sequencing targets witchweed and other destructive parasitic plants

Speech to Bono concerning Monsanto by Marenka
Bono and Monsanto Forum for Conscious Debate and Discovery on Facebook https://www.facebook.com/BonoMonsanto?ref=hl {You can join in supporting the objective...

By: Marenka Cerny

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Speech to Bono concerning Monsanto by Marenka - Video

Alien Genetic Engineering of YOU
Some interesting facts regarding human DNA strange artefacts that contradict the Darwinian theory of Human evolution. You have to see it to believe it.. Are ...

By: Dennis4706

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Alien Genetic Engineering of YOU - Video