Archive for the ‘Gene Therapy Research’ Category

SAN FRANCISCO--Genetic engineering could hold the key to artificially creating semiconductors in a lab. According to technology news site Ars Technica, a team of academics at the University of California, Santa Barbara is looking at ways to create synthetic proteins that could form new structures of silicon dioxide to make computer chips with.

These chips would then be used in all kinds of electronics.

The proteins could also form titanium dioxide, used in solar cells.

The process is a bit different from regular genetic engineering because it uses synthetic cells made of the randomly combined genes of two related silicateins replete with random mutations, surrounded by a nucleus of minute plastic beads.

The artificial cells are put through the proverbial wringer, killing many along the way. Those that survive the process have their genes cherry picked by the scientists from either the silicon or titanium dioxide-forming proteins.

The results were somewhat surprising, with researchers finding not just the original silicateins used to form the artificial cell in the first place, but also another, different gene.

Tests on the new gene found it contained a silica-forming protein which has been dubbed silicatein X1, which may prove useful in the making of folded sheets of silica-protein fibers.

Silica skeletons of radiolaria in false color

Now that scientists know its possible to create entirely different silica proteins, the next step will be to change the conditions in order to achieve things like semiconductor performance.

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Genetic engineering for synthetic semiconductors

Patients who have genetic testing done to detect their risk for multiple health conditions do not use more health services after testing than those who elect not to be checked, says a study published online May 17 in Genetics in Medicine.

Genetic tests increasingly are being marketed directly to patients, raising concerns among some physicians that they could cause a spike in patients requesting unnecessary screening and procedures, said Robert J. Reid, MD, PhD, lead study author and associate investigator with Group Health Research Institute in Seattle.

Certainly, there is a lot of concern in the country that doing indiscriminate testing of individuals around their genetic susceptibility will alarm them and increase demand, he said.

Researchers studied 1,599 insured patients between age 25 and 40 from the Henry Ford Health System in Detroit. Of those, 217 opted to get genetic tests. Patients who received the tests had more specialty physician visits before the checks than the untested group, but the study found no change in overall use of health care services among those who had the evaluations done and those who did not (ncbi.nlm.nih.gov/pubmed/22595941/).

Researchers analyzed health care usage by participants for 12 months before and 12 months after genetic testing. Dr. Reid said the study took a conservative approach. It looked only at screening and procedures associated with four of eight conditions whose risk could be detected from the multiplex genetic susceptibility tests: type 2 diabetes mellitus, atherosclerotic coronary heart disease, colorectal cancer and lung cancer. Also, the tests were thoroughly explained to all study participants something that doesnt necessarily happen in everyday practice, Dr. Reid said.

They certainly had a fair amount of material on which to base their decision, and they had follow-up to help them understand the results, he said. In most cases there is not a lot of counseling beforehand or a lot of explanation afterward.

One surprising factor was how few patients opted to have the testing done, Dr. Reid said.

Blacks were significantly less likely than whites to choose testing, as were those with just a high school education or less. The age group studied could be a factor, as younger individuals may feel that such tests offer little value at that stage in their lives, he said.

More research needs to be done to determine how genetic tests impact behavior in larger groups of patients. Such tests may have a positive impact by motivating some patients to make healthier lifestyle choices.

If someone is told they are at risk for heart disease or diabetes, it might prompt them to maintain a healthy body weight, try to lower their cholesterol or stop smoking, Dr. Reid said. I think that is the next stage to see if it promotes positive health behavior.

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Genetic testing doesn’t drive up demand for more health services

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/3lsg2r/forwardtime_popul) has announced the addition of John Wiley and Sons Ltd's new book "Forward-Time Population Genetics Simulations: Methods, Implementation, and Applications" to their offering.

The only book available in the area of forward-time population genetics simulationsapplicable to both biomedical and evolutionary studies

The rapid increase of the power of personal computers has led to the use of serious forward-time simulation programs in genetic studies. Forward-Time Population Genetics Simulations presents both new and commonly used methods, and introduces simuPOP, a powerful and flexible new program that can be used to simulate arbitrary evolutionary processes with unique features like customized chromosome types, arbitrary nonrandom mating schemes, virtual subpopulations, information fields, and Python operators.

The book begins with an overview of important concepts and models, then goes on to show how simuPOP can simulate a number of standard population genetics modelswith the goal of demonstrating the impact of genetic factors such as mutation, selection, and recombination on standard Wright-Fisher models. The rest of the book is devoted to applications of forward-time simulations in various research topics.

Key Topics Covered:

1. Basic concepts and models

2. Simulation of population genetics models

3. Ascertainment bias in population genetics

4. Observing properties of evolving populations

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Research and Markets: Forward-Time Population Genetics Simulations: Methods, Implementation, and Applications

07-06-2012 07:39 Cell being the smallest part of any organism, is a building block of life. Cell therapies often focus on the treatment of hereditary diseases, with methods of gene therapy. The journal describes biology of a cell and the process of pioneering new cells into a tissue in order to negotiate a disease.

Originally posted here:
OMICS Group :: Journal of Cell Science

Regulated information June 8, 2012

TiGenix obtains national reimbursement in the Netherlands for breakthrough cartilage therapy ChondroCelect

Leuven (BELGIUM) - June 8, 2012 - TiGenix (NYSE Euronext: TIG) announced today that its innovative cartilage repair therapy ChondroCelect has obtained national reimbursement in the Netherlands. The Dutch National Health Authority (NZa) has formally announced that ChondroCelect is to receive national reimbursement retroactively per January 1, 2012. Previously ChondroCelect was made available in the Netherlands under a risk-sharing scheme.

"We are delighted with the decision of the NZa to reimburse ChondroCelect, and look forward to working with Dutch orthopedic centers of excellence and health insurers to routinely make this breakthrough therapy available to the right patients in the Netherlands," said Eduardo Bravo, CEO of TiGenix. "Dutch clinicians and scientists have been instrumental in ChondroCelect`s development and four Cartilage Expert Centers in the Netherlands have already gained extensive experience with the procedure. After having obtained national reimbursement in Belgium last year, this constitutes another major step in improving patient access to this innovative therapy. We remain optimistic that we can obtain national reimbursement in other European countries later this year."

For more information: Eduardo Bravo Chief Executive Officer eduardo.bravo@tigenix.com

Claudia D`Augusta Chief Financial Officer claudia.daugusta@tigenix.com Hans Herklots Director Investor & Media Relations hans.herklots@tigenix.com +32 16 39 60 97

About TiGenix

TiGenix NV (NYSE Euronext Brussels: TIG)is a leading European cell therapy companywith a marketed product for cartilage repair, ChondroCelect, and a strongpipeline with clinical stage allogeneic adult stem cell programsfor the treatment ofautoimmune and inflammatory diseases.TiGenixis based out of Leuven (Belgium) and has operations in Madrid (Spain), and Sittard-Geleen (theNetherlands). For more information please visitwww.tigenix.com.

About ChondroCelect

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TiGenix : national reimbursement in the Netherlands obtained for breakthrough cartilage therapy ChondroCelect®

06-06-2012 19:15 A research team led by Dr. Seung Hoon Lee took part in a multinational genome research project, consisting of researchers from fifty different nations. The project's findings identifying 56 genes involved in osteoporosis and fracture risk were published on April16th in Nature Genetics. In the largest-scale genetic research project to date, genetic testing was done on 210000 individuals from around the world. The study included clinical data from Korea, such as bone density measures and DNA samples from fourteen hundred patients. The study was able to identify 56 genetic variants, including WNT16, that influence bone density, of which 14 were associated with fracture risk. Dr. Seung Hoon Lee / Dept. of Endocrinology/Metabolism If individuals with high fracture risk can be identified by detecting this kind of high-risk gene, in addition to other clinical risk factors and bone density measurements in accordance with current treatment standards, the study suggests that prevention and treatment using individually-tailored drugs will be possible. Osteoporosis is a skeletal disease of increased risk of fracture due to weakened bone strength. Although this age-related disease is silent and asymptomatic until fractures occur, it has a high incidence and devastating consequences. By identifying genes related to osteoporosis and fracture risk, this multinational genetic study is expected to lead to new breakthroughs in the treatment of osteoporosis.

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Genes associated with osteoporosis and fracture risk identified - Video

Public release date: 7-Jun-2012 [ | E-mail | Share ]

Contact: Jim Fessenden james.fessenden@umassmed.edu 508-856-2000 University of Massachusetts Medical School

WORCESTER, MA Degeneration of the axon and synapse, the slender projection through which neurons transmit electrical impulses to neighboring cells, is a hallmark of some of the most crippling neurodegenerative and brain diseases such as amyotrophic lateral sclerosis (ALS), Huntington's disease and peripheral neuropathy. Scientists have worked for decades to understand axonal degeneration and its relation to these diseases. Now, researchers at the University of Massachusetts Medical School are the first to describe a gene dSarm/Sarm1 responsible for actively promoting axon destruction after injury. The research, published today online by Science, provides evidence of an exciting new therapeutic target that could be used to delay or even stop axon decay.

"This discovery has the potential to have a profound impact on our understanding of neurodegenerative diseases, much like the discovery of apoptosis (programmed cell death) fundamentally changed our understanding of cancer," said Marc R. Freeman, PhD, associate professor of neurobiology at the University of Massachusetts Medical School and lead investigator on the study. "Identification of this gene allows us to start asking exciting new questions about the role of axon death in neurodegenerative diseases. For example, is it possible that these pathways are being inappropriately activated to cause premature axon death?"

For more than a century, scientists believed that injured axons severed from the neuron cell body passively wasted away due to a lack of nutrients. However, a mouse mutation identified in the early 1990s called slow Wallerian degeneration (Wlds) was able to suppress axon degeneration for weeks. This finding forced scientists to reassess Wallerian degeneration, the process through which an injured axon degenerates, as a passive process and consider the possibility that an active program of axon auto-destruction, akin to apoptotic death, was at work instead.

If Wallerian degeneration was an active process, hypothesized Dr. Freeman, a Howard Hughes Medical Institute Early Career Scientist, then it should be possible through forward genetic screens in Drosophila to identify mutants exhibiting Wlds-like axon protection. Freeman and colleagues screened more than 2,000 Drosophila mutants for ones that exhibited long-term survival of severed axons. Freeman says this was a heroic effort on the part of his colleagues. The screen took place over the next two and a half years, and involved seven students and post-docs in the Freeman labJeannette M. Osterloh, A. Nicole Fox, PhD, Michelle A. Avery, PhD, Rachel Hackett, Mary A. Logan, PhD, Jennifer M. MacDonald, Jennifer S. Zeigenfusswho performed the painstaking and labor-intensive experiments needed on each Drosophila mutant to identify flies that suppressed axonal degeneration after nerve injury.

Through these tests, they identified three mutants (out of the 2,000 screened) where severed axons survived for the lifespan of the fly. Next generation sequencing and chromosome deficiency mapping techniques were then used to isolate the single gene affected in all three dSarm. These were loss-of-function alleles, meaning that Drosophila unable to produce the dSarm/Sarm1 molecule exhibited prolonged axon survival for as many as 30 days after injury. Freeman and colleagues went on to show that mice lacking Sarm1, the mammalian homolog of dSarm, also displayed remarkable preservation of injured axons. These findings provided the first direct evidence that Wallerian degeneration was driven by a conserved axonal death program and not a passive response to axon injury.

"For 20 years people have been looking for a gene whose normal function is to promote axon degeneration," said Osterloh, first author on the study. "Identification of the dSarm/Sarm1 gene has enormous therapeutic potential, for example as a knockdown target for patients suffering from diseases involving axonal loss."

The next step for Freeman and colleagues is to identify additional genes in the axon death pathway and investigate whether any have links with specific neurodegenerative diseases. "We're already working with scientists at UMMS to understand the role axon death plays in ALS and Huntington's disease," said Freeman. "We are very excited about the possibility that these findings could have broad therapeutic potential in many neurodegenerative diseases."

###

Originally posted here:
Scientists identify first gene in programmed axon degeneration

ScienceDaily (June 7, 2012) A team of UC Davis investigators has found that a genetic mutation may play an important role in the development of prostate cancer. The mutation of the so-called p53 (or Tp53) gene was previously implicated in late disease progression, but until now has never been shown to act as an initiating factor. The findings may open new avenues for diagnosing and treating the disease.

The study was published online in the journal Disease Models & Mechanisms and will appear in the November 2012 print edition in an article titled, "Initiation of prostate cancer in mice by Tp53R270H: Evidence for an alternate molecular progression."

"Our team found a molecular pathway to prostate cancer that differs from the current conventional wisdom of how the disease develops," said Alexander Borowsky, associate professor of pathology and laboratory medicine and principal investigator of the study. "With this new understanding, research can go in new directions to possibly develop new diagnostics and refine therapy."

Prostate cancer is the leading cancer diagnosis in men in the United States. Although it is curable in about 80 percent of men with localized disease, the rate is much lower if the cancer is highly virulent and has spread beyond the prostate gland.

The investigators developed a mouse model genetically engineered to have a mutation in the "tumor suppressor" gene, p53, specifically in the cells of the prostate gland. These mice were significantly more likely to develop prostate cancer than control mice without the mutation, and provided the first indication that the p53 mutation could be involved in the initiation of prostate cancer. They also note that the mutation of p53 in the prostate differs from loss or "knock-out" of the gene, which suggests that the mechanism is more complicated than simply a "loss of tumor suppression" and appears to involve an actively oncogenic function of the mutant gene.

The p53 gene encodes for a protein that normally acts as a tumor suppressor, preventing the replication of cells that have suffered DNA damage. Mutation of the gene, which can occur through chemicals, radiation or viruses, causes cells to undergo uncontrolled cell division. The p53 mutation has been implicated in the initiation of other malignancies, including breast, lung and esophageal cancers.

Other studies have associated p53 mutation with disease progression in prostate cancer, but this is the first to find that it can have a role in the early initiation of prostate cancer, as well.

Until now, understanding of the role of p53 was that mutation occurred exclusively as a late event in the course of prostate cancer. Based on the findings in the new mouse model that the researchers developed, p53 mutation not only can initiate prostate cancer but might also be associated with early progression toward more aggressive forms of the disease.

Genetic mutations can initiate cancers in a variety of ways. Those include promotion of uncontrolled cell growth and loss of the gene's normal cell growth-suppressor functions. Exactly how the p53 mutation promotes the initiation and progression of prostate cancer remains to be clarified and is a focus of current research by the UC Davis team. They also are trying to gain an understanding of how the p53 mutation affects the effectiveness of standard treatments for prostate cancer, such as radiation and hormone therapy.

Another application of the discovery could be the development of a new diagnostic test for prostate cancer based on the presence of the p53 mutation as a biomarker.

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New role for p53 genetic mutation -- initiation of prostate cancer

Scientists map babys genetic code in womb

By John von Radowitz

Friday, June 08, 2012

An unborn babys whole genetic code has been mapped in the womb using DNA taken from its parents.

The technique could in future make it possible to swiftly scan for some 3,500 genetic disorders before birth, without physically disturbing either foetus or mother.

But scientists acknowledge the ability to sequence a babys whole genome in the womb has as yet unresolved ethical implications.

It could produce a wealth of data relating to a babys future health. At the same time, difficult questions may be raised about the moral case for termination.

Most pre-natal genetic screening currently involves tapping fluid from the foetal sac, or taking placental samples. Such invasive methods can only identify a small number of birth defects including Downs syndrome, and spina bifida.

They also pose risks for both mother and child. But there are thousands of rarer genetic conditions that are seldom spotted until they start producing symptoms.

The new research involved analysing DNA shed by the foetus and floating in the mothers bloodstream. Blood sample DNA from the mother was also studied as well as DNA extracted from the fathers saliva.

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Scientists map baby’s genetic code in womb

06-06-2012 13:09 Mesenchymal stem cell homing to tissue damage, umbilical cord stem cells historically used for anti-aging, mesenchymal stem cells role in immune system modulation, inflammation reduction and stimulating tissue regeneration, donor stem cell safety and testing, the role of HLA matching in donated umbilical cord-derived stem cells, umbilical cord blood safety data and historical use in blood transfusions, allogeneic stem cell persistence in human mothers. Treatment information at More information on Dr. Riordan at

Link:
Neil Riordan PhD - Stem Cell Therapy for Spinal Cord Injury (Part 3 of 5) || Stem Cell Treatments - Video

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/ws7n9p/analysis_of_micror) has announced the addition of Frost & Sullivan's new report "Analysis of MicroRNA Tools and Services Market in Europe" to their offering.

This Frost & Sullivan research titled Analysis of MicroRNA Tools and Services Market in Europe starts from the base year of 2010 with forecasts running through 2017. It offers a comprehensive market overview including key challenges, drivers and restraints, while providing valuable recommendations to market participants. The market segmentation is based on microRNA (miRNA) research in life science. This research service gives an overall analysis of miRNA tools such as qRT-PCR, microarray and functional analysis and services including expression profiling and phenotypic screening.

Market Overview

Expanded MicroRNA Research to Result in Increased Uptake of Related Research Tools

A number of large pharmaceutical and biotech companies are keen to invest in life science research. Advances in genomic technologies and molecular biology segments will boost the miRNA research and tools market in the future. MicroRNA is set to unveil a new era in molecular diagnostics and in the development of effective therapeutics.

The adoption of miRNA research in different fields is, in turn, widening the use of related miRNA tools across an ever-expanding spectrum of applications. MicroRNA profiling has already been adopted in cancer research, stem cell research, developmental biology and neuroscience, notes the analyst of this research. This has caused many other fields to develop an interest in auditing their gene expression analyses or epigenetic research by profiling miRNAs. Recently, more research and development has been promoted in finding the utility and role of miRNAs in the field of cardiovascular research, plant science, virology, endocrinology and genetic disease. As researchers discover new miRNAs and study functions, additional research fields may realise that miRNAs can play a role in their disciplines.

Market Sectors

Expert Frost & Sullivan analysts thoroughly examine the following market sectors in this research:

- miRNA tools( qRT-PCR, microarray and functional analysis)

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Research and Markets: Analysis of MicroRNA Tools and Services Market in Europe 2012

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/w4spkx/life_sciences_pcr) has announced the addition of the "Life Sciences (Pcr, CellCulture, In-Vitro Diagnostics, Expression & Transfection) & Analytical Reagents (Chromatography, MassSpectrometry, Electrophoresis, FlowCytometry) Market Applications (Protein Purification, Gene Expression, Dna & Rna Analys" report to their offering.

Biotechnology (life science and analytical) reagents are the substances or compounds used to detect or synthesize another substance in order to provide a test reading. These reagents are used in the field of research, diagnosis, bioscience, and education.

The life sciences and analytical reagents market report studies the life science and analytical reagents market, by technology, end-users, and applications. The life sciences and analytical reagents market, by technology studied in this report are segmented as life science reagents and analytical reagents; of which life science segment accounted for the largest share of 59.37% of the total market in 2011. The global life science and analytical reagents market was valued at $40,308.8 million in 2011 and is expected to reach $59,319.2 million by 2016; growing at a CAGR of 8% from 2011 to 2016.

The life sciences and analytical reagents market is driven by the increasing use of reagents in therapeutics, basic research and commercial applications. The demand for biotechnology reagents is mainly dependent upon the growth of the biotechnology instrumentation market. The biotechnology instrumentation market continues to witness significant growth due to an increase in the number of biotechnology firms around the globe and increase in research and development expenditure by the biotechnology companies, thus augmenting the demand for biotechnology instruments. Continual product developments are being witnessed in various industries, such as pharmaceutical/bio-pharmaceutical, agri-biotech, and food and beverages; this is expected to facilitate market growth.

Key Topics Covered:

1 Introduction

2 Executive Summary

3 Market Overview

4 Life Sciences & Analytical Reagents Market, By Technology

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Research and Markets: Life Sciences & Analytical Reagents Market

MADISON, Wis., June 7, 2012 /PRNewswire/ --Cellular Dynamics International, Inc. (CDI), the world's largest commercial producer of human induced pluripotent stem (iPS) cell lines and tissue cells, today announced the launch of its MyCell Services. These services include novel iPS cell line reprogramming, genetic engineering and differentiation of iPS cells into commercially available iCell terminal tissue cells (for example, heart or nerve cells).

"CDI's mission is to be the top developer and manufacturer of standardized human cells in high quantity, quality and purity and to make these cells widely available to the research community. Our MyCell Services provide researchers with unprecedented access to the full diversity of human cellular biology," said Bob Palay, CDI Chief Executive Officer. "The launch of MyCell Services furthers CDI founder and stem cell pioneer Jamie Thomson's vision to enable scientists worldwide to easily access the power of iPSC technology, thus driving breakthroughs in human health."

Over the past 2 years, CDI has launched iCell Cardiomyocytes, iCell Neurons and iCell Endothelial Cells for human biology and drug discovery research. MyCell Services leverage CDI's prior investment in building an industrial manufacturing platform that can handle the parallel production of multiple iPSC lines and tissue cells, manufacturing billions of cells daily.

Chris Parker, CDI Chief Commercial Officer, commented, "Not all studies requiring human cells can be accomplished by using cells from a limited set of normal, healthy donors. Researchers may need iPS cells or tissue cells derived from specific ethnic or disease populations, and MyCell Services enable them to take advantage of our deep stem cell expertise and robust industrial manufacturing pipeline to do so. Previously, scientists had to create and differentiate iPS cells themselves. Such activities consume significant laboratory time and resources, both of which could be better applied to conducting experiments that help us better understand human biology. CDI's MyCell Services enable scientists to re-direct those resources back to their experiments."

CDI pioneered the technique to create iPS cells from small amounts of peripheral blood, although iPS cells can be created from other tissue types as well. Additionally, CDI's episomal reprogramming method is "footprint-free," meaning no foreign DNA is integrated into the genome of the reprogrammed cells, alleviating safety concerns over the possible use of iPS cells in therapeutic settings. These techniques have been optimized for manufacture of over 2 billion human iPS cells a day, and differentiated cells at commercial scale with high quality and purity to match the research needs.

Modeling Genetic Diversity

CDI has several projects already underway using MyCell Services to model genetic diversity of human biology. The Medical College of Wisconsin and CDI received a $6.3M research grant from the National Heart, Lung, and Blood Institute (NHLBI), announced July 2011, for which CDI's MyCell Services will reprogram an unprecedented 250 iPS cell lines from blood samples collected from Caucasian and African-American families in the Hypertension Genetic Epidemiology Network (HyperGEN) study. In addition, MyCell Services will differentiate these iPS cells into heart cells to investigate the genetic mechanisms underlying Left Ventricular Hypertrophy, an increase of the size and weight of the heart that is a major risk factor for heart disease and heart failure.

Researchers are also using CDI's MyCell Services to generate iPS cells and liver cells from individuals with drug induced liver injury (DILI), toward an eventual goal of identifying genetic factors linked to idiosyncratic liver toxicity. "The most problematic adverse drug event is sudden and severe liver toxicity that may occur in less than one in one thousand patients treated with a new drug, and thus may not become evident until the drug is marketed. This type of liver toxicity is not predicted well by usual preclinical testing, including screening in liver cultures derived from random human donors," said Paul B. Watkins, M.D., director of with The Hamner - University of North Carolina Institute for Drug Safety Sciences. "The ability to use iPS cell technology to prepare liver cultures from patients who have actually experienced drug-induced liver injury, and for whom we have extensive genetic information, represents a potential revolution in understanding and predicting this liability."

Screening Human Disease

While most diseases are multi-systemic, focus typically centers on only one organ system. For example, congenital muscular dystrophy (CMD) is a group of rare genetic diseases with a focus on skeletal muscle, yet other systems, including heart, eye, brain, diaphragm and skin, can be involved. Understanding the molecular mechanisms underlying complex disease phenotypes requires access to multiple tissue types from a single patient. While some systems are readily accessible for taking a biopsy sample, for example skin, other organs are not.

Continue reading here:
Cellular Dynamics Launches MyCell™ Services

A few blogs ago I asked, "Where, in fact, do 'the good ones' really come from?" By "good ones" I meant useful genome changes in evolution. This question stimulated some debate about whether it was possible to distinguish good changes from bad changes before they occur.

In the abstract, this may seem an overwhelmingly difficult problem. But if we think a bit about the highly organized state of the genome and non-random natural genetic engineering, biasing changes toward "good ones" becomes more conceivable.

I have already discussed purposeful, targeted changes in the immune system. The immune system illustrates how efficiently cells can target DNA restructuring by recognizing specific sequences and coupling DNA changes to transcription (copying DNA sequence into RNA).

Some evolutionists object that a somatic process like antibody synthesis provides no model for germline changes in evolution. So let's examine natural genetic engineering events in microbial cells. We'll look at mobile genetic elements targeted in ways that increase their evolutionary potential.

Mobile genetic elements come in many forms. Some operate purely as DNA. Others make an RNA copy and reverse transcribe it back into DNA as it inserts at a new location. Elements that move, or transpose, to multiple new locations are called "transposons" or "retrotransposons" (if they use an RNA intermediate).

Other mobile elements only insert in particular locations by a process called "site-specific" recombination. In bacterial evolution, this process is used in specialized structures called "integrons" that capture casettes containing protein coding sequences for antibiotic resistance, pathogenicity, and other functions.

What all mobile elements share are proteins that aid them to cut and splice DNA chains so that they can construct novel sequences, much as human genetic engineers do in their test tubes. These proteins have various names, such as "recombinase," "transposase," and "integrase." It is the specificity of the cutting reactions involving these proteins that determines where a mobile element moves in the genome.

One fascinating case of highly biased integration is the bacterial transposon Tn7. Tn7 has two specialized proteins to target its transposition. The TnsD protein directs Tn7 to insert into a special "attTn7" site in the chromosomes of many bacterial species where it does not disrupt any host functions and so causes no deleterious effects.

Another, more interesting protein, TnsE, directs Tn7 to insert into replicating DNA molecules. The reason this is important is that transmissible plasmids replicate their DNA as they transfer from one cell to another. TnsE targeting to plasmids in transit to new cells thus enhances the spread of Tn7 and the resistances it carries to many different kinds of bacteria.

Tn7 carries its antibiotic resistance determinants in an integron. Integrons and their recombinase proteins are likewise specialized to participate in plasmid spreading through bacterial populations. Plasmids enter new cells as single-stranded DNA. We learned just in 2005 that integron site-specific recombinases are special in operating on single-stranded DNA, not double-stranded molecules like previously studied recombinases. Moreover, integron recombinase synthesis is triggered by the entrance of single-stranded DNA into a cell. So integron activity is intimately linked in more than one way to plasmid transfer.

See original here:
James A. Shapiro: Can Cells Bias Natural Genetic Engineering Toward Useful Evolutionary Outcomes?

SEATTLE -- Researchers at the University of Washington have assembled the first comprehensive genetic map of an unborn child -- a development that could help usher in a new era of prenatal testing.

By analyzing fetal DNA circulating in the mother's blood, the scientists were able to sequence the baby's genome 18 weeks into the pregnancy. The technique also worked at eight weeks, with slightly lower sensitivity.

Because the approach requires only a blood sample from the mother and saliva from the father, it poses none of the miscarriage risk associated with invasive tests such as amniocentesis. And while most existing prenatal tests are designed to check for single disorders, including Down syndrome, a full-gene scan has the power to reveal a wide range of potential problems before birth, said lead author Jacob Kitzman, a doctoral student in genetics.

"It's much more comprehensive."

The procedure is still several years away from commercialization, project leader Jay Shendure said.

But the UW study, published in the June 6 issue of Science Translational Medicine, marks a significant step forward in technology that's been developing over the past several years -- and which worries some people, said Marcy Darnovsky of the Center for Genetics and Society in Berkeley, Calif.

"I think it's a game-changer," she said. Cheap, safe genome sequencing could give parents the power to practice a kind of eugenics, preselecting children based on desirable traits.

"It could become a routine part of prenatal testing ... which raises questions about what people will do with the information," Darnovsky said.

Shendure cautioned against expecting too much -- at least in the near future. Scientists may be able to sequence the 3 billion DNA units that make up each person's genetic heritage, but they still don't understand the genetic basis of most common diseases.

"The capacity of genomics to generate data is outstripping our ability to interpret it in useful ways," he said.

Read this article:
Researchers assemble genetic map of an unborn child

By contrast, the scientists say their new test would identify far more conditions, caused by genetic errors.

However, they warned it raised many ethical questions because the results could be used as a basis for abortion.

These concerns were last night amplified by pro-life campaigners, who said widespread use of such a test would inevitably lead to more abortions.

The American scientists were able to map the babys genetic code principally from tiny traces free-floating DNA, which makes its way into the mothers blood.

Blood sample DNA from the mother was also studied as well as DNA extracted from the father's saliva.

Fitting pieces of the genetic jigsaw together, scientists in the US were able to reconstruct the entire genetic code of an unborn baby boy.

They were then able to see what spontaneous genetic mutations had arisen.

Such natural mutations - called de novo mutations - are responsible for the majority of genetic defects.

By checking their prediction of the babys genetic code with actual DNA taken after the birth, the team from the University of Washington in Seattle, found they were able to identify 39 of 44 such mutations in the child.

De novo mutations are thought to play a role in a number of complex conditions such as autism and schizophrenia.

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Unborn babies could be tested for 3,500 genetic faults

Researchers at the University of Washington have sequenced the entire genome of a fetus. The scientific advance could help detect certain diseases in the womb, but some experts worry that the trove of genetic information may prove more scary and overwhelming than useful.

Suspended in the blood of a pregnant woman along with some added information from a dad-to-bes saliva lurks enough fetal DNA to map out an unborn babys entire genetic blueprint.

It may sound like something conjured by Jules Verne, but it happened at the University of Washington: a professor and his graduate student used DNA samples from the parents of a baby boy who was still in utero and reconstructed his entire genetic makeup from A to Z.

The account, published Wednesday in Science Translational Medicine, takes prenatal testing to new heights, promising a motherlode of genetic information about a child who had not even been born along with a corresponding trove of data that even experts dont yet know how to interpret.

Jacob Kitzman, lead author and a graduate student in the department of genome sciences at the University of Washington (UW), was excited but cautious about his teams achievement. There have been a lot of steps toward this, but this is the first time capturing the whole genome, says Kitzman. The fact that this technology is now on the path to becoming clinically feasible is a good opportunity for a broader discussion of the implications.

Figuring out how to communicate the vast cache of information uncovered by genome sequencing remains controversial, since much of it still isnt clinically useful. But although researchers dont understand the significance of the entirety of the information revealed through whole-genome sequencing, they do know that certain genes are responsible for Mendelian, or more simple, single-gene disorders that includes more than 3,000 conditions such as cystic fibrosis, Tay-Sachs disease and some muscular dystrophies that affect 1% of pregnancies. Prenatal sequencing would allow parents to learn before delivery if their child has one of these diseases, many of which are debilitating or fatal. While genetic screening of parents before pregnancy can also identify carriers, and an increasing number of prenatal DNA-based tests can determine early in pregnancy whether developing babies have specific conditions such as Down syndrome, whole-genome sequencing is the most sophisticated way to examine a persons entire genetic code.

(MORE:Down Syndrome: With Breakthroughs in Testing, a Choice Becomes Tougher)

Prenatal genome sequencing could potentially replace more invasive procedures such as amniocentesis or chorionic villus sampling to detect recessive Mendelian disorders on average, we all carry 20 to 30 recessive genes but it is not yet precise enough to take the place of these tests when looking for other chromosomal conditions. Nor is it a foolproof gauge of risk for many other complex diseases a category that includes most cancers and common conditions such as diabetes and heart disease because theyre influenced by multiple genes and environmental factors. Great, says Thomas Murray, president of the Hastings Center bioethics institute, we can sequence the genome of a fetus. What the hell does it tell us? Much less than most people probably believe.

Kitzman concurs. Its a really big challenge for the field, figuring out how to communicate to clinicians not only the results but the uncertainty that goes along with those results, he says. Theres no easy answer.

In this particular situation, Kitzman and Jay Shendure, an associate professor of genome sciences at UW, sidestepped the thorny issue of assessing disease risk and sharing that information with parents because the expectant couple was anonymous. Kitzman doesnt know their identity, only that they consented to have their biological samples used for genome sequencing. Their son was born healthy and full-term.

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Genetic Motherlode: Scientists Decode an Unborn Baby's DNA

Prospective parents might soon be able to screen their unborn babies for thousands of genetic disorders, according to a study published by Science Translations Medicine.

This is potentially a two-edged sword. Although it might pick up more curable conditions, some experts worry that it may lead to more abortions

American scientists were able to map the babys genetic code form tiny traces of free-floating DNA in blood from the babys mother, who was 18 weeks pregnant. They were also able to pinpoint if the mutations came from the mother or fathers side.

If the technique is refined and the technology becomes inexpensive, as many experts predict, this type of prenatal testing could allow doctors to screen unborn babies for 3,500 genetic disorders by taking a blood sample from the mother and a swab of saliva from the father.

Now, the only genetic disorder routinely testing is Down Syndrome.

On the positive side, picking up genetic problems early may lead to better treatments, sometimes while the baby is still a fetus, sometimes right after birth and that might prevent complications, said NBC4 health expert Dr. Bruce Hensel.

Some experts believe the finding is a double-edged sword, and could potentially raise ethical concerns.

It might give peace of mind if (parents) dont find problems. On the other hand, it could lead to dilemmas what do you do about them can you treat them, might it lead to more abortions? Hensel said.

The genetic predictions in the study were confirmed by analyzing umbilical cord blood collected at the babys birth.

The test is not being used yet, and experts said the methods will have to refined before the screenings are widely used.

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Study: Testing Unborn Babies for Genetic Disorders

Public release date: 6-Jun-2012 [ | E-mail | Share ]

Contact: Elizabeth Streich estreich@columbia.edu 212-305-3689 Columbia University Medical Center

New York, NY (June 6, 2012) A clinical study has demonstrated that a new drug, a targeted molecular therapy called vismodegib (trade name Erivedge), can dramatically shrink basal cell skin cancers and prevent the formation of new ones, in patients with basal cell nevus syndrome (BCNS). This rare genetic condition causes dozens, and sometimes hundreds or thousands, of skin cancers on each patient's body. The primary treatment option is surgical removal. These study results are significant as they indicate the possibility of an alternative treatment with oral medication; although side effects remain a consideration.

The phase II clinical study, led by researchers at NewYork-Presbyterian Hospital/Columbia University Medical Center (NYPH/CUMC) and Children's Hospital of Oakland Research Institute (CHORI), was published today in the online edition of the New England Journal of Medicine.

"In its current formulation, vismodegib is appropriate only for BCNS patients with very large numbers of basal cell skin cancers. Still, this is a huge step forward, pointing to the day when we can offer every one of these patients an alternative to repeated surgery, which can be disfiguring and burdensome," said study co-leader David R. Bickers, MD, the Carl Truman Nelson Professor and chairman of dermatology at CUMC and director of dermatology at NewYork-Presbyterian Hospital/CUMC. The study was co-led by Ervin H. Epstein, Jr., MD, a senior scientist at CHORI.

The study is the first to evaluate vismodegib in patients with BCNS. Forty-two patients were randomized to receive either vismodegib (taken orally) or a placebo, for a maximum of 18 months. Overall, the study tracked more than 2,000 existing surgically eligible basal cell skin cancers (SEBs) and documented 694 new SEBs, on the 42 patients.

Patients taking vismodegib experienced an average of 2.3 new SEBs, compared with 29 for patients in the placebo group. Among patients taking the drug, the diameter of clinically significant skin cancers decreased an average of 65 percent, compared with 11 percent among controls. In light of these findings, the independent data and safety monitoring board appointed to oversee this trial recommended switching all patients into the treatment group.

"In many patients, we observed a dramatic reduction in the size of the lesions within one to two months," said Dr. Bickers.

BCNS, also called Gorlin syndrome, encompasses multiple defects that involve the skin, nervous system, eyes, endocrine glands, and bones. The hallmark of BCNS is the appearance of basal cell carcinomas, a slow-growing form of skin cancer, at or around puberty.

BCNS has been linked to mutations in a gene called PTCH1. PTCH1 is the primary inhibitor of a signaling pathway called sonic hedgehog, which helps ensure proper segmentation of the developing embryo. At birth, PTCH1 activity causes most sonic hedgehog signaling to cease. When PTCH1 is mutated, however, sonic hedgehog signaling continues postnatally. The result can be abnormal cell growth and proliferation, setting the stage for tumor formation.

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New drug found effective against rare form of basal cell skin cancer

06-06-2012 09:13 Alan McHughen, Bureau of Intelligence and Research, deliver remarks on "What everyone needs to know about modern genetics, or, Who's getting into your genes?" at the Jefferson Science Distinguished Lecture Series on Current Issue in Science and Technology at the Marshall Center in Washington, DC on February 28, 2012. [Go to for more video and text transcript.]

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Alan McHughen Delivers Remarks on Modern Genetics - Video

06-06-2012 15:26 To register for this complimentary webinar, please visit: Join us in a discussion of single-cell NSC profiling and identification of profiles of other cells not differentiating in the NSC pathway. We all know that tissues are composed of heterogeneous mixtures of cells. But what does that mean when we take gene expression measurements from homogenized samples? Are we accurately accounting for the small but critical changes occurring in individual cells? View this insightful webinar and see how single-cell analysis is transforming life science research.

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Innovation in Single-Cell Gene Expression Analysis- webinar preview - Video

ScienceDaily (June 6, 2012) An Indiana University biologist has shown that natural variation in measures of the brain's ability to process steroid hormones predicts functional variation in aggressive behavior.

The new work led by Kimberly A. Rosvall, a postdoctoral fellow and assistant research scientist in the IU Bloomington College of Arts and Sciences' Department of Biology, has found strong and significant relationships between aggressive behavior in free-living birds and the abundance of messenger RNA in behaviorally relevant brain areas for three major sex steroid processing molecules: androgen receptor, estrogen receptor and aromatase.

"Individual variation is the raw material of evolution, and in this study we report that free-living birds vary in aggression and that more aggressive individuals express higher levels of genes related to testosterone processing in the brain," she said. "We've long hypothesized that the brain's ability to process steroids may account for individual differences in hormone-mediated behaviors, but direct demonstrations are rare, particularly in unmanipulated or free-living animals."

Rosvall said the study shows that aggression is strongly predicted by individual variation in gene expression of the molecules that initiate the genomic effects of testosterone. The new work, "Neural sensitivity to sex steroids predicts individual differences in aggression: implications for behavioral evolution," was published June 6 in Proceedings of The Royal Society B.

The findings are among the first to show that individual variation in neural gene expression for three major sex steroid processing molecules predicts individual variation in aggressiveness in both sexes in nature, results that should have broad implications for understanding the mechanisms by which aggressive behavior may evolve.

"On the one hand, we have lots of evidence to suggest that testosterone is important in the evolution of all kinds of traits," Rosvall noted. "On the other hand, we know that individual variation is a requirement for natural selection, but individual variation in testosterone does not always predict behavior. This conundrum has led to debate among researchers about how hormone-mediated traits evolve."

To find such strong relationships between behavior and individual variation in the expression of genes related to hormone-processing is exciting because it tells scientists that evolution could shape behavior via changes in the expression of these genes, as well as via changes in testosterone levels themselves.

The team measured natural variation in aggressiveness toward the same sexes in male and female free-living dark-eyed juncos (Junco hyemalis) early in the breeding season. The dark-eyed junco is a North American sparrow that is well studied with respect to hormones, behavior and sex differences. By comparing individual differences in aggressiveness (flyovers or songs directed at intruders) to circulating levels of testosterone and to neural gene expression for the three major sex steroid processing molecules, the researchers were able to quantify measures of sensitivity to testosterone in socially relevant brain areas: the hypothalamus, the ventromedial telencephalon and the right posterior telencephalon.

Their results suggest selection could shape the evolution of aggression through changes in the expression of androgen receptor, estrogen receptor and aromatase in both males and females, to some degree independently of circulating levels of testosterone. They found, for example, that males that sing more songs at an intruder have more mRNA for aromatase and estrogen receptor in the posterior telencephalon, and also that males and females that dive-bomb an intruder more frequently have more androgen receptor, estrogen receptor and aromatase mRNA in brain tissues including the medial amygdala, an area of the brain that's known to control aggression in rodents and other birds. mRNA are single-stranded copies of genes that are translated into protein molecules.

The work reveals there is ample variation in hormone signal and in gene expression on which selection may act to affect aggressiveness. It also establishes a prerequisite for the evolution of testosterone-mediated characteristics through changes in localized gene expression for the key molecules that process sex steroids, and suggests that trait evolution can occur with some degree of independence from circulating testosterone levels.

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Variations in sex steroid gene expression can predict aggressive behaviors

Public release date: 6-Jun-2012 [ | E-mail | Share ]

Contact: Lindsay Morton lmorton@plos.org 415-935-2094 Public Library of Science

Psychoactive medications in water affect the gene expression profiles of fathead minnows in a way that mimics the gene expression patterns associated with autism spectrum disorder in genetically susceptible humans, according to research published June 6 in the open access journal PLoS ONE. These results suggest a potential environmental trigger for autism spectrum disorder in this vulnerable population, the authors write.

The researchers, led by Michael A. Thomas of Idaho State University, exposed the fish to three psychoactive pharmaceuticals fluoxetine, a selective serotonin reuptake inhibitor, or SSR1; venlafaxine, a serotonin-norepinephrine reuptake inhibitor, and carbamazepine, used to control seizures at concentrations comparable to the highest estimated environmental levels.

They found that the only gene expression patterns affected were those associated with idiopathic autism spectrum disorders, caused by genetic susceptibility interacting with unknown environmental triggers. These results suggest that exposure to environmental psychoactive pharmaceuticals may play a role in the development of autism spectrum disorder in genetically predisposed individuals.

Lead researcher Michael A. Thomas remarks, "While others have envisioned a causal role for psychotropic drugs in idiopathic autism, we were astonished to find evidence that this might occur at very low dosages, such as those found in aquatic systems."

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Citation: Thomas MA, Klaper RD (2012) Psychoactive Pharmaceuticals Induce Fish Gene Expression Profiles Associated with Human Idiopathic Autism. PLoS ONE 7(6): e32917. doi:10.1371/journal.pone.0032917

Financial Disclosure: MAT was supported by a PhRMA Foundation Sabbatical Fellowship grant, National Institutes of Health Grant Number P20 RR016454 from the INBRE Program of the National Center for Research Resources, and grant number URC-FY2010-05 from the University Research Committee of Idaho State University. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing Interest Statement: The authors have declared that no competing interests exist.

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Fish show autism-like gene expression in water with psychoactive pharmaceuticals

Public release date: 6-Jun-2012 [ | E-mail | Share ]

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

New Rochelle, NY, June 6, 2012Awareness of the risks of heart disease and signs of a heart attack vary greatly among women of different racial and ethnic groups and ages. New data that clearly identify these disparities in heart health awareness are presented in an article in Journal of Women's Health, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Women's Health website at http://www.liebertpub.com/jwh.

In a pooled analysis from two American Heart Association surveys, Black and Hispanic women were 66% less likely than white women to be aware that heart disease is the leading cause of death in women, report Heidi Mochari-Greenberger, MPH, PhD, Lori Mosca, MD, MPH, PhD, New York-Presbyterian Hospital/Columbia University Medical Center (New York, NY), and Kerri Miller, MA, Harris Interactive (Amherst, NH). Women younger than 55 years of age were also less well-informed about heart disease risk. Overall among women, awareness was low of the most common signs of heart attack, which tend to differ from those in men, according to the article "Racial/Ethnic and Age Differences in Women's Awareness of Heart Disease."

"Clearly, education that is targeted to racial/ethnic minority and younger women about heart disease risk is needed, as well as education of all women about the signs and symptoms of a heart attack," says Susan G. Kornstein, MD, Editor-in-Chief of Journal of Women's Health, Executive Director of the Virginia Commonwealth University Institute for Women's Health (Richmond, VA), and President of the Academy of Women's Health.

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About the Journal

Journal of Women's Health, published monthly, is a core multidisciplinary journal dedicated to the diseases and conditions that hold greater risk for or are more prevalent among women, as well as diseases that present differently in women. The Journal covers the latest advances and clinical applications of new diagnostic procedures and therapeutic protocols for the prevention and management of women's healthcare issues. Tables of content and a sample issue may be viewed on the Journal of Women's Health website at http://www.liebertpub.com/jwh. Journal of Women's Health is the Official Journal of the Academy of Women's Health.

About the Society

Academy of Women's Health (http://academyofwomenshealth.org) is an interdisciplinary, international association of physicians, nurses, and other health professionals who work across the broad field of women's health, providing its members with up-to-date advances and options in clinical care that will enable the best outcomes for their women patients. The Academy's focus includes the dissemination of translational research and evidence-based practices for disease prevention, diagnosis, and treatment for women across the lifespan.

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Racial and ethnic disparities in awareness of heart disease risk in women

7 June 2012

Councils protect their growers from GE

In the vacuum of inaction left by the National Government, local councils are having to lead the way in keeping New Zealand free of genetic engineering, the Green Party said today.

Hastings District Council have given official support to the GE free movement, voting unanimously in support of a proposal to declare the district GE free.

This is an exciting move made by the Hastings District Council but they have been forced to take this action because the National Government is refusing to, said the Green Party GE spokesperson Steffan Browning.

This region by region approach will be able to protect some growers but is not the real solution New Zealand needs.

The growers in the Hawkes Bay have identified that they need to be able to reap the significant branding benefits of being able to market GE free food, said Mr Browning.

These producers are receiving demand for GE free products and we need to be protecting their market for them

There are not sufficient liability protections for non GE growers should their produce get contaminated.

Farmers in Australia are already experiencing loss of income due to contamination by GE crops.

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Councils protect their growers from Genetic Engineering