James interviews Dr. Deanna Minich of PMLI and Food Spirit
Deanna Minich, PhD is an innovator in the world of food as medicine and VP of Education at the Personalized Medicine Lifestyle Institute. We look at the futu...

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Prof. Timothy O #39;Brien, Director of REMEDI - The Centre for Cell Manufacturing Ireland
Prof. Timothy O #39;Brien, Director of REMEDI, speaks about regenerative medicine ahead of the launch of the Centre for Cell Manufacturing Ireland http://www.nuigalway....

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Regenerative medicine with combination of cells and biomaterials
Tissue engineer Dr Jess Frith is combining cells with biomaterials to reconstruct body tissues in the lab, on the path to one day potentially treating osteop...

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When it comes to finding cures for heart disease scientists are working to their own beat. That's because they may have finally developed a tissue model for the human heart that can bridge the gap between animal models and human patients. These models exist for other organs, but for the heart, this has been elusive. Specifically, the researchers generated the tissue from human embryonic stem cells with the resulting muscle having significant similarities to human heart muscle. This research was published in the February 2014 issue of The FASEB Journal.

"We hope that our human engineered cardiac tissues will serve as a platform for developing reliable models of the human heart for routine laboratory use," said Kevin D. Costa, Ph.D., a researcher involved in the work from the Cardiovascular Cell and Tissue Engineering Laboratory, Cardiovascular Research Center, Icahn School of Medicine at Mt. Sinai, in New York, NY. "This could help revolutionize cardiology research by improving the ability to efficiently discover, design, develop and deliver new therapies for the treatment of heart disease, and by providing more efficient screening tools to identify and prevent cardiac side effects, ultimately leading to safer and more effective treatments for patients suffering from heart disease."

To make this advance, Costa and colleagues cultured human engineered cardiac tissue, or hECTs, for 7-10 days and they self-assembled into a long thin heart muscle strip that pulled on the end-posts and caused them to bend with each heart beat, effectively exercising the tissue throughout the culture process. These hECTs displayed spontaneous contractile activity in a rhythmic pattern of 70 beats per minute on average, similar to the human heart. They also responded to electrical stimulation. During functional analysis, some of the responses known to occur in the natural adult human heart were also elicited in hECTs through electrical and pharmacological interventions, while some paradoxical responses of hECTs more closely mimicked the immature or newborn human heart. They also found that these human engineered heart tissues were able to incorporate new genetic information carried by adenovirus.

"We've come a long way in our understanding of the human heart," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal, "but we still lack an adequate tissue model which can be used to test promising therapies and model deadly diseases. This advance, if it proves successful over time, will beat anything that's currently available."

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Tissue that is typically discarded in routine hip replacement operations may offer a rich untapped source of stem cells that could be banked for later use in regenerative medicine, where patients' own cells are used to treat disease or repair failing organs.

This was the implication of a new study led by the University of New South Wales (UNSW) in Australia, published online recently in the journal Stem Cells Translational Medicine.

Study leader Prof. Melissa Knothe Tate and colleagues say, given the tens of thousands of hip replacements performed every year, their findings could have "profound implications" for clinical use.

Currently, to grow new bone or tissue after an infection, injury or the removal of a tumor, if the patient has not preserved stem cells in a cell bank (which is the case for the vast majority of older adults), the stem cells have to come from a donor, or the patient has to undergo surgery to have them harvested from their own bone marrow.

Prof. Knothe Tate explains how their study findings, which now need to be tested clinically, could offer a new source of stem cells for older patients:

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The development of human embryonic stem cells, which have the ability to form any cell in the body, may enable us to repair tissues damaged by injury or disease. Initially, these cells could only be obtained through methods that some deemed ethically unacceptable, but researchers eventually developed a combination of genes that could reprogram most cells into an embryonic-like state. That worked great for studies, but wasn't going to work for medical uses, since one of the genes involved has been associated with cancer.

Researchers have since been focusing on whittling down the requirements needed for getting a cell to behave like a stem cell. Now, researchers have figured out a radically simplified process: expose the cells to acidic conditions, then put them in conditions that stem cells grow well in. After a week, it's possible to direct these cells into a state that's even more flexible than embryonic stem cells.

The catalyst for this work is rather unusual. The researchers were motivated by something that works in plants: expose individual plant cells to acidic conditions, grow them in hormones that normally direct plant development, and you can get a whole plant back out. But we're talking about plants here, which evolved with multicellularity and with specialized tissues in a lineage that's completely separate from that of animals. So there's absolutely no reason to suspect that animal cells would react in a similar way to acid treatmentand a number of reasons to expect they wouldn't.

And yet the researchers went ahead and tried anyway. And, amazingly, it worked.

The treatments weren't especially harshonly a half-hour in a pH of 5.45.8. Afterward, the cells were placed in the same culture medium that stem cells are grown in. Many of the cells died, and the ones that were left didn't proliferate like stem cells do. But, over the course of a week, the surviving cells began to activate the genes that are normally expressed by stem cells. This was initially tried with precursors to blood cells, but it turned out to work with a huge variety of tissues: brain, skin, muscle, fat, bone marrow, lung, and liver (all of them obtained from micethis hasn't been tried with human cells yet).

While these cells didn't divide like stem cells, they did behave like them. Injecting them into embryos showed that they were incorporated into every tissue in the body, meaning they had the potential to form any cell. That suggests they are a distinct class of cell from the other ones we're aware of (the researchers call them STAP cells).

But, if they don't grow in culture, it's hard to use or study them. So, the authors tried various combinations of hormones and growth factors that stem cells like. One combination got some of the STAP cells to grow, after which they behaved very much like embryonic stem cells. But a second combination of growth factors got the cells to contribute to non-embryonic tissues, like the placenta, as well. So, in this sense, they seem to be even more flexible than embryonic stem cells, and seem more akin to one of the first cells formed after fertilization.

The people behind this development have done a tremendous amount of work, so much that it was spread across two papers. Still, like many good results, it raises lots of other questions. Many cells in our bodies get exposed to acidic conditions every daywhy do those manage to stably maintain their identity? A related question is what goes on at a molecular level inside the cell after acid treatment. Understanding that will help us learn more about the stem cell fate itself.

And then there are the practical questions. How close are these STAP cells to an actual embryonic cell, in terms of the state of its DNA and gene expression? And, if there are differences, are they significant enough to prevent these cells from being used in safe and efficient medical treatments?

January 30, 2014. DOI: 10.1038/nature12968, 10.1038/nature12969 (About DOIs).

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Newswise Cancer drugs that recruit antibodies from the bodys own immune system to help kill tumors have shown much promise in treating several types of cancer. However, after initial success, the tumors often return.

A new study from MIT reveals a way to combat these recurrent tumors with a drug that makes them more vulnerable to the antibody treatment. This drug, known as cyclophosphamide, is already approved by the Food and Drug Administration (FDA) to treat some cancers.

Antibody drugs work by marking tumor cells for destruction by the bodys immune system, but they have little effect on tumor cells that hide out in the bone marrow. Cyclophosphamide stimulates the immune response in bone marrow, eliminating the reservoir of cancer cells that can produce new tumors after treatment.

Were not talking about the development of a new drug, were talking about the altered use of an existing therapy, says Michael Hemann, the Eisen and Chang Career Development Associate Professor of Biology, a member of MITs Koch Institute for Integrative Cancer Research, and one of the senior authors of the study. We can operate within the context of existing treatment regimens but hopefully achieve drastic improvement in the efficacy of those regimens.

Jianzhu Chen, the Ivan R. Cottrell Professor of Immunology and a member of the Koch Institute, is also a senior author of the paper, which appears in the Jan. 30 issue of the journal Cell. The lead author is former Koch Institute postdoc Christian Pallasch, now at the University of Cologne in Germany.

Finding cancers hiding spots

Antibody-based cancer drugs are designed to bind to proteins found on the surfaces of tumor cells. Once the antibodies flag the tumor cells, immune cells called macrophages destroy them. While many antibody drugs have already been approved to treat human cancers, little is known about the best ways to deploy them, and what drugs might boost their effects, Hemann says.

Antibodies are very species-specific, so for this study, the researchers developed a strain of mice that can develop human lymphomas (cancers of white blood cells) by implanting them with human blood stem cells that are genetically programmed to become cancerous. Because these mice have a human version of cancer, they can be used to test drugs that target human tumor cells.

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Stem Cell Therapy: Non-Surgical Treatment for Neck Pain Whiplash
An informative guide to how Platelet Rich Plasma can heal the tough minority of whiplash cases where traditional treatments do not offer significant relief. For more information, visit http://www.stemcell...

By: StemCell ARTS

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Stress before conception can cause changes to a woman's eggs These changes can lead to genetic differences in her future children Even stress during the woman's teens can affect her future offspring

By Emma Innes

PUBLISHED: 10:56 EST, 31 January 2014 | UPDATED: 10:58 EST, 31 January 2014

A woman's levels of stress even before conception can influence her child's ability to deal with stressful situations

All women know that their lifestyle during pregnancy can have important effects on their childs future health.

Now research suggests that a womans levels of stress even before conception can influence her childs ability to deal with stressful situations.

Research has shown that stress before conception can cause genetic changes to children because it can cause changes in the mother-to-bes eggs.

The research, conducted by the University of Haifa, in Israel, was carried out on rats but scientists believe the conclusions can be applied to humans.

Researcher Hiba Zaidan said: The systemic similarity in many instances between us and rats raises questions about the transgenerational influences in humans as well.

If until now we saw evidence only of behavioural effects, now weve found proof of effects at the genetic level.

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Macaques in China are the first primates born with genomes engineered by precision gene-targeting methods.

Prime cuts: The faint ladder-rung patterns in an image of a DNA gel show that genome editing successfully modified a gene in two macaque infants (central columns), but not in an untreated animal (right column). The left column shows a size standard.

Researchers at Nanjing Medical University and Yunnan Key Laboratory of Primate Biomedical Research in Kunming, China, have created genetically modified monkeys using a new method of DNA engineering known as Crispr. The infant macaques show that targeted genome editing is feasible in primatesa potential boon for scientists studying complex diseases, including neurological ones, and an advance that suggests that the method could one day work in humans. The work was reported in the journal Cell on Thursday.

Scientists have previously used the new genome-editing technique to delete, insert, and modify DNA in human cells and other animal cells grown in petri dishes. The method has also been used to create gene modifications in whole animals such as mice, rats, and zebrafish. The new study shows for the first time that Crispr can create viable primates with genomes modified at specific targeted genes.

The Chinese researchers injected single-cell macaque embryos with RNAs to guide the genome-editing process. The team modified three genes in the monkeys: one that regulates metabolism, another that regulates immune cell development and a third that regulates stem cells and sex determination, says study coauthor Wezhi Ji, a researcher at the Yunnan Key Laboratory of Primate Biomedical Research. The researchers found that the genome-editing tools created multiple changes in their target genes at different stages of embryonic development. The infant monkeys are too young for the team to yet determine if the genetic changes have an effect on physiology or behavior, says Ji. But, he adds, data from this species should be very useful for curing human disease and improving human health.

Researchers have previously created a handful of transgenic monkeys, such as a rhesus macaque that produces the disease-causing version of theHuntingtons gene. Researchers at Emory University in Atlanta created this avatar of human disease by injecting a virus into macaque eggs. The virus delivered a disease-version of the human Huntingtons gene into a random location in the monkeys genome.

Primate pioneers: Twin infant macaques whose genomes were modified within three different genes.

Crispr, on the other hand, can be used to insert, delete, or rewrite a DNA sequence at a specific location within a genome. Like the random viral insertion used by the Emory team, the Crispr method employed by Ji and colIeagues can create genetically modified animals in a single generation, an important consideration for researchers working with animals that can take three years to reach sexual maturity and are expensive and difficult to rear.

Others say they are anxious to use Crispr to create their own monkeys. Robert Desimone, director of MITs McGovern Brain Institute for Brain Research, says he and colleagues are planning on using genome editing to create modified monkeys. He says its possible the success of the Chinese researchers will encourage other groups to use primates in their work. Although mice are giving us tremendous insight into basic brain biology and the biology of the disease, theres still a big gap in between the mouse brain and the monkey brain, says Desimone.

For example, he says, lots of drugs that work in mice to treat disease dont work in humans. Desimone says hes hoping that some success in monkeys will interest drug companies in neurosciencealluding to a recent trend of large drug companies abandoning research on brain diseases because the work often proved unsuccessful. The hope is that disease and drug research in monkeys will more likely lead to therapies in humans because the primates share complex behaviors and social structures. We are cautiously optimistic, says Desimone.

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Monkeys Modified with Genome Editing

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A joint research team led by an NUI Galwayscientist has found that changes in a little-known gene called ULK4 were observed in individuals with schizophrenia.

A rare risk factor which is associated with mental illnesses like schizophrenia has been identified by a joint research team led by an NUI Galway (NUIG) scientist.

The research team has found that changes in a little-known gene called ULK4 were observed in individuals with schizophrenia.

The findings are published today in the Journal of Cell Science.

Prof Sanbing Shen of NUIGs Regenerative Medicine Institute, who led the research, says that this could contribute to more effective treatment of the condition in time.

The multi-institutional study examined a database of up to 7,000 people, half of whom had schizophrenia and half of whom did not.

Many genetic risk factors have been associated with schizophrenia and other mental illnesses such as bipolar disorder and depression, but Prof Shen and his team were able to characterise how the ULK4 gene functions in the brain.

He and his colleagues found that when levels of ULK4 were decreased, through mutation or deletion, the neuronal (brain) cells tend to function less well.

This leads to reduced synaptic function and other changes that are also known as risk factors of schizophrenia.

Prof Shen said ULK4 is essential for the formation of the nerve fibres which connect the two sides of the brain.

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Risk factor linked to schizophrenia identified by NUI Galway scientist

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PARIS, Jan. 31 (UPI) -- Female development in the fetus is activated by the FOXL2 gene, blocking male gene expression, meaning the default of sex of a fetus is not female.

Researchers at the INRA, in Paris, France, have identified the FOXL2 gene as responsible for female differentiation.

Females were long believed to be the "default" sex of a fetus, with a gene on the Y chromosome leading to male differentiation. But in some cases an XX fetus, programmed to be female, fails to develop ovaries and instead is born with male characteristics.

On analyzing the genes of such fetuses, researches identified the FOXL2 gene, which acts like a "defender of the ovary," silencing the male genes as the ovary develops and well into adulthood. These findings have been published in the journal Current Biology.

Using goat embryos, researchers silenced the FOXL2 gene and witnessed that XX fetuses developed testes instead of ovaries, explaining the development of male characteristics in XX fetuses.

The FOXL2 gene had previously been linked to premature menopause in young women. Techniques are being developed based on the goat model to treat certain types of infertility.

[INRA] [Current Biology]

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Female differentiation in the fetus is not default, has to be activated

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Niu et al., Cell

Twin cynomolgus monkeys born in China are the first with mutations in specific target genes.

The ultimate potential of precision gene-editing techniques is beginning to be realised. Today, researchers in China report the first monkeys engineered with targeted mutations1, an achievement that could be a stepping stone to making more realistic research models of human diseases.

Xingxu Huang, a geneticist at the Model Animal Research Center of Nanjing University in China, and his colleagues successfully engineered twin cynomolgus monkeys (Macaca fascicularis) with two targeted mutations using the CRISPR/Cas9 system a technology that has taken the field of genetic engineering by storm in the past year. Researchers have leveraged the technique to disrupt genes in mice and rats2, 3, but until now none had succeeded in primates.

"This is an important step," says Feng Zhang, a synthetic biologist who was not involved in the study, but who has helped to develop CRISPR technology at the Massachusetts Institute of Technology in Cambridge. "It shows that the system is working."

Transgenic mice have long dominated as models for human diseases, in part because scientists have honed a gene-editing method for the animals that uses homologous recombination rare, spontaneous DNA-swapping events to introduce mutations. The strategy works because mice reproduce quickly and in large numbers, but the low rates of homologous recombination make such a method unfeasible in creatures such as monkeys, which reproduce slowly.

"We need some non-human primate models," says Hideyuki Okano, a stem-cell biologist at Keio University in Tokyo. Human neuropsychiatric disorders can be particularly difficult to replicate in the simple nervous systems of mice, he says.

Previous attempts to genetically modify primates have relied on viral methods4, 5, which create mutations efficiently, but at unpredictable locations and in uncontrolled numbers. Prospects for primates brightened with the emergence of the CRISPR/Cas9 gene-editing system, which uses customizable snippets of RNA to guide the DNA-cutting enzyme Cas9 to the desired mutation site.

Huang and his team first tested the technology in a monkey cell line, disrupting each of three genes with 1025% success. Encouraged, the scientists subsequently targeted the three genes simultaneously in more than 180 single-celled monkey embryos. Ten pregnancies resulted from 83 embryos that were implanted, one of which led to the birth of a pair with mutations in two genes: Ppar-, which helps to regulate metabolism, and Rag1, which is involved in healthy immune function.

Stem-cell researcher Rudolf Jaenisch of the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, calls the result an interesting demonstration, but says that it offers little scientific insight. "The next step is to see if we can learn anything from it," says Jaenisch, who pioneered the use of transgenic mice in the 1970s.

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A central question has been answered regarding a protein that plays an essential role in the bacterial immune system and is fast becoming a valuable tool for genetic engineering. A team of researchers with the Lawrence Berkeley National Laboratory (Berkeley Lab) and the University of California (UC) Berkeley have determined how the bacterial enzyme known as Cas9, guided by RNA, is able to identify and degrade foreign DNA during viral infections, as well as induce site-specific genetic changes in animal and plant cells. Through a combination of single-molecule imaging and bulk biochemical experiments, the research team has shown that the genome-editing ability of Cas9 is made possible by the presence of short DNA sequences known as "PAM," for protospacer adjacent motif.

"Our results reveal two major functions of the PAM that explain why it is so critical to the ability of Cas9 to target and cleave DNA sequences matching the guide RNA," says Jennifer Doudna, the biochemist who led this study. "The presence of the PAM adjacent to target sites in foreign DNA and its absence from those targets in the host genome enables Cas9 to precisely discriminate between non-self DNA that must be degraded and self DNA that may be almost identical. The presence of the PAM is also required to activate the Cas9 enzyme."

With genetically engineered microorganisms, such as bacteria and fungi, playing an increasing role in the green chemistry production of valuable chemical products including therapeutic drugs, advanced biofuels and biodegradable plastics from renewables, Cas9 is emerging as an important genome-editing tool for practitioners of synthetic biology.

"Understanding how Cas9 is able to locate specific 20-base-pair target sequences within genomes that are millions to billions of base pairs long may enable improvements to gene targeting and genome editing efforts in bacteria and other types of cells," says Doudna who holds joint appointments with Berkeley Lab's Physical Biosciences Division and UC Berkeley's Department of Molecular and Cell Biology and Department of Chemistry, and is also an investigator with the Howard Hughes Medical Institute (HHMI).

Doudna is one of two corresponding authors of a paper describing this research in the journal Nature. The paper is titled "DNA interrogation by the CRISPR RNA-guided endonuclease Cas9." The other corresponding author is Eric Greene of Columbia University. Co-authoring this paper were Samuel Sternberg, Sy Redding and Martin Jinek.

Bacterial microbes face a never-ending onslaught from viruses and invasive snippets of nucleic acid known as plasmids. To survive, the microbes deploy an adaptive nucleic acid-based immune system that revolves around a genetic element known as CRISPR, which stands for Clustered Regularly Interspaced Short Palindromic Repeats. Through the combination of CRISPRs and RNA-guided endonucleases, such as Cas9, ("Cas" stands for CRISPR-associated), bacteria are able to utilize small customized crRNA molecules (for CRISPR RNA) to guide the targeting and degradation of matching DNA sequences in invading viruses and plasmids to prevent them from replicating. There are three distinct types of CRISPR-Cas immunity systems. Doudna and her research group have focused on the Type II system which relies exclusively upon RNA-programmed Cas9 to cleave double-stranded DNA at target sites.

"What has been a major puzzle in the CRISPR-Cas field is how Cas9 and similar RNA-guided complexes locate and recognize matching DNA targets in the context of an entire genome, the classic needle in a haystack problem," says Samuel Sternberg, lead author of the Nature paper and a member of Doudna's research group. "All of the scientists who are developing RNA-programmable Cas9 for genome engineering are relying on its ability to target unique 20-base-pair long sequences inside the cell. However, if Cas9 were to just blindly bind DNA at random sites across a genome until colliding with its target, the process would be incredibly time-consuming and probably too inefficient to be effective for bacterial immunity, or as a tool for genome engineers. Our study shows that Cas9 confines its search by first looking for PAM sequences. This accelerates the rate at which the target can be located, and minimizes the time spent interrogating non-target DNA sites."

Doudna, Sternberg and their colleagues used a unique DNA curtains assay and total internal reflection fluorescence microscopy (TIRFM) to image single molecules of Cas9 in real time as they bound to and interrogated DNA. The DNA curtains technology provided unprecedented insights into the mechanism of the Cas9 target search process. Imaging results were verified using traditional bulk biochemical assays.

"We found that Cas9 interrogates DNA for a matching sequence using RNA-DNA base-pairing only after recognition of the PAM, which avoids accidentally targeting matching sites within the bacterium's own genome," Sternberg says. "However, even if Cas9 somehow mistakenly binds to a matching sequence on its own genome, the catalytic nuclease activity is not triggered without a PAM being present. With this mechanism of DNA interrogation, the PAM provides two redundant checkpoints that ensure that Cas9 can't mistakenly destroy its own genomic DNA."

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A new gene-editing technique could lead to more useful animal models of disease, and perhaps one day more effective gene therapy for humans

Genetically modified long-tailed macaques. Credit: Cell, Niu et al.

Like many babies, the wide-eyed twins are cute. The fact that they are macaque monkeys is almost beside the point. What is not beside the point, however, is their genetic heritage. These baby macaques are, as reported inCell, the first primates to have been genetically modified using an extremely precise gene-editing tool based on the so-called CRISPR/Cas system.

Conducted by researchers in China, the new study is significant because it paves the way for the custom development of laboratory monkeys with genetic profiles that are similar to those found in humans with certain medical disorders. Although mice and rats have long been the animals of choice when creating living models of human disease, they have not been very helpful for studying neurological conditions such as autism and Alzheimers disease; the differences between rodent and human brains are just too great.

To be sure, a few other genetically modified monkeys have been born over the past decade and a half, but the methods used to alter their DNA were not as efficient or as easy to use as the CRISPR/Cas technology. The amount of genome engineering in monkeys is pretty small, says George Church, a professor of genetics at Harvard Medical School.So yes, this [paper] is a pretty big deal.

CRISPR stands for clustered regularly interspaced short palindromic repeats and refers to what at first glance appear to be meaningless variations and repeats in the sequence of molecular letters (A, T, C and G) that make up DNA. These CRISPR patterns are found in many bacteria and most archaea (an ancient group of bacteria that is now considered to be different enough from other one-celled organisms to merit is own taxonomic kingdom, along with bacteria, protists, fungi, plants and animals).

First identified in bacteria in 1987, CRISPR elements started being widely used to create genetic engineering tools only in 2013. It took that long to figure out that the patterns actually served a purpose, determine out what that purpose washelping archaea and bacteria to recognize and defend themselves against virusesand then adapt that original function to a new goal.

Basically, biologists learned that certain proteins associated with the CRISPR system (dubbed, straightforwardly enough, CRISPR-associated, or Cas, proteins) act like scissors that cut any strands of DNA they come across. These cutting proteins, in turn, are guided to specific strands of DNA by complementary pieces of RNA (a sister molecule to DNA). The bacteria generate specific guide strands of RNA whenever they encounter a virus that is starting to hijack their cellular machinery. The guide-RNA complements the viral DNA, which is how the Cas proteins know where to cut. The bacteria then keep a copy of the viral DNA in their own genetic sequence between two CRISPR elements for future reference in case a similar virus tries to cause trouble later on.

In the past couple of years researchers have learned how to trick the Cas proteins into targeting and slicing through a sequence of DNA of their own choosing. By developing strands of RNA that precisely complement the part of the DNA molecule that they want to change, investigators can steer the Cas proteins to a predesignated spot and cut out enough genetic material to permanently disrupt the usual expression of the DNA molecule at that location.

In essence, scientists have turned a bacterial self-defense mechanism into an incredibly precise gene-editing tool. By some accounts CRISPR technology has been successfully tried out on 20 different kinds of higher organisms (meaning higher than bacteria) in just the past year or so.

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New Biotech Makes It Much Easier to Genetically Modify Monkeys

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News Release

Short DNA sequences known as PAM (shown in yellow) enable the bacterial enzyme Cas9 to identify and degrade foreign DNA, as well as induce site-specific genetic changes in animal and plant cells. The presence of PAM is also required to activate the Cas9 enzyme. (Illustration by KC Roeyer.)

A central question has been answered regarding a protein that plays an essential role in the bacterial immune system and is fast becoming a valuable tool for genetic engineering. A team of researchers with the Lawrence Berkeley National Laboratory (Berkeley Lab) and the University of California (UC) Berkeley have determined how the bacterial enzyme known as Cas9, guided by RNA, is able to identify and degrade foreign DNA during viral infections, as well as induce site-specific genetic changes in animal and plant cells. Through a combination of single-molecule imaging and bulk biochemical experiments, the research team has shown that the genome-editing ability of Cas9 is made possible by the presence of short DNA sequences known as PAM, for protospacer adjacent motif.

Our results reveal two major functions of the PAM that explain why it is so critical to the ability of Cas9 to target and cleave DNA sequences matching the guide RNA, says Jennifer Doudna, the biochemist who led this study. The presence of the PAM adjacent to target sites in foreign DNA and its absence from those targets in the host genome enables Cas9 to precisely discriminate between non-self DNA that must be degraded and self DNA that may be almost identical. The presence of the PAM is also required to activate the Cas9 enzyme.

With genetically engineered microorganisms, such as bacteria and fungi, playing an increasing role in the green chemistry production of valuable chemical products including therapeutic drugs, advanced biofuels and biodegradable plastics from renewables, Cas9 is emerging as an important genome-editing tool for practitioners of synthetic biology.

Understanding how Cas9 is able to locate specific 20-base-pair target sequences within genomes that are millions to billions of base pairs long may enable improvements to gene targeting and genome editing efforts in bacteria and other types of cells, says Doudna who holds joint appointments with Berkeley Labs Physical Biosciences Division and UC Berkeleys Department of Molecular and Cell Biology and Department of Chemistry, and is also an investigator with the Howard Hughes Medical Institute (HHMI).

Jennifer Doudna and Samuel Sternberg used a combination of single-molecule imaging and bulk biochemical experiments to show how the RNA-guided Cas9 enzyme is able to locate specific 20-base-pair target sequences within genomes that are millions to billions of base pairs long. (Photo by Roy Kaltschmdit)

Doudna is one of two corresponding authors of a paper describing this research in the journal Nature. The paper is titled DNA interrogation by the CRISPR RNA-guided endonuclease Cas9. The other corresponding author is Eric Greene of Columbia University. Co-authoring this paper were Samuel Sternberg, Sy Redding and Martin Jinek.

Bacterial microbes face a never-ending onslaught from viruses and invasive snippets of nucleic acid known as plasmids. To survive, the microbes deploy an adaptive nucleic acid-based immune system that revolves around a genetic element known as CRISPR, which stands for Clustered Regularly Interspaced Short Palindromic Repeats. Through the combination of CRISPRs and RNA-guided endonucleases, such as Cas9, (Cas stands for CRISPR-associated), bacteria are able to utilize small customized crRNA molecules (for CRISPR RNA) to guide the targeting and degradation of matching DNA sequences in invading viruses and plasmids to prevent them from replicating. There are three distinct types of CRISPRCas immunity systems. Doudna and her research group have focused on the Type II system which relies exclusively upon RNA-programmed Cas9 to cleave double-stranded DNA at target sites.

What has been a major puzzle in the CRISPRCas field is how Cas9 and similar RNA-guided complexes locate and recognize matching DNA targets in the context of an entire genome, the classic needle in a haystack problem, says Samuel Sternberg, lead author of the Nature paper and a member of Doudnas research group. All of the scientists who are developing RNA-programmable Cas9 for genome engineering are relying on its ability to target unique 20-base-pair long sequences inside the cell. However, if Cas9 were to just blindly bind DNA at random sites across a genome until colliding with its target, the process would be incredibly time-consuming and probably too inefficient to be effective for bacterial immunity, or as a tool for genome engineers. Our study shows that Cas9 confines its search by first looking for PAM sequences. This accelerates the rate at which the target can be located, and minimizes the time spent interrogating non-target DNA sites.

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Running with genetic scissors: how a breakthrough technology works

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Advances in molecular biology and human genetics, coupled with the completion of the Human Genome Project and the increasing power of quantitative genetics to identify disease susceptibility genes, are contributing to a revolution in the practice of medicine. In the 21st century, practicing physicians will focus more on defining genetically determined disease susceptibility in individual patients. This strategy will be used to prevent, modify, and treat a wide array of common disorders that have unique heritable risk factors such as hypertension, obesity, diabetes, arthrosclerosis, and cancer.

The Division of Genetic Medicine provides an academic environment enabling researchers to explore new relationships between disease susceptibility and human genetics. The Division of Genetic Medicine was established January 1, 1999 under the leadership of its founding Director, Alfred L. George, Jr., M.D.,and an accelerated plan is underway to establish a core group of faculty, and develop both research and clinical programs. Equipped with state-of-the-art research tools and facilities, our faculty is advancing knowledge of the common genetic determinants of cancer, epilepsy, congenital gastrointestinal disorders, and heart disease. The Division supports the operation of high-throughput DNA Sequencing and Allele-Typing core facilities that are available to other Vanderbilt University faculty and researchers from other institutions. We also work jointly with the Vanderbilt-Ingram Cancer Center to support a Family Cancer Risk Service for counseling patients and their families who have an inherited predisposition to various malignancies.

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PUBLIC RELEASE DATE:

30-Jan-2014

Contact: Scott LaFee slafee@ucsd.edu 619-543-6163 University of California - San Diego

In a study published in the January 31, 2014 issue of Science, an international team led by scientists at the University of California, San Diego School of Medicine report doubling the number of known causes for the neurodegenerative disorder known as hereditary spastic paraplegia. HSP is characterized by progressive stiffness and contraction of the lower limbs and is associated with epilepsy, cognitive impairment, blindness and other neurological features.

Over several years, working with scientific colleagues in parts of the world with relatively high rates of consanguinity or common ancestry, UC San Diego researchers recruited a cohort of more than 50 families displaying autosomal recessive HSP the largest such cohort assembled to date. The scientists analyzed roughly 100 patients from this cohort using a technique called whole exome sequencing, which focuses on mapping key portions of the genome. They identified a genetic mutation in almost 75 percent of the cases, half of which were in genes never before linked with human disease.

"After uncovering so many novel genetic bases of HSP, we were in the unique position to investigate how these causes link together. We were able to generate an 'HSP-ome,' a map that included all of the new and previously described causes," said senior author Joseph G. Gleeson, MD, Howard Hughes Medical Institute investigator, professor in the UC San Diego departments of Neurosciences and Pediatrics and at Rady Children's Hospital-San Diego, a research affiliate of UC San Diego.

The HSP-ome helped researchers locate and validate even more genetic mutations in their patients, and indicated key biological pathways underlying HSP. The researchers were also interested in understanding how HSP relates to other groups of disorders. They found that the HSP-ome links HSP to other more common neurodegenerative disorders, such as Alzheimer's disease and amyotrophic lateral sclerosis.

"Knowing the biological processes underlying neurodegenerative disorders is seminal to driving future scientific studies that aim to uncover the exact mechanisms implicated in common neurodegenerative diseases, and to indicate the path toward development of effective treatments," said Gleeson.

"I believe this study is important for the neurodegenerative research community," said co-lead author Gaia Novarino, PhD, a post-doctoral scholar in Gleeson's lab. "But more broadly, it offers an illustrative example of how, by utilizing genomics in specific patient populations, and then building an 'interactome,' we greatly expand knowledge around unknown causes of disease."

"This is very exciting since identifying the biological processes in neurological disorders is the first step toward the development of new treatments," agreed co-lead author Ali G. Fenstermaker. "We identified several promising targets for development of new treatments."

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Scientists discover new genetic forms of neurodegeneration

Recommendation and review posted by Bethany Smith

In a study published in the January 31, 2014 issue of Science, an international team led by scientists at the University of California, San Diego School of Medicine report doubling the number of known causes for the neurodegenerative disorder known as hereditary spastic paraplegia. HSP is characterized by progressive stiffness and contraction of the lower limbs and is associated with epilepsy, cognitive impairment, blindness and other neurological features.

Over several years, working with scientific colleagues in parts of the world with relatively high rates of consanguinity or common ancestry, UC San Diego researchers recruited a cohort of more than 50 families displaying autosomal recessive HSP -- the largest such cohort assembled to date. The scientists analyzed roughly 100 patients from this cohort using a technique called whole exome sequencing, which focuses on mapping key portions of the genome. They identified a genetic mutation in almost 75 percent of the cases, half of which were in genes never before linked with human disease.

"After uncovering so many novel genetic bases of HSP, we were in the unique position to investigate how these causes link together. We were able to generate an 'HSP-ome,' a map that included all of the new and previously described causes," said senior author Joseph G. Gleeson, MD, Howard Hughes Medical Institute investigator, professor in the UC San Diego departments of Neurosciences and Pediatrics and at Rady Children's Hospital-San Diego, a research affiliate of UC San Diego.

The HSP-ome helped researchers locate and validate even more genetic mutations in their patients, and indicated key biological pathways underlying HSP. The researchers were also interested in understanding how HSP relates to other groups of disorders. They found that the HSP-ome links HSP to other more common neurodegenerative disorders, such as Alzheimer's disease and amyotrophic lateral sclerosis.

"Knowing the biological processes underlying neurodegenerative disorders is seminal to driving future scientific studies that aim to uncover the exact mechanisms implicated in common neurodegenerative diseases, and to indicate the path toward development of effective treatments," said Gleeson.

"I believe this study is important for the neurodegenerative research community," said co-lead author Gaia Novarino, PhD, a post-doctoral scholar in Gleeson's lab. "But more broadly, it offers an illustrative example of how, by utilizing genomics in specific patient populations, and then building an 'interactome,' we greatly expand knowledge around unknown causes of disease."

"This is very exciting since identifying the biological processes in neurological disorders is the first step toward the development of new treatments," agreed co-lead author Ali G. Fenstermaker. "We identified several promising targets for development of new treatments."

Story Source:

The above story is based on materials provided by University of California, San Diego Health Sciences. Note: Materials may be edited for content and length.

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New genetic forms of neurodegeneration discovered

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AP Psychology: EvolutionaryPsych Genetics or Environment with Mrs. Rice
AP Psychology: EvolutionaryPsych Genetics or Environment with Mrs. Rice For our Genetics or Enviornment chart Activity in class.

By: Amanda Rice

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AP Psychology: EvolutionaryPsych Genetics or Environment with Mrs. Rice - Video

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Hagmann Report On Full Spectrum Survival How Tattoos Change Genetics 10 14 2013
we have great shows here coast to coast am ALTERNATIVE shows these guys gave me the ok to post there shows so dont repost them they will take them down Stay ...

By: InframeAlternative

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Hagmann Report On Full Spectrum Survival & How Tattoos Change Genetics 10 14 2013 - Video

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Genetics Since Mendel

By: Christie Ariail

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Genetics Since Mendel - Video

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Population genetics - Founder effect problem solution
In population genetics, the founder effect is the loss of genetic variation that occurs when a new population is established by a very small number of indivi...

By: GeneticsLessons

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Population genetics - Founder effect problem solution - Video

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In 2006 I helped my 25-year-old son Jamal locate his biological families. I hoped this reunion would help him overcome some of the challenges he was wrestling with on his path to adulthood. I was thrilled when the families of both his white mother and his black father welcomed him. But I was unprepared for the discovery of how much he had in common with his birth parents: not just appearance, but also many personality traits, talents and problems.

When I adopted in 1981, I believed -- like many social scientists and adoption professionals at that time -- that nurture was everything, each infant a blank slate awaiting parental inscription. Even when Jamal was a young child, I recognized that this idea was too simple, that my son had many attributes different from those of anyone else in my family. Still, I was surprised by these reunion revelations.

The adoption theory that I'd absorbed over the years never mentioned genetic heritage. Jamal's difficulty finding his way as a young adult, I was told, might stem from a number of psychological factors. First was the loss of a birth mother with whom he had bonded in utero -- a "primal wound" that supposedly made it difficult for him to bond with an adoptive mother. This idea never resonated with me, for we always had a close connection, with a lot of emotional and verbal sharing. Even in our most troubled times, we never lost contact, and he often confided in me. If anything, I saw him as too close to me, his only parent.

More compelling was the idea that he had been affected by the fetal environment of a stressed teenage birth mother, who probably drank and smoked. This, possibly combined with a weak sense of self deriving from a loss of ethnicity and family history, especially prevalent in the transracially adopted, might help to explain why he chose a life outside the mainstream, one that for many years involved heavy marijuana and alcohol use.

None of these theories, however, prepared me for the shock of finding that my son's birth mother and father -- out of touch with each other for 25 years -- had both struggled with drug addiction throughout their lives. I was especially surprised because in my phone conversations and a visit with them, I had seen that they (like Jamal) were charming and intelligent people. I learned, however, that substance abuse had taken a toll on their lives, especially the father's.

Reunion has helped Jamal secure a stronger sense of self, especially since he found mixed-race heritage on both sides. His mother married another black man and had three more biracial children, and his father's extended family is multiracial as well. But reunion also added many complications to his life as he has tried to reconcile the heritage of what he calls his "three families." Only gradually, through moving to Louisiana for six months and living first with his birth mother and then with his birth father, did Jamal acknowledge their shared substance abuse problems. This realization led him for the first time to enter a recovery program, something his birth parents have never done. He sought to overcome the negative part of his birth heritage so that he could build on the positive. Recently, I asked Jamal how he was different from his birth father.

"Not a heck of a lot," he replied. "But I have better tools."

Jamal's reunion experience led me to undertake my own search, a quest to understand genetics and how they might impact adoption. Perhaps I hoped to find that nature is everything, and that I could let go of my parental guilt for his problems. As a social scientist with little biological education, I began by looking at science journalism, then turned to the original research. I found that genetics alone could explain neither Jamal's positive behavior nor his addiction; genes provide only probabilistic propensities, not predetermined programming. They provide probabilities for behavior and risk factors for disease but do not indicate whether any individual will sustain a behavior or succumb to a particular mental or physical disorder, or how severe the disease might be.

I found other research that surprised me, especially an interdisciplinary field that I'd never heard of, called behavioral genetics. Though it's not focused on adoption per se, many of its findings are based on the study of adoptees. While I had not known about this field by name, I had heard of some of its more infamous practitioners, like those at the turn of the century who advocated selective breeding and forced sterilization. I also knew about a few more recent behavioral geneticists who published controversial studies of racial differences in IQ. But now I discovered that behavioral genetics had gained legitimacy as a science for its studies on individual differences.

Behavioral genetics tries to explain how much of the variation among individuals' cognitive and psychological traits can be attributed to genetic heritage and how much is due to the environment. Their major methodology is a natural experiment that separates genetic heritage and environment by comparing the similarities and differences among adoptees, adoptive parents, and biological parents, and also between biological and adoptive siblings. In addition, behavioral genetics studies identical twins raised apart. In studies over a number of years in many different countries, researchers concur that identical twins separated at birth and adopted into different families, compared with identical twins raised together by their biological parents, are still very similar on a number of measures of personality, temperament, intelligence, interests and susceptibility to physical and mental disease. Additionally, identical twins raised apart are more similar than fraternal twins raised together.

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Adoption and Genetics: Implications for Adoptive Parents ...

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PUBLIC RELEASE DATE:

29-Jan-2014

Contact: Shaun Mason smason@mednet.ucla.edu 310-206-2805 University of California - Los Angeles

Scientists from UCLA's Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research were today awarded grants totaling more than $3.5 million by California's stem cell agency for their ongoing efforts to advance revolutionary stem cell science in medicine.

Recipients of the awards from the California Institute of Renerative Medicine (CIRM) included Lili Yang ($614,400), who researches how stem cells become rare immune cells; Denis Evseenko ($1,146,468), who is studying the biological niche in which stem cells grow into cartilage; Thomas Otis and Bennet Novitch ($1,148,758), who are using new techniques to study communication between nerve and muscle cells in spinal muscular atrophy; and Samantha Butler ($598,367), who is investigating the molecular elements that drive stem cells to become the neurons in charge of our sense of touch.

"These basic biology grants form the foundation of the revolutionary advances we are seeing in stem cell science," said Dr. Owen Witte, professor and director of the Broad Stem Cell Research Center. "Every cellular therapy that reaches patients must begin in the laboratory with ideas and experiments that will lead us to revolutionize medicine and ultimately improve human life. That makes these awards invaluable to our research effort."

The awards are part of CIRM's Basic Biology V grant program, which fosters cutting-edge research on significant unresolved issues in human stem cell biology, with a focus on unravelling the key mechanisms that determine how stem cells decide which cells they will become. By learning how such mechanisms work, scientists can develop therapies that drive stem cells to regenerate or replace damaged or diseased tissue.

Lili Yang: Tracking special immune cells

The various cells that make up human blood all arise from hematopoietic stem cells. These include special white blood cells called T cells, the "foot soldiers" of the immune system that attack bacteria, viruses and other disease-causing invaders. Among these T cells is a smaller group, a kind of "special forces" unit known as invariant natural killer T cells, or iNKT cells, which have a remarkable capacity to mount immediate and powerful responses to disease when activated and are believed to be important to the immune system's regulation of infections, allergies, cancer and autoimmune diseases such as Type I diabetes and multiple sclerosis.

The iNKT cells develop in small numbers in the blood generally accounting for less than 1 percent of blood cells but can differ greatly in numbers among individuals. Very little is known about how blood stem cells produce iNKT cells.

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Stem cell agency's grants to UCLA help set stage for revolutionary medicine

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