Archive for the ‘Gene Therapy Research’ Category

Scientists have identified a gene variant that seems to strongly raise the risk for Alzheimer's disease, giving a fresh target for research into treatments for the mind-robbing disorder.

The problem gene is not common less than 1 percent of people are thought to have it but it roughly triples the chances of developing Alzheimer's compared with people with the normal version of the gene. It also seems to harm memory and thinking in older people without dementia.

The main reason scientists are excited by the discovery is that what this gene does, and how, might reveal what causes Alzheimer's and ways to prevent it. The gene helps the immune system control inflammation in the brain and clear junk such as the sticky deposits that are the hallmark of the disease. Mutations in the gene might impair these tasks, so treatments to restore the gene's function and quell inflammation might help.

"It points us to potential therapeutics in a more precise way than we've seen in the past," said Dr. William Thies, chief medical and scientific officer of the Alzheimer's Association, which had no role in the research.

It is described in a study by an international group published online Wednesday by the New England Journal of Medicine.

About 35 million people worldwide have dementia, and Alzheimer's is the most common type. In the U.S., about 5million have Alzheimer's. Medicines such as Aricept and Namenda temporarily ease symptoms. There is no known cure.

Until now, only one gene ApoE has been found to have a big impact on Alzheimer's risk. About 17 percent of the population has at least one copy of the problem version of this gene but nearly half of all people with Alzheimer's do. Other genes that have been tied to the disease raise risk only a little, or cause the less common type of Alzheimer's that develops earlier in life, before age 60.

The new gene, TREM2, already has been tied to a couple of other forms of dementia. Researchers led by deCODE Genetics of Iceland homed in on a version of it they identified through mapping the entire genetic code of more than 2,200 Icelanders.

Further tests on 3,550 Alzheimer's patients and more than 110,000 people without dementia in several countries, including the United States, found that the gene variant was more common in Alzheimer's patients.

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Gene triples risk for Alzheimer's, new study shows

CTVNews.ca Staff Published Wednesday, Nov. 14, 2012 10:00PM EST Last Updated Thursday, Nov. 15, 2012 9:24AM EST

A rare mutation of a gene thats normally linked to inflammation could triple the risk of Alzheimers disease, according to new research from an international team of scientists.

Less than 1 per cent of the population has the gene variant, called TREM2. Scientists hope that by studying the gene they will better understand how Alzheimers attacks the brain -- and find a way to stop it.

Their findings were published Wednesday in the New England Journal of Medicine.

About 30 million people around the world have Alzheimers, and that number is expected to rise to 35 million in the next three years.

The incurable disease first destroys the minds ability to remember. Over time, as brain cells are attacked, symptoms worsen and patients lose more of their mental abilities until they are entirely dependent on caregivers.

Until now, its been commonly thought that the disease is caused by Amyloid plaques -- a sticky, toxic material. Based on this theory, pharmaceutical companies have spent hundreds of millions of dollars testing medications to treat Alzheimers, but most attempts have failed clinical studies.

The new research suggests those experimental treatments were pointed in the wrong direction, and that TREM2s role suggests inflammation could be the main culprit.

What we are now finding out from genetic study is that inflammation is an important part of the disease itself, Dr. Peter St. George-Hyslop of the University of Toronto told CTV News. It starts early, and it is part of the way the disease actually happens.

TREM2 has been previously linked to other forms of dementia, and was first found by researchers with Iceland-based deCODE Genetics Inc., who mapped the genetic code of 2,200 people.

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Gene variant could play central role in Alzheimer's disease

Thursday November 15, 2012

Scientists have identified a new gene variant that seems to strongly raise the risk for Alzheimers disease, giving a fresh target for research into treatments for the mind-robbing disorder.

The problem gene is not common -- less than 1 percent of people are thought to have it -- but it roughly triples the chances of developing Alzheimers compared to people with the normal version of the gene. It also seems to harm memory and thinking in older people without dementia.

The main reason scientists are excited by the discovery is what this gene does, and how that might reveal what causes Alz heimers and ways to prevent it. The gene helps the immune system control inflammation in the brain and clear junk such as the sticky deposits that are the hallmark of the disease. Mutations in the gene may impair these tasks, so treatments to restore the genes function and quell inflammation may help.

"It points us to potential therapeutics in a more precise way than weve seen in the past," said Dr. William Thies, chief medical and scientific officer of the Alz heimers Association, which had no role in the research. Years down the road, this discovery will likely be seen as very important, he predicted.

It is described in a study by an international group published online Wednesday by the New England Journal of Medicine.

About 35 million people worldwide have dementia, and Alz heimers

Until now, only one gene -- ApoE -- has been found to have a big impact on Alzheimers risk. About 17 percent of the population has at least one copy of the problem version of this gene but nearly half of all people with Alzheimers do. Other genes that have been tied to the disease raise risk only a little, or cause the less common type of Alzheimers that develops earlier in life, before age 60.

The new gene, TREM2, already has been tied to a couple other forms of dementia. Researchers led by deCODE Genetics Inc. of Iceland honed in on a version of it they identified through mapping the entire genetic code of more than 2,200 Icelanders.

Further tests on 3,550 Alzheimers patients and more than 110,000 people without dementia in several countries, including the United States, found that the gene variant was more common in Alzheimers patients.

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Gene triples risk for Alzheimer's disease, scientists say

REYKJAVIK, Iceland--(BUSINESS WIRE)--

deCODE Genetics and Illumina, global leaders in analyzing and understanding the human genome, together with scientists from the National Hospital of Iceland and collaborators from Holland, Germany and the United States, reported today in the New England Journal of Medicine the identification of just the second gene variant found to confer high risk of acquiring the more common, late-onset form of Alzheimers disease. The newly discovered variant was also found to predict poorer cognitive function in older individuals who do not have Alzheimers disease.

The discovery of variant TREM2 is important because it confers high risk for Alzheimers and because the genes normal biological function has been shown to reduce immune response that may contribute to the disease, said study lead author Kari Stefnsson, M.D., Dr. Med., CEO of deCODE Genetics. These combined factors make TREM2 an attractive target for drug development.

While a number of common, low-risk variants have been reported to associate with late-onset Alzheimers, the 4 allele of Apolipoprotein E, originally discovered as a risk factor for the disease in 1993, has been the most important sequence variant because of its prevalence in the population and the size of its effect on risk.

TREM2, while rarer in the general population than the ApoE 4 allele, confers comparable risk of the disease and plays a significant role in the central nervous system. In preclinical studies, TREM2 has been found to regulate the clearing of cell debris and amyloid protein, a component of theamyloid plaquesassociated withAlzheimer's disease. TREM2 has also been shown to excersize a regulatory control of inflammation, which has been associated with Alzheimers and cognitive decline.

Our findings strongly implicate variant TREM2 in the pathogenesis of Alzheimers disease, said Dr. Stefnsson. Reduced TREM2 activity may lead to brain damage through increased inflammatory response.

Big Data Research

Focusing specifically on variants likely to impact protein function, and thereby honing in on potential targets for drug development, deCODEs scientists sought additional high-risk variants for Alzheimers disease.

Through the companys genome sequencing and genotyping, deCODE researchers identified approximately 41 million markers, including 191,777 functional variants, from 2,261 Icelandic samples. These variants were then analyzed against the genomes of 3,550 persons with Alzheimers disease and a control population over the age of 85 without a diagnosis of the disease. The association analysis used to identify the variant TREM2 in the Icelandic population was then replicated against other control populations with Alzheimers disease maintained in the United States, Germany, the Netherlands and Norway.

Using this approach, we have recently reported variants that greatly influence the risk of developing other diseases, including ovarian cancer, gliomas, gout and sick sinus syndrome, said Dr. Stefnsson. So-called big data research has evolved to a new level of sophistication due to new research tools, access to expanded and high quality genomic data sets, and certainly the profound analytic skill level of investigators now combining sequence data and biological knowledge to find drug targets.

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deCODE Genetics, Multinational Research Team Find Gene Variant Conferring High Risk for Common, Late-Onset Form of ...

By Nicole Giese Rura

Whitehead Institute researchers report that common assumptions employed in the generation and interpretation of data from global gene expression analyses can lead to seriously flawed conclusions about gene activity and cell behavior in a wide range of current biological research.

Expression analysis is one of the most commonly used methods in modern biology, says Whitehead Member Richard Young. So we are concerned that flawed assumptions may affect the interpretation of many biological studies.

Much of todays interpretation of gene expression data relies on the assumption that all cells being analyzed have similar total amounts of messenger RNA (mRNA), the roughly 10% of a cells RNA that acts as a blueprint for protein synthesis. However, some cells, including aggressive cancer cells, produce several times more mRNA than other cells. Traditional global gene expression analyses have typically ignored such differences.

Weve highlighted this common assumption in gene expression analysis that potentially affects many researchers, says Tony Lee, a scientist in Youngs lab and a corresponding author of the article published in this weeks issue of Cell. We provided a concrete example of the problem and a solution that can be implemented by investigators.

Members of the Young lab recently uncovered the flaw while investigating genes expressed in cancer cells expressing high levels of c-Myc, a gene regulator known to be highly expressed in aggressive cancer cells. When comparing cells with high and low c-Myc levels, they were surprised to find very different results using different approaches to gene expression analysis. Further investigation revealed that there were striking differences in the total amounts of RNA from the high and low c-Myc -containing cells, yet these differences were masked by commonly used experimental and analytical methods.

The different results we saw from different methods of gene expression analysis were shocking, and led us to reinvestigate the whole process on several platforms, says Jakob Lovn, postdoctoral reseacher in Youngs lab and co-author of the Cell paper. We then realized that the common assumption that cells contain similar levels of mRNA is badly flawed and can lead to serious misinterpretations, particularly with cancer cells that can have very different amounts of RNA.

In addition to delineating this problem, the Whitehead scientists also describe a remedy. By using synthetically produced mRNAs, called RNA spike-ins, as standardized controls, researchers can compare experimental data and eliminate assumptions about total cell RNA amounts. The remedy applies to all three gene expression analysis platforms they studied.

Although the researchers believe the use of RNA spike-ins should become the new standard for global gene expression analyses, questions are likely to persist about the interpretations of much prior research.

There are over 750,000 expression datasets in public databases, and because they generally lack information about the cell numbers used in the analysis, it is unclear whether they can be re-examined in order to validate the original interpretation says David Orlando, a scientist in the Young lab. It may be necessary to reinvestigate some important concepts.

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Whitehead Scientists Identify Major Flaw In Standard Approach To Global Gene Expression Analysis

Scientists have identified a new gene variant that seems to strongly raise the risk for Alzheimer's disease, giving a fresh target for research into treatments for the mind-robbing disorder.

The problem gene is not common less than 1 per cent of people are thought to have it but it roughly triples the chances of developing Alzheimer's compared to people with the normal version of the gene. It also seems to harm memory and thinking in older people without dementia.

The main reason scientists are excited by the discovery is what this gene does, and how that might reveal what causes Alzheimer's and ways to prevent it. The gene helps the immune system control inflammation in the brain and clear junk such as the sticky deposits that are the hallmark of the disease. Mutations in the gene may impair these tasks, so treatments to restore the gene's function and quell inflammation may help.

"It points us to potential therapeutics in a more precise way than we've seen in the past," said Dr. William Thies, chief medical and scientific officer of the Alzheimer's Association, which had no role in the research. Years down the road, this discovery will likely be seen as very important, he predicted.

It is described in a study by an international group published online Wednesday by the New England Journal of Medicine.

About 35 million people worldwide have dementia, and Alzheimer's is the most common type. In the U.S., about 5 million have Alzheimer's. Medicines such as Aricept and Namenda just temporarily ease symptoms. There is no known cure.

Until now, only one gene ApoE has been found to have a big impact on Alzheimer's risk. About 17 per cent of the population has at least one copy of the problem version of this gene but nearly half of all people with Alzheimer's do. Other genes that have been tied to the disease raise risk only a little, or cause the less common type of Alzheimer's that develops earlier in life, before age 60.

The new gene, TREM2, already has been tied to a couple other forms of dementia. Researchers led by deCODE Genetics Inc. of Iceland honed in on a version of it they identified through mapping the entire genetic code of more than 2,200 Icelanders.

Further tests on 3,550 Alzheimer's patients and more than 110,000 people without dementia in several countries, including the United States, found that the gene variant was more common in Alzheimer's patients.

"It's a very strong effect," raising the risk of Alzheimer's by three to four times about the same amount as the problem version of the ApoE gene does, said Dr. Allan Levey, director of an Alzheimer's program at Emory University, one of the academic centres participating in the research.

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New gene triples risk for Alzheimer's disease; may give clues into causes

CHICAGO (Reuters) - Two international teams of scientists have identified a rare mutation in a gene linked with inflammation that significantly increases the risk for the most common form of Alzheimer's disease, the first such discovery in at least a decade.

The findings, published on Wednesday in the New England Journal of Medicine, offer new insights into the underpinnings of Alzheimer's, a deadly, brain-wasting disease that robs people of their memories, their independence and their lives.

In separate studies, teams led by privately held deCode Genetics and John Hardy of University College London found that people with a mutation in a gene called TREM2 were four times as likely to have Alzheimer's as people who did not have the gene.

"It quadruples the risk of Alzheimer's," said Dr. Kari Stefansson of Reykjavik-based deCode in a telephone interview.

The level of risk compares with ApoE4, the best-known genetic cause of late-onset Alzheimer's, the form of the disease that occurs in older adults.

But this new gene variant is 10 times more rare than ApoE4, which is present in about 40 percent of people with late-onset Alzheimer's.

Rare or not, scientists say the discovery represents a big breakthrough for Alzheimer's research.

"This is one of the most common, most devastating illnesses in humans and we still don't have a very good understanding of what causes the disease," said Dr. Allan Levey, director of the Emory Alzheimer's Disease Center of Excellence in Atlanta, which helped confirm the deCode findings.

"In my mind, this is very important. It gives us another important clue as to one of the biological factors that contribute to causing the disease," he said.

Despite numerous costly attempts, drug companies have been stymied in their efforts to develop drugs that can alter the steady course of Alzheimer's, which affects more than 5 million Americans and costs the United States more than $170 billion annually to treat.

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Scientists identify new risk gene for Alzheimer's

Scientists have identified a new gene variant that seems to strongly raise the risk for Alzheimer's disease, giving a fresh target for research into treatments for the mind-robbing disorder.

The problem gene is not common less than 1 percent of people are thought to have it but it roughly triples the chances of developing Alzheimer's compared to people with the normal version of the gene. It also seems to harm memory and thinking in older people without dementia.

The main reason scientists are excited by the discovery is what this gene does, and how that might reveal what causes Alzheimer's and ways to prevent it. The gene helps the immune system control inflammation in the brain and clear junk such as the sticky deposits that are the hallmark of the disease. Mutations in the gene may impair these tasks, so treatments to restore the gene's function and quell inflammation may help.

"It points us to potential therapeutics in a more precise way than we've seen in the past," said Dr. William Thies, chief medical and scientific officer of the Alzheimer's Association, which had no role in the research. Years down the road, this discovery will likely be seen as very important, he predicted.

It is described in a study by an international group published online Wednesday by the New England Journal of Medicine.

About 35 million people worldwide have dementia, and Alzheimer's is the most common type. In the U.S., about 5 million have Alzheimer's. Medicines such as Aricept and Namenda just temporarily ease symptoms. There is no known cure.

Until now, only one gene ApoE has been found to have a big impact on Alzheimer's risk. About 17 percent of the population has at least one copy of the problem version of this gene but nearly half of all people with Alzheimer's do. Other genes that have been tied to the disease raise risk only a little, or cause the less common type of Alzheimer's that develops earlier in life, before age 60.

The new gene, TREM2, already has been tied to a couple other forms of dementia. Researchers led by deCODE Genetics Inc. of Iceland honed in on a version of it they identified through mapping the entire genetic code of more than 2,200 Icelanders.

Further tests on 3,550 Alzheimer's patients and more than 110,000 people without dementia in several countries, including the United States, found that the gene variant was more common in Alzheimer's patients.

"It's a very strong effect," raising the risk of Alzheimer's by three to four times about the same amount as the problem version of the ApoE gene does, said Dr. Allan Levey, director of an Alzheimer's program at Emory University, one of the academic centers participating in the research.

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New gene triples risk for Alzheimer's disease

Advances In Applied Microbiology
ll4.me Advances In Applied Microbiology From the Reviews of Previous Volumes"No laboratory scientist, field worker or technical administrator can afford to pass it up.2- ASM NEWS"The topics are well supported by an extensive bibliography and provide a rich source of current information."- BIOPHARMKey Features* Genetic engineering* Genetic manipulation* Bioprocessing and fermentation* Using microbes for producing Publisher: Academic Press Illustration: N Language: ENG Title: Advances in Applied Microbiology Pages: 00290 (Encrypted PDF) On Sale: 1995-10-10 SKU-13/ISBN: 9780120026418 Category: Science : Life Sciences - Microbiology Category: Science : Life Sciences - Molecular Biology Category: Technology Engineering : Food Science From the Reviews of Previous Volumes"No laboratory scientist, field worker or technical administrator can afford to pass it up.2- ASM NEWS"The topics are well supported by an extensive bib science, life sciences, microbiology, molecular biologyFrom:davidaguilar565Views:0 0ratingsTime:00:10More inPeople Blogs

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Lipid Biotechnology
ll4.me Lipid Biotechnology Discussing a variety of lipid-active enzymes from animal, plant, fungal, and microbial sources, Lipid Biotechnology covers modern techniques in genetic engineering. This text presents the latest advances in supercritical fluid technology, biocatalysis, bioprocess engineering, and crop breeding. Lipid Biotechnology offers a thorough review of the most recent principles and approaches used in the development and design of lipids for cosmetic, industrial and pharmaceutical, and food products. The authors provide in-depth analyses of the structure, metabolic and enzymatic functions and mechanisms, defensive and catalytic properties, industrial uses, and other applications of oxilipins, lipases, and other fatty acids. Related discussions include reaction conditions, reactor design, immobilization technology, and large-scale manufacturing. Publisher: Marcel Dekker Illustration: N Language: ENG Title: Lipid Biotechnology Pages: 00000 (Encrypted PDF) On Sale: 2002-01-22 SKU-13/ISBN: 9780824744182 Category: Technology Engineering : General Discussing a variety of lipid-active enzymes from animal, plant, fungal, and microbial sources, Lipid Biotechnology covers modern techniques in genetic engineering. This text presents the latest advan technology, engineering, generalFrom:aidataylor326Views:0 0ratingsTime:00:10More inPeople Blogs

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Lipid Biotechnology - Video

Fighting For Human Rights
ll4.me Fighting For Human Rights In a world that is increasingly disillusioned with formal politics, this book identifies activism as a key means of realising human rights and as a new form of politics. People are no longer prepared to wait for governments and international institutions for act on human rights concerns. "Fighting for Human Rights" documents and compares successful high profile campaigns to cancel debt, ban landmines, and set up the International Criminal Court as well as emerging campaigns that focus on HIV/Aids, genetic engineering, environmental justice, democratization, and blood diamonds. Motivated diverse international movements, these campaigns aim to establish international agreements that will become the basis for processes of monitoring and enforcement. Publisher: Routledge Illustration: N Language: ENG Title: Fighting for Human Rights Pages: 00000 (Encrypted PDF) On Sale: 2004-07-14 SKU-13/ISBN: 9780415312929 Category: Political Science : Political Freedom Security - Civil Rig Category: Political Science : International Relations - General Category: Social Science : General In a world that is increasingly disillusioned with formal politics, this book identifies activism as a key means of realising human rights and as a new form of politics. People are no longer prepared social science, generalFrom:barrynielsen9854Views:0 0ratingsTime:00:13More inPeople Blogs

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Biotechnology And The Integrity Of Life: Taking Public Fears Seriously Ashgate Studies In Applied Et
ll4.me Biotechnology And The Integrity Of Life: Taking Public Fears Seriously Ashgate Studies In Applied Ethics - Michael Hauskeller Genetic engineering is still considered morally wrong by a large proportion of the public. Yet many scientists are puzzled about the public concern over a technology that, in their view, promises great benefits to humans and does not seem to cause more harm to animals than other practices which are rarely questioned. In this book, Michael Hauskeller takes public fears seriously and offers the idea of #39;biological integrity #39; as a clarifying principle which can then be analyzed to show that seemingly irrational public concerns about genetic engineering are not so irrational and that a philosophically sound justification of those concerns can indeed be given.Author: Hauskeller, Michael Publisher: Ashgate Gower Illustration: N Language: ENG Title: Biotechnology and the Integrity of Life: Taking Public Fears Seriously Ashgate Studies in Applied Ethics Pages: 00174 (Encrypted PDF) On Sale: 2007-12-01 SKU-13/ISBN: 9780754660446 Category: Social Science : General Category: History : General Genetic engineering is still considered morally wrong by a large proportion of the public. Yet many scientists are puzzled about the public concern over a technology that, in their view, promises grea michael hauskeller, history, generalFrom:lilliangoodin9854Views:0 0ratingsTime:00:13More inPeople Blogs

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Biotechnology And The Integrity Of Life: Taking Public Fears Seriously Ashgate Studies In Applied Et - Video

Applications Of Plant Cell And Tissue Culture - Ciba Foundation Symposium
ll4.me Applications Of Plant Cell And Tissue Culture - Ciba Foundation Symposium This work deals with basic plant physiology and cytology, and addresses the practical exploitation of plants, both as crops and as sources of useful compounds produced as secondary metabolites. Covers problems of commercial exploitation, socio-legal aspects of genetic engineering of crop plants, and of the difficulties of marketing natural compunds produced by cells under artificial conditions.Author: CIBA Foundation Symposium Publisher: Wiley Illustration: N Language: ENG Title: Applications of Plant Cell and Tissue Culture Pages: 00280 (Encrypted PDF) On Sale: 2008-04-30 SKU-13/ISBN: 9780471918868 Category: Science : Life Sciences - Botany This work deals with basic plant physiology and cytology, and addresses the practical exploitation of plants, both as crops and as sources of useful compounds produced as secondary metabolites. Covers ciba foundation symposium, science, life sciences, botanyFrom:barrynielsen9854Views:0 0ratingsTime:00:10More inPeople Blogs

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Planet X Ancient Texts
Publisher of Mysterious World books, Doug Elwell, discussed his research on ancient references to Planet X which connects the work of Zecharia Sitchin to Biblical writings. He noted that astronomers have actually been looking for Planet X for "over 100 years" and clarified that the use of #39;X #39; is merely to denote that the object remains, so far, unknown. "It #39;s not some cheesy science fiction thing," he declared, "it #39;s a legitimate scientific endeavor." Elwell described his interpretation of Planet X as a combination of mainstream science theories on the object along with the voluminous work of Zecharia Sitchen. According to Elwell #39;s research, Planet X circles through our solar system about every 2000 years and crosses through the asteroid belt. Elwell observed that numerous ancient texts appear to allude to Planet X and asserted that the object is actually the "core concept behind the Bible." He noted that, in the Bible, Jesus said that, much like his birth, his return would be preceded by the arrival of a bright star, which Elwell interprets, in both cases, to be Planet X. Additionally, he said that if we "take mythology at face value," various ancient cultures wrote about their highest deities facing off in battle against a "dragon" of some kind. All of these references, Elwell theorized, suggest a "cosmic war" between God and the fallen angels. Wikipedia Zecharia Sitchin was an Azerbaijani-born American author of books proposing an explanation for human origins ...From:DiscloseTruthTVViews:64 1ratingsTime:01:42:10More inEducation

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Planet X

Fresh Prince of Bel-Air Rap (Brave New World Theme)
English rap; block 2-2, Ms.Lin Creative Project: Brave New World Rap VERSE 1: Brave new world in London city, overpopulated with the technology. While genetic engineering is on top of the globe, citizens consume soma while enjoying the show. Perfect Prime example of a dystopia, with various types of drugs causing fake euphoria, and a formula to reproduce and clone. Set in castes that are divided into four separate zones. Alpha, beta gamma then the epsilons. Emotionless beings, their minds all gone. Admiring Henry Ford for his brilliance, pray on! And the rest are sent to an island like Saint John Game on! World controllers in control, alienating human minds to reach their ultimate goal. All peace, a perfect society that functions, ironic how the end result is sad and corrupted. VERSE 2: Here we go Imma tell a bit of the story We have a girl named Lenina seeming pretty horny. Then a guy named John moves into the city acting pretty lost, I feel a tad bit sorry. But it #39;s alright, he gets a new name and some fame, unknowingly starting to get sucked in the game. What a shame, he came, and, endured pain, but sadly it was something that he could not tame. How insane, he later moves out, and in the rain wanting to erase all the memories from his brain. Nonetheless in the end he could not take it, with his feet dangling in the air feeling forsaken. So the moral of the story is to be aware, technology might be something we cannot bear. See ,we all want peace deep within, but this ...From:Jackie ChanViews:4 1ratingsTime:01:46More inMusic

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Fresh Prince of Bel-Air Rap (Brave New World Theme) - Video

Public release date: 13-Nov-2012 [ | E-mail | Share ]

Contact: Chris Chipello christopher.chipello@mcgill.ca 514-398-4201 McGill University

As they develop, vertebrate embryos form vertebrae in a sequential, time-controlled way. Scientists have determined previously that this process of body segmentation is controlled by a kind of "clock," regulated by the oscillating activity of certain genes within embryonic cells. But questions remain about how precisely this timing system works.

A new international cross-disciplinary collaboration between physicists and molecular genetics researchers advances scientists' understanding of this crucial biological timing system. The study, co-authored by McGill University Prof. Paul Franois and Ohio State University Prof. Sharon L. Amacher and published in Developmental Cell, sheds light on the clock mechanism by providing the first real-time, visual evidence of how it operates at the level of individual cells.

While previous scientific studies have examined the oscillation phenomenon in the tissue of mouse embryos, the McGill and Ohio State researchers were able to observe and analyze it in single cells. To do so, they genetically modified zebrafish a freshwater fish whose body is nearly transparent during early development, making its anatomy easy to observe. The researchers used a fluorescent marker in the transgenic fish and developed software tools to monitor the concentration of a certain "cyclic" protein, whose production rises and falls with the oscillating expression of the molecular clock genes.

It is known that cells communicate with neighboring cells through a messaging system known as the Notch signaling pathway. In their experiments with the zebrafish, the researchers cut off this inter-cellular communication network enabling them to see how that would affect the oscillation pattern in individual cells and their neighbors.

These experiments revealed that cyclic protein concentrations in individual cells of the zebrafish continued to rise and fall, indicating that they continued to oscillate. With the inter-cellular signaling pathway blocked, however, the oscillations were no longer synchronized among neighboring cells. The cellular clocks were still ticking, in other words, but not in unison. This finding confirms that the Notch pathway serves to coordinate timing among cells a crucial role, since the cells must act in concert in order to form vertebrae.

By observing normal zebrafish embryos, the researchers were also able to show that cells desynchronize their oscillations while performing cellular division, then later resynchronize with their neighbors as they proceed collectively to form vertebrae.

"In humans, defects in Notch signaling are associated with congenital developmental disorders called spondylocostal dysostosis, that are typified by scoliosis and trunk dwarfism caused by malformed ribs and vertebrae," Amacher notes. "Studies such as ours may provide insight into potential therapies for human disease. It is likely that many cells in our bodies - stem cells, cancer cells - have similar molecular oscillators that regulate response to environmental signals. By unraveling such molecular clocks, we can understand how to modify them and thus change the number of oscillating cells that respond to differentiating signals, providing tremendous insight for studies in stem cell and cancer biology and tissue engineering."

"The formation of the vertebral column is very important, because everything follows from that" in the development of vertebrates, Franois adds. A physicist, he developed the computer tools used to analyze video footage of the zebrafish embryos. Francois's research focuses on the modeling of physical properties of gene networks and their evolution a field that has emerged at the nexus of biology and physics in recent years, following sequencing of the human genome and rapid growth in scientists' understanding of the processes inside cells.

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Study sheds light on genetic 'clock' in embryonic cells

Public release date: 13-Nov-2012 [ | E-mail | Share ]

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

New Rochelle, NY, November 13, 2012The average incidence of traumatic brain injury (TBI) among service members deployed in Middle East conflict zones has increased 117% in recent years, mainly due to proximity to explosive blasts. Therapeutic exposure to a high oxygen environment was hoped to minimize the concussion symptoms resulting from mild TBI, but hyperbaric oxygen (HBO2) treatment may not offer significant advantages, according to an article in Journal of Neurotrauma, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Neurotrauma website at http://www.liebertpub.com/neu.

A prospective trial conducted at the U.S. Air Force School of Aerospace Medicine evaluated the benefits of HBO2 therapy on post-concussion symptoms in 50 military servicepersons who had suffered at least one combat-related mild TBI. The study, "The Effect of Hyperbaric Oxygen on Symptoms Following Mild Traumatic Brain Injury," compared the results following 30 sessions of either HBO2 (2.4 atmospheres absolute pressure) or sham treatment over an 8-week period.

George Wolf, MD and Leonardo Profenna, MD, U.S. Air Force School of Aerospace Medicine (San Antonio, TX), David Cifu, MD and William Carne, PhD, Virginia Commonwealth University (Richmond), and Laura Baugh, MD, Uniformed Services University of the Health Sciences Department of Neurology (Bethesda, MD), present data demonstrating that both patient groups showed significant improvement in concussion assessment and cognitive testing scores over the course of the study.

"This is a particularly important communication that addresses a continued area of controversy, particularly as it relates to the treatment of our military personnel sustaining mild traumatic brain injury," says John T. Povlishock, PhD, Editor-in-Chief of Journal of Neurotrauma and Professor, VCU Neuroscience Center, Medical College of Virginia, Richmond. "While the authors stress that based upon their findings, larger multi-center, randomized, controlled, double-blinded clinical trials should be conducted, the compelling data in this communication does not support any therapeutic value for hyperbaric oxygen treatment, striking a cautionary note for those involved in the care and management of this patient population."

###

About the Journal

Journal of Neurotrauma is an authoritative peer-reviewed journal published 24 times per year in print and online that focuses on the latest advances in the clinical and laboratory investigation of traumatic brain and spinal cord injury. Emphasis is on the basic pathobiology of injury to the nervous system, and papers and reviews evaluate preclinical and clinical trials targeted at improving the early management and long-term care and recovery of patients with traumatic brain injury. Journal of Neurotrauma is the Official Journal of the National Neurotrauma Society and the International Neurotrauma Society. Complete tables of content and a sample issue may be viewed on the Journal of Neurotrauma website at http://www.liebertpub.com/neu.

About the Publisher

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Should hyperbaric oxygen therapy be used to treat combat-related mild traumatic brain injury?

Public release date: 13-Nov-2012 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, November 12, 2012--Radiolabeled agents are powerful tools for targeting and killing cancer cells and may help improve outcomes and lengthen survival times of patients with advanced disease that has spread beyond the initial tumor site. Effective therapy for metastatic cancer requires a combination of treatments, and the benefits of adding radionuclide therapy are explored in three studies published in Journal of Clinical Investigation, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The articles are available free on the Journal of Clinical Investigation website.

"The preliminary therapeutic results reported in these case studies using radionuclide multimodality approaches are encouraging," says Co-Editor-in-Chief Donald J. Buchsbaum, PhD, Division of Radiation Biology, Department of Radiation Oncology, University of Alabama at Birmingham. "The outcomes described in these small, single center studies must be confirmed in larger trials before they can be translated into widespread oncology practice."

J. Harvey Turner, MD, FRACP, The University of Western Australia, Fremantle, coauthored two of the case studies and, in the Perspective article "Multimodality Radionuclide Therapy of Progressive Disseminated Lymphoma and Neuroendocrine Tumors as a Paradigm for Cancer Control," he states that the synergistic effects that can be achieved by combining chemotherapy and radionuclides "has the potential to enhance efficacy and minimize toxicity." Although advanced forms of lymphoma and neuroendocrine tumors are usually incurable, multimodal treatment approaches may be able to stop or slow tumor progression, achieve durable remission, prolong patient survival, and improve their quality of life.

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Paul Kruger, Julian Cooney, and J. Harvey Turner report that more patients survived longer and were free of disease when a radioimmunotherapeutic agent was added to their treatment regimen in the article "Iodine-131 Rituximab Radioimmunotherapy with BEAM Conditioning and Autologous Stem Cell Transplant Salvage Therapy for Relapsed/Refractory Aggressive Non-Hodgkin Lymphoma."

Phillip Claringbold, Richard Price, and J. Harvey Turner added a lutetium-177 labeled peptide to the therapeutic regimen of a group of patients with advanced neuroendocrine cancer and described substantially improved tumor control rates with no significant side effects. They report their findings in "Phase I-II Study of Radiopeptide 177Lu-Octreotate in Combination with Capecitabine and Temozolomide in Advanced Low-Grade Neuroendocrine Tumors."

About the Journal

Journal of Clinical Investigation, published 10 times a year in print and online, is under the editorial leadership of Editors Donald J. Buchsbaum, PhD, Division of Radiation Biology, Department of Radiation Oncology, University of Alabama at Birmingham, and Robert K. Oldham, MD, Lower Keys Cancer Center, Key West, FL. Journal of Clinical Investigation is the only journal with a specific focus on cancer biotherapy, including monoclonal antibodies, cytokine therapy, cancer gene therapy, cell-based therapies, and other forms of immunotherapy. The Journal includes extensive reporting on advancements in radioimmunotherapy and the use of radiopharmaceuticals and radiolabeled peptides for the development of new cancer treatments. Topics include antibody drug conjugates, fusion toxins and immunotoxins, nanoparticle therapy, vascular therapy, and inhibitors of proliferation signaling pathways.

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Can the addition of radiolabeled treatments improve outcomes in advanced metastatic disease?

Amarillo, TX -- New research at WTAMU is putting the school at the forefront of genetic engineering.

Scientists at WT are celebrating the successful birth of a cloned calf - their second this year. And these two recent successes represent major strides toward improving stock lines, and ultimately, our food supply.

The word "cloning" tends to make many people uneasy, but in this sense, "cloning" is really just an expedited form of selective breeding.

"Alpha," a young bull, and "Gamma," a days-old heifer, were recently born using a process called somatic cell nuclear transfer. In simplest terms, that means putting a reprogrammed cell into a surrogate mother. The idea is that by systematically improving the gene pool, you can create better and stronger breeds, as WTAMU Associate Professor of Animal Science Dr. Ty Lawrence explains,

"We hope to create a new breed of cattle that currently does not exist. And this new breed of cattle will be a piece of the best of the best of the best from all existing breeds and their crosses."

By isolating the most desirable traits, researchers can create higher-yield cattle more resistant to drought and disease, as veterinarian Dr. Greg Veneklasen says,

"It's not just about meat; this is about genetic disease, this is about infectious disease. This is a model that we've created that we can use ... we can use this model for many different things."

And each new model is a step closer toward creating the ideal food animal.

Alpha and Gamma, for instance, are both Yield Grade One Prime beef, which represents about one in 15,000 cattle.

And advances like these are putting WTAMU on the map, as Dr. Don Topliff says,

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WT cloning research advances field

Research of James Millonig, PhD, Featured in Video at Award Ceremony on November 8

Newswise Piscataway, NJ Research that contributed to the development of a new genetic test for Autism Spectrum Disorder (ASD) has earned scientists at the University of Medicine and Dentistry of New Jersey (UMDNJ)-Robert Wood Johnson Medical School and Rutgers, The State University of New Jersey, the coveted Edison Patent Award from the Research & Development Council of New Jersey. The award recognizes a UMDNJ patent (U.S. Patent 7,629,123) for research that established an association between Engrailed Homeobox 2, (EN2), a gene involved in human development, and susceptibility for autism and related disorders. Diagnostic tools developed through this research have been used, in part, to test for the risk of autism in children who have siblings already diagnosed with the disorder.

As a New Jersey-based health and sciences institution and participating site in the CDCs autism study, we are very proud of this patent and its recognition by the Research & Development Council of New Jersey, said James Millonig, PhD, associate professor of neuroscience and cell biology and a member of the Center for Advanced Biotechnology and Medicine at Robert Wood Johnson Medical School.

In families where one child has been diagnosed with ASD, there is an increased risk that siblings also will be diagnosed with the disorder, providing evidence of a genetic component in the development of autism. This predisposition in siblings is the basis for research that established the link between EN2 and autism led by Dr. Millonig, in collaboration with Linda Brzustowicz, MD, professor and chair of genetics at Rutgers, The State University of New Jersey, and Neda Gharani, PhD, senior research scientist at the Coriell Institute.

The patented research recognized in the medical diagnostic category by the Research & Development Council of New Jersey, relates to compositions that can be used to help determine the predisposition, onset, or presence of ASD in children. Additional research by the team has shown that the ASD-associated genetic variant is functional and increases EN2 levels. Therapeutic methods for treating a child diagnosed with, or at-risk for, developing ASD, by adjusting the level or activity of EN2 also are included in the patent.

Diagnosis of ASD through professionally-developed observational techniques generally does not occur before age 3. It is the hope of the research team that the gene-based approach they have patented may lead to accurate diagnoses even sooner.

Earlier diagnosis means earlier treatment, which has enormous potential to improve social and communicative delays, thereby enhancing a childs ability to assimilate into the mainstream. said Dr. Millonig. Reducing the severity of symptoms related to Autism Spectrum Disorder, and possible the incidence of it, also may lead to lower costs for long-term treatment.

The Research & Development Council of New Jersey presented the award to Dr. Millonig and his team on Thursday, November 8. The presentation included a short video about the patent and Dr. Millonigs research, which can be found at: http://tinyurl.com/aaby5cs.

About UMDNJ-ROBERT WOOD JOHNSON MEDICAL SCHOOL As one of the nations leading comprehensive medical schools, UMDNJ-Robert Wood Johnson Medical School is dedicated to the pursuit of excellence in education, research, health care delivery, and the promotion of community health. In cooperation with Robert Wood Johnson University Hospital, the medical schools principal affiliate, they comprise one of the nation's premier academic medical centers. In addition, Robert Wood Johnson Medical School has 34 other hospital affiliates and ambulatory care sites throughout the region.

As one of the eight schools of the University of Medicine and Dentistry of New Jersey with 2,800 full-time and volunteer faculty, Robert Wood Johnson Medical School encompasses 22 basic science and clinical departments, hosts centers and institutes including The Cancer Institute of New Jersey, the Child Health Institute of New Jersey, the Center for Advanced Biotechnology and Medicine, the Environmental and Occupational Health Sciences Institute, and the Stem Cell Institute of New Jersey. The medical school maintains educational programs at the undergraduate, graduate and postgraduate levels for more than 1,500 students on its campuses in New Brunswick, Piscataway, and Camden, and provides continuing education courses for health care professionals and community education programs. To learn more about UMDNJ-Robert Wood Johnson Medical School, log on to rwjms.umdnj.edu. Find us online at http://www.Facebook.com/RWJMS and http://www.twitter.com/UMDNJ_RWJMS.

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Research into Genetic Link of Autism Spectrum Disorder Earns Prestigious Edison Patent Award from the Research ...

November 15, 2012 Courtesy of Matt Solovey

By Michael Martin Garrett

Researchers from the Penn State College of Medicine at Hershey Medical Center have recently completed a study that found that zebrafish can be used to test the effects of genetic mutations in humans.

[Zebrafish] genes are similar enough that if [someone] mutates the genes or knocks them down, what will happen is very similar to what will happen in humans, said lead researcher Dr. Keith Cheng.

In the future, the process and results of the study may be used to test the functions of genetic mutations, Cheng said.

This kind of research, being able to functionally test human mutations in a living model organism, can lend much support to the developing field of personalized medicine, Steven Wentzel , a Penn State graduate student and researcher on the study, wrote in an email.

Wentzel wrote that many scientific studies have identified numerous genes that are linked to various diseases, but by being able to test individual genetic mutations we can gain insight into what roles they may play in human disease, allowing us to prioritize treatment targets.

Cheng said there are many different combinations of mutations, and these mutations can be very small, with the difference of only a single amino acid between two versions of the same gene.

Everybody knows that were going to be carrying our DNA sequence around in our iPhones soon, but were not going to know what all of our mutations mean, Cheng said.

According to the abstract of the study, the approach may be extended to other model systems and could contribute to the understanding of the relationships between DNA sequence variation, human biology and disease.

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Penn state researchers study genetic mutations in Zebrafish

Washington, November 15 (ANI): A mutation in an immune system gene may contribute to a person's risk of developing Alzheimer's disease, Canadian researchers have found.

Using data from 25,000 people, researchers from the Faculty of Medicine and University College London's Institute of Neurology discovered that a rare genetic mutation in the TREM2 gene - which helps trigger immune system responses - is also associated with increased risk of Alzheimer's.

The discovery supports an emerging theory about the role of the immune system in the disease.

"This discovery provides an increasingly firm link between brain inflammation and increased risk for Alzheimer's," says Dr. Peter St George-Hyslop, director of University of Toronto's Tanz Centre for Research in Neurodegenerative Diseases.

"This is an important step towards unraveling the hidden causes of this disease, so that we can develop treatments and interventions to end one of the 21st century's most significant health challenges."

The team began by sequencing the genes of 1,092 people with Alzheimer's and a control group of 1,107 healthy people. The results showed several mutations in the TREM2 gene occurred more frequently in people who had the disease than in those without the disease. One mutation - known as R47H - had a particularly strong association with the disease.

The mutation makes a patient three times more likely to develop the disease, although it affects just 0.3 per cent of the population.

"While the genetic mutation we found is extremely rare, its effect on the immune system is a strong indicator that this system may be a key player in the disease," says Dr. Rita Geurreiro from UCL, the study's lead author.

The study has been published in the New England Journal of Medicine. (ANI)

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Genetic mutation linked to Alzheimer's disease

Sanofi-Institut Pasteur 2012 Awards: Interview of Professor Peter Palese
Peter Palese is Professor and Chairman of the Department of Microbiology of the Mount Sinai School of Medicine in New York City. He is honored for his fundamental work on the genetics of influenza viruses.From:sanofiaventisTVenViews:5 1ratingsTime:01:41More inScience Technology

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Sanofi-Institut Pasteur 2012 Awards: Interview of Professor Peter Palese - Video

True Strength Now - The Real Deal Strength Building Strength Gain Routine By Todd Walsh (truestrengthtodd)
xxsurl.com True Strength Now - The Real Deal Strength Building Strength Gain Routine By Todd Walsh (truestrengthtodd) True Strength Now - The Real Deal Strength Building Strength Gain Routine By Todd Walsh (truestrengthtodd) This is me deadlifting 405 lbs 3 times. Looks pretty easy rightb Give it a try. Home | Contact TRUE STRENGTH NOW! A strength training program that will make you STRONGER THAN YOU HAVE EVER BEEN. A 10 week program that can change your life. By Todd Walsh A regular 41 year old guy who takes getting strong very seriously The truth is genetics determine how strong you can get. The good news is that most people (99%) have never even come close to their true strength potential. The routine included in my e-Book will help you unlock the strength within you. I know, you #39;ve been told through the media and magazines that there is a trick to being strong, or a supplement that can make you strong. The plain truth is that to be strong you need to be dedicated and you need a good routine. There just isn #39;t an easy way or short cut. There are however easier ways and good routines that can make all the difference in helping you achieve your strength goals. What I can do is show you how to get as strong as you can possibly be by introducing you to a simply fantastic strength gain routine. So, how strong can you getb The only way to answer you is to tell you how strong I am. Well... at my last body composition test I was 20% body fat and was slightly dehydrated ...From:lessanders396Views:0 0ratingsTime:01:57More inPeople Blogs

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True Strength Now - The Real Deal Strength Building

Humans Getting Dumber As Species
A scientist claims humans are potentially getting dumber as a species. Are humans getting dumber as a species? Stanford University professor Gerald Crabtree #39;s research into human kind #39;s intelligence suggests that due to the low level of competition for basic necessities in the modern world, the best and brightest aren #39;t the only ones naturally selected for survival and procreation anymore. Civilization and modern medicine allow for even the dumbest and most physically unfit to survive and pass their genes on to the next generation. In the distant past, survival wasn #39;t so easy. The Darwinian concept of evolution dictates that only the people who could navigate the complexities of life on earth would be able to live on and provide for their offspring. Crabtree says: "New developments in genetics, anthropology, and neurobiology... make a clear prediction that our intellectual and emotional abilities are genetically surprisingly fragile." When comparing genomes of parents and their children, it turns out that there are somewhere between 25 and 65 DNA mutations between each generation. Other scientists oppose Crabtree #39;s ideas saying that there is no real way to test his theory. What do you think? Are humans getting dumber due to the conveniences of modern life?From:geobeatsViews:4 7ratingsTime:01:14More inEducation

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Humans Getting Dumber As Species - Video