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New research published Thursday in the journal Neuron sheds new light on the molecular causes of Alzheimers disease, while also revealing a potential new therapy which could help prevent cognitive decline and brain damage during the early stages of the neurodegenerative disorder.

The study focuses on a variant of a gene known as CD33, which typically contributes to Alzheimers disease by inhibiting the ability of a bodys immune cells to remove toxic molecules from the brain. Those toxins, which are known as beta-amyloid plaques, form between neurons in the brain. Past studies have linked those plaques to neuron death and cognitive deficits such as impaired memory, the researchers explained.

Too much CD33 activity appears to promote late-onset Alzheimers by preventing support cells from clearing out toxic plaques, key risk factors for the disease, explained senior author Dr. Rudolph Tanzi of Massachusetts General Hospital and Harvard University. Future medications that impede CD33 activity in the brain might help prevent or treat the disorder.

Before our study, nothing was known about the function of CD33 in the brain. Moreover, our findings suggest that pharmaceutical inactivation of CD33 represents a potentially powerful new therapy for the treatment and prevention of Alzheimers disease, and perhaps other neurodegenerative disorders, he added. Our findings raise the exciting possibility that the inability of microglia to degrade beta-amyloid in Alzheimers disease could be reversed therapeutically by inhibition of CD33 activity.

Tanzi and his colleagues first became interested in CD33 variations during 2008 research into genes that contribute to late-onset Alzheimers disease. They knew the gene made a protein which regulated the immune system, but its function within the brain was unclear. In order to learn more about how it could contribute to the neurodegenerative condition, they looked at human genetics, biochemistry and human brain tissue, laboratory mice and cell-based experiments, the researchers explained.

They discovered the CD33 gene regulates the clearing of a toxic protein known as amyloid beta (A-beta) in the brains of Alzheimers patients. As part of the Neuron study, Tanzi and his co-authors describe a protective variant of CD33 which promotes clearance of the protein. They also illustrate how reducing the genes expression in immune cells known as microglia boosts their ability to clear-away A-beta, raising the hope the brains immune system could be aided with A-beta removal if CD33 activity is blocked.

In the current study, the researchers first found that CD33 activity was significantly higher in microglia cells in brain samples from Alzheimers patients than in cells from non-demented controls, Massachusetts General Hospital explained in a statement. Moreover, they showed that the presence of a version of the gene that protected against Alzheimers disease reduced CD33 protein levels in the brain. Importantly, the same protective version of CD33 was found to reduce levels of A-beta 42 the primary constituent of the amyloid plaques that characterize the disease.

Increased numbers of CD33-containing microglia were also linked to higher a-beta levels and total beta-amyloid plaque levels. Their research was conducted using an Alzheimers mouse model, and according to Tanzi, their findings indicate inhibiting CD33 activity in a human patients brain could ultimately become a powerful new approach to treating and possibly preventing Alzheimers disease.

In related research, published online Thursday in the journal Cell, an international team of researchers report they located a network of genes involved in the inflammatory response in the brain which is a critical component in late-onset Alzheimers disease (LOAD).

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Studies Detail Genetic Mechanisms That Could Improve Alzheimer's Treatment

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Apr. 25, 2013 An international research consortium led by the Universitat Autnoma de Barcelona (UAB), the CIBERER and the University of Wurzburg (Germany) has discovered a gene that can cause three totally different diseases, depending on how it is altered.

The researchers, using next-generation massive ultrasequencing techniques, have sequenced the over 20,000 genes of a Fanconi anemia patient's genome. By adopting this strategy they have succeeded in identifying pathogenic mutations responsible for this disease in the ERCC4 gene, which had already been linked to two other rare diseases: xeroderma pigmentosum and a type of progeria. The latter are characterised by heightened sensitivity to sunlight, susceptibility to skin cancer and, in the case of progeria, premature aging. Fanconi anemia, on the other hand, is characterised by progressive anemia, congenital malformations and a high risk of developing leukemia and mouth tumours. The ERCC4 gene can therefore be responsible for three different diseases.

The researchers have shown that this gene is involved in two DNA repair mechanisms by which cells maintain the stability of the genome, in such a way that the balance between these two repair systems will determine which of the three diseases the patient will contract. "This is a rather exceptional case, since there are few precedents of a single gene being involved in two independent physiological mechanisms and causing three clinically different diseases," points out UAB professor Dr Jordi Surralls.

These findings, published today in the American Journal of Human Genetics, as well as improving the diagnosis and genetic characterisation of rare diseases, will allow new therapeutic strategies to be applied, like gene therapy or the selection of healthy, compatible embryos to cure siblings through umbilical cord transplants. The findings add to our knowledge of the two DNA repair mechanisms, which are so important for maintaining the stability of our genes and preventing cancer in the general population. In fact, the researchers point to the importance of going on to study this gene's possible role in breast cancer and ovarian cancer.

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Discovery of a gene that controls three different diseases

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Apr. 25, 2013 RNA molecules, made from DNA, are best known for their role in protein production. MicroRNAs (miRNAs), however, are short (~22) nucleotide RNA sequences found in plants and animals that do not encode proteins but act in gene regulation and, in the process, impact almost all biological processes -- from development to physiology to stress response.

Present in almost in every cell, microRNAs are known to target tens to hundreds of genes each and to be able to repress, or "silence," their expression. What is less well understood is how exactly miRNAs repress target gene expression.

Now a team of scientists led by geneticists at the University of California, Riverside has conducted a study on plants (Arabidopsis) that shows that the site of action of the repression of target gene expression occurs on the endoplasmic reticulum (ER), a cellular organelle that is an interconnected network of membranes -- essentially, flattened sacs and branching tubules -- that extends like a flat balloon throughout the cytoplasm in plant and animal cells.

"Our study is the first to demonstrate that the ER is where miRNA-mediated translation repression occurs," said lead researcher Xuemei Chen, a professor of plant cell and molecular biology and a Howard Hughes Medical Institute-Gordon and Betty Moore Foundation Investigator. "To understand how microRNAs repress target gene expression, we first need to know where microRNAs act in the cell. Until now no one knew that membranes are essential for microRNA activity. Our work shows that an integral membrane protein, AMP1, is required for the miRNA-mediated target gene repression to be successful. As AMP1 has counterparts in animals, our findings in plants could have broader implications."

Study results appear today in the journal Cell.

Simply put, DNA makes RNA, and then RNA makes proteins. Specifically, RNA encodes genetic information that can be "translated" into the amino acid sequence of proteins. But noncoding RNAs -- RNAs that do not encode proteins -- are increasingly found to act in numerous biological processes. MicroRNAs are a class of noncoding RNAs whose main function is to downregulate gene expression.

Research on miRNAs has increased tremendously since they were first identified about 20 years ago. In the case of diseases, if some genes are up- or down-regulated, miRNAs can be used to change the expression of these genes to fight the diseases, thus showing therapeutic potential.

MicroRNAs are known to regulate target genes by two major modes of action: they either destabilize the target RNAs, leading to their degradation, or they do not impact the stability of the target RNAs, but simply prevent them from being translated into proteins -- a process known as translation inhibition. The end result of translation inhibition is that the genes do not get expressed. Just how miRNAs cause translational inhibition of their target genes is not well understood.

"We were surprised that the ER is required for the translational inhibition activity of miRNAs," Chen said. "This new knowledge will expedite our understanding of the mechanism of gene silencing. Basically, now we know where to look: the ER. We also suspect it is the rough ER portions that are involved."

Chen explained that the ER has two types: rough and smooth. Rough ER, which synthesizes and packages proteins, looks bumpy; smooth ER, which acts in lipid synthesis and protein secretion, resembles tubes. The ER protein AMP1, she said, is anchored in the rough ER.

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Key cellular organelle involved in gene silencing identified

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Mapping out how an Alzheimers gene works could lead to new treatments.

So far, nearly two dozen genes scattered across four chromosomes have been linked to an increased risk of Alzheimers disease. But identifying such genetic risk factors doesnt mean that researchers fully understand how they contribute to cognitive decline and dementia. And that understanding is often crucial to turning genetic information into effective treatments.

Now a group of scientists report in the journal Neuron that they have pieced together the back story of one gene, known as CD33, that could lead to exciting new ways of removing the amyloid plaques that build up in the brains of Alzheimers patients and cause so many problems with memory and cognitive functions.

(MORE: New Research on Understanding Alzheimers)

Dr. Rudolph Tanzi, director of the genetics and aging research unit at Massachusetts General Hospital and professor of neurology at Harvard Medical School, and his team first identified CD33 in 2008, and at the time, he says, We had no idea what this thing did. And in the [scientific research] literature, little was known about it. So we started from scratch.

Beginning with studies of the where the gene was expressed, he found that a subset of brain cells known as microglia seemed to show high levels of CD33, which makes receptors that pop up on the surface of the cells to bind to neuronal debris, including the residue of inflammatory reactions, and dead and dying nerve cells. CD33 functions as a molecular housekeeper, patrolling the nervous system for any material that doesnt belong and could impair normal brain function. That includes the deposits of amyloid protein that build up in the brains of Alzheimers patients, eventually forming sticky plaques that compromise normal nerve function before destroying them.

(MORE: First Genes Linked to Higher Risk of Alzheimers Disease Among African-Americans)

But when Tanzis team looked at the brains of patients who had died of Alzheimers, they found that CD33 also had a darker side. In patients with a higher burden of amyloid plaques, CD33 also appeared in excess. And so did tons of dead neurons. At some point, as the amyloid is making the cells sick, and forming tangles as lots of neurons are dying, the microglia put on their battle gear and turn radical, killing whatever they think is attacking the brain, says Tanzi. The result is friendly fire, and they start to kill so many neurons that the microglia are now detrimental; they are no longer clearing but theyre rounding up nerve cells and shooting out free radicals and causing a lot of damage.

Instead of engulfing and removing the amyloid, microglia armed with CD33 were targeting healthy nerves instead. To confirm that, Tanzis team conducted a series of tests with cells in culture and in animals, and found that when microglia were stripped of CD33, they went back to performing their housekeeping duties as expected, sniffing out amyloid and pulling the protein out of circulation. Mice genetically engineered to develop Alzheimers plaques but without CD33 showed lower levels of amyloid plaques in their brains than animals with the gene, suggesting that the CD33 was clearing the protein away.

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How an Alzheimer's Gene Could Lead to New Treatments

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The Mesothelioma Applied Research Foundation announced today that the educational video covering the BAP1 gene, which is the first gene discovered in mesothelioma, is now available on the organizations website.

Alexandria, VA (PRWEB) April 26, 2013

BAP1 is the first gene discovered in mesothelioma and researchers have just begun embarking on trials to better understand its incidence.

In germ line mutations (inherited mutations), this gene is thought to be extremely rare but has been found to have associations with uveal melanoma (melanoma of the eye), renal cell carcinoma (kidney cancer) and an unpigmented nevi (a skin lesion without color). It is thought that approximately 25% of mesothelioma patients will have somatic mutations (those that occur spontaneously) of this gene.

According to the executive director of the Mesothelioma Applied Research Foundation, Mary Hesdorffer, Nurse Practitioner, this gene has much potential for mesothelioma patients.

Currently, the research goal of the BAP1 gene is for prevention and early detection of mesothelioma, says Ms. Hesdorffer.

According to her, this means that, for example, asbestos exposed individuals who carry the gene can be studied to determine if a cancer signal can be picked up before the development of mesothelioma.

The idea is that down the line, if you have a germ line mutation, you and your immediate family will be screened for cancers associated with this gene in the hope of picking up an early malignancy. If the gene is found to be defective, researchers will be looking for ways to turn it off and avoid the malignancy entirely," added Ms. Hesdorffer.

The Mesothelioma Applied Research Foundation had an entire session devoted to the BAP1 gene at the 2013 Symposium.

Mesothelioma is a malignant tumor of the lining of the lung, abdomen, or heart known to be caused by exposure to asbestos. Medical experts consider it one of the most aggressive and deadly of all cancers. Approximately 3,000 Americans are diagnosed with mesothelioma every year and an estimated one-third were exposed while serving in the Navy or working in Navy shipyards.

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New Mesothelioma Gene Discovered: Educational Video Available

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DUBLIN--(BUSINESS WIRE)--

Research and Markets has announced the addition of the "MediPoint: Predictive Breast Cancer Gene Testing - Current and Future Players" report to their offering.

This report focuses on the predictive breast cancer gene testing markets in the US and Europe, and future markets in China, India and Brazil, identifying and competitively assessing current marketed and pipeline products and emerging technologies.

This report identifies the unmet needs in the market, provides an understanding of physician perception of predictive breast cancer gene testing, and future trends. To successfully market new gene tests, companies need to offer gene tests that address the current unmet needs of current predictive breast cancer gene tests and show better efficacy and cost effectiveness to the gene tests currently in the market. This report will identify the opportunities for this technology.

Scope

- Investigation of current and future market competition for predictive breast cancer gene testing.

- Competitor assessment.

- Coverage of key market players and company profiles including business description, financial overview and SWOT analysis.

- Strategic assessment of the device sector through market impact analysis, future market scenario and company analysis.

- Direct quotes from Key Opinion Leaders (KOL) as well as oncologists, geneticists and genetic counselors already using these gene tests.

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Research and Markets: MediPoint: Predictive Breast Cancer Gene Testing - Current and Future Players

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The Stream - The baby blueprint
Follow The Stream on Al Jazeera: http://stream.aljazeera.com/story/201304192241-0022689 YOUTUBE: http://www.youtube.com/show/thestream TWITTER: https://twitt...

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The Stream - The baby blueprint - Video

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A Beginners Guide to Genetic Engineering
Science Talent Search 2013.

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A Beginners Guide to Genetic Engineering - Video

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ALM207 Genetic engineering lecture two
This is a video on the topic Genetic engineering lecture Two. This is part of the topic of technology in Plant and Animal breeding, which is offered in the Agricultural Degree at NMIT. For...

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Dr Rasheed Genetic Engineering 23-4

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Dr Rasheed Genetic Engineering 23-4 - Video

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New Gift - Supriyo Sen - GE FOCUS FOWARD
Subscribe to the GE Channel: http://full.sc/12xcByI In today #39;s context of biological and ecological destruction caused by chemical farming, industrial agricu...

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New Gift - Supriyo Sen - GE FOCUS FOWARD - Video

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Genetic Engineering: Somewhat Defined
These are my comrades explaining their own impromptu definition of genetic engineering.

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Genetic Engineering on Genetically Modified Food
"A multimedia project for the 2013 Student Bio Expo by Abbey Landicho and Lucy Lu." This audio slideshow is about the topic Genetic Engineering about Genetic...

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Genetic Engineering on Genetically Modified Food - Video

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Genetic engineering The world_s greatest scam_ 1)

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Public release date: 25-Apr-2013 [ | E-mail | Share ]

Contact: Kathryn Ruehle kruehle@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, April 25, 2013Delving into controversial and unsettling subjects such as the gender basis of violence, the new refereed journal Violence and Gender, launching in fall 2013, will explore the difficult issues that are vital to threat assessment and prevention of the epidemic of violence. Edited by Mary Ellen O'Toole, PhD, Violence and Gender is the first and only peer-reviewed journal focusing on the understanding, prediction, and prevention of acts of violence, and will be published online with Open Access options and in print by Mary Ann Liebert, Inc., publishers.

"We have an urgent imperative," says Mary Ann Liebert, President and CEO of the company that bears her name. "There are differences in the way men and women exhibit violent behavior, and they need to be better understood and addressed to prevent tragic acts of murder and massive, often irreversible, injury. It is a serious public health issue."

Violence and Gender will be the international forum for the critical examination of biological, genetic, behavioral, psychological, racial, ethnic, and cultural factors as they relate to the gender of perpetrators of violence. Papers in the Journal will cover topics such as gender biology; genetics; psychopathy; mental health; planned predatory behavior; testosterone, hormones, and neurochemicals; nature vs. nurture; films, television, and video games; and pyromania.

The Editor-in-Chief of Violence and Gender, Mary Ellen O'Toole, PhD, is recognized as the FBI's leading expert in psychopathy. Her expertise is in criminal investigative analysis, offender behavior, targeted school violence, workplace violence, and threat assessment. How gender impacts these subjects must be better understood to prevent the growing number and nature of violent episodes.

"We are becoming immune to tragic events such as Columbine," Dr. O'Toole says. "The mandate for this journal to help us better understand and hopefully prevent these tragedies is absolute."

Dr. O'Toole has helped develop a better understanding of infamous offenders, including Green River Killer Gary Ridgway and Unabomber Ted Kaczynski, and high-profile crimes, such as the Columbine shootings, Zodiac serial murder case, and 2002 Salt Lake City Olympics bombing.

"I spent my career studying the criminal violent mind," says Dr. O'Toole, "and now gratuitous violence is at an all-time high. This violence is well-planned, lethal, and extremely callous. The offenders are nearly always male. Does gender really make a difference in the commission of violent crime? It's time for a journal to take on this question."

Violence and Gender will be a primary resource for psychologists and mental health providers; sociologists; criminologists; educators; cultural anthropologists; probation, parole, and corrections officers; and law enforcement professionals at federal, state, local, and international agencies that assess threats and deal with violent behaviors.

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Violence and Gender Journal launching fall 2013

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Even as the final report of the Supreme Court-appointed Technical Expert Committee (TEC) on open field trials of genetically modified crops is awaited, 51 independent international scientists with expertise in genetic engineering and biosafety protocols have approved the panels Interim Report. The report has called for a 10-year moratorium on open field trials of Bt food crops until adequate regulatory mechanisms and safety standards are put in place.

With Bt brinjal being the first-ever food crop sought to be introduced in India, its dossier went through international appraisal and evoked much interest throughout the world.

The TEC report attracted attention because of intense polarisation over the use of GM agri-biotechnologies in food and the environment and the large number of public and private researchers, investors and companies engaged in developing GM crops and associated Intellectual Property Rights claims, the renowned GM scientists said in a statement.

Since the Interim Report was made public, the Union Agriculture Ministry filed an affidavit in the Supreme Court in favour of GM technology. After hearing the Ministry, the court appointed a sixth member on the panel.

This was opposed by Aruna Rodrigues, lead PIL petitioner, through her lawyer Prashant Bhushan, who said that in the matter of regulation of GM crops, the Ministry of Environment and Forests stood over the Agriculture Ministry.

Underscoring the need for science to operate free of commercial and political goals, the scientists said the review of previous approvals in India for Bt crops left the TEC in no doubt that India was not ready to make reliable safety judgments because of failures in procedure, inadequate attention to development of competent and independent regulatory bodies and lack of appropriate management of conflict of interest among scientific consultants.

The TEC provided competence and independence to achieve credibility. The science used by the TEC is sound and its recommendations are reasonable. It has not imposed any new rules or suggested a moratorium on research. It has simply called for adequate standards to be established, said the 51 signatories, including fellows of Royal Societies or National Academies of Science, scientists representing a range of research disciplines including plant genetic engineering and the creation of first GM food crop, tomato, in the U.S., which was later withdrawn for health concerns.

The TEC made 11 specific recommendations for properly regulating the development and commercialisation of genetically modified crops in India.

It recommended that product testing outside of the laboratory [field trials] be stopped until a comprehensive and effective process for such testing could be implemented. Except for a ban on testing GM crops for which India is a centre of biodiversity or origin, all testing can restart as soon as the government provides a robust and proper procedure, the statement said.

Taking note of the concerns expressed by the scientists, three eminent citizens the former Supreme Court judge, V.R. Krishna Iyer; the former Election Commissioner, J.M. Lyngdoh; and the former Chief Justice of the Delhi High Court, A.P. Shah endorsed and forwarded their statement to Prime Minister Manmohan Singh and UPA chairperson Sonia Gandhi.

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Global scientists back 10-year moratorium on field trials of Bt food crops

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How TPP will hurt America
On Wednesday, the Senate Finance Committee met to discuss the opportunities and challenges the Trans-Pacific Partnership could pose on the United States. The...

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FORT MYERS NeoGenomics is winning market share.

That was one of the major takeaways from an earnings call it held for investors Thursday.

The Fort Myers-based company, focused on genetic testing for cancer, saw its test volume grow by 19 percent in the first quarter. Along with that growth came record quarterly revenue of $15.7 million, up 3 percent from a year ago.

Another takeaway? The company continues to aggressively develop new tests, adding to its already extensive menu of choices.

Innovation is very important to what we do. We are in an era of personalized medicine and we are introducing a lot of new molecular tests that are not only helping the company to grow, but also helping physicians diagnose and treat cancer better, said Douglas VanOort, the companys chairman and CEO, in a phone interview after the call.

NeoGenomics handles testing for pathologists, clinicians, oncologists and hospitals throughout the country.

The company reported profits of $300,000 for the first quarter, down from $603,000 a year ago.

During the conference call, VanOort highlighted the companys efforts to become more efficient and to regain profitability in the aftermath of a big regulatory change. The change, related to its Medicare billing practices, has cost the company about $1.3 million quarterly since it took effect last year. The company expects to overcome that hurdle later this year.

In the first quarter, the average revenue per test decreased by 13 percent from a year ago, primarily because of the regulatory change. But through newfound efficiencies, the company cut its cost per test by 5 percent from the fourth quarter, and its down 12 percent from a year ago.

We are not cutting costs, VanOort said in the phone interview. We are just finding more efficient ways to do what we do.

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Fort Myers-based genetic testing company sees record quarterly revenue

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Newswise New Brunswick, NJ Your genetic makeup can help determine how well your body will respond to weight loss efforts aimed at controlling high blood pressure, a new study confirms.

The multi-institutional study, led by researchers at The Cardiovascular Institute, part of the University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, may help clarify how hypertension develops and progresses in certain individuals and also identify people for whom weight loss programs are most likely to help reduce blood pressure. Results were published in the current issue of Hypertension 2013;61:857-863.

The Trial of Nonpharmacologic Interventions in the Elderly (TONE) looked at 21 polymorphisms that have been identified as relating to hypertension, obesity, and diabetes mellitus to see what impact weight loss and sodium-reduction programs would have on blood pressure. Polymorphisms are the elements of a persons DNA that make it different from anothers and allow for diversity in such varied areas as eye color, hair texture, and even blood type. The TONE study identified several polymorphisms that relate to weight sensitivity with regard to hypertension, according to principal investigator John B. Kostis, MD, John G. Detwiler professor of cardiology, professor of medicine and pharmacology, associate dean for cardiovascular research, and director of The Cardiovascular Institute of Robert Wood Johnson Medical School.

The study sheds some light on an issue that has received little attention in the past, the researchers said.

There are more than a thousand papers discussing the question of what the impact is on blood pressure of decreasing the amount of salt you consume in your dietwhat is called salt sensitivity. But, there is nobody talking about weight sensitivity, and weight loss is equally or more important in controlling blood pressure, Dr. Kostis said.

Our work describes the variability of blood pressure drop in response to weight loss, according to a number of genetic polymorphisms, added William J. Kostis, PhD, MD, clinical and research fellow in medicine, Massachusetts General Hospital, Cardiology Division, alumnus of Robert Wood Johnson Medical School, and member of The Cardiovascular Institute, who was the first author of the study.

Participants in the TONE studyindividuals age 60 to 80 who were already taking one or two anti-hypertensive medicationswere randomly assigned to one of four interventions: Intensive dietary intervention focused on sodium reduction Weight loss program Combination of weight loss and sodium-reduction programs Attention control, in which individuals attended meetings that discussed dentistry, podiatry, or other topics unrelated to hypertension, weight loss, or sodium reduction

Regardless of the intervention, participants levels of anti-hypertensive medication remained the same throughout, to remove medication changes as a variable.

The study showed that both weight loss, if individuals are overweight, and decreased sodium intake may each lead to lower blood pressure, and the combination of weight loss and sodium restriction is more effective than either strategy alone, noted Dr. William Kostis.

Physicians can put these findings to use today through a blood test or even saliva test that measures genotype, Dr. John Kostis said. They can compare the patients genetic background with the polymorphisms that have been identified in the study and counsel patients accordingly, offering advice as to which type of intervention may be more successful in lowering that patients blood pressure, he said.

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New Study Confirms Link between Weight Loss and Blood Pressure for Individuals with Specific Genetic Polymorphisms

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Undoing aging: Aubrey de Grey at TEDxDanubia 2013
Aubrey de Grey is a biomedical gerontologist and the Chief Science Officer of SENS Foundation, a charity dedicated to combating the aging process. He is also...

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Rett #39;s Syndrome: Finding a Cure Through Gene Therapy
A lab research project for the student bio expo 2013 by Mimansa Dogra I explore Rett #39;s Syndrome and the causes of this disorder, as well as treatments than c...

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NEW YORK, April 24, 2013 /PRNewswire/ -- Reportlinker.com announces that a new market research report is available in its catalogue:

Stem Cell Therapy Market in Asia-Pacific to 2018 - Commercialization Supported by Favorable Government Policies, Strong Pipeline and Increased Licensing Activity

http://www.reportlinker.com/p01075729/Stem-Cell-Therapy-Market-in-Asia-Pacific-to-2018---Commercialization-Supported-by-Favorable-Government-Policies-Strong-Pipeline-and-Increased-Licensing-Activity.html#utm_source=prnewswire&utm_medium=pr&utm_campaign=Biological_Therapy

Stem Cell Therapy Market in Asia-Pacific to 2018 - Commercialization Supported by Favorable Government Policies, Strong Pipeline and Increased Licensing Activity

Summary

GBI Research, the leading business intelligence provider, has released its latest research "Stem Cell Therapy Market in Asia-Pacific to 2018 - Commercialization Supported by Favorable Government Policies, Strong Pipeline and Increased Licensing Activity". The report provides an in-depth analysis on stem cell research and development in India, China, Japan, South-Korea and Singapore. The report market analysis and forecasts for CABG, LSCT, Type 1 DM, Type 2 DM, Hearticellgram, Cerecellgram, Cartistem and Cupistem. The report also provides information on trends and pipelines. In addition to this, the report covers market drivers and challenges for stem cell research market.

This report is built using data and information sourced from proprietary databases, primary and secondary research and in-house analysis by GBI Research's team of industry experts.

GBI Research analysis finds the stem cell therapy market was valued at $545m in 2012, and is projected to grow at a Compound Annual Growth Rate (CAGR) of 10% from 2012 to 2018, to attain a value of $972m in 2018. The market is poised for significant growth in the forecast period due to the anticipated launch of JCR Pharmaceuticals' JR-031 (2014) in Japan and FCB Pharmicell's Cerecellgram (CCG) (2015) in South Korea. The research is mainly in early stages, with the majority of the molecules being in early stages of development (Phase I/II and Phase II). Phase I/II and Phase II contribute 67% of the pipeline. Stem cell research is dominated by hospitals/universities/institutions, which contribute 63% of the molecules in the pipeline. The dominance of institutional research is attributable to uncertain therapeutic outcomes in stem cell research.The major companies conducting research in India include Reliance Life Sciences and Stempeutics Research Pvt Ltd, among others. The major institutions include PGIMER and AIIMS.

Scope

- Country analysis of regulatory framework of India, China, South-Korea, Japan and Singapore - In-depth information and analysis on the pipeline products expected to bring a shift to the market positions of the leading manufacturers. - Market characterization data for stem cell research for CABG, LSCT, Type 1 DM, Type 2 DM, Hearticellgram, Cerecellgram, Cartistem and Cupistem. - Key drivers and restraints that have a significant impact on the market. - Competitive landscape of stem cell research in Asia-Pacific. The key companies discussed in this report are Stempeutics, Reliance Lifesciences, International Stem cell services, Shenzhen Beike Biotechnology, JCR Pharmaceuticals, ES Cells International, Stem Cell Technologies i, Pharmicell and Medipost - Key M&A activities, licensing agreements, that have taken place between stem cell companies in 2007 till date.

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Stem Cell Therapy Market in Asia-Pacific to 2018 - Commercialization Supported by Favorable Government Policies ...

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The Stem Cell Institute, located in Panama City, Panama, will present an informational umbilical cord stem cell therapy seminar on Saturday, May 11, 2013 in Miami, Florida at the Conrad Hotel from 1:00 pm to 4:00 pm.

Miami, Florida (PRWEB) April 24, 2013

Speakers and topics include:

"Umbilical cord stem cells: regeneration, repair, inflammation and autoimmunity" - Neil Riordan, PhD

Dr. Riordan is the Founder of the Stem Cell Institute and Medistem Panama Inc.

Dr. Paz is the Medical Director at the Stem Cell Institute. Dr. Paz practiced internal medicine in the United States for over a decade before joining the Stem Cell Institute in Panama.

Dr. Lowe is a psychiatrist at Amen Clinics in New York City.

Raymond Cralle is a physical therapist at Cralle Physical Therapy in Delray Beach, Florida.

After the talks, our speakers and stem cell therapy patients will be on hand to share their personal experiences and answer questions.

Admission is free but space is limited and registration is required. For venue information and to register and reserve your tickets today, please visit: http://scimiamiseminar.eventbrite.com/ or call Cindy Cunningham, Patient Events Coordinator, at 1 (800) 980-7836.

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Stem Cell Institute Public Seminar on Adult Stem Cell Therapy in Miami, Florida May 11th, 2013

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Public release date: 25-Apr-2013 [ | E-mail | Share ]

Contact: Sue McGreevey smcgreevey@partners.org 617-724-2764 Massachusetts General Hospital

Massachusetts General Hospital (MGH) investigators have determined that one of the recently identified genes contributing to the risk of late-onset Alzheimer's disease regulates the clearance of the toxic amyloid beta (A-beta) protein that accumulates in the brains of patients with the disease. In their report receiving advance online publication in Neuron, the researchers describe a protective variant of the CD33 gene that promotes clearance of A-beta from the brain. They also show that reducing expression of CD33 in immune cells called microglia enhances their ability to clear away A-beta protein, raising the possibility that blocking CD33 activity could help the brain's immune system remove A-beta.

"Our findings show, for the first time, a "switch" that controls how fast microglial cells can clear A-beta protein from the brain as we age CD33 is the key," says Rudolph Tanzi, PhD, director of the Genetics and Aging Unit in the MGH Department of Neurology and senior author of the Neuron paper. "If we can find a way of safely inactivating CD33 on microglia, we should be able to slow the accumulation of A-beta in aging brains and hopefully reduce risk for Alzheimer's disease."

In 2008, as part of the Alzheimer's Genome Project, Tanzi's team identified four novel genes containing variants that increased the risk of late-onset Alzheimer's, the most common form of the devastating neurological disorder. One of these was CD33. The protein was known to play a role in regulation of the innate immune system the body's first line of defense against infection but how it might function in the brain and possibly contribute to Alzheimer's risk was not known.

In the current study, the researchers first found that CD33 activity was significantly higher in microglia cells in brain samples from Alzheimer's patients than in cells from non-demented controls. Moreover, they showed that the presence of a version of the gene that protected against Alzheimer's disease reduced CD33 protein levels in the brain. Importantly, the same protective version of CD33 was found to reduce levels of A-beta 42 the primary constituent of the amyloid plaques that characterize the disease. Greater numbers of CD33-containing microglia also were associated with higher levels of A-beta 42 and more plaques overall.

In an Alzheimer's mouse model, knocking out the CD33 gene improved the ability of microglia in the brain to clear away A-beta 42 and reduced the presence of amyloid plaques. Experiments with cultured microglia showed that increasing CD33 expression on the cells' surface inhibited their ability to take up A-beta 42, while reducing CD33 activity led to greater clearance of A-beta 42.

"Collectively these experiments indicate that CD33 directly modulates the ability of microglial cells to clear A-beta 42 from the brain." says Tanzi. "Our findings raise the possibility that inhibiting CD33 activity in the brain could represent a potentially powerful new approach to treating and possibly preventing Alzheimer's disease."

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Primary support for the study includes grants from the Cure Alzheimer's Fund and National Institutes of Health grants R37MH060009, P01AG15379, R01AG08487 and P50AG05134. In addition to Tanzi, the Kennedy Professor of Neurology at Harvard Medical School, co-authors of the Neuron paper are lead author Ana Griciuc, PhD, of the MGH Genetics and Aging Research Unit; Antonio Parrado, Andrea Lesinski, Caroline Asselin, Kristina Mullin, Basavaraj Hooli, PhD, and Se Hoon Choi, PhD, MGH Genetics and Aging Unit; and Alberto Serrano-Pozo, MD, and Bradley Hyman, MD, PhD, MGH Alzheimer's Disease Research Laboratory.

Read more:
Alzheimer's risk gene presents potential treatment target

Recommendation and review posted by Bethany Smith

Gene Sperling, President Obamas top economic adviser, sketched out a hopeful scenario on Thursday for the next round of budget negotiations.

Not only is there the possibility of passing a budget to fund the government through the normal congressional process rather than lurching from crisis to crisis with stopgap measures, but Sperling also sees a building of trust over the dinners Obama has hosted with groups of lawmakers in recent weeks.

Trust at least that there can be conversations that can be kept quiet. Trust that the president is willing to compromise, that hes willing toas weve seeneven take some disagreement from his own supporters, Sperling, who is director of the White House National Economic Council, said at an event hosted by Allstate, The Atlantic and National Journal.

That's a positive outlook for a process that has been thoroughly twisted in recent years--and, as National Journalrecently reported, for which the path forward is anything but clear.

Sperling offered one place where there wont be any friendly, quiet talks hosted by the White House. Earlier this year, Congress voted to suspend the U.S. debt ceiling until May 18, at which point the Treasury Department is expected to take so-called extraordinary measures to push back the date for a few months when the country exceeds its borrowing limit and goes into default. Then, it will be up to lawmakers to raise the ceiling.

In the summer of 2011, the debate over raising the nations debt limit became a looming crisis as Republicans tried to use the talks to demand spending cuts the White House refused to make. The dragged-out negotiations ultimately hit confidence, caused markets to tank and ultimately cost the U.S. its top, triple-A credit rank from ratings agency Standard & Poors. It is not remembered by most as a shining example of Washington at work.

This time, Sperling said, We just have to be very clear: The era of threatening default as a budget [negotiating] tactic is over, Sperling said. The president is not going to negotiate on this.

Suspending rather than raising the debt ceiling this winter allowed Republicans to sidestep a politically thorny issue. But negotiations this summer could heat up again, although it's not clear to what degree. Earlier this month, analysts at political risk research and consulting firm Eurasia Group wrote that "early signals indicate that this summer's debt ceiling fight will present less risk and less opportunity for fiscal reform than that of 2011." Some House Republicans have proposed prioritizing the nations payments in the event lawmakers cant agree to raise the U.S. borrowing limit before it is reached. Sperling rejected that idea. It is default by any other name, he said Thursday.

And although Sperling sounded a hopeful note about negotiations occuring through regular processes and growing trust among lawmakers, he acknowledged that any negotiations over the budget could be derailed by intransigence. I think we have to recognize that if people, you know, particularly in the House, are completely unwilling to compromise, theres nothing any of us can do, he said.

Originally posted here:
Gene Sperling, Top Econ Adviser: “The Era of Threatening Default Is Over”

Recommendation and review posted by Bethany Smith