Archive for the ‘Gene Therapy Research’ Category

(MENAFN - Arab Times) Ministry of Health (MoH) employees holding PhD degrees announced that they will participate in the sit-in demonstration carried out by the Labor Union of Health Ministry, reports Al-Seyassah daily.

In the press release, they said they are protesting against the fact that they are receiving the same salary scale and benefits as any other ministry employee with lower qualifications and if necessary, they are ready to even burn their PhD certificates at the sit-in to get the benefits they deserve according to their qualifications.

The sit-in will be carried out in front of Health Ministry headquarters in Sulaibikhat at 10 am on Tuesday, March 20, 2012.

The number of PhD holders has exceeded 100 considering the participation of PhD holders from other ministries as well.

Meanwhile, the MoH has banned stem cell therapy in the country until the committee tasked to set the standards for the treatment completes its work, reports Al-Anba daily quoting Director of Health License Department Dr Marzouq Al-Bader.

Al-Bader disclosed the ministry had earlier formed the committee to ensure the stem cell procedures are carried out in an appropriate manner to protect the patients. He added the ministry will also issue a decision soon to regulate the use of antibiotics in the private health sector.

Meanwhile, Al-Bader confirmed the ministry has endorsed around 51,000 female doctors in private hospitals and health centers. He said the ministry closely monitors the performance of female doctors and those found to have violated the law will be referred to the Medical Council for the necessary action.

On the issuance of licenses through the Internet, Al-Bader revealed his department has asked the ministry to activate the e-link system for this purpose.

He said the ministry has asked the Kuwait Municipality to issue permit for the construction of a building fit for the department's operations.

Meanwhile, the Medical Emergency Department at the Ministry of Health has affirmed its readiness to deal with emergency cases that may arise due to a series of dust storms engulfing the country.

Read this article:
Stem cell therapy banned in Kuwait

Washington, Mar 19 (ANI): A compound used in traditional Japanese medicine, honokiol (HNK), plays a role in blocking key protein in inflammatory brain damage, a new study led by Indian origin scientist has suggested.

Microglia are the first line defence of the brain and are constantly looking for infections to fight off.

Overactive microglia can cause uncontrolled inflammation within the brain, which can in turn lead to neuronal damage.

New research shows that HNK is able to down-regulate the production of pro-inflammatory cytokines and inflammatory enzymes in activated microglia via Klf4, a protein known to regulate DNA.

Scientists from the National Brain Research Centre, Manesar, India, used lipopolysaccharide (LPS), a molecule present on the surface of bacteria, to stimulate an immune response from microglia cells.

LPS mimics the effect of a bacterial infection and the microglia cells spring into action, releasing proinflammatory cytokines, such as TNFa.

Activation of microglia also stimulates the production of nitric oxide (NO) and Cox-2, which co-ordinate the immune response, leading to inflammation.

However uncontrolled inflammation can lead to neuronal death and permanent brain damage.

Microglial inflammation is also observed in several neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and multiple sclerosis.

The team led by Dr Anirban Basu found that the inflammatory response was mediated by Klf4, a 'transcription' factor which binds directly to DNA to enhance or impede gene expression.

The rest is here:
Japanese traditional therapy may help prevent inflammatory brain damage

London, March 19 (ANI): Researchers have revealed how a mutation in a single gene is responsible for the inability of neurons to effectively pass along appetite suppressing signals from the body to the right place in the brain, which results in obesity caused by a voracious appetite.

Researchers at Georgetown University Medical Center suggested there might be a way to stimulate expression of that gene to treat obesity caused by uncontrolled eating.

The research team specifically found that a mutation in the brain-derived neurotrophic factor (Bdnf) gene in mice does not allow brain neurons to effectively pass leptin and insulin chemical signals through the brain.

In humans, these hormones, which are released in the body after a person eats, are designed to "tell" the body to stop eating. But if the signals fail to reach correct locations in the hypothalamus, the area in the brain that signals satiety, eating continues.

"This is the first time protein synthesis in dendrites, tree-like extensions of neurons, has been found to be critical for control of weight," said the study's senior investigator, Baoji Xu, Ph.D., an associate professor of pharmacology and physiology at Georgetown.

"This discovery may open up novel strategies to help the brain control body weight," he noted.

Xu has long investigated the Bdnf gene. He has found that the gene produces a growth factor that controls communication between neurons.

For example, he has shown that during development, BDNF is important to the formation and maturation of synapses, the structures that permit neurons to send chemical signals between them.

The Bdnf gene generates one short transcript and one long transcript. He discovered that when the long-form Bdnf transcript is absent, the growth factor BDNF is only synthesized in the cell body of a neuron but not in its dendrites. The neuron then produces too many immature synapses, resulting in deficits in learning and memory in mice.

Xu also found that the mice with the same Bdnf mutation grew to be severely obese.

Read this article:
Gluttony gene that makes you eat more even when you are full identified

A single gene's effect on the brain can result in non-stop eating, research has shown.

Scientists believe the "gluttony gene" may be responsible for cases of obesity caused by out-of-control appetite.

The Bdnf gene variant was studied in mice. It was found to prevent brain neurons from transmitting signals that tell the body it has eaten enough.

"This discovery may open up novel strategies to help the brain control body weight," said lead researcher Dr Baoki Xu, from Georgetown University Medical Centre in the United States.

Hunger and satiety, the sensation of "feeling full", are governed by a complex balance of hormonal and neuronal signals.

Two hormones in particular, leptin and insulin, released in the body after a meal play a key role.

Their chemical signals activate neurons in the hypothalamus region of the brain that trigger satiety. But if the connection is not made, the craving for food continues.

"Short" versions of the Bdnf gene block the leptin and insulin signals and prevent the "stop eating" message passing through the brain to the correct appetite-suppressing locations, say the scientists.

The research is reported in the journal Nature Medicine.

Bdnf makes a protein that is synthesised in dendrites, the branch-like "fingers" that project from nerve cells. Dendrites carry the synapses that neurons use to communicate to each other.

The rest is here:
'Gluttony gene' may explain out-of-control appetite

At 102, Saul Belson has escaped many of the diseases that easily kill men 30 and 40 years his junior.

It may be luck, or the fact that he tried to eat healthy and was never a smoker or a drinker. Or, it might be genetics.

Belson is part of a set of those not just living, but living life well and with no or few health problems, over age 100.

Hes hoping to be selected as a genomic pioneer in a gene sequencing competition.

A hundred centenarians are being chosen worldwide to voluntarily contribute their DNA to the Archon Genomics X PRIZE competition, presented by Medco, a health care and research company based in New Jersey.

It is a competition of world-class teams from genotyping companies that will compete to quickly, accurately and affordably sequence the genomes of the 100 centenarians.

The grand prize to the winning genotyping company is $10 million. It is being funded by philanthropists and sponsors.

Ive always been very interested in science, Belson said. If Ive got something good, Im willing to share it.

Belson was born in London on Sept. 12, 1909, to Russian immigrant parents. They came to Chicago when he was 5 years old.

Belson spent most of his professional life working in the dental industry as a designer, making false teeth for Boston Dental in Chicago. He moved to Sakonnet Bay Manor in Tiverton six years ago after his wife, Dora, died, and to be closer to his son, Harold.

Follow this link:
Tiverton centenarian recruited for genetics contest that could unlock secrets of longevity

London, March 19 (ANI): Scientists have now found answer to why some patients fail to respond to some of the most successful cancer drugs.

Tyrosine kinase inhibitor drugs (TKIs) work effectively in most patients to fight certain blood cell cancers, such as chronic myelogenous leukemia (CML), and non-small-cell lung cancers (NSCLC) with mutations in the EGFR gene.

These precisely targeted drugs shut down molecular pathways that keep these cancers flourishing and include TKIs for treating CML, and the form of NSCLC with EGFR genetic mutations.

Now, a multi-national research team led by scientists at Duke-NUS Graduate Medical School in Singapore, working with the Genome Institute of Singapore (GIS), Singapore General Hospital and the National Cancer Centre Singapore, has discovered that there is a common variation in the BIM gene in people of East Asian descent that contributes to some patients' failure to benefit from these tyrosine kinase inhibitor drugs.

"Because we could determine in cells how the BIM gene variant caused TKI resistance, we were able to devise a strategy to overcome it," said S. Tiong Ong, M.B.B. Ch., senior author of the study and associate professor in the Cancer and Stem Cell Biology Signature Research Programme at Duke-NUS and Division of Medical Oncology, Department of Medicine, at Duke University Medical Center.

"A novel class of drugs called the BH3-mimetics provided the answer," he said.

"When the BH3 drugs were added to the TKI therapy in experiments conducted on cancer cells with the BIM gene variant, we were able to overcome the resistance conferred by the gene. Our next step will be to bring this to clinical trials with patients," Ong added.

Yijun Ruan, Ph.D., a co-senior author of this study and associate director for Genome Technology and Biology at GIS said: "We used a genome-wide sequencing approach to specifically look for structural changes in the DNA of patient samples. This helped in the discovery of the East Asian BIM gene variant. What's more gratifying is that this collaboration validates the use of basic genomic technology to make clinically important discoveries."

If the drug combination does override TKI resistance in people, this will be good news for those with the BIM gene variant, which occurs in about 15 percent of the typical East Asian population. By contrast, no people of European or African ancestry were found to have this gene variant.

"While it's interesting to learn about this ethnic difference for the mutation, the greater significance of the finding is that the same principle may apply for other populations," said Patrick Casey, Ph.D., senior vice dean for research at Duke-NUS and James B. Duke Professor of Pharmacology and Cancer Biology.

Read the rest here:
Gene variant in East Asians could explain resistance to cancer drugs

Could lead to treatments for obesity

By Tamara Cohen

PUBLISHED: 14:28 EST, 18 March 2012 | UPDATED: 14:28 EST, 18 March 2012

The secret to staying slim may be all in your genes.

Scientists believe they have found the gluttony gene which fails to tell your brain when you are full.

In tests on mice, they showed that a mutation on a single gene broke down communication in the body and led to non-stop eating and rapid weight gain.

Gut buster: Scientists believe they have uncovered a gene which makes you eat even when are full because it breaks down communication between the body and the brain

But the good news is, they hope identifying the gene could help with treatments for obesity which affects nearly one in four adults in the UK.

Researchers at Georgetown University Medical Centre in the U.S. studied variations in the Bdnf gene in mice.

See original here:
Georgetown University Medical Centre: Scientists discover 'greedy gene¿ that makes you eat more even when you are full

A single gene's effect on the brain can result in non-stop eating, research has shown.

Scientists believe the "gluttony gene" may be responsible for cases of obesity caused by out-of-control appetite. The Bdnf gene variant was studied in mice. It was found to prevent brain neurons from transmitting signals that tell the body it has eaten enough.

"This discovery may open up novel strategies to help the brain control body weight," said lead researcher Dr Baoki Xu, from Georgetown University Medical Centre in the US.

Hunger and satiety, the sensation of "feeling full", are governed by a complex balance of hormonal and neuronal signals. Two hormones in particular, leptin and insulin, released in the body after a meal play a key role.

Their chemical signals activate neurons in the hypothalamus region of the brain that trigger satiety. But if the connection is not made, the craving for food continues.

"Short" versions of the Bdnf gene block the leptin and insulin signals and prevent the "stop eating" message passing through the brain to the correct appetite-suppressing locations, say the scientists.

The research is reported online in the journal Nature Medicine.

Bdnf makes a protein that is synthesised in dendrites, the branch-like "fingers" that project from nerve cells. Dendrites carry the synapses that neurons use to communicate to each other.

"If there is a problem with the Bdnf gene, neurons can't talk to each other and the leptin and insulin signals are ineffective, and appetite is not modified," said Dr Xu.

Previous work by Dr Xu has shown that Bdnf is important for the formation and maturation of synapses during development. Mice born without the correct "long" version of the gene suffer impaired learning and memory. They also grow to be severely obese.

Read more:
Scientists 'discover gluttony gene'

This is a guest post from M. A. Loera Snchez from the iGEM team UANL 2012. I have carried out a few small grammar edits but otherwise the essay is all his work, and I would like to thank him for the opportunity to host it on my blog. All references are below the main text.

The mainstream fronts of synthetic biology

What I cannot build, I cannot understand.

This phrase by the genius physicist Richard Feynman is cleverly encrypted into the genetic code of the first bacterial cells with an artificial genome that have ever existed.

Actually the quote says what I cannot create, but maybe the scientists at the JCVI who are behind this tremendous breakthrough- preferred to save some base pairs to avoid the use of the word create and its tricky implications.They published this work in 2010 and opened a whole new world of possibilities and made it completely clear to anyone what we mean when we talk about Synthetic Biology and what its ultimate purpose should be: to understand life by building it.

Although the term Synthetic Biology has been around since the mid-1970s, the definition of it has been very vague: some people would call Synthetic Biology anything related to general genetic engineering procedures; others, perhaps more rightfully, would claim to be doing Synthetic Biology because of working with DNA synthesis or making bacteria behave like tiny computers. Even the 2010 report by the US Presidencial Comission for the Study of Bioethical Issues has to define the term considering different points of view (that of the molecular biology, the chemist and the engineer) and states that the activities related to Synthetic Biology are considered by some to be just extensions of already existing fields, like Molecular Biology, Genetic Engineering and Microbiology.

I remember (oh, the shame!) being skeptic about the possibility of something so oxymoronic being, well true. I still turn red when I recall that I kind of corrected the person who first said Synthetic Biology to me by telling her that what she wanted to say was maybe Systems Biology.

So what is it really?

Well, my work in Bio! has been devoted to dig into the deeps of Synthetic Biology and the iGEM competition, and throughout this time I began to notice what I would call the mainstream fronts of Synthetic Biology. These are the main orientations that so called Synthetic Biology projects would take and by enlisting them, I think it will be easier to clarify the distinctive characteristics of this field.

Front 1: DNA synthesis

Read the original post:
The mainstream fronts of Synthetic Biology: Guest post

ScienceDaily (Mar. 18, 2012) A multinational research team led by scientists at Duke-NUS Graduate Medical School has identified the reason why some patients fail to respond to some of the most successful cancer drugs.

Tyrosine kinase inhibitor drugs (TKI) work effectively in most patients to fight certain blood cell cancers, such as chronic myelogenous leukemia (CML), and non-small-cell lung cancers (NSCLC) with mutations in the EGFR gene.

These precisely targeted drugs shut down molecular pathways that keep these cancers flourishing and include TKIs for treating CML, and the form of NSCLC with EGFR genetic mutations.

Now the team at Duke-NUS Graduate Medical School in Singapore, working with the Genome Institute of Singapore (GIS), Singapore General Hospital, and the National Cancer Centre Singapore, has discovered that there is a common variation in the BIM gene in people of East Asian descent that contributes to some patients' failure to benefit from these tyrosine kinase inhibitor drugs.

"Because we could determine in cells how the BIM gene variant caused TKI resistance, we were able to devise a strategy to overcome it," said S. Tiong Ong, MBBCh, senior author of the study and associate professor in the Cancer and Stem Cell Biology Signature Research Programme at Duke-NUS and Division of Medical Oncology, Department of Medicine, at Duke University Medical Center.

"A novel class of drugs called the BH3-mimetics provided the answer," Ong said. "When the BH3 drugs were added to the TKI therapy in experiments conducted on cancer cells with the BIM gene variant, we were able to overcome the resistance conferred by the gene. Our next step will be to bring this to clinical trials with patients."

Said Yijun Ruan, PhD, a co-senior author of this study and associate director for Genome Technology and Biology at GIS: "We used a genome-wide sequencing approach to specifically look for structural changes in the DNA of patient samples. This helped in the discovery of the East Asian BIM gene variant. What's more gratifying is that this collaboration validates the use of basic genomic technology to make clinically important discoveries."

The study was published online in Nature Medicine on March 18.

If the drug combination does override TKI resistance in people, this will be good news for those with the BIM gene variant, which occurs in about 15 percent of the typical East Asian population. By contrast, no people of European or African ancestry were found to have this gene variant.

"While it's interesting to learn about this ethnic difference for the mutation, the greater significance of the finding is that the same principle may apply for other populations," said Patrick Casey, PhD, senior vice dean for research at Duke-NUS and James B. Duke Professor of Pharmacology and Cancer Biology.

See original here:
Genetic variation in East Asians found to explain resistance to cancer drugs

Public release date: 18-Mar-2012 [ | E-mail | Share ]

Contact: Karen Mallet km463@georgetown.edu Georgetown University Medical Center

Washington, D.C. -- Researchers at Georgetown University Medical Center have revealed how a mutation in a single gene is responsible for the inability of neurons to effectively pass along appetite suppressing signals from the body to the right place in the brain. What results is obesity caused by a voracious appetite.

Their study, published March 18th on Nature Medicine's website, suggests there might be a way to stimulate expression of that gene to treat obesity caused by uncontrolled eating.

The research team specifically found that a mutation in the brain-derived neurotrophic factor (Bdnf) gene in mice does not allow brain neurons to effectively pass leptin and insulin chemical signals through the brain. In humans, these hormones, which are released in the body after a person eats, are designed to "tell" the body to stop eating. But if the signals fail to reach correct locations in the hypothalamus, the area in the brain that signals satiety, eating continues.

"This is the first time protein synthesis in dendrites, tree-like extensions of neurons, has been found to be critical for control of weight," says the study's senior investigator, Baoji Xu, Ph.D., an associate professor of pharmacology and physiology at Georgetown.

"This discovery may open up novel strategies to help the brain control body weight," he says.

Xu has long investigated the Bdnf gene. He has found that the gene produces a growth factor that controls communication between neurons.

For example, he has shown that during development, BDNF is important to the formation and maturation of synapses, the structures that permit neurons to send chemical signals between them. The Bdnf gene generates one short transcript and one long transcript. He discovered that when the long-form Bdnf transcript is absent, the growth factor BDNF is only synthesized in the cell body of a neuron but not in its dendrites. The neuron then produces too many immature synapses, resulting in deficits in learning and memory in mice.

Xu also found that the mice with the same Bdnf mutation grew to be severely obese.

See the original post:
Researchers reveal how a single gene mutation leads to uncontrolled obesity

Washington, March 17 (ANI): New biotechnological and chemical methods will facilitate efficient production of chemicals, materials and fuels from renewable natural resources, such as agricultural or industrial waste materials, say researchers.

The Academy of Finland Centre of Excellence (CoE) in White Biotechnology - Green Chemistry Research is focusing on the research and development of microbial cells, or cell factories, for producing new useful compounds from sugars in plant biomass.

These compounds can be used, for example, for manufacturing bioplastics or in medical applications.

"By means of gene technology, we can modify microbial metabolism and thereby produce organic acids for a wide range of industrial applications. They can be used, among other things, for manufacturing new plastic and textile materials, or packaging technologies," explained Merja Penttila, Research Professor and Director of the Centre of Excellence from VTT Technical Research Centre of Finland.

New methods play a key role when various industries are developing environmentally friendly and energy-efficient production processes.

Use of renewable natural resources, such as agricultural or industrial waste materials, to replace oil-based raw materials will make industries less dependent of fossil raw materials and, consequently, reduce carbon dioxide emissions into the atmosphere.

The CoE also develops highly sensitive measuring methods and investigates microbial cell functions at molecular level.

"We need this information to be able to develop efficient bioprocesses for the future. For instance, we build up new micro- and nanoscale instruments for measuring and controlling microbial productivity in bioreactors during production," said Penttila.

The metabolism of microbes is modified so that they will convert plant biomass sugars into sugar acids and their derivatives.

These compounds can potentially serve as raw materials for new types of polyesters, whose properties - such as water solubility and extremely rapid degradation into natural substances - can be used, for example, in medicine.

More:
Soon, gene technology to produce novel plastics and textiles from waste

A NEW stem cell therapy treatment to develop new bones for patients with bone loss and new skin for recipients of plastic surgery has been developed, doctors from Shanghai No.9 People's Hospital announced yesterday.

In the procedure, medical staff use a special machine to collect stem cells from a patient's blood. The stem cells adhere to a base made of a special biological material.

The stem cells are then transplanted into the patient's body, where they grow into either new bones or skin tissue, while the base is absorbed by the human body.

"So far the practice has been successful in treating patients with bone and skin loss," said Dr Dai Kerong from Shanghai Jiao Tong University's translational medicine institute at Shanghai No.9 hospital. "The stem cell technology will be used to develop corneas for blind people as well as treating heart attack and stroke patients by developing new heart and cerebral tissue."

The technology is patented in China and abroad and will be licensed within one or two years, according to Dai.

China has established 51 translational medicine centers to boost the introduction of laboratory research into clinical use.

The complicated procedures and documentation required often prevent doctors from introducing lab success into clinical practice.

Dai said one reagent developed by No. 9 hospital's doctors for in vitro fertilization received a license in Europe within six months and has been used in clinical practice "while this would take at least five years in China."

See the original post here:
Eastday-Big stem cell breakthrough

15-03-2012 13:24 Video created as class project by JTC-345 students featuring Dr. Gene Kelly, CSU faculty member and Associate Director for Research and Development at the School of Global Environmental Sustainability.

Go here to read the rest:
COLORADO STATE UNIVERSITY - Enviance March Madness Contest - Gene Kelly - Video

Public release date: 15-Mar-2012 [ | E-mail | Share ]

Contact: Jennifer Ganton jganton@ohri.ca 613-798-5555 x73325 Ottawa Hospital Research Institute

A team of researchers from the Ottawa Hospital Research Institute (OHRI) and the University of Ottawa (uOttawa) has been awarded $367,000 from the Canadian Institutes of Health Research (CIHR) and $75,000 from the Stem Cell Network to lead the first clinical trial in the world of a stem cell therapy for septic shock. This deadly condition occurs when an infection spreads throughout the body and over-activates the immune system, resulting in severe organ damage and death in 30 to 40 per cent of cases. Septic shock accounts for 20 per cent of all Intensive Care Unit (ICU) admissions in Canada and costs $4 billion annually. Under the leadership of Dr. Lauralyn McIntyre, this new "Phase I" trial will test the experimental therapy in up to 15 patients with septic shock at The Ottawa Hospital's ICU.

The treatment involves mesenchymal stem cells, also called mesenchymal stromal cells or MSCs. Like other stem cells, they can give rise to a variety of more specialized cells and tissues and can help repair and regenerate damaged organs. They also have a unique ability to modify the body's immune response and enhance the clearance of infectious organisms. They can be found in adult bone marrow and other tissues, as well as umbilical cord blood, and they seem to be easily transplantable between people, because they are more able to avoid immune rejection.

There has been a great deal of interest in using MSCs to treat disease, with most research so far focused on heart disease, stroke, inflammatory bowel disease and blood cancers. Hundreds of patients with these diseases have already been treated with MSCs through clinical trials, with results suggesting that these cells are safe in these patients, and have promising signs of effectiveness. MSCs are still considered experimental however, and have not been approved by Health Canada as a standard therapy for any disease.

In recent years, a number of animal studies have suggested that MSCs may also be able to help treat septic shock. For example, a recent study by Dr. Duncan Stewart, CEO and Scientific Director of OHRI (and also a co-investigator on the new clinical trial) showed that treatment with these cells can triple survival in a mouse model of this condition.

"Mesenchymal stem cell therapy appears promising in animal studies, but it will require many years of clinical trials involving hundreds of patients to know if it is safe and effective," said Dr. Lauralyn McIntyre, a Scientist at the OHRI, ICU Physician at The Ottawa Hospital, Assistant Professor of Medicine at uOttawa and a New Investigator with CIHR and Canadian Blood Services. "This trial is a first step, but it is a very exciting first step."

As with all "Phase I" trials, the main goal of this study is to evaluate the safety of the therapy and determine the best dose for future studies. The 15 patients in the treatment group will receive standard treatments (such as fluids, antibiotics and blood pressure control), plus a planned intravenous dose of 0.3 to 3 million MSCs per kg of body weight. The MSCs will be obtained from the bone marrow of healthy donors and purified in the OHRI's Good Manufacturing Practice Laboratory in the Sprott Centre for Stem Cell Research. The researchers also plan to evaluate 24 similar septic shock patients who will receive standard treatments only (no MSCs). All patients will be rigorously monitored for side effects, and blood samples will be taken at specific time points to monitor the cells and their activity. This trial will not be randomized or blinded and it will not include enough patients to reliably determine if the therapy is effective. It will be conducted under the supervision of Health Canada and the Ottawa Hospital Research Ethics Board, and will have to be approved by both of these organizations before commencing.

"The OHRI is rapidly becoming known as a leader in conducting world-first clinical trials with innovative therapies such as stem cells," said Dr. Duncan Stewart, CEO and Scientific Director of OHRI, Vice-President of Research at The Ottawa Hospital and Professor of Medicine at uOttawa. "This research is truly pushing the boundaries of medical science forward, and is providing the citizens of Ottawa with access to promising new therapies."

"The Canadian Institutes of Health Research (CIHR) is very pleased to support this clinical trial," said Dr. Jean Rouleau, Scientific Director of the CIHR Institute of Circulatory and Respiratory Health. "The work of Dr. McIntyre and her colleagues will not only add to our growing knowledge of the benefits of stem-cell therapies, but will hopefully lead to treatments that can help save the lives of patients where currently, our treatment options are less than optimal."

Read this article:
Ottawa researchers to lead world-first clinical trial of stem cell therapy for septic shock

OTTAWA A team of Canadian researchers has been awarded $442,000 to test the world's first experimental stem-cell therapy aimed at patients who suffer from septic shock, a runaway infection of the bloodstream that's notoriously difficult to treat.

The federal grant will allow researchers from the Ottawa Hospital Research Institute to use mesenchymal stem cells, found in the bone marrow of healthy adults, to treat as many as 15 patients with septic shock.

The deadly infection occurs when toxic bacteria spreads rapidly throughout the body and over-activates the immune system, leading to multiple organ failure and death in up to 40 per cent of cases.

One in five patients admitted to intensive-care units suffers from septic shock, making it the most common illness among a hospital's sickest of the sick.

Existing treatments focus on early diagnosis and intervention before organs start to fail. Patients with septic shock require aggressive resuscitation measures, large doses of intravenous antibiotics and, often, ventilators to help them breathe.

Yet because the infection can creep up on patients rapidly and cause unpredictable complications, death from septic shock remains relatively common.

The experimental therapy aims to use donor stem cells, grown and purified at the Ottawa laboratory, to dial down the body's hyperactive immune response and reduce the cascade of inflammation that leads to organ failure.

Early results from animal studies even raise the possibility that mesenchymal cells could eliminate the bacteria that causes septic shock, although the impact on humans is not yet known.

"It's a unique feature of the stem cells," said Dr. Lauralyn McIntyre, the intensive-care physician who is leading the trial. "Certainly no other therapy in the past, other than antibiotics, has impacted the bacterial load in the system."

As with other stem cells, mesenchymal cells can turn into a variety of more specialized cells and tissues that help repair and regenerate damaged organs. And because mesenchymal cells are derived from adults, they sidestep the ethical issues arising from the destruction of human embryos needed to make embryonic stem cells.

Read the original:
Canadian researchers receive grant to test stem-cell therapy for septic shock

OTTAWA A team of Ottawa researchers has been awarded $442,000 to test the worlds first experimental stem-cell therapy aimed at patients who suffer from septic shock, a runaway infection of the bloodstream thats notoriously difficult to treat.

The federal grant will allow researchers from the Ottawa Hospital Research Institute to use mesenchymal stem cells, found in the bone marrow of healthy adults, to treat as many as 15 patients with septic shock.

The deadly infection occurs when toxic bacteria spreads rapidly throughout the body and over-activates the immune system, leading to multiple organ failure and death in up to 40 per cent of cases.

One in five patients admitted to intensive-care units suffers from septic shock, making it the most common illness among a hospitals sickest of the sick.

Existing treatments focus on early diagnosis and intervention before organs start to fail. Patients with septic shock require aggressive resuscitation measures, large doses of intravenous antibiotics and, often, ventilators to help them breathe.

Yet because the infection can creep up on patients rapidly and cause unpredictable complications, death from septic shock remains relatively common.

The experimental therapy aims to use donor stem cells, grown and purified at the Ottawa laboratory, to dial down the bodys hyperactive immune response and reduce the cascade of inflammation that leads to organ failure.

Early results from animal studies even raise the possibility that mesenchymal cells could eliminate the bacteria that causes septic shock, although the impact on humans is not yet known.

Its a unique feature of the stem cells, said Dr. Lauralyn McIntyre, the intensive-care physician who is leading the trial. Certainly no other therapy in the past, other than antibiotics, has impacted the bacterial load in the system.

Like other stem cells, mesenchymal cells can turn into a variety of more specialized cells and tissues that help repair and regenerate damaged organs. And because mesenchymal cells are derived from adults, they sidestep the ethical issues arising from the destruction of human embryos needed to make embryonic stem cells.

Read more from the original source:
Ottawa researchers receive grant to test stem-cell therapy for septic shock

Al-Omran, who is an associate professor and consultant vascular surgeon at KSU, is widely published in many respectable peer-reviewed journals such as the New England Journal of Medicine, PNAS, JBC, Circulation and Nature Communication.

"This is an important initial step in implementing this innovative treatment for cardiovascular diseases. The treatment is still experimental and in the animal phase, so the next step is to move from the experimental phase to application on patients through more research processes that will take several years," Al-Omran told Arab News, underscoring the significance of this research.

Al-Omran explained the idea behind this research was conceived about seven years ago when he was in his general surgery training at University of Toronto working with breast cancer patients.

This question launched the research that Al-Omran and Verma undertook where they experimented on mice by removing the BRCA1 gene and administering Doxorubicin.

Al-Omran, who is focused on risk reduction and prevention of cardiovascular diseases despite being a surgeon, added: "Cardiovascular diseases is the leading cause of death worldwide, and this research will pave the way for developing therapies that treat and prevent these diseases. This will also be potentially useful for prevalent conditions such as hypertension and diabetes among others."

When asked about the future of research in Saudi Arabia, Al-Omran lauded King Saud University for its strategic research programs such as the Research Chairs Program, International Twinning Program, and Attracting Outstanding Faculty and Researchers Program.

She added this patent is the embodiment of the university's vision of harnessing the benefits of international collaboration in research and education that will ultimately speed up information and technology exchange and the transfer of medical discoveries from the laboratory bench to patients' bedside.

"More than 50 percent of our postgraduate medical trainee and students abroad are already enrolled in formal research programs such as Master's and Ph.D, programs alongside their clinical training," said Al-Omran.

He said he intends to continue his research on the BRCA1 gene in order to move on from the experimental phase to the application of the therapy on patients after going through the necessary experiments and ethical approval.

Arab News 2012

The rest is here:
Leading Business Intelligence on the Middle East & North Africa

SILVER SPRING, Md.--(BUSINESS WIRE)--

Nuvilex, Inc. (OTCQB:NVLX), an emerging biotechnology provider of cell and gene therapy solutions through its ongoing acquisition of the assets of SG Austria, realizes the important role for Cell-in-a-Box technology, and what it offers the medical community, and aims today to discuss the potential it will serve as a treatment option for a variety of solid tumors.

As discussed previously, the Cell-in-a-Box technology involves the encapsulating, or encasing of live cells in a specially created cotton-based capsule. The cell-type chosen, in the case of cancer treatment it is a cytochrome P450 expressing cell, is chosen for the disease and then is ultimately placed beside or within the target tumor while the cells remain inside the capsule. For cancer, once a patient receives the drug to be converted, the encapsulated cells transform this into an active chemotherapeutic. As a result, a high concentration of the drug is provided locally to the tumor.

Although the original human clinical trials were limited to pancreatic cancer tumors, later work showed the Cell-in-a-Box encapsulation technology has great potential for use in other solid tumors. The work also pointed toward encapsulated cells expressing more than one drug-activating enzyme as being of potential value in treating other cancers, indicating the possibility of combination drug therapies targeted by one or more encapsulated cell product(s) being placed in or near the tumor to cause a high level of chemotherapy at the site its intended for.

Most chemotherapy drugs affect both normal and cancerous tissue, which is why they are so toxic to naturally fast-growing cells in the body, such as hair follicles and intestinal cells. By using encapsulated cytochrome P450 expressing cells to convert the drug locally and then placing them close to or in a tumor, much less active drug is available to cause harm to healthy normal cells and instead its localized high concentration remains in the tumor region, irrespective of solid tumor type being treated, and thereby can increase elimination of the tumor cells.

Dr. Robert Ryan, Chief Executive Officer of Nuvilex, added, The work that continues to be advanced by SG Austria expands the possible use of the Cell-in-a-Box technology beyond pancreatic cancer. When combined with the potential downstream affect on micro metastases through use of encapsulated cells, we can realistically imagine being able to treat cancers across a broad spectrum. Our goal is to minimize normal cell and tissue damage, reduce the life-threatening side effects, and yet bring about elimination of a persons cancer. Over the past year and through today, we have continued to research new ways to improve on the quality and quantity of the products we will be driving forward, including the pancreatic cancer treatment, all of which are designed to increase the quality of our lives through effective use of live cell encapsulation.

About Nuvilex

Nuvilex, Inc. (OTCQB:NVLX.PK - News) is an emerging international biotechnology provider of clinically useful therapeutic live encapsulated cells and services for encapsulating live cells for the research and medical communities. Through our effort, all aspects of our corporate activities alone, and especially in concert with SG Austria, are rapidly moving toward completion, including closing our agreement. One of our planned offerings will include cancer treatments using the companys industry-leading live-cell encapsulation technology.

Safe Harbor Statement

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 involving risks and uncertainties. Results, events and performances could vary from those contemplated. These statements involve risks and uncertainties which may cause actual results, expressed or implied, to differ from predicted outcomes. Risks and uncertainties include product demand, market competition, and Nuvilexs ability to meet current or future plans. Investors should study and understand all risks before making an investment decision. Readers are recommended not to place undue reliance on forward-looking statements or information. Nuvilex is not obliged to publicly release revisions to any forward-looking statement, to reflect events or circumstances afterward, or to disclose unanticipated occurrences, except as required under applicable laws.

Follow this link:
Completed Clinical Trial Further Indicates Cell-in-a-Box® Encapsulation Technology Has the Potential to Treat a Wide ...

Editor's Choice Academic Journal Main Category: Heart Disease Also Included In: Genetics;Medical Devices / Diagnostics Article Date: 16 Mar 2012 - 9:00 PDT

email to a friend printer friendly opinions

Current Article Ratings:

Using a gene analysis tool called the Cardiochip, the researchers examined a specific gene variant associated with inflammation and heart disease. The chip was designed by Brendan J. Keating, Ph.D., co-author of the study and a researcher in the Center for Applied Genomics at The Children's Hospital of Philadelphia.

Even though researchers are aware of the association between inflammation and atherosclerosis - a disorder in which fat, cholesterol, and other fatty deposits build up in the walls of arteries - they have been unable to find an inflammatory agent that causes the diseases, until now. In addition, researchers did not know whether a drug targeted at reducing inflammation might treat the disease.

The team focused on the signaling protein interleukin-6 receptor (IL6R). IL6R is found in the blood and increases inflammatory responses.

Keating explained:

The meta-analysis study was conducted by the IL6R Mendelian Randomization Analysis Consortium, and international team of investigators led by Dr. Juan Pablo Casas, Professor Aroon. D. Hingorani, and Dr. Daniel I. Swerdlow, all of University College London, UK.

The researchers examined data from 40 previous studies that involved almost 133,500 individuals from Europe and the United States. Mendelian randomization is a research technique that utilizes knowledge of genes and biological mechanisms in order to figure out the likely effects of a new medication before a clinical trial is conducted, with its potential risk of adverse effects and high cost.

In the same issue of The Lancet, an associated report conducted by the IL6R Genetics Consortium and Emerging Risk Factors Collaboration, discovered that a genetic variant of the IL6R gene, which carries the code for the IL6R protein, decreases inflammation and therefore reduces the risk of heart disease.

Read more:
Gene Chip May Help Prevent Heart Disease

A team of Stanford researchers has unveiled the most detailed biological profile of a human being done so far: a peek at one man's genetic foundation, along with snapshots, taken dozens of times over the course of a year, of the millions of proteins and other molecules that are in constant flux in his body.

In a stroke of shocking good luck - for the scientists, if not necessarily the patient - the profile subject developed Type 2 diabetes during the study, allowing researchers to follow in real time the molecular changes that took place as the illness progressed.

It also allowed the subject, Stanford geneticist Michael Snyder, to catch his diabetes early and stop it, most likely months or even years before he would have been diagnosed without the genetic profiling.

"This is the first time someone's actually analyzed the genome of a healthy person, predicted disease risk, and then by following him, actually saw a disease develop," said Snyder, who in addition to being the subject of the study was the senior author.

Snyder's profile and an analysis of the results were published today in the journal Cell. Snyder, chairman of the genetics department at Stanford, is not named in the published study because of privacy rules, but he volunteered to identify himself.

The research provides some of the first proof that detailed genetic profiling - beyond just DNA sequencing - could be used someday not just to predict an individual's chances of developing disease, but also to identify the smallest molecular changes that show when a person starts to become ill, said experts in personalized medicine.

The first human genome - a map of all of the DNA in a human cell - was announced in 2000. Seven or eight years later geneticists began mapping the genomes of specific individuals. Such personal genomic sequencing is expected to become widely available this year, at a cost of several thousand dollars.

Using genetic information to help diagnose and treat patients is still a very new field, although it's growing rapidly. Certain key genes have been found to greatly increase the risk of breast cancer, for example, or the deadly Huntington's disease, and doctors will regularly test for those genes when someone is diagnosed with an illness or when a close family member is known to have a disease.

But for most people, DNA sequencing and other biological profiling isn't yet useful - subjects would end up with a lot of unwieldy information that is mostly beyond modern scientific understanding or far too expensive to analyze.

"What they did (at Stanford) is much more interesting from a scientific basis than a practical basis," said Dr. David Witt, a medical geneticist at Kaiser San Jose. "And that gets to the heart of personalized medicine: It's not ready for prime time."

The rest is here:
Stanford gene researchers see diabetes develop

15-03-2012 12:52 Personalized Medicine: trends and prospects for the new science of genetic testing and molecular diagnostics Overview of new working paper -- Mapping the Future of Genetic Testing and Molecular Diagnostics: A payer's perspective on integrating personalized care into clinical practice Review of results of survey of consumers and physicians about genetic testing Deneen Vojta, UnitedHealth Group

Read more:
Personalized Medicine, UnitedHealth Group - Video

15-03-2012 14:59 What is the relationship between implementation guidelines and reimbursement? Are payers the ultimate gatekeeper? Is it worth educating healthcare providers and patients? • Appropriate uses of genetic testing • Evidence-based guidelines and flexibility • Clinical management of new technology • Best practices (eg, breast cancer) Moderator: Robert Green, Harvard Medical School Robert McCormack, Veridex/J&J Thomas Musci, Novartis Diagnostics Greg Feero, Maine - Dartmouth Family Medicine Residency and NHGRI Deborah Heine, Claire Altman Heine Foundation

See the original post here:
Integrating new genetic testing technologies into clinical pathways - Video

15-03-2012 16:33 This panel will consider the context for evidence, rather than the level of evidence, needed to move innovative technology into a clinical setting and how we will generate the needed evidence. Which evidence questions must be answered pre- market and which, if any, can be answered post-market? It will consider the often mismatched evidence requirements of patients, clinicians, test developers, regulators and payers. Collectively, we should define a burden of evidence that's appropriate for the balances of risk and speed that is appropriate in this space. This will require community-wide cooperation to collect and analyze data residing in many different places -- inside pharmaceutical companies, inside diagnostics companies and payers -- to measure outcomes and define the best use of diagnostics, and innovative methodologies to generate evidence (both in process and results). Moderator: Adam Berger, Institute of Medicine Patricia Deverka, Center for Medical Technology Policy Stanley Lapidus, SynapDx Susan Friedman, Facing Our Risk of Cancer Empowered David Clifford, PatientsLikeMe Roger Klein, University of South Florida Medical School

Continue reading here:
Evidence - Video

A team of Stanford researchers has unveiled the most detailed biological profile of a human being done so far: a peek at one man's genetic foundation, along with snapshots, taken dozens of times over the course of a year, of the millions of proteins and other molecules that are in constant flux in his body.

In a stroke of shocking good luck - for the scientists, if not necessarily the patient - the profile subject developed Type 2 diabetes during the study, allowing researchers to follow in real time the molecular changes that took place as the illness progressed.

It also allowed the subject, Stanford geneticist Michael Snyder, to catch his diabetes early and stop it, most likely months or even years before he would have been diagnosed without the genetic profiling.

"This is the first time someone's actually analyzed the genome of a healthy person, predicted disease risk, and then by following him, actually saw a disease develop," said Snyder, who in addition to being the subject of the study was the senior author.

Snyder's profile and an analysis of the results were published today in the journal Cell. Snyder, chairman of the genetics department at Stanford, is not named in the published study because of privacy rules, but he volunteered to identify himself.

The research provides some of the first proof that detailed genetic profiling - beyond just DNA sequencing - could be used someday not just to predict an individual's chances of developing disease, but also to identify the smallest molecular changes that show when a person starts to become ill, said experts in personalized medicine.

The first human genome - a map of all of the DNA in a human cell - was announced in 2000. Seven or eight years later geneticists began mapping the genomes of specific individuals. Such personal genomic sequencing is expected to become widely available this year, at a cost of several thousand dollars.

Using genetic information to help diagnose and treat patients is still a very new field, although it's growing rapidly. Certain key genes have been found to greatly increase the risk of breast cancer, for example, or the deadly Huntington's disease, and doctors will regularly test for those genes when someone is diagnosed with an illness or when a close family member is known to have a disease.

But for most people, DNA sequencing and other biological profiling isn't yet useful - subjects would end up with a lot of unwieldy information that is mostly beyond modern scientific understanding or far too expensive to analyze.

"What they did (at Stanford) is much more interesting from a scientific basis than a practical basis," said Dr. David Witt, a medical geneticist at Kaiser San Jose. "And that gets to the heart of personalized medicine: It's not ready for prime time."

Original post:
Stanford man's genetic profile yields surprises