Clearwater, FL (PRWEB) August 20, 2014

Botanica Day Spa has unveiled their first-ever stem cell facial. Utilizing the new and popular stem cell line from Pevonia, the anti-aging treatment effectively targets fine lines and wrinkles and naturally repairs the skin. The spa also recently announced August specials, highlighting the new service by offering clients a complimentary dermaplaning session with the purchase of the stem cell facial.

Pevonia continues to be a global leader in natural, botanical-based skincare and aging solutions. The Stem Cells Phyto-Elite collection, launched just last month, features two unique plant-based stem cell sources for skin repair and the reversal of signs of aging. According to Pevonia, the new line contains a concentration of stem cells that may be up to ten times higher than any other currently available product. Stem cells from the Argan tree work to improve skin elasticity while stem cells from the European Comfrey Root speed up skin cell renewal. Take a few moments to learn more about the science: What is a plant stem cell?

Aging appears in different ways, but commonly its seen in the form of wrinkles, loss of elasticity and progressively thinner skin over time, said Gen Obolensky, owner at Botanica Day Spa and an aesthetician/facialist herself. All of these common signs of aging are the result of our skin producing fewer and fewer new skin cells over time. Age reversal treatments generally target only the symptoms of slower cell turnover, so its very exciting to be able to offer innovative products that work from inside the skin at the root of what causes these signs of aging.

Obolensky recognizes the buzz surrounding stem cell beauty treatments, adding, Botanicas stem cell facial uses the new Stem Cells Phyto-Elite line which offers a wide range of age reversal benefits. It cleanses, exfoliates, tones, hydrates and brightens while stimulating faster skin cell repairall of which is backed by clinical research and testing, conducted by a respected skincare leader.

In addition to their offer of a no-cost dermaplaning with the stem cell facial, Botanica recently announced more August spa specials including:

Botanica expects appointment spots to fill up quickly with this special offer. To schedule your stem cell facial treatment, call 727-441-1711 or book online today!

ABOUT BOTANICA DAY SPA Located in downtown Clearwater, Botanica Day Spa specializes in natural treatments for the body, skin and nails. Recognized in 2013 as first runner-up for Creative Loafings Best of the Bay awards, Botanica was voted first runner-up for Best Day Spa and first place for Best Mani/Pedi. Botanica was also voted Best of Tampa Bay for Brazilian bikini waxing, eyebrow shaping and therapeutic massage by CitySearch in 2010. With an emphasis on the use of organic and natural product lines in a cutting edge beauty services setting, Botanicas staff is comprised of 12 fully licensed aestheticians, nail technicians, massage therapists and makeup artists offering a full menu of luxury spa services. The spa celebrates its twentieth year in business in 2014. For more information, please visit http://www.BotanicaDaySpa.com.

Visit link:
New Stem Cell Facial Unveiled at Botanica Day Spa

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

20-Aug-2014

Contact: Ashley Culver ashley.culver@vanderbilt.edu 615-322-4747 Vanderbilt University Medical Center

Vanderbilt-led research, as part of an international, multicenter trial, found regular blood transfusion therapy significantly reduces the recurrence of silent strokes and strokes in children with sickle cell anemia who have had pre-existing silent strokes, according to study results released today in the New England Journal of Medicine.

Michael R. DeBaun, M.D., MPH, director of the Vanderbilt-Meharry Sickle Cell Disease Center of Excellence and professor of Pediatrics, was the principal investigator of the more than $20 million, federally-funded trial, the largest of its kind in children with sickle cell. Nearly 100,000 people in the United States are living with sickle cell disease, a group of inherited blood disorders.

Sickle cell disease most commonly affects African-Americans, occurring in one of every 396 births in this ethnic group. In patients with the disease, red blood cells are abnormal hard, sticky and shaped like a crescent moon. When the sickle cells travel through small blood vessels, they can decrease the normal blood flow to all organs of the body, causing many complications including pain that require hospitalization for treatment, lung disease and a shortened life span.

Silent strokes are frequent in sickle cell anemia (the most common form of sickle cell disease), occurring in approximately 3 percent of school-age children with the disease, and can cause poor school performance and limit performance of complex tasks. The only way to diagnose a silent stroke is with magnetic resonance imaging (MRI) of the brain. Once a child has had a silent stroke, he is at a much higher risk for more dangerous overt strokes and new or enlarged silent stokes.

Results of the 10-year trial led by DeBaun, which involved 29 clinical centers in the United States, France, Canada and the United Kingdom, appear in the Aug. 21 issue of NEJM.

The Silent Cerebral Infarct Transfusion (SIT) Trial looked at the efficacy of blood transfusion therapy for children with sickle cell anemia to prevent repeat cerebral infarcts (overt strokes and silent strokes). Researchers found that monthly blood transfusions reduced the recurrence of silent strokes and strokes by 58 percent in children with pre-existing silent strokes when compared to children who were not transfused. The actual benefit of transfusion therapy is probably higher because 15 percent of the children who were assigned to receive blood transfusion therapy either never received the transfusion or only received transfusions for a brief period, but were counted as if they were transfused, referred to as "intention to treat analysis."

"The success of the trial is a tribute to over 1,000 families of children who were screened with an MRI of the brain and the almost 200 families of children who committed to monthly visits for three years. The successful recruitment, adherence and retention of black families, many of whom were working poor, to an arduous, complex trial, should lay to rest the misperception that blacks are not willing participants in research," said DeBaun, J.C. Peterson M.D. Professor of Pediatric Pulmonology. "The results of the trail indicate members of the community are interested in research, when they are well-informed, empowered to make their own decision, and have a trusting relationship with the health care provider who is independent of their participation in the study," DeBaun continued.

View original post here:
Regular blood transfusions can reduce repeat strokes in children with sickle cell disease

Recommendation and review posted by Bethany Smith

Researchers at Utah's Huntsman Cancer Institute have identified a specific gene mutation that helps regulate chronic myeloid leukemia, giving patients a normal life and normal life expectancy.

Jordan Allred, Deseret News

Enlarge photo

SALT LAKE CITY A common blood cancer is meeting its match with a new discovery amid ongoing research at the University of Utah's Huntsman Cancer Institute.

Researchers have identified a specific gene mutation that drives chronic myeloid leukemia, allowing them to potentially develop treatments that could help the 20 to 30 percent of patients for whom medication does not work.

The cancer which, unlike most cancers, starts in the bone marrow and invades the blood can be managed with drugs called tyrosine kinase inhibitors. The medication helps patients lead fairly normal lives, giving them a 95 percent survival rate in the past five years.

But some patients with chronic myeloid leukemia become resistant to the available drug.

"Fortunately, the problems we are studying affect a minority of chronic myeloid leukemia patients, but still, this leaves some patients with no good treatment option at all," said lead author and Huntsman investigator Thomas O'Hare. "Our goal is to have a tyrosine kinase inhibitor option for every patient."

The trouble with this type of leukemia is that cancer cells build up in the blood and prevent the body from working how it should. In rare cases, it can evolve into a more voracious cancer that could impact vital organs in the body.

The American Cancer Society estimates that nearly 6,000 new cases of chronic myeloid leukemia will be diagnosed this year. The cancer is more common in adults but occurs rarely in children; however, treatment is the same.

See the rest here:
Utah researchers tackle gene mutation resistance in leukemia patients

Recommendation and review posted by Bethany Smith

11 hours ago The green anole lizard (Anolis carolinensis), when caught by a predator, can lose its tail and then grow it back. Researchers have discovered the genetic 'recipe' as to how this happens. Credit: Joel Robertson

By understanding the secret of how lizards regenerate their tails, researchers may be able to develop ways to stimulate the regeneration of limbs in humans. Now, a team of researchers from Arizona State University is one step closer to solving that mystery. The scientists have discovered the genetic "recipe" for lizard tail regeneration, which may come down to using genetic ingredients in just the right mixture and amounts.

An interdisciplinary team of scientists used next-generation molecular and computer analysis tools to examine the genes turned on in tail regeneration. The team studied the regenerating tail of the green anole lizard (Anolis carolinensis), which when caught by a predator, can lose its tail and then grow it back.

The findings are published today in the journal PLOS ONE.

"Lizards basically share the same toolbox of genes as humans," said lead author Kenro Kusumi, professor in ASU's School of Life Sciences and associate dean in the College of Liberal Arts and Sciences. "Lizards are the most closely-related animals to humans that can regenerate entire appendages. We discovered that they turn on at least 326 genes in specific regions of the regenerating tail, including genes involved in embryonic development, response to hormonal signals and wound healing."

Other animals, such as salamanders, frog tadpoles and fish, can also regenerate their tails, with growth mostly at the tip. During tail regeneration, they all turn on genes in what is called the 'Wnt pathway'a process that is required to control stem cells in many organs such as the brain, hair follicles and blood vessels. However, lizards have a unique pattern of tissue growth that is distributed throughout the tail.

"Regeneration is not an instant process," said Elizabeth Hutchins, a graduate student in ASU's molecular and cellular biology program and co-author of the paper. "In fact, it takes lizards more than 60 days to regenerate a functional tail. Lizards form a complex regenerating structure with cells growing into tissues at a number of sites along the tail."

"We have identified one type of cell that is important for tissue regeneration," said Jeanne Wilson-Rawls, co-author and associate professor with ASU's School of Life Sciences. "Just like in mice and humans, lizards have satellite cells that can grow and develop into skeletal muscle and other tissues."

"Using next-generation technologies to sequence all the genes expressed during regeneration, we have unlocked the mystery of what genes are needed to regrow the lizard tail," said Kusumi. "By following the genetic recipe for regeneration that is found in lizards, and then harnessing those same genes in human cells, it may be possible to regrow new cartilage, muscle or even spinal cord in the future."

The researchers hope their findings will help lead to discoveries of new therapeutic approaches to spinal cord injuries, repairing birth defects, and treating diseases such as arthritis.

See the rest here:
How lizards regenerate their tails: Researchers discover genetic 'recipe'

Recommendation and review posted by Bethany Smith

16 hours ago by Keith Hautala

University of Kentucky biologist Randal Voss is sequencing the genome of salamanders. Though we share many of the same genes, the salamander genome is massive compared to our own, about 10 times as large.

Voss's research focuses on axolotls, salamanders with amazing regenerative ability.

"It's hard to find a body part they can't regenerate: the limbs, the tail, the spinal cord, the eye, and in some species, the lens, half of their brain has been shown to regenerate," Voss said."I'm very fortunate to have a colleague in the department, Jeramiah Smith, who's an expert at the ability to put small pieces of DNA together to kind of recreate the puzzle, which is the genome. We have funding from the National Institute of Health and the Department of Defense to sequence the axolotl genome and provide this blueprint for the first time."

With a partner at the University of Dayton, Voss is looking at the loss of regenerative ability in the eye as a salamander ages.

"Early on in life, axolotls can regenerate their lens. But at some point in time, around 28 days after they hatch, that plasticity goes away and they can't regenerate the lens," Voss said. "So, I've been working with that group trying to identify the genes that might explain that."

Voss is also starting a new collaboration with an orthopedic surgeon at UK to study knee joint regeneration.

This video is not supported by your browser at this time.

"Over the course of say 10 to 15 days, the salamander will successfully regenerate a complete joint. That blows the orthopedic surgeon's mind because that would be the Holy Grail in their field to understand how to orchestrate joint regeneration in a human."

Explore further: Researchers cohere research cluster focusing on genetic mechanisms underscoring regeneration

Read more here:
Sequencing the genome of salamanders

Recommendation and review posted by Bethany Smith

17 hours ago

The hospital germ Pseudomonas aeruginosa wraps itself into the membrane of human cells: A team led by Dr. Thorsten Eierhoff and Junior Professor Dr. Winfried Rmer from the Institute of Biology II, members of the Cluster of Excellence BIOSS Centre for Biological Signalling Studies of the University of Freiburg, has identified a novel mechanism of bacterial invasion: Pseudomonas aeruginosa uses lipids in the cell membrane to make its way into host cells. The protein LecA on the surface of the bacteria binds to sugar on special lipid molecules, so-called Gb3 lipids, which are present in the outer membrane of human cells. When the germ docks onto a cell, the LecA molecules of the bacteria and the Gb3 lipids of the host membrane interlock - like a zipper. In this way, the cell envelope wraps itself around the germ step by step and conveys it into the cell's interior. Rmer and Eierhoff found evidence of the new mechanism in synthetic membranes as well as in cultures of human lung cells. They published their findings in the journal Proceedings of the National Academy of Sciences.

Pseudomonas aeruginosa can cause serious inflammations of the skin and the lung in patients with a weakened immune system, particularly in those suffering from the genetic disorder cystic fibrosis. When the bacteria enter human cells, Gb3 lipids bind to LecA proteins and bend the membrane. This bond is enough to wrap up the bacterium, calculated Prof. Dr. Christian Fleck from Wageningen University, Netherlands. He was co-author of this study. Researchers were previously only familiar with methods of bacterial invasion involving the manipulation of signals in the host cell. These signals control actin fibers, the cell's muscles: The fibers bend the cell envelope from inside and form membrane bubbles into which the bacteria are absorbed.

In order to prove that the process runs without actin, the researchers observed the effect of Pseudomonas bacteria on synthetic membrane bubbles. The bubbles contained neither actin nor other cellular components - only the lipid Gb3. The in vitro membrane folded in and closed in around the bacteria when they docked onto the surface. However, the wrapping process only took place when the bacteria produced the protein LecA. "The experiment shows that Pseudomonas uses this lipid zipper to make its way into cells without manipulating actin," says Eierhoff. The researchers demonstrated that LecA and Gb3 are also important for bacterial invasion in human lung cells: When the pair of molecules was missing, the number of germs that infiltrated the cells was reduced by up to 70 percent. These findings enabled Rmer's research group to identify a potential agent against Pseudomonas aeroginosa.

Explore further: Researchers find agent against hospital germ pseudomonas aeruginosa

More information: T. Eierhoff, B. Bastian, R. Thuenauer, J. Madl, A. Audfray, S. Aigal, S.Juillot, G. E. Rydell, S. Mller, S. de Bentzmann, A. Imberty, C. Fleck and W. Rmer (2014) "A lipid zipper triggers bacterial invasion." PNAS DOI: 10.1073/pnas.1402637111

No admission for bacteria: Scientists from the University of Freiburg have succeeded in preventing Pseudomonas bacteria from entering host cells with the help of a sugar complex. Dr. Thorsten Eierhoff and ...

How do bacteria overcome the barrier of the outer membrane to gain access to the cells of the body? That is the question addressed by junior professor Dr. Winfried Rmer and his colleagues Kevin Trndle ...

The epithelium lines the organs of the human body. In the skin and the intestine as well as in the kidney, this cell layer forms a barrier that regulates the exchange of molecules like hormones and nutrients. ...

Biologists at the Ruhr-Universitt Bochum (RUB) have discovered new mechanisms used by bacteria to manufacture lipids, i.e. fat molecules, for the cell membrane. Those mechanisms are a combination of familiar ...

View post:
Researchers discover new strategy germs use to invade cells

Recommendation and review posted by Bethany Smith

Illumina CEO Jay Flatley

When Renee Valints daughter Shelby was born in 2000, she seemed weak, like a rag doll. Shelby learned to walk and talk, but she did so slowly, missing developmental milestones. By age 4 she was confined to a wheelchair, and she started using a computerized voice to communicate in the fifth grade. Desperate, Renee took her from Phoenix to the Mayo Clinic in Rochester, Minn. for one last week of tests and discussion with some of the countrys top doctors.

They all put up their hands and said, We have no idea whats wrong with her, says Renee. At that point she couldnt even move. I bathed her, fed her. She couldnt even swallow. I had to thicken her liquids so she could swallow without choking. It was like a nightmare. That was it. There was nowhere else to go.

But then doctors at the Translational Genomics Research Institute in Phoenix used a new technologyDNA sequencingto look at Shelbys genes. Based in part on what they found, they guessed that she might respond to the same dopamine-boosting medicines that are given to Parkinsons patients. Three months later Shelby got up out of her wheelchair. The next day she walked to school, and she hasnt used the wheelchair since. Now she likes to dance.

Stories like this are creating an exploding market for DNA-sequencing machines. Major cancer centers are using them as a standard way to pick medicines for patients who have little other hope. DNA sequencers now allow disorders like Down syndrome and other conditions to be detected in a fetus using a vial of the mothers blood. They are replacing older, more expensive methods of genetic testing.

And the change is coming at breakneck speed. How fast? In the 1980s and 1990s the PC revolution was driven by an insight that legendary Intel cofounder and chairman Gordon Moore had as a researcher in 1965: The number of transistors on an integrated circuit doubles every two years. This was not a law of science but of will: It was a target for engineers to hit.

But over the past 13 years the cost of sequencing DNA has dropped 1,000 times more than Moores Law, from $100 million per human genome to only $1,000.

The only thing more extraordinary than the growth rate of the sequencing revolution is that the beneficiary is a single company, Illumina of San Diego, and most of the credit for the rate of change can be laid at the feet of one entrepreneur, Chief Executive Jay Flatley. Thanks largely to Flatleys leadership, Illumina emerged as the dominant maker of DNA sequencers eight years ago and has maintained 80% market share despite an assault by several well-funded competitors.

Since 2008 Illuminas sales and profit have both increased 147%, to $1.42 billion and $125 million, respectively, as the stock increased 617% and the companys market capitalization reached $23 billion.

We have predictors of market sizes, says Flatley, 61. Anything weve done so far says that in our time horizon, which is five or ten years, if we remain the leader in sequencing we can grow our company with a much more fantastic return on investment than anything else.

See the article here:
Flatley's Law: How One Company Is Creating Medicine's Genetic Revolution

Recommendation and review posted by Bethany Smith

A new gene therapy developed by researchers at the University of Missouri School of Medicine has shown to protect mice from a life-threatening heart condition caused by muscular dystrophy.

"This is a new therapeutic avenue," said Yi Lai, PhD, the leading author of the study and assistant research professor in the MU School of Medicine's Department of Molecular Microbiology and Immunology. "This is just a first step, but we hope this could lead to a treatment for people with this devastating heart condition, which is a leading cause of death for people with Duchenne muscular dystrophy."

About one in 3,500 children, mostly boys, are born with Duchenne muscular dystrophy (DMD). They experience a progressive wasting away of muscles, starting in the legs and pelvis. Children with DMD have difficulty walking, and most need wheelchairs by age 12.

As DMD depletes the skeletal muscles, it also causes the heart to decay. A weakened heart kills up to 40 percent of people with DMD, usually by their 20s or early 30s. DMD originates with mutations in a single gene. For more than two decades, researchers have explored using gene therapy, an experimental treatment, to replace the flawed gene with a healthy copy.

The recent MU study, however, did not try to replace the faulty gene. The researchers targeted a different gene -- one involved with the heart's built-in system for responding to heart attacks and other emergencies.

This targeted gene expresses a protein called nNOS. During short-term stresses, nNOS activates briefly to help regulate the heart. The MU researchers altered the gene to enable more efficient transfer of the nNOS gene to mouse hearts.

Seven months after the gene therapy, the mice who received the treatment showed significantly improved overall heart health. On most disease indicators, the researchers found that the treatment protected their hearts from the damage of DMD.

"The study showed for the first time that a modified nNOS gene could be delivered through gene therapy to protect the hearts of mice from Duchenne muscular dystrophy," said Dongsheng Duan, PhD, co-author of the study and Margaret Proctor Mulligan Professor in Medical Research at the MU School of Medicine.

"Since nNOS protects against multiple heart diseases, this method could one day be extended to the treatment of other heart diseases, such as heart failure or a heart attack," Duan said.

The technique is in an early stage of development and will require more research before potential applications in humans are explored.

Read more:
Gene therapy protects mice from lethal heart condition, researchers find

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

19-Aug-2014

Contact: Derek Thompson thompsonder@health.missouri.edu 573-882-3323 University of Missouri-Columbia

COLUMBIA, Mo. A new gene therapy developed by researchers at the University of Missouri School of Medicine has been shown to protect mice from a life-threatening heart condition caused by muscular dystrophy.

"This is a new therapeutic avenue," said Yi Lai, Ph.D., the leading author of the study and assistant research professor in the MU School of Medicine's Department of Molecular Microbiology and Immunology. "This is just a first step, but we hope this could lead to a treatment for people with this devastating heart condition, which is a leading cause of death for people with Duchenne muscular dystrophy."

About one in 3,500 children, mostly boys, are born with Duchenne muscular dystrophy (DMD). They experience a progressive wasting away of muscles, starting in the legs and pelvis. Children with DMD have difficulty walking, and most need wheelchairs by age 12.

As DMD depletes the skeletal muscles, it also causes the heart to decay. A weakened heart kills up to 40 percent of people with DMD, usually by their 20s or early 30s. DMD originates with mutations in a single gene. For more than two decades, researchers have explored using gene therapy, an experimental treatment, to replace the flawed gene with a healthy copy.

The recent MU study, however, did not try to replace the faulty gene. The researchers targeted a different gene one involved with the heart's built-in system for responding to heart attacks and other emergencies.

This targeted gene expresses a protein called nNOS. During short-term stresses, nNOS activates briefly to help regulate the heart. The MU researchers altered the gene to enable more efficient transfer of the nNOS gene to mouse hearts.

Seven months after the gene therapy, the mice who received the treatment showed significantly improved overall heart health. On most disease indicators, the researchers found that the treatment protected their hearts from the damage of DMD.

Excerpt from:
Gene therapy protects mice from lethal heart condition, MU researchers find

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

19-Aug-2014

Contact: Sarah McDonnell s_mcd@mit.edu 617-253-8923 Massachusetts Institute of Technology

CAMBRIDGE, MA -- MIT chemical engineers have devised a new implantable tissue scaffold coated with bone growth factors that are released slowly over a few weeks. When applied to bone injuries or defects, this coated scaffold induces the body to rapidly form new bone that looks and behaves just like the original tissue.

This type of coated scaffold could offer a dramatic improvement over the current standard for treating bone injuries, which involves transplanting bone from another part of the patient's body a painful process that does not always supply enough bone. Patients with severe bone injuries, such as soldiers wounded in battle; people who suffer from congenital bone defects, such as craniomaxillofacial disorders; and patients in need of bone augmentation prior to insertion of dental implants could benefit from the new tissue scaffold, the researchers say.

"It's been a truly challenging medical problem, and we have tried to provide one way to address that problem," says Nisarg Shah, a recent PhD recipient and lead author of the paper, which appears in the Proceedings of the National Academy of Sciences this week.

Paula Hammond, the David H. Koch Professor in Engineering and a member of MIT's Koch Institute for Integrative Cancer Research and Department of Chemical Engineering, is the paper's senior author. Other authors are postdocs M. Nasim Hyder and Mohiuddin Quadir, graduate student Nomie-Manuelle Dorval Courchesne, Howard Seeherman of Restituo, Myron Nevins of the Harvard School of Dental Medicine, and Myron Spector of Brigham and Women's Hospital.

Stimulating Bone Growth

Two of the most important bone growth factors are platelet-derived growth factor (PDGF) and bone morphogenetic protein 2 (BMP-2). As part of the natural wound-healing cascade, PDGF is one of the first factors released immediately following a bone injury, such as a fracture. After PDGF appears, other factors, including BMP-2, help to create the right environment for bone regeneration by recruiting cells that can produce bone and forming a supportive structure, including blood vessels.

Efforts to treat bone injury with these growth factors have been hindered by the inability to effectively deliver them in a controlled manner. When very large quantities of growth factors are delivered too quickly, they are rapidly cleared from the treatment site so they have reduced impact on tissue repair, and can also induce unwanted side effects.

Continue reading here:
Engineering new bone growth

Recommendation and review posted by Bethany Smith

By Estel Grace Masangkay

With help from the zebrafish, a team of Australian researchers has uncovered how hematopoietic stem cells (HSC) renew themselves, considered by many to be the holy grail of stem cell research.

HSCs are a significant type of stem cell present in the blood and bone marrow. These are needed for the replenishment of the bodys supply of blood and immune cells. HSCs already play a part in transplants in patients with blood cancers such as leukemia and myeloma. The stem cells are also studied for their potential to transform into vital cells including muscle, bone, and blood vessels.

Understanding how HSCs form and renew themselves has potential application in the treatment of spinal cord injuries, degenerative disorders, even diabetes. Professor Peter Currie, of the Australian Regenerative Medicine Institute at Victorias Monash University, led a research team to discover a crucial part of HSCs development. Using a high-resolution microscopy, Prof. Curies team caught HSCs on film as they formed inside zebrafish embryos. The discovery was made while the researchers were studying muscle mutations in the aquatic animal.

Zebrafish make HSCs in exactly the same way as humans do, but whats special about these guys is that their embryos and larvae develop free living and not in utero as they do in humans. So not only are these larvae free-swimming, but they are also transparent, so we could see every cell in the body forming, including HSCs, explained Prof. Currie.

While playing the film back, the researchers noticed that a buddy cell came along to help the HSCs form. Called endotome cells, they aided pre-HSCs to turn into HSCs. Prof. Currie said, Endotome cells act like a comfy sofa for pre-HSCs to snuggle into, helping them progress to become fully fledged stem cells. Not only did we identify some of the cells and signals required for HSC formation, we also pinpointed the genes required for endotome formation in the first place.

The next step for the researchers is to locate the signals present in the endotome cells that trigger HSC formation in the embryo. This can help scientists make different blood cells on demand for blood-related disorders. Professor Currie also pointed out the discoverys potential for correcting genetic defects in the cell and transplanting them back in the body to treat disorders.

The teams work was published in the international journal Nature.

View post:
Stem Cell Research Holy Grail' Uncovered, Thanks to Zebrafish

Recommendation and review posted by Bethany Smith

Since Maria Buhl's son was diagnosed with leukemia in 1995, she has looked for a way to make a difference with the bone marrow donor registry.

In September, the Delmar resident's vision will be realized when the Guilderland YMCA and the Guilderland Public Library pair up to host a Be the Match Bone Marrow Donor Drive. Joining the donor registry is as simple as getting a cheek swab and filling out paperwork.

According to the website http://bethematch.org, one in 500 people who sign up become donors in one of two ways: Peripheral blood stem cell donation or bone marrow donation. A PBSC donor receives injections of a medication that increases the number of blood-forming cells in their bloodstream. In a procedure a bit more complicated than a standard blood donation, blood is drawn from one arm and passed through a machine that separates out the blood-forming cells. The remaining blood is then returned through the other arm.

In bone marrow donations, which are done in a hospital operating room under anesthesia, needles are used to withdraw liquid marrow from the back of the pelvic bone.

Most donors are able to return to work, school and other activities within a week after donation, according to bethematch.org.

While at Albany Medical Center during her son's treatment, Buhl noticed a flier about a bone marrow drive in Albany. She registered and promptly forgot about it. Her son never needed a transplant, but she wanted to be able to help someone else. Buhl's son is now 21 and healthy. It wasn't until September 2013, 18 years later, that Buhl received an email saying she was a potential donor.

"I was overwhelmed with emotions and read the email at work so I had to excuse myself for a minute," she said.

A few days later, Buhl called the registry to confirm her identity and asked how they still had her information. The registry is so dedicated to tracking donors, they purchase any public records of people who fall off the grid, Buhl said.

In December 2013, she received another email telling her she would not need to donate, because the patient either found a better match, no longer was eligible for a match or decided not to pursue the treatment.

"I was so energized by being chosen that I felt deflated once I wasn't needed anymore," she said. "But who knows what will happen in the future?"

Excerpt from:
Hope runs deep

Recommendation and review posted by Bethany Smith

Ruxolitinib (trade name: Jakavi) has been approved since August 2012 for the treatment of adults with myelofibrosis. In an early benefit assessment pursuant to the Act on the Reform of the Market for Medicinal Products (AMNOG), the German Institute for Quality and Efficiency in Health Care (IQWiG) examined whether this new drug offers an added benefit over the appropriate comparator therapy specified by the Federal Joint Committee (G-BA).

According to the results, there is an indication of considerable added benefit in comparison with "best supportive care" (BSC) because ruxolitinib is better at relieving symptoms. Moreover, a hint of an added benefit with regard to survival can be derived from the dossier. Its extent is non-quantifiable, however.

Bone marrow is replaced by connective tissue

Myelofibrosis is a rare disease of the bone marrow, in which the bone marrow is replaced by connective tissue. As a consequence of this so-called fibrosis, the bone marrow is no longer able to produce enough blood cells. Sometimes the spleen or the liver takes over some of the blood production. Then these organs enlarge and can cause abdominal discomfort and pain. The typical symptoms also include feeling of fullness, night sweats and itching. Some patients with myelofibrosis develop leukemia.

Stem cell transplantation is currently the only option to cure myelofibrosis. The drug ruxolitinib aims to relieve the symptoms of myelofibrosis.

G-BA specifies appropriate comparator therapy

Ruxolitinib is an option for patients with so-called primary or secondary myelofibrosis whose spleen is already enlarged (splenomegaly) or who have other disease-related symptoms.

The G-BA specified "best supportive care" (BSC) as appropriate comparator therapy. BSC means a therapy that provides the patient with the best possible, individually optimized, supportive treatment to alleviate symptoms and improve quality of life. This also includes adequate pain therapy.

Relevant study ongoing until 2015

In its assessment, IQWiG could include one randomized controlled trial (RCT) conducted in 89 centres in Australia, Canada and the United States (COMFORT-I). The 309 patients in total were either treated with ruxolitinib plus BSC or with placebo plus BSC.

Read this article:
Ruxolitinib for myelofibrosis: Indication of considerable added benefit

Recommendation and review posted by Bethany Smith

18 hours ago We can compare this process to the layers of an onion. Transcription factors are at the heart of process efficiency, while epigenetic factors form the outer layers that protect the mechanism from attacks and environmental change. Credit: Elodie Legrand and Sophie Jarriault

How can a specialized cell change its identity? A team from the Institut de Gntique et de Biologie Molculaire et Cellulaire (CNRS/INSERM/Universit de Strasbourg) investigated a 100% effective natural example of this phenomenon, which is called transdifferentiation. This process, by which some cells lose their characteristics and acquire a new identity, could be more generally involved in tissue or organ regeneration in vertebrates, and is a promising research avenue for regenerative medicine. This study identifies the role of epigenetic factors involved in this conversion, underlines the dynamic nature of the process, and shows the key mechanisms for effective transdifferentiation. This work, conducted in collaboration with the Institut Curie, was published on August 15, 2014 in Science.

Our body is constituted of cells that acquired characteristics during development and that fulfill a precise function in each organ: we call these differentiated cells. Generally cells maintain their specificity until they die, but it has been proven that some cells can change state and acquire new functions. This is rare but is found in many species and is called "transdifferentiation".

The team studied this process in C. elegans, a small transparent nematode, where a rectal cell transforms naturally into a motor neuron. This change from one cell type into another occurs without cell division, by a succession of well defined steps that always lead to the same result. The researchers investigated the factors that make the conversion process so stable.

The team had elucidated the role of several transcription factors in this transdifferentiation. But these new results have shown the role of so-called "epigenetic" factors that can modulate gene expression. Two protein complexes are involved in the mechanism. These enzymes act on a histone and when a mutation changes their action, the transdifferentiation stops and the rectal cell no longer transforms into a neuron.

The researchers observed that the two complexes act at different steps and that their role may change as a function of the transcription factors with which they are associated. These results underline the importance of the correct chain of steps for each of these molecules: the dynamic nature of the transdifferentiation mechanism is essential to its stability.

The respective role of genetic and epigenetic factors in biological processes is a hotly debated subject. This work shows how each of these factors acts in transdifferentiation: transcription factors handle initiation and progress whereas epigenetic factors guarantee the constant result. The study even goes further, showing that under "normal" conditions, the epigenetic factors are incidental (even when they are absent the conversion occurs relatively efficiently) but that they are indispensable when there are environmental stressors. So they have a crucial role in maximizing the mechanism's efficacy and ensuring that it remains stable in the face of external variations.

Transdifferentiation is a phenomenon that is poorly understood. It may be involved in the organ regeneration that we observe in some organisms, for example newts, which can reconstruct their eye lens after injury. These results bring key new information to help us understand how to control this process and may open the path to promising therapies, in particular in the field of regenerative medicine.

Explore further: One step closer to cell reprogramming

More information: Sequential Histone Modifying Activities Determines the Robustness of Transdifferentiation; S. Zuryn, A. Ahier, M. Portoso, E. Redhouse White, M.C. Morin, R. Margueron, S. Jarriault; Science; August 15, 2014.

Continued here:
From rectal cells to neurons: Keys to understanding cell transdifferentiation

Recommendation and review posted by Bethany Smith

A promising technique for synthetic biology is fraught with risks.

Kenneth Oye

Genes in sexually reproducing organisms typically have a 50 percent chance of being inherited. Some genes have naturally evolved methods of improving these odds; these are called gene drives. The genomes of almost every sexually reproducing species contain either active gene drives or remnants of drives. Ten years ago, Austin Burt of Imperial College London proposed designing drives to alter genes in natural populations of mosquitoes. But the difficulty of precisely editing genomes to create engineered drives stymied the realization of Burts vision. This is about to change.

The recent development of a powerful genome editing tool called CRISPR/Cas9 allows scientists to insert, replace, delete, and regulate genes. Since Cas9 can cut essentially any gene and works in most organisms, it could in principle be used to make gene drives in any sexually reproducing organism. CRISPR gene-drive laboratory experiments in yeast and mosquitoes are under way. Development of purpose-built gene drives in the next few years is very likely.

Unlike most applications of biological engineering, gene drives have the potential to propagate changes throughout populations of organisms with short reproduction cycles. And that creates the potential for powerful positive and negative effects. Gene drives could be used to make it harder for mosquitoes to carry malaria and dengue fever, or they could be used to suppress populations of invasive species such as Asian carp. But they could also be misusedfor example, to increase the ability of insects to carry diseases, or to suppress populations of economically significant crops and livestock.

Im less worried about those kinds of deliberate misuses than I am by the unintended environmental consequences. The truth is that we dont fully understand the interactions between gene drives and the environment, or the mutations possible in drive-bearing organisms.

In July, along with other researchers from MIT, Harvard, and other institutions around the world, I published an article in Science that recommends 10 steps biological engineers, environmental scientists, and policy analysts need to take before releasing gene drives. These include research to improve our understanding of drives properties and side effects, measures to address identified risks, and hedges in case the initial assessments are wrong.

Gene drives dont fit into any existing regulatory frames. There are no environmental regulations that would cover the use of gene drives consistently around the world. So the bottom line is that we need to move cautiously. Scientists need time to evaluate the risks and develop safeguards. Legislators need time to evaluate regulatory arrangements. And the public deserves time for an informed debate.

Kenneth Oye is an associate professor of political science and engineering systems at MIT.

Read the rest here:
Proceed with Caution

Recommendation and review posted by Bethany Smith

18 hours ago San Diego State University graduate student Yan Wei Lim is exploring coral reefs in the southern Line Islands. Credit: Rob Edwards, SDSU computer scientist

Daylight was breaking over the central Pacific and coffee brewing aboard the MY Hanse Explorer. Between sips, about a dozen scientists strategized for the day ahead. Some would don wetsuits and slip below the surface to collect water samples around the southern Line Islands' numerous coral reefs. Others would tinker with the whirring gizmos and delicate machinery strewn throughout the 158-foot research vessel. All shared a single goal: Be the first research group to bring a DNA sequencer out into the field to do remote sequencing in real time. Against an ocean of odds, they succeeded.

This three-week, five-island expedition took place last year with a research crew including San Diego State University computer scientist Rob Edwards, biologist Forest Rohwer, postdoctoral scholar Andreas Haas and graduate student Yan Wei Lim. They were accompanied by several other researchers from the San Diego region and around the world. The researchers published an account of their trip and methods today in the journal PeerJ.

Line Island investigations

Biologists and computer scientists at SDSU have been traveling to the Line Islands for the last decade, collecting and analyzing the coral habitat to better understand what organisms live there, how they compete for resources, and what effects their presence has on the reef's ecosystem. It always bothered Edwards that they had to wait until they were back home, on the other side of the world, before they could look at their data and develop new hypotheses.

"If only we had had that data out in the field, we could have asked those questions there and then," Edwards said.

That inkling grew into an ambitious plan to somehow, some way bring out to sea a cumbersome and expensive piece of equipment designed to analyze a sample's DNA makeup and spit out detailed information about its genome.

The project initially had its doubters.

"People are a little bit hesitant to take a half-million-dollar piece of equipment into the middle of the Pacific if you're not sure it's going to be coming back," Edwards said.

This video is not supported by your browser at this time.

See the article here:
Sequencing at sea: Real-time DNA sequencing in a remote field location

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

19-Aug-2014

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

New Rochelle, August 19, 2014A new ovoid structure discovered in the Nakhla Martian meteorite is made of nanocrystalline iron-rich clay, contains a variety of minerals, and shows evidence of undergoing a past shock event from impact, with resulting melting of the permafrost and mixing of surface and subsurface fluids. Based on the results of a broad range of analytical studies to determine the origin of this new structure, scientists present the competing hypotheses for how this ovoid formed, point to the most likely conclusion, and discuss how these findings impact the field of astrobiology in a fascinating article published in Astrobiology, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available Open Access on the Astrobiology website.

In the article, "A Conspicuous Clay Ovoid in Nakhla: Evidence for Subsurface Hydrothermal Alteration on Mars with Implications for Astrobiology," Elias Chatzitheodoridis, National Technical University of Athens, Greece, and Sarah Haigh and Ian Lyon, the University of Manchester, UK, describe the use of tools including electron microscopy, x-ray, and spectroscopy to analyze the ovoid structure. While the authors do not believe the formation of this structure involved biological materials, that is a possible hypothesis, and they note that evidence exists supporting the presence of niche environments in the Martian subsurface that could support life.

"This study illustrates the importance of correlating different types of datasets when attempting to discern whether something in rock is a biosignature indicative of life," says Sherry L. Cady, PhD, Editor-in-Chief of Astrobiology and Chief Scientist at the Pacific Northwest National Laboratory. "Though the authors couldn't prove definitively that the object of focus was evidence of life, their research strategy revealed a significant amount of information about the potential for life to inhabit the subsurface of Mars."

###

About the Journal

Astrobiology, led by Editor-in-Chief Sherry L. Cady, Chief Scientist at the Pacific Northwest National Laboratory, and a prominent international editorial board comprised of esteemed scientists in the field, is the authoritative peer-reviewed journal for the most up-to-date information and perspectives on exciting new research findings and discoveries emanating from interplanetary exploration and terrestrial field and laboratory research programs. The Journal is published monthly online with Open Access options and in print. Complete tables of content and a sample issue may be viewed on the Astrobiology website.

About the Publisher

See the original post here:
Life on Mars? Implications of a newly discovered mineral-rich structure

Recommendation and review posted by Bethany Smith

17 hours ago Amy Brunner

Two Virginia Tech researchers have received a $1.4 million grant to investigate the genetic regulatory networks that will allow an important bioenergy crop to be bred so it will grow in less than ideal soils and climate.

Populus, a genus of fast-growing trees commonly known as cottonwoods and aspens, is being grown for bioenergy because it produces a significant amount of biomass in two years and will re-grow robustly when cut at just above ground level. Woody biomass can be converted to liquid fuels, such as ethanol.

"The goal is to develop the species so it will not become dormant in conditions that would stress other crops, such as high temperature, drought, or marginal soil nutrients," said Amy Brunner, associate professor of molecular genetics in the College of Natural Resources and Environment and an affiliate of the Fralin Life Science Institute. "It is important that bioenergy crops not require prime agricultural land."

"We don't want biomass production to compete with food production," she continued. "The aim is to minimize inputs, develop varieties that grow in different environments, and maximize biomass production."

Brunner and Jason Holliday, assistant professor of forest genetics and biotechnology in the college and a fellow Fralin Life Science Institute affiliate, received the grant from the U.S. Department of Agriculture National Institute of Food and Agriculture and the U.S. Department of Energy Office of Biological and Environmental Research. Their project is one of 10 grants awarded as part of the national strategy of sustainable biofuels production.

"The college made the decision to enter into the specialized and highly competitive research arena of molecular genetics, and Drs. Brunner and Holliday are making important contributions to the body of molecular genetics science of tree species," said Paul Winistorfer, dean of the college. "Developing alternative approaches to biofuel crops and their adaptation and success to a changing climate is a strategic and important contribution to our future energy needs."

Brunner and Holliday are experimenting with the FT2 gene, which regulates vegetative growth. "In addition to seasonal dormancy, which happens when days get shorter, a common response to stress by woody plants is to stop growing and wait for things to get better, which is important to natural populations' ability to survive adverse conditions," said Brunner.

"Jason and I are melding our expertise to understand growth and dormancy transitions," she continued. "We will identify specific control points that can be manipulated to maximize growth in different environments."

The FT2 gene integrates signals regarding environmental conditions, such as day length and drought, to control shoot growth or regrowth after harvest.

Read more:
Forestry geneticists develop tree biomass crop to grow on marginal lands

Recommendation and review posted by Bethany Smith

11 hours ago by Brendan M. Lynch

It's not a monkey. It's not a lemur. It's not an African Bush Baby or even a Madagascan Mouse. Meet the Philippine tarsier: a tiny, adorable and downright "cool" primate from Southeast Asia.

"It's really not like any animals that Americans are familiar with," said Rafe Brown, curator-in-charge at the University of Kansas' Biodiversity Institute. "A tarsier has giant eyes and ears; an extremely cute, furry body; a long tail with a furry tuft at the end; and interesting expanded fingers and toe tips that look a bit like the disks on the digits of tree frogs."

Brown said the tarsier (tar-SEER) has become the "flagship" iconic species for promoting environmental stewardship and ecotourism in the Philippines, a nation suffering from large-scale destruction of natural habitat.

"They're threatened with habitat loss due to development, mining and deforestation from the timber industry," Brown said. "On Bohol, where they are a big part of the tourist economy, literally thousands of animals are taken out of the wild, essentially harassed by tourists, and die in captivity due to the stress and inability of their captors to feed them an appropriate diet of live small animals. Tarsiers must eat an enormous amount every night to fuel their high metabolism."

Because of threats to the tarsier, conservation efforts are mounting for the charismatic animal. But these have been thwarted by a lack of research: Too little has been known about the tarsier's taxonomic diversity; there have been too few field studies; and a scarcity of genetic samples and voucher specimens in biodiversity repositories has left advocates of the tarsier in the dark. In short, to save the tarsier, experts have needed to know much more about the species.

"Basically, we can not legally protect something if we do not know that it exists," Brown said.

Today, research by Brown and colleagues published by the journal PLOS ONE will shed new light on the animal's genetic diversity and distribution. Additionally, the KU researchers have verified the presence of a new variety of tarsier, one heretofore only suspected to existthe Dinagat-Caraga tarsier.

"Previously tarsiers were one species, divided into three named subspecies," Brown said. "Our data disagree with that subspecies arrangement and instead demonstrate that the Philippine tarsiers are divided into three genetic unitsbut these units are from different localities than the named taxa. So our data provide an objective way to restructure conservation efforts and point the resources where they need to go, in order to really have an effective impact on preserving genetic diversity in the group."

Brown's student Anthony Barley performed genetic sequencing of the tarsiers' mitochondrial DNA at KU, while fellow student Karen Olsen characterized the nuclear microsatellite loci variation of the animals.

See the original post:
Philippine tarsier gets boost from Kansas research, and genetic proof of a new variety

Recommendation and review posted by Bethany Smith

Medical researchers have used DNA sequencing to identify a gene variant responsible for causing lupus in a young patient.

The development shows that for the first time, it is feasible for researchers to identify the individual causes of lupus in patients by using DNA sequencing, allowing doctors to target specific treatments to individual patients.

Lupus is a chronic autoimmune disease that affects one in 700 Australians, predominantly young and middle aged women.

Medical researchers at the Centre for Personalised Immunology, based at the John Curtin School of Medical Research (JCSMR), sequenced the genes of a young girl who suffered a stroke when she was four as a result of her lupus.

"We can now target her specific disease, and make treatments that will benefit her throughout her life," said lead researcher Dr Julia Ellyard, from the JCSMR.

Researchers identified a variant in the TREX1 gene. This mutation caused the patient's cells to produce a molecule called interferon-alpha. Clinical trials are already underway for drugs to target interferon-alpha in adults.

Dr Jeff Chaitow, head of rheumatology, a co-investigator and the patient's treating clinician at Sydney's The Children's Hospital at Westmead, said his young patient, now 10 years old, still needs regular steroids and immune suppressive drugs each day.

"New targeted therapy would be a major benefit in controlling her disease," he said.

Professor Carola Vinuesa, Co-director of the Centre for Personalised Immunology, said research was showing lupus was primarily caused by defects in only one or a few genes.

"This is the new age of personalised medicine," she said.

Read more here:
Genetic key to lupus shows potential of personalized medicine

Recommendation and review posted by Bethany Smith

(DGAP-Media / 19.08.2014 / 10:21) Tissue specific optimized AAV Plasmids are now available to make research & therapy more targeted Gene Therapy development progresses with tissue specific AAV Plasmids developed by Europe's leading commercial supplier of viral vectors, SIRION Biotech in Munich. Munich, 19 August 2014, viral vectors are a new class of biologics that help treat diseases caused by defective gene function / proteins ("gene therapy"). More than 20 companies worldwide the majority of which originate in the United States are applying viral vectors to conduct clinical studies. A key hurdle when applying viral vectors is to limit the transduction (gene transfer) to the appropriate cells of a specific tissue without affecting their surrounding environment. But, how can an expression system differentiate between tissue or even cell type? SIRION Biotech, in cooperation with U of Munich (LMU) and U of Cologne, has developed a line of viral vectors with specific promotors that are only active in a specific set of targetetd cells to initiate the desired gene expression. Using this method, the gene of interest is only being expressed in the targeted tissue which is relevant for the desired therapy. This improves the effectiveness of the therapy and also addresses safety concerns by reducing the likelihood of side effects. Recently the company announced a new line of cell specific AAV construction plasmids, controlling expression in brain & retinal sensory cells, liver, cardiac and skeletal muscle. They are based on the commonly used AAV 2 single strand serotype and contain a classical multiple-cloning-site (MCS) for easy, customized manipulation by the experimenter. SIRION Biotech is offering such plasmids as kits at affordable pricing of $ 900 and $ 1.300, making it available to a broad academic and industrial audience. The packages include the AAV construction plasmids, vector maps and additional control vectors equipped with an ubiquitous promotor. About SIRION Biotech http://www.SIRION-Biotech.com SIRION Biotech started in Munich in 2007 with the idea of enabling novel cell models closer to reality than ever before. This required the assembly of an all-encompassing, novel viral vector platform. Both, designing de novo viral vectors and the subsequent creation of custom cell models will pave the way for superior compound development in the life sciences. Many of SIRION's viral vectors are being used to conducting clinical studies. SIRION's technologies have been validated in over 400 single projects with more than 150 academic and industrial partners. As a result, cell models for drug discovery and development have become highly reliable, as have the use of new viral vectors in gene therapy and vaccine studies. Contact SIRION: SIRION BIOTECH GmbH Dr. Christian Thirion Am Klopferspitz 19 D-82152 Martinsried Tel.: +49-89-700 961 99-15 eMail: Thirion@SIRION-Biotech.com http://www.SIRION-Biotech.com End of Media Release =-------------------------------------------------------------------- Issuer: Sirion Biotech GmbH Key word(s): Research/Technology 19.08.2014 Dissemination of a Press Release, transmitted by DGAP - a service of EQS Group AG. The issuer is solely responsible for the content of this announcement. The DGAP Distribution Services include Regulatory Announcements, Financial/Corporate News and Press Releases. Media archive at http://www.dgap-medientreff.de and http://www.dgap.de =-------------------------------------------------------------------- 282835 19.08.2014

(END) Dow Jones Newswires

August 19, 2014 04:21 ET (08:21 GMT)

Read the rest here:
Tissue specific optimized AAV Plasmids are now available to make research & therapy more targeted

Recommendation and review posted by Bethany Smith

Scientists at Washington State University have identified a crucial step in DNA repair that could lead to targeted gene therapy for hereditary diseases such as "children of the moon" and a common form of colon cancer.

Such disorders are caused by faulty DNA repair systems that increase the risk for cancer and other conditions.

The findings are published in this week's Proceedings of the National Academy of Sciences. The study was funded by the National Institute of Environmental Health Sciences.

Regents Professor Michael Smerdon and post-doctoral researcher Peng Mao found that when DNA is damaged, a specific protein must first be "unbuckled" to allow easy access for the DNA "repair crew." Without this unbuckling, entry to the damaged site is hampered by the compact arrangement of genes and protein in chromosomes called chromatin.

Smerdon and Mao's finding is one of the first to document details of how this repair process takes place in chromatin.

Daily demands for DNA repair

Each human cell sustains a range of assaults that can create up to 100,000 DNA injuries every day, said Smerdon. The cells must repair this damage by continually -- and quickly -- producing replacement DNA and proteins.

Like a tiny locomotive, an enzyme called RNA polymerase runs up and down the DNA copying genetic information. When it comes to a gene whose protein is needed by the cell, it stops and unwinds the double-stranded DNA, copies one strand and sends it off to machinery to manufacture the new protein. And all is well.

But when DNA is damaged by UV radiation or harmful substances, it forms an impenetrable mass that stalls the RNA polymerase, said Smerdon. Like a boulder on the railroad tracks, the lifeless lump blocks all protein production from that gene. Unless quickly repaired, the cell could die.

In healthy people, an enzyme repair crew travels along with the RNA polymerase and instantly rushes in to excise the damage and clear the tracks. This is called transcription-coupled repair, or TCR, an aspect of one of four known DNA repair systems. Smerdon said that even a partial deficiency in any of the repair systems could lead to life-threatening disorders.

See the article here:
Crucial step in DNA repair identified by researchers

Recommendation and review posted by Bethany Smith

Contact Information

Available for logged-in reporters only

Newswise A new study by Barbara Beltz, the Allene Lummis Russell Professor of Neuroscience at Wellesley College, and Irene Sderhll of Uppsala University, Sweden, published in the August 11 issue of the journal Developmental Cell, demonstrates that the immune system can produce cells with stem cell properties, using crayfish as a model system. These cells can, in turn, create neurons in the adult animal. The flexibility of immune cells in producing neurons in adult animals raises the possibility of the presence of similar types of plasticity in other animals.

We have been suspicious for some time that the neuronal precursor cells (stem cells) in crayfish were coming from the immune system, Beltz wrote. The paper contains multiple lines of evidence that support this conclusion, in addition to the experiments showing that blood cells transferred from a donor to a recipient animal generate neurons.

Beltz, whose research focuses on the production of new neurons in the adult nervous system, uses the crustacean brain as the model system because the generations of precursor cells are spatially segregated from one another. According to Beltz, this separation is crucial because it allowed the researchers to determine that the first generation precursors do not self-renew. For the Developmental Cell study, the cells of one crayfish were labeled and this animals blood was used for transfusions into another crayfish. They found that the donor blood cells could generate neurons in the recipient.

In many adult organisms, including humans, neurons in some parts of the brain are continually replenished. While this process is critical for ongoing health, dysfunctions in the production of new neurons may also contribute to several neurological diseases, including clinical depression and some neurodegenerative disorders.

Beltz notes, of course, that it is difficult to extrapolate from crayfish to human disease. However, because of existing research suggesting that stem cells harvested from bone marrow also can become neural precursors and generate neurons, she says it is tempting to suggest that the mechanism proposed in crayfish may also be applicable in evolutionarily higher organisms, perhaps even in humans.

Prior studies conducted in both humans and mice and published about a decade ago, showed that bone marrow recipients who had received a transplant from the opposite gender had neurons with the genetic signature of the opposite sex. The implication was that cells from the bone marrow generated those neurons. However, it is currently thought that neuronal stem cells in mammals, including humans, are self-renewing and therefore do not need to be replenished. Thus, these findings have not been interpreted as contributing to a natural physiological mechanism.

Every experiment we did confirmed the close relationship between the immune system and adult neurogenesis, Beltz said. Often when one is doing research, experiments can be fussy or give variable results. But for this work, once we started asking the right questions, the experiments worked first time and every time. The consistency and strength of the data are remarkable.

Our findings in crayfish indicate that the immune system is intimately tied to mechanisms of adult neurogenesis, suggesting a much closer relationship between the immune system and nervous system than has been previously appreciated, said Sderhll. If further studies demonstrate a similar relationship between the immune system and brain in mammals, these findings would stimulate a new area of research into immune therapies to target neurological diseases.

Go here to read the rest:
Blood Cells Generate Neurons in Crayfish; Could Have Implications for Treatment of Neurodegenerative Disorders

Recommendation and review posted by Bethany Smith

August 18, 2014

Image Caption: Melbourne researchers have revealed the critical importance of highly specialized immune cells, called natural killer cells, in killing melanoma cells that have spread to the lungs. These natural killer cells could be harnessed to hunt down and kill cancers that have spread in the body. Dr. Nick Huntington (left), Rebecca Delconte (center) and Dr. Priyanka Sathe led the team from the Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Credit: Walter and Eliza Hall Institute of Medical Research

Walter and Eliza Hall Institute of Medical Research

Melbourne researchers have revealed the critical importance of highly specialized immune cells, called natural killer cells, in killing melanoma cells that have spread to the lungs. These natural killer cells could be harnessed to hunt down and kill cancers that have spread in the body.

The team, from the Walter and Eliza Hall Institute, also found natural killer cells were critical to the bodys rejection of donor bone marrow transplants and in the runaway immune response during toxic shock syndrome.

The discoveries came after the team showed that a protein called MCL-1 was crucial for survival of natural killer cells, in research published today in the journal Nature Communications. The discovery will help to determine how natural killer cells can be manipulated to fight cancers and other disorders.

Dr Nick Huntington, Dr Priyanka Sathe and Ms Rebecca Delconte from the Molecular Immunology division said MCL-1 could be a target for boosting or depleting natural killer cell populations to treat disease. Natural killer cells are immune predators, scouring the body in search of foreign invaders such as viruses, and sensing changes in our own cells that are associated with cancer.

Dr Huntington said the team showed natural killer cells were needed to fight off invading tumor cells that had spread past the original cancer site.

We discovered MCL-1 is absolutely essential for keeping natural killer cells alive, Dr Huntington said. Without natural killer cells, the body was unable to destroy melanoma metastases that had spread throughout the body, and the cancers overwhelmed the lungs.

Knowing how important natural killer cells are for detecting and destroying cancer cells as they spread suggests they would be a good target for boosting immune defenses to treat cancer.

See the article here:
Specialized Immune Cells Could Stop Cancer Spread

Recommendation and review posted by Bethany Smith

Living Cell Technologies Limited

CAN: 104 028 042

ASX: LCT

OTCQX: LVCLY

ASX ANNOUNCEMENT

Successful second implant of NTCELL for Parkinsons

18 August 2014 Sydney, Australia and Auckland, New Zealand Living Cell Technologies Limited today announced that a second patient has been successfully implanted at Auckland City Hospital in the clinical trial of the regenerative cell therapy NTCELL for Parkinsons disease. LCT plans to complete the patient treatment phase of the study this year.

The Phase I/IIa clinical trial is an open-label investigation of the safety and clinical effects of NTCELL in patients who can no longer respond to current therapy. The trial is directed by Dr Barry Snow MBChB, FRACP, FRCPC, an internationally recognised clinician and researcher in Parkinsons disease who leads the Auckland Movement Disorders Clinic at the Auckland District Health Board.

Dr Ken Taylor, CEO of LCT says, A great deal of hard work, preclinical research and scientific endeavour has gone into the discovery and development of NTCELL. Our innovative approach is the first to target regeneration of brain cells for patients who are failing the current conventional treatment for Parkinsons disease.

Ends

See the original post:
Successful second implant of NTCELL for Parkinsons

Recommendation and review posted by Bethany Smith