SALT LAKE CITY, May 2, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) announced today that its Analyst and Investor Day for research analysts and institutional investors will take place on Thursday, May 9, 2013 at 9:00 a.m. EST in New York City. Peter D. Meldrum, president and chief executive officer of Myriad, will host the event that also will include other key members of Myriad's executive team. The focus of the meeting will be on Myriad's diagnostic product pipeline and the Company's strategic growth initiatives.

A live webcast of Myriad's Analyst and Investor Day can be accessed by visiting the investor relations section of the Company's website at http://investor.myriad.com/index.cfm. A replay of this presentation will be archived on the Myriad website for approximately one month following the completion of the analyst day.

About Myriad Genetics

Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patients' lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's portfolio of molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Read the original post:
Myriad Genetics Announces 2013 Analyst and Investor Day

Recommendation and review posted by Bethany Smith

SEATTLE, WA--(Marketwired - May 2, 2013) - Atossa Genetics, Inc. (NASDAQ: ATOS), The Breast Health Company, has signed an agreement with Millennium HealthCare Inc. (PINKSHEETS: MHCC) for the distribution by Millennium Medical Devices of Atossa's ForeCYTE Breast Health devices, which consist of the patented MASCT pump and ForeCYTE patient collection kits. Millennium has submitted an initial order for 10,000 ForeCYTE collection kits, which it intends to market to managed-care networks, healthcare clinics and physician practices in the New York Metro Area and Northern New Jersey.

Atossa's MASCT system is used by physicians and nurses to collect a small amount of nipple aspirate fluid for analysis by the National Reference Laboratory for Breast Health with the ForeCYTE Breast Health Test.

The ForeCYTE test, intended for the 110 million women in the U.S. ages 18-73, is a painless, quick and non-invasive procedure that can be performed in a physician's office. ForeCYTE can provide vital early detection of cancer or pre-cancerous conditions that may progress to cancer over an approximately eight-year period before cancer can be detected by mammography or other means. Millennium HealthCare, through its wholly-owned operating subsidiaries, provides primary care physicians practices, physician groups and healthcare facilities of all sizes with cutting edge medical devices focused primarily on preventive care through early detection.

Dr. Steven Quay, Chairman, CEO & President of Atossa Genetics, said, "We are extremely pleased that Millennium HealthCare will be distributing the ForeCYTE Breast Health devices to its healthcare practitioners. Millennium shares our passion about providing life-saving diagnostics to its healthcare professionals and we look forward to working closely with the Millennium team."

Chris Amandola, President of Millennium HealthCare, stated, "According to a recent American Cancer Society report, there were over 200,000 new cases of invasive breast cancer among women in 2011. Excluding cancers of the skin, breast cancer is the most common cancer among women, accounting for nearly 1 in 3 cancers diagnosed in the U.S. Our distribution channels are excited by the prospect that Atossa's non-invasive test can offer physicians a simple and cost-effective preventive care solution to their patients for the early detection of precursors to breast cancer."

Dominick Sartorio, CEO of Millennium HealthCare, commented, "Our team continues to explore the marketplace for new medical devices that can have a meaningful impact on improving patient care. Atossa Genetics' management team has done an outstanding job of advancing breast health care through their innovative medical devices and we look forward to a long relationship building together."

Just as the Pap smear has reduced cervical cancer rates by more than 70 percent, becoming the most successful screening test in medicine, the goal of Atossa Genetics is to reduce the stubbornly high rate of breast cancer through the early detection and treatment of the precursor changes that lead to breast cancer.

About Atossa Genetics, Inc.

Atossa Genetics, Inc. (NASDAQ: ATOS), The Breast Health Company, based in Seattle, WA, is focused on preventing breast cancer through the commercialization of patented, FDA-designated Class II diagnostic medical devices and patented, laboratory developed tests (LDT) that can detect precursors to breast cancer up to eight years before mammography.

In addition to the ForeCYTE Breast Health Test, Atossa markets the ArgusCYTE Breast Health Test, a blood test for recurrence in breast cancer survivors that provides a "liquid biopsy" for circulating cancer cells and a tailored treatment plan for patients and their caregivers. For additional information, please visit http://www.atossagenetics.com.

More here:
Atossa Genetics Signs Distribution Agreement With Millennium HealthCare

Recommendation and review posted by Bethany Smith

London, United Kingdom (Reuters) - British scientists are stepping up clinical tests of gene therapy in a bid to help people with advanced heart failure pump blood more efficiently. Researchers said on Tuesday they planned to enroll patients into two new clinical trials using Mydicar, a gene therapy treatment made by privately held US biotech company Celladon. After more than 20 years of research, the ground-breaking method for fixing faulty genes is starting to deliver, with European authorities approving the first gene therapy for an rare metabolic disease last November.

In the case of heart failure, the aim is to insert a gene called SERCA2a directly into heart cells using a modified virus, delivered via a catheter infusion. Lack of SERCA2a leads to ever weaker pumping in people with heart failure.

Although drugs offer some relief, there is currently no way of restoring heart function and the prognosis for those with advanced disease is worse than for many cancers.

One of the studies, led by scientists at Imperial College London, is part of a wider mid-stage Phase II project sponsored by Celladon that involves 200 patients worldwide, some of whom have already been treated in the United States and Denmark.

The second trial, which is due to start in the summer, will test the same treatment in 24 British patients already fitted with mechanical heart pumps to see how the approach may help in this particular setting.

It promises to be a long haul, with extensive Phase III studies still needed once results of the current mid-stage tests are received, which Celladon expects in the first half of 2015. Gene therapy has experienced a series of advances and setbacks over the decades. The most notable blow came in 1999 when an Arizona teenager died in a gene therapy experiment. More recent results, however, have been promising in fields ranging from immune system diseases to blindness.

''It is a great example of the slow burn of good laboratory science translating into a potential clinical treatment,'' said Peter Weissberg, medical director of the British Heart Foundation, which is co-funding the second trial.

Because gene therapy replaces or boosts the activity of a faulty gene, it offers the possibility of a one-time ''fix'' - and that creates an economic challenge.

Any gene therapy is bound to be expensive, since a single dose could last a lifetime and the manufacturer will have just one shot at recouping its investment.

But Alexander Lyon of Imperial College, lead investigator on both studies, said it could be a cost-effective solution in heart failure if it avoided the need for interventions such as heart transplants at 200,000 pounds ($300,000) each.

Read this article:
Health: Gene therapy

Recommendation and review posted by Bethany Smith

WALTHAM, Mass.--(BUSINESS WIRE)--

ViaCord, PerkinElmers family cord blood and tissue preservation business, is collaborating with the Center for International Blood and Marrow Transplant Research (CIBMTR) to collect, maintain and publish research from ViaCords cord blood stem cell transplants. This collaboration will expand knowledge of cord blood-derived stem cell applications throughout the medical and research community. To date, CIBMTRs large network of transplant centers has resulted in the development of a clinical database of more than 30,000 cord blood transplant recipients for clinical decision-making, use in studies, and other research purposes with the goal of making a profound impact on the survival of cord blood transplant patients around the world. CIBMTR will work directly with ViaCord to collect and analyze data to better understand the quality and any outcome metrics of ViaCords released cord blood stem cell units as well as how the units are being used.

Collaborating with CIBMTR, which has established the industry standard for collecting data around hematopoietic cellular therapy and regenerative medicine, allows us to simultaneously gain insights into the effectiveness of the cord blood stem cell units we have released for use as well as outcomes from their clinical application, said Morey Kraus, Chief Scientific Officer, ViaCord. We are then able to incorporate data from our transplanted units into the larger database, which may be accessed for other CIBMTR studies by the medical and scientific community to further their research and understanding of cord blood stem cells.

ViaCord is working with CIBMTR to collect and publish data as well as identify outcomes unique to related or autologous (stem cells from the same patient) transplants. The collaboration will also enable the analysis of umbilical cord units released for potential future use in autologous cell therapy and regenerative medicine clinical trials, including Cerebral Palsy, Type 1 Diabetes and others.

The science of cord blood and cord tissue stem cells is growing at a rapid pace, said J. Douglas Rizzo, M.D., M.S., Associate Scientific Director, CIBMTR. We are excited to collaborate with ViaCord to provide data and analytic expertise that will assist the development of the field through research.

ViaCord's family cord blood banking services currently offers expectant families the opportunity to preserve their baby's umbilical cord blood for potential medical use by the child or a related family member. Families are also preserving their babys umbilical cord tissue because research suggests that one day these special cells may have the potential to treat medical conditions that are untreatable today. ViaCord has preserved the umbilical cord blood of more than 300,000 newborns. Twenty years ago, cord blood stem cells were used to treat just one disease, Fanconi's anemia. Today, cord blood stem cells have been used in the treatment of nearly 80 diseases, including cancers, certain blood disorders and immunodeficiencies. Please visit http://www.viacord.com for more information.

Factors Affecting Future Performance This press release contains "forward-looking" statements within the meaning of the Private Securities Litigation Reform Act of 1995, including, but not limited to, statements relating to estimates and projections of future earnings per share, cash flow and revenue growth and other financial results, developments relating to our customers and end-markets, and plans concerning business development opportunities and divestitures. Words such as "believes," "intends," "anticipates," "plans," "expects," "projects," "forecasts," "will" and similar expressions, and references to guidance, are intended to identify forward-looking statements. Such statements are based on management's current assumptions and expectations and no assurances can be given that our assumptions or expectations will prove to be correct. A number of important risk factors could cause actual results to differ materially from the results described, implied or projected in any forward-looking statements. These factors include, without limitation: (1) markets into which we sell our products declining or not growing as anticipated; (2) fluctuations in the global economic and political environments; (3) our failure to introduce new products in a timely manner; (4) our ability to execute acquisitions and license technologies, or to successfully integrate acquired businesses and licensed technologies into our existing business or to make them profitable, or successfully divest businesses; (5) our failure to adequately protect our intellectual property; (6) the loss of any of our licenses or licensed rights; (7) our ability to compete effectively; (8) fluctuation in our quarterly operating results and our ability to adjust our operations to address unexpected changes; (9) significant disruption in third-party package delivery and import/export services or significant increases in prices for those services; (10) disruptions in the supply of raw materials and supplies; (11) the manufacture and sale of products exposing us to product liability claims; (12) our failure to maintain compliance with applicable government regulations; (13) regulatory changes; (14) our failure to comply with healthcare industry regulations; (15) economic, political and other risks associated with foreign operations; (16) our ability to retain key personnel; (17) significant disruption in our information technology systems; (18) our ability to obtain future financing; (19) restrictions in our credit agreements; (20) our ability to realize the full value of our intangible assets; (21) significant fluctuations in our stock price; (22) reduction or elimination of dividends on our common stock; and (23) other factors which we describe under the caption "Risk Factors" in our most recent quarterly report on Form 10-Q and in our other filings with the Securities and Exchange Commission. We disclaim any intention or obligation to update any forward-looking statements as a result of developments occurring after the date of this press release.

About the Center for International Blood and Marrow Transplant Research(CIBMTR) A combined research program of the National Marrow Donor Program and the Medical College of Wisconsin, the CIBMTR facilitates critical, cutting-edge research that has led to increased survival and an enriched quality of life for thousands of patients. The CIBMTR collaborates with the global scientific community to advance hematopoietic cell transplantation and cellular therapy research worldwide. The prospective and observational research is accomplished through scientific and statistical expertise, a large network of transplant centers and clinical database of more than 350,000 transplant recipients.

About PerkinElmer, Inc. PerkinElmer, Inc. is a global leader focused on improving the health and safety of people and the environment. The company reported revenue of approximately $2.1 billion in 2012, has about 7,500 employees serving customers in more than 150 countries, and is a component of the S&P 500 Index. Additional information is available through 1-877-PKI-NYSE, or at http://www.perkinelmer.com.

Original post:
ViaCord® to Advance Cord Blood Stem Cell Therapy Research through Collaboration with the Center for International ...

Recommendation and review posted by simmons

BRITISH scientists are stepping up clinical tests of gene therapy in a bid to help people with advanced heart failure pump blood more efficiently.

Researchers say they plan to enrol patients into two new clinical trials using Mydicar, a gene therapy treatment made by privately held US biotech company Celladon.

After more than 20 years of research, the groundbreaking method for fixing faulty genes is starting to deliver, with European authorities approving the first gene therapy for rare metabolic disease last November.

In the case of heart failure, the aim is to insert a gene called Serca2a directly into heart cells using a modified virus, delivered via a catheter infusion. Lack of Serca2a leads to ever weaker pumping in people with heart failure.

Although drugs offer some relief, there is currently no way of restoring heart function and the prognosis for those with advanced disease is worse than for many cancers.

One of the studies, led by scientists at Imperial College London, is part of a wider midstage phase 2 project sponsored by Celladon that involves 200 patients worldwide, some of whom have already been treated in the US and Denmark.

The second trial, which is due to start in July, will test the same treatment in 24 British patients already fitted with mechanical heart pumps to see how the approach may help in this particular setting.

It promises to be a long haul, with extensive phase 3 studies still needed once results of the current mid-stage tests are received, which Celladon expects in the first half of 2015.

Gene therapy has experienced a series of advances and setbacks over the decades. The most notable blow came in 1999 when an Arizona teenager died in a gene therapy experiment. More recent results, however, have been promising in fields ranging from immune system diseases to blindness.

"It is a great example of the slow burn of good laboratory science translating into a potential clinical treatment," says Dr Peter Weissberg, medical director of the British Heart Foundation, which is co-funding the second trial.

Original post:
Another piece in the puzzle of how to heal broken hearts

Recommendation and review posted by Bethany Smith

London, April 30 (ANI): A Northwestern University study has shed light on how a mouse instinctively avoids a cat, when it smells the feline.

The study involving olfactory receptors, which underlie the sense of smell, provides evidence that a single gene is necessary for the behavior.

A research team led by neurobiologist Thomas Bozza has shown that removing one olfactory receptor from mice can have a profound effect on their behavior. The gene, called TAAR4, encodes a receptor that responds to a chemical that is enriched in the urine of carnivores.

While normal mice innately avoid the scent marks of predators, mice lacking the TAAR4 receptor do not.

The study reveals something new about our sense of smell: individual genes matter.

Unlike our sense of vision, much less is known about how sensory receptors contribute to the perception of smells. Color vision is generated by the cooperative action of three light-sensitive receptors found in sensory neurons in the eye. People with mutations in even one of these receptors experience color blindness.

"It is easy to understand how each of the three color receptors is important and maintained during evolution," said Bozza, an author of the paper, "but the olfactory system is much more complex."

In contrast to the three color receptors, humans have 380 olfactory receptor genes, while mice have more than 1,000. Common smells like the fragrance of coffee and perfumes typically activate many receptors.

"The general consensus in the field is that removing a single olfactory receptor gene would not have a significant effect on odor perception," said Bozza, an assistant professor of neurobiology in the Weinberg College of Arts and Sciences.

Bozza and his colleagues tested this assumption by genetically removing a specific subset of olfactory receptors called trace amine-associated receptors, or TAARs, in mice. Mice have 15 TAARs. One is expressed in the brain and responds to amine neurotransmitters and common drugs of abuse such as amphetamine. The other 14 are found in the nose and have been coopted to detect odors.

Read this article:
Gene necessary for mice to avoid cats discovered

Recommendation and review posted by Bethany Smith

DUBLIN--(BUSINESS WIRE)--

Research and Markets has announced the addition of the "MediPoint: Predictive Breast Cancer Gene Testing - EU Analysis and Market Forecasts" report to their offering.

MediPoint: Predictive Breast Cancer Gene Testing - EU Analysis and Market Forecasts

Breast cancer is the most common form of cancer in women in both the developed and developing world. The incidence of breast cancer is increasing due to the increased life span and increasing adoption of Western lifestyle risk factors. Predictive breast cancer gene tests can be used to identify women who are at increased risk of developing hereditary breast cancer. The Predictive Breast Cancer Gene Testing market has seen exponential growth in the US, dominated by Myriad Genetics. Gene testing in Europe is mostly carried out by the state funded health sector, but increasingly private companies are offering breast cancer gene tests to physicians. Myriad Genetics' position in the market is dependent on it being the leading provider of the most common breast cancer mutations. By the end of our forecast period, the competitive landscape will experience significant change due to the erosion of Myriad Genetics' position, as a result of the expiry of key patents, and the emergence of alternative molecular technologies.

Scope

- An overview of Breast Cancer, which includes epidemiology, etiology, symptoms, diagnosis, pathology and treatment guidelines.

- Annualized EU Breast Cancer Gene Testing market revenue and future forecasts from 2009 to 2011, forecast for 7 years to 2018.

- Investigation of current and future market competition for Breast Cancer Gene Testing

- Insightful review of the key industry drivers, restraints and challenges as well as predicted impact of key events.

- Competitor assessment including device approval analysis and device sales forecasts.

See original here:
Research and Markets: MediPoint: Predictive Breast Cancer Gene Testing - EU Analysis and Market Forecasts

Recommendation and review posted by Bethany Smith

Feds Were Watching Tamerlan Tsarnaev and Mother Long Before the Bombing
About 18 months before the Boston Marathon bombings, the CIA added the mother of the two suspects to a terrorism database after Russian authorities raised co...

By: TheAlexJonesChannel

Link:
Feds Were Watching Tamerlan Tsarnaev and Mother Long Before the Bombing - Video

Recommendation and review posted by Bethany Smith

Bilderberg Sleuth Jim Tucker Remembered
Alex broadcasts from the road. He pays tribute to Bilderberg sleuth Jim Tucker, who passed away last week at the age of 78. He also covers the latest attack ...

By: TheAlexJonesChannel

See the original post:
Bilderberg Sleuth Jim Tucker Remembered - Video

Recommendation and review posted by Bethany Smith

Dear EarthTalk: What is the Monsanto Protection Act and why are environmentalists so upset about it?

Rita Redstone

Milwaukee, Wisc.

The so-called Monsanto Protection Act is actually a provision (officially known as Section 735) within a recently passed Congressional spending bill, H.R. 933, which exempts biotech companies from litigation regarding the making, selling and distribution of genetically engineered seeds and plants.

President Barack Obama signed the bill and its controversial rider into law in March, much to the dismay of environmentalists. It means that Monsanto and other companies that supply the majority of the nation's crop seeds can continue to produce genetically engineered products regardless of any potential court orders stating otherwise. Opponents of genetically engineered foods believe that giving such companies a free reign over the production of such potentially dangerous organisms regardless of judicial challenge is a bad idea -- especially given how little we still know about the biological and ecological implications of widespread use of genetically engineered crops.

Today, more than 90 percent of the corn, soybeans, cotton, sugar beets and canola planted in the U.S. is derived from seeds genetically engineered by Monsanto and other companies to resist pests and thus increase yields. Aviva Shen of the ThinkProgress blog reports that, instead of reducing farmers' use of toxic pesticides and herbicides, genetically engineered seeds are having the opposite effect in what has become a race to keep faster and faster developing "superweeds" and "superbugs" at bay. With Congress and the White House refusing to regulate genetically engineered crops, the court system has remained a last line of defense for those fighting the widespread adoption of genetic engineering -- until now, that is, thanks to H.R. 933.

Monsanto isn't the only seed company heavily into genetic engineering, but it is the biggest and most well-known and spends millions of dollars each year on lobbyists to keep it that way. Critics point out that the company has spent decades stacking government agencies with its executives and directors. "Monsanto's board members have worked for the EPA, advised the U.S. Department of Agriculture and served on President Obama's Advisory Committee for Trade Policy and Negotiations," reports the group Food & Water Watch. "The prevalence of Monsanto's directors in these highly influential positions begs a closer look at how they're able to push the pro-genetically engineered agenda within the government and influence public opinion."

"The judicial review process is an essential element of U.S law and serves as a vital check on any Federal Agency decision that may negatively impact human health, the environment or livelihoods," reports Food Democracy Now! "Yet this provision seeks an end-run around such judicial review by preemptively deciding that industry can set its own conditions to continue to sell biotech seeds, even if a court may find them to have been wrongfully approved."

Another concern of safe food advocates now is getting the government to require food makers to list genetically engineered ingredients clearly on product labels so consumers can make informed choices accordingly. "Not only is (genetically engineered) labeling a reasonable and common sense solution to the continued controversy that corporations like Monsanto, DuPont and Dow Chemical have created by subverting our basic democratic rights," adds Food Democracy Now!, "but it is a basic right that citizens in 62 other countries around the world already enjoy, including Europe, Russia, China, India, South Africa and Saudi Arabia."

CONTACTS: ThinkProgress, http://www.thinkprogress.org; Food & Water Watch, http://www.foodandwaterwatch.org; Food Democracy Now!, http://www.fooddemocracynow.org.

Follow this link:
EarthTalk / Efforts to regulate genetic engineering of crops sacked

Recommendation and review posted by Bethany Smith

Researchers studying a genetic mutation, which causes sudden cardiac death, may have discovered a genetic link between German, Danish and Newfoundland families.

Dr. Hendrick Milting, a genetics researcher at the Heart and Diabetes Center North Rhine-Westphalia in Bad Oeynhausen, Germany, has been doing work with a gene mutation for arrhythmogenic right ventricular, or ARVC, a form of heart disease that usually appears in early adulthood and causes sudden cardiac death.

It has affected many members of a German family.

That mutation is the same one that genetic researchers at Memorial University identified in 2008 as affecting 24 Newfoundland families adding up to 1,200 people over several generations.

Not only did Milting discover the Newfoundland research, he also found a similar mutation in a Danish family.

"By chance at the same time, a group in Copenhagen found a similar family in Denmark. We decided to make a genetic fingerprint of these families and we found that all these families are connected," said Milting.

"So they have a common root."

Milting has come to Memorial University to work with genetic researchers Dr. Kathy Hodgkinson, Dr. Terry Lynn Young, and Dr. Sean Connors at the Faculty of Medicine.

He has also planned to meet with history, folklore, geography, and anthropology experts to try to find out more about how the German and Danish families could be linked to the Newfoundland family, which, like many Newfoundland families, was thought to be of English and Irish descent.

"What we have is a piece of DNA that gives us history written in a DNA code," said Hodgkinson.

More:
Genetic mutation shared by Newfoundland, German, Danish families

Recommendation and review posted by Bethany Smith

CAMBRIDGE, Mass., April 30, 2013 /PRNewswire/ -- Metamark Genetics, Inc., a leader in the discovery of novel molecular prognostic and diagnostic tests for cancer, today announced that industry veteran Shawn M. Marcell has been named the company's new president and chief executive officer. Mr. Marcell succeeds interim executive Michael Kauffman, M.D., who will remain on Metamark's board of directors.

Metamark lead director Gregory C. Critchfield, M.D., said, "We are excited to welcome Shawn to Metamark as the company prepares to launch its first prognostic test, for prostate cancer. Shawn's broad and deep experience in life sciences, and his success in bringing innovative products to market, make him the ideal leader for Metamark as it grows into to a commercial organization." Dr. Critchfield added, "We also would like to thank Michael Kauffman for his leadership during this important time in the company's evolution."

"Metamark's strategy to develop novel prognostic and diagnostic tests based on advanced quantitative histologic analysis has the potential to transform approaches to cancer and other major diseases," said Mr. Marcell. "I am thrilled to join the company and look forward to working with the entire team as we build a leading commercial stage molecular diagnostics company."

Mr. Marcell has nearly three decades of diverse executive, commercial and operational experience in life science and technology businesses. Most recently, he was the lead executive, serving as general manager of Hologic's (HOLX) wholly owned LIFECODES subsidiary, which was acquired by Immucor. He headed commercial operations at Sequenom (SQNM), which acquired SensiGen, where he served as president and CEO. Mr. Marcell has both CLIA laboratory and product launch experience and has had additional key management roles with Redpoint Bio, Prima Facie, Centocor and Abbott Diagnostics.

Mr. Marcell has been adjunct faculty and lecturer in Entrepreneurial Programs at the Wharton School and has served on numerous for-profit and non-profit boards.

About Metamark

Metamark Genetics is a privately held biotechnology company founded in 2007 to develop new function- based prognostic and diagnostic tests aimed at improving cancer care. The company's proprietary genomic and proteomic discovery platforms have yielded significant discoveries in several disease areas, including prostate, colon and breast cancers. During 2013, Metamark plans to commercialize ProMarkTM its lead prostate cancer prognostic test through its Cambridge, MA CLIA-certified laboratory. For more information, please visit the company's Website at http://www.metamarkgenetics.com.

MetamarkTM and ProMarkTM are trademarks of Metamark Genetics, Inc.

More here:
Metamark Genetics Board of Directors Appoints Shawn M. Marcell President and Chief Executive Officer

Recommendation and review posted by Bethany Smith

Public release date: 30-Apr-2013 [ | E-mail | Share ]

Contact: Phyllis Edelman pedelman@genetics-gsa.org 301-634-7302 Genetics Society of America

Bethesda, MDApril 30, 2013 Listed below are the selected highlights for the May 2013 issue of the Genetics Society of America's journal, GENETICS. The May issue is available online at http://www.genetics.org/content/current. Please credit GENETICS, Vol. 194, MAY 2013, Copyright 2013.

Please feel free to forward to colleagues who may be interested in these articles on a wide array of topics including: developmental and behavioral genetics; genome integrity and transmission; genetics of complex traits; cellular genetics; and population and evolutionary genetics.

ISSUE HIGHLIGHTS

Developmental and Behavioral Genetics An organelle gatekeeper function for Caenorhabditis elegans UNC-16 (JIP3) at the axon initial segment, pp. 143-161 S. L. Edwards, S.-c. Yu, C. M. Hoover, B. C. Phillips, J. E. Richmond, and K. G. Miller Nerve cell bodies have a vastly different organelle composition than axons. This article (see accompanying commentary by Zheng and Nonet, pp. 35-37) provides insight into the basis of this difference. The authors report the discovery of a previously unrecognized organelle gatekeeper function, mediated by UNC-16 (JIP3 in humans), that acts at the axon initial segment to restrict the flow of Golgi and endosomal organelles into the synaptic region of axons.

Genome Integrity and Transmission Novel proteins required for meiotic silencing by unpaired DNA and siRNA generation in Neurospora crassa, pp. 91-100 T. M. Hammond, H. Xiao, E. C. Boone, L. M. Decker, S. A. Lee, T. D. Perdue, P. J. Pukkila, and P. K. Shiu and Identification of small RNAs associated with meiotic silencing by unpaired DNA, pp. 279-284 T. M. Hammond, W. G. Spollen, L. M. Decker, S. M. Blake, G. K. Springer, and P. K. Shiu Genes unpaired during meiosis are silenced in Neurospora by a mechanism known as meiotic silencing by unpaired DNA (MSUD). Two articles in this issue of GENETICS report the identification of novel players in this process, including small RNAs and the first nuclear MSUD protein. This protein is not required for meiosis, providing the first indication that MSUD is not necessarily coupled to sexual development.

Genome Integrity and Transmission Intragenomic conflict between the two major knob repeats of maize, pp. 81-89 L. B. Kanizay, P. S. Albert, J. A. Birchler, and R. K. Dawe Large genomes are often replete with tandem repeats. Why do they exist? Here the authors investigate the distribution of tandem repeats in maize heterochromatic domains called knobs. The data suggest an intragenomic conflict whereby one family of repeats suppresses proliferation of the other. Similar competition may underlie the formation and maintenance of many tandem repeat arrays.

Genome Integrity and Transmission Nonrandom distribution of interhomolog recombination events induced by breakage of a dicentric chromosome in Saccharomyces cerevisiae, pp. 69-80 W. Song, M. Gawel, M. Dominska, P. W. Greenwell, E. Hazkani-Covo, K. Bloom, and T. D. Petes This article presents the first high-resolution mapping of the positions of chromosome breaks that result from the bridge-fusion-breakage cycles of dicentric chromosomes. Sites of recombination between a dicentric chromosome and its normal homolog revealed the locations of breaks in the dicentric chromosome, which were distributed in a quasi-random fashion between the two centromeres.

Genetics of Complex Traits Systems genetics of environmental response in the mature wheat embryo, pp. 265-277 J. D. Munkvold, D. Laudencia-Chingcuanco, and M. E. Sorrells This article illustrates the utility of network approaches for understanding gene expression by environment interaction, even in organisms with highly complex genomes. A unique Weighted Gene Co-Expression Network Analysis approach was used to compare gene expression networks in mature wheat embryos from two distinct growing environments across a segregating population. This approach identified environmentally conserved and unique co-expression modules and their genetic control.

Go here to read the rest:
Genetics Society of America's GENETICS journal highlights for May 2013

Recommendation and review posted by Bethany Smith

The technique, which has been 20 years in development, could help the 750,000 people in the UK living with heart failure.

The condition results from damage to the heart left over from a heart attack or side-effects of powerful chemotherapy drugs. After the heart is starved of oxygen, cells die and the remaining heart cells become fatigued.

"Once heart failure starts, it progresses into a vicious cycle where the pumping becomes weaker and weaker, as each heart cell simply cannot respond to the increased demand." said Alex Lyon, a cardiologist at the Royal Brompton hospital in London who is leading the trial in the UK.

"Our goal is to fight back against heart failure by targeting and reversing some of the critical molecular changes arising in the heart when it fails," he said.

People with heart failure can find it difficult to walk long distances or climb stairs. The disease is usually progressive, with heart function gradually weakening over time. The only solutions are heart transplant or surgically implanted pumps to maintain blood flow.

The gene therapy adds a repair gene to failing heart cells which produces more of a protein called SERCA2a which regulates the availability of calcium in the heart. Without ample supplies of calcium, heart muscles are unable to contract properly or relax properly between contractions - two key symptoms of heart failure.

Tests on human cells in the laboratory at Imperial College in London and in animals have shown that the SERCA2a gene can be repaired, and reverses some of the symptoms of heart failure.

A US biotech company Celladon has patented a method for inserting the gene into human hearts. They are co-sponsoring the UK element of the trial along with the British Heart Foundation which funded much of the basic research involved.

The technique uses a harmless virus similar related to the common cold. The DNA from the virus is removed and replaced with SERCA2a gene. This virus is then injected into the heart where it infects heart cells. The cells' own machinery then decodes the SERCA2a gene, making more of the calcium regulating protein that is missing in failing hearts.

"When the gene is repaired it produces more of the functional protein and the problem is reversed," said Dr Lyon.

Read more from the original source:
Gene therapy hope for heart failure patients

Recommendation and review posted by Bethany Smith

The first of 200 patients from around the world will be treated at the Golden Jubilee National Hospital, Clydebank, and the Royal Brompton Hospital, London, in the next three to six weeks.

All suffer from severe chronic heart failure, due to the after-effects of heart attacks and inherited conditions.

Doctors will randomly treat half the patients with a harmless virus carrying a corrective gene. The rest will receive an inactive placebo treatment.

Previous research suggests that a protein produced by the gene can restore function to failing hearts, and reduce the risk of death and the need for heart transplants.

Lead investigator Dr Alexander Lyon, consultant cardiologist at the Royal Brompton, said: "Our goal is to fight back against heart failure by targeting and reversing some of the critical molecular changes arising in the heart when it fails."

The Cupid 2 trial is taking place in conjunction with US biotech company Celladon, which has patented the treatment.

The therapy involves injecting the virus directly into the heart via a catheter. As the virus infects the heart cells, it implants the corrective gene.

This has the effect of increasing levels of a protein called SERCA2a, which plays a key role in a vital signalling mechanism involving calcium.

"When the heart muscle is injured it activates a series of compensatory changes, but over time fatigue sets in which results in the natural version of this gene switching off," said Dr Lyon. "When the gene is repaired it produces more of the functional protein and the problem is reversed."

Contextual targeting label:

Excerpt from:
Gene hope for heart patients

Recommendation and review posted by Bethany Smith

More than 200 people with heart failure are to receive a pioneering form of gene therapy to try to get their hearts beating properly again. "This is the first ever gene therapy trial to target heart failure," says lead investigator Alexander Lyon of Imperial College London.

Heart failure results after damage to the heart muscle causes it to deteriorate, which in turn progressively weakens cells that govern heartbeat. The result is serious fatigue due to the heart's inability to pump blood efficiently. Each year in the UK alone it affects 120,000 people who have never had the condition before, killing a third of them within 12 months.

Doctors will inject participants with harmless viruses that ferry a gene called SERCA2a into their heart muscle. The gene codes for a protein that recycles calcium within heart muscle cells, vital for driving each heartbeat and priming the next one.

In damaged cells, this recycling is impaired. By loading new copies of the gene the aim is to compensate for this decline. "The gene therapy will reset the calcium control," says Lyon.

A preliminary trial of the same therapy three years ago in 39 people demonstrated that it is safe and delivers benefits. Those who got the highest dose of the virus, for example, spent only a tenth as long in hospital as those given a placebo (Circulation, doi.org/bzvxst). The impending follow-up trial will recruit 200 people split equally between the US and Europe.

In a separate trial of the same therapy, doctors will treat 24 people who already have temporary mechanical implants to aid heartbeat while they await heart transplants.

If you would like to reuse any content from New Scientist, either in print or online, please contact the syndication department first for permission. New Scientist does not own rights to photos, but there are a variety of licensing options available for use of articles and graphics we own the copyright to.

Only subscribers may leave comments on this article. Please log in.

Only personal subscribers may leave comments on this article

Subscribe now to comment.

See the article here:
Gene therapy to repair failing hearts starts trial

Recommendation and review posted by Bethany Smith

Patients with severe heart failure are to be treated with gene therapy for the first time in Britain.

Earlier clinical trials have suggested the treatment could reverse damaging changes inside cardiac cells that weaken the muscle and reduce the ability of the heart to pump blood.

The condition affects 750,000 people in the UK and is often fatal.

Doctors backed by the British Heart Foundation will give 100 patients an infusion of a harmless virus that has been genetically engineered to carry an extra gene, called SERCA2a.

The virus infects cardiac cells. Once inside, the gene becomes activated and makes a protein crucial to normal beating of the heart.

Dr Alexander Lyon, consultant cardiologist at The Royal Brompton Hospital, is leading the Cupid 2 trial.

He said: "When the heart muscle is injured it activates a series of compensatory changes, but over time fatigue sets in which results in the natural version of this gene switching off.

"When the gene is repaired it produces more of the functional protein and the problem is reversed."

The first patients will be given the treatment in the next three to six weeks at hospitals in London and Glasgow.

They will be tracked and compared to another group of study volunteers who will receive a dummy treatment.

See original here:
Heart Failure: First UK Gene Therapy Trial

Recommendation and review posted by Bethany Smith

The first attempt in Britain to treat heart failure patients with gene therapy is to begin within weeks, as part of study aimed at improving the lives of up to a million people in the UK who suffer the debilitating and potentially fatal condition.

Click HERE to view 'how to treat a failing heart' graphic

Two clinical trials are planned for a few dozen British patients who will be deliberately exposed to a virus carrying a synthetic copy of a human gene known to be involved in boosting heartbeat.

The first trial will be carried out at the Royal Brompton Hospital in London and the Golden Jubilee National Hospital in Glasgow. The patients will be part of a group of 200 from around the world who will have the virus injected via a cardiac catheter inserted through a vein in the leg. A second trial at the Harefield and Papworth hospitals will be based entirely within the UK and involve 24 patients with chronic heart failure who are already fitted with an "artificial heart" known as a left ventricular assist device, which helps to pump blood around the body.

The aim in both trials is to inject additional copies of a healthy gene, known to be responsible for a key protein involved in regulating the rhythmic contraction of the heart muscle. It is hoped that the extra genes will remain active within a patient's heart for many months or even years.

Scientists believe the approach could lead to a significant improvement in the efficiency of the diseased heart to pump blood around the body so improving the quality of life of thousands of patients with progressive heart failure who develop serious ailments as well as severe fatigue.

Scientists warned that it will still be several years before the technique can be made widely available. They do not want to raise hopes unduly as many previous gene therapy trials on patients with a range of other illnesses have failed to live up to expectations.

However, the heart researchers said they are optimistic that the gene technique will improve the quality of life in at least some of the patients, who would otherwise suffer deteriorating health and life expectancy a third of patients die within a year of diagnosis.

"Once heart failure starts, it progresses into a vicious cycle where the pumping becomes weaker and weaker, as each heart cell simply cannot respond to the increased demand," said Alexander Lyon, a consultant cardiologist at the Royal Brompton.

"Our goal is to fight back against heart failure by targeting and reversing some of the critical molecular changes arising in the heart when it fails."

Read the original:
Gene therapy to offer up to 1m heart patients new lease of life

Recommendation and review posted by Bethany Smith

The first attempt in Britain to treat heart failure patients with gene therapy is to begin within weeks, as part of study aimed at improving the lives of up to a million people in the UK who suffer the debilitating and potentially fatal condition.

Click HERE to view 'how to treat a failing heart' graphic

Two clinical trials are planned for a few dozen British patients who will be deliberately exposed to a virus carrying a synthetic copy of a human gene known to be involved in boosting heartbeat.

The first trial will be carried out at the Royal Brompton Hospital in London and the Golden Jubilee National Hospital in Glasgow. The patients will be part of a group of 200 from around the world who will have the virus injected via a cardiac catheter inserted through a vein in the leg. A second trial at the Harefield and Papworth hospitals will be based entirely within the UK and involve 24 patients with chronic heart failure who are already fitted with an "artificial heart" known as a left ventricular assist device, which helps to pump blood around the body.

The aim in both trials is to inject additional copies of a healthy gene, known to be responsible for a key protein involved in regulating the rhythmic contraction of the heart muscle. It is hoped that the extra genes will remain active within a patient's heart for many months or even years.

Scientists believe the approach could lead to a significant improvement in the efficiency of the diseased heart to pump blood around the body so improving the quality of life of thousands of patients with progressive heart failure who develop serious ailments as well as severe fatigue.

Scientists warned that it will still be several years before the technique can be made widely available. They do not want to raise hopes unduly as many previous gene therapy trials on patients with a range of other illnesses have failed to live up to expectations.

However, the heart researchers said they are optimistic that the gene technique will improve the quality of life in at least some of the patients, who would otherwise suffer deteriorating health and life expectancy a third of patients die within a year of diagnosis.

"Once heart failure starts, it progresses into a vicious cycle where the pumping becomes weaker and weaker, as each heart cell simply cannot respond to the increased demand," said Alexander Lyon, a consultant cardiologist at the Royal Brompton.

"Our goal is to fight back against heart failure by targeting and reversing some of the critical molecular changes arising in the heart when it fails."

View original post here:
Gene therapy to offer heart patients new lease of life

Recommendation and review posted by Bethany Smith

Public release date: 28-Apr-2013 [ | E-mail | Share ]

Contact: Hilary Glover hilary.glover@biomedcentral.com 44-020-319-22370 BioMed Central

Injection of human stem cells into mice with tumors slowed down tumor growth, finds research published in BioMed Central's open access journal Stem Cell Research & Therapy. Human mesenchymal stem cells (MSC), isolated from bone marrow, caused changes in blood vessels supplying the tumor, and it is this modification of blood supply which seems to impact tumor growth.

The use of stem cells in treating cancer has been controversial, with some studies finding that stem cells force tumors to enter programmed cell death. However other studies find that stem cells actually promote tumor growth by inducing infiltration of new blood vessels. In attempting to sort out this puzzle researchers from INSERM groups at Universit Joseph Fourier in collaboration with CHU de Grenoble investigated the impact of MSC on already established subcutaneous or lung metastasis in mice.

For both the subcutaneous and lung tumors, injection of MSC reduced cell division, consequently slowing the rate of tumor growth. Part of the mode of action of stem cells therefore appears to be due to with angiogenesis, but the mechanism behind this is still unclear.

Claire Rome who led this study explained, "We found that MSC altered vasculature inside the tumor - although new blood vessels were generated, overall they were longer and fewer than in untreated tumors. This could be restricting the oxygen and nutrients to the tumor, limiting cell division." She continued, "Our study confirms others which propose that stem cells, in particular MSC, might be one way forwards in treating cancer."

Commenting on this study Celia Gomes, from the University of Coimbra, said, "One of the interesting questions this study raises is when MSC promote tumor growth and when they restrict it. The answer seems to be timing this study looks at already established tumors, while others, which find that MSC increase growth, tend to be investigating new tumors. This is a first step in the path to identifying exactly which patients might benefit from stem cell therapy and who will not."

###

Media Contact

Dr Hilary Glover Scientific Press Officer, BioMed Central Tel: +44 (0) 20 3192 2370 Mob: +44 (0) 778 698 1967 Email: hilary.glover@biomedcentral.com

Visit link:
Clarifying the effect of stem cell therapy on cancer

Recommendation and review posted by simmons

ALLENDALE, N.J., April 29, 2013 (GLOBE NEWSWIRE) -- NeoStem, Inc. (NYSE MKT:NBS) and its subsidiary, Progenitor Cell Therapy LLC ("PCT"), announced today the execution of a Services Agreement with Sentien Biotechnologies, Inc. ("Sentien") under which PCT will provide services to support Sentien's development of its cell therapy product, including technology transfer, staff training, and manufacturing.

Sentien is developing an allogeneic cell therapy product consisting of bone marrow derived mesenchymal stem cells seeded onto a medical device for critical care indications. Sentien has engaged PCT for manufacture of the final formulation of its cell therapy product and intends to transfer and implement Sentien's master cell bank, product working cell bank and product manufacturing processes to PCT. These cell banks will be prepared according to Good Manufacturing Practices ("GMP") guidelines and implemented by PCT to create a cell therapy product for Sentien's Investigational New Drug ("IND") submission to the FDA. Upon obtaining an IND, Sentien intends to have PCT manufacture GMP compliant grade materials to support Sentien's Phase I clinical trial.

"We are excited to enter into this agreement with Sentien, an innovator for acute organ failure," said Robert A. Preti, PhD, President and Chief Scientific Officer of PCT. PCT is an internationally recognized contract development and manufacturing organization with facilities in Allendale, New Jersey and Mountain View, California. The company has expertise in GMP manufacture for cell therapies, including dendritic cells, stem cells and T cells. Notably, PCT provided manufacturing for the pivotal studies for Dendreon's Provenge(R), the first cell therapy approved for cancer treatment.

About NeoStem, Inc.

NeoStem, Inc. ("NeoStem" or the "Company") is a leader in the emerging cellular therapy industry. Our business model includes the development of novel proprietary cell therapy products as well as operating a contract development and manufacturing organization ("CDMO") providing services to others in the regenerative medicine industry. The combination of a therapeutic development business and revenue-generating service provider business provides the Company with capabilities for cost effective in-house product development and immediate revenue and cash flow generation. http://www.neostem.com

Forward-Looking Statements for NeoStem, Inc.

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements reflect management's current expectations, as of the date of this press release, and involve certain risks and uncertainties. Forward-looking statements include statements herein with respect to the successful execution of the Company's business strategy, including with respect to the Company's research and development and clinical evaluation efforts for cellular therapies, including with respect to AMR-001, the future of the regenerative medicine industry and the role of stem cells and cellular therapy in that industry and the Company's ability to successfully grow its contract development and manufacturing business. The Company's actual results could differ materially from those anticipated in these forward- looking statements as a result of various factors. Factors that could cause future results to materially differ from the recent results or those projected in forward-looking statements include the "Risk Factors" described in the Company's Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 11, 2013 and in the Company's periodic filings with the Securities and Exchange Commission. The Company's further development is highly dependent on future medical and research developments and market acceptance, which is outside its control.

Read the original here:
NeoStem's Subsidiary, Progenitor Cell Therapy, Enters Into a Services Agreement With Sentien Biotechnologies, Inc.

Recommendation and review posted by Bethany Smith

Apr. 29, 2013 University of North Carolina researchers have discovered that disrupting a gene that acts as a regulatory switch to turn on other genes can keep blood vessels from forming and developing properly.

Further study of this gene -- a "transcription factor" called CASZ1 -- may uncover a regulatory network that influences the development of cardiovascular disease. A number of other studies have already shown a genetic link between mutations in CASZ1 and hypertension.

The UNC research, which was carried out in a frog model as well as human cells, will be published April 29, 2013, in the journal Developmental Cell.

"There has been a lot of interest in studying the vasculature because of its role in a wide range of disease states, as well as human development. But there are very few transcription factors that are known to affect the vasculature. To find a new one is quite unique, and then to be able to link it up to a known network of vascular development is surprising and encouraging," said senior study author Frank Conlon, PhD, an associate professor of genetics in the UNC School of Medicine.

During vascular development, specialized cells coalesce into three-dimensional "cords" that then hollow out to provide a path for transporting blood throughout the body. This process involves the complex coordination of molecular entities like growth factors and signaling molecules, defects that have been associated with human illnesses such as cancer, stroke, and atherosclerosis.

Conlon has long been interested in understanding how these various molecular players come together in the cardiovascular system. In 2008, his laboratory showed that a gene called CASZ1 is involved in the development of heart muscle. In this study, he and his colleagues decided to look for its role in the development of blood vessels.

Marta S. Charpentier and Kathleen S. Christine, lead authors of the study and graduate students in Conlon's laboratory, removed CASZ1 from frog embryos and looked to see how its absence affected the development of the vasculature. Without CASZ1, the frogs failed to form branched and functional blood vessels. When they removed the CASZ1 gene from cultured human cells, Charpentier and Christine saw similar defects: the cells did not sprout or branch correctly due to their inability to maintain proper adhesions with the surrounding extracellular matrix.

"If you take out CASZ1, these cultured human cells try to migrate by sending out these filopodia or little feet, but what happens is it is like someone nails down the back end of those growing vessels. They try to move and keep getting thinner and thinner, and like an elastic band it gets to be too much and just snaps back. It appears to cause an adhesion defect that makes the cells too sticky to form normal vessels," said Conlon.

CASZ1 is a transcription factor, a master switch that controls when and where other genes are expressed. Therefore, Charpentier and Christine did a series of experiments to explore CASZ1's influence on a known vascular network, involving other genes called Egfl7 and RhoA. When Charpentier and Christine added the Egfl7 gene to her CASZ1-depleted cells, the defect in blood vessel formation went away, suggesting that the two genes are connected. They then showed that CASZ1 directly acts on the Egfl7 gene, and that this activity in turn activates the RhoA gene, which is known to be required for cellular behaviors associated with adhesion and migration.

Transcription factors themselves are so essential that they are generally considered to be "undruggable," but the researchers say that further studies into how specific transcription factors work and the targets they control could eventually lead to new drug candidates.

The rest is here:
Molecular role of gene linked to blood vessel formation uncovered

Recommendation and review posted by Bethany Smith

Public release date: 29-Apr-2013 [ | E-mail | Share ]

Contact: Megan Fellman fellman@northwestern.edu 847-491-3115 Northwestern University

When a mouse smells a cat, it instinctively avoids the feline or risks becoming dinner. How? A Northwestern University study involving olfactory receptors, which underlie the sense of smell, provides evidence that a single gene is necessary for the behavior.

A research team led by neurobiologist Thomas Bozza has shown that removing one olfactory receptor from mice can have a profound effect on their behavior. The gene, called TAAR4, encodes a receptor that responds to a chemical that is enriched in the urine of carnivores. While normal mice innately avoid the scent marks of predators, mice lacking the TAAR4 receptor do not.

The study, published April 28 in the journal Nature, reveals something new about our sense of smell: individual genes matter.

Unlike our sense of vision, much less is known about how sensory receptors contribute to the perception of smells. Color vision is generated by the cooperative action of three light-sensitive receptors found in sensory neurons in the eye. People with mutations in even one of these receptors experience color blindness.

"It is easy to understand how each of the three color receptors is important and maintained during evolution," said Bozza, an author of the paper, "but the olfactory system is much more complex."

In contrast to the three color receptors, humans have 380 olfactory receptor genes, while mice have more than 1,000. Common smells like the fragrance of coffee and perfumes typically activate many receptors.

"The general consensus in the field is that removing a single olfactory receptor gene would not have a significant effect on odor perception," said Bozza, an assistant professor of neurobiology in the Weinberg College of Arts and Sciences.

Bozza and his colleagues tested this assumption by genetically removing a specific subset of olfactory receptors called trace amine-associated receptors, or TAARs, in mice. Mice have 15 TAARs. One is expressed in the brain and responds to amine neurotransmitters and common drugs of abuse such as amphetamine. The other 14 are found in the nose and have been coopted to detect odors.

Read more:
Cat and mouse: A single gene matters

Recommendation and review posted by Bethany Smith

Public release date: 29-Apr-2013 [ | E-mail | Share ]

Contact: Tom Hughes tahughes@unch.unc.edu 919-966-6047 University of North Carolina Health Care

CHAPEL HILL, N.C. University of North Carolina researchers have discovered that disrupting a gene that acts as a regulatory switch to turn on other genes can keep blood vessels from forming and developing properly.

Further study of this gene a "transcription factor" called CASZ1 may uncover a regulatory network that influences the development of cardiovascular disease. A number of other studies have already shown a genetic link between mutations in CASZ1 and hypertension.

The UNC research, which was carried out in a frog model as well as human cells, will be published April 29, 2013, in the journal Developmental Cell.

"There has been a lot of interest in studying the vasculature because of its role in a wide range of disease states, as well as human development. But there are very few transcription factors that are known to affect the vasculature. To find a new one is quite unique, and then to be able to link it up to a known network of vascular development is surprising and encouraging," said senior study author Frank Conlon, PhD, an associate professor of genetics in the UNC School of Medicine.

During vascular development, specialized cells coalesce into three-dimensional "cords" that then hollow out to provide a path for transporting blood throughout the body. This process involves the complex coordination of molecular entities like growth factors and signaling molecules, defects that have been associated with human illnesses such as cancer, stroke, and atherosclerosis.

Conlon has long been interested in understanding how these various molecular players come together in the cardiovascular system. In 2008, his laboratory showed that a gene called CASZ1 is involved in the development of heart muscle. In this study, he and his colleagues decided to look for its role in the development of blood vessels.

Marta S. Charpentier and Kathleen S. Christine, lead authors of the study and graduate students in Conlon's laboratory, removed CASZ1 from frog embryos and looked to see how its absence affected the development of the vasculature. Without CASZ1, the frogs failed to form branched and functional blood vessels. When they removed the CASZ1 gene from cultured human cells, Charpentier and Christine saw similar defects: the cells did not sprout or branch correctly due to their inability to maintain proper adhesions with the surrounding extracellular matrix.

"If you take out CASZ1, these cultured human cells try to migrate by sending out these filopodia or little feet, but what happens is it is like someone nails down the back end of those growing vessels. They try to move and keep getting thinner and thinner, and like an elastic band it gets to be too much and just snaps back. It appears to cause an adhesion defect that makes the cells too sticky to form normal vessels," said Conlon.

Here is the original post:
UNC research uncovers molecular role of gene linked to blood vessel formation

Recommendation and review posted by Bethany Smith

Apr. 29, 2013 When a mouse smells a cat, it instinctively avoids the feline or risks becoming dinner. How? A Northwestern University study involving olfactory receptors, which underlie the sense of smell, provides evidence that a single gene is necessary for the behavior.

A research team led by neurobiologist Thomas Bozza has shown that removing one olfactory receptor from mice can have a profound effect on their behavior. The gene, called TAAR4, encodes a receptor that responds to a chemical that is enriched in the urine of carnivores. While normal mice innately avoid the scent marks of predators, mice lacking the TAAR4 receptor do not.

The study, published April 28 in the journal Nature, reveals something new about our sense of smell: individual genes matter.

Unlike our sense of vision, much less is known about how sensory receptors contribute to the perception of smells. Color vision is generated by the cooperative action of three light-sensitive receptors found in sensory neurons in the eye. People with mutations in even one of these receptors experience color blindness.

"It is easy to understand how each of the three color receptors is important and maintained during evolution," said Bozza, an author of the paper, "but the olfactory system is much more complex."

In contrast to the three color receptors, humans have 380 olfactory receptor genes, while mice have more than 1,000. Common smells like the fragrance of coffee and perfumes typically activate many receptors.

"The general consensus in the field is that removing a single olfactory receptor gene would not have a significant effect on odor perception," said Bozza, an assistant professor of neurobiology in the Weinberg College of Arts and Sciences.

Bozza and his colleagues tested this assumption by genetically removing a specific subset of olfactory receptors called trace amine-associated receptors, or TAARs, in mice. Mice have 15 TAARs. One is expressed in the brain and responds to amine neurotransmitters and common drugs of abuse such as amphetamine. The other 14 are found in the nose and have been coopted to detect odors.

Bozza's group has shown that the TAARs are extremely sensitive to amines -- a class of chemicals that is ubiquitous in biological systems and is enriched in decaying materials and rotting flesh. Mice and humans typically avoid amines since they have a strongly unpleasant, fishy quality.

Bozza's team, including the paper's lead authors, postdoctoral fellow Adam Dewan and graduate student Rodrigo Pacifico, generated mice that lack all 14 olfactory TAAR genes. These mice showed no aversion to amines. In a second experiment, the researchers removed only the TAAR4 gene. TAAR4 responds selectively to phenylethylamine (PEA), an amine that is concentrated in carnivore urine. They found that mice lacking TAAR4 fail to avoid PEA, or the smell of predator cat urine, but still avoid other amines.

Original post:
Cat and mouse: One gene is necessary for mice to avoid predators

Recommendation and review posted by Bethany Smith