Archive for the ‘Gene Therapy Research’ Category

~Varying Perspectives Represented and Best Practices Shared by Experts~

Newswise The 4th Annual Consumer Genetics Conference, a yearly forum designed to spark influential conversation on the current state of personal genomics and to shape the future of the field, is being held October 3-5 at the Seaport Hotel in Boston, Massachusetts. This event will bring together the fields preeminent researchers, clinicians, government regulators and industry leaders, who will provide their perspectives on the direction of this field, and the crucial topics surrounding its implications to clinical health and medicine.

In this highly interactive forum, panel participants will represent a broad spectrum of viewpoints, and will engage in an open discussion on best practices and policies, as well as new advancements and challenges. Through the course of this dynamic exchange, the future of consumer-based genetics will be explored, examined, and shaped.

The deadline to take advantage of discounted early bird registration rates is Friday, September 7.

Major themes to be covered at this conference will include: Personal Genomics, Third-Generation Sequencing, Molecular Diagnostics, Investment & Funding Opportunities, Genome Interpretation, The Future of Personalized Medicine, Big Data, Prenatal/Neonatal & Disease Diagnostics, Empowering Patients, Nutrition, Food Genetics & Cosmetics

Keynote speakers and featured presenters will include:

Diana Bianchi, M.D., Executive Director, Mother Infant Research Institute, Tufts Medical Center Kenneth Chahine, Ph.D., J.D., Senior Vice President and General Manager, DNA, Ancestry.com Brian T. Naughton, Ph.D., Founding Scientist, 23andMe Nathan Pearson, Ph.D., Director of Research, Knome, Inc. John Quackenbush, Ph.D., Professor, Biostatistics and Computational Biology, Cancer Biology Center for Cancer Computational Biology, Dana-Farber Cancer Institute Heidi L. Rehm, Ph.D., FACMG, Chief Laboratory Director, Molecular Medicine, Partners HealthCare Center for Personalized Genetic Medicine; Assistant Professor of Pathology, Harvard Medical School Lee Silver, Ph.D., Professor of Molecular Biology and Public Affairs, Woodrow Wilson School, Princeton University

For more information on the 4th Annual Consumer Genetics Conference, including registration and a full program schedule, please visit http://www.consumergeneticsconference.com.

Media are invited to attend this conference and meet and interview speakers on-site. Registration can be obtained by emailing Lynn Blenkhorn at lynn.blenkhorn@fkhealth.com, or by calling: 508-851-0930. If you cannot attend but you would like to speak with one of the presenters, we would be pleased to organize a phone interview on the day of their presentation.

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Consumer Genetics Conference 2012 Features Preeminent Leaders in Industry, Academia, Medicine and Government to ...

ScienceDaily (Sep. 5, 2012) That low bone density causes osteoporosis and a risk of fracture is common knowledge. But an excessively high bone density is also harmful. The most serious form of excessively high bone density is a rare, hereditary disease which can lead to the patient's death by the age of only five. Researchers at Lund University in Sweden are now trying to develop gene therapy against this disease.

In order for the body to function, a balance is necessary between the cells that build up the bones in our skeletons and the cells that break them down. In the disease malignant infantile osteopetrosis, MIOP, the cells that break down the bone tissue do not function as they should, resulting in the skeleton not having sufficient cavities for bone-marrow and nerves.

"Optic and auditory nerves are compressed, causing blindness and deafness in these children. Finally the bone marrow ceases to function and, without treatment, the child dies of anemia and infections," explains Carmen Flores Bjurstrm. She has just completed a thesis which presents some of the research at the division for Molecular Medicine and Gene Therapy in Lund.

The researchers' work focuses on finding alternatives to the only treatment currently available against MIOP, namely a bone-marrow transplant. This treatment can be effective, but it is both risky and dependent on finding a suitable donor.

Gene therapy requires no donor, as stem cells are taken from the patients themselves. Once the cells' non-functioning gene has been replaced with a healthy copy of itself, the stem cells are put back into the patient.

Great hopes have been placed on gene therapy as a treatment method but the work has proven to be more difficult than expected. The method is used today for certain immunodeficiency diseases, and has also been applied to a blood disorder called thalassemia.

"So far, the method is not risk-free. Since it is impossible to control where the introduced gene ends up, there is a certain risk of it ending up in the wrong place and giving rise to leukemia. This is why gene therapy is only used for serious diseases for which there is no good treatment," says Carmen Flores Bjurstrm.

The Lund researchers have conducted experiments with gene therapy in both patient cells and laboratory animals. The next step is to conduct trials on patients. The trials will probably take place at the hospital in Ulm, Germany, which currently treats the majority of children in Europe suffering from MIOP.

MIOP is a rare disease: in Sweden a child is born with the condition approximately once every three years. Worldwide, the incidence of the disease is one case for every 300 000 births. It is, however, more common in Costa Rica where 3-4 children per 100 000 births have the disease.

"But there are several other genetic mutations that lead to other osteopetrosis diseases. If we manage to treat MIOP, it may become possible to treat these other conditions as well," hopes Carmen Flores Bjurstrm along with her supervisor, Professor Johan Richter.

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Can gene therapy cure fatal diseases in children?

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

AlloCure, Inc. today announced that it has initiated a phase 2 clinical trial of AC607, the companys mesenchymal stem cell therapy, as a potential treatment for acute kidney injury (AKI). The randomized, double-blind, placebo-controlled, multi-center trial, designated ACT-AKI (AC607 Trial in Acute Kidney Injury) (NCT01602328), will enroll 200 cardiac surgery subjects at leading tertiary care centers in the United States.

ACT-AKI follows the positive results from a phase 1 AC607 trial in cardiac surgery subjects, which showed an excellent safety profile and encouraging data on the incidence of AKI and hospital length of stay, said Robert M. Brenner, M.D., AlloCure President and Chief Executive Officer. We have worked closely with leaders in the field on the design of ACT-AKI, and trial initiation represents an important milestone for AlloCure and the patients we collectively serve.

AC607 is a promising therapeutic candidate for AKI, for which effective therapies are greatly needed, said Richard J. Glassock, M.D., Emeritus Professor of Medicine at the Geffen School of Medicine at the University of California, Los Angeles. The initiation of ACT-AKI represents a critical step in the development of an innovative therapy for this all-too-common, serious and costly medical condition, for which no approved treatments currently exist beyond supportive care.

About AC607

AC607 is a novel biologic therapy under development for the treatment of AKI. AC607 also possesses potential applications in other grievous illnesses. AC607 comprises allogeneic bone marrow-derived mesenchymal stem cells that are harvested from healthy adult donors and then expanded via a mature and state-of-the art manufacturing process. AC607 homes to the site of injury where it mediates powerful anti-inflammatory and organ repair processes via the secretion of beneficial paracrine factors, without differentiation and repopulation of the injured kidney. Importantly, AC607 avoids recognition by the hosts immune system, enabling administration in an off the shelf paradigm without the need for blood or tissue typing.

About AlloCure

AlloCure, Inc. is a privately held, clinical-stage biotechnology company focused on the treatment of kidney disease. The company is a leader in the AKI field and is pioneering the development of the first effective therapy for the treatment of AKI. The companys headquarters is located in Burlington, MA. For more information about AlloCure, please visit the companys web site at http://www.allocure.com.

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AlloCure Begins Phase 2 Clinical Trial in Acute Kidney Injury

NEW YORK, Sept. 4, 2012 (GLOBE NEWSWIRE) -- NeoStem, Inc. (NYSE MKT:NBS) ("NeoStem" or the "Company"), a rapidly emerging market leader in the fast growing cell therapy market, today announced that Company management will present at three investor conferences in September.

The 19th Annual Newsmakers in the Biotech Industry - BioCentury & Thomson Reuters

Rodman & Renshaw Annual Global Investment Conference

National Investment Banking Association Conference

About NeoStem, Inc.

NeoStem, Inc. continues to develop and build on its core capabilities in cell therapy capitalizing on the paradigm shift that we see occurring in medicine. In particular, we anticipate that cell therapy will have a large role in the fight against chronic disease and in lessening the economic burden that these diseases pose to modern society. We are emerging as a technology and market leading company in this fast developing cell therapy market. Our multi-faceted business strategy combines a state-of-the-art contract development and manufacturing subsidiary, Progenitor Cell Therapy, LLC ("PCT") with a medically important cell therapy product development program, enabling near and long-term revenue growth opportunities. We believe this expertise and existing research capabilities and collaborations will enable us to achieve our mission of becoming a premier cell therapy company.

Our contract development and manufacturing service business supports the development of proprietary cell therapy products. NeoStem's most clinically advanced therapeutic, AMR-001, is being developed at Amorcyte, LLC ("Amorcyte"), which we acquired in October 2011. Amorcyte is developing a cell therapy for the treatment of cardiovascular disease and is enrolling patients in a Phase 2 trial to investigate AMR-001's efficacy in preserving heart function after a heart attack. Athelos Corporation ("Athelos"), which is approximately 80%-owned by our subsidiary, PCT, is collaborating with Becton-Dickinson in the early clinical exploration of a T-cell therapy for autoimmune conditions. In addition, pre-clinical assets include our VSELTM Technology platform as well as our mesenchymal stem cells product candidate for regenerative medicine. Our service business and pipeline of proprietary cell therapy products work in concert, giving us a competitive advantage that we believe is unique to the biotechnology and pharmaceutical industries. Supported by an experienced scientific and business management team and a patent and patent pending (IP) portfolio, we believe we are well positioned to succeed.

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 or its partners' successful development of AMR-001 and other cell therapeutics, the size of the market for such products, its competitive position in such markets, the Company's ability to successfully penetrate such markets and the market for its CDMO business, and the efficacy of protection from its patent portfolio, as well as the future of the cell therapeutics industry in general, including the rate at which such industry may grow. Forward looking statements also include statements with respect to satisfying all conditions to closing the disposition of Erye, including receipt of all necessary regulatory approvals in the PRC. The Company's actual results could differ materially from those anticipated in these forward- looking statements as a result of various factors, including but not limited to (i) the Company's ability to manage its business despite operating losses and cash outflows, (ii) its ability to obtain sufficient capital or strategic business arrangement to fund its operations, including the clinical trials for AMR-001, (iii) successful results of the Company's clinical trials of AMR-001 and other cellular therapeutic products that may be pursued, (iv) demand for and market acceptance of AMR-001 or other cell therapies if clinical trials are successful and the Company is permitted to market such products, (v) establishment of a large global market for cellular-based products, (vi) the impact of competitive products and pricing, (vii) the impact of future scientific and medical developments, (viii) the Company's ability to obtain appropriate governmental licenses and approvals and, in general, future actions of regulatory bodies, including the FDA and foreign counterparts, (ix) reimbursement and rebate policies of government agencies and private payers, (x) the Company's ability to protect its intellectual property, (xi) the company's ability to successfully divest its interest in Erye, and (xii) matters described under the "Risk Factors" in the Company's Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 20, 2012 and in the Company's other periodic filings with the Securities and Exchange Commission, all of which are available on its website. The Company does not undertake to update its forward-looking statements. The Company's further development is highly dependent on future medical and research developments and market acceptance, which is outside its control.

Originally posted here:
NeoStem to Present at Three Investor Conferences in September

September spotlights childhood cancer, which remains the leading cause of death by disease of young Americans. At St. Jude Childrens Research Hospital, doctors and scientists are working to change that statistic

Newswise (MEMPHIS, Tenn. September 4, 2012) As St. Jude Childrens Research Hospital celebrates its 50th anniversary and marks September as Childhood Cancer Awareness Month, investigators are focused on the future.

Although survival rates for childhood cancer have soared to about 80 percent nationally since the hospital opened in 1962, cancer remains the leading cause of death by disease for U.S. children between infancy and age 15. The cause of many childhood cancers remains uncertain. For some cancers, drug development has stalled. For others, successful treatment leaves survivors at increased risk for second cancers and other problems that threaten their health and well-being.

In response to such challenges, St. Jude launched the most ambitious effort yet to identify the causes of some of the most difficult and poorly understood childhood cancers. Known as the St. Jude Childrens Research Hospital Washington University Pediatric Cancer Genome Project, the three-year endeavor is using 21st century technology to decipher the complete normal and cancer genomes of 600 young patients with some of the toughest cancers. The human genome is stored in the DNA found in nearly all cells and provides the instructions needed to assemble and sustain a person.

We expect the Pediatric Cancer Genome Project to catalyze global research in childhood cancer and improve our ability to diagnose, monitor and treat young patients with therapies that target the mutations identified as driving their disease, said Dr. William E. Evans, St. Jude director and chief executive officer. The project is designed to complement larger government efforts focused on adult cancers, which are often quite different from the cancers that strike children and adolescents.

To help realize that goal, published and unpublished whole genome sequencing data from the project are now freely available online to the global scientific community. We hope other researchers will use this rich resource for insight into childhood cancer as well as other diseases of children and adults, said James Downing, M.D., St. Jude scientific director and the projects leader at St. Jude.

The privately funded Pediatric Cancer Genome Project has already yielded remarkable surprises, Downing added. These discoveries are pointing us toward new therapeutic options for children, he said.

The findings include clues to understanding and possibly improving treatment of several cancers, including an aggressive subtype of acute lymphoblastic leukemia (ALL). The subtype is known as early T-cell precursor ALL or ETP-ALL. Although overall long-term survival is now 94 percent for ALL patients treated at St. Jude, the prognosis is much worse for patients with ETP-ALL. The new findings suggest patients in this subgroup might benefit from the addition of drugs developed for treatment of the blood cancer acute myeloid leukemia (AML).

In other studies, Pediatric Cancer Genome Project investigators reported evidence that drugs already under development for adult cancers and other diseases might help in fighting certain childhood tumors. The cancers include the eye tumor retinoblastoma as well as subtypes of the most common childhood brain tumor medulloblastoma.

Pediatric Cancer Genome Project researchers have also identified new mutations at work in an aggressive brain tumor as well as in adolescents and young adults with a tumor of the sympathetic nervous system called neuroblastoma. The results are fueling efforts to find new, more selective therapies for these cancers.

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Gene Sequencing Project Builds the Foundation for Next Generation of Childhood Cancer Care

ScienceDaily (Sep. 4, 2012) Researchers have discovered two gene variants that raise the risk of the pediatric cancer neuroblastoma. Using automated technology to perform genome-wide association studies on DNA from thousands of subjects, the study broadens understanding of how gene changes may make a child susceptible to this early childhood cancer, as well as causing a tumor to progress.

"We discovered common variants in the HACE1 and LIN28B genes that increase the risk of developing neuroblastoma. For LIN28B, these variants also appear to contribute to the tumor's progression once it forms," said first author Sharon J. Diskin, Ph.D., a pediatric cancer researcher at The Children's Hospital of Philadelphia. "HACE1 and LIN28B are both known cancer-related genes, but this is the first study to link them to neuroblastoma."

Diskin and colleagues, including senior author John M. Maris, M.D., director of the Center for Childhood Cancer Research at Children's Hospital, published the study online Sept. 2 in Nature Genetics.

Striking the peripheral nervous system, neuroblastoma usually appears as a solid tumor in the chest or abdomen. It accounts for 7 percent of all childhood cancers, and 10 to 15 percent of all childhood cancer deaths.

The study team performed a genome-wide association study (GWAS), comparing DNA from 2,800 neuroblastoma patients with that of nearly 7,500 healthy children. They found two common gene variants associated with neuroblastoma, both in the 6q16 region of chromosome 6. One variant is within the HACE1 gene, the other in the LIN28B gene. They exert opposite effects: HACE1 functions as a tumor suppressor gene, hindering cancer, while LIN28B is an oncogene, driving cancer development.

The current study showed that low expression of HACE1, a tumor suppressor gene, and high expression of LIN28B, an oncogene, correlated with worse patient survival. To further investigate the gene's role, the researchers used genetic tools to decrease LIN28B's activity, and showed that this inhibited the growth of neuroblastoma cells in culture.

The new research builds on previous GWAS work by Children's Hospital investigators implicating other common gene variants as neuroblastoma oncogenes. As in the current study, these gene variants show a double-barreled effect, both initiating cancer and provoking its progression.

"In addition to broadening our understanding of the heritable component of neuroblastoma susceptibility, we think this research may suggest new therapies," Diskin added. "Our follow-up studies will focus on how we may intervene on these genes' biological pathways to develop more effective treatments."

Financial support for this study came from the National Institutes of Health (grants CA124709, CA151869, HD026979, and CA136979), the Giulio D'Angio Endowed Chair, the Alex's Lemonade Stand Foundation, Andrew's Army Foundation, the PressOn Foundation, the Abramson Family Cancer Research Institute, Fondazione Italiana per la Lotta al Neuroblastoma and Associazione Italiana per la Ricerca sul Cancro, and the Center for Applied Genomics at The Children's Hospital of Philadelphia. Co-authors with Diskin and Maris included researchers from institutions in Naples, Rende and Rome, Italy.

In addition to their positions at Children's Hospital, both Diskin and Maris are on the faculty of the Perelman School of Medicine at the University of Pennsylvania.

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New gene variants raise risk of neuroblastoma, influence tumor progression

Most random gene expression signatures are significantly associated with breast cancer outcome, according to a research team at Universit Libre de Bruxelles.

The Belgian group, which presented its work in PLoS Computational Biology last year, compared 48 published breast cancer outcome signatures to those comprising random genes and found that 28 of the breast cancer signatures, or 60 percent, were "not significantly better outcome predictors than random signatures of identical size," while 11, or 23 percent, were actually poorer predictors than the median random signature.

These findings prompted a review that appeared in Bioessays this month, as well as a commentary published in June in the journal Breast Cancer Research.

Bertrand Jordan, author of the Bioessays review, called the paper "provocative and iconoclastic," as it "states that many published interpretations of expression profiling experiments are not really significant."

Jordan, who is an emeritus research director at the French National Center for Scientific Research, told BioArray News this week that the paper makes a "strong statement" that "seems to be backed by fairly solid data" and "deserved more exposure than it had received" initially.

In addition to the review and commentary, Vincent Detours, a computational biologist at ULB and corresponding author on the PLoS Computational Biology paper, said that he has received "encouragement" from other researchers since it first appeared.

"My impression is that many people were aware of the issue or felt uncomfortable about the proliferation of signatures, and were pleased to see their concerns addressed," Detours told BioArray News last week.

An 'Iconoclastic' Paper

As Detours noted in an opinion article published last December in The Scientist, the accumulation of signatures with all sorts of biological meaning, but nearly identical prognostic values, had "already looked suspicious" to him, coauthors David Venet and Jacques Dumont, and others as far back as 2007.

After collecting from the literature some signatures with as little connection to cancer as possible, the authors discovered that the signature of the blood cells of Japanese patients who were told jokes after lunch, and a signature derived from the microarray analysis of the brains from mice that suffered social defeat were both associated with breast cancer outcome by any statistical standards.

Link:
'Provocative' Paper Sparks Debate on Relevance of Breast Cancer Gene Expression Signatures

Greg Stock wrote a book about the future of human genetic engineering. (Photo courtesy of Greg Stock.)

While perhaps not yet a majority many parents says they would bioengineer their children if they could, to create the perfect, or more perfect child. Now, that parental dream is closer to reality, but no one is quite sure what the implications may be.

Nearly a decade after the human genome was decoded, scientists are only now beginning to understand its implications.

One of the leading thinkers in this field is the biotech entrepreneurGregory Stock. A biophysicist by training, his 2002 bookRedesigning Humans: Our Inevitable Genetic Futuremakes the case that full-scale genetic engineering is on the way whether we like it or not.

And, Stock believes, if the U.S. doesnt lead the way in developing those advances, other nations will.

Between a third and two-thirds of the population and even higher if you look at China or Thailand and other eastern cultures of parents say if they could enhance the genetics of their children, enhance their either cognitive or physical capabilities, they would absolutely do it," he said.

But engineering traits to improve people remains a thorny issue.

It sounds so compelling, take out a little bit of this, that, its going to be the best of you, Stock said. But actually, we don't have a clue what creates exceptional capabilities."

While Stocks attitude is full-speed ahead, he admits, its going to get weird."

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Author argues U.S. must lead way on bioengineering

5 September 2012

GE not in our best interest

The United States State Department and American multinational companies have been pushing for the release of genetically engineered food into the New Zealand environment at a biotechnology conference being held in Rotorua this week, the Green Party said today.

The ABIC 2012 conference being held in Rotorua is dubbed the World Cup of biotechnology and has seen a huge push from vested interests for GE release into the environment despite public opposition to such a move.

The primary benefactors of Genetic Engineering (GE) are US corporate interests not New Zealand farmers, Green Party primary production spokesperson Steffan Browning said.

The GE focused ABIC 2012 conference in Rotorua this week, is clearly part of a strong push towards GE farming in Aotearoa New Zealand by large multinational companies and Washington.

The US State Department presence at the Rotorua conference shows that pushing GE is part of US foreign policy as much as it is in the interests of big corporates like DuPont and Monsanto.

Consumers around the world dont want a bar of GE and if New Zealand wants to continue reaping the benefits of exporting high value-added produce, we need to steer clear.

GE will not enable more exports it risks locking our produce out of markets and tarnishing our clean green brand. GE is not smart, green economics.

We can add more value to our agricultural exports by leveraging our clean, safe, 100% Pure brand.

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Genetic Engineering not in our best interest

Public release date: 4-Sep-2012 [ | E-mail | Share ]

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

New Rochelle, NY, September 4, 2012The use of RNA in nanotechnology applications is highly promising for many applications, including the development of new therapeutic compounds. Key technical challenges remain, though, and the challenges and opportunities associated with the use of RNA molecules in nanotechnology approaches are presented in a review article in Nucleic Acid Therapeutics, a peer-reviewed journal from Mary Ann Liebert, Inc. The article is available free online at the Nucleic Acid Therapeutics website.

Peixuan Guo and colleagues, University of Kentucky, Lexington, highlight the ability of RNA to self-assemble into nanoparticles with diverse structures. In "Uniqueness, Advantages, Challenges, Solutions, and Perspectives in Therapeutics Applying RNA Nanotechnology," the authors provide a detailed description of the main challenges faced by the RNA therapeutics industry, including the chemical and thermodynamic instability of the molecules, potential safety and side effect issues, difficulties in delivery and specific targeting, and low yield and high production costs in manufacturing.

"The remarkable structural and enzymatic properties of RNA continue to astound us," says Executive Editor Fintan Steele, PhD, SomaLogic, Inc., Boulder, CO. "It is exciting to see those properties increasingly realized for the benefit of human health and welfare, as described by Dr. Guo and his colleagues."

###

Nucleic Acid Therapeutics is under the editorial leadership of Co-Editors-in-Chief Bruce A. Sullenger, PhD, Duke Translational Research Institute, Duke University Medical Center, Durham, NC, and C.A. Stein, MD, PhD, City of Hope National Medical Center, Duarte, CA; and Executive Editor Fintan Steele, PhD, SomaLogic, Boulder, CO.

About the Journal

Nucleic Acid Therapeutics is an authoritative, peer-reviewed journal published bimonthly in print and online that focuses on cutting-edge basic research, therapeutic applications, and drug development using nucleic acids or related compounds to alter gene expression. Nucleic Acid Therapeutics is the Official Journal of the Oligonucleotide Therapeutics Society. Complete tables of content and a free sample issue may be viewed online at the Nucleic Acid Therapeutics website.

About the Publisher

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Realizing the promise of RNA nanotechnology for new drug development

TUESDAY, Sept. 4 (HealthDay News) -- Not only is Internet addiction a legitimate compulsion, it may have the same genetic component as nicotine addiction, a new study suggests.

Out of nearly 850 people interviewed about their Internet habits, German researchers evaluated 132 who showed signs of being hooked to the Web, while another 132 without problematic Internet behavior were selected as a control group.

The addicted users said that all their thoughts revolved around the Internet during the day, and they felt that their well-being was harmed if they couldn't go online. The participants' average age was 25.

The study authors conducted a genetic analysis and discovered that the people with Internet addiction were more likely than others to have a genetic mutation on the CHRNA4 gene, which is known to play a major role in nicotine addiction.

The gene mutation was more common in women with online addiction than in men with the problem, according to the study. But the researchers said further research is needed to confirm this because numerous surveys have found that men are more prone to Internet addiction than women.

The study was recently published in the Journal of Addiction Medicine. The study found an association between the gene mutation and addiction, but it did not prove a definitive link.

Overall, the findings show "that Internet addiction is not a figment of our imagination," study author Christian Montag, of the department for differential and biological psychology at the University of Bonn, said in a university news release.

While more research is needed to further analyze the link between this gene mutation and online addiction, the study "shows that there are clear indications for genetic causes of Internet addiction," Montag said.

Learning more about how genetics influences Internet addiction could lead to better treatments, he noted.

Noting that these addicted Internet users reported only occasional problems in everyday life because of overuse of the Internet, the researchers said extreme users should be evaluated in future research.

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Could Internet Addiction Be Genetic?

Public release date: 4-Sep-2012 [ | E-mail | Share ]

Contact: Dean Forbes dforbes@fhcrc.org 206-667-2896 Fred Hutchinson Cancer Research Center

SEATTLE A team of scientists led by a bone marrow transplant researcher at Fred Hutchinson Cancer Research Center has shed new light on why most bone marrow transplant patients who receive tissue-matched cells from unrelated donors still suffer acute graft-versus-host disease (GVHD). The answer appears to lie in the discovery of previously undetected genetic differences in the DNA of patients and unrelated marrow donors.

The laboratory-based study findings by Effie Petersdorf, M.D., and colleagues soon will be translated to the clinic when a Hutchinson Center transplant protocol the first of its kind opens at Seattle Cancer Care Alliance later this year to test patients and donors for these genetic differences. The goal is to further refine the tissue-matching process to reduce the incidence of GVHD, which affects about 80 percent of patients and has been a longtime, vexing challenge for transplant doctors.

GVHD occurs when the donor immune system (the graft) begins to circulate in the patient's bloodstream and recognizes the host's (the patient's) tissue as foreign. When this happens, the new immune system attacks the recipient's tissues such as the liver, gastrointestinal system and skin.

Bone marrow and stem cell transplants are used to treat a variety of malignant blood diseases such as leukemia. Hematopoietic cell transplantation was pioneered at the Hutchinson Center in the 1970s and continues to be a major focus of research and clinical trials to improve survival and reduce side effects.

Published recently in Science Translational Medicine, the study details how researchers identified two specific single-nucleotide polymorphisms, also called SNPs (pronounced "snips"), within the major histocompatibility complex (MHC) in human DNA that are markers for either acute GVHD or disease-free survival. These markers are distinct from the human leukocyte antigens (HLA), found on the same chromosome as the MHC, that are traditionally used to match recipients and donors, a process called tissue typing.

Researchers found that if a patient and donor have different SNPs, the patient was at increased risk of GVHD or a lower chance of disease-free survival. The scientists surmised that genes located near these SNPs must be involved in that process.

"The question I wanted to ask with this study is whether there could be genes we don't know about that are located close to the major histocompatibility complex that could be influencing GVHD risk," said Petersdorf, a member of the Hutchinson Center's Clinical Research Division. "Now that we know what to test for we can begin screening for the presence of the SNPs in patients and donors and select the optimal donor whose SNP profile will benefit the patient the most."

SNP genotyping is only beneficial for patients when they have multiple matched unrelated donors in order to determine which donor is the optimal match. Fortunately, this is fairly common, according to the study. Of 230 patients who had two or more HLA-matched donors, significant percentages also had at least one donor who was SNP-matched.

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New genetic clues to why most bone marrow transplant patients develop graft-versus-host disease

Discovery will lead to new screening protocol to better match patients & donors

Newswise SEATTLE A team of scientists led by a bone marrow transplant researcher at Fred Hutchinson Cancer Research Center has shed new light on why most bone marrow transplant patients who receive tissue-matched cells from unrelated donors still suffer acute graft-versus-host disease (GVHD). The answer appears to lie in the discovery of previously undetected genetic differences in the DNA of patients and unrelated marrow donors.

The laboratory-based study findings by Effie Petersdorf, M.D., and colleagues soon will be translated to the clinic when a Hutchinson Center transplant protocol the first of its kind opens at Seattle Cancer Care Alliance later this year to test patients and donors for these genetic differences. The goal is to further refine the tissue-matching process to reduce the incidence of GVHD, which affects about 80 percent of patients and has been a longtime, vexing challenge for transplant doctors.

GVHD occurs when the donor immune system (the graft) begins to circulate in the patients bloodstream and recognizes the hosts (the patients) tissue as foreign. When this happens, the new immune system attacks the recipients tissues such as the liver, gastrointestinal system and skin.

Bone marrow and stem cell transplants are used to treat a variety of malignant blood diseases such as leukemia. Hematopoietic cell transplantation was pioneered at the Hutchinson Center in the 1970s and continues to be a major focus of research and clinical trials to improve survival and reduce side effects.

Published recently in Science Translational Medicine, the study details how researchers identified two specific single-nucleotide polymorphisms, also called SNPs (pronounced snips), within the major histocompatibility complex (MHC) in human DNA that are markers for either acute GVHD or disease-free survival. These markers are distinct from the human leukocyte antigens (HLA), found on the same chromosome as the MHC, that are traditionally used to match recipients and donors, a process called tissue typing.

Researchers found that if a patient and donor have different SNPs, the patient was at increased risk of GVHD or a lower chance of disease-free survival. The scientists surmised that genes located near these SNPs must be involved in that process.

The question I wanted to ask with this study is whether there could be genes we dont know about that are located close to the major histocompatibility complex that could be influencing GVHD risk, said Petersdorf, a member of the Hutchinson Centers Clinical Research Division. Now that we know what to test for we can begin screening for the presence of the SNPs in patients and donors and select the optimal donor whose SNP profile will benefit the patient the most.

SNP genotyping is only beneficial for patients when they have multiple matched unrelated donors in order to determine which donor is the optimal match. Fortunately, this is fairly common, according to the study. Of 230 patients who had two or more HLA-matched donors, significant percentages also had at least one donor who was SNP-matched.

A SNP is a base change that involves two or more of the four bases (A, C, T and G) that comprise DNA, and is the simplest form of DNA variation on the human genome. SNPs serve as signposts or markers for nearby genes that are the actual drivers for the effect that they have on disease.

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Researchers Uncover New Genetic Clues to Why Most Bone Marrow Transplant Patients Develop Graft-Versus-Host Disease

ScienceDaily (Sep. 4, 2012) Fanconi anemia is a recessive genetic disorder affecting 1 in 350,000 babies, which leaves cells unable to repair damaged DNA. This lack of repair puts Fanconi anemia patients at high risk for developing a variety of cancers, especially leukemias and head and neck cancer.

Cruelly, the condition also nixes the use of an entire class of cancer drugs, namely drugs like mitomycin C, by encouraging DNA to crosslink together like sticky strands of bread dough -- generally, healthy cells can repair a few crosslinks whereas cancer cells cannot and so are killed. However, Fanconi anemia patients are unable to repair the damage done to healthy or cancerous cells done by these drugs and so treatment with mitomycin C is frequently fatal.

A University of Colorado Cancer Center study funded by the Fanconi Anemia Research Fund explored the effectiveness of a novel agent in preventing cancer in this population -- namely, resveratrol as found in red wine. The results of this study will be presented at the 24th annual Fanconi Anemia Research Fund Scientific Symposium, September 27-30 at the Grand Hyatt Hotel in Denver, Colo.

In fact, the findings may go far past Fanconi anemia.

"One of the Fanconi genes that is lost is BRCA2 -- the same genetic loss that causes many breast cancers," says Robert Sclafani, PhD, investigator at the University of Colorado Cancer Center and professor of biochemistry and molecular genetics at the CU School of Medicine. "So one mystery is why Fanconi anemia patients don't get breast cancer. In Fanconi, every cell in the body is missing that gene -- Fanconi is a very rare thing but it's telling us something about cancers that aren't so rare."

Sclafani's had already shown the effectiveness of resveratrol in treating head and neck cancer, and in this study explored the effect of resveratrol in Fanconi cell lines -- could it prevent cancer by eliminating the cancer cells in Fanconi patients?

"It turns out that regular Fanconi cells aren't sensitive to resveratrol in the way they're sensitive to drugs like mitomycin C," Sclafani says. Instead, Sclafani hopes that additional mutations found in Fanconi head and neck cancer cells but not in regular Fanconi cells will make the cancer cells sensitive to resveratrol in a way normal Fanconi cells are not. His recent results will be presented at the upcoming meeting.

"It's an interesting population," says Sclafani, "and one that may hold information about many kinds of cancer."

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Rare genetic disease offers insight into common cancers

Not only have great strides been made in human genetics but also in animal genetics. This is important because such genetic information is not only helpful to the animal, but it frequently can also be applied to humans.

A recent article in the New England Journal of Medicine discussed how genetic research from one type of animal, the dog, has been helpful in better understanding the genetics of certain inherited disorders that are present in both dogs and humans.

It is generally easier to do genetic research on dogs than on people. Dogs reproduce many litters, therefore, more animals are available to study.Compared with dogs who are bred much closer, purebreds, there is more genetic heterogeneity present in humans. This results in a greater number of uncontrolled variables being present in people than in dogs. Such genetic heterogeneity or variables can make it more difficult to interpret the results of genetic studies.

There are many genetic disorders that affect the bones of dogs. Hip dysplasia is frequently found in larger dogs.

Another condition that affects the bones and is also present in both humans and dogs is chondrodysplasia. About 20 breeds of dogs have this condition and as a result they have disproportionately short legs. Examples are dachshunds, corgis and basset hounds.

By studying dogs that are affected with chondrodysplasia, researchers were able to uncover the gene that is responsible for this skeletal abnormality and also the chromosome where it is located.

This information is now being applied to patients with this condition by the geneticists who care for them.

Genetic studies are now underway on dogs who have other human conditions such as cancer, epilepsy, lupus erythematosus and narcolepsy, to name just a few.

But as gene research on humans has been helpful in understanding genetic diseases in people, the same is true of gene research involving animals.

Determining the genetic cause of a disease, be it a human or an animal, brings researchers one big step closer to finding ways to treat and prevent the disorder.

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Dr. Murray Feingold: Animal genetics help scientists understand diseases

Not only have great strides been made in human genetics but also in animal genetics. This is important because such genetic information is not only helpful to the animal, but it frequently can also be applied to humans.

A recent article in the New England Journal of Medicine discussed how genetic research from one type of animal, the dog, has been helpful in better understanding the genetics of certain inherited disorders that are present in both dogs and humans.

It is generally easier to do genetic research on dogs than on people. Dogs reproduce many litters, therefore, more animals are available to study. Compared to dogs who are bred much closer, purebreds, there is more genetic heterogeneity present in humans. This results in a greater number of uncontrolled variables being present in people than in dogs. Such genetic heterogeneity or variables can make it more difficult to interpret the results of genetic studies.

There are many genetic disorders that affect the bones of dogs. Hip dysplasia is frequently found in larger dogs.

Another condition that affects the bones and is also present in both humans and dogs is chondrodysplasia. About 20 breeds of dogs have this condition and as a result they have disproportionately short legs. Examples are dachshunds, corgis and basset hounds.

By studying dogs that are affected with chondrodysplasia, researchers were able to uncover the gene that is responsible for this skeletal abnormality and also the chromosome where it is located.

This information is now being applied to patients with this condition by the geneticists who care for them.

Genetic studies are now underway on dogs who have other human conditions such as cancer, epilepsy, lupus erythematosus and narcolepsy, to name just a few.

But as gene research on humans has been helpful in understanding genetic diseases in people, the same is true of gene research involving animals.

Determining the genetic cause of a disease, be it a human or an animal, brings researchers one big step closer to finding ways to treat and prevent the disorder.

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Feingold: Animal genetics help scientists understand diseases

Rutherford, NJ, Sept. 4, 2012 (GLOBE NEWSWIRE) -- Cancer Genetics, Inc. (CGI), a leader in oncology-focused personalized medicine, today announced that Inc. magazine ranked the company #232 among private Healthcare companies, and #2859 overall on its sixth annual Inc. 500|5000 list, an exclusive ranking of the nation's fastest-growing private companies. The list represents a comprehensive look at the most important segment of the economy--America's independent entrepreneurs. This was the first year the Company has been on the list, and is among the first oncology-focused molecular diagnostic companies on the list.

Panna Sharma, CEO of Cancer Genetics, Inc. says "Our team takes tremendous pride in being among other great companies and in our ability to scale our unique focus on personalizing the diagnosis for cancer patients. This recognition by Inc. results from the dedication of CGI's employees and our commitment towards paving the way of personalized medicine in oncology."

In a stagnant economic environment, median growth rate of 2012 Inc. 500|5000 companies remains an impressive 97 percent. The companies on this year's list report having created over 400,000 jobs in the past three years, and aggregate revenue among the honorees reached $299 billion.

Complete results of the Inc. 5000, including company profiles, methodology and an interactive database that can be sorted by industry, region, and other criteria, can be found at http://www.inc.com/5000.

"Now, more than ever, we depend on Inc. 500/5000 companies to spur innovation, provide jobs, and drive the economy forward. Growth companies, not large corporations, are where the action is," says Inc. editor Eric Schurenberg.

About Cancer Genetics, Inc.

Cancer Genetics, Inc. (CGI) is an emerging leader in the field of personalized medicine, offering products and services that enable cancer diagnostics as well as treatments that are tailored to the specific genetic profile of the individual. CGI is committed to maintaining the standard of clinical excellence through its investment in outstanding facilities and equipment. Our reference laboratory is both CLIA certified and CAP accredited and GLP compliant. In addition we have approvals and accreditations from the states of Florida, Maryland, New York, and New Jersey. The company has been built on a foundation of world-class scientific knowledge and IP in solid and blood-borne cancers, as well as strong research collaborations with major cancer centers such as Memorial Sloan-Kettering and the National Cancer Institute.

For further information, http://www.cancergenetics.com.

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Cancer Genetics, Inc. Named To the 2012 Inc. 500|5000 List

Mice with olfactory defects can have their sense of smell restored through gene therapy.

D. AUBREY/SCIENCE PHOTO LIBRARY

Gene therapy can fix a defective sense of smell in mice by repairing problems with the hair-like structures on their olfactory neurons, researchers report this week in Nature Medicine1. The study suggests that abnormalities in these structures, called cilia, can be treated, but how the findings can be applied to other organs is unclear.

Cilia are found on the surfaces of many types of cell, and they affect various functions, including sensory perception, movement and cell signaling. Damage to cilia as a result of genetic mutation can cause kidney and liver cysts, extra digits, obesity, blindness and hearing loss in mammals.

The mutations and cellular mechanisms that contribute to such ciliopathies have been well studied, but there's been very little work done in the area of therapeutics, says study leader Jeffrey Martens, a pharmacologist at the University of Michigan in Ann Arbor.

Martens and his colleagues used mice in which a mutant protein causes effects similar to polycystic kidney disease in humans. Mutation of this protein, called intraflagellar transport 88 (IFT88), disrupts cilia expression and function, causing impaired growth, extra digits, blindness and brain abnormalities2. These mice, called Oak Ridge polycystic kidney (ORPK) mice, die by early adulthood.

Because olfactory dysfunction is a common effect of ciliopathy, the researchers examined the olfactory neurons of ORPK mice. In healthy mice, numerous cilia project from the olfactory neurons, but ORPK mice had fewer cilia, and those that remained were shortened and malformed. As expected, these mice also had a deficient sense of smell.

To reverse this defect, the authors inserted a functional IFT88 protein into an adenovirus and then injected the virus into the noses of ORPK mice. The injection restored normal cilia number and structure as well as sense of smell.

Because ORPK mice die young, the authors were unable to conduct behavioural tests in adult mice, but they found that newborn mice injected with IFT88 were better at suckling and feeding both associated with smell. ORPK mice are usually one-quarter the size of normal mice by three weeks of age, but treated pups showed a 60% increase in body weight.

The demonstration that a ciliopathy can be reversed is impressive, says Joseph Gleeson, a neurogeneticist at the University of California, San Diego, but its unclear whether results in the olfactory system will translate to other organs. Olfactory neurons continually regenerate, which is not true of all cells affected by ciliopathies, and some defects may be permanent if cilia do not function correctly during development, Gleeson says.

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Gene therapy restores sense of smell to mice

Editor's Choice Main Category: Ear, Nose and Throat Also Included In: Genetics Article Date: 03 Sep 2012 - 11:00 PDT

Current ratings for: New Discovery Offers Hope For People Who Can't Smell

3.33 (3 votes)

4 (1 votes)

The experts believe that fixing congenital anosmia, which is medical language for not being able to smell anything, may eventually lead to curing similar medical issues which also come from the cilia or small hair-like pieces which reside on the outside of cells and are present in diseases involving the kidneys, eyes, and other parts of the body.

According to the report, it may take a while for the evidence to be able to help humans and it will eventually be extremely significant for individuals who have lost the ability to smell because of some type of medical problem, and not so much for people who can't smell because of trauma to the nose, or simply old age. However, the new findings help researchers to understand anosmia on the cellular level, which gives hope to anyone who does not have a sense of smell that someday their ability to smell may be restored.

Jeffery Martens, Ph.D., senior author of the study commented:

The rodents involved in the study possessed some genetic defect that affected a protein named IFT88. This defect made the individuals have less- than-normal amounts of cilia in their bodies. When this problem occurs in mice, it results in early death and poor feeding habits, while for humans it can be fatal.

IFT88 genes were implanted into the cells in the mice when the researchers gave them a common cold virus which had plenty of normal DNA. This made it easy for the virus to infect them, and therefore, the researchers could insert the virus into the cells of the mice.

After this, the experts were able to analyze the feeding habits of the mice, as well as how they were growing, and the neuron signals which assist in the smelling process.

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New Discovery Offers Hope For People Who Can't Smell

(CBS News) There may be hope for people who are unable to smell. Using gene therapy, scientists have successfully restored the sense of smell in mice that had a genetic mutation that took away their olfactory senses.

Smell disorders or olfactory dysfunction affect one to two percent of people living in North America, according to the National Institute of Deafness and Other Communication Disorders (NIDCD). They partially funded the study along with the National Institute on Diabetes and Digestive and Kidney Diseases (NIDDK), the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), and the National Eye Institute (NEI).

However, smell problems increase with age. A study showed that about 25 percent of men between the ages of 60 to 69 and 11 percent of women in that age group had developed a problem with their sense of smell, NIDCD said.

Scientist hypothesize that olfactory dysfunction may be due to a group of genetic disorders called ciliopathies, which include diseases such as polycystic kidney disease and retinitis pigmentosa, an inherited degenerative eye disease that causes severe vision impairment and blindness. Problems with cilia, antenna-like projections on cells that help sense what's around, are the root of these distorders. The cilia are found on olfactory sensory neurons where are located in tissue high up in the nasal cavity in the olfactory system.

In order to see if they could reintroduce the sense of smell, researchers from the University of Michigan tested mice that had a mutated version of the IFT88 gene. When working normally, the gene creates the IFT88 protein which is necessary for the in the development of cilia. Without it, cilia function decreases especially in the olfactory system. The same genetic problem in humans causes congenital anosmia, the inability to smell from birth.

They injected the subjects with an adenovirus - in this case, a version of the common cold virus - with the missing normal IFT88 sequence. Theoretically, it would "infect" the mice's DNA and insert the correct gene into the cells. The mice were given the therapy for three days via the nose and then given 10 days to allow the IFT88 protein to grow.

Two weeks after the three-day treatment, the mice had gained 60 percent of their body weight meaning they were eating more. Often, mice missing the protein are underweight because their lack of smell gives them less motivation to eat. Other tests showed that the neurons connected to smell were working correctly when the mice were exposed to amyl acetate, a strong-smelling chemical also called banana oil.

"Using gene therapy in a mouse model of cilia dysfunction, we were able to rescue and restore olfactory function, or sense of smell," says senior author Jeffrey Martens, an associate professor of pharmacology at University of Michigan, said in a press release. "Essentially, we induced the neurons that transmit the sense of smell to regrow the cilia they'd lost."

The authors said they hope to continue their research on mice who are completely lacking the IFT88 protein and see if there is a way to use the therapy to restore the sense of smell to people who were born with anosmia.

"These results could lead to one of the first therapeutic options for treating people with congenital anosmia," Dr. James F. Battey, Jr., director of the National Institute on Deafness and Other Communications Disorders (NIDCD), said in a press release. "They also set the stage for therapeutic approaches to treating diseases that involve cilia dysfunction in other organ systems, many of which can be fatal if left untreated."

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Scientists restore sense of smell to mice who were born with genetic abnormality

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/55tpk9/cardiovascular_dru) has announced the addition of Jain PharmaBiotech's new report "Cardiovascular Drug Delivery - Technologies, Markets and Companies" to their offering.

Drug delivery to the cardiovascular system is different from delivery to other systems because of the anatomy and physiology of the vascular system; it supplies blood and nutrients to all organs of the body. Drugs can be introduced into the vascular system for systemic effects or targeted to an organ via the regional blood supply. In addition to the usual formulations of drugs such as controlled release, devices are used as well. This report starts with an introduction to molecular cardiology and discusses its relationship to biotechnology and drug delivery systems.

Drug delivery to the cardiovascular system is approached at three levels: (1) routes of drug delivery; (2) formulations; and finally (3) applications to various diseases. Formulations for drug delivery to the cardiovascular system range from controlled release preparations to delivery of proteins and peptides. Cell and gene therapies, including antisense and RNA interference, are described in full chapters as they are the most innovative methods of delivery of therapeutics. Various methods of improving systemic administration of drugs for cardiovascular disorders are described including use of nanotechnology.

Cell-selective targeted drug delivery has emerged as one of the most significant areas of biomedical engineering research, to optimize the therapeutic efficacy of a drug by strictly localizing its pharmacological activity to a pathophysiologically relevant tissue system. These concepts have been applied to targeted drug delivery to the cardiovascular system. Devices for drug delivery to the cardiovascular system are also described.

Role of drug delivery in various cardiovascular disorders such as myocardial ischemia, hypertension and hypercholesterolemia is discussed. Cardioprotection is also discussed. Some of the preparations and technologies are also applicable to peripheral arterial diseases. Controlled release systems are based on chronopharmacology, which deals with the effects of circadian biological rhythms on drug actions.A full chapter is devoted to drug-eluting stents as treatment for restenosis following stenting of coronary arteries.Fifteen companies are involved in drug-eluting stents.

New cell-based therapeutic strategies are being developed in response to the shortcomings of available treatments for heart disease. Potential repair by cell grafting or mobilizing endogenous cells holds particular attraction in heart disease, where the meager capacity for cardiomyocyte proliferation likely contributes to the irreversibility of heart failure. Cell therapy approaches include attempts to reinitiate cardiomyocyte proliferation in the adult, conversion of fibroblasts to contractile myocytes, conversion of bone marrow stem cells into cardiomyocytes, and transplantation of myocytes or other cells into injured myocardium.

Advances in molecular pathophysiology of cardiovascular diseases have brought gene therapy within the realm of possibility as a novel approach to treatment of these diseases. It is hoped that gene therapy will be less expensive and affordable because the techniques involved are simpler than those involved in cardiac bypass surgery, heart transplantation and stent implantation. Gene therapy would be a more physiologic approach to deliver vasoprotective molecules to the site of vascular lesion. Gene therapy is not only a sophisticated method of drug delivery; it may at time need drug delivery devices such as catheters for transfer of genes to various parts of the cardiovascular system.

The cardiovascular drug delivery markets are estimated for the years 2011 to 2021 on the basis of epidemiology and total markets for cardiovascular therapeutics. The estimates take into consideration the anticipated advances and availability of various technologies, particularly drug delivery devices in the future. Markets for drug-eluting stents are calculated separately. Role of drug delivery in developing cardiovascular markets is defined and unmet needs in cardiovascular drug delivery technologies are identified.

Selected 80 companies that either develop technologies for drug delivery to the cardiovascular system or products using these technologies are profiled and 77 collaborations between companies are tabulated. The bibliography includes 200 selected references from recent literature on this topic. The report is supplemented with 27 tables and 7 figures.

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Research and Markets: Cardiovascular Drug Delivery - Technologies, Markets and Companies - Updated 2012 Report

LONDON (ShareCast) - Tuesday has a bit of an agricultural feel to it, with animal genetics company Genus (Xetra: 762548 - news) and veterinary health-care company Dechra Pharmaceuticals set to update the market.

Peel Hunt says emerging markets growth should be offsetting higher feed prices at Genus. It is forecasting a 15% improvement in profits, with strong growth across a number of emerging markets.

The key issue currently is the rise in feed prices, Peel Hunt believes. "This will have a direct impact on Genus's feed costs of around 1m, but it will also affect its customers. Some customers may well struggle in the short term, but generally higher feed prices are good news for Genus as it accelerates the trend to industrialisation of the industry and reinforces the benefits of genetics in improving feed conversion," the broker predicts.

"We expect to hear more about plans in China, particularly with the announcement of the major JV [joint venture] with Besun, which will deliver genetics to 10m slaughter pigs when in full operation," the broker added.

As for Dechra, the market is expecting profit before tax of 31.1m on revenue of 420.2m. Earnings per share are tipped to rise 19% to 37.03p, paving the way for the full-year dividend to be upped to around 12.16p from 10.97p last year.

US health-care software developer Craneware (Other OTC: CRWRF.PK - news) issued a profit warning in July which does not seem to have done the share price any long term harm, possibly because the group said that the lowering of earnings guidance was because of deal slippage. Analysts will be looking to see if there has been any more signs since then of customers delaying putting pen to paper on new deals.

Abbot ale brewer Greene King (Other OTC: GRKGF.PK - news) issues an interim management statement, and Panmure Gordon thinks the pubs group will have made a robust start to the new financial year, despite the wettest summer since 1912 in the UK.

"We forecast 3.5% LFL [like-for-like] sales growth in managed pubs and 2.5% growth in average EBITDA [earnings before interest, tax, depreciation and amortisation] in its tenanted pubs," the broker revealed.

"Core (Berlin: LJ1.BE - news) brand brewing volumes should be broadly flat," Panmure Gordon added.

Sticking with the boozy theme, pubs group Spirit Pub Company issues a pre-close interim management statement and Panmure Gordon expects the group to reiterate it is comfortable with market expectations of full-year profit before tax of 51.5m.

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Tuesday preview: Genus, Dechra, Greene King

Scientists restored sense of smell to mice bred to have human genetic disorder Has potential to help patients with dementia, which has been linked to loss of smell

By Daily Mail Reporter

PUBLISHED: 03:52 EST, 3 September 2012 | UPDATED: 06:01 EST, 3 September 2012

People born without a sense of smell could enjoy their first aromas, after a scientific breakthrough.

Researchers managed to reverse the problem in mice bred to have the human genetic disorder called congenital anosmia.

They may be able to adapt the procedure to reverse loss of smell caused by ageing or disease.

Floral scent: A new technique could restore the sense of smell

The technique regrows parts of cells known as cilia that are essential for olfactory function, according to a study published online in Mature Medicine.

Dr James Battey, director of the National Institute on Deafness and Other Communications Disorders (NIDCD) in the US, said: 'These results could lead to one of the first therapeutic options for treating people with congenital anosmia.

'They also set the stage for therapeutic approaches to treating diseases that involve cilia dysfunction in other organ systems, many of which can be fatal if left untreated.'

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Anosmia: Gene therapy offers new hope after restoring sense in mice

Public release date: 2-Sep-2012 [ | E-mail | Share ]

Contact: Emmanouil Dermitzakis emmanouil.dermitzakis@unige.ch 41-223-795-483 Universit de Genve

Genetic disease risk differences between one individual and another are based on complex aetiology. Indeed, they may reflect differences in the genes themselves, or else differences at the heart of the regions involved in the regulation of these same genes.

By gene regulation we mean the decision that the cell makes as to when, where and at what level to activate or suppress the expression of a gene. In theory, two people could thus share a gene that is perfectly identical and yet show differences in their predisposition to a disease due to genetic differences concerning the regulation (overexpression or underexpression) of this same gene.

Numerous teams are currently trying to draw up a map of regions involved in gene regulation. Not an easy task, but invaluable since it allows us to understand all the genetic causes that can explain the predisposition to certain diseases.

Working with twins

Emmanouil Dermitzakis, Louis-Jeantet Professor at the Faculty of Medicine and member of the NCCR Frontiers in Genetics and the Institute of Genetics and Genomics of Geneva (IGE3), is a specialist in what is called the genetics of complex traits. With an international team co-led by Professor Tim Spector (Kings College), Professor Mark McCarthy (Oxford University) and Dr. Panos Deloukas (Wellcome Trust Sanger Institute), he publishes a study highlighting thousands of these genetic variants that seem to explain individual differences in gene expression.

For this work, the researchers used samples of three different tissue types (adipose tissue, skin and blood cells) collected from more than 800 homozygotic (identical) and dizygotic twins.

"Identifying variants which control the activity of many genes is a greater challenge than we anticipated but we are developing appropriate tools to uncover them and understand their contribution to disease," comments Panos Deloukas. "Modern human genetics combined with samples donated by the participants in studies such as TwinsUK is making great strides towards finding the genetic culprits behind human disease."

The method researchers followed allowed them to uncover nearly 358 variants apparently involved in the predisposition to certain diseases including quantifying the contribution of rare regulatory variants that was previously not possible to identify by conventional analysis methods.

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A new light shed on genetic regulation's role in the predisposition to common diseases

Public release date: 2-Sep-2012 [ | E-mail | Share ]

Contact: Robin Latham lathamr@nidcd.nih.gov 301-496-7243 NIH/National Institute on Deafness and Other Communication Disorders

Scientists funded by the National Institutes of Health have restored the ability to smell in a mouse model of a human genetic disorder that causes congenital anosmiathe inability to smell from birth. The approach uses gene therapy to regrow cilia, cell structures that are essential for olfactory function. The study was funded by four parts of NIH: the National Institute on Deafness and Other Communications Disorders (NIDCD), the National Institute on Diabetes and Digestive and Kidney Diseases (NIDDK), the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), and the National Eye Institute (NEI). It was published online in the September 2, 2012, issue of the journal Nature Medicine.

"These results could lead to one of the first therapeutic options for treating people with congenital anosmia," said James F. Battey, Jr., M.D., Ph.D., director of NIDCD. "They also set the stage for therapeutic approaches to treating diseases that involve cilia dysfunction in other organ systems, many of which can be fatal if left untreated."

Olfactory dysfunction can be a symptom of a newly recognized class of genetic disorders, known as ciliopathies, which include diseases as diverse as polycystic kidney disease and retinitis pigmentosa, an inherited, degenerative eye disease that causes severe vision impairment and blindness. The disorders are caused by defects in cilia, antenna-like projections on cells that help them sense their environment. Scientists believe that nearly every cell in the body has the capacity to grow one or more cilia. In the olfactory system, multiple cilia project from olfactory sensory neurons, sensory cells that are found in the olfactory epithelium, tissue high up in the nasal cavity. Receptors that bind odorants are localized on the cilia, which is why a loss of cilia results in a loss in the ability to smell.

The team of researchers, led by Jeffrey R. Martens, Ph.D., at the University of Michigan, Ann Arbor, and Jeremy C. McIntyre, Ph.D., a post-doctoral fellow in Martens' laboratory, worked with a mouse model carrying a mutation in the IFT88 gene. The mutation causes a decrease in the IFT88 protein, which leads to a dramatic reduction in cilia function in several different organ systems, including the olfactory system.

The researchers used an adenovirus to introduce a healthy copy of the gene as a way to restore IFT88 protein levels in the mice. They wanted to see if the reintroduction of the lost protein could restore cilia to the olfactory sensory neurons and return the ability to smell. For three consecutive days, the mice received intranasal gene delivery therapy and then were allowed 10 days for the infected sensory neurons to express the viral-encoded IFT88 protein. After that time, the mice were tested with increasing concentrations of an odorant (amyl acetate). Their responses were measured at the cellular, tissue, and synaptic levels, which all indicated that the mice had regained olfactory function.

"By restoring the protein back into the olfactory neurons, we could give the cell the ability to regrow and extend cilia off the dendrite knob, which is what the olfactory neuron needs to detect odorants," said McIntyre.

The change in olfactory function also has implications in the feeding behavior of the mice. The mouse model the scientists used is born underweight and its anosmia interferes with the motivation to eat, which in many mammals, including humans, is driven by smell. Treatment with adenovirus therapy increased bodyweight by 60 percent in treated compared to untreated mice, indicating that the restored olfactory function was motivating feeding.

The researchers plan to continue their work by developing another mouse model to look at the impact on olfactory function and the potential for restoring function when the IFT88 gene is completely missing, rather than just mutated. Future studies could begin to plot a way to bring this therapeutic tactic to human study volunteers, which could eventually restore the sense of smell, and a better quality of life, to people who are born with anosmia. Further research could also advance the treatments for other ciliopathies, as these findings show that gene therapy is a viable option for the functional rescue of cilia in established, already differentiated cells.

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NIH-funded researchers restore sense of smell in mice using genetic technique