In promoting the health care law, President Barack Obama is repeating his persistent and unsubstantiated assurance that Americans who like their health insurance can simply keep it. Republican rival Mitt Romney says quite the opposite, but his doomsday scenario is a stretch.
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Published: Friday, June 29, 2012, 12:09 a.m.
To read more about the Affordable Care Act, go to our national news page.
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By MICHAEL FALCONE (@michaelpfalcone) and AMY WALTER (@amyewalter) NOTABLES: WORD SEARCH: Based on interviews with Obama administration officials and Republican leaders over the weekend, it was evident that the race to define last week’s Supreme Court decision — on favorable terms for each side —...
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Health Care Ruling Turns 'Tax' Into A Four-Letter Word (The Note)
Credit: Tetra images/Getty Images
By MICHAEL FALCONE (@michaelpfalcone) and AMY WALTER (@amyewalter)
NOTABLES:
And another group, Crossroads GPS, announced this weekend they would be unveiling specific ads targeting House and Senate candidates on the health care issue. Heres one calling on North Dakota Senate candidate Heidi Heitkamp to support repeal of the law. The ad is titled Tax, and was updated to reflects the courts ruling. WATCH: http://bit.ly/LUFyaE
THE NOTE:
Its a bird, its a plane! Its a tax, its a penalty!
Ever since last Thursdays Supreme Court decision that ruled the Obama administrations signature health care reform law constitutional, both Democrats and Republicans laced up their running shoes for a sprint to the dictionary.
The keyword: tax.
Republicans want to bake the idea that the health care law imposes a tax into the cake. While Democrats, on the other hand, are loathe to refer to it in those terms.
White House Chief of Staff Jack Lew insisted, repeatedly, in interviews this weekend that under the law refusal to buy insurance would amount to a penalty and Obama campaign aides echoed the White House line, calling it a a free loader penalty.
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You can now see Indystar.com in a format specifically designed for your tablet. Experience the best local news, video, and photos in a beautiful finger-friendly interface.
You will only see this screen once. You can always browse directly to Tablet.Indystar.com or Indystar.com depending on which version you want to see.
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Editor's Choice Main Category: Smoking / Quit Smoking Also Included In: Immune System / Vaccines Article Date: 02 Jul 2012 - 11:00 PDT
Current ratings for: Vaccine For Blocking Nicotine Chemicals Before They Reach The Brain Shows Promise
The study, published in the journal Science Translational Medicine describes that a single dose of the novel vaccine protects mice against a life-long addiction against nicotine.
The vaccine uses the animal's liver as a production site to continuously produce antibodies that instantly gobble up nicotine the moment it enters the bloodstream, and therefore prevents the chemical from reaching the brain and heart.
Leading researcher, Dr. Ronald G. Crystal, chairman and professor of Genetic Medicine at Weill Cornell Medical College explains:
He continues saying: "Our vaccine allows the body to make its own monoclonal antibodies against nicotine, and in that way, develop a workable immunity."
Dr. Crystal stated that the reason why earlier nicotine vaccines failed in clinical trials was because they all directly deliver nicotine antibodies. Their effect only lasted a few weeks and therefore required repeated, costly injections. He adds that this impractical, passive vaccine also delivered inconsistent results, which could potentially be because each person may require a different dose, particularly if the person starts to smoke again.
Crystal says:
He adds that evidence has shown that 70 to 80% of smokers who try to quit pick up the habit again within six months.
Around 20% of American adults smoke, and what keeps smokers addicted is the nicotine in the tobacco, and not the 4,000 chemicals in the burning cigarette that cause smoking-related health problems and which lead to one in every five deaths in the U.S.
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Vaccine For Blocking Nicotine Chemicals Before They Reach The Brain Shows Promise
Public release date: 2-Jul-2012 [ | E-mail | Share ]
Contact: Christine Bauquis christine@eshre.eu 32-499-258-046 European Society of Human Reproduction and Embryology
Istanbul, 2 July 2012: Preimplantation genetic diagnosis (PGD) for the breast cancer genes BRCA1/2 is now feasible and established, with good success rates for those treated, according to investigators from the reproduction, oncology and genetics centres of the university hospitals of Maastricht and Brussels. The results follow a review of the largest number of PGD treatments for BRCA1/2 in Europe and were presented today at the annual meeting of ESHRE (European Society of Human Reproduction and Embryology) by Professor Willem Verpoest from the Centre for Reproductive Medicine at Vrije Universiteit Brussel, Belgium.
Behind his vote of confidence lie 145 PGD cycles for BRCA1/2 mutations performed in 70 couples at the two centres (a mean of 2.1 cycles per woman). Almost 60% of the mutation carriers were female, two-thirds with a BRCA1 mutation. Just over one quarter (26.2%) of female carriers had undergone a prophylactic bilateral mastectomy.
Following IVF, 717 embryos were found suitable for genetic analysis, and of these 43.1% were diagnosed as affected by the mutation, with 40.7% unaffected and thus suitable for transfer (the remainder had an abnormal genotype or the analysis was inconclusive). Hence, 62.1% of the PGD cycles led to fresh embryo transfer - with 3.6% transferred from one or two frozen-thawed unaffected embryos - resulting in 42 pregnancies in 40 women. Pregnancy rates were 41.4% per fresh embryo transfer and 23.1% per frozen. The overall pregnancy rate was 29%.
The series also included three cases of PGD on embryos previously cryopreserved for fertility preservation prior to chemotherapy, and these too resulted in two ongoing pregnancies.
Two female BRCA1 carriers were diagnosed with breast cancer within three months of the PGD treatment, despite breast screening shortly before treatment. One had a history of breast cancer, the other patient hadn't. The former patient went on to have healthy twins three years after the second breast surgery and chemotherapy, and following frozen/thawed embryo transfer.
So far, PGD for BRCA1 and BRCA2 gene mutations has been considered controversial. While most PGD procedures are indicated to remove completely the risk of inherited sex-linked and single-gene diseases (such as cystic fibrosis) in the children of affected couples, PGD for the breast cancer mutations cannot remove the risk completely - because the 10% background risk of breast cancer remains, even after PGD. Moreover, breast and ovarian cancers are usually of late onset, with prevention and therapeutic options constantly improving - so the chances of successful treatment, and many years of healthy life, are high.
Nor is breast cancer inevitable for a woman (or man) carrying a BRCA1/2 mutation. The controversy thus rests on the fact that a mutation in the BRCA genes increases susceptibility to breast or ovarian cancer, but does not reflect an inevitability for developing the diseases. However, with female carriers of a mutation in either gene having a lifetime risk of 60-80% for breast cancer, and a risk of 30-60% (BRCA1) or 5-20% (BRCA2) for ovarian cancer, many authorities have recognised the gravity of the risk and accepted a BRCA gene mutation as an indication for PGD.
So far, only five pregnancies after PGD for BRCA1/2 have been reported since the first was described in 2008.(1) The slow uptake reflects not just the controversial nature of the procedure, but also concerns over patient selection and the safety of hormonal stimulation for IVF in women at risk themselves of breast and ovarian cancers.
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The prevention of hereditary breast and ovarian cancer by PGD is 'feasible'
July 2, 2012
Lawrence LeBlond for redOrbit.com Your Universe Online
At least three genetic mutations found in the human brain have been linked to enlarged brain size (megalencephaly) and a number of disorders, including cancer, epilepsy and autism, according to new research led by Seattle Childrens Research Institute.
The mutations were found in the genes AKT3, PIK3R2 and PIK3CA. The mutations were also linked to vascular disorders and skin growth disorders, said the researchers. The study, published in the online edition of the journal Nature Genetics on June 24, offers important implications for the future of medicine through the research findings.
Study leaders, geneticist William Dobyns, MD, and Jean-Baptiste Rivire, PhD, discovered through their research additional proof that the genetic makeup of a person is not completely determined at the moment of conception. The new evidence ties in with previous research that recognized that genetic changes can occur after conception, although considered quite rare.
The researchers also discovered the genetic causes of these human diseases, including developmental disorders, may also directly lead to new possibilities for treatment.
AKT3, PIK3R2 and PIK3CA are found in all humans, but only when they are mutated do they lead to the diseases and disorders. PIK3CA is known as a cancer-related gene, and appears to make cancer more aggressive. Boston Childrens Hospital researchers recently found a common link between the PIK3CA gene and a rare condition known as CLOVES syndrome.
James Olson, MD, PhD, a pediatric cancer expert at Seattle Childrens and Fred Hutchinson Cancer Research Center acknowledged the two decades-worth of work that led to the findings.
This study represents ideal integration of clinical medicine and cutting-edge genomics, said Olson, who was not involved in the latest research. I hope and believe that the research will establish a foundation for successfully using drugs that were originally developed to treat cancer in a way that helps normalize intellectual and physical development of affected children.
He noted that the team did an excellent job by deep sequencing exceptionally rare familial cases and unrelated cases to identify the culprit pathway. He further noted that the three genes all encode core components of the phosphatidylinositol-3-kinase/AKT pathway, the culprit pathway, as referenced by his work.
Excerpt from:
Gene Mutations Associated With Enlarged Brain Size, Disorders
Newswise Researchers at Moffitt Cancer Center working with colleagues at three other institutions have validated a link between a rare genetic variant and the risk of glioma, the most common and lethal type of brain tumor. The validation study also uncovered an association between the same rare genetic variant and improved rates of survival for patients with glioma.
The study, the first to confirm a rare susceptibility variant in glioma, appeared in a recent issue of the Journal of Medical Genetics, a journal published by the British Medical Association.
"Glioma is a poorly understood cancer with high morbidity and devastating outcomes," said study lead author Kathleen M. Egan, Sc.D., interim program leader of Cancer Epidemiology and vice chair of the Department of Cancer Epidemiology. "However, the discovery of the association of the TP53 genetic variant rs78378222 with glioma provides new insights into these tumors and offers better prospects for identifying people at risk."
According to the authors, their study "genotyped' the single nucleotide polymorphism (SNP, or "snip") rs78378222 in TP53, an important tumor suppressor gene. The researchers said the SNP disrupts the TP53 signal and, because of its activity, has been linked to a variety of cancers. This study linked the presence of the rare form of rs78378222 to deadly glioma.
The researchers conducted a large, clinic-based, case-control study of individuals age 18 and older with a recent glioma diagnosis. A total of 566 glioma cases and 603 controls were genotyped for the rs78378222 variant.
Study results reveal that the odds of developing glioma were increased 3.5 times among the rare variant allele carriers. However, when researchers examined the impact of rs78378222 on survival, they found an approximately 50 percent reduction in death rates for those who were variant allele carriers.
"That the variant increased survival chances was an unexpected finding," Egan said. "It is tempting to speculate that the presence of the risk allele could direct tumor development into a less aggressive path."
The researchers concluded that their study results "may shed light on the etiology and progression of these tumors."
In addition to researchers from Moffitt, researchers from The University of Alabama at Birmingham, Emory School of Medicine and Vanderbilt University participated in the study and co-authored the paper.
The study was supported by funding from Public Health Service Grants R01CA11674 from the National Cancer Institute and the U.S. Department of Health and Human Services, as well as institutional funding from Moffitt and the Vanderbilt-Ingram Cancer Center.
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Moffitt Cancer Center Study Validates Activity of Rare Genetic Variant in Glioma
ScienceDaily (July 2, 2012) Researchers at Moffitt Cancer Center working with colleagues at three other institutions have validated a link between a rare genetic variant and the risk of glioma, the most common and lethal type of brain tumor. The validation study also uncovered an association between the same rare genetic variant and improved rates of survival for patients with glioma.
The study, the first to confirm a rare susceptibility variant in glioma, appeared in a recent issue of the Journal of Medical Genetics, a journal published by the British Medical Association.
"Glioma is a poorly understood cancer with high morbidity and devastating outcomes," said study lead author Kathleen M. Egan, Sc.D., interim program leader of Cancer Epidemiology and vice chair of the Department of Cancer Epidemiology. "However, the discovery of the association of the TP53 genetic variant rs78378222 with glioma provides new insights into these tumors and offers better prospects for identifying people at risk."
According to the authors, their study "genotyped' the single nucleotide polymorphism (SNP, or "snip") rs78378222 in TP53, an important tumor suppressor gene. The researchers said the SNP disrupts the TP53 signal and, because of its activity, has been linked to a variety of cancers. This study linked the presence of the rare form of rs78378222 to deadly glioma.
The researchers conducted a large, clinic-based, case-control study of individuals age 18 and older with a recent glioma diagnosis. A total of 566 glioma cases and 603 controls were genotyped for the rs78378222 variant.
Study results reveal that the odds of developing glioma were increased 3.5 times among the rare variant allele carriers. However, when researchers examined the impact of rs78378222 on survival, they found an approximately 50 percent reduction in death rates for those who were variant allele carriers.
"That the variant increased survival chances was an unexpected finding," Egan said. "It is tempting to speculate that the presence of the risk allele could direct tumor development into a less aggressive path."
The researchers concluded that their study results "may shed light on the etiology and progression of these tumors."
In addition to researchers from Moffitt, researchers from The University of Alabama at Birmingham, Emory School of Medicine and Vanderbilt University participated in the study and co-authored the paper.
The study was supported by funding from Public Health Service Grants R01CA11674 from the National Cancer Institute and the U.S. Department of Health and Human Services, as well as institutional funding from Moffitt and the Vanderbilt-Ingram Cancer Center.
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Technology company Tegal Corp. said Monday it will buy CollabRx Inc., which develops technology that is used in genetic-based medicine.
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In February last year, The New York Times published an interview with my University of Chicago colleague Janet Rowley. Janet is deservedly famous for finding a repeated chromosome rearrangement in certain types of leukemia. This was one of the earliest indications that genome changes in cancer cells do not occur randomly.
In the interview, Janet explained how she discovered this particular chromosome change, now called the "Philadelphia Chromosome." She was just looking through the microscope, motivated by her curiosity to know more about these tumor cells.
Janet pointed out that she might well not be able to repeat her discovery in today's scientific environment. She was practicing what she called "observationally driven research." Today, she said, granting agencies don't support that kind of work. "That's the kiss of death if you're looking for funding today. We're so fixated now on hypothesis-driven research that if you do what I did, it would be called a 'fishing expedition,' a bad thing."
In other words, you have to know what kind of result to expect before the funding agencies will give you money to look for it. Surprises are not fundable. But "surprise" is just another word for "discovery." As Janet put it, "I keep saying that fishing is good. You're fishing because you want to know what's there."
Let's look at how we would "fish" for complex genomic novelty through natural genetic engineering. I can think of two approaches. There will definitely turn out to be more.
One approach was included in my book. The idea was to do interspecific hybridization with a well-characterized organism, like the mustard weed Arabidopsis, and follow what happens with the genetically unstable hybrid progeny.
We know that interspecific hybridization and genome duplication lead to high levels of genomic and phenotypic variation. DNA sequencing has found evidence of genome duplication at many critical points of evolutionary divergence, especially in plants. There is a fine Scientific American article by the famous 20th-century evolutionist G. Ledyard Stebbins entitled "Cataclysmic Evolution," which describes how hybridization between two wild grasses can recreate the origin of flour wheat.
The hybrid progeny can be followed, and those plants that develop significant new traits, such as flower patterns, can then be analyzed. Sequencing the whole Arabidopsis genome in a short time is now feasible. The sequence data will let the Arabidopsis genome speak for itself in telling us how the new traits evolved.
We can then look for multiple changes that show signs of coordination in the underlying natural genetic engineering events. Such coordinated events might be insertions of the same or related mobile elements at distinct locations in the genome or the addition of the same domains to more than one protein in the network responsible for development of the novel trait.
The second "fishing" approach to asking how a novel feature can evolve would use a microbe, as suggested in the previous blog on experimental evolution. In this case, however, the changes would not be pre-targeted to a number of different sites in the genome.
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Public release date: 1-Jul-2012 [ | E-mail | Share ]
Contact: Mika OnoScripps Research Institute scientists develop alternative to gene therapy mikaono@scripps.edu 858-784-2052 Scripps Research Institute
LA JOLLA, CA July 1, 2012 Scientists at The Scripps Research Institute have discovered a surprisingly simple and safe method to disrupt specific genes within cells. The scientists highlighted the medical potential of the new technique by demonstrating its use as a safer alternative to an experimental gene therapy against HIV infection.
"We showed that we can modify the genomes of cells without the troubles that have long been linked to traditional gene therapy techniques," said the study's senior author Carlos F. Barbas III, who is the Janet and Keith Kellogg II Professor of Molecular Biology and Chemistry at The Scripps Research Institute.
The new technique, reported in Nature Methods on July 1, 2012, employs zinc finger nuclease (ZFN) proteins, which can bind and cut DNA at precisely defined locations in the genome. ZFNs are coming into widespread use in scientific experiments and potential disease treatments, but typically are delivered into cells using potentially risky gene therapy methods.
The Scripps Research scientists simply added ZFN proteins directly to cells in a lab dish and found that the proteins crossed into the cells and performed their gene-cutting functions with high efficiency and minimal collateral damage.
"This work removes a major bottleneck in the efficient use of ZFN proteins as a gene therapy tool in humans," said Michael K. Reddy, who oversees transcription mechanism grants at the National Institutes of Health's (NIH) National Institute of General Medical Sciences, which helped fund the work, along with an NIH Director's Pioneer Award. "The directness of Dr. Barbas's approach of 'simply' testing the notion that ZFNs could possess an intrinsic cell-penetrating ability is a testament to his highly creative nature and further validates his selection as a 2010 recipient of an NIH Director's Pioneer Award."
Questioning Assumptions
ZFNs, invented in the mid-1990s, are artificial constructs made of two types of protein: a "zinc-finger" structure that can be designed to bind to a specific short DNA sequence, and a nuclease enzyme that will cut DNA at that binding site in a way that cells can't repair easily. The original technology to make designer zinc finger proteins that are used to direct nucleases to their target genes was first invented by Barbas in the early 1990s.
Scientists had assumed that ZFN proteins cannot cross cell membranes, so the standard ZFN delivery method has been a gene-therapy technique employing a relatively harmless virus to carry a designer ZFN gene into cells. Once inside, the ZFN gene starts producing ZFN proteins, which seek and destroy their target gene within the cellular DNA.
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Scripps Research Institute Scientists Develop Alternative to Gene Therapy
London, July 2 : Scientists at The Scripps Research Institute have found a surprisingly simple and safe method to disrupt specific genes within cells.
They highlighted the medical potential of the new technique by demonstrating its use as a safer alternative to an experimental gene therapy against HIV infection.
"We showed that we can modify the genomes of cells without the troubles that have long been linked to traditional gene therapy techniques," said the study's senior author Carlos F. Barbas III, who is the Janet and Keith Kellogg II Professor of Molecular Biology and Chemistry at The Scripps Research Institute.
The new technique employs zinc finger nuclease (ZFN) proteins, which can bind and cut DNA at precisely defined locations in the genome. ZFNs are coming into widespread use in scientific experiments and potential disease treatments, but typically are delivered into cells using potentially risky gene therapy methods.
The Scripps Research scientists simply added ZFN proteins directly to cells in a lab dish and found that the proteins crossed into the cells and performed their gene-cutting functions with high efficiency and minimal collateral damage.
ZFNs, invented in the mid-1990s, are artificial constructs made of two types of protein: a "zinc-finger" structure that can be designed to bind to a specific short DNA sequence, and a nuclease enzyme that will cut DNA at that binding site in a way that cells can't repair easily. The original technology to make designer zinc finger proteins that are used to direct nucleases to their target genes was first invented by Barbas in the early 1990s.
Scientists had assumed that ZFN proteins cannot cross cell membranes, so the standard ZFN delivery method has been a gene-therapy technique employing a relatively harmless virus to carry a designer ZFN gene into cells. Once inside, the ZFN gene starts producing ZFN proteins, which seek and destroy their target gene within the cellular DNA.
One risk of the gene-therapy approach is that viral DNAeven if the virus is not a retrovirusmay end up being incorporated randomly into cellular DNA, disrupting a valuable gene such as a tumor-suppressor gene. Another risk with this delivery method is that ZFN genes will end up producing too many ZFN proteins, resulting in a high number of "off-target" DNA cuts.
In the new study, Barbas and his colleagues set out to find a safer ZFN delivery method that didn't involve the introduction of viruses or other genetic material into cells. They experimented initially with ZFN proteins that carry extra protein segments to help them penetrate cell membranes, but found these modified ZFNs hard to produce in useful quantities. Eventually, the scientists recognized that the zinc-finger segments of ordinary ZFNs have properties that might enable the proteins to get through cell membranes on their own.
Next, the team showed how the new technique could be used in a ZFN-based strategy against HIV infection.
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New technique offers safer alternative to gene therapy for HIV treatment
ScienceDaily (July 1, 2012) Scientists at The Scripps Research Institute have discovered a surprisingly simple and safe method to disrupt specific genes within cells. The scientists highlighted the medical potential of the new technique by demonstrating its use as a safer alternative to an experimental gene therapy against HIV infection.
"We showed that we can modify the genomes of cells without the troubles that have long been linked to traditional gene therapy techniques," said the study's senior author Carlos F. Barbas III, who is the Janet and Keith Kellogg II Professor of Molecular Biology and Chemistry at The Scripps Research Institute.
The new technique, reported in Nature Methods on July 1, 2012, employs zinc finger nuclease (ZFN) proteins, which can bind and cut DNA at precisely defined locations in the genome. ZFNs are coming into widespread use in scientific experiments and potential disease treatments, but typically are delivered into cells using potentially risky gene therapy methods.
The Scripps Research scientists simply added ZFN proteins directly to cells in a lab dish and found that the proteins crossed into the cells and performed their gene-cutting functions with high efficiency and minimal collateral damage.
"This work removes a major bottleneck in the efficient use of ZFN proteins as a gene therapy tool in humans," said Michael K. Reddy, who oversees transcription mechanism grants at the National Institutes of Health's (NIH) National Institute of General Medical Sciences, which helped fund the work, along with an NIH Director's Pioneer Award.
Questioning Assumptions
ZFNs, invented in the mid-1990s, are artificial constructs made of two types of protein: a "zinc-finger" structure that can be designed to bind to a specific short DNA sequence, and a nuclease enzyme that will cut DNA at that binding site in a way that cells can't repair easily. The original technology to make designer zinc finger proteins that are used to direct nucleases to their target genes was first invented by Barbas in the early 1990s.
Scientists had assumed that ZFN proteins cannot cross cell membranes, so the standard ZFN delivery method has been a gene-therapy technique employing a relatively harmless virus to carry a designer ZFN gene into cells. Once inside, the ZFN gene starts producing ZFN proteins, which seek and destroy their target gene within the cellular DNA.
One risk of the gene-therapy approach is that viral DNA -- even if the virus is not a retrovirus -- may end up being incorporated randomly into cellular DNA, disrupting a valuable gene such as a tumor-suppressor gene. Another risk with this delivery method is that ZFN genes will end up producing too many ZFN proteins, resulting in a high number of "off-target" DNA cuts. "The viral delivery approach involves a lot of off-target damage," said Barbas.
In the new study, Barbas and his colleagues set out to find a safer ZFN delivery method that didn't involve the introduction of viruses or other genetic material into cells. They experimented initially with ZFN proteins that carry extra protein segments to help them penetrate cell membranes, but found these modified ZFNs hard to produce in useful quantities. Eventually, the scientists recognized that the zinc-finger segments of ordinary ZFNs have properties that might enable the proteins to get through cell membranes on their own.
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NEW YORK, July 2, 2012 /PRNewswire/ --Reportlinker.com announces that a new market research report is available in its catalogue:
Gene Therapy Market to 2018 - Product Development Slowed by Clinical Failures, Close Regulatory Surveillance and High Compliance Standards
This report is built using data and information sourced from proprietary databases, primary and secondary research, and in-house analysis by GBI Research's team of industry experts.
Gene therapies are biological compounds, which modify or replace disease-causing genes. These therapies are the new therapeutic class aimed at treating diseases associated with genetic mutations. Gene therapy promises to provide new treatments for a large number of inherited and acquired diseases. The basic concept of gene therapy is to introduce a piece of genetic material into target cells, which will result in either a cure for the disease or a slowdown in the progression of the disease. It involves the transfer of a functional gene copy into specific cells of an individual in order to repair a faulty gene copy. It may be used to replace a defective gene, or to introduce a new gene to cure a condition.
For example, mutations in genes on the X chromosome lead to X chromosome-linked genetic diseases such as Duchenne muscular dystrophy and hemophilia. Since males have only one copy of the genes from this chromosome, there is no other normal copy available to fulfill a defective gene's function which is present on the X chromosome. If the normal copy of the mutated gene is delivered in the nucleus externally through a delivery agent, the cells can produce the normal gene products and the disease would be treated.
From a commercial perspective, there is a huge unmet need in oncology and autoimmune diseases, amongst others, that could further drive growth of the pharmaceutical and biotech industry. The unmet need is largely driven by the lack of efficacious and safe therapeutic products based on conventional pharmaceutical and biotech research. Gene therapy is a new therapeutic category that has the potential to satisfy this unmet need, especially considering how efficacious and safe this therapeutic category is expected to be.
GBI Research's analysis suggests that therapies developed using gene therapy technology can address the majority of the unmet needs prevailing in the current pharmaceutical market. The inherent structure of gene therapies and their potential to replace the functions of defective genes make them highly effective to knockdown any gene that was previously unapproachable by conventional therapies. Gene therapies are poised to become the next most promising class of drugs in the pharmaceutical industry. Currently there are only three approved products, namely Gendicine, Oncorine and Rexin-G, with a collective market little above $2.8m. Since first movers always have the competitive edge, many large pharmaceutical and biotechnology companies have already commenced their R&D activities on gene therapies.
This report provides insights into the major unmet needs prevailing in the current pharmaceutical industry, and points to gene therapies as the solution to these unmet needs. The report also elucidates the promising late-stage gene therapy pipeline, and provides insights into the gene therapeutics R&D pipeline and funding opportunities.
- Analysis of the leading therapeutic segments for which clinical development in gene therapy is being conducted.
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Clay Dean spends his days imagining the future. You might soon be driving what he dreams.
As executive director of General Motors' advanced global design department, he is currently envisioning the roads of 2040, and what he sees is very different from today.
We are on the verge, he says, of a renaissance, an era in which car design will change the look of our roads, the way we commute to work, how much stress we endure throughout the day, even our impact on the planet.
"Today, it is all possible," says Dean, who sees Walt Disneys vision of futurism as a model. "It is an exciting time to be a designer."
This month marks 85 years since GM became the first automaker to create a department devoted entirely to body design. That department now finds itself at a crossroads: as GM, the worlds biggest automaker, and other major American manufacturers seek to regain the country's confidence and engage younger buyers - and even expand their business to more distant, untapped markets - innovating at a pace beyond what most car companies are used to will be key.
GM hopes its history will be instructive. The company's first design chief, Hollywood coachbuilder Harley Earl, added colors beyond the then-standard black and is credited with the idea of the "concept car" - as in, a sexy, wild-looking design (albeit one that people may not actually be able to drive). By the time Earl retired in 1958, he had some truly progressive designs to his name, too, from the 1938 Buick Y-Job, with its hidden headlamps and electric windows, to the 1956 Firebird II, which included a guidance system that GM said would soon be integrated with the "highway of the future," enabling the car to drive itself.
This hasnt quite come to pass.
Even if automakers push through innovative new products, it's unclear if people will buy them. The most popular cars today aren't known for their radical styling. The Toyota Camry has been the best-selling car in the U.S. for every year since 1997 except one.
Nor is it certain the automakers will manufacture anything too out of the box. Take the Chevy Volt, the advanced hybrid battery-powered car that has won accolades and awards for its design, but almost didn't happen. It took the persistence of one top executive to convince the company's board that the idea made financial sense.
These are the kinds of challenges the Big Three U.S. automakers have struggled to meet for decades. The flying cars promised more than half a century ago remain far from dealers' lots, but with their companies' futures anything but certain, designers at GM, Ford and Chrysler now seem to feel a new urgency as they grapple with new material compositions, shifting transportation needs and, not least, the legacies of their predecessors, which loom large around them as they work to make Americans fall back in love with the automobile.
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Futuristic Car Design Is Already In the Works At The Detroit Automakers
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The American soft-drink industry does not want you to think about fatness. The American soft-drink industry wants you to erase all soda-related images of fatness from your mind. Erase the anonymously obese bodies parading down city streets on the nightly news. Erase the memory of those subway ads with fatty substances oozing out of soda bottles. Erase the text that accompanied them, the obesity ...
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In an effort to prevent the passage of legislation like the Stop Online Piracy Act (SOPA), as well as ISP blockades, various Internet groups today joined forces to launch the Declaration of Internet Freedom, a set of principles organizers hope will be embraced by lawmakers, private companies, and average Web users alike.
The effort - organized by Free Press, Harvard's Kennedy School, Techdirt.com, Reddit, and Ben Huh's Cheezburger network - invites Web users to "stand for a free and open Internet."
The declaration covers five basic principles: Expression (don't censor the Internet); Access (Promote universal access to fast and affordable networks); Openness (keep the Internet an open network where everyone is free to connect, communicate, write, read, watch, speak, listen, learn, create and innovate); Innovation (protect the freedom to innovate and create without permission. Don't block new technologies, and don't punish innovators for their users' actions); and Privacy (protect privacy and defend everyone's ability to control how their data and devices are used).
During a conference call with reporters this afternoon, Josh Levy, the Internet campaign director at Free Press, said the groups have been working since Jan. 18 - Internet blackout day - to "figure out what comes next and how do we marshal the energy of more than 13 million Internet users ... who now realize that the open Internet is a fragile thing."
In opposition to SOPA and its Senate counterpart, the PROTECT IP Act (PIPA), various Internet sites went dark in January for one day, prompting the demise of SOPA and PIPA. The bills aimed to stop "rogue" overseas websites that traffic in pirated goods, but detractors argued that they would make it easy to cut off access to legitimate websites.
"This is about building political power for Internet users [by rallying] millions of people around a very basic set of principles," Levy continued. "When it comes time to build policy, we can stand up and say Internet users need a seat at the table."
Cheezburger's Huh said that come Election Day, supporters will look to elect those who adhere to the Internet freedom principles. The group isn't looking to back a specific candidate per se, he said, but "from this comes the legislation and lobbying and representatives."
"This helps establish a baseline, so when you have something like SOPA and PIPA," lawmakers know where supporters stand, said Mike Masnick, CEO and founder of Techdirt.
When asked if the Declaration of Internet Freedom was targeted more at the government or ISPs, Levy said the group did not have a "defined target" because both sectors cross-pollinate so much when it comes to the Web.
What's next? The group is asking Web users to chime in on the principles and make suggestions for how they might be approved. There will be forums on Reddit as well as TechDirt and Cheezburger, where organizers will collect peoples' thoughts.
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