Plain cigarette packaging: pro-smoking groups and Ukip condemn move

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The government is to give MPs a vote before May on regulations forcing tobacco firms to introduce plain packaging Photograph: Department of Health

Pro-smoking groups, Ukip and libertarian MPs have all condemned the governments surprise decision to bring forward a law on plain cigarette packaging before the general election.

Health minister Jane Ellison said on Wednesday night that the government would give MPs a vote before May on regulations forcing tobacco firms to introduce plain packaging and before the end of a consultation exercise about the idea.

Farage, the Rothmans-smoking leader of the UK Independence party, said the proposal represented meddling in the free market that would damage the economy. Condemning the move in a tweet, he said: Plain packaging is an appalling intrusion into consumer choice and the operation of the free market. Jobs and tax revenue would suffer.

Writing in the Independent, Farage said: I call it a deliberate and nonsensical imposition on a market worth around 12bn to the Treasury, and which keeps around 66,000 people in jobs.

But forget the financials, or the employment figures, as Labour are so willing to do. Instead, lets focus on the evidence. Does plain packaging really stop people smoking? The best example we have is in Australia, where since plain packaging was introduced in 2012, household expenditure on tobacco has actually increased. And so has the black market in cigarettes.

These are the effects of banning things that should be readily available to responsible adults in a free society. Not, as the meddlesome politicians will try to tell you, a response that they would like to see. But rather quite the opposite.

Ukip MP Mark Reckless, who defected to the party last year, tweeted: Plain packs for cigarettes as enshrining overseas aid at 7% GDP unites Cons with left wing quangocrats against public. Only @UKIP will fight.

The vote is likely to see some libertarian Tories voting against the measure. Philip Davies, the Conservative MP for Shipley in West Yorkshire, echoed Ukips concerns.

He told the Daily Mail that the governments announcement was a triumph for the nanny state. Davies added: This flies in the face of every Conservative principle.

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Plain cigarette packaging: pro-smoking groups and Ukip condemn move

UAB Research Probes Molecular Basis of Rare Genetic Disorder

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Newswise BIRMINGHAM, Ala. An international group co-led by University of Alabama at Birmingham researcher Mary MacDougall, Ph.D., has unraveled the molecular basis for the rare, inherited genetic disorder, Singleton-Merten Syndrome (SMS). Individuals with SMS develop extreme, life-threatening calcification of the aorta and heart valves, early-onset periodontitis and root resorption of the teeth, decreases in bone density, and loss of bone tissue at the tips of fingers and toes.

The cause of SMS is a missense mutation that changes a single amino acid in the protein MDA5 from arginine to glutamine, MacDougall and colleagues are reporting today (Jan. 22) in the online version of The American Journal of Human Genetics. That change in MDA5 which detects viral double-stranded RNA as part of the innate immunity system causes increased induction of interferon beta. Thus SMS is recognized as an innate autoimmune disease for the first time.

The autoimmunity finding was startling, said MacDougall, associate dean for research, James R. Rosen Chair of Dental Research, and professor in the Department of Oral and Maxillofacial Surgery at the UAB School of Dentistry, and director of UABs Global Center for Craniofacial, Oral and Dental Disorders. She and Frank Rutsch, M.D., Department of General Pediatrics, Muenster University Childrens Hospital, Germany, are co-first authors of the paper, A Specific IFIH1 Gain-of-function Mutation Causes Singleton-Merten Syndrome.

Because of the unusual dental problems in SMS patients, Rutsch had contacted MacDougall 10 years ago to probe the molecular mechanisms of the syndrome. MacDougall is an internationally respected research leader in craniofacial developmental biology and dental genetics, particularly the molecular basis and mechanisms associated with human dental genetic disorders that alter tooth number, formation and hard tissue structure. Such investigations of differentiation during tooth and bone formation have broad applications across medical research.

SMS is an autosomal-dominant disorder, meaning the mutation is not carried on the sex chromosomes, and a single copy of the mutation in the gene IFIH1 that encodes MDA5 can cause disease. Rutsch identified three SMS-affected families, and researchers in Cologne, Germany performed whole-exome DNA sequencing and targeted Sanger sequencing to identify the mutation. The same mutation was found in 10 different patients.

MacDougalls group at UAB analyzed the dental features of patients and created cell lines from SMS individuals and controls. Several of the dental pulp cell lines came from an extracted, forming third-molar that was shipped from Germany to Alabama by FedEx.

Functional studies by the UAB group found that: MDA5 as measured by immunohistochemistry of human heart, skin and cartilage tissue, or demineralized developing mouse teeth was present in all target tissues that are altered in SMS. Presence of the SMS- IFIH1 mutant gene increased interferon beta gene expression by 20-fold, and correcting the single mutation of the SMS-IFIH1 back to normal reduced expression to control levels. The SMS- IFIH1 mutant gene had a greater response, as measured by interferon beta induction, when challenged with double-stranded RNA, as compared with the normal gene. Whole blood of SMS individuals and the cell lines developed from the SMS tooth had higher expression of interferon signature genes, compared with control individuals and cells.

Thus, the altered gene is a gain-of-function mutation. Recently, IFIH1 has been linked to several autoimmune disorders, including Aicardi-Goutieres syndrome, though those individuals show brain and developmental defects.

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UAB Research Probes Molecular Basis of Rare Genetic Disorder

Treatment restores sociability in autism mouse model

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Among the problems people with Autism spectrum disorders (ASD) struggle with are difficulties with social behavior and communication. That can translate to an inability to make friends, engage in routine conversations, or pick up on the social cues that are second nature to most people. Similarly, in a mouse model of ASD, the animals, like humans, show little interest in interacting or socializing with other mice.

One drug, risperidone, works in both humans and mice with ASD to treat other symptoms of the disorder -- including repetitive behaviors--but no medication has been found to help socialization.

Now researchers at UCLA have treated ASD mice with a neuropeptide--molecules used by neurons to communicate with each other--called oxytocin, and have found that it restores normal social behavior. In addition, the findings suggest that giving oxytocin as early as possible in the animal's life leads to more lasting effects in adults and adolescents. This suggests there may be critical times for treatment that are better than others.

The study appears in the January 21 online edition of the journal Science Translational Medicine.

Mouse models of neuropsychiatric diseases provide a platform for understanding the mechanisms behind disorders and development of new therapies, noted Daniel Geschwind, a UCLA professor of psychiatry, neurology and human genetics, and senior author of the study. In 2011, Geschwind and his colleagues developed a mouse model for ASD by knocking out a gene called CNTNAP2 (contactin-associated protein-like 2), which scientists believe plays an important role in the brain circuits responsible for language and speech. Previous research has linked common CNTNAP2 variants to heightened autism risk in the general population, while rare variants can lead to an inherited form of autism called cortical dysplasia-focal epilepsy syndrome (CDFE).

It's known that the oxytocin is involved in regulating various aspects of social behavior. Among its other roles, oxytocin neurons in the brain's hypothalamus interact with several other brain regions, including the amygdala, hippocampus, and frontal cortex, where they influence such behaviors as fear, memory, and social behavior.

"The oxytocin system is a key mediator of social behavior in mammals, including humans, for maternal behavior, mother-infant bonding, and social memory," said Geschwind, who holds UCLA's Gordon and Virginia MacDonald Distinguished Chair in Human Genetics and is the director of the Center for Autism Research and Treatment at the Semel Institute for Neuroscience and Human Behavior at UCLA. "So it seemed like a natural target for us to go after."

In the ASD mice, the researchers found a decrease in the number of oxytocin neurons in the hypothalamus and, overall, a decrease in oxytocin levels throughout the brain. But when they administered oxytocin to the ASD mice, sociability, defined as time spent interacting normally with other mice, was restored. Then, using a second strategy, the researchers also found that by giving the mice melanocortin, an agonist (which binds to specific receptors on a cell to activate it) caused a natural release of oxytocin from brain cells, which also improved social deficits.

"The study shows that a primary deficit in oxytocin may cause the social problems in these mice, and that correcting this deficit can correct social behavior," said Geschwind. "We were surprised as well to discover a relationship between the cntnap2 protein and oxytocin--the absence of cntnap2 effected oxytocin neurons in the hypothalamus."

The biggest surprise, though, said Geschwind, was finding that early postnatal administration of the oxytocin led to longer positive effects upon social behavior when measured several weeks later. "This suggests that there may be critical windows of time for treatment that are better than others."

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Treatment restores sociability in autism mouse model

Research probes molecular basis of rare genetic disorder

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An international group co-led by University of Alabama at Birmingham researcher Mary MacDougall, Ph.D., has unraveled the molecular basis for the rare, inherited genetic disorder, Singleton-Merten Syndrome (SMS). Individuals with SMS develop extreme, life-threatening calcification of the aorta and heart valves, early-onset periodontitis and root resorption of the teeth, decreases in bone density, and loss of bone tissue at the tips of fingers and toes.

The cause of SMS is a missense mutation that changes a single amino acid in the protein MDA5 from arginine to glutamine, MacDougall and colleagues are reporting today (Jan. 22) in the online version of The American Journal of Human Genetics. That change in MDA5 -- which detects viral double-stranded RNA as part of the innate immunity system -- causes increased induction of interferon beta. Thus SMS is recognized as an innate autoimmune disease for the first time.

"The autoimmunity finding was startling," said MacDougall, associate dean for research, James R. Rosen Chair of Dental Research, and professor in the Department of Oral and Maxillofacial Surgery at the UAB School of Dentistry, and director of UAB's Global Center for Craniofacial, Oral and Dental Disorders. She and Frank Rutsch, M.D., Department of General Pediatrics, Muenster University Children's Hospital, Germany, are co-first authors of the paper, "A Specific IFIH1 Gain-of-function Mutation Causes Singleton-Merten Syndrome.

Because of the unusual dental problems in SMS patients, Rutsch had contacted MacDougall 10 years ago to probe the molecular mechanisms of the syndrome. MacDougall is an internationally respected research leader in craniofacial developmental biology and dental genetics, particularly the molecular basis and mechanisms associated with human dental genetic disorders that alter tooth number, formation and hard tissue structure. Such investigations of differentiation during tooth and bone formation have broad applications across medical research.

SMS is an autosomal-dominant disorder, meaning the mutation is not carried on the sex chromosomes, and a single copy of the mutation in the gene IFIH1 that encodes MDA5 can cause disease. Rutsch identified three SMS-affected families, and researchers in Cologne, Germany performed whole-exome DNA sequencing and targeted Sanger sequencing to identify the mutation. The same mutation was found in 10 different patients.

MacDougall's group at UAB analyzed the dental features of patients and created cell lines from SMS individuals and controls. Several of the dental pulp cell lines came from an extracted, forming third-molar that was shipped from Germany to Alabama by FedEx.

Functional studies by the UAB group found that: MDA5 -- as measured by immunohistochemistry of human heart, skin and cartilage tissue, or demineralized developing mouse teeth -- was present in all target tissues that are altered in SMS. Presence of the SMS- IFIH1 mutant gene increased interferon beta gene expression by 20-fold, and correcting the single mutation of the SMS-IFIH1 back to normal reduced expression to control levels. The SMS- IFIH1 mutant gene had a greater response, as measured by interferon beta induction, when challenged with double-stranded RNA, as compared with the normal gene. Whole blood of SMS individuals and the cell lines developed from the SMS tooth had higher expression of interferon signature genes, compared with control individuals and cells.

Thus, the altered gene is a gain-of-function mutation. Recently, IFIH1 has been linked to several autoimmune disorders, including Aicardi-Goutieres syndrome, though those individuals show brain and developmental defects.

The UAB research team included Changming Lu and Olga Mamaeva, research associates for the Institute of Oral Health Research in the UAB School of Dentistry, and Heidi Erlandsen, a former dental school instructor.

MacDougall is continuing SMS gene research at UAB, including probing the impact of its dysregulation of 30 genes that are involved in tooth formation and dentin mineralization; using it as a paradigm for patients with other diseases, such as periodontitis and aggressive periodontitis; screening glaucoma patients for the mutation, since early-onset glaucoma is one phenotype seen in some SMS individuals; and looking for altered microbiomes and oral biomes in SMS individuals.

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Research probes molecular basis of rare genetic disorder

Day 2 Wow 3 Pounds lost in One Day| Sugar and Salt Slows Fat Loss -James Knight – Video

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Day 2 Wow 3 Pounds lost in One Day| Sugar and Salt Slows Fat Loss -James Knight
Join the Facebook Group (plans and recipes) Day 2 Wow 3 Pounds lost in One Day| Sugar and Salt Slows Fat Loss - Barry Anderson | James Knight 90 Day Weight Loss Challenge WEIGHT...

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Day 2 Wow 3 Pounds lost in One Day| Sugar and Salt Slows Fat Loss -James Knight - Video

Health-care unions grapple with bargaining report

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The provinces four health-care unions have instructed their legal teams to work together to make the Dorsey report work for everyone.

A news release issued jointly by the Canadian Union of Public Employees, Nova Scotia Government & General Employees Union, Nova Scotia Nurses Union and Unifor said the decision comes from a meeting on Tuesday with a goal of getting the best outcomes for the 24,000 health-care member affected by the Liberal governments Health Authorities Act.

Dorsey ruled the government could reduce the number of bargaining units to four: clerical, health care, nursing and support. The government has indicated a desire for each of the four unions to represent one of the new units.

In a move the unions heralded, Dorsey said where there is no clear majority for one union health care and support those affected could form an amalgamated union for the purpose of negotiations.

Further hearings are set for the week of Feb. 2 to discuss that idea and what will happen with the nursing and clerical units. Although opinions have changed throughout the process, the prevailing desire from the unions is amalgamated unions be used for all negotiations, with unions retaining their members.

Health and Wellness Minister Leo Glavine said Wednesday the governments position is that amalgamated unions are only for cases without a clear majority. He was particularly firm in the case of the nursing bargaining unit.

We want to be able to provide nurses with the greatest degree of mobility and we feel that, again, if we retain two (unions) there will be limitations within the way they will operate.

The Dorsey report said only the clerical bargaining unit has a union with a proper majority, in that case the NSGEU. That union has said it would be willing to wave that majority in favour of an amalgamated bargaining unit if it means unions can keep their respective members.

Glavine isnt interested in that option.

If theres a clear majority and if thats the way the bargaining agent can be determined, then thats absolutely the direction that we would go.

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Health-care unions grapple with bargaining report

New study finds 8 genetic 'errors' that cause aging of brain

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NEW DELHI: A global team of about 300 scientists studied over 30,000 brain scans of people from 33 countries and found that eight common genetic mutations are behind the aging of brain. This was the largest collaborative study of the brain to date and its findings could lead to targeted therapies and interventions for Alzheimer's disease, autism and other neurological conditions.

The study known as the Enhancing Neuro Imaging Genetics through Meta Analysis (ENIGMA) Network was led by researchers from the Keck School of Medicine of the University of Southern California (USC) and involved 190 institutions. The findings are published on Jan 21 in Nature. This is the first high-profile study since the National Institutes of Health (NIH) of the US launched its Big Data to Knowledge (BD2K) centers of excellence in 2014.

"ENIGMA's scientists screen brain scans and genomes worldwide for factors that help or harm the brainthis crowd-sourcing and sheer wealth of data gives us the power to crack the brain's genetic code," said Paul Thompson, professor at Keck School of Medicine and principal investigator of ENIGMA. "Our global team discovered eight genes that may erode or boost brain tissue in people worldwide. Any change in those genes appears to alter your mental bank account or brain reserve by 2 or 3 percent. The discovery will guide research into more personalized medical treatments for Alzheimer's, autism, depression and other disorders."

The study could help identify people who would most benefit from new drugs designed to save brain cells, but more research is necessary to determine if the genetic mutations are implicated in disease.

The ENIGMA researchers screened millions of "spelling differences" in the genetic code to see which ones affected the size of key parts of the brain in magnetic resonance images (MRIs) from 30,717 individuals. The MRI analysis focused on genetic data from seven regions of the brain that coordinate movement, learning, memory and motivation. The group identified eight genetic variants associated with decreased brain volume, several found in over one-fifth of the world's population. People who carry one of those eight mutations had, on average, smaller brain regions than brains without a mutation but of comparable age; some of the genes are implicated in cancer and mental illness.

In October 2014, the NIH invested nearly $32 million in its Big Data Initiative, creating 12 research hubs across the United States to improve the utility of biomedical data. USC's two BD2K centers of excellence, including ENIGMA, were awarded a total of $23 million over four years.

"The ENIGMA Center's work uses vast datasets as engines of biomedical discovery; it shows how each individual's genetic blueprint shapes the human brain," said Philip Bourne, Ph.D., associate director for data science at the NIH. "This 'Big Data' alliance shows what the NIH Big Data to Knowledge (BD2K) Program envisions achieving with our 12 Centers of Excellence for Big Data Computing."

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Investigator Offers Lessons From Precision Medicine's Cancer Debacle

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The endeavor known as precision medicine, which Obama singled out in his State of the Union Address, may sound futuristic, but its been around long enough for people to have screwed it up, and badly. One of the worst medical scandals this century started with cancer researchers at Duke promising something that sounded a little too good to be true and ended with retracted papers, dead patients and lawsuits.

But precision medicine is obviously moving forward. To learn more about it, and what lessons the past has to offer, I caught up with Keith Baggerly, whose dogged investigations uncovered the problem with the Duke project. Baggerly is a professor in the Department of Bioinformatics and Computational Biology and Division of Quantitative Sciences at UT MD Anderson Cancer Center. (He is also a witness in a pending lawsuit filed by patients and their families.)

Though precision medicine has different meanings, medical researchers tend to use that term or personalized medicine to refer to the use of individual DNA differences in tailoring treatments to patients. The strategy is being driven by advances in the ability to quickly and cheaply read the sequences of code characters in DNA and by the growing use of big data to find patterns. As described in this Philadelphia Inquirer story, a number of big data cancer initiatives are gathering momentum.

The dream of precision medicine has been particularly tantalizing for cancer treatment, since cancer cells are just ordinary cells with broken DNA mutations that change the cells instructions and cause them to run amok.

And so, in 2006, cancer researchers around the word took notice when a team led by Dr. Anil Potti at Duke claimed in the prestigious journal Nature Medicine that theyd created a highly complex mathematical system that could assess a given patients tumor and determine from its genetic make-up exactly which drugs would give that patient the best odds of survival. While investigations have revealed fraud on the part of Anil Potti, many other people made mistakes in ignoring whistle blowers and allowing the technique to be used on cancer patients in a clinical trial.

While some avenues of precision medicine could lead to new, prohibitively expensive drugs used for rare subsets of patient, the Duke technique promised to chart the best course among existing treatments said Baggerly.

It would be based on the DNA in individual patients tumors. And it didnt just apply to one kind of cancer but to cancers across the board. Instead of telling a patient there was a 70% chance a drug would work to kill her tumor, he said, they could find out ahead of time if she was in the other 30% and prescribe an alternative course of treatment.

Doctors were excited and thought if the system worked, they owed it to their own patients to adopt a form of it, he said. Several groups asked Baggerly to look into it. One danger with the approach, he said, was that it was impossible to know how the technique worked. The data were so big they were measuring thousands of things per patient and there was this perception that the analysis of such data sets would be complex, he said. In most medical tests, theres some understanding of how they work. Thats true in some of the early advances in precision medicine. In some cases of melanoma, for example, theres a break in a particular gene called BRAF, and drugs that target cells with that broken gene. Theres a mechanistic understanding of how it all works.

But with the Duke project, he said, nobody has a good intuition of what 50 or 60 things are doing at once. And so there was no way for intuition to tell anyone whether it worked at all. When Baggerly started to re-analyze how the Duke researchers created the system in the first place, it didnt work. Was he using the system wrong or was there something wrong with the system?

As he investigated further, he found egregious errors that should have prevented it from working. The team had relied on cancer cell samples that had various degrees of resistance to an array of drugs. Those had been mislabeled. Some were reversed, so that the cells that were most resistant were labelled as the least.

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Investigator Offers Lessons From Precision Medicine's Cancer Debacle