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Government needs to adopt a share first mentality for departmental data. Its easy exchange should be the default, not the arduous and exceptional result of lengthy administrative and legal battles to pry data from legacy computer systems and siloed departments.

Departments within a single government entity should be able to freely use data that’s been scrubbed of sensitive personal information, although clear policies concerning the process for anonymizing the information, as well as how long and under what conditions it will be archived, are necessary.

Unfortunately, concerns about exchanging sensitive personal information, particularly as it relates to human services or student data governed by such federal privacy laws as the Health Insurance Portability and Protection Act and the Family Educational Rights and Privacy Act, too often override the free exchange of information. My involvement in these areas, even as a mayor or deputy mayor over the last two decades, has always been somewhere between frustrating and excruciating. Information that would actually help a client often goes unused due to obstacles more rooted in folklore than in law.

A data-sharing program in Missouri, which includes the departments of Health and Senior Services, Mental Health, and Social Services, stands as one example of how effective data sharing allows for improved delivery of care and saving of taxpayer dollars. Hospital use by clients of the state’s Medicaid program fell by 20 percent as of last year, and emergency room visits fell by 12 percent. The decline in emergency room visits alone saves the state $8 million annually. Data sharing accounts for much of the credit for these efficiencies.

The sharing of health data, in particular, often needs a legal framework that both allows access that meets individual departments’ needs and ensures compliance with privacy laws and regulations. Minneapolis utilizes a streamlined process that makes legal resources available specifically for these kinds of discussions. The city clerk’s office and representatives from individual departments work with the city’s legal counsel to vet data as necessary and set any legally mandated boundaries. This city’s open-data policy encourages all other types of data to be open automatically, limiting complex legal discussions to an as-needed basis.

The resulting project equipped officials with data analytics that allowed them to identify populations with the highest risk factors for infant mortality and target preventive strategies, including referring mothers who had missed prenatal appointments because they could not find rides to public transportation resources.

Opening up data across departments by default facilitates a comprehensive, ongoing set of collaborative discoveries that are not slowed by needless negotiations that create transaction friction. Whether it is done by running data through a dedicated team at the Minneapolis clerk’s office on an as-needed basis or a governor calling in counsel to mediate, as in Indiana, there are strategies aplenty for governments to navigate confidentiality laws and open up departmental data.

In addition, federal privacy laws in many cases are less restrictive than imagined by state or local officials who often act in unrealistic fear of the consequences of a misstep. In March, the U.S. Department of Education released a manual with guidance about sharing student data while maintaining privacy. It breaks down some of the myths about the Family Educational Rights and Privacy Act, including the perception that it effectively prevents most data sharing. The manual also proposes several strategies, including depersonalization of data, so that it can be legally shared, and it highlights the ability of data sharing to help schools better serve students.

A comprehensive approach to data sharing must include policy transparency that enhances trust and reduces the chances of future embarrassment. The benefits of data-driven governance are well worth the time it takes to explain the process to the public. But these benefits can only be realized with an open first approach, effective and efficient anonymization practices, and a problem-solving legal adviser with the authority to make decisions and overcome misperceptions about legal restrictions.

In the end, the risks that come from not sharing data across a governmental enterprise greatly exceed the risks of finding ways to use the data to provide more efficient and effective services. The default setting should be the open one.

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What can be done when the body launches an immune attack against its own tissue? The autoimmune disease multiple sclerosis is the most common disabling neurological condition to affect young adults, with over 85,000 people affected in the UK, over 250,000 in the USA, and about 2.5 million people worldwide. Multiple sclerosis occurs when the protective sheath around nerve fibres in the central nervous system, called myelin, is damaged. Depending on the part affected, this leads to disturbances of vision, movement, sensation and basic bodily functions such as bladder control.

Researchers at Cambridge have pioneered the use of monoclonal antibodies to identify an effective treatment for multiple sclerosis. Antibodies provide a natural defence mechanism against invading foreign substances. In the 1980s, Nobel Prizewinning research at the Laboratory of Molecular Biology in Cambridge showed that monoclonal antibodies, designed to target specific antigens, could be produced in almost unlimited quantities. Researchers from the Department of Pathology seized on this discovery and went a step further to create ‘humanised’ monoclonal antibodies for use as medicines. The first, Campath-1H, went on to be developed as a treatment for chronic lymphatic leukaemia.

A team at the Department of Clinical Neurosciences entered this area of research in 1991, and has since continued to study Campath-1H by painstakingly investigating its effects in multiple sclerosis. Building up from single case studies in individual patients, a large Phase II international multi-centre trial was completed in 2007. Interim results at the end of two years were announced in September 2006, and confirmed what the Cambridge-based investigators had recognised for several years.

Given early in the course of relapsing-remitting multiple sclerosis, Campath-1H causes a significant reduction in the occurrence of new episodes – by more than 90% in this trial. Campath-1H appears to stop the development of multiple sclerosis in its tracks, by inhibiting new tissue injury in the central nervous system. Remarkably, these long-term effects are achieved following only one week of exposure to Campath-1H every 12-18 months. But as with all potential new advances, treatment is not uncomplicated. Surprisingly, in this context, although the autoimmune process of multiple sclerosis seems to be suppressed, a range of other conditions – also autoimmune in their mechanisms – emerge as a complication of treatment; nevertheless the patients still consider the benefits of Campath-1H to outweigh the risks of these treatable disorders. Phase III studies of alemtuzumab (as Campath-1H is now known) are due to be launched in 2007, highlighting how coordinated and interactive research within a university environment can lead to the development of effective clinical treatments.

Cambridge researchers have simultaneously been exploring other avenues of potential therapy for patients with multiple sclerosis, by developing techniques that may enable the brain to repair damaged myelin and nerve cells itself. Using adult stem cells, which are derived from a patient’s own tissues – not necessarily of brain origin – scientists at the Cambridge Centre for Brain Repair (Department of Clinical Neurosciences) have recently begun a MRC funded trial into the effects of autologous adult bone marrow stem cells in patients with multiple sclerosis.

While recent changes in the patterns of obesity in the population are certainly driven by environmental changes, the heritability of obesity is extremely strong. Thus, identical twins who are brought up in different families, will usually have very similar amounts, and distribution, of body fat in adult life, bearing little resemblance to the families into which they were adopted.

Researchers at the Institute of Metabolic Science have played a world-leading role in identifying genes that can influence human body weight. By focusing on a cohort of children with extreme obesity from an early age, they have discovered a number of gene mutations that lead directly to obesity. Thus far, all of the genes discovered have had their normal function in the hypothalamus, the area of the brain concerned with control of appetite and energy expenditure. These genes have been shown to influence the drive to eat, as well as feeding behaviour. In particular, one genetic defect, though rare, is dramatically curable with a daily injection of a recombinant protein called leptin. This condition is a graphic demonstration that obesity in humans can be purely biologically driven and amenable to mechanism-based therapy. Researchers in the Department of Pharmacology study hypothalamic anatomy and function in an effort to determine how defects in neurocircuitry lead to excess food consumption beyond metabolic need. In particular, hypothalamic neurons – both in isolation and inside their native neural networks – are assessed to explore how they generate their electrical signals, how these signals are communicated to other brain areas, and how they are altered by physiological and pharmacological stimuli.

Another obesity disorder, known as melanocortin 4 receptor deficiency, is one of the most common Mendelian disorders in humans. It is present in 5- 6% of severely obese children and 0.5- 1% of obese adults. Remarkably, the functional properties of the mutant receptor in vitro can predict spontaneous food intake behaviour at a test meal in individuals carrying these genetic defects. Further research at Cambridge has also clearly implicated the neurotrophin system in the regulation of human appetite and body weight. Collaborative research with the MRC Epidemiology Unit in Cambridge and the Sanger Institute at Hinxton is currently exploring the genetic basis of more common forms of obesity in the population, using large-scale population resources and high throughput genomics combined with expertise in functional biology.

A programme of research sponsored by the Woco Foundation has brought researchers from the Institute of Metabolic Science and the Department of Psychiatry together to explore the biology underlying higher cognitive processes involved in food seeking behaviour. Using a combination of psychometric and functional imaging studies applied to individuals with known genetic lesions in the appetitive pathways, Cambridge scientists are beginning to gain novel and exciting insights into the interactions between the homeostatic and hedonic control of food intake.

Degenerative brain diseases have an enormous impact on our aging society. Alzheimer’s disease progressively robs its victims of their memory. Parkinson’s disease leads to impairments in movement. Frontotemporal dementia causes bewildering changes in a person’s thoughts and behaviour. Huntington’s disease painstakingly deprives a person of their ability to walk, talk, think and reason, often as early as in their mid 30s and 40s.

In all of these degenerative brain diseases, the time from the onset of symptoms until death can be as many as ten or twenty years, with many sufferers’ lives characterised by a total loss of independence in their final years. The staggering emotional toll that these diseases have on their victims and their families, as well as the economic cost to society, has led neuroscientists all over the world to strive to identify effective prevention and treatment strategies.

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The genetic codes of mice, chimpanzees and humans all share remarkable similarities. Ninety-nine percent of mouse genes match a sequence in the human genome. So what makes the three species so different? Clearly the complexity of the genome lies in how the genes interact and are regulated. Understanding longterm changes in gene regulation, and especially how they occur after birth, is critical in determining the impact that nutrition and other environmental factors have on healthy development and adult life. Moreover, since most of the development of the human brain occurs after birth, there is considerable interest in trying to identify how social and environmental changes can affect brain functioning and lead to alterations in gene expression that span across generations.

Epigenetics is the study of how a set of reversible heritable changes in the functioning of a gene can occur without any alterations to the DNA sequence. These changes may be induced spontaneously, in response to environmental factors, or in response to the presence of a particular gene. Studies of animal behaviour have shown that the offspring of a mother with good nurturing skills are more likely to be good parents themselves. Importantly, well-nurtured animals show long-term brain changes, especially in an area called the hippocampus, where genes that respond to stress are silenced in the presence of good mothering. This epigenetic effect is passed on to the next generation and continues until the cycle of good mothering is broken.

The contribution of genetics to the understanding of cognition and psychiatric disorders has tended to focus on gene polymorphisms. However, although there are increasing numbers of genetic polymorphisms under investigation, they are still unable to account for much of the variance seen in many psychiatric illnesses. In contrast, gene-environment interactions can account for much more of the aetiology of psychiatric disorders. For example, schizophrenia is only 50% concordant in genetically identical (monozygotic) twins, while the severity of different ‘life-events’ is known to predispose some people to certain psychiatric disorders. It is now established in animal and human studies that some environmental events can induce long-term developmental changes in chromatin structure through various mechanisms such as histone de-acetylation and DNA methylation of non-coding sequences, which produce long-term silencing of transcription. Since most human brain development occurs postnatally, the brain more than any other organ is under strong social and environmental influences that can have long-lasting effects on brain function and wellbeing.

The study of epigenetic marks on chromosomes was pioneered in Cambridge, with studies of genomic imprinting and gene expression. This type of regulation is unique to mammals, and it may play an important role in brain development and evolution. Cambridge has fostered a strong multi-disciplinary approach to epigenetics, especially in terms of its relevance to neuroscience. Currently, researchers from the Gurdon Institute, Physiology, Development & Neuroscience, and the Department of Zoology, in collaboration with the Babraham Institute, are undertaking complex functional studies on imprinted genes for brain development, brain evolution and behaviour. The aim of this exciting research is to have a greater understanding of foetal programming and postnatal social influences on well-being.

http://www.neuroscience.cam.ac.uk/research/cameos/GeneticBrain.php

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