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Genetics Arkive











New Research Develops New Risk Score That Is Far More Effective for Diabetes Diagnosis



|| January 21: 2019: University of Exeter News || ά. A new way of screening babies and adults for future risk of Type One Diabetes will be much more effective at identifying the condition than the current methods, new research has concluded. Researchers at the University of Exeter and the Pacific Northwest Research Institute in Seattle have developed a new risk score, which takes into account detailed genetic information known to increase the chances of Type One Diabetes.

This could be used to help identity babies at highest risk of developing the condition in the future. The score, may, also, be used at the time of Diabetes diagnosis to help decide, if, someone has Type One or Type Two Diabetes, which need very different treatments. In a study published on Thursday, January 17 in Diabetes Care, the research team found that their new risk score, the T1DGRS2, which uses detailed analysis of key regions of the genome, was nearly twice as efficient at identifying babies at high risk of Type One Diabetes as existing methods, which use more simplistic measures.

The research, funded by Diabetes UK, found the new test was, also, better at predicting Type One Diabetes in adults in the general population. The Senior Author of the research Dr Richard Oram, said, "Prediction of what diseases we, might, get in the future is an important area and Type One Diabetes has a strong genetic element, that we are now able to measure very well.

Measurement of the Type One Diabetes genetic risk score could help predict who will develop the condition from early life could help with research into potential early life interventions and with classifying diabetes correctly at diagnosis."

To develop the test, the researchers analysed genetic variation and gene interactions across the entire genome in 6,581 people with Type One Diabetes in the Type One Diabetes Genetics Consortium. They compared that to 9,247 control participants. This helped them incorporate all known and recently-discovered genetic elements, that can indicate Type One Diabetes. They, then, conducted simulations to see how their test compared to current genetic methods of diagnosis and screening.

Type One Diabetes develops when the body’s own immune system attacks insulin-producing beta cells in the pancreas. The immune attack, usually, begins several years before the symptoms of Type One Diabetes appear. Being able to identify who’s will develop the condition before its onset could help parents and doctors identify the condition before it becomes severe and help the development of effective treatments to prevent the disease occurring.

Current methods of early diagnosis involve measuring of islet auto-antibodies, proteins in the blood, indicating beta cell destruction. However, monitoring auto-antibodies is expensive and difficult in young children. The Exeter team recently discovered that half of all cases of Type One Diabetes develop in adulthood and can, often, be misdiagnosed. But the new risk score can help distinguish between Type One and Type Two Diabetes, helping healthcare professionals to make the right diagnosis.

Co-author Dr William Hagopian, from the Pacific Northwest Research Institute in Seattle, said, ‘’Gathering all this genetic information together allows the test to perform better. This makes prediction of Type One Diabetes among all children much more affordable in public health settings. Parents can be warned to watch for early symptoms to avoid hospitalisation for life-threatening complications. Kids with the greatest future risk can get access to research trials to develop ways to delay or prevent progression to clinical diabetes."

Ms Anna Morris, the Assistant Director of Research Strategy and Partnership at Diabetes UK, said, "It's exciting to see the power of genetics being harnessed to help predict who might develop Type One Diabetes in the future, particularly, from a young age. If, successful, this approach could help to reduce someone's risk of being misdiagnosed or developing complications during diagnosis.

In the future, this research could, also, open up new insights into what could be done to stop Type One Diabetes from progressing."

The Paper: Development and Standardisation of an Improved Type One Diabetes Genetic Risk Score for Use in Newborn Screening and Incident Diagnosis: Published in Diabetes Care: Seth A. Sharp, Stephen S. Rich, Andrew R. Wood, Samuel E. Jones, Robin N. Beaumont, James W. Harrison, Darius A. Schneider, Jonathan M. Locke, Jess Tyrrell, Michael N. Weedon, William A. Hagopian,and Richard A. Oramω.

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New Research Gains New Insights Into How Genes are Activated


















|| January 14: 2019: Karolinska Institutet News || ά. In a study, published in Nature, researchers at Karolinska Institutet present a new method for analysing how instructions in the genome control how our genes are activated in individual cells. The results give new insights into how the genome encodes for its own use, which increases our basic understanding of how genes are activated in different types of cell in the body in both good and ill health.

Almost, all cells in the body have the same set of DNA and can, in principle, become any kind of cell. What distinguishes the cells is the way, in which, the genes in our DNA are used. All the DNA in a cell is called the genome, our genetic material but, only, a very small part of a human’s genome consists of genes. Instead, extensive areas of the genome are used to regulate when and in which cells nearby genes are active. These regions contain ‘enhancers’ and the gene sequences located right next to the genes, ‘promoters’.

In a diseased body, these regions are, often, mutated and a deeper understanding of the function of these regions would bring light to the course of the disease in question. In order for a gene to be used, it, must be, translated from DNA to copies of RNA. RNA is similar to DNA but its structure is slightly different and it can be used as a template for producing protein. The translation of DNA to RNA is called transcription.

There are still many things, that are not clearly understood about how transcription takes place and how it is regulated. For example, if, a gene is used by a cell, the gene’s DNA is not translated to RNA all the time. That would require too much energy. Instead, the transcription takes places in bursts, when the transcription machinery is recruited and several RNA molecules are produced in a short time. The transcription of each gene can be characterised on the basis of the kinetics of this process, that is, the frequency of the bursts and the number of molecules produced during the bursts.

”It used to be difficult to measure the kinetics and how many RNA molecules had been produced by a gene in an individual cell. The methods, that have existed up to now were only able to follow a few genes at a time. Moreover, mammals have two sets of, almost, all their genes so it has been difficult to distinguish between the RNA, that comes from the mother’s version of the gene and that from the father’s version.” says Professor Rickard Sandberg, at the Department of Cell and Molecular Biology at Karolinska Institutet, who has led the study in question.

In the study, the researchers used a method, which they had developed themselves to sequence RNA in individual cells. The method makes it possible to measure the number of RNA molecules for, almost, all the genes used in a cell.

The researchers sequenced cells of connective tissue and embryonal stem cells from a crossbreed of two distantly related mice. With the help of the natural variation found in the genes of the two different types of mouse, the researchers were able to distinguish between the sequenced RNA from the mother’s and the father’s versions of the gene and in that way measure the transcription exactly. They, then, used a mathematical model to make estimations, for each of the version, of how often the gene is transcribed and how much RNA is, then, produced.

”We discovered that enhancers did affect how often a gene was transcribed in the two different cell types but not how many RNA molecules were produced. We, also, found that certain DNA sequences located at the beginning of a gene can influence how much RNA is produced in a burst. In that way, we have begun to chart how the genome encodes for its own use.” says Mr Anton Larsson, the First Author of the study and a doctoral student in Professor Rickard Sandberg’s research group.

”It will be possible to make wide use of our method to chart at a much deeper level how different proteins affect the transcription process.” says Professor Rickard Sandberg.

The research was funded with support from the European Research Council, the Swedish Research Council, the Knut and Alice Wallenberg Foundation and the Vallee Foundation.

The Paper: Genomic encoding of transcriptional burst kinetics: Anton Larsson, Per Johnsson, Michael Hagemann-Jensen, Leonard Hartmanis, Omid R. Faridani, Björn Reinius, Åsa Segerstolpe, Chloe M. Rivera, Bing Ren and Rickard Sandberg: Published in Nature Online January 02: 2018:::ω.

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A Large International Study Discovers 11 New Epilepsy Genes





|| December 18: 2018: University of Eastern Finland News || ά. The results from a new study tripled the number of known genetic associations for Epilepsy and implicated 11 new genes. Epilepsy is a common neurological condition with a controversial past.  The cause was unknown and, often, shrouded in mystery.  We now understand that the cause is largely genetic, however, little is known about the specific genes, responsible for the most common forms of the disorder. 

This is, particularly, important, when we consider that a third of the 65 million patients worldwide will not become seizure free, using current treatment options. To find new Epilepsy genes, a large study was undertaken by more than 150 researchers from multiple centres in the UK, Europe, USA, Brazil, Hong Kong and Australia as part of the International League Against Epilepsy Consortium on Complex Epilepsies. The DNA of more than 15,000 people with the illness was compared to the DNA of 30,000 healthy controls.

The results tripled the number of known genetic associations for Epilepsy and implicated 11 new genes. These genes have a number of different functions in the human body, including, regulating signal transduction between brain cells, converting vitamin-B6 into its active form and controlling expression of genes in the brain.

The researchers found that the majority of current anti-epileptic drugs directly target one or more of the associated genes and identified an additional 166 drugs, that do the same.

These drugs are promising new candidates for Epilepsy therapy as they directly target the genetic basis of the disease. With these findings, the researchers hope that in the future more people with Epilepsy will achieve seizure freedom.

KUH Epilepsy Centre and the University of Eastern Finland were critical to this effort by contributing samples of 422 patients with focal Epilepsy, accurately and clinically diagnosed and with high-quality brain imaging data and samples of 293 controls.

This line of research is continuing as part of an Epilepsy bio-marker study, funded by the Saastamoinen Foundation and led by Professor Reetta Kälviäinen at UEF. The study seeks to identify genetic and other predictors of Epilepsy in order to enable better targeted and more personalised treatments.

For further information contact: Professor Reetta Kälviäinen: Tele: +358 405839249: email: reetta.kalviainen at

The Paper: Genome-wide mega-analysis identifies 16 loci and highlights diverse biological mechanisms in the common epilepsies: The International League Against Epilepsy Consortium on Complex Epilepsies: Published in Nature Communications: Volume 9, Article number: 5269:2018:::ω. 

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For Stories Published in Genetics in Year Gamma Arkive












Life's Laurel Is You In One-Line-Poetry A Heaven-Bound Propagated Ray Of Light Off The Eye Of The Book Of Life: Love For You Are Only Once



Life: You Are The Law The Flow The Glow: In Joys In Hurts You Are The Vine-Songs On The Light-Trellis


























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