Daily Archives: May 2, 2017

Now that scientists have mapped the barley genome, better beer could be the result – Digital Trends

Posted: May 2, 2017 at 10:35 pm

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Now that scientists have mapped the barley genome, better beer could be the result - Digital Trends

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Researchers unravel barley’s genome – food in canada

Posted: at 10:35 pm

Gatersleben, Germany A group of researchers has mapped the entire genome of barley.

Sci-News.com (Science News) reports that the International Barley Sequencing Consortium (IBSC) announced the news in late April.

Barley, says Sci-News.com, is the worlds fourth most important cereal crop after wheat, rice and

Image: ThinkStock

maize. IBSC has published its work in the journal Nature.

Barley, says the story on Sci-News.com April 27, 2017, is cultivated in all temperate regions from the Arctic Circle to the tropics. Its known for its tolerance to cold, drought, alkali and salinity.

Barley is found in breakfast cereals and all-purpose flour and it helps bread rise, says Sci-News.com. Malted barley also gives beer its colour, body, protein and the natural sugars needed for fermentation.

In a statement, the IBSC says the mapping of barleys genome can lead to higher yields, improved pest and disease resistance and enhanced nutritional value.

It will also facilitate the development of new and better barley varieties able to cope with the demands of climate change. It should also help in the fight against cereal crop diseases, which cause millions in losses every year.

Barley, says IBSC, was first cultivated more than 15,000 years ago. It belongs to the Triticeae family, which includes wheat and rye, and that together provides around 30 per cent of the calories consumed worldwide.

In the statement, IBSC writes the sequencing will accelerate research in barley and its close relative wheat. Armed with this information breeders and scientists will be much better placed to deal with the challenge of effectively addressing the food security agenda under the constraints of a rapidly changing environment.

For more on barley and IBSC, click here.

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Researchers unravel barley's genome - food in canada

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UCPEA Classification Salary & Longevity Schedule …

Posted: at 10:35 pm

FY17

Effective July 1, 2016

Click on the Payroll Title for a listing of job titles by level.

Salary Schedule

Longevity Payment

Minimum

Midpoint

Maximum

10 Years Service (25% of full allotment)

15 Years Service (50% of full allotment)

20 Years Service (75% of full allotment)

25 Year Service (100% of full allotment)

$38,769

$52,144

$65,237

$208.50

$417.00

$625.50

$834.00

$39,993

$53,797

$67,598

$215.25

$430.50

$645.75

$861.00

$41,449

$55,762

$70,075

$223.00

$446.00

$669.00

$892.00

$43,076

$57,955

$72,834

$231.75

$463.50

$695.25

$927.00

$46,072

$62,002

$77,930

$248.00

$496.00

$744.00

$992.00

$50,540

$68,039

$85,529

$272.25

$544.50

$816.75

$1,089.00

$55,471

$74,692

$93,913

$298.75

$597.50

$896.25

$1,195.00

$60,578

$81,586

$102,594

$326.25

$652.50

$978.75

$1,305.00

$65,758

$88,582

$111,398

$354.25

$708.50

$1,062.75

$1,417.00

$71,513

$96,349

$121,188

$385.50

$771.00

$1,156.50

$1,542.00

$77,852

$104,901

$131,958

$419.50

$839.00

$1,258.50

$1,678.00

$87,074

$117,332

$147,607

$469.25

$938.50

$1,407.75

$1,877.00

NOTE: As the result of the Board of Trustees approval to extend the current UCPEA contract, the July 1, 2015 salary schedule for the UCPEA bargaining unit will remain in effect for fiscal year 2017 or until such time as a successor agreement is ratified and approved by the Board of Trustees and Legislature, whichever occurs first.

LONGEVITY: Employees in the bargaining unit shall be eligible for longevity increments in accordance with Connecticut General Statutes. The full longevity payment shall be 1.6% of the mid-point of the range according to the salary schedule.

UCP Levels by Job Family

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UCPEA Classification Salary & Longevity Schedule ...

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Stool microbes predict advanced liver disease – Medical Xpress

Posted: at 10:35 pm

May 2, 2017 Credit: CC0 Public Domain

Nonalcoholic fatty liver disease (NAFLD)a condition that can lead to liver cirrhosis and cancerisn't typically detected until it's well advanced. Even then, diagnosis requires an invasive liver biopsy. To detect NAFLD earlier and more easily, researchers in the NAFLD Research Center at University of California San Diego School of Medicine, Human Longevity, Inc. and the J. Craig Venter Institute report that the unique microbial makeup of a patient's stool sampleor gut microbiomecan be used to predict advanced NAFLD with 88 to 94 percent accuracy.

The proof-of-concept study, which involved 135 participants, is published May 2 in Cell Metabolism.

"We estimate that as many as 100 million adults and children in the U.S. may have NAFLD. Determining exactly who has or is at risk for the disease is a critical unmet medical need," said first author Rohit Loomba, MD, professor of medicine in the Division of Gastroenterology, director of the NAFLD Research Center and a faculty member in the Center for Microbiome Innovation at UC San Diego. "There are about 50 new NAFLD drugs in the pipeline, including about five that will likely be approved for use in the next two years. If we are better able to diagnose this condition, we will be better at enrolling the right types of patients in these trials, and ultimately will be better equipped to prevent and treat it."

The precise cause of NAFLD is unknown, but diet and genetics play substantial roles. Up to 50 percent of obese people are believed to have NAFLD. As mounting evidence continues to suggest that the makeup of a person's gut microbiome may influence his or her risk for obesity, Loomba and team began to wonder if the gut microbiome might also be linked to obesity-associated liver disease. If so, they hypothesized that a stool-based "read-out" of what's living in a person's gut might provide insight into his or her NAFLD status.

To answer these questions, Loomba and team examined two different patient groups. The first group included 86 patients with NAFLD, as diagnosed by biopsy. Of these, 72 had mild/moderate NAFLD and 14 had advanced disease. Collaborators at Human Longevity, Inc. sequenced the microbial genes extracted from each participant's stool sample and used that information to determine which species were living where, and the relative abundance of each. The researchers found 37 bacterial species that distinguished mild/moderate NAFLD from advanced disease, allowing them to predict which patients had advanced disease with 93.6 percent accuracy.

The team validated this finding with a second study group that included 16 patients with advanced NAFLD and 33 healthy people as controls. In this case, they found nine bacterial species whose relative numbers allowed them to distinguish NAFLD patients from the healthy volunteers, with 88 percent accuracy. Seven of these bacterial species overlapped with the signature 37 used in the previous group.

There are four main types of bacteria found in the human gut: Firmicutes, Proteobacteria, Bacteroidetes and Actinobacteria. Loomba and team found that patients with advanced NAFLD tend to have more Proteobacteria and fewer Firmicutes in their stool than those with early stage NAFLD. At the species level, one major difference the researchers found was in the abundance of E. colithese bacteria were three-fold more common in advanced NAFLD patients than early stage patients.

"We believe our study sets the stage for a potential stool-based test to detect advanced liver fibrosis based simply on microbial patterns," said senior author Karen E. Nelson, PhD, president of the J. Craig Venter Institute, "or at least help us minimize the number of patients who have to undergo liver biopsies."

While Loomba estimates that a stool-based microbiome diagnostic might cost $1,500 if it were on the market today, he predicts that cost will lower to less than $400 in the next five years due to advances in genomic sequencing and analysis technologies.

While excited, the researchers caution that so far this new diagnostic approach has only been tested in a relatively small patient group at a single, highly specialized medical center. The team is now applying for grant funding to expand their study in a larger cohort across multiple sites. Even if successful, a stool-based test for NAFLD wouldn't be available to patients for at least five years, they said. Loomba also points out that while a distinct set of microbial species may be associated with advanced NAFLD, this study does not suggest that the presence or absence of these microbes causes NAFLD or vice versa.

"We are looking forward to further studies to assess the role, if any, these microbial species play in gut permeability, liver inflammation and cross-talk with other factors to induce liver injury, and ultimately influence disease progression in NAFLD," said study co-author David A. Brenner, MD, vice chancellor of UC San Diego Health Sciences and dean of UC San Diego School of Medicine.

"Understanding the microbiome, just as sequencing the human genome, is one part of the puzzle on human health and disease," said study co-author J. Craig Venter, PhD, co-founder and executive chairman of Human Longevity, Inc. "New technologies, such as machine learning, are allowing for tremendous advances to interpret these data."

Explore further: Many diabetics don't know they have serious liver disease

More information: Rohit Loomba et al, Gut Microbiome-Based Metagenomic Signature for Non-invasive Detection of Advanced Fibrosis in Human Nonalcoholic Fatty Liver Disease, Cell Metabolism (2017). DOI: 10.1016/j.cmet.2017.04.001

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Stool microbes predict advanced liver disease - Medical Xpress

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How Scientists Think CRISPR Will Change Medicine – TIME

Posted: at 10:35 pm

With the advent of CRISPR , a new way to edit DNA, the field of genomic technology has never been more exciting. The implications have yet to be seen, but scientists could theoretically snip out a person's genetic risk for disease. But it's also never been a more anxiety-inducing time. Some experts argue innovations in genomics are moving forward at a pace faster than our ability to parse their potential consequences.

In a panel discussion at Fortune s Brainstorm Health conference in San Diego, scientists discussed the promises and perils of this breakthrough technologysome of which they're already starting to see.

I think CRISPR is a very exciting discovery, said J. Craig Venter, co-founder of the health company Human Longevity, Inc. and one of the first scientists to sequence the human genome. Venter is using genome sequencing as a way to help predict a persons risk for disease and offer more personalized treatment with a physical exam called the Health Nucleus : an eight-hour, $25,000 inside-and-out doctors appointment that includes whole-genome sequencing, high-tech scanning and early diagnostics.

So far the company has sequenced more than 40,000 human genomes. Of the people that complete the Health Nucleus, one in 40 will discover they have a serious cancer they didn't know about, he said.

Yet some experts are skeptical that exhaustive testing always translates to better health. Dr. Eric Topol, founder and director of Scripps Translational Science Institute, called for a more reserved way forward in his remarks at the conference, arguing that too much scanning can lead to more false positive results and potentially unnecessary interventions. We have to prove that doing tests are truly associated with positive outcomes, Topol said. We have to be much more discriminative about the tests that we do.

Some companies are taking a more tempered approach: inexpensive testing that looks for specific genes known to substantially increase a persons risk for disease. Color Genomics, a genetics company that has brought down the cost of genetic testing, focuses on cancer and offers affordable tests for the BRCA1 and BRCA2 genes, which can significantly raise a womans risk for breast and ovarian cancer. It changes the equation in terms of treating disease, said Othman Laraki, co-founder and CEO of Color Genomics.

As for finding and fixing genetic problems well before they even arise? The scientists on the panel agreed that they're not there yet, and that current iterations of CRISPR may not be quite as precise as the hype has claimed. For now, that may be for the best. Editing human embryos with CRISPR should be a long way off, said Venter. Not something we do next week.

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What the Death of the World’s Oldest Human Means for Longevity – Inverse

Posted: at 10:35 pm

The oldest man in the world died on Sunday at his home in Indonesia. Sodimejo, known to many as Mbah Gotho, claimed to be 146 years old. While the Indonesian government only started tracking births in 1900, Sodimejo has identification papers that say he was born in December 1870. And though his age was called into question in 2016, Indonesian authorities have confirmed the validity of his documents. If theyre right, he was the oldest person on record.

This would mean that the oldest human was 24 years older than what we have previously even thought possible for aging. And in a world filled with people obsessed with living forever, people are hungry for the keys to slowing the inexorable process of bodily and mental decay.

Unfortunately, Sodimejo doesnt appear to have had many answers that doctors could bottle. A lifelong smoker, he cited patience and close relationships with loved ones as the keys to his longevity. Nevertheless, besides the whole smoking thing, this is good advice, even if it is a little underwhelming.

But having a positive attitude doesnt seem to sufficiently explain Sodimejos long life. His case, if true, would upend conventional wisdom about human lifespans. So what could account for it?

One possible explanation for why Sodimejo lived from 1870 to 2017 is not totally unique to him: Improvements in public health and sanitation affect everyone. When he was born, most people didnt have electricity, running water, or access to science-based health care. Shortly before he died, though, he spent several days in a modern hospital. This is a huge change from the era of his birth.

The common causes of death during much of Sodimejos life such as water-borne pathogens, tuberculosis, or even infections that settle in minor scrapes are now considered to be almost completely preventable. So while many people who were born around the same time as Sodimejo may have fallen victim to illnesses or accidents that are now treated as routine, he beat the odds for a man born in 1870.

But that doesnt seem to explain his whole situation. Other people in his peer group also dodged preventable diseases before they were curable, so if we choose to explain his long life as beating the odds, we still need another way to explain why he outlived his peers by so long.

In 2016, scientists said that the upper limit for human aging is 115 years old and that this limit is fixed and subject to natural constraints. The matter is far from settled, though; other researchers in the field vigorously disagreed about whether there could be a fixed upper limit to human aging at all. Directly contradicting that study in the same year that it was published, Jeanne Calment, who at the time was the worlds oldest person, died at 122 years old.

Besides, while seemingly irreversible physical changes like slowed mitochondrial regeneration and telomere shortening set in as we age, a fixed limit on aging doesnt seem to make sense in light of average human lifespans that continue to increase each year.

So, the possibility that the limit to human aging does not exist remains. This doesnt mean that all humans will live for a super long time because human illnesses vary in who they affect and are often unpredictable. It could simply mean that Sodimejo is on the far end of the bell curve, where outliers live. If thats the case, then whats to stop others from joining him there? We could be witnessing an era in which the maximum human lifespan simply continues to increase, and not just for the super rich.

Then again, its also entirely possible that Sodimejo wasnt actually 146 years old.

Peter is a writer living in New York. He is preoccupied with Star Wars and memes, but he writes about climate change, chatbots and ants. You may have seen his work in Popular Science, New Scientist and Motherboard.

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Oldest human might have reached 146 or it was a very long con – Next Big Future

Posted: at 10:35 pm

An Indonesian man claimed to be 146 years old the longest living human ever. He died in his village in Central Java.

According to his papers, Sodimedjo, also known as Mbah Ghoto (grandpa Ghoto), was born in December 1870.

But Indonesia only started recording births in 1900 and there have been mistakes before.

Yet officials told the BBC his papers were valid, based on documents he provided and interviews with him. He was taken to hospital on 12 April because of deteriorating health. Six days later he insisted on checking out to return home.

Mbah was an Indonesian Christian man who unverifiably claimed to be the oldest person ever recorded. In May 2010, Solopos reported that enumerators of that years census had recorded his age next birthday as 142, which would make him 19 years older than the official oldest recorded person, Jeanne Calment, who died in 1997. He outlived ten siblings, four wives and all his children. The Liputan 6 website reported that Mbah Gothos estimated age was 140, that he could not remember his date of birth but claimed to remember the construction of a sugar factory built in Sragen in 1880.

Indonesian officials at the local record office confirm the birth date. There is no independent, third-party verification of his claimed age, which is required for the longevity claim to be recognized by record authorities such as Guinness World Records. Robert Young of the Gerontology Research Group said the claimed age was fiction, unbelievable and in the same category as Sasquatch [Bigfoot], the Yeti, and the Loch Ness Monster. The 2010 Liputan 6 story noted others of a similar claimed age including a woman named Maemunah and known as Ambu Unah, supposedly born in 1867, in Cimanuk, Pandeglang Regency.

There are living supercentenarian cases, in descending order of claimed age, with full birth and review dates, have been updated within the past two years, but have not had their claimed age validated by an independent body such as the Gerontology Research Group or Guinness World Records. Only claims over 115 years but under 130 years are included in the list. See longevity myths for claims over 130 years, such as Mbah Gotho.

Maria Lucimar Pereira, is a native of Feij and was born on September 3, 1890. She is of the Kaxinaw ethnic group and lives in Aldeia Grota. She is believed to be 126 and has better documentation than Mbah. Marias claim has not been independently verified.

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The Patients Association: New Report Highlights True Personal and Public Cost of Psoriasis, and Spotlights Variation … – Yahoo Finance

Posted: at 10:34 pm

HARROW, England, May 3, 2017 /PRNewswire/ --

"Research shows that far from being just a skin disease, psoriasis ruins lives - and has the potential to shorten them too." Katherine Murphy, Chief Executive of the Patients Association

Today, Wednesday 3 May 2017, the Patients Association, in partnership with LEO Pharma, released a new report highlighting the debilitating effect psoriasis can have on up to two million people battling the condition in the UK[8] and Ireland[9]. Despite the World Health Organisation (WHO) recognising psoriasis as an area of focus,[10] and recent advancement in treatments, the PSO What? Report underscores the need for improvement in the health and experiences of people living with psoriasis.

(Photo: http://mma.prnewswire.com/media/507020/Katherine_Murphy_The_Patients_Association.jpg )

The PSO What? report, led by the Patients Association in collaboration with the expert PSO What? Taskforce, which brought together patients, healthcare professionals and charities, reinforces that far from being 'just a skin condition', psoriasis is a serious, sometimes lifelong condition impacting emotional and mental wellbeing, as well as physical health[10]. "This new report highlights the need to take action now to address the significant burden psoriasis places on individuals with psoriasis, and inspire those who may have previously given up to take control of their condition, as well as raise the priority of psoriasis care in the health service", said Katherine Murphy, Chief Executive of the Patients Association. "We are therefore asking people to pledge their personal and practical support to drive real change by visiting http://www.PSO-What.com."

She added: "A third of people with psoriasis we surveyed do not regularly visit their GP each year and contrasting healthcare guidelines mean that doctors have no clear direction for when exactly to ask their psoriasis patients back into the consulting room. We are therefore using this report to ask that every individual with psoriasis has the opportunity to discuss their care with a healthcare practitioner, and undergo screening for associated conditions at regular reviews, at least once a year. "

Alongside the personal toll of psoriasis, figures show the disease places a heavy burden on the health service - with nearly a quarter of the population having sought a GP consultation on skin matters in England and Wales; up to 5% on psoriasis alone.[5],[6] Despite this, some GPs in the UK have only received five days of undergraduate dermatological training.[7] Inevitably, there is a risk that these practitioners may not be afforded the depth of knowledge required to treat psoriasis specifically. The problem is exacerbated due to the lack of consultants to support GPs, with only 650 dermatologists to provide more specialist care.[6] This is particularly concerning given that people with psoriasis are at risk of developing other serious associated conditions,[10] including psoriatic arthritis,[10] cardiovascular disease,[4],[11],[12],[13] inflammatory bowel disease (IBD)[10], liver disease[10], complications with vision[14] and some cancers.[3],[15]

The survey conducted as part of the PSO What? initiative also reveals that the condition negatively affects the quality of life of 93% of the people surveyed and that less than half (45%) feel well supported by their doctor.[1] Jacqueline McCallum from Hertfordshire was diagnosed with psoriasis over 30 years ago: "Psoriasis is a horrible disease to live with on a daily basis. In the past it has made me depressed and affected my self-esteem, which has limited my personal and professional life. However, I've regularly struggled to even get a GP appointment to discuss my psoriasis because the receptionists do not think it is a serious enough condition, and do not understand the significant impact it has on my wider health and wellbeing. They see my psoriasis plaques, but not me."

Dr Angelika Razzaque, GPwSI Dermatology and Vice Chair of the Primary Care Dermatology Society (PCDS), comments: "The onus is on the GP community to continually review how we're treating the psoriasis itself, and to look beyond the skin to screen for associated complications such as depression, cardiovascular disease and diabetes. Regular reviews, at least annually, can safeguard against further psoriasis complications. Psoriasis affects everyone differently, but people can live full and happy lives providing they regularly see their doctor, and medical professionals are adequately trained to offer an effective and personalised approach to treatment. My advice to patients is not to give up, there is always a way to get help."

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Dr Anthony Bewley, Consultant Dermatologist at Whipps Cross and St Bart's NHS Trust comments, "We, as healthcare professionals need to move far away from the misconception that psoriasis is 'just a skin condition'. The PSO What? Taskforce invites patients to demand more from their health care professionals, to be more empowered, and to make sure that healthcare professionals do not undermine the experience of living with psoriasis. There needs to be a true dialogue between a patient and their doctor in order to achieve the best outcomes for them individually; each person has different needs, experiences and expectations of what they want in order to live well.'

The cost of psoriasis to the UK economy is substantial, coming in at over 1.07 billion in lost productivity alone, while figures show that just a 10% reduction in sickness absence due to psoriasis, would deliver a 50 million boost.[16] Dr Angelika Razzaque continues: "By 'treating to prevent', we're reducing the risk of life-limiting complications for the patient, helping to tackle sickness absence in the workplace, and reducing the potential burden on the health system later down the line."

PSO What? will you do differently? To find out more visit the PSO What? website (http://www.PSO-What.com) and pledge to do one thing differently to help make a difference for the nearly 2 million people living with psoriasis in the UK[8] and Ireland.[9]

Notes to the editor

About the PSO What? Initiative

The PSO What? initiative is a partnership programme led by The Patients Association and LEO Pharma, in collaboration with the expert PSO What? Taskforce. LEO Pharma has provided core funding, editorial input and undertaken survey-based research to support the development of the PSO What? Report.

The PSO What? Taskforce is a multidisciplinary group representing people living with psoriasis, psoriasis advocacy and professional groups, and healthcare professionals. A full list of Taskforce members can be found in the report.

The Taskforce met in 2016 to discuss the challenges currently facing people living with psoriasis as well as those who care and commission services for them, including key themes and issues around which change could be effected for the benefit of people living with the condition. The pledge of each member of the Taskforce is to continue to have a voice and drive positive change for psoriasis and develop resources and programmes to facilitate this.

As part of the PSO What? initiative a survey was conducted amongst psoriasis sufferers and healthcare professionals in the UK and Ireland. The survey results and further desk research helped inform some of the key findings of the PSO What? Report. These include:

Psychological impact of psoriasis

Standards of care

Impact on employment

To read the full Report visit the PSO What? website: http://www.PSO-What.com

References

1. Data on file. LEO Pharma. DERM-004 MAR 2017

2. NHS Choices. Psoriatic Arthritis Overview. Available at: http://www.nhs.uk/conditions/psoriatic-arthritis/Pages/Introduction.aspx.Last accessed April 2017

3. Pouplard C, Brenaut E, Horreau C, et al. Risk of cancer in psoriasis: a systematic review and meta-analysis of epidemiological studies. JEADV. 2013;27(Suppl 3):36-46.

4. Gelfand JM, Niemann AL, Shin DB, et al. Risk of myocardial infarction in patients with psoriasis. JAMA. 2016;296:1735-41

5. King's Fund. How can dermatology services meet current and future patient needs while ensuring that quality of care is not compromised and that access is equitable across the UK? Source report, 7 March 2014.

6. Schofield JK, Grindlay D, Williams HC. Skin conditions in the UK: a health needs assessment. 2009. Centre for Evidence Based Dermatology, University of Nottingham.

7. Primary Care Commissioning. Quality standards for dermatology. Providing the right care for people with skin conditions. July 2011. Available at: https://www.bad.org.uk/shared/get-file.ashx?itemtype=document&id=795

8. Mental Health Foundation, Psoriasis Association. See psoriasis: look deeper. Recognising the life impact of psoriasis. 2012.

9. Irish Skin Foundation. Securing the future for people with skin disease. Submission to Oireachtas Committee on the Future of Healthcare (Dil ireann). August 2016.

10. World Health Organization. Global report on psoriasis. 2016. World Health Organization. Available at: http://apps.who.int/iris/bitstream/10665/204417/1/9789241565189_eng.pdf. Last accessed January 2017.

11. Ahlehoff O, Gislason GH, Jorgensen CH, et al. Psoriasis and risk of atrial fibrillation and ischaemic stroke: a Danish nationwide cohort study. Eur Heart J. 2012;33:2054-64.

12. Lowes MA, Suarez-Farinas M, Kreuger JG. Immunology of psoriasis. Ann Rev Immunol. 2014;32:227-35.

13. Langan SM, Seminara NM, Shin DB, et al. Prevalence of metabolic syndrome in patients with psoriasis: a population-based study in the United Kingdom. J Invest Dermatol.

14. Fraga NA, Oliveira MF, Follador I, et al. Psoriasis and uveitis: a literature review. An Bras Dermatol. 2012;87:877-83.

15. Lebwohl M. Psoriasis. Lancet. 2003;361:1197-204.

16. Bajorek Z, Hind A, Bevan S. The impact of long term conditions on employment and the wider UK economy. 2016.

17. Kurd SK, TROXE B, Crits-Christoph P, Gelfand JM. The risk of depression, anxiety and suicidality in patients with psoriasis: a population-based cohort study. Ann Dermatol. 2019;146:891-5

18. Gupta MA, Schork NJ, Gupta AK. Suicidal ideation in psoriasis. Int J Dermatol. 1993;32:188-90.

19. Changing Faces. Report highlights stigma faced by psoriasis patients. Available at: https://www.changingfaces.org.uk/report-highlights-stigma-faced-psoriasis-patients. Last accessed March 2017

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The Patients Association: New Report Highlights True Personal and Public Cost of Psoriasis, and Spotlights Variation ... - Yahoo Finance

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This Founder is using Synbio to Revolutionize Genetic Medicine – Labiotech.eu (blog)

Posted: at 10:34 pm

Oxford Genetics founder and CEO Ryan Cawood told me about his companys improvements to DNA design for better biologicals.

Last month at Synbiobeta, I caught up with Ryan Cawood, who created one of the most successful synthetic biology companies around, Oxford Genetics. Our direction actually took off from this conference, he told me. We saw that the cost of DNA synthesis is going to be driven down, so this was not a market for us to compete in.

Instead of focusing on making DNA engineering cheaper, Cawood decided to explore how to improve the quality of its products. Specific inspiration came in the form of frustration as he was trying to finish his PhD in genetics at Oxford University

I was making gene therapy plasmids, and they were increasingly hard to test because we just couldnt make them. They were 50 to 100 kilobases for different viruses with no standardization one section camefrom Spain, one section from the US, and one from the back of the freezerit was a sort of genetic car crash, as my PI, Len Seymour, called it.

As a company, we set out to improve this by focusing on DNA design we now help other companies working on therapeutics develop them better with SnapFast, a lego-like core DNA system.

In 2011, I formed the company by taking out bank loan. Then I negotiated a lab bench from local company in return for gene engineering for them. Finally, I built a website. Ive since obtained seven grants and connected with solid investors. Mercia Technologies has invested three times now the first time was in 2013 and on this next round, someone else will probably come in as well.

Len, my former lab PI, is still on the board as one of the cofounders. He was actually involved in founding two biotech companies before hand, one for oncolytic viruses (PsiOxus Therapeutics) and one for protein expression (The Native Antigen Company).

Cawoods lightning talk at Synbiobeta: fromsynthetic biology, Oxford Genetics is building up to improve biological drugsto reachpersonalised versions.

Well, our trajectory and plan was to build better DNA tech for the design and synthesis to discover and manufacture biologicals better. Fundamentally, youre always trying to build a tool to develop these better.

What Id like to see from the field is a major advancement of human therapeutics. There are four major challenges in biological development that were working to address: discovery, design, production and delivery basically every step.

We think Snapfast DNA will improve all of them because DNA is an integral part of each. So, we can absolutely use synbio to improve cell and gene therapies and biologics.

People who work in the area think of synbio as making things in algae, or making new genetic circuits etc, but dont necessarily see consequences for human health. The field has a huge role to play in tying the genetics of an individual human to a therapeutic treatment based on DNA. At the moment, there is no such pairing were a long way from that, but with synbio well get there.

We take a sort of blunt hammer approach now: its very inefficient therapeutically, and its a very inefficient use of government funds. By funding a better understanding of people, youll see significant gains intreatmentefficiencies.

The current approach is far too retrospective at the moment: we give a drug and then try to figure out why it worked in some people afterwards, or we just carry on giving it everyone knowing only a few people will benefit, in the future I hope we can predict efficacy and act upon that calculation.

Im still very much motivated by the therapeutic side of synthetic biology. Not everyone working at the company has a background in human genetics some come from working on archaea, but they all are oriented towards working towards therapeutics. Even my PA has first class degree in genetics.

DNA foundries are all the rage in synbio now, but we were much more interested in biology than physical manufacture that is, were much more focused on end goal versus how you get there. This thinking has changed the company a lot: instead of just making things, were designing things.

Images from Oxford Genetics,author at Synbiobeta, 04 April 2017, Mercia, & Sergei Drozd, Saibarakova Ilona /shutterstock.com

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Smoking-related heart disease tied to effects of a single gene – Medical Xpress

Posted: at 10:33 pm

May 1, 2017 Credit: Vera Kratochvil/public domain

Researchers have found a genetic explanation for how smoking can lead to coronary heart disease (CHD). Many people have a protective gene type that reduces levels of an enzyme connected to artery-clogging fatty plaques and CHD. However, in people carrying this gene, smoking counteracts the protective effect.

"Our finding suggest that interventions to inhibit this enzyme would be particularly beneficial for smokers, and they may also prove useful for anyone at heightened risk of coronary heart disease," said study leader Muredach P. Reilly, MBBCH, MSCE, the Herbert and Florence Irving Professor of Medicine (in Cardiology) and director of the Irving Institute for Clinical and Translational Research at Columbia University Medical Center (CUMC).

The study, the largest of its kind, was published online today in the journal Circulation.

Cigarette smoking is known to cause about one in five cases of CHD, and is linked to approximately 1.6 million deaths worldwide each year. But the precise mechanisms by which smoking leads to CHD has not been clear. To learn more about how genetics affect the interplay between smoking and heart disease, the researchers pooled genetic data on more than 140,000 people from 29 previous studies. They analyzed 45 small regions of the genome that have been previously associated with a heightened risk of CHD. They hypothesized that for some of these regions, the associated heart risk would be different in smokers than in non-smokers.

The analysis showed that a change in a single DNA "letter" on chromosome 15, near the gene that expresses an enzyme (ADAMTS7) produced in blood vessels, was associated with a 12 percent reduction in heart risk in non-smokers. However, smokers with this same variation had only a 5 percent lower risk of CHDreducing by over half the protective effect of this genetic variation.

DNA variations located near a gene sometimes inhibit the gene's activity, causing below-normal levels of the protein it produces. In this case, the researchers discovered that the single-letter DNA variation that protected patients from CHD resulted in a significant decline in the production of ADAMTS7.

In a separate recent mouse study, Dr. Reilly's lab demonstrated that genetic deletion of ADAMTS7 reduced the buildup of fatty plaques in arteries, suggesting that blocking the production or function of this enzyme might be a way to lower the risk of CHD.

In the current study, when the researchers applied a liquid extract of cigarette smoke to coronary artery cells, the cells' production of ADAMTS7 more than doubled, supporting the conclusion that smoking may counteract the genetic protection from CHD by increasing the level of ADAMTS7 in the artery wall.

"This has been one of the first big steps towards solving the complex puzzle of gene-environment interactions that lead to CHD," said lead author Danish Saleheen, PhD, assistant professor of biostatistics and epidemiology at the Perelman School of Medicine at the University of Pennsylvania.

In future studies, the researchers hope to establish exactly how the ADAMTS7 variants protect against CHD, how cigarette smoking affects the activity of the gene that produces the enzyme, and whether reducing or inhibiting ADAMTS7 can slow the progression of atherosclerosis due to cigarette smoking.

"This study is an important example of the emerging field of precision medicine and precision public health," said Dr. Reilly. "Through these large-scale genetic studies, we're beginning to understand the genetic variations that drive risk in response to certain environmental exposures or lifestyle behaviors. Not everyone reacts the same to the same exposures or behaviors. For example, some people who don't exercise develop diabetes while others do not. So, instead of saying there are rules for everybody, we can specify which interventions will be especially beneficial for specific populations or individuals and focus our health resources more efficiently."

The study is titled, "Loss of Cardio-Protective Effects at the ADAMTS7 Locus Due to Gene-Smoking Interactions."

Explore further: Scientists identify new therapeutic target for coronary heart disease

More information: Danish Saleheen et al. Loss of Cardio-Protective Effects at theLocus Due to Gene-Smoking Interactions, Circulation (2017). DOI: 10.1161/CIRCULATIONAHA.116.022069 , circ.ahajournals.org/content/early/2017/04/20/CIRCULATIONAHA.116.022069

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