Publications

Publication: Kidney International

Lia Bally, Philipp Gubler, Hood Thabit, Sara Hartnell, Yue Ruan, Malgorzata E. Wilinska, Mark L. Evans, Mariam Semmo, Bruno Vogt, Anthony P. Coll, Christoph Stettler, Roman Hovorka
https://doi.org/10.1016/j.kint.2019.03.006

Summary:
In a post hoc analysis of a randomised controlled clinical trial, researchers compared the efficacy of fully automated closed-loop insulin delivery vs. usual care in patients undergoing hemodialysis while in hospital.
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Publication: Brain

David Howett, Andrea Castegnaro, Katarzyna Krzywicka, Johanna Hagman, Deepti Marchment, Richard Henson, Miguel Rio, John A King, Neil Burgess, Dennis Chan


Summary:

This research showed that a virtual reality test of spatial navigation was more effective at identifying patients with mild cognitive impairment (MCI) due to Alzheimer’s disease (AD) than gold standard tests of memory and thinking currently used in clinic and research studies. More here

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Publication: PLOS Medicine

David Wastlund, Alexandros A. Moraitis, Alison Dacey, Ulla Sovio, Edward C. F. Wilson, Gordon C. S. Smith

16 April 2019

Despite the relative ease with which breech presentation can be identified through ultrasound screening, the assessment of foetal presentation at term is often based on clinical examination only. Due to limitations in this approach, many women present in labour with an undiagnosed breech presentation, with increased risk of foetal morbidity and mortality. This study sought to determine the cost effectiveness of universal ultrasound scanning for breech presentation near term (36 weeks of gestational age [wkGA]) in nulliparous women.

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Publication: Frontiers in Immunology

Manu Chhabra, Jawaher Alsughayyir, M. Saeed Qureshi, Mekhola Mallik, Jason M. Ali, Ivonne Gamper, Ellen L. Moseley, Sarah Peacock, Vasilis Kosmoliaptsis, Martin J. Goddard, Michelle A. Linterman, Reza Motallebzadeh and Gavin J. Pettigrew

23 January 2019


Summary:

Different profiles of alloantibody responses are observed in the clinic, with those that persist, often despite targeted treatment, associated with poorer long-term transplant outcomes. Although such responses would suggest an underlying germinal center (GC) response, the relationship to cellular events within the allospecific B cell population is unclear. Here we examine the contribution of germinal center (GC) humoral alloimmunity to chronic antibody mediated rejection (AMR)…

This work is composed of two parts, of which this is Part II. Please read also Part I: Alsughayyir et al., 2019.

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Publication: Frontiers in Immunology

Jawaher Alsughayyir, Manu Chhabra, M. Saeed Qureshi, Mekhola Mallik, Jason M. Ali, Ivonne Gamper, Ellen L. Moseley, Sarah Peacock, Vasilis Kosmoliaptsis, Martin J. Goddard, Michelle A. Linterman, Reza Motallebzadeh, Gavin J. Pettigrew

22 January 2019


Summary:

Humoral alloimmunity is now recognized as a major determinant of transplant outcome. MHC glycoprotein is considered a typical T-dependent antigen, but the nature of the T cell alloresponse that underpins alloantibody generation remains poorly understood. This paper examines how the relative frequencies of alloantigen-specific B cells and helper CD4 T cells influence the humoral alloimmune response and how this relates to antibody-mediated rejection (AMR).

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Publication: BMJ Open

John OO AyorindeDominic M Summers, Laura Pankhurst, Emma Laing, Alison J Deary, Karla Hemming, Edward CF Wilson, Victoria Bardsley, Desley A Neil, Gavin J Pettigrew

17 January 2019


Summary:

Most potential kidney transplant donors in the UK are aged over 60 years, yet increasing donor age is associated with poorer graft survival and function. Urgent preimplantation kidney biopsy can identify chronic injury, and may aid selection of better ‘quality’ kidneys from this group. However, the impact of biopsy on transplant numbers remains unproven. The PreImplantation Trial of Histopathology In renal Allografts (PITHIA) study will assess whether the introduction of a national, 24 hours, digital histopathology service increases the number, and improves outcomes, of kidneys transplanted in the UK from older deceased donors.

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Publication: Journal of Hepatology

Rhiannon Taylor, Elisa Allen, James A. Richards, Mingzheng A. Goh, James Neuberger, David Collett, Gavin J. Pettigrew, Liver Advisory Group to NHS Blood and Transplant

11 January 2019


Summary:

This study looks at patients who require a liver transplant to save their lives; this liver can be donated by a person who has died either after their heart has stopped (donation after cardiac death – DCD) or after the brain has been injured and can no longer support life (donation after brainstem death – DCB). We know that livers donated after brainstem death function better than those after cardiac death, but there are not enough of these livers for everyone, so we wished to help patients decide whether it was better for them to accept an early offer of a DCD liver than waiting longer to receive a “better” liver from a DBD donor. We found that patients were more likely to survive if they accepted the offer of a liver transplant as soon as possible (DCD or DBD), especially if their liver disease was very severe.

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Publication: American Journal of Transplantation

Ines G. Harper, Olivera Gjorgjimajkoska, Jacqueline H. Y. Siu, Jasvir Parmar, Arend Mulder, Frans H. J. Claas, Sarah A. Hosgood, Michael L. Nicholson, Reza Motallebzadeh, Gavin J. Pettigrew

12 December 2018


Summary:

Tissue resident lymphocytes are present within many organs, and are presumably transferred at transplantation, but their impact on host immunity is unclear. Here, we examine whether transferred donor natural regulatory CD4 T cells (nT‐regs) inhibit host alloimmunity and prolong allograft survival.

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Publication: Journal of Autoimmunity

M. Saeed Qureshi, Jawaher Alsughayyir, Manu Chhabra, Jason M. Ali, Martin J. Goddard, Christopher A. Devine, Thomas M. Conlon, Michelle A. Linterman, Reza Motallebzadeh, Gavin J.Pettigrew

7 December 2018


Summary:

The development of humoral autoimmunity following organ transplantation is increasingly recognised, but of uncertain significance. We examine whether autoimmunity contributes independently to allograft rejection.

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Publication: Frontiers in Immunology

Jacqueline H. Y. Siu, Veena Surendrakumar, James A. Richards and Gavin J. Pettigrew

5 November 2018


Summary:

Transplantation is unusual in that T cells can recognize alloantigen by at least two distinct pathways: as intact MHC alloantigen on the surface of donor cells via the direct pathway; and as self-restricted processed alloantigen via the indirect pathway. Direct pathway responses are viewed as strong but short-lived and hence responsible for acute rejection, whereas indirect pathway responses are typically thought to be much longer lasting and mediate the progression of chronic rejection. However, this is based on surprisingly scant experimental evidence, and the recent demonstration that MHC alloantigen can be re-presented intact on recipient dendritic cells—the semi-direct pathway—suggests that the conventional view may be an oversimplification.

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Publication:

Jason M. Ali, Margaret C. Negus, Thomas M. Conlon, Ines G. Harper, M. Saeed Qureshi, Reza Motallebzadeh, Richard Willis, Kourosh Saeb-Parsy, Eleanor M. BoltonJ. Andrew Bradley, Gavin J. Pettigrew

9 February 2016


Summary:

MHC alloantigen is recognized by two pathways: “directly,” intact on donor cells, or “indirectly,” as self-restricted allopeptide. The duration of each pathway, and its relative contribution to allograft vasculopathy, remain unclear. Using a murine model of chronic allograft rejection, we report that direct-pathway CD4 T cell alloresponses, as well as indirect-pathway responses against MHC class II alloantigen, are curtailed by rapid elimination of donor hematopoietic antigen-presenting cells. In contrast, persistent presentation of epitope resulted in continual division and less-profound contraction of the class I allopeptide-specific CD4 T cell population, with approximately 10,000-fold more cells persisting than following acute allograft rejection. This expanded population nevertheless displayed sub-optimal anamnestic responses and was unable to provide co-stimulation-independent help for generating alloantibody. Indirect-pathway CD4 T cell responses are heterogeneous. Appreciation that responses against particular alloantigens dominate at late time points will likely inform development of strategies aimed at improving transplant outcomes.

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Publication: Frontiers in Behavioural Neuroscience

George Savulich, Emily Thorp, Thomas Piercy, Katie A Peterson, John D Pickard, Barbara J Sahakian.

21 Jan 2019


Summary:

A new ‘brain training’ game designed by researchers at the University of Cambridge improves users’ concentration, according to new research published today. The scientists behind the venture say this could provide a welcome antidote to the daily distractions that we face in a busy world.

A team from the Behavioural and Clinical Neuroscience Institute at the University of Cambridge, has developed and tested ‘Decoder’, a new game that is aimed at helping users improve their attention and concentration. The game is based on the team’s own research and has been evaluated scientifically.

In a study published in the journal Frontiers in Behavioural Neuroscience Professor Sahakian and colleague Dr George Savulich have demonstrated that playing Decoder on an iPad for eight hours over one month improves attention and concentration. This form of attention activates a frontal-parietal network in the brain. Read the full story here

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Publication: Oxford Academic

Lisa Pennells, Stephen Kaptoge, AngelaWood, Mike Sweeting , Xiaohui Zhao, Ian White, Stephen Burgess, Peter Willeit, Thomas Bolton, Karel G.M. Moons, Yvonne T. van der Schouw, Randi Selmer, Kay-Tee Khaw, Vilmundur Gudnason, Gerd Assmann, Philippe Amouyel, Veikko Salomaa, Mika Kivimaki, Børge G. Nordestgaard, Michael J. Blaha, Lewis H. Kuller, Hermann Brenner, Richard F. Gillum, Christa Meisinger, Ian Ford, MatthewW. Knuiman, Annika Rosengren, Debbie A. Lawlor, Henry Vo¨ lzke, Cyrus Cooper, Alejandro Marı´n Iba~nez, Edoardo Casiglia, Jussi Kauhanen, Jackie A. Cooper, Beatriz Rodriguez, Johan Sundstro¨m, Elizabeth Barrett-Connor, Rachel Dankner, Paul J. Nietert, KarinaW. Davidson, Robert B.Wallace, Dan G. Blazer, Cecilia Bjo¨ rkelund, Chiara Donfrancesco, Harlan M. Krumholz, Aulikki Nissinen, Barry R. Davis, Sean Coady, Peter H.Whincup, Torben Jørgensen, Pierre Ducimetiere, Maurizio Trevisan, Gunnar Engstro¨m, Carlos J. Crespo, TomW. Meade,  Marjolein Visser, Daan Kromhout, Stefan Kiechl, Makoto Daimon, Jackie F. Price, Agustin Go´mez de la Ca´mara, JWouter Jukema, Benoıˆt Lamarche, Altan Onat, Leon A. Simons, Maryam Kavousi, Yoav Ben-Shlomo, John Gallacher, Jacqueline M. Dekker, Hisatomi Arima, Nawar Shara, RobertW. Tipping, Ronan Roussel, Eric J Brunner, Wolfgang Koenig, Masaru Sakurai, Jelena Pavlovic, Ron T. Gansevoort, Dorothea Nagel, Uri Goldbourt, Elizabeth L.M. Barr, Luigi Palmieri, Inger Njølstad, Shinichi Sato,W.M. Monique Verschuren, Cherian V. Varghese, Ian Graham, Oyere Onuma, Philip Greenland, MarkWoodward, Majid Ezzati, Bruce M. Psaty, Naveed Sattar, Rod Jackson, Paul M. Ridker, Nancy R. Cook, Ralph B. D’Agostino, Sr, Simon G Thompson, John Danesh, Emanuele Di Angelantonio

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Publication: BMJ

Loes CA Rutten-Jacobs, Susanna C Larsson,, Rainer Malik,, Kristiina Rannikmäe, MEGASTROKE consortium, International Stroke Genetics Consortium, Cathie L Sudlow, Martin Dichgans, Hugh S Markus, professor2, Matthew Traylor


Summary:

Researchers investigated whether a genetic risk score for stroke is associated with actual (“incident”) stroke in a large population of British adults.

They developed a genetic risk score based on 90 gene variants known to be associated with stroke from 306,473 white men and women in the UK Biobank – a database of biological information from half a million British adults.

Participants were aged between 40 and 73 years and had no history of stroke or heart attack. Adherence to a healthy lifestyle was based on four factors: non-smoker, diet rich in fruit, vegetables and fish, not overweight or obese (body mass index less than 30), and regular physical exercise.

A high genetic risk combined with an unfavourable lifestyle profile was associated with a more than twofold increased risk of stroke compared with a low genetic risk and a favourable lifestyle. Full story here

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Publication: Nature

Baland Jalal, Annette Brühl, Claire O’Callaghan, Thomas Piercy, Rudolf N. Cardinal, Vilayanur S. Ramachandran and Barbara J. Sahakian


Summary:

A ‘brain training’ app could help people who suffer from obsessive compulsive disorder (OCD) manage their symptoms, which may typically include excessive handwashing and contamination fears.

One of the most common types of OCD, affecting up to 46% of OCD patients, is characterised by severe contamination fears and excessive washing behaviour. Excessive washing can be harmful as sometimes OCD patients use spirits, surface cleansers or even bleach to clean their hands. The behaviours can have a serious impact on people’s lives, their mental health, their relationships and their ability to hold down jobs.

Cambridge researchers developed a new treatment to help people with contamination fears and excessive washing. The intervention, which can be delivered through a smartphone app, involves patients watching videos of themselves washing their hands or touching fake contaminated surfaces. Read the full story here

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Publication: Journal of the American College of Cardiology

Michael Inouye, Gad Abraham, Christopher P. Nelson, Angela M. Wood, Michael J. Sweeting, Frank Dudbridge, Florence Y. Lai, Stephen Kaptoge, Marta Brozynska, Tingting Wang, Shu Ye, Thomas R. Webb, Martin K. Rutter, Ioanna Tzoulaki,Riyaz S. Patel, Ruth J.F. Loos, Bernard Keavney, Harry Hemingway, John Thompson, Hugh Watkins, Panos Deloukas,Emanuele Di Angelantonio, Adam S. Butterworth, John Danesh, Nilesh J. Samani


Summary:

Genetic factors have long been known to be major contributors of someone’s risk of developing coronary heart disease – the leading cause of heart attacks. Currently to identify those at risk doctors use scores based on lifestyle and clinical conditions associated with coronary heart disease such as cholesterol level, blood pressure, diabetes and smoking. But these scores are imprecise, age-dependent and miss a large proportion of people who appear ‘healthy’, but will still develop the disease.

The ‘big-data’ GRS technique takes into account 1.7 million genetic variants in a person’s DNA to calculate their underlying genetic risk for coronary heart disease.

The team analysed genomic data of nearly half a million people from the UK Biobank research project aged between 40-69 years. This included over 22,000 people who had coronary heart disease.

The GRS was better at predicting someone’s risk of developing heart disease than each of the classic risk factors for coronary heart disease alone. The ability of the GRS to predict coronary heart disease was also largely independent of these known risk factors. This showed that the genes which increase the risk of coronary heart disease don’t simply work by elevating blood pressure or cholesterol, for example.

People with a genomic risk score in the top 20 per cent of the population were over four-times more likely to develop coronary heart disease than someone with a genomic risk score in the bottom 20 per cent. Read the full press release

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Publication: Nature Genetics

Geoff Macintyre, Teodora E. Goranova, Dilrini De Silva, Darren Ennis, Anna M. Piskorz, Matthew Eldridge, Daoud Sie, Liz-Anne Lewsley, Aishah Hanif, Cheryl Wilson, Suzanne Dowson, Rosalind M. Glasspool, Michelle Lockley, Elly Brockbank, Ana Montes, Axel Walther, Sudha Sundar, Richard Edmondson, Geoff D. Hall, Andrew Clamp, Charlie Gourley, Marcia Hall, Christina Fotopoulou, Hani Gabra, James Paul, Anna Supernat, David Millan, Aoisha Hoyle, Gareth Bryson, Craig Nourse, Laura Mincarelli, Luis Navarro Sanchez, Bauke Ylstra, Mercedes Jimenez-Linan, Luiza Moore, Oliver Hofmann, Florian Markowetz, Iain A. McNeish and James D. Brenton


Summary:

Researchers have found distinct patterns of DNA rearrangement that are linked to patient outcomes.

In this study of ovarian cancer samples from over 500 women, the research team harnessed big data processing techniques to look for broad patterns in the genetic readouts from ovarian cancer cells.

Rather than focusing on the detail of each individual mistake in the DNA, they designed powerful computer algorithms to scan the genetic data, finding seven distinct patterns.

They showed that each pattern, or “signature”, represented a different mechanism of DNA mutation. Taken together, these signatures were able to make sense of the chaos seen in ovarian cancer genomes. Read the full story here

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Publication: The Lancet

Michael J Sweeting, Katya L Masconi, PhD, Edmund Jones, PhD, Pinar Ulug, PhD, Matthew J Glover, MSc, Prof Jonathan A Michaels, MChir, Prof Matthew J Bown, MD, Prof Janet T Powell, MD, Prof Simon G Thompson, DSc


Summary:

The NHS introduced ultrasound screening in men aged 65 and over in 2009 to detect and treat the condition – which arises when the main blood vessel swells in the abdomen, and is symptomless until the point of rupture. Since the launch, the programme has been successfully screening and identifying men at risk of an AAA.

Researchers wanted to see if UK women – who are less likely to have AAAs – could also benefit from a similar screening programme. Read the full press release here

 

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Publication: The Lancet

Gemma D Banham, MRCP(UK), Shaun M Flint, FRACP,  Nicholas Torpey, FRCP, Paul A Lyons, PhD, Don N Shanahan, MSc, Adele Gibson, BSc, Prof Christopher J E Watson, FRCS, Ann-Marie O’Sullivan, MRes, Joseph A Chadwick, Katie E Foster, PhD, Rachel B Jones, FRCP, Luke R Devey, MRCSEd, Anna Richards, MRCP(UK), Prof Lars-Peter Erwig, MD, Prof Caroline O Savage,FMedSci, Prof Kenneth G C Smith, FMedSci, Robert B Henderson, PhD, Menna R Clatworthy, FRCP†,


Summary:

Transplantation is the best form of treatment for most patients with end-stage renal failure, but long-term graft survival is limited by the development of antibodies against the graft. There is therefore a major unmet need to find immunosuppressants that target humoral alloimmunity.

Researchers investigated the use of Belimumab, a monoclonal antibody that binds the B cell pro-survival cytokine BAFF, in kidney transplant recipients.

The study found that the use of belimumab was not associated with any excess risk of infection, and led to a reduction in antibody-producing plasmablasts, activated memory B cells, new IgG antibody formation and in non-HLA IgG antibodies associated with poor graft outcomes. Remarkably, belimumab treatment spared regulatory B cells – a cell type associated with transplant tolerance, with an increase in IL10-producing B cells observed.

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Publication: The Lancet

Angela M Wood PhD, P, Stephen Kaptoge, PhD, Adam S Butterworth, PhD, Peter Willeit, MD, Samantha Warnakula, PhD, Thomas Bolton, MMath, Ellie Paige, PhD, Dirk S Paul, PhD, Michael Sweeting, PhD, Stephen Burgess, PhD, Steven Bell, PhD, William Astle, PhD, David Stevens, MSc, Albert Koulman, PhD, Randi M Selmer, PhD, Prof W M Monique Verschuren, PhD, Prof Shinichi Sato, MD, Prof Inger Njølstad, MD, Prof Mark Woodward, PhD, Prof Veikko Salomaa, MD, Prof Børge G Nordestgaard, MD, Prof Bu B Yeap, MBBS, Prof Astrid Fletcher, PhD, Prof Olle Melander, MD, Prof Lewis H Kuller, MD, Beverley Balkau, PhD, Prof Michael Marmot, FMedSci, Prof Wolfgang Koenig, MD, Prof Edoardo Casiglia, MD, Prof Cyrus Cooper, FMedSci, Volker Arndt, MD, Prof Oscar H Franco, MD, Patrik Wennberg, MD, Prof John Gallacher, PhD, Agustín Gómez de la Cámara, MD, Prof Henry Völzke, MD, Christina C Dahm, PhD, Caroline E Dale, PhD, Manuela M Bergmann, PhD, Carlos J Crespo, PhD, Prof Yvonne T van der Schouw, PhD, Prof Rudolf Kaaks, MD, Leon A Simons, MD, Pagona Lagiou, MD, Josje D Schoufour, PhD, Jolanda M A Boer, PhD, Prof Timothy J Key, DPhil, Beatriz Rodriguez, MD, Conchi Moreno-Iribas, PhD, Karina W Davidson, PhD, James O Taylor, MD, Carlotta Sacerdote, PhD, Prof Robert B Wallace, MD, J Ramon Quiros, MD, Prof Rosario Tumino, MD, Dan G Blazer II, MD, Prof Allan Linneberg, MD, Makoto Daimon, MD, Salvatore Panico, MD, Barbara Howard, PhD, Guri Skeie, PhD, Prof Timo Strandberg, MD, Prof Elisabete Weiderpass, PhD, Prof Paul J Nietert, PhD, Prof Bruce M Psaty, MD, Prof Daan Kromhout, PhD, Elena Salamanca-Fernandez, MSc, Prof Stefan Kiechl, MD, Prof Harlan M Krumholz, MD, Sara Grioni, BSc, Domenico Palli, MD, José M Huerta, PhD, Prof Jackie Price, MD, Prof Johan Sundström, MD, Larraitz Arriola, MD, Prof Hisatomi Arima, MD, Ruth C Travis, DPhil, Prof Demosthenes B Panagiotakos, PhD, Anna Karakatsani, MD, Prof Antonia Trichopoulou, MD, Tilman Kühn, PhD, Prof Diederick E Grobbee, MD, Elizabeth Barrett-Connor, MD, Natasja van Schoor, MD, Prof Heiner Boeing, PhD, Prof Kim Overvad, MD, Prof Jussi Kauhanen, MD, Prof Nick Wareham, MD, Claudia Langenberg, MD, Prof Nita Forouhi, PhD, Maria Wennberg, PhD, Prof Jean-Pierre Després, DPhil, Prof Mary Cushman, MD, Jackie A Cooper, MSc, Prof Carlos J Rodriguez, MD, Masaru Sakurai, MD, Jonathan E Shaw, PhD, Prof Matthew Knuiman, PhD, Trudy Voortman, PhD, Prof Christa Meisinger, MD, Anne Tjønneland, MD, Prof Hermann Brenner, MD, Luigi Palmieri, PhD, Jean Dallongeville, MD, Prof Eric J Brunner, PhD, Prof Gerd Assmann, MD, Maurizio Trevisan, MD, Richard F Gillum, MD, Prof Ian Ford, PhD, Prof Naveed Sattar, FMedSci, Mariana Lazo, MD, Prof Simon G Thompson, FMedSci, Pietro Ferrari, PhD, Prof David A Leon, PhD, Prof George Davey Smith, MD, Prof Richard Peto, FRS, Prof Rod Jackson, PhD, Prof Emily Banks, PhD, Emanuele Di Angelantonio, MD, Prof John Danesh,


Summary:

Regularly drinking more than the recommended UK guidelines for alcohol could take years off your life, according to new research from the University of Cambridge. The study shows that drinking more alcohol is associated with a higher risk of stroke, fatal aneurysm, heart failure and death.

The authors say their findings challenge the widely held belief that moderate drinking is beneficial to cardiovascular health, and support the UK’s recently lowered guidelines. The study compared the health and drinking habits of over 600,000 people in 19 countries worldwide and controlled for age, smoking, history of diabetes, level of education and occupation.

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Publication: Nature Communications

Stefan Gräf, Matthias Haimel, Marta Bleda, Charaka Hadinnapola, Laura Southgate, Wei Li, Joshua Hodgson, Bin Liu, Richard M. Salmon, Mark Southwood, Rajiv D. Machado, Jennifer M. Martin, Carmen M. Treacy, Katherine Yates, Louise C. Daugherty, Olga Shamardina, Deborah Whitehorn, Simon Holden, Micheala Aldred, Harm J. Bogaard, Colin Church, Gerry Coghlan, Robin Condliffe, Paul A. Corris, Cesare Danesino, Mélanie Eyries, Henning Gall, Stefano Ghio, Hossein-Ardeschir Ghofrani, J. Simon R. Gibbs, Barbara Girerd, Arjan C. Houweling, Luke Howard, Marc Humbert, David G. Kiely, Gabor Kovacs, Robert V. MacKenzie Ross, Shahin Moledina, David Montani, Michael Newnham, Andrea Olschewski, Horst Olschewski, Andrew J. Peacock, Joanna Pepke-Zaba, Inga Prokopenko, Christopher J. Rhodes, Laura Scelsi, Werner Seeger, Florent Soubrier, Dan F. Stein, Jay Suntharalingam, Emilia M. Swietlik, Mark R. Toshner, David A. van Heel, Anton Vonk Noordegraaf, Quinten Waisfisz, John Wharton, Stephen J. Wort, Willem H. Ouwehand, Nicole Soranzo, Allan Lawrie, Paul D. Upton, Martin R. Wilkins, Richard C. Trembath & Nicholas W. Morrell


Summary:

Pulmonary Arterial Hypertension (PAH) is a fatal lung disease and causes the walls of the arteries become thick and stiff, narrowing the space for blood to pass through and increasing blood pressure then leading to heart failure.

The disease kills 50% of those affected within five years, but little was known about what caused the condition in some people. Now experts say they have discovered five genes that cause the illness and could pave the way for more treatments.

Scientists carried out the largest ever genetic study of the disease by analysing the genomes – the unique sequence of a person’s DNA – of more than 1,000 PAH patients for whom the cause of the illness was unknown.

They found that mutations in five genes were responsible for causing the illness in these people, including in four genes that were not previously known to be involved in the disease. In people with the condition these genes fail to effectively produce the proteins that are required for the structure, function and regulation of the body’s tissues, researchers found.

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Publication: Annals

Linda M. O’Keeffe, PhD; Anna Ramond, DPharm; Clare Oliver-Williams, PhD; Peter Willeit, MD; Ellie Paige, PhD; Patrick Trotter, MBChB; Jonathan Evans, MBChB; Jonas Wadström, MD; Michael Nicholson, MD; Dave Collett, PhD; Emanuele Di Angelantonio, MD


Summary:

Living kidney donors are not at increased risk for some health outcomes previously of concern, but do seem at risk for worse blood pressure and kidney function than nondonors. In addition, female donors seem to be at increased risk for preeclampsia.

A team lead by researchers reviewed 52 published studies comprising more than 100,000 living kidney donors and more than 110,000 nondonors to assess the mid- and long-term health risks associated with living kidney donation in adults.

The data showed that kidney donors had higher diastolic blood pressure, poorer renal function, and higher risk for ESRD than nondonors. Female donors had an almost two-fold higher risk than nondonors for pregnancy-related complications, such as preeclampsia.

There was no evidence that living kidney donors had higher risk for mortality, cardiovascular disease, or type 2 diabetes, or reduced quality of life.

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Publication: Nature Cell Biology

Vasileios I. Floros, Angela Pyle, Sabine Dietmann, Wei Wei, Walfred W. C. Tang, Naoko Irie, Brendan Payne, Antonio Capalbo, Laila Noli, Jonathan Coxhead, Gavin Hudson, Moira Crosier, Henrik Strahl, Yacoub Khalaf, Mitinori Saitou, Dusko Ilic, M. Azim Surani & Patrick F. Chinnery

 15 Jan 2018; DOI: 10.1038/41556-017-0017-8


Summary:

Researchers have shown for the first time how children can inherit a severe – potentially fatal – mitochondrial disease from a healthy mother. The study reveals that healthy people harbour mutations in their mitochondrial DNA and explains how cases of severe mitochondrial disease can appear unexpectedly in previously unaffected families.

Mitochondrial diseases caused by mutations in mitochondrial DNA are rare, affecting approximately 1 in 10,000 births, but can cause severe conditions. Mitochondria are the powerhouses inside our cells, producing energy and carrying their own DNA instructions (separate from the DNA in the nucleus of every cell) and are inherited from a person’s mother via the egg.

In this study, the researchers found that a variety of mutations were present in the mitochondrial DNA in the developing egg cells of all 12 of the human embryos studied, showing that low levels of mitochondrial DNA mutations are carried by healthy humans.

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Publication: Brain

Thomas E Cope, Timothy Rittman, Robin J Borchert, P Simon, JonesDeniz Vatansever, Kieren Allinson Luca Passamonti, Patricia Vazquez Rodriguez, W Richard Bevan-Jones, John T O’Brien, James B Rowe

Brain, awx347,

Published: 05 January 2018


Summary:
Recent advances in brain imaging have enabled scientists to show for the first time that a key protein which causes nerve cell death spreads throughout the brain in Alzheimer’s disease – and hence that blocking its spread may prevent the disease from taking hold.
A team led by scientists describe using a combination of imaging techniques to examine how patterns of tau relate to the wiring of the brain in 17 patients with Alzheimer’s disease, compared to controls.
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Publication: J Neurol

Underwood BR, Green-Thompson ZW, Pugh PJ, Lazic SE, Mason SL4, Griffin J, Jones PS, Rowe JB, Rubinsztein DC7,4, Barker RA.

2017 Oct 26. doi: 10.1007/s00415-017-8647-0. [Epub ahead of print]

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Publication: The Lancet Neurology

Prof Andrew I R Maas*,’Correspondence information about the author Prof Andrew I R MaasEmail the author Prof Andrew I R Maas, Prof David K Menon*,’Correspondence information about the author Prof David K MenonEmail the author Prof David K Menon, P David Adelson, Nada Andelic, Michael J Bell, Antonio Belli, Peter Bragge, Alexandra Brazinova, András Büki, Randall M Chesnut, Giuseppe Citerio, Mark Coburn, D Jamie Cooper, A Tamara Crowder, Endre Czeiter, Marek Czosnyka, Ramon Diaz-Arrastia, Jens P Dreier, Ann-Christine Duhaime, Ari Ercole, Thomas A van Essen, Valery L Feigin, Guoyi Gao, Joseph Giacino, Laura E Gonzalez-Lara, Russell L Gruen, Deepak Gupta, Jed A Hartings, Sean Hill, Ji-yao Jiang, Naomi Ketharanathan, Erwin J O Kompanje, Linda Lanyon, Steven Laureys, Fiona Lecky, Harvey Levin, Hester F Lingsma, Marc Maegele, Marek Majdan, Geoffrey Manley, Jill Marsteller, Luciana Mascia, Charles McFadyen, Stefania Mondello, Virginia Newcombe, Aarno Palotie, Paul M Parizel, Wilco Peul, James Piercy, Suzanne Polinder, Louis Puybasset, Todd E Rasmussen, Rolf Rossaint, Peter Smielewski, Jeannette Söderberg, Simon J Stanworth, Murray B Stein, Nicole von Steinbüchel, William Stewart, Ewout W Steyerberg, Nino Stocchetti, Anneliese Synnot, Braden Te Ao, Olli Tenovuo, Alice Theadom, Dick Tibboel, Walter Videtta, Kevin K W Wang, W Huw Williams, Lindsay Wilson, Kristine Yaffe for the show InTBIR Participants and Investigators

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Publication: Proceedings of National Academy of Sciences

Deniz Vatansever, David K. Menon, and Emmanuel A. Stamatakis

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Publication: Lancet

Schormair, B., Zhao, C., Bell, S. et al.

Lancet Neurology; 10th October 2017; DOI: 10.1016/S1474-4422(17)30327-7


Summary:

A new study into the genetics underlying restless legs syndrome has identified 13 previously-unknown genetic risk variants, while helping inform potential new treatment options for the condition.

Studies of families and twins have shown that there is a strong genetic component to the disorder and led to the discovery of six genetic variants that increased the risk of developing the condition.

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Astle WJ, Elding H, Jiang T, Allen D, Ruklisa D, Mann AL, Mead D, Bouman H, Riveros-Mckay F, Kostadima MA, Lambourne JJ, Sivapalaratnam S, Downes K, Kundu K, Bomba L, Berentsen K, Bradley JR, Daugherty LC, Delaneau O, Freson K, Garner SF, Grassi L, Guerrero J, Haimel M, Janssen-Megens EM, Kaan A, Kamat M, Kim B, Mandoli A, Marchini J, Martens JH, Meacham S, Megy K, O’Connell J, Petersen R, Sharifi N, Sheard SM, Staley JR, Tuna S, van der Ent M, Walter K, Wang SY, Wheeler E, Wilder SP, Iotchkova V, Moore C, Sambrook J, Stunnenberg HG, Di Angelantonio E, Kaptoge S, Kuijpers TW, Carrillo-de-Santa-Pau E, Juan D, Rico D, Valencia A, Chen L, Ge B, Vasquez L, Kwan T, Garrido-Martín D, Watt S, Yang Y, Guigo R, Beck S, Paul DS, Pastinen T, Bujold D, Bourque G, Frontini M, Danesh J, Roberts DJ, Ouwehand WH, Butterworth AS, Soranzo N.

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Di Angelantonio E, Bhupathiraji SN, Wormser D, Gao P, Kaptoget S, Berrington de Gonzalez A, Cairns BJ, Huxley R, Jackson CL, Joshy G, Lewington S, Manson JE, Murphy N, Patel AV, Samet JM, Woodward M, Zheng W, Zhou M, Bansal N, Barricarte A, Carter B, Cerhan JR, Collins R, Davey Smith G, Franco OH, Green J, Halsey J, Hildebrand JS, Jung KJ, Korda RJ, McLerran DF, Moore SC, O’Keeffe LM, Paige E, Ramond A, Reeves GK, Rolland B, Sacerdote C, Sattar N, Sofanopoulou E,Stevens J, Thun M, Ueshima H, Yang L, Duk Yun Y, Willeit P, Banks E, Beral V, Chen Z, Gapstur SM, Gunter MJ, Hartge P, Jee SH, Lam T-H, Peto R, Potter JD, Willet WC, Thompson SG, Danesh J*, Hu FB*.

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Willeit P, Kaptoge S, Welsh P, Butterworth AS, Chowdury R, Spackman S, Pennells L,Gao P, Burgess S, Freitag DF, Sweeting M, Wood AM, Cook NR, Judd S, Trompet S, Nambi V, Hecht Olsen M, Everett BM, Kee F, Ärnlöv J, Salomaa V, Levy D, Kauhanen J, Laukkanen JA, Kavousi M, Ninomiya T, Casas J-P, Daniels LB, Lind L, Kistorp CN, Rosenberg J, Mueller T, Rubattu S, Panagiotakos DB, Franco OH, de Lemos JA, Luchner A, St Marien K, Kizer JR, Kiechl S, Salonen JT, Wannamethee SG, Nordestgaard BG, Anderson J, Jørgensen T, Melander O, Ballantyne CM, DeFilippi C, Ridker PM, Cushman M, Rosamond WD, Thompson SG, Gudnason V, Sattar N, Danesh J, Di Angelantonio E.

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Zanoni P, Khetarpal SA, Larach DB, Hancock-Cerutti WF, Millar JS, Cuchel M, DerOhannessian S, Kontush A, Surendran P, Saleheen D, Trompet S, Jukema JW, De Craen A, Deloukas P, Sattar N, Ford I, Packard C, Majumder Aa, Alam DS, Di Angelantonio E, Abecasis G, Chowdhury R, Erdmann J, Nordestgaard BG, Nielsen SF, Tybjærg-Hansen A, Schmidt RF, Kuulasmaa K, Liu DJ, Perola M, Blankenberg S, Salomaa V, Männistö S, Amouyel P, Arveiler D, Ferrieres J, Müller-Nurasyid M, Ferrario M, Kee F, Willer CJ, Samani N, Schunkert H, Butterworth AS, Howson JM, Peloso GM, Stitziel NO, Danesh J, Kathiresan S, Rader DJ; CHD Exome+ Consortium; CARDIoGRAM Exome Consortium; Global Lipids Genetics Consortium.

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