Welsh National School Of Medicine Research Articles

Championing for better management of individuals with lower limb ulceration

British Journal of Community NursingVol. 28, No. Sup6 EditorialChampioning for better management of individuals with lower limb ulcerationSamantha HollowaySamantha HollowayE-mail Address: [email protected]Reader, Programme Director for MSc in Wound Healing and Tissue Repair, Cardiff University School of Medicine; President, International Skin Tear Advisory Panel (ISTAP); Chair, European Wound Management Association (EWMA) Education Committee and EWMA Teacher NetworkSearch for more papers by this authorSamantha HollowayPublished Online:1 Jun 2023https://doi.org/10.12968/bjcn.2023.28.Sup6.S5AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References Callam MJ, Harper DR, Dale JJ, Ruckley CV. Chronic ulcer of the leg: clinical history. Br Med J (Clin Res Ed). 1987;294(6584):1389-1391. https://doi.org/10.1136/bmj.294.6584.1389 Crossref, Medline, Google ScholarGuest JF, Ayoub N, McIlwraith T, Uchegbu I, Gerrish A, Weidlich D, Vowden K, Vowden P. Health economic burden that wounds impose on the National Health Service in the UK. BMJ Open. 2015;5(12):e009283. https://doi.org/10.1136/bmjopen-2015-009283 Crossref, Medline, Google ScholarGuest JF, Ayoub N, McIlwraith T et al.. Health economic burden that different wound types impose on the UK's National Health Service. Int Wound J. 2017a;14(2):322-330. https://doi.org/10.1111/iwj.12603 Crossref, Medline, Google ScholarGuest JF, Vowden K, Vowden P. The health economic burden that acute and chronic wounds impose on an average clinical commissioning group/health board in the UK. J Wound Care. 2017b;26(6):292-303. https://doi.org/10.12968/jowc.2017.26.6.292 Link, Google ScholarLegs Matter. Legs matter-stand up for legs. 2023. https://legsmatter.org/ (accessed 4 May 2023) Google ScholarLohmann Rauscher. Squeeze in being bold. 2023. https://lohmann-rauscher.co.uk/squeeze-in-being-bold (accessed 4 May 2023) Google ScholarNational Wound Care Strategy Programme. Lower limb. 2023. https://www.nationalwoundcarestrategy.net/lower-limb/ (accessed 4 May 2023) Google ScholarNational Wound Care Strategy Programme. About the programme. 2023. https://www.nationalwoundcarestrategy.net/ (accessed 4 May 2023) Google Scholar FiguresReferencesRelatedDetails 1 June 2023Volume 28Issue Sup6ISSN (print): 1462-4753ISSN (online): 2052-2215 Metrics History Published online 1 June 2023 Published in print 1 June 2023 Information© MA Healthcare LimitedPDF download

Abstract P4-08-22: Expression of Dual Specific Phosphatase-7 (DUSP7/PYST2) and it’s Connection with Salt Inducible Kinases (SIKs) and Downstream MKKs in breast cancer

Abstract Expression of Dual Specific Phosphatase-7 (DUSP7/PYST2) and it’s Connection with Salt Inducible Kinases (SIKs) and Downstream MKKs in breast cancer Wenxiao Ji1, Emily Ling Xin1,2, Lin Ye1, Eleri Davies3, Wen G. Jiang1, Tracey A. Martin1 1CCMRC, Cardiff University School of Medicine, Cardiff, Wales, UK 2Breast Centre, Peking University First Hospital, Xicheng District, Beijing, China 3Wales Breast Centre, University Llandough Hospital, Cardiff CF64 2XX, UK Introduction. DUSP7 is a member of the large Dual specific phosphatase family, able to regulate the phosphorylation of both tyrosine and serine/threonine protein kinases. The role of DUSP7 in cancer is not clear, however, it has been identified as a possible target for therapy in cancers including breast cancer. It has also been reported as having value in prognosis of certain cancers, such as haematological malignancies, breast cancer and certain types of gynaecological cancer. The signalling network for DUSP7 is not fully established but is known to connect to ERKs and MAP2Ks. DUSP7 also appears to be linked with salt inducible kinases (SIKs), a small family of kinases linked with progression and response to therapies in breast cancer. Thus, DUSP7 and salt inducible kinases may interact with each other and with the downstream kinases including MAP2Ks and STK11 to influence the clinical course of breast cancer. The present study explored if the pattern of DUSP7 together with salt inducible kinases and the downstream MKKs in breast cancer. Methods. The expression of DUSP7 was quantified in a cohort of breast cancer tissues (both normal mammary tissues and breast cancer tissues). The expression of the potential downstream kinases including MKK1, MKK2, MKK3, MKK4 and STK11 was also quantified. The expression profile of these molecule, together with the salt inducible kinases reported to be aberrant in our previous studies, were analysed against clinical and outcome information. Results. Breast cancer tissues expressed high levels of DUSP7 compared with normal mammary tissues, although not statistically significant. When we explored the relationship between DUSP7 and other potential related molecules in the database of the cohort, we found a highly significant correlation between DUSP7 and SIK1 (r=0.385, p< 0.001), SIK2 (r=0.590, p< 0.001), but not SIK3 (r=0.158, p>0.05). Together with SIK1 and SIK2 (known to link to drug sensitivity), DUSP7, MKK1 (MAP2K1) and MKK3 (MAP2K3) appear to form a gene signature that is of significant value in predicting the overall survival of the patients (ROC 0.723, p=0.001). This allowed us to significantly distinguish between those with good OS and poor OS (p< 0.001, Hazard Ration (HR) =1.443 (95%CI 1.154-1.804)). Multivariate analysis has shown that this signature is independent in predicting overall survival (p=0.013, HR=1.432). The signature is more significant in predicting OS in ER(-) tumours (p< 0.001) than ER(+) tumours (p=0.61). The same is seen when predicting OS with triple negative breast cancers (TNBC) (p< 0.001) than non-TNBC tumours (p=0.044). The gene signature also predicted disease free outcome (p=0.007, HR=1.266 (95% CI 1.065-1.504)). Conclusion. The dual specific phosphatase DUSP7 together with potentially correlated salt inducible kinases (SIK-1 and SIK-2) and downstream MKKs (MKK-1 and MKK3) have important clinical value in breast cancer. This provides support that DUSP7 may be a valuable therapeutic target in breast cancer. Citation Format: WENXIAO JI, Ling Xin, Eleri Davies, Wen G. Jiang, Lin Ye. Expression of Dual Specific Phosphatase-7 (DUSP7/PYST2) and it’s Connection with Salt Inducible Kinases (SIKs) and Downstream MKKs in breast cancer [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P4-08-22.

Dr. Leslie H. Blumgart - A 'Living Legend' and 'The Professor'.

Dr Leslie Blumgart, a name that requires no introduction, was a pioneer and one of the most influential figures in hepatobiliary and pancreatic surgery. His methods and innovations have revolutionized the way these pathologies are being approached. He was one of the pioneering surgeons in the world who sought to make hepatopancreaticobiliary surgery a recognized specialty. His work took this field from a place with frequent and drastic complications to a safer and more effective zone. He was born to Harold Herman Blumgart and Hilda Blumgart on December 7, 1931, in South Africa. He did his schooling at Jepp High School in Johanessburg and was initially trained as a dentist at Witwatersrand University in Johanessburg in 1954, where he completed his graduation. He later moved to England, where he received his medical degree and surgical training at the University of Sheffield and graduated with an MBChB and MD. He accepted his first academic position as Lecturer and Deputy Director, Department of Surgery, Welsh National School of Medicine, Cardiff, from 1970 to 1972. He subsequently moved to the Glasgow Royal Infirmary as the St. Mungo Professor of Surgery from 1972 to 1979. He then served as Professor Director and Honorary Consultant Surgeon for the Department of Surgery at the Royal Postgraduate Medical School, University of London and Honorary Consultant, Hammersmith Hospital, London, 1979–1986. He was later recruited as Professor and Director of the Department of Visceral and Transplantation Surgery, University of Bern in Switzerland from 1986 to1991. In 1991, he accepted the position of Chief of the Hepatopancreaticobiliary Service in the Department of Surgery at Memorial Sloan Kettering Cancer Centre, New York, and was the holder of the Enid Haupt Chair. He was promoted to director of the program on hepatobiliary diseases in 1995. Dr Blumgart has authored over 600 peer-reviewed papers, edited 15 books, and written over 150 book chapters1. He has authored a number of books, including Blumgart’s Surgery of the Liver, Biliary Tract, and Pancreas2, currently in its 7th edition, and the Video Atlas: Liver, Biliary & Pancreatic Surgery. He has served on the editorial boards of 14 major journals in surgery, gastroenterology, and oncology. He has lectured widely as a visiting professor in the United States and abroad, delivering over 200 lectures and orations.He was a founding member of the International Biliary Association (now the International Hepato-Pancreatico-Biliary Association) and later rose to become its president. In more recent years, he was honored by the International Hepato-Pancreatico-Biliary Association as a ‘living legend.’ He was also a member of the Society for Surgery of the Alimentary Tract, the United States of America, the Hong Kong Surgical Society, the Hellenic Surgical Society, the Los Angeles Surgical Society, and the Yugoslav Society of Surgery. Following his significant contributions to surgical oncology, and in particular to Hepatopancreaticobiliary surgery, Dr Blumgart was awarded the Lifetime Achievement Award during the opening session of 34th Congress of the European Society of Surgical Oncology in partnership with British Association of Surgical Oncologists, 2014. Some of the many laurels he received during his career are honorary fellowships from multiple surgical colleges around the world, including the Royal Colleges of Surgeons in Edinburgh (Glasgow), the French Surgical Association, the Austrian Society of Surgery and the Italian Society of Surgery. He was also awarded the Acral Medal of the Swedish Society of Surgery. ‘The Professor,’ as he was called by his trainees, was a dominant figure in the evolution of hepatopancreaticobiliary surgery around the world for almost 50 years. He had built a great hepatopancreaticobiliary surgery academic and clinical program at Memorial Sloan Kettering Cancer Centre since 1991 and had trained a generation of surgical oncologists and hepatopancreaticobiliary surgeons who now carry forward his legacy. Dr Blumgart also generated a video library of complex hepatopancreaticobiliary procedures which he used in simplifying the training of many surgeons for many years. Watercolor painting and wood carving were his lesser-well known talents, which he pursued after he retired from clinical practice. Dr Blumgart recently passed away on September 27, 2022, and is survived by his wife Sarah Blumgart, and his children and grandchildren. Ethical approval None. Sources of funding None. Authors’ contribution H.A.: resources, writing – original draft, visualization. N.G.: conceptualization, validation, supervision. Conflict of interest disclosure The author declare that they have no conflict of interest. Research registration unique identifying number (UIN) None. Guarantor Nikhil Gupta and Himanshu Agrawal.

Abstract P2-16-09: Dual Specific Phosphatase-7 (DUSP7/PYST2) and its role in regulating vascular endothelial functions

Abstract Dual Specific Phosphatase-7 (DUSP7/PYST2) and its role in regulating vascular endothelial functions Wenxiao Ji, Wen G. Jiang, Lin Ye, Tracey A. Martin CCMRC, Cardiff University School of Medicine, Cardiff, Wales, UK Introduction. Dual specific phosphatases (DUSPs) are a large family of enzyme able to trigger tyrosine phosphorylation, and phosphorylation of serine and/or threonine. This feature of a dual phosphorylation pattern by DUSPs, renders them with diverse roles in cells, from cytoskeletal regulation of cell migration, regulation of multiple kinases in cell signalling, to regulation of proteins such as microtubules and cell growth. We have investigated DUSP family members, in particular DUSP-7 (otherwise known as PYST2), identified from our studies as being one of prominent DUSPs found to be highly aberrant in certain cancer types including gastric cancer and pancreatic cancer. In breast cancer cells, DUSP7 has been reported as a potential factor linked to drug sensitivity. The role played by DUSP7 in vascular endothelial cells has been poorly studied. Here, we present our findings on the role of DUSP-7 in the regulation of biological functions of vascular endothelial cells. Methods. Human vascular endothelial cells were used in the present study. Cell sub-models were created by knock down of DUSP7. The cells were evaluated for their biological response to loss of DUSP7, including proliferation, migration, matrix adhesion and response to downstream signalling. DUSP7 responses to various exogenous factors were also evaluated by a protein kinase platform. Results. Knock down of DUSP7 in human endothelial cells rendered them manifesting significantly reduced matrix adhesiveness (p< 0.05) and most strikingly, reduced cellular migration (P< 0.0001, control versus DUSP7 knock down). Interestingly, there was little change with the rate of cell growth. When cells were tested by inhibiting a tight junctional molecule, HAVcR1, the endothelial cells responded with markedly reduced DUSP7 (reduction of 46%). Likewise, the cells were also exhibited reduced levels of DUSP7 after being challenged by exogenous metastasis related Kisspeptin, indicating that DUSP7 may participated the wide network of signalling and functional regulations shared with the tight junction regulator HAVcR1 and possibly utilising Mitogen-activated protein kinase 3 (MAPK3 or Extracellular signal regulated kinase-1). Conclusion. Dual specific phosphatase-7 has an important role to play in vascular endothelial cells, primarily on cell matrix adhesion and cellular migration. A possible route of regulation is by targeting the extracellular signalling network. Citation Format: WENXIAO JI, Wen G. Jiang, Lin Ye, Tracey A. Martin. Dual Specific Phosphatase-7 (DUSP7/PYST2) and its role in regulating vascular endothelial functions [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P2-16-09.

Abstract P2-26-20: Marvel D3 and its associated junctional proteins in breast cancer

Abstract Marvel D3 and its associated junctional proteins in breast cancer Wenxiao Ji, Wen G. Jiang, Tracey A. Martin CCMRC, Cardiff University School of Medicine, Cardiff, Wales, UK Introduction. Marvel (Membrane Associated Domain Containing) proteins are a small family of proteins that are concentrated at the tight junction (TJ) region of epithelial and endothelial cells. They are important players in the formation and regulation of TJs. The Marvel protein family has three members, Marvel-D1, Marvel-D2 and Marvel-D3, all known to be TJ components. Marvel-D3 is more prominent in TJ regulation, by interacting widely with other proteins that co-localised at TJs. In the present study, we have examined the expression of Marvel-D3 and its splicing variants, their relationship with other known interactive TJ partners in breast cancer and in disease progression and clinical outcome. Methods. Marvel-D3 and its variants were quantified in a breast cancer cohort that contained both normal and tumour tissues. The expression was analysed together with the known Marvel-D3 interactive molecules available in our database of the same cohort. The profile of the expression of the molecules was also integrated to search for a pattern of the expression that may have clinical significance including the survival of the patients. Results. Marvel-D3 had significantly high levels in breast cancer tissues than normal tissues (p=0.011). The difference between normal and tumour tissues for two Marvel-D3 variants were not statistically significant. Of all the known Marvel-D3 interactive proteins that were available for analyses, we identified thirteen with viability in integrated analyses; they include the JAM family members, Marvel-D2, occludin, the zonula occluden family members, small number of the claudin family members and cingulin, all being important TJ components. The integrated expression of these Marvel-D3 partners presented a highly significant predictive power for the overall survival of the patients (RUC=0.821, p< 0.0001). Stratifying the patients based on the profile has a significant value in evaluating survival (survival rate 95.7% with favourable expression versus 57.1% unfavourable, during the followup period). This predictive power is independent of other clinical and hormonal receptor status (p< 0.001, HR=1.226 (95% CI 1.094-1.373)). We have also noted that this predictive value is applicable to subtypes of the breast cancer and hormone receptor status with similar predictive power. Conclusion. Expression of Marvel-D3, a TJ component, together with its interactive TJ partners, including both transmembrane and intracellular subcoat proteins, form an important clinical indicator for clinical progression of breast cancer. Citation Format: WENXIAO JI, Wen G. Jiang, Tracey A. Martin. Marvel D3 and its associated junctional proteins in breast cancer [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P2-26-20.

Professor David Brynmor Thomas

Professor David Brynmor Thomas

Family-Based Designs that Disentangle Inherited Factors from Pre- and Postnatal Environmental Exposures: In Vitro Fertilization, Discordant Sibling Pairs, Maternal versus Paternal Comparisons, and Adoption Designs.

Identifying environmental risk and protective exposures that have causal effects on health is an important scientific goal. Many environmental exposures are nonrandomly allocated and influenced by dispositional factors including inherited ones. We review family-based designs that can separate the influence of environmental exposures from inherited influences shared between parent and offspring. We focus on prenatal exposures. We highlight that the family-based designs that can separate the prenatal environment from inherited confounds are different to those that are able to pull apart later-life environmental exposures from inherited confounds. We provide a brief review of the literature on maternal smoking during pregnancy and offspring attention-deficit/hyperactivity disorder (ADHD) and conduct problems; these inconsistencies in the literature make a review useful and this illustrates that results of family-based genetically informed studies are inconsistent with a causal interpretation for this exposure and these two offspring outcomes.

Brian Frost-Smith: physician, author, and horologist

Brian Frost-Smith was born in Liverpool, in the year of the general strike, to Jane and Percy, both teachers at Appleby Grammar School. At the age of 11 he developed...

John Gwyn Thomas

John Gwyn Thomas (“Gwyn”) was born and educated in Denbigh. After national service he entered the Welsh National School of Medicine in Cardiff, where he met Mari Beddow. They married...

Anthony David Griffiths

Anthony David Griffiths (“Tony”) was born on 5 March 1937 in Merthyr Tydfil. Tony’s mother, Eira (nee Lewis), was a haberdasher and needlewoman, and his father, Trefor, and grandfather were...

William Charles Donald Lovett

William Charles Donald Lovett (“Donald”) was born in Ystradowen in the Vale of Glamorgan, the eldest son of two school teachers. He was educated at Caerleon, where his father was...

Getting to the core of medicine: Developing undergraduate forensic medicine and pathology teaching

Teaching and learning of forensic medicine and pathology in the undergraduate medical curriculum has been in decline for decades in the UK, and yet graduates are expected to be able to recognise, and protect, those who are most vulnerable in society – i.e. at risk of abuse or neglect - a matter highly relevant to the role of the forensic medical practitioner.When Cardiff University School of Medicine created a new ‘learner-centred’ undergraduate curriculum, championing case-based discussion in small groups, and earlier clinical contact, residual teaching on ‘the pathology of trauma’ disappeared. An opportunity to create a new course for the year 3 core curriculum, however, led to re-emergence of forensic medicine and pathology, with a focus on identification, and protection, of the ‘vulnerable patient’.This paper describes the development process of the first two iterations of that course, and the influence of ‘listening to the student voice’.Forensic medicine and pathology remain relevant in undergraduate medical education; effective, and ethical, safeguarding of the vulnerable is an essential ‘core’ skill of the modern medical graduate, and forensic medical practitioners can play an integral role in the preparation of medical students for their future clinical practice.

John Stuart Morris

John Stuart Morris was born in Merthyr Tydfil. He qualified from the Welsh National School of Medicine in 1963. At medical school he met Lucy, who became his wife. After...

Basic and clinical science posters: Type 1 diabetes

Aims and objectives: Interventional trials in new‐onset Type 1 diabetes rely on recruiting patients within a short time window, aiming for optimal residual c‐peptide levels. Conducting these trials is dependent on improving current recruitment strategies. We aimed to identify the factors influencing effective recruitment to interventional trials of new‐onset Type 1 diabetes. Methods: Factors and measures influencing recruitment to new‐onset Type 1 diabetes trials were examined for all referrals to the Diabetes Research Group at Cardiff University School of Medicine between January and December 2015. Results: From 65 patient referrals, 61.6% of were from local hospitals and 38.4% from other diabetes research networks. 81.5% of referred patients responded to the initial contact, 86.8% of them showed an interest in research. Forty four out of 45 patients who could commit their time to trials had Type 1 diabetes. Only 43.2% of these patients were eligible and willing to take part in the trials. Inconvenience, distance and work commitments counted for 52% of the reasons for unsuitability; leaving 13 patients. Only three out of 18 willing and eligible patients participated in trials after they received the information sheet. Conclusion: Recruiting patients with new‐onset Type 1 diabetes to clinical trials within a short time after diagnosis is challenging for patients and research teams. More than half of the recruitment barriers can be modified by taking extra steps to facilitate participation. Further studies including surveys on big cohorts of newly‐diagnosed patients are required to study the factors influencing recruitment with potential input when designing future trials.

Douglas B Brewer

Douglas Bertram Brewer was an eminent renal pathologist. He was important in the development both of the understanding of kidney diseases and of the specialty of renal biopsy pathology—for example,...

In Memoriam: David A. Flockhart, 1952–2015

We lost David Flockhart on Thanksgiving Day, 2015. He was 63 years old, and had battled cancer for more than a year. David Flockhart was a pioneer and innovator in the field of pharmacogenetics. His conceptual contributions to pharmacogenomics date back more than 20 years, when most of us were learning to recognize the word. He is best known for his work on the pharmacogenomics of breast cancer, and the responsiveness of the disease to tamoxifen and aromatase inhibitor treatment. He also made major contributions to understanding the genetic basis for individual variations in pharmacokinetics and clinical response to warfarin, clopidogrel, opiates, antiretroviral drugs, and antidepressants. Despite his conviction of the importance of medical genetics and pharmacogenomics, David retained a critical and questioning outlook, cautioning us about the limitations of the discipline, and the potential downside of widespread or routine genetic profiling. David's scientific work was consistently insightful and of high scientific merit, but his overall objective always was to improve the length and quality of life of ill patients. As such, his impact on both biomedical science and clinical patient care was broad and profound. David was a native of Scotland—the oldest of five children born to D. Ross Flockhart and Pamela Ellison Flockhart. Following his early education in Aberdeen and Edinburgh, he received his undergraduate degree from the University of Bristol in 1973, and his Ph.D. in biochemistry from the Welsh National School of Medicine in 1976. David came to Nashville in 1976, serving first as post-doctoral research associate, then as assistant professor, in the Department of Physiology at Vanderbilt University through 1984. David's soul was set on becoming a physician—he wanted to assure that the science had an impact on humanity. He enrolled at the University of Miami School of Medicine, graduating in 1987. He did his residency training in internal medicine at Georgetown University, finishing as chief medical resident at the Fairfax Hospital in 1991. His voluntary shouldering of the chief residency position—one of medicine's thankless and relentless tasks—says a great deal about David's dedication to patient care and medical education. The same dedication persisted throughout the rest of his career. Following residency, David stayed on for fellowship training in clinical pharmacology at the legendary Georgetown University Division of Clinical Pharmacology, with Ray Woosley as his mentor. David joined the faculty in 1993, and rose to tenured associate professor in 1999. He was named Chair and Chief of the Division in 2000, and was a consistent advocate for and supporter of the discipline of clinical pharmacology. Craig Brater recruited David to Indiana University School of Medicine in 2001, where he became Professor of Medicine, Pharmacology, and Medical Genetics, and Director of Clinical Pharmacology. He was appointed as the Gladstein Chair in Cancer Genomics in 2007, and Director of the Indiana University Institute for Personalized Medicine in 2011. David Flockhart was a national and international leader in cancer pharmacogenomics. He served on or directed numerous scientific symposia, workshops, and policy-making advisory groups. He served as Principal Investigator for the NIH Pharmacogenetics Research Network, and for the Consortium on Breast Cancer Pharmacogenomics. He participated as visiting scientist or guest speaker at the invitation of numerous academic institutions, medical and scientific societies, hospitals, and government agencies. The quality and impact of David's work has been recognized by his peers through awards such as the Rawls-Palmer Progress in Medicine Award from the American Society for Clinical Pharmacology and Therapeutics (2011), and the Nathaniel T. Kwit Distinguished Service Award from the American College of Clinical Pharmacology (2009). With no hesitation, he accepted our invitation to serve on the Editorial Board of Clinical Pharmacology in Drug Development, despite a number of existing editorial board commitments. Above all, David remained devoted to his patients and his students. He was kind and compassionate to the patients under his care, and spent as much time as necessary to assure their best possible treatment. To his students and trainees he was equally devoted, enthusiastic, careful, and thorough. He always believed that scientific advances had to be translated into improved patient care. David loved his family. He loved music, and took great pride in his Scottish beginnings. He retained the quaint Scottish lilt to his speech. David Flockhart was a great scientist, colleague, and friend. We will miss him.

A Novel Student-Led Approach to Multiple-Choice Question Generation and Online Database Creation, With Targeted Clinician Input

Problem: Multiple-choice questions (MCQs) are the main method of assessing medical student knowledge. As a result there is a high demand from medical students for formative MCQs. However, teaching staff rarely have the time or incentive to develop high-quality formative questions, focusing instead on material for high-stakes assessments. Intervention: We have developed a novel student-led approach involving an interactive online question database, created by medical students for medical students. We adopted a staged approach to create an online bank of formative MCQ questions. First, students write MCQs following a standardized format. Questions are then peer-reviewed by other students, discussing relevant clinical topics, guidelines, and journals to improve question quality. The questions are then scrutinized by specialist doctors and academics. Next, questions are piloted online. Finally, question performance is evaluated statistically. This 5-stage student-led process produced a bank of more than 200 MCQs in three months. Context: This intervention was carried out by two final-year medical student leads at Cardiff University School of Medicine, UK. Final-year students were recruited to write and peer-review questions, and senior content specialists were recruited from the department. After piloting and evaluation of the questions, the question bank was made available as a learning resource to all medical students at Cardiff University. Outcome: Objective analysis of the created MCQs (discrimination indices and distractor analysis) indicated that the random sample of questions piloted were of high quality. When the questions were made available as online tests to approximately 600 students, usage data revealed that 2,800 tests were taken over a 3-month period, indicating that the resource was popular. In addition, subjective feedback from students question writers/reviewers was gathered via free text feedback forms and was invariably positive. We plan to continue the question generation process in Cardiff and would encourage other medical schools to adopt this approach. Lessons Learned: Our 5-stage approach can generate a large volume of high-quality MCQs, addressing the demand from students for formative MCQ questions, with minimal teaching staff input. The project's benefits go beyond the creation of the resource, as involving students in the writing, review, and presentation of questions itself is useful pedagogically.

Motor neurone disease: through patient and practitioner eyes

The inaugural joint conference of the Motor Neurone Disease Association (MND Association) and the Royal College of Nursing (RCN) was held on 5 November 2014 at the RCN headquarters in London. The conference is to be followed by a programme of educational open lectures on different aspects of MND throughout 2015 and then with an e-learning package, to be released in 2016. The aim of the event was to highlight the importance of individualised patient care. The day focused on: how the different roles within the multidisciplinary health-care team come together to provide the highest quality of care; and how to increase understanding of this complex and devastating disease. The four themes of the event were management of: cognitive; limb; respiratory; and bulbar symptoms. The theme of palliative care and support ran through all sessions. The meeting was attended by a varied group of health professionals, including specialist and non-specialist nurses, palliative and hospice nurses, occupational therapists, general practitioners and consultants. The talks, delivered by different practitioners within the healthcare team, provided an overall picture of the multiple aspects of care involved for MND patients at all stages of the disease. The meeting was opened by speeches from Sally Light, Chief Executive of the MND Association, Peter Carter, Chief Executive and General Secretary of the RCN, and Baroness Finlay of Llandaff, Professor of Palliative Medicine at Cardiff University School of Medicine, patron of the MND Association and independent crossbench member of the House of Lords. Baroness Findlay importantly reminded the audience that caring for patients with MND or any other disease, is about doing everything one can, regardless of one’s specific role in the health-care team, to ensure the patient feels valued. These words set the scene for what was a fascinating day of talks, sharing knowledge and catching up. The morning session began with a thought-provoking keynote lecture, also by Baroness Finlay, on choices at end of life and how the care team could have a positive influence in these discussions. Lucy Davies, a GP and clinical support fellow for rare diseases from the Royal College of General Practitioners described the difficulty of diagnosing Jennifer Franklin

ADHD Genes Also Influence Social, Cognitive Behaviors

Back to table of contents Previous article Next article Professional NewsFull AccessADHD Genes Also Influence Social, Cognitive BehaviorsNick ZagorskiNick ZagorskiSearch for more papers by this authorPublished Online:20 Nov 2014https://doi.org/10.1176/appi.pn.2014.11b24AbstractGenetic variants associated with a clinical diagnosis of ADHD correlate with lower attention, memory, and social language skills in children without the disorder.While clinicians have to make categorical decisions when diagnosing attention-deficit/hyperactivity disorder (ADHD), the traits that are characteristic of this disorder—inattentiveness, restlessness, impulsivity—occur at varying levels in every person.The question has been whether ADHD represents just an extreme of this natural spectrum or an abnormal state of inattention or impulsivity. Ruane Prize recipient Anita Thapar, M.B.B.Ch., Ph.D., presents her research at the Brain and Behavior Research Foundation symposium on how genetic variants for ADHD risk influence other behavioral traits.Mike CinelliSome new genetic studies suggest the former scenario may be the case. A team led by Anita Thapar, M.B.B.Ch., Ph.D., a professor at the Cardiff University School of Medicine in Wales, found that a cluster of risk genes often found in children with ADHD was also associated with behavioral and cognitive traits among the general population.The group used the Avon Longitudinal Study of Parents and Children (ALSPAC), a large study that has been monitoring children and their parents since 1991. They obtained genetic data for more than 8,200 ALSPAC children and gave each one a polygenic risk score based on the number of ADHD-associated gene variants they possessed Thapar had previously found that higher risk scores—composed from a library of thousands of individual variations that individually have a negligible effect on risk—were higher in children with a clinical ADHD diagnosis than in healthy controls. The new analysis in the ALSPAC group showed that a higher risk score also correlated with more inattention and hyperactivity in children without ADHD, as well as with traits such as pragmatic language, working memory, and IQ.“What’s interesting is that these traits are not typical diagnostic features of ADHD,” Thapar told Psychiatric News. “So these ADHD risk genes make contributions to other neurocognitive behaviors.”So in addition to providing molecular evidence to support the idea of ADHD as just one end of a broad behavioral spectrum, the findings also highlight the overlap between ADHD and related childhood disorders like autism spectrum disorder (ASD) and the new DSM-5 category of social communication disorder.Other behaviors found in patients with ASD, such as social cognition and facial emotion recognition, were not associated with these risk genes, however.Thapar, who was the recipient of this year’s Brain and Behavior Research Foundation’s Ruane Prize for Outstanding Achievement in Child and Adolescent Research for her contributions to ADHD genetics, hopes that continued analysis and refinement of these risk scores may help identify children with potential learning or attention difficulties, even if they do not manifest as clinical ADHD. However, as a child clinician herself, she stressed the importance of not extrapolating the results too far in regard to how ADHD is diagnosed and treated. “These findings are exciting, but as clinicians, we cannot prescribe treatments based on what may happen in the future; our decision making can be based only on what we see and what we know,” she said.These genetic studies were published as two related papers in Biological Psychiatry and the Journal of Child Psychology and Psychiatry. The work was funded by the United Kingdom Medical Research Council and the Wellcome Trust. ■An abstract of “Genetic Risk for Attention-Deficit/Hyperactivity Disorder Contributes to Neurodevelopmental Traits in the General Population” can be accessed here. An abstract of “Neurocognitive Abilities in the General Population and Composite Genetic Risk Scores for Attention-Deficit/Hyperactivity Disorder” is available here. ISSUES NewArchived

Barrie Patrick Marmion

Barrie Patrick Marmion excelled as a clinical microbiologist, medical researcher and academic, mentor to many younger colleagues, and outstanding human being. His professional life and activity stretched more than 70...