1,007 research outputs found
Ferguson-Smith, Malcolm: transcript of a video interview (06-Jun-2015)
No full textInterview with Professor Malcolm Ferguson-Smith, conducted by Ms Emma M. Jones, for the History of Modern Biomedicine Research Group, 06 June 2015, in Glasgow. Transcribed by Mrs Debra Gee, and edited by Professor Tilli Tansey and Mr Alan Yabsley. The project management was undertaken by Mr Adam Wilkinson. Professor Malcolm Ferguson-Smith (b. 1931) is Emeritus Professor of Pathology, University of Cambridge. He graduated in medicine at Glasgow University in 1955 and, while undertaking postgraduate training there in pathology, was introduced to research on sex chromatin under Bernard Lennox. An interest in Klinefelter’s syndrome in 1957 to 1958 led to his appointment as Fellow in Medicine at Johns Hopkins University, Baltimore, in 1959, where he established the first chromosome diagnostic service in the USA, and undertook cytogenetic research into Turner syndrome. Research interests include molecular cytogenetics, karyotype evolution, vertebrate sex determination and comparative genomics. He is joint author of 'Essential Medical Genetics'.The History of Modern Biomedicine Research Group is funded by the Wellcome Trust, which is a registered charity (no. 210183). The current interview has been funded by the Wellcome Trust Strategic Award entitled “Makers of modern biomedicine: testimonies and legacy” (2012-2017; awarded to Professor Tilli Tansey)
Book Review of Confederate Outlaw: Champ Ferguson and the Civil War in Appalachia
No full textReview of: Confederate Outlaw: Champ Ferguson and the Civil War in Appalachia. By Brian D. McKnight. Conflicting Worlds: New Dimensions of the American Civil War. (Baton Rouge: Louisiana State University Press, 2011. Pp. [xvi], 252. $34.95, ISBN 978-0-8071-3769-7.)
Excerpt:
Civil War scholars have produced a number of noteworthy studies of guerrilla warfare in recent years. These historians have reassessed the origins of guerrilla violence, its impact on local communities, its role in the overall war effort, and some of its notorious figures. In Confederate Outlaw: Champ Ferguson and the Civil War in Appalachia, Brian D. McKnight addresses not only the infamous guerrilla Champ Ferguson but also the larger context of the war in southern Appalachia. The author argues that fluid loyalties, extreme paranoia, and opportunism defined Ferguson\u27s war in the Upper Cumberland region [...
A Computational Investigation into the Authorship of Sister Peg
No full textThis article engages with the longstanding debate over the authorship of the Scottish Militia pamphlet Sister Peg (1761). While previous evidence is born out of rigorous historical research, a debate remains between whether Adam Ferguson or David Hume was the author. This article uses computational stylometry to statistically investigate this question, with the aim of complementing existing historical evidence rather than overturning it. In doing this it concludes that the work was not written solely by David Hume and, instead, Adam Ferguson is likely to be the sole author or there was a more complicated history of co-authorship
Haemorrhagic kidney syndrome of Atlantic salmon, Salmo salar L.
No full textThis report describes a new syndrome affecting farmed Atlantic salmon on the Canadian east coast that has resulted in increased morbidity and mortality in affected stocks. The major pathological findings are apparent only microscopically and include renal interstitial haemorrhage and acute tubular necrosis and tubular casting. As a result, the disease has become known as haemorrhagic kidney syndrome (HKS). Affected fish are lethargic and anorectic, and lark external lesions. Clinically, HKS fish are anaemic, hypoproteinaemic and hyperosmolalic, with increased serum concentrations of sodium and chloride. At necropsy, internal changes ranged from apparently normal to include one or several of the following: swelling and/or patchy reddening of the kidney, pale gills, exophthalmos, serosanguinous ascites, darkening of the posterior intestine and splenomegaly. Ultrastructurally, viral inclusions were found in the cytoplasm of erythrocytes of HKS fish, and there were unusual electron-dense inclusions within the tips of renal tubular microvilli of HKS fish. The significance and relevance of the ultrastructural findings to HKS are unknown. Virus isolation was attempted using CHSE, RTG-2, FH-10, BE and EPC cell lines; no virus was isolated. Bacteriological analysis failed to reveal significant pathogens. Analysis of tissues for heavy metals and pesticides was negative. Assays for clostridial toxins, lipopolysaccharide and verotoxins were negative. The aetiology of HKS remains unresolved.PT: J; CR: AHNE W, 1989, VIRUSES LOWER VERTEB, V3 ARMSTRONG R, 1993, CAN VET J, V34, P312 AUSTIN B, 1993, BACTERIAL FISH PATHO BOVO G, 1995, DIS AQUAT ORGAN, V21, P115 CONFER AW, 1995, THOMSONS SPECIAL VET, P209 DANNEVIG BH, 1995, J GEN VIROL, V76, P1353 EATON WD, 1993, J GEN VIROL, V74, P2299 EVENSEN O, 1991, RES VET SCI, V51, P215 FERGUSON HW, 1982, VET PATHOL, V19, P687 FOOTT JS, 1992, J AQUAT ANIM HEALTH, V4, P306 HETRICK FM, 1993, ANN REV FISH DIS, V3, P187 KIMURA T, 1986, DIS AQUAT ORGAN, V1, P209 KIMURA T, 1989, VIRUSES LOWER VERTEB, V3 KOSKI P, 1992, BULL EUR ASSN FISH P, V12, P177 LAMAS J, 1995, J FISH DIS, V18, P425 MEIER W, 1994, ANN REV FISH DIS, V4, P359 NOUGAYREDE P, 1992, B EUROPEAN ASS FISH, V12, P5 PINTO RA, 1992, J AQUATIC ANIMAL HLT, V4, P292 ROBERTS RJ, 1994, RECENT ADV AQUACULTU, V5 SANO T, 1995, AQUACULTURE, V132, P43 SMITH LS, 1975, MISCELLANEOUS SPECIA, V27 SPEILBERG L, 1995, VET PATHOL, V32, P466 THOESEN JC, 1994, BLUE BOOK SUGGESTED TISHER CC, 1989, RENAL PATHOLOGY CLIN, V1 WADDELL TE, 1996, INFECT IMMUN, V64, P1714 WOLF K, 1988, FISH VIRUSES FISH VI WOOD CM, 1995, PHYSL ECOLOGY PACIFI; NR: 27; TC: 29; J9: J FISH DISEASES; PG: 11; GA: 170XZSource type: Electronic(1
Author Correction: Results of the phase IIa RADICAL trial of the FGFR inhibitor AZD4547 in endocrine resistant breast cancer (Nature Communications, (2022), 13, 1, (3246), 10.1038/s41467-022-30666-0)
No full text\ua9 The Author(s) 2023.In the original version of this article, the following author (Veronica Ferguson) was omitted from the author list. Author list, Author contributions and competing interests statements have now been updated in both the PDF and HTML versions of the article
Impact of obesity on cardiovascular disease
No full textObesity is associated with increased risk of cardiovascular disease (CVD), heart failure, diabetes, cancer, and ultimately all-cause mortality. Obesity is causally related to dyslipidemia, hypertension, and diabetes, all strong CVD risk factors, and so causally related to CVD risk. In fact, a substantial part of the risk imparted by obesity on CVD outcomes operates via traditional risk factors. Obese men are almost twice as likely and women almost two and half times as likely to develop hypertension. Obese individuals are around 50% more likely to have a stroke and have around 6–12 times higher risks of developing type 2 diabetes compared to those with a normal BMI.
Obesity is also linked to greater risk for development of heart failure. Yet, there appears to be an obesity paradox in established heart failure such that the risk of death is lower in overweight and mildly obese individuals than in those with normal weight. Such observations are likely partially driven by reverse causality whereby disease-specific issues drive weight loss rather than higher weight per se being protective.
While obesity is most commonly defined by BMI, the importance of body fat distribution and markers such as waist circumference, waist: hip ratio, visceral and ectopic fat volumes are becoming better appreciated. The concept of harmful fat distribution is therefore topical and recent evidence suggest those who can store more fat subcutaneously (and so delay their ectopic depot expansions until much heavier) have lesser diabetes and cardiovascular risks. This paradigm may also largely explain men’s greater risks for both chronic conditions at similar BMI’s to women.
Trials of weight loss add strong support for causal links between adiposity and CVD; for example, the best evidence suggests that losing around 1 kg reduces SBP by around 1 mmHg. Weight loss also improves lipid profiles with reduced total cholesterol, LDL-cholesterol, and in particular triglyceride levels. Weight loss of around 5 kg reduces the risk of obese individuals progressing to impaired glucose tolerance and type 2 diabetes. In those with type 2 diabetes, 5 to <10% intentional weight loss is associated with 3.5 times increased odds of obtaining a 0.5% reduction in HbA1c. Not surprisingly, substantial weight loss has been associated with significantly lower mortality from several causes.
This chapter will show how the best epidemiological evidence, using methods to lessen the impact of reverse causality, supports strong graded links between adiposity and CVD. It will also examine and explain the apparent obesity paradox of heart failure. The chapter will then describe the effect on CVD outcomes of robust lifestyle and surgical intervention studies and trials. Finally, we will also explain how genetics data have helped support causal associations between increasing BMI and CVD, including understanding better the causal links between regional adiposity and CVD.
In conclusion, several lines of evidence, including observational, trial, and genetic, collectively support causal links between obesity, cardiovascular morbidity and mortality, and all-cause mortality
Impact of Obesity on Cardiovascular Disease
No full textObesity is associated with increased risk of cardiovascular disease (CVD), heart failure, diabetes, cancer, and ultimately all-cause mortality. Obesity is causally related to dyslipidemia, hypertension, and diabetes, all strong CVD risk factors, and so causally related to CVD risk. In fact, a substantial part of the risk imparted by obesity on CVD outcomes operates via traditional risk factors. Obese men are almost twice as likely and women almost two and half times as likely to develop hypertension. Obese individuals are around 50% more likely to have a stroke and have around 6–12 times higher risks of developing type 2 diabetes compared to those with a normal BMI.
Obesity is also linked to greater risk for development of heart failure. Yet, there appears to be an obesity paradox in established heart failure such that the risk of death is lower in overweight and mildly obese individuals than in those with normal weight. Such observations are likely partially driven by reverse causality whereby disease-specific issues drive weight loss rather than higher weight per se being protective.
While obesity is most commonly defined by BMI, the importance of body fat distribution and markers such as waist circumference, waist: hip ratio, visceral and ectopic fat volumes are becoming better appreciated. The concept of harmful fat distribution is therefore topical and recent evidence suggest those who can store more fat subcutaneously (and so delay their ectopic depot expansions until much heavier) have lesser diabetes and cardiovascular risks. This paradigm may also largely explain men’s greater risks for both chronic conditions at similar BMI’s to women.
Trials of weight loss add strong support for causal links between adiposity and CVD; for example, the best evidence suggests that losing around 1 kg reduces SBP by around 1 mmHg. Weight loss also improves lipid profiles with reduced total cholesterol, LDL-cholesterol, and in particular triglyceride levels. Weight loss of around 5 kg reduces the risk of obese individuals progressing to impaired glucose tolerance and type 2 diabetes. In those with type 2 diabetes, 5 to <10% intentional weight loss is associated with 3.5 times increased odds of obtaining a 0.5% reduction in HbA1c. Not surprisingly, substantial weight loss has been associated with significantly lower mortality from several causes.
This chapter will show how the best epidemiological evidence, using methods to lessen the impact of reverse causality, supports strong graded links between adiposity and CVD. It will also examine and explain the apparent obesity paradox of heart failure. The chapter will then describe the effect on CVD outcomes of robust lifestyle and surgical intervention studies and trials. Finally, we will also explain how genetics data have helped support causal associations between increasing BMI and CVD, including understanding better the causal links between regional adiposity and CVD.
In conclusion, several lines of evidence, including observational, trial, and genetic, collectively support causal links between obesity, cardiovascular morbidity and mortality, and all-cause mortality
Identification of the Kna/Knb polymorphism and a method for Knops genotyping
No full textDNA mutations resulting in the McCoy and Swain-Langley polymorphisms have been identified on complement receptor 1 (CR1)-a ligand for rosetting of Plasmodium falciparum-infected RBCs. The molecular identification of the Kna/Knb polymorphism was sought to develop a genotyping method for use in the study of the Knops blood group and malaria
Measuring business value and sustainability performance
No full textThe integration of corporate sustainability within operations remains an important and fundamental challenge for business. This paper first consolidates and then builds upon the EABIS-supported activities of Cranfield School of Management with business practitioners. It focuses on the performance and evaluation criteria relating to determining corporate responsibility (CR) value.
The paper begins by categorising components of CR in terms of decision-making levels and business case requirements. It then describes a methodology for establishing CR issues with the prioritisation of stakeholders before linking this relationship onto business benefits and shareholder value drivers. Using illustrated models and worked examples, sections within the paper provide further practical advice and guidance for developing and populating elements within the framework. Additional sections then complement the application of the CR Value-chain framework, with a chapter on performance measurement that explores the key performance measure characteristics required to underpin the performance element of the framework. The final chapter describes decision-making support tools, such as financial appraisals and risk evaluations, which also underpin the shareholder value approach and should be integrated within this corporate sustainability value management framework.
A key purpose of this approach is to support the integration of sustainability performance management processes and systems within business practice. It explores methods for making more explicit the issues surrounding CR and financial value. It also provides useful approaches for helping businesses select, measure and evaluate performance for internal CR strategies, policies and processes. Some analytical methods are considered for identifying the costs and benefits from sustainability-related issues, projects and new ventures, including discussions with regard to harmonising existing business functions.
This paper serves to provide an early prototype for future approaches towards integrated sustainability performance management systems.The European Academy for Business and Society, IBM, Johnson & Johnson, Microsoft, Shell and Unileve
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