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Head and Neck Cancer: United Kingdom National Multidisciplinary Guidelines, Sixth Edition
- Jarrod J Homer, Stuart C Winter, Elizabeth C Abbey, Hiba Aga, Reshma Agrawal, Derfel ap Dafydd, Takhar Arunjit, Patrick Axon, Eleanor Aynsley, Izhar N Bagwan, Arun Batra, Donna Begg, Jonathan M Bernstein, Guy Betts, Colin Bicknell, Brian Bisase, Grainne C Brady, Peter Brennan, Aina Brunet, Val Bryant, Linda Cantwell, Ashish Chandra, Preetha Chengot, Melvin L K Chua, Peter Clarke, Gemma Clunie, Margaret Coffey, Clare Conlon, David I Conway, Florence Cook, Matthew R Cooper, Declan Costello, Ben Cosway, Neil J A Cozens, Grant Creaney, Daljit K Gahir, Stephen Damato, Joe Davies, Katharine S Davies, Alina D Dragan, Yong Du, Mark R D Edmond, Stefano Fedele, Harriet Finze, Jason C Fleming, Bernadette H Foran, Beth Fordham, Mohammed M A S Foridi, Lesley Freeman, Katherine E Frew, Pallavi Gaitonde, Victoria Gallyer, Fraser W Gibb, Sinclair M Gore, Mark Gormley, Roganie Govender, J Greedy, Teresa Guerrero Urbano, Dorothy Gujral, David W Hamilton, John C Hardman, Kevin Harrington, Samantha Holmes, Jarrod J Homer, Deborah Howland, Gerald Humphris, Keith D Hunter, Kate Ingarfield, Richard Irving, Kristina Isand, Yatin Jain, Sachin Jauhar, Sarra Jawad, Glyndwr W Jenkins, Anastasios Kanatas, Stephen Keohane, Cyrus J Kerawala, William Keys, Emma V King, Anthony Kong, Fiona Lalloo, Kirsten Laws, Samuel C Leong, Shane Lester, Miles Levy, Ken Lingley, Gitta Madani, Navin Mani, Paolo L Matteucci, Catriona R Mayland, James McCaul, Lorna K McCaul, Pádraig McDonnell, Andrew McPartlin, Valeria Mercadante, Zoe Merchant, Radu Mihai, Mufaddal T Moonim, John Moore, Paul Nankivell, Sonali Natu, A Nelson, Pablo Nenclares, Kate Newbold, Carrie Newland, Ailsa J Nicol, Iain J Nixon, Rupert Obholzer, James T O'Hara, S Orr, Vinidh Paleri, James Palmer, Rachel S Parry, Claire Paterson, Gillian Patterson, Joanne M Patterson, Miranda Payne, L Pearson, David N Poller, Jonathan Pollock, Stephen Ross Porter, Matthew Potter, Robin J D Prestwich, Ruth Price, Mani Ragbir, Meena S Ranka, Max Robinson, Justin W G Roe, Tom Roques, Aleix Rovira, Sajid Sainuddin, I J Salmon, Ann Sandison, Andy Scarsbrook, Andrew G Schache, A Scott, Diane Sellstrom, Cherith J Semple, Jagrit Shah, Praveen Sharma, Richard J Shaw, Somiah Siddiq, Priyamal Silva, Ricard Simo, Rabin P Singh, Maria Smith, Rebekah Smith, Toby Oliver Smith, Sanjai Sood, Francis W Stafford, Neil Steven, Kay Stewart, Lisa Stoner, Steve Sweeney, Andrew Sykes, Carly L Taylor, Selvam Thavaraj, David J Thomson, Jane Thornton, Neil S Tolley, Nancy Turnbull, Sriram Vaidyanathan, Leandros Vassiliou, John Waas, Kelly Wade-McBane, Donna Wakefield, Amy Ward, Laura Warner, Laura-Jayne Watson, H Watts, Christina Wilson, Stuart C Winter, Winson Wong, Chui-Yan Yip, Kent Yip
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- Journal:
- The Journal of Laryngology & Otology / Volume 138 / Issue S1 / April 2024
- Published online by Cambridge University Press:
- 14 March 2024, pp. S1-S224
- Print publication:
- April 2024
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57 CSF Markers of AD-Related Pathology Relate to aMCI among People with HIV
- Judith D. Lobo, Erin E. Sundermann, Laura M. Campbell, Ben Gouaux, Scott Letendre, Mark W. Bondi, David J. Moore
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- Journal:
- Journal of the International Neuropsychological Society / Volume 29 / Issue s1 / November 2023
- Published online by Cambridge University Press:
- 21 December 2023, pp. 53-54
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Objective:
Older people with HIV (PWH) are at-risk for Alzheimer’s disease (AD) and its precursor, amnestic mild cognitive impairment (aMCI). Identifying aMCI among PWH is challenging because memory impairment is also common in HIV-associated neurocognitive disorders (HAND). The neuropathological hallmarks of aMCI/AD are amyloid-ß42 (Aß42) plaque and phosphorylated tau (p-tau) accumulation. Neurofilament light chain protein (NfL) is a marker of neuronal injury in AD and other neurodegenerative diseases. In this study, we assessed the prognostic value of the CSF AD pathology markers of lower Aß42, and higher p-tau, p-tau/Aß42 ratio, and NfL levels to identify an aMCI-like profile among older PWH and differentiating it from HAND. We assessed the relationship between aMCI and HAND diagnosis and AD biomarker levels
Participants and Methods:Participants included 74 PWH (Mean age=48 [SD=8.5]; 87.4% male, 56.5% White) from the National NeuroAIDS Tissue Consortium (NNTC). CSF Aß42, Aß40, p-tau and NfL were measured by commercial immunoassay. Participants completed a neurocognitive evaluation assessing the domains of learning, recall, executive function, speed of information processing, working memory, verbal fluency, and motor. Memory domains were assessed with the Hopkins Verbal Learning Test-Revised and the Brief Visuospatial Memory Test-Revised, and aMCI was defined as impairment (<1.0 SD below normative mean) on two or more memory outcomes among HVLT-R and BVMT-R learning, delayed recall and recognition with at-least one recognition impairment required. HAND was defined as impairment (<1.0 SD below normative mean) in 2 or more cognitive domains. A series of separate linear regression models were used to examine how the levels of CSF p-tau, Aß42, p-tau/Aß42 ratio, and NfL relate to aMCI and HAND status while controlling for demographic variables (age, gender, race and education). Covariates were excluded from the model if they did not reach statistical significance.
Results:58% percent of participants were diagnosed with HAND, 50.5% were diagnosed with aMCI. PWH with aMCI had higher levels of CSF p-tau/Aß42 ratio compared to PWH without aMCI (ß=.222, SE=.001, p=.043) while controlling for age (ß=.363, p=.001). No other AD biomarker significantly differed by aMCI or HAND status.
Conclusions:Our results indicate that the CSF p-tau/Aß42 ratio relates specifically to an aMCI-like profile among PWH with high rates of cognitive impairment across multiple domains in this advanced HIV disease cohort. Thus, the p-tau/Aß42 ratio may have utility in disentangling aMCI from HAND and informing the need for further diagnostic procedures and intervention. Further research is needed to fully identify, among a broader group of PWH, who is at greatest risk for aMCI/AD and whether there is increased risk for aMCI/AD among PWH as compared to those without HIV.
Long-term data for endemic frog genera reveal potential conservation crisis in the Bale Mountains, Ethiopia
- David J. Gower, Roman K. Aberra, Silvia Schwaller, Malcolm J. Largen, Ben Collen, Stephen Spawls, Michele Menegon, Breda M. Zimkus, Rafael de Sá, Abebe A. Mengistu, Fikirte Gebresenbet, Robin D. Moore, Samy A. Saber, Simon P. Loader
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Populations of many frogs have declined alarmingly in recent years, placing nearly one third of the > 6,000 species under threat of extinction. Declines have been attributed largely to habitat loss, environmental degradation and/or infectious diseases such as chytridiomycosis. Many frogs undergo dramatic natural population fluctuations such that long-term data are required to determine population trends without undue influence of stochastic factors. We present long-term quantitative data (individuals encountered per person hour of searching) for four monotypic frog genera endemic to an Afromontane region of exceptional importance but growing conservation concern: one endemic to the Ethiopian highlands (Spinophrynoides osgoodi) and three endemic to the Bale Mountains (Altiphrynoides malcolmi, Balebreviceps hillmani, Ericabatrachus baleensis), collected during 15 field trips to the Bale Mountains between 1971 and 2009. Only a single confirmed sighting of S. osgoodi has been made since 1995. The other three species have also declined, at least locally. E. baleensis appears to have been extirpated at its type locality and at the same site B. hillmani has declined. These declines are in association with substantial habitat degradation caused by a growing human population. Chytrid fungus has been found on several frog species in Bale, although no dead or moribund frogs have been encountered. These results expose an urgent need for more amphibian surveys in the Bale Mountains. Additionally, we argue that detrimental human exploitation must be halted immediately in at least some parts of the Harenna Forest if a conservation crisis is to be averted.
Chapter Thirteen - Plant secondary metabolite polymorphisms and the extended chemical phenotype
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- By Glenn R. Iason, Ecological Sciences Group, The James Hutton Institute, Ben D. Moore, Ecological Sciences Group, The James Hutton Institute, Jack J. Lennon, Ecological Sciences Group, The James Hutton Institute, Jenni A. Stockan, Ecological Sciences Group, The James Hutton Institute, Graham H. R. Osler, Ecological Sciences Group, The James Hutton Institute, Colin D. Campbell, Ecological Sciences Group, The James Hutton Institute, David A. Sim, Ecological Sciences Group, The James Hutton Institute, Joan R. Beaton, Ecological Sciences Group, The James Hutton Institute, Joanne R. Russell, The James Hutton Institute
- Edited by Glenn R. Iason, Marcel Dicke, Wageningen Universiteit, The Netherlands, Susan E. Hartley, University of York
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- Book:
- The Ecology of Plant Secondary Metabolites
- Published online:
- 05 August 2012
- Print publication:
- 19 April 2012, pp 247-268
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Summary
Introduction
As it was originally proposed, the extended phenotype comprised ‘all effects of a gene upon the world’ (Dawkins, 1989) and portrayed how the effects of a gene borne by an organism influenced its biotic and abiotic environments. The consideration of indirect genetic effects, in which an organism’s phenotype becomes part of the selective environment of conspecifics (Wolf et al., 1998), was developed rigorously in the population genetics context and the concept subsequently extended to include effects on heterospecifics (Whitham et al., 2003). The extended phenotype concept has been adopted as a framework by some evolutionary biologists and ecologists to study the roles of plant secondary metabolites (PSMs) since Whitham et al. (2003) used heritable variation in tissue tannin concentrations among Populus species and hybrids to develop the concept of community and ecosystem genetics (Antonovics, 1992).
Many studies of how genetically determined variation in plant traits, including PSMs, drive associated community phenotypes and processes, have been based on differences between hybrids (Dungey et al., 2000; Hochwender & Fritz, 2004; Bailey et al., Chapter 14). Fewer studies have investigated the effects on extended phenotypes of continuously varying PSMs or between known genotypes within a species (Whitham et al., 2006; Schweitzer et al., 2008; Barbour et al., 2009; O’Reilly-Wapstra et al., Chapter 2). A convenient approach to identification and utilisation of genotypic variation for the study of multiple effects of PSMs is provided by the use of genetic polymorphisms. A polymorphism can be defined as occurring when a trait such as a morphological or biochemical character exists in two or more distinct forms in a randomly mating population within a species (Ford, 1975). The approach is particularly useful in species that cannot be readily cloned. Here, we review examples of how intra-specific variation in a particular group of PSMs, the monoterpenes, has informed our understanding of how PSMs can play multiple ecological roles and mediate the extended phenotype of plants. The monoterpenes are a group of low-molecular-weight, volatile terpenoids which form a very diverse group in terms of number of compounds, structure and function (Gershenzon & Dudareva, 2007). We use variation within species which are polymorphic for concentrations or presence of monoterpenes to provide an insight into their ecological ramifications and larger-scale consequences, against the background of intra-specific variation in other traits.
Chapter Twelve - Integrating the effects of PSMs on vertebrate herbivores across spatial and temporal scales
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- By Ben D. Moore, Ecological Sciences Group, The James Hutton Institute, Jane L. DeGabriel, School of Biological Sciences, University of Aberdeen
- Edited by Glenn R. Iason, Marcel Dicke, Wageningen Universiteit, The Netherlands, Susan E. Hartley, University of York
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- The Ecology of Plant Secondary Metabolites
- Published online:
- 05 August 2012
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- 19 April 2012, pp 226-246
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Summary
Introduction
Since Fraenkel (1959) proposed a leading role for plant secondary metabolites (PSMs) in the interactions between plants and herbivores, science has achieved broad insight into the diversity of PSMs and herbivores’ counter-adaptations to them (Freeland & Janzen, 1974; Foley et al., 1999; Foley & Moore, 2005). However, the more we learn about the distributions and functions of PSMs in natural systems, the sharper the limitations of our understanding become. In countless plant–herbivore interactions, ecologists have identified PSMs that act as feeding deterrents, toxins, digestibility reducers, feeding or oviposition cues, and signals for communicating to neighbouring plants and natural enemies of herbivores. However, most studies focus on the interaction between single species of herbivore and plant, usually with observations of captive animals fed diets containing PSMs under highly simplified conditions. Although such approaches are a necessary first step in isolating and characterising the actions of PSMs, they greatly oversimplify the complex interactions that occur between wild herbivores and plants. The next challenge for ecologists is to ‘scale up’ the roles of PSMs in plant–herbivore interactions, as we understand them from controlled experiments at small temporal scales, to predict ecological interactions at greater temporal and spatial extents.
A captive herbivore may commonly eat less as PSM concentrations in its food increase, but can this predict the foraging decisions of a wild animal within its home range, or, ultimately the distributions and abundances of plant and herbivore species and genotypes? Scaling up has an obvious spatial component, because wild animals forage more extensively than do captive animals, but it also has a temporal component. Experiments usually describe plant–herbivore interactions over very short time intervals, but in nature they are continuous and the effects of PSMs can be long-lasting (Cheeke, 1998). Animal feeding preferences are dynamic and often change with season or reproductive state, or through the ongoing process of refinement of conditioned flavour aversions (Provenza, 1996). With increasing spatial extent and finer spatial grain size comes greater complexity in the interactions between plants and animals; PSMs are rarely distributed evenly throughout landscapes, and understanding how this influences plant–animal interactions requires approaches adopted from resource ecology, foraging theory and spatial ecology and often an extensive, high-resolution picture of the foodscapes within which animals forage (van Langevelde & Prins, 2008).
The relationship of social function to depressive and negative symptoms in individuals at clinical high risk for psychosis
- C. M. Corcoran, D. Kimhy, M. A. Parrilla-Escobar, V. L. Cressman, A. D. Stanford, J. Thompson, S. Ben David, A. Crumbley, S. Schobel, H. Moore, D. Malaspina
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- Journal:
- Psychological Medicine / Volume 41 / Issue 2 / February 2011
- Published online by Cambridge University Press:
- 06 May 2010, pp. 251-261
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Background
Social dysfunction is a hallmark symptom of schizophrenia which commonly precedes the onset of psychosis. It is unclear if social symptoms in clinical high-risk patients reflect depressive symptoms or are a manifestation of negative symptoms.
MethodWe compared social function scores on the Social Adjustment Scale-Self Report between 56 young people (aged 13–27 years) at clinical high risk for psychosis and 22 healthy controls. The cases were also assessed for depressive and ‘prodromal’ symptoms (subthreshold positive, negative, disorganized and general symptoms).
ResultsPoor social function was related to both depressive and negative symptoms, as well as to disorganized and general symptoms. The symptoms were highly intercorrelated but linear regression analysis demonstrated that poor social function was primarily explained by negative symptoms within this cohort, particularly in ethnic minority patients.
ConclusionsAlthough this study demonstrated a relationship between social dysfunction and depressive symptoms in clinical high-risk cases, this association was primarily explained by the relationship of each of these to negative symptoms. In individuals at heightened risk for psychosis, affective changes may be related to a progressive decrease in social interaction and loss of reinforcement of social behaviors. These findings have relevance for potential treatment strategies for social dysfunction in schizophrenia and its risk states and predict that antidepressant drugs, cognitive behavioral therapy and/or social skills training may be effective.