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Search Results: 1 - 10 of 461850 matches for " A. A.;Hyslop "
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Prothetely in the Elaterid Genus Melanotus
J. A. Hyslop
Psyche , 1916, DOI: 10.1155/1916/91392
The Host of Zelia Vertebrata (Diptera, Dexlidae)
J. A. Hyslop
Psyche , 1916, DOI: 10.1155/1916/60584
Common Names and Taxonomy
J. A. Hyslop
Psyche , 1929, DOI: 10.1155/1929/69072
Elateridae and Throscidae of the Stanford University Expedition of 1911 to Brazil
J. A. Hyslop
Psyche , 1916, DOI: 10.1155/1916/52350
Observations on the Life History of Meracantha Contracta (Beauv)
J. A. Hyslop
Psyche , 1915, DOI: 10.1155/1915/68180
Development of sustainable georesources for the built environment in the United Kingdom
McMillan, Andrew A.,Hyslop Ewan K.
Estonian Journal of Earth Sciences , 2008,
Abstract: The character of the UK’s built heritage has been largely determined by the country’s diverse geology. Indigenous natural stone forms a major component of the nation’s pre-1919 building stock. Stone has been used traditionally for roofing, roads, pavements, bridges, engineering works, and all forms of walling. Today it is mostly employed as thin panel cladding to concrete frameworks in modern construction and is now increasingly being used in large volumes for new city streetscapes.This paper outlines the material requirements for the repair and maintenance of the stone-built heritage and illustrates a range of initiatives across the UK aimed at safeguarding and redeveloping indigenous resources. The importance, particularly for the repair and conservation sector, of selecting appropriate replacement stone is being recognized by architectural and conservation professionals and by local authority officials. There is also increasing recognition of the importance to the economy of the local character of the built environment in terms of its value to tourism and to architectural, historical, and cultural identity. The paper also examines the historical sources of information on stone in the UK and offers recommendations for databasing and disseminating stone resource information. This may assist the redevelopment of a healthy indigenous stone industry and ensure that the unique built heritage character of the UK is maintained and enhanced.
Coalescence of nanoscale metal clusters: Molecular-dynamics study
Shaun C. Hendy,Simon A. Brown,Michael Hyslop
Physics , 2003, DOI: 10.1103/PhysRevB.68.241403
Abstract: We study the coalescence of nanoscale metal clusters in an inert-gas atmosphere using constant-energy molecular dynamics. The coalescence proceeds via atomic diffusion with the release of surface energy raising the temperature. If the temperature exceeds the melting point of the coalesced cluster, a molten droplet forms. If the temperature falls between the melting point of the larger cluster and those of the smaller clusters, a metastable molten droplet forms and freezes.
Serum Monocyte Chemoattractant Protein-1 in Pancreatic Cancer
Jennifer Sullivan,Qiaoke Gong,Terry Hyslop,Harish Lavu,Galina Chipitsyna,Charles J. Yeo,Hwyda A. Arafat
Journal of Oncology , 2011, DOI: 10.1155/2011/518394
Abstract: Background/Aims. Pancreatic ductal adenocarcinoma (PDA) has etiological association with chronic inflammation. Elevated circulating levels of inflammatory mediators, such as monocyte chemoattractant protein-1 (MCP-1), are found in obese individuals. We hypothesized that serum MCP-1 levels are elevated in obese PDA patients. Methods. ELISA was used to analyze MCP-1 serum levels in PDA ( ) and intraductal papillary mucinous neoplasms (IPMN) ( ). Recursive partitioning statistical analysis investigated the relationship between log MCP-1 and clinicopathological parameters. Results. Log MCP-1 values were significantly ( ) elevated in patients with BMI ≥ 37.5. In patients with BMI < 37.5, average log MCP-1 values were significantly elevated in PDA patients when compared to IPMN patients. Within the IPMN group, higher log MCP-1 levels correlated with increased age. Recursive partitioning analysis of IPMN versus PDA revealed a strategy of predicting characteristics of patients who are more likely to have cancer. This strategy utilizes log MCP-1 as the primary factor and also utilizes smoking status, gender, and age. Conclusion. MCP-1 is a promising biomarker in pancreatic cancer. The potential of using MCP-1 to distinguish PDA from IPMN patients must be studied in larger populations to validate and demonstrate its eventual clinical utility. 1. Introduction With an estimated 35, 420 deaths in 2008, pancreatic cancer is the fourth leading cause of cancer death in the United States [1]. Pancreatic cancer has an overall five-year survival rate of only 4%, as fewer than 10% of patients' tumors are confined to the pancreas at the time of diagnosis. In most cases, the cancer has progressed to the point where surgical resection is impossible. In a disease that is still considered most often incurable, there remains a need for new strategies for prevention and novel methods for early diagnosis. One factor that is believed to have an important role in the development of pancreatic cancer is obesity. Obesity is defined as a body mass index (BMI) > 30, and in the United States, more than 30% of the population is classified as obese [2]. Several studies have shown that the adipose tissue is an active source of inflammatory mediators, suggesting that obesity causes a chronic, low-level inflammatory state [3]. This is thought to contribute to the development of many of the comorbidities found in obese patients, such as atherosclerosis, diabetes, and cancer [4, 5]. This concept is supported by studies that have observed altered chemokine levels and deceased cancer mortality
Selection of optimal reference genes for normalization in quantitative RT-PCR
Inna Chervoneva, Yanyan Li, Stephanie Schulz, Sean Croker, Chantell Wilson, Scott A Waldman, Terry Hyslop
BMC Bioinformatics , 2010, DOI: 10.1186/1471-2105-11-253
Abstract: We propose a robust approach for selecting optimal subset(s) of reference genes with the smallest variance of the corresponding normalizing factors. The normalizing factor variance estimates are based on the estimated unstructured covariance matrix of all available candidate reference genes, adjusting for all possible correlations. Robustness is achieved through bootstrapping all candidate reference gene data and obtaining the bootstrap upper confidence limits for the variances of the log-transformed normalizing factors. The selection of the reference gene subset is optimized with respect to one of the following criteria: (A) to minimize the variability of the normalizing factor; (B) to minimize the number of reference genes with acceptable upper limit on variability of the normalizing factor, (C) to minimize the average rank of the variance of the normalizing factor. The proposed approach evaluates all gene subsets of various sizes rather than ranking individual reference genes by their stability, as in the previous work. In two publicly available data sets and one new data set, our approach identified subset(s) of reference genes with smaller empirical variance of the normalizing factor than in subsets identified using previously published methods. A small simulation study indicated an advantage of the proposed approach in terms of sensitivity to identify the true optimal reference subset in the presence of even modest, especially negative correlation among the candidate reference genes.The proposed approach performs comprehensive and robust evaluation of the variability of normalizing factors based on all possible subsets of candidate reference genes. The results of this evaluation provide flexibility to choose from important criteria for selecting the optimal subset(s) of reference genes, unless one subset meets all the criteria. This approach identifies gene subset(s) with smaller variability of normalizing factors than current standard approaches, particularly
Prevention of Alzheimer's disease in high risk groups: statin therapy in subjects with PSEN1 mutations or heterozygosity for apolipoprotein E epsilon 4
Daniel A Pollen, Stephen Baker, Douglas Hinerfeld, Joan Swearer, Barbara A Evans, James E Evans, Richard Caselli, Ekaterina Rogaeva, Peter St George-Hyslop, Majaz Moonis
Alzheimer's Research & Therapy , 2010, DOI: 10.1186/alzrt55
Abstract: To date, there have been no systematic treatment studies on subjects with presenilin (PSEN) mutations [1] who inherit an autosomal dominant form of early onset familial Alzheimer's disease (AD). The principal objective of this review is to summarize the existing published pilot studies that address the issues of presymptomatic intervention in early onset familial AD and to compare these results with analogous treatment studies in hyperlipidemic subjects who are heterozygous for apolipoprotein Eε4 (ApoEε4). Our decision to focus on studies of presymptomatic rather than symptomatic subjects was based on the premise that most putative therapies for AD are likely to have more demonstrable effects on normal subjects compared to those with overt AD whose brains have already been subject to extensive neurodegenerative changes. We also recognize that it is not yet known whether any preventative opportunities that may arise as a consequence of an understanding of the pathogenesis of PSEN1 mutations will be applicable to the vastly larger number of cases of mild cognitive impairment and late onset AD (LOAD).Both groups of subjects exhibit early increased brain deposition of amyloid-beta 42 (Aβ42), which many researchers [2,3] have proposed is either a direct or intermediary toxic agent in the genesis of the neurodegeneration that subsequently leads to AD. Homozygotes for ApoEε4 are at far greater risk for late onset AD than are heterozygotes, but we did not identify a sufficiently large enough group of the former to comprise a separate study group. Decreases in cerebral spinal fluid (CSF) Aβ42 levels precede cognitive decline in subjects with PSEN1 mutations [4,5]. Consequently, in these subjects there is a window of opportunity - estimated as at least 4 to 12 years - to evaluate the ability of any putative prophylactic therapy to decrease, arrest or reverse abnormalities in Aβ42 metabolism many years before clinical symptoms of AD occur. For example, increased levels of CSF
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