222 research outputs found
Letter From Charles Jenkinson to Francis Mairs Huntington-Wilson, September 8, 1909
The document is a carbon copy of a typed letter from Charles Jenkinson to Francis Mairs Huntington-Wilson regarding personal correspondence that he has missed during his vacation.https://digitalcommons.ursinus.edu/fmhw_other/1169/thumbnail.jp
Letter From Charles Jenkinson to John Edward Jones, September 8, 1909
The document is a carbon copy of a typed letter from Charles Jenkinson to John Edward Jones concerning a leave of absence request for his Deputy Consul General.https://digitalcommons.ursinus.edu/fmhw_other/1170/thumbnail.jp
Letter From Charles Jenkinson to Carl Lumholtz, September 1, 1909
The document is a carbon copy of a typed letter from Charles Jenkinson to Carl Lumholtz concerning a letter of introduction provided by Jose Yves Limantour.https://digitalcommons.ursinus.edu/fmhw_other/1165/thumbnail.jp
Note From Charles Jenkinson to Francis Mairs Huntington-Wilson, December 30, 1909
The document is a typed note from Charles Jenkinson to the Assistant Secretary of State regarding a visit from Senator Henry Cabot Lodge.https://digitalcommons.ursinus.edu/fmhw_other/1196/thumbnail.jp
Pancreatic insufficiency, digestive enzyme supplementation, and postnatal growth in preterm babies
Background: Optimising postnatal growth facilitates better long-term neonatal neurodevelopmental outcomes. Early postnatal growth is often hindered by a variety of factors unique to the extrauterine environment and digestive immaturity both contributing to reduced enteral feed tolerance during the first few days and weeks after birth. Preterm infants display varying levels of pancreatic insufficiency that are related to gestational age and providing digestive enzyme supplementation, may be one way in which to improve postnatal growth in enterally fed preterm babies.
Summary: In this review, we explore which exocrine pancreatic enzymes are deficient in preterm babies, the methods by which exocrine pancreatic function is measured, potential avenues by which digestive enzyme replacement might improve postnatal growth failure, and which babies might benefit most from this intervention.
Key Messages: Pancreatic exocrine function exhibits developmental immaturity in extremely preterm infants and may contribute to postnatal growth failure. Stool elastase is a simple, non-invasive method of assessing pancreatic function in preterm infants. Available evidence does not currently support routine use of digestive enzyme supplementation in preterm infants
Analysis of UK and European NOx and VOC emission scenarios in the Defra model intercomparison exercise
This is a PDF file of an unedited manuscript that has been accepted for publication. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertainSimple emission scenarios have been implemented in eight United Kingdom air quality models with the aim of assessing how these models compared when addressing whether photochemical ozone formation in southern England was NOx- or VOC-sensitive and whether ozone precursor sources in the UK or in the Rest of Europe (RoE) were the most important during July 2006. The suite of models included three Eulerian-grid models (three implementations of one of these models), a Lagrangian atmospheric dispersion model and two moving box air parcel models. The assignments as to NOx- or VOC-sensitive and to UK- versus RoE-dominant, turned out to be highly variable and often contradictory between the individual models. However, when the assignments were filtered by model performance on each day, many of the contradictions could be eliminated. Nevertheless, no one model was found to be the 'best' model on all days, indicating that no single air quality model could currently be relied upon to inform policymakers robustly in terms of NOx- versus VOC-sensitivity and UK- versus RoE-dominance on each day. It is important to maintain a diversity in model approaches.Peer reviewedFinal Accepted Versio
Assessing Reliability of Myocardial Blood Flow After Motion Correction With Dynamic PET Using a Bayesian Framework
The estimation of myocardial blood flow (MBF) in dynamic PET can be biased by many different processes. A major source of error, particularly in clinical applications, is patient motion. Patient motion, or gross motion, creates displacements between different PET frames as well as between the PET frames and the CT-derived attenuation map, leading to errors in MBF calculation from voxel time series. Motion correction techniques are challenging to evaluate quantitatively and the impact on MBF reliability is not fully understood. Most metrics, such as signal-to-noise ratio (SNR), are characteristic of static images, and are not specific to motion correction in dynamic data. This study presents a new approach of estimating motion correction quality in dynamic cardiac PET imaging. It relies on calculating a MBF surrogate, K 1 , along with the uncertainty on the parameter. This technique exploits a Bayesian framework, representing the kinetic parameters as a probability distribution, from which the uncertainty measures can be extracted. If the uncertainty extracted is high, the parameter studied is considered to have high variability - or low confidence - and vice versa. The robustness of the framework is evaluated on simulated time activity curves to ensure that the uncertainties are consistently estimated at the multiple levels of noise. Our framework is applied on 40 patient datasets, divided in 4 motion magnitude categories. Experienced observers manually realigned clinical datasets with 3D translations to correct for motion. K 1 uncertainties were compared before and after correction. A reduction of uncertainty after motion correction of up to 60% demonstrates the benefit of motion correction in dynamic PET and as well as provides evidence of the usefulness of the new method presented
Multi-site genetic analysis of diffusion images and voxelwise heritability analysis : a pilot project of the ENIGMA–DTI working group
The ENIGMA (Enhancing NeuroImaging Genetics through Meta-Analysis) Consortium was set up to analyze brain measures and genotypes from multiple sites across the world to improve the power to detect genetic variants that influence the brain. Diffusion tensor imaging (DTI) yields quantitative measures sensitive to brain development and degeneration, and some common genetic variants may be associated with white matter integrity or connectivity. DTI measures, such as the fractional anisotropy (FA) of water diffusion, may be useful for identifying genetic variants that influence brain microstructure. However, genome-wide association studies (GWAS) require large populations to obtain sufficient power to detect and replicate significant effects, motivating a multi-site consortium effort. As part of an ENIGMA–DTI working group, we analyzed high-resolution FA images from multiple imaging sites across North America, Australia, and Europe, to address the challenge of harmonizing imaging data collected at multiple sites. Four hundred images of healthy adults aged 18–85 from four sites were used to create a template and corresponding skeletonized FA image as a common reference space. Using twin and pedigree samples of different ethnicities, we used our common template to evaluate the heritability of tract-derived FA measures. We show that our template is reliable for integrating multiple datasets by combining results through meta-analysis and unifying the data through exploratory mega-analyses. Our results may help prioritize regions of the FA map that are consistently influenced by additive genetic factors for future genetic discovery studies. Protocols and templates are publicly available at (http://enigma.loni.ucla.edu/ongoing/dti-working-group/)
The GALNT9, BNC1 and CCDC8 genes are frequently epigenetically dysregulated in breast tumours that metastasise to the brain.
Tumour metastasis to the brain is a common and deadly development in certain cancers; 18-30 % of breast tumours metastasise to the brain. The contribution that gene silencing through epigenetic mechanisms plays in these metastatic tumours is not well understood
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