Prospective Evaluation of Doppler Sonography to Detect the Twinkling Artifact Versus Unenhanced Computed Tomography for Identifying Urinary Tract Calculi

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135595/1/jum201231101619.pd

Liver imaging reporting and data system: An expert consensus statement

The increasing incidence and high morbidity and mortality of hepatocellular carcinoma (HCC) have inspired the creation of the Liver Imaging Reporting and Data System (LI-RADS). LI-RADS aims to reduce variability in exam interpretation, improve communication, facilitate clinical therapeutic decisions, reduce omission of pertinent information, and facilitate the monitoring of outcomes. LI-RADS is a dynamic process, which is updated frequently. In this article, we describe the LI-RADS 2014 version (v2014), which marks the second update since the initial version in 2011

Local tumor progression patterns after radiofrequency ablation of colorectal cancer liver metastases

PURPOSE:We aimed to evaluate patterns of local tumor progression (LTP) after radiofrequency ablation (RF ablation) of colorectal cancer liver metastases (CRCLM) and to highlight the percentage of LTP not attributable to lesion size or RF ablation procedure-related factors (heat sink or insufficient ablation margin).METHODS:CRCLM treated by RF ablation at a single tertiary care center from 2004–2012, with a minimum of six months of postprocedure follow-up, were included in this retrospective study. LTP morphology was classified as focal nodular (270°), or crescentic (90°–270°). Initial metastasis size, minimum ablation margin size, morphology of LTP, presence of a heat sink, and time to progression were recorded independently by two radiologists.RESULTS:Thirty-two of 127 RF ablation treated metastases (25%) with a mean size of 23 mm (standard deviation 12 mm) exhibited LTP. Fifteen of 32 LTPs (47%) were classified as focal nodular, with seven having no procedure-related factor to explain recurrence. Ten of 32 LTPs (31%) were circumferential, with four having no procedure-related factor to explain recurrence. Seven of 32 LTPs (22%) were crescentic, with two having no procedure-related factor to explain recurrence. Of the 13 lesions without any obvious procedure-related reason for LTP, six (46%) were <3 cm in size.CONCLUSION:Although LTP in RF ablation treated CRCLM can often be explained by procedure-related factors or size of the lesion, in this study up to six (5%) of the CRCLM we treated showed LTP without any reasonable cause

ECFA Detector R&D Panel, Review Report

Two special calorimeters are foreseen for the instrumentation of the very forward region of an ILC or CLIC detector; a luminometer (LumiCal) designed to measure the rate of low angle Bhabha scattering events with a precision better than 10$^{-3}$ at the ILC and 10$^{-2}$ at CLIC, and a low polar-angle calorimeter (BeamCal). The latter will be hit by a large amount of beamstrahlung remnants. The intensity and the spatial shape of these depositions will provide a fast luminosity estimate, as well as determination of beam parameters. The sensors of this calorimeter must be radiation-hard. Both devices will improve the e.m. hermeticity of the detector in the search for new particles. Finely segmented and very compact electromagnetic calorimeters will match these requirements. Due to the high occupancy, fast front-end electronics will be needed. Monte Carlo studies were performed to investigate the impact of beam-beam interactions and physics background processes on the luminosity measurement, and of beamstrahlung on the performance of BeamCal, as well as to optimise the design of both calorimeters. Dedicated sensors, front-end and ADC ASICs have been designed for the ILC and prototypes are available. Prototypes of sensor planes fully assembled with readout electronics have been studied in electron beams.Comment: 61 pages, 51 figure

Infrastructure for Detector Research and Development towards the International Linear Collider

The EUDET-project was launched to create an infrastructure for developing and testing new and advanced detector technologies to be used at a future linear collider. The aim was to make possible experimentation and analysis of data for institutes, which otherwise could not be realized due to lack of resources. The infrastructure comprised an analysis and software network, and instrumentation infrastructures for tracking detectors as well as for calorimetry.Comment: 54 pages, 48 picture

LI-RADS: A Conceptual and Historical Review from Its Beginning to Its Recent Integration into AASLD Clinical Practice Guidance

The Liver Imaging Reporting and Data System (LI-RADS®) is a comprehensive system for standardizing the terminology, technique, interpretation, reporting, and data collection of liver observations in individuals at high risk for hepatocellular carcinoma (HCC). LI-RADS is supported and endorsed by the American College of Radiology (ACR). Upon its initial release in 2011, LI-RADS applied only to liver observations identified at CT or MRI. It has since been refined and expanded over multiple updates to now also address ultrasound-based surveillance, contrast-enhanced ultrasound for HCC diagnosis, and CT/MRI for assessing treatment response after locoregional therapy. The LI-RADS 2018 version was integrated into the HCC diagnosis, staging, and management practice guidance of the American Association for the Study of Liver Diseases (AASLD). This article reviews the major LI-RADS updates since its 2011 inception and provides an overview of the currently published LI-RADS algorithms

Disruption of the Autophagy-Lysosome Pathway Is Involved in Neuropathology of the nclf Mouse Model of Neuronal Ceroid Lipofuscinosis

Variant late-infantile neuronal ceroid lipofuscinosis, a fatal lysosomal storage disorder accompanied by regional atrophy and pronounced neuron loss in the brain, is caused by mutations in the CLN6 gene. CLN6 is a non-glycosylated endoplasmic reticulum (ER)-resident membrane protein of unknown function. To investigate mechanisms contributing to neurodegeneration in CLN6 disease we examined the nclf mouse, a naturally occurring model of the human CLN6 disease. Prominent autofluorescent and electron-dense lysosomal storage material was found in cerebellar Purkinje cells, thalamus, hippocampus, olfactory bulb and in cortical layer II to V. Another prominent early feature of nclf pathogenesis was the localized astrocytosis that was evident in many brain regions and the more widespread microgliosis. Expression analysis of mutant Cln6 found in nclf mice demonstrated synthesis of a truncated protein with a reduced half-life. Whereas the rapid degradation of the mutant Cln6 protein can be inhibited by proteasomal inhibitors, there was no evidence for ER stress or activation of the unfolded protein response in various brain areas during postnatal development. Age-dependent increases in LC3-II, ubiquitinated proteins, and neuronal p62-positive aggregates were observed, indicating a disruption of the autophagy-lysosome degradation pathway of proteins in brains of nclf mice, most likely due to defective fusion between autophagosomes and lysosomes. These data suggest that proteasomal degradation of mutant Cln6 is sufficient to prevent the accumulation of misfolded Cln6 protein, whereas lysosomal dysfunction impairs constitutive autophagy promoting neurodegeneration

Histological and transcriptome-wide level characteristics of fetal myofiber hyperplasia during the second half of gestation in Texel and Ujumqin sheep

<p>Abstract</p> <p>Background</p> <p>Whether myofibers increase with a pulsed-wave mode at particular developmental stages or whether they augment evenly across developmental stages in large mammals is unclear. Additionally, the molecular mechanisms of myostatin in myofiber hyperplasia at the fetal stage in sheep remain unknown. Using the first specialized transcriptome-wide sheep oligo DNA microarray and histological methods, we investigated the gene expression profile and histological characteristics of developing fetal ovine longissimus muscle in Texel sheep (high muscle and low fat), as a myostatin model of natural mutation, and Ujumqin sheep (low muscle and high fat). Fetal skeletal muscles were sampled at 70, 85, 100, 120, and 135 d of gestation.</p> <p>Results</p> <p>Myofiber number increased sharply with a pulsed-wave mode at certain developmental stages but was not augmented evenly across developmental stages in fetal sheep. The surges in myofiber hyperplasia occurred at 85 and 120 d in Texel sheep, whereas a unique proliferative surge appeared at 100 d in Ujumqin sheep. Analysis of the microarray demonstrated that immune and hematological systems' development and function, lipid metabolism, and cell communication were the biological functions that were most differentially expressed between Texel and Ujumqin sheep during muscle development. Pathways associated with myogenesis and the proliferation of myoblasts, such as calcium signaling, chemokine (C-X-C motif) receptor 4 signaling, and vascular endothelial growth factor signaling, were affected significantly at specific fetal stages, which underpinned fetal myofiber hyperplasia and postnatal muscle hypertrophy. Moreover, we identified some differentially expressed genes between the two breeds that could be potential myostatin targets for further investigation.</p> <p>Conclusions</p> <p>Proliferation of myofibers proceeded in a pulsed-wave mode at particular fetal stages in the sheep. The myostatin mutation changed the gene expression pattern in skeletal muscle at a transcriptome-wide level, resulting in variation in myofiber phenotype between Texel and Ujumqin sheep during the second half of gestation. Our findings provide a novel and dynamic description of the effect of myostatin on skeletal muscle development, which contributes to understanding the biology of muscle development in large mammals.</p

Proteomic mapping of differentially vulnerable pre-synaptic populations identifies regulators of neuronal stability in vivo.

Synapses are an early pathological target in many neurodegenerative diseases ranging from well-known adult onset conditions such as Alzheimer and Parkinson disease to neurodegenerative conditions of childhood such as spinal muscular atrophy (SMA) and neuronal ceroid lipofuscinosis (NCLs). However, the reasons why synapses are particularly vulnerable to such a broad range of neurodegeneration inducing stimuli remains unknown. To identify molecular modulators of synaptic stability and degeneration, we have used the Cln3-/- 33 mouse model of a juvenile form of NCL. We profiled and compared the molecular composition of anatomically-distinct, differentially-affected pre-synaptic populations from the Cln3-/- 35 mouse brain using proteomics followed by bioinformatic analyses. Identified protein candidates were then tested using a Drosophila CLN3 model to study their ability to modify the CLN3-neurodegenerative phenotype in vivo. We identified differential perturbations in a range of molecular cascades correlating with synaptic vulnerability, including valine catabolism and rho signalling pathways. Genetic and pharmacological targeting of key ‘hub’ proteins in such pathways was sufficient to modulate phenotypic presentation in a Drosophila CLN3 model. We propose that such a workflow provides a target rich method for the identification of novel disease regulators which could be applicable to the study of other conditions where appropriate models exist