91 research outputs found
The Effect of Tag Positioning on Passive Radio Frequency Identification (RFID) Performance: Case of Food Beverages
Smart packaging containing sensors could be considered the natural progression in packaging innovation for many consumer products. The goal of implementing sensors into the packaging is to improve product traceability and sustainability and to increase product shelf-life. Radio-frequency identification (RFID) systems have already been adopted for traceability purposes in many supply chains including apparel, electronics, pharmaceuticals, and food. The Ultra-High Frequency (UHF) range is widely used for those purposes. However, to improve the adoption of this technology several challenges need to be overcome. The goal of this research was to determine the best configuration for attaching a passive UHF RFID tag to different beverage bottles. To do this, three different packaging materials (polyethylene terephthalate (PET), clear glass, and Tetrapak®) which are commonly used in the beverage industries, and three commercially available passive UHF RFID tags with different designs were used. The influence of the RFID positioning (bottom or top) on the performance of tags using empty and water-filled bottles was assessed. Power on tag Forward and Theoretical Read Range were used as the indicators of the tag performance.
The results of this study confirmed that tag positioning affects the performance of the RFID system. In order to have the best passive UHF RFID tag performance, packaging and labeling industries should consider the effect of tag design, packaging material, and food composition
Diffuse laser illumination for Maxwellian view Doppler holography of the retina
We describe the advantages of diffuse illumination in laser holography for
ophthalmology. The presence of a diffusing element introduces an angular
diversity of the optical radiation and reduces its spatial coherence, which
spreads out the energy distribution of the illumination beam in the focal plane
of the eyepiece. The field of view of digitally computed retinal images can
easily be increased as the eyepiece can be moved closer to the cornea to obtain
a Maxwellian view of the retina without compromising ocular safety. Compliance
with American and European safety standards for ophthalmic devices is more
easily obtained by preventing the presence of a laser hot spot observed in
front of the cornea in the absence of a scattering element. Diffuse laser
illumination does not introduce any adverse effects on digitally computed laser
Doppler images.Comment: 9 page
Coulomb dissociation of N 20,21
Neutron-rich light nuclei and their reactions play an important role in the creation of chemical elements. Here, data from a Coulomb dissociation experiment on N20,21 are reported. Relativistic N20,21 ions impinged on a lead target and the Coulomb dissociation cross section was determined in a kinematically complete experiment. Using the detailed balance theorem, the N19(n,γ)N20 and N20(n,γ)N21 excitation functions and thermonuclear reaction rates have been determined. The N19(n,γ)N20 rate is up to a factor of 5 higher at
Biomarkers to identify and isolate senescent cells
This paper was accepted for publication in the journal Ageing Research Reviews and the definitive published version is available at http://dx.doi.org/10.1016/j.arr.2016.05.003.Aging is the main risk factor for many degenerative diseases and declining health. Senescent cells are part of the underlying mechanism for time-dependent tissue dysfunction. These cells can negatively affect neighbouring cells through an altered secretory phenotype: the senescence-associated secretory phenotype (SASP). The SASP induces senescence in healthy cells, promotes tumour formation and progression, and contributes to other age-related diseases such as atherosclerosis, immune-senescence and neurodegeneration. Removal of senescent cells was recently demonstrated to delay age-related degeneration and extend lifespan. To better understand cell aging and to reap the benefits of senescent cell removal, it is necessary to have a reliable biomarker to identify these cells. Following an introduction to cellular senescence, we discuss several classes of biomarkers in the context of their utility in identifying and/or removing senescent cells from tissues. Although senescence can be induced by a variety of stimuli, senescent cells share some characteristics that enable their identification both in vitro and in vivo. Nevertheless, it may prove difficult to identify a single biomarker capable of distinguishing senescence in all cell types. Therefore, this will not be a comprehensive review of all senescence biomarkers but rather an outlook on technologies and markers that are most suitable to identify and isolate senescent cells
CXCR4 involvement in neurodegenerative diseases
Neurodegenerative diseases likely share common underlying pathobiology. Although prior work has identified susceptibility loci associated with various dementias, few, if any, studies have systematically evaluated shared genetic risk across several neurodegenerative diseases. Using genome-wide association data from large studies (total n = 82,337 cases and controls), we utilized a previously validated approach to identify genetic overlap and reveal common pathways between progressive supranuclear palsy (PSP), frontotemporal dementia (FTD), Parkinson's disease (PD) and Alzheimer's disease (AD). In addition to the MAPT H1 haplotype, we identified a variant near the chemokine receptor CXCR4 that was jointly associated with increased risk for PSP and PD. Using bioinformatics tools, we found strong physical interactions between CXCR4 and four microglia related genes, namely CXCL12, TLR2, RALB, and CCR5. Evaluating gene expression from post-mortem brain tissue, we found that expression of CXCR4 and microglial genes functionally related to CXCR4 was dysregulated across a number of neurodegenerative diseases. Furthermore, in a mouse model of tauopathy, expression of CXCR4 and functionally associated genes was significantly altered in regions of the mouse brain that accumulate neurofibrillary tangles most robustly. Beyond MAPT, we show dysregulation of CXCR4 expression in PSP, PD, and FTD brains, and mouse models of tau pathology. Our multi-modal findings suggest that abnormal signaling across a 'network' of microglial genes may contribute to neurodegeneration and may have potential implications for clinical trials targeting immune dysfunction in patients with neurodegenerative diseases
Recommended from our members
Genetic variation across RNA metabolism and cell death gene networks is implicated in the semantic variant of primary progressive aphasia
The semantic variant of primary progressive aphasia (svPPA) is a clinical syndrome characterized by neurodegeneration and progressive loss of semantic knowledge. Unlike many other forms of frontotemporal lobar degeneration (FTLD), svPPA has a highly consistent underlying pathology composed of TDP-43 (a regulator of RNA and DNA transcription metabolism). Previous genetic studies of svPPA are limited by small sample sizes and a paucity of common risk variants. Despite this, svPPA\xe2\x80\x99s relatively homogenous clinicopathologic phenotype makes it an ideal investigative model to examine genetic processes that may drive neurodegenerative disease. In this study, we used GWAS metadata, tissue samples from pathologically confirmed frontotemporal lobar degeneration, and in silico techniques to identify and characterize protein interaction networks associated with svPPA risk. We identified 64 svPPA risk genes that interact at the protein level. The protein pathways represented in this svPPA gene network are critical regulators of RNA metabolism and cell death, such as SMAD proteins and NOTCH1. Many of the genes in this network are involved in TDP-43 metabolism. Contrary to the conventional notion that svPPA is a clinical syndrome with few genetic risk factors, our analyses show that svPPA risk is complex and polygenic in nature. Risk for svPPA is likely driven by multiple common variants in genes interacting with TDP-43, along with cell death,x` working in combination to promote neurodegeneration
- …