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

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

The Limits of Visual Resolution

Visual resolution, the ability to see fine spatial detail, emerges from the capacities of both the eye and the brain. A great deal of insight into the anatomical and physiological basis of human visual resolution has been gained since Helmholtz first proposed his sampling theory of visual resolution. Anatomical, physiological and psychophysical investigations have revealed in great detail the properties of the biological structures underlying visual resolution and identified many of the optical, retinal, and cortical factors that govern the limits of visual resolution. However, technological limitations have long prevented researchers from examining both the structure and function of the visual system simultaneously in the living eye. The microscopic photoreceptors of the retina have been inaccessible to optical examination, preventing high quality measurements of both visual resolution and retinal anatomy from being obtained in the same eyes. The present studies investigated the relationship between the optical, retinal, and cortical factors that govern visual resolution in humans. These experiments employed adaptive optics scanning laser ophthalmoscopy (AOSLO) as a tool to study how these factors govern visual resolution in normal and diseased eyes. The AOSLO is an ideal tool for studying the limits of vision because of its ability to present complex stimuli to the retina that are of higher optical quality than the visual system has ever experienced, while simultaneously imaging the underlying cone photoreceptor mosaic on a microscopic scale.Adaptive optics correction of ocular aberrations allowed observers to achieve immediate and significant improvements in visual resolution. Training was not required to achieve this benefit, which allowed the resolving capacity of the retinal and cortical visual system to be assessed unobstructed by the optics of the eye. Not all participants in these studies benefited to the same extent from AO correction. Visual resolution was found to be significantly poorer in low myopia as compared to emmetropia, despite the similar optical quality afforded by AO correction, showing that retinal and cortical changes in myopia caused the observed deficit. Simultaneous imaging and visual resolution testing determined the precise relationship between the spatial sampling limit of the cone mosaic and visual resolution across the human fovea. These studies revealed that the spatial sampling limit of the cone mosaic largely governs visual resolution at the center of the fovea for normal eyes, but that outside the foveal center visual resolution falls off at a greater rate than predicted by cone spacing and is governed by the spatial sampling limit of the mosaic of midget retinal ganglion cells.Significant differences between otherwise normally appearing observers were revealed using AOSLO, showing the power of visual resolution testing after AO correction for detecting small changes in the visual system resulting from disease. Significant retinal changes were revealed in female carriers of a rare X-linked genetic mutation in the L and M opsin gene array that causes blue cone monochromacy (the loss of all L and M cone function) in affected males. Retinal findings from AO imaging provided insight into the development and function of the carrier retina. Although carriers had visual resolution within the normal range when tested clinically, visual resolution testing in AOSLO revealed significantly reduced visual resolution compared to normal eyes. Resolution testing across the fovea in normal and diseased eyes provided insight into the relationship between cones, ganglion cells and visual resolution across the visual field. Retinal imaging showed that carriers had fairly normal cone topography despite peak cone density that was ~50% lower than normal; showing that cones destined to express a non-functional photopigment degenerated early in development. Drastic reductions in visual resolution across the fovea in the carrier are best explained by ganglion cell loss that resulted from the loss of cones in the carrier. The relationship between resolution and the spatial sampling limit of the carrier cone mosaic was similar to what was predicted for normal eyes, suggesting an organizing principle in the visual system whereby cone density is the primary determinant of the retinal circuitry that governs visual resolution across the visual field. Together, these studies provide an important contribution to the understanding of the limits of human visual resolution