Experimental characterization of the twin-eye laser mouse sensor

This paper proposes the experimental characterization of a laser mouse sensor used in some optical mouse devices. The sensor characterized is called twin-eye laser mouse sensor and uses the Doppler effect to measure displacement as an alternative to optical flow-based mouse sensors. The experimental characterization showed similar measurement performances to optical flow sensors except in the sensitivity to height changes and when measuring nonlinear displacements, where the twin-eye sensor offered better performance. The measurement principle of this optical sensor can be applied to the development of alternative inexpensive applications that require planar displacement measurement and poor sensitivity to -axis changes such as mobile robotics.The authors acknowledge the support of the Government of Catalonia (Comissionat per a Universitats i Recerca, Departament d’Innovació, Universitats i Empresa) and the European Social Fund

Development of advanced control strategies for Adaptive Optics systems

Atmospheric turbulence is a fast disturbance that requires high control frequency. At the same time, celestial objects are faint sources of light and thus WFSs often work in a low photon count regime. These two conditions require a trade-off between high closed-loop control frequency to improve the disturbance rejection performance, and large WFS exposure time to gather enough photons for the integrated signal to increase the Signal-to-Noise ratio (SNR), making the control a delicate yet fundamental aspect for AO systems. The AO plant and atmospheric turbulence were formalized as state-space linear time-invariant systems. The full AO system model is the ground upon which a model-based control can be designed. A Shack-Hartmann wavefront sensor was used to measure the horizontal atmospheric turbulence. The experimental measurements yielded to the Cn2 atmospheric structure parameter, which is key to describe the turbulence statistics, and the Zernike terms time-series. Experimental validation shows that the centroid extraction algorithm implemented on the Jetson GPU outperforms (i.e. is faster) than the CPU implementation on the same hardware. In fact, due to the construction of the Shack-Hartmann wavefront sensor, the intensity image captured from its camera is partitioned into several sub-images, each related to a point of the incoming wavefront. Such sub-images are independent each-other and can be computed concurrently. The AO model is exploited to automatically design an advanced linear-quadratic Gaussian controller with integral action. Experimental evidence shows that the system augmentation approach outperforms the simple integrator and the integrator filtered with the Kalman predictor, and that it requires less parameters to tune

A 2-pyridone-amide inhibitor targets the glucose metabolism pathway of Chlamydia trachomatis.

UnlabelledIn a screen for compounds that inhibit infectivity of the obligate intracellular pathogen Chlamydia trachomatis, we identified the 2-pyridone amide KSK120. A fluorescent KSK120 analogue was synthesized and observed to be associated with the C. trachomatis surface, suggesting that its target is bacterial. We isolated KSK120-resistant strains and determined that several resistance mutations are in genes that affect the uptake and use of glucose-6-phosphate (G-6P). Consistent with an effect on G-6P metabolism, treatment with KSK120 blocked glycogen accumulation. Interestingly, KSK120 did not affect Escherichia coli or the host cell. Thus, 2-pyridone amides may represent a class of drugs that can specifically inhibit C. trachomatis infection.ImportanceChlamydia trachomatis is a bacterial pathogen of humans that causes a common sexually transmitted disease as well as eye infections. It grows only inside cells of its host organism, within a parasitophorous vacuole termed the inclusion. Little is known, however, about what bacterial components and processes are important for C. trachomatis cellular infectivity. Here, by using a visual screen for compounds that affect bacterial distribution within the chlamydial inclusion, we identified the inhibitor KSK120. As hypothesized, the altered bacterial distribution induced by KSK120 correlated with a block in C. trachomatis infectivity. Our data suggest that the compound targets the glucose-6-phosphate (G-6P) metabolism pathway of C. trachomatis, supporting previous indications that G-6P metabolism is critical for C. trachomatis infectivity. Thus, KSK120 may be a useful tool to study chlamydial glucose metabolism and has the potential to be used in the treatment of C. trachomatis infections

Biomedical Photoacoustic Imaging and Sensing Using Affordable Resources

The overarching goal of this book is to provide a current picture of the latest developments in the capabilities of biomedical photoacoustic imaging and sensing in an affordable setting, such as advances in the technology involving light sources, and delivery, acoustic detection, and image reconstruction and processing algorithms. This book includes 14 chapters from globally prominent researchers , covering a comprehensive spectrum of photoacoustic imaging topics from technology developments and novel imaging methods to preclinical and clinical studies, predominantly in a cost-effective setting. Affordability is undoubtedly an important factor to be considered in the following years to help translate photoacoustic imaging to clinics around the globe. This first-ever book focused on biomedical photoacoustic imaging and sensing using affordable resources is thus timely, especially considering the fact that this technique is facing an exciting transition from benchtop to bedside. Given its scope, the book will appeal to scientists and engineers in academia and industry, as well as medical experts interested in the clinical applications of photoacoustic imaging

Immunophenotyping of Lymphoid Cells in Autism

Research into the cause of autism continues without any clear-cut answers. However, recent studies suggest that abnormalities of the immune system are associated with this disorder and autism results from failure of the immune system to regulate itself. Proper immune regulation requires that the host have the appropriate number and percentage of each population of lymphocytes and monocytes. These populations can be distinguished from one another with monoclonal antibodies that react with unique protein structures on the cell surface designated as the cluster of differentiation (CD) antigens. This investigation studied the possibility that the immune abnormalities seen in autism are due to a change in the lymphocytes or monocytes in the subjects with autism . The autistic subjects as compared to age- and sex-matched control subjects exhibited several changes in their cell populations. These included a depression of total lymphocytes, CD2+ (total T cells), CD4+ (helper T cells), and CD4+CD45RA+ (the antigen-inexperienced, suppressor inducer subset of helper T cells). Also analyzed were the siblings of the autistic subjects. A reduced percentage of CD4+ cells was seen in the male siblings as compared to unrelated males. Analyses also compared the cells of mothers and fathers of the autistic subjects with controls of mothers and fathers of normal children. No differences were seen in any of the markers used. Findings in the literature show an increase in memory cells and a decrease in naive cells as a function of age. The data gathered in these experiments uphold this concept and are consistent with the idea that CD45RA and CDw29 are maturational states of helper T cells. The quantitation of different immune markers on lymphoid cells seems to have been useful in the further characterization and investigation of the immune mechanism relevant to the syndrome of autism. Differences in some of the cell types were observed and may account for some of the immune abnormalities seen in autism. These differences may be the result or the cause of the syndrome. Further investigation seems necessary before a direct pathological link can be found between the body\u27s immunity and autism

Histopathology of human ischemic retinopathies

Retinal ischemia is a key feature in sight threatening eye diseases such as retinopathy of prematurity (ROP) or diabetic retinopathy (DR). Whilst the longterm consequences of ROP and DR are well described, our understanding of the early pathobiological events is much less clear. In particular cellular changes during the early stages of these disease are poorly studied so far. Most of our current insights about the pathobiological events are derived from animal models, with little confirmation in humans. The aim of this thesis is therefore to fill this gap by carefully characterizing vascular features and cellular damage in post-mortem tissue from patients with early stages of ROP and DR. To better understand the early cellular events in ROP, post-mortem eyes from postnatal, premature infants were collected. Different vascular phenotypes could be distinguished in whole mount retinal vasculature stains. Differences in branching profiles and capillary free zone morphology implicated different levels of oxygen exposure in the infants studied. Furthermore, characterizing a hyperplastic ridge, distal to the edge of the growing vascular plexus, revealed a correlation between the retinal astrocyte marker PAX2 and increased expression of vascular endothelial growth factor (VEGF). This suggests that retinal astrocytes make an important, but so far overlooked, contribution to the pathology in ROP. To better understand early stages of DR, eyes from diabetic donors without diagnosed DR were collected. Whole mount imaging revealed an indistinguishable retinal vasculature phenotype compared to controls, confirming the absence of DR. However, detailed quantification of vessel profiles on retinal cross sections demonstrated a 5-fold increase in acellular (and presumed non-perfused) capillaries (7-fold in the deeper plexuses) in retinas from diabetics without DR. Interestingly, localized capillary dropout of individual capillaries in the deeper plexuses did not correlated with a reduction of cells in the vicinity of the non-perfused capillaries. Instead, there was a panretinal loss of cells in the inner nuclear layer (INL) in diabetic retina, suggesting an ischemia independent mechanism for INL cell loss in diabetic retina

Visualizing the stimulation of encephalitogenic T cells in gut associated lymphoid tissue as a trigger of autoimmunity

Autoantigen-specific encephalitogenic T cells exist in the healthy immune repertoire. In case of CNS autoimmunity, such as multiple sclerosis (MS), cells penetrate into the central nervous system (CNS), where they get activated by local antigen presenting cells, and induce inflammation. However, the triggering mechanisms that provoke CNS infiltration of pre-existing autoreactive T cells are largely unknown. Recent studies have shown evidence that microbiota induce proliferation of encephalitogenic T cells in gut associated lymphatic tissues (GALT) before CNS infiltration in the spontaneous experimental autoimmune encephalomyelitis (EAE), an animal model of MS. In this study, the activation and subsequent behaviour of encephalitogenic T cells in the GALT are investigated. Myelin oligodendrocyte glycoprotein (MOG) specific T cells from transgenic mice are retrovirally transduced with FRET-based calcium activation sensors and adoptively transferred to recipient mice. T cells in the lamina propria and Peyer’s patches are imaged in vivo with two-photon microscopy and the calcium fluctuation is quantified to detect T cell activation. Moreover, migrating T cells in the efferent lymphatic vessels of GALT were analysed in order to elucidate phenotypic changes due to in vivo stimulation. Intravital imaging reveals that encephalitogenic T cells, but not polyclonal T cells, display continuous calcium signaling in the lamina propria. In contrast, encephalitogenic T cells in the Peyer’s patch show only brief calcium signaling. The continuous calcium signaling is diminished by administration of anti-MHC class II blocking antibody. This observation suggests that the calcium signaling of encephalitogenic T cells is mediated by antigen presenting cells. Additionally, the role of commensal microbiota is highlighted through the fact encephalitogenic T cells do not show continuous calcium signaling in germ free mice, which suggests the influence of microbiota. The increased number of IL17A and IFN producing T cells were detected in efferent lymph from mesenteric lymph nodes, further suggests the stimulation of T cells in the GALT. This phenotype, in addition to the enhanced number of CD44+ encephalitogenic T cells, suggests that microbiota induced stimulation in the GALT influences the migration of encephalitogenic T cells in CNS autoimmunity. In summary, the following study reveals pre-existing encephalitogenic T cells are capable of being stimulated in the lamina propria of ileum. The stimulation is dependent upon an intact gut microbiota compartment and may enhance migration of encephalitogenic T cells