Status of Uncooled Infrared Detector Technology at ULIS, France

The high level of accumulated expertise by ULIS and CEA/LETI on uncooled microbolometers made from amorphous silicon enables ULIS to develop uncooled IRFPA with 17 µm pixel-pitch to enable the development of small power, small weight and power (SWaP) and high performance IR systems. Key characteristics of amorphous silicon based uncooled IR detector is described to highlight the advantage of this technology for system operation. A full range of products from 160 x 120 to 1024 x 768 has been developed and we will focus the paper on the ¼ VGA with 17 µm pixel pitch. Readout integrated circuit (ROIC) architecture is described highlighting innovations that are widely on-chip implemented to enable an easier operation by the user. The detector configuration (integration time, windowing, gain, scanning direction), is driven by a standard I²C link. Like most of the visible arrays, the detector adopts the HSYNC/VSYNC free-run mode of operation driven with only one master clock (MC) supplied to the ROIC which feeds back pixel, line and frame synchronisation. On-chip PROM memory for customer operational condition storage is available for detector characteristics. Low power consumption has been taken into account and less than 60 mW is possible in analogue mode at 60 Hz. A wide electrical dynamic range (2.4V) is maintained despite the use of advanced CMOS node. The specific appeal of this unit lies in the high uniformity and easy operation it provides. The reduction of the pixel-pitch turns this TEC-less ¼ VGA array into a product well adapted for high resolution and compact systems. Noise equivalent temperature difference (NETD) of 35 mK and thermal time constant of 10 ms have been measured leading to 350 mK.ms figure of merit. We insist on NETD trade-off with wide thermal dynamic range, as well as the high characteristics uniformity and pixel operability, achieved thanks to the mastering of the amorphous silicon technology coupled with the ROIC design. This technology node associated with advanced packaging technique, paves the way to compact low power system.Defence Science Journal, 2013, 63(6), pp.545-549, DOI:http://dx.doi.org/10.14429/dsj.63.5753

FUS and TARDBP but Not SOD1 Interact in Genetic Models of Amyotrophic Lateral Sclerosis

Mutations in the SOD1 and TARDBP genes have been commonly identified in Amyotrophic Lateral Sclerosis (ALS). Recently, mutations in the Fused in sarcoma gene (FUS) were identified in familial (FALS) ALS cases and sporadic (SALS) patients. Similarly to TDP-43 (coded by TARDBP gene), FUS is an RNA binding protein. Using the zebrafish (Danio rerio), we examined the consequences of expressing human wild-type (WT) FUS and three ALS–related mutations, as well as their interactions with TARDBP and SOD1. Knockdown of zebrafish Fus yielded a motor phenotype that could be rescued upon co-expression of wild-type human FUS. In contrast, the two most frequent ALS–related FUS mutations, R521H and R521C, unlike S57Δ, failed to rescue the knockdown phenotype, indicating loss of function. The R521H mutation caused a toxic gain of function when expressed alone, similar to the phenotype observed upon knockdown of zebrafish Fus. This phenotype was not aggravated by co-expression of both mutant human TARDBP (G348C) and FUS (R521H) or by knockdown of both zebrafish Tardbp and Fus, consistent with a common pathogenic mechanism. We also observed that WT FUS rescued the Tardbp knockdown phenotype, but not vice versa, suggesting that TARDBP acts upstream of FUS in this pathway. In addition we observed that WT SOD1 failed to rescue the phenotype observed upon overexpression of mutant TARDBP or FUS or upon knockdown of Tardbp or Fus; similarly, WT TARDBP or FUS also failed to rescue the phenotype induced by mutant SOD1 (G93A). Finally, overexpression of mutant SOD1 exacerbated the motor phenotype caused by overexpression of mutant FUS. Together our results indicate that TARDBP and FUS act in a pathogenic pathway that is independent of SOD1

WNK1/HSN2 Mutation in Human Peripheral Neuropathy Deregulates <em>KCC2</em> Expression and Posterior Lateral Line Development in Zebrafish (<em>Danio rerio</em>)

<div><p>Hereditary sensory and autonomic neuropathy type 2 (HSNAII) is a rare pathology characterized by an early onset of severe sensory loss (all modalities) in the distal limbs. It is due to autosomal recessive mutations confined to exon “HSN2” of the WNK1 (with-no-lysine protein kinase 1) serine-threonine kinase. While this kinase is well studied in the kidneys, little is known about its role in the nervous system. We hypothesized that the truncating mutations present in the neural-specific HSN2 exon lead to a loss-of-function of the WNK1 kinase, impairing development of the peripheral sensory system. To investigate the mechanisms by which the loss of WNK1/HSN2 isoform function causes HSANII, we used the embryonic zebrafish model and observed strong expression of WNK1/HSN2 in neuromasts of the peripheral lateral line (PLL) system by immunohistochemistry. Knocking down wnk1/hsn2 in embryos using antisense morpholino oligonucleotides led to improper PLL development. We then investigated the reported interaction between the WNK1 kinase and neuronal potassium chloride cotransporter KCC2, as this transporter is a target of WNK1 phosphorylation. <em>In situ</em> hybridization revealed <em>kcc2</em> expression in mature neuromasts of the PLL and semi-quantitative RT–PCR of wnk1/hsn2 knockdown embryos showed an increased expression of <em>kcc2</em> mRNA. Furthermore, overexpression of human KCC2 mRNA in embryos replicated the wnk1/hsn2 knockdown phenotype. We validated these results by obtaining double knockdown embryos, both for wnk1/hsn2 and kcc2, which alleviated the PLL defects. Interestingly, overexpression of inactive mutant KCC2-C568A, which does not extrude ions, allowed a phenocopy of the PLL defects. These results suggest a pathway in which WNK1/HSN2 interacts with KCC2, producing a novel regulation of its transcription independent of KCC2's activation, where a loss-of-function mutation in WNK1 induces an overexpression of KCC2 and hinders proper peripheral sensory nerve development, a hallmark of HSANII.</p> </div

All-weather vision for automotive safety: which spectral band?

SIA Vision 2016 - International Conference Night Drive Tests and Exhibition, Paris, FRANCE, 13-/10/2016 - 14/10/2016The AWARE (All Weather All Roads Enhanced vision) French public funded project is aiming at the development of a low cost sensor fitting to automotive and aviation requirements, and enabling a vision in all poor visibility conditions, such as night, fog, rain and snow. In order to identify the technologies providing the best all-weather vision, we evaluated the relevance of four different spectral bands: Visible RGB, Near-Infrared (NIR), Short-Wave Infrared (SWIR) and Long-Wave Infrared (LWIR). Two test campaigns have been realised in outdoor natural conditions and in artificial fog tunnel, with four cameras recording simultaneously.This paper presents the detailed results of this comparative study, focusing on pedestrians, vehicles, traffic signs and lanes detection

KCC2 is overexpressed in WNK1/HSN2 knockdown embryos.

<p>A) RT-PCR against <i>slc12a5</i> (coding for kcc2) shows higher levels of RNA in WNK1/HSN2 knockdown embryos when compared with WT at 72 hpf as well as at 24 hpf. We overexpressed human KCC2 mRNA in WT embryos (morphology presented in (B)) to validate this result and were able to replicate the WNK1/HSN2 knockdown phenotype as assayed by (C) the number of structural and functional hair cells in PLL neuromasts and by (D) the 4-di-2-ASP score. We also validated this result by obtaining a partial rescue of the WNK1/HSN2 knockdown phenotype by knocking down kcc2 using MO1-slc12a5 in WNK1/HSN2 embryos (double knockdown-KD experiments). The embryos lacking kcc2 have morphological defects and a lower 4-di-2-ASP score (D) due to their smaller length (B), but double knockdown embryos, which are also morphologically abnormal and smaller in size have a significantly higher 4-di-2-ASP score (D) indicative of a partial rescue. For (C) The number of neuromasts counted per condition is indicated in the boxes and the total number of embryos obtained per condition is indicated in parenthesis at the bottom of the box plots. For (D), the total number of embryos is indicated in the boxes. (E) Overexpression of inactive mutant KCC2-C568A mimics hKCC2 overexpression and WNK1/HSN2 knockdown phenotype by producing PLL defects as assayed by 4-di-2-ASP vital dye staining. This indicates that WNK1/HSN2 interacts with KCC2 and regulates its transcription independent of the cotransporter's activation. Neuromast scores were tabulated as previously done and presented as a box plot. The number of neuromasts counted per condition is indicated in the boxes. Scale bar: 100 µm.</p