6 research outputs found
Optical Character Recognition from Images
No full textAnalysis of document images for information extraction has become very prominent in recent past. Wide variety of information, which has been conventionally stored on paper, is now being converted into electronic form for better storage and intelligent processing. This needs processing of documents using image analysis, processing methods. This article provides an overview of various methods used for digital image processing using three main components: Pre-processing, Feature extraction and the Classification. Pre-processing feature extraction and classification. Classification is an important step in Office Automation, Digital Libraries, and other document image analysis applications
Built-in Self Repair Approach by Module Relocation for FPGA Based Reconfigurable Systems
No full textAbstractSystems that are installed in harsh environment conditions are continuously exposed to radiations, temperature variations and pressure variations which cause fast circuit degradation and malfunctioning. FPGAs are used as the core component in many such systems especially in mission critical and safety critical applications. To ensure reliable and prolonged system functioning until mission completion, proper fault recovery techniques need to be incorporated in to the system during the design phase itself. Traditional self-repairing schemes utilize spare cells to replace faulty cells. So, the number of spare cells increases with the number of faults to be repaired which creates high area overhead. Dynamic runtime partial reconfiguration has been considered to be a promising technique that helps improve the flexibility and efficiency of FPGA based systems. The key concept behind self-repairing scheme discussed in this paper is faulty module relocation to enable better use of resources and scheduling of repair for different modules to maintain system operation until mission completion or up to the required lifetime with maximum efficiency. The paper presents an efficient self-repairing scheme for FPGAs which can handle higher number of faults with better resource utilization and lesser overheads
Efficacy, safety, and immunogenicity of a booster regimen of Ad26.COV2.S vaccine against COVID-19 (ENSEMBLE2) : results of a randomised, double-blind, placebo-controlled, phase 3 trial
No full textBackground Despite the availability of effective vaccines against COVID-19, booster vaccinations are needed to maintain vaccine-induced protection against variant strains and breakthrough infections. This study aimed to investigate the efficacy, safety, and immunogenicity of the Ad26.COV2.S vaccine (Janssen) as primary vaccination plus a booster dose.
Methods ENSEMBLE2 is a randomised, double-blind, placebo-controlled, phase 3 trial including crossover vaccination after emergency authorisation of COVID-19 vaccines. Adults aged at least 18 years without previous COVID-19 vaccination at public and private medical practices and hospitals in Belgium, Brazil, Colombia, France, Germany, the Philippines, South Africa, Spain, the UK, and the USA were randomly assigned 1:1 via a computer algorithm to receive intramuscularly administered Ad26.COV2.S as a primary dose plus a booster dose at 2 months or two placebo injections 2 months apart. The primary endpoint was vaccine efficacy against the first occurrence of molecularly confirmed moderate to severe-critical COVID-19 with onset at least 14 days after booster vaccination, which was assessed in participants who received two doses of vaccine or placebo, were negative for SARS-CoV-2 by PCR at baseline and on serology at baseline and day 71, had no major protocol deviations, and were at risk of COVID-19 (ie, had no PCR-positive result or discontinued the study before day 71). Safety was assessed in all participants; reactogenicity, in terms of solicited local and systemic adverse events, was assessed as a secondary endpoint in a safety subset (approximately 6000 randomly selected participants). The trial is registered with ClinicalTrials.gov, NCT04614948, and is ongoing.
Findings Enrolment began on Nov 16, 2020, and the primary analysis data cutoff was June 25, 2021. From 34 571 participants screened, the double-blind phase enrolled 31 300 participants, 14 492 of whom received two doses (7484 in the Ad26.COV2.S group and 7008 in the placebo group) and 11 639 of whom were eligible for inclusion in the assessment of the primary endpoint (6024 in the Ad26.COV2.S group and 5615 in the placebo group). The median (IQR) follow-up post-booster vaccination was 36 center dot 0 (15 center dot 0-62 center dot 0) days. Vaccine efficacy was 75 center dot 2% (adjusted 95% CI 54 center dot 6-87 center dot 3) against moderate to severe-critical COVID-19 (14 cases in the Ad26.COV2.S group and 52 cases in the placebo group). Most cases were due to the variants alpha (B.1.1.7) and mu (B.1.621); endpoints for the primary analysis accrued from Nov 16, 2020, to June 25, 2021, before the global dominance of delta (B.1.617.2) or omicron (B.1.1.529). The booster vaccine exhibited an acceptable safety profile. The overall frequencies of solicited local and systemic adverse events (evaluated in the safety subset, n=6067) were higher among vaccine recipients than placebo recipients after the primary and booster doses. The frequency of solicited adverse events in the Ad26.COV2.S group were similar following the primary and booster vaccinations (local adverse events, 1676 [55 center dot 6%] of 3015 vs 896 [57 center dot 5%] of 1559, respectively; systemic adverse events, 1764 [58 center dot 5%] of 3015 vs 821 [52 center dot 7%] of 1559, respectively). Solicited adverse events were transient and mostly grade 1-2 in severity.
Interpretation A homologous Ad26.COV2.S booster administered 2 months after primary single-dose vaccination in adults had an acceptable safety profile and was efficacious against moderate to severe-critical COVID-19. Studies assessing efficacy against newer variants and with longer follow-up are needed. Funding Janssen Research & Development.
Copyright (c) 2022 The Author(s). Published by Elsevier Ltd
Control of Fusarium oxysporum f.sp. lycopersici by supernatants with siderophores of Acinetobacter sp.
No full textIlustracionesEl marchitamiento vascular del tomate causado por Fusarium oxysporum f. sp. lycopersici (Fol) es una de las enfermedades más limitantes del cultivo. El uso de fungicidas sistémicos y variedades resistentes a ciertas razas del patógeno no ha sido suficiente para su manejo. En este estudio se aislaron microrganismos productores de sideróforos con potencial biocontrolador sobre la cepa Fol59. Los aislamientos fueron obtenidos de muestras provenientes de la rizósfera y filósfera de árboles de cacao silvestre de cinco zonas de la Amazonía Colombiana. Los quince aislamientos seleccionados por su eficiencia en la síntesis de sideróforos, fueron clasificados dentro de los géneros Acinetobacter sp. (9), Bacillus sp. (2), Delftia sp. (1), Serratia sp. (1), Pseudomonas sp. (1) y Herbaspirillum sp. (1). La aplicación previa a la infección con Fol59 de los sobrenadantes con alto contenido de sideróforos (SodSid), de cinco de los aislamientos de Acinetobacter sp., logró disminuir el AUDPC de la severidad de la enfermedad hasta en un 45 %, siendo el aislamiento CBIO117 el que mayor actividad biocontroladora generó. Finalmente, se observó que los SodSid de Acinetobacter CBIO117 indujeron la expresión de los genes PR1 y ERF1 marcadores de las vías hormonales del Ácido Salicílico y Etileno en la planta respectivamente, pero no del gen (MYC2), factor de transcripción de los genes de defensa dependientes del Ácido Jasmónico. Sin embargo, en las plantas estimuladas con los SodSid CBIO117 e infectadas con Fol59 se indujo la expresión de manera diferencial del gen MYC2, destacando la activación de la defensa dependiente del ácido Jasmónico. Estos resultados demuestran el potencial biocontrolador que tienen los sobrenadantes con sideróforos secretados por aislamientos del género Acinetobacter sp. en la disminución del marchitamiento vascular del tomate, actuando como posibles elicitores de la respuesta de defensa de la planta. (texto tomado de la fuente)The vascular wilt disease of tomato caused by Fusarium oxysporum f. sp. lycopersici (Fol) is one of the most limiting diseases of this crop. The use of systemic fungicides and varieties resistant to certain races of the pathogen have not provided an adequate control. In this study, siderophore-producing microorganisms with biocontrol potential against Fol were isolated from rhizosphere and phyllosphere samples taken from wild cocoa trees in five different locations of the Colombian Amazon. The fifteen isolates selected for being representative of the sampling zones and showing greater production of siderophores were classified within the genera Acinetobacter sp. (9), Bacillus sp. (2), Delftia sp. (1), Serratia sp. (1), Pseudomonas sp. (1) y Herbaspirillum sp. (1). The application before infection with Fol59 of supernatants with a high content of siderophores (SodSid) from five Acinetobacter sp. isolates caused a reduction in the AUDPC of the disease severity of up to 45%, being CBIO117 the isolate which showed greater biocontrol activity. Finally, it was confirmed that SodSid Acinetobacter CBIO117 generated an induction in the expression of PR1 and ERF1 genes, markers of the Salicylic Acid and Ethylene hormonal pathways in the plant, respectively. In contrast the gene (MYC2), a transcription factor of the Jasmonic Acid-dependent defense genes was not expressed. However, in plants stimulated with SodSid CBIO117 and infected with Fol59, MYC2 gene expression was differentially induced, highlighting the activation of the Jasmonic acid-dependent defense that possibly led to counteracting the infection process of the pathogen and reducing the severity of the disease. Our results demonstrate the biotechnological potential of siderophore-producing isolates of the genus Acinetobacter sp. for the control of plant pathogens, eliciting the defensive response in the plant.MaestríaMagíster en Ciencias AgrariasÁrea Curricular en Producción Agraria Sostenibl
Whole-genome sequencing reveals host factors underlying critical COVID-19
No full textAltres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
Stratified analyses refine association between TLR7 rare variants and severe COVID-19
No full textSummary: Despite extensive global research into genetic predisposition for severe COVID-19, knowledge on the role of rare host genetic variants and their relation to other risk factors remains limited. Here, 52 genes with prior etiological evidence were sequenced in 1,772 severe COVID-19 cases and 5,347 population-based controls from Spain/Italy. Rare deleterious TLR7 variants were present in 2.4% of young (<60 years) cases with no reported clinical risk factors (n = 378), compared to 0.24% of controls (odds ratio [OR] = 12.3, p = 1.27 × 10−10). Incorporation of the results of either functional assays or protein modeling led to a pronounced increase in effect size (ORmax = 46.5, p = 1.74 × 10−15). Association signals for the X-chromosomal gene TLR7 were also detected in the female-only subgroup, suggesting the existence of additional mechanisms beyond X-linked recessive inheritance in males. Additionally, supporting evidence was generated for a contribution to severe COVID-19 of the previously implicated genes IFNAR2, IFIH1, and TBK1. Our results refine the genetic contribution of rare TLR7 variants to severe COVID-19 and strengthen evidence for the etiological relevance of genes in the interferon signaling pathway
