User-friendly automatic transcription of low-resource languages: Plugging ESPnet into Elpis

This paper reports on progress integrating the speech recognition toolkit ESPnet into Elpis,a web front-end originally designed to provide access to the Kaldi automatic speech recognition toolkit. The goal of this work is to makeend-to-end speech recognition models avail-able to language workers via a user-friendlygraphical interface. Encouraging results are reported on (i) development of an ESPnet recipe for use in Elpis, with preliminary resultson data sets previously used for training acoustic models with the Persephone toolkit alongwith a new data set that had not previously been used in speech recognition, and (ii) in-corporating ESPnet into Elpis along with UIe nhancements and a CUDA-supported Docker file

Los servicios en los esquemas de integración: algunas consideraciones y opciones para Centroamérica: versión provisional

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The Imported Fever Service; a UK-wide system for improved management and diagnosis of fever in returned travellers

Background: Poor integration of diagnostic services can delay the diagnosis of febrile illness in returning travelers, with significant clinical and public health consequences. The Imported Fever Service (IFS) was established in 2012 as a national specialist diagnostic and clinical advice service for acute imported fevers. We summarise the first 9 months' activity. Methods: The IFS is a collaboration between the Rare and Imported Pathogens Laboratory, the Hospital for Tropical Diseases and the Liverpool School of Tropical Medicine. It combines 24-hour clinical advice and diagnostic services capable of rapidly detecting ‘exotic’ pathogens, including VHFs. For each referral a panel of tests, based on the patient's travel is performed and relevant clinical data are collected. Results: Between June 2012 and February 2013, 143 cases were referred from 84 UK centres. 43 (30%) diagnoses were made following referral to the service. Patients had travelled to Africa (32%), Asia (24%) and Europe (15%). Presenting complaints included neurological (24%), undifferentiated fever (23%) and respiratory (14%). The IFS diagnosed: murine typhus (n=7), spotted fever, dengue (n=4 each), Q fever, sandfly fever, leptospirosis (n=3 each), Tick-Borne encephalitis, scrub typhus, hantavirus and CCHF (1-2 cases each). The service helped infection control and public health responses to CCHF and autochthonous hantavirus cases. Conclusions: Referral to the IFS resulted in rapid diagnosis of illness in 30% of returned travellers with otherwise undiagnosed fever. These diagnoses informed critical clinical, infection control and public health decisions and demonstrate the IFS model is feasible, effective and could be reproduced in other countries

Chromosome contacts in activated T cells identify autoimmune disease candidate genes

Abstract Background Autoimmune disease-associated variants are preferentially found in regulatory regions in immune cells, particularly CD4+ T cells. Linking such regulatory regions to gene promoters in disease-relevant cell contexts facilitates identification of candidate disease genes. Results Within 4 h, activation of CD4+ T cells invokes changes in histone modifications and enhancer RNA transcription that correspond to altered expression of the interacting genes identified by promoter capture Hi-C. By integrating promoter capture Hi-C data with genetic associations for five autoimmune diseases, we prioritised 245 candidate genes with a median distance from peak signal to prioritised gene of 153 kb. Just under half (108/245) prioritised genes related to activation-sensitive interactions. This included IL2RA, where allele-specific expression analyses were consistent with its interaction-mediated regulation, illustrating the utility of the approach. Conclusions Our systematic experimental framework offers an alternative approach to candidate causal gene identification for variants with cell state-specific functional effects, with achievable sample sizes

Transcriptional, epigenetic and metabolic signatures in cardiometabolic syndrome defined by extreme phenotypes.

Funder: The National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre and NIHR Rare Disease Translational Research CollaborationFunder: NIHR Leicester Biomedical Research Centre and the John and Lucille Van Geest FoundationFunder: British Heart Foundation Cambridge Centre of ExcellenceFunder: NIHR Cambridge Biomedical Research CentreFunder: NHS Health Education EnglandFunder: Isaac Newton fellowshipBACKGROUND: This work is aimed at improving the understanding of cardiometabolic syndrome pathophysiology and its relationship with thrombosis by generating a multi-omic disease signature. METHODS/RESULTS: We combined classic plasma biochemistry and plasma biomarkers with the transcriptional and epigenetic characterisation of cell types involved in thrombosis, obtained from two extreme phenotype groups (morbidly obese and lipodystrophy) and lean individuals to identify the molecular mechanisms at play, highlighting patterns of abnormal activation in innate immune phagocytic cells. Our analyses showed that extreme phenotype groups could be distinguished from lean individuals, and from each other, across all data layers. The characterisation of the same obese group, 6 months after bariatric surgery, revealed the loss of the abnormal activation of innate immune cells previously observed. However, rather than reverting to the gene expression landscape of lean individuals, this occurred via the establishment of novel gene expression landscapes. NETosis and its control mechanisms emerge amongst the pathways that show an improvement after surgical intervention. CONCLUSIONS: We showed that the morbidly obese and lipodystrophy groups, despite some differences, shared a common cardiometabolic syndrome signature. We also showed that this could be used to discriminate, amongst the normal population, those individuals with a higher likelihood of presenting with the disease, even when not displaying the classic features

Heritage under attack : motives for targeting cultural property during armed conflict

Although attacks on cultural property have caused international outcry, our understanding of this phenomenon is still limited. In particular, little research has been directed towards exploring the motivations for such attacks. Therefore, we ask: What are the motives for attacking sites, buildings or objects representing cultural heritage? By combining insights from peace and conflict research with findings from heritage studies we present a typology of motivations for attacking cultural property. We identify four, not mutually exclusive, broad groups of motives: (i) attacks related to conflict goals, in which cultural property is targeted because it is connected to the issue the warring parties are fighting over (ii), military-strategic attacks, in which the main motivation is to win tactical advantages in the conflict (iii), signalling attacks, in which cultural property is targeted as a low-risk target that signals the commitment of the aggressor, and (iv) economic incentives where cultural property provides funding for warring parties. Our typology offers a theoretical structure for research about why, when, and by whom, cultural property is targeted. This is not only likely to provide academic benefits, but also to contribute to the development of more effective tools for the protection of cultural property during armed conflict