dataesr/scientific-paragraphs-categorization huggingface dataset:
The timing of vaccination, number of doses, and vaccine type were not analysed in this study, preventing us from drawing conclusions about the relation between vaccination and post-COVID-19 effects or disentangling the normal weaning down of symptoms from the protective effects of vaccination. The clinical relevance of our clustering results was supported by retrospective questionnaire data about the lived experience of post-COVID-19 condition. The main result from this analysis was that symptom clusters we identified differed in their relation to individuals' daily activities. We found that specific symptom profiles, such as clusters wild-B (mainly associated with systemic symptoms) and wild-test-C (mainly associated with respiratory symptoms), were related to more severe forms of post-COVID-19 conditions, which probably led people to seek medical help and to report prolonged effects on their daily lives.
Data sharing Data collected in the COVID Symptom Study app are shared with other health researchers through the UK National Health Service-funded Health Data Research UK and Secure Anonymised Information Linkage consortium, housed with the UK Secure Research Platform (Swansea, UK). Anonymised data can be made available to researchers, provided that they share their protocols and their research is in the public interest. Requests for access should be made via the Health Data Research Innovation Gateway (https://web. www. healthdatagateway. org/dataset/fddcb382-3051-4394-8436-b92295f14259).
Acknowledgments We thank the study participants (including those who shared opinions about our work and how could we improve it to understand symptom progression and recovery) and the  CSS Biobank  volunteer advisory panel for their feedback on the significance of this work. This research was partly funded by the  Wellcome Trust  ( 215010/Z/18/Z ), the  Wellcome Engineering and Physical Sciences Research Council Centre for Medical Engineering at King's College London  ( WT 203148/Z/16/Z ),  Engineering and Physical Sciences Research Council  ( EP/T022205/1 ), and the  UK Department of Health  via the  UK National Institute for Health and Care Research comprehensive Biomedical Research Centre  award to Guy's & St Thomas's  NHS Foundation  Trust in partnership with  King's College London  and  King's College Hospital NHS Foundation Trust.
Further support was provided by the  Chronic Disease Research Foundation  ( CDRF-22/2020 ) and the  UK Department of Health  via the  National Core Studies , an initiative funded by  UK Research and Innovation , the  National Institute for Health and Care Research , and the  Health and Safety Executive. The  COVID-19 Longitudinal Health and Wellbeing National Core Study  was funded by the  UK Medical Research Council  ( MC_PC_20030 ,  COV-LT-0009 ). The work was further supported by a grant from the  UK Department of Health and Social Care  to ZOE. We also acknowledge support from the  UK Research and Innovation London Medical Imaging and Artificial Intelligence Centre for Value-Based Healthcare. Investigators also received support from the  Wellcome Flagship Programme  ( WT213038/Z/18/Z  and  WT212904/Z/18/Z ), the  UK Medical Research Council , the  British Heart Foundation , the  UK Alzheimer's Society  ( AS-JF-17-011 ), the  EU , the  NIHR , and the  NIHR -funded BioResource,  Clinical Research Facility and Biomedical Research Centre at Guy 's and  St Thomas's NHS Foundation Trust  (in partnership with  King's College London ).
19  Bench to bedside: How basic research informs treatment in genetic epilepsies. Functional analyses of genetic variants can help us identify molecular mechanisms underlying genetic epilepsies. In turn, details of these pathogenic mechanisms can inform treatment with available anti-seizure medications and spur development of new therapies for genetic epilepsies that are refractory to current treatments. For example, we have tools to study the properties of sodium currents generated by variants in sodium channel genes identified in DS (SCN1A) and SCN8Arelated developmental and epileptic encephalopathy (DEE). 20 These studies revealed that DS is caused mostly by loss-offunction variants of SCN1A. In contrast, SCN8A-related DEE is caused by gain-of-function variants of SCN8A. These data explain why sodium channel blockers are contraindicated for Dravet syndrome but may be helpful for SCN8A-related DEE.
The essential outcomes included many nonseizure outcomes: anxiety, depression, suicidality, memory and attention, sleep quality, somnolence, and-for infants and young children-neurodevelopmental outcomes. The ICHOM Epilepsy Sets ensure that outcomes that are relevant to people with epilepsy, their representatives, and health care providers are measured. They also facilitate harmonization of outcome measurement, and if widely implemented should reduce outcome measurement heterogeneity and therefore facilitate comparative research and big-data science. 31, 32  Behavioral health across the spectrum of epilepsy. Behavioral health comorbidities are common in persons with epilepsy (PWE), can worsen ASM side effects, and are associated with poor health-related quality of life (HRQoL). 33  In addition, 30% to 60% of PWE are nonadherent to ASMs.
Utilization of various mechanisms of action is KEY to avoid side effects from pharmacokinetic interactions. 57  If a new medication is started and is more efficacious, evaluate and possibly reduce previous treatment to improve tolerance and retention. It was also discussed that the use of lower doses and slower titrations in the elderly may improve tolerance and reduce side effects. Consider nonpharmacologic methods: surgery, neuromodulation, and diet therapy. Neuromodulation does not produce the same side effects as medication and in fact has shown improvements in cognition, memory, and mood. The use of neuromodulation can help reduce polypharmacy. The data from the RNS allows providers to identify the efficacy of new medication early to determine clinical benefit of titration and possibly guide the reduction of other anti-seizure medication.
" Dr Maturu presented resource-rich and resource-spare opportunities in opening up a pregnancy clinic for women with epilepsy and shared insights on how to create and sustain such a clinic. The importance of establishing relationships early on, benefits immensely, assisting in sustainability with assuring that key stakeholders are aware of services and support to women with Epilepsy that become pregnant. Dr Velez Ruiz shared data supporting the models of care. 87  Participants were able to take key implications of practice away with the understanding that data can drive change and the viability and sustainability for such clinics. Co-Chairperson Shanna Guilfoyle, PhD, invited speakers back to the stage and recognized our advocates, as well as the speakers overall. Audience participants were able to address questions and discussions continued after the completion of this symposium.
Underutilization is particularly true for epilepsies where seizure freedom is not expected, or the etiology remains following surgery (i. e. , genetic epilepsies). Surgery for genetic epilepsy can result in significant seizure reduction and improvements in quality of life and development. Genetic conditions wherein the epileptogenic source is a focal brain malformation (i. e. , tuberous sclerosis complex and DEPDC5-related epilepsy) experience seizure-free rates exceeding 50% in many studies. 111, 112  Early surgical therapy is also associated with improved developmental trajectories. Conditions without structural epileptogenic sources, such as channelopathies, have been described as poor surgical candidates, yet data is often biased toward the expectation of seizure freedom. 113  Instead, it is imperative to consider the palliative benefits of surgery in this group.
Procedures such as corpus callosotomy demonstrate response rates often exceeding those of medications approved for these conditions, in addition to improvements in nonseizure outcomes. 114  Data from the Pediatric Epilepsy Research Consortium's Surgery Database found two-thirds of patients with genetic etiology experienced >50% seizure reduction following surgery. 115  While nonlesional genetic etiologies were often palliative procedures, 35% had >90% seizure reduction at a mean 11-month follow-up. Therefore, surgery must be considered a viable treatment option for genetic epilepsies in the absence of precision medical treatments with better disease-modifying effects. Tailored epilepsy imaging strategies for personalized care, focusing on structural MRI, was presented by Dr Irene Wang. The talk centered around 3 important aspects that imaging could help with lesion presence, border, and characteristics.
The importance of using dedicated MRI protocol and reviewing guidelines was addressed. The utilization of voxel-based and surface-based MRI postprocessing methods has shown great promise (and in some cases proven essential) for lesion detection and delineation in everyday clinical care. Emerging advanced techniques such as 7 T and MR fingerprinting (MRF) 116 may detect previously unseen lesions in patients with nonlesional 3 T MRI. Lesion characteristics such as FCD subtypes and epileptogenicity may be interrogated by multimodal MRI and MRF. Machine/deep learning studies using multicenter, large data sets, may soon be used for individual detection/prediction on local datasets. 117, 118  It is hoped that the integrative use of advanced MRI and postprocessing in everyday care will substantially improve the individualized yield of structural MRI.
From its founding in 1936 as the "American League Against Epilepsy" with 69 members,  136  the AES now has >4000 members. The AES annual meeting provides a venue for the community of members with diverse interests to meaningfully interact. The AES Fellows Program involves 105 fellows who receive complementary annual meeting attendance, with special career development and mentoring programming. Finally, the AES provided nearly US$1. 3 million for research grant funding in 2022, 87% of which was for early career grants. Therefore, AES provides a collegial environment, mentorship, and funding that is vital for our early career clinical investigators. What is next after early career funding. Dr Adam Hartman discussed funding opportunities for investigators who have completed studies supported by early career foundation funding (e.
g. , the Susan Spencer Scholarship). The National Institute of Neurological Disorders and Stroke (NINDS) and other Institutes and Centers at the NIH support a variety of career development awards for junior faculty. Funding mechanisms include the K-series (e. g. , K01, K08, K22, K23) but NINDS also supports applicants from diverse and underrepresented backgrounds through additional funding mechanisms (e. g. , K01, K22). Other grants support those who are transitioning to independence (e. g. , K02, K99/R00). National Institute of Neurological Disorders and Stroke provides diversity supplements in the form of short-and long-term investigator research supplements. Some private foundations and patient advocacy groups provide similar support. The NIH Lasker Clinical Scholars program aims to increase the number of clinical and translational researchers through a combination of intramural (NIH) and extramural mechanisms.
The incidence of childhood epilepsy is highest in the first years of life. Genetic and structural etiologies abound in this age group and resistance to anti-seizure medications (ASM) is common, leading to significant adverse consequences for cognitive and behavioral development. The Agency for Healthcare Research and Quality recently highlighted significant knowledge gaps for the treatment of early life epilepsies, including the absence of data for the effectiveness of currently available medications, the effectiveness of nonpharmacologic treatments, and the harms of these treatments used early in life. 183  This symposium highlighted multiple innovative and collaborative efforts to broaden research into early life epilepsies in an effort to eliminate knowledge gaps and improve outcomes.
[196] [197] [198]  Early work from PELHS includes the development of a novel quality of life measure for use in clinical care, and the development, iteration, and deployment of a standard electronic health record form optimized to support clinical workflows. As these data are collected, we anticipate an increasing pace of discovery to optimize clinical care for these vulnerable children. What we don't know can hurt others: Disparities in treatment of infantile spasms. The National Infantile Spasms Consortium, a collaborative, prospective, multicenter database, investigated important questions in disparities in the treatment of infantile spasms. 199 There were 25 centers from across the country and 555 infants with new-onset infantile spasms included. Children who identified as Black/non-Hispanic had a lower odds of receiving a standard treatment course for infantile spasms (P ¼.
Disseminating practice-changing findings can be accomplished by leveraging learning health care systems. Future work should focus on modernizing data management strategies and developing cloud-based data solutions with autonomous deidentification and standardization of data. This would significantly lower the barriers to doing multicentered research. Debate: Early surgery versus waiting for a second ASM failure-Con. Epilepsy surgery is accepted for the management of drugresistant focal epilepsy that persists despite 2 adequate ASM trials. 201 However, expedited epilepsy surgery is not without risk. Although complication rates have decreased over the last > 30 years, complications remain an unavoidable consequence of epilepsy surgery and include the risk of bleeding, infection, and persistent neurologic deficits.
210 SCN8A registry. Pathogenic variants at the voltage-gated sodium channel gene, SCN8A, are associated with a wide spectrum of epilepsy phenotypes ranging from benign familial infantile seizures to mild-to-severe developmental and epileptic encephalopathies. Clinical features include mild to severe developmental impairment and multiple seizure types, including generalized tonic-clonic and absence seizures, focal seizures, and infantile/epileptic spasms. One of the major challenges facing clinicians and researchers is to identify genotype-phenotype correlations that may improve prognosis, guide treatment decisions, and ultimately lead to precision medicine approaches. The SCN8A Registry is a patient-driven online database collecting data on children with SCN8A-related disorders. The range of data types collected provides an opportunity to perform genotype-phenotype correlation analyses and to develop methods to classify patients based on clinical features associated with gene variants.
Acknowledgments The authors would like to thank the AES staff including  Eileen Murray, MM , CAE,  Shawna Strickland, PhD, CAE, RRT ,  FAARC ,  Susan Oliver, MBA ,  Cristina Graham ,  JoLynn Amsden ,  Amy Kephart, MPH ,  CAE  for their support and all the committee members in charge of program planning of the Annual American Epilepsy Society Meeting.
All records used in this work can be accessed in the publicly available BOLD dataset DS-LONO2: dx. doi. org/10. 5883/DS-LONO2). When this work begun, there were 12 taxa recognized in the CLC corresponding to the 11 species and one subspecies recognized in the revision of subfamily Hemileucinae by  [24]. We databased records for all specimens (730 in total) in the MNHN collection and organized them based on their general habitus (wing pattern) and their geographical origin to sort specimens as candidate representatives of the many species described after 2002. Then we selected individuals of both sexes within each of the sorted sets of specimens and processed them through DNA barcoding (see below) to compare them with DNA barcodes available from other sources (including the type specimens of most of the recently described taxa).
All DNA barcode records used in this study, including both specimen (e. g. , voucher repository, identification, collecting data, GPS coordinates) and sequence data (e. g. , electropherograms, DNA sequence, GenBank accession numbers), are integrated into the BOLD dataset DS-LONO2 (dx. doi. org/10. 5883/DS-LONO2; available from the Barcode of Life Datasystems (BOLD,www. boldsystems. org; [42]   [43]. The DNA barcode dataset comprises 839 records, for specimens originating from 20 countries. We used BOLD analytical tools to compute genetic distances (using default parameters, BOLD sequence alignment option and computation of uncorrected p-distances after filtering out 31 records with DNA sequences shorter than 400bp), and to represent them in the form of a Neighbor Joining (NJ) tree. For visualization purposes, the BOLD NJ tree was imported as Newick format and edited into iToL v4  [43].
Spatial distribution and coincidence with areas of epidemiological relevance Once our database was assembled, we georeferenced those records that lacked coordinates using the locality reported on specimen labels. We used Google Earth and various online gazetteers, atlases, and traveler blogs to retrieve geographical coordinates as precisely as possible. Epidemiological information was gathered from published case reports or through Google searches using the terms "Lonomia accidents" and "lonomism" in both English and Spanish. Additional information from Brazil was obtained from the National Information System SINAN (http://portalsinan. saude. gov. br/dados-epidemiologicos-sinan) and information from Colombia was provided by the National Institute of Health. Municipality boundaries were gathered from GADM data (version 3.
Species delimitation and taxonomic account Our assembled database (DS-LONO2: dx. doi. org/10. 5883/DS-LONO2) comprises 1,212 records of Lonomia specimens. Of these records, 69% (839 records) have DNA barcode sequences and represent all species (52) and subspecies (5) listed as valid in  [25] , except for "Lonomia albiguttata Ko ¨hler, 1928", which we consider to be just an incorrect subsequent spelling of Lonomia albigutta Walker, 1855 (currently placed as a junior subjective synonym of L. obliqua). The three most recently described species, Lonomia cayennensis Brechlin & Meister, 2019, Lonomia moniqueae Brechlin & Meister, 2019, and Lonomia rubroguyana Brechlin & Meister, 2019, as well as Lonomia diabolus Draudt, 1929, recently raised to species status by  [33]  from subspecies status within L.
Three subspecies were proposed by  [45]  and are here retained as they form distinct, though shallow, genetic clusters that are geographically segregated: Our results also lead us to propose the following taxonomic changes: Lonomia (1) Lonomia oroiana Brechlin, Meister & Ka ¨ch, 2013 syn. nov. is here synonymized with Lonomia manabiana Brechlin, Meister & Ka ¨ch, 2013; under the Principle of the First Reviser as both species were described in the same publication. The DNA barcodes of holotype specimens of both species are nearly identical (p-distance of 0. 6%), the male adult habitus and genitalia are morphologically very similar  [46] , and the species occupy the same biogeographical region, west of the Ecuadorian Andean cordillera. Additional morphological comparisons and The inner map shows the distribution of 1019 georeferenced records of the genus Lonomia compiled in our database and gray areas represent the biomes where species with medical importance have been found.
Red and orange symbols in the map, and branches in the neighbor joining tree depict the species of confirmed (red) or suspected (orange) medical importance; these are listed and numbers after the species name refer to their position on the tree. Black dots depict all the other species in the genus. Country border shape file available at: (https://gadm. org/data. html); terrestrial ecoregions of the world available at: (https://www. worldwildlife. org/publications/terrestrial-ecoregions-ofthe-world). All species of the genus are numbered in the circular tree from 1 to 60 (clockwise, starting from top-left end of the tree) in reference to species as numbered in S1 Table. This tree was built using 808 DNA barcode records of more than 400bp in the public BOLD dataset DS-LONO2; branch lengths are proportional to genetic divergences (uncorrected p-distances).
achelous, L. rubroguyana, L. cayennensis and L. camox (S1 and S2 Figs). Peru has the highest species richness, and accidents have been recorded in Junı ´n in 2006, and in Huanuco in 2010 and 2017 when antivenom was used (S2 Table ). The species reported to be present here are:  (1)   In Venezuela, from 1960 to 1967, five accidents of hemorrhagic syndrome caused by contact with venomous caterpillars were recorded in Bolivar state  [8]. Lonomia achelous was, as usual, recorded as the causal agent  [8]  but only one species, Lonomia moniqueae Brechlin & Meister, 2019, has been collected in that state (S1 Fig). In 1996, caterpillar colonies were collected from Tapirira guinanensis tree trunks in Anzoategui and Bolivar states  [48]  but we have no Lonomia collection records from Anzoategui in our database (Fig  2).
Indeed, in face of the recent inflation of species names in the genus and more generally within the Saturniidae family  [25]  some taxonomists have chosen to ignore many of these taxa (e. g. [49] ), because of the lack of access to the necessary information (genetic data or actual specimens for study) for a critical evaluation of their validity. In this context, the DNA barcodes collated here (publicly available in BOLD dataset DS-LONO2: dx. doi. org/10. 5883/DS-LONO2) represent a new and invaluable resource for the identification of Lonomia species involved in accidents. DNA barcoding is cheap  [37] ,  [50] , and relatively simple to implement, and caterpillar tissues (e. g. , thoracic legs, head capsule) can be processed to provide a rapid and reliable identification for decision making by practitioners.
This tree was built using 808 DNA barcode records of more than 400bp in the public BOLD dataset DS-LONO2; branch lengths are proportional to genetic divergences (uncorrected p-distances). Colored background areas of the tree represent the three species-groups recognized in this work: the electra-group (blue), obliqua-group (yellow), and achelous-group (green). Left side picture: Lonomia sp. adult (live unidentified specimen from Costa Rica; courtesy of Armin Dett). Right side picture: Lonomia camox 6th instar caterpillar (photo by RR). A traditional vertical representation of this tree is also available at https://itol. embl. de/export/921881233420241575572285.
Acknowledgments We wish to give special thanks to our local collaborators at the field sites in  Tanimboca Natural Reserve and Secretarı ´a de Salud (Amazonas), Senderos del Canajagu ¨a (Meta) , and  La Victoria ,  Caoba Natural Reserve , and  Eudes Baca  and his family (Magdalena), who supported this research with their motivation of contributing to scientific knowledge, aware that ultimately it can be translated into benefits for the people living in areas at risk. In the same spirit, we want to thank:  Gabriel Colorado ,  Maria Elisa Peichoto  and  Pedro Sarmiento , who contributed specimens for barcode identification; the team at  CIMPAT  and the  Department of Biological Sciences , who were always prompt to support sample processing;  Giovanni Randazzo , for imaging documentation during fieldwork and  Alessandro Giusti  ( NHMUK ) for images of the holotype of L.
This work was funded by  Vicerrectorı ´a de Investigaciones , and  Facultad de Ciencias   INV-2020-105-2030 ,  Universidad de Los Andes  (Granted to CG). Pontificia Universidad Javeriana, Facultad de Estudios Ambientales y Rurales ,  PPTA 7996  (Granted to ARAS). Humboldt Institute through the collaboration agreement  16-220  (Granted to MAG). French National Research Agency (ANR) SPHINX  grant no. ANR-16-CE02-0011-01  (to RR, TD) and  French Foundation of Research on Biodiversity  (FRB; www. fondationbiodiversite. fr) and CESAB synthesis centre to ACTIAS project (to RR, LBM, IJK, TD). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.