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Alejandro Azofeifa Diana Valencia Carmen J. Rodriguez Maritza Cruz Devin Hayes Edn Montaez-Bez Betzaida Tejada-Vera Joshua E. Villafae-Delgado Jessica J. Cabrera Miguel Valencia-Prado 《Public health reports (Washington, D.C. : 1974)》2021,136(3):354
ObjectivesUsing the Council of State and Territorial Epidemiologists (CSTE) classification guidelines, we characterized coronavirus disease 2019 (COVID-19)–associated confirmed and probable deaths in Puerto Rico during March–July 2020. We also estimated the total number of possible deaths due to COVID-19 in Puerto Rico during the same period.MethodsWe described data on COVID-19–associated mortality, in which the lower bound was the sum of confirmed and probable COVID-19 deaths and the upper bound was excess mortality, estimated as the difference between observed deaths and average expected deaths. We obtained data from the Puerto Rico Department of Health COVID-19 Mortality Surveillance System, the Centers for Disease Control and Prevention’s National Electronic Disease Surveillance System Base System, and the National Center for Health Statistics.ResultsDuring March–July 2020, 225 COVID-19–associated deaths were identified in Puerto Rico (119 confirmed deaths and 106 probable deaths). The median age of decedents was 73 (interquartile range, 59-83); 60 (26.7%) deaths occurred in the Metropolitana region, and 140 (62.2%) deaths occurred among men. Of the 225 decedents, 180 (83.6%) had been hospitalized and 93 (41.3%) had required mechanical ventilation. Influenza and pneumonia (48.0%), sepsis (28.9%), and respiratory failure (27.1%) were the most common conditions contributing to COVID-19 deaths based on death certificates. Based on excess mortality calculations, as many as 638 COVID-19–associated deaths could have occurred during the study period, up to 413 more COVID-19–associated deaths than originally reported.ConclusionsIncluding probable deaths per the CSTE guidelines and monitoring all-cause excess mortality can lead to a better estimation of COVID-19–associated deaths and serve as a model to enhance mortality surveillance in other US jurisdictions. 相似文献
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Knorst Jessica Klöckner Brondani Bruna Tomazoni Fernanda Vargas Andressa Weber Cósta Marina Dutra da Silva Godois Leonardo Mendes Fausto Medeiros Ardenghi Diego Machado Ardenghi Thiago Machado 《Quality of life research》2021,30(6):1685-1691
Quality of Life Research - As people around the world are facing the Covid-19 outbreak, their perception of oral health problems could be changed. This study aimed to evaluate the immediate effects... 相似文献
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Wen Chen Jessica M. Gullett Rebecca E. Tweedell Thirumala-Devi Kanneganti 《European journal of immunology》2023,53(11):2250235
Regulated cell death (RCD) triggered by innate immune activation is an important strategy for host survival during pathogen invasion and perturbations of cellular homeostasis. There are two main categories of RCD, including nonlytic and lytic pathways. Apoptosis is the most well-characterized nonlytic RCD, and the inflammatory pyroptosis and necroptosis pathways are among the best known lytic forms. While these were historically viewed as independent RCD pathways, extensive evidence of cross-talk among their molecular components created a knowledge gap in our mechanistic understanding of RCD and innate immune pathway components, which led to the identification of PANoptosis. PANoptosis is a unique innate immune inflammatory RCD pathway that is regulated by PANoptosome complexes upon sensing pathogens, pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs) or the cytokines produced downstream. Cytosolic innate immune sensors and regulators, such as ZBP1, AIM2 and RIPK1, promote the assembly of PANoptosomes to drive PANoptosis. In this review, we discuss the molecular components of the known PANoptosomes and highlight the mechanisms of PANoptosome assembly, activation and regulation identified to date. We also discuss how PANoptosomes and mutations in PANoptosome components are linked to diseases. Given the impact of RCD, and PANoptosis specifically, across the disease spectrum, improved understanding of PANoptosomes and their regulation will be critical for identifying new therapeutic targets and strategies. 相似文献
99.
Valentina Mazzotta Alessandro Cozzi Lepri Francesca Colavita Silvia Rosati Eleonora Lalle Claudia Cimaglia Jessica Paulicelli Ilaria Mastrorosa Serena Vita Lavinia Fabeni Alessandra Vergori Gaetano Maffongelli Fabrizio Carletti Simone Lanini Emanuela Caraffa Eugenia Milozzi Raffaella Libertone Pierluca Piselli Enrico Girardi AnnaRosa Garbuglia Francesco Vaia Fabrizio Maggi Emanuele Nicastri Andrea Antinori INMI COVID- Outpatient Treatment Study Group 《Journal of medical virology》2023,95(1):e28186
100.
Lisanne E. de Koning Jessica Warnink-Kavelaars Marion A. van Rossum Diederik Bosman Leonie A. Menke Fransiska Malfait Rosa de Boer Jaap Oosterlaan Raoul H. H. Engelbert Lies Rombaut And the Pediatric Heritable Connective Tissue Disorders Study Group 《American journal of medical genetics. Part A》2023,191(7):1792-1803
The aim of the present study was to investigate the nature and prevalence of nonspecific somatic symptoms, pain and catastrophizing in children with Heritable Connective Tissue Disorders (HCTD), and to determine their association with disability. This observational, multicenter study included 127 children, aged 4–18 years, with Marfan syndrome (MFS) (59%), Loeys-Dietz syndrome (LDS) (8%), Ehlers-Danlos syndromes (EDS) (12%) and hypermobile Ehlers-Danlos syndrome (hEDS) (23%). The assessments included the Children's Somatization Inventory or parent proxy (CSI, PCSI), pain visual-analogue scale (VAS), SUPERKIDZ body diagram, Pain Catastrophizing Scale Child or parent proxy (PCS-C, PCS-P) and Childhood Health Assessment Questionnaire (CHAQ-30). Data from children aged ≥8 years were compared to normative data. In children ≥ 8 years (n = 90), pain was present in 59%, with a median of 4 (IQR = 3–9) pain areas. Compared to normative data, the HCTD group reported significantly higher on the CSI (p ≤ 0.001, d = 0.85), VAS pain intensity (p ≤ 0.001, d = 1.22) and CHAQ-30 (p ≤ 0.001, d = 1.16) and lower on the PCS-C (p = 0.017, d = −0.82) and PCS-P (p ≤ 0.001, d = −0.49). The intensity of nonspecific somatic symptoms and pain explained 45% of the variance in disability (r2 = 0.45 F(2,48) = 19.70, p ≤ 0.001). In children ≤ 7 years (n = 37), pain was present in 35% with a median of 5(IQR = 1–13) pain areas. The mean(SD) VAS scores for pain intensity was 1.5(2.9). Functional disability was moderately correlated to the number of pain areas (r = 0.56, p ≤ 0.001), intensity of nonspecific somatic symptoms (r = 0.63, p ≤ 0.001) and pain (r = 0.83, p ≤ 0.001). In conclusion, this study supports the need for comprehensive assessment of nonspecific somatic symptoms, pain, and disability in children with HCTD to allow tailored treatment. 相似文献