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3.
Tommaso Francesco Aiello; Jon Salmanton-Garcia; Francesco Marchesi; Barbora Weinbergerova; Andreas Glenthoj; Jens Van Praet; Francesca Farina; Julio Davila-Valls; Sonia Martín-Pérez; Shaimaa El-Ashwah; Martin Schönlein; Iker Falces-Romero; Jorge Labrador; Uluhan Sili; Caterina Buquicchio; Antonio Vena; Gaetan Plantefeve; Verena Petzer; Monika M. Biernat; Tobias Lahmer; Ildefonso Espigado; Jaap A. van Doesum; Ola Blennow; Klára Piukovics; Carlo Tascini; Michael Samarkos; Yavuz M. Bilgin; Luana Fianchi; Federico Itri; Toni Valkovic; Nicola S. Fracchiolla; Michelina Dargenio; Moraima Jimenez; Ferenc Magyari; Alberto Lopez-Garcia; Lucia Prezioso; Natasa Čolovic; Evgenii Shumilov; Ghaith Abu-Zeinah; Esperanza Lavilla-Rubira; Mario Virgilio Papa; Tomás-José Lopez-Gonzalez; László Imre Pinczes; Fatih Demirkan; Natasha Ali; Caroline Besson; Guillemette Fouquet; Alessandra Romano; Jose Angel Hernández-Rivas; Maria Ilaria del Principe; Avinash Aujayeb; Maria Merelli; Sylvain Lamure; Joyce Marques De Almeida; Maria Gomes da Silva; Noha Eisa; Joseph Meletiadis; Ikhwan Rinaldi; Olimpia Finizio; Ozren Jakšić; Mario Delia; Summiya Nizamuddin; Monia Marchetti; Marina Machado; Martin Cernan; Nicola Coppola; Eleni Gavriilaki; Chiara Cattaneo; Ana Groh; Zlate Stojanoski; Nurettin Erben; Nikola Pantic; Gustavo-Adolfo Mendez; Roberta Di Blasi; Stef Meers; Cristina De Ramon; Nathan C. Bahr; Ziad Emarah; Gina Varricchio; Milche Cvetanoski; Ramón Garcia-Sanz; Mirjana Mitrovic; Raphaël Lievin; Michaela Hanakova; Zdeněk Racil; Maria Vehreschild; Athanasios Tragiannidis; Raquel Nunes Rodrigues; Daniel Garcia-Bordallo; Raul Cordoba; Alba Cabirta; Anna Nordlander; Emanuele Ammatuna; Elena Arellano; Dominik Wolf; Romane Prin; Alessandro Limongelli; Martina Bavastro; Gökçe Melis Çolak; Stefanie K. Grafe; Ditte Stampe Hersby; Laman Rahimli; Oliver A. Cornely; Carolina Garcia-Vidal; Livio Pagano.
ssrn; 2023.
Preprint en Inglés | PREPRINT-SSRN | ID: ppzbmed-10.2139.ssrn.4473151
5.
medrxiv; 2022.
Preprint en Inglés | medRxiv | ID: ppzbmed-10.1101.2022.01.21.22269423

RESUMEN

Background: SARS-CoV-2 is spread primarily through droplets and aerosols. Exhaled aerosols are generated in the lung periphery by reopening of collapsed airways. Aerosol measuring may detect highly contagious individuals ("super spreaders or super-emitters") and discriminate between SARS-CoV-2 infected and non-infected individuals. This is the first study comparing exhaled aerosols in SARS-CoV-2 infected individuals and healthy controls. Design: A prospective observational cohort study in 288 adults, comprising 64 patients testing positive by SARS CoV-2 PCR before enrollment, and 224 healthy adults testing negative (matched control sample) at the University Hospital Frankfurt, Germany, from February to June 2021. Study objective was to evaluate the concentration of exhaled aerosols during physiologic breathing in SARS-CoV-2 PCR-positive and -negative subjects. Secondary outcome measures included correlation of aerosol concentration to SARS-CoV-2 PCR results, change in aerosol concentration due to confounders, and correlation between clinical symptoms and aerosol. Results: There was a highly significant difference in respiratory aerosol concentrations between SARS-CoV-2 PCR-positive (median 1490.5/L) and -negative subjects (median 252.0/L; p<0.0001). There were no significant differences due to age, sex, smoking status, or body mass index. ROC analysis showed an AUC of 0.8918. Conclusions: Measurements of respiratory aerosols were significantly elevated in SARS-CoV-2 positive individuals and may become a helpful tool in detecting highly infectious individuals via a noninvasive breath test. Clinical Trial Number: ClinicalTrials.gov Identifier: NCT04739020.


Asunto(s)
Síndrome Respiratorio Agudo Grave
6.
researchsquare; 2020.
Preprint en Inglés | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-127621.v1

RESUMEN

Coronavirus 2 (SARS-CoV-2) infection and the resulting COVID-19 illness vary from asymptomatic disease, mild upper respiratory tract infection, pneumonia1, to a life-threatening multi-organ failure with case fatality rates ranging from 0.27–13.4%2,3. Despite increasing knowledge of the clinical and immunological features underlying COVID-191,4−6, biological variables explaining the course of infection and its severity remain elusive. At the entry site of SARS-CoV2, the oropharyngeal microbiome represents a hub integrating viral and immune signals at the start of the infection7–10. To evaluate the role of the oropharyngeal microbiome in COVID-19, we performed a multi-center, cross-sectional clinical study analyzing the oropharyngeal microbial metagenomes in healthy adults, patients with non-SARS-CoV-2 infections, or with mild, moderate and severe COVID-19 encompassing a total of 345 participants. Significantly reduced microbiome diversity and high dysbiosis were observed in hospitalized patients with severe COVID-19, which was further associated with a loss of microbial genes and metabolic pathways. In this cohort, diversity measures were also associated with need for intensive care treatments as major clinical parameters in COVID-19. We further applied random forest machine learning to unravel microbial features for segregating clinical outcomes in hospitalized cases, and observed oropharyngeal microbiome abundances of Haemophilus or Streptococcus species as most important features. These findings provide insights into the role of the oropharyngeal microbiome in SARS-CoV-2 infection, and may suggest new biomarkers for COVID-19 severity.


Asunto(s)
Síndrome Respiratorio Agudo Grave , Infecciones por Haemophilus , Disbiosis , Infecciones del Sistema Respiratorio , COVID-19
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