Increasing diagnostic possibilities using the geneLEAD VIII platform for detection of SARS-CoV-2

At the time SARS-CoV-2 was identified as the cause of coronavirus disease 2019 (COVID-19) no in vitro diagnostic (IVD) tests were available since it was a new virus. Very shortly after the release of the genomic sequence of SARS-CoV-2, laboratory-developed tests (LDTs) were developed, made available and implemented in several laboratories in the Netherlands and globally. In this study, the performance of an E-gene Sarbeco specific realtime reverse-transcriptase PCR (RT-PCR) was verified on the open modus of the geneLEAD VIII sample-to-answer platform. The results obtained from 134 clinical samples, of which 63 had been tested positive, showed almost complete concordance compared to the same PCR on the routine diagnostic systems and that was validated according to the national reference standard. The only discordant sample tested positive using the routine diagnostic workflow with a cycle threshold (CT) value of 37.7, while the sample tested negative using the geneLEAD VIII workflow. In addition, good performance was achieved in analyzing a blinded SARS-CoV-2 external quality assurance (EQA) panel. Implementation of the geneLEAD VIII platform as routine diagnostic tool resulted in testing 871 clinical samples with 115 positive results. In conclusion, the geneLEAD VIII SARSCoV-2 workflow presented in this study showed excellent diagnostic performance and with a rapid turnaround time of approximately two hours it proved a valuable option for STAT SARS-CoV-2 testing in the absence of (rapid, CE-IVD) point-of-care testing platforms.Molecular basis of virus replication, viral pathogenesis and antiviral strategie

Endothelial dysfunction and low-grade inflammation are associated with greater arterial stiffness over a 6-year period

Endothelial dysfunction and low-grade inflammation are associated with cardiovascular disease. Arterial stiffening plays an important role in cardiovascular disease and, thus, may be a mechanism through which endothelial dysfunction and/or low-grade inflammation lead to cardiovascular disease. We investigated the associations between, on the one hand, biomarkers of endothelial dysfunction (soluble endothelial selectin, thrombomodulin, and both vascular and intercellular adhesion molecules 1 and von Willebrand factor) and of low-grade inflammation (C-reactive protein, serum amyloid A, interleukin 6, interleukin 8, tumor necrosis factor-α and, soluble intercellular adhesion molecule 1) and, on the other hand, arterial stiffness over a 6-year period, in 293 healthy adults (155 women). Biomarkers were combined into mean z scores. Carotid, femoral, and brachial arterial stiffness and carotid-femoral pulse wave velocity were determined by ultrasonography. Measurements were obtained when individuals were 36 and 42 years of age. Associations were analyzed with generalized estimating equation and adjusted for sex, height, and mean arterial pressure. The endothelial dysfunction z score was inversely associated with femoral distensibility (β:-0.51 [95% CI:-0.95 to-0.06]) and compliance coefficients (β:-0.041 [95% CI:-0.076 to-0.006]) but not with carotid or brachial stiffness or carotid-femoral pulse wave velocity. The low-grade inflammation z score was inversely associated with femoral distensibility (β:-0.51 [95% CI:-0.95 to-0.07]) and compliance coefficients (β:-0.050 [95% CI:-0.084 to-0.016]) and with carotid distensibility coefficient (β:-0.910 [95% CI:-1.810 to-0.008]) but not with brachial stiffness or carotid-femoral pulse wave velocity. Biomarkers of endothelial dysfunction and low-grade inflammation are associated with greater arterial stiffness. This provides evidence that arterial stiffening may be a mechanism through which endothelial dysfunction and low-grade inflammation lead to cardiovascular disease

Corrigendum: UP'S: A Cohort Study on Recovery in Psychotic Disorder Patients: Design Protocol (Front. Psychiatry, (2021), 11, (609530), 10.3389/fpsyt.2020.609530)

© 2021 van Aken, Bakia, Wierdsma, Voskes, Van Weeghel, van Bussel, Hagestein, Ruissen, Leendertse, Sewbalak, van der Draai, Hammink, Mandos, van der Gaag, Bonebakker, Van Der Feltz-Cornelis and MulderIn the original article, reference (100) was incorrectly written as “de Sonneville L. Amsterdamse neuropsychologische taken: wetenschappelijke en klinische toepassingen. Tijdschr voor Neuropsychol. (2005) 10:27–41”. It should be “Corcoran R, Mercer G, Frith CD. Schizophrenia, symptomatology and social inference: investigating “theory of mind” in people with schizophrenia. Schizophr Res. (1995) 17:5–13.” The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated