Pilot Study: Safety and Performance Validation of an Ingestible Medical Device for Collecting Small Intestinal Liquid in Healthy Volunteers.

The connection between imbalances in the human gut microbiota, known as dysbiosis, and various diseases has been well established. Current techniques for sampling the small intestine are both invasive for patients and costly for healthcare facilities. Most studies on human gut microbiome are conducted using faecal samples, which do not accurately represent the microbiome in the upper intestinal tract.

Comparison of Elecsys and Liaison immunoassays to determine Epstein-Barr virus serological status using further diagnostic approaches to clarify discrepant results.

Serological markers for Epstein-Barr virus (EBV) infection are commonly used to diagnose infectious mononucleosis and establish a serological status in pretransplant patients. This study prospectively assessed 1043 serum specimens sent to the laboratory for physician-ordered EBV testing. The three markers-antiviral capsid antigen (VCA) immunoglobulin M (IgM), anti-VCA immunoglobulin G (IgG), and anti-Epstein-Barr nuclear antigen (EBNA) antibodies-were tested using the Elecsys and the Liaison immunoassays.

Fine Analysis of Lymphocyte Subpopulations in SARS-CoV-2 Infected Patients: Differential Profiling of Patients With Severe Outcome.

COVID-19 is caused by the human pathogen severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in widespread morbidity and mortality. CD4 T cells, CD8 T cells and neutralizing antibodies all contribute to control SARS-CoV-2 infection. However, heterogeneity is a major factor in disease severity and in immune innate and adaptive responses to SARS-CoV-2.

Complement Alternative and Mannose-Binding Lectin Pathway Activation Is Associated With COVID-19 Mortality.

Background: The SARS-CoV-2 infection triggers excessive immune response resulting in increased levels of pro-inflammatory cytokines, endothelial injury, and intravascular coagulopathy. The complement system (CS) activation participates to this hyperinflammatory response. However, it is still unclear which activation pathways (classical, alternative, or lectin pathway) pilots the effector mechanisms that contribute to critical illness.