Geotechnical controls on erodibility in fluvial impact erosion

Bedrock incision by rivers is commonly driven by the impacts of moving bedload particles. The speed of incision is modulated by rock properties, which is quantified within a parameter known as erodibility that scales the erosion rate to the erosive action of the flow. Although basic models for the geotechnical controls on rock erodibility have been suggested, large scatter and trends in the remaining relationships indicate that they are incompletely understood. Here, we conducted dedicated laboratory experiments measuring erodibility using erosion mills. In parallel, we measured uniaxial compressive strength, tensile strength, Young's modulus, bulk density, and the Poisson's ratio for the tested lithologies. We find that under the same flow conditions, erosion rates of samples from the same lithology can vary by a factor of up to 60. This indicates that rock properties that may vary over short distances within the same rock can exert a strong control on its erosional properties. The geotechnical properties of the tested lithologies are strongly cross-correlated, preventing a purely empirical determination of their controls on erodibility. The currently prevailing model predicts that erosion rates should scale linearly with Young's modulus and inversely with the square of the tensile strength. We extend this model using first-principle physical arguments, taking into account the geotechnical properties of the impactor. The extended model provides a better description of the data than the existing model. Yet, the fit is far from satisfactory. We suggest that the ratio of mineral grain size to the impactor diameter presents a strong control on erodibility that has not been quantified so far. We also discuss how our laboratory results upscale to real landscapes and long timescales. For both a revised stream power incision model and a sediment-flux-dependent incision model, we suggest that long-term erosion rates scale linearly with erodibility and that, within this theoretical framework, relative laboratory measurements of erodibility can be applied at the landscape scale.</p

Disease Severity, Fever, Age, and Sex Correlate With SARS-CoV-2 Neutralizing Antibody Responses

Clinical trials on the use of COVID-19 convalescent plasma remain inconclusive. While data on safety is increasingly available, evidence for efficacy is still sparse. Subgroup analyses hint to a dose-response relationship between convalescent plasma neutralizing antibody levels and mortality. In particular, patients with primary and secondary antibody deficiency might benefit from this approach. However, testing of neutralizing antibodies is limited to specialized biosafety level 3 laboratories and is a time- and labor-intense procedure. In this single center study of 206 COVID-19 convalescent patients, clinical data, results of commercially available ELISA testing of SARS-CoV-2 spike-IgG and -IgA, and levels of neutralizing antibodies, determined by plaque reduction neutralization testing (PRNT), were analyzed. At a medium time point of 58 days after symptom onset, only 12.6% of potential plasma donors showed high levels of neutralizing antibodies (PRNT50 >= 1:320). Multivariable proportional odds logistic regression analysis revealed need for hospitalization due to COVID-19 (odds ratio 6.87; p-value 0.0004) and fever (odds ratio 3.00; p-value 0.0001) as leading factors affecting levels of SARS-CoV-2 neutralizing antibody titers in convalescent plasma donors. Using penalized estimation, a predictive proportional odds logistic regression model including the most important variables hospitalization, fever, age, sex, and anosmia or dysgeusia was developed. The predictive discrimination for PRNT50 >= 1:320 was reasonably good with AUC: 0.86 (with 95% CI: 0.79-0.92). Combining clinical and ELISA-based pre-screening, assessment of neutralizing antibodies could be spared in 75% of potential donors with a maximal loss of 10% of true positives (PRNT50 >= 1:320)

SARS-CoV-2 T Cell Response in Severe and Fatal COVID-19 in Primary Antibody Deficiency Patients Without Specific Humoral Immunity

Morbidity and mortality of COVID-19 is increased in patients with inborn errors of immunity (IEI). Age and comorbidities and also impaired type I interferon immunity were identified as relevant risk factors. In patients with primary antibody deficiency (PAD) and lack of specific humoral immune response to SARS-CoV-2, clinical disease outcome is very heterogeneous. Despite extensive clinical reports, underlying immunological mechanisms are poorly characterized and levels of T cellular and innate immunity in severe cases remain to be determined. In the present study, we report clinical and immunological findings of 5 PAD patients with severe and fatal COVID-19 and undetectable specific humoral immune response to SARS-CoV-2. Reactive T cells to SARS-CoV-2 spike (S) and nucleocapsid (NCAP) peptide pools were analyzed comparatively by flow cytometry in PAD patients, convalescents and naive healthy individuals. All examined PAD patients developed a robust T cell response. The presence of polyfunctional cytokine producing activated CD4(+) T cells indicates a memory-like phenotype. An analysis of innate immune response revealed elevated CD169 (SIGLEC1) expression on monocytes, a surrogate marker for type I interferon response, and presence of type I interferon autoantibodies was excluded. SARS-CoV-2 RNA was detectable in peripheral blood in three severe COVID-19 patients with PAD. Viral clearance in blood was observed after treatment with COVID-19 convalescent plasma/monoclonal antibody administration. However, prolonged mucosal viral shedding was observed in all patients (median 67 days) with maximum duration of 127 days. PAD patients without specific humoral SARS-CoV-2 immunity may suffer from severe or fatal COVID-19 despite robust T cell and normal innate immune response. Intensified monitoring for long persistence of SARS-CoV-2 viral shedding and (prophylactic) convalescent plasma/specific IgG as beneficial treatment option in severe cases with RNAemia should be considered in seronegative PAD patients