Effects of very early hyperoxemia on neurologic outcome after out-of-hospital cardiac arrest: A secondary analysis of the TTM-2 trial.

Purpose: Hyperoxemia is common in patients resuscitated after out-of-hospital cardiac arrest (OHCA) admitted to the intensive care unit (ICU) and may increase the risk of mortality. However, the effect of hyperoxemia on functional outcome, specifically related to the timing of exposure to hyperoxemia, remains unclear.

Methods: The secondary analysis of the Target Temperature Management 2 (TTM-2) randomized trial.

Plasma phosphorylated tau (p-tau231) and total tau (t-tau) as prognostic markers of neurological outcome after cardiac arrest - a multicentre study.

Purpose: We studied the promising Alzheimer biomarker plasma tau phosphorylated at threonine 231 (p-tau231) in a cohort of cardiac arrest patients who survived to intensive care to predict long-term neurological outcomes. We also compared it to total tau (t-tau), which has demonstrated predictive abilities of neurological outcome post-cardiac arrest.

Methods: This observational multicentre cohort study included 425 patients admitted to intensive care after cardiac arrest.

DMI fungicide resistance in Zymoseptoria tritici is unlinked to geographical origin and genetic background: a case study in Europe.

Background: The hemibiotrophic fungus Zymoseptoria tritici causing Septoria tritici blotch (STB), is a devastating foliar pathogen of wheat worldwide. A common group of fungicides used to control STB are the demethylation inhibitors (DMIs). DMI fungicides restrict fungal growth by inhibiting the sterol 14-α-demethylase, a protein encoded by CYP51 gene and essential for maintaining fungal cell permeability.

B cell receptor dependent enhancement of dengue virus infection.

Dengue virus (DENV) is the causative agent of dengue, a mosquito-borne disease that represents a significant and growing public health burden around the world. A unique pathophysiological feature of dengue is immune-mediated enhancement, wherein preexisting immunity elicited by a primary infection can enhance the severity of a subsequent infection by a heterologous DENV serotype. A leading mechanistic explanation for this phenomenon is antibody dependent enhancement (ADE), where sub-neutralizing concentrations of DENV-specific IgG antibodies facilitate entry of DENV into FcγR expressing cells such as monocytes, macrophages, and dendritic cells.