Targeted rescue of synaptic plasticity improves cognitive decline in sepsis-associated encephalopathy.

Sepsis-associated encephalopathy (SAE) is a frequent complication of severe systemic infection resulting in delirium, premature death, and long-term cognitive impairment. We closely mimicked SAE in a murine peritoneal contamination and infection (PCI) model. We found long-lasting synaptic pathology in the hippocampus including defective long-term synaptic plasticity, reduction of mature neuronal dendritic spines, and severely affected excitatory neurotransmission.

Mechanisms controlling membrane recruitment and activation of the autoinhibited SHIP1 inositol 5-phosphatase.

Signal transduction downstream of growth factor and immune receptor activation relies on the production of phosphatidylinositol-(3,4,5)-trisphosphate (PI(3,4,5)P) lipids by PI3K. Regulating the strength and duration of PI3K signaling in immune cells, Src homology 2 domain-containing inositol 5-phosphatase 1 (SHIP1) controls the dephosphorylation of PI(3,4,5)P to generate phosphatidylinositol-(3,4)-bisphosphate. Although SHIP1 has been shown to regulate neutrophil chemotaxis, B-cell signaling, and cortical oscillations in mast cells, the role that lipid and protein interactions serve in controlling SHIP1 membrane recruitment and activity remains unclear.

Improving an existing proxy-based approach for floodplain denitrification assessment to facilitate decision making on restoration.

Excess nitrogen (N) from agricultural sources is a major contributor to the water pollution of rivers in Europe. Floodplains are of tremendous importance as they can permanently remove nitrate (NO) from the environment by releasing reactive N to the atmosphere in its gaseous forms (NO, N) during denitrification. However, the quantitative assessment of this ecosystem function is still challenging, particularly on the national level.

Mechanisms controlling membrane recruitment and activation of autoinhibited SHIP1.

Signal transduction downstream of growth factor and immune receptor activation relies on the production of phosphatidylinositol-(3,4,5)-trisphosphate (PI(3,4,5)P ) lipids by phosphoinositide-3-kinase (PI3K). Regulating the strength and duration of PI3K signaling in immune cells, Src homology 2 domain-containing inositol 5-phosphatase 1 (SHIP1) controls the dephosphorylation of PI(3,4,5)P to generate PI(3,4)P . Although SHIP1 has been shown to regulate neutrophil chemotaxis, B-cell signaling, and cortical oscillations in mast cells, the role that lipid and protein interactions serve in controlling SHIP1 membrane recruitment and activity remains unclear.

3D-printing of the polymer/insect-repellent system poly(l-lactic acid)/ethyl butylacetylaminopropionate (PLLA/IR3535).

The polymer/solvent system poly(l-lactic acid)/ethyl butylacetylaminopropionate (PLLA/IR3535) is regarded as an insect-repellent-delivery system, serving, e.g., for fighting mosquito-borne tropical diseases.