Unraveling the effects of low protein-phenol binding affinity on the structural properties of beta-lactoglobulin.

Non-covalent interactions of phenolics with proteins cannot always be readily identified, often leading to contradictory results described in the literature. This results in uncertainties as to what extent phenolics can be added to protein solutions (for example for bioactivity studies) without affecting the protein structure. Here, we clarify which tea phenolics (epigallocatechin gallate (EGCG), epicatechin and gallic acid) interact with the whey protein β-lactoglobulin by combining various state-of-the-art-methods.

Myeloid-Specific Deletion of Diacylglycerol Lipase α Inhibits Atherogenesis in ApoE-Deficient Mice.

Background: The endocannabinoid 2-arachidonoylglycerol (2-AG) is a known modulator of inflammation. Despite its high concentration in vascular tissue, the role of 2-AG in atherogenesis has not yet been examined.

Methods: ApoE-deficient mice were sublethally irradiated and reconstituted with bone marrow from mice with a myeloid-specific knockout of the 2-AG synthesising enzyme diacylglycerol lipase α (Dagla) or control bone marrow with an intact 2-AG biosynthesis.

IL-5 release of CD4+ non-effector lymphocytes is increased in COPD--modulating effects of moxifloxacin and dexamethasone.

T-lymphocytes are crucial in chronic obstructive pulmonary disease (COPD) pathogenesis. Especially T(H)1-lymphocytes are involved in local and systemic inflammation in COPD, yet the role of T(H)2-mediated immune-responses in COPD pathogenesis is poorly understood. The objective of this study was to examine IL-5 expression in T(H)2-lymphocytes in smokers with and without COPD ex vivo compared with non-smokers and to evaluate the effects of bacterial endotoxin (lipopolysaccharide, LPS) as well as two drugs often used for treatment of COPD exacerbation, corticosteroids and moxifloxacin.

The T-helper cell type 1 immune response to gram-negative bacterial infections is impaired in COPD.

Rationale: The increased susceptibility to bacterial infections in chronic obstructive pulmonary disease (COPD) is critical for exacerbations. Toll-like receptor-4 (TLR4) detects bacteria via LPS and induces IFN-γ-based immune responses. The direct responsiveness of Th1 lymphocytes to LPS is disputed because they lack surface expression of the TLR4 coreceptor CD14.

[Ventilator-induced diaphragmatic dysfunction (VIDD)].

Although life-saving, mechanical ventilation is associated with numerous complications. Recently, it was shown in animal models that controlled mechanical ventilation (CMV) can cause the so-called ventilator-induced diaphragmatic dysfunction (VIDD). The decrease in diaphragmatic strength proceeds along with prolonged mechanical ventilation.