The expansion of multiple drug resistant (MDR) strains of presents an immense threat for public health. Annually, this microorganism causes thousands of lethal nosocomial infections worldwide. Currently, it has been shown that certain strains of lactic acid bacteria (LAB) can efficiently inhibit growth of and the formation of its biofilms; however, the active principle of such action remains unknown. In the current article, the growth inhibition of MDR by two LAB- LR1 and F-is demonstrated, and the nature of this inhibition studied at the level of exoproteome. This article shows that the exoproteomes of studied LAB contains both classically and non-classically secreted proteins. While for LR1 the substantial portion of classically secreted proteins was presented by cell-wall-degrading enzymes, for F only one out of four classically secreted proteins was presented by cell-wall hydrolase. Non-classically secreted proteins of both LAB were primarily metabolic enzymes, for some of which a possible moonlighting functioning was proposed. These results contribute to knowledge regarding antagonistic interaction between LAB and pathogenic and opportunistic microorganisms and set new perspectives for the use of LAB to control the spread of these microorganisms.
Research towards regenerative dentistry focused on developing scaffold materials whose high performance induces cell adhesion support and guides tissue growth. An early study investigated the proliferation abilities and attachment of human periodontal ligament fibroblasts (HPLFs) on two bovine pericardium membranes with different thicknesses, 0.2 mm and 0.
Background: Duchenne muscular dystrophy (DMD) is a devastating disease characterized by progressive muscle wasting that leads to diminished lifespan. In addition to the inherent weakness of dystrophin-deficient muscle, the dysfunction of resident muscle stem cells (MuSC) significantly contributes to disease progression.
Methods: Using the mdx mouse model of DMD, we performed an in-depth characterization of disease progression and MuSC function in dystrophin-deficient skeletal muscle using immunohistology, isometric force measurements, transcriptomic analysis and transplantation assays.
Aims: This study aimed to explore the role and underlying mechanisms of brain-derived exosomes in traumatic brain injury-induced acute lung injury (TBI-induced ALI), with a particular focus on the potential regulation of ferroptosis through miRNAs and Scd1.
Methods: To elucidate TBI-induced ALI, we used a TBI mouse model. Exosomes were isolated from the brains of these mice and characterized using TEM and NTA.
Background: Inclusion body myositis (IBM) is the most prevalent muscle disease in adults for which no current treatment exists. The pathogenesis of IBM remains poorly defined. In this study, we aimed to explore the interplay between inflammation and mitochondrial dysfunction in IBM.
Objectives: To explore the effect and the probable mechanisms of JLD in the treatment of type 2 diabetes mellitus (T2DM) - associated cognitive impairment (TDACI).
Methods: The effect of JLD in combating TDACI was assessed in T2DM model mice by conducting Morris water maze (MWM) behaviour testing. Active components and their putative targets, as well as TDACI-related targets, were collected from public databases.
