Proper micro-environment alleviates mortality in laboratory mouse breeding induced by litter overlap and older dams.

The ongoing worldwide effort to reduce animal numbers in research often omits the issue of pre-weaning mortality in mouse breeding. A conservative estimate of 20% mortality would mean approximately 1.1 M mice die annually in the EU before scientific use.

Optimized Depilation Method and Comparative Analysis of Hair Growth Cycle in Mouse Strains.

In mice, hair growth follows a mosaic or wavy patterning. Therefore, synchronization of the hair growth cycle is required to adequately evaluate any trichogenic interventions pre-clinically. Depilation is the established method for synchronizing the growth phase of mouse hair follicles.

Metabolism and bioenergetics in the pathophysiology of organ fibrosis.

Fibrosis is the tissue scarring characterized by excess deposition of extracellular matrix (ECM) proteins, mainly collagens. A fibrotic response can take place in any tissue of the body and is the result of an imbalanced reaction to inflammation and wound healing. Metabolism has emerged as a major driver of fibrotic diseases.

Application of the FTIR technique as a non-invasive tool to discriminate Portuguese olive oils with Protected Designation of Origin.

Three Portuguese olive oils with PDO ('Azeite do Alentejo Interior', 'Azeites da Beira Interior' and 'Azeite de Trás-os-Montes') were studied considering their physicochemical quality, antioxidant capacity, oxidative stability, total phenols content, gustatory sensory sensations and Fourier transform infrared (FTIR) spectra. All oils fulfilled the legal thresholds of EVOOs and the PDO's specifications. Olive oils from 'Azeite da Beira Interior' and 'Azeite de Trás-os-Montes' showed greater total phenols contents and antioxidant capacities, while 'Azeites da Beira Interior' presented higher oxidative stabilities.

Ataxia with giant axonopathy in Acbd5-deficient mice halted by adeno-associated virus gene therapy.

Acyl-CoA binding domain containing 5 (ACBD5) is a critical player in handling very long chain fatty acids (VLCFA) en route for peroxisomal β-oxidation. Mutations in ACBD5 lead to the accumulation of VLCFA and patients present retinal dystrophy, ataxia, psychomotor delay and a severe leukodystrophy. Using CRISPR/Cas9, we generated and characterized an Acbd5 Gly357* mutant allele.