Biology subjects

White, J. D.

Publications and source records attributed to White, J. D..

3 recordsLinked to original sources

bioRxiv2018

Facial masculinity does not appear to be a condition-dependent male ornament in humans and does not reflect MHC heterozygosity

Facial masculinity is thought to be a condition-dependent male ornament, reflecting immunocompetence in humans. To test this hypothesis, we calculated an objective measure of facial masculinity/femininity using three-dimensional images in a large sample (N = 1,233) of people of European ancestry. We show that facial masculinity is positively correlated with adult height in both males and females. This suggests that variation in growth contributes, at least in part, to variation in facial masculinity, which is characteristic of condition-dependent traits. However, facial masculinity scales with growth similarly in males and females, suggesting that facial masculinity is not specifically a male ornament. Additionally, we measured immunocompetence via heterozygosity at the major histocompatibility complex (MHC), a well known genetic marker of immunity. We show that while height is positively correlated with MHC heterozygosity, facial masculinity is not. Thus, facial masculinity does not reflect immunocompetence measured by MHC heterozygosity in humans as thought previously. Overall, we find no support for the idea that facial masculinity is a condition-dependent male ornament that has evolved to indicate immunocompetence.

evolutionary biology↗

bioRxiv2018

Low dose resveratrol promotes hypertrophy in wildtype skeletal muscle and reduces damage in skeletal muscle of exercised mdx mice.

Duchenne muscular dystrophy (DMD) is a progressive and fatal neuromuscular disorder for which there is no treatment. Therapies to restore dystrophin deficiency are not ready for clinical use and long-term efficiency is yet to be established. Therefore, there is a need to develop alternative strategies to treat DMD. Resveratrol is a nutraceutical with anti-inflammatory properties and previous studies have shown that high doses can benefit mdx mice. We treated 4-week-old mdx and wildtype mice with low-dose resveratrol (5mg/kg bodyweight/day) for 15 weeks. A voluntary exercise protocol was added to test if low dose resveratrol could reduce exercise-induced damage. We showed that resveratrol promoted skeletal muscle hypertrophy in the wildtype mice. There was no change in markers of pathology in the mdx mice; however, the low-dose resveratrol reduced exercised induced damage. Gene expression of immune cell markers such as CD86, CD163 and PCNA was reduced; however signalling targets associated with resveratrols mechanism of action of action including SIRT1 and NF-{kappa}B were unchanged. In conclusion, low-dose resveratrol was not effective in reducing disease pathology; however, its ability to promote hypertrophy in wildtype skeletal muscle could have direct applications to the livestock industry or in sports medicine.

physiology↗

bioRxiv2018

Benfotiamine reduces pathology and improves muscle function in mdx mice.

Duchenne Muscular Dystrophy (DMD) is a progressive and fatal neuromuscular disease which arises from mutations in the dystrophin gene (DMD) that result in the absence or severe reduction of the cytoskeletal protein dystrophin. In addition to the primary dystrophin defect, secondary processes such as inflammation, calcium influx, dysregulated autophagy and fibrosis exacerbate dystrophic pathology and thus increase disease progression. While therapies to restore dystrophin deficiency are being developed, strategies which target these secondary processes could be of benefit to patients. Benfotiamine is a lipid soluble precursor to thiamine that can reduce secondary processes such as inflammation and oxidative stress in diabetic patients. As such we tested it in the mdx mouse model of DMD and found that benfotiamine reduced multiple markers of dystrophic pathology and improved grip strength. In addition, members of the utrophin and dystrophin glycoprotein complexes were significantly increased at the sarcolemma which could improve cell adhesion. We also demonstrated that benfotiamine treatment lowered the expression of macrophage markers and pro-inflammatory cytokines suggesting that benfotiamine is reducing dystrophic pathology by acting on inflammatory processes.

physiology↗