Human physical characteristics and their perception by the brain are under pressure by natural selection to optimize reproductive success. Men and women have different strategies to appear attractive and have different interests in identifying beauty in people. Nevertheless, men and women from all cultures agree on who is and who is not attractive, and throughout the world attractive people show greater acquisition of resources and greater reproductive success than others. The brain employs at least three modules, composed of interconnected brain regions, to judge facial attractiveness: one for identification, one for interpretation and one for valuing. Key elements that go into the judgment are age and health, as well as symmetry, averageness, face and body proportions, facial color and texture. These elements are all Costly Signals of reproductive fitness because they are difficult to fake. However, people deceive others using tricks such as coloring hair, cosmetics and clothing styles, while at the same time they also focus on detecting fakes. People may also deceive themselves, especially about their own attractiveness, and use self-signally actions to demonstrate to themselves their own true value. The neuroscience of beauty is best understood by considering the evolutionary pressures to maximize reproductive fitness.

Concerns over existing sunscreen filters have reinforced the need to examine supplemental sun protection or repair of sun damage. Technology to enhance DNA repair has been available in skincare and sunscreen products for several decades, but skepticism and lack of familiarity with the supporting data remain prevalent. Here, we address six of the main questions raised by medical professionals regarding the efficacy of DNA repair enzymes in sun protection. These include the mode of delivery and mechanism of action, the effect on cellular responses and the amelioration of pre-cancers, cancers and photoaging. The conclusions are that topical DNA repair enzymes do enhance removal of DNA damage and reduce the appearance of new actinic keratoses as well as increase regression of existing lesions. Support for prevention of photoaging and skin cancer is significant but could be strengthened or disproven with additional research.

Palmitoylation is a lipid modification involving the attachment of palmitic acid to a cysteine residue, thereby affecting protein function. We investigated the effect of palmitoylation of tyrosinase, the rate-limiting enzyme in melanin synthesis, using a human three-dimensional skin model system and melanocyte culture. The palmitoylation inhibitor, 2-bromopalmitate, increased melanin content and tyrosinase protein levels in melanogenic cells by suppressing tyrosinase degradation. The palmitoylation site was Cysteine⁵⁰⁰ in the C-terminal cytoplasmic tail of tyrosinase. The nonpalmitoylatable mutant, tyrosinase (C500A), was slowly degraded and less ubiquitinated than wild-type tyrosinase. Screening for the Asp-His-His-Cys (DHHC) family of proteins for tyrosinase palmitoylation suggested that DHHC2, 3, 7, and 15 are involved in tyrosinase palmitoylation. Knockdown of DHHC2, 3, or 15 increased tyrosinase protein levels and melanin content. Determination of their subcellular localization in primary melanocytes revealed that DHHC2, 3, and 15 were localized in the endoplasmic reticulum, Golgi apparatus, and/or melanosomes, whereas only DHHC2 was localized in the melanosomes. Immunoprecipitation showed that DHHC2 and DHHC3 predominantly bind to mature and immature tyrosinase, respectively. Taken together, tyrosinase palmitoylation at Cysteine⁵⁰⁰ by DHHC2, 3, and/or 15, especially DHHC2 in trans-Golgi apparatus and melanosomes and DHHC3 in the endoplasmic reticulum and cis-Golgi apparatus, regulate melanogenesis by modulating tyrosinase protein levels.