The present disclosure provides a biosignature that distinguishes Lyme disease, including early Lyme disease, from STARI. The present disclosure also provides methods for detecting Lyme disease and STARI, as well as methods for treating subjects diagnosed with Lyme disease or STARI.

The present invention relates inter alia to therapeutic agents for use in the treatment of melanoma, methods of diagnosing an increased risk of metastasis in a subject suffering from melanoma, methods of treating such subjects, diagnostic assays and kits. More particularly, in certain embodiments the invention relates to identifying whether a subject suffering from melanoma has an increased risk of metastasis by determining the expression of Ambra-1 and Loricrin in a tissue sample obtained from the subject.

A polypeptide contains laminin beta-4 and a carrier contains the polypeptide. An antibody, preferably autoantibody, is against laminin beta-4. Furthermore, use of the polypeptide, carrier or autoantibody for the diagnosis of a disease, and a method with the step of detecting an autoantibody against laminin beta-4 in a sample are described.

The present invention relates to methods of preventing or treating skin necroptosis diseases, including administering to subjects receptor-interacting protein kinase-3 (RIP3)-mixed lineage kinase domain-like protein (MLKL) pathway blockers or dabrafenib, and method of diagnosing of skin necroptosis diseases, including detecting phosphorylated MLKL. The RIP3-MLKL pathway blockers according to the present invention directly suppress RIP3 overexpressing in skin necroptosis diseases, or inhibit phosphorylation and translocation to plasma membranes of MLKL, subsequently induced therefrom, thereby effectively preventing skin cell death via necroptosis. Thus, the present invention can prevent or treat a variety of skin diseases caused by necroptosis.

A method can be used for analyzing digital images of skin lesions. The images include pixels distributed over a lesion area. Sets of values including a first discrimination value indicative of a weighted average of the image pixels with weighing at the border of the lesion, a second discrimination value indicative of skewness and kurtosis of the distribution of the image pixels, a third discrimination value indicative of the ratio of symmetry and gray-level power of the distribution of the image pixels and calculated. A total additive score of the values in the sets of values is provided and compared with a total score threshold. The first, second and third discrimination values are compared with respective first, second and third discrimination threshold values. An output classification for the image analyzed is provided as a function of the results of the comparing.

The present invention relates to a method for diagnosing a degradation of esthetic qualities of the skin, based on a measurement of the level of expression of the gene encoding FLG2. The present invention also relates to a method for the cosmetic treatment of skin. The present invention also relates to a method for identifying a compound for reducing and/or slowing the degradation of esthetic quality of the skin, and a kit.

A method evaluating a skin cleansing composition for an ability to treat a skin condition, can include a) identifying a target skin condition or lack of target skin condition on a skin sample; b) taking a baseline measurement of a Microbial index of Skin Health via a Microbial index of Skin Health Method; c) performing a wash protocol with the cleansing composition via the Wash Protocol Method; and d) taking a second measurement of the Microbial Skin Health Measurement after the Wash Protocol; wherein an increase from the baseline Microbial Skin Health Index of 5 or more signifies the cleansing product is efficacious for treatment of the identified skin condition.

Disclosed herein are methods of treating or preventing an autoimmune skin disorder and/or inflammatory skin disorder, skin tumor and obesity in a subject in need thereof by administering an inhibitor capable of inhibiting the activation of inflammasome NLRP1, NLRP1 mutants, an agent that prevents the secretion of stress responsive secreted factors, known pro-inflammatory cytokines, keratinocytes differentiation markers, inflammasome-dependent cytokines, and growth factors in the skin and an agent that reduces the effect of inflammasome-dependent cytokines. The invention encompasses the use of an activator of NLRP1, such as talabostat, specifically for treating skin tumors. Also enclosed herein are methods of determining the likelihood of a subject in developing an autoimmune skin disorder and/or inflammatory skin disorder comprising detecting NLRP1 mutation in a sample obtained from the subject. An inflammasome sensor NLRP1 mutant and compositions for treatment are also disclosed.

The present invention relates to an in vitro method for identifying a skin wound in an individual as being a non-healing skin wound or healing skin wound, in vitro methods for monitoring the healing of a skin wound in an individual, methods for screening for compounds suitable for modulating skin wound healing, as well as kits related thereto.

Agents which contain at least one D-amino acid selected from the group consisting of D-arginine, D-histidine, D-leucine, D-tyrosine, D-valine, D-allo-threonine, D-lysine, D-tryptophan, D-allo-isoleucine, D-asparagine, D-phenylalanine, and D-glutamine as an active ingredient are effective for improving the function of the horny layer.