The present invention relates to a method for diagnosing esthetic degradations of skin, in particular linked to pollution, in a subject, comprising a step (a) of determining, in a skin sample of the subject, the level of at least one marker chosen from the group constituted of (i) bacteria of the species Propionibacterim acnes, bacteria of the family Micrococcaceae, bacteria of the genus Brachybacterium, bacteria of the genus Brevibacterium, bacteria of the order Burkholderiales, bacteria of the genus Parococcus, bacteria of the family Rhodobacteraceae and bacteria of the genus Fusobacterium, and (ii) metabolites of these bacteria chosen from 3-hydroxy-3-methylglutarate, 3-methylglutarate/2-methylglutarate, 4-guanidinobutanoate, 4-imidazoleacetate, 5-oxoproline, aconitrate, adipate, alanine, alpha-cetoglutarate, arabonate/xylonate, azelate, beta-citrylglutamate, choline, cis-urocanate, citraconate/glutaconate, fructose, fumarate, gamma-glutamylalanine, gamma-glutamylglutamine, gamma-glutamylglycine, gamma-glutamylisoleucine, gamma-glutamylleucine, gamma-glutamylsérine, gamma-glutamylthréonine, gamma-glutamyltryptophane, gamma-glutamylvaline, glutarate, glycerate, glycerol-3-phosphate, glycine, isovalerylglycine, kynurenate, lactate, linoleoyl ethanolamide, malate, maleate, malonate, maltose, methionine sulfoxide, methylsuccinate, N-acetylalanine, N-acetylarginine, N-acetylaspartate, N-acetylglycine, N-acetylhistidine, N-acetylphenylalanine, N-acetylthréonine, N-acetylvaline, oleamide, ornithine, palmitamide, pimelate, proline, salicylate, sebacate, serine, suberate, succinate, undecanedioate and S-amino-omega caprolactam.

The present invention relates to a method of identifying a subgroup of patients suffering from diffuse cutaneous systemic sclerosis (dcSSc) which subgroup of patients benefits from a treatment with at least one sGC stimulator and/or sGC activator in a higher degree than patients not belonging to this subgroup.

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.

The present invention provides a method for determining a sensitivity to ultraviolet light non-invasively and immediately. A method for determining a UV sensitivity is provided involving: a step of irradiating the skin of a test subject with ultraviolet light to determine the UV sensitivity using the amount of biophotons to be detected within a specific period after the irradiation, wherein 50% or more of the specific period overlaps a period from 1 to 3 minutes after the irradiation.

The present invention relates to a method of diagnosis or prognosis of a non-healing or chronic wound comprising the step of determining the ratio of carnitine to ceramide and/or ceramide derivative in a sample, or the level of at least one metabolite in a sample.

The present invention relates to a pharmaceutical composition for preventing or treating hypertrophic scars. The present inventors have found that the inhibition of expression of TXNDC5, PRRC1, S100A11, Galectin 1, Filamin A, eIF-5A, Annexin A2, and FABP5 can be a new target for improving and treating hypertrophic scars. In the present invention, TXNDC5-, PRRC1-, S100A11-, Galectin 1-, Filamin A-, eIF-5A-, Annexin A2-, and FABP5-specific siRNAs were constructed to determine the probability of treating the hypertrophic scars. As a result, the knockdown of the protein or a gene encoding the protein induces apoptosis in the hypertrophic scars and reduces collagen expression, which can be very useful in treating wounds.

A method can be used for detecting, in a sample, an autoantibody binding to a polypeptide having the sequence SEQ ID NO: 1, SEQ ID NO: 11 or SEQ ID NO: 24. A carrier containing said polypeptide and an autoantibody binding to said polypeptide are useful. The autoantibody may be used for the diagnosis of a disease, and a method can be used for isolating an autoantibody binding to said polypeptide. The polypeptide and a kit containing said polypeptide are useful, and can be used for the manufacture of a kit or medical device. A method involves contacting a medical or diagnostic device containing said polypeptide with a buffered solution containing an antibody binding specifically to said polypeptide. A sample containing said autoantibody as a positive control and a diluted sample containing said autoantibody are useful.

Biomarkers for diagnosing the disease activity, disease severity or disease type of severe cutaneous adverse drug reactions (SCARs) such as drug-induced hypersensitivity syndrome and Stevens-Johnson syndrome/toxic epidermal necrolysis are provided. Also provided is a method of testing SCARs, comprising measuring the expression of at least one protein selected from the group consisting of stratifin, TNF receptor superfamily member 8 (CD30/TNFRSF8), interleukin-1 receptor antagonist (IL-1Ra), and TNF receptor superfamily member 6B (DcR3/TNFRSF6B) in a sample derived from a subject.

A method of selecting skin treatment regimens, ingredients and compositions that includes measuring the levels of particular small molecule metabolites on skin both before and after product application and testing for a change in small molecule metabolite levels is disclosed.

The current disclosure provides antibodies that bind to peptides associated with the primary immunodeficiency disorders (PIDD) Wiskott-Aldrich Syndrome (WAS) and X-linked agammaglobulinemia (XLA). The antibodies can be used in peptide immunoaffinity enrichment coupled to selected reaction monitoring mass spectrometry (immuno-SRM) assays for clinical diagnosis and newborn screening of WAS and XLA, among other uses.