The invention in relates in part to a method for rejuvenating hair follicles, the method comprising the steps of: (1) obtaining androgen non-inhibited cells from hair follicle tissue; (2) culturing the androgen non-inhibited cells to produce an expanded population of androgen-non-inhibited cells; and (3) implanting the expanded population of androgen non-inhibited cells proximal to miniaturised and/or miniaturising hair follicles.

A method for manufacturing a skin chip according to an exemplary embodiment of the present disclosure may include: a step of forming first and second PDMS layers disposed on both surfaces of a porous membrane and each having a microfluidic channel through which a culture medium is transferred to both surfaces of the porous membrane; a step of forming first and second MEA substrate layers disposed on the outer surfaces of the first and second PDMS layers, respectively, and having metal electrodes for measurement of TEER arranged at positions corresponding to the channels; and a step of forming first and second PMMA layers disposed on the outer surfaces of the first and second MEA substrate layers, respectively. In the method for manufacturing a skin chip according to in an exemplary embodiment of the present disclosure, the porous membrane may be made of a polycarbonate having pores of a predetermined size.

Compositions and methods for stimulating proliferation and/or migration of melanocytes in order to re-pigment skin regions, using ROCK inhibitors and optionally SIK inhibitors.

The present invention relates to the treatment of sensory neuropathy induced by a marine neurotoxic poisoning. The invention further encompasses an in vitro method for producing a neuro-cutaneous model allowing to study the cellular and/or molecular mechanisms involved in said neuropathy, a neuro-cutaneous model obtainable according to said method, and applications thereof.

Methods of screening rinse-off personal care compositions can include the use of explant skin in combination with measurements for moisture and/or cell proliferation.

The present disclosure provides, in various aspects, a method of forming a prefabricated innervated pre-vascularized pre-laminated (PIPP) flap having a stoma or lumen. The method includes providing a cell construct including skin cells and/or mucosa cells. The method further includes forming an integrated in vivo composite at a donor site by grafting the cell construct onto a muscle. The method further includes stabilizing the composite on an obturator component. The method further includes developing a microvascular system in the composite by retaining it in vivo at the donor site for a predetermined period of time. The method further includes removing the obturator component from the stoma or lumen. In certain aspects, the present disclosure also provides a method of restoring a defect including damaged or surgically removed soft tissue using a PIPP flap. In certain aspect, the present disclosure also provides an obturator component for maintaining the stoma or lumen.

Disclosed herein are synthetic leathers, artificial epidermal layers, artificial dermal layers, layered structures, products produced therefrom and methods of producing the same.

A method for decellularization of a skin tissue according to an embodiment of the present invention comprises: a step of preparing a skin tissue to be decellularized; a peeling preparation step of treating the skin tissue with a first solution containing trypsin; and a peeling step of removing subcutaneous fat from the skin tissue after the peeling preparation step.

The present invention provides a pigmentation skin model that comprises: a first cell group containing fibroblasts damaged by light irradiation, said first cell group being seeded on a first cell culture substratum; and a second cell group containing melanocytes and keratinocytes, said second cell group being applied onto the first cell group. The present invention also provides a method for producing the pigmentation skin model, and a method for evaluating a factor for treating or preventing pigmentation of the skin, said method comprising using the pigmentation skin model.

The present invention relates to a method of using family and/or regulatory members of the PD-1/PD-L1 pathway as predictive markers for risk of skin cancer development and as targets for therapeutic prevention of pre-malignant (or pre-cancerous) skin lesions and non-melanoma skin cancer (NMSC). This invention will allow for quantitative measurements of UV-induced expression of PD-1/PD-Li signaling pathway family members (e.g., PD-1, PD-L1, PD-L2) and/or PD-1/PD-L1 regulatory factors including AP-1 and NFκB family members in skin tissue of individuals to determine an individual's 1) risk for skin cancer development and 2) appropriate prophylactic treatment strategy to prevent skin cancer development. This information will facilitate identification of those patients at risk for pre-malignant (or pre-cancerous) skin lesions or subsequent NMSC lesions who would benefit from a PD-1/PD-L1 pathway suppressing therapy to prevent skin cancer development.