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Research 721–750 of 1000+
- Lack of Collagen VI Promotes Wound-Induced Hair Growth
- Cicatricial Alopecia Research Foundation meeting, May 2016: Progress towards the diagnosis, treatment and cure of primary cicatricial alopecias
- An Update on Drug-Induced Pigmentation
- Female Adolescent Hair Disorders
- Effects of porcine acellular dermal matrix treatment on wound healing and scar formation: Role of Jag1 expression in epidermal stem cells
- Vogt-Koyanagi-Harada Disease: A Narrative Review
- Acne and acneiform eruptions
- EDA Fibronectin Microarchitecture and YAP Translocation During Wound Closure
- Side effects of common acne treatments
- Artificial Hair: By the Dawn to Automatic Biofibre® Hair Implant
- Localized Telogen Effluvium after Face Lift Surgery
- TREATMENT PEARLS FROM EUROPE
- Telogen hair loss and androgenetic‐like alopecia in GAPO syndrome
- Targeting the Wnt pathways for therapies
- Human epithelial hair follicle stem cells and their progeny: Current state of knowledge, the widening gap in translational research and future challenges
- Post-menopausal frontal fibrosing alopecia
- Transplantation of bone-marrow-derived mesenchymal and epidermal stem cells contribute to wound healing with different regenerative features
- Hair loss
- Cell-free adipose extract inhibits hypertrophic scar formation through collagen remodeling and antiangiogenesis
- Wound healing
- Idiopathic Hirsutism*
- Superficial granulomatous pyoderma: A localized vegetative form of pyoderma gangrenosum
- Fibroproliferative genes are preferentially expressed in central centrifugal cicatricial alopecia
- Alopecia.
- Chemical pharmacotherapy options for managing adult acne
- An overview of zinc and its importance in dermatology-Part II: The association of zinc with some dermatologic disorders
- Filamin A Mediates Wound Closure by Promoting Elastic Deformation and Maintenance of Tension in the Collagen Matrix
- Cosmetic Procedures in the Treatment of Alopecia
- Frontal Fibrosing Alopecia
- Primary cicatricial alopecias are characterized by dysregulation of shared gene expression pathways