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Research 331–360 of 537
- Alopecia: managing the basics
- Hormonal Treatment for Skin Androgen-Related Disorders
- Lab Quality Management and Methodology
- Sex hormones and related compounds, including hormonal contraceptives
- Systemic Corticosteroids in Vitiligo
- Medical Management Options for Hair Loss
- 9. Immunology and Genetics
- Dermatological manifestations associated with pregnancy
- Allergens and Irritants
- Journal Watch
- Spironolactone treatment of porphyria cutanea tarda-associated hirsutism
- Cytostatics and immunosuppressive drugs
- Self-medication by Jockeys
- Targeted overexpression of parathyroid hormone-related peptide in chondrocytes causes chondrodysplasia and delayed endochondral bone formation.
- Tooth Development Associated with Mutations in Hereditary Vitamin D–Resistant Rickets
- Clinical Snippets
- Hereditary 1,25-dihydroxyvitamin D-resistant rickets with alopecia resulting from a novel missense mutation in the DNA-binding domain of the vitamin D receptor
- Tacrolimus in Dermatologic Disorders
- The impact of VDR expression and regulation in vivo
- Mucocutaneous manifestations of acquired hypoparathyroidism: An observational study
- Presence of a Deletion Mutation (c.716delA) in the Ligand Binding Domain of the Vitamin D Receptor in an Indian Patient with Vitamin D-Dependent Rickets Type II
- APECED: JAK Inhibition in an Adult Case with Long-Term Follow-up
- Genotype–Phenotype Correlation in Children With Congenital Adrenal Hyperplasia due to 21‐Hydroxylase Deficiency Using Next Generation Sequencing
- Medical Management of Female Pattern Hair Loss
- Evolution and Function of Vitamin D
- Parathyroid Hormone-related Protein in Normal and Neoplastic Canine Tissues: Immunohistochemical Localization and Biochemical Extraction
- Wedelolactone inhibits breast cancer-induced osteoclastogenesis by decreasing Akt/mTOR signaling
- A unique insertion/duplication in the VDR gene that truncates the VDR causing hereditary 1,25-dihydroxyvitamin D-resistant rickets without alopecia
- Hepatic and dermatologic manifestations of chronic hypervitaminosis A in adults. Report of two cases
- An N-Ethyl-N-Nitrosourea Induced Corticotropin-Releasing Hormone Promoter Mutation Provides a Mouse Model for Endogenous Glucocorticoid Excess