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Research 31–60 of 1000+
- Prevalence of Low Serum Vitamin D Levels in Patients Presenting With Androgenetic Alopecia: A Review
- Role of Trichoscopy in diagnosing Genotrichosis—A Report of Two Cases
- Two siblings with vitamin-D-dependent rickets type II: No recurrence of rickets for 14 years after cessation of therapy
- Congenital atrichia associated with situs inversus and mesocardia
- Overview of popular cosmeceuticals in dermatology
- Atrichia with papular lesions
- New aspects of vitamin D metabolism and action — addressing the skin as source and target
- Successful Treatment of Alopecia Areata with Topical Calcipotriol
- Suppression of Vitamin D Receptor and Induction of Retinoid X Receptor α Expression During Squamous Differentiation of Cultured Keratinocytes
- Vitamin D and its Analogs in Treatment of Mild to Moderate Alopecia Areata: Systematic Review and Meta-Analysis.
- Vitamin D and the Skin: An Update for Dermatologists
- Investigation of Diffuse Hair Fall Case Due to Vitamin D Deficiency: A Case Report and Literature Review
- 25 Hydroxyvitamin D 1 α-Hydroxylase Is Required for Optimal Epidermal Differentiation and Permeability Barrier Homeostasis
- ANALYSIS OF THE RELATION BETWEEN ALOPECIA AND RESISTANCE TO 1,25‐DIHYDROXYVITAMIN D
- Noncalcemic actions of 1,25-dihydroxyvitamin D3 and clinical applications
- Hair follicle expression of 1,25-dihydroxyvitamin D3 receptors during the murine hair cycle
- Rickets and Alopecia with Resistance to 1,25-Dihydroxyvitamin D: Two Different Clinical Courses with Two Different Cellular Defects*
- VITAMIN D RESISTANT RICKETS WITH ALOPECIA: A FORM OF END ORGAN RESISTANCE TO 1,25 DIHYDROXY VITAMIN D
- Vitamin D-dependent rickets type II. Defective induction of 25-hydroxyvitamin D3-24-hydroxylase by 1,25-dihydroxyvitamin D3 in cultured skin fibroblasts.
- Hereditary 1,25-Dihydroxyvitamin D Resistant Rickets due to a Mutation Causing Multiple Defects in Vitamin D Receptor Function
- 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
- Vitamin D-dependent rickets type II: extreme end organ resistance to 1,25-dihydroxy vitamin D3 in a patient without alopecia
- Tryptophan Missense Mutation in the Ligand‐Binding Domain of the Vitamin D Receptor Causes Severe Resistance to 1,25‐Dihydroxyvitamin D
- Hereditary 1,25‐Dihydroxyvitamin D–Resistant Rickets Due to an Opal Mutation Causing Premature Termination of the Vitamin D Receptor
- Analysis of 1,25-Dihydroxyvitamin D3 Receptors (VDR. in Basal Cell Carcinomas
- Proliferation and Differentiation of Cultured Human Keratinocytes is Modulated by 1,25(OH)<sub>2</sub>D<sub>3</sub> and Synthetic Vitamin D<sub>3</sub> Analogues in a Cell Density‐, Calcium‐ and Serum‐Dependent Manner*
- The vitamin D receptor functions as a transcription regulator in the absence of 1,25-dihydroxyvitamin D3
- A unique insertion/duplication in the VDR gene that truncates the VDR causing hereditary 1,25-dihydroxyvitamin D-resistant rickets without alopecia
- Two New Unrelated Cases of Hereditary 1,25-Dihydroxyvitamin D-resistant Rickets with Alopecia resulting from the same Novel Nonsense Mutation in the Vitamin D Receptor Gene
- Evidence for 1,25-Dihydroxyvitamin D3-independent Transactivation by the Vitamin D Receptor