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Research 211–240 of 221
- SKIN MANIFESTATIONS OF RHEUMATOLOGICAL DISEASES
- E-Poster
- Alopecia Universalis Treated With Tofacitinib: The Role of JAK/STAT Inhibitors in Hair Regrowth
- Genetics and Epigenetics of Polycystic Ovary Syndrome
- Bioinformatic analysis of gene expression data reveals Src family protein tyrosine kinases as key players in androgenetic alopecia
- Dermatoses in overweight and obese children and their relationship with insulin and skin color
- Hair & Cutaneous Development
- Subject Index
- TONGUE, RED
- ZALCITABINE
- NEFAZODONE
- Impact of Combined Baricitinib and FTI Treatment on Adipogenesis in Hutchinson–Gilford Progeria Syndrome and Other Lipodystrophic Laminopathies
- How to diagnose a lipodystrophy syndrome
- Syndromes of Severe Insulin Resistance (SSIRs)
- Progeria (Hutchinson-Gilford Syndrome): Literature Review and Clinical Case
- A rare LMNA missense mutation causing a severe phenotype of mandibuloacral dysplasia type A: a case report
- Atypical Progeroid Syndrome due to Heterozygous Missense LMNA Mutations
- Case report: A novel splice-site mutation of MTX2 gene caused mandibuloacral dysplasia progeroid syndrome: the first report from China and literature review
- Cicatricial Alopecia Research Foundation meeting, May 2016: Progress towards the diagnosis, treatment and cure of primary cicatricial alopecias
- Integration of Biochemical and Mechanical Signals at the Nuclear Periphery: Impacts on Skin Development and Disease
- All Roads Go to the Nucleus: Integration of Signaling/Transcription Factor-Mediated and Epigenetic Regulatory Mechanisms in the Control of Skin Development and Regeneration
- Premature aging syndromes: From patients to mechanism
- Hutchinson-Gilford Progeria Syndrome—Current Status and Prospects for Gene Therapy Treatment
- Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin
- High-throughput Sequencing to Identify Monogenic Etiologies in a Preselected Polycystic Ovary Syndrome Cohort
- Dunnigan-Type Familial Partial Lipodystrophy: Understanding and Treating the Syndrome
- Biological Features Implies Potential Use of Autologous Adipose-Derived Stem/Progenitor Cells in Wound Repair and Regenerations for the Patients with Lipodystrophy
- A 10 Mb duplication in chromosome band 5q31.3–5q33.1 associated with late-onset lipodystrophy, ichthyosis, epilepsy and glomerulonephritis
- Treatment of Lipodystrophy with Troglitazone
- Loss of adipocyte phospholipase gene PLAAT3 causes lipodystrophy and insulin resistance due to inactivated arachidonic acid-mediated PPARγ signaling