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This report describes the first known case of Kaposi's varicelliform eruption occurring after a follicular unit extraction procedure, possibly linked to surgical trauma and post-surgical steroid use.

This narrative review suggests that intermediate filaments like vimentin and keratin play a significant role in various stages of viral infection, presenting potential antiviral intervention targets.

The KDM1 gene helps Venus flytraps close by managing potassium ions.

In this study, a novel VDR gene mutation was identified in a child with HVDRR, and the researchers observed that high-dose intravenous calcium therapy led to significant and sustained improvement in rickets symptoms.

A boy with a rare birthmark called verrucous hemangioma needed careful timing for surgery due to its size and depth.

This review discusses the use of very low-calorie ketogenic diets for obesity management and provides recommendations for nutrition experts, but reports no new clinical results.

In this study, eight patients with hereditary vitamin D-resistant rickets who share a specific VDR mutation showed improved clinical symptoms except alopecia after up to 11 years of treatment.

This study describes a patient with hereditary vitamin D resistant rickets (HVDRR) who, despite having a truncated vitamin D receptor, did not exhibit typical hair or skin abnormalities, suggesting possible compensation via interactions with other proteins.

The study reports that the AVET system showed higher efficiency in transfecting cultured human keratinocytes compared to SuperFect and PrimeFector, with AVET reaching levels of enzyme activity similar to normal cells in keratinocytes from lamellar ichthyosis patients.

This study suggests that the vitamin D receptor and hairless gene may directly regulate each other via a transcriptional mechanism, potentially explaining phenotypic similarities between atrichia and VDRRIIa rickets.

This abstract reviews hereditary vitamin D-resistant rickets, a rare genetic condition causing severe early childhood rickets, and reports no new results; effective treatment typically requires high doses of calcium to address hypocalcemia and secondary hyperparathyroidism.

This study created a humanized mouse model of hereditary vitamin D-resistant rickets that lacks alopecia, indicating the mutant receptor's potential to explore the syndrome's characteristics beyond vitamin D binding.

This study described the clinical and genetic features of two Iranian siblings with hereditary vitamin D resistant rickets, identifying a specific VDR gene mutation contributing to their symptoms.

This study reported a case of hereditary vitamin D–resistant rickets caused by a single heterozygous missense mutation in the VDR gene, showing dominant-negative effects and reduced response to 1,25-dihydroxyvitamin D3.

This study found that many participants with hair loss, or Khalitya, exhibited dietary incompatibilities and low calcium levels, aligning Ayurvedic concepts with modern dietary risk factors.

In this study, a Chinese Han family with hereditary vitamin D-resistant rickets was found to have a homozygous missense mutation in the VDR gene, and the affected individual uniquely responded well to treatment with oral calcium and low-dose calcitriol.

This study reports that the recombinant expression vector pcDNA3.1-KK demonstrates specific expression in the skin of newborn mice.

This study found that using histidine-tryptophan-ketoglutarate solution with adenosine triphosphate and deferoxamine for hair graft preservation significantly reduced postsurgical shedding compared to Ringer solution, enhancing patient satisfaction.

This study explored Ayurvedic treatments for Khalitya (Alopecia areata) and found that using Virechana Karma, along with systemic medicines and Rasayan drugs, may be extremely beneficial in managing this condition.

This study identified a new type II cytokeratin, named K6hf, exclusively expressed in the companion layer of the human hair follicle, distinguishing it from other keratins and suggesting a unique biochemical role.

This study observed that in varicella, the varicella-zoster virus spreads to dermal endothelial cells before reaching keratinocytes, whereas in herpes zoster, it first involves cutaneous nerves and pilosebaceous units.

This study suggests that varicella-zoster virus infection in skin cells may play a role in segmental vitiligo's progression and depigmentation.

This study found that the vitamin D-VDR system is crucial for mineral and bone metabolism post-weaning and identified missense mutations in 1alpha-hydroxylase causing type I rickets.

This study characterized two siblings with hereditary vitamin D resistant rickets and a mutation in the vitamin D receptor, finding no immune-related disorders despite a defective T cell response to vitamin D.

This study introduced the KRDQN predictive framework, which outperformed existing methods in predicting adverse drug reactions and provided interpretable insights into drug mechanisms, aiding pharmacovigilance and clinical decision-making.

This study found that both GHK-Cu liposome and GHK-Cu promoted hair growth and increased VEGF expression in a mouse model of alopecia.

In this study, researchers identified two types of potassium channels, BK and Kv4.2, in rat Merkel cells and reported that these channels play important roles in repolarizing action potentials and maintaining resting membrane potentials, potentially influencing tactile encoding in these cells.

This study found that a novel R343H mutation in the vitamin D receptor gene impairs its transcription activity, contributing to hereditary vitamin D-resistant rickets and alopecia in the affected family.

This study highlights Ayurveda's holistic approach to managing hair loss, known as Khalitya, through lifestyle changes, purification therapies, and targeted medications, addressing the condition's association with modern sedentary lifestyles and poor dietary habits.

This study demonstrated that both HR isoforms are expressed in keratinocytes, but HRDelta1072-1126 lacks corepressor activity and may act as a coactivator by inhibiting HDAC recruitment to the VDR transcriptional complex.