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10 rezultatima
Human leukocyte antigen-DQB1*03 alleles are associated with alopecia areata.
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Alopecia areata (AA) is characterized by hair loss in patches (patchy AA), over the entire scalp (AT, totalis), or universally (AU). An autoimmune mechanism has been hypothesized, because the inflammatory infiltrate targeted to the hair follicles includes activated T cells. To investigate whether or
Cellular activity in the dermis surrounding the hair bulb in alopecia areata.
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The metabolic activity of the cells in the connective tissue surrounding the hair bulb has been studied by radioautography in alopecia areata and in normal scalp, using in vitro incorporation of tritiated thymidine, uridine, histidine, leucine and proline. In alopecia areata, the hair bulbs are
Enteral calcium infusion used successfully as treatment for a patient with hereditary vitamin D resistant rickets (HVDRR) without alopecia: a novel mutation.
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BACKGROUND
We report a novel mutation in a case of hereditary vitamin D resistant rickets (HVDRR) without alopecia and successful management of this condition with the intravenous formulation of calcium chloride delivered via gastric tube.
METHODS
A 22 month old male (length -3.4 SDS; weight -2.1
Modulation of dermal cell activity during hair growth in the rat.
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Interaction between connective tissue cells and hair growth in the rat has been studied by radioautography after in vivo and in vitro pulse labelling with thymidine, uridine, histidine, leucine and proline. The connective tissue, which surrounds and integrates the hair bulbs as a unit, contains
Scd1ab-Xyk: a new asebia allele characterized by a CCC trinucleotide insertion in exon 5 of the stearoyl-CoA desaturase 1 gene in mouse.
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We describe here a spontaneous, autosomal recessive mutant mouse suffering from skin and hair defects, which arose in the outbred Kunming strain. By haplotype analysis and direct sequencing of PCR products, we show that this mutation is a new allele of the asebia locus with a naturally occurring
Activation of Nrf2 in keratinocytes causes chloracne (MADISH)-like skin disease in mice.
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The transcription factor Nrf2 is a key regulator of the cellular stress response, and pharmacological Nrf2 activation is a promising strategy for skin protection and cancer prevention. We show here that prolonged Nrf2 activation in keratinocytes causes sebaceous gland enlargement and seborrhea in
The effect of L-3, 4-dehydroproline on the antitumor activity and toxicity of bleomycin.
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Pulmonary fibrosis is a serious side effect that limits the therapeutic utility of bleomycin (BLM). Recently, it has been demonstrated that L-3, 4-dehydroproline (DHP), a proline analog, significantly reduced the extent of pulmonary fibrosis in rats administered BLM intratracheally. The present
Mutations in AEC syndrome skin reveal a role for p63 in basement membrane adhesion, skin barrier integrity and hair follicle biology.
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BACKGROUND
AEC (ankyloblepharon-ectodermal defects-clefting) syndrome is an autosomal dominant ectodermal dysplasia disorder caused by mutations in the transcription factor p63. Clinically, the skin is dry and often fragile; other features can include partial eyelid fusion (ankyloblepharon),
Hereditary long QT syndrome due to autoimmune hypoparathyroidism in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome.
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Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED), also known as autoimmune polyglandular syndrome type I, is a rare autosomal recessively inherited disorder characterized by variable combinations of endocrine and nonendocrine symptoms. In this report, we describe two 20- and
Dipeptidyl peptidase IV inhibition for the treatment of type 2 diabetes: potential importance of selectivity over dipeptidyl peptidases 8 and 9.
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Dipeptidyl peptidase (DPP)-IV inhibitors are a new approach to the treatment of type 2 diabetes. DPP-IV is a member of a family of serine peptidases that includes quiescent cell proline dipeptidase (QPP), DPP8, and DPP9; DPP-IV is a key regulator of incretin hormones, but the functions of other
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