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Open Access Publications from the University of California

Scholarly Works (8 results)

  • Article
  • Peer Reviewed
Dermatology Online Journal, Volume 10, Issue 3 (2004)
    • Article
    • Peer Reviewed
    Dermatology Online Journal, Volume 22, Issue 11 (2016)
    Atypical complete DiGeorge syndrome (DGS) is an extremely rare congenital disease characterized by an eczematous dermatitis, lymphadenopathy, and an oligoclonal T-cell proliferation. Because its initial presentation may be confused with other types of eczematous dermatitis, diagnosis and treatment are usually delayed. We describe herein a case of an infant with atypical complete DGS to draw attention to the clinical and histopathological findings that lead us to the diagnosis.
      Cover page: Dermatological clues to the diagnosis of atypical complete DiGeorge syndromeCreative Commons 'BY-NC-ND' version 4.0 license
      • Article
      • Peer Reviewed
      Dermatology Online Journal, Volume 26, Issue 10 (2020)
      Pseudoatrophoderma colli is a rare entity described in the same time period as confluent and reticular papillomatosis of Gougerot-Carteaud and the two conditions have certain similarities. Pseudoatrophoderma colli is clinically characterized by lesions with an atrophic and wrinkled appearance, which are mainly located on the trunk and neck (hence the name colli). Few references exist in the literature and most of them are very old. Histopathological findings are nonspecific, showing mild hyperkeratosis, thinning of the stratum granulosum, and acanthosis and papillomatosis in some areas. In the papillary dermis there is vascular dilatation with a sparse inflammatory lymphohistiocytic perivascular infiltrate. Fragmentation of elastic tissue has been described only in one case. There is no specific treatment, with variable responses to diverse therapies including ultraviolet light, vitamin A, lactic acid and minocycline. We describe in detail two patients with pseudoatrophoderma colli and show histology. The first patient was treated with minocycline 100mg per day for two months and the second patient was treated with lymecycline 600mg per day for three months and 300mg per day for another two months. Both patients demonstrated a good response within the first month of treatment.
        Cover page: Pseudoatrophoderma colli: distinct entity or just a variant of confluent and reticular papilomatosis of Gougerot-CarteaudCreative Commons 'BY-NC-ND' version 4.0 license
        • Article
        • Peer Reviewed
        Dermatology Online Journal, Volume 29, Issue 3 (2023)
        Calcipotriol (calcipotriene) is a synthetic vitamin D3 derivative that is a standard treatment option for psoriasis. It is generally well tolerated with minimal side effects. Due to its ability to reduce keratinocyte proliferation and induce keratinocyte differentiation as well as its immunomodulatory effects, calcipotriol has been used to treat a variety of skin disorders such as atopic dermatitis, actinic keratoses, lichen planus, seborrheic keratoses, and vitiligo [1]. We surveyed the literature examining the use of calcipotriol for non-psoriatic dermatologic disease.
          Cover page: Non-psoriatic uses of calcipotriol: a concise updated reviewCreative Commons 'BY-NC-ND' version 4.0 license
          • Article
          • Peer Reviewed
          UC San Francisco Previously Published Works (2013)
          Psoriasis is a chronic, inflammatory skin disease caused by a combination of environmental and genetic factors. The Tnip1 gene encodes A20 binding and inhibitor of NF-κB-1 (ABIN-1) protein and is strongly associated with susceptibility to psoriasis in humans. ABIN-1, a widely expressed ubiquitin-binding protein, restricts TNF- and TLR-induced signals. In this study, we report that mice lacking ABIN-1 specifically in dendritic cells (DCs), ABIN-1(fl) CD11c-Cre mice, exhibit perturbed immune homeostasis. ABIN-1-deficient DCs display exaggerated NF-κB and MAPK signaling and produce more IL-23 than do normal cells in response to TLR ligands. Challenge of ABIN-1(fl) CD11c-Cre mice with topical TLR7 ligand leads to greater numbers of Th17 and TCRγδ T cells and exacerbated development of psoriaform lesions. These phenotypes are reversed by DC-specific deletion of the TLR adaptor MyD88. These studies link ABIN-1 with IL-23 and IL-17, and they provide cellular and molecular mechanisms by which ABIN-1 regulates susceptibility to psoriasis.
            Cover page: Cutting Edge: ABIN-1 Protects against Psoriasis by Restricting MyD88 Signals in Dendritic Cells
            • Article
            • Peer Reviewed
            UC Davis Previously Published Works (2022)
            A 3-months old Chinese shar-pei puppy with ichthyosis was investigated. The dog showed generalized scaling, alopecia and footpad lesions. Histopathological examinations demonstrated a non-epidermolytic hyperkeratosis. The parents of the affected puppy did not show any skin lesions. A trio whole genome sequencing analysis identified a heterozygous de novo 3 bp deletion in the KRT1 gene in the affected dog. This variant, NM_001003392.1:c.567_569del, is predicted to delete a single asparagine from the conserved coil 1A motif within the rod domain of KRT1, NP_001003392.1:p.(Asn190del). Immunohistochemistry demonstrated normal levels of KRT1 expression in the epidermis and follicular epithelia. This might indicate that the variant possibly interferes with keratin dimerization or another function of KRT1. Missense variants affecting the homologous asparagine residue of the human KRT1 cause epidermolytic hyperkeratosis. Histologically, the investigated Chinese shar-pei showed a non-epidermolytic ichthyosis. The finding of a de novo variant in an excellent functional candidate gene strongly suggests that KRT1:p.Asn190del caused the ichthyosis phenotype in the affected Chinese shar-pei. To the best of our knowledge, this is the first description of a KRT1-related non-epidermolytic ichthyosis in domestic animals.
              Cover page: A de novo variant in the keratin 1 gene (KRT1) in a Chinese shar-pei dog with severe congenital cornification disorder and non-epidermolytic ichthyosis
              • Thesis
              • Peer Reviewed
              UC San Francisco Electronic Theses and Dissertations (2013)

              Heterologous expression of ABIN-1 (A20 Binding and Inhibitor of NF-kB-1, gene name Tnip1), like A20, was suggested to restrict TNF-induced inflammation and cell death. ABIN-1's physiological function was unknown. To interrogate ABIN-1's roles in vivo, we generated ABIN-1-deficient mice. ABIN-1 was required for successful embryonic development. TNF-deficiency rescued this lethality, demonstrating that ABIN-1 restricts potentially lethal TNF-induced signals. ABIN-1-/- TNF-/- mice develop a striking immune phenotype, suggesting that ABIN-1 restricts TNF-independent signals. ABIN-1-/- TNF-/- RAG-1-/- mice have splenomegaly, which supports that ABIN-1 expression in innate cells preserves immune quiescence. ABIN-1-/- fetal liver chimera develop partially cell-intrinsic widespread immune activation, suggesting that ABIN-1-/- hematopoietic cells are sufficient for exaggerated immune activation.

              Aberrant immune activation contributes to the pathogenesis of multiple autoimmune and inflammation-exacerbated diseases. The Tnip1 gene is strongly associated with susceptibility to psoriasis in humans. Psoriasis is a chronic, inflammatory skin disease caused by a combination of environmental and genetic factors. We demonstrated that mice lacking ABIN-1 specifically in dendritic cells (DCs), ABIN-1Flox CD11c-Cre mice, exhibited perturbed immune homeostasis. ABIN-1 deficient DCs displayed exaggerated NF-kB and MAP kinase signaling and produced more IL-23 than normal cells in response to TLR ligands. Challenge of ABIN-1Flox CD11c-Cre mice with topical TLR7 ligand lead to greater numbers of TH17 and gamma delta T cells and exacerbated development of psoriaform lesions. These phenotypes were reversed by DC-specific deletion of the TLR adaptor MyD88. These studies link ABIN-1 with IL-23 and IL-17, and provide cellular and molecular mechanisms by which ABIN-1 regulates susceptibility to psoriasis. They support that ubiquitin sensor ABIN-1 regulates cell survival and restricts proinflammatory signals in DC to protect against psoriasis.

                Cover page: Roles of Ubiquitin Sensor ABIN-1 In The Immune System
                • Article
                • Peer Reviewed
                UC Davis Previously Published Works (2018)
                Cutaneous squamous cell carcinoma (cSCC) is the second most common form of human cancer and has an increasing annual incidence. Although most cSCC is cured with office-based therapy, advanced cSCC poses a significant risk for morbidity, impact on quality of life, and death. This document provides evidence-based recommendations for the management of patients with cSCC. Topics addressed include biopsy techniques and histopathologic assessment, tumor staging, surgical and nonsurgical management, follow-up and prevention of recurrence, and management of advanced disease. The primary focus of these recommendations is on evaluation and management of primary cSCC and localized disease, but where relevant, applicability to recurrent cSCC is noted, as is general information on the management of patients with metastatic disease.
                  Cover page: Guidelines of care for the management of cutaneous squamous cell carcinoma
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