David Paslin
University of California, San Francisco
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by David Paslin.
Journal of The American Academy of Dermatology | 1981
David Paslin
A 10-year-old boy developed an asymptomatic, pigmented, flat-topped papule on the thigh. Biopsy revealed intravascular papillary endothelial hyperplasia in a dilated capillary of the superficial dermal plexus. This vascular abnormality was not accompanied by demonstrable thrombotic material or by angioma. Pathogenetically, intravascular papillary endothelial hyperplasia in this case appears to represent a primary rather than a reactive endothelial proliferation.
Experimental Dermatology | 2013
Courtney Phillips; Mina Kalantari-Dehaghi; Steve Marchenko; Alex I. Chernyavsky; Valentin Galitovskiy; Vivian Gindi; Sookhee Chun; David Paslin; Sergei A. Grando
Grovers disease (GD) is a transient or persistent, monomorphous, papulovesicular, asymptomatic or pruritic eruption classified as non‐familial acantholytic disorder. Contribution of autoimmune mechanisms to GD pathogenesis remains controversial. The purpose of this study was to investigate antibody‐mediated autoimmunity in 11 patients with GD, 4 of which were positive for IgA and/or IgG antikeratinocyte antibodies by indirect immunofluorescence. We used the most sensitive proteomic technique for an unbiased analysis of IgA‐ and IgG‐autoantibody reactivities. Multiplex analysis of autoantibody responses revealed autoreactivity of all 11 GD patients with cellular proteins involved in the signal transduction events regulating cell development, activation, growth, death, adhesion and motility. Semiquantitative fluorescence analysis of cultured keratinocytes pretreated with sera from each patient demonstrated decreased intensity of staining for desmoglein 1 and/or 3 and PCNA, whereas 4 of 10 GD sera induced BAD expression, indicating that binding of autoantibodies to keratinocytes alters expression/function of their adhesion molecules and activates apoptosis. We also tested the ability of GD sera to induce visible alterations of keratinocyte shape and motility in vitro but found no specific changes. Thus, our results demonstrated that humoral autoimmunity in GD can be mediated by both IgA and IgG autoantibodies. At this point, however, it is impossible to conclude whether these autoantibodies cause or are caused by the disease. Antidesmoglein antibodies may be triggered by exposure to immune system of sequestered antigens due to disintegration of desmosomes during primary acantholysis. Clarifying aetiology of GD will help improve treatment, which currently is symptomatic and of marginal effectiveness.
International Journal of Dermatology | 2004
David Paslin; Esther Krug
Background The study of skin barrier constituents may require collection of much stratum corneum. Existing methods are inadequate and/or difficult.
Journal of The American Academy of Dermatology | 1989
David Paslin
A 30-year-old atopic lactating woman developed a peculiar plaquelike dermatitis of nipples and areolae after infection with Staphylococcus aureus. Histologic examination showed an eosinophilic and plasma cellular edematous psoriasiform dermatitis. This constellation of findings seems distinct from other clinicopathologic states induced by staphylococci.
Cancer | 1977
David Paslin
Ten strains of anaerobic Corynebacteria were compared in their effect on survival of C57BL/6 mice, bearing subcutaneously inoculated B16 melanomas. The corynebacterial suspensions were injected intralesionally twice weekly for five injections. Significant permanent tumor regression was not obtained. Significant prolongation of surival was observed in mice treated with seven of the corynebacterial strains.
Archives of Dermatological Research | 2015
David Paslin; Erik Reykjalin; Elias Tsadik; Lionel Schour; Alexander H. Lucas
Inflammation in atopic dermatitis is mediated in part by the chemokine CCL1 and its receptor, CCR8. Recombinant Molluscum contagiosum viral protein (rMC148p), a cc-chemokine homolog, inhibits CCL1-induced chemotaxis of cells expressing CCR8. rMC148p was prepared using the baculovirus/Sf9 insect cell expression system. The recombinant MC148 fusion protein (rMC148fp), rMC148-TAT-6xHis, was similarly prepared by adding base sequences onto the PCR primers to fuse TAT and 6xHis to rMC148p at the carboxyl terminus. rMC148fp retains the capacity of rMC148p to inhibit CCL1-induced chemotaxis. Furthermore, unlike rMC148p, topically applied rMC148fp penetrates stratum corneum of human neonatal foreskins and concentrates along the basal and lower spinous cell layers of the epidermis. rMC148fp may be a safe and effective agent in the treatment of atopic dermatitis and other CCR8-mediated disorders.
British Journal of Dermatology | 1976
David Paslin
The present study was undertaken to compare the antitumour effects of intralesionally administered Corynebacterium granulosum, Corynebacterium parvum, BCG and saline on a hamster melanoma. Forty‐eight golden hamsters were inoculated subcutaneously with Fortners melanotic melanoma no. 1. Twenty‐four animals bore palpable tumours which were left in situ. The remaining twentyfour animals bore palpable tumours which were excised. No non‐excised group animal showed primary tumour regression. In the excised group, the tumours generally recurred at the excision site in the C. parvum, BCG and saline‐treated animals. By contrast, the incidence of recurrence was significantly reduced by intralesional injections of C. granulosum.
Archives of Dermatology | 1977
David Paslin; Michael E. Norman
Journal of the National Cancer Institute | 1974
David Paslin; Nikolay V. Dimitrov; Charles L. Heaton
Archives of Dermatology | 1985
David Paslin