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1 y syndrome versus erythrodermic inflammatory dermatoses.
2 mpared to normal skin or benign inflammatory dermatoses.
3 viding an animal model of human neutrophilic dermatoses.
4 ey were used topically to treat inflammatory dermatoses.
5 a phenotype resembling acquired inflammatory dermatoses.
6 e complex genetic basis of many inflammatory dermatoses.
7 nical management of the complex inflammatory dermatoses.
8 s of the heterogeneous group of neutrophilic dermatoses.
9 y contributes to inflammatory and autoimmune dermatoses.
10  resembling those seen in human neutrophilic dermatoses.
11  to prevent or treat certain common neonatal dermatoses.
12 ammation that occurs during photo-aggravated dermatoses.
13 functions in the progression of inflammatory dermatoses.
14 egulated in psoriasis and other inflammatory dermatoses.
15  infections, and chronic inflammatory vulvar dermatoses.
16 s associated with malignancies and inherited dermatoses.
17 itigate photoaging, and treat photosensitive dermatoses.
18 hed control individuals with noninflammatory dermatoses, 127 controls undergoing allergy testing for
19 o many aspects of the so-called neutrophilic dermatoses, a heterogeneous group of skin diseases with
20           Subepidermal autoimmune blistering dermatoses (AIBD) are prototypic autoantibody-mediated d
21                        In autoimmune bullous dermatoses (AIBD), autoantibodies induce blisters on ski
22 nt cytokine expression in autoimmune bullous dermatoses (AIBDs), cytokine-targeting therapies have no
23 s up-regulated in situ in hyperproliferative dermatoses-an innate mechanism to repair and restore epi
24 res for lesional skin of patients with these dermatoses and healthy control skin.
25 n a comparison of patients with inflammatory dermatoses and patients with isolated lesions, patients
26 Case reports of infection, tattoo-associated dermatoses, and allergic reactions to tattoos continue t
27                                 Neutrophilic dermatoses are a group of complex heterogeneous autoinfl
28 zary syndrome and erythrodermic inflammatory dermatoses can be challenging, and a number of studies h
29 ssor, which invites therapeutic targeting in dermatoses characterized by excessive Krt17 expression.
30                                 Neutrophilic dermatoses comprise a wide spectrum of inflammatory dise
31 synthase protein in a number of inflammatory dermatoses, coupled with the induction of an intense cut
32 uld lead to new forms of topical therapy for dermatoses (e.g., psoriasis, atopic dermatitis, and irri
33 isolated lesions, patients with inflammatory dermatoses had higher scale scores, and (ii) in an explo
34 ecognition that DM can resemble other common dermatoses highlights the need for a cutaneous biopsy to
35   With regard to the management of factitial dermatoses in children, it is of paramount importance fo
36 ng the diagnosis and management of factitial dermatoses in children.
37 function could also drive other inflammatory dermatoses, including psoriasis.
38 feature of psoriasis and other proliferative dermatoses is accumulation in the skin of the unusual ar
39 ed efficacy in the treatment of inflammatory dermatoses, likely due to decreased inflammation and enh
40  in the pediatric population, photosensitive dermatoses may begin prior to adulthood.
41                                 Inflammatory dermatoses of the lower extremity are often misdiagnosed
42                     Importance: Inflammatory dermatoses of the lower extremity are often misdiagnosed
43                    Because many inflammatory dermatoses result from defects in cutaneous barrier func
44  has been evaluated for the life-threatening dermatoses Stevens-Johnson syndrome and toxic epidermal
45 bnormal Krt17 expression is a key feature of dermatoses such as psoriasis and pachyonychia congenita,
46 To date, it has been recognized that several dermatoses such as psoriasis, atopic dermatitis, Mal de
47 oplasms but also for various T cell-mediated dermatoses such as psoriasis.
48 ficial in stress-induced, barrier-associated dermatoses, such as psoriasis and atopic dermatitis.
49 ld be able to recognize the common factitial dermatoses that are seen in the pediatric population.
50 rather than aggravate cutaneous inflammatory dermatoses through the anti-inflammatory activity of inc
51  19 patients with erythrodermic inflammatory dermatoses were analyzed for cell surface proteins by fl
52  immunobullous disorders, and other pustular dermatoses were considered.
53 ation could alter the course of inflammatory dermatoses, which invariably exhibit an increased SC pH.
54 3 inhibition can lead to clinically distinct dermatoses, which suggests the effect of FLT3 inhibition
55 rom patients with erythrodermic inflammatory dermatoses with 100% specificity.

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