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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  resembling those seen in human neutrophilic dermatoses.
10  to prevent or treat certain common neonatal dermatoses.
11 ammation that occurs during photo-aggravated dermatoses.
12 functions in the progression of inflammatory dermatoses.
13 egulated in psoriasis and other inflammatory dermatoses.
14 y contributes to inflammatory and autoimmune dermatoses.
15  infections, and chronic inflammatory vulvar dermatoses.
16 s associated with malignancies and inherited dermatoses.
17 rity of aged humans do not have inflammatory dermatoses.
18 roperties used for treatment of inflammatory dermatoses.
19 cal development in NS and other inflammatory dermatoses.
20 mples from unique patients with inflammatory dermatoses.
21 itigate photoaging, and treat photosensitive dermatoses.
22 hed control individuals with noninflammatory dermatoses, 127 controls undergoing allergy testing for
23 o many aspects of the so-called neutrophilic dermatoses, a heterogeneous group of skin diseases with
24 nt education on the nuanced presentations of dermatoses across different skin types, leading to poten
25           Subepidermal autoimmune blistering dermatoses (AIBD) are prototypic autoantibody-mediated d
26                        In autoimmune bullous dermatoses (AIBD), autoantibodies induce blisters on ski
27 nt cytokine expression in autoimmune bullous dermatoses (AIBDs), cytokine-targeting therapies have no
28 s up-regulated in situ in hyperproliferative dermatoses-an innate mechanism to repair and restore epi
29 res for lesional skin of patients with these dermatoses and healthy control skin.
30 ular and molecular landscape of neutrophilic dermatoses and implicates dermal immune-acting fibroblas
31 n a comparison of patients with inflammatory dermatoses and patients with isolated lesions, patients
32 n lesions have been reported as neutrophilic dermatoses and vasculitis.
33 Case reports of infection, tattoo-associated dermatoses, and allergic reactions to tattoos continue t
34                                 Neutrophilic dermatoses are a group of complex heterogeneous autoinfl
35 itis, hidradenitis suppurativa, neutrophilic dermatoses, autoimmune blistering disease, and Netherton
36 zary syndrome and erythrodermic inflammatory dermatoses can be challenging, and a number of studies h
37 ssor, which invites therapeutic targeting in dermatoses characterized by excessive Krt17 expression.
38 herited, heterogeneous group of rare genetic dermatoses characterized by mucocutaneous fragility and
39                                 Neutrophilic dermatoses comprise a wide spectrum of inflammatory dise
40 synthase protein in a number of inflammatory dermatoses, coupled with the induction of an intense cut
41 ated clinical benefit in pruritus-associated dermatoses (e.g. atopic dermatitis, bullous pemphigoid,
42 uld lead to new forms of topical therapy for dermatoses (e.g., psoriasis, atopic dermatitis, and irri
43                    Like other hypopigmentary dermatoses - for example, vitiligo, psoriasis, and lepro
44 isolated lesions, patients with inflammatory dermatoses had higher scale scores, and (ii) in an explo
45 ecognition that DM can resemble other common dermatoses highlights the need for a cutaneous biopsy to
46   With regard to the management of factitial dermatoses in children, it is of paramount importance fo
47 ng the diagnosis and management of factitial dermatoses in children.
48 ogram nonvolar to volar skin to reduce stump dermatoses in patients with limb loss using prosthetics.
49                 Visual clinical diagnosis of dermatoses in people of color (PoC) is a considerable ch
50 revolutionized the treatment of inflammatory dermatoses, including atopic dermatitis and psoriasis.
51 nd KLK-5 were found to be altered in various dermatoses, including atopic dermatitis, psoriasis, and
52 function could also drive other inflammatory dermatoses, including psoriasis.
53 feature of psoriasis and other proliferative dermatoses is accumulation in the skin of the unusual ar
54  and is deeply intertwined with inflammatory dermatoses like atopic dermatitis.
55 ed efficacy in the treatment of inflammatory dermatoses, likely due to decreased inflammation and enh
56                Adequate treatment of bullous dermatoses may be associated with a decrease in mental h
57  in the pediatric population, photosensitive dermatoses may begin prior to adulthood.
58                     Importance: Inflammatory dermatoses of the lower extremity are often misdiagnosed
59                                 Inflammatory dermatoses of the lower extremity are often misdiagnosed
60 cluding those with existing chronic pruritic dermatoses or systemic diseases known to cause pruritus,
61 ents with cutaneous vasculitis, neutrophilic dermatoses, or chondritis.
62 uently include thyroid disease, neutrophilic dermatoses, polyarthritis, connective tissue diseases, v
63 ession diagnosis among patients with bullous dermatoses ranged from 11.4% to 28%.
64 ressive symptoms among patients with bullous dermatoses ranged from 40% to 80%.
65 f skin ECs and their underlying mechanism in dermatoses remain to be determined.
66                    Because many inflammatory dermatoses result from defects in cutaneous barrier func
67  has been evaluated for the life-threatening dermatoses Stevens-Johnson syndrome and toxic epidermal
68 ty of KLKs may also be pathological in other dermatoses such as atopic dermatitis (AD).
69 y stages because of similarities with benign dermatoses such as atopic dermatitis (AD).
70 s, malignancies, neuropathic conditions, and dermatoses such as atopic dermatitis.
71                        Although inflammatory dermatoses such as psoriasis and atopic dermatitis predi
72 bnormal Krt17 expression is a key feature of dermatoses such as psoriasis and pachyonychia congenita,
73 To date, it has been recognized that several dermatoses such as psoriasis, atopic dermatitis, Mal de
74 oplasms but also for various T cell-mediated dermatoses such as psoriasis.
75 ficial in stress-induced, barrier-associated dermatoses, such as psoriasis and atopic dermatitis.
76 hing features compared to other neutrophilic dermatoses, such as pyoderma gangrenosum, remain poorly
77 ld be able to recognize the common factitial dermatoses that are seen in the pediatric population.
78 s of secondary malignancies and inflammatory dermatoses that may occur with extremity lymphedema.
79 rather than aggravate cutaneous inflammatory dermatoses through the anti-inflammatory activity of inc
80  19 patients with erythrodermic inflammatory dermatoses were analyzed for cell surface proteins by fl
81  immunobullous disorders, and other pustular dermatoses were considered.
82 ation could alter the course of inflammatory dermatoses, which invariably exhibit an increased SC pH.
83 3 inhibition can lead to clinically distinct dermatoses, which suggests the effect of FLT3 inhibition
84 rom patients with erythrodermic inflammatory dermatoses with 100% specificity.