ライフサイエンスコーパス: eczematous

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1 sociated with eczematous drug eruptions (ie, eczematous and interface dermatitis) was also performed.

2 The most represented forms of non-eczematous contact dermatitis include the erythema multi

3 ription 3 (STAT3) mutations has a history of eczematous dermatitis and elevated IgE; however, clinica

4 sis fungoides were compared with 18 cases of eczematous dermatitis by multiparametric image cytometry

5 medical history who first presented with an eczematous dermatitis on her torso, extremities, and but

6 It is an eczematous dermatitis that differs in timing and appeara

7 model ADAM17-deficiency in human, developed eczematous dermatitis with naturally occurring dysbiosis

8 vis sequentially emerged during the onset of eczematous dermatitis, and antibiotics specific for thes

9 a possible target for future therapeutics in eczematous dermatitis.

10 than 90% of cases, this eruption is pruritic eczematous dermatitis.

11 frequently included low-grade infections and eczematous dermatitis.

12 and triggers the appearance of spongiosis in eczematous dermatitis.

13 s AD, atopic eczema (AE), and multiple other eczematous disorders.

14 conventionally thought to be associated with eczematous drug eruptions (ie, eczematous and interface

15 ents of advanced age presenting with chronic eczematous eruptions of uncertain etiology.

16 mice lead to the development of spontaneous eczematous inflammation and address the aberrant immunol

17 oreactivity; and experimental elicitation of eczematous lesions after provocation.

18 n AD-like phenotype, with the development of eczematous lesions containing inflammatory dermal cellul

19 transepidermal water loss and development of eczematous lesions in these specific pathogen-free NC/Tn

20 rans-epidermal water loss and development of eczematous lesions in these SPF NC/Tnd mice, which norma

21 es, such as IL-22, was demonstrated in acute eczematous lesions independent of their pathogenesis.

22 Diagnosis is based upon the distribution of eczematous lesions rather than the appearance of individ

23 eous T-cell lymphoma (CTCL) may present with eczematous lesions, mycosis fungoides (MF), or as exfoli

24 3, and tenascin C were observed in all acute eczematous lesions, while a correlation of IL-17+ T cell

25 notype characterized by xerosis and pruritic eczematous lesions; dermal infiltration of CD4+ T cells,

26 causes congenital exfoliative erythroderma, eczematous-like lesions, and atopic manifestations.

27 Eczematous mice exhibited lower natural killer (NK) cell

28 ervations in these patients have varied from eczematous or urticarial to papular or nodular skin lesi

29 ic contact dermatitis usually presents as an eczematous process, clinically characterized by erythema

30 ruption comprising 2 distinct components: an eczematous reaction and a wave of melanocytic proliferat

31 exanthemata as a consequence of exaggerated eczematous reactions to topical and systemic allergens.

32 In contrast, weak acidification of eczematous skin in conventionally housed NC/Tnd mice red

33 In contrast, weak acidification of eczematous skin in conventionally housed NC/Tnd mice red

34 Virus infection of eczematous skin induced severe primary erosive skin lesi

35 to a similar clinical pattern, that is, the eczematous skin lesion, but showing distinct progression

36 med to investigate IL-17 expression in acute eczematous skin lesions and correlate it with markers of

37 Eczematous skin lesions of atopic dermatitis (AD) as wel

38 act and Staphylococcal enterotoxin B induced eczematous skin lesions.

39 itus sine materia (no primary skin lesions), eczematous, urticarial, papular, and/or nodular skin les

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