ライフサイエンスコーパス: microabscess

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1 ation with lymphocytes, and disappearance of microabscess.

2 s epidermotropic and produces intraepidermal microabscesses.

3 n the liver and an increase in the number of microabscesses.

4 tes become heavily infected and develop into microabscesses.

5 amatically increased PMN trafficking to skin microabscesses and lungs after ischemia-reperfusion, whe

6 s, hyperkeratosis, intraepidermal neutrophil microabscesses, and increased T helper type 1 (Th1)/Th17

7 However, not all hepatic microabscesses are due to CMV infection.

8 The microabscesses are smaller and more numerous than in CMV

9 leukocytes, rather than forming disseminated microabscesses as seen for the wild type.

10 epidermis and superficial dermis, subcorneal microabscesses, basement membrane degradation, and angio

11 widespread polymorphonuclear leukocyte-rich microabscesses but without change in cytotoxic T-lymphoc

12 Munro's microabscesses contain polymorphonuclear leukocytes and

13 The persistence of leukocytes within liver microabscesses correlated with enhanced colonization and

14 macrophages, and numerous neutrophil-filled microabscesses developed, followed by tissue destruction

15 nflammatory cells and tissue damage, such as microabscesses, edema, and necrosis progressed following

16 keratinocytes is essential for neutrophilic microabscess formation and contributes to hyperprolifera

17 S mice with purified CD8(+) T cells restored microabscess formation and epidermal hyperproliferation.

18 nsplant patients with necrotizing lesions or microabscess formation at allograft biopsy.

19 e infected with Listeria had similar hepatic microabscess formation in terms of histologic appearance

20 cation of imiquimod in vivo led to epidermal microabscess formation, acanthosis, and increased IL-1al

21 n RAS was expressed on a Rag1-/- background, microabscess formation, inducible nitric oxide synthase

22 1alpha and IL-1R1 signaling is essential for microabscess formation, neutrophil recruiting chemokine

23 n, we explored the role of IL-1 signaling in microabscess formation.

24 Neutrophil-rich microabscesses formed beneath the stratum corneum.

25 Disseminated microabscesses in major organs were found in animals tre

26 yperplasia, and the presence of eosinophilic microabscesses in the epithelium) were examined by revie

27 the liver, about 95% are granulomas with 5% microabscesses involving intrahepatic infection.

28 Parenchymal microabscesses (MA) in liver transplant biopsies are fre

29 In 1992, we described "mini" microabscess (MMA) syndrome, a distinct clinical syndrom

30 The number and area of microabscesses on the ears of E-/P-deficient mice were d

31 led hyperplasia of the epidermis, subcorneal microabscesses, orthohyperkeratosis, parakeratosis, and

32 Microabscess, severe necrosis, and early calcification w

33 calized with Thy-1(+) EC of small vessels in microabscesses, suggesting an interaction between CD97 a

34 Histopathologically, disseminated septic microabscesses surrounded by necrotic foci were found ex

35 is characterized in the liver by parenchymal microabscesses, usually containing CMV-infected cells.

36 Atypical lymphocytes in epidermal Pautrier microabscesses were positive for HTLV-1.

37 s is particularly evident in the edge of the microabscess, where hepatocytes are not yet destroyed by

38 the equilibrium between granulomas and liver microabscesses, with massive transfer of the infection t

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