ライフサイエンスコーパス: cigarette smoke condensate

1 ively modulated by exogenous stimuli such as cigarette smoke condensate.

2 -1beta, PMA, LPS, H(2)O(2), doxorubicin, and cigarette smoke condensate.

3 cetate, okadaic acid, hydrogen peroxide, and cigarette smoke condensate also was suppressed.

4 agent, referred to as CSC, was isolated from cigarette smoke condensate and shown to prime purified h

5 lter epithelial morphology, including IL-13, cigarette smoke condensate, and retinoic acid deficiency

6 orbol 12-myristate 13-acetate, H(2)O(2), and cigarette smoke condensate as well as that induced by TN

7 In mice, paternal exposure to cigarette smoke condensate (CSC) causes molecular defect

8 ere cultured in normal media with or without cigarette smoke condensate (CSC) for up to 9 months unde

9 Cigarette smoke condensate (CSC) increases expression of

10 Cigarette smoke condensate (CSC) is comprised of thousan

11 Cigarette smoke condensate (CSC) is the particulate matt

12 that exposure of esophageal cancer cells to cigarette smoke condensate (CSC) led to upregulation of

13 d the effect of hydrogen peroxide (H2O2) and cigarette smoke condensate (CSC) on histone acetylation:

14 In this study, we investigated the effect of cigarette smoke condensate (CSC) on the characteristics

15 f pregnant p(un) mice to cigarette smoke and cigarette smoke condensate (CSC) on the frequency of bla

16 Following exposure to carcinogens: cigarette smoke condensate (CSC) or N-nitrosamine-4-(met

17 epithelial cell line, MCF10A, for 72 h with cigarette smoke condensate (CSC) resulted in a transform

18 ntly demonstrated that long-term exposure of cigarette smoke condensate (CSC) to HIV-uninfected (U937

19 vious studies have shown that treatment with cigarette smoke condensate (CSC) transforms normal breas

20 In earlier studies, we have shown that cigarette smoke condensate (CSC), a surrogate for cigare

21 d in primary bronchial epithelium exposed to cigarette smoke condensate (CSC), and alteration of mir-

22 (NHBE) resulted in significant inhibition of cigarette smoke condensate (CSC)-induced cell proliferat

23 ng adenocarcinoma H1299 cells, we found that cigarette smoke condensate (CSC)-induced NF-kappaB activ

24 lls cultured in normal media with or without cigarette smoke condensate (CSC).

25 cells cultured in the presence or absence of cigarette smoke condensate (CSC).

26 cells exhibit similar molecular responses to cigarette smoke condensate ex vivo and in vivo.

27 The neutral fraction of cigarette smoke condensate had most of the carcinogenic

28 s factor (TNF), phorbol ester, okadaic acid, cigarette smoke condensate, hydrogen peroxide, and inter

29 rom immortalized HBE cells after exposure to cigarette smoke condensate in vivo.

30 A549 cell exposure to cigarette smoke condensate increased these enhancer mark

31 (e.g. phorbol 12-myristate 13-acetate, H2O2, cigarette smoke condensate, interleukin-1beta, lipopolys

32 It was concluded from these studies that cigarette smoke condensate is primarily a tumor-promotin

33 sate were also performed, and indicated that cigarette smoke condensate leads to genome instability i

34 arcinogenic and inflammatory agents, such as cigarette smoke condensate, phorbol 12-myristate 13-acet

35 y tumor necrosis factor (TNF), okadaic acid, cigarette smoke condensate, phorbol myristate acetate, a

36 tronger SMAD3 epigenetic repression, because cigarette smoke condensate selectively increased SMAD3 p

37 benzo[a]pyrene (BaP) is a major component of cigarette smoke condensate that has received significant

38 pressed NF-kappaB activated by a carcinogen (cigarette smoke condensate), tumor promoters (phorbol my

39 by lipopolysaccharide, interleukin-1beta, or cigarette smoke condensate was completely suppressed in

40 bronchial epithelial cell lines treated with cigarette smoke condensate were also performed, and indi