ライフサイエンスコーパス: OHP

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1 OHP oxidation results in the disruption of the Y36'-C22-

2 enzymatic product 17-hydroxyprogesterone (17-OHP).

3 Treatment of WT mice with 17-OHP was sufficient to induce liver injury that reproduce

4 -y cluster-randomized trial, we developed an OHP INT with Navajo input that was delivered by trained

5 e, we describe the structures of reduced and OHP-oxidized OhrR, visualizing the structural mechanism

6 ease in collagen deposition (as reflected by OHP content) in the PTFE tubes without an effect on tota

7 OxyR regulon yet is specifically induced by OHPs.

8 art site was sufficient for ohr induction by OHPs.

9 bition assays and showed enhanced killing by OHPs in liquid culture.

10 ancer (OCCs), 88 oro-/hypopharyngeal cancer (OHPs), and 193 laryngeal cancer cases] were available fo

11 (i.e., >/=3 child OHP events, >/=1 caregiver OHP events, and >/=3 fluoride varnish).

12 INT adherence was 53% (i.e., >/=3 child OHP events, >/=1 caregiver OHP events, and >/=3 fluoride

13 f convective drying (CDP) and ohmic heating (OHP) were assayed.

14 In r/r livers, however, OHP content remained elevated at peak fibrosis levels.

15 ptimal resistance to organic hydroperoxides (OHPs) but not to hydrogen peroxide or paraquat.

16 at upon oxidation by organic hydroperoxides (OHPs) forms an intersubunit disulphide bond with residue

17 ignificantly (43%) decreased hydroxyproline (OHP) content.

18 mplantation and analyzed for hydroxyproline (OHP, nmol/cm catheter, an index of collagen accumulation

19 r in CDP (46.6-110.1mg/100g protein) than in OHP (13.7-42.0mg/100g protein) samples, probably due to

20 ates the initial influx of DDP, CBDCA, and L-OHP and is a major determinant of responsiveness to DDP

21 cantly sensitized these cells to TRAIL and L-OHP.

22 , also sensitized these cells to TRAIL and L-OHP.

23 of CBDCA and reduced the initial uptake of L-OHP by 68% but had no effect on the influx of transplati

24 of TRAIL in RKO and HT29 cells and that of L-OHP in HT29 cells.

25 ugs at low concentrations, accumulation of L-OHP is not dependent on CTR1 at higher concentrations.

26 ned for DDP and CBDCA, but accumulation of L-OHP was no longer CTR1-dependent.

27 When exposed to DDP, CBDCA, or L-OHP at 2 microM, accumulation in the CTR1-/- cells was o

28 ncreasing concentrations of DDP, CBDCA, or L-OHP for 1 h.

29 further sensitize these cells to TRAIL- or L-OHP-induced cell death; however, exposure caused the dow

30 eutic approaches that include oxaliplatin (L-OHP) have brought the median survival rate to 22 months,

31 n (DDP), carboplatin (CBDCA), oxaliplatin (L-OHP), and transplatin.

32 DP), carboplatin (CBDCA), and oxaliplatin (L-OHP).

33 We conclude that L-OHP is a substrate for some other cellular entry mechani

34 t to CBDCA, but only 1.7-fold resistant to L-OHP.

35 The diagnosis of OHP requires a multidisciplinary approach and relies on

36 hrR, visualizing the structural mechanism of OHP induction.

37 trated to contribute to the decomposition of OHPs.

38 nt in cells treated with a sublethal dose of OHPs but not in cells treated with paraquat.

39 Organic-inorganic halide perovskite (OHP) materials, for example, CH3 NH3 PbI3 (MAPbI3 ), hav

40 Occupational hypersensitivity pneumonitis (OHP) is an immunologic lung disease resulting from lymph

41 d, tribally delivered oral health promotion (OHP) intervention (INT) at reducing caries increment in

42 the expression of a peroxidase that reduces OHPs to their less toxic alcohols.

43 Diagnostic criteria adapted to OHP are proposed.

44 r was induced up to 15-fold upon exposure to OHPs, and this induction was independent of OxyR.

45 otype correlated with hypersusceptibility to OHPs, suggesting overlapping or compensatory functions o

46 A Deltaohr mutant was hypersusceptible to OHPs in disk inhibition assays and showed enhanced killi

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