ライフサイエンスコーパス: oxypurinol

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1 ocked by the xanthine oxidase (XO) inhibitor oxypurinol.

2 creased myocyte width in SHHF was reduced by oxypurinol.

3 1 months) and SHHF (19 to 21 months) rats to oxypurinol (1 mmol/L; n=4 and n=15, respectively) or pla

4 hese afferents was determined by infusion of oxypurinol (10 mg kg(-1), I.V.), an inhibitor of xanthin

5 one under nonischemic conditions and also by oxypurinol (100 micromol/L), a potent inhibitor of XO.

6 obtained by allopurinol, 175 mg kg-1 and by oxypurinol, 40 mg kg-1.

7 roxide dismutase (SOD; 250 and 1000 U/ml) or oxypurinol (50 and 200 microM), a potent xanthine oxidas

8 Patients (n = 405) were randomized to oxypurinol (600 mg/day) or placebo.

9 ndered the enzyme resistant to inhibition by oxypurinol, achieving approximately 50% inhibition.

10 cin administration, (2) partially reduced by oxypurinol administration, (3) reduced by decreasing mus

11 Oxypurinol also largely restored normal mitochondrial mo

12 ors of xanthine oxidoreductases (allopurinol oxypurinol, amflutizole and BOF 4272), which block all o

13 Oxypurinol and catalase inhibited phase-1 adhesion, sugg

14 Oxypurinol and Tempol diminished the leak in NOS1(-/-) c

15 endipitous findings identify allopurinol and oxypurinol as the lead compounds of a novel class of ino

16 ortantly, the XOR inhibitors allopurinol and oxypurinol attenuate dysfunction caused by XOR in these

17 did not change cardiac architecture in WKY, oxypurinol attenuated decreased FS and elevated LV end-d

18 (Oxypurinol Compared With Placebo for Class III-IV NYHA C

19 In addition, SUA reduction to oxypurinol correlated with favorable clinical response.

20 Whereas placebo and oxypurinol did not change cardiac architecture in WKY, o

21 Oxypurinol did not produce clinical improvements in unse

22 ) inhibition of xanthine oxidoreductase with oxypurinol does not inhibit nitrite-dependent vasodilati

23 y, the overall inhibition constant (K(i)) of oxypurinol for HS6B-XO was 2-5-fold greater than for fre

24 Thus, the inhibition kinetics of oxypurinol for XO was determined using saturating concen

25 Oxypurinol further reduced reactive oxygen species gener

26 NO, and the molybdenum-binding XO inhibitor oxypurinol inhibited this NO formation, indicating that

27 The molybdenum-binding XO inhibitor, oxypurinol, inhibited both nitrite and NO production, in

28 th HS6B and cell models substantially limits oxypurinol inhibition of XO, an event that has important

29 with indomethacin and xanthine oxidase with oxypurinol) on superoxide release by the contracting dia

30 ation of the xanthine oxidase (XO) inhibitor oxypurinol or aldehyde oxidase (AO) inhibitor raloxifene

31 sened did not differ between those receiving oxypurinol or placebo.

32 Tempol, oxypurinol, or SB203850 decreased O2- in all groups to l

33 ncubation with Tiron, ascorbic acid, Tempol, oxypurinol, or SB203850, an inhibitor of p38 kinase, but

34 ll lines that react to ALP or its metabolite oxypurinol (OXP) from HLA-B*58:01(+) and HLA-B*58:01(-)

35 (>9.5 mg/dl, n = 108) responded favorably to oxypurinol (p = 0.02 for interaction term), whereas oxyp

36 ulated kinase were restored toward normal by oxypurinol (P<0.05 versus placebo-SHHF).

37 Within the entire oxypurinol patient cohort, those characterized as either

38 nol (p = 0.02 for interaction term), whereas oxypurinol patients with SUA <9.5 mg/dl exhibited a tren

39 d whether a xanthine oxidase (XO) inhibitor, oxypurinol, produces clinical benefits in patients with

40 Addition of either apocyanin or oxypurinol reduced LAA O2*-, implying that NADPH and xan

41 Oxypurinol reduced serum uric acid (SUA) by approximatel

42 We conclude that allopurinol and oxypurinol sensitize the cardiac myofilaments to Ca2+.

43 We observed that oxypurinol significantly decreased the activity of cardi

44 Our findings indicate that oxypurinol treatment largely prevented mitochondrial def

45 reased XOR mRNA expression and activity, and oxypurinol treatment reduced XOR activity and superoxide

46 The XO inhibitor oxypurinol was administered to CryAB(R120G) mice for a p

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