ライフサイエンスコーパス: SITS

1 f 3365, OR 5.55, 95% CI 4.01-7.70, p<0.0001; SITS-MOST definition 124 [3.7%] vs 19 [0.6%], OR 6.67, 9

2 -isothiocyanostrilbene-2,2'-disulfonic acid (SITS, 2 mM), 5-nitro-2-(3-phenyl-propylamino)benzoic aci

3 sothiocyanatostilbene-2,2'-disulphonic acid (SITS) and 4,4'-diisothiocyanostilbene-2,2'-disulphonic a

4 sothiocyanatostilbene-2,2'-disulphonic acid (SITS) as well as by the Na+ -H+ exchange inhibitor amilo

5 isothiocyanostilbene-2, 2'-disulphonic acid (SITS).

6 The disulfonic stilbenes (DIDS and SITS) had markedly different effects and were found to g

7 endent, and inhibited by stilbenes (DIDS and SITS).

8 in both cAMP-stimulated HCO3- secretion and SITS-sensitive current in NBC1-/- proximal colon.

9 Specific anion cotransport blockers, such as SITS, DIDS, furosemide, or bumetanide, when simultaneous

10 omatic intracerebral haemorrhage (defined by SITS-MOST criteria) occurred in 20 (2%) versus 15 (2%) p

11 of symptomatic intracerebral haemorrhage (by SITS-MOST definition, 1/52 [2%] tenecteplase vs 2/51 [4%

12 It was inhibited by SITS (0.3-1 mM), NPPB (30-300 microM) and niflumic acid

13 The 'leak' cation fluxes were inhibited by SITS, dipyridamole and NS1652, chemically diverse inhibi

14 ompletely inhibited by amiloride, but not by SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfo

15 pylamino)benzoic acid) but was unaffected by SITS (4-acetamido-4'-isothiocyanatostilbene- 2,2'-disulp

16 and 4,4'-dinitrostilbene-2,2'-disulphonate (SITS).

17 creased with increasing stroke severity: for SITS-MOST intracerebral haemorrhage the absolute excess

18 using either the chloride channel inhibitor SITS or medium with a reduced chloride concentration.

19 the broad spectrum anion transport inhibitor SITS, and is not accompanied by detectable changes in in

20 , after a brief preincubation with 20 microM SITS at 4 degrees C, were warmed to 24 degrees C, and th

21 a+/H+ antiporter blocker, amiloride, but not SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfo

22 1-7.70]; absolute excess 5.5% [4.6-6.4]); of SITS-MOST haemorrhage (124 [3.7%] of 3391 vs 19 [0.6%] o

23 In the absence of SITS and CCCP, dehydration was limited by the diffusiona

24 95% confidence interval [CI] = 0.72-2.11 per SITS-MOST; aOR = 1.26, 95% CI = 0.82-1.70 per European C

25 f Thrombolysis in Stroke Monitoring Study's (SITS-MOST) haemorrhage within 24-36 h (type 2 parenchyma

26 fe Implementation of Thrombolysis in Stroke (SITS) International Stroke Thrombolysis Register.

27 of Thrombolysis in Stroke-Monitoring Study (SITS-MOST), which included a parenchymal hematoma type 2

28 The SITS-insensitive component of phi(E) was alkali shifted

29 rrhage within 7 days and, separately, by the SITS-MOST definition of parenchymal type 2 haemorrhage w

30 propensity score-matched (PSM) data from the SITS-ISTR.

31 ulates the SITS-insensitive but inhibits the SITS-sensitive acid extrusion.

32 e of CO(2)/HCO(-)(3), hypoxia stimulates the SITS-insensitive but inhibits the SITS-sensitive acid ex

33 was alkali shifted by 0.20-0.30, whereas the SITS-sensitive component of phi(E) was depressed in the