• The response was inhibited by the apical Cl- channel blocker, diphenylamine-dicarboxylic acid, and the Ca2+-activated Cl- channel blocker, disulfonic acid stilbene, indicating that Cl- may pass through two types of Cl- channels on the apical side. (nih.gov)
  • One of the first molecules described to inhibit RAD51 was the 4,4 -diisothiocyanato-stilbene-2,2 -disulfonic acid (DIDS) molecule. (univ-nantes.fr)
  • This group of compounds includes amino acids and fatty acids. (lookformedical.com)
  • Organic compounds that contain 1,2-diphenylethylene as a functional group. (nih.gov)
  • Extracellular nucleotides and DIDS, however, had no or only partial effects on D-[3H]aspartate release from cells swollen by hypotonic medium, but such release was inhibited by NPPB, dideoxyforskolin, and tamoxifen. (nih.gov)
  • Activated by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) in a sustained intracellular acidification-dependence manner. (nih.gov)
  • [ 12 ] In addition, the activities of ClC-K1 and ClC-K2 were inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), 9-anthracene carboxylic acid and 2-(p-chlorophenoxy)propionic acid derivatives. (medscape.com)
  • Using fluorescence pH(i) imaging, we show that cancer-derived cell lines (colorectal HCT116 and HT29, breast MDA-MB-468, pancreatic MiaPaca2, and cervical HeLa) extrude acid by H(+) efflux and HCO(3)(-) influx, largely sensitive to dimethylamiloride and 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS), respectively. (ox.ac.uk)
  • With depth, acid extrusion became relatively more DIDS-sensitive because the low extracellular pH at the spheroid core inhibits H(+) flux more than HCO(3)(-) flux. (ox.ac.uk)
  • Involved in pH regulation to eliminate acids generated by active metabolism or to counter adverse environmental conditions. (nih.gov)
  • Bile acids (BAs) are natural end products of cholesterol metabolism (12). (pancreapedia.org)
  • The sulfated form of TLC (TLCS) causes Ca 2+ signalling in pancreatic acinar cells via an inositol 1,4,5-trisphosphate (IP 3 )-dependent mobilization of sequestered intracellular Ca 2+ (49). (pancreapedia.org)
  • changes of intracellular Na + concentrations ([Na + ] i ) induced by readmission of different external K + concentrations ([K + ] o ) to tissues depleted of K + by 4‐h exposure to K + ‐free solution. (comprehensivephysiology.com)
  • Intracellular pH (pH(i)), a major modulator of cell function, is regulated by acid/base transport across membranes. (ox.ac.uk)
  • p = 0.363), with higher grade 3-4 hematologic toxicity. (bvsalud.org)
  • Unfortunately, we do not know the concentration of bile acids that can reach the pancreatic ductal cells under pathological conditions. (pancreapedia.org)
  • The major BAs in humans are chenodeoxycholic acid (CDCA) and cholic acid (CA), which are known as primary BAs since they are synthesized in the liver (46). (pancreapedia.org)
  • Secondary bile acids such as deoxycholic acid (DCA) and lithocholic acid (LCA) are produced in the colon by bacterial dehydroxylation of the primary BAs. (pancreapedia.org)
  • It has been shown that one of the most toxic BAs to acinar cells is the secondary BA, taurolithocholic acid (TLC) that forms from LCA after re-absorption from the intestine. (pancreapedia.org)
  • When HCO(3)(-) flux was pharmacologically inhibited, acid extrusion in multicellular HT29 and HCT116 spheroids (∼10,000 cells) was highly non-uniform and produced low pH(i) at the core. (ox.ac.uk)
  • This is because H(+) transporters require extracellular mobile pH buffers, such as CO(2)/HCO(3)(-), to overcome low H(+) ion mobility and chaperone H(+) ions away from cells. (ox.ac.uk)
  • CO(2)/HCO(3)(-) exerts a dual effect: as substrate for membrane-bound HCO(3)(-) transporters and as a mobile buffer for facilitating extracellular diffusion of H(+) ions extruded from cells. (ox.ac.uk)
  • PMID- 9339686 OWN - NLM STAT- MEDLINE DA - 19971114 DCOM- 19971114 LR - 20061115 PUBM- Print IS - 0028-3878 (Print) VI - 49 IP - 4 DP - 1997 Oct TI - Higher neonatal cerebral blood flow correlates with worse childhood neurologic outcome. (nih.gov)
  • Controversy exists regarding the effects of such low CBF on subsequent neurologic function. (nih.gov)
  • Bupivacaine may bind with low affinity to the Ca channel and also affect an unidentified metabolic component that modulates Ca channel function. (nih.gov)
  • Follow-up information at ages 4 to 12 years was obtained on all 26 subjects. (nih.gov)