|1.||Renard, Patricia: 3 articles (01/2003 - 01/2002)|
|2.||Ninane, Noelle: 3 articles (01/2003 - 01/2002)|
|3.||Raes, Martine: 3 articles (01/2003 - 01/2002)|
|4.||Michiels, Carine: 3 articles (01/2003 - 01/2002)|
|5.||Buck, Leslie Thomas: 2 articles (10/2010 - 09/2005)|
|6.||Mottet, Denis: 2 articles (01/2003 - 11/2002)|
|7.||Michel, Gaetan: 2 articles (01/2003 - 11/2002)|
|8.||Wang, Yue: 1 article (09/2015)|
|9.||Dufour, Inès: 1 article (09/2015)|
|10.||Iwata, Yuko: 1 article (09/2015)|
|1.||Brain Ischemia (Cerebral Ischemia)
12/01/2006 - "BAPTA-AM is the acetoxymethylester of the calcium chelator BAPTA and has demonstrated efficacy in several animal models of cerebral ischemia. "
11/15/2010 - "BAPTA free acid was identified as the main metabolic product of 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(actoxymethyl ester) (BAPTA-AM), a neuroprotective agent in cerebral ischemia, in rats. "
10/22/2004 - "Like hypoxia, BAPTA stimulated HIF-1-dependent transcription by increasing the activity of the C-terminal transactivation domain of HIF-1alpha and greatly enhanced expression of the HIF-1 target gene CA9. "
11/01/1997 - "Loading hearts with BAPTA prior to anoxia failed to reduce NA overflow (1561 +/- 147 vs 1496 +/- 206 pmol/g over 40 min). "
12/01/1996 - "Hypoxia in the absence of external Ca2+ did not cause any detectable signs of damage in BAPTA-loaded slices. "
11/01/1997 - "1. Ischaemia and anoxia induce excessive noradrenaline (NA) release in the heart by a mechanism independent of both nerve activity and extracellular Ca2+. The present study was designed to examine the potential role of intracellular Ca2+ mobilization in anoxic NA release in the heart by chelating intracellular free Ca2+. 2. In normoxic hearts, preloading with an intracellular free Ca2+ chelator (BAPTA) reduced neuronal NA release by 65%, confirming the effectiveness of the loading protocol. "
10/22/2004 - "Knock down of HIF-1alpha mRNA and protein by small interference RNA for HIF-1alpha revealed that both hypoxia and the BAPTA-induced gene expression of CA9 were strictly dependent on HIF-1alpha. "
11/01/2011 - "Furthermore, I(Ca,L) increased with time after patch rupture in LDS cardiomyocytes dialyzed with pipette solution containing BAPTA whereas not at EDS. "
09/01/1988 - "4. When several minutes had elapsed following rupture of the patch, to allow a substantial amount of BAPTA into the cell (ca. 10 mM in the patch pipette), the second component was slowed by a factor of about 20-fold, while the first component continued to have the same rapid time course as the solution change. "
03/01/1986 - "Similar results were obtained when EGTA was used in place of BAPTA, and also in the few cases when successful rupture of the outer segment membrane was obtained. "
03/01/1986 - "When the patch pipette contained no added calcium and 10 mM of the calcium chelator BAPTA (1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid) (free Ca2+ ca. 10(-9) M) rupture of the patch led, over a period of a few minutes, to an increase in mean dark current, an increased duration of responses, a substantial increase in flash sensitivity, and a pronounced overshoot in the recovery phase, but with virtually no change in the rising phase of the response to bright flashes. "
08/01/2001 - "The L-type Ca2+ current [I(Ca(L))] increases with time after patch rupture in guinea pig ventricular myocytes dialyzed with pipette solutions containing > or =20 mM 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid ([BAPTA]pip). "
09/01/2015 - "In fibres overexpressing TRPV2-DN as well as in fibres in which Ca(2+) transients were abolished by the Ca(2+) chelator BAPTA, the level of P-SPAK(Ser373) in response to hyperosmotic shock was reduced, suggesting a modulation of SPAK phosphorylation by intracellular Ca(2+) . "
08/01/1998 - "The intracellular Ca2+ chelator, BAPTA, also inhibited the RVD response to hypotonic shock. "
01/01/2000 - "Removal of external Ca2+ and treatment with BAPTA or H89 prior to exposure to sublethal heat shock that reduced the amount of HSP-72 and -90 production still protected cells from subsequent thermal injury. "
01/01/2000 - "The synthesis of both HSP-72 and -90 was attenuated when cells were exposed to heat shock in medium devoid of Ca2+ or pretreated with the calcium chelator BAPTA for 30 min prior to heat shock. "
09/01/1999 - "Pretreatment of the cells with BAPTA or GF-109203X for 30 min or a sublethal heat shock to allow HSP-72 overexpression led to an attenuation of the increase in [Ca2+]i by a subsequent heat shock. "
02/08/2008 - "Ischemia-induced functional deterioration at Purkinje neurons was accompanied by cytoplasm Ca(2+) rise and prevented by BAPTA infusion. "
01/01/1999 - "Neither intracellular BAPTA, a Ca2+ chelator, nor incubation of the slices in low-Ca2+-containing solutions affected the ischemia-induced depolarization, whereas it was reduced by lowering the external Na+ concentration. "
10/26/2005 - "Ischemia in Ca2+-free (plus BAPTA) perfusate resulted in a smaller but consistent Ca2+ increase monitored by Oregon Green 488 BAPTA-1, indicating release from intracellular sources. "
07/01/2005 - "Low extracellular calcium (100 nM) or increase of intracellular calcium buffering ability by BAPTA-acetoxymethyl ester significantly reduced ischemia-induced neuronal damage. "
12/01/2006 - "The intracellular calcium chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, 1mM, but not the N-methyl-d-asparate receptor antagonist, MK-801, 1muM, prevented the translocation of beta(1) isoform observed during ischemia. "
|2.||1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester
|5.||gluconic acid (gluconate)
|6.||barium chloride (barium dichloride)
|7.||1,2- bis(2- aminophenoxy)ethane- N,N,N',N'- tetraacetic acid (BAPTA)
|8.||Egtazic Acid (EGTA)
|9.||Messenger RNA (mRNA)
|10.||Calmodulin (Calcium-Dependent Activator Protein)
|4.||Coronary Artery Bypass (Coronary Artery Bypass Surgery)