Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.22.61 (caspase-8)
 6,833 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Layered double hydroxide of Mg-Al-carbonate system (MACH) was prepared and its heat-treated product (MACHT) was obtained by calcination at 500 degrees C. The resulting materials were used as an adsorbent for removal of color from synthetic textile wastewater (STW) and textile wastewater (TWW). Batch kinetic study showed that these materials are an efficient adsorbent for textile dye. The maximum adsorption capacities between 16 to 32 mg of dyes per g of adsorbent was obtained by fitting the adsorption data to the Langmuir adsorption Isotherm. It was found that the adsorption capacity of MACHT is higher than MACH.
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PMID:The use of Mg/Al layered double hydroxide for color removal of textile wastewater. 1141 39

Bicarbonate transport (BT) has been previously shown to participate in apoptosis induced by various stress factors. However, the precise role of BT in ischaemia-induced apoptosis is still unknown. To investigate this subject, rat coronary endothelial cells (EC) were exposed to simulated ischaemia (glucose free anoxia at Ph 6.4) for 2 hrs and cells undergoing apoptosis were visualized by nuclear staining or by determination of cas-pase- 3 activity. To inhibit BT, EC were either treated with the inhibitor of BT 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS, 300 mumol/l) or exposed to ischaemia in bicarbonate free, 4-(2-hydroxyethyl)-I-piperazi-neethanesulphonic acid (HEPES)-buffered medium. Simulated ischaemia in bicarbonate-buffered medium (Bic) increased caspase-3 activity and the number of apoptotic cell (23.7 + 1.4%versus 5.1 + 1.2% in control). Omission of bicarbonate during ischaemia further significantly increased caspase-3 activity and the number of apoptotic cells (36.7 1.7%). Similar proapoptotic effect was produced by DIDS treatment during ischaemia in Bic, whereas DIDS had no effect when applied in bicarbonate-free, HEPES-buffered medium (Hep). Inhibition of BT was without influence on cytosolic acidification during ischaemia and slightly reduced cytosolic Ca(2+) accumulation. Initial characterization of the underlying mechanism leading to apoptosis induced by BT inhibition revealed activation of the mitochondrial pathway of apoptosis, i.e., increase of cytochrome C release, depolarization of mitochondria and translocation of Bax protein to mitochondria. In contrast, no activation of death receptor-dependent pathway (caspase-8 cleavage) and endoplasmic reticulum- dependent pathway (caspase-12 cleavage) was detected. In conclusion, BT plays an important role in ischaemia-induced apoptosis of coronary EC by suppression of mitochondria-dependent apoptotic pathway.
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PMID:Importance of bicarbonate transport for ischaemia-induced apoptosis of coronary endothelial cells. 1776 Aug 41