Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.99.3 (PRE)
 1,923 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirteen patients undergoing cardiac surgery were studied to examine whether beta-adrenergic desensitization occurs in the perioperative period surrounding cardiac surgery, using peripheral blood lymphocytes as a model. Lymphocytes were isolated before induction of anesthesia (PRE) and on the morning of the first postoperative day (POST). Cyclic adenosine monophosphate (cAMP) production from the lymphocytes was assayed in the untreated (BASAL) state, and after treatment with 5 microM isoproterenol, 10 microM prostaglandin E1, or 20 mM sodium fluoride with 10 microM AlCl3 (NaF). All cAMP values are reported as picomoles per 10(6) cells, mean +/- SEM. BASAL cAMP production did not change significantly between the PRE and POST samples (PRE, 1.2 +/- 0.1; POST, 1.0 +/- 0.1). Isoproterenol-stimulated cAMP was significantly lower postoperatively (PRE, 8.36 +/- 0.9; POST, 5.1 +/- 0.5; P less than 0.005). Prostaglandin E1-stimulated cAMP did not change (PRE, 21.7 +/- 2.4; POST, 25.3 +/- 2.5), and NaF-stimulated cAMP was increased postoperatively (PRE, 8.8 +/- 1.6; POST, 14.3 +/- 2.0; P less than 0.05). These findings suggest that cardiac surgery and/or cardiopulmonary bypass results in significant desensitization of the beta-adrenergic receptor/adenylate cyclase system of lymphocytes, which may parallel changes in the adrenergic response of other organ systems.
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PMID:Cardiac surgery causes desensitization of the beta-adrenergic receptor system of human lymphocytes. 130 62

It has been postulated that at least part of the loss of cognitive function in aging may be the result of deficits in Ca(2+) recovery (CAR) and increased oxidative/inflammatory (OX/INF) stress signaling. However, previous research showed that aged animals supplemented with blueberry (BB) extract showed fewer deficits in CAR, as well as motor and cognitive functional deficits. A recent subsequent experiment has shown that DA- or Abeta(42)-induced deficits in CAR in primary hippocampal neuronal cells (HNC) were antagonized by BB extract, and (OX/INF) signaling was reduced. The present experiments assessed the most effective BB polyphenol fraction that could protect against OX/INF-induced deficits in CAR, ROS generation, or viability. HNCs treated with BB extract, BB fractions (e.g., proanthocyanidin, PAC), or control medium were exposed to dopamine (DA, 0.1 mM), amyloid beta (Abeta(42), 25 muM) or lipopolysaccharide (LPS, 1 microg/mL). The results indicated that the degree of protection against deficits in CAR varied as a function of the stressor and was generally greater against Abeta(42) and LPS than DA. The whole BB, anthocyanin (ANTH), and PRE-C18 fractions offered the greatest protection, whereas chlorogenic acid offered the lowest protection. Protective capabilities of the various fractions against ROS depended upon the stressor, where the BB extract and the combined PAC (high and low molecular weight) fraction offered the best protection against LPS and Abeta(42) but were less effective against DA-induced ROS. The high and low molecular weight PACs and the ANTH fractions enhanced ROS production regardless of the stressor used, and this reflected increased activation of stress signals (e.g., P38 MAPK). The viability data indicated that the whole BB and combined PAC fraction showed greater protective effects against the stressors than the more fractionated polyphenolic components. Thus, these results suggest that, except for a few instances, the lesser the polyphenolic fractionation, the greater the effects, especially with respect to prevention of ROS and stress signal generation and viability.
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PMID:Differential protection among fractionated blueberry polyphenolic families against DA-, Abeta(42)- and LPS-induced decrements in Ca(2+) buffering in primary hippocampal cells. 2059 78