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A Reshef

Publications and source records attributed to A Reshef.

103 records · Page 6Linked to original sources

The adenosine-induced mechanism for the acquisition of ischemic tolerance in primary rat neuronal cultures.

Neurons can be preconditioned by various procedures to resist ischemic insult. The preconditioning mechanism induced by adenosine ("the adenosine mechanism") was characterized in primary rat neuronal cultures, employing a model of chemical ischemia. The protective mechanism, initiated by activation of adenosine receptors, consists of a signal transduction pathway, involving activation of protein kinase C (PKC) and opening of ATP-sensitive potassium (K(ATP)) channels. Direct activation (and inhibition) of PKC, as well as opening of K(ATP) channels, also confers protection. The opening of the K(ATP) channels mediates the signal activated by the adenosine receptors, and probably also that activated by PKC. The acquired ischemic resistance lasts up to 5 days, depending on the activating substance. The adenosine-activated cascade of events leading to ischemic tolerance in neurons is similar to that operating in cardiomyocytes.

Adenosine↗

The use of acid phosphatase test papers for DNA profiling.

The acid phosphatase (AP) test is a routine assay used to screen casework items for the possible presence of semen. This colour test is carried out on filter paper which is retained after testing. Two-year-old AP test papers were found to contain sufficient DNA for short tandem repeat (STR) profiling. Prior to polymerase chain reaction (PCR) amplification, the DNA was preferentially separated into sperm depleted and sperm enriched cell fractions. The implication of these findings for past and present cases is discussed.

Acid Phosphatase↗

Expression of lipoprotein lipase mRNA in rat heart is localized mainly to mesenchymal cells as studied by in situ hybridization.

The expression of lipoprotein lipase mRNA (LPL mRNA) was studied in rat hearts by use of a sulfur-35-labeled antisense mRNA probe. Rats were studied under three conditions: fed, fasted, and injected with cholera toxin (an irreversible agonist of adenylate cyclase) and then fasted. The highest LPL activity was found in the hearts of cholera toxin-injected, fasted rats. After injection of cholera toxin, LPL mRNA levels were 3.5-fold higher than those from fed rats. Using in situ hybridization, we studied the site of expression of LPL mRNA under the same three experimental conditions. In sections of hearts from cholera toxin-injected, fasted rats, concentrations of autoradiographic grains, representing the site of LPL mRNA, were seen over interstitial elements, which comprise capillary and perivascular cells. A more diffuse and sparse reaction was seen over cardiac myocytes and was not always distinguishable from background. A similar but much less definitive localization was seen in sections of hearts from fasted rats. The present results indicate that in the rat heart, the main site of LPL synthesis and processing, especially after stimulation with an irreversible agonist of adenylate cyclase, is localized to interstitial elements rather than to adult cardiac myocytes.

Adenylyl Cyclase Inhibitors↗