Share This Author
Hallucinogenic drug interactions at human brain 5-HT2 receptors: implications for treating LSD-induced hallucinogenesis
The hypothesis that the hallucinogenic effects of these drugs in humans are mediated in whole or in part via 5-HT2 receptors is supported and treatment with 5- HT2 receptor antagonists may be effective in reversing the halluc inogenic effects caused by the ingestion, of LSD and LSD-like drugs.
The value of serial plasma nuclear and mitochondrial DNA levels in patients with acute ischemic stroke.
Multiple effects of 1-[β-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole hydrochloride (SKF 96365) on Ca2+ signaling in MDCK cells: depletion of thapsigargin-sensitive Ca2+ store…
- C. Jan, C. Ho, S. -. Wu, C. Tseng
- Biology, ChemistryNaunyn-Schmiedeberg's Archives of Pharmacology
- 25 January 1999
It is found that besides its well-known inhibitory action on capacitative Ca2+ entry in many cell types, in MDCK cells SKF 96365 exerted multiple and complex effects on Ca2- signaling.
Inhibitory effects of berberine on voltage- and calcium-activated potassium currents in human myeloma cells.
The value of leukocyte adhesion molecules in patients after ischemic stroke
The expressions of leukocyte adhesion molecules on admission are significantly increased in patients with acute ischemic stroke and higher neutrophil PSGL-1 expression on admission may imply a higher risk for END and that monocyte Mac-1expression on admission reflects the severity of isChemic stroke on admission.
Cardiovascular effects of nitric oxide and adenosine in the nucleus tractus solitarii of rats.
A reciprocal attenuation of adenosine receptor antagonist and NO synthase inhibitor on L-arginine and adenosines responses, respectively, in the NTS is demonstrated and implicate an interaction between NO andAdenosine in central cardiovascular regulation.
Safrole-induced cellular Ca2+ increases and death in human osteosarcoma cells.
Mechanism of rise and decay of thapsigargin-evoked calcium signals in MDCK cells.
Multiple effects of econazole on calcium signaling: depletion of thapsigargin-sensitive calcium store, activation of extracellular calcium influx, and inhibition of capacitative calcium entry.
Calmidazolium-induced rises in cytosolic calcium concentrations in Madin Darby canine kidney cells.
Calmidazolium induced internal Ca(2+) release in a manner dependent on phospholipases C- and A(2)-coupled events and thapsigargin-sensitive Ca( 2+) store was the source of calmidrazolium-induced Ca(1+) release.