Disease relevance of EPN 300

• Diabetics with mild or no distal polyneuropathy (DPN) had a median EPN score of 2.4 compared with 4.7 in those with overt DPN (p less than 0.0001) [1].
• In order to detail the characteristics of end-point (EPN) and rebound nystagmus (RN), two series of experiments were performed with infrared oculography for measurement of horizontal eye movements [2].
• Thus, EPN enables us to reveal the intrinsic toxicity of hydrophilic molecules which have a limited access to their intracellular targets [3].
• EPN impaired embryonic growth and was highly teratogenic: 37-42% of the surviving embryos at 18 days were abnormal with cervical and axial scoliosis as well as severe edema [4].
• It might be difficult to determine the point at which pyelonephritis develops into EPN or perinephric abscess [5].

High impact information on EPN 300

• Data reported here demonstrate that loss of Pyk2 kinase function results in induction of cell motility and migration in EPN cells, a line of non-transformed epithelial cells derived from human normal prostate tissue [6].
• A previous study on a double mutant EPN of hAFP suggested that the Ca(2+)-binding site of hAFP was the ice-binding site [7].
• The electropermeabilization (EPN) of living cells allows the uptake of non-permeant molecules and can reveal their potential activity on cells without the constraints of the plasma membrane crossing [3].
• Differential metabolism of O-ethyl O-4-nitrophenyl phenylphosphonothioate by rat and chicken hepatic microsomes [8].
• Malathion A and B esterases of mouse liver--II. Effect of EPN in vitro and in vivo [9].

Biological context of EPN 300

• For this reason, the effects of topical egg application on EPN were examined on mallard (Anas platyrhynchos) embryo development [4].
• Kinetic and distribution studies showed that EPN was eliminated from the tissues and plasma according to exponential kinetics [10].
• Delayed neurotoxicity was produced in cats following the administration of either a single dermal dose of 22.5 to 225 mg/kg (0.2 to 5.0 times the LD50) or subchronic (90 days) administration of 0.5 to 2.0 mg/kg of technical grade O-ethyl O-4-nitrophenyl phenylphosphonothioate (EPN) [11].
• RESULTS: In NPEC and in EPN treated with RA for up to 24 h, Western blot analyses of Erk1/2 phosphorylation show that RA causes a rapid activation of Erk1/2 within 5 min, which is maintained for 30 min, followed by a return to basal levels [12].
• Cell death due to the EPN procedure was less than 4% and more than 90% of cells were permeabilized [13].

Anatomical context of EPN 300

• Relative residence (RR) of EPN relative to plasma was longest in the sciatic nerve and shortest in the kidney [10].
• The disposition studies showed that EPN was the major compound identified 0.5 day after administration in the brain, spinal cord, sciatic nerve, adipose tissue, plasma, muscle, liver, and kidney [10].
• Only traces of EPN were detected in the urine and feces [10].
• After 70 passages, EPN cells did not undergo "Hayflike crisis" and were free of fibroblast contamination and were thus subcloned and characterized [14].
• Thus, the somatic projection to EPN seems to course directly from the thalamus or the reticular formation but not through the CN [15].

Associations of EPN 300 with other chemical compounds

• Equation (3) accurately predicted AChE inhibition by methamidophos, coumaphos and EPN, but not by acephate [16].
• When an inhibition study with the developed sensor was undertaken at the optimized AChE immobilization with varying concentrations of a model organophosphorus pesticide EPN and carbamate one carbofuran, a sensitive detection for them was possible with the limit of detection corresponding to 1.55x10(-8) and 1.30x10(-9)M, respectively [17].
• Selectivity of the ELISA indicates that the monoclonal antibody can readily distinguish the target pesticide from other structurally related analogs and some metabolites (oxon forms), with the exception of ethyl O-(p-nitrophenyl) phenyl phosphonothionate (EPN), parathion-methyl, and parathion [18].
• The EG complex was easily dissociated by administration of OPs, i.e. fenitrothion, EPN, phenthionate, and bis-beta-nitrophenyl phosphate (BNPP), and resulting beta-G dissociated was released into blood, leading to the rapid and transient increase of plasma beta-G level with a concomitant decrease of liver microsomal beta-G level [19].
• Thus, the single administration of EPN (O-ethyl O-p-nitrophenylphenylphosphonothioate), acephate and chlorpyrifos increased plasma BG activity in approximately 100-fold the control level in rats [20].

Gene context of EPN 300

• We examined the effect of estrogens on mitogen-activated protein kinase (MAPK) in EPN cells, a line of epithelial cells derived from human normal prostate [21].
• EPN cells in culture, as prostate epithelial cells in vivo, express high-molecular weight cytokeratin and Pyk2, whereas they do not express desmin [14].
• Xenobiotic-metabolizing capacity was temperature dependent, with enzymatic activity increasing as the temperature was increased from 28 to 34 to 37 degrees C, was inducible by Aroclor 1254 (a chemical inducer of cytochrome P450-dependent monooxygenase activity), and was reduced by EPN (an inhibitor of P450 activity) [22].
• Recoveries from 50 g unpolished rice samples fortified with 5-50 micrograms diazinon, 6-30 micrograms parathion, 8-40 micrograms fenitrothion and IBP, 10-50 micrograms dimethoate and fenthoate, 20-100 micrograms malathion, or 40-200 micrograms EPN ranged from 75.7 to 95.8% [23].

Analytical, diagnostic and therapeutic context of EPN 300

• Physiological disposition and metabolism of O-ethyl-O-4-nitrophenyl phenylphosphonothioate in male cats following a single dermal administration [10].
• Delayed neurotoxicity of O-ethyl O-4-nitrophenyl phenylphosphonothioate: subchronic (90 days) oral administration in hens [24].
• Electropermeabilization (EPN), also termed electroporation, is a physical method to overcome the barrier of the cell membrane by applying short and intense electric pulses [13].
• On the other hand, the spreading depression by microinjection of KCl 3M into the CN does not modify the ERs in EPN, but the spreading depression in EPN does modify the CN response [15].

References