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https://www.selleckchem.com/products/icg-001.html The study aims to investigate maternal serum levels of asymmetric dimethylarginine (ADMA) in preeclampsia. Serum samples were collected from 57 women with preeclamptic pregnancies and 30 women with normal pregnancies during the third trimester. ADMA levels were measured with the ELISA method. ADMA levels in preeclamptic pregnancies were significantly higher when compared with normal pregnancies (2.35 ± 3.20 nmol/l versus 0.35 ± 0.10 nmol/l; p  less then  .05). ADMA levels show a significant positive correlation with systolic and diastolic pressure, urea, and creatinine but a negative correlation with proteinuria. ADMA levels have a significant strong correlation with PE. ADMA levels are significantly higher in preeclamptic pregnancy compared with normal pregnancy.1. The absorption, distribution, metabolism, elimination, and drug-drug interaction (DDI) potential of the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib was characterised in vitro.2. Rucaparib showed moderate cellular permeability, moderate human plasma protein binding (70.2%), and slow metabolism in human liver microsomes (HLMs). In HLMs, cytochrome P450 (CYP) 1A2 and CYP3A contributed to the metabolism of rucaparib to its major metabolite M324 with estimated fractions of metabolism catalysed by CYP (fm,CYP) of 0.27 and 0.64, respectively. Rucaparib reversibly inhibited CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3As (IC50, 3.55, 12.9, 5.42, 41.6, and 17.2-22.9 µM [2 substrates], respectively), but not CYP2B6 or CYP2C8 (>190 µM). No time-dependent inhibition of any CYP was observed. In cultured human hepatocytes, rucaparib showed concentration-dependent induction of CYP1A2 mRNA and downregulation of CYP3A4 and CYP2B6 mRNA. In transfected cells expressing drug transporters, rucaparib was a substrate for P-gp and BCRP, but not for OATP1B1, OATP1B3, OAT1, OAT3, or OCT2. Rucaparib inhibited P-gp and BCRP (IC50, 169 and 55 µM, respectively) and slightly inh

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