ABSTRACT
Ferroptosis is a form of iron-dependent regulated cell death. Evidence of its existence and the effects of its inhibitors on subarachnoid hemorrhage (SAH) is still lacking. In the present study, we found that liproxstatin-1 protected HT22 cells against hemin-induced injury by protecting mitochondrial functions and ameliorating lipid peroxidation. In in vivo experiments, we demonstrated the presence of characteristic shrunken mitochondria in ipsilateral cortical neurons after SAH. Moreover, liproxstatin-1 attenuated the neurological deficits and brain edema, reduced neuronal cell death, and restored the redox equilibrium after SAH. The inhibition of ferroptosis by liproxstatin-1 was associated with the preservation of glutathione peroxidase 4 and the downregulation of acyl-CoA synthetase long-chain family member 4 as well as cyclooxygenase 2. In addition, liproxstatin-1 decreased the activation of microglia and the release of IL-6, IL-1β, and TNF-α. These data enhance our understanding of cell death after SAH and shed light on future preclinical studies.
ABSTRACT
To describe the development and implementation of pharmaceutical care services in an in-patient setting, and to examine the effectiveness of pharmacist interventions. A single-center, 2-phase [pre-/post-intervention phase] design was performed in an intensive care unit [ICU] of a university-affiliated hospital. Patients in the post-intervention phase [March 2011 to June 2011] received pharmaceutical care from a clinical pharmacist, while patients in the pre-intervention phase [December 2010 to March 2011] received routine medical care. The pre- and post-intervention phases were then compared to evaluate the outcomes of pharmacist interventions. During the 3-month study period, the clinical pharmacist made 232 interventions for 416 admitted patients; of these, 202 [87.1%] were accepted by physicians or nurses, and dosage adjustment [n=83, [35.8%]] was the type of intervention implemented most often. In the group that received the participation of pharmacists, medication errors per patient decreased from 1.68 to 0.46 [p 0.001]; medication errors, of incorrect dose or dosing interval, were markedly improved [decreased from 0.87 to 0.14; p<0.001], the drug cost per patientday decreased from $347.43 to $307.36 [p=0.095], and the length of ICU stay did not change significantly [6.14 days versus 5.93 days; p=0.14]. The presence of the pharmacist in the ICU resulted in significant reduction of medication errors and had potential drug-cost-saving effects, but did not have an influence on decreasing the length of ICU stay
Subject(s)
Humans , Male , Female , Middle Aged , Aged , Aged, 80 and over , Intensive Care Units , Pharmacists , Medication ErrorsABSTRACT
To assess the influence of cyclosporin A (CsA) and tacrolimus (FK506) on mycophenolic acid (MPA) and correlation analysis of the pharmacokinetic parameters and patient characteristics, clinical outcome in Chinese kidney transplant recipients, the pharmacokinetics of 1000 mg mycophenolate mofetil (MMF) twice daily was measured by high-performance liquid chromatography (HPLC). PKS (Pharmaceutical Kinetics Software) 1.0.2 software package was used for the calculation of pharmacokinetic parameters. The mean C(max), t(max), and AUC((0-12))were (21.88+/-10.52) microg/ml, (1.20+/-0.95) h, and (52.546+/-13.215) microg.h/ml, respectively. The level of AUC((0-12)) in the FK506 group was significantly higher than that in the CsA group. MPA appeared not to be affected by renal function. MPA AUC((0-12)) showed statistically significant difference according to the patient's gender.
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Cyclosporine , Immunosuppressive Agents , Pharmacokinetics , Kidney Transplantation , Physiology , Mycophenolic Acid , Pharmacokinetics , TacrolimusABSTRACT
<p><b>OBJECTIVE</b>To study the determination of desloratadine in human serum and its pharmacokinetics in healthy volunteers.</p><p><b>METHODS</b>A single oral dose of 10 mg desloratadine was given to 18 healthy volunteers. The serum concentrations of desloratadine were determined by HPLC-MS assay. The pharmacokinetics parameters of desloratadine tablets were calculated with program 3P97.</p><p><b>RESULT</b>The main pharmacokinetics parameters of desloratadine tablets were as followsút(max)(1.611 +/-0.366)h, C(max) (4.455+/-1.990)microg x L(-1), AUC(0-t) (58.50+/-21.34)microg x L(-1) x h(-1), AUC(0-infinity) (60.59+/-22.32)microg x L(-1) x h(-1), t(1/2(ke)) (20.303+/-5.833)h, Ke (0.0372+/-0.0116)h(-1) and CL(0.1838+/-0.0563)L x h(-1).</p><p><b>CONCLUSION</b>Desloratadine tablet is absorbed quicker in the 18 healthy volunteers than the reports and its peak blood concentration reached at 1.5 h after oral administration with t(1/2) 20 h.</p>