Search results for: RLMS

Authors: Marina Kartseva, Polina Kuznetsova

Abstract:

In our work, we estimate the contribution of inequality of opportunity to inequality in the health of the Russian population aged 25 to 74 years. The empirical basis of the study is the nationally representative data of the RLMS for 2018. Individual health is measured using a self-reported status on five-point scale. The startconditions are characterized by parental education and place of birth (country, type of settlement). Personal efforts to maintain health include the level of education, smoking status, and physical activity. To understand how start opportunities affect an individual's health, we use the methodology proposed in (Trannoy et al., 2010), which takes into account both direct and indirect (through the influence on efforts) effects. Regression analysis shows that all other things being equal, the starting capabilities of individuals have a significant impact on their health. In particular, parental education has a positive effect on self-reported health. Birth in another country, in another settlement, and in an urban area, on the contrary, reduceself-reported health. This allows to conclude that there exists an unfair inequality in health, namely inequality caused by factors that are independent of a person's own efforts. We estimate the contribution of inequality of opportunity to inequality in health using a nonparametric approach (Checchi, Peragine, 2010; Lazar, 2013). According to the obtained results, the contribution of unfair inequality as 72-74% for the population as a whole, being slightly higher for women (62-74% and 60-69% for men and women, respectively) and for older age (59- 62% and 67-75% for groups 25-44 years old and 45-74 years old, respectively). The obtained estimates are comparable with the results for other countries and indicate the importance of the problem of inequality of opportunities in health in Russia.

Keywords: inequality of opportunity, inequality in health, self-reported health, efforts, health-related lifestyle, Russia, RLMS

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Authors: Adnan A. Kadi, Nasser S. Al-Shakliah, Haitham Al-Rabiah

Abstract:

Zorifertinib is a novel, potent, oral, a small molecule used to treat non-small cell lung cancer (NSCLC). zorifertinib is an Epidermal Growth Factor Receptor (EGFR) inhibitor and has good blood–brain barrier permeability for (NSCLC) patients with EGFR mutations. zorifertinibis currently at phase II/III clinical trials. The current research reports the characterization and identification of in vitro, in vivo and reactive intermediates of zorifertinib. Prediction of susceptible sites of metabolism and reactivity pathways (cyanide and GSH) of zorifertinib were performed by the Xenosite web predictor tool. In-vitro metabolites of zorifertinib were performed by incubation with rat liver microsomes (RLMs) and isolated perfused rat liver hepatocytes. Extraction of zorifertinib and it's in vitro metabolites from the incubation mixtures were done by protein precipitation. In vivo metabolism was done by giving a single oral dose of zorifertinib(10 mg/Kg) to Sprague Dawely rats in metabolic cages by using oral gavage. Urine was gathered and filtered at specific time intervals (0, 6, 12, 18, 24, 48, 72,96and 120 hr) from zorifertinib dosing. A similar volume of ACN was added to each collected urine sample. Both layers (organic and aqueous) were injected into liquid chromatography ion trap mass spectrometry(LC-IT-MS) to detect vivozorifertinib metabolites. N-methyl piperizine ring and quinazoline group of zorifertinib undergoe metabolism forming iminium and electro deficient conjugated system respectively, which are very reactive toward nucleophilic macromolecules. Incubation of zorifertinib with RLMs in the presence of 1.0 mM KCN and 1.0 Mm glutathione were made to check reactive metabolites as it is often responsible for toxicities associated with this drug. For in vitro metabolites there were nine in vitro phase I metabolites, four in vitro phase II metabolites, eleven reactive metabolites(three cyano adducts, five GSH conjugates metabolites, and three methoxy metabolites of zorifertinib were detected by LC-IT-MS. For in vivo metabolites, there were eight in vivo phase I, tenin vivo phase II metabolitesofzorifertinib were detected by LC-IT-MS. In vitro and in vivo phase I metabolic pathways wereN- demthylation, O-demethylation, hydroxylation, reduction, defluorination, and dechlorination. In vivo phase II metabolic reaction was direct conjugation of zorifertinib with glucuronic acid and sulphate.

Keywords: in vivo metabolites, in vitro metabolites, cyano adducts, GSH conjugate

Procedia PDF Downloads 177