Author: Dr. Bashar Mudhaffar Abdullah

This study aims to estimate a simple, rapid and sensitive method for a trace amount of atropine (ATR) in medicinal compounds. Two approaches were followed to accomplish this aim, i.e., spectrophotometric determination of pure ATR and pharmaceutical preparations using SbI42− ion as a new reagent. The procedure involves the implementation of an ion-association complex with this alkaloid. The resulting complex was extracted and detected spectrophotometrically at 492 nm. Appropriate parameters were investigated, including the ion SbI42− concentration and the pH value of the complex formation. Using chloroform to extract the complex, taking into consideration extraction time and volume of solvent used. The calibration graph is linear in the ranges of 0.5–5.0 × 10−3 M. Precision, accuracy, detection limit, and RSD %, as well as relative standard deviation (n = 5), were calculated. The test sensitivity was 0.013 μg cm−2. Several interference additives were studied by investigating the effect of equal and duplicate quantities of some common excipients on selectivity, such as starch, glucose, lactose, glycerin, and talc. The molar ratio of the SbI42−_ATR was determined. The amount of ATR in the pharmaceutical tablets and eye drop preparation was calculated using Erel at ratios of 2.24 and 2.75%, respectively.

The study of anaemia is a well-developed discipline where the concepts of precision medicine have, in part, been researched extensively. This review discusses the treatment of ery thropoietin (EPO) deficiency anaemia and resistance in cases of chronic kidney disease (CKD). Traditionally, erythropoietin-stimulating agents (ESAs) and iron supplementation have been used to manage anaemia in cases of CKD. However, these treatments pose potential risks, including cardiovascular and thromboembolic events. Newer treatments have emerged to address these risks, such as slow-release and low-dosage intravenous iron, oral iron supplementation, and erythropoietin iron combination therapy. Another novel approach is the use of hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs). This review highlights the need for precision medicine targeting the genetic components of EPO deficiency anaemia in CKD and discusses individual variability in genes such as the erythropoietin gene (EPO), the interleukin-gene (IL-), and the hypoxia-inducible factor gene (HIF). Pharmacogenetic testing aims to provide targeted therapies and interventions that are tailored to the specific characteristics of an individual, thus optimising treatment outcomes and minimising resistance and adverse effects. This article concludes by suggesting that receptor modification has the potential to revolutionise the treatment outcomes of patients with erythropoietin deficiency anaemia through the integration of the mentioned approach.

Type 2 diabetes mellitus (T2DM) is characterized by impaired insulin secretion on a background of insulin resistance (IR). IR and T2DM are associated with atherosclerotic coronary artery disease (CAD). The mechanisms of IR and atherosclerosis are known to share similar genetic and environmental roots. Endothelial dysfunction (ED) detected at the earliest stages of IR might be the origin of atherosclerosis progression. ED influences the secretion of pro-inflammatory cytokines and their encoding genes. The genes and their single nucleotide polymorphisms (SNPs) act as potential genetic markers of IR and atherosclerosis. This review focuses on the link between IR, T2DM, atherosclerosis, CAD, and the potential genetic markers CHI3L1, CD36, LEPR, RETN, IL-18, RBP-4, and RARRES2 genes