The majority of the well-known pharmacogenomics research used in the medical sciences contributes to our understanding of medication interactions. It has a significant impact on treatment and drug development. The broad use of pharmacogenomics is required for the progress of therapy. The main focus is on how genes and an intricate gene system affect the body’s reaction to medications. Novel biomarkers that help identify a patient group that is more or less likely to respond to a certain medication have been discovered as a result of recent developments in the field of clinical therapeutics. It aims to improve customized therapy by giving the appropriate drug at the right dose at the right time and making sure that the right prescriptions are issued. A combination of genetic, environmental, and patient variables that impact the pharmacokinetics and/or pharmacodynamics of medications results in interindividual variance in drug response. Drug development, illness susceptibility, and treatment efficacy are all impacted by pharmacogenomics. The purpose of this work is to give a review that might serve as a foundation for the creation of new pharmacogenomics applications, techniques, or strategies.

To understand complex diseases, high-throughput data are generated at large and multiple levels. However, extracting meaningful information from large datasets for comprehensive understanding of cell phenotypes and disease pathophysiology remains a major challenge. Despite tremendous advances in understanding molecular mechanisms of cancer and its progression, current knowledge appears discrete and fragmented. In order to render this wealth of data more integrated and thus informative, we have developed a GECIP toolbox to investigate the crosstalk and the responsible genes’/proteins’ connectivity of enriched pathways from gene expression data. To implement this toolbox, we used mainly gene expression datasets of prostate cancer, and the three datasets were GSE17951, GSE8218, and GSE1431. The raw samples were processed for normalization, prediction of differentially expressed genes, and the prediction of enriched pathways for the differentially expressed genes. The enriched pathways have been processed for crosstalk degree calculations for which number connections per gene, the frequency of genes in the pathways, sharing frequency, and the connectivity have been used. For network prediction, protein–protein interaction network database FunCoup2.0 was used, and cytoscape software was used for the network visualization. In our results, we found that there were enriched pathways 27, 45, and 22 for GSE17951, GSE8218, and GSE1431, respectively, and 11 pathways in common between all of them. From the crosstalk results, we observe that focal adhesion and PI3K pathways, both experimentally proven central for cellular output upon perturbation of numerous individual/distinct signaling pathways, displayed highest crosstalk degree. Moreover, we also observe that there were more critical pathways which appear to be highly significant, and these pathways are HIF1a, hippo, AMPK, and Ras. In terms of the pathways’ components, GSK3B, YWHAE, HIF1A, ATP1A3, and PRKCA are shared between the aforementioned pathways and have higher connectivity with the pathways and the other pathway components. Finally, we conclude that the focal adhesion and PI3K pathways are the most critical pathways, and since for many other pathways, high-rank enrichment did not translate to high crosstalk degree, the global impact of one pathway on others appears distinct from enrichment.

Background: Iron deficiency anemia (IDA) is a global health problem affecting the quality of life of more than 2 billion individuals. The current practice guidelines diagnose and monitor IDA via conventional hematological and iron biomarkers, which take several months before they are corrected under an iron-treatment plan. Reticulocyte hemoglobin equivalent (Ret-He) is used as a marker in most new hematology analyzers to assess iron incorporation into erythrocyte hemoglobin directly. This study aims to examine the efficacy of Ret-He as a marker for iron deficiency (ID) and IDA and investigate whether Ret-He is sensitive to iron therapy. Methods: Two blood samples were drawn from 182 participants for CBC and iron profile measurements. Follow-up samples were drawn from participants with a confirmed diagnosis of ID and/or IDA. Results: Ret-He levels were lower in the ID and IDA groups compared to the control (p < 0.0001), and lower in the IDA group compared to the ID group (p < 0.0001). Ret-He was correlated with ferritin at ID level (<30.0 mg/mL; r = 0.39) and severe IDA (<13.0 ng/mL; p-value < 0.01, r = 0.57). Cut-off values of <28.25 pg for ID and <21.55 pg for IDA showed a higher specificity and sensitivity (ID; AUC: 0.99, sensitivity: 92.73%, specificity: 97.87%) and (IDA; AUC: 0.94, sensitivity: 90.63%, specificity: 92.31%). Finally, Ret-He successfully reflected the iron therapy (p < 0.001) when compared to hemoglobin (Hb) (p = 0.1). Conclusions: Ret-He is a potential marker for detecting and diagnosing different stages of ID with high validity and is very sensitive in reflecting the iron incorporation in a short time.

Immunization is the ultimate objective to ensure safe return, for schools and jobs to be open. Fortunately, the government of Saudi Arabia had announced that Clinical trials for SARS-CoV-2 will start in August 2020. There is need to evaluate immune response among vaccinated individuals and recovered patients. The market is full of different commercial tests promoted for the health care providers. An accurate selection of tests is crucial specially that are approved by international authorities the FDA-CDC. By August 2020, forty-seven serology tests were authorized by the FDA-CDC under the -EAU emergency. The accuracy and reliability of the serological tests is reflected by the sensitivity and specificity of the test. However, serological testing has an inherent problem of false positive and false negative that are associated with tests. Therefore, the sensitivity and specificity values are not enough indicators for the interpretation of the results specially in variation of the prevalence rate. The positive predictive value (PPV) was calculated from sensitivity and specificity of 47 tests at different prevalence rates to show its effect on the interpretation of results at different populations. In conclusion, it is time to use serological testing for the public to return to normal life. Selecting the proper serological kit depends heavily on the specificity, more than the sensitivity, of the test and the prevalence of the disease among the group tested. In lower prevalence population use two kits to increase the PPV and reliability of the results.

Infectious diseases remain a leading cause of morbidity and mortality worldwide, driven by a wide range of potential infectious agents, including bacteria, viruses, fungi, protozoa, and helminths. These pathogens can invade and multiply within human hosts, causing illnesses that range from mild to life-threatening. Emerging and re-emerging infectious diseases, such as COVID-19, Ebola, and antibiotic-resistant bacterial infections, highlight the dynamic interaction between humans, microbes, and environmental factors. Zoonotic transmission, global travel, urbanization, and climate change contribute to the increased incidence and spread of infectious agents. Understanding the biology, transmission pathways, and pathogenic mechanisms of these agents is crucial for developing effective prevention, diagnosis, and treatment strategies. This review provides an overview of major classes of infectious agents, the diseases they cause, and the global challenges in managing infectious threats to public health.

The Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway is an essential cell signaling system that plays a significant role in the production of blood cells and regulates the growth, differentiation, and function of immune cells. Numerous hematological disorders can result from mutations that target this system, which can cause an excess of these cell types. This commentary perspectives JAKs in leukemia and also in chronic myeloid leukemia. This commentary also covers the relevant mutations and drug-targets for JAKs as well as the current therapeutic strategies for preventing constitutive, cytokine-independent pathway activation.