Background: Bacopa monnieri is an herbal plant used predominantly in Ayurvedic medicine. Though this plant has pharmacological properties, it is pivotal to acknowledge its antioxidant capacity and toxicological properties which are not well established. Objectives: The principal aim of this study is to elucidate the antioxidant capacity and toxicological properties of B. monnieri leaf extracts in the early life stages of Danio rerio (zebrafish) embryos. Methods: This was a comparative identification of the antioxidant capacities of five different extracts of aqueous, ethanol, acetone, chloroform, and petroleum ether of B. monnieri leaf by investigating through in vitro antioxidant assays such as Diphenyl-1-Picrylhydrazyl (DPPH), azinobis[3-Ethylbenzothiazoline-6-Sulfonate] (ABTS), ferric reducing antioxidant power (FRAP), and total antioxidant capacity (TAC) and enzymatic assays such as SOD, CAT, Px, AO, and PPO. Additionally tested for the qualitative and quantitative estimation of phytochemicals. Furthermore, the Fish Embryo Toxicity (FET) assay has been performed to analyze the developmental deformities, lethal and sublethal toxic effects, hatch rate, heart rate, and survival of zebrafish embryos upon treatment with the aqueous plant extract. Result: The results showed the availability of polyphenols and non-phenolic macromolecules. Total phenol and flavonoid content were greater in the aqueous extract and tannin content was higher in ethanol extract. Among the five extracts, the aqueous extract showed greater antioxidant and free radical scavenging activities. Furthermore, the investigation addressed the toxicological effects of aqueous extract on zebrafish embryos that resulted in the least developmental abnormalities and delayed hatching rate at greater concentrations along with 100% mortality at 96 h Post Fertilization (hpf) of higher concentrations. Conclusion: The results indicate that B. monnieri may serve a strong prophylactic action against reactive oxygen species-related diseases with the least sublethal effects.

Acute myeloid leukemia (AML) is a severe blood cancer in myeloid cells which is found to be developed due to mutation in genes that causes dysregulation in the gene’s expression, affecting the cellular function and signaling pathways. STK24 is a protein belonging to the Germinal Center Kinase III (GCK III) sub-family, found to be related to many intracellular and intercellular processes. In the following study the expression of the gene STK24 is studied using the web-based tool TNM plot, in which the expression is found dysregulated in AML with a significant p-value of 9.76e - 23. In addition to expression analysis, survival analysis is carried out, the dysregulated expression of STK24 is found to be related to lower overall survivable outcome indicated by significant p-value of 1.6e - 05 with median survival for lower expression of the STK24 for 10.7 month time. In the protein-protein interaction analysis, the targeted protein STK24 was found to interact with several proteins, among them some of the proteins which are found to be related to AML pathogenesis are PDCD10, PPP2R1B, STK11, TCP1, STK25, STK26 and STRN3 with combined score between .5 to 1.00. Among the interacting proteins 20 proteins are found to have higher interaction efficiency which is represented in circular format. A correlation study of the target protein STK24 with AML and glutamine metabolism related protein FLT3, NPM1, RUNX1, RARA, IDH1, IDH2, GLS, SLC1A5, GLUD1 and SLC7A11 showed a significant correlation with Pearson’s coefficient r value between -1 to 1 and p-value < 0.05. With the analysis of expression and survival and protein-protein interaction and gene correlation it can be indicated that STK24 may have a role in pathogenesis in AML. But to conclude the study, further expression of the gene STK24 in the AML is needed to prove its correlation with the disease progression and further in vitro and in vivo analysis are needed to be carried out.

Kinases are essential for signaling pathways that affects biological processes. The kinase inhibitors potential as therapeutic medicines to prolong lifespan has been brought to light by recent research which includes aging and longevity, one is mTOR modulation. For instance, it has demonstrated that mTOR inhibition mimics the effects of caloric restriction, a tried-and-true strategy for increasing lifespan in animals. These inhibitors can control pathways related to inflammation, stress reactions, and DNA repair—essential to the aging. Preclinical research on small-molecule inhibitors that target kinases, including PI3K, JNK, and IGF-1 has shown promise. These substances can decrease build-up of cellular damage, alleviate illnesses, and increase longevity. Though these are encouraging, the intricacy of kinase networks and off-target consequences make it difficult to translate insights into safe and efficient. To optimize kinase inhibitors for anti-aging therapies, more study is required, with a particular emphasis on safety, effectiveness, and avoiding adverse effects.

Myeloid leukaemia (ML) is a cancer that occurs by the accumulation of abnormally multiplied myeloid cells in bone marrow, peripheral blood, and other related tissue. MST3 is a gene of the GCK family that has a role in apoptosis, along with other cellular functions like cellular differentiation, cell cycle, metabolism, and others. Objectives: The objectives of this study were to count RBCs and WBCs, study MST3 expression in ML and control samples, and perform an in silico correlation study on the KRAS and NRAS genes. Methods: The counting of RBCs and WBCs was carried out using a hemacytometer, the expression of MST3 was studied using RT-PCR, and a correlation study was carried out using GEPIA. Results: RBC and WBC levels in ML differed from the control levels, and the expression of MST3 was found to be upregulated in ML in comparison to controls, with a 2.90–8.65-fold change, with a significant p-value > 0.05. A positive correlation in expression was also found between MST3 and KRAS and NRAS genes, with a significant r value correlation. Conclusions: From this study, it could be deduced that MST3 might have a role in ML pathogenesis, but further research is needed to study its role in the progression of the disease.

Neurodegenerative diseases represent a significant global health burden, characterized by the progressive deterioration of neuronal dysfunction and complex molecular pathologies. Traditional omics approaches have provided valuable insights into the genetic, transcriptomic, and proteomic alterations involved; however, they often lack spatial resolution, obscuring the tissue-specific and cellular-contextual dynamics of disease progression. Spatial multi-omics technologies integrate spatial transcriptomics, proteomics, epigenomics, and metabolomics to enable high-resolution mapping of molecular features within intact tissues. This chapter explores recent advancements in spatial multi-omics technologies and also the role of spatial multi-omics involving metabolomics, epigenomics, and their application to neurodegenerative disease models, as well as the challenges and future directions in translating these insights into clinical impact.