Infertility has a remarkable global impact affecting approximately about 48 million couples worldwide. One of the most contended concerns in reproductive biology is the prospective influence of psychological stress on pregnancy rates. Individuals struggling to conceive face a stupendous amount of emotional turbulence and have a greater risk for psychological vulnerability. Both stress and infertility reinforce the impact of each other; hence, there exists a reciprocal relationship. Stress may be the major contributor to subsequent infertility. Infertility treatments may enhance stress levels as well as reduce treatment outcomes. The biological mechanisms that interlink stress and infertility are the outcome of the hormonal actions at the brain level, where they stimulate or suppress the hypothalamic-pituitary-adrenal axis (HPA) and have a potential influence on the secretion of the respective hormone by the reproductive organs and the pregnancy outcomes. Sex hormones play an essential role in reproductive biology as well as in general physiology where they generate the cycle and provide a potential environment for pregnancy. This article reviews the impact of stress on reproductive rates and the implications of sex hormones on infertility. Additionally, it suggests strategies to overcome the stress conditions and the scenarios that may lead to stress.

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.