Multiple myeloma (MM) is a malignant hematological disease. The disease is characterized by the clonal proliferation of malignant plasma cells in the bone marrow. MM accounts for 1.3% of all malignancies and has been increasing in incidence all over the world. Various genetic abnormalities, mutations, and translocation, including epigenetic modifications, are known to contribute to the disease’s pathophysiology. The prognosis is good if detected early, or else the outcome is very bad if distant metastasis has already occurred. Conventional treatment with drugs poses a challenge when there is drug resistance. In the present review, we discuss multiple myeloma and its treatment, drug resistance, the molecular basis of epigenetic regulation, the role of natural products in epigenetic regulators, diet, physical activity, addiction, and environmental pollutants, which may be beneficial for clinicians and researchers.

The circadian system in the human body responds to daily environmental changes to optimise behaviour according to the biological clock and also influences various physiological processes. The suprachiasmatic nuclei are located in the anterior hypothalamus of the brain, and they synchronise to the 24 h light/dark cycle. Human physiological functions are highly dependent on the regulation of the internal circadian clock. Skeletal muscles comprise the largest collection of peripheral clocks in the human body. Both central and peripheral clocks regulate the interaction between the musculoskeletal system and energy metabolism. The skeletal muscle circadian clock plays a vital role in lipid and glucose metabolism. The pathogenesis of osteoporosis is related to an alteration in the circadian rhythm. In the present review, we discuss the disturbance of the circadian rhythm and its resultant effect on the musculoskeletal system. We also discuss the nutritional strategies that are potentially effective in maintaining the system’s homeostasis. Active collaborations between nutritionists and physiologists in the field of chronobiological and chrononutrition will further clarify these interactions. This review may be necessary for successful interventions in reducing morbidity and mortality resulting from musculoskeletal disturbances.

Background/Objectives: Nutritional status significantly influences cardiac surgery outcomes, with malnutrition contributing to poorer results and increased complications. This study addresses the critical gap in understanding by exploring the relationship between pre-operative nutritional status and post-operative cognitive dysfunction (POCD) in adult cardiac patients. Methods: A comprehensive search across key databases investigates the prevalence of malnutrition in pre-operative cardiac surgery patients, its effects, and its association with POCD. Factors exacerbating malnutrition, such as chronic illnesses and reduced functionality, are considered. The study also examines the incidence of POCD, its primary association with CABG procedures, and the impact of malnutrition on complications like inflammation, pulmonary and cardiac failure, and renal injury. Discussions: Findings reveal that 46.4% of pre-operative cardiac surgery patients experience malnutrition, linked to chronic illnesses and reduced functionality. Malnutrition significantly contributes to inflammation and complications, including POCD, with an incidence ranging from 15 to 50%. CABG procedures are particularly associated with POCD, and malnutrition prolongs intensive care stays while increasing vulnerability to surgical stress. Conclusions: The review underscores the crucial role of nutrition in recovery and advocates for a universally recognized nutrition assessment tool tailored to diverse cardiac surgery patients. Emphasizing pre-operative enhanced nutrition as a potential strategy to mitigate inflammation and improve cognitive function, the review highlights the need for integrating nutrition screening into clinical practice to optimize outcomes for high-risk cardiac surgery patients. However, to date, most data came from observational studies; hence, there is a need for future interventional studies to test the hypothesis that pre-operative enhanced nutrition can mitigate inflammation and improve cognitive function in this patient population.

Postoperative cognitive dysfunction (POCD) is cognitive decline after surgery. The authors hypothesized that gene-level changes could be involved in the pathogenesis of POCD. The present study evaluated the incidence of POCD and its associated differentially expressed genes. This was a prospective cohort study conducted on high-risk coronary artery bypass graft patients aged 40 to 75 years. POCD classification was based on a one standard deviation decline in the postoperative scores compared to the preoperative scores. The differentially expressed genes were identified using microarray analysis and validated using quantitative RT-PCR. Forty-six patients were recruited and completed the study. The incidence of POCD was identified using a set of neurocognitive assessments and found to be at 17% in these high-risk CABG patients. Six samples were selected for the gene expression analyses (3 non-POCD and 3 POCD samples). The findings showed five differentially expressed genes in the POCD group compared to the non-POCD group. The upregulated gene was ERFE, whereas the downregulated genes were KIR2DS2, KIR2DS3, KIR3DL2, and LIM2. According to the results, the gene expression profiles of POCD can be used to find potential proteins for POCD diagnostic and predictive biomarkers. Understanding the molecular mechanism of POCD development will further lead to early detection and intervention to reduce the severity of POCD, and hence, reduce the mortality and morbidity rate due to the condition.