The world’s population is ageing at an accelerated pace. Ageing is a natural, physiological but highly complex and multifactorial process that all species in the Tree of Life experience over time. Physical and mental disabilities, and age‐related diseases, would increase along with the increasing life expectancy. Ginger (Zingiber officinale) is a plant that belongs to the Zingiberaceae family, native to Southeast Asia. For hundreds of years, ginger has been consumed in various ways by the natives of Asian countries, both as culinary and medicinal herb for the treatment of many diseases. Mounting evidence suggests that ginger can promote healthy ageing, reduce morbidity, and prolong healthy lifespan. Ginger, a well‐known natural product, has been demonstrated to possess antioxidant, anti‐inflammatory, anticancer, and antimicrobial properties, as well as an outstanding antiviral activity due to a high concentration of antiviral compounds. In this review, the current evidence on the potential role of ginger and its active compounds in the prevention of ageing is discussed.

The current study aimed to describe the fabrication of a composite patch by incorporating marine algae powders (MAPs) into poly-lactic acid (PLA) for bone tissue engineering. The prepared composite patch was functionalized with the co-polymer, poly (2-hydroxyethyl methacrylate-co-ethylene glycol dimethacrylate) (p(HEMA-co-EGDMA)) via initiated chemical vapor deposition (iCVD) to improve its wettability and overall biocompatibility. The iCVD functionalized MAP–PLA composite patch showed superior cell interaction of human osteoblasts. Following the surface functionalization by p(HEMA-co-EGDMA) via the iCVD technique, a highly hydrophilic patch was achieved without tailoring any morphological and structural properties. Moreover, the iCVD modified composite patch exhibited ideal cell adhesion for human osteoblasts, thus making the proposed patch suitable for potential biomedical applications including bone tissue engineering, especially in the fields of dentistry and orthopedy.

In recent years much attention has been focused on the role of glutathione (GSH) and GSH-related enzymes such as glutathione peroxidase (GSH Px), glutathione reductase (GSH Red), and glutathione S-transferase (GST) in the inhibition of free radical-induced carcinogenesis. In this study, erythrocyte GSH levels and activities of GSH Px, GSH Red, and GST were determined in patients with colorectal tumors (n = 20, mean age 54.5 - 8.3 yr). Erythrocyte GSH Red and GST activities were significantly higher in patients with colorectal tumors. Erythrocyte GSH levels and GSH Px activities were found to be significantly decreased in the patients. When the patients were classified based on their clinical grading (Dukes classifications), there was no significant difference in studied parameters between Dukes B and Dukes C. Our results suggest that oxidative stress may play an important role in colorectal tumorigenesis and that these events have no effect on the clinical grading of the colorectal tumor.

The aim of this study was to investigate how myeloperoxidase (MPO) G-463A gene polymorphism and enzyme levels varied among patients with chronic lymphocytic leukemia (CLL) and multiple myeloma (MM) and to find the relationship between the MPO gene, enzyme levels, and clinical parameters. We studied the sera from 40 healthy volunteers, patients with CLL (n = 34) and MM (n = 28). In subjects with homozygote GG genotype, MPO levels were higher in the patients with both CLL and MM than in the control group. This difference was statistically significant in patients with CLL. In conclusion, homozygote GG genotype is found to be associated with an increasing amount of serum MPO. In accordance with the results of the study, we assess that the increase in the MPO enzyme level in the patient groups with CLL and MM generated bactericidal effects as well as the increased formation of ROP, thus setting off a pro-cell death pathway and playing a role on the pathogenesis of lymphoproliferative malignancies through this mechanism.