Ribosomal computing: implementation of the computational method.

BACKGROUND: Several computational and mathematical models of protein synthesis have been explored to accomplish the quantitative analysis of protein synthesis components and polysome structure. The effect of gene sequence (coding and non-coding region) in protein synthesis, mutation in gene sequence, and functional model of ribosome needs to be explored to investigate the relationship among protein synthesis components further. Ribosomal computing is implemented by imitating the functional property of protein synthesis. RESULT: In the proposed work, a general framework of ribosomal computing is demonstrated by developing a computational model to present the relationship between biological details of protein synthesis and computing principles. Here, mathematical abstractions are chosen carefully without probing into intricate chemical details of the micro-operations of protein synthesis for ease of understanding. This model demonstrates the cause and effect of ribosome stalling during protein synthesis and the relationship between functional protein and gene sequence. Moreover, it also reveals the computing nature of ribosome molecules and other protein synthesis components. The effect of gene mutation on protein synthesis is also explored in this model. CONCLUSION: The computational model for ribosomal computing is implemented in this work. The proposed model demonstrates the relationship among gene sequences and protein synthesis components. This model also helps to implement a simulation environment (a simulator) for generating protein chains from gene sequences and can spot the problem during protein synthesis. Thus, this simulator can identify a disease that can happen due to a protein synthesis problem and suggest precautions for it.

Deeper insight into ferroptosis: association with Alzheimer's, Parkinson's disease, and brain tumors and their possible treatment by nanomaterials induced ferroptosis.

Ferroptosis is an emerging and novel type of iron-dependent programmed cell death which is mainly caused by the excessive deposition of free intracellular iron in the brain cells. This deposited free iron exerts a ferroptosis pathway, resulting in lipid peroxidation (LiPr). There are mainly three ferroptosis pathways viz. iron metabolism-mediated cysteine/glutamate, and LiPr-mediated. Iron is required by the brain as a redox metal for several physiological activities. Due to the iron homeostasis balance disruption, the brain gets adversely affected which further causes neurodegenerative diseases (NDDs) like Parkinson's and Alzheimer's disease, strokes, and brain tumors like glioblastoma (GBS), and glioma. Nanotechnology has played an important role in the prevention and treatment of these NDDs. A synergistic effect of nanomaterials and ferroptosis could prove to be an effective and efficient approach in the field of nanomedicine. In the current review, the authors have highlighted all the latest research in the field of ferroptosis, specifically emphasizing on the role of major molecular key players and various mechanisms involved in the ferroptosis pathway. Moreover, here the authors have also addressed the correlation of ferroptosis with the pathophysiology of NDDs and theragnostic effect of ferroptosis and nanomaterials for the prevention and treatment of NDDs.