Lithium salts have strong medical properties in neurological disorders such as bipolar disorder and lithium-responsive headaches. They have recently gathered attention due to their potential preventive effect in viral infections. Though the therapeutic effect of lithium was documented by Cade in the late 1940s, its underlying mechanism of action is still disputed. Acute lithium exposure has an activating effect on excitable organic tissue and organisms, and is highly toxic. Lithium exposure is associated with a strong metabolic response in the organism, with large changes in phospholipid and cholesterol expression. Opposite to acute exposure, this metabolic response alleviates excessive cellular activity. The presence of lithium ions strongly affects lipid conformation and membrane phase unlike other alkali ions, with consequences for membrane permeability, buffer property and excitability. This review investigates how lithium ions affect lipid membrane composition and function, and how lithium response might in fact be the body's attempt to counteract the physical presence of lithium ions at cell level. Ideas for further research in microbiology and drug development are discussed.

Receptor-ligand binding on contacting cells dictates the extent of transmembrane signaling through membrane receptors during cell communication, influencing both the physiological and pathological activities of cells. This process is integral to fundamental biological mechanisms including signal transduction, cancer metastasis, immune responses, and inflammatory cascades, all of which are profoundly influenced by the cell microenvironment. This article provides an overview of the kinetic theory of receptor-ligand binding and examines methods for measuring this interaction, along with their respective advantages and disadvantages. Furthermore, it comprehensively explores the factors that impact receptor-ligand binding, encompassing protein-membrane interactions, the bioelectric microenvironment, auxiliary factors, hydrogen bond strength, pH levels, cis and trans interactions between ligands and receptors. The application of receptor-ligand binding kinetics in various diseases such as immunity, cancer, and inflammation are also discussed. Additionally, the investigation into how functional substances alter receptor-ligand binding dynamics within specific cellular microenvironments presents a promising new approach to treating related diseases.

The exceptional differentiation abilities of stem cells make them ideal candidates for cell replacement therapies. Considering their great potential, researchers should understand how stem cells interact with other cell types. The production of high-quality differentiated cells is crucial for favorable treatment and makes them an ideal choice for clinical applications. Label-free stem cell monitoring approaches are anticipated to be more effective in this context, as they ensure quality of differentiation while preserving the therapeutic potential. Electric cell-substrate impedance sensing (ECIS) is a nonintrusive technique that enables cell quantification through continuous monitoring of adherent cell behavior using electronic transcellular impedance measurements. This technique also facilitates the study of cell growth, motility, differentiation, drug effects, and cell barrier functions. Therefore, numerous studies have identified ECIS as an effective method for monitoring stem cell quality and differentiation. In this review, we discuss the current understanding of ECIS's achievements in examining cell behaviors and the potential applications of ECIS arrays in preclinical stem cell research. Moreover, we highlight our present knowledge concerning ECIS's contributions in examining cell behaviors and speculate about the future uses of ECIS arrays in preclinical stem cell research. This review also aims to stimulate research on electrochemical biosensors for future applications in regenerative medicine.

DNA is the macromolecule responsible for storing the genetic information of a cell and it has intrinsic properties such as deformability, stability and curvature. DNA Curvature plays an important role in gene transcription and, consequently, in the subsequent production of proteins, a fundamental process of cells. With recent advances in bioinformatics and theoretical biology, it became possible to analyze and understand the involvement of DNA Curvature as a discriminatory characteristic of gene-promoting regions. These regions act as sites where RNAp (ribonucleic acid-polymerase) binds to initiate transcription. This review aims to describe the formation of Curvature, as well as highlight its importance in predicting promoters. Furthermore, this article provides the potential of DNA Curvature as a distinguishing feature for promoter prediction tools, as well as outlining the calculation procedures that have been described by other researchers. This work may support further studies directed towards the enhancement of promoter prediction software.

Collective cell migration is the primary mode of cellular movement during embryonic morphogenesis, tissue repair and regeneration, and cancer invasion. Distinct from single-cell migration, collective cell migration involves complex intercellular signaling cascades and force transmission. Consequently, cell collectives exhibit intricate and diverse migration patterns under the influence of the microenvironment in vivo. Investigating the patterns and mechanisms of collective cell migration within complex environmental factors in vitro is essential for elucidating collective cell migration in vivo. This review elucidates the influence of physical and chemical factors in vitro microenvironment on the migration patterns and efficiency of cell collectives, thereby enhancing our comprehension of the phenomenon. Furthermore, we concisely present the effects of characteristic properties of common biomaterials on collective cell migration during tissue repair and regeneration, as well as the features and applications of tumor models of different dimensions (2D substrate or 3D substrate) in vitro. Finally, we highlight the challenges facing the research of collective cell migration behaviors in vitro microenvironment and propose that modulating collective cell migration may represent a potential strategy to promote tissue repair and regeneration and to control tumor invasion and metastasis.

The origin of life and its evolution are generally taught as occurring by abiogenesis and gene-centric neo-Darwinism. Significant biological evolutionary changes are preserved and given direction (descent with modification) by Darwin's (Spencer's) natural selection by survival of the fittest. Only survival of the fittest (adapted/broadened) is available to provide a 'naturalistic' direction to prefer one outcome/reaction over another for abiogenesis. Thus, assembly of first life must reach some threshold (the first minimal cell) before 'survival of the fittest' (the only naturalistic explanation available) can function as Darwin proposed for biological change. We propose the novel concept that the requirement for co-origination of vitamins with enzymes is a fundamental, but overlooked, problem that survival of the fittest (even broadly redefined beyond Darwin) cannot reasonably overcome. We support this conclusion with probability calculations. We focus on the stage of evolution involving the transition from non-life to the first, minimal living cell. We show that co-origination of required biochemical processes makes the origin of life probabilistically absurdly improbable even when all assumptions are chosen to unreasonably favor evolutionary theories.

Animal diseases are a major concern to animal welfare, human health and the global economy. Early detection, prevention and control of these animal diseases are crucial to ensure sustainability of livestock sector, to reduce farm losses and protecting public health. Points of care (POC) devices are small, portable instruments that provide rapid results thus reduce the risk of disease transmission and enable early intervention. CRISPR based diagnostics offer more accurate and efficient solution for monitoring animal health due to their quick response, can detect very low level of pathogenic organism or disease markers and specificity. These diagnostics are particularly useful in the in area with limited resources or access to common diagnostic methods, especially in developing countries. The ability of electrochemical sensors to detect accurately very low analyte concentration makes them suitable for POC diagnostics and field application. CRISPR base electrochemical biosensors show great potential in revolutionizing disease detection and diagnosis including animal health. However, challenges, such as achieving selectivity and sensitivity, need to be addressed to enhance the competitiveness of these biosensors. Currently, most CRISPR based bioassay research focuses on nucleic acid target detection, but researchers exploring to monitor small organic/inorganic non-nucleic acid molecules like toxins and proteins. Emerging diagnostics would be centered on CRISPR-Cas system will offer great potential as an accurate, specific and effective means to identify microorganism, virus, toxins, small molecules, peptides and nucleic acid related to various animal health disorders particularly when integrated into electrochemical biosensing platform.

This review delves into the reversible process of DNA compaction, vital for cellular functions like replication and transcription. The study highlights how various cations assist in the condensation of DNA chains, highlighting their specificity. The impact of the ionic environment on chromatin characteristics is discussed, emphasizing the roles of mono- and divalent cations in neutralizing DNA charge and promoting compaction. Trivalent ions induce significant compaction, while divalent ions also contribute, albeit less strongly. Charge inversion, facilitated by high concentrations of multivalent counterions, affects DNA condensation dynamics. Manipulating solution pH and dielectric constant can alter charge inversion bidirectionally. The hydrophobic effect driven by organic cations plays a crucial role in DNA compaction. The review underscores the implications of charge inversion, including macroscopic phase separation and DNA precipitation, driven by the binding of cationic micelles to DNA.

Superfamily of cytochromes P450 (CYPs) is composed of heme-thiolate-containing monooxygenase enzymes, which play crucial roles in the biosynthesis, bioactivation, and detoxification of a variety of organic compounds, both endogenic and exogenic. Majority of CYP monooxygenase systems are multi-component and contain various redox partners, cofactors and auxiliary proteins, which contribute to their diversity in both prokaryotes and eukaryotes. Recent progress in bioinformatics and computational biology approaches make it possible to undertake whole-genome and phylogenetic analyses of CYPomes of a variety of organisms. Considerable variations in sequences within and between CYP families and high similarity in secondary and tertiary structures between all CYPs along with dramatic conformational changes in secondary structure elements of a substrate binding site during catalysis have been reported. This provides structural plasticity and substrate promiscuity, which underlie functional diversity of CYPs. Gene duplication and mutation events underlie CYP evolutionary diversity and emergence of novel selectable functions, which provide the involvement of CYPs in high adaptability to changing environmental conditions and dietary restrictions. In our review, we discuss the recent advancements and challenges in the elucidating the evolutionary origin and mechanisms underlying the CYP monooxygenase system diversity and plasticity. Our review is in the view of hypothesis that diversity of CYP monooxygenase systems is translated into the broad metabolic profiles, and this has been acquired during the long evolutionary time to provide structural plasticity leading to high adaptative capabilities to environmental stress conditions.

With the progress of modern science and technology, magnetic therapy technology develops rapidly, and many types of magnetic therapy methods continue to emerge, making magnetic therapy one of the main techniques of physiotherapy. With the continuous development of magnetic field research and clinical applications, magnetic therapy, as a non-invasive brain stimulation therapy technology, has attracted much attention due to its potential in the treatment of motor dysfunction, cognitive impairment and speech disorders in patients with neurodegenerative diseases. However, the role of magnetic fields in the prognosis and treatment of neurodegenerative diseases and their mechanisms remain largely unexplored. In this paper, the therapeutic effect and neuroprotective mechanism of the magnetic field on neurodegenerative diseases are reviewed, and the new magnetic therapy techniques are also summarized. Although the neuroprotective mechanism of magnetic field cannot be fully elaborated, it is helpful to promote the application of magnetic field in neurodegenerative diseases and provide a new theoretical basis for the related magnetic field research in the later period.

Diabetic foot ulcers, as one of the chronic wounds, are a serious challenge in the global healthcare system which have shown notable growth in recent years. DFU is associated with impairment in various stages of wound healing, including angiogenesis. Aberrant expression of microRNAs (miRNAs) involved in the disruption of the balance between angiogenic and anti-angiogenic factors, plays a crucial role in angiogenesis dysfunction. Alteration in the expression of angiomiRNAs (angiomiRs) have the potential to function as biomarkers in chronic wounds. Additionally, considering the rising importance of therapeutic RNAs, there is potential for utilizing angiomiRs in wound healing to induce angiogenesis. This review aims to explore angiogenesis in chronic wounds and investigate the mechanisms mediated by pro- and anti-angiomiRs in the context of diabetic foot ulcers.

Sugar serves as the primary energy source for mammals, with glucose metabolism facilitating energy acquisition in human cells. The proper functioning of intracellular glucose metabolism is essential for the maintenance of orderly and healthy physiological activities. Tumor cells, characterized by uncontrolled growth, exhibit dysregulated proliferation and apoptosis processes, leading to abnormal alterations in glucose metabolism. Specifically, tumor cells exhibit a shift towards aerobic glycolysis, resulting in the production of lactic acid that can be utilized as a metabolic intermediate for sustained tumor cell growth. This article provides a comprehensive overview of the enzymes involved in glucose metabolism and the alterations in gene expression that occur during tumor progression. It also examines the current research on targeting abnormal glucose metabolism processes for tumor treatment and discusses potential future directions for utilizing glucose metabolism as a therapeutic target.

In the bloodstream or other physiological fluids, "circulating cells and sub-cellular bio-particles" include many microscopic biological elements such as circulating tumor cells (CTCs), cell-free DNA (cfDNA), exosomes, microRNAs, platelets, immune cells, and proteins are the most well-known and investigated. These structures are crucial biomarkers in healthcare and medical research for the early detection of cancer and other disorders, enabling treatment to commence before the onset of clinical symptoms and enhancing the efficacy of treatments. As the size of these biomarkers to be detected decreases and their numbers in body fluids diminishes, the detection materials, ranging from visual inspection to advanced microscopy techniques, begin to become smaller, more sensitive, faster, and more effective, thanks to developing nanotechnology. This review first defines the circulating cells and subcellular bio-particles with their biological, physical, and mechanical properties and second focuses on their diagnostic importance, including their most recent applications as biomarkers, the biosensors that are utilized to detect them, the present obstacles that must be surmounted, and prospective developments in the domain. As technology advances and biomolecular pathways are deepens, diagnostic tests will become more sensitive, specific, and thorough. Finally, integrating recent advances in the diagnostic use of circulating cells and bioparticles into clinical practice is promising for precision medicine and patient outcomes.

This review dives into the complex dynamics of bone remodeling, combining biological insights with mathematical perspectives to better understand this fundamental aspect of skeletal health. Bone, being a crucial part of our body, constantly renews itself, and with the growing number of individuals facing bone-related issues, research in this field is vital. In this review, we categorized and classified most common mathematical models used to simulate the mechanical behavior of bone under different loading and health conditions, shedding light on the evolving landscape of bone biology. While current models have effectively captured the essence of healthy bone remodeling, the ever-expanding knowledge in bone biology suggests an update in mathematical methods. Knowing the role of the skeleton in whole-body physiology, and looking at the recent discoveries about activities of bone cells emphasize the urgency of refining our mathematical descriptions of the bone remodeling process. The underexplored impact of bone diseases like osteoporosis, Paget's disease, or breast cancer on bone remodeling also points to the need for intensified research into diverse disease types and their unique effects on bone health. By reviewing a range of bone remodeling models, we show the necessity for tailor-made mathematical models to decipher their roots and enhance patient treatment strategies. Collaboration among scientists from various domains is pivotal to surmount these challenges, ensuring improved accuracy and applicability of mathematical models. Ultimately, this effort aims to deepen our understanding of bone remodeling processes and their broader implications for diverse health conditions.

Lipid homeostasis plays a pivotal role in cellular growth, necessitating the engagement of numerous lipid metabolism genes and the cohesive functioning of organelles. While the nucleus is traditionally recognized for its genetic roles, emerging evidence highlights its significant contribution to lipid homeostasis maintenance. Certain nuclear membrane proteins or associated proteins have the capacity to directly catalyze lipid synthesis or modification processes. Mutations in the genes encoding these proteins can lead to disrupted lipid metabolism, contributing to a spectrum of metabolic disorders. This article provides a comprehensive reviews of the investigations exploring the interplay between nuclear membrane proteins and lipid metabolism. Additionally, it delves into the heterogeneity of the nuclear membrane, positioning it as a novel therapeutic target for managing metabolic disorders and mitigating adverse drug reactions.

Osteosarcoma (OS) represents the primary form of bone cancer observed in paediatric and adolescent populations. Nearly 10%-15% of patients have metastases at diagnosis, and the 5-year survival rate was less than 20%. Although numerous investigators have offered significant efforts, the survival rates for patients with OS have remained almost unchanged over the past three decades. The most pervasive and abundant modification of internal transcripts in eukaryotic messenger RNAs (mRNAs) is N6-methyladenosine (m6A), and it is regulated by m6A methylation regulators. A number of recent studies have demonstrated that m6A modifications can regulate the biological activities of tumour cells and are intimately linked with cancer development, prognosis, drug resistance, and therapy. N6-methyladenosine modification of Non-coding RNA (ncRNA) has likewise shown a broad potential in gene regulation and tumor biology. Epigenetic changes induced by mRNAs and ncRNAs methylation are important for a better understanding of OS development and targeted drug development. Therefore, this paper summarises the biological functions of m6A-modified regulators in osteosarcoma and the role of mutual regulation between m6A and ncRNAs in osteosarcoma. Furthermore, the potential clinical applications of m6A modifications in OS are presented for consideration. It provides new directions for the future research and clinical treatment strategies of osteosarcoma.

Transfer RNA-derived small RNAs (tsRNAs), a recently identified subclass of small non-coding RNAs (sncRNAs), emerge through the cleavage of mature transfer RNA (tRNA) or tRNA precursors mediated by specific enzymes. The tumor necrosis factor (TNF) protein, a signaling molecule produced by activated macrophages, plays a pivotal role in systemic inflammation. Its multifaceted functions include the capacity to eliminate or hinder tumor cells, enhance the phagocytic capabilities of neutrophils, confer resistance against infections, induce fever, and prompt the production of acute phase proteins. Notably, four TNF-related tsRNAs have been conclusively linked to distinct diseases. Examples include 5'tiRNA-Gly in skeletal muscle injury, tsRNA-21109 in systemic lupus erythematosus (SLE), tRF-Leu-AAG-001 in endometriosis (EMs), and tsRNA-04002 in intervertebral disk degeneration (IDD). These tsRNAs exhibit the ability to suppress the expression of TNF-α. Additionally, KEGG analysis has identified seven tsRNAs potentially involved in modulating the TNF pathway, exerting their influence across a spectrum of non-cancerous diseases. Noteworthy instances include aberrant tiRNA-Ser-TGA-001 and tRF-Val-AAC-034 in intrauterine growth restriction (IUGR), irregular tRF-Ala-AGC-052 and tRF-Ala-TGC-027 in obesity, and deviant tiRNA-His-GTG-001, tRF-Ser-GCT-113, and tRF-Gln-TTG-035 in irritable bowel syndrome with diarrhea (IBS-D). This comprehensive review explores the biological functions and mechanisms of tsRNAs associated with the TNF signaling pathway in both cancer and other diseases, offering novel insights for future translational medical research.

Cancer is a pernicious and pressing medical problem; moreover, it is a failure of multicellular morphogenesis that sheds much light on evolutionary developmental biology. Numerous classes of pharmacological agents have been considered as cancer therapeutics and evaluated as potential carcinogenic agents; however, these are spread throughout the primary literature. Here, we briefly review recent work on ion channel drugs as promising anti-cancer treatments and present a systematic review of the known cancer-relevant effects of 109 drugs targeting ion channels. The roles of ion channels in cancer are consistent with the importance of bioelectrical parameters in cell regulation and with the functions of bioelectric signaling in morphogenetic signals that act as cancer suppressors. We find that compounds that are well-known for having targets in the nervous system, such as voltage-gated ion channels, ligand-gated ion channels, proton pumps, and gap junctions are especially relevant to cancer. Our review suggests further opportunities for the repurposing of numerous promising candidates in the field of cancer electroceuticals.

Basing on logical assumptions and necessary steps of complexification along biological evolution, we propose here an evolutionary path from molecules to cells presenting four ages and three major transitions. At the first age, the basic biomolecules were formed and become abundant. The first transition happened with the event of a chemical symbiosis between nucleic acids and peptides worlds, which marked the emergence of both life and the process of organic encoding. FUCA, the first living process, was composed of self-replicating RNAs linked to amino acids and capable to catalyze their binding. The second transition, from the age of FUCA to the age of progenotes, involved the duplication and recombination of proto-genomes, leading to specialization in protein production and the exploration of protein to metabolite interactions in the prebiotic soup. Enzymes and metabolic pathways were incorporated into biology from protobiotic reactions that occurred without chemical catalysts, step by step. Then, the fourth age brought origin of organisms and lineages, occurring when specific proteins capable to stackle together facilitated the formation of peptidic capsids. LUCA was constituted as a progenote capable to operate the basic metabolic functions of a cell, but still unable to interact with lipid molecules. We present evidence that the evolution of lipid interaction pathways occurred at least twice, with the development of bacterial-like and archaeal-like membranes. Also, data in literature suggest at least two paths for the emergence of DNA biosynthesis, allowing the stabilization of early life strategies in viruses, archaeas and bacterias. Two billion years later, the eukaryotes arouse, and after 1,5 billion years of evolution, they finally learn how to evolve multicellularity via tissue specialization.

Symbiogenesis has been systematically exploited to understand consciousness as the aggregate of our physiology. The Symbiogenic mechanism for assimilation of factors in the environment formulates the continuum from inside the cell to the Cosmos, both consciousness and cosmology complying with the Laws of Nature. Since Symbiogenesis is 'constructive', whereas eliminating what threatens us is 'destructive', why do we largely practice Symbiogenesis? Hypothetically, Symbiogenesis recursively simulates the monism of our origin, recognizing 'something bigger than ourselves'. That perspective explains many heretofore unexplained aspects of consciousness, such as mind, epigenetic inheritance, physiology, behaviors, social systems, mathematics, the Arts, from an a priori perspective. Moreover, there is an energetic continuum from Newtonian to Quantum Mechanics, opening up to a novel way of understanding the 'true nature of our being', not as 'materialism', but instead being the serial homeostatic control of energy. The latter is consistent with the spirit of Claude Bernard and Walter B. Cannon's perspectives on physiology. Such a paradigm shift is overdue, given that materialism is causing the destruction of the Earth and ourselves.

The liver has the function of regulating metabolic equilibrium in the human body, and the majority of liver disorders are chronic conditions that can significantly impair health. Recent research has highlighted the critical role of long noncoding RNAs (lncRNAs) in liver disease pathogenesis. LncRNA H19, an endogenous noncoding single-stranded RNA, exerts its influence through epigenetic modifications and affects various biological processes. This review focuses on elucidating the key molecular mechanisms underlying the regulation of H19 during the progression and advancement of liver diseases, aiming to highlight H19 as a potential therapeutic target and provide profound insights into the molecular underpinnings of liver pathologies.