Anthocyanins, natural pigments known for their vibrant hues and beneficial properties, undergo intricate genetic control. However, red vegetables grown in plant factories frequently exhibit reduced anthocyanin synthesis compared to those in open fields due to factors like inadequate light, temperature, humidity, and nutrient availability. Comprehending these factors is essential for optimizing plant factory environments to enhance anthocyanin synthesis. This review insights the impact of physiological and genetic factors on the production of anthocyanins in red lettuce grown under controlled conditions. Further, we aim to gain a better understanding of the mechanisms involved in both synthesis and degradation of anthocyanins. Moreover, this review summarizes the identified regulators of anthocyanin synthesis in lettuce, addressing the gap in knowledge on controlling anthocyanin production in plant factories, with potential implications for various crops beyond red lettuce.

In the contemporary epoch, cancer stands as the predominant cause of premature global mortality, necessitating a focused exploration of molecular markers and advanced therapeutic strategies. N6-methyladenosine (m6A), the most prevalent mRNA modification, undergoes dynamic regulation by enzymes referred to as methyltransferases (writers), demethylases (erasers), and effective proteins (readers). Despite lacking methylation activity, RNA-binding motif protein 15 (RBM15), a member of the m6A writer family, assumes a crucial role in recruiting the methyltransferase complex (MTC) and binding to mRNA. Although the impact of m6A modifications on cancer has garnered widespread attention, RBM15 has been relatively overlooked. This review briefly outlines the structure and operational mechanism, and delineates the unique role of RBM15 in various cancers, shedding light on its molecular basis and providing a groundwork for potential tumor-targeted therapies.

Over a long period of evolution, plants have developed self-protection mechanisms, such as leaving seeds, dropping leaves, growing thorns, producing specific substances or emitting special odors to repel insects. Although studies on the taxonomic characteristics, functions and application of spines in spiny plants have been reported in China and abroad, a systematic overview of plant spines is currently lacking. This study therefore identifies the characteristics and types of plant spines based on domestic and international research on plant spines to provide clear criteria or bases for determining the types of plant spines. In addition, the functions, regulatory mechanisms, and factors influencing the formation of spines and the prospects for their development and application are described and summarized. This study will help to improve the understanding of the types, functions and regulatory mechanisms of plant spines and provide new ideas for the genetic improvement of plants from spiny to nonspiny varieties.

Recent studies have reported that HOXB-AS3 (HOXB Cluster Antisense RNA 3) is an intriguing molecule with dual functionality as a long noncoding RNA (lncRNA) and putative coding peptide in tumorigenesis and progression. The significant expression alterations of HOXB-AS3 were detected in diverse cancer types and closely correlated with clinical stage and patient survival. Furthermore, HOXB-AS3 was involved in a spectrum of biological processes in solid tumors and hematological malignancies, such as stemness, lipid metabolism, migration, invasion, and tumor growth. This review comprehensively analyzes its clinical relevance for diagnosis and prognosis across human tumors and summarizes its functional role and regulatory mechanisms in different malignant tumors, including liver cancer, acute myeloid leukemia, ovarian cancer, lung cancer, endometrial carcinoma, colon cancer, and oral squamous cell carcinoma. Overall, HOXB-AS3 emerges as a promising biomarker and novel therapeutic target in multiple human tumors.

This paper aims to explore the possibility of employing large language models (LLMs) - a type of artificial intelligence (AI) - in clinical pharmacology, with a focus on its possible misuse in bioweapon development. Additionally, ethical considerations, legislation and potential risk reduction measures are analysed. The existing literature is reviewed to investigate the potential misuse of AI and LLMs in bioweapon creation. The search includes articles from PubMed, Scopus and Web of Science Core Collection that were identified using a specific protocol. To explore the regulatory landscape, the OECD.ai platform was used. The review highlights the dual-use vulnerability of AI and LLMs, with a focus on bioweapon development. Subsequently, a case study is used to illustrate the potential of AI manipulation resulting in harmful substance synthesis. Existing regulations inadequately address the ethical concerns tied to AI and LLMs. Mitigation measures are proposed, including technical solutions (explainable AI), establishing ethical guidelines through collaborative efforts, and implementing policy changes to create a comprehensive regulatory framework. The integration of AI and LLMs into clinical pharmacology presents invaluable opportunities, while also introducing significant ethical and safety considerations. Addressing the dual-use nature of AI requires robust regulations, as well as adopting a strategic approach grounded in technical solutions and ethical values following the principles of transparency, accountability and safety. Additionally, AI\'s potential role in developing countermeasures against novel hazardous substances is underscored. By adopting a proactive approach, the potential benefits of AI and LLMs can be fully harnessed while minimizing the associated risks.

Head and neck squamous cell carcinoma (HNSCC), a common malignancy of the head and neck, is associated with a rapid progression, a high mortality rate and unsatisfactory curative effects. The treatment efficacy is unsatisfactory due to chemotherapeutic drug resistance, the lack of ideal therapeutic agents, as well as the absence of clinical prognostic models. Thus, the identification of novel potential therapeutic targets for its diagnosis and treatment is vital. Ferroptosis is an iron‑dependent regulatory cell death mode different from traditional cell death modes, such as apoptosis and autophagy, and has notable therapeutic potential in cancer treatment. The study of ferroptosis in HNSCC is expected to solve this bottleneck problem. In the present review, the findings, characteristics and regulatory mechanisms of ferroptosis are summarized, with emphasis on the factors and drugs that regulate ferroptosis in HNSCC, in order to provide theoretical basis for the targeted therapy of ferroptosis in HNSCC.

Adaptive evolution is a process in which variation that confers an evolutionary advantage in a specific environmental context arises and is propagated through a population. When investigating this process, researchers have mainly focused on describing advantageous phenotypes or putative advantageous genotypes. A recent increase in molecular data accessibility and technological advances has allowed researchers to go beyond description and to make inferences about the mechanisms underlying adaptive evolution. In this systematic review, we discuss articles from 2016 to 2022 that investigated or reviewed the molecular mechanisms underlying adaptive evolution in vertebrates in response to environmental variation. Regulatory elements within the genome and regulatory proteins involved in either gene expression or cellular pathways have been shown to play key roles in adaptive evolution in response to most of the discussed environmental factors. Gene losses were suggested to be associated with an adaptive response in some contexts. Future adaptive evolution research could benefit from more investigations focused on noncoding regions of the genome, gene regulation mechanisms, and gene losses potentially yielding advantageous phenotypes. Investigating how novel advantageous genotypes are conserved could also contribute to our knowledge of adaptive evolution.

UNASSIGNED: Effective treatments for the ongoing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic are limited. The virus has evolved strategies to evade the immune system or hijack immune responses to facilitate infection and escape immune surveillance. Mechanistically, SARS-CoV-2 takes advantage of TLR4 and cytokine-induced integrins to promote its entrance into the cell. Furthermore, the activation of pattern recognition receptors (PRR)-mediated signaling pathways is compromised by SARS-CoV-2 non-structural proteins (NSPs), accessory protein open reading frames (ORFs), and structural proteins upon infection, contributing to viral infection and replication. Host factors necessary for cellular protein synthesis, metabolism, and viral replication can also be inhibited by the SARS-CoV-2 proteins. Exploring specific mechanisms would optimize the therapy methods and benefit drug research and development.
UNASSIGNED: We describe pathways and mechanisms by which SARS-CoV-2 evades immune system; these include the mechanisms that operate during virus entry, signaling pathways involved, and processes at RNA and protein levels.
UNASSIGNED: Increased understanding of how viruses interfere with immune responses would provide more evidence for drug development. Drugs targeting conserved viral proteins to inhibit their replication or host factors to enhance immune responses would minimize the impact of virus mutations and prepare for future coronavirus outbreaks.

Long noncoding RNAs (lncRNAs) are a class of RNA molecules that are greater than 200 nt in length and do not have protein-coding capabilities or encode micropeptides only. LncRNAs are involved in the regulation of cell proliferation, differentiation, apoptosis and other biological processes, and are closely associated with the occurrence, recurrence and metastasis of a variety of malignant hematologic diseases. This article summarizes the function, regulatory mechanism and potential clinical application of lncRNAs in leukemia. In general, lncRNAs regulate the occurrence and development of leukemia and the multi-drug resistance in chemotherapy through epigenetic modification, ribosomal RNA transcription, competitive binding with miRNA, modulating glucose metabolic pathway, and activating tumor-related signaling pathway. Studies on lncRNAs provide new references for understanding the pathogenesis of leukemia, uncovering new prognostic markers and potential therapeutic targets, and addressing the problems of drug resistance and post-treatment recurrence in patients in clinical treatment of leukemia.

Tight junctions (TJs) are an important component of cell connectivity; they maintain cell polarity, permeability and adhesion, and participate in the regulation of cell proliferation and differentiation. The claudin (CLDN) family is integral to TJs, and CLDN6 is an important member of this family. Abnormal expression of CLDN6 can destroy the integrity of TJs through various mechanisms and can serve multiple roles in the occurrence and development of tumours. CLDN6 is widely expressed in various tumours but rarely expressed in healthy adult tissues. The aim of this review is to critically examine the recent literature on CLDN6, including its structure, expression in different tumours, regulatory mechanisms and therapeutic prospects. Although some conclusions are controversial, in certain tumours, such as liver, ovarian, endometrial and oesophageal cancer, and atypical teratoid/rhabdoid tumours, research consistently shows that CLDN6 is expressed in tumour tissues but is not expressed or is expressed at low levels in surrounding tissues. In these tumours, CLDN6 has potential as a carcinoembryonic antigen and a therapeutic target.