Caenorhabditis elegans (C. elegans) has emerged as an outstanding model organism for investigating the aging process due to its shortened lifespan, well-defined genome, and accessibility of potent genetic tools. This review presents the current findings on chronological aging and photoaging in C. elegans, exploring the elaborate molecular pathways that control these processes. The progression of chronological aging is characterized by a gradual deterioration of physiological functions and is influenced by an interaction of genetic and environmental factors, including the insulin/insulin-like signaling (IIS) pathway. In contrast, photoaging is characterized by increased oxidative stress, DNA damage, and activation of stress response pathways induced by UV exposure. Although the genetic mechanisms of chronological aging in C. elegans have been characterized by extensive research, the pathways regulating photoaging are comparatively less well-studied. Here, we provide an overview of the current understanding of aging research, including the crucial genes and genetic pathways involved in the aging and photoaging processes of C. elegans. Understanding the complex interactions between these factors will provide invaluable insights into the molecular mechanisms underlying chronological aging and photoaging and may lead to novel therapeutic approaches and further studies for promoting healthy aging in humans.

Background Burkholderia pseudomallei, a Gram-negative pathogen, causes melioidosis. Although various clinical laboratory identification methods exist, culture-based techniques lack comprehensive evaluation. Thus, this systematic review and meta-analysis aimed to assess the diagnostic accuracy of culture-based automation and non-automation methods. Methods Data were collected via PubMed/MEDLINE, EMBASE, and Scopus using specific search strategies. Selected studies underwent bias assessment using QUADAS-2. Sensitivity and specificity were computed, generating pooled estimates. Heterogeneity was assessed using I2 statistics. Results The review encompassed 20 studies with 2,988 B. pseudomallei samples and 753 non-B. pseudomallei samples. Automation-based methods, particularly with updating databases, exhibited high pooled sensitivity (82.79%; 95% CI 64.44-95.85%) and specificity (99.94%; 95% CI 98.93-100.00%). Subgroup analysis highlighted superior sensitivity for updating-database automation (96.42%, 95% CI 90.01-99.87%) compared to non-updating (3.31%, 95% CI 0.00-10.28%), while specificity remained high at 99.94% (95% CI 98.93-100%). Non-automation methods displayed varying sensitivity and specificity. In-house latex agglutination demonstrated the highest sensitivity (100%; 95% CI 98.49-100%), followed by commercial latex agglutination (99.24%; 95% CI 96.64-100%). However, API 20E had the lowest sensitivity (19.42%; 95% CI 12.94-28.10%). Overall, non-automation tools showed sensitivity of 88.34% (95% CI 77.30-96.25%) and specificity of 90.76% (95% CI 78.45-98.57%). Conclusion The study underscores automation's crucial role in accurately identifying B. pseudomallei, supporting evidence-based melioidosis management decisions. Automation technologies, especially those with updating databases, provide reliable and efficient identification.

Caenorhabditis elegans has served as a model for the unfolded protein response of the endoplasmic reticulum (UPR-ER) and, separately, the oxidative stress response coordinated by SKN-1/Nrf. The oxidative protein folding in the ER generates reactive oxygen species, which is one reason why these systems are frequently studied together. Additionally, numerous stressors activate both pathways simultaneously. Although these molecular chaperones are critical to both processes, current research rarely considers them as an integrative concept, instead categorizing the interaction strictly within different pathway mechanisms. This review focuses on the chaperone systems themselves, including the HSP-4 and protein disulfide isomerases that are located in the ER, the HSP-70 family that resides in the cytoplasm and is controlled by HSF-1, and HSP-6 and HSP-60 that function in the mitochondria and are regulated by ATFS-1. Oxidative stress interacts with each compartment in a manner that is mechanistically distinct. This corresponds to direct redox chemistry in the ER, transcriptional coupling by SKN-1, and compartment-specific ROS-sensing evidence in the mitochondria and cytoplasm. Oxidative stress and chaperone induction converge through multiple independent pathways rather than a single sequential pathway, and this convergence deteriorates with age in a pathway- and tissue-specific manner, as shown by studies focusing on translational chaperone loss, particulate matter exposure, and proteasome-mediated degradation. Finally, we address some outstanding issues, such as the translational relevance to human diseases associated with ER stress and the functioning of redox-regulated chaperone mechanisms in C. elegans.

Stress can reshape the epigenome through changes in DNA methylation, histone modifications, chromatin accessibility, and non-coding RNA regulation. Much is known about how these changes arise during stress, yet their fate once the initiating stimulus has subsided is less clear. Some alterations are rapidly reversed, whereas others recover only partially or at selected loci, and a subset persists long after the acute response has ended. This review examines the mechanisms and contextual factors that shape post-stress recovery and persistence. We consider how stress interacts with cell identity, chromatin context, metabolic state, DNA damage and repair, and the machinery responsible for rebuilding epigenetic organization. We use epigenetic recovery capacity as a conceptual framework describing the extent and rate at which altered epigenetic features return toward a defined pre-stress or homeostatic state. We propose that this capacity, together with stress burden and locus susceptibility, may shape post-stress fate. Persistence itself does not necessarily constitute epigenetic memory. Some persistent states may remain functionally neutral, whereas others may be engaged during adaptive or maladaptive responses. We further outline an evidence framework that distinguishes epigenetic persistence from functional and causal epigenetic memory and discuss the potential for redirecting maladaptive post-stress trajectories.

Selenium (Se) is a trace element with a narrow margin between beneficial effects and stress from toxic effects. The determinants of the transition from selenium adequacy to toxicity remain unknown. Moreover, the roles of selenoproteins and other adaptive responses also remain unclear. The effects of dynamic and localized redox fluctuations on survival and neurodegeneration also require further investigation. To better understand the underlying mechanisms, several studies utilized the nematode Caenorhabditis elegans (C. elegans) as a model. This review systematically addresses pivotal mechanistic controversies. Thioredoxin reductase-1 (TRXR-1) is the only protein in a small amount of the selenoproteome, and it also has a fully conserved selenocysteine insertion mechanism. Moreover, this systematic review also incorporates the current understanding of the molecular factors that determine selenium homeostasis, ranging from neurotoxicological diseases to biosynthetic circumstances. TRXR-1 supports health benefits such as enhance lipid metabolism, longevity, and stress response. During acute selenium toxicity, TRXR-1 is not needed for survival. Instead, cells defend against adverse effects by using the HIF-1 pathway. Reactive oxygen species (ROS) and hydrogen sulfide (H₂S) inhibit the prolyl hydroxylase EGL-9 in high-selenium conditions, stabilizing HIF-1 and initiating a transcriptional detoxification process independent of the selenoprotein mechanism. Finally, this review also discuss selective neurotoxicity, a condition in which degeneration that occurs solely in cholinergic ventral cord motor neurons plays a distinctive and precarious role among trace elements.