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Planarians are widely used as water quality indicator species to provide early warning of harmful pollution in aquatic ecosystems. However, the impact of microplastics on freshwater planarians remains poorly investigated. Here we simulated waterborne microplastic exposure in the natural environments to examine the effect on the antioxidant defense system and microbiota in Dugesia japonica . The results showed that exposure to microplastics significantly changed the levels of antioxidant enzymes, including superoxide dismutase, catalase, and glutathione S-transferase, indicating that microplastic exposure induces oxidative stress in planarians. High-throughput 16S rRNA gene sequencing results revealed that exposure to microplastics altered the diversity, abundance, and composition of planarian microbiota community. At phylum level, the relative abundance of the dominant phyla Proteobacteria and Bacteroidetes changed significantly after microplastic exposure. At genus level, the abundance of dominant genera also changed significantly, including Curvibacter and unclassified Chitinophagales . Predictive functional analysis showed that the microbiota of microplastic-exposed planarians exhibited an enrichment in genes related to fatty acid metabolism. Overall, these results showed that microplastics can cause oxidative stress and microbiota dysbiosis in planarians, indicating that planarians can serve as an indicator species for microplastic pollution in freshwater systems.

Climate change has a profound impact on the phenology and growth of vegetation, which in turn influences the distribution and behavior of animal communities, including prey species. This dynamic shift significantly affects predator survival and activities. This study utilizes the MaxEnt model to explore how climate change impacts the distribution of the North China leopard (Panthera pardus japonensis) in the Ziwuling region of Gansu Province, China. As an endemic subspecies and apex predator, the North China leopard is vital for maintaining the structure and function of local ecosystems. Unfortunately, its population faces several threats, including habitat change, interspecies competition, and human encroachment, all of which are compounded by the ongoing effects of climate change. To assess the requirement and quality of habitat for this species, we conducted a population survey in the Ziwuling area from May 2020 to June 2022, utilizing 240 infrared cameras, which identified 46 active leopard sites. Using the MaxEnt model, we simulated habitat suitability and future distribution under different climate change scenarios based on nine environmental variables. Our results indicate that the population distribution of North China leopards is primarily influenced by the mean diurnal range (Bio2), with additional sensitivity to isothermal conditions (Bio3), temperature seasonality (Bio4), maximum temperature of the warmest month (Bio5), and annual temperature range (Bio7). We also evaluated habitat suitability across three socioeconomic pathways (SSP126, SSP245, and SSP585) for three time intervals: the 2050s (2041–2060), the 2070s (2061–2080), and the 2090s (2081–2100). The findings suggest a significant decline in high-suitability habitat for North China leopards, while areas of medium and low suitability are projected to increase. Understanding these distributional changes in North China leopards will enhance our comprehension of the region’s biogeography and inform conservation strategies aimed at mitigating the impacts of climate change.

Perimenopause represents a key transition from a reproductive to non-reproductive state in women, characterized by physiological and psychological changes. Mood disturbances during this period, such as depression, anxiety and cognitive decline, are increasingly understood as complex neuroendocrine and metabolic disorders. Mitochondrial homeostasis carries out a key role in the pathophysiology of these affective symptoms. Disruptions in mitochondrial biogenesis, mitophagy and calcium regulation contribute to synaptic dysfunction and neuroimmune changes. These mitochondrial alterations interact with inflammatory pathways and hormonal signals, exacerbating neuropsychiatric symptoms. A more comprehensive understanding of the molecular mechanisms of mitochondrial dysfunction in menopausal mood disorders unveils potential therapeutic strategies, including mitochondria-targeted antioxidants, hormone replacement therapy, and lifestyle interventions designed to restore mitochondrial integrity and cerebral bioenergetic function.

Soybean, a typical short-day crop, is sensitive to photoperiod, which is a major limiting factor defining its north-to-south cultivation range. The long-juvenile (LJ) trait is controlled primarily by the J locus which has been used for decades by soybean breeders to delay flowering and improve grain yield in tropical regions. The J gene encodes an ortholog of the Arabidopsis Evening Complex (EC) component EARLY FLOWERING 3 ( ELF3 ). To identify modifiers of J , we conducted a forward genetic screen and isolated a mutant ( eoj57 ) that in combination with j has longer flowering delay compared with j single mutant plants. Map-based cloning and genome re-sequencing identified eoj57 (designated as GmLUX2 ) as an ortholog of the Arabidopsis EC component LUX ARRHYTHMO ( LUX ). To validate that GmLUX2 is a modifier of J , we used trans-complementation and identified a natural variant allele with a similar phenotype. We also show that GmLUX2 physically interacts with GmELF3a/b and binds DNA, whereas the mutant and natural variant are attenuated in both activities. Transcriptome analysis shows that the GmLUX2-GmELF3a complex co-regulates the expression of several circadian clock-associated genes and directly represses E1 expression. These results provide mechanistic insight into how GmLUX2-GmELF3 controls flowering time via synergistic regulation of gene expression. These novel insights expand our understanding of the regulation of the EC complex, and facilitate the development of soybean varieties adapted for growth at lower latitudes.

The aberrant activation of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signalling pathway is involved in spinal cord injury (SCI) progression. Electroacupuncture (EA) stimulation is effective in alleviating SCI, but the mechanism is poorly understood. An SCI model was constructed by cord contusion at T10, and AG490 (a JAK2 inhibitor) served as a positive control in this study. We evaluated the effects of EA on locomotor activity and spinal damage in SCI rats. The effects of EA on astrocytes and microglia and on the JAK2/STAT3 signalling pathway in the cells were investigated. Behavioural tests showed that hind limb motor function of rats was improved after EA stimulation. The therapeutic effects of EA stimulation in restoring motor function, alleviating injured spinal cords, and inhibiting spinal cord neuronal apoptosis in SCI rats, were similar to those of AG490. Increased STAT3 activation was observed in astrocytes and microglia in the spinal cord of SCI rats, and this was reversed by EA stimulation. EA alleviated astrogliosis and inhibited microglia M1 polarisation in SCI rat spinal cords. In addition, RNA expression levels of pro-inflammatory factors IL-6, CXCL1, and TNF-α in rat spinal cords were suppressed by EA stimulation, while the expression level of the anti-inflammatory factor heme oxygenase 1 was increased. Meanwhile, the expression of p-JAK2, p-STAT3, and JAK2/STAT3 downstream targets SOCS3 and COX-2 in the spinal cord of SCI rats was inhibited by EA stimulation. Interestingly, the observed effects were comparable to those treated with EA. Our findings demonstrate that EA stimulation ameliorates SCI in rats and exerts an inhibitory effect on the JAK2/STAT3 signalling pathway.

Histone modifications, such as methylation and demethylation, play an important role in regulating chromatin structure and gene expression. The JmjC domain-containing proteins, an important family of histone lysine demethylases (KDMs), play a key role in maintaining homeostasis of histone methylation . In this study, we performed a comprehensive analysis of the ( ) gene family in the soybean genome and identified 48 genes ( ) distributed unevenly across 18 chromosomes. Phylogenetic analysis showed that these JmjC domain-containing genes can be divided into eight groups. within the same phylogenetic group share similar exon/intron organization and domain composition. In addition, 16 duplicated gene pairs were formed by a -specific whole-genome duplication (WGD) event approximately 13 million years ago (Mya). By investigating the expression profiles of these gene pairs in various tissues, we showed that the expression pattern is conserved in the polyploidy-derived JmjC duplicates, demonstrating that the majority of were preferentially retained after the most recent WGD event and suggesting important roles for demethylase duplications in soybean evolution. These results shed light on the evolutionary history of this family in soybean and provide insights into the which will be helpful to reveal their functions in controlling soybean development.

Histone modifications, such as methylation and demethylation, have crucial roles in regulating chromatin structure and gene expression. Lysine-specific histone demethylases (LSDs) belong to the amine oxidase family, which is an important family of histone lysine demethylases (KDMs), and functions in maintaining homeostasis of histone methylation. Here, we identified six LSD-like (LDL) genes from the important leguminous soybean. Phylogenetic analyses divided the six GmLDLs into four clusters with two highly conserved SWRIM and amine oxidase domains. Indeed, demethylase activity assay using recombinant GmLDL proteins in vitro demonstrated that GmLDLs have demethylase activity toward mono- and dimethylated Lys4 but not trimethylated histone 3, similar to their orthologs previously reported in animals. Using real-time PCR experiments in combination with public transcriptome data, we found that these six GmLDL genes exhibit comparable expressions in multiple tissues or in response to different abiotic stresses. Moreover, our genetic variation investigation of GmLDL genes among 761 resequenced soybean accessions indicates that GmLDLs are well conserved during soybean domestication and improvement. Taken together, these findings demonstrate that GmFLD, GmLDL1a, and GmLDL1b are bona fide H3K4 demethylases towards H4K4me1/2 and GmLDLs exist in various members with likely conserved and divergent roles in soybeans.

Many products contain silver nanoparticles, which are adsorbed by living organisms and then go through biological barriers. In particular, penetration of silver nanoparticles through the placental barrier is likely to damage the offspring. Here, we review hazards of silver nanoparticles with focus on exposure during pregnancy, toxicokinetics at maternal and fetal layers, ex vivo and in vivo placenta transfer models, and factors affecting the transfer. Exposure occurs by oral uptake, inhalation, dermal contact, and systemic administration. Toxicokinetics include absorption, distribution in tissues, metabolism and excretion. The accumulation efficiency is primarily influenced by the mode of exposure. Injection exhibits the highest bioavailability, followed by inhalation and oral uptake. Particles within the range of tens of nanometers are capable of crossing the placenta, according to an ex vivo placental perfusion model. In contrast, larger particles in the range of hundreds of nanometers are expelled outside. Due to the size restriction of the trophoblast channel, which typically ranges from 15 to 25 nm, it is possible for silver nanoparticles with an average size of around 20 nm to passively enter the placenta through the pericellular pathway, such as diffusion. On the other hand, larger silver nanoparticles may be delivered to the placenta through endocytosis, which can occur via phagocytosis, receptor-mediated or independent mechanisms.

Summary Epigenetic variations, including DNA methylation and small RNAs, are crucial for plant stress adaptation. However, their association with soybean adaptation to natural environments remains unclear. Through multi‐omics analyses, we investigate soybeans from distinct geographical regions (Northern China: HH43, Southern China: HX3, and Wm82) and grown under contrasting South Winter (SW) and South Summer (SS) conditions in China. Transcriptomic clustering classifies soybeans into two distinct groups based on SW and SS. Methylome demonstrates increased CHH methylation in SW, accompanied by HDA6 up‐regulation, leading to chromatin compaction and transcriptional repression. Substantial Copia retrotransposons and DNA transposons are also repressed in SW. Interestingly, DNA methylation predominantly influences down‐regulated/up‐regulated COR genes for HH43 and HX3 through increased/decreased DNA methylation, respectively. In contrast, lower CG/CHG methylation in SW coincided with reduced DNA methyltransferases expression. Notably, non‐CG methylation contributes more to DSR in adaptive traits under selective pressure. Such as the E2 domesticated gene exhibits lower CHG methylation within the gene body region and down‐regulated expression in SW for HH43. Furthermore, 22‐nt siRNA are substantially degraded in SW, and GmDCL2a/2b mutation results in increased plant sensitivity to low temperatures. These highlight the dynamic interplay between DNA methylation, small RNAs and gene expression in soybean adaptation to natural environments.

Human exposure to environmental arsenic induces cardiovascular diseases such as arrhythmias, hypertension, and arteriosclerosis. Here, we review the toxicological and cardiovascular impacts of arsenic in in vitro cardiac and vascular models. The mechanism of arsenic-induced cardiovascular impairments includes oxidative stress, epigenetic modifications, chromatin instability, subcellular damage, and premature aging. The different types of cardiac and vascular cells exhibit distinct responses to arsenic exposure. Arsenic causes arrhythmias, which involve alteration of cardiomyocyte potassium channels and, in turn, repolarization issues. This is mainly due to redox signals that cause epigenetic modifications of potassium channels. On the other hand, vascular lesions, such as damage to blood vessels, occur mainly due to an imbalance in redox levels. This imbalance leads to premature senescence of cells and stop the cell cycle. Furthermore, intracellular accumulation of calcium and ferrous ions plays a major role in arsenic-induced vascular cell apoptosis and cardiomyocyte ferroptosis, respectively.