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Parkinson's disease (PD) is a neurodegenerative disorder characterized by degeneration of dopaminergic neurons associated with dysregulation of iron homeostasis in the brain. Ferroptosis is an iron-dependent cell death process that serves as a significant regulatory mechanism in PD. However, its underlying mechanisms are not yet fully understood. By performing RNA sequencing analysis, we found that the main iron storage protein ferritin heavy chain 1 (FTH1) is differentially expressed in the rat 6-hydroyxdopamine (6-OHDA) model of PD compared with control rats. Our present work demonstrates that FTH1 is involved in iron accumulation and the ferroptosis pathway in this model. Knockdown of FTH1 in PC-12 cells significantly inhibited cell viability and caused mitochondrial dysfunction. Moreover, FTH1 was found to be involved in ferritinophagy, a selective form of autophagy involving the degradation of ferritin by ferroptosis. Overexpression of FTH1 in PC-12 cells impaired ferritinophagy and downregulated microtubule-associated protein light chain 3 and nuclear receptor coactivator 4 expression, ultimately suppressing cell death induced by ferroptosis. Consistent with these findings, the ferritinophagy inhibitors chloroquine and bafilomycin A1 inhibited ferritin degradation and ferroptosis in 6-OHDA-treated PC-12 cells. This entire process was mediated by the cyclic regulation of FTH1 and ferritinophagy. Taken together, these results suggest that FTH1 links ferritinophagy and ferroptosis in the 6-OHDA model of PD, and provide a new perspective and potential for a pharmacological target in this disease.

Artificial reefs (ARs) are important for habitat restoration and exhibit clear spatial gradient effects. However, most studies focus on AR groups, neglecting the ecological functions and mechanisms of individual AR units at a local scale. This limits a deeper understanding and optimization of the ecological effects of ARs. This study employed high-throughput sequencing to examine the seasonal and spatial variations in sediment microbial communities surrounding AR units. The results showed that microbial community distributions in sediments varied significantly with seasons, reef distance, and reef structure. The community structure varied significantly across seasons at different reef distances, with the most unique structure observed at 3 m (1.5-times the reef height). In May, microbial community spatial changes were mainly driven by sediment organic matter (OM), while in November and February, although the spatial enrichment patterns of microbial groups changed seasonally, they were not strongly affected by functional types (aerobic or anaerobic). The Neutral Community Model (NCM) showed lower levels of R2 and Nm at 0 m and 3 m, which are relatively consistent with the flow field effects (upwelling and reverse eddy currents). Key environmental factors and their regulatory effects vary with distance from the reef.

The modification of methyltransferase-like (METTL) enzymes plays important roles in various cellular responses by regulating microRNA expression. However, how m6A modification is involved in stress granule (SG) formation in the early stage of acute ischemic stroke by affecting the biogenesis processing of microRNAs remains unclear. Here, we established a middle cerebral artery occlusion (MCAO) model in rats and an oxygen-glucose deprivation/reperfusion (OGD/R) model in primary cortical neurons and PC12 cells to explore the potential mechanism between m6A modification and SG formation. The in vivo results showed that the level of infarction and apoptosis increased while SG formation decreased significantly within the ischemic cortex with improved reperfusion time after 2 h of ischemia. Consistent with the in vivo data, an inverse association between the apoptosis level and SG formation was observed in PC12 cells during the reperfusion period after 6 h of OGD stimulation. Both in vivo and in vitro results showed that the expression of METTL3 protein, m6A and miR-335 was significantly decreased with the reperfusion period. Overexpression of the METTL3 and METTL3 gene-knockdown in PC12 cells were achieved via plasmid transfection and CRISPR-Cas9 technology, respectively. Overexpression or knockdown of METTL3 in oxygen-glucose deprivation of PC12 cells resulted in functional maturation of miR-335, SG formation and apoptosis levels. In addition, we found that miR-335 enhanced SG formation through degradation of the mRNA of the eukaryotic translation termination factor (Erf1). In conclusion, we found that METTL3-mediated m6A methylation increases the maturation of miR-335, which promotes SG formation and reduces the apoptosis level of injury neurons and cells, and provides a potential therapeutic strategy for AIS.

In this study, we investigate a delayed reaction-diffusion predator-prey system with the effect of toxins. We first investigate whether the internal equilibrium exists. We then provide certain requirements for the presence of Turing and Hopf bifurcations by examining the corresponding characteristic equation. We also study Turing-Hopf and Hopf bifurcations brought on by delays. Finally, numerical simulations that exemplify our theoretical findings are provided. The quantitatively obtained properties are in good agreement with the findings that the theory had predicted. The effects of toxins on the system are substantial, according to theoretical and numerical calculations.

Predictive industrial maintenance promotes proactive scheduling of maintenance to minimize unexpected device anomalies/faults. Almost all current predictive industrial maintenance techniques construct a model based on prior knowledge or data at build-time. However, anomalies/faults will propagate among sensors and devices along correlations hidden among sensors. These correlations can facilitate maintenance. This paper makes an attempt on predicting the anomaly/fault propagation to perform predictive industrial maintenance by considering the correlations among faults. The main challenge is that an anomaly/fault may propagate in multiple ways owing to various correlations. This is called as the uncertainty of anomaly/fault propagation. This present paper proposes a correlation-based event routing approach for predictive industrial maintenance by improving our previous works. Our previous works mapped physical sensors into a soft-ware-defined abstraction, called proactive data service. In the service model, anomalies/faults are encapsulated into events. We also proposed a service hyperlink model to encapsulate the correlations among anomalies/faults. This paper maps the anomalies/faults propagation into event routing and proposes a heuristic algorithm based on service hyperlinks to route events among services. The experiment results show that, our approach can reach 100% precision and 88.89% recall at most.

Seagrasses are marine flowering plants found in tropical and sub-tropical areas that live in coastal regions between the sea and land. All seagrass species evolved from terrestrial monocotyledons, providing the opportunity to study plant adaptation to sea environments. Here, we sequenced the chloroplast genomes (cpGenomes) of three Zostera species, then analyzed and compared their cpGenome structures and sequence variations. We also performed a phylogenetic analysis using published seagrass chloroplasts and calculated the selection pressure of 17 species within seagrasses and nine terrestrial monocotyledons, as well as estimated the number of shared genes of eight seagrasses. The cpGenomes of Zosteraceae species ranged in size from 143,877 bp ( Zostera marina ) to 152,726 bp ( Phyllospadix iwatensis ), which were conserved and displayed similar structures and gene orders. Additionally, we found 17 variable hotspot regions as candidate DNA barcodes for Zosteraceae species, which will be helpful for studying the phylogenetic relationships and interspecies differences between seagrass species. Interestingly, nine genes had positive selection sites, including two ATP subunit genes ( atpA and atpF ), two ribosome subunit genes ( rps4 and rpl20 ), two DNA-dependent RNA polymerase genes ( rpoC1 and rpoC2 ), as well as accD , clpP , and ycf2 . These gene regions may have played key roles in the seagrass adaptation to diverse environments. The Branch model analysis showed that seagrasses had a higher rate of evolution than terrestrial monocotyledons, suggesting that seagrasses experienced greater environmental pressure. Moreover, a branch-site model identified positively selected sites (PSSs) in ccsA , suggesting their involvement in the adaptation to sea environments. These findings are valuable for further investigations on Zosteraceae cpGenomes and will serve as an excellent resource for future studies on seagrass adaptation to sea environments.

Parkinson's disease (PD) is a neurodegenerative disease characterized by the selective loss of dopaminergic neurons in the substantia nigra (SN). In a previous study, the authors demonstrated that ferritin heavy chain 1 (FTH1) inhibited ferroptosis in a model of 6-hydroxydopamine (6-OHDA)-induced PD. However, whether and how microRNAs (miRNAs/miRs) modulate FTH1 in PD ferroptosis is not yet well understood. In the present study, in vivo and in vitro models of PD induced by 6-OHDA were established. The results in vivo and in vitro revealed that the levels of the ferroptosis marker protein, glutathione peroxidase 4 (GPX4), and the PD marker protein, tyrosine hydroxylase (TH), were decreased in the model group, associated with a decreased FTH1 expression and the upregulation of miR-335. In both the in vivo and in vitro models, miR-335 mimic led to a lower FTH1 expression, exacerbated ferroptosis and an enhanced PD pathology. The luciferase 3′-untranslated region reporter results identified FTH1 as the direct target of miR-335. The silencing of FTH1 in 6-OHDA-stimulated cells enhanced the effects of miR-335 on ferroptosis and promoted PD pathology. Mechanistically, miR-335 enhanced ferroptosis through the degradation of FTH1 to increase iron release, lipid peroxidation and reactive oxygen species (ROS) accumulation, and to decrease mitochondrial membrane potential (MMP). On the whole, the findings of the present study reveal that miR-335 promotes ferroptosis by targeting FTH1 in in vitro and in vivo models of PD, providing a potential therapeutic target for the treatment of PD.

Seed development is a crucial phase in the life cycle of seed-propagated plants. As the only group of angiosperms that evolved from terrestrial plants to complete their life cycle submerged in marine environments, the mechanisms underlying seed development in seagrasses are still largely unknown. In the present study, we attempted to combine transcriptomic, metabolomic, and physiological data to comprehensively analyze the molecular mechanism that regulates energy metabolism in Zostera marina seeds at the four major developmental stages. Our results demonstrated that seed metabolism was reprogrammed with significant alteration of starch and sucrose metabolism, glycolysis, the tricarboxylic acid cycle (TCA cycle), and the pentose phosphate pathway during the transition from seed formation to seedling establishment. The interconversion of starch and sugar provided energy storage substances in mature seeds and further acted as energy sources to support seed germination and seedling growth. The glycolysis pathway was active during Z. marina germination and seedling establishment, which provided pyruvate for TCA cycle by decomposing soluble sugar. Notably, the biological processes of glycolysis were severely inhibited during Z . marina seed maturation may have a positive effect on seed germination, maintaining a low level of metabolic activity during seed maturation to preserve seed viability. Increased acetyl-CoA and ATP contents were accompanied with the higher TCA cycle activity during seed germination and seedling establishment, indicating that the accumulations of precursor and intermediates metabolite that can strengthen the TCA cycle and facilitate energy supply for Z . marina seed germination and seedling growth. The large amount of oxidatively generated sugar phosphate promotes fructose 1,6-bisphosphate synthesis to feed back to glycolysis during seed germination, indicating that the pentose phosphate pathway not only provides energy for germination, but also complements the glycolytic pathway. Collectively, our findings suggest these energy metabolism pathways cooperate with each other in the process of seed transformation from maturity to seedling establishment, transforming seed from storage tissue to highly active metabolic tissue to meet the energy requirement seed development. These findings provide insights into the roles of the energy metabolism pathway in the complete developmental process of Z . marina seeds from different perspectives, which could facilitate habitat restoration of Z . marina meadows via seeds.

Photocrosslinked methacrylated hyaluronic acid (MeHA) hydrogels support chondrogenesis of encapsulated human mesenchymal stem cells (hMSCs). However, the covalent crosslinks formed via chain polymerization in these hydrogels are hydrolytically non-degradable and restrict cartilage matrix spatial distribution and cell spreading. Meanwhile, cells are known to remodel their surrounding extracellular matrix (ECM) by secreting catabolic enzymes, such as MMPs. Hydrogels that are created with bifunctional crosslinkers containing MMP degradable peptide sequences have been shown to influence hMSC differentiations. However, crosslinks formed in the MMP-degradable hydrogels of these previous studies are also prone to hydrolysis, thereby confounding the effect of MMP-mediated degradation. The objective of this study is to develop a MMP-sensitive but hydrolytically stable hydrogel scaffold and investigate the effect of MMP-mediated hydrogel degradation on the chondrogenesis of the encapsulated hMSCs. Hyaluronic acid macromers were modified with maleimide groups and crosslinked with MMP-cleavable peptides or control crosslinkers containing dual thiol groups. The chondrogenesis of the hMSCs encapsulated in the hydrolytically stable MMP-sensitive HA hydrogels were compared with that of the MMP-insensitive HA hydrogels. It was found that hMSCs encapsulated in the MMP-sensitive hydrogels switched to a more spreaded morphology while cells in the MMP-insensitive hydrogels remained in round shape. Furthermore, hMSCs in the MMP-sensitive hydrogels expressed higher level of chondrogenic marker genes but lower level of hypertrophic genes compared to cells in the MMP-insensitive hydrogels. As a result, more cartilage specific matrix molecules but less calcification was observed in the MMP-degradable hydrogels than in the MMP-insensitive hydrogels. Findings from this study demonstrate that cell-mediated scaffold degradation regulates the chondrogenesis and hypertrophy of hMSCs encapsulated in HA hydrogels.

Background Several methods can assist in detecting early esophageal cancer (EEC) and staging esophageal cancer (EC) invasion depth. Objective To evaluate the accuracy of magnifying endoscopy with narrow-band imaging (ME-NBI) plus endoscopic ultrasonography (EUS) for diagnosing EC. Methods We searched the PubMed, Embase, Cochrane Library, and China National Knowledge Infrastructure (CNKI) databases for relevant studies. The Quality Assessment of Diagnostic Accuracy Studies 2 (QADAS2) was used to assess the studies’ methodological quality. The sensitivity, specificity, positive likelihood (LR+), negative likelihood (LR−), and diagnostic odds ratio (DOR) were calculated, and the summary receiver operating characteristic (SROC) curves were drawn to evaluate the diagnostic performance. Results Seven studies were included. The meta-analysis suggested that the pooled sensitivity, specificity, LR+, LR−, and DOR of ME-NBI plus EUS for diagnosing EC were 0.947 (95% confidence interval [CI], 0.901–0.975), 0.894 (95% CI , 0.847–0.931), 7.989 (95% CI , 4.264–14.970), 0.066 (95% CI , 0.035–0.124), and 137.96 (95% CI , 60.369–315.27), respectively. Those values for staging the invasive depth were 0.791 (95% CI , 0.674–0.881), 0.943 (95% CI , 0.906–0.968), 13.087 (95% CI , 7.559–22.657), 0.226 (95% CI , 0.142–0.360), and 61.332 (95% CI , 27.343–137.57). The areas under the curves (AUCs) for diagnosis and staging were 0.97 and 0.95, respectively. Conclusions ME-NBI plus EUS might be an adequate diagnostic and staging modality for EC. Due to the study limitations, more large-scale, high-quality studies are needed to confirm the diagnostic accuracy of ME-NBI plus EUS.