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Background Alkaline stress poses severe threats to sustainable triticale production. However, lack of molecular and metabolic data restricts the efficient breeding and field management of triticale cultivated in alkaline soils. The aim of this study was to explore the genotypical effects on modifications of transcriptional and metabolic profile in triticale, and find out the prospective genes and metabolites responsible for alkaline tolerance. Results In this study, we compared the root development in two triticale cultivars with contrasting alkali tolerance, and found that root number, length, surface area and biomass were reduced, but the average root diameter was increased in triticale subjected to alkaline stress. The stress effect was extremely significant in the alkali-sensitive cultivar. Comparative transcriptomic and metabolomic analyses revealed that the genotype effect on alkaline stress resistance was predominantly connected with metabolism of amino acids and flavonoids, as well as the featuring biosynthesis of benzoxazinoid and brassinosteroid. Simultaneous regulation of genes and metabolites involved in betalains, dopa and a group of other pathways in the two cultivars were suggested to be basic alkaline stress responses in triticale. Additionally, expression of key genes involved in these processes and typical alkaline stress responses in plants were examined and the subset including AT1 - PIP2 , RGI1 , SAUR215 , SCaBP3 indicated their implication in alkali tolerance in triticale. Conclusions These gene, metabolite, and pathway resources depict the internal responsive atlas of triticale under alkaline stress. Those involved in the metabolism of key amino acids, flavonoids, and betalains as mentioned above represent prior targets for future genetic studies and breeding of stress-tolerant triticale germplasm to cope with alkaline stress.

Prion diseases are a group of fatal neurodegenerative disorders characterized by the abnormal folding of cellular prion proteins into pathogenic forms. The development of these diseases is intricately linked to oxidative stress and mitochondrial dysfunction. Irisin, an endogenous myokine, has demonstrated considerable neuroprotective potential due to its antioxidative properties. However, the protective effects of irisin against prion diseases have yet to be clarified. Our findings indicate that treatment with exogenous irisin can mitigate the apoptosis induced by PrP 106–126. Additionally, irisin significantly reduces oxidative stress and alleviates the mitochondrial dysfunction triggered by PrP 106–126 . Furthermore, irisin treatment targets uncoupling protein 2 (UCP2) and activates the AMPK-Nrf2 pathway, substantially improving oxidative stress and mitochondrial dysfunction in N2a cells induced by PrP 106–126 . These results suggest that irisin represents a novel and promising therapeutic approach for treating prion diseases. Highlights PrP 106–126 induces mitochondrial dysfunction in a mtROS-dependent manner. Irisin alleviates PrP 106–126 -induced oxidative stress via UCP2 activation. UCP2 mediates irisin-induced AMPK-Nrf2 activation. Inhibition of oxidative stress rescues PrP 106–126 -induced cell death. PrP 106–126 exposure induces ROS accumulation, leading to mitochondrial dysfunction and cell death. Irisin has a protective effect against PrP 106–126 toxicity and depends on the activation of the UCP2-AMPK signaling pathway.

A persistent accumulation of damaged mitochondria is part of prion disease pathogenesis. Normally, damaged mitochondria are cleared via a major pathway that involves the E3 ubiquitin ligase parkin and PTEN-induced kinase 1 (PINK1) that together initiate mitophagy, recognize and eliminate damaged mitochondria. However, the precise mechanisms underlying mitophagy in prion disease remain largely unknown. Using prion disease cell models, we observed PINK1-parkin-mediated mitophagy deficiency in which parkin depletion aggravated blocked mitochondrial colocalization with LC3-II-labeled autophagosomes, and significantly increased mitochondrial protein levels, which led to inhibited mitophagy. Parkin overexpression directly induced LC3-II colocalization with mitochondria and alleviated defective mitophagy. Moreover, parkin-mediated mitophagy was dependent on PINK1, since PINK1 depletion blocked mitochondrial Parkin recruitment and reduced optineurin and LC3-II proteins levels, thus inhibiting mitophagy. PINK1 overexpression induced parkin recruitment to the mitochondria, which then stimulated mitophagy. In addition, overexpressed parkin and PINK1 also protected neurons from apoptosis. Furthermore, we found that supplementation with two mitophagy-inducing agents, nicotinamide mononucleotide (NMN) and urolithin A (UA), significantly stimulated PINK1-parkin-mediated mitophagy. However, compared with NMN, UA could not alleviate prion-induced mitochondrial fragmentation and dysfunction, and neuronal apoptosis. These findings show that PINK1-parkin-mediated mitophagy defects lead to an accumulation of damaged mitochondria, thus suggesting that interventions that stimulate mitophagy may be potential therapeutic targets for prion diseases.

Prion diseases caused by the cellular prion protein (PrP C ) conversion into a misfolded isoform (PrP Sc ) are associated with multiple mitochondrial damages. We previously reported mitochondrial dynamic abnormalities and cell death in prion diseases via modulation of a variety of factors. Optic atrophy 1 (OPA1) is one of the factors that control mitochondrial fusion, mitochondrial DNA (mtDNA) maintenance, bioenergetics, and cristae integrity. In this study, we observed downregulation of OPA1 in prion disease models in vitro and in vivo, mitochondria structure damage and dysfunction, loss of mtDNA, and neuronal apoptosis. Similar mitochondria findings were seen in OPA1-silenced un-infected primary neurons. Overexpression of OPA1 not only alleviated prion-induced mitochondrial network fragmentation and mtDNA loss, decrease in intracellular ATP, increase in ADP/ATP ratio, and decrease in mitochondrial membrane potential but also protected neurons from apoptosis by suppressing the release of cytochrome c from mitochondria to cytosol and activation of the apoptotic factor, caspase 3. Our results demonstrated that overexpression of OPA1 alleviates prion-associated mitochondrial network fragmentation and cristae remodeling, mitochondrial dysfunction, mtDNA depletion, and neuronal apoptosis, suggesting that OPA1 may be a novel and effective therapeutic target for prion diseases.

Objective To determine the dose correlation between point B and metastatic lymph nodes in cervical cancer treated with three‐dimensional (3D) high‐dose‐rate (HDR) brachytherapy. Methods A retrospective study was conducted involving 30 cervical cancer patients with lymph node metastases who completed 3D HDR brachytherapy at Liaoning Cancer Hospital and Institute from May 2019 to November 2020. Brachytherapy was performed with a Fletcher applicator at a prescribed dose of 28 Gy/4 f. Computed tomography images of the external irradiation target were fused with delineated images of the brachytherapy target on the MIM system. The minimum dose received by 90% of the volume (D90) was read on the MIM system for all metastatic lymph nodes and the point B dose was read for the brachytherapy target area. In total, 78 metastatic lymph nodes from 30 patients with cervical cancer were included in this study, including para‐aortic, common iliac, external iliac, internal iliac, obturator, and inguinal lymph nodes. Paired t‐tests and Pearson correlation coefficient analyses were performed to examine the difference in the equivalent dose between each group of metastatic lymph nodes and point B. Results The mean equivalent point B dose was 6.69 ± 1.08 Gy. There were significant differences in dose between point B and the para‐aortic, common iliac, external iliac, internal iliac, and inguinal lymph nodes (p < 0.05), with a weak positive correlation (r < 0.4). There was no statistically significant difference in dose between obturator lymph nodes and point B (p = 0.3999), with a positive correlation (r = 0.65). Conclusion 3D HDR brachytherapy contributed significantly to pelvic lymph node doses in cervical cancer patients with lymph node metastasis, but less to para‐aortic and inguinal lymph node doses. The dose at point B grossly overestimated the mean dose to pelvic lymph nodes; only the dose to obturator lymph nodes was similar to that of point B, with a slightly positive correlation. 3D high‐dose‐rate brachytherapy contributes significantly to pelvic lymph nodes in cervical cancer patients with lymph nodes metastases.

Recent years have witnessed a surge in the publication of dozens of genome assemblies for Triticeae crops, which have significantly advanced gene-related research in wheat, rye, and triticale. However, this progress has also introduced challenges in selecting universally efficient and applicable reference genomes for genotypes with distant or ambiguous phylogenetic relationships. In this study, we assessed the completeness and accuracy of genome assemblies for wheat, rye, and triticale using comparative benchmarking universal single-copy orthologue (BUSCO) analysis and transcript mapping approaches. BUSCO analysis revealed that the proportion of complete genes positively correlated with RNA-seq read mappability, while the frequency of internal stop codons served as a significant negative indicator of assembly accuracy and RNA-seq data mappability in wheat. By integrated analysis of alignment rate, covered length, and total depth from RNA-seq data, we identified the assemblies of SY Mattis, Lo7, and SY Mattis plus Lo7 as the most robust references for gene-related studies in wheat, rye, and triticale, respectively. Furthermore, we recommend that the D genome sequence be incorporated in reference assemblies in bioinformatic analyses for triticale, as introgression, translocation, and substitution of the D genome into triticale genome frequently occurs during triticale breeding. The frequency of internal stop codons could help in evaluating correctness of assemblies published in the future, and other findings are expected to support gene-related research in wheat, rye, triticale, and other closely related species.

Proper mitochondrial performance is imperative for the maintenance of normal neuronal function to prevent the development of neurodegenerative diseases. Persistent accumulation of damaged mitochondria plays a role in prion disease pathogenesis, which involves a chain of events that culminate in the generation of reactive oxygen species and neuronal death. Our previous studies have demonstrated that PINK1/Parkin-mediated mitophagy induced by PrP 106−126 is defective and leads to an accumulation of damaged mitochondria after PrP 106−126 treatment. Externalized cardiolipin (CL), a mitochondria-specific phospholipid, has been reported to play a role in mitophagy by directly interacting with LC3II at the outer mitochondrial membrane. The involvement of CL externalization in PrP 106−126 -induced mitophagy and its significance in other physiological processes of N2a cells treated with PrP 106−126 remain unknown. We demonstrate that the PrP 106−126 peptide caused a temporal course of mitophagy in N2a cells, which gradually increased and subsequently decreased. A similar trend in CL externalization to the mitochondrial surface was seen, resulting in a gradual decrease in CL content at the cellular level. Inhibition of CL externalization by knockdown of CL synthase, responsible for de novo synthesis of CL, or phospholipid scramblase-3 and NDPK-D, responsible for CL translocation to the mitochondrial surface, significantly decreased PrP 106−126 -induced mitophagy in N2a cells. Meanwhile, the inhibition of CL redistribution significantly decreased PINK1 and DRP1 recruitment in PrP 106−126 treatment but had no significant decrease in Parkin recruitment. Furthermore, the inhibition of CL externalization resulted in impaired oxidative phosphorylation and severe oxidative stress, which led to mitochondrial dysfunction. Our results indicate that CL externalization induced by PrP 106−126 on N2a cells plays a positive role in the initiation of mitophagy, leading to the stabilization of mitochondrial function.

The perennial legume alfalfa (Medicago sativa L.) is of high value in providing cheap and high-nutritive forages. Due to a lack of tillage during the production period, the soil in which alfalfa grows prunes to become compacted through highly mechanized agriculture. Compaction deteriorates the soil’s structure and fertility, leading to compromised alfalfa development and productivity. However, the way alfalfa responses to different levels of soil compaction and the underlying molecular mechanism are still unclear. In this study, we systematically evaluated the effects of gradient compacted soil on the growth of different cultivars of alfalfa, especially the root system architecture, phytohormones and internal gene expression profile alterations. The results showed that alfalfa growth was facilitated by moderate soil compaction, but drastically inhibited when compaction was intensified. The inhibition effect was universal across different cultivars, but with different severity. Transcriptomic and physiological studies revealed that the expression of a set of genes regulating the biosynthesis of lignin and flavonoids was significantly repressed in compaction treated alfalfa roots, and this might have resulted in a modified secondary cell wall and xylem vessel formation. Phytohormones, like ABA, are supposed to play pivotal roles in the regulation of the overall responses. These findings provide directions for the improvement of field soil management in alfalfa production and the molecular breeding of alfalfa germplasm with better soil compaction resilience.

This study investigated the efficiency of biochar in eliminating Cd(II) and Pb(II) ions from slurries generated from construction-derived waste materials. The construction waste slurry samples consisted of genuinely contaminated sludge sediments. To improve the adsorption capacity of biochar for metal ions, coconut shell-derived biochar was subjected to hydrochloric acid treatment. The modified biochar demonstrated an improved porous structure and showed a higher concentration of oxygen-containing functional groups compared to the untreated biochar. After a 48 h contact with the contaminated slurry, the treated biochar attained removal efficiencies of 21.15% for Cd(II) and 19.43% for Pb(II). The kinetic study of the adsorption process conformed to a pseudo-second-order model. Density functional theory (DFT) computations clarified the adsorption mechanism of Cd(II) and Pb(II) by carboxyl (-COOH) and hydroxyl (-OH) functional groups. The findings demonstrated that functional groups contribute lone-pair electrons for the adsorption of heavy metal ions. The carboxyl (-COOH) functional group exhibited a greater affinity for binding Cd(II) and Pb(II) ions than the hydroxyl (-OH) group, which explains the improved adsorption efficiency seen in biochar treated with hydrochloric acid. These findings offer theoretical validation for the use of hydrochloric acid-modified biochar as an efficient adsorbent for the remediation of sludge contaminated with Cd(II) and Pb(II).

In the intelligent transformation of spraying operations, the investigation into the robotic spraying process holds significant importance. The spraying process, however, falls within the realm of experience-driven technology, characterized by high complexity, diverse parameters, and coupling effects. Moreover, the quality of manual spraying processes relies entirely on manual experience. Thus, the crux of the intelligent transformation of spraying robots lies in establishing a mapping model between the spraying process and the resultant spraying quality. To address the challenge of intelligently transforming empirical spraying processes and achieving the mapping from the spraying process to spraying quality, an algorithm employing an enhanced extreme learning machine-based neural network is proposed for predicting spraying process parameters with respect to the evaluation index of spraying quality. In this approach, an algorithmic model based on the Extreme Learning Machine (ELM) neural network is initially constructed utilizing five spraying process parameters: spraying speed, spraying height, spraying width pressure, atomization pressure, and oil spraying pressure. Two spraying quality evaluation indexes, namely average film thickness at the center point and surface roughness, are also incorporated. Subsequently, the prediction neural network is optimized using the K-means improved predator optimization algorithm (KHPO) to enhance the model’s prediction accuracy. This optimization step aims to improve the efficiency of the model in predicting spraying quality based on the specified process parameters. Finally, data collection and model validation for the spraying quality prediction algorithm are conducted using a designed robotic automated waterborne paint spraying experimental system. The experimental results demonstrate a significant reduction in the prediction error of the KHPO-ELM neural network model for the average film thickness center point, showcasing a decrease of 61.95% in comparison to the traditional ELM neural network and 50.81% in comparison to the BP neural network. Likewise, the improved neural network model yields a 2.31% decrease in surface roughness prediction error compared to the traditional ELM neural network and a substantial 54.0% reduction compared to the BP neural network. Consequently, the KHPO-ELM neural network, incorporating the prediction algorithm, effectively facilitates the prediction of multi-spraying process parameters for the center point of average film thickness and surface roughness in automated robot spraying. Notably, the prediction algorithm exhibits a commendable level of accuracy in these predictions.