Construction of an ER stress-related prognostic signature for predicting prognosis and screening the effective anti-tumor drug in osteosarcoma.

BACKGROUND: Osteosarcoma is the most common malignant primary bone tumor in infants and adolescents. The lack of understanding of the molecular mechanisms underlying osteosarcoma progression and metastasis has contributed to a plateau in the development of current therapies. Endoplasmic reticulum (ER) stress has emerged as a significant contributor to the malignant progression of tumors, but its potential regulatory mechanisms in osteosarcoma progression remain unknown. METHODS: In this study, we collected RNA sequencing and clinical data of osteosarcoma from The TCGA, GSE21257, and GSE33382 cohorts. Differentially expressed analysis and the least absolute shrinkage and selection operator regression analysis were conducted to identify prognostic genes and construct an ER stress-related prognostic signature (ERSRPS). Survival analysis and time dependent ROC analysis were performed to evaluate the predictive performance of the constructed prognostic signature. The "ESTIMATE" package and ssGSEA algorithm were utilized to evaluate the differences in immune cells infiltration between the groups. Cell-based assays, including CCK-8, colony formation, and transwell assays and co-culture system were performed to assess the effects of the target gene and small molecular drug in osteosarcoma. Animal models were employed to assess the anti-osteosarcoma effects of small molecular drug. RESULTS: Five genes (BLC2, MAGEA3, MAP3K5, STC2, TXNDC12) were identified to construct an ERSRPS. The ER stress-related gene Stanniocalcin 2 (STC2) was identified as a risk gene in this signature. Additionally, STC2 knockdown significantly inhibited osteosarcoma cell proliferation, migration, and invasion. Furthermore, the ER stress-related gene STC2 was found to downregulate the expression of MHC-I molecules in osteosarcoma cells, and mediate immune responses through influencing the infiltration and modulating the function of CD8+ T cells. Patients categorized by risk scores showed distinct immune status, and immunotherapy response. ISOX was subsequently identified and validated as an effective anti-osteosarcoma drug through a combination of CMap database screening and in vitro and in vivo experiments. CONCLUSION: The ERSRPS may guide personalized treatment decisions for osteosarcoma, and ISOX holds promise for repurposing in osteosarcoma treatment.

Associations between cortical bone-to-implant contact and microstructure derived from CBCT and implant primary stability.

OBJECTIVES: To evaluate the associations between the cortical bone-to-implant contact (CBIC), bone microstructure derived from cone-beam computed tomography (CBCT), and the primary stability of the implant. MATERIALS AND METHODS: Twenty-two patients with 65 implants were enrolled in this study. The peak insertion torque values (ITVs) were measured during implant insertion, and the implant stability quotient (ISQ) values were measured immediately after implant placement and 3 months after surgery. The profiles of the peri-implant bone structure were outlined using the volumetric reconstruction of the CBCTs and superimposition of the virtual models, and the features of CBIC and bone microstructure parameters were measured. The linear mixed effects model and generalized estimating equation were used to explore the predictors for implant primary stability. RESULTS: The average ITV, baseline, and secondary ISQ values were 31.44 ± 6.54 N·cm, 73.34 ± 7.39, and 80.32 ± 4.58, respectively. Statistically significant correlations were found between ITV and surface area of CBIC (r = .340, p = .006), bone volume fraction (r = .294, p = .017), and bone surface fraction (r = -.278, p = .039). Implants with buccolingual CBIC had a higher ITV than implants without CBIC (p = .016). None of the parameters were associated with baseline and secondary ISQ values in generalized estimating equation analysis (all p > .05). CONCLUSIONS: Within the limitations of the study, preoperative CBCT measurements might enable the prediction of ITV and therefore of implant primary stability values.

Effects of NLRP3 on implants placement. / NLRP3ç‚Žç—‡å°ä½“å¯¹ç§æ¤ä½“æ¤å ¥çš„å½±å“.

Bone stability is precisely controlled by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. When the balance is broken, the integrity of the bone structure will be destroyed. Inflammasomes are important protein complexes in response to pathogen-related molecular models or injury-related molecular models, which can promote the activation and secretion of proinflammatory cytokines and activate a local inflammatory response. NOD-like receptor thermal protein domain associated protein (NLRP) 3 inflammasome can promote bone resorption through the activation of the proinflammatory cytokines interleukin (IL)-1ß, IL-18 and the induction of caspase-1-mediated pyroptosis. Inhibiting the production of NLRP3 inflammasome may be beneficial to improve comfort and bone stability. The presence of metal particles and microorganisms around implants can activate NLRP3 and promote bone absorption. NLRP3 inflammasome plays an important role in the maintenance of bone stability around implants, however, most studies focus on orthopedic implants and periodontitis. This article reviews the effects of NLRP3 inflammasome on bone formation, resorption and pain induced by implants, and the possibility of NLRP3 as a target for preventing peri-implantitis is discussed.

Stereoselective Synthesis of Tetrasubstituted Olefins via Visible-Light-Promoted Iodine-Mediated Homo-Coupling of Diazo.

A visible-light-promoted iodine-mediated homo-coupling of diazo was first described. A series of tetrasubstituted olefins were synthesized in high yields and with low to high Z-selectivities from phenyldiazoacetates. For 3-diazooxindoles, isoindigo derivatives were provided in moderate to high yields and with excellent E-selectivities. Experimental results showed that the reaction proceeded through a diiodo intermediate. The synthetic usefulness of this reaction was illustrated by the synthesis of maleimide derivatives and dispiro epoxy.

Silica nanoparticles cause spermatogenesis dysfunction in mice via inducing cell cycle arrest and apoptosis.

The widespread use of silica nanoparticles (SiNPs) has increased the risk of human exposure, which raised concerns about their adverse effects on human health, especially the reproductive system. Previous studies have shown that SiNPs could cause damage to reproductive organs, but the specific mechanism is still unclear. In this study, to investigate the underlying mechanism of male reproductive toxicity induced by SiNPs, 40 male mice at the age of 8 weeks were divided into two groups and then intraperitoneally injected with vehicle control or 10 mg/kg SiNPs per day for one week. The results showed that SiNPs could damage testicular structure, perturb spermatogenesis and reduce serum testosterone levels, leading to a decrease in sperm quality and quantity. In addition, the ROS level in the testis of exposed mice was significantly increased, followed by imbalance of the oxidative redox status. Further study revealed that exposure to SiNPs led to cell cycle arrest and apoptosis, as shown by downregulation of the expression of positive cell cycle regulators and the activation of TNF-α/TNFR Ⅰ-mediated apoptotic pathway. The results demonstrated that SiNPs could cause testicles injure via inducing oxidative stress and DNA damage which led to cell cycle arrest and apoptosis, and thereby resulting in spermatogenic dysfunction.

Effect of drought on photosynthesis, total antioxidant capacity, bioactive component accumulation, and the transcriptome of Atractylodes lancea.

BACKGROUND: Atractylodes lancea (Thunb.) DC, a medicinal herb belonging to the Asteraceae family, often faces severe drought stress during its growth. Until now, there has been no research on the effect of drought stress on the quality formation of A. lancea. Therefore, the present study aimed to study the effects of drought stress on A. lancea through physical and chemical analysis, and to reveal the related molecular mechanisms via transcriptome analysis. RESULTS: The photosynthesis was markedly inhibited under drought stress. There were alterations to photosynthetic parameters (Pn, Gs, Ci) and chlorophyll fluorescence (Fv/Fm, NPQ), and the chlorophyll content decreased. Twenty genes encoding important regulatory enzymes in light and dark reactions, including the Rubisco gene of the Calvin cycle, were significantly downregulated. After exposure to drought stress for more than 4 days, the activities of four antioxidative enzymes (SOD, POD CAT and APX) began to decrease and continued to decrease with longer stress exposure. Meanwhile, most of the genes encoding antioxidative enzymes were downregulated significantly. The downregulation of 21 genes related to the respiratory electron transport chain indicated that the blocked electron transfer accelerated excessive ROS. The MDA content was significantly elevated. The above data showed that 15 days of drought stress caused serious oxidative damage to A. lancea. Drought stress not only reduced the size and dry weight of A. lancea, but also lowered the amount of total volatile oil and the content of the main bioactive components. The total volatile oil and atractylodin content decreased slightly, whereas the content of atractylon and ß-eudesmol decreased significantly. Moreover, ten significantly downregulated genes encoding sesquiterpene synthase were mainly expressed in rhizomes. CONCLUSIONS: After exposed to drought stress, the process of assimilation was affected by the destruction of photosynthesis; stress tolerance was impaired because of the inhibition of the antioxidative enzyme system; and bioactive component biosynthesis was hindered by the downregulation of sesquiterpene synthase-related gene expression. All these had negative impacts on the quality formation of A. lancea under drought stress.

Succession of the Resident Soil Microbial Community in Response to Periodic Inoculations.

To maintain the beneficial effects of microbial inoculants on plants and soil, repeated inoculation represents a promising option. Until now, the impacts of one-off inoculation on the native microbiome have been explored, but it remains unclear how long and to what extent the periodic inoculations would affect the succession of the resident microbiome in bulk soil. Here, we examined the dynamic responses of plant growth, soil functions, and the resident bacterial community in the bulk soil to periodic inoculations of phosphate-solubilizing and N2-fixing bacteria alone or in combination. Compared to single-strain inoculation, coinoculation better stimulated plant growth and soil nutrients. However, the benefits from inoculants did not increase with repeated inoculations and were not maintained after transplantation to a different site. In response to microbial inoculants, three patterns of shifts in the bacterial composition were observed: fold increase, fold decrease, and resilience. The periodic inoculations impacted the succession course of resident bacterial communities in bulk soil, mainly driven by changes in soil pH and nitrate, resulting in the development of three main cluster types throughout the investigation. The single and mixed inoculants transiently modulated the variation in the resident community in association with soil pH and the C/N ratio, but finally, the community established and showed resilience to subsequent inoculations. Consequently, the necessity of repeated inoculations should be reconsidered, and while the different microbial inoculants showed distinct impacts on resident microbiome succession, the communities ultimately exhibited resilience.IMPORTANCE Introducing beneficial microbes to the plant-soil system is an environmentally friendly approach to improve the crop yield and soil environment. Numerous studies have attempted to reveal the impacts of inoculation on the rhizosphere microbiome. However, little is known about the effectiveness of periodic inoculations on soil functioning. In addition, the long-term impact of repeated inoculations on the native community remains unclear. Here, we track the succession traits of the resident microbiome in the bulk soil across a growing season and identify the taxon clusters that respond differently to periodic inoculation. Crucially, we compare the development of the resident community composition with and without inoculation, thus providing new insight into the interactions between resident microbes and intruders. Finally, we conclude that initial inoculation plays a more important role in influencing the whole system, and the native microbial community exhibits traits of resilience, but no resistance, to the subsequent inoculations.

Untargeted and targeted gingival metabolome in rodents reveal metabolic links between high-fat diet-induced obesity and periodontitis.

AIM: To characterize gingival metabolome in high-fat diet (HFD)-induced obesity in mice with/without periodontitis. METHODS: HFD-induced obesity mouse model was established by 16-week feeding, and a lean control group was fed with low-fat diet (n = 21/group). Both models were induced for periodontitis on the left sides by molar ligation for 10 days, whereas the right sides were used as controls. Gingival metabolome and arginine metabolism were analysed by non-targeted/targeted liquid chromatography-mass spectrometry. RESULTS: Of 2247 reference features, presence of periodontitis altered 165 in lean versus 885 in HFD mice; and HFD altered 525 in absence versus 1435 in presence of periodontitis. Compared with healthy condition, periodontitis and HFD had distinct effects on gingival metabolome. Metabolomic impacts of periodontitis were generally greater in HFD mice versus lean controls. K-medoids clustering showed that HFD amplified the impacts of periodontitis on gingival metabolome in both intensity and extensity. Ten metabolic pathways were enriched, including 2 specific to periodontitis, 5 specific to HFD and 3 shared ones. Targeted validation on arginine metabolism confirmed the additive effects between HFD and periodontitis. CONCLUSION: The obese population consuming excessive HFD display amplified metabolic response to periodontitis, presenting a metabolic susceptibility to exacerbated periodontal destruction.

[Dendrobium officinale cliff epiphytic cultivation method].

To solve the issues of costly planting of facility cultivation method and inferior efficacy than wild herbs of Dendrobium officinale, the cliff epiphytic cultivation method was studied. To research the growth, agronomic traits, yield, polysaccharide and alcohol-soluble extract contents were measured on the D. officinale from different water regulation and cliff slope gradients treatments. The results showed that D. officinale epiphytic at 85 degrees-90 degrees cliff and sprayed water 1-2 h x d(-1) at the growing season can get better growth and obtain high yield, and the morphology has no different from wild cliff D. officinale, even in the environments without shade. The contents of polysaccharide and alcohol-soluble extract are closely related to the physiological ages, but significantly higher than the facility cultivation. It is possible that environmental stresses benefit the accumulation of polysaccharides, alcohol-soluble extract and other efficient ingredients.

Ceramide metabolism-related prognostic signature and immunosuppressive function of ST3GAL1 in osteosarcoma.

Osteosarcoma is the most common primary malignant bone tumor with elevated disability and mortality rates in children and adolescents and the therapeutic effect for osteosarcoma has remained stagnant in the past 30 years. Emerging evidence has shown ceramide metabolism plays a vital role in tumor progression, but its mechanisms in osteosarcoma progression remain unknown. Through consensus clustering and LASSO regression analysis based on the osteosarcoma cohorts from TARGET database, we constructed a ceramide metabolism-related prognostic signature including ten genes for osteosarcoma, with ST3GAL1 exhibiting the highest hazard ratio. Biological signatures analysis demonstrated that ceramide metabolism was associated with immune-related pathways, immune cell infiltration and the expression of immune checkpoint genes. Single-cell profiling revealed that ceramide metabolism was enriched in myeloid, osteoblast and mesenchymal cells. The interaction between TAMs and CD8+ T cells played an essential role in osteosarcoma. ST3GAL1 regulated the SPP1-CD44 interaction between TAMs and CD8+ T cells and IL-10 secretion in TAMs through α2,3 sialic acid receptors, which inhibited CD8+ T cell function. IHC analysis showed that ST3GAL1 expression correlated with the prognosis of osteosarcoma patients. Co-culture assay revealed that upregulation of ST3GAL1 in tumor cells regulated the differentiation of TAMs and cytokine secretion. Collectively, our findings demonstrated that ceramide metabolism was associated with clinical outcome in osteosarcoma. ST3GAL1 facilitated tumor progression through regulating tumor immune microenvironment, providing a feasible therapeutic approach for patients with osteosarcoma.

Silybin protected from avermectin-induced carp (Cyprinus carpio) nephrotoxicity by regulating PPAR-γ-involved inflammation, oxidative stress, ferroptosis and autophagy.

Avermectin, a widely used deworming drug, poses a significant threat to fisheries. Silybin is recognized for its antioxidant and anti-inflammatory properties. The kidney, being crucial for fish survival, plays a vital role in maintaining ion balance, nitrogen metabolism, and hormone regulation. While residual avermectin in water could pose a risk to carp (Cyprinus carpio), it remains unclear whether silybin can alleviate the renal tissue toxicity induced by avermectin in this species. In current study, we developed a model of long-term exposure of carp to avermectin to investigate the potential protective effect of silybin against avermectin-induced nephrotoxicity. The results indicated that avermectin induced renal inflammation, oxidative stress, ferroptosis, and autophagy in carp. Silybin suppressed the mRNA transcript levels of pro-inflammatory factors, increased catalase (CAT) activity, reduced glutathione (GSH) activity, diminished reactive oxygen species (ROS) accumulation in renal tissues, and promoted the activation of the Nrf2-Keap1 signaling pathway. Furthermore, the transcript levels of ferroptosis-associated proteins, including gpx4 and slc7a11, were significantly reduced, while those of cox2, ftl, and ncoa4 were elevated. The transcript levels of autophagy-related genes, including p62 and atg5, were also regulated. Network pharmacological analysis revealed that silybin inhibited ROS accumulation and mitigated avermectin-induced renal inflammation, oxidative stress, ferroptosis, and autophagy in carp through the involvement of PPAR-γ. Silybin exerted its anti-inflammatory effect through the NF-κB pathway and antioxidant effect through the Nrf2-Keap1 pathway, induced renal cell iron efflux through the SLC7A11/GSH/GPX4, and suppressed autophagy initiation via the PI3K/AKT pathway. This study provides evidence of the protective effect of silybin against avermectin-induced nephrotoxicity in carp, highlighting its potential as a therapeutic agent to alleviate the adverse effects of avermectin exposure in fish.

A diagnostic signature developed based on the necroptosis-related genes and its association with immune infiltration in osteosarcoma.

Introduction: Osteosarcoma is a bone-derived malignancy that often leads to lung metastasis and death. Material and methods: The RNA-seq data of TARGET-osteosarcoma were collected from TARGET database. GSE16088 and GSE12865 datasets of osteosarcoma x from Gene Expression Database (GEO) were donwloaded. ConsensusClusterPlus was used for molecular subtype classification. Univariate Cox and Lasso regression was employed to develop a risk model. To analyze the regulatory effects of model feature genes on the malignant phenotype of osteosarcoma cell lines, qRT-PCR, Transwell and wound healing assays were performed. The abundance of immune cell infiltration was assessed using MCP-Counter, Gene Set Enrichment Analysis (GSEA), and ESTIMATE. The Tumor Immune Dysfunction and Exclusion (TIDE) software was employed to evaluate immunotherapy and response to conventional chemotherapy drugs. Results: Three clusters (C1, C2 and C3) were classified using 39 necroptosis score-associated genes. In general, C1 and C2 showed better prognosis outcome and lower death rate than C3. Specifically, C2 could benefit more from immunotherapy, while C3 was more sensitive to traditional medicines, and C1 had higher immune cell infiltration. Next, an 8-gene signature and a risk score model were developed, with a low risk score indicating better survival and immune cell infiltration. ROC analysis showed that 1-, 3-, and 5-year overall survival of osteosarcoma could be correctly predicted by the risk score model. Cellular experiments revealed that the model feature gene IFITM3 promoted the osteosarcoma cell migration and invasion. Furthermore, the overall survival of osteosarcoma patients from TARGET and validation datasets can be accurately evaluated using the nomogram model. Conclusions: Our prognostic model developed using necroptosis genes could facilitate the prognostic prediction for patients suffering from osteosarcoma, offering potential osteosarcoma targets.

Targeting NAT10 inhibits osteosarcoma progression via ATF4/ASNS-mediated asparagine biosynthesis.

Despite advances in treatment, the prognosis of patients with osteosarcoma remains unsatisfactory, and searching for potential targets is imperative. Here, we identify N4-acetylcytidine (ac4C) acetyltransferase 10 (NAT10) as a candidate therapeutic target in osteosarcoma through functional screening. NAT10 overexpression is correlated with a poor prognosis, and NAT10 knockout inhibits osteosarcoma progression. Mechanistically, NAT10 enhances mRNA stability of activating transcription factor 4 (ATF4) through ac4C modification. ATF4 induces the transcription of asparagine synthetase (ASNS), which catalyzes asparagine (Asn) biosynthesis, facilitating osteosarcoma progression. Utilizing virtual screening, we identify paliperidone and AG-401 as potential NAT10 inhibitors, and both inhibitors are found to bind to NAT10 proteins. Inhibiting NAT10 suppresses osteosarcoma progression in vivo. Combined treatment using paliperidone and AG-401 produces synergistic inhibition for osteosarcoma in patient-derived xenograft (PDX) models. Our findings demonstrate that NAT10 facilitates osteosarcoma progression through the ATF4/ASNS/Asn axis, and pharmacological inhibition of NAT10 may be a feasible therapeutic approach for osteosarcoma.

Catalytic performance and mechanism study of the isomerization of 2,5-dichlorotoluene to 2,4-dichlorotoluene.

This work investigates the influence of catalyst HZSM-5 on the isomerization of 2,5-dichlorotoluene (2,5-DCT) to produce 2,4-dichlorotoluene (2,4-DCT). We observe that hydrothermal treatment leads to a decrease in total acidity and Brønsted/Lewis ratio of HZSM-5 while generating new secondary pores. These characteristics result in excellent selectivity for post-hydrothermal modified HZSM-5 in the isomerization reaction from 2,5-DCT to 2,4-DCT. Under atmospheric pressure at 350 °C, unmodified HZSM-5 achieves a selectivity of 66.4% for producing 2,4-DCT, however after hydrothermal modification the selectivity increases to 78.7%. Density Functional Theory (DFT) calculations explore the thermodynamic aspects of adsorption between the HZSM-5 surface and 2,4-DCT. The kinetic perspective investigates the mechanism involving proton attack on the methyl group of 2,5-DCT followed by rearrangement leading to formation of 2,4-DCT during isomerization. The consistency between simulation and experimental results provides evidence for the feasibility of isomerizing 2,5-DCT to 2,4-DCT. This work fills the gap in the low value-added product 2,5-DCT isomer conversion, indicating its significant practical application potential and provides a valuable reference and guidelines for industrial research in this field.

Stomach as the target organ of Rickettsia heilongjiangensis infection in C57BL/6 mice identified by click chemistry.

Spotted fever group rickettsiae (SFGR) are obligate intracellular bacteria that cause spotted fever. The limitations of gene manipulation pose great challenges to studying the infection mechanisms of Rickettsia. By combining bioorthogonal metabolism and click chemistry, we developed a method to label R. heilongjiangensis via azide moieties and achieved rapid pathogen localization without complex procedures. Moreover, we constructed a C57BL/6 mice infection model by simulating tick bites and discovered that the stomach is the target organ of R. heilongjiangensis infection through in vivo imaging systems, which explained the occurrence of gastrointestinal symptoms following R. heilongjiangensis infection in some cases. This study offers a unique perspective for subsequent investigations into the pathogenic mechanisms of SFGR and identifies a potential target organ for R. heilongjiangensis.

FBXO5-mediated RNF183 degradation prevents endoplasmic reticulum stress-induced apoptosis and promotes colon cancer progression.

Endoplasmic reticulum (ER) stress induces the unfolded protein response (UPR), and prolonged ER stress leads to cell apoptosis. Despite increasing research in this area, the underlying molecular mechanisms remain unclear. Here, we discover that ER stress upregulates the UPR signaling pathway while downregulating E2F target gene expression and inhibiting the G2/M phase transition. Prolonged ER stress decreases the mRNA levels of E2F2, which specifically regulates the expression of F-Box Protein 5(FBXO5), an F-box protein that functions as an inhibitor of the anaphase-promoting complex/cyclosome (APC/C) ubiquitin ligase complex. Depletion of FBXO5 results in increased ER stress-induced apoptosis and decreased expression of proteins related to PERK/IRE1α/ATF6 signaling. Overexpression of FBXO5 wild-type (not its ΔF-box mutant) alleviates apoptosis and the expression of the C/EBP Homologous Protein (CHOP)/ATF. Mechanistically, we find that FBXO5 directly binds to and promotes the ubiquitin-dependent degradation of RNF183, which acts as a ubiquitin E3 ligase in regulating ER stress-induced apoptosis. Reversal of the apoptosis defects caused by FBXO5 deficiency in colorectal cancer cells can be achieved by knocking down RNF183 in FBXO5-deficient cells. Functionally, we observed significant upregulation of FBXO5 in colon cancer tissues, and its silencing suppresses tumor occurrence in vivo. Therefore, our study highlights the critical role of the FBXO5/RNF183 axis in ER stress regulation and identifies a potential therapeutic target for colon cancer treatment.

Hybrid electron microscopy-FRET imaging localizes the dynamical C-terminus of Tfg2 in RNA polymerase II-TFIIF with nanometer precision.

TFIIF-a general transcription factor comprising two conserved subunits can associate with RNA polymerase II (RNAPII) tightly to regulate the synthesis of messenger RNA in eukaryotes. Herein, a hybrid method that combines electron microscopy (EM) and Förster resonance energy transfer (FRET) is described and used to localize the C-terminus of the second TFIIF subunit (Tfg2) in the architecture of RNAPII-TFIIF. In the first stage, a poly-histidine tag appended to the Tfg2 C-terminus was labeled with nickel-NTA nanogold and a seven-step single particle EM protocol was devised to obtain the region accessible by the nanogold in 3D, suggesting the Tfg2 C-terminus is proximal to the clamp of RNAPII. Next, the C-termini of the Rpb2 and the Rpb4 subunits of RNAPII, adjacent to the clamp, were selected for placing FRET satellites to enable the nano-positioning (NP) analysis, by which the localization precision was improved such that the Tfg2 C-terminus was found to dwell on the clamp ridge but could move to the clamp top during transcription. Because the tag receptive to the EM or FRET probes can be readily introduced to any protein subunit, this hybrid approach is generally applicable to complement cryo-EM study of many protein complexes to nanometer precision.

Morphological, physiological, and secondary metabolic responses of Taraxacum officinale to salt stress.

Salt stress has a major effect on growth and secondary metabolism in medicinal plants, however, the effect of salt stress on Taraxacum officinale F. H. Wigg. is still scarce. In this study, we evaluated the effects of salt stress on the physiology, morphology, phenolic acid accumulation, and expression of genes involved in phenolic acid biosynthesis in T. officinale. We found that plants grew well at 1 g kg-1 NaCl, and the state of photosystem Ⅱ (PSⅡ) and the organization of the chloroplasts at 0.5 g kg-1 NaCl showed no significant differences compared with the control. However, 2 g kg-1 and 4 g kg-1 NaCl inhibited growth and accelerated leaf senescence. At 4 g kg-1 NaCl, the fresh and dry weights decreased to 28% and 42% of the control, while chlorosis and necrosis were observed on the leaves. Furthermore, up-regulation of the expression of ToC3'H corresponded with an increase in the levels of caffeoylquinic acids (chlorogenic acid and isochlorogenic acid A) at NaCl concentration ≤ 1 g kg-1. Expressions of four phenolic acid biosynthesis genes, ToC4H, To4CL, ToHCT, and ToHQT, were down-regulated with increasing NaCl concentrations, consistent with the observed decreases in caftaric and cichoric acids. In summary, cultivation of T. officinale under mild salt stress (NaCl ≤ 1 g kg-1) is feasible and facilitates the accumulation of caffeoylquinic acids; thus this species may be recommended for saline soils.

Reproductive toxicity investigation of silica nanoparticles in male pubertal mice.

Silica nanoparticles (SiNPs), one of the most produced nanoparticles (NPs) in the world, are used in all aspects of life. The increased application of SiNPs, especially in medicine, has raised considerable concern regarding their toxicological impact. Previous studies have shown that SiNPs can pass through the reproductive barrier and cause reproductive organ dysfunction by destroying Sertoli cells, Leydig cells, and germ cells. However, little is known about the mechanism of SiNPs-induced reproductive toxicity. In the present study, 5-week-old male mice were intraperitoneally administered SiNPs per day for 1 week at a dose of 0.2 mg per mouse. The results showed that SiNPs could cause damage to the structure of the testis and the epididymis and change the reproductive organ coefficients, leading to decreases of 56.1% and 55.3% in the rates of sperm concentration and motility and an increase of 168.8% in the rate of sperm abnormality. Moreover, the serum testosterone level obviously decreased from 18.77 to 5.23 µg/ml after exposure, and the transcription statuses of some key genes involved in the synthesis and transport of testosterone in the testis were also affected. Additional experiments showed that SiNPs exposure during puberty induced oxidative stress and an inflammatory response, as shown by the changed activity of superoxide dismutase (SOD), increased contents of malondialdehyde (MDA), and excess expression of proinflammatory factors, including TNF-α and IL-1ß. Furthermore, the administration of SiNPs caused DNA damage and cell apoptosis, which were presented by the increased apoptotic cells in the sections of testis and epididymis and activation of the TNF-α/TNFR I-mediated pro-apoptotic pathway. In conclusion, these results indicate that SiNPs exposure during puberty significantly damaged the structure and function of the testis and epididymis by inducing oxidative stress and cell apoptosis. This study provides novel insight into SiNPs-induced reproductive toxicity during puberty, which warrants a more careful assessment of SiNPs before their application in juvenile supplies.

Power Batteries Health Monitoring: A Magnetic Imaging Method Based on Magnetoelectric Sensors.

With the popularity of electric vehicles, the ever-increasing demand for high-capacity batteries highlights the need for monitoring the health status of batteries. In this article, we proposed a magnetic imaging technique (MIT) to investigate the health status of power batteries nondestructively. This technique is based on a magnetic sensor array, which consists of a 16-channel high-performance magnetoelectric sensor, and the noise equivalent magnetic induction (NEB) of each channel reaches 3-5 pT/Hz1/2@10 Hz. The distribution of the magnetic field is imaged by scanning the magnetic field variation of different positions on the surface. Therefore, the areas of magnetic anomalies are identified by distinguishing different magnetic field abnormal results. and it may be possible to classify the battery failure, so as to put forward suggestions on the use of the battery. This magnetic imaging method expands the application field of this high-performance magnetoelectric sensor and contributes to the battery's safety monitoring. Meanwhile, it may also act as an important role in other nondestructive testing fields.