Exploring the relationship between sleep patterns and depression among Chinese middle school students: a focus on sleep quality vs. sleep duration.

Objective: This study aims to explore the relationship between sleep patterns and depressive symptoms among adolescents, examining variations in depressive symptoms across different sleep qualities, durations, and habits. Method: A cross-sectional survey was conducted, gathering data from 8,775 Chinese adolescents on their demographics, lifestyle habits, sleep quality and duration, and depressive symptoms. The association between sleep parameters and depressive symptoms was analyzed using multivariate logistic regression. Findings: The findings reveal a significant correlation between sleep quality/duration and depressive symptoms. Specifically, adolescents with poor sleep quality had higher depressive scores (mean score = 14.62, standard deviation = 5.71), significantly exceeding those with better sleep quality (mean score = 11.54, standard deviation = 4.69). Adolescents with shorter sleep duration also showed significantly higher depressive scores than those with moderate sleep duration. Importantly, adolescents experiencing both poor sleep quality and shorter sleep duration were at a significantly increased risk of depressive symptoms (OR = 4.04, 95% CI: 3.53-4.62, P < 0.001). Further analysis indicated that older age and lower family economic status were independent predictors of a higher risk of adolescent depression (OR = 1.22, 95% CI: 1.08-1.38, P = 0.001), whereas factors such as gender, ethnicity, residence, being an only child, and parental education levels were not statistically significant. Conclusion: Among Chinese adolescents, poor sleep quality and shorter sleep duration are independent predictors of higher depressive symptom scores. Adolescents experiencing both of these conditions simultaneously have a significantly increased risk of depressive symptoms. Furthermore, older age and lower family economic status are also significantly related to an increased risk of depression in adolescents. These findings emphasize the importance of improving sleep quality and optimizing sleep duration for the prevention of adolescent depression. They also suggest the need for a comprehensive approach that addresses the multifaceted factors influencing adolescent mental health, including sleep patterns and socioeconomic disparities.

Patients with chronic ankle instability exhibit increased sensorimotor cortex activation and correlation with poorer lateral balance control ability during single-leg stance: a FNIRS study.

Introduction: Chronic Ankle Instability (CAI) is a musculoskeletal condition that evolves from acute ankle sprains, and its underlying mechanisms have yet to reach a consensus. Mounting evidence suggests that neuroplastic changes in the brain following ankle injuries play a pivotal role in the development of CAI. Balance deficits are a significant risk factor associated with CAI, yet there is a scarcity of evidence regarding the sensorimotor cortical plasticity related to balance control in affected individuals. This study aims to evaluate the differences in cortical activity and balance abilities between patients with CAI and uninjured individuals during a single-leg stance, as well as the correlation between these factors, in order to elucidate the neurophysiological alterations in balance control among patients with CAI. Methods: The study enrolled 24 patients with CAI and 24 uninjured participants. During single-leg stance, cortical activity was measured using a functional near-infrared spectroscopy (fNIRS) system, which included assessments of the pre-motor cortex (PMC), supplementary motor area (SMA), primary motor cortex (M1), and primary somatosensory cortex (S1). Concurrently, balance parameters were tested utilizing a three-dimensional force platform. Results: Independent sample t-tests revealed that, compared with the uninjured individuals, the patients with CAI exhibited a significant increase in the changes of oxyhemoglobin concentration (ΔHbO) during single-leg stance within the left S1 at Channel 5 (t = 2.101, p = 0.041, Cohen's d = 0.607), left M1 at Channel 6 (t = 2.363, p = 0.022, Cohen's d = 0.682), right M1 at Channel 15 (t = 2.273, p = 0.029, Cohen's d = 0.656), and right PMC/SMA at Channel 11 (t = 2.467, p = 0.018, Cohen's d = 0.712). Additionally, the center of pressure root mean square (COP-RMS) in the mediolateral (ML) direction was significantly greater (t = 2.630, p = 0.012, Cohen's d = 0.759) in the patients with CAI. Furthermore, a moderate positive correlation was found between ML direction COP-RMS and ΔHbO2 in the M1 (r = 0.436; p = 0.033) and PMC/SMA (r = 0.488, p = 0.016), as well as between anteroposterior (AP) direction COP-RMS and ΔHbO in the M1 (r = 0.483, p = 0.017). Conclusion: Patients with CAI demonstrate increased cortical activation in the bilateral M1, ipsilateral PMC/SMA, and contralateral S1. This suggests that patients with CAI may require additional brain resources to maintain balance during single-leg stance, representing a compensatory mechanism to uphold task performance amidst diminished lateral balance ability in the ankle joint.

Study on Plastic Constitutive Relation and Ductile Fracture Criterion of AM60B Magnesium Alloy.

It is currently a challenge to accurately predict the deformation and fracture behavior of metal parts in automobile crashes. Many studies have shown that the deformation and fracture behavior of materials are significantly affected by the stress state during automobile crashes with complex stress state characteristics. In order to further promote the application of die-cast magnesium alloys in automobiles, it is particularly important to study the material deformation and fracture behavior of die-cast magnesium alloys. In this paper, the mechanical properties of the AM60B die-cast magnesium alloy sheet under four stress states (shear, tension, R10 notch tension, and cupping) were designed and tested. Based on the von Mises isotropic constitutive model and Swift weighted Hockett-Sherby hardening model, the plastic constitutive model of die-cast magnesium alloy was established. Based on the plastic model and the fracture model (JC, MMC, and DIEM) considering the influence of three stress states, the deformation and fracture behavior of the AM60B die-cast magnesium alloy front-end members in three-point bending were predicted by experiments and finite element simulation. The experimental results show that the deformation mode and loading-displacement curve trend of the AM60B die-cast magnesium alloy front members are the same, the crack initiation point and crack initiation time are the same, and the crack shape is similar. The results show that the complex stress state constitutive model parameters and the DIEM fracture model obtained in this paper can accurately predict the deformation and fracture failure behavior of the AM60B die-cast magnesium alloy sheet.

Botulinum Toxin to Improve the Prognosis of Skin Transplantation: A Short Narrative Review.

Skin transplantation is a traditional and well-established method of repairing skin loss, especially deep second-degree postburn wounds. Complications often happen amid the healing process, including necrosis and skin contracture, which has raised widespread concern from patients and doctors. Since the first recorded medical application of botulinum toxin for strabismus, accumulating evidence has enclosed all-round potential of botulinum toxin, more than aesthetic management. In recent decades, botulinum toxin also has been revealed to improve the prognosis of skin grafts. This literature review aims to briefly summarize the history and latest advances of its use for skin transplantation.

Exploring the modulatory impact of isosakuranetin on Staphylococcus aureus: Inhibition of sortase A activity and α-haemolysin expression.

The ubiquity of methicillin-resistant Staphylococcus aureus (MRSA) and the mounting prevalence of antibiotic resistance necessitate the identification of novel therapeutic approaches to reduce the selective pressure of antibiotics. Targeting bacterial virulence factors, such as the pivotal Sortase A (SrtA) in S. aureus for adhesion and invasion, and the salient toxin α-Hemolysin (Hla), offers a sophisticated approach to attenuate pathogenicity without bacterial elimination. Herein, we report the discovery of a flavonoid, isosakuranetin, which inhibits the activity of S. aureus SrtA. A fluorescence resonance energy transfer assay revealed that isosakuranetin exhibited a low IC50 of 21.20 µg/mL. Furthermore, isosakuranetin significantly inhibited SrtA-related virulence properties, such as bacterial adhesion to fibrinogen, biofilm formation, and invasion of A549 cells. We employed fluorescence quenching and molecular docking to determine the interactions between isosakuranetin and SrtA, revealing the key amino acid sites for binding. Importantly, isosakuranetin inhibited the haemolytic activity of S. aureus in vitro at a concentration of 32 µg/mL. Moreover, isosakuranetin effectively suppressed the transcription and expression of Hla in a dose-dependent manner and regulated the transcription of RNAIII, the upstream operator of Hla. Notably, isosakuranetin demonstrated in vivo efficacy in a mouse model of S. aureus-induced pneumonia by significantly improving survival rates and reducing lung damage. This is a valuable finding, as isosakuranetin's dual inhibitory effects on SrtA and haemolytic activity, as well as its anti-virulence activity against MRSA, make it an excellent candidate for therapeutic development.

[Relationship between MTHFR Gene Polymorphism(C677T) and Adverse Reactions of High-Dose Methotrexate in Pediatric Patients with Acute Lymphoblastic Leukemia].

OBJECTIVE: To explore the effects of methylenetetrahydrofolate reductase (MTHFR) C677T gene polymorphism on the adverse reactions of high-dose methotrexate (MTX) in pediatric patients with acute lymphoblastic leukemia (ALL). METHODS: A total of 69 children with ALL admitted to the department of Pediatrics of Sun Yat-sen Memorial Hospital of Sun Yat-sen University from November 2018 to October 2020 were included in this study. The clinical data of the children were collected, leukocytes were isolated from their peripheral blood, and MTHFR genotyping was performed by digital fluorescence molecular hybridization techniques. The adverse reactions and plasma drug concentration of MTX were monitored during the chemotherapy. Moreover, the effect of MTHFR gene polymorphism on MTX adverse reactions and plasma drug concentration were analyzed. RESULTS: Among the middle and high risk children, compared with the wildtype group (CC genotype), patients with MTHFR C677T mutations (CT+TT genotypes) had a higher risk of leukopenia (OR=2.38), neutropenia (OR=2.2), anemia (OR=1.83) and hepatoxicity (OR=1.98). However, no significant difference was found in the MTX plasma concentration between the MTHFR C677T mutantion group and the wildtype group at different timepoints (24 h, 48 h and 72 h). Multivariate analysis revealed that the plasma concentration of MTX (48 h), clinical risk level of ALL and MTHFR C677T gene polymorphism were independent factors for the adverse reactions of high-dose MTX. CONCLUSION: The MTHFR C677T mutations may be associated with myelosuppression and hepatotoxicity in children with ALL after high-dose MTX treatment.

Intestinal ACE2 regulates glucose metabolism in diet-induced obese mice through a novel gut-islet axis mediated by tryptophan.

OBJECTIVE: Angiotensin-converting enzyme 2 (ACE2) plays a vital role in regulating intestinal tryptophan (Trp) transport and maintaining Trp homeostasis. This study aimed to investigate the functional relationship between intestinal ACE2 and Trp in the regulation of glucose metabolism under metabolic stress. METHODS: ACE2-knockout mice and mice with adeno-associated virus-mediated overexpression of ACE2 were fed with a high-fat diet for 12 weeks to establish a high-fat-induced metabolic stress model. They were subjected to a Trp gavage intervention for another 4 weeks. RESULTS: Here, it is reported that ACE2 regulates intestinal Trp absorption by stabilizing neutral amino acid transporter B0 AT1. Notably, in ACE2-knockout mice, it was found that B0 AT1 and serum Trp levels were significantly reduced, which was not reversed by Trp supplementation. However, mice receiving adeno-associated virus-ACE2 did the opposite and showed significantly improved glycolipid metabolism. It was then confirmed that Trp potentiated glucagon-like peptide 1 production from intestinal and islet α-cells. Meanwhile, Trp-treated MIN6 cells ameliorated mitochondrial function and safely guarded MIN6 cells against reactive oxygen species exposure. CONCLUSIONS: This study highlights an essential role of ACE2 in the maintenance of systemic metabolism to optimize the function of the islets through a novel gut-islet axis mediated by Trp. These results provide proof-of-concept evidence for treating obesity and diabetes.

Identification of FGF13 as a Potential Biomarker and Target for Diagnosis of Impaired Glucose Tolerance.

Early identification of pre-diabetes provides an opportunity for intervention and treatment to delay its progression to type 2 diabetes mellitus (T2DM). We aimed to identify the biomarkers of impaired glucose tolerance (IGT) through bioinformatics analysis. The GSE76896 dataset, including non-diabetic (ND), IGT, and T2DM clinical samples, was deeply analyzed to identify 309 Co-DEGs for IGT and T2DM. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses indicated that inflammatory responses and the PI3K-AKT signaling pathway are important patho-physiological features of IGT and T2DM. Protein-protein interaction (PPI) network analysis and cytoHubba technolgy identified seven hub genes: namely, CCL2, CXCL1, CXCL8, EDN1, FGF13, MMP1, and NGF. The expression and ROC curves of these hub genes were validated using the GSE38642 dataset. Through an immunofluorescence assay, we found that the expression of FGF13 in islets of mice in the HFD and T2DM groups was significantly lower than in the control group. Similarly, the level of FGF13 in the sera of IGT and T2DM patients was lower than that in the healthy group. Together, these results suggest that FGF13 can be treated as a novel biomarker of IGT, which may provide new targets for the diagnosis and treatment of pre-diabetes and T2DM.

A bioinspired antibacterial and photothermal membrane for stable and durable clean water remediation.

Solar-driven steam generation has been considered as a prevalent and sustainable approach to obtain clean fresh water. However, the presence of microorganisms in seawater may cause the biofouling and degradation of polymeric photothermal materials and clog the channels for water transportation, leading to a decrease in solar evaporation efficiency during long-term usage. Herein, we have reported a facile strategy to construct a robust cellulose membrane device coated by tobramycin-doped polydopamine nanoparticles (PDA/TOB@CA). The PDA/TOB@CA membrane not only exhibited synergistic antibacterial behaviors with long-term and sustained antibiotic release profiles, but also achieved a high water evaporation rate of 1.61 kg m-2 h-1 as well as an evaporation efficiency of >90%. More importantly, the high antibacterial activity endowed the PDA/TOB@CA membrane with superb durability for stable reuse over 20 cycles, even in microbe-rich environments. Therefore, we envision that this study could pave a new pathway towards the design and fabrication of robust antibacterial and photothermal materials for long-term and stable clean water production.

Isovitexin Protects Mice from Methicillin-Resistant Staphylococcus aureus-Induced Pneumonia by Targeting Sortase A.

The rise of methicillin-resistant Staphylococcus aureus (MRSA) has resulted in significant morbidity and mortality, and clinical treatment of MRSA infections has become extremely difficult. Sortase A (SrtA), a virulence determinant that anchors numerous virulence-related proteins to the cell wall, is a prime druggable target against S. aureus infection due to its crucial role in the pathogenicity of S. aureus. Here, we demonstrate that isovitexin, an active ingredient derived from a variety of traditional Chinese medicines, can reversibly inhibit SrtA activity in vitro with a low dose (IC50=24.72 µg/ml). Fluorescence quenching and molecular simulations proved the interaction between isovitexin and SrtA. Subsequent point mutation experiments further confirmed that the critical amino acid positions for SrtA binding to isovitexin were Ala-92, Ile-182, and Trp-197. In addition, isovitexin treatment dramatically reduced S. aureus invasion of A549 cells. This study shows that treatment with isovitexin could alleviate pathological injury and prolong the life span of mice in an S. aureus pneumonia model. According to our research, isovitexin represents a promising lead molecule for the creation of anti-S. aureus medicines or adjuncts.

Angiotensin-converting enzyme 2 improves hepatic insulin resistance by regulating GABAergic signaling in the liver.

The angiotensin-converting enzyme 2 (ACE2)/angiotensin 1-7/MAS axis and the gamma-aminobutyric acid (GABA)ergic signaling system have both been shown to have the dual potential to improve insulin resistance (IR) and hepatic steatosis associated with obesity in the liver. Recent studies have demonstrated that ACE2 can regulate the GABA signal in various tissues. Notwithstanding this evidence, the functional relationship between ACE2 and GABA signal in the liver under IR remains elusive. Here, we used high-fat diet-induced models of IR in C57BL/6 mice as well as ACE2KO and adeno-associated virus-mediated ACE2 overexpression mouse models to address this knowledge gap. Our analysis showed that glutamate decarboxylase (GAD)67/GABA signaling was weakened in the liver during IR, whereas the expression of GAD67 and GABA decreased significantly in ACE2KO mice. Furthermore, exogenous administration of angiotensin 1-7 and adeno-associated virus- or lentivirus-mediated overexpression of ACE2 significantly increased hepatic GABA signaling in models of IR both in vivo and in vitro. We found that this treatment prevented lipid accumulation and promoted fatty acid ß oxidation in hepatocytes as well as inhibited the expression of gluconeogenesis- and inflammation-related genes, which could be reversed by allylglycine, a specific GAD67 inhibitor. Collectively, our findings show that signaling via the ACE2/A1-7/MAS axis can improve hepatic IR by regulating hepatic GABA signaling. We propose that this research might indicate a potential strategy for the management of diabetes.

[Clinical effect of digital impression combined with all-ceramic denture on restoration of 60 patients with dental defects].

PURPOSE: To analyze the clinical effect of digital impression combined with all-ceramic denture restoration on patients with dental defects. METHODS: A study was conducted on 120 patients with dental defects admitted to Dongfeng Stomatological Hospital from June 2018 to June 2020. The two groups of patients were randomly divided into digital imprinting modules and silicone rubber imprinting modules using a random number table method. There were 60 cases in each group. The silicone rubber imprint module used traditional silicone impression combined with all-ceramic denture restoration, while the digital imprint module used digital impression combined with all-ceramic denture restoration.The clinical efficacy of the two groups was observed. Gingival index (GI), periodontal index (PI) before dental restoration, during dental restoration and 6 monthes after dental restoration were compared. The adjacent surface contact conditions, occlusion and adverse reactions of the two groups were compared. SPSS 22.0 software package was used for statistical analysis. RESULTS: The two groups of patients selected grade A and grade B for the evaluation of the restoration when the restoration was completed. The number of patients who chose grade A for the digital imprint module was more than that of the silicone rubber imprint module,but there was no significant difference(P＞0.05). Six months after the tooth was worn, GI and PI indexes of the two groups of patients increased. GI and PI indexes of the silicone rubber stamping module were significantly higher than those of the digital stamping module(P＜0.05). When dental restoration was completed and 6 months after the tooth was replaced, the pass rate of contact between the adjacent surfaces of the imprinting module patients was significantly higher than that of the silicone rubber imprinting module(P＜0.05). When dental restoration was completed, the occlusion of the digital imprinting module patients was significantly better than that of the silicone rubber imprinting module(P＜0.05). Six months after wearing the denture, there was no significant difference in occlusion between the two groups of patients(P＞0.05). When dental models of the two groups of patients were taken, the incidence of adverse reactions in patients with digital imprints was significantly lower than that of silicone rubber imprints(P＜0.05). CONCLUSIONS: The use of digital impressions combined with all-ceramic restorations to repair patients with dental defects can effectively improve the treatment effect, improve prognostic GI and PI indexes of the patients, increase the pass rate of the adjacent surface contact and occlusion of the tooth, and reduce the process of dental restoration. The incidence of adverse reactions are minimal, with good prognostic effects. It is worthy of clinical application.

No Evidence of Bacterial Symbionts Influencing Host Specificity in Aphis gossypii Glover (Hemiptera: Aphididae).

The cotton-melon aphid, Aphis gossypii Glover, is a polyphagous insect pest with many host-specialized biotypes, such as the Cucurbitaceae- and Malvaceae-specialized (CU and MA) biotypes. Bacterial symbionts were reported to determine the host range in some aphids. Whether this is the case in A. gossypii remains unknown. Here, we tested the host specificity of the CU and MA biotypes, compared the host specificity between the wingless and winged morph within the same biotype, and analyzed the composition of the bacterial symbionts. The reproduction of the CU and MA biotypes reduced by 66.67% and 82.79%, respectively, on non-native hosts, compared with on native hosts. The composition of bacterial symbionts was not significantly different between the CU and MA biotypes, with a Buchnera abundance >95% in both biotypes. Meanwhile, the winged morph produced significantly more nymphs than the wingless morph on non-native hosts, and the Buchnera abundance in the winged morph was only about 10% of that in the wingless morph. There seemed to be a relationship between the Buchnera abundance and host specificity. We regulated the Buchnera abundance by temperature and antibiotics, but did not find that a low Buchnera abundance resulted in the high reproduction on non-native hosts. We conclude that the host specificity of A. gossypii is not controlled by specific bacterial symbionts or by Buchnera abundance.

Comparative Proteomic Analysis of Drug Trichosanthin Addition to BeWo Cell Line.

Trichosanthin (TCS) is a traditional Chinese herbal medicine used to treat some gynecological diseases. Its effective component has diverse biological functions, including antineoplastic activity. The human trophoblast cell line BeWo was chosen as an experimental model for in vitro testing of a drug screen for anticancer properties of TCS. The MTT method was used in this study to get a primary screen result. The result showed that 100 mM had the best IC50 value. Proteomics analysis was then performed for further investigation of the drug effect of TCS on the BeWo cell line. In this differential proteomic expression analysis, the total proteins extracted from the BeWo cell line and their protein expression level after the drug treatment were compared by 2DE. Then, 24 unique three-fold differentially expressed proteins (DEPs) were successfully identified by MALDI-TOF/TOF MS. Label-free proteomics was run as a complemental method for the same experimental procedure. There are two proteins that were identified in both the 2DE and label-free methods. Among those identified proteins, bioinformatics analysis showed the importance of pathway and signal transduction and gives us the potential possibility for the disease treatment hypothesis.

Dihydrohomoplantagin and Homoplantaginin, Major Flavonoid Glycosides from Salvia plebeia R. Br. Inhibit oxLDL-Induced Endothelial Cell Injury and Restrict Atherosclerosis via Activating Nrf2 Anti-Oxidation Signal Pathway.

Oxidized low-density lipoprotein (oxLDL)-induced endothelium injury promotes the development of atherosclerosis. It has been reported that homoplantaginin, a flavonoid glycoside from the traditional Chinese medicine Salvia plebeia R. Br., protected vascular endothelial cells by inhibiting inflammation. However, it is undetermined whether homoplantaginin affects atherosclerosis. In this study, we evaluated the effect of homoplantaginin and its derivative dihydrohomoplantagin on oxLDL-induced endothelial cell injury and atherosclerosis in apoE-/- mice. Our results showedthat both dihydrohomoplantagin and homoplantaginin inhibited apoptosis and the increased level of ICAM-1 and VCAM-1 in oxLDL-stimulated HUVECs and the plaque endothelium of apoE-/- mice. Additionally, both of them restricted atherosclerosis development of apoE-/- mice. Mechanistic studies showed that oxLDL-induced the increase in ROS production, phosphorylation of ERK and nuclear translocation of NF-κB in HUVECs was significantly inhibited by the compounds. Meanwhile, these two compounds promoted Nrf2 nuclear translocation and increased the anti-oxidation downstream HO-1 protein level in HUVECs and plaque endothelium. Notably, knockdown of Nrf2 by siRNA abolished the cell protective effects of compounds and antagonized the inhibition effects of them on ROS production and NF-κB activation in oxLDL-stimulated HUVECs. Collectively, dihydrohomoplantagin and homoplantaginin protected VECs by activating Nrf2 and thus inhibited atherosclerosis in apoE-/- mice.

GKK1032B from endophytic Penicillium citrinum induces the apoptosis of human osteosarcoma MG63 cells through caspase pathway activation.

Chemical investigation of the culture extract of an endophytic Penicillium citrinum from Dendrobium officinale, afforded nine citrinin derivatives (1-9) and one peptide-polyketide hybrid GKK1032B (10). The structures of these compounds were determined by spectroscopic methods. The absolute configurations of 1 and 2 were determined for the first time by calculation of electronic circular dichroism (ECD) data. Among them, GKK1032B (10) showed significant cytotoxicity against human osteosarcoma cell line MG63 with an IC50 value of 3.49 µmol·L-1, and a primary mechanistic study revealed that it induced the apoptosis of MG63 cellsvia caspase pathway activation.

MiR-873-5p modulates progression of tongue squamous cell carcinoma via targeting SEC11A.

OBJECTIVE: To explore the effect of miR-873-5p on proliferation, apoptosis, migration, and invasion of tongue squamous cell carcinoma (TSCC) by targeting SEC11A. METHODS: Tongue squamous cell carcinoma tissues were collected and performed by qRT-PCR and Western blotting to determine the expression of miR-873-5p and SPC18. SCC9 and CAL-27 cells were transfected and divided into Mock, mimic NC, miR-873-5p mimic, SEC11A, and miR-873-5p mimic + SEC11A groups. Then, a series of experiments including cell count kit 8 (CCK-8), wound healing, Transwell, and flow cytometry were conducted. Besides, Western blotting was used to detect the expression of SPC18 and EGFR pathway-related proteins. RESULTS: MiR-873-5p was downregulated while SPC18 was upregulated in TSCC, and miR-873-5p was negatively correlated with SPC18. Dual luciferase reporter gene assay confirmed SEC11A to be a target of miR-873-5p. Cell proliferation, migration, and invasion of SCC9 and CAL-27 cells in miR-873-5p mimic group were decreased with increased cell apoptosis, presenting with downregulations of SPC18 and EGFR pathway-related proteins, while cells in SEC11A group manifested totally different changes. Moreover, the inhibitory effect of miR-873-5p mimic on TSCC cell growth was abolished by SEC11A overexpression. CONCLUSION: Overexpression of miR-873-5p may suppress cell proliferation, migration, and invasion, but facilitate apoptosis in TSCC via targeting SEC11A.

Plant pathogen-mediated rapid acclimation of a host-specialized aphid to a non-host plant.

Polyphagous aphids often consist of host-specialized lineages, which have greater fitness on their native hosts than on others. The underlying causes are important for understanding of the evolution of diet breadth and host shift of aphids. The cotton-melon aphid Aphis gossypii Glover is extremely polyphagous with many strict host-specialized lineages. Whether and how the lineage specialized on the primary host hibiscus shifts to the secondary host cucumber remains elusive. We found that the hibiscus-specialized lineage suffered high mortality and gave birth to very few nymphs developing into yellow dwarfs on fresh cucumber leaves, and did not inflict any damage symptoms on cucumber plants. The poor performance did not improve with prolonged exposure to cucumber; however, it did significantly improve when the cucumber leaves were pre-infected with a biotrophic phytopathogen Pseudoperonospora cubensis. More importantly, the hibiscus-specialized lineage with two-generation feeding experience on pre-infected cucumber leaves performed as well as the cucumber-specialized lineage did on fresh cucumber leaves, and inflicted typical damage symptoms on intact cucumber plants. Electrical penetration graph (EPG) indicated that the hibiscus-specialized lineage did not ingest phloem sap from fresh cucumber leaves but succeeded in ingesting phloem sap from pre-infected cucumber leaves, which explained the performance improvement of the hibiscus-specialized lineage on pre-infected cucumber leaves. This study revealed a new pathway for the hibiscus-specialized lineage to quickly acclimate to cucumber under the assistance of the phytopathogen. We considered that the short feeding experience on pre-infected cucumber may activate expression of effector genes that are related to specific host utilization. We suggest to identify host-specific effectors by comparing proteomes or/and transcriptomes of the hibiscus-specialized lineage before and after acclimating to cucumber.

Malus rootstocks affect copper accumulation and tolerance in trees by regulating copper mobility, physiological responses, and gene expression patterns.

We investigated the roles of rootstocks in Cu accumulation and tolerance in Malus plants by grafting 'Hanfu' (HF) scions onto M. baccata (Mb) and M. prunifolia (Mp) rootstocks, which have different Cu tolerances. The grafts were exposed to basal or excess Cu for 20 d. Excess Cu-treated HF/Mb had less biomass, and pronounced root architecture deformation and leaf ultrastructure damage than excess Cu-challenged HF/Mp. Root Cu concentrations and bio-concentration factor (BCF) were higher in HF/Mp than HF/Mb, whereas HF/Mb had higher stem and leaf Cu concentrations than HF/Mp. Excess Cu lowered root and aerial tissue BCF and translocation factor (Tf) in all plants; however, Tf was markedly higher in HF/Mb than in HF/Mp. The subcellular distribution of Cu in the roots and leaves indicated that excess Cu treatments increased Cu fixation in the root cell walls, which decreased Cu mobility. Compared to HF/Mb, HF/Mp sequestered more Cu in its root cell walls and less Cu in leaf plastids, nuclei, and mitochondria. Moreover, HF/Mp roots and leaves had higher concentrations of water-insoluble Cu compounds than HF/Mb, which reduced Cu mobility and toxicity. Fourier transform infrared spectroscopy analysis showed that the carboxyl, hydroxyl and acylamino groups of the cellulose, hemicellulose, pectin and proteins were the main Cu binding sites in the root cell walls. Excess Cu-induced superoxide anion and malondialdehyde were 28.6% and 5.1% lower, but soluble phenolics, ascorbate and glutathione were 10.5%, 41.9% and 17.7% higher in HF/Mp than HF/Mb leaves. Compared with HF/Mb, certain genes involved in Cu transport were downregulated, while other genes involved in detoxification were upregulated in HF/Mp roots and leaves. Our results show that Mp inhibited Cu translocation and mitigated Cu toxicity in Malus scions by regulating Cu mobility, antioxidant defense mechanisms, and transcription of key genes involved in Cu translocation and detoxification.

Semaphorin 4A restricts tumor progression by inhibiting angiogenesis of oral squamous cell carcinoma cells.

OBJECTIVE: To investigate the effects of Semaphorin 4A (Sema4A) on the angiogenesis, migration and invasion of oral squamous cell carcinoma (OSCC) cells. METHODS: Sema4A expression in OSCC patients was detected by Immunohistochemistry, and its relationship with clinicopathological features and prognosis of patients was analyzed. The mRNA and protein expression of Sema4A in primary human oral keratinocytes (HOKs) and OSCC cells (SCC-25, HSC-3, CAL-27) were determined by Western blotting and qRT-PCR. After HOKs, HSC-3 cells and SCC-25 cells transfected with Control/Sema4A CRISPR activation plasmid, the migration and invasion abilities were detected by Wound healing and Transwell invasion. Tube formation assay was also performed on endothelial cells and the contents of VEGF and bFGF were quantified using qRT-PCR and ELISA. RESULTS: Cytoplasmic Sema4A expression was related to T classification, clinical stage and nodal metastasis of OSCC patients. Patients with low cytoplasmic Sema4A expression showed the higher microvessel density (MVD) and the poorer prognosis in OSCC. Compared with HOK, OSCC cells (SCC-25, HSC-3, CAL-27) declined apparently in Sema4A expression, which was much more significant in metastatic HSC-3 and SCC-25 cells. After HOKs, HSC-3 cells and SCC-25 cells transfected with Sema4A over-expression plasmid, the invasion and migration abilities were decreased. Besides, overexpression of Sema4A could significantly inhibit the tube formation of HUVEC induced by OSCC cells with reductions of angiogenic factors (VEGF and bFGF). CONCLUSION: Over-expression of Sema4A could restrict tumor progression through inhibiting the angiogenesis, invasion and migration of OSCC cells.