Insights into the response of nitrogen metabolism to sulfamethoxazole contamination in constructed wetlands with varied substrates.

This study conducted an analysis of the variations in nitrogen metabolism pathways within constructed wetlands (CWs) using zeolite (CW-Z), ceramsite (CW-C), and lava (CW-L) under high concentration sulfamethoxazole (SMX) stress. The introduction of SMX hindered the formation of hydrogen bonds on the substrate surfaces; however, these surfaces still maintained a dense and thick biofilm. CW-Z exhibited superior removal efficiencies for ammonium nitrogen (NH4+-N) and nitrate nitrogen (NO3--N) compared to CW-C and CW-L, with removal rates of 92.54 ± 2.88 % and 89.39 ± 6.74 %, respectively. Interestingly, the proportion of genes involved in nitrification, denitrification and nitrate reduction genes in CW-C (36.05 %) were higher than that in CW-C (29.81 %) and CW-L (29.70 %) but the interactions among nitrogen functional bacteria in CW-Z were much more complex. Further analysis of the nitrogen metabolism pathway indicated that under CW-Z enhanced dissimilatory nitrate reduction SMX stress, while CW-L enhanced assimilatory nitrate reduction process compared to CW-C.

In Situ Polymerized 1,3-Dioxolane Electrolyte for Integrated Solid-State Lithium Batteries.

Solid-state lithium batteries are promising and safe energy storage devices for mobile electronics and electric vehicles. In this work, we report a facile in situ polymerization of 1,3-dioxolane electrolytes to fabricate integrated solid-state lithium batteries. The in situ polymerization and formation of solid-state dioxolane electrolytes on interconnected carbon nanotubes (CNTs) and active materials is the key to realizing a high-performance battery with excellent interfacial contact among CNTs, active materials and electrolytes. Therefore, the electrodes could be tightly integrated into batteries through the CNTs and electrolyte. Electrons/ions enable full access to active materials in the whole electrode. Electrodes with a low resistance of 4.5â€…Ω â–¡-1 and high lithium-ion diffusion efficiency of 2.5×10-11  cm2 s-1 can significantly improve the electrochemical kinetics. Subsequently, the batteries demonstrated high energy density, amazing charge/discharge rate and long cycle life.

Metal-Organic Framework-Derived Carbon/Carbon Nanotubes Mediate Impedance Matching for Strong Microwave Absorption at Fairly Low Temperatures.

The use of magnetic particles and carbon materials, particularly those with compatible dielectric and magnetic loss, is crucial in managing microwave pollution. However, the mismatched impedance of currently available absorbers constrains their practical applications. Herein, we demonstrate the potential of a metal-organic framework (MOF)-derived composite whose impedance matching is optimized through spraying and immersion of MOF precursors in carbon nanotube socks followed by carbonization. The composite presents extremely strong microwave absorption with a reflection loss of -30 dB, a thin thickness of 1.5 mm, and a wide frequency bandwidth of 7.8 GHz. The excellent absorption can still be maintained even at a fairly low temperature of -40 °C. Such results are primarily attributed to the synergistic effect between the hierarchical architecture and multiple components that greatly optimizes the impedance matching. We believe that the composite is a promising microwave absorber that can help to solve the critical electromagnetic wave pollution.

A Dendrite-Free Lithium/Carbon Nanotube Hybrid for Lithium-Metal Batteries.

Lithium (Li) metal is promising in the next-generation energy storage systems. However, its practical application is still hindered by the poor cycling performance and serious safety issues for the consequence of dendritic Li. Herein, a dendrite-free Li/carbon nanotube (CNT) hybrid is proposed, which is fabricated by direct coating molten Li on CNTs, for Li-metal batteries. The favorable thermodynamic and kinetic conditions are the powerful force to drive the rapid lift upwards and infusion of molten Li into CNTs network, which is the key to form a uniform metallic layer in Li/CNTs hybrid. The obtained hybrid indicates super-stable functions even at an ultrahigh current density of 40 mA cm-2 for 2000 cycles with a stripping/plating capacity of 2 mAh cm-2 in symmetric cells. Subsequently, this hybrid also demonstrates a significantly decreased resistance, excellent cycling stability at high current density and flexibility in the full Li-S battery. This work provides valuable concepts in fabricating Li anodes toward Li-metal batteries and beyond for their high-level services.

Sp1 promotes cell migration and invasion in oral squamous cell carcinoma by upregulating Annexin A2 transcription.

Oral squamous cell carcinoma (OSCC) is a common malignant tumor with high metastatic potential in head and neck. Revealing the mechanism of OSCC metastasis will benefit the prognosis and prevention of OSCC. Sp1 is a transcription factor involved in the progression of several tumors. Annexin A2 functions as an oncogene, and there are three putative Sp1 binding sites in the Annexin A2 promoter region. Therefore, we hypothesized that Sp1 could regulate OSCC metastasis by regulating Annexin A2 expression. Quantitative real-time PCR (qRT-PCR) and Western blot were used to evaluate Sp1 or Annexin A2 expression. Transwell assays were used to evaluate the migration and invasion capacity of OSCC cells. Luciferase assays and Chromatin immunoprecipitation assays were used to verify whether Sp1 regulate Annexin A2 at the transcriptional level. We found that the expression of Sp1 increased in OSCC tissues compared to paired adjacent normal tissues, and the overexpression of Sp1 was associated with tumor metastasis. Furthermore, Sp1 promoted cell migration and invasion through Annexin A2. In addition, we verified that Sp1 controls Annexin A2 expression at the transcriptional level and identified the binding sites involved. Our study suggests that Sp1/Annexin A2 expression could be a promising prognostic biomarker and therapeutic target for OSCC metastasis.

Integrin-α5 promoted the progression of oral squamous cell carcinoma and modulated PI3K/AKT signaling pathway.

BACKGROUND: Integrin-α5 (ITGA5) gene has been reported to be critical for the progression of several cancers. However, the effects of ITGA5 in oral squamous cell carcinoma (OSCC) remain unclear. METHODS: We firstly used bioinformatics methods to analyze the ITGA5 gene expression based on the public dataset. HO1-N-1 and SCC-9 cells with silenced ITGA5 were constructed using siRNA. Then, we determined the biological functions of ITGA5 in OSCC cells using cell counting kit-8 (CCK-8) assay, colony formation assay, wound healing assay and transwell assays. The expression of PI3K, p-PI3K, AKT, p-AKT, ERK and pERK were determined by western blot. RESULTS: Our results revealed that ITGA5 expression was up-regulated in OSCC. The biological experiments further confirmed that ITGA5 expression was higher in OSCC cell lines. Moreover, we found that knockdown of ITGA5 inhibited the proliferation, migration and invasion of OSCC cells. The expression of phosphorylated-(p) PI3K, p-AKT and p-ERK obviously decreased after knockdown of ITGA5 in OSCC cells. CONCLUSION: In summary, ITGA5 could promote the progression of OSCC via activating the PI3K/AKT signaling pathway, and it can be regarded as a potential biomarker for OSCC treatment.

The efficacy of polidocanol sclerotherapy in mucocele of the minor salivary gland.

OBJECTIVES: Mucocele of the minor salivary gland is usually caused when the duct is injured, mucus leaks into the tissue space and the mucous gland are obstructed, which lead to cystic lesion formation and dilatation. Currently, there are multiple therapeutic methods available with various outcomes. This study aims to provide clinical evidence of polidocanol sclerotherapy for the treatment of mucocele of the minor salivary gland. METHODS: In this study, we injected polidocanol into 112 patients who were diagnosed with mucocele of the minor salivary gland and evaluated the treatment efficacy and safety systematically. RESULTS: Of the 122 cases, 102 cases were cured, eight cases showed remarkable remission, and two cases had partial remission. No recurrence was found during follow-up, and none of the cases showed an invalid effect, resulting in a total cure rate of 91.07%. No severe side effects were observed during treatment or the follow-up period. No significant difference in efficacy between different genders was found (P = 0.490). Polidocanol sclerotherapy for mucocele on the lower lip was more effective compared to mucocele on the inferior surface of the lingual apex (P = 0.035). CONCLUSION: Polidocanol sclerotherapy showed satisfying curative effects for mucocele of the minor salivary gland without causing side effects of anesthesia, trauma, or severe pain.

[Clinicopathological and prognostic significance of PD-L1 expression in oral squamous cell carcinoma: a meta analysis].

PURPOSE: To determine the prognostic role of high PD-L1 in patients with oral squamous cell carcinoma. METHODS: Electronic databases, such as PubMed, Embase and Cochrane library, were searched to identify studies evaluating PD-L1 expression and overall survival (OS) in these patients. RevMan 5.3 software was used for meta-analysis. RESULTS: A total of 12 studies that involved 1595 patients were included. Pooled hazard ratio (HR) 1.02 (95%CI= 0.93-1.11,P=0.71) indicated that the association between PD-L1 expression and overall survival (OS) was not significant. The pooled odds ratios (ORs) indicated that PD-L1 expression was associated with gender (OR=0.64, 95%CI=0.48-0.85, P=0.002), differentiation (OR=0.58, 95%CI=0.37-0.90, P=0.01) and HPV infection (OR=1.91, 95%CI=1.13-3.23, P=0.02). However, PD-L1 had no correlation with tumour size, and lymph node status. CONCLUSIONS: PD-L1 expression may not be an independent predictor of prognosis of patients with OSCC. Well-designed large cohort studies are needed to confirm these findings.

Inhibition of autophagy augments apoptosis in human oral squamous cell carcinoma under nutrient depletion.

There has been little research conducted regarding autophagy in oral squamous cell carcinoma (OSCC). Given the prevalence of oral cancers which are OSCC and the severe side effects of current treatments, there is a pressing need to develop effective alternative therapies. In this study, we have endeavored to explore the biological characteristics of oral squamous cell carcinoma cell line KB cells, in particular with regard to the role played by autophagy in their survival. Autophagy was activated by nutrient depletion via culturing cells in Earle's balanced salts (EBSS) and was measured via indices relating to Beclin 1, microtubule-associated protein light chain 3 (MAPLC3, LC3), p62, and Green fluorescent protein-light chain 3 plasmid transfection (GFP-LC3). Cell death and apoptosis induced by nutrient depletion was measured using both MTT assay and flow cytometry (FCM). Compared to initial levels at 0 h, Beclin 1 density in EBSS-treated cells was found to have increased at 6, 12, and 18 h in a time-dependent manner and was found to have subsequently declined at 24 and 48 h. p62 levels, LC3-II/LC3-I ratio, and GFP-LC3 levels increased at 6, 12, 18, 24, and 48 h in a time-dependent manner. 3-methyladenine (3-MA) was found to inhibit autophagy and the expression of Beclin 1 and significantly enhanced nutrient depletion-induced apoptosis and death. We concluded that nutrient depletion enhances OSCC cell autophagy in time-course patterns and that the inhibition of autophagy augments apoptosis in OSCC cells. We also deduced that Beclin 1 takes part in the development and progression of autophagy, potentially playing an important role in the crosstalk between apoptosis and autophagy in OSCC cells. These findings suggest that nutrient depletion may be an effective way to explore autophagy and that autophagy inhibitors should be investigated as a potential novel agent for the adjuvant treatment of human OSCC.

Lentivirus-based RNA silencing of Nemo-like kinase (NLK) inhibits the CAL 27 human adenosquamos carcinoma cells proliferation and blocks G0/G1 phase to S phase.

BACKGROUND: The Nemo-like kinase (NLK) is a serine/threonine-protein kinase that involved in a number of signaling pathways regulating cell fate. Variation of NLK has been shown to be associated with the risk of cancer. However, the function of NLK in oral adenosquamous carcinoma cells line CAL-27 is unknown. METHODS: In this study, we evaluated the function of NLK in CAL-27 cells by using lentivirus-mediated RNA silence. The targeted gene expression, cell proliferation and cell cycle are investigated by RT-PCR, western-blot, MTT method, colony forming assay and flow cytometry analysis respectively. RESULTS: After NLK silencing, the number of colonies was significantly reduced (54 ± 5 colonies/well compared with 262 ± 18 colonies/well in non-infected or 226 ± 4 colonies/well in negative control group (sequence not related to NLK sequence with mismatched bases). Using crystal violet staining, we also found that the cell number per colony was dramatically reduced. The RNA silencing of NLK blocks the G0/G1 phase to S phase progression during the cell cycle. CONCLUSIONS: These results suggest that NLK silencing by lentivirus-mediated RNA interference would be a potential therapeutic method to control oral squamous carcinoma growth.

Limits to sustained energy intake. XVIII. Energy intake and reproductive output during lactation in Swiss mice raising small litters.

Limits to sustained energy intake (SusEI) during lactation in Swiss mice have been suggested to reflect the secretory capacity of the mammary glands. However, an alternative explanation is that milk production and food intake are regulated to match the limited growth capacity of the offspring. In the present study, female Swiss mice were experimentally manipulated in two ways - litter sizes were adjusted to be between 1 and 9 pups and mice were exposed to either warm (21°C) or cold (5°C) conditions from day 10 of lactation. Energy intake, number of pups and litter mass, milk energy output (MEO), thermogenesis, mass of the mammary glands and brown adipose tissue cytochrome c oxidase activity of the mothers were measured. At 21 and 5°C, pup mass at weaning was almost independent of litter size. Positive correlations were observed between the number of pups, litter mass, asymptotic food intake and MEO. These data were consistent with the suggestion that in small litters, pup requirements may be the major factor limiting milk production. Pups raised at 5°C had significantly lower body masses than those raised at 21°C. This was despite the fact that milk production and energy intake at the same litter sizes were both substantially higher in females raising pups at 5°C. This suggests that pup growth capacity is lower in the cold, perhaps due to pups allocating ingested energy to fuel thermogenesis. Differences in observed levels of milk production under different conditions may then reflect a complex interplay between factors limiting maternal performance (peripheral limitation and heat dissipation: generally better when it is cooler) and factors influencing maximum pup growth (litter size and temperature: generally better when it is hotter), and may together result in an optimal temperature favouring reproduction.

Apoptotic effect of MG-132 on human tongue squamous cell carcinoma.

The aim of this study was to investigate the apoptotic effect of a proteasome inhibitor MG-132 on Tca-8113, a cell line of human tongue squamous cell carcinoma. Tca-8113 cells were treated with 10, 20, and 30µM of MG-132, or 5µM thapsigargin. Apoptosis rate was determined with annexin V/propidium iodide double staining. Expression of E3ubiquitin-protein ligase was determined by ELISA, and Grp78 and caspase-12 mRNA, and Grp78 and caspase-12 protein was assessed by RT-PCR and Western blot, respectively. Apoptosis was observed 18h after MG-132 treatment. The apoptotic rate in the 10, 20, and 30µM MG-132 group was 13.5, 19.6 and 34.7%, respectively, which was higher than in the thapsigargin (8.5%, P<0.01) or control group (0.5%, P<0.01). The expression of E3 ubiquitin-protein ligase in the 10, 20, and 30µM MG-132 group was 28.75±2.28, 18.16±0.65, 8.85±0.72, respectively, which was lower than in the thapsigargin (38.96±0.33, P<0.05 or 0.01) or control (40.88±4.52, P<0.05 or 0.01) group. The levels of Grp78 and capase-12 mRNA, Grp78 and caspase-12 protein in the MG-132 groups were higher than in the control group (P<0.01). In conclusion, MG-132 induces apoptosis in Tca-8113 cells in a concentration-dependent manner. The MG-132-induced apoptosis may involve downregulation of E3 ubiquitin ligase, and upregulation of Grp78 and caspase-12.

[Apoptosis induced by MG-132 in Tca-8113 cells].

PURPOSE: To explore the apoptotic effect of ubiquitin-proteasome inhibitor (PI) MG-132 on human tongue squamous cell carcinoma cell line (Tca-8113 cell) through endoplasmic reticulum stress. METHODS: Tca-8113 cells were cultured in RPMI 1640 medium supplemented with 10% fetal calf serum, the exponential cells were divided into 5 groups.The cell culture medium was added to 1640 (negative control group), thapsigargin 5 µmol/L (positive control group), and 10,20,30 µmol/L (MG-132 group). After 24 h, the following experiments were carried out: morphological change of apoptotic cells was observed by Hoechst 33258 fluorescent staining under fluorescent microscope, apoptotic rate of cells was determined with annexin V-FITC/PI double staining by flow cytometry, the GRP78 mRNA level was determined by RT-PCR, the expression of caspase-12 protein was evaluated by Western blot, the human ubiquitin-protein ligase E3 concentration was detected by ELISA. The data was analyzed using SPSS16.0 software package. RESULTS: Typical morphological change of apoptosis in Tca-8113 cells was observed 24 hours after treating with 10.0, 20.0, 30.0 µmol/L MG-132 and positive control group; The apoptotic rate of MG-132 groups gradually increased with MG-132 concentration; The GRP78 mRNA level was up-regulated; The expression of caspase-12 increased was demonstrated by Western blot; The expression of the human ubiquitin-protein ligase E3 in MG-132 groups was 28.75 ± 2.28, 18.16 ± 0.65 and 8.85 ± 0.72. CONCLUSIONS: MG-132 can induce apoptosis of Tca-8113 cells through endoplasmic reticulum stress; MG-132 can inhibit the expression of human ubiquitin ligase E3.