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Backgrounds: Anincreasing people are suffering from sensorineural hearing loss (SNHL) and facing great psychological and physical stress. Although the extract of extract of Ginkgo biloba (EGb) has been widely used to treat SNHL for many years, underlying pharmacological mechanisms remain unclear. Methods: Active ingredients of EGb and compounds targets were retrieved from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). SNHL-related genes were obtained from GeneCards. Venny 2.1 was used to select common targets between active ingredients of EGb and SNHL, and Gene ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. Cytoscape was used to construct a network map to assess the relationship between active ingredients, interacting targets, and signaling pathways, and Chem3D, AutoDock Tools, and PyMol were employed to perform molecular docking between active ingredients and hub genes. Besides, House Ear Institute-Organ of Corti 1 (HEI-OC1) cells were treated with cisplatin and EGb to verify target genes by quantitative Real-time PCR (q-PCR). Results: Venny diagram showing that SNHL and EGb had a total of 64 intersecting targets (core targets). The results of GO and KEGG analysis indicated that 64 core targets were involved in regulating of biological process, stabilization of cell membranes and organelles, protein binding, and diverse signaling pathways. According to the cytoscape and PPI network analyses, three genes (GSK3B, NOS3 and AKT1) and nine kinds of corresponding ingredients (kaempferol, quercetin, sesamin, luteolin, isorhamnetin, isogoycyrol, laricitrin, syringetin and chryseriol) were picked. Molecular docking demonstrates protein binding models for intersection genes and effective ingredients. Eventually, the results of q-PCR experiments further revealed that GSK3B, NOS3 and AKT1 genes exerted their functions in treatment of SNHL by EGb. Conclusions: Our findings indicate the mechanisms of action of EGb in treating SNHL. There are five active components, including luteolin, quercetin, isorhamnetin, kaempferol, and sesamin. Those ingredients exert their effects through regulating three genes (GSK3B, NOS3 and AKT1), which are involved in the PI3K-Akt signaling pathway.

Background Previous investigations indicated that transmembrane protein 16A (TMEM16A) mediates the pathogenesis and malignant of many tumors through regulating multiple pathways. However, whether TMEM16A could regulate autophagy via mammalian target of rapamycin (mTOR) pathway to modulate hypopharyngeal squamous cell carcinoma (HSCC) occurrence and development or not is still unclear. Methods The expression of TMEM16A in HSCC and metastatic lymph nodes was detected by immunohistochemistry and western blot. TMEM16A was overexpressed or knocked down in FaDu cell line to evaluate its effects on the biological function by cell colony formation experiment, wound healing assay, trans well assay, and invasion assay. TMEM16A was knocked down or over expression in FaDu cells to test apoptosis and autophagy related protein and autophagosome formation by western blot, transmission electron microscopy and immunofluorescence. Results In the present study, we observe that the expression level of TMEM16A in HSCC and metastatic lymph nodes are significantly higher than that in normal tissues. The results of in-vitro experiments showed that silencing TMEM16A significantly inhibited the proliferation, invasion and migration of HSCC cells. Silencing TMEM16A inhibited tumor formation in xenografted mice. Further experiments demonstrated that knocking down TMEM16A in HSCC cells could block the activation of mTOR, and thus promote the initiation of the autophagic death by activating sequestosome-1 (SQSTM1/P62) and protein light chain 3II (LC3II). Conclusion Therefore, TMEM16A displays an important effect on autophagy in HSCC, which may provide a potential therapeutic target for the treatment of HSCC.

Nuclear modifier genes have been proposed to modify the phenotypic expression of mitochondrial DNA mutations. Using a targeted exome-sequencing approach, here we found that the p.191Gly>Val mutation in mitochondrial tyrosyl-tRNA synthetase 2 (YARS2) interacts with the tRNASer(UCN) 7511A>G mutation in causing deafness. Strikingly, members of a Chinese family bearing both the YARS2 p.191Gly>Val and m.7511A>G mutations displayed much higher penetrance of deafness than those pedigrees carrying only the m.7511A>G mutation. The m.7511A>G mutation changed the A4:U69 base-pairing to G4:U69 pairing at the aminoacyl acceptor stem of tRNASer(UCN) and perturbed tRNASer(UCN) structure and function, including an increased melting temperature, altered conformation, instability, and aberrant aminoacylation of mutant tRNA. Using lymphoblastoid cell lines derived from symptomatic and asymptomatic members of these Chinese families and control subjects, we show that cell lines harboring only the m.7511A>G or p.191Gly>Val mutation revealed relatively mild defects in tRNASer(UCN) or tRNATyr metabolism, respectively. However, cell lines harboring both m.7511A>G and p.191Gly>Val mutations displayed more severe defective aminoacylations and lower tRNASer(UCN) and tRNATyr levels, aberrant aminoacylation, and lower levels of other tRNAs, including tRNAThr, tRNALys, tRNALeu(UUR), and tRNASer(AGY), than those in the cell lines carrying only the m.7511A>G or p.191Gly>Val mutation. Furthermore, mutant cell lines harboring both m.7511A>G and p.191Gly>Val mutations exhibited greater decreases in the levels of mitochondrial translation, respiration, and mitochondrial ATP and membrane potentials, along with increased production of reactive oxygen species. Our findings provide molecular-level insights into the pathophysiology of maternally transmitted deafness arising from the synergy between tRNASer(UCN) and mitochondrial YARS mutations.

Background The enlarged vestibular aqueduct (EVA), associated with mutations in the SLC26A4 gene, characterized by non-syndromic hearing loss, is an autosomal recessive disorder. Here, we intended to investigate genetic causes of hearing loss in a Han Chinese man. Method First, whole-exome sequencing was performed to identify the gene mutations responsible for hearing loss in the proband. Sanger sequencing was used to verify the candidate mutations detected in the family. Next, we collected blood samples and clinical data from the three-generation pedigree. Finally, SLC26A4 mRNA and protein expression levels were detected by qPCR and western blotting. Result The proband suffered from bilateral progressive sensorineural hearing loss with EVA. The sequence analysis of SLC26A4 revealed that the proband and his sister both harbored a compound heterozygous mutation of c.2168A > G/c.2029C > T, inherited from their father and mother respectively. c.2029C > T mutation has not been recorded in the relevant literature previously. Relative mRNA levels of the SLC26A4 gene in individuals carrying a compound heterozygous mutation were significantly lower compared to a heterozygous mutation. SLC26A4 protein levels of 293t cells which transfected with recombinant plasmids [GV219-SLC26A4-mut (c.2029C > T) and GV219-SLC26A4-mut (c.2168A > G/c.2029C > T)] were significantly lower than normal control recombinant plasmids (GV219-SLC26A4-wt). Conclusion This study found a novel heterozygous mutation c.2029 (exon17) C > T compound with c.2168 (exon19) A > G in the SLC26A4 gene in a patient with EVA. The c.2029 (exon17) C > T mutation is proved to be pathogenic. This finding broadens the spectrum of variants in SLC26A4 gene.

Background MicroRNA (miR)-146a, as an important immune regulatory factor with an anti-inflammatory effect, plays a crucial role in regulatory T cells (Tregs) differentiation and function in allergic rhinitis (AR). The present study aimed to investigate the regulatory mechanism employed by miR-146a to control Tregs differentiation and function in AR. Methods Expression of miR-146a and STAT5b in peripheral blood mononuclear cells (PBMCs) and nasal mucosa from patients with AR was detected by qPCR and western blotting. Tregs were quantified by flow cytometry in miR-146a knockdown or STAT5b knockdown PBMCs. FOXP3, IL-10, and TGF-β levels were detected by western blotting or ELISA in miR-146a knockdown or STAT5b overexpressing PBMCs, as well as in STAT5b knockdown PBMCs overexpressing miR-146a. The effect of miR-146a on STAT5b was observed by luciferase assay and knockdown experiments. Results Levels of miR146a and STAT5b in the nasal mucosa or PBMCs were significantly lower in the AR group than in the control group. There were significantly fewer Tregs in miR-146a knockdown or STAT5b knockdown PBMCs compared to control PBMCs. Expression of FOXP3, IL-10, and TGF-β was decreased in the miR-146a knockdown group but increased in the STAT5b overexpression group. In contrast, miR-146a overexpression increased the levels of these factors, but knockdown of STAT5b significantly inhibited this effect. Luciferase assay and knockdown experiments showed that miR-146a bound directly to STAT5b. Conclusions miR-146a enhances Tregs differentiation and function in AR by positively targeting STAT5b.

Mitochondrial tRNA processing defects were associated with human diseases but their pathophysiology remains elusively. The hypertension-associated m.4401A>G mutation resided at a spacer between mitochondrial tRNAMet and tRNAGln genes. An in vitro processing experiment revealed that the m.4401A>G mutation caused 59% and 69% decreases in the 5′ end processing efficiency of tRNAGln and tRNAMet precursors, catalyzed by RNase P, respectively. Using human umbilical vein endothelial cells-derived cybrids, we demonstrated that the m.4401A>G mutation caused the decreases of all 8 tRNAs and ND6 and increases of longer and uncleaved precursors from the Light-strand transcript. Conversely, the m.4401A>G mutation yielded the reduced levels of tRNAMet level but did not change the levels of other 13 tRNAs, 12 mRNAs including ND1, 12S rRNA and 16S rRNA from the Heavy-strand transcript. These implicated the asymmetrical processing mechanisms of H-strand and L-strand polycistronic transcripts. The tRNA processing defects play the determined roles in the impairing mitochondrial translation, respiratory deficiency, diminishing membrane potential, increasing production of reactive oxygen species and altering autophagy. Furthermore, the m.4401A>G mutation altered the angiogenesis, evidenced by aberrant wound regeneration and weaken tube formation in mutant cybrids. Our findings provide new insights into the pathophysiology of hypertension arising from mitochondrial tRNA processing defects.

To explore the role of DNA methyltransferase 1 (DNMT1) in development and progression of hypopharyngeal squamous carcinoma.A total of 32 hypopharyngeal squamous carcinoma biopsy samples and 20 normal tissue specimens were collected. Immunohistochemical staining, quantitative real-time polymerase chain reaction, and Western blot were performed for expression analysis. The mRNA and protein expression in the specimens and subcellular localization were analyzed. hypopharyngeal squamous carcinoma cells (FaDu) were used for small interfering RNA of DNMT1, and proliferation, cell cycle, and apoptosis were determined in the transfected cells. Furthermore, metastatic ability and methylation status of OOur results showed that DNMT1 was overexpressed, while MGMT was down expressed in hypopharyngeal squamous carcinoma. DNMT1 overexpression and MGMT down expression were significantly associated with poorly differentiated tumors, lymph node metastasis, and clinical stage. DNMT1 and MGMT were majorly distributed in the nucleus. Furthermore, knockdown of DNMT1 inhibited proliferation and metastasis, induced apoptosis and G1 phase arrest in FaDu cells, and upregulated MGMT expression to reverse methylation status of MGMT promoter.This study for the first time demonstrated the clinical value and the role of DNMT1 and MGMT in the biological function of hypopharyngeal squamous carcinoma. This work suggested that DNMT1 might serve as a potential therapeutic target for patients with hypopharyngeal squamous carcinoma.

Objective Previous studies have reported a correlation between coronavirus disease-2019 (COVID-19) and asthma. However, data on whether asthma constitutes a risk factor for COVID-19 and the prevalence of asthma in COVID-19 cases still remains scant. Here, we interrogated and analyzed the association between COVID-19 and asthma. Methods In this study, we systematically searched PubMed, Embase, and Web of Science databases for studies published between January 1, to August 28, 2020. We included studies that reported the epidemiological and clinical features of COVID-19 and its prevalence in asthma patients. We excluded reviews, animal trails, single case reports, small case series and studies evaluating other coronavirus-related illnesses. Raw data from the studies were pooled into a meta-analysis. Results We analyzed findings from 18 studies, including asthma patients with COVID-19. The pooled prevalence of asthma in COVID-19 cases was 0.08 (95% CI, 0.06-0.11), with an overall I2 of 99.07%, p

Mammalian mitochondrial tRNA (mt-tRNA) plays a central role in the synthesis of the 13 subunits of the oxidative phosphorylation complex system (OXPHOS). However, many aspects of the context-dependent expression of mt-tRNAs in mammals remain unknown. To investigate the tissue-specific effects of mt-tRNAs, we performed a comprehensive analysis of mitochondrial tRNA expression across five mice tissues (brain, heart, liver, skeletal muscle, and kidney) using Northern blot analysis. Striking differences in the tissue-specific expression of 22 mt-tRNAs were observed, in some cases differing by as much as tenfold from lowest to highest expression levels among these five tissues. Overall, the heart exhibited the highest levels of mt-tRNAs, while the liver displayed markedly lower levels. Variations in the levels of mt-tRNAs showed significant correlations with total mitochondrial DNA (mtDNA) contents in these tissues. However, there were no significant differences observed in the 2-thiouridylation levels of tRNALys, tRNAGlu, and tRNAGln among these tissues. A wide range of aminoacylation levels for 15 mt-tRNAs occurred among these five tissues, with skeletal muscle and kidneys most notably displaying the highest and lowest tRNA aminoacylation levels, respectively. Among these tissues, there was a negative correlation between variations in mt-tRNA aminoacylation levels and corresponding variations in mitochondrial tRNA synthetases (mt-aaRS) expression levels. Furthermore, the variable levels of OXPHOS subunits, as encoded by mtDNA or nuclear genes, may reflect differences in relative functional emphasis for mitochondria in each tissue. Our findings provide new insight into the mechanism of mt-tRNA tissue-specific effects on oxidative phosphorylation.

The present study aimed to explore the role of TGF-β1-mediated epithelial-mesenchymal transition (EMT) in the pathogenesis of tympanosclerosis. Sprague Dawley rats were injected with inactivated Streptococcus pneumoniae suspension to establish a rat model of tympanosclerosis. The rats were sacrificed 8 weeks after the model was established. H&E and von Kossa staining was used to observe the morphological changes of middle ear mucosa. Western blotting was used to detect the expression of TGF-β1 and EMT-associated proteins in the mucosa samples. Middle ear mucosal epithelial cells of rats were collected to establish a primary culture. The cultured cells were stimulated with TGF-β1 and the expression of EMT-associated proteins was detected by western blotting and immunofluorescence. In addition, the cells were treated with TGF-β receptor type I/II inhibitor and the expression level of EMT-associated proteins was detected by western blotting. Sclerotic lesions appeared on 72.4% of tympanic membranes, and marked inflammation, inflammatory cell infiltration and fibrosis were found in the middle ear mucosa of rat models of tympanosclerosis. In middle ear mucosa of rats with tympanosclerosis, the expression of mesenchymal cell markers increased and that of epithelial cell markers decreased compared with the control group. TGF-β1 stimulated the activation of the EMT pathway in middle ear mucosal epithelial cells, resulting in an increased expression of fibronectin and N-cadherin. In addition, a decreased expression level of EMT-associated proteins was observed when TGF-β1 was inhibited. In conclusion, the present study indicated that TGF-β1-mediated EMT may play an important role in the pathogenesis of tympanosclerosis.

The pathophysiology underlying spiral ganglion cell defect–induced deafness remains elusive. Using the whole exome sequencing approach, in combination with functional assays and a mouse disease model, we identified the potentially novel deafness-causative MAP1B gene encoding a highly conserved microtubule-associated protein. Three novel heterozygous MAP1B mutations (c.4198A>G, p.1400S>G; c.2768T>C, p.923I>T; c.5512T>C, p.1838F>L) were cosegregated with autosomal dominant inheritance of nonsyndromic sensorineural hearing loss in 3 unrelated Chinese families. Here, we show that MAP1B is highly expressed in the spiral ganglion neurons in the mouse cochlea. Using otic sensory neuron–like cells, generated by pluripotent stem cells from patients carrying the MAP1B mutation and control subject, we demonstrated that the p.1400S>G mutation caused the reduced levels and deficient phosphorylation of MAP1B, which are involved in the microtubule stability and dynamics. Strikingly, otic sensory neuron–like cells exhibited disturbed dynamics of microtubules, axonal elongation, and defects in electrophysiological properties. Dysfunctions of these derived otic sensory neuron–like cells were rescued by genetically correcting MAP1B mutation using CRISPR/Cas9 technology. Involvement of MAP1B in hearing was confirmed by audiometric evaluation of Map1b heterozygous KO mice. These mutant mice displayed late-onset progressive sensorineural hearing loss that was more pronounced in the high frequencies. The spiral ganglion neurons isolated from Map1b mutant mice exhibited the deficient phosphorylation and disturbed dynamics of microtubules. Map1b deficiency yielded defects in the morphology and electrophysiology of spiral ganglion neurons, but it did not affect the morphologies of cochlea in mice. Therefore, our data demonstrate that dysfunctions of spiral ganglion neurons induced by MAP1B deficiency caused hearing loss., Dysfunctions of spiral ganglion neurons caused by Map1b deficiency leads to sensorineural hearing loss.

Objective To explore the role of DNA methyltransferase 1 (DNMT1) in development and progression of hypopharyngeal squamous carcinoma. Design A total of 32 hypopharyngeal squamous carcinoma biopsy samples and 20 normal tissue specimens were collected. Immunohistochemical staining, quantitative real-time polymerase chain reaction, and Western blot were performed for expression analysis. The mRNA and protein expression in the specimens and subcellular localization were analyzed. hypopharyngeal squamous carcinoma cells (FaDu) were used for small interfering RNA of DNMT1, and proliferation, cell cycle, and apoptosis were determined in the transfected cells. Furthermore, metastatic ability and methylation status of O6-methylguanine-DNAmethyl-transferase (MGMT) promoter was assessed. Results Our results showed that DNMT1 was overexpressed, while MGMT was down expressed in hypopharyngeal squamous carcinoma. DNMT1 overexpression and MGMT down expression were significantly associated with poorly differentiated tumors, lymph node metastasis, and clinical stage. DNMT1 and MGMT were majorly distributed in the nucleus. Furthermore, knockdown of DNMT1 inhibited proliferation and metastasis, induced apoptosis and G1 phase arrest in FaDu cells, and upregulated MGMT expression to reverse methylation status of MGMT promoter. Conclusions This study for the first time demonstrated the clinical value and the role of DNMT1 and MGMT in the biological function of hypopharyngeal squamous carcinoma. This work suggested that DNMT1 might serve as a potential therapeutic target for patients with hypopharyngeal squamous carcinoma.

The deafness-associated m.12201T>C mutation affects the A5-U68 base-pairing within the acceptor stem of mitochondrial tRNAHis. The primary defect in this mutation is an alteration in tRNAHisaminoacylation. Here, we further investigate the molecular mechanism of the deafness-associated tRNAHis12201T>C mutation and test whether the overexpression of the human mitochondrial histidyl-tRNA synthetase gene (HARS2) in cytoplasmic hybrid (cybrid) cells carrying the m.12201T>C mutation reverses mitochondrial dysfunctions. Using molecular dynamics simulations, we demonstrate that the m.12201T>C mutation perturbs the tRNAHisstructure and function, supported by decreased melting temperature, conformational changes, and instability of mutated tRNA. We show that the m.12201T>C mutation-induced alteration of aminoacylation tRNAHiscauses mitochondrial translational defects and respiratory deficiency. We found that the transfer ofHARS2into the cybrids carrying the m.12201T>C mutation raises the levels of aminoacylated tRNAHisfrom 56.3 to 75.0% but does not change the aminoacylation of other tRNAs. Strikingly,HARS2overexpression increased the steady-state levels of tRNAHisand of noncognate tRNAs, including tRNAAla, tRNAGln, tRNAGlu, tRNALeu(UUR), tRNALys, and tRNAMet, in cells bearing the m.12201T>C mutation. This improved tRNA metabolism elevated the efficiency of mitochondrial translation, activities of oxidative phosphorylation complexes, and respiration capacity. Furthermore,HARS2overexpression markedly increased mitochondrial ATP levels and membrane potential and reduced production of reactive oxygen species in cells carrying the m.12201T>C mutation. These results indicate thatHARS2overexpression corrects the mitochondrial dysfunction caused by the tRNAHismutation. These findings provide critical insights into the pathophysiology of mitochondrial disease and represent a step toward improved therapeutic interventions for mitochondrial disorders.

Aim This study investigated the relation of serum carbohydrate antigen 199 (CA 19–9) levels to the clinical characteristics and chronic complications of patients newly diagnosed with type 2 diabetes mellitus (T2DM).Methods A total of 371 patients newly diagnosed with T2DM and 133 healthy people with consecutively matched age were compared. The 371 patients with T2DM were divided into four groups by quartiles based on their serum CA 19–9 levels, in which clinical characteristics and chronic complications, such as diabetic retinopathy (DR), diabetic nephropathy, and macrovascular complications were compared. Logistic regression analysis was used to evaluate the risk factors of DR.Results Among the 371 patients newly diagnosed with T2DM, 60 had elevated CA 19–9 levels (16.17%). The frequencies of elevated serum CA 19–9 were 24.39% (30 of 123) for females and 12.10% (30 of 248) for males, in which the values for females were higher than those for males (PConclusions Serum CA 19–9 levels were correlated with HbA1c and DR in patients newly diagnosed with T2DM. The elevated serum CA 19–9 levels, high FC-P, and FBG levels were important risk factors for DR in patients newly diagnosed with T2DM.

Nuclear modifier genes have been proposed to modify the phenotypic expression of mitochondrial DNA mutations. Using a targeted exome-sequencing approach, here we found that the p.191Gly>Val mutation in mitochondrial tyrosyl-tRNA synthetase 2 (YARS2) interacts with the tRNA(Ser(UCN)) 7511A>G mutation in causing deafness. Strikingly, members of a Chinese family bearing both the YARS2 p.191Gly>Val and m.7511A>G mutations displayed much higher penetrance of deafness than those pedigrees carrying only the m.7511A>G mutation. The m.7511A>G mutation changed the A4:U69 base-pairing to G4:U69 pairing at the aminoacyl acceptor stem of tRNA(Ser(UCN)) and perturbed tRNA(Ser(UCN)) structure and function, including an increased melting temperature, altered conformation, instability, and aberrant aminoacylation of mutant tRNA. Using lymphoblastoid cell lines derived from symptomatic and asymptomatic members of these Chinese families and control subjects, we show that cell lines harboring only the m.7511A>G or p.191Gly>Val mutation revealed relatively mild defects in tRNA(Ser(UCN)) or tRNA(Tyr) metabolism, respectively. However, cell lines harboring both m.7511A>G and p.191Gly>Val mutations displayed more severe defective aminoacylations and lower tRNA(Ser(UCN)) and tRNA(Tyr) levels, aberrant aminoacylation, and lower levels of other tRNAs, including tRNA(Thr), tRNA(Lys), tRNA(Leu(UUR)), and tRNA(Ser(AGY)), than those in the cell lines carrying only the m.7511A>G or p.191Gly>Val mutation. Furthermore, mutant cell lines harboring both m.7511A>G and p.191Gly>Val mutations exhibited greater decreases in the levels of mitochondrial translation, respiration, and mitochondrial ATP and membrane potentials, along with increased production of reactive oxygen species. Our findings provide molecular-level insights into the pathophysiology of maternally transmitted deafness arising from the synergy between tRNA(Ser(UCN)) and mitochondrial YARS mutations.

EDTA functionalized magnetic graphene oxide (EDTA-mGO), a good adsorbent for Pb(II), Hg(II) and Cu(II), was synthesized in the present work. It was characterized by SEM, FTIR, BET, XRD, XPS, TGA and zeta potential analysis. Contact time, adsorbent dose, pH and initial concentration were optimized to improve the removal efficiency. Most importantly, EDTA-mGO displayed better adsorption performance than EDTA-GO, EDTA-Fe3O4 and mGO. The adsorption of Pb(II), Hg(II) and Cu(II) mainly depend on the metal chelation of EDTA and the electrostatic attractions of abundant functional groups on GO surface. Besides, good magnetic performance of EDTA-mGO makes it easy to achieve the solid–liquid separation. The magnetic separation process only took 25 s. The adsorption kinetic data described well with the pseudo-second-order model and the equilibrium data fitted well to Freundlich and Temkin isotherms. The maximum adsorption capacity was 508.4 mg g−1 for Pb(II), 268.4 mg g−1 for Hg(II) and 301.2 mg g−1 for Cu(II) from Langmuir isotherm. Thermodynamic studies (ΔG 0, ΔS > 0) implied an endothermic and spontaneous adsorption process in nature. Furthermore, the excellent reproducibility indicated that EDTA-mGO has a promising application in water treatment.

Xanthate functionalized magnetic graphene oxide (Fe3O4-xGO) was successfully synthesized through linking xanthate groups to a kind of graphenes magnetic material (Fe3O4-GS). Fe3O4-xGO was found to be an ideal adsorbent for Hg(II) and methylene blue removal with a higher adsorption capacity. The synthesized adsorbent was characterized by SEM, TEM, FTIR, XRD, and BET respectively. Fe3O4-xGO can be simply recovered from water with magnetic separation at low magnetic field within only 1min. The adsorption capacity was found to be 118.55mg g(-1) for Hg(2+) (contact time for 180min, pH at 7 and temperature at 25°C) and 526.32mg g(-1) for methylene blue (contact time for 120min, pH at 5.5 and temperature at 25°C), respectively. Kinetic data showed good correlation with pseudo-second-order equation and the Langmuir model was found to fit for the isotherm data, which showed the contaminant sorption was accomplished mainly via chelation or ion exchange. The results of thermodynamic studies (ΔG0, ΔH0, ΔS0) illustrate that the adsorption process was endothermic and spontaneous in nature. The experimental results suggest that Fe3O4-xGO has the potential applications in the environmental management.

Magnetic carbonate hydroxyapatite/graphene oxide (M-CHAP/GO) was successfully prepared by loading magnetic carbonate hydroxyapatite (M-CHAP) onto graphene oxide sheets and was found to be an ideal adsorbent for heavy metal (Pb(II)) and dye (methylene blue). The obtained adsorbent was characterized by SEM, FTIR, XRD, BET, TGA, XPS and zeta potential, respectively. M-CHAP/GO nano-particles possessed a favorable and stable morphology. Moreover, the good magnetic properties of M-CHAP/GO made it simple to recover from water with magnetic separation. The equilibrium adsorption capacity was 277.7 mg g−1 for Pb(II) and 546.4 mg g−1 for methylene blue under the optimal conditions. The pseudo-second-order equation and the Langmuir model showed good correlation with the experimental data and explained well the mechanism of adsorption. It was found that the adsorption process was accomplished mainly via chelation and ion exchange. Thermodynamic studies (ΔG 0, ΔS > 0) implied that the adsorption process was endothermic and spontaneous in nature. The other adsorption mechanisms are further researched in this article. All the experimental results show that M-CHAP/GO nano-particles have potential application in the future of environmental management.

In this paper, carboxymethyl functionalized chitosan was used for the synthesis of a magnetic polysaccharide–graphene oxide composite (SCGO). Compared with the magnetic chitosan–graphene oxide composite reported before, adsorption capacity in this research had improved significantly. The calculated maximum adsorption capacity values for methylene blue (MB) and malachite green (MG) were 358.4 mg g−1 and 289.1 mg g−1, respectively. The morphology, chemical properties and physical structure of SCGO were characterized by scanning electron microscopy (SEM), Fourier transform infrared spectroscopy (FTIR) and X-ray powder diffraction (XRD). The influence factors which included pH, adsorbent dose, ionic strength and contact time on the adsorption properties of MB and MG onto SCGO were investigated. The adsorption kinetics of MB and MG on SCGO were well-described by pseudo-second order kinetic models. The experimental data of the isotherm followed the Temkin isotherm model and the Langmuir model, respectively. Thermodynamic analysis was also performed to calculate the changes in free energy (ΔG), enthalpy (ΔH), and entropy (ΔS). The results obtained from this research suggested that SCGO was a potential adsorbent for effective removal of methylene blue and malachite green.

Magnetic hydroxypropyl chitosan/graphene oxide (MHCGO) composites have been synthesized and employed as adsorbent for removal of lead ions from aqueous solution. X-ray powder diffraction, Fourier transform infrared spectrum, and scanning electron microscope showed that the MHCGO composites were fabricated successfully. The effects of adsorbent dosage, pH, and contact time on the adsorption of lead ions have been discussed, and the optimal adsorption conditions have been acquired. The results indicated that the adsorption of lead ions on MHCGO was dependent on pH with the optimum pH nearly 5.5. The adsorption process was fairly quick and the time to reach adsorption equilibrium is 100 min. The adsorption kinetics could be described by the pseudo-second-order model very well. Adsorption data fitted well with Freundlich model. The effect of temperature on lead ions adsorption was studied and was shown to be spontaneous.

In this study, a novel, amino-functionalized magnetic composite of CoFe2O4-chitosan-graphene (MCGS) had been successfully synthesized. The crystal phase, surface morphology and structure of the MCGS were investigated by powder X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FTIR), zeta potential measurement, and Brunauer–Emmett–Teller (BET) surface area. The adsorptive characteristics of the MCGS which was intended for removal of Hg(II) from aqueous solutions were deeply studied. The results showed that the adsorption efficiency increased with the increasing of pH and reached the highest point at pH 7.0. The Hg(II) adsorption kinetics on MCGS was consistent with the pseudo second-order process. Langmuir and Freundlich isotherm models were employed to analyze the experimental data, and the Langmuir model was fitted better with a maximum adsorption capacity of 361.0 mg/g at pH 7.0 and 323 K. Thermodynamic studies illustrated that the adsorption process was endothermic and spontaneous.

A novel magnetic nano-composite was synthesized by a simple method of coprecipitation through embedding ferroferric oxide into magnesium hydroxyapatite (MgHAp/Fe3O4) to remove Cu2 + from aqueous solution. The obtained adsorbent was characterized by scanning electron microscopy (SEM), energy dispersive spectrometer (EDS), Brunauer–Emmett–Teller (BET) surface area measurement and Fourier transform infrared spectroscopy (FTIR). Mg2 + and Cu2 + possess the same electrical charge and similar ionic radius, which is especially beneficial to their exchange in hydroxyapatites. Static adsorption experiments indicated that the maximal immobilization capacity of Cu2 + reached to 305 mg/g on the optimum adsorption conditions (dosage of 0.32 mg/mL, contact time for 90 min, pH at 5.9 and temperature at 25 °C). Adsorption kinetics including the pseudo-first order and pseudo-second order kinetic models were researched and the data fitted better with the pseudo-second order kinetic model (R2 = 0.99). For adsorption isotherms, Freundlich isotherm was proved to be the best correlation (R2 > 0.99) compared with the Henry and Langmuir isotherms. The thermodynamic parameters (ΔG

A method of co-precipitation was used to synthesize a novel magnetic nano-composite strontium hydroxyapatite/ferroferric oxide (SrHAp/Fe3O4) by embedding ferroferric oxide into strontium hydroxyapatite and this SrHAp/Fe3O4 was utilized as adsorbent to remove Pb2 + from aqueous solutions. The morphology features at the micro level of the obtained adsorbent were characterized by scanning electron microscopy (SEM), transmission electron microscopy (TEM), Brunauer–Emmett–Teller (BET) surface area and Fourier transform infrared (FTIR). The maximal immobilization capacity of Pb2 + reached to 1249 mg/g at the optimum adsorption conditions (dosage of 0.2 mg/mL, contact time for 20 min, pH at 4.5 and temperature at 25 °C). Adsorption of Pb2 + onto SrHAp/Fe3O4 agreed well with the pseudo-second order model (R2 = 0.9997). For adsorption isotherms, the Freundlich isotherm was provided to be the best correlation (R2 = 0.9862) compared to the Henry and Langmuir isotherms. The thermodynamic parameters (ΔG

Magnetic cobalt ferrite (CoFe 2 O 4 )-reduced graphene oxide (rGO) nanocomposites (CoFe 2 O 4 -rGO) were developed as an adsorbent to remove Pb(II) and Hg(II) from aqueous solution. The CoFe 2 O 4 -rGO was prepared by a facile approach and characterized by X-ray diffraction (XRD), Brunauer–Emmett–Teller (BET) surface area and Zeta potential measurement. In this work, contact time, adsorbent dose, and solution pH temperature were optimized. The sorption kinetics and isotherm model fitting studies, demonstrated that data fit well to pseudo-second order kinetics and Langmuir isotherm models. The highest adsorption equilibrium for Pb(II) were 299.4 mg/g at pH of 5.3 and 25 °C; while for Hg(II) were 157.9 mg/g at pH of 4.6 and 25 °C. Due to magnetic property, CoFe 2 O 4 -rGO could be simply recovered from water by magnetic separations at low magnetic field within 2 min.

In order to investigate the effects of flagellin secreted by bacteria associated with pine wood nematode (Bursaphelenchus xylophilus) on pine cells, suspension cells of Pinus thunbergii were treated with flagellin of Pseudomonas fluorescens GcM5-1A, and some physiological indices were determined. Superoxide anions radical (·O2 −) in treated suspension cells increased with prolongation of treatment time, with maximum content of 1,282 μmol g−1 FW at 30 h, but the content of H2O2 gradually decreased as compared with that in the control group. Maximum content of malondialdehyde (MDA) and free proline, which is 1.72 times and 1.49 times of that in the control, respectively, appeared when suspension cells were treated for 12 h, after that both of the contents decreased gradually. The activities of superoxide dismutase (SOD), peroxidase (POD) and catalases (CAT) also increased at the primary stage of treatment and then decreased compared with those of the control.

Leber's hereditary optic neuropathy (LHON) is the most common mitochondrial disease. Mitochondrial modifiers are proposed to modify the phenotypic expression of primary LHON-associated mitochondrial DNA (mtDNA) mutations. In this study, we demonstrated that the LHON susceptibility allele (m.14502T > C, p. 58I > V) in the ND6 gene modulated the phenotypic expression of primary LHON-associated m.11778G > A mutation. Twenty-two Han Chinese pedigrees carrying m.14502T > C and m.11778G > A mutations exhibited significantly higher penetrance of optic neuropathy than those carrying only m.11778G > A mutation. We performed functional assays using the cybrid cell models, generated by fusing mtDNA-less ρo cells with enucleated cells from LHON patients carrying both m.11778G > A and m.14502T > C mutations, only m.14502T > C or m.11778G > A mutation and a control belonging to the same mtDNA haplogroup. These cybrids cell lines bearing m.14502T > C mutation exhibited mild effects on mitochondrial functions compared with those carrying only m.11778G > A mutation. However, more severe mitochondrial dysfunctions were observed in cell lines bearing both m.14502T > C and m.11778G > A mutations than those carrying only m.11778G > A or m.14502T > C mutation. In particular, the m.14502T > C mutation altered assemble of complex I, thereby aggravating the respiratory phenotypes associated with m.11778G > A mutation, resulted in a more defective complex I. Furthermore, more reductions in the levels of mitochondrial ATP and increasing production of reactive oxygen species were also observed in mutant cells bearing both m.14502T > C and m.11778G > A mutation than those carrying only 11778G > A mutation. Our findings provided new insights into the pathophysiology of LHON that were manifested by interaction between primary and secondary mtDNA mutations.

© 2015 Elsevier B.V. Multifunctional hyperbranched polyamine modified graphene oxide (HPA-GO) was successfully prepared and characterized by Fourier transform infrared spectroscopy (FTIR), thermogravimetric analysis (TGA), X-ray diffraction (XRD), zeta potential and scanning electron microscope (SEM) analyses. HPA-GO exhibited excellent adsorption performance for the removal of a heavy metal (Pb(II)) and a dye (methylene blue (MB)). The equilibrium adsorption capacity was 819.7 mg g-1 for Pb(II) and 740.7 mg g-1 for MB under the optimal conditions. The pseudo-second order equation and the Langmuir model exhibited good correlation with the adsorption kinetic and isotherm data, respectively, for these two pollutants. The thermodynamic results (ΔG0, ΔS>0) implied that the adsorption process of Pb(II) and MB was feasible, endothermic and spontaneous in nature. A possible adsorption mechanism has been proposed where chelation and electrostatic attraction dominated the adsorption of Pb(II) and π-π stacking interactions and electrostatic attraction dominated the adsorption of MB. In addition, the excellent reproducibility endowed HPA-GO with the potential for application in water treatment.

With Phone Gap method, developers can use Web technical which correspond to the W3C standard developing native mobile application. According to call the API of Phone Gap, Web applications can communicate with the SDK API of the mobile platform which using by the developers, and then, they can use the native functions of the mobile platform. Phone Gap provides a method to develop plugins and import plugins, this method makes developers develop their own plugins or import new plugins to meet their special demands. According to the contrast testing, the mobile applications using Phone Gap method have a better performance than the applications using Web View method. Phone Gap Technical Introduction Phone Gap is an open source framework currently developed and maintained by the United States Adobe company. Using Phone Gap can be used HTML, CSS, JavaScript and HTML5+CSS3 prepared by the APP Web to build a cross platform for mobile applications. The main prospects is by acting as a bridge between JavaScript and native code with phone gap, not only to web application project conveniently packaged for local applications, but also by other local characteristics of the phone gap plug-in called Android devices, such as camera, geographic information, local network settings, and developers can according to the specific hardware needs and business requirements to develop phone gap plug-ins for their own equipment. Technical Principle and Implementation Process of Phone gap Cross Platform Principle of Phone Gap. Using phone gap technology and developers by using CSS and HTML to design the UI and control the program logic; at the same time, use JavaScript to call the API and the corresponding Platform SDK to interact, to activate the phone's GPS, motion, gravity sensors and other functions. Phone Gap prepared using the program will be packaged and installed on the phone, when the application is loaded into the phone's browser control to resolve the implementation of [4]. Phone gap framework for developers to provide a series of API, the API can be invoked in the JavaScript code; in the actual development process, through these API calls, phone gap program can interact with the developers use the Mobile Platform SDK API, and the actual call of the platform of local functions. After the development is completed, the user uses the application, the developer uses HTML technology Web, CSS and JavaScript files will be in the form of "mirror image" is packaged and released to the user's mobile platform. In actual operation, the Web browser embedded in the platform is analyzed and implemented, so as to realize the function of a development, multi platform operation. Phone Gap currently supports almost all mobile applications, such as iOS, Android, Phone Windows, blackberry and WebOS, etc.. Phone Gap Adopt JavaScript Call Java Process. The Phone Gap technology discussed in this paper will take the Android platform as an example, and based on the Phone Gap 1.6, 2.3.6 Android version to explore and test. Below through a simple Hello World program description in the Android platform based on Phone Gap development of the application of the principle of operation. The specific development process will be introduced in the next section. 6th International Conference on Sensor Network and Computer Engineering (ICSNCE 2016) © 2016. The authors Published by Atlantis Press 520 The following JavaScript code to achieve through the Phone Gap call Android device on the vibration notification function, when the program is running, the user clicks on the main program of the "shock 2 seconds" button, the device will continue to vibrate for 2 seconds. And the realization of this function, only need to use the same as the preparation of Web applications, in the HTML page to add the following line of JavaScript code. And the introduction of phonegap.js and phonegap.jar two class library support. // vibrate for 2 seconds. Function vibrate () {navigator. notification. Vibrate (2000);} Consider the user to click on the "2 seconds" button on the main program; the JavaScript code is how to call the API Android. When the user clicks on the button, the Notification. prototype. vibrate method in the phonegap.js will receive the call, and then call the Phone Gap. exec method. As shown in the following code section: Notification.prototype.vibrate = function (mills) {Phone Gap. exec(null, null, "Notification", "vibrate", [mills]);}; Phone Gap. Exec method is called, it will call prompt (stringify JSON. (args), "+JSON." stringify gap: ([service, action, callback ID, true]) method to complete the communication between JavaScript and Java. At this point, the Web View component of the Android system will attempt to pop up a window. Using Web Chrome Client provided API Android can intercept this action Web View. Specific to the Phone Gap 1.6 is the inheritance of the com. Phone gap. Cordova Chrome Client on Js Prompt class in the Web Chrome Client method. Execution of plugin Manager. exec (service, action, callbackId, message, async,) methods in the on Js Prompt method. At this point, Plug Manager will be based on the received parameters, will be distributed to a specific command Plugin, that is, the plug-in. About Phone Gap plug-in, will be described in the next section. In this case, the received plugin is Notification; the received action is vibrate; the parameter is 2000 Ms. Thus, Phone Gap call this. vibrate in the Notification (args. get Long (0)) method, notify the device vibration 2000 Ms. In the notification class vibrate method does not return a value, but in other phone gap plugins, common success and error two basic return value, to return a JSON object form, in order to inform the user, program execution state. And this return value can be captured and output on the main program page. Therefore, the summary of the JavaScript Phone Gap call Java process, as shown below. Figure 1. The communication process between JavaScript and Phone Gap in Java Phone Gap Adopt Java Call JavaScript Process. Phone Gap to achieve a callback server, the server is responsible for the callback JavaScript code; the server has a JavaScript code queue, in the src/com/phone gap/CallbackServer.java file: /** * The list of JavaScript statements to be sent to JavaScript.

The octavinyl polyhedral oligomeric silsesquioxane (POSS) grafted polypropylene (PP) was first prepared by reactive blending. The structure and properties of physical blending and reactive blending composites of PP/POSS were investigated by wide-angle X-ray diffraction (WAXD), differential scanning calorimetry (DSC), dynamic mechanical analysis (DMA). WAXD analysis shows that the POSS in the reactive blending composites has better compatibility with PP than in the physical blending composites. The β-form crystalline hence disappears even the non-reactive POSS can act as an effective β-nucleating agents. DSC analysis shows the reactive blending composites have higher crystalline temperature while POSS in the physical blending composites have little effect on the crystalline temperature. The modulus of reactive blending composites increases in the presence of POSS, while that of the physical blending composites decreases with increasing POSS content.

Polypropylene (PP)/octavinyl polyhedral oligomeric silsesquioxane (POSS) composites were prepared by two different processing methods: reactive blending and physical blending, and the crystallization behavior of PP and PP/POSS composites was studied by means of differential scanning calorimetry and polarized optical microscope. The results showed that the crystallization of PP in PP/POSS composites was strongly influenced by the different processing methods. POSS particles can act as effective nucleating agent, accelerating the crystallization of PP. The crystallization rate increased more dramatically for the reactive blending composite due to the stronger nucleating effect of PP grafted POSS. © 2008 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 46: 1762–1772, 2008

Carbon black (CB)-filled immisicible thermoplastic/thermosetting polymer blends consisting of polypropylene (PP) and Novolac resin were reported in this paper. The PP/Novolac/CB blends with varied compositions and different processing sequences were prepared by melt-mixing method. The CB distribution, conductive mechanism and the relationship between morphology and electrical properties of the PP/Novolac/CB blends were investigated. Scanning electron microscopy (SEM), optical microscopy and extraction experiment results showed that in PP/Novolac blends CB particles preferentially localized in the Novolac phase, indicating CB has a good affinity with Novolac resin. The incorporation of CB changed the spherical particles of the dispersed Novolac phase into elongated structure. With increasing Novolac content, the elongation deformation of Novolac phase became more obvious and eventually the blends developed into co-continuous structure, which form double percolation and decrease the percolation threshold. When CB was initially blended with PP and followed by the addition of Novolac resin, the partial migration of CB from PP to the Novolac phase was possibly occurred. The addition of Novolac to PP evidently increases the storage modulus G ′, loss modulus G ″ and complex viscosity η ∗ . The addition of CB to PP/Novolac blends further increase η ∗ , and it increases with increasing CB loading, which was related to the change of composite morphology.

The rheological behavior of polypropylene/novolac blends was investigated with special reference to the effects of the blend ratio, compatibilization, and dynamic cure. The polypropylene and all the polypropylene/novolac blends presented evidence of shear-thinning behavior. The novolac, compatibilizer, and dynamic cure had dramatic effects on the rheological behavior of the polypropylene. Various rheological plots, including plots of the viscosity, storage modulus, loss modulus, and loss angle, Han plots, and Cole–Cole plots, were used to analyze the polypropylene/novolac blends. The results showed that the compatibilization together with the dynamic cure could increase the viscosity and modulus because of the formation of a grafting polymer between the maleic anhydride grafted polypropylene and the curing novolac resin. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007

In this article, the dynamic vulcanization process was applied to polypropylene (PP)/Novolac blends compatibilized with maleic anhydride-grafted PP (MAH-g-PP). The influences of dynamic cure, content of MAH-g-PP, Novolac, and curing agent on mechanical properties of the PP/Novolac blends were investigated. The results showed that the dynamically cured PP/MAH-g-PP/Novolac blend had the best mechanical properties among all PP/Novolac blends. The dynamic cure of Novolac improved the modulus and stiffness of the PP/Novolac blends. The addition of MAH-g-PP into dynamically cured PP/Novolac blend further enhanced the mechanical properties. With increasing Novolac content, tensile strength, flexural modulus, and flexural strength increased significantly, while the elongation at break dramatically deceased. Those blends with hexamethylenetetramine (HMTA) as a curing agent had good mechanical properties at HMTA content of 10 wt %. Scanning electron microscopy (SEM) analysis showed that dynamically cured PP/MAH-g-PP/Novolac blends had finer domains than the PP/MAH-g-PP/Novolac blends. Thermogravimetric analysis (TGA) results indicated that the incorporation of Novolac into PP could improve the thermal stability of PP. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007

The crystallization, melting behavior, and morphology of Polypropylene (PP) and PP/Novolac blends were studied by scanning electron microscopy, wide angle X-ray diffraction, differential scanning calorimetry, and polarized optical microscope. The results showed that the crystallization of PP in PP/Novolac blends was strongly influenced by crystallization temperature, particles size of Novolac, crosslinking, and compatibilizer maleic anhydride-grafted PP. The Novolac resin could not only affect the crystal structure, but also acted as effective nucleating agents, accelerating the crystallization of PP in the PP/Novolac blends. And the smaller the Novolac particles were, the more effective were the nucleating agent for PP crystallization. Avrami equation was used to analyze the isothermal crystallization kinetics of PP and PP/Novolac blends. The influences of curing and compatibilizer on the crystallization behavior of PP were rather complicated. The crystallization thermodynamics were estimated using the Hoffman theory. The incorporation of cured Novolac and compatibilizer evidently decreased the chain folding energy of PP. © 2006 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 44: 3288–3303, 2006