Synthesis of core-shell silicon-carbon nanocomposites via in-situ molten salt-based reduction of rice husks: A promising approach for the manufacture of lithium-ion battery anodes.

Silicon (Si) has gained substantial interest as a potential component of lithium-ion battery (LIB) anodes due to its high theoretical specific capacity. However, conventional methods for producing Si for anodes involve expensive metal reductants and stringent reducing environments. This paper describes the development of a calcium hydride (CaH2)-aluminum chloride (AlCl3) reduction system that was used for the in-situ low-temperature synthesis of a core-shell structured silicon-carbon (Si-C) material from rice husks (RHs), and the material was denoted RHs-Si@C. Moreover, as an LIB anode, RHs-Si@C exhibited exceptional cycling performance, exemplified by 90.63 % capacity retention at 5 A g-1 over 2000 cycles. Furthermore, the CaH2-AlCl3 reduction system was employed to produce Si nanoparticles (Si NPs) from RHs (R-SiO2, where SiO2 is silica) and from commercial silica (C-SiO2). The R-SiO2-derived Si NPs exhibited a higher residual silicon oxides (SiOx) content than the C-SiO2-derived Si NPs. This was advantageous, as there was sufficient SiOx in the R-SiO2-derived Si NPs to mitigate the volumetric expansion typically associated with Si NPs, resulting in enhanced cycling performance. Impressively, Si NPs were fabricated on a kilogram scale from C-SiO2 in a yield of 82 %, underscoring the scalability of the low-temperature reduction technique.

Two-State Hydrogen Atom Transfer Reactivity of Unsymmetric [Cu2(O)(NO)]2+ Complexes.

We report the temperature-dependent spin switching of dicopper oxo nitrosyl [Cu2(O)(NO)]2+ complexes and their influence on hydrogen atom transfer (HAT) reactivity. Electron paramagnetic resonance (EPR) and Evans method analysis suggest that [Cu2(O)(NO)]2+ complexes transition from the S = 1/2 to the S = 3/2 state around ca. 202 K. At low temperatures (198 K) where S = 3/2 dominates, a strong correlation between the rate of HAT (kHAT) and the population of the S = 1/2 state was identified (R2 = 0.988), suggesting that the HAT by [Cu2(O)(NO)]2+ complexes proceeds by the S = 1/2 isomer. Installation of functional groups that introduce an unsymmetric secondary coordination environment accelerates the HAT rates through perturbation of the spin equilibria. Given the often unsymmetric coordination sphere of bimetallic active sites in natural proteins, we anticipate that similar strategies could be employed by metalloenzymes to control HAT reactions.

Nanostructured MoS2 with Interlayer Controllably Regulated by Ionic Liquids/Cellulose for High-Capacity and Durable Sodium Storage Properties.

Low intrinsic conductivity and structural instability of MoS2 as an anode of sodium-ion batteries limit the liberation of its theoretical capacity. Herein, density functional theory simulations for the first time optimize MoS2 interlayer distance between 0.80 and 1.01 nm for sodium storage. 1-Butyl-3-methyl-imidazolium acetate ([BMIm]Ac) induces cellulose oligomers to intercalate MoS2 interlayers for achieving controllable distance by changing the mass ratio of cellulose to [BMIm]Ac. Based on these findings, porous carbon loading the interlayer-expanded MoS2 allowing Na+ to insert with fast kinetics is synthesized. A carbon layer derived from [BMIm]Ac and cellulose coating the composite prevents the MoS2 from contacting electrolytes, leading to less sulfur loss for a more reversible specific capacity. Meanwhile, MoS2 and carbon have a strong interfacial connection through MoN binding, contributing to enhanced structural stability. As expected, while cycling 250 times at 0.1 A g-1 , the MoS2 -porous carbon composite displays an optimal reversible capacity at 517.79 mAh g-1 as a sodium-ion batteries anode. The cyclic test of 1.0 A g-1 also shows considerable stability (310.74 mAh g-1 after 1000 cycles with 86.26% retentive capacity). This study will open up new possibilities of modifying MoS2 that serves as an applicable material as sodium-ion battery anode.

Reductive NO Coupling at Dicopper Center via a [Cu2(NO)2]2+ Diamond-Core Intermediate.

Treatment of a dicopper(I,I) complex with excess amounts of NO leads to the formation of a dicopper dinitrosyl [Cu2(NO)2]2+ complex capable of (i) releasing two equivalents of NO reversibly in 90% yield and (ii) reacting with another equivalent of NO to afford N2O and dicopper nitrosyl oxo species [Cu2(NO)(O)]2+. Resonance Raman characterization of the [Cu2(NO)2]2+ complex shows a 15N-sensitive N═O stretch at 1527.6 cm-1 and two Cu-N stretches at 390.6 and 414.1 cm-1, supporting a symmetric diamond-core structure with bis-µ-NO ligands. The conversion of [Cu2(NO)2]2+ to [Cu2(NO)O]2+ occurs via a rate-limiting reaction with NO and bypasses the dicopper oxo intermediate, a mechanism distinct from that of diFe-mediated NO reduction to N2O.

Controlling the Direction of S-Nitrosation versus Denitrosation: Reversible Cleavage and Formation of an S-N Bond within a Dicopper Center.

Iron and copper enzymes are known to promote reversible S-nitrosation/denitrosation in biology. However, it is unclear how the direction of S-N bond formation/scission is controlled. Herein, we demonstrate the interconversion of metal-S-nitrosothiol adduct M(RSNO) and metal nitrosyl thiolate complex M(NO)(SR), which may regulate the direction of reversible S-(de)nitrosation. Treatment of a dicopper(I,I) complex with RSNO leads to a mixture of two structural isomers: dicopper(I,I) S-nitrosothiol [CuICuI(RSNO)]2+ and dicopper(II,II) nitrosyl thiolate [CuIICuII(NO)(SR)]2+. The Keq between these two structural isomers is sensitive to temperature, the solvent coordination ability, and counterions. Our study illustrates how copper centers can modulate the direction of RS-NO bond formation and cleavage through a minor perturbation of the local environment.

Direct copolymerization of ethylene with protic comonomers enabled by multinuclear Ni catalysts.

Ethylene/polar monomer coordination copolymerization offers an attractive way of making functionalized polyolefins. However, ethylene copolymerization with industrially relevant short chain length alkenoic acid remain a big challenge. Here we report the efficient direct copolymerization of ethylene with vinyl acetic acid by tetranuclear nickel complexes. The protic monomer can be extended to acrylic acid, allylacetic acid, ω-alkenoic acid, allyl alcohol, and homoallyl alcohol. Based on X-ray analysis of precatalysts, control experiments, solvent-assisted electrospray ionization-mass spectrometry detection of key catalytic intermediates, and density functional theory studies, we propose a possible mechanistic scenario that involves a distinctive vinyl acetic acid enchainment enabled by Ni···Ni synergistic effects. Inspired by the mechanistic insights, binuclear nickel catalysts are designed and proved much more efficient for the copolymerization of ethylene with vinyl acetic acid or acrylic acid, achieving the highest turnover frequencies so far for both ethylene and polar monomers simultaneously.

Direct NO Reduction by a Biomimetic Iron(II) Pyrazolate MOF.

A novel metal-organic framework (MOF) containing one-dimensional, Fe2+ chains bridged by dipyrazolate linkers and N,N-dimethylformamide (DMF) ligands has been synthesized. The unusual chain-type metal nodes feature accessible coordination sites on adjacent metal centers, resulting in motifs that are reminiscent of the active sites in non-heme diiron enzymes. The MOF facilitates direct reduction of nitric oxide (NO), producing nearly quantitative yields of nitrous oxide (N2 O) and emulating the reactivity of flavodiiron nitric oxide reductases (FNORs). The ferrous form of the MOF can be regenerated via a synthetic cycle involving reduction with cobaltocene (CoCp2 ) followed by reaction with trimethylsilyl triflate (TMSOTf).

NAT10 as a potential prognostic biomarker and therapeutic target for HNSCC.

BACKGROUND: Increasing evidence has demonstrated the critical roles of mRNA modification regulators on multiple types of cancers. However, it is still poorly known about the prognostic and therapeutic value of mRNA modification regulators in HNSCC. METHODS: The gene expression profile of 36 mRNA modification regulators and their corresponding clinical data were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). Stepwise regression in R with both directions was used to construct a model for the prognosis of HNSCC. Univariate Cox regression survival analysis was performed to identify the most significant risk gene. Gene set enrichment analysis (GSEA) was applied to determine the cancer-associated pathways with NAT10. Immunohistochemistry (IHC) staining was performed to evaluate the expression of NAT10 in formalin fixed paraffin-embedded (FFPE) samples of HNSCC. Univariate and multivariate Cox regression survival analysis performed to identify the independent risk factors associated with the OS of patients with HNSCC. HNSCC cell lines (Cal-27, FaDu, and Detroit-562) were transfected with short interfering RNA (siRNA) targeting NAT10 or treated with Remodelin, a small-molecule inhibitor of NAT10. Knockdown efficiency of siRNA was assessed by quantitative real-time PCR (qRT-PCR) and western blotting. In addition, CCK-8 assay, scratch assay and transwell assay were used to examine the proliferation, migration, and invasion abilities of the three HNSCC cell lines after NAT10 was inhibited genetically and pharmaceutically. Cell cycle and cell apoptosis assays were performed by flow cytometry. Finally, the therapeutic value of Remodelin in HNSCC was evaluated via a patient-derived xenograft (PDX) model. The statistical analysis was performed with SPSS 23.0. RESULTS: A risk prediction model containing 10 mRNA modification regulators was constructed and showed prognostic value in HNSCC. NAT10 was further identified as a key risk gene and independent prognostic factor in TCGA HNSCC dataset. The GSEA analysis suggested that high NAT10 expression was associated with MYC, E2F, G2M checkpoint, mTORC1, DNA repair and oxidative phosphorylation pathways. NAT10 protein expression was significantly up-regulated in tumour cells compared to normal epithelial cells in FFPE samples and increased NAT10 protein expression was correlated with poor overall survival of 267 HNSCC patients. Genetic depletion of NAT10 using siRNA or chemical inhibition of NAT10 using Remodelin resulted in reduced cell proliferation, migration and invasion abilities in Cal-27, FaDu and Detroit-562 cells. Knockdown of NAT10 using siRNA significantly increased cell cycle arrest in S/G2-phase. Remodelin significantly inhibited tumour growth and tumour cell proliferation in the PDX model of HNSCC. CONCLUSIONS: NAT10 could be a potential prognostic marker and a therapeutic target for HNSCC.

Redox-Neutral S-nitrosation Mediated by a Dicopper Center.

A redox-neutral S-nitrosation of thiol has been achieved at a dicopper(I,I) center. Treatment of dicopper (I,I) complex with excess NO. and thiol generates a dicopper (I,I) di-S-nitrosothiol complex [CuI CuI (RSNO)2 ]2+ or dicopper (I,I) mono-S-nitrosothiol complex [CuI CuI (RSNO)]2+ , which readily release RSNO in 88-94 % yield. The S-nitrosation proceeds by a mixed-valence [CuII CuIII (µ-O)(µ-NO)]2+ species, which deprotonates RS-H at the basic µ-O site and nitrosates RS- at the µ-NO site. The [CuII CuIII (µ-O)(µ-NO)]2+ complex is also competent for O-nitrosation of MeOH. A rare [CuII CuII (µ-NO)(OMe)]2+ intermediate was isolated and fully characterized, suggesting the S-nitrosation may proceed through the intermediary of analogous [CuII CuII (µ-NO)(SR)]2+ species. This redox- and proton-neutral S-nitrosation process is the first functional model of ceruloplasmin in mediating S-nitrosation of external thiols, with implications for biological copper sites in the interconversion of NO. /RSNO.

Dicopper µ-Oxo, µ-Nitrosyl Complex from the Activation of NO or Nitrite at a Dicopper Center.

Treatment of a dicopper(I,I) complex with nitric oxide produces a dicopper µ-oxo, µ-nitrosyl complex [LCu2(µ-O)(µ-NO)]2+, representing the first structurally characterized µ-oxo, µ-nitrosyl metal complex. This compound can also be synthesized from the reaction of nitrite with an [LCuIICuI]3+ synthon. Full characterization of the thermal-sensitive [LCu2(µ-O)(µ-NO)]2+ complex with IR, EPR, and X-ray crystallography suggests a localized mixed-valent CuIII, CuII, O2-, NO- formulation. The [Cu2(µ-O)(µ-NO)]2+ core efficiently oxidizes exogenous substrates, such as phosphine, cyclohexadienes, and isochroman to afford phosphine oxide, benzene, and 1-isochromanone. Since both nitrite and nitric oxide are proposed oxidants in denitrifying methane oxidation, the oxidative reactivity of [Cu2(µ-O)(µ-NO)]2+ core is potentially relevant to anaerobic methane oxidation observed in methanotrophic archaea.

Repurposing Ponatinib as a Potent Agent against KIT Mutant Melanomas.

Rationale: Mutations in KIT, a major cancer driver gene, are now considered as important drug targets for the treatment of melanomas arising from mucosal and acral tissues and from chronically sun-damaged sites. At present, imatinib is the only targeted drug for KIT-mutation-bearing melanomas that is recommended by the National Comprehensive Cancer Network (NCCN) Clinical Practice guidelines. Patients with KIT mutations, however, are either insensitive or rapidly progress to imatinib insensitivity, which restricts its clinical use. Thus, effective inhibitors of KIT-mutation-bearing melanomas are urgently needed. Methods: A cohort of patient-derived tumor xenograft (PDX) models and corresponding PDX-derived cells (PDCs) from patients with melanomas harboring KIT mutations (KITV560D, KITK642E and KITD816V) were established, characterized, and then used to test the in vitro and, subsequently, in vivo inhibitory effects of a panel of known KIT inhibitors. Results: Ponatinib was more potent than imatinib against cells bearing KIT mutations. In vivo drug efficacy evaluation experiments showed that ponatinib treatment caused much stronger inhibition of KIT-mutation-bearing melanomas than did imatinib. Mechanistically, molecular dynamics (MD) simulations revealed a plausible atomic-level explanation for the observation that ponatinib has a higher affinity for the KITD816V mutant protein than does imatinib. Conclusions: Our study of KIT-mutation-and KITWT-bearing melanomas demonstrates that ponatinib is a far more potent inhibitor than is imatinib for KIT-mutation-bearing melanomas and thus underscores that ponatinib should be given priority consideration for the design of precision treatments for melanoma patients triaged to have KIT mutations. Moreover, our work provides a rationale for undertaking clinical trials to examine the repurposing of ponatinib, which is already approved for use in leukemia, for use in treating a large subset of melanoma patients.

Analysis of Mucosal Melanoma Whole-Genome Landscapes Reveals Clinically Relevant Genomic Aberrations.

PURPOSE: Unlike advances in the genomics-driven precision treatment of cutaneous melanomas, the current poor understanding of the molecular basis of mucosal melanomas (MM) has hindered such progress for MM patients. Thus, we sought to characterize the genomic landscape of MM to identify genomic alterations with prognostic and/or therapeutic implications. EXPERIMENTAL DESIGN: Whole-genome sequencing (WGS) was performed on 65 MM samples, including 63 paired tumor blood samples and 2 matched lymph node metastases, with a further droplet digital PCR-based validation study of an independent MM cohort (n = 80). Guided by these molecular insights, the FDA-approved CDK4/6 inhibitor palbociclib was tested in an MM patient-derived xenograft (PDX) trial. RESULTS: Besides the identification of well-recognized driver mutations of BRAF (3.1%), RAS family (6.2%), NF1 (7.8%), and KIT (23.1%) in MMs, our study also found that (i) mutations and amplifications in the transmembrane nucleoporin gene POM121 (30.8%) defined a patient subgroup with higher tumor proliferation rates; (ii) enrichment of structural variations between chromosomes 5 and 12 defined a patient subgroup with significantly worse clinical outcomes; (iii) over 50% of the MM patients harbored recurrent focal amplification of several oncogenes (CDK4, MDM2, and AGAP2) at 12q13-15, and this co-occurred significantly with amplification of TERT at 5p15, which was verified in the validation cohort; (iv) the PDX trial demonstrated robust antitumor effects of palbociclib in MMs harboring CDK4 amplification. CONCLUSIONS: Our largest-to-date cohort WGS analysis of MMs defines the genomic landscape of this deadly cancer at unprecedented resolution and identifies genomic aberrations that could facilitate the delivery of precision cancer treatments.See related commentary by Shoushtari, p. 3473.

[Blockage of mTOR signaling pathway by homoharringtonine inhibits proliferation and induces apoptosis of HT29 human colorectal tumor cells].

Objective To investigate the molecular mechanisms underlying the effect of homoharringtonine (HHT) on the proliferation and apoptosis in HT29 human colorectal tumor cells. Methods HT29 cells were treated by 0, 0.007812, 0.015625, 0.03125, 0.0625, 0.125, 0.25, 0.5, 1, 2, 4, 8 µg/mL HHT for 24, 48 and 72 hours. CCK-8 assay was used to assess the cell viability. Colony formation assay was performed to detect the cell proliferation ability. Flow cytometry was used to analyze cell apoptosis. Hoechst33258 fluorescent staining was used to observe the morphology of the cell nuclei. The real-time quantitative PCR was used to detect the mRNA expressions of BAX, Bcl2, caspase-3, caspase-9, mammalian target of rapamycin (mTOR), PI3K, pyruvate dehydrogenase kinase-1 (PDK1), protein kinase B (AKT), raptor, rictor. The protein levels of Bax, Bcl2, pro-caspase-3, cleaved caspase 3 (c-caspase-3), pro-caspase-9, cleaved caspase-9 (c-caspase- 9), poly(ADP-ribose)polymerase (PARP), cleaved PARP (c-PARP), mTOR, raptor, rictor, PI3K, PDK1, AKT, p-AKT were detected by Western blotting. Results Compared with the control group, the proliferation of HT29 cells was inhibited when treated with HHT. Meanwhile, the nuclear fragmentation, chromatin condensation, and apoptotic body of the cells could be observed. Treatment of HHT could increase the mRNA expressions of BAX/Bcl2, caspase-3, caspase-9 and raptor, and decrease PI3K, AKT and rictor in the HT29 cells. The protein levels of pro-caspase-3, pro-caspase-9, PARP, PI3K, PDK1, AKT, mTOR, and rictor were down-regulated, and the c-caspase-3, c-caspase-9, c-PARP, BAX and raptor were up-regulated. Conclusion HHT has the function of inhibiting the HT29 cell proliferation and inducing its apoptosis by blockage of mTOR signaling pathway.

Nickel-Catalyzed Propylene/Polar Monomer Copolymerization.

Nickel complexes bearing bidentate alkylphophine-phenolate ligands were synthesized and applied to the polymerization of propylene and the copolymerization of propylene and polar monomers. Therein, the use of bulky alkyl substituents on the phosphorus atom was crucial for the formation of highly regioregular polypropylenes. Theoretical calculations suggested that the 1,2-insertion of propylene is favored over the 2,1-insertion in these nickel-catalyzed (co)polymerization reactions. The substituent at the ortho position relative to the oxido group greatly influences the polymerization activity, the molecular weight, and stereoregularity of the polypropylenes. This method delivers moderately isotactic ([mm] ≤ 68%) crystalline polypropylenes. The present system represents the first example for a nickel-catalyzed regiocontrolled copolymerization of propylene and polar monomers such as but-3-en-1-ol, but-3-en-1-yl acetate, and tert-butyl allylcarbamate.

Targeting and Regulating of an Oncogene via Nanovector Delivery of MicroRNA using Patient-Derived Xenografts.

In precision cancer nanomedicine, the key is to identify the oncogenes that are responsible for tumorigenesis, based on which these genetic drivers can be each specifically regulated by a nanovector-directed, oncogene-targeted microRNA (miRNA) for tumor suppression. Fibroblast Growth Factor Receptor 3 (FGFR3) is such an oncogene. The molecular tumor-subtype harboring FGFR3 genomic alteration has been identified via genomic sequencing and referred to as the FGFR3-driven tumors. This genomics-based tumor classification provides further rationale for the development of the FGFR3-targeted miRNA replacement therapy in treating patients with FGFR3 gene abnormity. However, successful miRNA therapy has been hampered by lacking of an efficient delivery vehicle. In this study, a nanovector is developed for microRNA-100 (miR-100) -mediated FGFR3 regulation. The nanovector is composed of the mesoporous magnetic clusters that are conjugated with ternary polymers for efficient miRNA in-vivo delivery. The miRNA-loading capacity of the nanovector is found to be high due to the polycation polymer functionalized mesoporous structure, showing excellent tumor cell transfection and pH-sensitive miRNA release. Delivery of miR-100 to cancer cells effectively down-regulates the expression of FGFR3, inhibits cell proliferation, and induces cell apoptosis in vitro. Patient-derived xenografts (PDXs) are used to evaluate the efficacy of miRNA delivery in the FGFR3-driven tumors. Notably, sharp contrasts are observed between the FGFR3-driven tumors and those without FGFR3 genomic alteration. Only the FGFR3-driven PDXs are significantly inhibited via miR-100 delivery while the non-FGFR3-driven PDXs are not affected, showing promise of precision cancer nanomedicine.

Overexpression of stathmin/oncoprotein 18 correlates with poorer prognosis and interacts with p53 in oral squamous cell carcinoma.

PURPOSE: The stathmin/oncoprotein 18 (STMN1) is overexpressed in various human cancers. The aim of our study was to investigate its clinical significance and interaction with p53 in oral squamous cell carcinoma (OSCC). MATERIALS AND METHODS: Stathmin expression was assessed by Oncomine, Gene Expression Omnibus (GEO) database, western blotting, and reverse transcription polymerase chain reaction. We investigated the relationship between stathmin expression and clinical characteristics among 109 OSCC patients by immunohistochemical staining. The prognosis factors were analyzed using univariate and multivariate analysis. Immunoprecipitation assay and The Cancer Genome Atlas (TCGA) analysis were used to detect the relationship between mutant p53 and stathmin. RESULTS: Stathmin was overexpressed in OSCC. In immunohistochemical analysis, high stathmin expression correlated with gender (P = 0.040), T stage (P = 0.015), TNM stage (P = 0.045), and pathological differentiation (P = 0.000). We found a correlation between the stathmin expression and overall survival (P = 0.027). Multivariate analysis suggested only lymph node metastasis (P = 0.007) and stathmin expression (P = 0.013) as independent prognostic factors. There was interaction between stathmin and p53 in OSCC cell lines with mutant p53 through immunoprecipitation assay. CONCLUSION: These results suggest that overexpression of stathmin could contribute to cancer progression/prognosis, and that interaction between p53 and stathmin may contribute to the gain-of-function of p53.

Charge Variants of an Avastin Biosimilar Isolation, Characterization, In Vitro Properties and Pharmacokinetics in Rat.

The similarity between a proposed biosimilar product and the reference product can be affected by many factors. This study is designed to examine whether any subtle difference in the distribution of the charge variants of an Avastin biosimilar can affect its in vitro potency and in vivo PK. Here, the acidic, basic and main peak fractions of a biosimilar product were isolated using high-performance cation-exchange chromatography and were subjected to various studies to compare their in vitro properties and in vivo PK profile. A serial of analytical methods, including size exclusion chromatography (SEC), imaged capillary isoelectric focusing (icIEF) capillary zone electrophoresis (CZE) and cation-exchange chromatography (CEX-HPLC) were also used to characterize the isolated charge variants. The kinetics constant was measured using a Biacore X100 system. The study indicates the biosimilar product has a high similarity with avastin in physicochemical properties. The potency in vitro and PK profile in rat of charge variants and biosimilar product are consistent with avastin.

Copolymerization of Ethylene and Polar Monomers by Using Ni/IzQO Catalysts.

The replacement of precious metals in catalysis by earth-abundant metals is currently one of the urgent challenges for chemists. Whereas palladium-catalyzed copolymerization of ethylene and polar monomers is a valuable method for the straightforward synthesis of functionalized polyolefins, the corresponding nickel-based catalysts have suffered from poor thermal tolerance and low molecular weight of the polymers formed. Herein, we report a series of neutral nickel complexes bearing imidazo[1,5-a]quinolin-9-olate-1-ylidene (IzQO) ligands. The Ni/IzQO system can catalyze ethylene polymerization at 50-100 °C with reasonable activity in the absence of any cocatalyst, whereas most known nickel-based catalysts are deactivated at this temperature range. The Ni/IzQO catalyst was successfully applied to the copolymerization of ethylene with allyl monomers to obtain the corresponding copolymers with the highest molecular weight reported for a Ni-catalyzed system.

[Expression and localization of FGFR family in squamous cell carcinoma of head and neck].

PURPOSE: To investigate the expression and localization of FGFR family in squamous cell carcinoma of head and neck (SCCHN) cell lines. METHODS: Total protein was extracted from 10 SCCHN cell lines and the expression of FGFR was detected by Western blot. The localization of FGFR was further demonstrated by immunofluorescence staining in SCC25 and HN4 cell lines. Gray value was measured by Image J. GraphPad Prism 5.01 software package was used for data processing and analysis. RESULTS: FGFR1 expression was detected in 6/10 cell lines and FGFR2, 3, 4 was detectable in all cell lines. The expression of FGFR1, 2, 4 was mainly in the nucleus and cytoplasm while FGFR3 was predominantly localized in cytoplasm. CONCLUSIONS: FGFR shows co-expression in SCCHN cell lines, which may be associated with the tumorigenesis and development of SCCHN.

A highly efficient and enantioselective intramolecular Cannizzaro reaction under TOX/Cu(II) catalysis.

An asymmetric intramolecular Cannizzaro reaction of aryl and alkyl glyoxals with alcohols has been realized with an unprecedented high level of enantioselectivity, on the basis of a newly developed congested TOX ligand and a gradual liberation protocol of active glyoxals from glyoxal monohydrates. Preliminary results suggested a mechanism of enantioselective addition of alcohols to glyoxals contributing most to the stereoselectivity, other than by the dynamic kinetic resolution of hemiacetal intermediates.