Coordination compound-derived Fe4N/Fe3N/Fe/CNT for efficient electrocatalytic oxygen evolution: a facile one-step synthesis in the absence of extra nitrogen source.

By annealing an Fe(III)-coordination compound (Fe-CC), [FeCl3(Hbta)2] (Hbta = benzotriazole) in the presence of a carbon nanotube precursor (PCNT) template, an Fe4N/Fe3N/Fe/CNT heterostructure was successfully synthesized without an extra nitrogen source. The decomposition of the Hbta in Fe-CC under high-temperature annealing can produce carbon sheets and reduced graphene oxide (rGO), and the presence of CNTs can alleviate the stacking of thein situ-generated carbon materials. Meanwhile, iron nitride nanoparticles (NPs) can be anchored on the carbon sheets, and the anchoring effect efficiently prevents the agglomeration of NPs and increases the amount of active catalytic sites for the oxygen evolution reaction (OER). Fe4N/Fe3N/Fe/CNT shows an excellent OER activity with a Tafel slope of 63 mV dec-1as well as overpotentials of 121 (η10) and 275 mV (η100) at 10 and 100 mA cm-2, respectively - far exceeding commercial RuO2and other catalysts. Density functional theory calculations show that the excellent OER performance of Fe4N/Fe3N/Fe/CNT is associated with the Fe4N/Fe3N heterojunction, which can improve the electron conductivity and boost the electron transfer from N to Fe. The Fe4N/Fe3N/Fe/CNT catalyst exhibits long-term OER activity during 100 h of electrolysis at 20 mA cm-2. This is related to the dual coatings of thein situ-generated thin carbon shell and few-layered rGO on the surface of the iron nitride NPs, which can protect the fast leaching of iron nitride during the OER process. Furthermore, the effects of the annealing temperature, the PCNT template and the heating rate on the calcined products were investigated.

Coordination Polymer-Derived Fe3N Nanoparticles for Efficient Electrocatalytic Oxygen Evolution.

Based on a coordination polymer, FeCl2(4,4'-bpy) (4,4'-bpy = 4,4'-bipyridine) and the carbon nanotube (CNT)/NaCl dual template, Fe3N nanoparticles (NPs) were synthesized via chemical thermolysis in the absence of an extra nitrogen source. The decomposition of 4,4'-bpy under high temperature produces thin carbon coating for Fe3N NPs. Also, the CNT template anchors the Fe3N NPs to avoid aggregation. The sample (denoted as Fe3N-C N) exhibits excellent electrocatalytic oxygen evolution reaction (OER) behavior even with a small molar ratio of Fe3N (Fe: 4.9 at. %), which can deliver a current density of 10 mA cm-2 at an overpotential of 218 mV with a Tafel slope of 84 mV dec-1 and long-term OER activity during 60 h electrolysis at 20 mA cm-2. Furthermore, the sample after 20 h electrolysis, denoted as Post-Fe3N-C N (20 h), displays enhanced OER activity with a smaller Tafel slope of 41 mV dec-1 and overpotentials of 195 and 327 mV at 10 and 100 mA cm-2, respectively, which is mainly due to the partial transformation of Fe3N into FeOOH. The OER mechanism is investigated by density functional theory calculations, and it is found that the surface partial oxidation of Fe3N leads to the effective OER electrolysis, which changes the electron density of the superficial atoms and induces the moderate adsorption for the intermediates.

Correlation between tripartite motif-containing protein 44 protein expression and the prognosis of postoperative patients exhibiting skin squamous cell carcinoma.

Tripartite motif-containing protein 44 (TRIM44) plays an important role in the development and progression of some human cancers; however, its role in skin squamous cell carcinoma (SCC) remains unknown. The aim of the present study was to investigate TRIM44 expression and clinicopathological significance of TRIM44 in SCC.Immunohistochemistry (IHC) technique, reverse transcriptase-polymerase chain reaction (RT-PCR) and western blot were performed to evaluate differences in TRIM44 protein expression in SCC and normal skin tissues.IHC showed that the positive rate of TRIM44 staining in SCC tissues 26.00% (9/30), while the positive rate of normal control group was 83.33% (25/30). The positive rate of TRIM44 staining in SCC tissues is significantly lower than normal skin tissue (P <.01). RT-PCR showed that the positive rates of TRIM44 mRNA expression in SCC tissues were 16.67% (5/30), but the positive rate of normal control group was 86.67% (26/30). TRIM44 mRNA expression in SCC group was significantly lower than that in the normal group (P <.01). Kaplan-Meier survival analysis showed that low expression was associated with poor overall survival in SCC patients (P =.004). Multi-factor survival analysis indicated that both low TRIM44 expression and tumor stage were independent factors affecting the overall survival of patients with SCC (P =.038 and P =.001, respectively). Low expression of TRIM44 in SCC was associated with staging (P =.009 and P =.008, respectively) and metastasis (P =.003 and P =.004, respectively).The levels of TRIM44 protein and TRIM44 mRNA in SCC are both lowly expressed which is strongly associated with tumor staging, metastasis, and poor survival. And it also is an independent factor affecting the overall survival of patients with SCC.

Clinical significance of the phosphorylation of MAPK and protein expression of cyclin D1 in human osteosarcoma tissues.

The aim of the present study was to investigate the significance of the phosphorylation of mitogen-activated protein kinase (MAPK) and the protein expression of cyclin D1 in human osteosarcoma tissues. Human osteosarcoma tissue samples were collected from 30 patients, benign bone tumor samples were collected from 30 patients, and normal bone tissues were collected from 10 individuals as controls. Immunohistochemistry was performed to measure the levels of phosphorylated (p)-MAPK and cyclin D1 protein in cases of human osteosarcoma. The results showed that the positive rates of MAPK and cyclin D1 in osteosarcoma were 86.67% (26/30) and 73.00% (22/30), respectively. The positive staining rates of MAPK and cyclin D1 in benign bone tumor tissues were 10.00% (3/30) and 3.30% (1/30), respectively. The positive rate in the normal bone tissues was 0% (0/30), which was significantly lower, compared with that of the cancerous bone tissue. The positive rates of MAPK and cyclin D1 in osteosarcoma were increased (P<0.05), and the expression of cyclin D1 and p­MAPK were positively correlated. The phosphorylation of MAPK may be important in the development of osteosarcoma, and the overactivation of MAPK may induce high expression of cyclin D1 and induce tumor cells to proliferate continuously.

Clinical significance of STAT3 and MAPK phosphorylation, and the protein expression of cyclin D1 in skin squamous cell carcinoma tissues.

The present study aimed to investigate the significance of the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and mitogen­activated protein kinase (MAPK), and the protein expression of cyclin D1, in skin squamous cell carcinoma (SCC) tissues. SCC specimens from the skin were collected from 30 patients, and normal skin tissues were collected from 10 individuals as a control. Immunohistochemistry was used to assess the protein expression levels of phosphorylated (p­)STAT3, p­MAPK and cyclin D1 in the SCC tissues. The levels of p­STAT3 protein were abnormally increased in SCC (P<0.05); however, no significant differences in the protein expression of p­MAPK were identified between the normal skin and the SCC specimens. The extent of the upregulation of the expression of p­STAT3 and cyclin D1 correlated with the depth of tumor invasion (P<0.05). A positive correlation existed between the expression of p­STAT3 and cyclin D1 in SCC. However, no association between the expression intensity of p­MAPK and cyclin D1 was identified in SCC. It is postulated that the activation of STAT3 may induce the overexpression of cyclin D1, which results in the persistent proliferation of these tumor cells in SCC.

Inhibitory effect of curcumin on invasion of skin squamous cell carcinoma A431 cells.

OBJECTIVE: To investigate the regulatory effect of curcumin on expression of signal transducer and activator of transcription 3 (STAT3) in skin squamous cell carcinoma tissues as well as possible mechanisms of curcumin in prevention and treatment of skin squamous cell carcinoma. MATERIALS AND METHODS: Highly invasive A431 cells were treated with curcumin at various doses .The cytotoxic effects of treatment with 5, 10, 15, 20, 25, 30, 35, 40 and 50 umol/L curcumin for 24, 48 and 72 hours on A431 cells were measured by MTT assay. The invasion capacity of cells treated with 5, 10 and 15 umol/L curcumin was measured by Transwell test, while adhesive ability was assessed by cell adhesion assay. The effects of 5,10 and 15 umol/L curcumin on expression levels of STAT3 were determined by Western blotting and on transcription levels of STAT3 mRNA by RT-PCR. RESULTS: Treatment with curcumin at a doses of more than 15 umol/L for more than 24 hour inhibited the growth of A431 cells in a time-and dose-dependent fashion (p<0.001). The doses of 15 umol/L and less for 24 hours showed no significant cytotoxic effects on the cells, survival rates being more than 85%.The invasion and adhesive abilities decreased gradually with the increasing curcumin concentration, 15 umol/L exerting the strongest inhibitory effects (p<0.05). Curcumin showed significant dose-dependent inhibitory effects on the transcription level of STAT3 mRNA (p<0.05). CONCLUSIONS: Curcumin may reduce the invasive ability of A431 cells by inhibiting the activation of STAT3 signal pathway and expression of STAT3 as a target gene in the pathway.

[The type IV secretion system encoded by the cag PAI of Helicobacter pylori].

Helicobacter pylori is a human-specific gastric pathogen that colonizes over half the world's population. Infection with this bacterium is associated with a spectrum of gastric pathologies ranging from mild gastritis to peptic ulcers and gastric cancer. A strong predictor of severe disease outcome is infection with a bacterial strain harbouring the cag (cytotoxin associated gene) pathogenicity island (PAI), a 40 kb stretch of DNA that encodes homologues of several components of a type IV secretion system (TFSS). One gene within the cag PAI, cagA, has been shown to encode a substrate for the TFSS which is translocated into host cells, inducing the dephosphrylation of host cell proteins and leading to changes in the morphology or shape of AGS gastric epithelial cells. Furthermore, the TFSS is involved in the induction of proinflammatory cytokines. It appeears to play a key role in H. pylori pathogenesis. Very little is known about the H. pylori cag PAI-encoded TFSS, the expression of Cag proteins in H. pylori, and the functions of individual proteins encoded by the cag PAI. Only by exploring the mechanistic details of the interplay between H. pylori and eukaryotic cells can we endeavour to understand how these cellular interactions play out at the tissue and organismal level during the lifelong coexistence of bacterium and host.

Type IV secretion system in Helicobacter pylori: a new insight into pathogenicity.

OBJECTIVE: To review the research progress on Type IV secretion system (T4SS) in Helicobacter pylori. DATA SOURCES: The data used in this review were identified by searching of PUBMED (1995 - 2007) online resources using the key terms 'Type IV secretion system' and 'Helicobacter pylori'. STUDY SELECTION: Mainly original articles and critical reviews written by major pioneer investigators of this field were selected. RESULTS: The research progress on T4SS in Helicobacter pylori was summarized. The structure and function was discussed. CONCLUSIONS: T4SS is not only involved in toxin secretion and injection of virulence factors into eukaryotic host target cells, but also involved in horizontal DNA transfer to other bacteria and eukaryotic cells, through DNA uptake from or release into the extracellular milieu. It provides a new insight into the pathogenicity of Helicobacter pylori and a novel target for antimicrobials development. However, many challenges remain for us in understanding the biological role of T4SS in Helicobacter pylori.