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1.
Chem Commun (Camb) ; 56(65): 9300-9303, 2020 Aug 21.
Artigo em Inglês | MEDLINE | ID: mdl-32666980

RESUMO

Two mixed-metal hydride clusters, corresponding to x = 3 and 4, were structurally characterized from a set of atomically precise heptanuclear clusters, CuxAg7-x(H){S2P(OiPr)2}6 (x = 1-6). An interstitial hydride lying at the center of a tricapped tetrahedral cage was located and refined anisotropically by using X-ray data, and its presence acertained by multinuclear NMR spectroscopy and DFT calculations.

2.
Front Oncol ; 9: 404, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31214489

RESUMO

Background: Although lung cancer incidence and mortality have been declining since the 1990s, the extent to which such progress has been made is unequal across population segments. Updated epidemiologic data on trends and patterns of disparities are lacking. Methods: Data on lung cancer cases and deaths during 1974 to 2015 were extracted from the Surveillance, Epidemiology, and End Results program. Age-standardized lung cancer incidence and mortality and their annual percent changes were calculated by histologic types, demographic variables, and tumor characteristics. Results: Lung cancer incidence decreased since 1990 (1990 to 2007: annual percent change, -0.9 [95% CI, -1.0%, -0.8%]; 2007 to 2015: -2.6 [-2.9%, -2.2%]). Among adults aged between 20 and 39 years, a higher incidence was observed among females during 1995 to 2011, after which a faster decline in female lung cancer incidence (males: -2.5% [-2.8%, -2.2%]; females: -3.1% [-4.7%, -1.5%]) resulted in a lower incidence among females. The white population had a higher incidence than the Black population for small cell carcinoma since 1987. Black females were the only group whose adenocarcinoma incidence plateaued since 2012 (-5.0% [-13.0%, 3.7%]). A higher incidence for squamous cell carcinoma was observed among Black males and females than among white males and females during 1974 to 2015. After circa 2005, octogenarians and older patients constituted the group with the highest lung cancer incidence. Incidence for localized and AJCC/TNM stage I lung cancer among octogenarians and older patients plateaued since 2009, while mortality continued to rise (localized: 1.4% [0.6%, 2.1%]; stage I: 6.7% [4.5%, 9.0%]). Conclusions: Lung cancer disparities prevail across population segments. Our findings inform effective approaches to eliminate lung cancer disparities by targeting at-risk populations.

3.
Mol Immunol ; 75: 144-50, 2016 07.
Artigo em Inglês | MEDLINE | ID: mdl-27289030

RESUMO

The purpose of this study was to evaluate the effects of GATA-6 on airway inflammation and remodeling and the underlying mechanisms in a murine model of chronic asthma. Female BALB/c mice were randomly divided into four groups: phosphate-buffered saline control (PBS), ovalbumin (OVA)-induced asthma group (OVA), OVA+ siNC and OVA+ siGATA-6. In this mice model, GATA-6 expression level was significantly elevated and the expression in Caveolin-1 (Cav-1) inversely correlated with the abundance of GATA-6 in OVA-induced asthma of mice. Silencing of GATA-6 gene expression upregulated Cav-1 expression. Additionally, downregulation of GATA-6 dramatically decreased OVA-challenged inflammation, infiltration, and mucus production. Moreover, silencing of GATA-6 resulted in decreased levels of immunoglobulin E (IgE) and inflammatory mediators and reduced inflammatory cell accumulation, as well as inhibiting the expression of important mediators including matrix metalloproteinase (MMP)-2 and MMP-9, TGF-ß1, and a disintegrin and metalloproteinase 8 (ADAM8) and ADAM33, which is related to airway remodeling. Further analysis confirmed that silencing of GATA-6 attenuated OVA-induced airway inflammation and remodeling through the TLR2/MyD88 and NF-κB pathway. In conclusion, these findings indicated that the downregulation of GATA-6 effectively inhibited airway inflammation and reversed airway remodeling via Cav-1, at least in part through downregulation of TLR2/MyD88/NF-κB, which suggests that GATA-6 represents a promising therapeutic strategy for human allergic asthma.


Assuntos
Remodelação das Vias Aéreas/imunologia , Asma/imunologia , Caveolina 1/biossíntese , Fator de Transcrição GATA6/biossíntese , Transdução de Sinais/imunologia , Animais , Asma/metabolismo , Western Blotting , Caveolina 1/imunologia , Modelos Animais de Doenças , Ensaio de Imunoadsorção Enzimática , Feminino , Fator de Transcrição GATA6/imunologia , Regulação da Expressão Gênica/imunologia , Técnicas de Silenciamento de Genes , Camundongos , Camundongos Endogâmicos BALB C , Fator 88 de Diferenciação Mieloide/imunologia , Fator 88 de Diferenciação Mieloide/metabolismo , NF-kappa B/imunologia , NF-kappa B/metabolismo , Reação em Cadeia da Polimerase , Receptor 2 Toll-Like/imunologia , Receptor 2 Toll-Like/metabolismo
4.
Chemistry ; 21(43): 15439-45, 2015 Oct 19.
Artigo em Inglês | MEDLINE | ID: mdl-26471449

RESUMO

The development of active, selective, and robust catalysts is a key issue in promoting the practical application of hydrazine monohydrate (N2 H4 ⋅H2 O) as a viable hydrogen carrier. Herein, the synthesis of a supported Ni-Pt bimetallic nanocatalyst on mesoporous ceria by a one-pot evaporation-induced self-assembly method is reported. The catalyst exhibits exceptionally high catalytic activity, 100 % selectivity, and satisfactory stability in promoting H2 generation from an alkaline solution of N2 H4 ⋅H2 O at moderate temperatures. For example, the Ni60 Pt40 /CeO2 catalyst enabled complete decomposition of N2 H4 ⋅H2 O to generate H2 at a rate of 293 h(-1) at 30 °C in the presence of 2 M NaOH, which compares favorably with the reported N2 H4 ⋅H2 O decomposition catalysts. Phase/structural analysis by XRD, TEM, and Auger electron spectroscopy was conducted to gain insight into the excellent catalytic performance of the Ni-Pt/CeO2 catalyst.

5.
Int J Clin Exp Med ; 7(4): 1190-6, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24955208

RESUMO

In our previous study, the upregulation of adipophilin in lung adenocarcinoma were identified compared with normal lung tissues by quantitative proteomics. In this study, our aim was to verify the result from quantitative proteomics, further investigate the relationship between adipophilin expression and clinicopathologic factors of lung cancer patients. The expression levels of adipophilin were examined in 10 pairs of lung adenocarcinoma and normal lung tissues using western blotting and the expression and cellular distribution of adipophilin were determined by IHC in 62 formalin-fixed and paraffin embedded primary lung cancer specimens. Adipophilin expression was significantly higher in lung adenocarcinoma specimens than in normal tissues and lung squamous cell carcinomas (P<0.05). There were no significant difference of adipophilin expression between lung squamous cell carcinomas and normal lung tissues. The expression of adipophilin in lung cancer did not correlate with any clinicopathologic factors such as lymph node metastasis, patients' age, gender, tumor size, grade, and TNM stage. In Conclusion, Adipophilin was upregulated in lung adenocarcinoma, suggesting that adipophilin play an important role in tumorigenesis of lung adenocarcinoma and may serve as a potential marker for lung adenocarcinoma.

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