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1.
Materials (Basel) ; 14(23)2021 Dec 06.
Artigo em Inglês | MEDLINE | ID: mdl-34885625

RESUMO

Gd and Yb elements have high chemical stability, which can stabilize the solid solution in ZrO2. Gd2O3 and Yb2O3 have high melting points, and good oxidation resistance in extreme environments, stable chemical properties. Therefore, Gd2O3 and Yb2O3 were added to ZrO2 to stabilize oxides, improve the high temperature stability, and effectively decrease the thermal conductivity at high temperature. In this work, 5 wt% Yb2O3 and 5 wt%, 10 wt%, 15 wt% Gd2O3 were doped into 8 wt% Y2O3 stabilized ZrO2 (8YSZ) powders as thermal barrier coating materials, and sintered at 1650 °C for 6 h, 12 h, 24 h. The effects of Gd2O3 addition on the microstructure, density, thermal conductivity, hardness, and fracture toughness of Gd2O3-Yb2O3-Y2O3-ZrO2 (GYYZO) bulk composite ceramics were investigated. It was found that the densification of the 8YSZ bulk and GYYZO bulk with 15 wt% Gd2O3 reached 96.89% and 96.22% sintered at 1650 °C for 24 h. With the increase of Gd2O3 addition, the hardness, elastic modulus and fracture toughness of the GYYZO bulk increased and the thermal conductivity and thermal expansion coefficient of the GYYZO bulk decreased. GYYZO bulk with 15 wt% Gd2O3 sintered at 1650 °C for 24h had the highest hardness, elastic modulus and fracture toughness of 15.61 GPa, 306.88 GPa, 7.822 MPa·m0.5, and the lowest thermal conductivity and thermal expansion coefficient of 1.04 W/(m·k) and 7.89 × 10-6/°C at 1100 °C, respectively. The addition of Gd2O3 into YSZ could not only effectively reduce the thermal conductivity but also improve the mechanical properties, which would improve the thermal barrier coatings' performances further.

2.
Ying Yong Sheng Tai Xue Bao ; 29(2): 651-658, 2018 Feb.
Artigo em Chinês | MEDLINE | ID: mdl-29692082

RESUMO

In recent years, the two issues of climate change including elevated CO2 etc., and resistance of transgenic Bt crops against non-target insect pests have received widespread attention. Elevated CO2 can affect the herbivorous insects. To date, there is no consensus about the effect of elevated CO2 on the suck-feeding insect pests (non-target insect pests of transgenic Bt crops). Its effects on the suck-feeding behavior have rarely been reported. In this study, CO2 levels were set up in artificial climate chamber to examined the effects of ambient (400 µL·L-1) and double-ambient (800 µL·L-1) CO2 levels on the suck-feeding behavior, growth, development, and reproduction of the non-target insect pest of transgenic Bt rice, brown planthopper, Nilaparvata lugens. The results showed that CO2 level significantly affected the egg and nymph duration, longevity and body mass of adults, and feeding behavior of the 4th and 5th instar nymphs, while had no effect on the fecundity of N. lugens. The duration of eggs and nymphs, and the longevity of female adults were significantly shortened by 4.0%, 4.2% and 6.6% respectively, the proportion of the macropterous adults was significantly increased by 11.6%, and the body mass of newly hatched female adults was significantly decreased by 2.2% by elevated CO2. In addition, elevated CO2 significantly enhanced the stylet puncturing efficiency of the 4th and 5th instar nymphs of N. lugens. The duration ofphloem ingestion of the N4b waveform was significantly prolonged by 60.0% and 50.1%, and the frequency significantly was increased by 230.0% and 155.9% for the 4th and 5th instar nymphs of N. lugens by elevated CO2, respectively. It was concluded that double-ambient CO2 could promote the growth and development of N. lugens through enhancing its suck-feeding, shorten the generation life-span and increase the macropertous adults' proportion of N. lugens. Thus, it could result in the occurrence of non-target rice planthopper N. lugens and make the transgenic Bt crops face with harm risk due to migration and diffusion of N. lugens under elevated CO2.


Assuntos
Dióxido de Carbono , Hemípteros , Plantas Geneticamente Modificadas , Comportamento de Sucção , Animais , Feminino , Ninfa , Oryza/genética
3.
Mol Hum Reprod ; 22(4): 252-60, 2016 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-26769260

RESUMO

STUDY HYPOTHESIS: What factors in mouse oocytes are involved in the ageing-related decline in oocyte quality? STUDY FINDING: The maternal effect gene Mater is involved in ageing-related oocyte quality decline in mice. WHAT IS KNOWN ALREADY: Premature loss of centromere cohesion is a hallmark of ageing-related oocyte quality decline; the maternal effect gene Mater (maternal antigen that embryos require, also known as Nlrp5) is required for preimplantation embryo development beyond the 2-cell stage, and mRNA expression of Mater decreases with maternal ageing. STUDY DESIGN, SAMPLES/MATERIALS, METHODS: Mater protein expression level in mature oocytes from 7 young (5-8 weeks old) to 7 old mice (41-68 weeks old) was compared by immunoblotting analysis. Wild-type and Mater-null mice were used to examine whether Mater is necessary for maintaining normal centromere cohesion by means of cytogenetic karyotyping, time-lapse confocal microscopy and immunofluorescence staining. MAIN RESULTS AND THE ROLE OF CHANCE: Mater protein is decreased in mature oocytes from old versus young mice (P = 0.0022). Depletion of Mater from oocytes leads to a reduction in centromere cohesion, manifested by precocious sister chromatid separation, enlargement of sister centromere distance and misalignment of chromosomes in the metaphase plate during meiosis I and II. LIMITATIONS, REASONS FOR CAUTION: This study was conducted in mice. Whether or not the results are applicable to human remains further elucidation. In addition, we were unable to confirm if the strain of mice (C57BL/6XSv129) at the age of 41-68 weeks old has the 'cohesin-loss' phenotype. WIDER IMPLICATIONS OF THE FINDINGS: Investigating Mater's functional mechanisms could provide fresh insights into understanding how the ageing-related oocyte quality decline occurs. LARGE SCALE DATA: N/A. STUDY FUNDING AND COMPETING INTERESTS: This work was supported by the research grant from Chinese NSFC to P.Z. (31071274). We have no conflict of interests to declare.


Assuntos
Envelhecimento/genética , Antígenos/genética , Proteínas do Ovo/genética , Oócitos/metabolismo , Animais , Antígenos/metabolismo , Centrômero/metabolismo , Centrômero/ultraestrutura , Cromátides/metabolismo , Cromátides/ultraestrutura , Proteínas do Ovo/metabolismo , Feminino , Expressão Gênica , Cariotipagem , Meiose , Camundongos , Camundongos Endogâmicos C57BL , Oócitos/citologia , Imagem com Lapso de Tempo
4.
Cell Stem Cell ; 16(6): 684-98, 2015 Jun 04.
Artigo em Inglês | MEDLINE | ID: mdl-25936915

RESUMO

Pluripotent stem cells (PSCs) hold great promise in cell-based therapy, but the genomic instability seen in culture hampers their full application. A greater understanding of the factors that regulate genomic stability in PSCs could help address this issue. Here we describe the identification of Filia as a specific regulator of genomic stability in mouse embryonic stem cells (ESCs). Filia expression is induced by genotoxic stress. Filia promotes centrosome integrity and regulates the DNA damage response (DDR) through multiple pathways, including DDR signaling, cell-cycle checkpoints and damage repair, ESC differentiation, and apoptosis. Filia depletion causes ESC genomic instability, induces resistance to apoptosis, and promotes malignant transformation. As part of its role in DDR, Filia interacts with PARP1 and stimulates its enzymatic activity. Filia also constitutively resides on centrosomes and translocates to DNA damage sites and mitochondria, consistent with its multifaceted roles in regulating centrosome integrity, damage repair, and apoptosis.


Assuntos
Dano ao DNA , Instabilidade Genômica , Células-Tronco Embrionárias Murinas/metabolismo , Proteínas/metabolismo , Animais , Apoptose/efeitos dos fármacos , Proteínas Mutadas de Ataxia Telangiectasia/metabolismo , Pontos de Checagem do Ciclo Celular/efeitos dos fármacos , Diferenciação Celular/efeitos dos fármacos , Transformação Celular Neoplásica/metabolismo , Transformação Celular Neoplásica/patologia , Centrossomo/efeitos dos fármacos , Centrossomo/metabolismo , Quinase do Ponto de Checagem 2/metabolismo , Reparo do DNA/efeitos dos fármacos , Instabilidade Genômica/efeitos dos fármacos , Camundongos , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Células-Tronco Embrionárias Murinas/citologia , Células-Tronco Embrionárias Murinas/efeitos dos fármacos , Mutagênicos/toxicidade , Fosforilação/efeitos dos fármacos , Fosfosserina/metabolismo , Poli(ADP-Ribose) Polimerases/metabolismo , Ligação Proteica/efeitos dos fármacos , Transporte Proteico/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Frações Subcelulares/efeitos dos fármacos , Frações Subcelulares/metabolismo , Regulação para Cima/efeitos dos fármacos
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