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| 1 | ROS-induced DNA damage and PARP-1 are required for optimal induction of starvation-induced autophagy显示文摘响应滋养的应力,房间开始能导致改编或死亡的一个 autophagy 节目。位于从饥饿发信号到 autophagy 的开始下面的机制充分没被理解。在当前的学习,我们证明 PARP-1 的缺席或 inactivation 强烈推迟导致饥饿的 autophagy。我们发现了那 DNA 损坏是由 γ 测量了的导致饥饿的 autophagy 的一个早事件; -H2AX 累积和彗星试金,与在两个参数显示减小的 PARP-1 猛烈房间。在饥饿期间,导致 ROS 的 DNA 损坏激活 PARP-1,导致 ATP 弄空(在滋养的剥夺以后的一个早事件) 。PARP-1 的缺席弄钝 AMPK 激活并且阻止了 mTOR 活动的完全的损失,导致在 autophagy 的延期。PARP-1 弄空在饥饿的房间赞成 apoptosis,建议在滋养的剥夺以后的 autophagy 和 PARP-1 激活的一个支持幸存的角色。在 PARP-1 变异的老鼠的出生不满一月的婴儿使遭到了到尖锐饥饿的 vivo 结果表演,也显示缺乏的肝 autophagy,暗示为在导致饥饿的 autophagy 的 PARP-1 的一个生理的角色。因此,表明小径的 PARP 是 autophagy 承诺追随者饥饿的起始的步骤的一个关键管理者。 | Jose Manuel Rodriguez-Vargas Maria Jose Ruiz-Magana Carmen Ruiz-Ruiz Jara Majuelos-Melguizo Andreina Peralta-Lea Maria Isabel Rodriguez Jose Antonio Munoz-Gaimez Mariano Ruiz de Almodovar Eva Siles Abelardo Lopez Rivas Marja Jaattela F Javier Oliver | 2012 | Cell Research2012，22，7： | 8 |
| 2 | Medical abortion and manual vacuum aspiration for legal abortion protect women's health and reduce costs to the health system:findings from Colombia显示文摘 | Maria Isabel Rodriguez Willis Simancas Mendoza Camilo GuerraPalacio | 2015 | Reproductive Health Matters2015，44，22： | 1 |
| 3 | Phenotypic characterization of idiosyncratic drug‐induced liver injury: The influence of age and sex显示文摘 | M. Isabel Lucena Raúl J. Andrade Neil Kaplowitz Miren García‐Cortes M. Carmen Fernández Manuel Romero‐Gomez Miguel Bruguera Hacibe Hallal Mercedes Robles‐Diaz Jose F. Rodriguez‐González Jose Maria Navarro Javier Salmeron Pedro Martinez‐Odriozola Ramón Pér | 2009 | Hepatology2009，，： | 1 |
| 4 | Effectiveness and safety of first-generation protease inhibitors in clinical practice:Hepatitis C virus patients with advanced fibrosis显示文摘AIM:To evaluates the effectiveness and safety of the first generation,NS3/4A protease inhibitors(PIs) in clinical practice against chronic C virus,especially in patients with advanced fibrosis. METHODS:Prospective study and non-experimental analysis of a multicentre cohort of 38 Spanish hospitals that includes patients with chronic hepatitis C genotype 1,treatment-na?ve(TN) or treatment-experienced(TE),who underwent triple therapy with the first generation NS3/4A protease inhibitors,boceprevir(BOC) and telaprevir(TVR),in combination with pegylated interferon and ribavirin. The patients were treatment in routine practice settings. Data on the study population and on adverse clinical and virologic effects were compiled during the treatment period and during follow up.RESULTS:One thousand and fifty seven patients were included,405(38%) were treated with BOC and 652(62%) with TVR. Of this total,30%(n = 319) were TN and the remaining were TE:28%(n = 298) relapsers,12%(n = 123) partial responders(PR),25%(n = 260) null-responders(NR) and for 5%(n = 57) with prior response unknown. The rate of sustained virologic response(SVR) by intention-to-treatment(ITT) was greater in those treated with TVR(65%) than in those treated with BOC(52%)(P < 0.0001),whereas by modified intention-to-treatment(m ITT) no were found significant differences. By degree of fibrosis,56% of patients were F4 and the highest SVR rates were recorded in the non-F4 patients,both TN and TE. In the analysis by groups,the TN patients treated with TVR by ITT showed a higher SVR(P = 0.005). However,by m ITT there were no significant differences between BOC and TVR. In the multivariate analysis by m ITT,the significant SVR factors were relapsers,IL28 B CC and non-F4; the type of treatment(BOC or TVR) was not significant. The lowest SVR values were presented by the F4-NR patients,treated with BOC(46%) or with TVR(45%). 28% of the patients interrupted the treatment,mainly by non-viral response(51%):this outcome was more frequent in the TE than in the TN patients(57% vs 40%,P = 0.01). With respect to severe haematological disorders,neutropaenia was more likely to affect the patients treated with BOC(33% vs 20%,P ≤ 0.0001),and thrombocytopaenia and anaemia,the F4 patients(P = 0.000,P = 0.025,respectively). CONCLUSION:In a real clinical practice setting with a high proportion of patients with advanced fibrosis,effectiveness of first-generation PIs was high except for NR patients,with similar SVR rates being achieved by BOC and TVR. | Javier Salmeron Carmen Vinaixa Ruben Berenguer Juan Manuel Pascasio Juan Jose Sanchez Ruano Miguel angel Serra Ana Gila Moises Diago Manuel Romero-Gomez Jose Maria Navarro Milagros Testillano Conrado Fernandez Dolores Espinosa Isabel Carmona Jose Antonio Pons Francisco Jorquera Francisco Javier Rodriguez Ramon Perez Jose Luis Montero Rafael Granados Miguel Fernandez Ana Belen Martin Paloma Munoz de Rueda Rosa Quiles | 2015 | World Journal of Gastroenterology2015，21，30： | 0 |
| 5 | Identification of IL11RA and MELK amplification in gastric cancer by comprehensive genomic profiling of gastric cancer cell lines显示文摘AIM To identify common copy number alterations on gastric cancer cell lines.METHODS Four gastric cancer cell lines(ACP02, ACP03, AGP01 and PG100) underwent chromosomal comparative genome hybridization and array comparative genome hybridization. We also confirmed the results by fluorescence in situ hybridization analysis using the bacterial artificial chromosome clone and quantitative real time PCR analysis.RESULTS The amplification of 9p13.3 was detected in all cell lines by both methodologies. An increase in the copy number of 9p13.3 was also confirmed by fluorescence in situ hybridization analysis. Moreover, the interleukin 11 receptor alpha(IL11RA) and maternal embryonic leucine zipper kinase(MELK) genes, which are present in the 9p13.3 amplicon, revealed gains of the MELK gene in all the cell lines studied. Additionally, a gain in the copy number of IL11 RA and MELK was observed in 19.1%(13/68) and 55.9%(38/68) of primary gastric adenocarcinoma samples, respectively. CONCLUSION The characterization of a small gain region at 9p13.3 in gastric cancer cell lines and primary gastric adenocarcinoma samples has revealed MELK as a candidate target gene that is possibly related to the development of gastric cancer. | Danielle Queiroz Calcagno Sylvia Santomi Takeno Carolina Oliveira Gigek Mariana Ferreira Leal Fernanda Wisnieski Elizabeth Suchi Chen Taíssa Maíra Thomaz Araújo Eleonidas Moura Lima Maria Isabel Melaragno Samia Demachki Paulo Pimentel Assumpcao Rommel Rodriguez Burbano Marília Cardoso Smith | 2016 | World Journal of Gastroenterology2016，22，43： | 0 |
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