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1430. Atezolizumab versus docetaxel for patients with previously treated non-small-cell lung cancer (POPLAR): a multicentre, open-label, phase 2 randomised controlled trial.
作者: Louis Fehrenbacher.;Alexander Spira.;Marcus Ballinger.;Marcin Kowanetz.;Johan Vansteenkiste.;Julien Mazieres.;Keunchil Park.;David Smith.;Angel Artal-Cortes.;Conrad Lewanski.;Fadi Braiteh.;Daniel Waterkamp.;Pei He.;Wei Zou.;Daniel S Chen.;Jing Yi.;Alan Sandler.;Achim Rittmeyer.; .
来源: Lancet. 2016年387卷10030期1837-46页
Outcomes are poor for patients with previously treated, advanced or metastatic non-small-cell lung cancer (NSCLC). The anti-programmed death ligand 1 (PD-L1) antibody atezolizumab is clinically active against cancer, including NSCLC, especially cancers expressing PD-L1 on tumour cells, tumour-infiltrating immune cells, or both. We assessed efficacy and safety of atezolizumab versus docetaxel in previously treated NSCLC, analysed by PD-L1 expression levels on tumour cells and tumour-infiltrating immune cells and in the intention-to-treat population.
1432. Effect on mortality of point-of-care, urine-based lipoarabinomannan testing to guide tuberculosis treatment initiation in HIV-positive hospital inpatients: a pragmatic, parallel-group, multicountry, open-label, randomised controlled trial.
作者: Jonny G Peter.;Lynn S Zijenah.;Duncan Chanda.;Petra Clowes.;Maia Lesosky.;Phindile Gina.;Nirja Mehta.;Greg Calligaro.;Carl J Lombard.;Gerard Kadzirange.;Tsitsi Bandason.;Abidan Chansa.;Namakando Liusha.;Chacha Mangu.;Bariki Mtafya.;Henry Msila.;Andrea Rachow.;Michael Hoelscher.;Peter Mwaba.;Grant Theron.;Keertan Dheda.
来源: Lancet. 2016年387卷10024期1187-97页
HIV-associated tuberculosis is difficult to diagnose and results in high mortality. Frequent extra-pulmonary presentation, inability to obtain sputum, and paucibacillary samples limits the usefulness of nucleic-acid amplification tests and smear microscopy. We therefore assessed a urine-based, lateral flow, point-of-care, lipoarabinomannan assay (LAM) and the effect of a LAM-guided anti-tuberculosis treatment initiation strategy on mortality.
1437. Adjuvant sunitinib or sorafenib for high-risk, non-metastatic renal-cell carcinoma (ECOG-ACRIN E2805): a double-blind, placebo-controlled, randomised, phase 3 trial.
作者: Naomi B Haas.;Judith Manola.;Robert G Uzzo.;Keith T Flaherty.;Christopher G Wood.;Christopher Kane.;Michael Jewett.;Janice P Dutcher.;Michael B Atkins.;Michael Pins.;George Wilding.;David Cella.;Lynne Wagner.;Surena Matin.;Timothy M Kuzel.;Wade J Sexton.;Yu-Ning Wong.;Toni K Choueiri.;Roberto Pili.;Igor Puzanov.;Manish Kohli.;Walter Stadler.;Michael Carducci.;Robert Coomes.;Robert S DiPaola.
来源: Lancet. 2016年387卷10032期2008-16页
Renal-cell carcinoma is highly vascular, and proliferates primarily through dysregulation of the vascular endothelial growth factor (VEGF) pathway. We tested sunitinib and sorafenib, two oral anti-angiogenic agents that are effective in advanced renal-cell carcinoma, in patients with resected local disease at high risk for recurrence.
1438. Gut bacteria dysbiosis and necrotising enterocolitis in very low birthweight infants: a prospective case-control study.
作者: Barbara B Warner.;Elena Deych.;Yanjiao Zhou.;Carla Hall-Moore.;George M Weinstock.;Erica Sodergren.;Nurmohammad Shaikh.;Julie A Hoffmann.;Laura A Linneman.;Aaron Hamvas.;Geetika Khanna.;Lucina C Rouggly-Nickless.;I Malick Ndao.;Berkley A Shands.;Marilyn Escobedo.;Janice E Sullivan.;Paula G Radmacher.;William D Shannon.;Phillip I Tarr.
来源: Lancet. 2016年387卷10031期1928-36页
Gut bacteria might predispose to or protect from necrotising enterocolitis, a severe illness linked to prematurity. In this observational prospective study we aimed to assess whether one or more bacterial taxa in the gut differ between infants who subsequently develop necrotising enterocolitis (cases) and those who do not (controls).
1440. Teratogenic effects of the Zika virus and the role of the placenta.
作者: Jennifer J Adibi.;Ernesto T A Marques.;Abigail Cartus.;Richard H Beigi.
来源: Lancet. 2016年387卷10027期1587-1590页
The mechanism by which the Zika virus can cause fetal microcephaly is not known. Reports indicate that Zika is able to evade the normal immunoprotective responses of the placenta. Microcephaly has genetic causes, some associated with maternal exposures including radiation, tobacco smoke, alcohol, and viruses. Two hypotheses regarding the role of the placenta are possible: one is that the placenta directly conveys the Zika virus to the early embryo or fetus. Alternatively, the placenta itself might be mounting a response to the exposure; this response might be contributing to or causing the brain defect. This distinction is crucial to the diagnosis of fetuses at risk and the design of therapeutic strategies to prevent Zika-induced teratogenesis.
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