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4. Planned Out-of-Hospital Birth and Birth Outcomes.
作者: Jonathan M Snowden.;Ellen L Tilden.;Janice Snyder.;Brian Quigley.;Aaron B Caughey.;Yvonne W Cheng.
来源: N Engl J Med. 2015年373卷27期2642-53页
The frequency of planned out-of-hospital birth in the United States has increased in recent years. The value of studies assessing the perinatal risks of planned out-of-hospital birth versus hospital birth has been limited by cases in which transfer to a hospital is required and a birth that was initially planned as an out-of-hospital birth is misclassified as a hospital birth.
13. Secukinumab, an Interleukin-17A Inhibitor, in Ankylosing Spondylitis.
作者: Dominique Baeten.;Joachim Sieper.;Jürgen Braun.;Xenofon Baraliakos.;Maxime Dougados.;Paul Emery.;Atul Deodhar.;Brian Porter.;Ruvie Martin.;Mats Andersson.;Shephard Mpofu.;Hanno B Richards.; .; .
来源: N Engl J Med. 2015年373卷26期2534-48页
Secukinumab is an anti-interleukin-17A monoclonal antibody that has been shown to control the symptoms of ankylosing spondylitis in a phase 2 trial. We conducted two phase 3 trials of secukinumab in patients with active ankylosing spondylitis.
14. Selexipag for the Treatment of Pulmonary Arterial Hypertension.
作者: Olivier Sitbon.;Richard Channick.;Kelly M Chin.;Aline Frey.;Sean Gaine.;Nazzareno Galiè.;Hossein-Ardeschir Ghofrani.;Marius M Hoeper.;Irene M Lang.;Ralph Preiss.;Lewis J Rubin.;Lilla Di Scala.;Victor Tapson.;Igor Adzerikho.;Jinming Liu.;Olga Moiseeva.;Xiaofeng Zeng.;Gérald Simonneau.;Vallerie V McLaughlin.; .
来源: N Engl J Med. 2015年373卷26期2522-33页
In a phase 2 trial, selexipag, an oral selective IP prostacyclin-receptor agonist, was shown to be beneficial in the treatment of pulmonary arterial hypertension.
15. Azithromycin versus Doxycycline for Urogenital Chlamydia trachomatis Infection.
作者: William M Geisler.;Apurva Uniyal.;Jeannette Y Lee.;Shelly Y Lensing.;Shacondra Johnson.;Raymond C W Perry.;Carmel M Kadrnka.;Peter R Kerndt.
来源: N Engl J Med. 2015年373卷26期2512-21页
Urogenital Chlamydia trachomatis infection remains prevalent and causes substantial reproductive morbidity. Recent studies have raised concern about the efficacy of azithromycin for the treatment of chlamydia infection.
16. Second Cancer Risk Up to 40 Years after Treatment for Hodgkin's Lymphoma.
作者: Michael Schaapveld.;Berthe M P Aleman.;Anna M van Eggermond.;Cécile P M Janus.;Augustinus D G Krol.;Richard W M van der Maazen.;Judith Roesink.;John M M Raemaekers.;Jan Paul de Boer.;Josée M Zijlstra.;Gustaaf W van Imhoff.;Eefke J Petersen.;Philip M P Poortmans.;Max Beijert.;Marnix L Lybeert.;Ina Mulder.;Otto Visser.;Marieke W J Louwman.;Inge M Krul.;Pieternella J Lugtenburg.;Flora E van Leeuwen.
来源: N Engl J Med. 2015年373卷26期2499-511页
Survivors of Hodgkin's lymphoma are at increased risk for treatment-related subsequent malignant neoplasms. The effect of less toxic treatments, introduced in the late 1980s, on the long-term risk of a second cancer remains unknown.
17. Resensitization to Crizotinib by the Lorlatinib ALK Resistance Mutation L1198F.
作者: Alice T Shaw.;Luc Friboulet.;Ignaty Leshchiner.;Justin F Gainor.;Simon Bergqvist.;Alexei Brooun.;Benjamin J Burke.;Ya-Li Deng.;Wei Liu.;Leila Dardaei.;Rosa L Frias.;Kate R Schultz.;Jennifer Logan.;Leonard P James.;Tod Smeal.;Sergei Timofeevski.;Ryohei Katayama.;A John Iafrate.;Long Le.;Michele McTigue.;Gad Getz.;Ted W Johnson.;Jeffrey A Engelman.
来源: N Engl J Med. 2016年374卷1期54-61页
In a patient who had metastatic anaplastic lymphoma kinase (ALK)-rearranged lung cancer, resistance to crizotinib developed because of a mutation in the ALK kinase domain. This mutation is predicted to result in a substitution of cysteine by tyrosine at amino acid residue 1156 (C1156Y). Her tumor did not respond to a second-generation ALK inhibitor, but it did respond to lorlatinib (PF-06463922), a third-generation inhibitor. When her tumor relapsed, sequencing of the resistant tumor revealed an ALK L1198F mutation in addition to the C1156Y mutation. The L1198F substitution confers resistance to lorlatinib through steric interference with drug binding. However, L1198F paradoxically enhances binding to crizotinib, negating the effect of C1156Y and resensitizing resistant cancers to crizotinib. The patient received crizotinib again, and her cancer-related symptoms and liver failure resolved. (Funded by Pfizer and others; ClinicalTrials.gov number, NCT01970865.).
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