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| 1 | RTOG 0211:a phase 1/2 study of radiation therapy with concurrent gefitinib for newly diagnosed glioblastoma patients显示文摘PURPOSE: To determine the safety and efficacy of gefitinib,an epidermal growth factor receptor(EGFR) tyrosine kinase inhibitor,in combination with radiation for newly diagnosed glioblastoma(GBM) patients.METHODS AND MATERIALS: Between March 21,2002,and May 3,2004,Radiation Therapy Oncology Group(RTOG) 0211 enrolled 31 and 147GBM patients in the phase 1 and 2 arms,respectively.Treatment consisted of daily oral gefinitnib started at the time of conventional cranial radiation therapy(RT) and continued post RT for 18 months or until progression.Tissue microarrays from 68 cases were analyzed for EGFR expression.RESULTS: The maximum tolerated dose(MTD) of gefitinib was determined to be 500 mg in patients on non-enzyme-inducing anticonvulsant drugs(non-EIAEDs).All patients in the phase 2 component were treated at a gefitinib dose of 500 mg;patients receiving EIADSs could be escalated to 750 mg.The most common side effects of gefitinib in combination with radiation were dermatologic and gastrointestinal.Median survival was 11.5 months for patients treated per protocol.There was no overall survival benefit for patients treated with gefitinib + RT when compared with a historical cohort of patients treated with RT alone,matched by RTOG recursive partitioning analysis(RPA) class distribution.Younger age was significantly associated with better outcome.Per protocol stratification,EGFR expression was not found to be of prognostic value for gefitinib + RT-treated patients.CONCLUSIONS: The addition of gefitinib to RT is well tolerated.Median survival of RTOG 0211 patients treated with RT with concurrent and adjuvant gefitinib was similar to that in a historical control cohort treated with radiation alone. | Chakravarti A Wang M Robins HI Lautenschlaeger T Curran WJ Brachman DG Schultz CJ Choucair A Dolled-Filhart M Christiansen J Gustavson M Molinaro A Mischel P Dicker AP Bredel M Mehta M | 2013 | 中国神经肿瘤杂志2013，11，1： | 8 |
| 2 | Pathophysiology of cerebral oedema in acute liver failure显示文摘Cerebral oedema is a devastating consequence of acute liver failure(ALF)and may be associated with the development of intracranial hypertension and death.In ALF,some patients may develop cerebral oedema and increased intracranial pressure but progression to lifethreatening intracranial hypertension is less frequent than previously described,complicating less than one third of cases who have proceeded to coma since the advent of improved clinical care.The rapid onset of encephalopathy may be dramatic with the development of asterixis,delirium,seizures and coma.Cytotoxic and vasogenic oedema mechanisms have been implicated with a preponderance of experimental data favouring a cytotoxic mechanism.Astrocyte swelling is the most consistent neuropathological finding in humans with ALF and ammonia plays a definitive role in the development of cytotoxic brain oedema.The mechanism(s)by which ammonia induces astrocyte swelling remains unclear but glutamine accumulation within astrocytes has led to the osmolyte hypothesis.Current evidence also supports an alternate‘Trojan horse’hypothesis,with glutamine as a carrier of ammonia into mitochondria,where its accumulation results in oxidative stress,energy failure and ultimately astrocyte swelling.Although a complete breakdown of the blood-brain barrier is not evident in human ALF,increased permeation to water and other small molecules such as ammonia has been demonstrated resulting from subtle alterations in the protein composition of paracellular tight junctions.At present,there is no fully efficacious therapy for cerebral oedema other than liver transplantation and this reflects our incomplete knowledge of the precise mechanisms underlying this process which remain largely unknown. | Teresa R Scott Victoria T Kronsten Robin D Hughes Debbie L Shawcross | 2013 | World Journal of Gastroenterology2013，19，48： | 8 |
| 3 | Strong prognostic value of nodal and bone marrow micro-involvement in patients with pancreatic ductal carcinoma receiving no adjuvant chemotherapy显示文摘AIM: To study the prognostic value of adjuvant chemo-therapy in patients with pancreatic, ductal adenocar-cinoma.METHODS: Lymph nodes from 106 patients with resectable pancreatic ductal adenocarcinoma were systematically sampled. A total of 318 lymph nodes classified histopathologically as tumor-free were examined using sensitive immunohistochemical assays. Forty-three (41%) of the 106 patients were staged as pT1/2, 63 (59%) as pT3/4, 51 (48%) as pN0, and 55 (52%) as pN1. The study population included 59 (56%) patients exhibiting G1/2, and 47 (44%) patients with G3 tumors. Patients received no adjuvant chemo- or radiation therapy and were followed up for a median of 12 (range: 3.5 to 139) mo.RESULTS: Immunostaining with Ber-EP4 revealed nodal microinvolvement in lymph nodes classified as “tumor free” by conventional histopathology in 73 (69%) out of the 106 patients. Twenty-nine (57%)of 51 patients staged histopathologically as pN0 had nodal microinvolvement. The five-year survival probability for pN0-patients was 54% for those without nodal microinvolvement and 0% for those with nodal microinvolvement. Cox-regression modeling revealed the independent prognostic effect of nodal microinvolvement on recurrence-free (relative risk 2.92, P = 0.005) and overall (relative risk 2.49, P = 0.009) survival.CONCLUSION: The study reveals strong and independent prognostic significance of nodal microinvolvement in patients with pancreatic ductal adenocarcinoma who have received no adjuvant therapy. The addition of immunohistochemical findings to histopathology reports may help to improve risk stratification of patients with pancreatic cancer. | Emre F Yekebas Dean Bogoevski Michael Bubenheim Bjrn-Christian Link Jussuf T Kaifi Robin Wachowiak Oliver Mann Asad Kutup Guellue Cataldegirmen Lars Wolfram Andreas Erbersdobler Christoph Klein Klaus Pantel Jakob R Izbicki | 2006 | World Journal of Gastroenterology2006，12，40： | 3 |
| 4 | Treatment of relapsing autoimmune pancreatitis with immunomodulators and rituximab: the Mayo Clinic experience显示文摘 | Phil A Hart Mark D Topazian Thomas E Witzig Jonathan E Clain Ferga C Gleeson Robin R Klebig Michael J Levy Randall K Pearson Bret T Petersen Thomas C Smyrk Aravind Sugumar Naoki Takahashi Santhi S Vege Suresh T Chari | 2013 | Gut2013，，11： | 2 |
| 5 | Treatment of relapsing autoimmune pancreatitis with immunomodulators and rituximab: the Mayo Clinic experience显示文摘 | Phil A Hart Mark D Topazian Thomas E Witzig Jonathan E Clain Ferga C Gleeson Robin R Klebig Michael J Levy Randall K Pearson Bret T Petersen Thomas C Smyrk Aravind Sugumar Naoki Takahashi Santhi S Vege Suresh T Chari | 2013 | Gut2013，，11： | 2 |
| 6 | Precision atomic gravimeter based on Bragg diffraction显示文摘 | P A Altin M T Johnsson V Negnevitsky G R Dennis R P Anderson J E Debs S S Szigeti K S Hardman S Bennetts G D McDonald L D Turner J D Close N P Robins | 2013 | New Journal of Physics2013，，2： | 2 |
| 7 | Molecular basis of inherited calcium channelopathies:role of mutations in pore-forming subunits显示文摘形成毛孔的高山哈电压门钙隧道的子单元包含响应房间去极位于钙流入下面的必要生物物理的机械。在有需要的辅助子单元的联合,这些毛孔子单元形成对从精子到神经原的多样的房间的生理学和药理学枢轴的钙隧道建筑群。不令人惊讶地,在毛孔子单元的变化产生多样的病理,称为的 channelopathies,那在联合到夜盲的刺激收缩从失败。在最后十年,进致病的机制的主要卓见从自发的出现的动物或诱发突变被导出。在平行,在我们从结构功能,规定和房间生物学观点的电压门离子隧道的活动方式的理解有可观的生长。这里,我们记录我们位于包含电压门钙隧道高山的 channelopathies 下面的变化的当前的理解哈在人和另外的种类的子单元。 | Lynn MCKEOWN Philip ROBIN Owen T JONES | 2006 | Acta Pharmacologica Sinica2006，27，7： | 2 |
| 8 | The efects of starvation and subsequent feeding on survival growth of Fulton channel sockeye salmon ( Oncorhynchus nerka) 显示文摘 | Bihon H T Robins G L | 1973 | J Fish Res Board1973，30，： | 1 |
| 9 | Superior per ovskite oxide-ion conductor strontium- and magnesium-doped La GaO3 显示文摘 | HUANG Ke-qin ROBIN S T Goodenough J B | 1998 | Journal of American Cemic Soc1998，81，10： | 1 |
| 10 | Wnt/β-catenin is essential forintestinal homeostasis and maintenance of intestinal stem cells显示文摘 | Fevr T Robine S Louvar D | 2007 | Mol Cell Biol2007，27，21： | 1 |
| 11 | Low-dose thoracoab- dominal irradiation for the treatment of refractory chronic graft- versus-host disease显示文摘 | Robin M Guardiola P Girinsky T | 2005 | Transplantation2005，80，5： | 1 |
| 12 | Developmental plasticity of Th17 and Treg cells显示文摘 | Yun Kyung Lee Ryuta Mukasa Robin D Hatton Casey T Weaver | 2009 | Current Opinion in Immunology2009，，3： | 1 |
| 13 | Invasion of bladder by t ramsitional cell carcinoma显示文摘 | Robin T Peter A Paul E | 1998 | Cancer1998，82，： | 1 |
| 14 | Three novel CYP21A2 mutations and their protein modelling in patients with classical 21-hydroxylase deficiency from northeastern Iran显示文摘 | Baradaran H A Vakili R Robins T | 2007 | Clin Endocrinol (Oxf)2007，67，3： | 1 |
| 15 | Mycoplasma hominis and ure- aplasma urealyticum in midtrimester amniotic fluid : Association with amniotic fluid cytokine levels and pregnancy outcome显示文摘 | Stephen T Robin B Steven S | 2004 | Am J Obstet Gyne- col2004，191，4： | 1 |
| 16 | Management of intermittent ovarian torsion by laparoscopic oophoropexy显示文摘 | Germain M Rarick T Robins E | 1996 | Obste Gynecol1996，88，4： | 1 |
| 17 | Safety and tolerability of intraputaminal delivery of CERE-120 (adeno-associated virus serotype 2–neurturin) to patients with idiopathic Parkinson’s disease: an open-label, phase I trial显示文摘 | William J Marks Jill L Ostrem Leonard Verhagen Philip A Starr Paul S Larson Roy AE Bakay Robin Taylor Deborah A Cahn-Weiner A Jon Stoessl C Warren Olanow Raymond T Bartus | 2008 | Lancet Neurology2008，，5： | 1 |
| 18 | Minimal sufficient causation and directed acyclic graphs 显示文摘 | VanderWeele T J Robins J M | 2009 | Annals of Statistics2009，37，3： | 1 |
| 19 | Specification, estimation and validation of a pedestrian walking behavior model显示文摘 | Robin T Antonini G Bierlaire M et el | 2009 | Transpor- tation Research Part 132009，43，1： | 1 |
| 20 | A 10-bit 50 MS/s pipelined ADC with capacitor-sharing and variable opamp 显示文摘 | BYUNG G L ROBIN M T | 2009 | IEEE JSSC2009，44，3： | 1 |
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