Institution
Monash University
Education•Melbourne, Victoria, Australia•
About: Monash University is a education organization based out in Melbourne, Victoria, Australia. It is known for research contribution in the topics: Population & Poison control. The organization has 35920 authors who have published 100681 publications receiving 3027002 citations.
Papers published on a yearly basis
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University of Queensland1, Princess Alexandra Hospital2, Royal Brisbane and Women's Hospital3, National University of Singapore4, Nanyang Technological University5, Tan Tock Seng Hospital6, Istanbul Medipol University7, King Saud bin Abdulaziz University for Health Sciences8, Sapienza University of Rome9, University of Udine10, Monash University11, American University of Beirut12, North Shore Hospital13, University of Sydney14, Westmead Hospital15, University of Cape Town16, University of Wollongong17, Illawarra Health & Medical Research Institute18, Wollongong Hospital19, Middlemore Hospital20, King Fahad Specialist Hospital21, St. Vincent's Health System22, University of Western Australia23, Fiona Stanley Hospital24, Sunnybrook Health Sciences Centre25, Mater Health Services26, QIMR Berghofer Medical Research Institute27, Deakin University28, Monash University, Clayton campus29
TL;DR: Among patients with E coli or K pneumoniae bloodstream infection and ceftriaxone resistance, definitive treatment with piperacillin-tazobactam compared with meropenem did not result in a noninferior 30-day mortality, and findings do not support use of piperACillin- tazobactsam in this setting.
Abstract: Importance Extended-spectrum β-lactamases mediate resistance to third-generation cephalosporins (eg, ceftriaxone) in Escherichia coli and Klebsiella pneumoniae. Significant infections caused by these strains are usually treated with carbapenems, potentially selecting for carbapenem resistance. Piperacillin-tazobactam may be an effective “carbapenem-sparing” option to treat extended-spectrum β-lactamase producers. Objectives To determine whether definitive therapy with piperacillin-tazobactam is noninferior to meropenem (a carbapenem) in patients with bloodstream infection caused by ceftriaxone-nonsusceptible E coli or K pneumoniae . Design, Setting, and Participants Noninferiority, parallel group, randomized clinical trial included hospitalized patients enrolled from 26 sites in 9 countries from February 2014 to July 2017. Adult patients were eligible if they had at least 1 positive blood culture with E coli or Klebsiella spp testing nonsusceptible to ceftriaxone but susceptible to piperacillin-tazobactam. Of 1646 patients screened, 391 were included in the study. Interventions Patients were randomly assigned 1:1 to intravenous piperacillin-tazobactam, 4.5 g, every 6 hours (n = 188 participants) or meropenem, 1 g, every 8 hours (n = 191 participants) for a minimum of 4 days, up to a maximum of 14 days, with the total duration determined by the treating clinician. Main Outcomes and Measures The primary outcome was all-cause mortality at 30 days after randomization. A noninferiority margin of 5% was used. Results Among 379 patients (mean age, 66.5 years; 47.8% women) who were randomized appropriately, received at least 1 dose of study drug, and were included in the primary analysis population, 378 (99.7%) completed the trial and were assessed for the primary outcome. A total of 23 of 187 patients (12.3%) randomized to piperacillin-tazobactam met the primary outcome of mortality at 30 days compared with 7 of 191 (3.7%) randomized to meropenem (risk difference, 8.6% [1-sided 97.5% CI, −∞ to 14.5%]; P = .90 for noninferiority). Effects were consistent in an analysis of the per-protocol population. Nonfatal serious adverse events occurred in 5 of 188 patients (2.7%) in the piperacillin-tazobactam group and 3 of 191 (1.6%) in the meropenem group. Conclusions and relevance Among patients with E coli or K pneumoniae bloodstream infection and ceftriaxone resistance, definitive treatment with piperacillin-tazobactam compared with meropenem did not result in a noninferior 30-day mortality. These findings do not support use of piperacillin-tazobactam in this setting. Trial Registration anzctr.org.au Identifiers:ACTRN12613000532707andACTRN12615000403538and ClinicalTrials.gov Identifier:NCT02176122
487 citations
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California Institute of Technology1, Agricultural Research Service2, University of Tsukuba3, University of Guelph4, University of Texas at Austin5, Princeton University6, Kuwait University7, University of Valencia8, University of Salamanca9, Agriculture and Agri-Food Canada10, University of Southern California11, European Academy of Bozen12, University of Grenoble13, Finnish Meteorological Institute14, National Autonomous University of Mexico15, University of Twente16, Comisión Nacional de Actividades Espaciales17, Vienna University of Technology18, Monash University19, Goddard Space Flight Center20, Massachusetts Institute of Technology21
TL;DR: The NASA Soil Moisture Active Passive (SMAP) mission has utilized a set of core validation sites as the primary methodology in assessing the soil moisture retrieval algorithm performance as mentioned in this paper.
487 citations
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TL;DR: Results appear to confirm earlier findings that public provision demonstrates less variability than private, and points to the future in terms of possible directions for research in efficiency measurement in health care and health.
Abstract: This paper reviews 188 published papers on frontier efficiency measurement. The techniques used are mainly based on non-parametric data envelopment analysis, but there is increasing use of parametric techniques, such as stochastic frontier analysis. Applications both to hospitals and wider health care areas are reviewed and summarised, and some meta-type analysis undertaken. Results appear to confirm earlier findings that public provision demonstrates less variability than private. The paper is meant as a resource in itself, but also points to the future in terms of possible directions for research in efficiency measurement in health care and health.
487 citations
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TL;DR: Early changes in ctDNA during first-line chemotherapy predict the later radiologic response and is detectable in a high proportion of treatment naïve mCRC patients.
487 citations
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TL;DR: It is demonstrated that a paracrine mechanism driven by DeltaEGFR is the primary means for recruiting wtEGFR-expressing cells into accelerated proliferation in vivo, and support the view that a minor tumor cell population can potently drive accelerated growth of the entire tumor mass, and thereby actively maintain tumor cell heterogeneity within a tumor mass.
Abstract: Human solid tumors frequently have pronounced heterogeneity of both neoplastic and normal cells on the histological, genetic, and gene expression levels. While current efforts are focused on understanding heterotypic interactions between tumor cells and surrounding normal cells, much less is known about the interactions between and among heterogeneous tumor cells within a neoplasm. In glioblastoma multiforme (GBM), epidermal growth factor receptor gene (EGFR) amplification and mutation (EGFRvIII/ΔEGFR) are signature pathogenetic events that are invariably expressed in a heterogeneous manner. Strikingly, despite its greater biological activity than wild-type EGFR (wtEGFR), individual GBM tumors expressing both amplified receptors typically express wtEGFR in far greater abundance than the ΔEGFR lesion. We hypothesized that the minor ΔEGFR-expressing subpopulation enhances tumorigenicity of the entire tumor cell population, and thereby maintains heterogeneity of expression of the two receptor forms in different cells. Using mixtures of glioma cells as well as immortalized murine astrocytes, we demonstrate that a paracrine mechanism driven by ΔEGFR is the primary means for recruiting wtEGFR-expressing cells into accelerated proliferation in vivo. We determined that human glioma tissues, glioma cell lines, glioma stem cells, and immortalized mouse Ink4a/Arf−/− astrocytes that express ΔEGFR each also express IL-6 and/or leukemia inhibitory factor (LIF) cytokines. These cytokines activate gp130, which in turn activates wtEGFR in neighboring cells, leading to enhanced rates of tumor growth. Ablating IL-6, LIF, or gp130 uncouples this cellular cross-talk, and potently attenuates tumor growth enhancement. These findings support the view that a minor tumor cell population can potently drive accelerated growth of the entire tumor mass, and thereby actively maintain tumor cell heterogeneity within a tumor mass. Such interactions between genetically dissimilar cancer cells could provide novel points of therapeutic intervention.
487 citations
Authors
Showing all 36568 results
Name | H-index | Papers | Citations |
---|---|---|---|
Bert Vogelstein | 247 | 757 | 332094 |
Kenneth W. Kinzler | 215 | 640 | 243944 |
David J. Hunter | 213 | 1836 | 207050 |
David R. Williams | 178 | 2034 | 138789 |
Yang Yang | 171 | 2644 | 153049 |
Lei Jiang | 170 | 2244 | 135205 |
Dongyuan Zhao | 160 | 872 | 106451 |
Christopher J. O'Donnell | 159 | 869 | 126278 |
Leif Groop | 158 | 919 | 136056 |
Mark E. Cooper | 158 | 1463 | 124887 |
Theo Vos | 156 | 502 | 186409 |
Mark J. Smyth | 153 | 713 | 88783 |
Rinaldo Bellomo | 147 | 1714 | 120052 |
Detlef Weigel | 142 | 516 | 84670 |
Geoffrey Burnstock | 141 | 1488 | 99525 |