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"Cutler, E. P"
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Art + fashion : collaborations and connections between icons
\"A volume of magnificent proportions, Art + Fashion is as exciting and elegant as the creative partnerships it celebrates. Spanning numerous eras, men and women's fashion, and a wide range of art mediums, these 25 collaborative projects reveal the astonishing work that results when luminaries from the art world (such as Pollock, Haring, and Hirst) come together with icons of the fashion world (including Saint Laurent, Westwood, McQueen). From 20th-century legends such as Elsa Schiaperelli and her famous lobster dress painted by Salvador Dalí to 21st-century trailblazers such as Cindy Sherman and her self-portraits in vintage Chanel, these electric and provocative pairings--represented in lavish visuals and thoughtful essays reflecting on the history of each project--brim with the energy and possibility of powerful forces uniting\"-- Provided by publisher.
Book
Tackling the Racial Intimacies that Fashioned a Generation
Tackling the Racial Intimacies that Fashioned a Generation Thuy Linh Nguyen Tu's The Beautiful Generation: Asian Americans and the Cultural Economy of Fashion, Durham, North Carolina, Duke University Press, 2011 With the academic equivalent of military prowess, assistant professor of Asian Pacific Studies at New York University Thuy Linh Nguyen Tu flanks the topic of Asian Americans in fashion. In her first chapter, \"Crossing the Assembly Line,\" Tu explores what factors facilitated the rise of second-generation Asian American design- ers and finds that, despite fashion's strict edict that the labor of creating a garment is separate from and not equal to their design, the line between creation and creativity is not impenetrable.
Journal Article
Meteorology and surface energy fluxes in the 2005-2007 ablation seasons at the Miage debris-covered glacier, Mont Blanc Massif, Italian Alps
During the 2005–2007 June–September ablation seasons, meteorological conditions were recorded on the lower and upper parts of the debris‐covered ablation zone of Miage Glacier, Italy. In 2005, debris temperature and subdebris ice melt were also monitored at 25 points with debris thickness of 0.04–0.55 m, spread over 5 km2 of the glacier. The radiative fluxes were directly measured, and near‐closure of the surface energy balance is achieved, providing support for the bulk aerodynamic calculation of the turbulent fluxes. Surface‐layer meteorology and energy fluxes are dominated by the pattern of incoming solar radiation which heats the debris, driving strong convection. Mean measured subdebris ice melt rates are 6–33 mm d−1, and mean debris thermal conductivity is 0.96 W m−1 K−1, displaying a weak positive relationship with debris thickness. Mean seasonal values of the net shortwave, net longwave, and debris heat fluxes show little variation between years, despite contrasting meteorological conditions, while the turbulent latent (evaporative) heat flux was more than twice as large in the wet summer of 2007 compared with 2005. The increase in energy output from the debris surface in response to increasing surface temperature means that subdebris ice melt rates are fairly insensitive to atmospheric temperature variations in contrast to debris‐free glaciers. Improved knowledge of spatial patterns of debris thickness distribution and 2 m air temperature, and the controls on evaporation of rainwater from the surface, are needed for distributed physically based melt modeling of debris‐covered glaciers.
Journal Article
HER kinase inhibition in patients with HER2- and HER3-mutant cancers
Somatic mutations of
ERBB2
and
ERBB3
(which encode HER2 and HER3, respectively) are found in a wide range of cancers. Preclinical modelling suggests that a subset of these mutations lead to constitutive HER2 activation, but most remain biologically uncharacterized. Here we define the biological and therapeutic importance of known oncogenic HER2 and HER3 mutations and variants of unknown biological importance by conducting a multi-histology, genomically selected, ‘basket’ trial using the pan-HER kinase inhibitor neratinib (SUMMIT; clinicaltrials.gov identifier NCT01953926). Efficacy in HER2-mutant cancers varied as a function of both tumour type and mutant allele to a degree not predicted by preclinical models, with the greatest activity seen in breast, cervical and biliary cancers and with tumours that contain kinase domain missense mutations. This study demonstrates how a molecularly driven clinical trial can be used to refine our biological understanding of both characterized and new genomic alterations with potential broad applicability for advancing the paradigm of genome-driven oncology.
In a basket trial design, the efficacy of the pan-HER kinase inhibitor neratinib is tested in patients with 21 different tumour types, and responses are determined by mutation and tissue type, and are restricted to HER2-mutant cancers.
Basket trial of HER inhibition
Mutations in, or overexpression of, HER2 and HER3 (members of the epidermal growth factor receptor (EGFR) family) are found in numerous cancer types. Here, the authors conduct a basket trial—a clinical trial whereby patients are given a targeted therapy based on the presence of a molecular marker rather than on their tumour type—to test the efficacy of neratinib, an irreversible inhibitor of all HER kinases. Neratinib was given to 141 patients with one of 21 different tumour types containing mutations in HER2 and HER3, including breast, lung, bladder and colorectal cancer. The results show that responses are determined by mutation and tissue type, and are restricted to HER2-mutant cancers. Clinical benefit is also conditioned by alterations in downstream signalling pathways. The results highlight the potential of basket trials in molecularly driven oncology.
Journal Article
Protective autophagy elicited by RAF→MEK→ERK inhibition suggests a treatment strategy for RAS-driven cancers
Pancreatic ductal adenocarcinoma (PDA) was responsible for ~ 44,000 deaths in the United States in 2018 and is the epitome of a recalcitrant cancer driven by a pharmacologically intractable oncoprotein, KRAS1–4. Downstream of KRAS, the RAF→MEK→ERK signaling pathway plays a central role in pancreatic carcinogenesis5. However, paradoxically, inhibition of this pathway has provided no clinical benefit to patients with PDA6. Here we show that inhibition of KRAS→RAF→MEK→ERK signaling elicits autophagy, a process of cellular recycling that protects PDA cells from the cytotoxic effects of KRAS pathway inhibition. Mechanistically, inhibition of MEK1/2 leads to activation of the LKB1→AMPK→ULK1 signaling axis, a key regulator of autophagy. Furthermore, combined inhibition of MEK1/2 plus autophagy displays synergistic anti-proliferative effects against PDA cell lines in vitro and promotes regression of xenografted patient-derived PDA tumors in mice. The observed effect of combination trametinib plus chloroquine was not restricted to PDA as other tumors, including patient-derived xenografts (PDX) of NRAS-mutated melanoma and BRAF-mutated colorectal cancer displayed similar responses. Finally, treatment of a patient with PDA with the combination of trametinib plus hydroxychloroquine resulted in a partial, but nonetheless striking disease response. These data suggest that this combination therapy may represent a novel strategy to target RAS-driven cancers.Targeted inhibition of RAF–MEK–ERK signaling induces autophagy through the LKB1–AMPK axis, creating a therapeutic vulnerability that can be exploited for treating patients with pancreatic cancer and potentially other RAS-mutant tumors.
Journal Article
Refining the role of de novo protein-truncating variants in neurodevelopmental disorders by using population reference samples
Mark Daly and colleagues use population reference samples to refine the role of
de novo
protein-truncating variants in neurodevelopmental disorders. They show that variants independently observed in population reference samples do not contribute substantively to neurodevelopmental risk, and they use a loss-of-function intolerance metric to identify a small subset of genes that contain the entire observed signal of associated
de novo
protein-truncating variants in these disorders.
Recent research has uncovered an important role for
de novo
variation in neurodevelopmental disorders. Using aggregated data from 9,246 families with autism spectrum disorder, intellectual disability, or developmental delay, we found that ∼1/3 of
de novo
variants are independently present as standing variation in the Exome Aggregation Consortium's cohort of 60,706 adults, and these
de novo
variants do not contribute to neurodevelopmental risk. We further used a loss-of-function (LoF)-intolerance metric, pLI, to identify a subset of LoF-intolerant genes containing the observed signal of associated
de novo
protein-truncating variants (PTVs) in neurodevelopmental disorders. LoF-intolerant genes also carry a modest excess of inherited PTVs, although the strongest
de novo
–affected genes contribute little to this excess, thus suggesting that the excess of inherited risk resides in lower-penetrant genes. These findings illustrate the importance of population-based reference cohorts for the interpretation of candidate pathogenic variants, even for analyses of complex diseases and
de novo
variation.
Journal Article
Phase 3 Trial of Crinecerfont in Adult Congenital Adrenal Hyperplasia
In adults with congenital adrenal hyperplasia, crinecerfont, a corticotropin-releasing factor type 1 receptor antagonist, lowered the mean glucocorticoid dose and decreased the mean androstenedione level.
Journal Article
Final Report of a Trial of Intensive versus Standard Blood-Pressure Control
In confirmation of a previous preliminary report, among patients who were at increased cardiovascular risk, targeting a systolic blood pressure less than 120 mm Hg, as compared with less than 140 mm Hg, resulted in lower rates of major adverse cardiovascular events, both during receipt of the randomly assigned therapy and after the trial.
Journal Article