Author
Deborah Lockridge
Bio: Deborah Lockridge is an academic researcher. The author has contributed to research in topics: Truck & Air brake. The author has an hindex of 3, co-authored 13 publications receiving 44 citations.
Papers
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TL;DR: In this article, Brakes must work harder than ever, but replacement brake linings may not be up to the task, and the authors suggest to replace the linings with a new one.
Abstract: Subtitle: Brakes must work harder than ever, but your replacement brake linings may not be up to the task.
27 citations
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TL;DR: In this paper, environmental and energy issues are hot topics on Capitol Hill. What they'll mean for trucking is anyone's guess. But you can count on one thing: they will have an effect.
Abstract: Subtitle: Environmental and energy issues are hot topics on Capitol Hill. What they'll mean for trucking is anyone's guess. But you can count on one thing: they will have an effect.
5 citations
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TL;DR: In this article, the authors pay attention to why drivers walk out the door and find that it may be even more important to pay attention why drivers leave the door than why they come in.
Abstract: Subtitle: We spend a lot of time trying to attract drivers -- but it may be even more important to pay attention to why drivers walk out the door.
4 citations
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TL;DR: In this paper, the authors report that ultra low sulfur diesel is causing unique problems in both cold weather operation and maintenance, and that issues with biodiesel could be even worse than diesel.
Abstract: Subtitle: Ultra low sulfur diesel is causing unique problems in both cold weather operation and maintenance. Issues with biodiesel could be even worse.
2 citations
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TL;DR: In this article, the authors show that today's transportation companies do whatever it takes to get the freight there, regardless of the cost of doing so, and they use 3PLs to transport the freight.
Abstract: Truckload, LTL, intermodal, private fleets, dedicated, warehousing, packaging, air freight, container ships, global, 3PL-- Today's transportation companies do whatever it takes to get the freight there.
1 citations
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TL;DR: A nanofluidic proteomic immunoassay (NIA) to quantify total and low-abundance protein isoforms in nanoliter volumes for the development of new therapeutics for cancer.
Abstract: Current methods of protein detection are insensitive to detecting subtle changes in oncoprotein activation that underlie key cancer signaling processes. The requirement for large numbers of cells precludes serial tumor sampling for assessing a response to therapeutics. Therefore, we have developed a nanofluidic proteomic immunoassay (NIA) to quantify total and low-abundance protein isoforms in nanoliter volumes. Our method can quantify amounts of MYC oncoprotein and B cell lymphoma protein-2 (BCL2) in Burkitt's and follicular lymphoma; identify changes in activation of extracellular signal-related kinases-1 (ERK1) and ERK2, mitogen-activated kinase-1 (MEK), signal transducer and activator of transcription protein-3 (STAT3) and STAT5, c-Jun N-terminal kinase (JNK) and caspase-3 in imatinib-treated chronic myelogeneous leukemia (CML) cells; measure an unanticipated change in the phosphorylation of an ERK2 isomer in individuals with CML who responded to imatinib; and detect a decrease in STAT3 and STAT5 phosphorylation in individuals with lymphoma who were treated with atorvastatin. Therefore, we have described a new and highly sensitive method for determining oncoprotein expression and phosphorylation in clinical specimens for the development of new therapeutics for cancer.
123 citations
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TL;DR: In this article, the authors examined how the targets of positive stereotypes evaluate others who express such stereotypic "compliments" toward group members and found that black participants evaluated a white student who praised the athletic ability of African Americans more negatively than a control condition.
104 citations
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TL;DR: The authors provide a framework to understand and synthesize the processes of person construal with the processes involved in intergroup relations, and explore the implications of the activation of these constructs for a range of social judgments including emotion identification, empathy, and intergroup behaviors.
Abstract: The primary aim of this chapter is to provide a framework to understand and synthesize the processes of person construal—early perceptions that lead to initial ingroup/outgroup categorizations—with the processes involved in intergroup relations. To this end, we review research examining the initial perception and categorization of ingroup and outgroup members and its downstream consequences. We first discuss bottom-up processes in person construal based on visual features (e.g., facial prototypicality and bodily cues), and then discuss how top-down factors (e.g., beliefs, stereotypes) may influence these processes. Next, we examine how the initial categorization of targets as ingroup or outgroup members influences identification, stereotyping, and group-based evaluations, and the relations between these constructs. We also explore the implications of the activation of these constructs for a range of social judgments including emotion identification, empathy, and intergroup behaviors. Finally, we describe a variety of well established and more recent strategies to reduce intergroup bias that target the activation of category-based knowledge, including intergroup contact, approach orientations, evaluative conditioning, and perspective taking.
101 citations
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TL;DR: The findings suggest that the rejection–aggression link is driven, in part, by the desire to return to affective homeostasis, and implicate aggression’s rewarding nature as an incentive for rejected individuals’ violent tendencies.
Abstract: How does emotion explain the relationship between social rejection and aggression? Rejection reliably damages mood, leaving individuals motivated to repair their negatively valenced affective state. Retaliatory aggression is often a pleasant experience. Rejected individuals may then harness revenge's associated positive affect to repair their mood. Across 6 studies (total N = 1,516), we tested the prediction that the rejection-aggression link is motivated by expected and actual mood repair. Further, we predicted that this mood repair would occur through the positive affect of retaliatory aggression. Supporting these predictions, naturally occurring (Studies 1 and 2) and experimentally manipulated (Studies 3 and 4) motives to repair mood via aggression moderated the rejection-aggression link. These effects were mediated by sadistic impulses toward finding aggression pleasant (Studies 2 and 4). Suggesting the occurrence of actual mood repair, rejected participants' affective states were equivalent to their accepted counterparts after an act of aggression (Studies 5 and 6). This mood repair occurred through a dynamic interplay between preaggression affect and aggression itself, and was driven by increases in positive affect (Studies 5 and 6). Together, these findings suggest that the rejection-aggression link is driven, in part, by the desire to return to affective homeostasis. Additionally, these findings implicate aggression's rewarding nature as an incentive for rejected individuals' violent tendencies. (PsycINFO Database Record
89 citations
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TL;DR: There is now strong evidence that cancers may have their origin in mutations that block the execution of critical steps in the process of normal differentiation, which means that cancer is not initially a disease of cell multiplication, but a Disease of differentiation.
Abstract: Despite the spectacular contributions to knowledge made by molecular biology during the last half century, cancer research has not delivered an agreed explanation of how malignant tumours originate. The models assiduously investigated in molecular terms largely reflect waves of fashion, and time has revealed their inadequacy: cancer is (1) not caused by the direct action of oncogenes, (2) not fully explained by the impairment of tumour suppressor genes, (3) not set in motion by mutations controlling the cell cycle, (4) not governed by the dependence of malignant tumours on an adequate blood supply and (5) not triggered by a failure of programmed cell death. But there is now strong evidence that cancers may have their origin in mutations that block the execution of critical steps in the process of normal differentiation. Cancer, thus seen, is not initially a disease of cell multiplication, but a disease of differentiation. The evidence for this point of view should now be explored.
80 citations