67 research outputs found

    Revised Pacific-Antarctic plate motions and geophysics of the Menard Fracture Zone

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    A reconnaissance survey of multibeam bathymetry and magnetic anomaly data of the Menard Fracture Zone allows for significant refinement of plate motion history of the South Pacific over the last 44 million years. The right-stepping Menard Fracture Zone developed at the northern end of the Pacific-Antarctic Ridge within a propagating rift system that generated the Hudson microplate and formed the conjugate Henry and Hudson Troughs as a response to a major plate reorganization ∼45 million years ago. Two splays, originally about 30 to 35 km apart, narrowed gradually to a corridor of 5 to 10 km width, while lineation azimuths experienced an 8° counterclockwise reorientation owing to changes in spreading direction between chrons C13o and C6C (33 to 24 million years ago). We use the improved Pacific-Antarctic plate motions to analyze the development of the southwest end of the Pacific-Antarctic Ridge. Owing to a 45° counterclockwise reorientation between chrons C27 and C20 (61 to 44 million years ago) this section of the ridge became a long transform fault connected to the Macquarie Triple Junction. Following a clockwise change starting around chron C13o (33 million years ago), the transform fault opened. A counterclockwise change starting around chron C10y (28 millions years ago) again led to a long transform fault between chrons C6C and C5y (24 to 10 million years ago). A second period of clockwise reorientation starting around chron C5y (10 million years ago) put the transform fault into extension, forming an array of 15 en echelon transform faults and short linking spreading centers

    Comment on "mantle flow drives the subsidence of oceanic plates"

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    Adam and Vidal (Reports, 2 April 2010, p. 83) reported sea-floor depth increasing as the square root of distance from the ridge along "mantle flow lines." However, their data actually support a depth-age relationship and "flattening" at older ages. We argue that no plausible physical mechanism supports their proposal that mantle flow drives subsidence

    Personality, psychological stress, and self-reported influenza symptomatology

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    <p>Abstract</p> <p>Background</p> <p>Psychological stress and negative mood have been related to increased vulnerability to influenza-like illness (ILI). This prospective study re-evaluated the predictive value of perceived stress for self-reported ILI. We additionally explored the role of the negative affectivity and social inhibition traits.</p> <p>Methods</p> <p>In this study, 5,404 respondents from the general population were assessed in terms of perceived stress, personality, and control variables (vaccination, vitamin use, exercise, etc.). ILI were registered weekly using self-report measures during a follow-up period of four weeks.</p> <p>Results</p> <p>Multivariable logistic regression analysis on ILI was performed to test the predictive power of stress and personality. In this model, negative affectivity (OR = 1.05, p = 0.009), social inhibition (OR = 0.97, p = 0.011), and perceived stress (OR = 1.03, p = 0.048) predicted ILI reporting. Having a history of asthma (OR = 2.33, p = < 0.0001) was also associated with ILI reporting. Older age was associated with less self-reported ILI (OR = 0.98, P = 0.017).</p> <p>Conclusion</p> <p>Elderly and socially inhibited persons tend to report less ILI as compared to their younger and less socially inhibited counterparts. In contrast, asthma, trait negative affectivity, and perceived stress were associated with higher self-report of ILI. Our results demonstrate the importance of including trait markers in future studies examining the relation between stress and self-report symptom measures.</p

    Feasibility and efficacy of addition of individualized-dose lenalidomide to chlorambucil and rituximab as first-line treatment in elderly and FCR-unfit patients with advanced chronic lymphocytic leukemia

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    Lenalidomide has been proven to be effective but with a distinct and difficult to manage toxicity profile in the context of chronic lymphocytic leukemia, potentially hampering combination treatment with this drug. We conducted a phase 1-2 study to evaluate the efficacy and safety of six cycles of chlorambucil (7 mg/m2 daily), rituximab (375 mg/m2 cycle 1 and 500 mg/m2 cycles 2-6) and individually-dosed lenalidomide (escalated from 2.5 mg to 10 mg) (induction-I) in first-line treatment of patients with chronic lymphocytic leukemia unfit for treatment with fludarabine, cyclophosphamide and rituximab. This was followed by 6 months of 10 mg lenalidomide monotherapy (induction-II). Of 53 evaluable patients in phase 2 of the study, 47 (89%) completed induction-I and 36 (68%) completed induction-II. In an intention-to-treat analysis, the overall response rate was 83%. The median progression-free survival was 49 months, after a median follow-up time of 27 months. The 2- and 3-year progression-free survival rates were 58% and 54%, respectively. The corresponding rates for overall survival were 98% and 95%. No tumor lysis syndrome was observed, while tumor flair reaction occurred in five patients (9%, 1 grade 3). The most common hematologic toxicity was grade 3-4 neutropenia, which occurred in 73% of the patients. In conclusion, addition of lenalidomide to a chemotherapy backbone followed by a fixed duration of lenalidomide monotherapy resulted in high remission rates and progression-free survival rates, which seem comparable to those observed with novel drug combinations including novel CD20 monoclonal antibodies or kinase inhibitors. Although lenalidomide-specific toxicity remains a concern, an individualized dose-escalation schedule is feasible and results in an acceptable toxicity profile. EuraCT number: 2010-022294-34

    Ordering the Classes

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