103 research outputs found

    Comparison of 2-way versus metered 3-way boom shut-off valves for automatic section control on agricultural sprayers

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    Modern spray rate controllers along with technologies such as automatic section control (ASC) provide benefits such as overlap reduction on agricultural sprayers. However, product (liquid) dynamics within the boom plumbing affect off-rate errors and application uniformity during rate changes and ASC actuation. Therefore, this study was conducted to compare nozzle flow stability and uniformity across the boom when using two different boom shut-off valves (2-way and metered 3-way) on an 18.3-m sprayer boom. Pressure transducers were mounted at 1) the boom manifold, 2) randomly at 12 nozzle bodies across the spray boom, and 3) upstream and downstream of the flow regulating valve. Effective system flow rate was measured using two flow meter(s), one located upstream of the boom control valves (2-way or metered 3-way) and another mounted to measure the tank return flow for the metered 3-way boom valve. Measured nozzle pressure was converted to nozzle flow using the manufacturer’s pressure-flow data. Results indicated that the 2-way boom versus metered 3-way valve response was significantly different. Significant differences in damping ratios were found when exiting (under-damped) and reentering (over-damped) of spray zones. For the metered 3-way boom valve configuration, nozzle flow settled faster (0.1 to 4.2 s) virtually eliminating off-rate errors whereas the 2-way boom valve configuration took up to 34.3 s to settle with off-rate errors ranging from 3.3% to 11.5%. The delayed nozzle flow settling times were associated with pressure settling (0.7 to 31.4 s) downstream of the regulating valve for the 2-way configuration. Ground speed and point row angle impacted nozzle flow settling times and off-rate errors. The increase in ground speed and point row angle increased nozzle flow settling time for the 2-way valve setup, except that acceleration decreased settling times when exiting spray zones. The delayed response contributed to off-rate time which decreased as the sprayer accelerated and point row angle decreased for both the 2-way (1.7 to 19.3 s) and metered 3-way (2.1 to 4.4 s) boom shut-off valve setups

    Tribute to Professor Doug Rendleman

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    A tribute to Professor Doug Rendleman, who served on the faculty of the Washington and Lee University School of Law from 1988 to 2020. Rendleman became Professor of Law, Emeritus in 2020

    Deletion of L-Selectin Increases Atherosclerosis Development in ApoE−/− Mice

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    Atherosclerosis is an inflammatory disease characterized by accumulation of leukocytes in the arterial intima. Members of the selectin family of adhesion molecules are important mediators of leukocyte extravasation. However, it is unclear whether L-selectin (L-sel) is involved in the pathogenesis of atherosclerosis. In the present study, mice deficient in L-selectin (L-sel−/−) animals were crossed with mice lacking Apolipoprotein E (ApoE−/−). The development of atherosclerosis was analyzed in double-knockout ApoE/L-sel (ApoE−/− L-sel−/−) mice and the corresponding ApoE−/− controls fed either a normal or a high cholesterol diet (HCD). After 6 weeks of HCD, aortic lesions were increased two-fold in ApoE−/− L-sel−/− mice as compared to ApoE−/− controls (2.46%±0.54% vs 1.28%±0.24% of total aortic area; p<0.05). Formation of atherosclerotic lesions was also enhanced in 6-month-old ApoE−/− L-sel−/− animals fed a normal diet (10.45%±2.58% vs 1.87%±0.37%; p<0.05). In contrast, after 12 weeks of HCD, there was no difference in atheroma formation between ApoE−/− L-sel−/− and ApoE−/− mice. Serum cholesterol levels remained unchanged by L-sel deletion. Atherosclerotic plaques did not exhibit any differences in cellular composition assessed by immunohistochemistry for CD68, CD3, CD4, and CD8 in ApoE−/− L-sel−/− as compared to ApoE−/− mice. Leukocyte rolling on lesions in the aorta was similar in ApoE−/− L-sel−/− and ApoE−/− animals. ApoE−/− L-sel−/− mice exhibited reduced size and cellularity of peripheral lymph nodes, increased size of spleen, and increased number of peripheral lymphocytes as compared to ApoE−/− controls. These data indicate that L-sel does not promote atherosclerotic lesion formation and suggest that it rather protects from early atherosclerosis

    Defects in Regulation of Local Immune Responses Resulting in Atherosclerosis

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    Atherosclerosis is nowadays generally accepted as an inflammatory disease but the mechanism of its origin and development have not yet been fully clarified. The present review focuses on the role of the local immune system as one of the key players in the pathogenesis of the complex process. Its part represented by vascular-associated lymphoid tissue (VALT) within the arterial wall participates directly in the vascular wall's homeostatis. Its inordinate activation during ontogenic development of an individual, this formerly defensive and physiologic mechanism transform into a pathological process resulting in an impairing inflammation. Hsp60, CRP and oxidized or otherwise modified LDL are serious candidates for triggering these pathological changes. The principal role is played by anti-Hsp60 antibodies and by shear stress originating on the surface of endothelium due to blood flow. The experimental and clinical data supporting this immunological hypothesis of atherosclerosis are discussed

    Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases

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    The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular "reactive oxygen species" (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation. We review the considerable and wide-ranging evidence for the involvement of this combination of (su)peroxide and poorly liganded iron in a large number of physiological and indeed pathological processes and inflammatory disorders, especially those involving the progressive degradation of cellular and organismal performance. These diseases share a great many similarities and thus might be considered to have a common cause (i.e. iron-catalysed free radical and especially hydroxyl radical generation). The studies reviewed include those focused on a series of cardiovascular, metabolic and neurological diseases, where iron can be found at the sites of plaques and lesions, as well as studies showing the significance of iron to aging and longevity. The effective chelation of iron by natural or synthetic ligands is thus of major physiological (and potentially therapeutic) importance. As systems properties, we need to recognise that physiological observables have multiple molecular causes, and studying them in isolation leads to inconsistent patterns of apparent causality when it is the simultaneous combination of multiple factors that is responsible. This explains, for instance, the decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference

    Another look at counting by weighing

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    Analysis of the time distribution and time sequence of behavioral acts.

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    A technique for analyzing the temporal structure between various initiations of a particular behavioral act has been developed using a parameter known as the K-function, the cornerstone of recent statistical research on spatial point processes and patterns. The technique has been extended to the study of the joint relationship of separate acts. Bootstrap methods are used to estimate the uncertainty in these measures. The usefulness of these techniques is demonstrated using data from studies of rats exposed to phenytoin and nitrous oxide
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