1,793 research outputs found

    Aquifer sensitivity map, Jo Daviess County, Illinois

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    Computer generated map./ "This map was prepared by the Illinois State Geological Survey, in cooperation with the Illinois Department of Commerce and Community Affairs and the Jo Daviess County Board. It is part of a suite of maps created to assist local government in addressing geologic questions concerning capable sites for landfill development. Maps produced for this study are intended for regional land use planning purposes. More detailed mapping is needed for site-specific considerations. This map has been reviewed for scientific accuracy and edited to meet the quality standards of maps in the ISGS Map Series."/ Includes text, references, 3 ancillary maps, and location map.Ope

    Land surface topography map, Jo Daviess County, Illinois

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    Rapid quenching effects in PVC films

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    Using a specially constructed microbalance for hydrostatic weighing, density changes in PVC thin films (with no additives, 30-100 micrometers thick), due to rapid quenching (approximately 300 C/sec) through the glass transition temperature, have been observed. The more severe the quench, the greater is the free volume content. Isobaric volume recovery of PVC has also been studied by volume dilatometry. Both show aging of relaxing molecular rearrangements takes place as a linear function of logarithmic aging time at room temperature. Distribution of retardation times and Primak's distributed activation energy spectra have been applied to the volume recovery data. The concomitant changes in mechanical properties of PVC after quenching have been monitored by tensile creep and stress-strain to failure. All reflect the presence of excess free volume content, due to rapid quenching

    Adolescent-to-parent violence : an audit of the prevalence in one sample and the response of agencies and professionals involved

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    Adolescent-to-parent violence (APV) is a growing concern. APV is challenging to define and there is a lack of clarity regarding who should respond to it and how. One child and adolescent mental health service (CAMHS) in England carried out an audit in a sample of 20 young people in whom violence and aggression had been identified as an issue. Among the findings, the audit showed that APV was present in all 20 cases. In almost one third of cases, there was no clear process or framework for multi-agency working and there was evidence of conflict between the agencies involved in the young people’s care. The audit highlights the challenges experienced by CAMHS professionals when encountering young people and families experiencing APV. Improved multi-agency working, a unified response from agencies and a clearer pathway of intervention for children, young people and families affected by APV are needed

    Regulation of Macrophage‐Derived Fibroblast Growth Factor Release by Arachidonate Metabolites

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    The macrophage is a source of many mediators with direct and indirect fibrogenic potential. In this study, release of macrophage‐derived fibroblast growth factor (MDGF) activity by murine peritoneal macrophages is examined with regard to its regulation by arachidonate metabolites. Upon stimulation with 10 μg/ml lipopolysaccharide (LPS), resident peritoneal macrophages from CBA/J mice released MDGF activity into media rapidly, reaching maximal levels in approximately 1 h. Lysates of these stimulated cells also revealed significantly increased cell‐associated MDGF activity, composing 45% of the total assayable activity. This activity, as assayed by radioactive thymidine incorporation by primary cultures of rat lung fibroblasts, was separable from interleukin‐1 (IL‐1) activity by reverse phase high performance liquid chromatography (HPLC). Furthermore, purified murine IL‐1 had no MDGF activity in this assay system. This stimulated MDGF release was enhanced by the cylooxygenase inhibitors indomethacin, Ibuprofen, and aspirin at micromolar concentrations, but inhibited in a dose‐dependent manner by prostaglandin E2 (PGE2). On the other hand, nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor was inhibitory at 0.1 and 0.4 μM but not at 2.5 μM. Zymosan‐stimulated macrophages also markedly increased MDGF release, albeit with a different time course which was characterized by a delay of approximately 7 h before peak levels were attained. Such stimulation, which is known to cause increased lipoxygenase activity, was also inhibited by 0.5 μM NDGA. In contrast, the lipoxygenase pathway products leukotrienes B4 (LTB4) and C4 (LTC4) stimulated MDGF release in a dose‐dependent (10‐10‐10‐8 M) manner, with LTC4 being more potent on a per unit dose basis. Stimulation by LTC4 was inhibited by the putative leukotriene receptor antagonist, FPL55712, while LTD4 and LTE4 did not stimulate MDGF release, thus suggesting the mediation of this effect by specific LTC4 receptors. These data suggest also that products of the cyclooxygenase and lipoxygenase pathways are potentially important both as exogenous (ie, derived from cells other than the macrophage itself) and auto‐ or self‐regulators of macrophage MDGF release. This, in turn, implies that cyclooxygenase products are antifibrogenic and important in maintaining or returning to the quiescent or normal state, whereas the lipoxygenase products are profibrogenic and important in induction of fibrosis or wound‐healing and tissue repair. Any alteration in the balance between these two pathways may result in either a desirable or a harmful outcome.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141690/1/jlb0106.pd

    The role of ILâ 5 in bleomycinâ induced pulmonary fibrosis

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    Eosinophils are known to express cytokines capable of promoting fibrosis. Interleukinâ 5 (ILâ 5) is important in regulating eosinophilopoiesis, eosinophil recruitment and activation. Lung ILâ 5 expression is elevated in pulmonary fibrosis, wherein the eosinophil is a primary source of fibrogenic cytokines. To determine the role of ILâ 5 in pulmonary fibrosis, the effects of antiâ ILâ 5 antibody were investigated in a model of bleomycinâ induced pulmonary fibrosis. Fibrosis was induced in mice by endotracheal bleomycin treatment. Animals were also treated with either antiâ ILâ 5 antibody or control IgG. Lungs were then analyzed for fibrosis, eosinophil influx, chemotactic activity, and cytokine expression. The results show that a primary chemotactic activity at the height of eosinophil recruitment is ILâ 5. Furthermore, antiâ ILâ 5 antibody caused significant reduction in lung eosinophilia, cytokine expression, and fibrosis. These findings taken together suggest an important role for ILâ 5 in pulmonary fibrosis via its ability to regulate eosinophilic inflammation, and thus eosinophilâ dependent fibrogenic cytokine production. J. Leukoc. Biol. 64: 657â 666; 1998.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141191/1/jlb0657.pd

    A spatiotemporal theory for MRI T2 relaxation time and apparent diffusion coefficient in the brain during acute ischaemia:Application and validation in a rat acute stroke model

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    The objective of this study is to present a mathematical model which can describe the spatiotemporal progression of cerebral ischaemia and predict magnetic resonance observables including the apparent diffusion coefficient (ADC) of water and transverse relaxation time T(2). This is motivated by the sensitivity of the ADC to the location of cerebral ischaemia and T(2) to its time-course, and that it has thus far proven challenging to relate observations of changes in these MR parameters to stroke timing, which is of considerable importance in making treatment choices in clinics. Our mathematical model, called the cytotoxic oedema/dissociation (CED) model, is based on the transit of water from the extra- to the intra-cellular environment (cytotoxic oedema) and concomitant degradation of supramacromolecular and macromolecular structures (such as microtubules and the cytoskeleton). It explains experimental observations of ADC and T(2), as well as identifying the rate of spread of effects of ischaemia through a tissue as a dominant system parameter. The model brings the direct extraction of the timing of ischaemic stroke from quantitative MRI closer to reality, as well as providing insight on ischaemia pathology by imaging in general. We anticipate that this may improve patient access to thrombolytic treatment as a future application

    Stroke onset time estimation from multispectral quantitative magnetic resonance imaging in a rat model of focal permanent cerebral ischaemia

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    Background Quantitative T2 relaxation magnetic resonance imaging allows estimation of stroke onset time. Aims We aimed to examine the accuracy of quantitative T1 and quantitative T2 relaxation times alone and in combination to provide estimates of stroke onset time in a rat model of permanent focal cerebral ischemia and map the spatial distribution of elevated quantitative T1 and quantitative T2 to assess tissue status. Methods Permanent middle cerebral artery occlusion was induced in Wistar rats. Animals were scanned at 9.4T for quantitative T1, quantitative T2, and Trace of Diffusion Tensor (Dav) up to 4 h post-middle cerebral artery occlusion. Time courses of differentials of quantitative T1 and quantitative T2 in ischemic and non-ischemic contralateral brain tissue (ΔT1, ΔT2) and volumes of tissue with elevated T1 and T2 relaxation times ( f1, f2) were determined. TTC staining was used to highlight permanent ischemic damage. Results ΔT1, ΔT2, f1, f2, and the volume of tissue with both elevated quantitative T1 and quantitative T2 (VOverlap) increased with time post-middle cerebral artery occlusion allowing stroke onset time to be estimated. VOverlap provided the most accurate estimate with an uncertainty of ±25 min. At all times-points regions with elevated relaxation times were smaller than areas with Dav defined ischemia. Conclusions Stroke onset time can be determined by quantitative T1 and quantitative T2 relaxation times and tissue volumes. Combining quantitative T1 and quantitative T2 provides the most accurate estimate and potentially identifies irreversibly damaged brain tissue. </jats:sec
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