569 research outputs found

    Land, Water, Infrastructure And People: Considerations Of Planning For Distributed Stormwater Management Systems

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    When urbanization occurs, the removal of vegetation, compaction of soil and construction of impervious surfaces—roofs, asphalt, and concrete—and drainage infrastructure result in drastic changes to the natural hydrological cycle. Stormwater runoff occurs when rain does not infiltrate into soil. Instead it ponds at the surface and forms shallow channels of overland flow. The result is increased peak flows and pollutant loads, eroded streambanks, and decreased biodiversity in aquatic habitat. In urban areas, runoff is typically directed into catch basins and underground pipe systems to prevent flooding, however such systems are also failing to meet modern environmental goals. Green infrastructure is the widely evocative idea that development practices and stormwater management infrastructure can do better to mimic the natural hydrological conditions through distributed vegetation and source control measures that prevent runoff from being produced in the first place. This dissertation uses statistics and high-resolution, coupled surface-subsurface hydrologic simulation (ParFlow.CLM) to examine three understudied aspects of green infrastructure planning. First, I examine how development characteristics affect the runoff response in urban catchments. I find that instead of focusing on site imperviousness, planners should aim to preserve the ecosystem functions of infiltration and evapotranspiration that are lost even with low density development. Second, I look at how the spatial configuration of green infrastructure at the neighborhood scale affects runoff generation. While spatial configuration of green infrastructure does result in statistically significant differences in performance, such differences are not likely to be detectable above noise levels present in empirical monitoring data. In this study, there was no evidence of reduced hydrological effectiveness for green infrastructure located at sag points in the topography. Lastly, using six years of empirical data from a voluntary residential green infrastructure program, I show how the spread of green infrastructure depends on the demographic and physical characteristics of neighborhoods as well as spatially-dependent social processes (such as the spread of information). This dissertation advances the science of green infrastructure planning at multiple scales and in multiple sectors to improve the practice of urban water resource management and sustainable development

    Elementary Mathematics and #BlackLivesMatter

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    The #BlackLivesMatter movement has opened up conversations in schools across the country about systemic racism, a “new” civil rights movement, and the treatment of children of color. In this article, a veteran elementary teacher uses the #BlackLivesMatter movement to help her students see the power of mathematics in their own lives, taking care to first connect with her school community so as not to incite trauma. Using an age-appropriate activity to investigate the feelings of anger felt by the Black community of Ferguson County, Missouri, shortly before the police murdered Michael Brown, we construct a conversation on what elementary mathematics learning looks like when framed around the guiding principles of #BlackLivesMatter. By utilizing and exploring the mathematics behind who gets into Peace Park, children connect various ways of recognizing inequity with mathematical observations, using mathematics as a tool to perceive and confront oppression

    Emission Inventory for PFOS in China: Review of Past Methodologies and Suggestions

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    Perfluorooctane sulfonate (PFOS) is a persistent, bioaccumulative, and toxic chemical that has the potential for long-range transport in the environment. Its use in a wide variety of consumer products and industrial processes makes a detailed characterization of its emissions sources very challenging. These varied emissions sources all contribute to PFOS' existence within nearly all environmental media. Currently, China is the only country documented to still be producing PFOS, though there is no China PFOS emission inventory available. This study reviews the inventory methodologies for PFOS in other countries to suggest a China-specific methodology framework for a PFOS emission inventory. The suggested framework combines unknowns for PFOS-containing product penetration into the Chinese market with product lifecycle assumptions, centralizing these diverse sources into municipal sewage treatment plants. Releases from industrial sources can be quantified separately using another set of emission factors. Industrial sources likely to be relevant to the Chinese environment are identified

    Co-targeting of DNA, RNA, and protein molecules provides optimal outcomes for treating osteosarcoma and pulmonary metastasis in spontaneous and experimental metastasis mouse models.

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    Metastasis is a major cause of mortality for cancer patients and remains as the greatest challenge in cancer therapy. Driven by multiple factors, metastasis may not be controlled by the inhibition of single target. This study was aimed at assessing the hypothesis that drugs could be rationally combined to co-target critical DNA, RNA and protein molecules to achieve "saturation attack" against metastasis. Independent actions of the model drugs DNA-intercalating doxorubicin, RNA-interfering miR-34a and protein-inhibiting sorafenib on DNA replication, RNA translation and protein kinase signaling in highly metastatic, human osteosarcoma 143B cells were demonstrated by the increase of γH2A.X foci formation, reduction of c-MET expression and inhibition of Erk1/2 phosphorylation, respectively, and optimal effects were found for triple-drug combination. Consequently, triple-drug treatment showed a strong synergism in suppressing 143B cell proliferation and the greatest effects in reducing cell invasion. Compared to single- and dual-drug treatment, triple-drug therapy suppressed pulmonary metastases and orthotopic osteosarcoma progression to significantly greater degrees in orthotopic osteosarcoma xenograft/spontaneous metastases mouse models, while none showed significant toxicity. In addition, triple-drug therapy improved the overall survival to the greatest extent in experimental metastases mouse models. These findings demonstrate co-targeting of DNA, RNA and protein molecules as a novel therapeutic strategy for the treatment of metastasis

    Physical assembly of Ag nanocrystals on enclosed surfaces in monocrystalline Si

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    Growth of thin crystals on external substrate surfaces by many different methods is a well-known technique, but its extension to inner, enclosed surfaces of large defects in monocrystalline materials has not yet been reported. The literature on thin film growth and defects in materials can be leveraged to fabricate new structures for a variety of applications. Here we show a physical process of nucleation and evolution of nanocrystalline silver inside voids in monocrystalline silicon. We found that the Ag growth is hetero-epitaxial using a coincident site lattice. Alignment of Ag and Si atomic planes is uniformly observed by high resolution transmission electron microscopy and macroscopically by channeling Rutherford backscattering spectrometry

    “I Got You”: Centering Identities and Humanness in Collaborations Between Mathematics Educators and Mathematicians

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    Existing literature widely reports on the value of collaborations between mathematicians and mathematics educators, and also how complex those collaborations can be. In this paper, we report on four collaborations that sought to address what mathematics is and who gets to do it. Drawing on the literature and from the careful and intentional work of the collaborators, we offer a framework to capture the richness of those collaborations – one that acknowledges the importance of acknowledging and welcoming the extensive personal and professional experience of each person involved in the collaboration – and a look at how collaborations built with that intentionality and acknowledgment can be impactful for students and institutions and be personally and professionally rewarding for the collaborators

    Reduced expression of alpha-1,2-mannosidase I extends lifespan in Drosophila melanogaster and Caenorhabditis elegans

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    Exposure to sub-lethal levels of stress, or hormesis, was a means to induce longevity. By screening for mutations that enhance resistance to multiple stresses, we identified multiple alleles of alpha-1,2-mannosidase I (mas1) which, in addition to promoting stress resistance, also extended longevity. Longevity enhancement is also observed when mas1 expression is reduced via RNA interference in both Drosophila melanogaster and Caenorhabditis elegans. The screen also identified Edem1 (Edm1), a gene downstream of mas1, as a modulator of lifespan. As double mutants for both mas1 and Edm1 showed no additional longevity enhancement, it appeared that both mutations function within a common pathway to extend lifespan. Molecular analysis of these mutants revealed that the expression of BiP, a putative biomarker of dietary restriction (DR), is down-regulated in response to reductions in mas1 expression. These findings suggested that mutations in mas1 may extend longevity by modulating DR

    Neurotrophin receptors expression and JNK pathway activation in human astrocytomas

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    <p>Abstract</p> <p>Background</p> <p>Neurotrophins are growth factors that regulate cell growth, differentiation and apoptosis in the nervous system. Their diverse actions are mediated through two different transmembrane – receptor signaling systems: Trk receptor tyrosine kinases (TrkA, TrkB, TrkC) and p75<sup>NTR </sup>neurotrophin receptor. Trk receptors promote cell survival and differentiation while p75<sup>NTR </sup>induces, in most cases, the activity of JNK-p53-Bax apoptosis pathway or suppresses intracellular survival signaling cascades. Robust Trk activation blocks p75<sup>NTR </sup>-induced apoptosis by suppressing the JNK-p53-Bax pathway. The aim of this exploratory study was to investigate the expression levels of neurotrophin receptors, Trks and p75<sup>NTR</sup>, and the activation of JNK pathway in human astrocytomas and in adjacent non-neoplastic brain tissue.</p> <p>Methods</p> <p>Formalin-fixed paraffin-embedded serial sections from 33 supratentorial astrocytomas (5 diffuse fibrillary astrocytomas, WHO grade II; 6 anaplastic astrocytomas, WHO grade III; 22 glioblastomas multiforme, WHO grade IV) were immunostained following microwave pretreatment. Polyclonal antibodies against TrkA, TrkB, TrkC and monoclonal antibodies against p75<sup>NTR </sup>and phosphorylated forms of JNK (pJNK) and c-Jun (pc-Jun) were used. The labeling index (LI), defined as the percentage of positive (labeled) cells out of the total number of tumor cells counted, was determined.</p> <p>Results</p> <p>Moderate to strong, granular cytoplasmic immunoreactivity for TrkA, TrkB and TrkC receptors was detected in greater than or equal to 10% of tumor cells in the majority of tumors independently of grade; on the contrary, p75<sup>NTR </sup>receptor expression was found in a small percentage of tumor cells (~1%) in some tumors. The endothelium of tumor capillaries showed conspicuous immunoreactivity for TrkB receptor. Trk immunoreactivity seemed to be localized in some neurons and astrocytes in non-neoplastic tissue. Phosphorylated forms of JNK (pJNK) and c-Jun (pc-Jun) were significantly co-expressed in a tumor grade-dependent manner (p < 0.05). Interestingly, a statistically significant (p < 0.05) reverse relationship between Trk receptors LIs and pc-Jun/pJNK LIs was noted in some glioblastomas multiforme.</p> <p>Conclusion</p> <p>In the context of astrocytomas, Trk receptors (TrkA, TrkB, TrkC) expression may promote tumor growth independently of grade. Furthermore, activation of JNK pathway may contribute to progression towards malignancy. Considering the fact that regional tumor heterogeneity may be a limiting factor for immunohistochemical studies, the significance of the reverse relationship between Trk receptors and pc-Jun/pJNK LIs with respect to biological behavior of human astrocytomas requires further evaluation.</p

    TLR 2 and 4 responsiveness from isolated peripheral blood mononuclear cells from rats and humans as potential chronic pain biomarkers

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    Background: Chronic pain patients have increased peripheral blood mononuclear cell Interkeukin-1β production following TLR2 and TLR4 simulation. Here we have used a human-to-rat and rat-to-human approach to further investigate whether peripheral blood immune responses to TLR agonists might be suitable for development as possible systems biomarkers of chronic pain in humans. Methods and Results: Study 1: using a graded model of chronic constriction injury in rats, behavioral allodynia was assessed followed by in vitro quantification of TLR2 and TLR4 agonist-induced stimulation of IL-1β release by PBMCs and spinal cord tissues (n = 42; 6 rats per group). Statistical models were subsequently developed using the IL-1β responses, which distinguished the pain/no pain states and predicted the degree of allodynia. Study 2: the rat-derived statistical models were tested to assess their predictive utility in determining the pain status of a published human cohort that consists of a heterogeneous clinical pain population (n = 19) and a pain-free population (n = 11). The predictive ability of one of the rat models was able to distinguish pain patients from controls with a ROC AUC of 0.94. The rat model was used to predict the presence of pain in a new chronic pain cohort and was able to accurately predict the presence of pain in 28 out of the 34 chronic pain participants. Conclusions: These clinical findings confirm our previous discoveries of the involvement of the peripheral immune system in chronic pain. Given that these findings are reflected in the prospective graded rat data, it suggests that the TLR response from peripheral blood and spinal cord were related to pain and these clinical findings do indeed act as system biomarkers for the chronic pain state. Hence, they provide additional impetus to the neuroimmune interaction to be a drug target for chronic pain.Yuen H. Kwok, Jonathan Tuke, Lauren L. Nicotra, Peter M. Grace, Paul E. Rolan, Mark R. Hutchinso
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