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  • 1
    Online Resource
    Online Resource
    The environmental impacts of home and community gardening.
    CABI Publishing ; 2016
    In:  CABI Reviews Vol. 2016 ( 2016-01), p. 1-14
    Details
    In: CABI Reviews, CABI Publishing, Vol. 2016 ( 2016-01), p. 1-14
    Abstract: Gardening has been practiced by humans for food and aesthetic purposes for thousands of years. As urbanization intensifies globally, gardening is increasing in both popularity and extent in urban and suburban regions of the world, thus increasing its impact on the environments. Here we discuss the health benefits and risks of home-grown vegetables followed by an in-depth examination of how home and community gardening impacts the biological and physical environments of the world with a focus on North America. In addition to offering multiple health benefits, gardens may promote biodiversity by providing critical habitats for a variety of native plant and animal species. At the same time, gardening has the potential to alter cycles of carbon, nutrients and water in urban and suburban areas, consequently contributing to global environmental changes. Conversely, gardening may have a range of adverse impacts on the environment, for instance, higher nutrient runoff and increased risk of eutrophication in aquatic ecosystems. Intensive lawn care, particularly in North America because of its large lawn areas, could divert essential resources, such as manpower, fertilizers and water, away from more ecologically and economically important activities. Exotic plants commonly grown in home gardens could escape cultivation and become noxious in their non-native habitats as already demonstrated by an increasing number of ornamental species, such as Callery pear and non-native honeysuckle, in the USA. As the world becomes more and more urbanized, the increasingly popular gardening will have greater impact on the abiotic and biotic environments of the world.
    Type of Medium: Online Resource
    ISSN: 1749-8848
    URL: Article
    DOI: 10.1079/PAVSNNR201611052
    Language: English
    Publisher: CABI Publishing
    Publication Date: 2016
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  • 2
    Online Resource
    Online Resource
    Image classification based on improved VLAD
    Springer Science and Business Media LLC ; 2016
    In:  Multimedia Tools and Applications Vol. 75, No. 10 ( 2016-5), p. 5533-5555
    Details
    In: Multimedia Tools and Applications, Springer Science and Business Media LLC, Vol. 75, No. 10 ( 2016-5), p. 5533-5555
    Type of Medium: Online Resource
    ISSN: 1380-7501 , 1573-7721
    URL: Article
    DOI: 10.1007/s11042-015-2524-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 1287642-2
    detail.hit.zdb_id: 1479928-5
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  • 3
    Online Resource
    Online Resource
    Su2028 Unique Expression of Adipose Triglyceride Lipase (ATGL) in Low Grade Colorectal Carcinoma
    Elsevier BV ; 2015
    In:  Gastroenterology Vol. 148, No. 4 ( 2015-04), p. S-578-S-579
    Details
    In: Gastroenterology, Elsevier BV, Vol. 148, No. 4 ( 2015-04), p. S-578-S-579
    Type of Medium: Online Resource
    ISSN: 0016-5085
    URL: Article
    DOI: 10.1016/S0016-5085(15)31957-0
    RVK:
    XA 44500
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2015
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  • 4
    Online Resource
    Online Resource
    Hydrogen peroxide stimulates macrophages and monocytes to actively release HMGB1
    Oxford University Press (OUP) ; 2007
    In:  Journal of Leukocyte Biology Vol. 81, No. 3 ( 2007-03-01), p. 741-747
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 81, No. 3 ( 2007-03-01), p. 741-747
    Abstract: High mobility group box 1 (HMGB1) can be actively secreted by macrophages/monocytes in response to exogenous and endogenous inflammatory stimuli (such as bacterial endotoxin, TNF-α, IL-1, and IFN-γ) or passively released by necrotic cells and mediates innate and adaptive inflammatory responses to infection and injury. Here, we demonstrated that a reactive oxygen species, hydrogen peroxide (H2O2), induces active and passive HMGB1 release from macrophage and monocyte cultures in a time- and dose-dependent manner. At nontoxic doses (e.g., 0.0125–0.125 mM), H2O2 induced HMGB1 cytoplasmic translocation and active release within 3–24 h. At higher concentrations (e.g., 0.25 mM), however, H2O2 exhibited cytotoxicity to macrophage and monocyte cell cultures and consequently, triggered active and passive HMGB1 release. In addition, H2O2 stimulated potential interaction of HMGB1 with a nuclear export factor, chromosome region maintenance (CRM1), in macrophage/monocyte cultures. Inhibitors specific for the JNK (SP600125) and MEK (PD98059), but not p38 MAPK (SB203580), abrogated H2O2-induced, active HMGB1 release. Together, these data establish an important role for oxidative stress in inducing active HMGB1 release, potentially through a MAPK- and CRM1-dependent mechanism.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    URL: Article
    DOI: 10.1189/jlb.0806540
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2007
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Alcohol enhances symptoms and propensity for infection in inflammatory bowel disease patients and a murine model of DSS-induced colitis
    Oxford University Press (OUP) ; 2018
    In:  Journal of Leukocyte Biology Vol. 104, No. 3 ( 2018-08-28), p. 543-555
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 104, No. 3 ( 2018-08-28), p. 543-555
    Abstract: Over 1.4 million Americans have been diagnosed with inflammatory bowel disease (IBD), and ulcerative colitis (UC) makes up approximately half of those diagnoses. As a disease, UC cycles between periods of remission and flare, which is characterized by intense abdominal pain, increased weight loss, intestinal inflammation, rectal bleeding, and dehydration. Interestingly, a widespread recommendation to IBD patients for avoidance of a flare period is “Don’t Drink Alcohol” as recent work correlated alcohol consumption with increased GI symptoms in patients with IBD. Alcohol alone not only induces a systemic pro-inflammatory response, but can also be directly harmful to gut barrier integrity. However, how alcohol could result in the exacerbation of UC in both patients and murine models of colitis has yet to be elucidated. Therefore, we conducted a retrospective analysis of patients admitted for IBD with a documented history of alcohol use in conjunction with a newly developed mouse model of binge alcohol consumption following dextran sulfate sodium (DSS)-induced colitis. We found that alcohol negatively impacts clinical outcomes of patients with IBD, specifically increased intestinal infections, antibiotic injections, abdomen CT scans, and large intestine biopsies. Furthermore, in our mouse model of binge alcohol consumption following an induced colitis flare, we found alcohol exacerbates weight loss, clinical scores, colonic shortening and inflammation, and propensity to infection. These findings highlight alcohol’s ability to potentiate symptoms and susceptibility to infection in UC and suggest alcohol as an underlying factor in perpetuating symptoms of IBD. This study builds on previous findings that alcohol has adverse effects in IBD and establishes these effects in a mouse model of colitis.
    Type of Medium: Online Resource
    ISSN: 1938-3673 , 0741-5400
    URL: Article
    DOI: 10.1002/JLB.4MA1217-506R
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2018
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Improving physical layer multicast by cooperative communications in heterogeneous networks
    Institute of Electrical and Electronics Engineers (IEEE) ; 2011
    In:  IEEE Wireless Communications Vol. 18, No. 3 ( 2011-06), p. 58-63
    Details
    In: IEEE Wireless Communications, Institute of Electrical and Electronics Engineers (IEEE), Vol. 18, No. 3 ( 2011-06), p. 58-63
    Type of Medium: Online Resource
    ISSN: 1536-1284
    URL: Article
    DOI: 10.1109/MWC.2011.5876501
    Language: Unknown
    Publisher: Institute of Electrical and Electronics Engineers (IEEE)
    Publication Date: 2011
    detail.hit.zdb_id: 2051681-2
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  • 7
    Online Resource
    Online Resource
    Monitoring a progressive collapse test of a spherical lattice shell using high‐speed videogrammetry
    Wiley ; 2017
    In:  The Photogrammetric Record Vol. 32, No. 159 ( 2017-09), p. 230-254
    Details
    In: The Photogrammetric Record, Wiley, Vol. 32, No. 159 ( 2017-09), p. 230-254
    Abstract: 在土木工程领域,结构连续性倒塌试验的监测始终是一项技术难题。本论文提出了一个新的视频测量方法来监测单层网壳结构,该方法由三个主要部分构成: 构建了一个由六台高速相机组成的视频测量系统来测量网壳的空间形态变化。 设计了一种特殊的人工标志来获取网壳每个节点中心的位置,并通过实验验证了该标志的可行性。 通过球面拟合和局部坐标变换解算了节点中心的三维位移。 与高精度全站仪的测量结果相比,本论文所提出的方法在人工标志空间定位中的偏差达到亚毫米级,且节点中心的定位偏差在1毫米左右。同时,通过与模型倒塌数值模拟的结果对比,进一步验证了本论文所提方法测量结果的可信性。
    Type of Medium: Online Resource
    ISSN: 0031-868X , 1477-9730
    URL: Issue
    URL: Article
    DOI: 10.1111/phor.2017.32.issue-159
    DOI: 10.1111/phor.12202
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2104419-3
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  • 8
    Online Resource
    Online Resource
    Proteomics analysis reveals diabetic kidney as a ketogenic organ in type 2 diabetes
    American Physiological Society ; 2011
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 300, No. 2 ( 2011-02), p. E287-E295
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 300, No. 2 ( 2011-02), p. E287-E295
    Abstract: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. To date, the molecular mechanisms of DN remain largely unclear. The present study aimed to identify and characterize novel proteins involved in the development of DN by a proteomic approach. Proteomic analysis revealed that 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase 2 (HMGCS2), the key enzyme in ketogenesis, was increased fourfold in the kidneys of type 2 diabetic db/db mice. Consistently, the activity of HMGCS2 in kidneys and 24-h urinary excretion of the ketone body β-hydroxybutyrate (β-HB) were significantly increased in db/db mice. Immunohistochemistry, immunofluorescence, and real-time PCR studies further demonstrated that HMGCS2 was highly expressed in renal glomeruli of db/db mice, with weak expression in the kidneys of control mice. Because filtered ketone bodies are mainly reabsorbed in the proximal tubules, we used RPTC cells, a rat proximal tubule cell line, to examine the effect of the increased level of ketone bodies. Treating cultured RPTC cells with 1 mM β-HB significantly induced transforming growth factor-β1 expression, with a marked increase in collagen I expression. β-HB treatment also resulted in a marked increase in vimentin protein expression and a significant reduction in E-cadherin protein levels, suggesting an enhanced epithelial-to-mesenchymal transition in RPTCs. Collectively, these findings demonstrate that diabetic kidneys exhibit excess ketogenic activity resulting from increased HMGCS2 expression. Enhanced ketone body production in the diabetic kidney may represent a novel mechanism involved in the pathogenesis of DN.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00308.2010
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2011
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Signaling for myocardial depression in hemorrhagic shock: roles of Toll-like receptor 4 and p55 TNF-α receptor
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 288, No. 3 ( 2005-03), p. R600-R606
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 288, No. 3 ( 2005-03), p. R600-R606
    Abstract: Hemorrhagic shock causes myocardial contractile depression. Although this myocardial disorder is associated with increased expression of tumor necrosis factor-α (TNF-α), the role of TNF-α as a myocardial depressant factor in hemorrhagic shock remains to be determined. Moreover, it is unclear which TNF-α receptor mediates the myocardial depressive effects of TNF-α. Toll-like receptor 4 (TLR4) regulates cellular expression of proinflammatory mediators following lipopolysaccharide stimulation and may be involved in the tissue inflammatory response to injury. The contribution of TLR4 signaling to tissue TNF-α response to hemorrhagic shock and TLR4’s role in myocardial depression during hemorrhagic shock are presently unknown. We examined the relationship of TNF-α production to myocardial depression in a mouse model of nonresuscitated hemorrhagic shock, assessed the influence of TLR4 mutation, resulting in defective signaling, on TNF-α production and myocardial depression, and determined the roles of TNF-α and TNF-α receptors in myocardial depression using a gene knockout (KO) approach. Hemorrhagic shock resulted in increased plasma and myocardial TNF-α (4.9- and 4.5-fold, respectively) at 30 min and induced myocardial contractile depression at 4 h. TLR4 mutation abolished the TNF-α response and attenuated myocardial depression (left ventricular developed pressure of 43.0 ± 6.2 mmHg in TLR4 mutant vs. 30.0 ± 3.6 mmHg in wild type, P 〈 0.05). TNF-α KO also attenuated myocardial depression in hemorrhagic shock, and the p55 receptor KO, but not the p75 receptor KO, mimicked the effect of TNF-α KO. The results suggest that TLR4 plays a novel role in signaling to the TNF-α response during hemorrhagic shock and that TNF-α through the p55 receptor activates a pathway leading to myocardial depression. Thus TLR4 and the p55 TNF-α receptor represent therapeutic targets for preservation of cardiac mechanical function during hemorrhagic shock.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00182.2004
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Activation state of stromal inflammatory cells in murine metastatic pancreatic adenocarcinoma
    American Physiological Society ; 2012
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 302, No. 9 ( 2012-05-01), p. R1067-R1075
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 302, No. 9 ( 2012-05-01), p. R1067-R1075
    Abstract: The histologic presence of macrophages (tumor-associated macrophages, TAMs) and neutrophils (tumor-associated neutrophils, TANs) has been linked to poor clinical outcomes for solid tumors. The exact mechanism for this association with worsened prognosis is unclear. It has been theorized that TAMs are immunomodulated to an alternatively activated state and promote tumor progression. Similarly, TANs have been shown to promote angiogenesis and tumor detachment. TAMs and TANs were characterized for activation state and production of prometastatic mediators in an immunocompetent murine model of pancreatic adenocarcinoma. Specimens from liver metastases were evaluated by immunofluorescence and immunoblotting. TAMS have upregulated expression of CD206 and CD163 markers of alternative activation, (4.14 ± 0.55-fold and 7.36 ± 1.13-fold over control, respectively, P 〈 0.001) but do not have increased expression of classically activated macrophage markers CCR2 and CCR5. TAMs also express oncostatin M (OSM). We found that TANs, not TAMs, predominantly produce matrix metalloproteinase-9 (MMP-9) in this metastatic tumor microenvironment, while MMP-2 production is pan-tumoral. Moreover, increased expression of VEGF colocalized with TAMs as opposed to TANs. TAMs and TANs may act as distinct effector cells, with TAMs phenotypically exhibiting alternative activation and releasing OSM and VEGF. TANs are localized at the invasive front of the metastasis, where they colocalize with MMP-9. Improved understanding of these interactions may lead to targeted therapies for pancreas adenocarcinoma.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00320.2011
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2012
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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