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1.
Ying Yong Sheng Tai Xue Bao ; 34(4): 1083-1090, 2023 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-37078328

RESUMO

Green space is a kind of resource welfare. The evaluation of green space equity based on green view index (GVI) is important to ensure the equitable distribution of green resources. Taking the central urban area of Wuhan as the research object, based on multi-source data such as Baidu Street View Map, Baidu Thermal Map, and satellite remote sensing images, we evaluated the equity of spatial distribution of GVI in Wuhan by using the locational entropy, Gini coefficient and Lorenz curve. The results showed that 87.6% of the points in the central urban area of Wuhan were below the level of poor green vision, which mainly concentrated in Wuhan Iron and Steel Industrial Base of Qingshan District and south of Yandong Lake. The number of points reaching an excellent level was the least (0.4%), mainly concentrated around the East Lake. The overall Gini coefficient of GVI in the central urban area of Wuhan was 0.49, which indicated that the distribution of GVI was heterogeneous. The Gini coefficient of Hongshan District was the largest at 0.64, indicating a huge gap in the distribution of GVI, while the Gini coefficient of Jianghan District was the smallest at 0.47, with a large gap in the distribution. The central urban area of Wuhan had the most low-entropy areas for 29.7% and the least high-entropy areas for 15.4%. There were two-level differences in entropy distribution within Hongshan District, Qingshan District, and Wuchang District. The nature of land use and the role of linear greenery were the main factors affecting the equity of green space in the study area. Our results could provide theoretical basis and planning reference for optimizing urban green space layout.


Assuntos
Indústrias , Parques Recreativos , Cidades , Lagos , Aço
2.
PLoS One ; 9(12): e115694, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25546475

RESUMO

Traumatic brain injury (TBI) triggers a series of neuroinflammatory processes that contribute to evolution of neuronal injury. The present study investigated the neuroprotective effects and anti-inflammatory actions of berberine, an isoquinoline alkaloid, in both in vitro and in vivo TBI models. Mice subjected to controlled cortical impact injury were injected with berberine (10 mg·kg(-1)) or vehicle 10 min after injury. In addition to behavioral studies and histology analysis, blood-brain barrier (BBB) permeability and brain water content were determined. Expression of PI3K/Akt and Erk signaling and inflammatory mediators were also analyzed. The protective effect of berberine was also investigated in cultured neurons either subjected to stretch injury or exposed to conditioned media with activated microglia. Berberine significantly attenuated functional deficits and brain damage associated with TBI up to day 28 post-injury. Berberine also reduced neuronal death, apoptosis, BBB permeability, and brain edema at day 1 post-injury. These changes coincided with a marked reduction in leukocyte infiltration, microglial activation, matrix metalloproteinase-9 activity, and expression of inflammatory mediators. Berberine had no effect on Akt or Erk 1/2 phosphorylation. In mixed glial cultures, berberine reduced TLR4/MyD88/NF-κB signaling. Berberine also attenuated neuronal death induced by microglial conditioned media; however, it did not directly protect cultured neurons subjected to stretch injury. Moreover, administration of berberine at 3 h post-injury also reduced TBI-induced neuronal damage, apoptosis and inflammation in vivo. Berberine reduces TBI-induced brain damage by limiting the production of inflammatory mediators by glial cells, rather than by a direct neuroprotective effect.


Assuntos
Berberina/uso terapêutico , Lesões Encefálicas/prevenção & controle , Neuroglia/metabolismo , Fármacos Neuroprotetores/uso terapêutico , Animais , Apoptose , Berberina/farmacologia , Barreira Hematoencefálica/efeitos dos fármacos , Barreira Hematoencefálica/metabolismo , Lesões Encefálicas/fisiopatologia , Células Cultivadas , Quimiocinas/genética , Quimiocinas/metabolismo , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Inflamação/tratamento farmacológico , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Fator 88 de Diferenciação Mieloide/genética , Fator 88 de Diferenciação Mieloide/metabolismo , NF-kappa B/genética , NF-kappa B/metabolismo , Neuroglia/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Fármacos Neuroprotetores/farmacologia , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Receptor 4 Toll-Like/genética , Receptor 4 Toll-Like/metabolismo
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