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Jiang, Xu,Ganesan, Palanivel,Rengarajan, Thamaraiselvan,Choi, Dong-Kug,Arulselvan, Palanisamy Elsevier 2018 BIOMEDICINE AND PHARMACOTHERAPY Vol.106 No.-
<P><B>Abstract</B></P> <P>Pathogenesis of Parkinson’s disease (PD) is undoubtedly a multifactorial phenomenon, with diverse etiological agents. Pro-inflammatory mediators act as a skew that directs disease progression during neurodegenerative diseases. Understanding the dynamics of inflammation and inflammatory mediators in preventing or reducing disease progression has recently gained much attention. Inflammatory neuro-degeneration is regulated via cytokines, chemokines, lipid mediators and immune cell subsets; however, individual cellular phenotypes in the Central Nervous System (CNS) acts in diverse ways whose persistent activation leads to unresolving inflammation often causing unfavorable outcomes in neurodegenerative disease like PD. Specifically, activation of cellular phenotypes like astrocytes, microglia, activation of peripheral immune cells requires different activation signals and agents like (cytokines, misfolded protein aggregates, infectious agents, pesticides like organophosphates, etc.,). However, what is unknown is how the different cellular phenotypes respond uniquely and the role of the factors they secrete alters the signal cascades in the complex neuron-microglial connections in the CNS. Hence, understanding the role of cellular phenotypes and the inflammatory mediators, the cross talk among the signals and their receptors can help us to identify the potential therapeutic target using natural products. In this review we have tried to put together the role of cellular phenotypes as a skew that favors PD progression and we have also discussed how the lack of experimental approaches and challenges that affects understanding the cellular targets that can be used against natural derivatives in alleviating PD pathophysiology. Together, this review will provide the better insights into the role of cellular phenotypes of neuroinflammation, inflammatory mediators and the orchestrating factors of inflammation and how they can be targeted in a more specific way that can be used in the clinical management of PD.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Distinct cellular Phenotypes acts uniquely in the pathogenesis of PD. </LI> <LI> Inflammation can be cause and consequence of PD pathogenesis. </LI> <LI> Flavonoids regulate multiple modulators of inflammation in mitigating PD pathology. </LI> <LI> Diverse intrinsic/extrinsic mediators converge together in glial activation in exacerbating PD pathology. </LI> </UL> </P>
BIOLOGICAL EFFECT OF INTRANASALLY INSTILLED TITANIUM DIOXIDE NANOPARTICLES ON FEMALE MICE
JIANGXUE WANG,YUFENG LI,WEI LI,BAI LI,YULIANG ZHAO,CHUNYING CHEN 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2008 NANO Vol.3 No.4
The toxicological effect of TiO2 nanoparticles with different crystal structure (80 nm for rutile and 155 nm for anatase) on female mice was investigated through intranasal instillation. After exposure for 30 days at the dose of 50 mg/kg body weight, no abnormal activity and mortality were observed with the normally increasing body weight of mice. The coefficients of tissues to body weight also show no obvious difference from the control except the increased coefficient of kidneys in mice exposed to 80 nm TiO2 nanoparticles. Titanium contents and histopathology examination indicate the no pathological response in the lung was induced by the increased TiO2 deposition, and the liver, heart, and spleen were not influenced. The severe pathology changes in kidneys suggest that TiO2 nanoparticles may be excreted out by kidneys via system circulation. However, the serum biochemical parameters were not changed compared with the control, whichmeans no obvious functional impairment induced by the nasal exposure for 30 days. In addition, the higher titanium contents in the brain tissues imply that the translocation and deposition of nanoparticles through intranasal instilling pathway is different from the other routes such as intratracheal inhalation or intratracheal instillation. The influence of deposited nanoparticles on central nervous system needs further investigation and is underway.
Spatial Spillover Effects of Transport Infrastructure in Chinese New Silk Road Economic Belt
Jian LI,Jiangxue WEN,Bao JIANG 국제이네비해양경제학회 2017 International Journal of e-Navigation and Maritime Vol.6 No.1
Based on the inner-effect mechanism of transport infrastructure and regional economic growth, this paper builds a specialized spatial weight matrix by utilizing the panel data from 31 provinces in New Silk Road Economic Belt (NSREB) and other areas from 2005 to 2014, and combines with the spatial panel model to analyze the spatial spillover effects of transport infrastructure. According to the analysis, the transport infrastructure plays an obvious lead role in regional economy growth alongside the NSREB, and the economic growth invigorates common development in surrounding regions. In addition, differences were observed among the different transport infrastructure with regard to their influences on regional economic development, as the highway transport affects regional economic growth to a larger degree than railway transport.
Miao Li,Shenfei Long,Qianqian Wang,Lianhua Zhang,Jiangxu Hu,Jie Yang,Zhibin Cheng,Xiang Shu Piao 아세아·태평양축산학회 2019 Animal Bioscience Vol.32 No.6
Objective: The objective of this study was to investigate effects of mixed organic acids (MOA) on nutrient digestibility, volatile fatty acids composition and intestinal microbiota in growing-finishing pigs fed high wheat bran diet. Methods: Six crossbred barrows (Duroc×Landrace×Yorkshire), with an average body weight 78.8±4.21 kg, fitted with T-cannulas at the distal ileum, were allotted to a double 3×3 Latin square design with 3 periods and 3 diets. Each period consisted of a 5-d adjustment period followed by a 2-d total collection of feces and then a 2-d collection of ileal digesta. The dietary treatments included a corn-soybean-wheat bran basal diet (CTR), mixed organic acid 1 diet (MOA1; CTR+3,000 mg/kg OA1), mixed organic acid 2 diet (MOA2; CTR+2,000 mg/kg OA2). Results: Pigs fed MOA (MOA1 or MOA2) showed improved (p<0.05) apparent total tract digestibility (ATTD) of gross energy, dry matter and organic matter, and pigs fed MOA2 had increased (p<0.05) ATTD of neutral detergent fiber compared to CTR. Dietary MOA supplementation decreased (p<0.05) pH value, and improved (p<0.01) concentrations of lactic acid and total volatile fatty acids (TVFA) in ileum compared to CTR. Pigs fed MOA showed higher (p<0.05) concentration of acetic acid, and lower (p<0.05) content of formic acid in feces compared to CTR. Pigs fed MOA1 had increased (p<0.05) concentration of TVFA and butyric acid in feces. Pigs fed MOA1 showed higher concentration of Lactobacillus and lower concentration of Escherichia in feces compared to CTR. Conclusion: Dietary supplementation of MOA 1 or 2 could improve nutrients digestibility, TVFA concentration and intestinal flora in growing-finishing pigs fed high fiber diet.