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In order to distinguish the research focus between different Library and Information Science (LIS) research institutions in China, we use the Keyword Activity Index (KAI) to identify their institution-specific keywords. The KAI, whose idea is borrowed from the Activity Index, measures whether an institution has alternatively comparative advantage in a particular topic according to its share in publications. In this study, a total of 65,653 papers from 19 core LIS journals in China during the period of 2000---2013 are collected. The top 8 most prolific LIS research institutions in China are selected for further investigation of the utility of KAI. Their institution-specific keywords are extracted based on the KAI values to represent their research focus and then clustered using co-word analysis; the research advantages of each institution are analyzed and compared according to these clusters. The reasons of their research advantages are analyzed based on their research function and research background.

This study aims to reveal the intellectual structure of Library and Information Science (LIS) in China during the period 2008---2012 utilizing co-word analysis. The status and trends of LIS in China are achieved by measuring the correlation coefficient of selected keywords extracted from relevant journals in the Chinese Journal Full-Text Database. In co-word analysis, multivariate statistical analysis and social network analysis are applied to obtain 13 clusters of keywords, a two-dimensional map, centrality and density of clusters, a strategic diagram and a relation network. Based on these results, the following conclusions can be drawn: (i) LIS in China has some established and well-developed research topics; (ii) a few emerging topics have a great potential for development; and (iii), the research topics in this LIS field are largely decentralized as a whole, where there are many marginal and immature topics.

This paper aims to reveal the relationship and structure of library and information science (LIS) journals in China. 24 core LIS journals in China are selected and the relevant data of journal co-citation are retrieved from Chinese Journal Full-Text Database constructed by China National Knowledge Infrastructure during the period of 1999---2009. By calculating mean co-citation frequencies and correlation coefficients, we find that there is a strong relationship among LIS journals in China. Utilizing the methods of cluster analysis, multidimensional scaling analysis and factor analysis, we analyze the data of journal co-citation. LIS journals in China are divided into four clusters. The relatedness among journals is shown manifestly through their locations in the two-dimensional map. A three-factor solution is obtained with the factor loading of each journal. Finally, we interpret and discuss the results to get some conclusions and also expect to describe the network characters of journal co-citation in future research.

L-glutamate plays a key role in neuronal cell death associated with many neurodegenerative conditions such as cerebral ischemia, hypoxia, Alzheimer's, Huntington's, and Parkinson's diseases. Selaginellin, a component extracted from Saussurea pulvinata (Hook.et Grev.) Maximo, was assessed for its ability to protect rat pheochromocytoma (PC12) cells against oxidative toxicity induced by glutamate. The differentiated PC12 cells were pretreated with various concentrations (10(-7), 3 x 10(-7), or 10(-6) M) of selaginellin for 1 h prior to exposure to L-glutamate. Selaginellin was shown to protect PC12 cells against glutamate toxicity, as determined by characteristic morphological features, lactate dehydrogenase release and cell viability, and apoptosis as evaluated by Hoechst 33342 staining assay and caspase-3 activity. In addition, the increase in levels of reactive oxygen species and decrease in klotho gene expression induced by glutamate were significantly reversed by selaginellin. Our study suggests that selaginellin has a neuroprotective effect against L-glutamate-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis via scavenging reactive oxygen species and up-regulating the expression of klotho gene.

Monocyte adhesion to activated vascular endothelial cells is the critical event in the initiation of atherosclerosis. Adhesion molecules are inflammatory markers, which are upregulated by oxidized low-density lipoprotein (ox-LDL) and play a pivotal role in atherogenesis. In present study, the effect of reinioside C, a major compound of Polygala fallax Hemsl., on adhesion of monocytes to endothelial cells induced by ox-LDL was investigated. The results showed that incubation of endothelial cells with ox-LDL (100 microg/mL) for 24 h markedly increased the expression of ICAM-1 and P-selectin and enhanced the adhesion of monocytes to endothelial cells. Pretreatment with reinioside C (1, 3, or 10 microM) dose-dependently decreased ox-LDL-induced upregulation of expression of ICAM-1 and P-selectin and the enhanced adhesion of monocytes to endothelial cells. To determine the role of NADPH oxidase/reactive oxygen species (ROS)/nuclear factor-kappaB (NF-kappaB) pathway, endothelial cells were treated with ox-LDL (100 microg/mL) for 2 h, and NADPH oxidase subunit (Nox 2 and p22phox) mRNA expression, intracellular ROS level, and NF-kappaB activity were measured. The results showed that reinioside C attenuated ox-LDL-induced NADPH oxidase subunit (Nox 2 and p22phox) mRNA expression, generation of ROS, and activation of NF-kappaB in endothelial cells in a dose-dependent manner; the two latter effects were inhibited by pyrollidine dithiocarbamate, the inhibitor of NF-kappaB. These findings suggest that reinioside C attenuates ox-LDL-induced expression of adhesion molecules (P-selectin and ICAM-1) and the adhesion of monocytes to endothelial cells by inhibiting NADPH oxidase/ROS/NF-kappaB pathway.

In the present study, we tested the protective effect of 3,4,5,6-tetrahydroxyxanthone, a synthetic xanthone derivative, on myocardial ischemia-reperfusion injury in rats. Ischemia-reperfusion injury was induced by 30 min of global ischemia and 30 min of reperfusion in isolated rat hearts or 30 min coronary artery occlusion and 120 min reperfusion in vivo, respectively. Heart rate, coronary flow (CF), left ventricular pressure (LVP), and its first derivative (+/- dp/dt (max)) were recorded, and the activity of creatine kinase in coronary effluent and tumor necrosis factor-alpha (TNF-alpha) content in myocardial tissues were measured in vitro. The activity of serum creatine kinase, the level of TNF-alpha and interleukin-6 (IL-6), and myocardial infarct size were measured in vivo. 3,4,5,6-tetrahydroxyxanthone (30, 100 or 300 microM) caused a significant improvement of cardiac function (LVP and +/- dp/dt (max)) and a decrease in the release of creatine kinase in coronary effluent as well as the level of TNF-alpha in myocardial tissues in vitro. 3,4,5,6-tetrahydroxyxanthone (0.5 or 1.0 mg/kg, i.v.) also markedly decreased infarct size and the release of creatine kinase and TNF-alpha, and increased serum IL-6 level in vivo. These results suggest that 3,4,5,6-tetrahydroxyxanthone possesses a protective effect on myocardial ischemia-reperfusion injury, and that the protective effects of 3,4,5,6-tetrahydroxyxanthone may be related to inhibition of TNF-alpha production and stimulation of IL-6 generation by inhibition of ROS production.

Previous investigations have indicated that the pharmacological effects of evodiamine, a major alkaloidal component of the dried, unripe fruit of Evodia rutaecarpa Bentham (Rutaceae), are associated with stimulation of calcitonin gene-related peptide (CGRP) release and CGRP prevents cardiac anaphylactic injury. In the present study, the protective effects of evodiamine on cardiac anaphylaxis were examined. Presensitized guinea-pig hearts challenged with specific antigen (bovine serum albumin) caused a marked decrease in coronary flow, left ventricular pressure and its derivatives (+/-dp/dt(max)), an increase in heart rate, and prolongation of P-R interval. Evodiamine (0.3 microM or 1 microM) markedly increased the content of CGRP in the coronary effluent concomitantly with a significant improvement of cardiac function and alleviation of the extension of P-R interval. Evodiamine at the concentration of 1 microM also inhibited the sinus tachycardia. The protective effect of evodiamine on cardiac anaphylaxis was abolished by CGRP(8-37), the selective CGRP receptor antagonist. These results suggest that evodiamine possesses a protective effect of cardiac anaphylactic injury and that the effect of evodiamine is related to stimulation of CGRP release.