ABSTRACT
OBJECTIVE: To evaluate the academic level and influence of "Chinese Journal of Applied Physiology" through statistical analysis for the fund sponsored articles published in the recent ten years. METHODS: The articles of "Chinese Journal of Applied Physiology" from 1999 to 2008 were investigated. The number and the percentage of the fund sponsored articles, the fund organization and the author region were quantitatively analyzed by using the literature metrology method. RESULTS: The number of the fund sponsored articles increased unceasingly. The ratio of the fund from local government significantly enhanced in the latter five years. Most of the articles were from institutes located at Beijing, Zhejiang and Tianjin. CONCLUSION: "Chinese Journal of Applied Physiology" has a fine academic level and social influence.
Subject(s)
Bibliometrics , Periodicals as Topic/statistics & numerical data , Physiology , ChinaABSTRACT
The effects of quinacrine (QA) on heat-induced neuronal injury have been explored, with the intention of understanding the mechanisms of QA protection. Primary cultivated striatum neurons from newborn rats were treated with QA 1h before heat treatment at 43 degrees C which lasted for another 1h, and necrosis and apoptosis were detected by Annexin-V-FITC and propidium iodide (PI) double staining. Neuronal apoptosis was determined using terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) techniques. Cell membrane fluidity, activity of cytosolic phospholipase A(2) (cPLA(2)) and the level of arachidonic acid (AA) were also examined. Membrane surface ultrastructure of striatum neurons was investigated by atomic force microscopy (AFM). Results showed that heat treatment induced great striatum neurons death, with many dying neurons undergoing necrosis rather than apoptosis. QA alone had little effect on the survival of striatum neurons, while QA pretreatment before heat treatment decreased necrosis. Heat treatment also resulted in decreased membrane fluidity and increased cPLA(2) activity as well as arachidonic acid level; these effects were reversed by QA pretreatment. QA pretreatment also significantly prevented damage to the membrane surface ultrastructure of heat-treated neurons. These results suggest that QA protects striatum neurons against heat-induced neuronal necrosis, and also demonstrate that inhibition of cPLA(2) activity and stabilization of membranes may contribute to protective effect of quinacrine.
Subject(s)
Hot Temperature , Neurons/drug effects , Quinacrine/pharmacology , Animals , Animals, Newborn , Apoptosis , Arachidonic Acid/metabolism , Microscopy, Atomic Force , Necrosis , Neurons/physiology , Phospholipases A2/metabolism , Rats , Rats, WistarABSTRACT
AIM: To observe the expressional alterations of colony stimulating factor-1 receptor (CSF-1R) after ischemic injury of cerebral cortex, and study the function of colony stimulating factor-1 (CSF-1)/CSF-1R signal during the process of ischemic injury and repair of central nervous system (CNS). METHODS: We examined the distribution and expression of CSF-1R in normal brain tissues and ischemic brain tissues by immunohistology and Western blot analysis. RESULTS: The expression of CSF-1R in neurons could be up-regulated by ischemic injury in CNS. CONCLUSION: CSF-1/CSF-1R might take part in the process of ischemic injury and repair.
Subject(s)
Cerebral Cortex/blood supply , Macrophage Colony-Stimulating Factor/physiology , Receptor, Macrophage Colony-Stimulating Factor/metabolism , Reperfusion Injury/metabolism , Animals , Brain Ischemia/pathology , Brain Ischemia/physiopathology , Female , Male , Mice , Mice, Inbred BALB C , Neurons/metabolism , Random Allocation , Receptor, Macrophage Colony-Stimulating Factor/genetics , Receptor, Macrophage Colony-Stimulating Factor/physiology , Reperfusion Injury/physiopathologyABSTRACT
AIM: To study the protective effect of Quinacrine(QA) on rat striatum neurons from the injury caused by heat environment treatment, to probe the relationship between cell membrane injury and cellular injury protection, and to seek the possibility of QA as a preventive agent to heat injury. METHODS: Primary cultured striatum neurons from newborn rats were pretreated with QA at different concentration for 1 h, and then heat-treated at 43 degrees C for another 1 h. Cell necrosis was detected by Trypan blue staining, and apoptosis was evaluated through Activated Caspase-3 dye and TdT dye. RESULTS: Heat treatment effected the survival of striatum neurons and resulted in great number of cell death, which was mainly mediated by cell necrosis process. It was shown that treatment of QA itself had little effect on the survival of striatum neurons, while QA pretreatment decreased cellular necrosis caused by following heat treatment. CONCLUSION: QA protects striatum neurons from heat environment injury at about 20 pmol/L, and the protection may mediated by reduction of necrosis.
