Problems and optimization of online book purchase recommendation system in academic library / 中华医学图书情报杂志

After the current studies, processes and types of online book purchase recommendation system in academic library were briefly described,its major problems at present were analyzed with suggestions put forward for its optimization, including improvement of its functions, establishment of its dynamic knowledge repository, improvement of its timeliness, enforcement of its electronic resources purchase and importance attached to its performance assessment.

Synthesis of pyrrolepyrazinones and study on their anti-inflammatory and analgesic activities / 中国药学杂志

OBJECTIVE: To study the structure-activity relationship (SAR) of pyrrolepyrazinones and search for novel nonsteroidal anti-inflammatory agents. METHODS: A series of pyrrolepyrazinone derivatives were synthesized. Their anti-inflammatory and analgesic activities were evaluated by xylene-induced ear edema and acetic acid-induced writhing in mice, respectively. RESULTS: Eleven new compounds were synthesized and confirmed by 1H-NMR and MS. Some of the target compounds showed anti-inflammatory and/or analgesic activities. CONCLUSION: Compound 14, which shows desirable anti-inflammatory activity and analgesic activity can be regarded as a valuable compound for further study.

The effects of autophagy on cell survival under different hypoxia / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the regulation of different hypoxia on cell survival and autophagy.</p><p><b>METHODS</b>PC12 cells were treated with different hypoxia. The cell survival was measured by MTT assay, expressions of LC3 and p62 were marked for autophagy detected by Western Blot, and the level of reactive oxygen species (ROS) was analyzed by flow cytometry.</p><p><b>RESULTS</b>The cell viability was different under different hypoxia: moderate hypoxia promoted cell viability, and severe hypoxia caused a decrease in cell viability; autophagy marker molecules, p62 and LC3-II expressions were different: moderate hypoxia increased p62 and LC3-II expressions, in contrast, severe hypoxia led to the decrease of p62 and LC3-II expressions; compared to normoxia, moderate hypoxia did not change the levels of ROS, while severe hypoxia increased the levels; 3-MA, the inhibitor of autophagy, elevated the levels of ROS in the three oxygen concentrations, additionally, the increased amplitudes in the moderate and severe hypoxia groups were higher than that in the normoxia group.</p><p><b>CONCLUSION</b>Moderate hypoxia promotes cell survival, severe hypoxia causes the cell death, and the autophagy activity may mediate the effects of different hypoxia.</p>

Effect of low glucose and/or hypoxia on the proliferation and metabolism of neural stem cells / 中国应用生理学杂志

<p><b>OBJECTIVE</b>Recent study demonstrated that hypoxia could regulate the proliferation and differentiation of neural stem cells in vitro. In the present study, effects of low glucose and/or hypoxia on the proliferation and metabolism of neural stem cells were investigated in vitro.</p><p><b>METHODS</b>The neural stem cells were isolated from the rat embryonic mesencephalon (E13.5), and exposed to different oxygen concentrations (low oxygen: 3% O2 or normoxia: 20% O2) and different glucose concentrations (high glucose concentration: 4.5 g/L and low glucose concentration: 1.4 g/L) for 3 days. The proliferation of neural stem cells were examined by CCK-8 assay. Furthermore, the content of glucose, lactate, and pyruvic acid in the medium were measured after cultured in different condition for 1, 3, 5 days.</p><p><b>RESULTS</b>Low oxygen and low glucose could increase the proliferation of neural stem cells respectively; in addition, the number of neurospheres under both low oxygen and glucose was the most among the four groups. The content of glucose and pyruvic acid in the medium from low oxygen or low glucose condition decreased, while the lactate concentration increased compared with the control group.</p><p><b>CONCLUSION</b>The results indicate the neural stem cells prefer grow under the low glucose and low oxygen condition, and that is mainly under going glycolysis to maintain its self-renew ability. This study may provide us a useful clue for application of neural stem cells transplantation.</p>

Extracellular signal-regulated kinase 1/2 is essential for the proliferation of neural stem cells derived from embryonic cortex / 生理学报

Extracellular signal-regulated kinase 1/2 (ERK1/2) pathway has been shown to be important for regulating cell proliferation and survival. The role of ERK1/2 signaling in the survival and growth of neural stem cells (NSCs) has not been addressed adequately. In this work, we aimed to provide evidence that proliferation of NSCs in vitro is controlled via ERK1/2-dependent pathway. NSCs were isolated from embryonic day 14.5 (E14.5) cortex of mouse forebrain. Cells were harvested at the desired times (1 d, 3 d and 5 d) and the total protein was extracted and analyzed by Western blot. It was observed that ERK1/2 was activated during the proliferation of NSCs. In addition, mitogen-activated protein kinase kinase (MEK) inhibitor PD98059, which directly prohibited ERK1/2 phosphorylation, inhibited the formation of neurospheres, and this inhibitory effect was dose-dependent. After treatment with 20 mumol/L PD98059, the growth of NSCs was also inhibited with time-dependence. These data indicate that ERK1/2 is essential for the proliferation of NSCs derived from mouse embryonic cortex.

Anti-hypoxia protective role of the effective component extracted from angelia injection / 中国应用生理学杂志

<p><b>AIM</b>To investigate anti-hypoxia protective roles of the effective component extracted from angelia injection using hypoxia injury model in mice and ECV304 cells separately.</p><p><b>METHODS</b>The survival time of mice was observed separately under normobaric and hypobaric hypoxia. The activity of ECV304 cells was tested by MTT assay, and the mortality rate was examined by Trypan blue exclusion assay to evaluate the pharmacodynamic effects.</p><p><b>RESULTS</b>After exposed to hypoxia the survival time of mice was increased in medicine groups,compared with the control groups (P < 0.05). The cell survival rate was decreased and the cell mortality rate was increased after cells were exposed to hypoxia,while the cell survival rate was significantly increased (P < 0.01), and the cell mortality rate was significantly decreased (P < 0.1) in the medicine groups compared with the control groups.</p><p><b>CONCLUSION</b>The effective component extracted from angelia injection can protect against the injury induced by hypoxia.</p>

Effects of hypoxia on the proliferation of embryonic stem cells / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effects of hypoxia on the proliferation of mouse embryonic stem cells (mouse ES cells) in vitro.</p><p><b>METHODS</b>We observed the proliferation of ES cells by hematometery and BrdU-labeled flow cytometry (FCM), and we also detected the expression of hypoxia inducible factor-1a (HIF-1a) by RT-PCR.</p><p><b>RESULTS</b>(1) The number of ES cells after culturing in the hypoxia environment (3% O2 and 10% O2) for 24 hours were lesser than those in normoxia (20% O2). (2) The number of ES cells significantly increased after intermittent hypoxia (3% O2) stimulus for 10 minutes per day for 4 days. (3) We also observed the relation between the expression of HIF-1a and the proliferation of ES cells by RT-PCR. The results showed that the expression of HIF-1a had no significant change after ES cells were culturing in hypoxia environment (3% O2 and 10% O2) for 24 hours or in intermittent hypoxia (3% O2 and 10% O2) for 4 days.</p><p><b>CONCLUSION</b>These results suggest that intermittent hypoxia (3% O2) can significantly promote the proliferation of ES cells in vitro, while persistent hypoxia inhibits those, and the mechanism of these should be addressed in further.</p>

Effect of CoCl2 pretreatment on Na + and K+ currents of the rat hippocampal neurons after acute hypoxia / 中国应用生理学杂志

<p><b>AIM</b>To study effect of CoCl2 pretreatment on the voltage-gated Na+ and K+ currents of the rat hippocampal neurons after acute hypoxia.</p><p><b>METHODS</b>Primarily cultured hippocampal neurons were divided into CoCl2 pretreated and non-pretreated groups. Patch clamp whole cell recording technique was used to examine Na+ and K+ currents of the hippocampal neurons.</p><p><b>RESULTS</b>After acute hypoxia, I(Na) and I(K) of the hippocampal neurons were significantly decreased and the threshold of I(Na) was right-shifted. Pretreatment of the neurons with CoCl2 inhibited the reduction of I(Na) and I(K).</p><p><b>CONCLUSION</b>CcCl2 pretreatment alleviates the acute hypoxia-induced changes of I(Na) and I(K), which may be one of the mechanisms for the protective effect of CoCl2 on neurons.</p>

Effects of oxygen-glucose deprivation on cultured rat hippocampal neurons / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effects of oxygen-glucose deprivation on cultured rat hippocampal neurons.</p><p><b>METHODS</b>The hippocampal neurons cultured for 12 d were exposed to combined oxygen-glucose deprivation for 0.5 - 4 h and then cultured with original medium in normoxia for 28 h. Necrotic neurons were identified by 0.4% trypan blue staining and apoptotic neurons were detected by a TUNEL technique. Meanwhile, the area, perimeter and circle diameter of cell bodies were measured respectively by a photography analysis system.</p><p><b>RESULTS</b>The percentage of necrotic cells in cultured hippocampal neurons increased significantly during oxygen-glucose deprivation, but the percentage of apoptotic cells increased significantly after 28 h oxygen-glucose recovery. Photography analysis showed that area, perimeter and circle diameter of the necrotic cell bodies were larger than those of the apoptotic ones.</p><p><b>CONCLUSION</b>Oxygen-glucose deprivation can lead to severe damage of cultured hippocampal neurons. The necrosis is major during acute oxygen-glucose deprivation, while the apoptosis is major 28 h after oxygen-glucose recovery.</p>

Establishment of the model of oxygen-glucose deprivation in vitro rat hippocampal neurons / 中国应用生理学杂志

<p><b>AIM</b>To establish the model of oxygen-glucose deprivation in vitro rat hippocampal neurons.</p><p><b>METHODS</b>The hippocampal neurons cultured for 12 d were exposed to combined oxygen-glucose deprivation for 0.5-4 h and then cultured with original medium in normoxia for 24 h. Auto-biochemical analyzer determined LDH activity. The change of neuronal morphology and neuron survival were observed by converted contrast microscope and assessed by photography analysis system. Neuron apoptosis was detected by using the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method.</p><p><b>RESULTS</b>The neurons swelled, LDH release increased and neuron survival decreased after gradually oxygen-glucose deprivation. The percentage of apoptosis increased obviously 24 h after recovering the supply of oxygen and glucose.</p><p><b>CONCLUSION</b>The model of oxygen-glucose deprivation in vitro rat hippocampal neurons is established successfully by using the modified ACSF (artificial cerebral spinal fluid) with serum and glucose free.</p>

Effects of hypoxic-preconditioning on anoxic-tolerance and Jun expression in cultured rat hippocampal neurons / 中国应用生理学杂志

<p><b>AIM</b>To study the effects of hypoxic preconditioning on anoxic tolerance and Jun expression in cultured rat hippocampal neurons after anoxia/reoxygenation.</p><p><b>METHODS</b>12 day cultured hippocampal neurons in control and hypoxic preconditioning group were exposed to anoxic environment (0.90L/L N2 + 0.10 L/L CO2) for 4 h, and then reoxygenated for either 24 h or 72 h. The neurons were immunocytochemically stained using the antiserum against Jun. The number of survival neurons and the percentage of Jun expressing neurons were investigated.</p><p><b>RESULTS</b>The percentage of Jun expressing neurons induced by anoxia in hypoxic-preconditioning group was significantly less than that in control group. The number of survival neurons was more in the hypoxic-preconditioning group than that in control group after anoxic reoxygenation.</p><p><b>CONCLUSION</b>Hypoxic-preconditioning can induce the development of anoxic-tolerance in cultured hippocampal neurons. The decrease in Jun expressing neurons in hippocampus may be an adaptive reaction to acute anoxia.</p>

Relationship between enhanced anoxic tolerance induced by hypoxic preconditioning and Na+, K+ currents in cultured hypothalamic cells / 中国应用生理学杂志

<p><b>AIM</b>To investigate the relationship between enhanced anoxic tolerance induced by hypoxic preconditioning and Na+, K+ currents.</p><p><b>METHODS</b>After hypoxic preconditioning and acute anoxia the I(Na), I(K) were measured in cultured hypothalamic cells by patch-clamp whole cell recording technique.</p><p><b>RESULTS</b>The amplification of Na+ currents did not been significantly changed, but the amplification of K+ currents was in hypoxic preconditioning neurons; acute anoxia lead to the inhibition of Na+, K+ currents in the two groups, while Na+, K+ currents in non-preconditioned control group were inhibited severity than hypoxic preconditioning group.</p><p><b>CONCLUSION</b>It is presumed enhanced anoxia tolerance induced by hypoxic preconditioning may be related to the opening of K+ channels.</p>

Effects of anoxia/reoxygenation on Fos and Jun expression and apoptosis in cultured rat hippocampal neurons / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effects of anoxia/reoxygenation on Fos and Jun expression and apoptosis in cultured rat hippocampal neurons.</p><p><b>METHODS</b>The hippocampal neurons cultured for 12 d were exposed to anoxia environment (90% N2 + 10% CO2) for 4 h and then reoxygenated for 24 h and 72 h. The neurons were immunocytochemically stained using the antiserum against Fos and Jun, and the apoptosis were detected by using the terminal deoxynucleotidyl transferase mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method and flow cytometric analysis.</p><p><b>RESULTS</b>The percentage of Fos and Jun positive neurons and apoptosis neurons in cultured hippocampal neurons after anoxia/reoxygenation increased than those in control.</p><p><b>CONCLUSION</b>The occurrence of neurons apoptosis is related to the increase in Fos and Jun expression in cultured hippocampal neurons after anoxia/reoxygenation.</p>

Effects of rhIL-6 on Bcl-2 and Bax expression and apoptosis after anoxia-reoxygenation in cultured rat hippocampal neurons / 生理学报

The purpose of the present study was to determine the effects of recombinant human interleukin-6 (rhIL-6) on the Bcl-2 and Bax expression and apoptosis after anoxia-reoxygenation in cultured rat hippocampal neurons. The control and rhIL-6 treated hippocampal neurons cultured for 12 d were exposed to anoxia environment (90% N2+10% CO2) for 2 and 4 h and then were reoxygenated for 24 and 72 h. The expression of Bcl-2 and Bax was revealed immunocytochemically using the antiserum against Bcl-2 and Bax. The apoptosis was examined by the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method and flow cytometric analysis. The results showed that in cultured hippocampal neurons the Bcl-2 expression decreased while Bax expression and the percentage of apoptotic neurons increased after anoxia-reoxygenation compared with those before anoxia. In comparison with the control, after anoxia-reoxygenation the Bcl-2 expression in hippocampal neurons was higher than that in rhIL-6 group; however the Bax expression and the percentage of the apoptosis were decreased in rhIL-6 group. It is suggested that rhIL-6 may play a role in protecting neurons from the damage induced by anoxia-reoxygenation.