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871.
中小功率内燃机空气滤清器的应用现状 总被引:1,自引:0,他引:1
综述了与空气滤清器研究有关的文献,主要包括空气滤清器的原理,研究现状及发展趋势,并在此基础上提出未来一些课题的可能研究方向. 相似文献
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873.
介绍几年来彰武县玉米精量播种技术的推广应用情况,通过与传统播种方式田间对比试验,证明采用精量播种技术种植玉米具有节本增效、省时省工、增产增收的优势,并指出玉米机械精量播种技术实施过程中的关键环节。 相似文献
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AIM: To study the influence of basic fibroblast growth factor(bFGF) on treating ed palatal perforation in rats. METHODS: bFGF was given to the early palatal perforation in rat. The granulation tissues in perforations were grossly and pathologically obserVed. RESULTS: The the of wound healing was significantly in- crease in the bFGF group (P<0.01 ). bFGF could obviously promote the proliferation of the granulation tissues and fibroblasts. The number of AgNORs granules in fibrablasts were 3.73 ±0.52 in the buy group and 2.11 ±0.31 in control group (P < 0.05). CONCLUSION: bFGF could promote the growth of granulation tissues and had a strong promotion on the wound healing in palatal perforation. It was helpful in repairing palatal perforation. 相似文献
878.
AIM and METHODS: To observe the effects of glucose-free and Mg2+-free in the extracellular fluid on the changes of [Ca 2+]i in the cerebro-cortical neurons damaged by 1mmol/L glutamate using laser confocal scanning microscope. RESULTS: Both frequency and amplitude of neuronal calcium oscillation induced by glutamate were lowered in glucose-free and Mg2+-free buffers. The basic [Ca2+]i concentration was lowered in the former case , but it was elevated in the latter case. CONCLUSION: Mg2+-free aggravates [Ca2+]i overload induced by 1mmol/L glutamate ,under certain conditions the glucose-free might resist damage role of glutamate and Mg2+-free. 相似文献
879.
AIM:To determine the relationship between ischemia, hypoxia and the production of vascular endothelial growth factor in rat myocardium and its basic mechanism. METHODS:(1) 28 Wistar rats were randomly divided into 4 groups: group A, normal control;group B, 1 day's acute myocardial infarction;group C, 3 day's acute myocardial infarction;group D, 7 day's acute myocardial infarction. (2) Rat cardiac myocytes cultured were primarily divided into some groups, hypoxia incubated 24 hours; PMA groups, hypoxia incubated 24 hours with PKC activator (PMA), A 0 ng/mL; B 10 ng/mL; C 100 ng/mL; D 1 000 ng/mL; Chelerythrine groups, hypoxia incubated 24 hours with PKC inhibitor (chelerythrine), A 0 nmol/L; B 10 nmol/L. (3) By computer scanned and quantitated, vascular endothelial growth factor (VEGF) protein was detected with immunohistochemical technique. RESULTS:The longer time of ischemia and hypoxia was, the higher the VEGF production.The relat ionship was found between the time of ischemia or hypoxia and the production of VEGF.The product ion of VEGF protein was further promoted by PMA with different concentrat ion, decreased by chelerythrine.CONCLUSION: Ischemia or hypoxia strongly stimulated the production of VEGF in myocardium, which played an important role in autoprotecting of ischemic or hypoxic myocardium. Hypoxia-induced PKC activation is one kind of basic mechanisms in this course. 相似文献
880.
AIM To investigate the activation of related repair pathways after bupivacaine-induced neuronal DNA damage by cDNA gene screening. METHODS The bupivacaine-induced SH-SY5Y neuronal damage and DNA damage model was established. The technique of cDNA microplate array was used to screen the 21 important regulatory factors in the DNA damage repair pathway. Post-analysis of these differentially expressed repair genes for the repair pathway enrichment and distribution was performed. The data were analyzed by GraphPad Prism 6 statistical software to compare differences between groups. RESULTS The viability of SH-SY5Y cells treated with bupivacaine at different concentrations (detected by CCK-8 assay) showed that the IC50 value of bupivacaine was 1.5 mmol/L. The comet assay related index (the comet tail) was increased (P <0.05), the phosphorylation level of γH2AX protein was increased (P <0.05), indicating that DNA damage in the SH-SY5Y cells was significantly aggravated after bupivacaine treatment. The results of cDNA microplate assay showed that compared withcontrol group, the differentially expressed genes after bupivacaine treatment were DNA-PKcs , PTEN , NTH1 , RAD9 , CSB , GADD45 , XPD, XPC-HR23B and P53 . The analysis showed that these repair genes were mainly concentrated in the following 3 repair mechanisms: base excision repair, nucleotide excision repair, and non-homologous reconstitution. CONCLUSION The repair genes differentially expressed after neuronal DNA damage caused by local anesthetics are mainly concentrated in the pathways of non-homologous end-joining, base excision repair and nucleotide excision repair. 相似文献