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61.
在相同条件下,从稻田直接收集的病粒中的稻粒黑粉病菌厚垣孢子不能萌发,而取之于仓库中的孢子能萌发。为探明其制约因素,对该病菌进行了光照和浸水时间试验。研究结果表明:稻粒黑粉病菌冬孢子形成后,必须经光照射后,方可进入休眠期;度过5~6个月休眠期的冬孢子,必须浸水48h以上才开始复苏;复苏后的冬孢子必须在光照条件下才能萌发。未完成后熟作用的冬孢子和完成后熟但尚未复苏的冬孢子即使在光照条件下也不能萌发。即稻粒黑粉病菌冬孢子必须经历后熟、休眠、复苏三个阶段后,在适宜的光照与温湿条件下,方可萌发。光照对其冬孢子具有双重作用,促使后熟进入休眠和刺激萌发。 相似文献
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盐池半荒漠风沙区土地沙漠化发生发展规律的研究 总被引:1,自引:0,他引:1
本文耐盐池半荒漠风沙区土地沙漠化发生发展规律进行了探讨,主要分析了在土地沙漠化的过程中土壤和植被的变化过程及其成因。 相似文献
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AIM: To explore interaction and biological behaviour changes of two kinds of cells-blastocysts and hepatocarcinoma cells in the same microenvironment. METHODS:The models of mouse blastocysts co-cultured with human hepatocarcinoma cell lines were established, then biological behaviours and mutual effects of the two kinds of cells in co-culture system were observed. RESULTS: Compared with control group, hepatocarcinoma cells with differently invasive and metastatic potential significantly enhanced the rates of blastocyst hatchment , attachment and outgrowth(P<0.05). There was no significant difference in those among hepatocarcinoma cells co-cultured groups (P>0.05). The blastocyst hatched and attached to hepatocarcinoma cells with differently invasive and metastatic potential. Then, differential trophoblasts invaded hepatocarcinoma cells. The clear-cut interfaces were gradually formed between both sides. Hepatocarcinoma cells on interface showed changes of growth direction and cell shapes and did not invade blastocysts. CONCLUSIONS: Hepatocarcinoma cells promoted blastocyst development. Blastocysts implanted and invaded hepatocarcinoma cells with differently invasive and metastatic potential in vitro, which indicate that blastocyst implantation in vitro does not relate with the kinds and differential level of interactional cells and the low selectivity maybe relate with high adaptability of early life. 相似文献
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AIM: To investigate the role of nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC) and protein kinase C (PKC) signaling in tumor necrosis factor-α (TNF-α)-induced cardioprotection against hypoxia/reoxygenation (H/R) injury. METHODS: Neonatal rat ventricular myocytes were pretreated with TNF-α or sodium nitroprusside (SNP) or L-arginine (L-Arg), respectively, for 12 h and then subjected to continuous hypoxia for 12 h, followed by reoxygenation for 6 h. The manganese superoxide dismutase (Mn-SOD) activity of the cells was measured after H/R. Myocyte injury was determined by the release of lactic dehydrogenase (LDH). RESULTS: TNF-α (105 U/L) significantly increased the Mn-SOD activity and decreased release of LDH from ventricular myocytes. The cardioprotection against H/R injury was induced by the pretreatment with SNP (5 μmol/L) or L-Arg (5 mmol/L), which was blocked by ODQ (10 μmol/L), the specific sGC inhibitor, and Chel (5 μmol/L), the specific PKC inhibitor. Pretreatment with L-NAME (100 μmol/L), ODQ, Chel, antoxidant 2-MPG (400 μmol/L) or tyrosine kinase inhibitor genistein (50 μmol/L) attenuated the increased Mn-SOD activity and reduced LDH level induced by TNF-α. CONCLUSION: The results suggest that NO may play a role in TNF-α-induced cardioprotection, which is mediated by sGC and PKC. 相似文献