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Exogenous application of salicylic acid (SA) reduces storage rots in a number of postharvest crops. SA's ability to protect sugarbeet (Beta vulgaris L.) taproots from common storage rot pathogens, however, is unknown. To determine the potential of SA to reduce storage losses caused by three common causal organisms of sugarbeet storage rot, freshly harvested roots were treated with 0.01, 0.1, 1.0 or 10 mM SA, inoculated with Botrytis cinerea, Penicillium claviforme, or Phoma betae, and evaluated for the severity of rot symptoms after incubation at 20 °C and 90% relative humidity. Roots were obtained from plants that received sufficient water or were water-stressed prior to harvest. Roots from water-stressed plants were included since water-stress increases sugarbeet root susceptibility to storage rot and SA mitigates drought effects in other plant species. SA at concentrations of 0.01–10 mM had no effect on the severity of storage rot caused by B. cinerea, P. claviforme, or P. betae in roots from plants that received sufficient water prior to harvest. However, SA at these same concentrations reduced the severity of rot symptoms for all three pathogens in roots from plants that were water stressed before harvest. For water-stressed roots, all concentrations of SA produced statistically equivalent reductions in the weight of rotted tissue for each pathogen, and on average, SA reduced rot severity due to B. cinerea, P. claviforme, and P. betae by 54, 45, and 58%, respectively. SA reduced rot from all three pathogens by reducing lesion size, but did not affect the incidence of infection. The ability of SA to reduce rot severity in water-stressed roots, but not in roots that received sufficient water before harvest suggests that SA alleviated the negative impact of water stress but did not directly protect sugarbeet roots against storage rots. 相似文献
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黄云战 《云南农业大学学报(自然科学版)》2000,15(4):349-352
对活塞销冲孔连皮在通用钻床上夹紧钻孔时的夹紧力、切削力进行初步分析计算,提出活塞销因钻削轴向力和扭矩的作用而产生滑移的原因,为合理设计专机选择可靠夹紧装置提供依据。 相似文献
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介绍了菲亚特轮式拖拉机拨叉加工中重点工序的夹具设计方法、夹具结构特点和使用原理,并提出了在设计该夹具时应注意的技术问题。 相似文献
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金针菇与凤尾菇科间原生质体融合研究 总被引：30，自引：5，他引：25
金针菇与凤尾菇皆属四极生异宗结合食用菌,其双核异核体菌株都具有锁关联合遗传标记本研究以金针菇和凤尾菇的双核异核菌株为亲本,将热灭活的凤尾菇原生质体,以ＰＥＧ为融合剂,在高下,高ＰＨ值条件下,与金针菇原生质体融合,结果从１３２９个再生菌株中选择出６株双亲细胞质和细胞核都融合的无锁状联合菌株,经融合核分裂技术处理后,融合核分裂成为具有锁状联合的双核菌株。 相似文献
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M.A. de Laat C.K. Clement C.M. McGowan M.N. Sillence C.C. Pollitt V.A. Lacombe 《Veterinary immunology and immunopathology》2014,157(1-2):78-86
Equine laminitis, a disease of the lamellar structure of the horse's hoof, can be incited by numerous factors that include inflammatory and metabolic aetiologies. However, the role of inflammation in hyperinsulinaemic laminitis has not been adequately defined. Toll-like receptor (TLR) activation results in up-regulation of inflammatory pathways and the release of pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α), and may be a pathogenic factor in laminitis. The aim of this study was to determine whether TLR4 expression and subsequent pro-inflammatory cytokine production is increased in lamellae and skeletal muscle during equine hyperinsulinaemia. Standardbred horses were treated with either a prolonged, euglycaemic hyperinsulinaemic clamp (p-EHC) or a prolonged, glucose infusion (p-GI), which induced marked and moderate hyperinsulinaemia, respectively. Age-matched control horses were treated simultaneously with a balanced electrolyte solution. Treated horses developed clinical (p-EHC) or subclinical (p-GI) laminitis, whereas controls did not. Skeletal muscle and lamellar protein extracts were analysed by Western blotting for TLR4, IL-6, TNF-α and suppressor of cytokine signalling 3 (SOCS3) expression. Lamellar protein expression of TLR4 and TNF-α, but not IL-6, was increased by the p-EHC, compared to control horses. A significant positive correlation was found between lamellar TLR4 and SOCS3. Skeletal muscle protein expression of TLR4 signalling parameters did not differ between control and p-EHC-treated horses. Similarly, the p-GI did not result in up-regulation of lamellar protein expression of any parameter. The results suggest that insulin-sensitive tissues may not accurately reflect lamellar pathology during hyperinsulinaemia. While TLR4 is present in the lamellae, its activation appears unlikely to contribute significantly to the developmental pathogenesis of hyperinsulinaemic laminitis. However, inflammation may have a role to play in the later stages (e.g., repair or remodelling) of the disease. 相似文献