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31.
螺杆结构对棉籽粉双螺杆挤压脱毒效果的影响 总被引:3,自引:1,他引:3
利用自行开发的双螺杆食品挤机对棉籽粉做了挤压脱棉酚试验,分析了11种螺杆结构中的捏合盘元件对脱毒效果的影响。试验中含水量、螺杆转速、喂料率及试验区温度分别设定为50%(w.b.),180r/min,12kg/h及120-130℃。结果表明:捏合盘的加入能有效改善脱毒效果,螺杆结构不同效果也不同。捏合盘长度、位置及两者交互效应都是影响脱毒效果的显著因素,捏合盘间距的影响则不显著。试验结果还表明,本研究选择的工艺条件及设备参数在棉籽粉挤压脱棉酚方面是合适的。 相似文献
32.
1997~1998年,研究了上海地区黑带食蚜蝇的生活史和生活习性.室内条件下该蝇一年发生5代左右.以蛹和成虫越冬.在6月上旬至9月下旬,以蛹在土壤中越夏.气温在24℃时,完成一世代需28.83天,其中卵期1.77天,幼虫期5.24天,蛹期6.49天和成虫(产卵前期)15.33天.一世代的发育起点温度为8.23℃,有效积温为449.05日度.一天中成虫数量高峰发生在上午10时,中午以后数量就下降.室外的成虫在飞行中交配,历时约1秒钟.田间雌蝇比例占47.6%.室内卵平均孵化率为42.51%。室内用25%蔗糖水饲育,雌、雄成虫寿命分别为15.8天和12.5天.越冬期的成虫寿命可长达2个月左右.在整个幼虫发育期间,平均每头幼虫可吃萝卜蚜276.4或桃粉蚜328.4头. 相似文献
33.
CMV和TMV病毒的侵染导致密纹片姜产量降低,品质下降,通过茎尖脱毒培养和筛选获得脱毒苗并建立快繁体系,以提高产量,改善品质。茎尖接种培养基为MS 6-BA1.0 ̄3.0mg/L NAA0.1mg/L,丛生芽快繁培养基为MS 6-BA2.0 ̄4.0mg/L,生根培养基为1/2MS。经过一年多的研究和培养,获得大量脱毒苗并应用于生产。本方法也适用于黄姜类其它品种的脱毒和快速繁殖。 相似文献
34.
肖汉明 《湖南农业大学学报(自然科学版)》2001,(3)
从自然哲学的视角重新探讨了老子的道德论,认为在宇宙论范围内的道与德,其内涵与人论、社会论的道与德既有区别又有联系,不可一概而论。在宇宙论范围内,道是宇宙的潜在状态,德是宇宙的实现状态。由道向德的嬗变,便是宇宙的发生与演变。老子的宇宙论,是在三代礼教崩溃的基础上产生的,是一种囊为古老的自然哲学形态的宇宙论,与科学意义上的现代宇宙学不能混同看待。 相似文献
35.
麻竹不同地理种源的生物量及抗逆性差异研究 总被引:1,自引:0,他引:1
本文研究了福建省麻竹在试验区的不同地理种源的生物量及抗逆性变化情况,以检验麻竹不同地理种源的引种效果。结果表明:参试种源在两个试验点的竹林系统生物量的分配情况为漳州:永泰>永春>宁德>华安>飞鸾>南靖>程溪;永安:永春>永安>永泰>宁德>华安>飞鸾>漳州>南平。在耐寒性差异分析中可知,永安和漳州点种源的耐寒性存在差异,永安造林区各种冻害程度更明显。抗病性差异分析中可知,各种源的差异不明显。从保存率差异来看,麻竹各种源在不同的试点的适应性有差异。漳州点平均造林成活率比永安点多1倍,根据两试点的造林成活率及发笋情况,表现较好、性状稳定的种源为永春、宁德等种源。华安与永泰种源仅在漳州表现较好。 相似文献
36.
甘蓝型油菜生物素羧基载体蛋白基因的克隆与结构分析 总被引:5,自引:0,他引:5
【目的】生物素羧基载体蛋白负责将羧基从生物素羧化酶转移到羧基转移酶上,对于长链脂肪酸的从头合成与种子含油量的形成具有十分重要的作用。本研究的目的是从甘蓝型油菜品种基因组DNA中分离生物素羧基载体蛋白(BCCP)基因的全长编码区序列,通过生物信息学分析揭示该基因的结构特征(包括内含子的数量、长度与分布,蛋白质保守区疏水性特征等)和功能关系。【方法】基因克隆采取同源序列法进行。【结果】分离得到的bccp基因全长均为1 600 bp左右,根据其结构特点可以分成3种类型,它们均包含5个内含子。bccp1基因编码的蛋白质具备完整的生物素化功能结构域,是唯一功能完整的基因序列;bccp2和bccp3由于移码突变造成蛋白合成提前终止,翻译的蛋白质均缺少生物素化结构域。【结论】本研究首次从中国冬油菜品种中克隆获得bccp基因的全长序列并揭示了其序列特征,为进一步利用该基因开展含油量的基因调控研究提供了科学依据。 相似文献
37.
38.
Tomonori KAMEDA Hideyuki NAKASHIMA Takumi TAKIZAWA Fumihito MIURA Takashi ITO Kinichi NAKASHIMA Takuya IMAMURA 《The Journal of reproduction and development》2021,67(6):369
Post-mitotic neurons do exhibit DNA methylation changes, contrary to the longstanding belief that the epigenetic pattern in terminally differentiated cells is essentially unchanged. While the mechanism and physiological significance of DNA demethylation in neurons have been extensively elucidated, the occurrence of de novo DNA methylation and its impacts have been much less investigated. In the present study, we showed that neuronal activation induces de novo DNA methylation at enhancer regions, which can repress target genes in primary cultured hippocampal neurons. The functional significance of this de novo DNA methylation was underpinned by the demonstration that inhibition of DNA methyltransferase (DNMT) activity decreased neuronal activity-induced excitatory synaptogenesis. Overexpression of WW and C2 domain-containing 1 (Wwc1), a representative target gene of de novo DNA methylation, could phenocopy this DNMT inhibition-induced decrease in synaptogenesis. We found that both DNMT1 and DNMT3a were required for neuronal activity-induced de novo DNA methylation of the Wwc1 enhancer. Taken together, we concluded that neuronal activity-induced de novo DNA methylation that affects gene expression has an impact on neuronal physiology that is comparable to that of DNA demethylation. Since the different requirements of DNMTs for germ cell and embryonic development are known, our findings also have considerable implications for future studies on epigenomics in the field of reproductive biology. 相似文献
39.
40.
AIM: To investigate the genetic cause of 2 Chinese families with Marfan syndrome. METHODS: The clinical and laboratory investigations were performed in the 2 unrelated Chinese families. Family 1 had 1 patient with cardiac problem. Family 2 had 2 patients:one died, and the other with respiratory and cardiac problems. Next generation sequencing and Sanger sequencing in the Marfan syndrome causal gene FBN1 were performed in the patient, his unaffected sister and the parents of family 1. Sanger sequencing covering all the exons and intron-exon boundaries were performed in the patient and the parents in family 2. Bioinformatic analysis was engaged in the variations unravelled. Fifty healthy individuals were also investigated in the same manner. RESULTS: Both patients were diagnosed with Marfan syndrome. A novel mutation c.4685G>A(p.Cys1562Tyr) was detected in the patient of family 1 but was absent in his parents and the unaffected sister. This is a previously unreported novel mutation. In the mutation a conserved Cys was substituted by a Tyr in amino acid 1562 affecting a TGF-β binding domain and the secondary structure in the encoded protein. We also detected the mutation c.3706T>C(p.Cys1236Arg) in the patient of family 2. It was absent in the unaffected parents, and therefore was a de novo mutation too. This mutation has been previously reported and known to be associated with neonatal Marfan syndrome. Both mutations were absent in the 50 healthy controls. We also compared the genotype and phenotypes of the 2 families. CONCLUSION: We report 2 de novo mutations in 2 Chinese families with Marfan syndrome. One of the 2 mutations is novel. The phenotype of the mutation c.4685G>A(p.Cys1562Tyr) in family 1 is associated with classical Marfan syndrome, while that of c.3706T>C(p.Cys1236Arg) in family 2 is with neonatal type of Marfan syndrome. De novo mutations may be a cause for a proportion of mutations underlying the disease. The novel mutation also expends the mutational spectrum of the FBN1 gene. 相似文献