连作对丹参生长的障碍效应

通过对1～4年不同连作年限地块丹参生长发育情况进行的连续调查分析,结果表明,连作严重危害丹参生长,主要表现在6～9月,丹参生长期的枯苗率大幅度上升,地上、地下部生长量下降,根系数量、直径和长度减小,产世降低。同时由于有效成分含量降低,根系外观畸形,造成商品率下降,从而影响丹参质量。通过对土壤pH测定发现．丹参连作障碍可能与土壤酸性增加有关。     

Polymorphism of ORM1 Is Associated with the Pharmacokinetics of Telmisartan

Background

The pharmacokinetics (PKs) and pharmacodynamics (PDs) of telmisartan varies among the individuals, and the main causes remain unknown. The aim of this study was to evaluate the impact of ORM1, as well as ABCC2, ABCB1, ABCG2 and SLCO1B3 polymorphisms, on the disposition of the drug and BP change after taking 40 mg telmisartan in 48 healthy Chinese males.

Method

A total of 48 healthy males were included in this trial. Every volunteer ingested a single dose of 40 mg telmisartan, and the plasma drug concentration and blood pressure (BP) were measured up to 48 h.

Result

In this study, the area under the plasma concentration-time curve (AUC) in the heterozygotes of ORM1 113AG was higher than that in the wild-type homozygotes, AUC_(0–48) (113AA vs. 113AG, 1,549.18±859.84 ng·h/ml vs. 2,313.54±1,257.71 ng·h/ml, P = 0.033), AUC_(0–∞) (113AA vs. 113AG, 1,753.13±1,060.60 ng·h/ml vs. 2,686.90±1,401.87 ng·h/ml, P = 0.016), and the change(%) of the diastolic blood pressure (DBP) from the baseline BP value also showed a significant difference between the ORM1 113AG and 113AA genotypes at 5 h after taking telmisartan (P = 0.026). This study also showed that the allele of ABCC2 C3972T would affected the disposition of telmsiartan and the DBP change significantly after taking the drug. However, the common SNPs of ABCG2 C421, ABCB1 C3435T, and SLCO1B3 T334G showed no impacts on the PKs of telmisartan or BP change(%) in our trial.

Conclusion

The ORM1 A113G polymorphism was associated with the PKs variability after taking telmsiartan, as well as ABCC2 C3972T. The heterozygotes of ORM1 113AG showed a larger AUC and a notable BP change(%) from the baseline compared with the wild-type.

Trial Registration

Chinese Clinical Trial Registry ChiCTR-TNC-10000898     

苹果园光能截获率的数学模型

应用气象学原理推导了不同纬度、不同栽植行向、不同树形的苹果园光能截获率的数学模型,给出在保证树冠基部外围日照时间大于25％总日照时间的条件下,生长季中充分截获光能的最佳树形、行距、冠高、冠径的优化组合方案。实例分析表明,计算结果与专家经验基本一致。本研究为果园合理栽植,充分利用光能,合理整形修剪提供理论依据与参考方案。     

采石场废弃地的早期植被与土壤种子库

调查了广州市白云山地区一个弃置 2 a的大型采石场的排土场、采石坑以及原用作破碎加工石料和成品贮运的平台等的土壤种子库和自然植被。这些废弃地的基质毫无结构 ,质地亦极端 ,排土场 60 %的颗粒直径小于 1 mm,碎石平台则主要由散落的碎石、石粉组成 ,粒径大于 5 mm占 5 0 %以上。3种类型废弃地的养分元素含量都很低 ,水溶性氮和磷含量分别为 0 .74～ 1 .43mg· kg- 1和 0 .0 32～ 0 .0 5 3mg· kg- 1。 3种废弃地在植被自然发生的程度及土壤种子库种子含量上也差异很大。排土场表面极不稳定 ,大大小小水蚀沟分布其上 ,水蚀和水土流失严重 ,基本上没有植物定居 ,土壤种子库接近零 (所有样品只检测到两种植物各 1株幼苗 ,换算成种子库的大小约当 33粒· m- 2 ) ;采石坑废弃地的自然植被较好 ,发展成以湿生植物为主的郁闭草地 ,边坡较为干旱而以禾草类为主 ,盖度亦达 1 0 0 % ,水环境的多样性促进了植物种类的多样性 ,计有 1 3科 30属 31种植物 ,土壤种子库的种子含量为 1 93± 46粒·m- 2 ,有 6个种 ;碎石贮运平台废弃地由于经车辆的反复辗压 ,表面异常坚实 ,废弃后早期只有在周边较疏松处及偶然出现的裂缝中有植物生长 ,总植被盖度小于 1 0 % ,种类也较少 ,只有 4科 9属 9种 ,然而其土壤种子库却是最     

草鱼呼肠孤病毒RNA聚合酶基因的表达与产物纯化

草鱼呼肠孤病毒是引起草鱼出血病的主要病原,隶属于呼肠孤病毒科水生呼肠孤病毒属.序列分析表明,GCRV S2 片段长为3 877核苷酸,编码一个分子量为138kDa 的蛋白VP2,具有RNA聚合酶性质.为进一步了解该病毒 RNA聚合酶特性,本研究在对GCRV RNA聚合酶基因(GCRV-RdRp)保守区(约1.5kb)重组质粒pR/RRp高效表达的基础上,分别构建了编码GCRV RNA聚合酶保守区N端与C端部分基因的 pR/RRpN及pR/RRpC重组表达载体,并在原核细胞中获得成功表达.筛选的重组表达菌株经IPTG诱导培养,得到分子量分别为98kDa、103kDa的目的表达融合蛋白.Western blot分析表明,该表达产物与兔抗GCRV-VP2血清呈阳性反应.通过ProBond柱亲和层析,纯化了融合有6个组氨酸的重组表达产物,并获得约90%纯的目的蛋白.上述结果为GCRV RNA聚合酶特性分析提供了依据.     

川西亚高山云杉人工林土壤质量性状演变

通过对川西亚高山云杉人工林不同演替阶段土壤肥力质量性状的研究 ,结果表明 ,人工云杉林土壤肥力退化与土壤有机质有关 ,在人工云杉林地中 ,随着抚育林龄的增加 ,土壤全 N、碱解 N、全 P、腐殖质、HA、FA、CEC、EB、微生物总数、细菌及真菌数量随有机质的减少而降低 ,土壤最大持水量、毛管持水量及总孔隙和毛管孔隙则先减少 ,之后随着云杉自疏而有上升的趋势 ,毛管持水量是决定林地自然含水量的主要因子。土壤 K素和酶活性变化较复杂 ,钾素主要与土壤母质有关 ,酶活性主要与林地微生态环境有关。土壤综合肥力评价表明 ,土壤综合肥力指标 (IFI)从人工云杉幼林向成熟林演替时 ,先迅速下降 ,之后随云杉自疏而缓慢上升 ,表现出非正“U”型的变化。解决当前人工成熟云杉林土壤退化的主要措施应因地制宜地进行间伐或轮伐 ,改善林地的微生态条件 ,尽量避免营造针叶纯林 ,建议营造针阔混交林。     

CGRP is essential for protection against alveolar epithelial cell necroptosis by activating the AMPK/L-OPA1 signaling pathway during acute lung injury

Alveolar epithelial cell (AEC) necroptosis is critical to disrupt the alveolar barrier and provoke acute lung injury (ALI). Here, we define calcitonin gene-related peptide (CGRP), the most abundant endogenous neuropeptide in the lung, as a novel modulator of AEC necroptosis in lipopolysaccharide (LPS)-induced ALI. Upon LPS-induced ALI, overexpression of Cgrp significantly mitigates the inflammatory response, alleviates lung tissue damage, and decreases AEC necroptosis. Similarly, CGRP alleviated AEC necroptosis under the LPS challenge in vitro. Previously, we identified that long optic atrophy 1 (L-OPA1) deficiency mediates mitochondrial fragmentation, leading to AEC necroptosis. In this study, we discovered that CGRP positively regulated mitochondrial fusion through stabilizing L-OPA1. Mechanistically, we elucidate that CGRP activates AMP-activated protein kinase (AMPK). Furthermore, the blockade of AMPK compromised the protective effect of CGRP against AEC necroptosis following the LPS challenge. Our study suggests that CRGP-mediated activation of the AMPK/L-OPA1 axis may have potent therapeutic benefits for patients with ALI or other diseases with necroptosis.