蛋白诱剂在梨园橘小实蝇绿色防控中的应用效果

为研究针对梨园橘小实蝇有效的绿色防控方法,于2019年在广西灌阳开展了橘小实蝇蛋白诱剂田间应用试验。结果表明,应用橘小实蝇蛋白诱剂及其配套的桶形诱捕器,对橘小实蝇具有较好的诱捕效果,持续作用时间长,在采收后期防治效果为59.07%,优于对照常规防治,减少化学农药使用1次,有利于控制橘小实蝇为害,减少化学农药使用量。

海南杨桃园和莲雾园诱集桔小实蝇比较研究

2021年3—11月,在海南省白沙县杨桃园和莲雾园,针对桔小实蝇成虫,设置塞拉诺克诱芯(蛋白诱剂为主)诱捕器,塞拉诺克诱芯+桶形诱捕器,95%甲基丁香酚+桶形诱捕器,空白诱芯+桶形诱捕器,黄色粘板等5个诱集处理,比较不同诱集处理的成虫、雌雄成虫数量,分析桔小实蝇发生情况,筛选桔小实蝇有效诱控方法。结果表明,桔小实蝇在供试杨桃园和莲雾园均发生3代,杨桃园桔小实蝇成虫、雌雄成虫数均显著高于莲雾园(p<0.05)。杨桃园和莲雾园中不同诱集处理的成虫、雌雄成虫数存在显著或极显著(p<0.01)差异。不同诱集处理的雌成虫数从高到低依次为塞拉诺克诱芯+桶形诱捕器>塞拉诺克诱芯诱捕器或95%甲基丁香酚+桶形诱捕器>黄粘板>空白诱芯+桶形诱捕器。不同诱集处理的雄成虫数从高到低依次为95%甲基丁香酚+桶形诱捕器>塞拉诺克诱芯+桶形诱捕器>塞拉诺克诱芯诱捕器或黄粘板>空白诱芯+桶形诱捕器。塞拉诺克诱芯处理的雌成虫占比均较高,超过60%。说明塞拉诺克诱剂对桔小实蝇雌成虫诱集效果好,较安全,可在生产上推广应用。

不同浓度啤酒废酵母酶解蛋白与硼砂组合对橘小实蝇的捕杀效果

于阳桃园和番石榴园，田间测定了不同浓度啤酒废酵母酶解蛋白与硼砂组合对橘小实蝇的诱捕和诱杀效果。结果表明：在诱捕和诱杀试验中，随着蛋白浓度和硼砂浓度的增加，酶解蛋白硼砂组合对橘小实蝇的捕杀数量呈逐渐增加趋势，以25g／L蛋白、0．09moL／L硼砂组合最高。通过诱捕和诱杀试验确定啤酒废酵母酶解蛋白的最佳田间使用浓度为20～25g／L，硼砂的添加量为0．06～0．12mol／L。

7种啤酒废酵母酶解液挥发性成分对橘小实蝇的引诱作用

测试了啤酒废酵母酶解液7种挥发性成分(3-甲基-1-丁醇、苯甲醛、乙酸辛酯、乙酸苯乙酯、辛酸乙酯、苯乙腈和苯乙醇)及其混合物对不同发育期橘小实蝇的引诱效果.结果显示,乙酸辛酯、乙酸苯乙酯和辛酸乙酯对橘小实蝇雌雄成虫的引诱作用显著;利用正交试验方法得到200μL·m L-1乙酸辛酯、200μL·m L-1乙酸苯乙酯和100μL·m L-1辛酸乙酯的混合物对橘小实蝇的引诱效果最好,引诱率达到88.6%.

Experimental and in silico studies on three hydrophobic charge-induction adsorbents for porcine immunoglobulin purification

Three hydrophobic charge-induction adsorbents with functional ligands of 4-mercapto-ethyl-pyridine, 2-mercapto-methyl-imidazole or 2-mercapto-benzimidazole were evaluated in the purification of porcine immunoglobulin from porcine blood. Adsorption isotherms were studied under different pH conditions. The adsorbent with 2-mercapto-methyl-imidazole as the ligand showed reasonable adsorption capacity(43.60 mg·g^(-1)gel)with great selectivity and it also showed the best elution performance in chromatographic studies. A multi-pH step elution process was proposed for the 2-mercapto-methyl-imidazole adsorbent, and the results showed that high immunoglobulin purity(94.3%) and a yield of 9.8 mg·(ml plasma)^(-1) could be achieved under the optimal condition of loading(pH 5.0)–pre-elution(pH 7.0)–elution(pH 3.8). Moreover, molecular simulation was employed to help in analyzing the binding mechanism between the ligands and immunoglobulin, and the results showed that both 2-mercapto-benzimidazole and 2-mercapto-methyl-imidazole ligands were docked on the same pocket(around TYR319 and LEU309) of the Fc fragment of immunoglobulin, with 2-mercaptobenzimidazole showing stronger binding interactions.

Inhibition Mechanism of Hydroxyproline-like Small Inhibitors to Disorder HIF-VHL Interaction by Molecular Dynamic Simulations and Binding Free Energy Calculations

Protein-protein interactions are vital for a wide range of biological processes.The interactions between the hypoxia-inducible factor and von Hippel Lindau(VHL)are attractive drug targets for ischemic heart disease.In order to disrupt this interaction,the strategy to target VHL binding site using a hydroxyproline-like(pro-like)small molecule has been reported.In this study,we focused on the inhibition mechanism between the pro-like inhibitors and the VHL protein,which were investigated via molecular dynamics simulations and binding free energy calculations.It was found that pro-like inhibitors showed a strong binding affinity toward VHL.Binding free energy calculations and free energy decompositions suggested that the modification of various regions of pro-like inhibitors may provide useful information for future drug design.

Proteasomal degradation unleashes the pro-death activity of androgen receptor

Androgen receptor （AR） is able to promote stress-induced cell death independently of its transcription activity in androgen-independent prostate cancer cells. Yet, the underlying mechanism is incompletely understood. Here, we report that stress-induced proteasomal degradation of AR contributes to its pro-death activity. Upon exposure to ul- traviolet fight and staurosporine, AR underwent proteasomal degradation. Blockade of AR degradation significantly suppressed stress-induced apoptosis in androgen-independent prostate cancer cells. Ectopic expression of the AR N-terminal （AR-N） domain, which lacks DNA- and ligand-binding abilities, led to cell death without any additional death stimuli. Truncation analysis revealed that AR-N domain contains several sub-domains that regulate the pro- death activity of AR, specifically the first 105 amino acids, which function as a minimal pro-death domain acting upstream of caspases. The pro-apoptotic activity of AR N-terminal fragments was suppressed by ectopic expression of Bcl-2 or selected caspase inhibitors. Thus, our results reveal a novel mechanism by which AR promotes stressinduced cell death in androgen-independent prostate cancer cells.

Cellular processing determinants for the activation of damage signals in response to topoisomerase I-linked DNA breakage

Recent studies have suggested an involvement of processing pathways for the initiation of cellular responses induced by topoisomerase-targeting drugs. Here, we showed that cellular exposure to camptothecin （CPT） induced formation of topoisomerase I cleavable complex （TOPlcc）, degradation of TOP1 and activation of DNA damage responses （DDR）. Transcription and proteasome-dependent proteolysis, but not replication, were involved in CPTo indneed TOPl degradation, while none of above three processing activities affected TOPlcc formation. Replication- and transcription-initiated proeessing （RIP and TIP） of TOPlee were identified as two independent pathways, which contribute distinctly to various CPT-activated DDR. Specifically, in cycling cells, RIP-processed TOPlec triggered the CPT-induced RPA pbosphorylation. At higher CPT dosages, the TIP pathway is required for other DDR activation, including ATM, p53 and Chkl/2 phosphorylation. The TIP pathway was further demonstrated to be S-phase independent by using three nonreplicating cell models. Furthermore, the effect of proteasome inhibitors mimicked that of transcription inhibition on the CPT-induced activation of DDR, suggesting the involvement of proteasome in the TIP pathway. Interestingly, the TIP pathway was important for TOPlcc-activated, but not ionization radiationactivated ATM, p53 and Chk2 phosphorylation. We have also found that pharmacological interferences of TIP and RIP pathways distinctively modulated the CPT-induced cell killing with treatments at low and high dosages, respec- tively. Together, our results support that both RIP and TIP pathways of TOPlcc are required for the activation of CPT-induced DDR and cytotoxicity.

Changes of proteins induced by anticoagulants can be more sensitively detected in urine than in plasma

The most fundamental property of biomarkers is change.But changes are hard to maintain in plasma since it is strictly controlled by homeostatic mechanisms of the body.There is no homeostatic mechanism for urine.Besides,urine is partly a filtration of blood,and systematic information can be reflected in urine.We hypothesize that change of blood can be reflected in urine more sensitively.Here we introduce the interference into the blood by two anticoagulants heparin or argatroban.Plasma and urine proteins were profiled by LC-MS/MS and then validated by Western blot in totally six SD female rats before and after the drug treatments.In argatroban treated group,with exactly the same experimental procedure and the same cutoff value for both plasma and urine proteins,62 proteins changed in urine,only one of which changed in plasma.In heparin treated group,27 proteins changed in urine but only three other proteins changed in plasma.Both LC-MS/MS and Western blot analyses demonstrated drug-induced increases in transferrin and hemopexin levels in urine but not in plasma.Our data indicates that urine may serve as a source for more sensitive detection of protein biomarkers than plasma.