试论环境地貌学的性质和应用

本文对环境地貌学的产生、学科性质、研究方法及果应用作了初步探讨、认为,随着人类改造自然的能力不断增长,地貌(?)环境意义急剧加大,环境地貌学也应运而生,它以统一的整体、环境观,把地貌作为人-地环境要素之一,对地貌的环境意义作理论探讨与实际应用.它运用传统的常规方法和新技术、新思想进行研究,其成果以各种地(?)图件和设计方案投入生产建设和环境整治.城市地貌研究集中体现了环境地貌学特点     

红霉素发酵过程前期参数相关分析及调控

对红霉素发酵过程前期调控策略进行了研究,从宏观代谢流的变化着手,对表征细胞代谢特征的参数进行了相关分析,对发酵前期的摄氧率(OUR)、二氧化碳释放率(CER)及呼吸商(RQ)相关变化及红霉素发酵前期CER与pH的变化进行了分析,确定了合适的调控方式,在工业规模发酵罐上通过控制发酵过程前期补糖速率等措施,使发酵平均水平从原来的4500u／mL提高到了6000u／mL。     

对苯二甲酸中微量杂质HPLC分析条件的优化

用离子交换高效液相色谱法分析对苯二甲酸中的微量杂质,并对该方法进行了系统的优化。通过选择流动相pH值使缓冲溶液的浓度降低至0．13mol／L,分析周期缩短至10min以下。结果表明：该方法的工作曲线相关系数在0．9998以上,回收率为98．7％～102．2％,相对标准偏差小于3．6％。     

A novel 72-kDa leukocyte-derived osteoglycin enhances the activation of toll-like receptor 4 and exacerbates cardiac inflammation during viral myocarditis

Background

Viral myocarditis can severely damage the myocardium through excessive infiltration of immune cells. Osteoglycin (OGN) is part of the small leucine-rich repeat proteoglycan (SLRP) family. SLRP’s may affect inflammatory and fibrotic processes, but the implication of OGN in cardiac inflammation and the resulting injury upon viral myocarditis is unknown.

Methods and results

This study uncovered a previously unidentified 72-kDa variant of OGN that is predominant in cardiac human and mouse samples of viral myocarditis. Its absence in mice significantly decreased cardiac inflammation and injury in Coxsackievirus-B3-induced myocarditis. It also delayed mortality in lipopolysaccharide-induced endotoxemia going along with a reduced systemic production of pro-inflammatory cytokines. This 72-kDa OGN is expressed in the cell membrane of circulating and resident cardiac macrophages and neutrophils. Co-immunoprecipitation and OGN siRNA experiments revealed that this 72-kDa variant activates the toll-like receptor-4 (TLR4) with a concomitant increase in IL-6, TNF-α, IL-1β, and IL-12 expression. This immune cell activation by OGN occurred via MyD88 and increased phosphorylation of c-jun. Finally, the 72-kDa chondroitin sulfate is the result of O-linked glycosylation of the 32-kDa protein core of OGN. In contrast, the 34-kDa dermatan sulfate-OGN, involved in collagen cross linking, was also the result of O-linked glycosylation.

Conclusion

The current study discovered a novel 72-kDa chondroitin sulfate-OGN that is specific for innate immune cells. This variant is able to bind and activate TLR4. The absence of OGN decreases cytokine production by both circulating and cardiac leukocytes upon (systemic) LPS exposure, and reduces cardiac inflammation and injury in viral myocarditis.

     

Substrate binding and catalytic mechanism of class B β-lactamases: a molecular modelling study

Increased resistance to β-lactam antibiotics is mainly due to β-lactamases whose production by pathogenic bacteria makes their broad activity spectrum especially frightening. X-ray structures of several zinc β-lactamases have revealed the coordination of the two metal ions, but their mode of action remains unclear. Geometry optimisation of stable complexes along the reaction pathway of benzylpenicillin hydrolysis highlighted a proton shuttle occurring from D120 of the Bacillus cereus β-lactamase to the β-lactam nitrogen via Zn2 which is central to the network. First, the Zn1 ion has a structural role maintaining Zn-bound waters, WAT1 and WAT2, either directly or through the Zn1 tetrahedrally coordinated histidine ligands. The Zn2 ion has a more catalytic role, stabilising the tetrahedral intermediate, accepting the β-lactam nitrogen atom as a ligand. The role of Zn2 and the flexibility in the coordination geometry of both Zn ions is of crucial importance for catalysis. Received 14 August 2001; received after revision 19 October 2001; accepted 30 October 2001     

Distribution of the blood flow supplied by the vertebral artery in rats: Anatomical,functional and pharmacological aspects

In rats, the vertebral artery makes only a minor contribution to the blood perfusion of the ponto-medullary area. This was measured with radioactive microspheres and was confirmed by methylmetacrylate casts and local injection of a centrally acting hypotensive drug.     

罗丹明B分子印迹聚合物的分子识别与结合特性的研究

以罗丹明 B为印迹分子 ,丙烯酰胺为功能单体 ,乙二醇二甲基丙烯酸酯为交联剂 ,制备了对罗丹明 B有较好选择性的印迹聚合物 .利用静态平衡结合法和 Scatchard分析法研究了此印迹聚合物的结合能力和选择性 ,结果表明 ,以丙烯酰胺为功能单体的印迹聚合物中形成了两类不同的结合位点 ,计算了离解常数分别为 1 .87×1 0 - 5和 4.2 4× 1 0 - 4mol/L.对比罗丹明 S和罗丹明 6G的结合特性 ,该印迹聚合物呈现了较好的选择性     

几种水文序列变异点诊断方法的性能比较

分别在正态分布和t分布假设下,通过改变样本容量、自由度、变异值、变点位置等参数用模拟试验的方法比较分析了3种常用的水文序列变异点检验方法的检验性能.结果表明,Pettitt检验法对于端点位置的均值变点具有最好的检验效果,BrownForsythe检验法适合小样本数据,秩和检验无明显优势.最后用这3种方法分析了西宁市1951年至2000年3月份的月均降水量序列,发现在1977年存在一个变异点.     

Redox-dependent thiol modifications: implications for the release of extracellular vesicles

Extracellular vesicles (EVs), including microvesicles and exosomes, are emerging as important regulators of homeostasis and pathophysiology. During pro-inflammatory and pro-oxidant conditions, EV release is induced. As EVs released under such conditions often exert pro-inflammatory and procoagulant effects, they may actively promote the pathogenesis of chronic diseases. There is evidence that thiol group-containing antioxidants can prevent EV induction by pro-inflammatory and oxidative stimuli, likely by protecting protein thiols of the EV-secreting cells from oxidation. As the redox state of protein thiols greatly impacts three-dimensional protein structure and, consequently, function, redox modifications of protein thiols may directly modulate EV release in response to changes in the cell’s redox environment. In this review article, we discuss targets of redox-dependent thiol modifications that are known or expected to be involved in the regulation of EV release, namely redox-sensitive calcium channels, N-ethylmaleimide sensitive factor, protein disulfide isomerase, phospholipid flippases, actin filaments, calpains and cell surface-exposed thiols. Thiol protection is proposed as a strategy for preventing detrimental changes in EV signaling in response to inflammation and oxidative stress. Identification of the thiol-containing proteins that modulate EV release in pro-oxidant environments could provide a rationale for broad application of thiol group-containing antioxidants in chronic inflammatory diseases.