导电材料强化微生物直接种间电子传递产甲烷的研究进展

厌氧条件下,微生物可以通过厌氧代谢产生甲烷(CH_4),由此衍生的厌氧消化技术可实现能源的回收利用。产CH_4的关键步骤是刺激发酵细菌和产甲烷古菌之间的有效电子转移,电活性微生物可以取代传统的氢/甲酸盐实现直接种间电子传递,其电子传递效率更高。添加导电材料可以促进直接种间电子传递并提高CH_4产率,是一种更有效的强化电子传递方式。本文在梳理直接种间电子传递发展和机理的基础上,综述了常见的促进直接种间电子传递的碳基和铁基导电材料,对其结构特征、电子传递机理、强化产CH_4和中间产物消耗等方面进行了系统总结。旨在为导电材料促进直接种间电子传递的研究提供参考,并探讨了未来可能的研究方向。     

产大米蛋白水解酶的菌株筛选、酶学性质及制备大米寡肽

【目的】旨在分离、筛选并鉴定具有大米蛋白降解作用的菌株及其关键蛋白酶,为高效制备大米寡肽提供制备酶及最优制备条件。【方法】以"水解圈"为评价指标,从粮食仓库附近土壤筛选获得具有降解大米蛋白能力的菌株;通过16S rRNA序列分析确定菌株归属;利用单因素实验获得最佳氮源并初步分析酶学性质;利用HPLC检测寡肽得率,并对制备条件进一步优化。【结果】经鉴定具有大米蛋白降解作用的菌株为沙雷氏菌(Serratia sp. JWG-D15),以大米蛋白为氮源培养菌株JWG-D15,蛋白酶So PRO产量最高,其最适温度40℃,最适pH 8.0;在加酶量20 U/mg,大米蛋白浓度40 mg/mL,40℃,4 h条件下寡肽得率最高72.38%。【结论】以大米蛋白为氮源培养菌株JWG-D15,蛋白酶So PRO产量最高;蛋白酶So PRO制得的大米寡肽,其得率是目前行业最高。本研究既丰富了大米寡肽的制备用酶的种类,又为深入大米寡肽产业化提供一定理论基础。     

A new fast algorithm for solving the minimum spanning tree problem based on DNA molecules computation

The minimum spanning tree (MST) problem is to find minimum edge connected subsets containing all the vertex of a given undirected graph. It is a vitally important NP-complete problem in graph theory and applied mathematics, having numerous real life applications. Moreover in previous studies, DNA molecular operations usually were used to solve NP-complete head-to-tail path search problems, rarely for NP-hard problems with multi-lateral path solutions result, such as the minimum spanning tree problem. In this paper, we present a new fast DNA algorithm for solving the MST problem using DNA molecular operations. For an undirected graph with n vertex and m edges, we reasonably design flexible length DNA strands representing the vertex and edges, take appropriate steps and get the solutions of the MST problem in proper length range and O(3m + n) time complexity. We extend the application of DNA molecular operations and simultaneity simplify the complexity of the computation. Results of computer simulative experiments show that the proposed method updates some of the best known values with very short time and that the proposed method provides a better performance with solution accuracy over existing algorithms.     

CCL2 increases αvβ3 integrin expression and subsequently promotes prostate cancer migration

Background

Chemokine ligand 2 (CCL2), also known as monocyte chemoattractant protein-1 (MCP-1), belongs to the CC chemokine family which is associated with the disease status and outcomes of cancers. Prostate cancer is the most commonly diagnosed malignancy in men and shows a predilection for metastasis to the bone. However, the effect of CCL2 on human prostate cancer cells is largely unknown. The aim of this study was to examine the role of CCL2 in integrin expression and migratory activity in prostate cancers.

Methods

Prostate cancer migration was examined using Transwell, wound healing, and invasion assay. The PKCδ and c-Src phosphorylations were examined by using western blotting. The qPCR was used to examine the mRNA expression of integrins. A transient transfection protocol was used to examine AP-1 activity.

Results

Stimulation of prostate cancer cell lines (PC3, DU145, and LNCaP) induced migration and expression of integrin αvβ3. Treatment of cells with αvβ3 antibody or siRNA abolished CCL2-increased cell migration. CCL2-increased migration and integrin expression were diminished by CCR2 but not by CCR4 inhibitors, suggesting that the CCR2 receptor is involved in CCL2-promoted prostate cancer migration. CCL2 activated a signal transduction pathway that includes PKCδ, c-Src, and AP-1. Reagents that inhibit specific components of this pathway each diminished the ability of CCL2 to effect cell migration and integrin expression.

Conclusions

Interaction between CCL2 and CCR2 enhances migration of prostate cancer cells through an increase in αvβ3 integrin production.

General significance

CCL2 is a critical factor of prostate cancer metastasis.     

High glucose induces vascular endothelial growth factor production in human synovial fibroblasts through reactive oxygen species generation

Background

Diabetes is an independent risk factor of osteoarthritis (OA). Angiogenesis is essential for the progression of OA. Here, we investigated the intracellular signaling pathways involved in high glucose (HG)-induced vascular endothelial growth factor (VEGF) expression in human synovial fibroblast cells.

Methods

HG-mediated VEGF expression was assessed with qPCR and ELISA. The mechanisms of action of HG in different signaling pathways were studied using Western blotting. Knockdown of proteins was achieved by transfection with siRNA. Chromatin immunoprecipitation assays were used to study in vivo binding of c-Jun to the VEGF promoter.

Results

Stimulation of OA synovial fibroblasts (OASF) with HG induced concentration- and time-dependent increases in VEGF expression. Treatment of OASF with HG increased reactive oxygen species (ROS) generation. Pretreatment with NADPH oxidase inhibitor (APO or DPI), ROS scavenger (NAC), PI3K inhibitor (Ly294002 or wortmannin), Akt inhibitor, or AP-1 inhibitor (curcumin or tanshinone IIA) blocked the HG-induced VEGF production. HG also increased PI3K and Akt activation. Treatment of OASF with HG increased the accumulation of phosphorylated c-Jun in the nucleus, AP-1-luciferase activity, and c-Jun binding to the AP-1 element on the VEGF promoter.

Conclusions

Our results suggest that the HG increases VEGF expression in human synovial fibroblasts via the ROS, PI3K, Akt, c-Jun and AP-1 signaling pathway.

General significance

We link high glucose on VEGF expression in osteoarthritis.     

Honokiol: A non-adipogenic PPARγ agonist from nature

Background

Peroxisome proliferator-activated receptor gamma (PPARγ) agonists are clinically used to counteract hyperglycemia. However, so far experienced unwanted side effects, such as weight gain, promote the search for new PPARγ activators.

Methods

We used a combination of in silico, in vitro, cell-based and in vivo models to identify and validate natural products as promising leads for partial novel PPARγ agonists.

Results

The natural product honokiol from the traditional Chinese herbal drug Magnolia bark was in silico predicted to bind into the PPARγ ligand binding pocket as dimer. Honokiol indeed directly bound to purified PPARγ ligand-binding domain (LBD) and acted as partial agonist in a PPARγ-mediated luciferase reporter assay. Honokiol was then directly compared to the clinically used full agonist pioglitazone with regard to stimulation of glucose uptake in adipocytes as well as adipogenic differentiation in 3T3-L1 pre-adipocytes and mouse embryonic fibroblasts. While honokiol stimulated basal glucose uptake to a similar extent as pioglitazone, it did not induce adipogenesis in contrast to pioglitazone. In diabetic KKAy mice oral application of honokiol prevented hyperglycemia and suppressed weight gain.

Conclusion

We identified honokiol as a partial non-adipogenic PPARγ agonist in vitro which prevented hyperglycemia and weight gain in vivo.

General significance

This observed activity profile suggests honokiol as promising new pharmaceutical lead or dietary supplement to combat metabolic disease, and provides a molecular explanation for the use of Magnolia in traditional medicine.