食用菌多糖的研究

食用菌多糖具有独特的生理特性和极高的药用价值,已成为当前药物研发的热点。从食用菌多糖的化学结构、提取分离、药用价值和应用等几个方面对其进行了全面的总结和展望。     

线艺建兰的组织培养和快速繁殖(简报)

以线艺建兰茎尖、腋芽为外植体,接种在1/2MS 6-BA 3.0mg/L NAA 0.3mg/L培养基上形成原球茎,原球茎在1/2MS 6-BA 0.1mg/L NAA 1.0mg/L培养基上可大量增殖,并伸长生长形成丛生型根状茎;根状茎在MS 6-BA 2.0mg/L PP333 1.0mg/L NAA 0.5mg/L培养基上可分化成小苗,分化率达46.3%;小苗在MS IBA 1.0mg/L GA 0.5mg/L 香蕉泥100g/L的培养基上生根壮苗,生根率达100%.     

Ergot alkaloids — Sources, structures and analytical methods

Natural sources,i.e. fungal strains and species producing ergot alkaloids (EA), are surveyed together with the chemical structures of EA and a list of new natural EA discovered in the last three decades. Other topics include new efficient chromatographic methods (HPLC) for the separation and isolation of new natural EA and also immunological methods of EA detection.     

Gas chromatographie determination of extracellular metabolites produced by baker’s yeast during glucose-induced acidification

Gas chromatographic separation of metabolites extruded during the medium acidification by resting baker’s yeast supplied with glucose is described. Silylation with bis(trimethylsilyl)trifluoroacetamide and trimethylchlorosilane and a direct chromatography on Chromosorb G-AW-DMCS with 2.5 % SE-52 in a programmed temperature interval of 80–220 °C (3 °C/min) made it possible to separate organic acids (lactic, pyruvic, succinic, glyceric, fumaric, malic), polyols (glycerol, arabinitol) and sugars (glucose). The yeast was found to extrude glycerol, lactic, malic, and succinic acid.     

吡咯喹啉醌合成及生产工艺研究进展

吡咯喹啉醌(pyrroloquinoline quinone, PQQ)是继烟酰胺和核黄素之后发现的第三类氧化还原酶辅因子,普遍存在于生物体中参与呼吸链电子传递,具有促进线粒体产生、清除自由基、增强细胞代谢和预防心肌损伤等生理功能,在医药、食品和农业领域具有广泛的应用前景。微生物发酵法是PQQ生产的主要方式,解析PQQ生物合成途径及其调控机制,通过代谢工程选育短周期、高产量的生产菌是PQQ工业化的研究方向之一。本文综述了PQQ的合成途径、高产菌株选育以及微生物发酵生产与分离纯化的研发工作,为深入阐释PQQ的生物合成机制和工业化生产菌株的选育提供参考。     

The FTD‐like syndrome causing TREM2 T66M mutation impairs microglia function,brain perfusion,and glucose metabolism

Genetic variants in the triggering receptor expressed on myeloid cells 2 (TREM2) increase the risk for several neurodegenerative diseases including Alzheimer's disease and frontotemporal dementia (FTD). Homozygous TREM2 missense mutations, such as p.T66M, lead to the FTD‐like syndrome, but how they cause pathology is unknown. Using CRISPR/Cas9 genome editing, we generated a knock‐in mouse model for the disease‐associated Trem2 p.T66M mutation. Consistent with a loss‐of‐function mutation, we observe an intracellular accumulation of immature mutant Trem2 and reduced generation of soluble Trem2 similar to patients with the homozygous p.T66M mutation. Trem2 p.T66M knock‐in mice show delayed resolution of inflammation upon in vivo lipopolysaccharide stimulation and cultured macrophages display significantly reduced phagocytic activity. Immunohistochemistry together with in vivo TSPO small animal positron emission tomography (μPET) demonstrates an age‐dependent reduction in microglial activity. Surprisingly, perfusion magnetic resonance imaging and FDG‐μPET imaging reveal a significant reduction in cerebral blood flow and brain glucose metabolism. Thus, we demonstrate that a TREM2 loss‐of‐function mutation causes brain‐wide metabolic alterations pointing toward a possible function of microglia in regulating brain glucose metabolism.