1.Extraction and characterization of antifungal substances produced by antagonistic Streptomyces S24.
Qisheng ZHOU ; Ningning CAO ; Nianquan QIU ; Benfeng ZHANG ; Nan ZHANG ; Xunli LIU
Chinese Journal of Biotechnology 2010;26(3):350-356
Streptomyces S24 has broad spectrum resistance to the Aspergillus in food and feed, such as Aspergillus flavus, Aspergillus niger, Asperegillus alutacells and so on. We studied the adsorption and desorption properties of antifungal substance from Streptomyces S24 on macroporous resins, screened the best elution solution and also investigated some physical and chemical characters of antifungal substance by determining the antifugal activity using oxford plate assay system. According to the analysis results, AB-8 resin offered the best adsorption and desorption capacity for antifungal substance and its saturated absorption capacity was 7.0822 x 10(4) microg/g, the optimal elution solution was 85% acetone and the dynamic desorption rate could reach 93.82%. The antifungal substance was stable to heat and alkali, not sensitive to organic solvents, and sensitive to ultraviolet rays and acid. Based on its ultraviolet spectrometry, the antifungal substance was identified as heptaene macrolide antibiotic.
Adsorption
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Antifungal Agents
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chemistry
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isolation & purification
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pharmacology
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Aspergillus
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drug effects
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Aspergillus flavus
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drug effects
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Aspergillus niger
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drug effects
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Streptomyces
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chemistry
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metabolism
2.Medium optimization for antagonistic Streptomyces S24 and its inhibition on Aspergillus flavus.
Qisheng ZHOU ; Xunli LIU ; Nan ZHANG ; Zhen SONG ; Nianquan QIU ; Benfeng ZHANG ; Hui GUO ; Changxu LÜ ; Jian YU
Chinese Journal of Biotechnology 2011;27(2):203-211
Streptomyces S24 has broad spectrum against Aspergillus spp. in food and feed, such as Aspergillus flavus, Aspergillus niger and Asperegillus alutacells. The objective of this study was to improve the production of antifungal substances produced by S24 and to test their inhibitory effects on Aspergillus flavus. By using one-factor-at-a-time experiment and orthogonal design method, we optimized the fermentation medium. The composition of an optimized medium for the production of antifungal substances contained (g/L): starch soluble, 10; Glucose, 40; yeast extract, 8; soybean powder, 24; KH2PO4 4; and CaCO3 0.8. As a result, the productivity of antifungal substances could reach to 10 235.45 microg/mL, and this value was 2.81 times higher than that of initial medium before optimization. Additionally, inhibitory effects of the products on Aspergillus flavus were analyzed. Antagonistic tests indicated that the antifungal substances greatly inhibited mycelium growth and spores germination of Aspergillus flavus. We observed through microscope that the mycelia grew abnormally, such as contorting, bulging, vacuole increasing and the cytoplasmic contents inside effusing and the spores appeared unusual, such as gathering, deforming, cytoplasmic contents inside effusing and fracturing.
Adsorption
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Antifungal Agents
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chemistry
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isolation & purification
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pharmacology
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Aspergillus flavus
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drug effects
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growth & development
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Aspergillus niger
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drug effects
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growth & development
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Culture Media
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chemistry
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Food Contamination
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prevention & control
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Streptomyces
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chemistry
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growth & development
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metabolism
3.Restoration of FMRP expression in adult V1 neurons rescues visual deficits in a mouse model of fragile X syndrome.
Chaojuan YANG ; Yonglu TIAN ; Feng SU ; Yangzhen WANG ; Mengna LIU ; Hongyi WANG ; Yaxuan CUI ; Peijiang YUAN ; Xiangning LI ; Anan LI ; Hui GONG ; Qingming LUO ; Desheng ZHU ; Peng CAO ; Yunbo LIU ; Xunli WANG ; Min-Hua LUO ; Fuqiang XU ; Wei XIONG ; Liecheng WANG ; Xiang-Yao LI ; Chen ZHANG
Protein & Cell 2022;13(3):203-219
Many people affected by fragile X syndrome (FXS) and autism spectrum disorders have sensory processing deficits, such as hypersensitivity to auditory, tactile, and visual stimuli. Like FXS in humans, loss of Fmr1 in rodents also cause sensory, behavioral, and cognitive deficits. However, the neural mechanisms underlying sensory impairment, especially vision impairment, remain unclear. It remains elusive whether the visual processing deficits originate from corrupted inputs, impaired perception in the primary sensory cortex, or altered integration in the higher cortex, and there is no effective treatment. In this study, we used a genetic knockout mouse model (Fmr1KO), in vivo imaging, and behavioral measurements to show that the loss of Fmr1 impaired signal processing in the primary visual cortex (V1). Specifically, Fmr1KO mice showed enhanced responses to low-intensity stimuli but normal responses to high-intensity stimuli. This abnormality was accompanied by enhancements in local network connectivity in V1 microcircuits and increased dendritic complexity of V1 neurons. These effects were ameliorated by the acute application of GABAA receptor activators, which enhanced the activity of inhibitory neurons, or by reintroducing Fmr1 gene expression in knockout V1 neurons in both juvenile and young-adult mice. Overall, V1 plays an important role in the visual abnormalities of Fmr1KO mice and it could be possible to rescue the sensory disturbances in developed FXS and autism patients.
Animals
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Disease Models, Animal
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Fragile X Mental Retardation Protein/metabolism*
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Fragile X Syndrome/metabolism*
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Humans
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Mice
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Mice, Knockout
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Neurons/metabolism*