用味精废液或造纸黑液生产有机肥时应注意的有关问题

介绍味精废液和造纸黑液的主要成分,用其生产有机肥的工艺过程、存在的问题及应注意的有关事项。     

An In Situ Assembled Trapping Gel Repairs Spinal Cord Injury by Capturing Glutamate and Free Calcium Ions

Spinal cord injury (SCI) can lead to devastating autonomic dysfunction. One of the most challenging issues for functional repair in SCI is the secondary damage caused by the increased release of glutamate and free Ca²⁺ from injured cells. Here, an in situ assembled trapping gel (PF-SA-GAD) is developed to sweep glutamate and Ca²⁺, promoting SCI repair. The hydrogel solution is a mixture of recombinant glutamate decarboxylase 67 (rGAD67) protein, sodium alginate (SA), and pluronic F-127 (PF-127). After intrathecal administration, temperature-sensitive PF-127 promoted in situ gelation. Glutamate (Glu) is captured and decarboxylated by rGAD67 into γ-aminobutyric acid (GABA). SA reacted with the free Ca²⁺ to generate gellable calcium alginate. Thereby, this in situ trapping gel retarded secondary neuron injury caused by Glu and free Ca²⁺ during SCI. In rat models of SCI, PF-SA-GAD reduces the lesion volume and inflammatory response after SCI, restores the motor function of rats with SCI. Together, the in situ assembled trapping gel is a long-term effective and minimally invasive sweeper for the direct elimination of glutamate and Ca²⁺ from injury lesions and can be a novel strategy for SCI repair by preventing secondary injury.     

Somatostatin,a Presynaptic Modulator of Glutamatergic Signal in the Central Nervous System

Somatostatin is widely diffused in the central nervous system, where it participates to control the efficiency of synaptic transmission. This peptide mainly colocalizes with GABA, in inhibitory, GABA-containing interneurons from which it is actively released in a Ca²⁺ dependent manner upon application of depolarizing stimuli. Once released in the synaptic cleft, somatostatin acts locally, or it diffuses in the extracellular space through “volume diffusion”, a mechanism(s) of distribution which mainly operates in the cerebrospinal fluid and that assures the progression of neuronal signalling from signal-secreting sender structures towards receptor-expressing targeted neurons located extrasynaptically, in a non-synaptic, inter-neuronal form of communication. Somatostatin controls the efficiency of central glutamate transmission by either modulating presynaptically the glutamate exocytosis or by metamodulating the activity of glutamate receptors colocalized and functionally coupled with somatostatin receptors in selected subpopulations of nerve terminals. Deciphering the role of somatostatin in the mechanisms of “volume diffusion” and in the “receptor-receptor interaction” unveils new perspectives in the central role of this fine tuner of synaptic strength, paving the road to new therapeutic approaches for the cure of central disorders.     

预排气UASB反应器处理味精废水

采用预排气UASB反应器在35℃下处理味精废水,通过预先排除床层产生的大部分气体控制污泥的上浮,使有机污染物的厌氧消化集中在床部完成,同时采取逐步驯化接种污泥和控制适宜的进水碱度等措施,可使厌氧微生物适应较高浓度的味精废水和毒性抑制物,反应器在高负荷下运行.反应器的水力停留时间为2 h～3 h,COD去除率可达70%～80%,COD容积负荷可达40 kg/(m3·d).     

有机溶剂透性化处理谷氨酸脱羧酶工程菌制备γ-氨基丁酸的研究

为了降低细胞壁和细胞膜的传质阻力对全细胞催化过程的不利影响,采用有机溶剂对表达重组谷氨酸脱羧酶(GAD)的工程菌BL21(DE3)-p ET28a-gad B进行了透性化处理。结果表明,菌体GAD表观催化活力的改善程度与有机溶剂的介电系数和疏水性具有较强相关性,低介电常数(6),高疏水性(log P0.68)的有机溶剂可以有效提高工程菌的GAD催化活性,其中最有效的透性化试剂为二甲苯(介电常数为2.4,log P为3.1)。当二甲苯的用量为5μL?mg?1(干重细胞)、处理时间5 min时,菌体表观催化活力达到最优值,为7.94 U?mg?1(干重细胞),是处理前表观催化活力的12.4倍。为了充分利用菌体的催化活力,采用海藻酸钙包埋的方法对二甲苯处理过的菌体进行固定化,结果发现固定化的透性化菌体可以较好地保持催化活力,反复催化10次后发现,第10次的GABA产率为第1次GABA产率的72.04%。研究为系统的选择有机溶剂来有效提高GAD工程菌表观催化活性提供了参考,同时制备的固定化的透性化菌体显示了良好工业应用前景。     

L-茶氨酸的合成研究

L 茶氨酸是绿茶的主要呈味成分 ,可由L 谷氨酸 γ 乙基酯 (Ⅰ)为原料 ,通过化学合成的方法得到。Ⅰ在吡啶溶液中与三苯基氯甲烷在 40℃下反应 48h ,接着与乙胺水溶液在室温下反应 48h ,再在乙酸水溶液中回流 5min脱去三苯甲基 ,得到L 茶氨酸 ,产率为 39% ,质量分数大于 98%     

Curcumin inhibits glutamate release from rat prefrontal nerve endings by affecting vesicle mobilization

Curcumin, one of the major constituents of Curcuma longa, has been shown to inhibit depolarization-evoked glutamate release from rat prefrontocortical nerve terminals by reducing voltage-dependent Ca(2+) entry. This study showed that curcumin inhibited ionomycin-induced glutamate release and KCl-evoked FM1-43 release, suggesting that some steps after Ca(2+) entry are regulated by curcumin. Furthermore, disrupting the cytoskeleton organization using cytochalasin D abolished the inhibitory action of curcumin on ionomycin-induced glutamate release. Mitogen-activated protein kinase kinase (MEK) inhibition also prevented the inhibitory effect of curcumin on ionomycin-induced glutamate release. Western blot analyses showed that curcumin decreased the ionomycin-induced phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and synaptic vesicle-associated protein synapsin I, the main presynaptic target of ERK. These results show that curcumin-mediated inhibition of glutamate release involves modulating downstream events by controlling synaptic vesicle recruitment and exocytosis, possibly through a decrease of MAPK/ERK activation and synapsin I phosphorylation, thereby decreasing synaptic vesicle availability for exocytosis.