木糖高效生物转化的新出路

木糖的高效利用是影响木质纤维资源生物炼制经济效益的关键因素之一,也是构建其工业化生产体系的必要前提,但是木糖生物转化面临着重要的技术瓶颈,必须寻求新的思路。基于对木糖利用的现状及产业发展的综合分析,提出了木糖高效发酵制取木糖酸的新出路,论述了本领域首要的科学和技术问题是发酵抑制物的控制与消除;针对抑制物的问题,提出了细胞生理生化、代谢流分析及分子生物学的多层次和多尺度解析的研究方法;在此基础上,基于系统论的观点提出了菌种选育、原料预处理、抑制物控制与脱除、木糖酸高效发酵的技术集成的研究思路。     

树干毕赤酵母和酿酒酵母混合糖发酵产乙醇

以树干毕赤酵母和酿酒酵母为发酵菌株,酸性蒸汽爆破玉米秸秆预水解液和纯糖模拟液为C源,采用固定化酵母细胞的方法,研究了酸爆玉米秸秆预水解液初始pH、N源种类及其浓度、3种发酵模式对树干毕赤酵母戊糖发酵的影响。结果表明:玉米秸秆预水解液适合发酵的初始pH范围为6.0～7.0;1.0 g/L的(NH4)2SO4作为N源,在40 g/L葡萄糖和25 g/L木糖培养基中发酵24 h,糖利用率达到99.47%,乙醇质量浓度为24.72 g/L,优于尿素和蛋白胨作为N源;3种模式的发酵体系中,以游离树干毕赤酵母和固定化酿酒酵母发酵性能最好,糖利用率和乙醇得率分别为99.43%和96.39%。     

利用反义RNA技术分析春化相关基因VER17在冬小麦花发育过程中的功能

为了研究小麦春化相关基因VER17的功能,应用反义RNA技术,将VER17基因的反义片段构建到载体pBI121上,通过花粉管通道法获取转基因小麦.对T0代转基因植株GUS染色以及PCR等分子鉴定,得到14株含反义VERJ7基因片段的阳性转基因植株.对T0代和T1代的表型观察结果显示,VER17反义转基因植株开花时间延迟,并且穗的顶部和基部小花出现明显的退化.表明春化相关基因VER17在小麦发育过程中可能起到促进植物开花以及穗顶端和基部花发育的作用,减少小花退化,同时对雄蕊的发育也有影响.     

研究生生物化学课程教学改革的尝试

针对化工和轻化工专业研究生生物化学的教学特点,从教学方法、教学内容和教学手段上进行了一些改革和尝试。     

佛坪自然保护区野生大熊猫交配行为的观察

On March 26 and 27, 2003, we observed six and five giant pandas assembled together respectively in Huodiba and Lijiagou districts of Sanguanmiao, Foping Nature Reserve, Shaanxi Province, China. The mating sites were located in the coniferous forest and mixed coniferous and deciduous forest, with steep slope and sparse shrubs and bamboos. Wind power was estimated over 3rd category in those two days. The competition and lighting among male pandas were observed, and the mating right with the female panda was mainly based on the hierarchical ordering. However, not all the winners during competition can be access to mating with the female panda. For wild giant panda, its mating system is maybe plastic, which perhaps is affected by environment, time and panda population itself. Cubs or sub-adults are observed oceurring at the mating site, which is considered to be linked with the learning of the reproductive behavior. Our results maybe provide a useful guideline to the management and breeding of giant pandas in the captivity.     

High IFN－α expression is associated with the induction of experimental autoimmune uveitis （EAU） in Fischer 344 rat

INTRODUCTIONThe CD4 T cells can be subdivided intoTh1 and Th2 subsets based on their secreted cy-tokine profile. Th1 cells characteristical1y secreteInterferonry (IFN--ry), whereas Th2 cells maiuly pro--duce IL--4[1]. IL-12 po1arizes the differentiation ofnaitre, CD4 T cells towards Th1 pathWay, in con-trast IL--4 directs T cell differentiation towards Th2pathWay The broken balance between Th1 and Th2immune responses and predominant Th1 responseare crucial factors in initiation…     

Cloning and characterization of a mouse liver-specific gene mfrep-1, upregulated in liver regeneration

Human fibrinogen-related protein-1/liver fibrinogen-related protein-1 (HFREP-1/LFIRE-1), a liver-specificprotein, is a member of fibrinogen superfamily that exerts various biological activities. However, the func-tion of HFREP-1/LFIRE-1 in liver remains unknown. Here we isolated its mouse ortholog gene-mousefibrinogen-related protein-1 (mfrep-1), which encoded 314 amino acids, exhibiting 80.4% similarity toHFREP-1/LFIRE-1. Northern blot analysis revealed that 1.2-kb mfrep-1 mRNA was detected selectivelyin mouse liver. To explore the function of MFREP-1, we examined the levels of mfrep-1 mRNA duringregeneration after 70% partial hepatectomy (PHx) in mice. mfrep-1 mRNA increased in the regeneratingliver and reached the first shoulder peak at 2-4 h after PHx. Cycloheximide pretreatment could suppress theinduction of mfrep-1, indicating the up-regulation of this gene need de novo protein synthesis. Its mRNAcontinued to elevate at 6 h thereafter and reached the second peak at 24 h. The enhanced expression ofmfrep-1 maintained high until 72 h and then declined slowly to the basal level. Immunohistochemistryassessment confirmed the up-regulated expression of MFREP-1 protein in parenchymal cells during liverregeneration. These data suggested that MFREP-1 might play an important role in liver regeneration andbe involved in the regulation of cell growth.     

Restoration of CD3+CD56+ cell level improves skin lesions in severe psoriasis: A pilot clinical study of adoptive immunotherapy for patients with psoriasis using autologous cytokine-induced killer cells

Psoriasis is a chronic inflammatory skin disorder mediated by the cells and molecules of both the innate and adaptive immune systems. Autologous cytokine-induced killer (CIK) cell infusion is considered an effective and safe cancer treatment and is licensed for this use in China. Accumulated evidence indicating that CD3⁺CD56⁺ cells are significantly decreased in psoriatic patients prompted us to investigate if the restoration of CD3⁺CD56⁺ cells may be beneficial for psoriatic patients. We designed a clinical trial for psoriasis treatment that involved CIK cell infusion because CIK cells include a large amount of CD3⁺CD56⁺ T cells (NCT01894373 at www.clinicaltrials.gov). Six patients with severe psoriasis were initially enrolled, and four of them exhibited markedly lower levels of CD3⁺CD56⁺ cells in their peripheral blood (PB) relative to healthy donors. CIK cell infusion-associated toxicity was not observed in any infusion. The percentage of CD3⁺CD56⁺ cells in the PB markedly increased and the psoriasis area and severity index (PASI) synchronously decreased in four patients with lower CD3⁺CD56⁺ cell contents, and two of them obtained a more than 4-month PASI75 after completing a four-cycle treatment. However, a decrease in the CD3⁺CD56⁺ cells was observed concomitantly with disease recurrence after short-term amelioration. In contrast, no obvious improvement was observed in the two patients with nearly normal CD3⁺CD56⁺ cells in the PB before treatment. These observations suggest that the normalization of the CD3⁺CD56⁺ cell level may improve the skin lesions of severe psoriasis and warrant further clinical trials for severe psoriasis using repeated CIK adoptive immunotherapy.     

兔脊髓α受体对血量扩张引起肾交感神经活动抑制和促钠排泄的作用

在窦主动脉去神经麻醉兔观察阻断脊髓α受体对血量扩张引起肾交感神经活动（RSNA）抑制和促钠排泄反应的影响。兔脊髓蛛网膜下腔注射a肾上腺素能受体阻断剂酚妥拉明与人工脑脊液后,血量扩张引起RSNA抑制分别为（－25．4±5．4）％与（－42．5±5.2）％（P＜0.05）;兔脊髓蛛网膜下腔注射α1受体阻断剂哌唑嗪与人工脑脊液后血量扩张引起RSNA抑制分别为（－29．3±6.1）％与（－42．5±5.2）％（P＜005）。结果表明,阻断脊髓α受体或α1受体均可减弱血量扩张引起RSNA抑制。脊髓注射哌唑嗪后血量扩张引起促钠排泄与利尿反应也显著减弱（P＜005）。