多花黄精总蛋白质提取工艺优化

对多花黄精主根与须根总蛋白质的提取工艺进行了研究.在对料液比、离心转速、NaCl溶液的浓度等进行单因素试验的基础上,通过正交试验确定了多花黄精主根与须根总蛋白质提取的最佳工艺条件,即对多花黄精主根蛋白质的提取最佳条件为料液比1:15、NaCl浓度0.10mol/L、转速为2500r/min;须根蛋白的提取最佳条件为料液比1:15、NaCl浓度0.20 mol/L、转速为4500r/min.在相同的提取条件下,多花黄精主根与须根的蛋白质得率差异显著.须根中蛋白质的含量与主根的差异性不显著,须根的利用价值也很高,有待于进一步开发利用.     

水分胁迫下不同油松种源SOD、POD、MDA及可溶性蛋白比较研究

采用盆栽控水试验方法,设置正常水分（T1,田间持水量的70%~80%）、轻度胁迫（T2,田间持水量的50%~60%）和严重胁迫（T3,田间持水量的30%~40%）3个水分梯度,对6个油松Pinus tabulaeformis Carr.种源幼苗（陕西洛南LN,陕西桥山QO,山西灵空山LK,山西芦芽山LY,河北雾灵山WL和辽宁千山QN）的保护酶参数进行了分析。结果表明,在T3下,各种源的可溶性蛋白质含量、超氧化物歧化酶（SOD）活性、过氧化物酶（POD）活性和丙二醛（MDA）含量差异均极显著（P〈0.01）;LK种源的可溶性蛋白质含量显著高于其它种源,种源LK、WL和LN依靠提高可溶性蛋白质含量来调节细胞渗透势以抵抗干旱胁迫的能力较强;种源QN和QO的SOD活性达到最大,它们通过增加SOD活性来清除O2.-用以抵抗膜脂过氧化的能力较强。整个水分处理过程中,种源LN和LY的POD活性均较高,而QN的POD活性较低,LN和LY通过增加POD活性分解H2O2对细胞破坏的能力较强;各油松种源的膜脂质过氧化程度在T3下均有所降低。     

You are What You Eat: Meat, Novel Protein Foods, and Consumptive Freedom

Animal husbandry has been accused ofmaltreating animals, polluting the environment, and soon. These accusations were thought to be answered whenthe Dutch research program ``Sustainable TechnologicalDevelopment' (STD) suggested a government-initiatedconversion from meat to novel protein foods (NPFs).STD reasoned that if consumers converted from meat toNPFs, non-sustainable animal husbandry would no longerbe needed. Whereas STD only worried about how toconstruct NPFs with a meat bite, this paper drawsattention to the presumed, but problematic, role forthe government in the execution of the STDsuggestions. Although vegetarians take the credo ``YouAre What You Eat' literally and accuse non-vegetariansof being beasts, a different interpretation is morepromising: eating meat has become a leading thread inmany lifestyles and narratives of self-identity. Sincethe freedom to follow your own lifestyle orconsumptive preferences is a core value incontemporary affluent societies, governmentintervention in the formation and satisfaction ofconsumer preferences for meat dishes is a precariousissue. Hence, NPFs might be interesting for a smallfraction of society, but we had better not expect toomuch from a government-initiated conversion from meatto NPFs as the answer to animal husbandry'sproblems.     

15株微藻对猪场养殖污水中氮磷的净化及其细胞营养分析

在实验室条件下调查了15株淡水微藻在猪场养殖污水中的生长性能、细胞组成及各微藻对污水中氮磷的去除效果.结果表明:15株微藻均可有效降低猪场养殖污水中的氮磷含量,但不同藻株对污水中不同形态氮的去除效果差异明显.多棘栅藻(Scenedesmus spinosus)SHOUF7、多棘栅藻(S.spinosus)SHOU-F8和四尾栅藻(S.quadricanda)SHOU-F35去除总氮效果最佳.多棘栅藻SHOU-F7、多棘栅藻SHOU-F8和斜生栅藻(S.obliquus)SHOU-F21去除硝态氮效果最好,最大去除率可达到100%.椭圆小球藻(Chlorella ellipsoidea)SHOU-F3、单生卵囊藻(Oocystis solitaria)SHOU-F5和四球藻(Tetrachlorella alternans)SHOU-F24去除氨态氮效果最好,最大去除率为97.82%.各株微藻对污水中总磷的去除率均很高,可达91.00%以上.利用猪场养殖污水培养的各株微藻细胞蛋白含量及脂肪酸组成差异显著,蛋白含量最高的为椭圆小球藻(Ch.ellipsoidea)SHOU-F3(43.90%),含量最低的为多棘栅藻SHOU-F8(23.87%);16∶0和18∶3n3在各株微藻中含量均较丰富.多棘栅藻SHOU-F7、多棘栅藻SHOU-F8、淡水小球藻(Chlorella sp.)SHOU-F19和针形纤维藻(A.acicularis)SHOU-F120的脂肪酸甲酯的理论烷基值超过47.因此,多棘栅藻SHOU-F7、多棘栅藻SHOU-F8和四尾栅藻SHOU-F35是净化猪场养殖污水的优良藻株,其中,多棘栅藻SHOU-F8是猪场养殖污水净化耦合微藻生物柴油生产的合适藻株.     

不同季节大气可吸入颗粒物(PM_(10))诱导小鼠原代培养神经元炎性及其级联损伤效应

为了探讨不同季节可吸入颗粒物(PM10)对神经元的损伤效应,本研究通过建立小鼠大脑皮层原代神经元体外染毒模型,考察了不同季节PM10对炎性因子诱导型一氧化氮合酶(iNOS)、环氧化酶-2(COX-2)和黏附分子(ICAM-1)表达水平的影响,并探讨了与之耦联的磷酸化Ca2+/钙调蛋白依赖性蛋白激酶Ⅱα(p-Ca MKⅡα)、环磷腺苷效应元件结合蛋白(p-CREB)及即早基因(c-jun、c-fos)的表达情况.结果表明,PM10暴露刺激神经元炎性细胞因子释放增加,显著上调p-Ca MKⅡα和p-CREB的水平,并刺激即早基因的高表达,且以冬季PM10的效应最为明显.由此提示,PM10暴露可能通过炎症反应机制激活Ca2+-Ca MK-CREB通路,进而刺激即早基因表达引发神经毒性作用,而冬季PM10中多环芳烃类物质负荷可能是造成效应季节性差异的主要原因.     

Implications of oxidative stress in occupational exposure to lead on a cellular level

The aim of this study was to determine oxidative alterations leading to cellular dysfunctions in Pb-exposed subjects by evaluating damage to all major classes of biomolecules in the cell, lipid peroxidation, protein and DNA damage and determine relationships between parameters of Pb toxicity and specific biomarkers of oxidative damage.

Analysis was conducted of smelter workers with high blood Pb and urine aminolevulinic acid levels and slightly elevated values of coproporphyrin and erythrocyte protoporphyrin IX. Significant decreases of thiol groups and increases in carbonyl groups as protein degradation end products, and of nitrite were detected. Elevated rates of lipid peroxidation and rises in the activities of the antioxidant enzymes Cu–Zn superoxide dismutase and catalase were also observed. Both enzymes showed positive correlations with the blood lead levels and urine coproporphyrin, while thiol groups correlated negatively with the same indices. The genotoxic potential of lead was manifested through an increased number of DNA-damaged cells. Increased activities of serum lactate dehydrogenase isoenzymes indicated cellular damage in the lungs, kidneys, and liver. These lead-induced impairments should be taken into consideration in the assessment of Pb-related health hazards.     

Microsatellite length polymorphisms associated with dispersal-related agonistic onset in male wild house mice (Mus musculus domesticus)

Dispersal propensity, reflecting one of the most decisive mammalian life history traits, has been suggested to vary heritably and to locally adapt to prevailing dispersal conditions in wild house mouse populations. Because individual dispersal propensity highly significantly covaries with the developmental timing of the onset of agonistic interactions between littermate brothers, we used agonistic onset as an endophenotype to explore the potential genetic basis of dispersal-related behavioral variation in male house mice. We found significant covariation of microsatellite marker compositions with the probability of fraternal pairs to exhibit agonistic relationships before the age of 2 months. In particular, the presence of two alleles associated with a serotonin transporter protein gene (Slc6a4) and a testosterone dehydrogenase gene (Cyp3a11), respectively, strongly covaried with the probability of early agonistic onset. These results are congruent with recent findings of microsatellite length polymorphisms marking regulatory variation of gene expression that is relevant for social behavior, including dispersal propensity development, in other mammals. Genetic variability for ontogenetic timing of agonistic onset would be in agreement with genotypic differentiation of the dispersive behavioral syndrome in natural populations that could lead to local adaptation.     

Molecular structure of extracellular poly(3-hydroxybutyrate) depolymerase fromAlcaligenes faecalis T1

The amino acid sequence of a peptide containing an active serine was examined with poly(3-hydroxybutyrate) (PHB) depolymerase ofAlcaligenes faecalis T1. The sequence Cys-Asn-Ala-Trp-Ala-Gly-Ser-Asn-Ala-Gly-Lys was obtained. This amino acid sequence around the active serine does not fit any reported sequence of other esterases and proteases. On the other hand, a segment of the amino acid sequence of PHB depolymerase ofA. faecalis was homologous to the type III sequence of fibronectin. Similar sequences have been reported in some type of bacterial chitinase and cellulases, and PHB depolymerase seems to have an overall similarity to these bacterial extracellular hydrolases.     

Molecular analysis of genomic DNA allows rapid,and accurate,prenatal diagnosis of peroxisomal D-bifunctional protein deficiency

Prenatal diagnosis was requested for a couple with a previous child affected by the peroxisomal disorder D-bifunctional protein deficiency. Prior analysis of the D-bifunctional protein cDNA sequence from the propositus had shown that it was missing 22 bp. This was subsequently attributed to a point mutation in the intron 5 donor site (IVS5+1G>C) of the D-bifunctional protein gene. Consistent with parental consanguinity, the patient was shown to be homozygous for this mutation, which is associated with loss of a Hph 1 restriction site in the genomic sequence. Prenatal testing of the fetus using genomic DNA isolated from uncultured amniocytes indicated that both alleles of the D-bifunctional protein had the IVS5+1G>C substitution. The peroxisomal defect was later confirmed biochemically using cultured amniocytes, which were found to have elevated levels of very long chain fatty acids (VLCFA). This is the first report of prenatal diagnosis of D-bifunctional protein deficiency using molecular analysis of genomic DNA. Copyright © 2002 John Wiley & Sons, Ltd.