ΛBMV中函数的F(a,q)平均逼近

设σｐ（ｆ，ｘ）＝∑∞ｋ＝０Ｃｋ（ｐ）Ｓｋ（Ｃｋ（ｐ）＞０）为ΛＢＭＶ中函数的Ｆｏｕｒｉｅｒ级数的Ｆ（ａ，ｑ）平均，这里Ｃｋ（ｐ）是满足一定条件的含参系数，本文作者给出了σｐ（ｆ，ｘ）－［ｆ（ｘ＋０）＋ｆ（ｘ－０）］／２的收敛速度．     

∧BMV中函数的F（a,q）平均逼近

设σｐ（ｆ，ｘ）＝＾∞∑ｋ＝０Ｃｋ（ｐ）Ｓｋ （Ｃｋ（ｐ）〉０）为∧ＢＭＶ中函数的Ｆｏｕｒｉｅｒ级数的Ｆ（ａ，ｑ）平均，这里Ｃｋ（ｐ）ｐ是满足一定条件的含参数系数，本文作者给出了σｐ（ｆ，ｘ）－［ｆ（ｘ＋０）＋ｆ（ｘ－０）］／２的收敛速度。     

迭代函数系自由变量的确定

利用最小二乘法建立了线性迭代函数系的竖直标度因子d的计算公式，以及非线性迭代函数系中关于y的非线性函数d(y)的系数d=(d1,d2,…,dn)^T的计算公式，从而使分形插值函数的确定更加客观。     

关于粗糙g-函数算子的一点注记

证明了对于（Ｓｎ－１）及适当的径向函数，为Ｌｐ－有界，其中１＜ｐ＜，该结果推广了已知的一些研究工作．     

空间C[0,1]的一个新的Schauder基

引入了区间［０，１］上一个新的标准正交系｛ｇａｌｋ（ｔ）｝∞０，证明了它在［０，１］上是一致有界的且是空间Ｃ［０，１］的Ｓｃｈａｕｄｅｒ基，同时｛ｇａｌｋ（ｔ）｝∞０的Ｌｅｂｅｓｇｕｅ函数｛Ｌ（Ｇ）ｎ（ｔ）｝在［０，１］上也是一致有界的，且｛ｇａｌｋ（ｔ）｝∞０还是［０，１］上的一个收敛系。     

星形函数系数的一个不等式

在α级星形函数族Ｓ＾＊（α）中选出一个子族Ｓ＾＊［α］，讨论了该子族中函数ｆ（ｚ）的第二、第三项系数不等式，并估计了其积分平均值。     

LFA-3和IL-2对机体免疫增强作用

以绵羊红细胞膜提取的ＬＦＡ－３和猪外周血单个核细胞（ＰＢＭＣ）所产生的ＩＬ－２，同时或分别与新城疫Ⅳ系疫苗胸肌注射２２日龄雏鸡，测定鸡体ＨＩ抗体效价及Ｅｔ花环形成率的变化，结果表明，ＬＦＡ－３组抗体效价与对照组（Ｄ组）差异极显著（ｐ＜０．０１），ＩＬ－２也可显著提高ＩＶ系苗免疫后ＨＩ抗体效价（ｐ＜０．０５），且两者的作用均具有剂量依赖性。Ｅｔ花环试验结果显示，ＬＦＡ－３和ＩＬ－２两者与Ｄ组差异不显著（Ｐ＞０．０５）。     

由一阶贝塞尔函数组成的两个正交系的证明

利用贝塞尔函数的微分与积分性质，给出了两个由一阶贝塞尔函数组成的线性函数系的正交性的证明，并给出了其长度表达式。     

n-3系多不饱和脂肪酸防治心血管疾病的研究进展

本文从流行病学的研究指出ｎ－３系多不饱和脂肪酸对心血管疾病的防治作用,并阐述ｎ－３系不多不饱和脂肪酸的作用机理及其对心血管疾病防治作用和一些影响因素。     

光度法直接测定钨合金中钍

研究了钨合金中钍的直接测定方法。在１．０ｍｏｌ／Ｌ硝酸和０．０８ｍｏｌ／Ｌ柠檬酸介质中，钍与３－［（２－羟基－３－羧基－５－磺基苯基）偶氮］－６－［（２－胂酸基苯基）偶氮］－４，５二羟基－２，７－萘二磺酸（ＡＳＡ－ＨＫＳ）发生灵敏的显色反应。钍与试剂形成１２绿色配合物，最大吸收波长为６７５ｎｍ，表观摩尔吸光系数为８．５４×１０４Ｌ／（ｍｏｌｃｍ）。钍含量在０～１．２ｍｇ／Ｌ范围内符合比耳定律。该方法的选择性是目前测定钍方法中较理想的，结果令人满意。     

淀粉磷酸酯取代度的分析方法

∶分光光度计法和磷钼酸喹啉容量法是测定淀粉磷酸酯取代度的常用方法．实验表明,磷钼酸喹啉容量法在数据精密度和重现性方面差于分光光度计法,且试剂配制繁琐．而分光光度计法可同时测多种未知样品,且操作方便,结果准确．     

Assembly interdependence among the S. cerevisiae bud neck ring proteins Elm1p,Hsl1p and Cdc12p

In Saccharomyces cerevisiae, a complex comprising more than 20 different polypeptides assembles in a ring at the neck between the mother cell and the bud. This complex functions to coordinate cell morphology with cell division. Relatively little is known about this control system, including the physical relationships between the components of the neck ring. This study addressed the assembly interactions of three components of the ring, specifically the protein kinases Elm1p and Hsl1p and the septin Cdc12p. Specific amino acid substitutions in each of these three proteins were identified that either cause or suppress a characteristic phenotype of abnormally elongated cells and delay in the G(2)-M transition. Each protein was fused to green fluorescent protein, and its ability to localize at the neck was monitored in vivo in cells of various genotypes. Localization of Hsl1p to the neck requires Elm1p function. Elm1p localized normally in the absence of Hsl1p, although a specific point mutation in Hsl1p clearly affected Elm1p localization. The cdc12-122 mutation prevented assembly of Elm1p or Hsl1p into the neck ring. Normal assembly of Cdc12p at the neck was dependent upon Elm1p and also, to a smaller extent, on Hsl1p. Ectopic localization of Cdc12p at the bud tip was observed frequently in elm1 mutants and also, to a lesser extent, in hsl1 mutants. Thus, Elm1p is a key factor in the assembly and/or maintenance of Hsl1p, as well as at least one septin, into the bud neck ring.     

Role of Tea1p, Tea3p and Pom1p in the determination of cell ends in Schizosaccharomyces pombe

Schizosaccharomyces pombe cells are rod-shaped and grow along a single axis from their two ends. Microtubules extend from the cell centre terminating at the cell ends. The ERM(ezrin/radixin/moesin)-like proteins Tea1p and Tea3p, and the Dyrk-like kinase Pom1p are cell end markers involved in the regulation of growth and microtubular dynamics at the cell ends. We have analysed the relative contribution of these three proteins to the determination of cell ends as sites both for cell growth and for microtubular termination. Pom1Delta, in combination with Tea1Delta or Tea3Delta, has the greatest difficulty in relocalizing actin to the cell ends following actin depolymerization and generates the most defective growth pattern. Tea1Delta, in combination with Pom1Delta or Tea3Delta, displays the highest number of microtubules bending round the cell ends. Tea1DeltaPom1Delta, which has the most defective growth pattern and microtubules, also displays the highest number of branched cells. We show that Tea1p, Tea3p and Pom1p all contribute, to different extents, to the determination of cell ends, as sites for both cell growth and microtubular termination. We also show that the fission yeast cell relies on both the positioning of landmarks and a properly organized microtubule cytoskeleton to direct cell growth.     

The Hsp90/Cdc37p chaperone system is a determinant of molybdate resistance in Saccharomyces cerevisiae

Saccharomyces cerevisiae lacks enzymes that contain the molybdopterin co‐factor and therefore any requirement for molybdenum as a trace mineral supplement. Instead, high molybdate levels are inhibitory to its growth. Low cellular levels of heat shock protein 90 (Hsp90), an essential chaperone, were found to enhance this sensitivity to molybdate. Certain Hsp90 point mutations and co‐chaperone protein defects that partially compromise the function of the Hsp90/Cdc37p chaperone system also rendered S. cerevisiae hypersensitive to high molybdate levels. Sensitivity was especially apparent with mutations close to the Hsp90 nucleotide binding site, with the loss of the non‐essential co‐chaperone Sti1p (the equivalent of mammalian Hop), and with the abolition of residue Ser14 phosphorylation on the essential co‐chaperone Cdc37p. While it remains to be proved that these effects reflect direct inhibition of the Hsp90 of the cell by the MoO₄²⁺ oxyanion in vivo; this possibility is suggested by molybdate sensitivity arising with a mutation in the Hsp90 nucleotide binding site that does not generate stress sensitivity or an impaired stress response. Molybdate sensitivity may therefore be a useful phenotype to score when studying mutations in this chaperone system. Copyright © 2009 John Wiley & Sons, Ltd.     

Technical note: p40 antibody as a replacement for p63 antibody in bovine mammary immunohistochemistry

Tumor protein 63 (p63) is a nuclear antigen found in basal epithelial cells. To date, 10 isoforms of p63 have been identified, falling into 2 major groups identified by presence or absence of an N-terminal transactivation domain (TAp63 and ΔNp63, respectively). Literature suggests that ΔNp63 is the predominant form expressed in basal epithelial cells and myoepithelial cells (MYEC). The mouse anti-p63 antibody, clone 4B1E12, has been used as a specific nuclear marker for bovine MYEC. Unfortunately, this antibody is no longer commercially available. A new mouse monoclonal antibody, clone BC28, specific to ΔNp63 (designated p40) has been developed. We hypothesized that the p40 antibody would be an appropriate substitution as a MYEC and epithelial basal cell marker. An array of archived formalin-fixed, paraffin-embedded bovine tissues were subjected to immunohistochemical staining for either p40 or p63, with a subset being dual stained for direct comparison. Positive staining for p40 and p63 was observed in serial sections of mammary, skin, rumen, salivary gland, ureter, and bladder. As predicted, negative staining for p40 and p63 was observed in testis and intestine. Dual staining for p40 and p63 in calf mammary (n = 4), lactating mammary (n = 4), rumen (n = 4), and skin (n = 4) showed nearly 100% agreement. Thus, we established that the mouse monoclonal antibody, clone BC28, is a suitable replacement for anti-p63, clone 4B1E12, as a marker of MYEC and basal epithelial cells in bovine tissues.     

Proteolytic processing of certain CaaX motifs can occur in the absence of the Rce1p and Ste24p CaaX proteases

The CaaX motif directs C‐terminal protein modifications that include isoprenylation, proteolysis and carboxylmethylation. Proteolysis is generally believed to require either Rce1p or Ste24p. While investigating the substrate specificity of these proteases, using the yeast a‐factor mating pheromone as a reporter, we observed Rce1p‐ and Ste24p‐independent mating (RSM) when the CKQQ CaaX motif was used in lieu of the natural a‐factor CVIA motif. Uncharged or negatively charged amino acid substitutions at the a₁ position of the CKQQ motif prevented RSM. Alanine substitutions at the a₂ and X positions enhanced RSM. Random mutagenesis of the CaaX motif provided evidence that RSM occurs with approximately 1% of all possible CaaX motif permutations. Combined mutational and genetic data indicate that RSM‐promoting motifs have a positively charged amino acid at the a₁ position. Two of nine naturally occurring yeast CaaX motifs conforming to this pattern promoted RSM. The activity of the isoprenylcysteine carboxyl methyltransferase Ste14p was required for RSM, indicating that RSM‐promoting CaaX motifs are indeed proteolysed. RSM was enhanced by the overexpression of Axl1p or Ste23p, suggesting a role for these M16A subfamily metalloproteases in this process. We have also determined that an N‐terminal extension of the a‐factor precursor, which is typically removed by the yeast M16A enzymes, is required for optimal RSM. These observations suggest a model that involves targeting of the a‐factor precursor to the peptidosome cavity of M16A enzymes where subsequent interactions between RSM‐promoting CaaX motifs and the active site of the M16A enzyme lead to proteolytic cleavage. Copyright © 2009 John Wiley & Sons, Ltd.     

Schizosaccharomyces pombe Pmf1p is structurally and functionally related to Mmf1p of Saccharomyces cerevisiae

A novel family of small proteins, termed p14.5 or YERO57c/YJGFc, has been identified. Independent studies indicate that p14.5 family members are multifunctional proteins involved in several pathways, e.g. regulation of translation or activation of the protease mu-calpain. We have previously shown that Mmf1p, a p14.5 of the budding yeast Saccharomyces cerevisiae, is localized in the mitochondria and influences mitochondrial DNA stability. In addition, we have demonstrated that Mmf1p is functionally related to p14.5 of mammalian cells. To explore further the evolutionary conservation of the mitochondrial function(s) of the p14.5s we have extended our study to the fission yeast, Schizosaccharomyces pombe. In this organism two p14.5 homologous proteins are present: Pmf1p (pombe mitochondrial factor 1) and Hpm1p (homologous Pmf1p factor 1). We have generated a specific Pmf1p antibody, which recognizes a single band of approximately 15 kDa in total cellular extracts. Cellular fractionation experiments indicate that Pmf1p localizes in the mitochondria as well as in the cytoplasm. We also show that Pmf1p shares several properties of S. cerevisiae Mmf1p. Indeed, Pmf1p restores the wild-type phenotype when expressed in delta mmf1 S. cerevisiae cells. Deletion of the leader sequence of Pmf1p abrogates its ability to localize in mitochondria and to functionally replace Mmf1p. Thus, these data together with our previous study show that the mitochondrial function(s) of the p14.5 family members are highly conserved in eukaryotic cells.     

The p53-, Bax- and p21-dependent inhibition of colon cancer cell growth by 5-hydroxy polymethoxyflavones

Scope: Previously, we reported that 5‐hydroxy polymethoxyflavones (5OH‐PMFs) isolated from orange, namely 5‐hydroxy‐6,7,8,3′,4′‐pentamethoxyflavone, 5‐hydroxy‐3,6,7,8,3′,4′‐hexamethoxyflavone (5HHMF) and 5‐hydroxy‐6,7,8,4′‐tetramethoxyflavone (5HTMF), potently induced apoptosis and cell‐cycle arrest in multiple human colon cancer cells. Herein, using isogenic variants of HCT116 human colon cancer cells, we investigated the effects of p53, Bax and p21 on the apoptosis and cell‐cycle arrest induced by different 5OH‐PMFs. Methods and results: Annexin V/PI co‐staining assay demonstrated that 5HHMF and 5HTMF significantly induced apoptosis in HCT116 (p53^+/+) cells but not in HCT116 (p53^?/?) cells. Furthermore, 5HHMF and 5HTMF significantly induced apoptosis in HCT116 (Bax^+/?) cells, whereas their pro‐apoptotic effects on HCT116 (Bax^?/?) cells were marginal. All three 5OH‐PMFs increased G0/G1 cell population of HCT116 (p53^+/+) cells, and these effects were abolished in HCT116 (p53^?/?) and HCT116 (p21^?/?) cells. Immunoblotting analysis showed that 5HHMF and 5HTMF increased the levels of cleaved caspase‐3, cleaved PARP in both HCT116 (p53^+/+) and HCT116 (Bax^+/?) cells and these effects were much weaker in HCT116 (p53^?/?) and HCT116 (Bax^?/?) cells. Conclusion: Our results demonstrated that 5OH‐PMFs, especially 5HHMF and 5HTMF, induce apoptosis and cell‐cycle arrest by p53‐, Bax‐ and p21‐dependent mechanism.     

Molecular characterization of Saccharomyces cerevisiae Sco2p reveals a high degree of redundancy with Sco1p

The Saccharomyces cerevisiae gene SCO1 has been shown to play an essential role in the transfer of copper to the Cu(A)-centre of the mitochondrial cytochrome c oxidase subunit Cox2p. By contrast, the function of Sco2p, the gene product of the highly homologous SCO2 gene, remains to be elucidated. Deletion of the SCO2 gene does not affect growth on a variety of carbon sources, including glycerol, lactate and ethanol. We report here, that Sco2p is anchored in the mitochondrial membrane by a single transmembrane segment and displays a similar tripartite structure as Sco1p. Most parts of Sco1p can be replaced by the homologous parts of Sco2p without loss of function. A short stretch of 13 amino acids, immediately adjacent to the transmembrane region, is crucial for Sco1p function and cannot be replaced by its Sco2p counterpart. We propose that this region is relevant for the correct spatial orientation of the C-terminal part of the protein. Immunoprecipitation and in vitro binding assays show that Sco2p interacts with the C-terminal portion of Cox2p. This interaction is neither dependent on bound copper ions nor on the presence of Sco1p. Furthermore we report on in vitro binding assays which show that Sco2p can form homomeric complexes, but also heteromeric complexes with Sco1p. Our data suggest that Sco2p is involved in the transfer of copper to Cox2p, but that this activity is insufficient for oxidative growth and not able to substitute for Sco1p activity.     

The role of two putative nitroreductases,Frm2p and Hbn1p,in the oxidative stress response in Saccharomyces cerevisiae

The nitroreductase family is comprised of a group of FMN‐ or FAD‐dependent enzymes that are able to metabolize nitrosubstituted compounds using the reducing power of NAD(P)H. These nitroreductases can be found in bacterial species and, to a lesser extent, in eukaryotes. There is little information on the biochemical functions of nitroreductases. Some studies suggest their possible involvement in the oxidative stress response. In the yeast Saccharomyces cerevisiae, two nitroreductase proteins, Frm2p and Hbn1p, have been described. While Frm2p appears to act in the lipid signalling pathway, the function of Hbn1p is completely unknown. In order to elucidate the functions of Frm2p and Hbn1p, we evaluated the sensitivity of yeast strains, proficient and deficient in both oxidative stress proteins, for respiratory competence, antioxidant‐enzyme activities, intracellular reactive oxygen species (ROS) production and lipid peroxidation. We found reduced basal activity of superoxide dismutase (SOD), ROS production, lipid peroxidation and petite induction and higher sensitivity to 4‐nitroquinoline‐oxide (4‐NQO) and N‐nitrosodiethylamine (NDEA), as well as higher basal activity of catalase (CAT) and glutathione peroxidase (GPx) and reduced glutathione (GSH) content in the single and double mutant strains frm2Δ and frm2Δ hbn1Δ. These strains exhibited less ROS accumulation and lipid peroxidation when exposed to peroxides, H₂O₂ and t‐BOOH. In summary, the Frm1p and Hbn1p nitroreductases influence the response to oxidative stress in S. cerevisae yeast by modulating the GSH contents and antioxidant enzymatic activities, such as SOD, CAT and GPx. Copyright © 2009 John Wiley & Sons, Ltd.