8 research outputs found

    Application of Chemical Modified Electrode in Drug Analysis

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    本研究利用全氟磺酸聚合物/含釕黃綠石氧化物(Nafion/Ru-oxide Pyrochlore)化學修飾電極偵測茶鹼(Theophylline)及兩種抗生素磺胺二 甲嘧啶(Sulfamethazine, SMZ), 磺胺二甲氧嘧啶(Sulfadimethoxine, SDM), 並對其在藥劑, 食品中的真實樣品做偵測. 茶鹼為強心, 利尿 劑, 亦有支氣管擴張, 冠動脈擴張, 平滑肌鬆弛功能. 以往皆是以層析方 法分析茶鹼, 本研究以化學修飾電極, 配合方波伏安法, 藉由修飾電極裡 的Ru-oxidePyrochlore對茶鹼的催化性, 以達到微量偵測的目的. 最佳的 方波條件為: 振幅30mV, 頻率45Hz, 預濃縮電位0V, 預濃縮時間15秒, 其 線性範圍為2至100uM, 偵測極限可達0.103uM(S/N=3), 再現性方面, 10uM 標準品連續偵測12次C.V.值1.34%, 並對紅茶, 綠茶等樣品進行標準品添 加校正曲線實驗, 其現性相關係數高達0.999. 本研究利用上述催化電 極, 進行對磺胺二甲嘧啶(SMZ)及磺胺二甲氧嘧啶(SDM)的偵測.磺胺劑為 常加在豬, 牛等家畜的飼料中以增加對疾病的抵抗能力的抗生素. 本研究 亦利用方波伏安法進行偵測. 偵測線性範圍分別為2-30uM, 2-25uM, 偵測 極限可達0.118uM, 0.129uM(S/N=3). 再現性方面, 20uM的SMZ與SDM標準 品連續偵測12次C.V.值分別為2.21%, 1.26%. 在實際樣品的偵測方面, 我 們選用了豬肉和牛奶來作實際樣品的偵測, 由於豬肉, 牛奶中可能未含有 磺胺劑, 或含量可能少於本實驗方法之偵測極限, 故並未有訊號出現. 但 添加少量磺胺劑後, 就有電流訊號產生, 且有很好的線性關係, 証明此電 極可應用於實際樣品的偵測

    Model of the effects on fitness (<i>w</i>) of a mutation.

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    <p><i>s<sub>f</sub></i>, <i>s<sub>m</sub></i> and <i>s<sub>a</sub></i> respectively denote the homozygous or hemizygous effect of a mutation <i>B</i> present in sexual females, males or asexual females, while <i>h<sub>f</sub></i>, <i>h<sub>m</sub></i> and <i>h<sub>a</sub></i> denote the dominance coefficients of <i>B</i> in these different types of individuals.</p

    Theoretical predictions of the genomic location of sex-biased genes in aphids.

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    <p>The preferred chromosomal locations of sexually antagonistic mutations (Prediction 1) are based on the simulations presented in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003690#pgen-1003690-g002" target="_blank">Figure 2</a>. Prediction 2: Predicted evolution of expression pattern of a gene bearing a sexually antagonist mutation after the evolution of a modifier that reduces the expression in the harmed sex (M, F and A refer to male, sexual female and asexual female, respectively, and the sign represents relative expression in each morph). The genomic locations of sex-biased genes (Predictions 3) were obtained by combining Predictions1 and 2. Theoretical predictions 3 were then tested with empirical data by looking at the genomic location of sex-biased genes, when considering different levels of fold-change in expression (2-, 5-, 10-fold difference). Observed number of genes for X and autosomes, frequency of X-linkage, % deviation from random expectation of X-linkage (<i>f</i><sub>(X)</sub> = 0.12) and its significance (Chi-square tests) are also given.</p

    Chromosomal location of genes differentially expressed between reproductive morphs.

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    <p>Frequency of X-linkage for genes with different rate of expression among males, sexual females and asexual females. Genes were classified according to their pattern of expression (M, F and A stand for male, sexual female and asexual female, respectively, and the sign represents relative expression in each morph) considering different minimal fold-change in expression between reproductive morphs (2-, 5- and 10-fold). The black line shows the expected frequency of X-linkage (based on genes supported by at least 5 reads over the eight libraries). Significance for deviation from the random expectation was calculated with Chi2-tests (* : <i>p</i><0.05, **: p<0.01, *** : <i>p</i><0.001). Theoretical predictions for the preferred genomic location of these different classes of genes (derived under the hypothesis that the evolution of sex-biased gene expression to restrict the product of a sexually antagonistic allele to the sex it benefits might solve intra-locus sexual conflicts) are shown on the top of the figure.</p

    Expression rate of X-linked and autosomal genes in males, sexual females and asexual females.

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    <p>Panels A to C: Log2 expression (RPKM+1) for autosomal and X-linked genes in the different reproductive morphs (males, sexual females, asexual females) for different cut-offs in gene expression. The white box for males represents X-linked genes with doubled expression to account for the haploid state of X chromosome in males. Difference in gene expression between X and autosomes within each morph was tested with Wilcoxon Rank sum tests.</p

    Annual life-cycle of the pea aphid and ploidy levels for autosomes (A) and sex-chromosome (X).

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    <p>Overwintering egg, diploid for both types of chromosomes (AA and XX) gives birth to an asexual female. After several cycles of apomictic parthenogenesis, asexual females produce sexual females and males. Males inherit the same autosomal genome as asexual females, but receive only one of the female Xs: hence they are diploid for the autosomes and haploid for the X (represented as AAX0). Ovules (haploid for both the autosomes and the X) are generated by a normal meiosis, but males produce only X-bearing sperm (AX). The fusion of male and female gametes restores the diploid level at both the X and the autosomes.</p

    Simulation of the accumulation of sexually antagonistic mutations on X chromosome and autosomes in aphids.

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    <p>Characteristics of mutations (in terms of their selection coefficients in males [<i>s<sub>m</sub></i>], in sexual females [<i>s<sub>f</sub></i>] and in asexual females [<i>s<sub>a</sub></i>]) that rise in frequency on the X more than on autosomes (panel A) or <i>vice-versa</i> (panel B) as a function of the dominance coefficient <i>h</i>. Our simulations predict that the X chromosome of aphids should be enriched in sexually antagonistic alleles beneficial for males whereas autosomes should be enriched in alleles favorable for asexual females under all dominance values.</p
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