33 research outputs found

    Development of new approaches to identify and characterise Campylobacter jejuni genes.

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    Campylobacter jejuni is now recognised as a major cause of food-borne enteritis. Characteristics of Campylobacter spp. make them less amenable to genetic analysis using standard molecular biology techniques. These problems can prevent the isolation and characterisation of campylobacter loci. In the absence of an efficient method for the generation of random mutations, the only mutagenesis strategy available is that which targets specific genes. The two approaches described were developed specifically for the analysis of specific genes. The polymerase chain reaction (PCR) with degenerate oligonucleotide primers (PCRDOP/inverse PCR mutagenesis (IPCRM) and inverse PCR strategies are designed to isolate and utilise small regions of DNA for the defined mutagenesis of targeted campylobacter genes. Moreover with the development of the IPCR mutagenesis, a small amount of sequence is the only requirement for the application of this approach. To evaluate the potential of both of these approaches, they were used to isolate and characterise potential virulence genes from C.jejuni. This study focused on the role of two classes of putative virulence determinants, stress response proteins of the HtrA family and response regulator proteins which are involved in the adaptation of bacteria to differing environmental stresses. A defined htrA mutant was constructed and phenotypic analysis established that this gene is not involved in the response to either temperature or oxidative stress, unlike many other homologues of HtrA. Three response regulator genes were isolated during this study, one of which is thought to encode CheY. Attempts to construct regX2 and regX3 mutants were unsuccessful. The flanking regions of htrA, regX2 and regX3 were isolated to facilitate the further characterisation of these loci. The work described in this study has verified that the PCRDOP/IPCRM and IPCR methodologies represent powerful approaches for the genetic analysis of Campylobacter spp

    Virgil, Aeneid 11, Pallas and Camilla, 1–224, 498–521, 532–596, 648–689, 725–835: Latin Text, Study Aids with Vocabulary, and Commentary (PDF)

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    A dead boy (Pallas) and the death of a girl (Camilla) loom over the opening and the closing part of the eleventh book of the Aeneid. Following the savage slaughter in Aeneid 10, the book opens in a mournful mood as the warring parties revisit yesterday’s killing fields to attend to their dead. One casualty in particular commands attention: Aeneas’ protégé Pallas, killed and despoiled by Turnus in the previous book. His death plunges his father Evander and his surrogate father Aeneas into heart-rending despair – and helps set up the foundational act of sacrificial brutality that caps the poem, when Aeneas seeks to avenge Pallas by slaying Turnus in wrathful fury. Turnus’ departure from the living is prefigured by that of his ally Camilla, a maiden schooled in the martial arts, who sets the mold for warrior princesses such as Xena and Wonder Woman. In the final third of Aeneid 11, she wreaks havoc not just on the battlefield but on gender stereotypes and the conventions of the epic genre, before she too succumbs to a premature death. In the portions of the book selected for discussion here, Virgil offers some of his most emotive (and disturbing) meditations on the tragic nature of human existence – but also knows how to lighten the mood with a bit of drag. This course book offers the original Latin text, vocabulary aids, study questions, and an extensive commentary. Designed to stretch and stimulate readers, Ingo Gildenhard’s volume will be of particular interest to students of Latin studying for A-Level or on undergraduate courses. It extends beyond detailed linguistic analysis to encourage critical engagement with Virgil’s poetry and the most recent scholarly thought. King's College, Cambridge, has generously contributed to this publication

    Virgil, Aeneid 11, Pallas and Camilla, 1–224, 498–521, 532–596, 648–689, 725–835: Latin Text, Study Aids with Vocabulary, and Commentary (XML)

    No full text
    A dead boy (Pallas) and the death of a girl (Camilla) loom over the opening and the closing part of the eleventh book of the Aeneid. Following the savage slaughter in Aeneid 10, the book opens in a mournful mood as the warring parties revisit yesterday’s killing fields to attend to their dead. One casualty in particular commands attention: Aeneas’ protégé Pallas, killed and despoiled by Turnus in the previous book. His death plunges his father Evander and his surrogate father Aeneas into heart-rending despair – and helps set up the foundational act of sacrificial brutality that caps the poem, when Aeneas seeks to avenge Pallas by slaying Turnus in wrathful fury. Turnus’ departure from the living is prefigured by that of his ally Camilla, a maiden schooled in the martial arts, who sets the mold for warrior princesses such as Xena and Wonder Woman. In the final third of Aeneid 11, she wreaks havoc not just on the battlefield but on gender stereotypes and the conventions of the epic genre, before she too succumbs to a premature death. In the portions of the book selected for discussion here, Virgil offers some of his most emotive (and disturbing) meditations on the tragic nature of human existence – but also knows how to lighten the mood with a bit of drag. This course book offers the original Latin text, vocabulary aids, study questions, and an extensive commentary. Designed to stretch and stimulate readers, Ingo Gildenhard’s volume will be of particular interest to students of Latin studying for A-Level or on undergraduate courses. It extends beyond detailed linguistic analysis to encourage critical engagement with Virgil’s poetry and the most recent scholarly thought. King's College, Cambridge, has generously contributed to this publication

    Association between child rash and wheeze and teacher-reported outcomes.

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    <p><sup>1</sup>Adjusted for child age and sex</p><p><sup>2</sup> Adjusted for variables in model 1 plus: maternal age, maternal education, financial difficulties, housing tenure</p><p><sup>3</sup> Adjusted for variables in model 2 plus: wheeze (in rash model) or rash (in wheeze model)</p><p>*compared to reference category, p<0.05</p><p>Association between child rash and wheeze and teacher-reported outcomes.</p

    Association between child rash and wheeze and child-reported outcomes.

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    <p><sup>1</sup>Adjusted for child age and sex</p><p><sup>2</sup> Adjusted for variables in model 1 plus: maternal age, maternal education, financial difficulties, housing tenure</p><p><sup>3</sup> Adjusted for variables in model 2 plus: wheeze (in rash model) or rash (in wheeze model)</p><p>*compared to reference category, p<0.05</p><p>Association between child rash and wheeze and child-reported outcomes.</p

    Study population characteristics.

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    <p><sup>1</sup> Teacher-reported outcomes were not imputed for the child-reported outcome study population</p><p>Study population characteristics.</p

    Adjusted associations of demographic, maternal, pregnancy and child characteristics with wheezing phenotypes in ALSPAC.

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    *<p>compared with never/infrequent wheezing (N = 5774) and using each child’s phenotype probability as weights.</p>±<p>Educated to school leaving certificate at 16 years (GCE level) or lower.</p>+<p>Chi-squared test across phenotypes.</p

    Description of study samples in each period with data on wheezing phenotypes.

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    ±<p>Educated to school leaving certificate at 16 years (GCE level) or lower.</p

    Adjusted associations of perinatal characteristics with wheezing phenotypes in ALSPAC.

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    *<p>compared with never/infrequent wheezing (N = 5642) and using each child’s phenotype probability as weights.</p>±<p>Not adjusted for each other but adjusted for preterm delivery (<37 weeks).</p>‡<p>Not adjusted for each other and not adjusted for birth weight/low birth weight (since birth weight does not influence gestational age).</p>+<p>Chi-squared test across phenotypes.</p

    Adjusted associations of postnatal characteristics with wheezing phenotypes in ALSPAC.

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    *<p>compared with never/infrequent wheezing (N = 4915) and using each child’s phenotype probability as weights.</p>+<p>Chi-squared test across phenotypes.</p
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