400 research outputs found

    Long-range angular correlations on the near and away side in p–Pb collisions at

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    Underlying Event measurements in pp collisions at s=0.9 \sqrt {s} = 0.9 and 7 TeV with the ALICE experiment at the LHC

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    Effect of color reconnection and rope formation on resonance production in p–p collisions in Pythia 8

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    Resonance production in proton–proton collisions at s=7\sqrt{s} = 7 TeV and 13 TeV have been investigated using a Pythia 8 event generator within the framework of microscopic processes including color reconnection and rope hadronization. Specifically, the observable effects of different modes of color reconnections on the ratio of yields of mesonic and baryonic resonances with respect to their stable counterpart have been explored as a function of mean charged particle multiplicity. A suppression in the ratio is observed as a function of the mean number of charged particles for mesonic resonances. The ϕ/K\phi /\mathrm {K} and ϕ/π{\phi /\pi } ratios show an enhancement for high-multiplicity events due to enhanced production of strange quarks via the microscopic process of rope hadronization in the partonic phase. The mechanism of the hadronization of color ropes together with the quark–gluon plasma (QCD)-based color reconnection of partons predicted an enhancement in the ratio for baryonic resonances to non-resonance baryons having similar quark content. The yield ratios of resonances are found to be independent of the collision energy and strongly dependent on event activity

    Molecular Evidence of Increased Resistance to Anti-Folate Drugs in <i>Plasmodium falciparum</i> in North-East India: A Signal for Potential Failure of Artemisinin Plus Sulphadoxine-Pyrimethamine Combination Therapy

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    <div><p>North-east India, being a corridor to South-east Asia, is believed to play an important role in transmitting drug resistant <i>Plasmodium falciparum</i> malaria to India and South Asia. North-east India was the first place in India to record the emergence of drug resistance to chloroquine as well as sulphadoxine/pyrimethamine. Presently chloroquine resistance is widespread all over the North-east India and resistance to other anti-malarials is increasing. In this study both <i>in vivo</i> therapeutic efficacy and molecular assays were used to screen the spectrum of drug resistance to chloroquine and sulphadoxine/pyrimethamine in the circulating <i>P. falciparum</i> strains. A total of 220 <i>P. falciparum</i> positives subjects were enrolled in the study for therapeutic assessment of chloroquine and sulphadoxine/pyrimethamine and assessment of point mutations conferring resistances to these drugs were carried out by genotyping the isolates following standard methods. Overall clinical failures in sulphadoxine/pyrimethamine and chloroquine were found 12.6 and 69.5% respectively, while overall treatment failures recorded were 13.7 and 81.5% in the two arms. Nearly all (99.0%) the isolates had mutant <i>pfcrt</i> genotype (76T), while 68% had mutant <i>pfmdr</i>-1 genotype (86Y). Mutation in <i>dhps</i> 437 codon was the most prevalent one while <i>dhfr</i> codon 108 showed 100% mutation. A total of 23 unique haplotypes at the <i>dhps</i> locus and 7 at <i>dhfr</i> locus were found while <i>dhps</i>-<i>dhfr</i> combined loci revealed 49 unique haplotypes. Prevalence of double, triple and quadruple mutations were common while 1 haplotype was found with all five mutated codons (<b><u>F/AGEGS/T</u></b>) at <i>dhps</i> locus. Detection of quadruple mutants (51I/59R/108N/164L) in the present study, earlier recorded from Car Nicobar Island, India only, indicates the presence of high levels of resistance to sulphadoxine/pyrimethamine in north-east India. Associations between resistant haplotypes and the clinical outcomes and emerging resistance in sulphadoxine/pyrimethamine in relation to the efficacy of the currently used artemisinin combination therapy are discussed.</p></div

    The frequency distribution of SNPs combination of <i>dhfr</i> alleles.

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    <p>Allelic combinations are in order of A16V, C50R N51I, C59R, S108N and I164L where bold and underlined allele denotes mutations. Values within bracket are the percentage of occurrences.</p><p>The frequency distribution of SNPs combination of <i>dhfr</i> alleles.</p
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