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P. D. van Helden

Researcher at Stellenbosch University

Publications -  147
Citations -  8111

P. D. van Helden is an academic researcher from Stellenbosch University. The author has contributed to research in topics: Mycobacterium tuberculosis & Tuberculosis. The author has an hindex of 55, co-authored 147 publications receiving 7717 citations. Previous affiliations of P. D. van Helden include University of the Western Cape & Medical Research Council.

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Exogenous Reinfection as a Cause of Recurrent Tuberculosis after Curative Treatment

TL;DR: DNA fingerprinting with restriction-fragment-length polymorphism analysis indicates that reinfection was the cause of the recurrence of tuberculosis after curative treatment of postprimary tuberculosis.
Journal Article

Differentiation of Mycobacterium tuberculosis complex by PCR amplification of genomic regions of difference.

TL;DR: A two-step, multiplex polymerase chain reaction (PCR) method based on genomic regions of difference allowed for rapid differentiation of members of the Mycobacterium tuberculosis complex, making it suitable for routine laboratories and surveillance purposes.
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A balancing act: efflux/influx in mycobacterial drug resistance.

TL;DR: The tubercle bacillus has become a central player in the epidemiology of diarrheal disease and its role in this disease has become increasingly important in the management of infectious disease outbreaks.
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Hypomethylation of DNA in pathological conditions of the human prostate

TL;DR: The overall 5-methylcytosine content of DNA from normal, benign hyperplastic, and neoplastic human prostate tissue was analyzed and the results suggest a correlation between hypomethylation and metastatic capacity.
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Putative Compensatory Mutations in the rpoC Gene of Rifampin-Resistant Mycobacterium tuberculosis Are Associated with Ongoing Transmission

TL;DR: A role for rpoC mutations in the transmission of multidrug-resistant tuberculosis is supported and illustrates how epistatic interactions between drug resistance-conferring mutations, compensatory mutations, and different strain genetic backgrounds might influence compensatory evolution in drug-resistant M. tuberculosis.