@article{pmid36832246,

title = {Performance of T-Track TB, a Novel Dual Marker RT-qPCR-Based Whole-Blood Test for Improved Detection of Active Tuberculosis},

author = {Johannes P Meier and Selina Möbus and Florian Heigl and Alexandra Asbach-Nitzsche and Hans Helmut Niller and Annelie Plentz and Korkut Avsar and Marion Heiß-Neumann and Bernhard Schaaf and Uwe Cassens and Bernd Seese and Daniel Teschner and Sabin Handzhiev and Uwe Graf and Christoph Lübbert and Monika Steinmaurer and Konstantina Kontogianni and Christoph Berg and Andreas Maieron and Stefan H Blaas and Ralf Wagner and Ludwig Deml and Sascha Barabas},

doi = {10.3390/diagnostics13040758},

issn = {2075-4418},

year  = {2023},

date = {2023-02-01},

urldate = {2023-02-01},

journal = {Diagnostics (Basel)},

volume = {13},

number = {4},

abstract = {Tuberculosis (TB) is one of the leading causes of death by an infectious disease. It remains a major health burden worldwide, in part due to misdiagnosis. Therefore, improved diagnostic tests allowing the faster and more reliable diagnosis of patients with active TB are urgently needed. This prospective study examined the performance of the new molecular whole-blood test T-Track TB, which relies on the combined evaluation of  and  mRNA levels, and compared it to that of the QuantiFERON-TB Gold Plus (QFT-Plus) enzyme-linked immunosorbent assay (ELISA). Diagnostic accuracy and agreement analyses were conducted on the whole blood of 181 active TB patients and 163 non-TB controls. T-Track TB presented sensitivity of 94.9% and specificity of 93.8% for the detection of active TB vs. non-TB controls. In comparison, the QFT-Plus ELISA showed sensitivity of 84.3%. The sensitivity of T-Track TB was significantly higher ( < 0.001) than that of QFT-Plus. The overall agreement of T-Track TB with QFT-Plus to diagnose active TB was 87.9%. Out of 21 samples with discordant results, 19 were correctly classified by T-Track TB while misclassified by QFT-Plus (T-Track TB-positive/QFT-Plus-negative), and two samples were misclassified by T-Track TB while correctly classified by QFT-Plus (T-Track TB-negative/QFT-Plus-positive). Our results demonstrate the excellent performance of the T-Track TB molecular assay and its suitability to accurately detect TB infection and discriminate active TB patients from non-infected controls.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36007550,

title = {MXD4/MAD4 Regulates Human Keratinocyte Precursor Fate},

author = {Julien Coutier and Frédéric Auvré and Gilles Lemaître and Jean-Jacques Lataillade and Jean-François Deleuze and Paul-Henri Roméo and Michèle T Martin and Nicolas O Fortunel},

doi = {10.1016/j.jid.2022.07.020},

issn = {1523-1747},

year  = {2023},

date = {2023-01-01},

urldate = {2023-01-01},

journal = {J Invest Dermatol},

volume = {143},

number = {1},

pages = {105--114.e12},

abstract = {Deciphering the pathways that regulate human epidermal precursor cell fate is necessary for future developments in skin repair and graft bioengineering. Among them, characterization of pathways regulating the keratinocyte (KC) precursor immaturity versus differentiation balance is required for improving the efficiency of KC precursor ex vivo expansion. In this study, we show that the transcription factor MXD4/MAD4 is expressed at a higher level in quiescent KC stem/progenitor cells located in the basal layer of human epidermis than in cycling progenitors. In holoclone KCs, stable short hairpin-RNA‒mediated decreased expression of MXD4/MAD4 increases MYC expression, whose modulation increases the proliferation of KC precursors and maintenance of their clonogenic potential and preserves the functionality of these precursors in three-dimensional epidermis organoid generation. Altogether, these results characterize MXD4/MAD4 as a major piece of the stemness puzzle in the human epidermis KC lineage and pinpoint an original avenue for ex vivo expansion of human KC precursors.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36482098,

title = {RNA-Seq comparative study reveals molecular effectors linked to the resistance of Pinna nobilis to Haplosporidium pinnae parasite},

author = {Pauline Salis and Claire Peyran and Titouan Morage and Simon de Bernard and Julien Nourikyan and Stéphane Coupé and Robert Bunet and Serge Planes},

doi = {10.1038/s41598-022-25555-x},

issn = {2045-2322},

year  = {2022},

date = {2022-12-01},

urldate = {2022-12-01},

journal = {Sci Rep},

volume = {12},

number = {1},

pages = {21229},

abstract = {With the intensification of maritime traffic, recently emerged infectious diseases have become major drivers in the decline and extinction of species. Since 2016, mass mortality events have decimated the endemic Mediterranean Sea bivalve Pinna nobilis, affecting ca. 100% of individuals. These events have largely been driven by Haplosporidium pinnae's infection, an invasive species which was likely introduced by shipping. While monitoring wild populations of P. nobilis, we observed individuals that survived such a mass mortality event during the summer of 2018 (France). We considered these individuals resistant, as they did not show any symptoms of the disease, while the rest of the population in the area was devastated. Furthermore, the parasite was not detected when we conducted a PCR amplification of a species-specific fragment of the small subunit ribosomal DNA. In parallel, the transcriptomic analysis showed evidence of some parasite RNA indicating that the resistant individuals had been exposed to the parasite without proliferating. To understand the underlying mechanisms of resistance in these individuals, we compared their gene expression with that of susceptible individuals. We performed de novo transcriptome assembly and annotated the expressed genes. A comparison of the transcriptomes in resistant and susceptible individuals highlighted a gene expression signature of the resistant phenotype. We found significant differential expressions of genes involved in immunity and cell architecture. This data provides the first insights into how individuals escape the pathogenicity associated with infection.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}