Clinical response to 2 protocols of aerosolized gentamicin in 46 dogs with Bordetella bronchiseptica infection (2012-2018).

Background: Bordetella bronchiseptica (Bb) infection commonly causes respiratory disease in dogs. Gentamicin delivered by aerosol maximizes local drug delivery without systemic absorption but clinical response to protocols remains undetermined.

Objectives: To compare the clinical response to 2 protocols of aerosolized delivery of gentamicin in bordetellosis.

Analysis of the lung microbiota in dogs with Bordetella bronchiseptica infection and correlation with culture and quantitative polymerase chain reaction.

Infection with Bordetella bronchiseptica (Bb), a pathogen involved in canine infectious respiratory disease complex, can be confirmed using culture or qPCR. Studies about the canine lung microbiota (LM) are recent, sparse, and only one paper has been published in canine lung infection. In this study, we aimed to compare the LM between Bb infected and healthy dogs, and to correlate sequencing with culture and qPCR results.

MPV17 does not control cancer cell proliferation.

MPV17 is described as a mitochondrial inner membrane channel. Although its function remains elusive, mutations in the MPV17 gene result in hepato-cerebral mitochondrial DNA depletion syndrome in humans. In this study, we show that MPV17 silencing does not induce depletion in mitochondrial DNA content in cancer cells.

Angiostrongylosis in dogs with negative fecal and in-clinic rapid serological tests: 7 Cases (2013-2017).

Background: Angiostrongylosis is considered as emerging disease in dogs in Belgium. Detection of first-stage larvae in feces using the Baermann method has an imperfect sensitivity.

Objectives: Investigation of efficacy of noninvasive blood and fecal diagnostic tests in comparison with PCR on bronchoalveolar lavage (BAL) material in a small series of coughing or dyspnoeic dogs naturally infected with Angiostrongylus vasorum.

Inhibition of mitochondrial genome expression triggers the activation of CHOP-10 by a cell signaling dependent on the integrated stress response but not the mitochondrial unfolded protein response.

Mitochondria-to-nucleus communication, known as retrograde signaling, is important to adjust the nuclear gene expression in response to organelle dysfunction. Among the transcription factors described to respond to mitochondrial stress, CHOP-10 is activated by respiratory chain inhibition, mitochondrial accumulation of unfolded proteins and mtDNA mutations. In this study, we show that altered/impaired expression of mtDNA induces CHOP-10 expression in a signaling pathway that depends on the eIF2α/ATF4 axis of the integrated stress response rather than on the mitochondrial unfolded protein response.