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resistance to a wide range of antimicrobial drugs, which complicates the treatment of these infections. S. aureus is also a common cause of hospital and community acquired infections. Mortality associated with severe S. aureus infections in the developing
: Prise en charge des diarrhées aiguës de l’enfant en milieu tropical . Med Trop 61 , 226 – 230 ( 2001 ) 4. Organisation Mondiale de la Santé (OMS) ( 2014 ): Antimicrobial Resistance: Global Report on
mtsai: Tetracycline resistance in Ureaplasma spp. and Mycoplasma hominis : prevalence in Bordeaux, France, from 1999 to 2002 and description of two tet(M) -positive isolates of M. hominis susceptible to tetracyclines. Antimicrob. Agents Chemother
) for the presence of the SA-specific staphylococcus protein A gene ( spa ), the two variants of the methicillin-resistance coding genes, mecA and mecC (formerly mecA LGA251 ), as well as pvl as a marker of the human-related virulence gene Panton
of nutrients well. It is also resistant against the attacks of the immune system. It has shown high resistance against azole-type antifungal medications. A protein called adhesin ensures its adhesion to the cell membrane. It easily produces biofilm on
biomarkers (hs-CRP and IL-6), while the weight loss caused by diets will reduce the concentration of such biomarkers. Because of the contradictory results of the mentioned studies, it is necessary to examine the effect of two types of resistance and
potential hepatotoxicity of these compounds given that resistance training (RT) is the main exercise modality practiced by AAS abusers [ 4 ]. However, to date, information about the effects of Su treatment and simultaneous RT on liver injury has been scarce
Introduction High-load resistance training with a mechanical load greater than 70% of one-repetition maximum (1RM) are generally required to increase muscle size and strength [ 1 ]. Similarly, low-load resistance training (20
, 11 ], was shown to promote neutrophil-mediated resistance and the spread of infection in vivo [ 12 ]. DNases would protect streptococci from being killed by neutrophil extracellular traps (NETs), by degrading this neutrophil-mediated antimicrobial
, are protected from stable C. jejuni colonization even following peroral infection with high bacterial loads [ 17 ]. This physiological colonization resistance provided by the intact complex murine gut microbiota is abrogated upon broad
