This assumption is likely tenuous and could potentially lead to inaccurate results while inter variability

Lraqi patient BKM120 carriers since there were MDR bacteria detected before the hospital opened. Additionally, MDR plasmids could be acquired by susceptible bacteria during treatment with antibiotics that can induce and select for horizontal transfer. Therefore, if the MDR bacteria were brought into hospitals by patient carriers this can be seen as a potential risk factor for initiating nosocomial contamination and spread, as seen in our study and also in other reports. This study also highlighted that multiple plasmids are found in these MDR bacteria, and can be a possible source of rearrangement of antimicrobial resistance genes into new combinations and new genetic elements such as plasmids with different Inc groups. Additionally, the presence of multiple replicon types in a single organism allows greater opportunity for dissemination of plasmids. In conclusion, this is the first report of the characteristics of the plasmids found in MDR Enterobacteriaceae compared to their susceptible counterparts isolated in Iraq. The large plasmids, carrying resistance genes and transfer-associated genes, may be potential factors for regional dissemination of antibiotic resistance. The eye provides a unique opportunity to image central nervous system tissue in vivo because of the transparent cornea and crystalline lens allowing direct optical visualization of the retina. The retina is laminated and highly organized neural tissue studied widely in neuroscience. It is affected in the many visually disabling and blinding diseases. Macular degeneration causes damage to the outer retina, including the rod and cone photoreceptors, and the retinal pigment epithelium in the outer retina, while glaucoma and other optic neuropathies cause damage to the retinal ganglion cells, situated in the inner retina. RGC axons form the optic nerve and in primates project primarily to targets in the lateral geniculate nuclei, but also others such as the superior colliculi and pretectal nuclei. In rodents, RGC axons synapse primarily in the superior colliculi, but project also to other minor targets. Because of their clinical significance, studies of optic neuropathies under experimental conditions are vital for understanding their pathophysiology and devising potential therapeutic strategies. Methods for estimating RGC loss after experimental damage, or RGC survival in neuroprotective studies, in rodents have relied almost exclusively on quantifying either retrogradely labeled RGC soma after application of a fluorescent tracer to the superior colliculus, or axons in optic nerve sections. Since introduction of the fluorescent tracer to the superior colliculus is invasive, potential retrograde damage may occur to RGCs confounding the results of the primary experiment. Additionally, since with this method quantification of RGC survival requires isolating the retina, each animal can provide only one time point and any longitudinal assessment assumes that the actual timecourse in an individual animal can be extrapolated from data points contributed cross-sectionally by multiple animals.

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