17 research outputs found
Occurrence and antimicrobial susceptibility of thermophilic Campylobacter species isolated from healthy children attending municipal care centers in Southern Ecuador
ABSTRACT The prevalence and antimicrobial susceptibility of Campylobacter jejuni and C. coli strains in healthy, well-nourished children of middle socioeconomic level from Southern Ecuador were determined. Among the 127 children studied, 17 (13.4%) harbored Campylobacter sp. corresponding to C. jejuni (7.1%) and C. coli (6.3%) with a higher concentration of C. jejuni among boys (8.6%) and C. coli (8.8%) among girls. C. jejuni showed high resistance to nalidixic acid and ciprofloxacin (77.8%), but susceptibility to all other antimicrobials tested. C. coli strains showed resistance to more antibiotics than C. jejuni strains including resistance to nalidixic acid (75%), ciprofloxacin (75%), erythromycin (12.5%) and ampicillin (28.6), but susceptible to gentamicin and amoxicillin/clavulanic acid
CD133+ adult human retinal cells remain undifferentiated in Leukaemia Inhibitory Factor (LIF)
<p>Abstract</p> <p>Background</p> <p>CD133 is a cell surface marker of haematopoietic stem and progenitor cells. Leukaemia inhibitory factor (LIF), sustains proliferation and not differentiation of embryonic stem cells. We used CD133 to purify adult human retinal cells and aimed to determine what effect LIF had on these cultures and whether they still had the ability to generate neurospheres.</p> <p>Methods</p> <p>Retinal cell suspensions were derived from adult human post-mortem tissue with ethical approval. With magnetic automated cell sorting (MACS) CD133<sup>+ </sup>retinal cells were enriched from post mortem adult human retina. CD133<sup>+ </sup>retinal cell phenotype was analysed by flow cytometry and cultured cells were observed for proliferative capacity, neuropshere generation and differentiation with or without LIF supplementation.</p> <p>Results</p> <p>We demonstrated purification (to 95%) of CD133<sup>+ </sup>cells from adult human postmortem retina. Proliferating cells were identified through BrdU incorporation and expression of the proliferation markers Ki67 and Cyclin D1. CD133<sup>+ </sup>retinal cells differentiated whilst forming neurospheres containing appropriate lineage markers including glia, neurons and photoreceptors. LIF maintained CD133<sup>+ </sup>retinal cells in a proliferative and relatively undifferentiated state (Ki67, Cyclin D1 expression) without significant neurosphere generation. Differentiation whilst forming neurospheres was re-established on LIF withdrawal.</p> <p>Conclusion</p> <p>These data support the evidence that CD133 expression characterises a population of cells within the resident adult human retina which have progenitor cell properties and that their turnover and differentiation is influenced by LIF. This may explain differences in retinal responses observed following disease or injury.</p
Lead induces oxidative stress and phenotypic markers of apoptosis in Saccharomyces cerevisiae
In the present work, the mode of cell death induced by Pb in Saccharomyces cerevisiae was studied.
Yeast cells Pb-exposed, up to 6 h, loss progressively the
capacity to proliferate and maintained the membrane
integrity evaluated by the fluorescent probes bis(1,3-
dibutylbarbituric acid trimethine oxonol) and propidium
iodide. Pb-induced death is an active process, requiring the
participation of cellular metabolism, since the simultaneous
addition of cycloheximide attenuated the loss of cell
proliferation capacity. Cells exposed to Pb accumulated
intracelullarly reactive oxygen species (ROS), evaluated by
2′,7′-dichlorodihydrofluorescein diacetate. The addition of
ascorbic acid (a ROS scavenger) strongly reduced the
oxidative stress and impaired the loss of proliferation
capacity in Pb-treated cells. Pb-exposed cells displayed
nuclear morphological alterations, like chromatin fragmentation, as revealed by diaminophenylindole staining. Together,
the data obtained indicate that yeast cells exposition
to 1 mmol/l Pb results in severe oxidative stress which can
be the trigger of programmed cell death by apoptosis