PubMed · 15132967
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Heinz Fehrenbach. 2004-05-15. Design-based counting.. https://doi.org/10.1164/ajrccm.169.10.962
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Flow cytometric signatures (i.e., light scatter, red and green fluorescence) were obtained for the active but non-culturable (ABNC) cells of E. coli and a coliform isolate H03N1, in seawater microcosms using BacLight, a live-dead assay kit from Molecular Probes (Eugene/Portland, OR). Previous studies have reported that there are two major adaptations, which cells undergo during the formation of ABNC states: cell wall toughening and DNA condensation. Therefore, we hypothesized that the matured ABNC forms should be more resistant to extreme temperature treatments (i.e., by freezing in liquid nitrogen and thawing at room temperature) than the normal and transition populations. It was shown that the membrane-compromised cells (comprising of normal wild-type and dead cells which are less resistant to rapid freeze thaw) could be differentiated from the matured ABNC using BacLight staining and fluorescence detection by flow cytometry. The population of ABNC cells, which could not be cultured using m-FC media (for the enumeration of fecal coliforms), was resuscitated in phosphate buffer saline followed by growth in Luria broth. Flow cytometry was thus able to detect and differentiate the ABNC cells against a mixed population comprising of culturable cells, transition populations, and dead cells. The results also showed that the formation of ABNC is as early as 2 days in seawater microcosms. By directly comparing the coliform levels enumerated by the BacLight based flow cytometry assays and m-FC technique, it was shown that the presence of coliforms can be undetected by the membrane filtration method.
Differences in lipid metabolism of tumor and normal tissues suggest a distinct response to available lipid compounds. In this study, the in vitro effects of five types of commercial parenteral lipid emulsions were investigated on human cell lines derived from normal fetal colon (FHC) or colon adenocarcinoma (HT-29). Changes of the cellular lipid fatty acid content, cell oxidative response, and the cell growth and death rates were evaluated after 48 h. No effects of any type of emulsions were detected on cell proliferation and viability. Compared to the controls, supplementation with lipid emulsions resulted in a multiple increase of linoleic and linolenic acids in total cell lipids, but the content of arachidonic, eicosapentaenoic, and docosahexaenoic acids decreased particularly in HT-29 cells. The concentration of emulsions which did not affected HT-29 cells increased the percentage of floating and subG0/G1 FHC cells probably due to their higher reactive oxygen species production and lipid peroxidation. Co-treatment of cells with antioxidant Trolox reduced the observed effects. Our results imply that lipid emulsions can differently affect the response of colon cells of distinct origin.
Populations of dendritic spines can change in number and shape quite rapidly as a result of synaptic activity. Here, we explore the consequences of such changes on the input-output properties of a dendritic branch. We consider two models: one for activity-dependent spine densities and the other for calcium-mediated spine-stem restructuring. In the activity-dependent density model we find that for repetitive synaptic input to passive spines, changes in spine density remain local to the input site. For excitable spines, the spine density increases both inside and outside the input region. When the spine stem resistances are relatively high, the transition to higher dendritic output is abrupt; when low, the rate of increase is gradual and resembles long-term potentiation. In the second model, spine density is held constant, but the stem dimensions are allowed to change as a result of stimulation-induced calcium influxes. The model is formulated so that a moderate amount of synaptic activation results in spine stem elongation, whereas high levels of activation result in stem shortening. Under these conditions, passive spines receiving modest stimulation progressively increase their spine stem resistance and head potentials, but little change occurs in the dendritic output. For excitable spines, modest stimulation frequencies cause a lengthening of both stimulated and neighboring spines and the stimulus eventually propagates. High-frequency stimulation that causes spines to shorten in the stimulated region decreases the amplitude of the dendritic output slightly or drastically, depending on initial spine densities and stem resistances.