Mrp1 is involved in lipid presentation and iNKT cell activation by Streptococcus pneumoniae

The CD1d pathway present lipid antigens resulting in the activation of iNKT cells but the complete pathway remains to be fully elucidated. Here, Chandra et al. use an siRNA screen and identify Mrp1 as crucial for CD1d lipid presentation and activation of iNKT in the context of Streptococcus pneumoniae infection

Erratum to: 36th International Symposium on Intensive Care and Emergency Medicine

[This corrects the article DOI: 10.1186/s13054-016-1208-6.]

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

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Regulation of intracellular free arachidonic acid in Aplysia nervous system

We have studied the regulation of arachidonic acid (AA) uptake, metabolism, and release in Aplysia nervous system. Following uptake of [ 3 H]AA, the distribution of radioactivity in intracellular and extracellular lipid pools was measured as a function of time in the presence or absence of exogenous AA. The greatest amount of AA was esterified into phosphatidylinositol (relative to pool size). We found that the intracellular free AA pool underwent rapid turnover, and that radioactive free AA and eicosanoids were released at a rapid rate into the extracellular medium, both in the presence and absence of exogenous AA. Most of the released radioactivity originated from phosphatidylinositol.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/48020/1/232_2005_Article_BF01868464.pd

Major intracellular cations and growth control: corres- pondence among magnesium content, protein synthesis, and the onset of dna synthesis in balb/c3t3 cells.

Omission of Ca(2+) from the medium of confluent BALB/c3T3 cells for a period of 17 hr causes a large decrease in the number of cells synthesizing DNA. This effect is reversed by raising the Mg(2+) concentration of the medium to 20 mM. However, if the [Mg(2+)] is greater than 20 mM (“ultra-high” Mg(2+)), there is again a decrease in the number of cells synthesizing DNA. The synthesis of protein has a similar dependence on Mg(2+) concentration in Ca(2+)-deficient medium, but it responds within 45 min of the shift in cation concentrations rather than the 10 hr that is required for the change in DNA synthesis to become apparent. Cells in the ultrahigh Mg(2+) concentrations that are at first inhibitory to protein synthesis later return to maximal protein synthesis. This delayed increase in protein synthesis is reflected in a delayed increase in DNA synthesis. Intracellular concentrations of Mg(2+) in Ca(2+)-deficient media increase in proportion to extracellular Mg(2+) concentrations. Cells in medium with 30 mM Mg(2+) have a high intracellular content of Mg(2+) at 3 hr but have decreased their intracellular content by 17 hr, a time at which protein synthesis has been restored to normal. Intracellular Na(+) and K(+) concentrations also change in Ca(2+)-deficient medium, but independent variation of these ions shows that protein synthesis is relatively insensitive to their concentration. Intracellular Ca(2+) remains fairly constant under all these conditions. The rate of protein synthesis of intact cells changes as a function of intracellular Mg(2+) content in a manner very similar to that which has been reported for cell-free systems. We conclude that protein synthesis is very sensitive to small changes in intracellular [Mg(2+)] within physiological range and that the onset of DNA synthesis is dependent on the rate of protein synthesis. Regulation of the availability of Mg(2+) within the cell therefore presents a plausible mechanism for growth control

Magnesium reverses inhibitory effects of calcium deprivation on coordinate response of 3T3 cells to serum

Deprivation of Ca(2+) in crowded cultures of 3T3 cells inhibits the onset of DNA synthesis. By raising [Mg(2+)] to 15 mM the inhibition produced by Ca(2+) deprivation can be fully overcome. Sparse cultures are not inhibited by a similar deprivation of Ca(2+), and therefore are not stimulated by supranormal [Mg(2+)]. The time course of stimulation of the onset of DNA synthesis by supranormal [Mg(2+)] in low [Ca(2+)] is the same as that produced by serum in physiological concentrations of Ca(2+) and Mg(2+). Concentrations of Mg(2+) > 20 mM in low [Ca(2+)] reverse the stimulation, and [Mg(2+)] ≥ 30 mM kills many cells. In contrast to the stimulation by 15 mM Mg(2+), supranormal [Ca(2+)] has no effect on the onset of DNA synthesis in cultures inhibited by Mg(2+) deprivation, if the formation of insoluble Ca-P(i) complexes is prevented. Neither Na(+) nor K(+) reproduces the effects of Mg(2+). The uptake of uridine is another parameter of the coordinate response of 3T3 cells to serum stimulation that is inhibited by Ca(2+) deprivation, and supranormal [Mg(2+)] also reverses this inhibition. The results support the thesis that the coordinate response of growth and metabolism to external effectors is regulated by the availability of Mg(2+) within the cell and that the inhibitory effects of Ca(2+) deprivation are indirect and caused by a reduction in the availability of Mg(2+)