A schematic diagram showing growth mechanism of CeO₂ nanotubes.

<p>A schematic diagram showing growth mechanism of CeO₂ nanotubes.</p

Synthesis strategy flow chart.

<p>Synthesis strategy flow chart.</p

(a)TEM image of as-prepared Ce(OH)CO₃ precursors and (b) SEM image of CeO₂ nanotubes.

<p>(a)TEM image of as-prepared Ce(OH)CO₃ precursors and (b) SEM image of CeO₂ nanotubes.</p

SEM images of the as-prepared CeO₂ products after different reaction time: (a)6h, (b)12h, (c)18h, (d) 24h, (e) 48h, (f) 54h, (g)60h.

<p>SEM images of the as-prepared CeO₂ products after different reaction time: (a)6h, (b)12h, (c)18h, (d) 24h, (e) 48h, (f) 54h, (g)60h.</p

Changes in 33 eyes with cysts at the last visit.

<p>Changes in 33 eyes with cysts at the last visit.</p

Population and preoperative refractive comparison of the cysts group and no cysts group.

<p>Population and preoperative refractive comparison of the cysts group and no cysts group.</p

The GAP Activity of Type III Effector YopE Triggers Killing of <i>Yersinia</i> in Macrophages

<div><p>The mammalian immune system has the ability to discriminate between pathogens and innocuous microbes by detecting conserved molecular patterns. In addition to conserved microbial patterns, the mammalian immune system may recognize distinct pathogen-induced processes through a mechanism which is poorly understood. Previous studies have shown that a type III secretion system (T3SS) in <i>Yersinia pseudotuberculosis</i> leads to decreased survival of this bacterium in primary murine macrophages by unknown mechanisms. Here, we use colony forming unit assays and fluorescence microscopy to investigate how the T3SS triggers killing of <i>Yersinia</i> in macrophages. We present evidence that <i>Yersinia</i> outer protein E (YopE) delivered by the T3SS triggers intracellular killing response against <i>Yersinia</i>. YopE mimics eukaryotic GTPase activating proteins (GAPs) and inactivates Rho GTPases in host cells. Unlike wild-type YopE, catalytically dead YopER144A is impaired in restricting <i>Yersinia</i> intracellular survival, highlighting that the GAP activity of YopE is detected as a danger signal. Additionally, a second translocated effector, YopT, counteracts the YopE triggered killing effect by decreasing the translocation level of YopE and possibly by competing for the same pool of Rho GTPase targets. Moreover, inactivation of Rho GTPases by <i>Clostridium difficile</i> Toxin B mimics the effect of YopE and promotes increased killing of <i>Yersinia</i> in macrophages. Using a Rac inhibitor NSC23766 and a Rho inhibitor TAT-C3, we show that macrophages restrict <i>Yersinia</i> intracellular survival in response to Rac1 inhibition, but not Rho inhibition. In summary, our findings reveal that primary macrophages sense manipulation of Rho GTPases by <i>Yersinia</i> YopE and actively counteract pathogenic infection by restricting intracellular bacterial survival. Our results uncover a new mode of innate immune recognition in response to pathogenic infection.</p></div

Change of J45 astigmatism of the 2 groups at pre-operation and at different postoperative visit periods.

<p>Change of J45 astigmatism of the 2 groups at pre-operation and at different postoperative visit periods.</p

Comparison of different <i>Y. pseudotuberculosis</i> strains for survival inside macrophages as determined by CFU assay.

<p>BMDMs were infected with the indicated strains at an MOI of 10 for 20 min, followed by gentamicin treatment to eliminate extracellular bacteria. At 1 h and 23 h post infection, the infected BMDMs were lysed, and serial dilutions were plated to determine the survival of intracellular bacteria by CFU assay. Ratios of CFU at 23 h/1 h are shown, determined as [23 h post infection CFU/1 h post infection CFU]. Results shown are the means from three independent experiments with duplicate infection wells. Error bars show standard deviations. (A)***, P<0.001 compared to IP17; (B) *, P<0.05 and ***, P<0.001 compared to IP6, as determined by one-way ANOVA.</p

Change of mean spherical equivalent in the 2 groups at pre-operate and different postoperative visit periods.

<p>Change of mean spherical equivalent in the 2 groups at pre-operate and different postoperative visit periods.</p