¹¹C <i>T</i>_1/2,wash values of the vascular or washout component in different tumor metabolic states (necrotic and active tumors).

<p>¹¹C <i>T</i>_1/2,wash values of the vascular or washout component in different tumor metabolic states (necrotic and active tumors).</p

Time-activity curves of ¹¹C induced by the vascular or washout component in different tumor metabolic states (necrotic and active tumors).

<p>Time-activity curves of ¹¹C induced by the vascular or washout component in different tumor metabolic states (necrotic and active tumors).</p

Axial view of the ¹¹C activity distributions at the beginning of PET acquisition (in the brain at the top, and in the muscle at the bottom).

<p>PET images were fused with X ray CT scan for a better injected point localization.</p

Time-activity curves of ¹¹C induced by the diffusion or tissular component in the brain, leg muscle and tumor.

<p>Time-activity curves of ¹¹C induced by the diffusion or tissular component in the brain, leg muscle and tumor.</p

¹¹C <i>T</i>_1/2,wash (and the corresponding standard deviation values) of the vascular or washout component in the brain, leg muscle and tumor.

<p>¹¹C <i>T</i>_1/2,wash (and the corresponding standard deviation values) of the vascular or washout component in the brain, leg muscle and tumor.</p

¹¹C <i>T</i>_1/2,tiss (and the corresponding standard deviation values) of the diffusion or tissular component in the brain, leg muscle and tumor.

<p>¹¹C <i>T</i>_1/2,tiss (and the corresponding standard deviation values) of the diffusion or tissular component in the brain, leg muscle and tumor.</p

Time-activity curves of ¹¹C induced by the vascular or washout component in the brain, leg muscle and tumor.

<p>Time-activity curves of ¹¹C induced by the vascular or washout component in the brain, leg muscle and tumor.</p

Lead induces Telomere-Induced Foci (TIFs).

<p>Results obtained with B3 cells following 24 h exposure with the indicated Pb(NO₃)₂ concentrations. <b>A.</b> Representative images obtained following IF-FISH. TIFs (yellow) represent co-localisation of γH2Ax (red) and telomere (green) signals. The upper panel shows a representative image of a single metaphase. The lower panel shows representative images of each type of staining pattern obtained from several metaphases <b>B.</b> Localisation of γH2Ax and telomere staining using IF-FISH. *<i>p</i><0.05, ** <i>p</i><0.01. The different combinations of staining are shown in the legend on the right.</p

Lead Exposure Induces Telomere Instability in Human Cells

<div><p>Lead (Pb) is an important environmental contaminant due to its widespread use over many centuries. While it affects primarily every organ system of the body, the most pernicious effects of Pb are on the central nervous system leading to cognitive and behavioral modification. Despite decades of research, the mechanisms responsible for Pb toxicity remain poorly understood. Recent work has suggested that Pb exposure may have consequences on chromosomal integrity as it was shown that Pb exposure leads to the generation of γH2Ax foci, a well-established biomarker for DNA double stranded break (DSB formation). As the chromosomal localization of γH2Ax foci plays an important role in determining the molecular mechanism responsible for their formation, we examined the localization of Pb-induced foci with respect to telomeres. Indeed, short or dysfunctional telomeres (uncapped or damaged telomeres) may be recognized as DSB by the DNA repair machinery, leading to “telomere-Induced Foci” (TIFs). In the current study, we show that while Pb exposure did not increase intra-chromosomal foci, it significantly induced TIFs, leading in some cases, to chromosomal abnormalities including telomere loss. The evidence suggests that these chromosomal abnormalities are likely due to perturbation of telomere replication, in particular on the lagging DNA strand. We propose a mechanism by which Pb exposure leads to the loss of telomere maintenance. As numerous studies have demonstrated a role for telomere maintenance in brain development and tissue homeostasis, our results suggest a possible mechanism for lead-induced neurotoxicity.</p></div

Lead induces mainly lagging strand instability.

<p><b>A.</b> Principle of telomere hybridization by CO-FISH. <b>B.</b> Mean telomere instability observed with B3 cells after 24 h exposure with indicated Pb(NO₃)₂ concentrations. *<i>p</i><0.05. Representative images obtained with B3 cells are shown in the inset.</p