Brain invasion is a biological hallmark of glioma that contributes to its aggressiveness and limits the potential of surgery and irradiation. Deregulated expression of adhesion molecules on glioma cells is thought to contribute to this process. Junctional adhesion molecules (JAMs) include several IgSF members involved in leukocyte trafficking, angiogenesis, and cell polarity. They are expressed mainly by endothelial cells, white blood cells, and platelets. Here, we report JAM-C expression by human gliomas, but not by their normal cellular counterpart. This expression correlates with the expression of genes involved in cytoskeleton remodeling and cell migration. These genes, identified by a transcriptomic approach, include poliovirus receptor and cystein-rich 61, both known to promote glioma invasion, as well as actin filament associated protein, a c-Src binding partner. Gliomas also aberrantly express JAM-B, a high affinity JAM-C ligand. Their interaction activates the c-Src proto-oncogene, a central upstream molecule in the pathways regulating cell migration and invasion. In the tumor microenvironment, this co-expression may thus promote glioma invasion through paracrine stimuli from both tumor cells and endothelial cells. Accordingly, JAM-C/B blocking antibodies impair in vivo glioma growth and invasion, highlighting the potential of JAM-C and JAM-B as new targets for the treatment of human gliomas.

Aim: Can monovoxel magnetic resonance spectroscopy (MRS) reliably follow tumour progression in low-grade glioma? Materials and Methods: 21 patients with low-grade glioma underwent at least 3 MRS. Results: For progression from a grade II to grade III tumour, a sensitivity of 57.1% and specificity of 60% were observed, with a positive predictive value (PPV) of 48.8% and a negative predictive value (NPV) of 54.5%. For progression under treatment, we obtained a sensitivity of 57.1% by N-acetylaspartate (NAA)/choline (Cho) and myoinositol/creatine (Cr) and a specificity of 100% by Cho/Cr and lipids, with a PPV of 80% and a NPV of 63.6%. Conclusion: We found that NAA/Cho is the best marker of tumour progression before therapy, with a sensitivity of 53.9%. For the therapeutic response, sensitivity was only 28.2%.

Cannabis consumption is temporally associated with the development of first episode psychosis (FEP). Whether or not the chronic use of this substance induces structural brain changes that may be responsible for the cognitive and psychological disturbances in this disorder is still matter of debate. To address this issue, we compared the magnetic resonance imaging (MRI)-assessed grey (GM) and white matter (WM) changes in young FEP patients between users versus non-users of cannabis. This prospective study included 50 consecutive FEP subjects: 33 users (22.7 ± 4.1 years, 4 women) and 17 non-users (23.9 ± 4.2 years, 10 women). Users were further divided into 15 heavy (23.3 ± 4.5 years, 2 women) and 18 light users (22.2 ± 3.8 years, 2 women) according to their lifetime cannabis use. Voxel-based-morphometry (VBM) analysis of GM and tract-based-spatial-statistics (TBSS) analysis of WM were performed. Age and gender were used as non-explanatory co-regressors. There were no supra-threshold differences between user and non-user groups for both GM and WM parameters. This was also the case when only heavy users were compared to non-users. Multivariate models controlling for age and gender confirmed these findings. We found no evidence for cannabis consumption related alterations in GM or WM in FEP subjects. Due to the strict correction for multiple comparisons and sample size, we cannot formally exclude subtle morphometric changes associated with cannabis consumption. However, even if present, such potential alterations would be of low magnitude.

Brain aging affects an increasing segment of the population and the role of chronic cerebrovascular disease is considered to be one of the main parameters involved. For this purpose we compared retrospectively MRI data with digitized subtraction angiography (DSA) data in a group of 50 patients focusing onto the watershed area of the carotid artery vascular territories. In order to evaluate the presence of white matter lesions (WML) in the hemispheric watershed areas, coronal fluid-attenuated inversion-recovery or axial T2 weighted MRI images of patients with symptomatic cerebrovascular insufficiency areas were compared with the capillary phase of DSA studies in anterior-posterior projection. Presence of cerebrovascular occlusive disease was evaluated on DSA using North American symptomatic carotid endarterectomy trial criteria and including evaluation of collateral vascular supply. Pathological MRI findings in the region of the watershed territories correlated overall in 66% of cases with a defect or delayed filling on DSA. In the case of asymmetrical MRI findings, there was a pathological finding of the capillary phase in the watershed area in 92% of DSA studies. Hypoperfusion in the capillary phase of the watershed area as seen on DSA correlated with the stenosis degree of the concerned carotid artery. Our findings suggest that asymmetrical findings of WML in the watershed areas as seen on MRI are caused by hemodynamic effect and a differentiation between small vessel disease and a consequence of distant stenosis may be possible under such conditions.

With dose tailored to body weight and automatic bolus triggering system, adjusting flow rate makes no difference in patients with regard to liver or portal vein enhancement, regardless of presence/absence of cirrhosis.