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In cases of mild to moderate suspicion of choledocholithiasis, the accuracies of endoscopic sonography and MR cholangiopancreatography are similar. Because MR cholangiopancreatography is noninvasive, it may be preferred for this indication.

The purpose of this study was to determine whether there is a significant association between function and well-being in children with cerebral palsy. To determine this, the authors used validated measures of function (Gillette Functional Assessment Questionnaire, Gross Motor Function Classification System, Gross Motor Function Measure, and walking speed) and correlated them to health-related quality of life (HRQOL) measures (Pediatric Outcomes Data Collection Instrument, Pediatric Quality of Life instrument). In a cross-sectional study of ambulatory children with mild to moderate cerebral palsy aged 10.2 +/- 3.2 years, mild to moderate decreases in function were found when compared with normative data. As the assessment of HRQOL comprises both functional well-being and psychosocial well-being, the authors decided to specify the aspect of well-being to which they were referring. It was found that the child's function was not correlated to psychosocial well-being. The children with mild cerebral palsy had greater effects on their psychosocial well-being than would be predicted by their functional disability. Functional measures were good at predicting the functional well-being but were weak at predicting the psychosocial arm of well-being.

DEP-1/CD148 is a receptor-like protein tyrosine phosphatase with antiproliferative and tumor-suppressive functions. Interestingly, it also positively regulates Src family kinases in hematopoietic and endothelial cells, where we showed it promotes VE-cadherin-associated Src activation and endothelial cell survival upon VEGF stimulation. However, the molecular mechanism involved and its biologic functions in endothelial cells remain illdefined. We demonstrate here that DEP-1 is phosphorylated in a Src-and Fyndependent manner on Y1311 and Y1320, IntroductionDEP-1/CD148 (also called PTP or PTPRJ) is a receptor-like protein tyrosine phosphatase (PTP) expressed in several cell types including epithelial, endothelial, and hematopoietic cells. 1 It encompasses an extracellular domain containing 8 fibronectin-type IIIlike motifs, a transmembrane domain, a single intracellular catalytic domain, and a short C-terminal tail. 2 Initial studies demonstrated that its expression increases with cell density and suggested a function in cell contact-mediated growth inhibition. 2,3 Overexpression of DEP-1 in cancer cells was also reported to inhibit their growth, while thyroid cell transformation was associated with its decreased expression, indicative of a role for DEP-1 as a tumor suppressor. 4-8 DEP-1 was further identified as the gene associated with the mouse colon cancer susceptibility locus (Scc1), and was found to be frequently deleted and mutated in human cancers. 9 These growth inhibitory functions of DEP-1 are consistent with the nature of some of its reported substrates, which include the PDGF-␤, HGF (Met), and VEGF (VEGFR2) receptors as well as Src family kinases (SFKs), ERK1/2, and the p85 subunit of PI3K. 10-18 DEP-1 also dephosphorylates proteins from the cell-cell junctional complexes including p120catenin, occludin, and ZO-1, which might impact biologic functions dependent on the loosening/strengthening of intercellular contacts. 11,14,19 VEGFR2 is a potent activator of the angiogenic response and is the main mediator of the mitogenic, chemotactic, permeability, and survival effects of VEGF in normal and tumor-associated vessels. 20 VE-cadherin adhesion complexes are important sites of VEGFdependent signaling in confluent cells, as activated VEGFR2 associates to these complexes to mediate Akt activation and cell survival. 21 DEP-1 was shown to colocalize to these sites and to attenuate the phosphorylation of VEGFR2, resulting in the impaired activation of ERK1/2 and the contact inhibition of endothelial cell proliferation. 13,22 However, DEP-1 was also reported to positively regulate VE-cadherin-associated Src and Akt and to promote VEGF-dependent endothelial cell survival. 15 Consistent with these distinct in vitro functions, inactivation of DEP-1 in mice via the swapping of its catalytic domain and C-terminal tail with GFP revealed both positive and negative regulatory effects in vascular development, and resulted in defective vessel remodeling and branching in addition to increased endothelial cell proliferati...

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