Imaging is essential in the diagnostic work-up of patients with orbital lesions. The position of an orbital lesion relative to the inferomedial muscular trunk of the ophthalmic artery determines endoscopic resectability, anticipated technical difficulty, and patient morbidity. Although the inferomedial muscular trunk is not readily identifiable on preoperative imaging, we hypothesize that it is spatially approximate to the location where the ophthalmic artery crosses the optic nerve. Our aim was to determine whether the ophthalmic artery-optic nerve crosspoint anatomically approximates the inferomedial muscular trunk in a cadaver study and can be appreciated on imaging of known posteromedial orbital lesions.
 
  Dissection was performed on 17 fresh-frozen cadaver orbits to assess the relationship between the inferomedial muscular trunk and ophthalmic artery-optic nerve crosspoint. Retrospective review of imaging in 9 patients with posteromedial orbital lesions assessed posteromedial orbital compartment characdial orbit demonstrates that the ophthalmic artery-optic nerve crosspoint closely approximates the inferomedial muscular trunk and can be seen in patients with posteromedial orbital lesions. Posteromedial intraconal fat effacement may help to localize these lesions. These findings may facilitate multidisciplinary communication and help predict lesion resectability and patient outcomes.
  Intracranial hemorrhage represents a severe complication of brain arteriovenous malformation treatment. The aim of this cohort was to report the rate of hemorrhagic complications after transvenous endovascular embolization and analyze the potential angioarchitectural risk factors as well as clinical outcomes.
 
  During an 11-year period, 57 patients underwent transvenous endovascular embolization. All cases of hemorrhagic complications were identified. We analyzed the following variables sex, age, hemorrhagic presentation, Spetzler-Martin grade, size of the AVM before the transvenous treatment, number of venous collectors, pattern of drainage, presence of dilated veins, and technical aspects. Univariate and multivariate multiple regression analyses were performed to evaluate the potential risk factors for procedure-related hemorrhagic complications.
 
  Hemorrhagic complications (either intraprocedural or periprocedural) unrelated to a perforation due to micronavigation occurred in 8 (14.0%) procedures. Signif.
  A 3D T1-weighted black-blood sequence was recently shown to improve the detection of contrast-enhancing lesions in the brain in patients with MS compared with a 3D T1-weighted MPRAGE sequence. We compared a contrast-enhanced 3D T1-weighted black-blood sequence with a dedicated orbital contrast-enhanced T1-weighted Dixon sequence in patients with acute optic neuritis.
 
  MR imaging data (3T) of 51 patients showing symptoms of acute optic neuritis were analyzed retrospectively, including whole-brain contrast-enhanced 3D T1-weighted black-blood and dedicated orbital coronal 2D or 3D contrast-enhanced T1-weighted Dixon sequences. Two neuroradiologists assessed the images for overall image quality, artifacts, diagnostic confidence, and visual contrast enhancement. Furthermore, the standardized contrast-to-noise ratio was calculated. The final diagnosis of acute optic neuritis was established on the basis of clinical presentation, visually evoked potentials, and optical coherence tomography.
 
  Thirty of 51 patienton of acute optic neuritis. Therefore, when used, it has the potential to considerably shorten total patient imaging time.
 Contrast-enhanced 3D T1-weighted black-blood imaging is comparable in accuracy and qualitative/quantitative features with dedicated orbital contrast-enhanced T1-weighted Dixon imaging for the detection of acute optic neuritis. Therefore, when used, it has the potential to considerably shorten total patient imaging time.VAR2CSA is the placental-malaria-specific member of the antigenically variant Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) family. It is expressed on the surface of Plasmodium falciparum-infected host red blood cells and binds to specific chondroitin-4-sulfate chains of the placental proteoglycan receptor. The functional ∼310 kDa ectodomain of VAR2CSA is a multidomain protein that requires a minimum 12-mer chondroitin-4-sulfate molecule for specific, high affinity receptor binding. However, it is not known how the individual domains are organized and interact to create the receptor-binding surface, limiting efforts to exploit its potential as an effective vaccine or drug target. Using small angle X-ray scattering and single particle reconstruction from negative-stained electron micrographs of the ectodomain and multidomain constructs, we have determined the structural architecture of VAR2CSA. The relative locations of the domains creates two distinct pores that can each accommodate the 12-mer of chondroitin-4-sulfate, suggesting a model for receptor binding. This model has important implications for understanding cytoadherence of infected red blood cells and potentially provides a starting point for developing novel strategies to prevent and/or treat placental malaria.RAS genes are the most commonly mutated in human cancers and play critical roles in tumor initiation, progression, and drug resistance. Identification of targets that block RAS signaling is pivotal to develop therapies for RAS-related cancer. As RAS translocation to the plasma membrane (PM) is essential for its effective signal transduction, we devised a high-content screening assay to search for genes regulating KRAS membrane association. We found that the tyrosine phosphatase PTPN2 regulates the plasma membrane localization of KRAS.  https://www.selleckchem.com/products/sbfi-26.html  Knockdown of PTPN2 reduced the proliferation and promoted apoptosis in KRAS-dependent cancer cells, but not in KRAS-independent cells. Mechanistically, PTPN2 negatively regulates tyrosine phosphorylation of KRAS, which, in turn, affects the activation KRAS and its downstream signaling. Consistently, analysis of the TCGA database demonstrates that high expression of PTPN2 is significantly associated with poor prognosis of patients with KRAS-mutant pancreatic adenocarcinoma. These results indicate that PTPN2 is a key regulator of KRAS and may serve as a new target for therapy of KRAS-driven cancer.