The analysis of representative state administrative databases of inpatient care records demonstrated improvements in mortality and amputation rates over time. However, a gender-related disparity in PAD outcomes remains that merits further investigation.

A mesenchymal transition occurs both during the natural evolution of glioblastoma (GBM) and in response to therapy. Here, we report that the adhesion G-protein-coupled receptor, GPR56/ADGRG1, inhibits GBM mesenchymal differentiation and radioresistance. GPR56 is enriched in proneural and classical GBMs and is lost during their transition toward a mesenchymal subtype. GPR56 loss of function promotes mesenchymal differentiation and radioresistance of glioma initiating cells both in vitro and in vivo. Accordingly, a low GPR56-associated signature is prognostic of a poor outcome in GBM patients even within non-G-CIMP GBMs. Mechanistically, we reveal GPR56 as an inhibitor of the nuclear factor kappa B (NF-κB) signaling pathway, thereby providing the rationale by which this receptor prevents mesenchymal differentiation and radioresistance. A pan-cancer analysis suggests that GPR56 might be an inhibitor of the mesenchymal transition across multiple tumor types beyond GBM.

Female gender is associated with more periprocedural complications, adjunctive arterial procedures, and increased endoleaks but does not affect long-term reinterventions or survival. Further studies are warranted to elucidate the effect of gender on outcomes. These data should be considered when selecting EVAR for men and women.

The incidence of ischemic colitis is decreased in patients undergoing EVAR vs open repair. The cause of the ischemia is multifactorial and seems to differ between patients in the early and late groups. Microembolization tends to produce severe ischemic colitis and is usually fatal. There should be a low threshold for performing endoscopy in any patient thought to have ischemic colitis after EVAR.

Metastatic prostate cancer is presently incurable. The oncogenic protein PTOV1, first described in prostate cancer, was reported as overexpressed and significantly correlated with poor survival in numerous tumors. Here, we investigated the role of PTOV1 in prostate cancer survival to docetaxel and self-renewal ability. Transduction of PTOV1 in docetaxel-sensitive Du145 and PC3 cells significantly increased cell survival after docetaxel exposure and induced docetaxel-resistance genes expression (ABCB1, CCNG2 and TUBB2B). In addition, PTOV1 induced prostatospheres formation and self-renewal genes expression (ALDH1A1, LIN28A, MYC and NANOG). In contrast, Du145 and PC3 cells knockdown for PTOV1 significantly accumulated in the G2/M phase, presented a concomitant increased subG1 peak, and cell death by apoptosis. These effects were enhanced in docetaxel-resistant cells. Analyses of tumor datasets show that PTOV1 expression significantly correlated with prostate tumor grade, drug resistance (CCNG2) and self-renewal (ALDH1A1, MYC) markers. These genes are concurrently overexpressed in most metastatic lesions. Metastases also show PTOV1 genomic amplification in significant co-occurrence with docetaxel-resistance and self-renewal genes. Our findings identify PTOV1 as a promoter of docetaxel-resistance and self-renewal characteristics for castration resistant prostate cancer. The concomitant increased expression of PTOV1, ALDH1A1 and CCNG2 in primary tumors, may predict metastasis and bad prognosis.

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An asymptomatic 53-year-old male was found to have a bruit on auscultation of his left carotid artery. Duplex ultrasound examination was performed, revealing a peak systolic velocity of 325 cm/s, end diastolic velocity of 142 cm/s, and an estimated stenosis of 80%-99% 2.12 cm distal to the bifurcation. Computed tomography angiogram with three-dimensional reconstructions was done, revealing a single-sided aberrant branch from the internal carotid artery (ICA), approximately 1 cm distal to the bifurcation, but proximal to the stenosis (A/Cover and B).On operative dissection, care was taken to preserve this branch (C), which proved to have significant back flow. Antegrade perfusion into the aberrant branch was preserved when patch closure of the arteriotomy was performed (D).Anomalous branches of the internal carotid artery have been described before. [1][2][3] As early as 1841, cases have been reported in which both the occipital and posterior auricular arteries originated from a branch of the extracranial ICA. Previously, angiography and color flow duplex scan have been used to image these anomalous vessels. This is the first reported computed tomography reconstruction outlining the proximal origin of an aberrant occipital branch correlating with operative images. Previous descriptions of anomalous branches of the ICA have shown branches originating distal to the stenosis. To our knowledge, this is the first description of an anomalous occipital branch originating proximal to the ICA stenosis.

No abstract