Pulmonary Embolism Response Teams (PERTs) have emerged to provide rapid multidisciplinary assessment and treatment of PE patients. However, descriptive institutional experience and preliminary outcomes data from such teams are sparse. PERT activations were identified through a retrospective review. Only confirmed submassive or massive PEs were included in the data analysis. In addition to baseline variables, the therapeutic intervention, length of stay (LOS), in-hospital mortality, and bleeding rate/severity were recorded. A total of 124 PERT activations occurred over 20 months: 43 in the first 10 months and 81 in the next 10. A total of 87 submassive (90.8%) and massive (9.2%) PE patients were included. The median age was 65 (51-75 IQR) years. Catheter-directed thrombolysis (CDT) was administered to 25 patients, systemic thrombolysis (ST) to six, and anticoagulation alone (AC) to 54. The median ICU stay and overall LOS were 6 (3-10 IQR) and 7 (4-14 IQR) days, respectively, with no association with any variables except a brain natriuretic peptide (BNP) >100 pg/mL ( p=0.008 ICU LOS; p=0.047 overall LOS). Twelve patients (13.7%) died in the hospital, nine of whom had metastatic or brain cancer, with a median overall LOS of 13 (11-17 IQR) days. There were five major bleeds: one in the CDT group, one in the ST group, and three in the AC group. Overall, (1) PERT activations increased after the first 10 months; (2) BNP >100 pg/mL was associated with a longer LOS; (3) rates of mortality and bleeding did not correlate with treatment; and (4) the majority of in-hospital deaths occurred in patients with advanced cancer.

Members of the Patatin-like Phospholipase Domain containing Protein A (PNPLA) family play key roles in triglyceride hydrolysis, energy metabolism, and lipid droplet (LD) homoeostasis. Here we report the identification of two distinct LD targeting motifs (LTM) for PNPLA family members. Transient transfection of truncated versions of human adipose triglyceride lipase (ATGL, also known as PNPLA2), PNPLA3/adiponutrin, or PNPLA5 (GS2-like) fused to GFP revealed that the C-terminal third of these proteins contains sequences that are sufficient for targeting to LDs. Furthermore, fusing the C-termini of PNPLA3 or PNPLA5 confers LD localization to PNPLA4, which is otherwise cytoplasmic. Analyses of additional mutants in ATGL, PNPLA5, and Brummer Lipase, the Drosophila homolog of mammalian ATGL, identified two different types of LTMs. The first type, in PNPLA5 and Brummer lipase, is a set of loosely conserved basic residues, while the second type, in ATGL, is contained within a stretch of hydrophobic residues. These results show that even closely related members of the PNPLA family employ different molecular motifs to associate with LDs.

Background and Purpose: Case reports suggest that unruptured intracranial aneurysms may serve as a nidus for thrombus formation and downstream embolic stroke. However, few data exist to support an association between unruptured aneurysms and ischemic stroke. Methods: We conducted a within-subjects case-control study of acute ischemic stroke patients prospectively enrolled in the Cornell AcutE Stroke Academic Registry (CAESAR) who had magnetic resonance imaging (MRI) of the brain and arterial imaging of the head within 14 days of admission. Reviewers blinded to the study hypothesis ascertained the presence of aneurysms from the neuroradiologist’s clinical report of the arterial imaging findings. McNemar’s test for paired data was used to compare the prevalence of unruptured aneurysms ipsilateral versus contralateral to the side of anterior circulation infarcts. Aneurysms of the anterior communicating artery or in the posterior circulation were not counted in the analysis. Results: Among 2,146 patients registered in CAESAR during 2011–2016, 1,541 met our inclusion criteria, of whom 176 (11.4%; 95% confidence interval [CI], 9.8–13.0%) had an intracranial aneurysm. The prevalence of aneurysms did not differ on the side ipsilateral versus contralateral to the infarction (risk ratio [RR], 1.2; 95% CI, 0.9–1.5). There was no significant association between aneurysms and ipsilateral stroke in secondary analyses of the 1,244 patients with stroke in a single anterior circulation territory (RR, 1.2; 95% CI, 0.8–1.9), the 619 patients with cryptogenic stroke (RR, 1.4; 95% CI, 0.9–2.0), or the 485 patients with cryptogenic stroke in a single anterior circulation territory (RR, 1.7; 95% CI, 0.8–3.3). Results were unchanged when counting only aneurysms larger than 3 mm (RR, 1.2; 95% CI, 0.8–1.9) or 5 mm in diameter (RR, 1.2; 95% CI, 0.9–1.5). Conclusions: Contrary to our hypothesis, we found no significant association between unruptured intracranial aneurysms and ipsilateral ischemic stroke.

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