tbuckley/cabot-search huggingface dataset:
TWMP-01. RESECTION OF SUPPLEMENTARY MOTOR AREA GLIOMAS: REVISITING SUPPLEMENTARY MOTOR SYNDROME AND THE ROLE OF THE FRONTAL ASLANT TRACT
Authors: Jacob Young, Andrew Gogos, Alex Aabedi, Ramin Morshed, Matheus Pereira, Samuel Lashof-Regas, Ziba Mansoori, Tracy Luks, Shawn Hervey-Jumper, Javier Villanueva-Meyer, Mitchel Berger
Journal: Neuro-Oncology (2021)

Abstract INTRODUCTION The supplemental motor area (SMA) is an eloquent region that is frequently a site for gliomas or the region is included in the resection trajectory to deeper lesions. METHODS Patient, tumor and outcome data were collected retrospectively from the UCSF tumor registry for patients who underwent surgical resection for newly diagnosed supratentorial diffuse glioma (WHO Grade II - IV) between 2010 and 2019 in the SMA region and the extent of SMA resection was determined by volumetric assessment. Tumors were registered to a standard brain atlas to create a frequency heat map of tumor volumes and resection cavities. RESULTS Although the volume of tumor within the SMA region did not correlate with the development of SMA syndrome, patients with SMA syndrome had larger resection cavities in the SMA region (25.4% SMA resection vs. 14.2% SMA resection, p = 0.039). The size of the resection cavity in the SMA region did not correlate with the severity of the SMA syndrome. Patients who developed SMA syndrome had cavities that were located more posteriorly in the SMA region and in the cingulate. When the frontal aslant tract (FAT) was preserved, 50% of patients developed SMA syndrome post-operatively; whereas 100% of patients who had disruption of the FAT during surgery developed SMA syndrome (p = 0.06). There was no difference in the overall survival for newly diagnosed glioblastoma patients with SMA syndrome compared to those without SMA syndrome (1.6 years vs. 3.0 years, p = 0.33). CONCLUSION For patients with SMA gliomas, larger resections and resections involving the posterior SMA region and posterior cingulate gyrus increased the likelihood of a post-operative SMA syndrome. Although SMA syndrome occurred in all cases where the FAT was resected, FAT preservation does not reliably avoid SMA syndrome post-operatively.
Effect of 7 vs 14 Days of Antibiotics Among Afebrile Men With Urinary Tract Infection
Authors: Joel Goldberg, John H. Powers
Journal: JAMA (2021)

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Abstract 116: T Cells Contribute To Diastolic Dysfunction And Cardiac Hypertrophy In A Preclinical Model Of Heart Failure With Preserved Ejection Fraction
Authors: Sasha Smolgovsky, Francisco Carrillo-Salinas, Marina Anastasiou, Kuljeet Kaur, Abraham Bayer, Mark Aronovitz, Robert M Blanton, Pilar Alcaide
Journal: Circulation Research (2021)

Introduction: Heart Failure with Preserved Ejection Fraction (HFpEF) is a prevalent cardiovascular syndrome with no curative therapies, characterized by diastolic dysfunction, preserved systolic function, and decreased expression of unfolded protein response (UPR) genes in the heart. Obesity and hypertension are risk factors for HFpEF and are intimately associated with systemic inflammation. However, the inflammatory mechanisms driving HFpEF remain largely unexplored. Hypothesis: We hypothesized that nitrosative stress induced by obesity and hypertension programs T cells to infiltrate the heart and drive cardiac pathology in HFpEF. Methods: Using a recently established model of HFpEF, we modeled obesity and hypertension in male C57/BL6 (wild-type, WT), T cell receptor alpha-deficient ( Tcra-/-), and Nur77-GFP reporter mice for T cell receptor engagement, using a high-fat diet (HFD) and L-NAME for 5 weeks, or standard chow (STD) as controls. Invasive hemodynamic analyses were used to assess cardiac function, and the heart and lymphoid organs were harvested to characterize immune cell populations by flow cytometry, histology, and gene expression of cardiac remodeling. Results: In WT mice, HFD/L-NAME induced significant cardiac infiltration of T cells alongside the hallmarks of HFpEF. HFD/L-NAME significantly expanded CD62 lo CD44 hi effector T cells in the mediastinal lymph nodes and spleen. Nur77-GFP mice revealed no antigen engagement by T cells in the heart, however, T cells sorted out of the lymphoid organs of HFpEF mice had significantly decreased gene expression of the UPR gene spliced X box-binding protein 1 (XBP1s) compared to controls, suggesting a T cell intrinsic dysregulation of the UPR, and T cell phenotypic changes independent of TCR engagement in the heart. Strikingly, Tcra-/- mice did not develop diastolic dysfunction or cardiomyocyte hypertrophy, demonstrating a novel role for T cells in this experimental model of HFpEF. Conclusions: We conclude diastolic dysfunction and cardiomyocyte hypertrophy in HFpEF is T cell dependent. Ongoing studies are determining whether the observed intrinsic T cell changes in XBP1s prime T cells for cardiac infiltration and effector function that results in diastolic dysfunction and HFpEF.
Abstract 11732: Hybrid Convergent Ablation of Atrial Fibrillation With Left Atrial Appendage Exclusion Improves Blood Pressure Control
Authors: Yury Malyshev, Ayaka Tsutsumi, Yisachar Greenberg, Felix Yang
Journal: Circulation (2021)

Introduction: Hybrid convergent ablation (HCA) of atrial fibrillation (AF) and left atrial appendage exclusion (LAAE) have evolved as alternative strategies to conventional rhythm control and stroke prevention, respectively. Recent data suggests that HCA and LAAE can substantially impact arrhythmia burden and hemodynamic profile. Hypothesis: We assessed the hypothesis that HCA with epicardial LAAE may reduce blood pressure (BP) and the number of medications required for its control. Methods: This is a retrospective study of 100 patients who underwent HCA with epicardial LAAE using AtriClip. Clinical outcomes were measured at 3 months and 1 year. Primary outcome was reduction in the number of BP medications compared to baseline. Secondary outcomes included dose reduction, composite of dose and number of medication reduction compared to baseline; changes in diastolic (DBP) and systolic BP (SBP). Results: At baseline, the mean number of BP reducing medications was 2.17 ± 1.3, SBP 130 ± 16.9 mmHg and DBP 80 ± 10.3 mmHg. The number of medications had decreased significantly both at 3 months (1.7 ± 1, p=0.005) and at 1 year (1.75 ± 1.1, p=0.015). 43% and 44% of patients had decreased the number of medications at 3 months and 1 year, respectively; 78% and 73% of patients had decreased the number and/or dose of medications compared to baseline at 3 months and 1 year, respectively. DBP was also significantly lower compared to baseline both at 3 months (75 ± 9.5 mmHg, p=0.00065) and 1 year (75 ± 10.6 mmHg, p=0.004). There was a trend towards lower SBP at 3 months (127 ± 16 mmHg, p=0.14) and 1 year (127 ± 15.8 mmHg, p=0.15). Conclusion: In conclusion, HCA with epicardial LAAE significantly decreases the number of BP medications required to control BP and significantly reduces DBP.
Abstract 12454: Prognostic Value of Computational Pressure-Flow Dynamics Derived Fractional Flow Reserve in Non-Culprit Vessels Among Patients Presenting With Acute Coronary Syndrome and Multivessel Disease
Authors: Ka Lam Calvin Leung, Lok Yee Lam, Kwan Yu LI, Shuk Yin Yu, Mei Zhen Wu, Qing Wen Ren, Pui Fai Wong, Yi Kei Tse, Si Yeung Yu, Hang Long Li, Yundi Feng, Yunlong Huo, Hung Fat Tse, Kai Hang Yiu
Journal: Circulation (2021)

Introduction: Computational pressure-flow dynamics derived fractional flow reserve (caFFR) is a novel index developed to assess the severity of myocardial ischemia in patients with coronary artery stenoses, without the requirement of invasive pressure wire and hyperemic stimulus needed in fractional flow reserve (FFR) measurement. In patients presenting with acute coronary syndrome (ACS), the non-culprit vessels are often diseased concomitantly, and the ischemia status of such vessels may affect clinical outcomes. In this study, we aimed to evaluate the prognostic value of caFFR in non-culprit vessels among ACS patients with multivessel disease. Methods: Patients presented with ACS and at least two vessels having ≥50% diameter stenosis were included, and the culprit vessel was identified for each patient. Analyses of caFFR were performed for the two non-culprit vessels of every patient. Based on the threshold of 0.8 adopted from FFR studies, patients were stratified into ischemic group if any non-culprit vessel caFFR was ≤0.8, and into non-ischemic group if none of the non-culprit vessels had caFFR≤0.8. The primary endpoint was major adverse cardiovascular events (MACE), defined as a composite of all-cause mortality, non-fatal myocardial infarction, and any subsequent revascularization. Results: A total of 293 patients (mean age 65.3±13.2, male 77.5%) were included, with 113 (38.6%) presented with STEMI, 119 (40.6%) presented with NSTEMI, and 41 (14.0%) presented with unstable angina. The ischemic group patients (n=176) had more obstructive lesions compared to non-ischemic group patients (n=117) (3.8±1.5 vs. 3.2±1.1, p&lt;0.001). The MACE event rate at 3 years was higher in ischemic group compared to non-ischemic group (28.4% vs. 15.4%; adjusted hazard ratio, 1.92; 95% confidence interval, 1.10-3.36; p=0.023). Conclusions: In ACS patients with multivessel disease, myocardial ischemia in non-culprit vessels assessed by caFFR was associated with adverse clinical outcomes in terms of MACE.
CircEAF2 counteracts Epstein-Barr virus-positive diffuse large B-cell lymphoma progression via miR-BART19-3p/APC/β-catenin axis
Authors: Chen-xing Zhao, Zi-xun Yan, Jing-jing Wen, Di Fu, Peng-peng Xu, Li Wang, Shu Cheng, Jian-da Hu, Wei-li Zhao
Journal: Molecular Cancer (2021)

Epstein-Barr virus (EBV) represents an important pathogenic factor of lymphoma and is significantly associated with poor clinical outcome of diffuse large B-cell lymphoma (DLBCL). Circular RNAs (circRNAs) play an essential role in lymphoma progression. However, the underlying mechanism of circRNA on DLBCL progression related to EBV remains largely unknown.CircRNA was screened by high-throughput sequencing in tumor samples of 12 patients with DLBCL according to EBV infection status. Expression of circEAF2, as well as the relationship with clinical characteristics and prognosis, were further analyzed in tumor samples of 100 DLBCL patients using quantitative real-time PCR. Gain- and loss-of-function experiments were conducted to investigate the biological functions of circEAF2 both in vitro and in vivo. The underlying mechanism of circRNA on DLBCL progression were further determined by RNA sequencing, RNA pull down assay, dual-luciferase reporter assay, rescue experiments and western blotting.We identified a novel circRNA circEAF2, which was downregulated in EBV + DLBCL and negatively correlated with EBV infection and DLBCL progression. In EBV-positive B lymphoma cells, circEAF2 overexpression induced lymphoma cell apoptosis and sensitized lymphoma cells to epirubicin. As mechanism of action, circEAF2 specifically targeted EBV-encoded miR-BART19-3p, upregulated APC, and suppressed downstream β-catenin expression, resulting in inactivation of Wnt signaling pathway and inhibition of EBV + DLBCL cell proliferation. In EBV-positive B-lymphoma murine models, xenografted tumors with circEAF2 overexpression presented decreased Ki-67 positivity, increased cell apoptosis and retarded tumor growth.CircEAF2 counteracted EBV + DLBCL progression via miR-BART19-3p/APC/β-catenin axis, referring circEAF2 as a potential prognostic biomarker. Therapeutic targeting EBV-encoded miRNA may be a promising strategy in treating EBV-associated lymphoid malignancies.
Abstract 12949: Mitral Valve Geometry and Remodeling in a Three Month Swine Model of Post-Infarction Heart Failure
Authors: Michael Silverman, Daisuke Onohara, Daniella Corporan, Dongyang Xu, Kirthana Sreerangathama Suresh, Muralidhar Padala
Journal: Circulation (2021)

Introduction: Mitral regurgitation (MR) following myocardial infarction (MI) is a known risk factor for increased hospitalizations and mortality. The longitudinal mitral valve remodeling in chronic ischemic MR (IMR) is not fully understood and a reproducible, large animal model is therefore needed. In this study, we establish a swine model of chronic IMR and investigate the consequent changes in mitral valve geometry. Methods: Yorkshire swine (n=7) were induced with an MI via targeted angiographic ethanol injection of the left circumflex coronary artery, and were followed to 3 months. Mitral valve geometry and MR grade were investigated at baseline, immediately after MI, and 3 months post MI ( Fig. A ). Epicardial echocardiography was performed under mini left thoracotomy for direct placement onto the left atrium, such that the entire left heart was imaged. Results: 3 months following MI, ejection fraction (EF) decreased compared to baseline (47.3 ± 8.4 vs 55.3 ± 6.5%, p=.03). Both effective regurgitant orifice area (EROA) and regurgitant volume (RV) increased compared to baseline (EROA: 12 ± .14 vs .01 ± .01cm 2 ; p=.001; RV: 18.7 ± 21.3 vs .14 ± .38ml; p=.001). Both tenting height (TH) and tenting area (TA) also increased compared to baseline (TH: 11.7 ± 2.8 vs 6.8 ± 0.7mm; p=.01; TA: 190 ± 66 vs 95 ± 16mm 2 ; p=.04), indicating tethering of the mitral valve. No differences were found in coaptation length (5.7 ± 1.4 vs 5.8 ± 0.8mm; p=.99) and anterior excursion angle (37.9 ± 10.5 vs 25.3 ± 11.9°; p=0.27). Posterior excursion angle decreased at 3 months following MI (25 ± 11.3 vs 39.6 ± 8.0°; p=.02), indicating restriction of the posterior leaflet ( Fig. B1-7 ) Conclusion: In this paired analysis of mitral valve and ventricular remodeling after posterolateral MI, consistent increase in EROA and RV were observed. This model mimics a clinically relevant situation, providing a platform for studying the effects of IMR correction on ventricular remodeling.
Abstract 10577: Dapagliflozin Improves Cardiac Function in Mice After Myocardial Infarction
Authors: Mohsin Haseeb, Chaitanya K Gavini, Quan Cao, Gregory Aubert
Journal: Circulation (2021)

Objective: We examined the effects of SGLT2 inhibition with Dapagliflozin (DAPA) on left ventricular ejection fraction (LVEF) and cardiomyocyte regeneration in mice after myocardial infraction (MI), a model for Heart Failure with reduced EF. Introduction: Neonatal mice can regenerate cardiomyocytes, but this ability is lost shortly after birth due in part to a switch from anaerobic glycolysis to fatty acid utilization. This switch is due to pyruvate dehydrogenase kinase 4 (PDK-4) inhibition of pyruvate dehydrogenase (PDH) dependent glycolysis. Empagliflozin use in mice after MI increases PDH activity and promotes glucose utilization. Hypothesis: DAPA use in mice after MI can improve LVEF by promoting cardiomyocyte regeneration secondary to increase PDH activity. Methods: A total of 49 mice, 8 weeks old, were randomized to LAD ligation (MI) or sham surgery (Sham). 72 hours after surgery, MI (n=19) and Sham (n=21) mice were randomized to PO DAPA (0.02 mg/ml) (MI-DAPA, Sham-DAPA) or vehicle (water) (MI-VEH, Sham-VEH). 20 mice were euthanized after each successive week (wk.) of treatment. Immunofluorescence, using Anti-phospho-Histone H3 (mitosis marker) (PH3)-Anti Cardiac Troponin T co-staining, was done at 2 wks. to assess regeneration. An echocardiogram was done at baseline, 72 hours after surgery, and weekly after treatment to assess LVEF. Results: At 1 wk. after MI, no significant change was observed between groups. At 2 wks., DAPA increased LVEF in MI mice (Sham-VEH 66.75%, SEM 1.18; Sham-DAPA 78.63%, SEM 2.82; MI-VEH 56.86%, SEM 4.80; MI-DAPA 74.3%, SEM 0.58%, p&lt;0.05). At 2 wks., MI increased % of PH3 positive cardiomyocyte nuclei (Sham-VEH 0%, SEM 0; MI-VEH 0.4268%, SEM 0.1259; p&lt;0.05). In DAPA treated mice no significant difference was observed as the % of PH3 positive cardiomyocyte increased in Sham-DAPA mice (Sham-DAPA 0.2253%, SEM 0.078; MI-DAPA 0.46%, SEM 0.07; p 0.47). Despite an increase in SHAM-VEH mice, no statistically significant difference was observed between SHAM-VEH and SHAM-DAPA. Conclusions: DAPA mitigate cardiac remodeling in mice after MI with increase LVEF after 2 wks. MI increases mitosis in cardiomyocytes after two wks. Despite a trend for increased mitosis with DAPA treatment for 2 wks., no significant change was seen.
Abstract 13594: Cyclosporine-A Reduces Myocardial Damage in Donation After Circulatory Death Hearts
Authors: Oluwatoyin E Akande, Qun Chen, Renee Cholyway, Stefano Toldo, Edward J Lesnefsky, Mohammed Quader
Journal: Circulation (2021)

Background: Mitochondria contribute to ischemia and reperfusion injury (IRI) in donation after circulatory death (DCD) donor hearts. Cyclosporine A (CyA), an inhibitor of mitochondrial permeability transition pore (MPTP) opening, limits IRI. CyA administration at the onset of reperfusion is essential for therapeutic efficacy. DCD heart transplantation (HTx) is a unique setting for controlled administration of CyA. Hypothesis: CyA administered to DCD hearts during reperfusion is cardioprotective. Methods: Under general anesthesia Sprague Dawley rats underwent simulated clinical DCD setup with a global ischemia of 25 minutes. Control beating-heart donor (CBD) hearts served as controls (n=10). Hearts were reanimated ex-vivo with Krebs-Henseleit buffer (KH) perfusion at 37 o C for 90 minutes. DCD hearts were randomly assigned to receive CyA (0.5mM) or DMSO added to KH buffer for the first 15 minutes of perfusion (n=10 each). The hearts were collected to measure oxidative phosphorylation (OXPHOS) and calcium retention capacity (CRC). Additional CBD (n=5) and DCD (with or without CyA, n=15) hearts underwent heterotopic HTx in recipient rats to measure developed pressure (DP) and rate pressure product (RPP) at 48 hours. Results: Compared to CBD hearts, OXPHOS in DCD hearts was significantly reduced. CyA improved OXPHOS and was similar to CBD hearts. CRC was reduced in DCD hearts compared to CBD hearts (317 vs.578nM/mg) and was increased with CyA treatment (413 vs. 317nM/mg; p&lt;0.05, Figure). Infarct size decreased significantly with CyA treatment (15% vs. 25%). In transplanted DCD hearts, DP and RPP were significantly reduced compared to CBD hearts (80 vs.153mmHg and 17639 vs. 29545mmHg*bpm). CyA treatment improved DP (124vs.80mmHg; p&lt;0.05) and RPP (35491vs.17639mmHg*bpm; p&lt;0.05) which was comparable to CBD hearts. Conclusions: CyA administered at reperfusion reduces mitochondrial damage, limits infarct size, and preserves function in transplanted DCD hearts.
Abstract 112: The 3CL Protease Of SARS-CoV2 Induces Sarcomeric Degradation Through Cleavage Of The Giant Protein Obscurin
Authors: Nora Yucel, Quentin McAfee, Maria G Paterlini, Zoltan Arany
Journal: Circulation Research (2021)

We hypothesized that the 3CL protease (3CLPro) is responsible for the sarcomere degradation observed in cardiomyocytes infected by SARS-COV2. Overexpression of 3CLPro, but not a catalytically inactive mutant, resulted in breakdown of sarcomeres characterized by intact Z-disk/thin filament subunits that has been recently reported (Perez-Bermejo, et al, 2021) in SARS-COV2 infection. To identify potential host protein targets of 3CLPro in an unbiased fashion we screened the human proteome using a cut-site scoring algorithm that we developed. Scoring, ie likelihood of 3CL protease cleavage, was based off experimental data (Chuck et al, 2010) previously published on the highly homologous (96%) 3CL protease from SARS-COV. This scoring was followed by refinement by secondary structure prediction to identify cut-sites that lie in unstructured regions that are thus thus more likely to be accessible to the protease. Using this method, we identified &gt;1000 potential high-likelihood cut sites across the proteome. Further filtering by proteins with cardiomyocyte expression showed 5 high-likelihood sites within the giant sarcomeric protein, Obscurin (OBSCN), as well as many other structural and signaling proteins which we experimentally validated. Expression of 3CLPro in IPSC cardiomyocytes resulted in significantly reduced OBSCN staining without alterations in Z-disk, thin filament, or thick filament proteins by both western blot and immunocytochemistry. In addition, imaging showed loss of OBSCN at sites with intact Z-disk/thin filament subunits. Thus we propose that activity of 3CLPro is a significant contributor to sarcomere breakdown in SARS-COV2 infection via degradation of Obscurin.
Evaluating Medical Therapy for Calcific Aortic Stenosis
Authors: Brian R. Lindman, Devraj Sukul, Marc R. Dweck, Mahesh V. Madhavan, Benoit J. Arsenault, Megan Coylewright, W. David Merryman, David E. Newby, John Lewis, Frank E. Harrell, Michael J. Mack, Martin B. Leon, Catherine M. Otto, Philippe Pibarot
Journal: Journal of the American College of Cardiology (2021)
Abstract 10093: Incidence of Sudden Cardiac Death After Percutaneous Coronary Intervention
Authors: Ryo Nakamaru, Nozomi Niimi, Taku Inohara, Yasuyuki Shiraishi, Nobuhiro Ikemura, Masahiro Suzuki, Shigetaka Noma, Yohei Numasawa, Keiichi Fukuda, Shun Kohsaka
Journal: Circulation (2021)

Introduction: Sudden cardiac death (SCD) remains a major concern for the patients that undergo percutaneous coronary intervention (PCI). We sought to investigate the incidence and contributing clinical factors of SCD after PCI. Methods: We analyzed 8791 consecutive patients who underwent PCI between 2008 and 2019 from 15 institutions, and evaluated the cumulative incidence of SCD after PCI. The cause of death was adjudicated by an independent event committee. SCD was defined as unexpected death without a non-cardiovascular case in a previously stable patient within 24 hours from the onset. Cox proportional hazards modeling was used with the Fine and Gray method to account for competing SCD risk. Results: In the present cohort, the mean age was 68.3±11.3 years, and the prevalence of previous heart failure (HF), which was ascertained from hospital records regardless of systolic function status, was 4.6%. Of these, 4592 (52.2%) underwent PCI for acute coronary syndrome (ACS). The cumulative incidence of all-cause death and SCD was 3.47% and 0.44%, respectively in 2 years. SCDs occurred more frequently immediately after PCI in ACS patients; however, the total incidence of SCD was similar in ACS and stable coronary artery disease (CAD) patients at 2 years (0.45% vs 0.44%, p = 0.91 for log-rank test) (Figure). Overall, presence of previous HF was associated with risk of SCD (crude incidence [vs. non-heart failure patients] 2.29 vs. 0.29%; adjusted hazard ratio 6.60, 95% CI 3.09-14.1, p&lt;0.01) rather than clinical presentation (e.g. ACS vs. stable CAD; adjusted hazard ratio 1.29, 95% CI 0.65-2.54, p=0.47). Conclusions: The cumulative incidence of SCD was ~0.5% in the contemporary multicenter PCI registry. Rather than the clinical presentation, the presence of previous HF was associated with a higher risk of SCD.