tbuckley/cabot-search huggingface dataset:
Abstract 453: The G Protein-coupled Estrogen Receptor GPER/GPR30 is a Potential Therapeutic Target for Cardiovascular Inflammation
Authors: Roxana Flores, Victor Nizet, Paul A Insel, Ross Corriden
Journal: Circulation Research (2016)

Abstract: Neutrophil extracellular traps (NETs), DNA-based structures that play an important role in pathogen killing/capture, are also thought to contribute to inflammatory disease and have been implicated in thrombosis. Pharmacological agents that can modulate the formation of extracellular traps are as-yet unknown. We hypothesized that targeting G protein-coupled receptors (GPCRs) may provide such agents and thereby could aid in treating inflammation in the cardiovascular system. Here, we investigated the role of the G protein-coupled estrogen receptor (GPER/GPR30), which has recently been shown to play a role in innate immune function (Cabas et al. J Immunol . 191: 4628-39 [2013]). Quantitative PCR revealed that GPER is highly expressed in human neutrophils isolated from healthy male and female donors. Fluorescent quantification of extracellular DNA using PicoGreen revealed that both selective (G-36) and general (raloxifene) antagonists of GPER, but not selective antagonists for the nuclear estrogen receptors ERa (MPP) or ERb (PHTPP) inhibited phorbol myristate acetate (PMA)-induced NET production by human neutrophils. These results were verified using high throughput imaging of fixed, SytoxGreen-stained neutrophils. The activity of GPER antagonists appeared to be independent of Erk1/2 signaling and reactive oxygen species (ROS) generation, pathways that are mediators of NET production. Immunocytochemistry revealed that G-36 treatment of neutrophils raises their concentration of cAMP, which can inhibit production of NETs. Taken together, our data suggest that GPER may be a novel therapeutic target for modulating NET production and inflammation in the cardiovascular system.
EFFECT OF DIAGNOSTIC INTERMITTENT HIGH MECHANICAL INDEX IMPULSES DURING AN ULTRASOUND ENHANCING AGENT INFUSION ON GLOBAL AND REGIONAL LONGITUDINAL STRAIN IN PATIENTS WITH ABNORMAL SYSTOLIC FUNCTION
Authors: Arif Albulushi, Lijun Qian, Daniel Mathers, Joan Olson, Feng Xie, Thomas Porter
Journal: Journal of the American College of Cardiology (2020)
COMORBIDITIES IN PULMONARY ARTERIAL HYPERTENSION (PAH): INSIGHTS FROM THE REAL-WORLD OPSUMIT® USERS (OPUS) REGISTRY
Authors: Sudarshan Rajagopal, Richard Channick, Kelly Chin, Nick H. Kim, Megan Flynn, Sandrine Leroy, Rose Ong, Graham Wetherill, Vallerie V. McLaughlin
Journal: Journal of the American College of Cardiology (2020)
Uncovering cognitive constraints is the bottleneck in resource-rational analysis
Authors: Cvetomir Dimov
Journal: Behavioral and Brain Sciences (2020)

Abstract A major constraint in resource-rational analysis is cognitive resources. Yet, uncovering the nature of individual components of the human mind has progressed slowly, because even the simplest behavior is a function of most (if not all) of the mind. Accelerating our understanding of the mind's structure requires more efforts in developing cognitive architectures.
ESTROGEN STABILIZES MITOCHONDRIAL MEMBRANE POTENTIAL IN ANGIOTENSIN-II CHALLENGED PORCINE AORTIC SMOOTH MUSCLE CELLS: RELEVANCE TO THE LOWER INCIDENCE AND LATER ONSET OF ABDOMINAL AORTIC ANEURYSM IN WOMEN
Authors: S. David Gertz, Ayelet Zuckerman, Dan Gilon, Ronen Beeri, Dean Nachman, Lilach Gavish
Journal: Journal of the American College of Cardiology (2020)
Leukemic phase of Richter transformation: A mimic of acute myeloid leukemia that responded to Ibrutinib monotherapy
Authors: Hui Liu, Yi Miao, Alessandra Ferrajoli, Guilin Tang, Timothy McDonnell, L. Jeffrey Medeiros, Shimin Hu
Journal: American Journal of Hematology (2020)

Richter transformation (RT) is defined as a histologic progression from chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) to a more aggressive lymphoma.This is most commonly diffuse large B-cell lymphoma (DLBCL), and rarely, classic Hodgkin lymphoma.RT occurs in approximately 2%-10% of patients with CLL/SLL with a transformation rate of 0.5%-1% per year. 1 Risk factors for RT include advanced Rai stage, lymph node size ≥3 cm, elevated serum lactate dehydrogenase (LDH), and the following features of the CLL cells: expression of CD38 and ZAP70, unmutated IGHV gene, TP53 aberrations, and lack of del(13)(q14). 2,3In most patients, RT manifests as DLBCL that is clonally related to previous CLL/SLL and IGHVunmutated. 1 Patients with clonally related RT respond poorly to conventional chemotherapy regimens and have a dismal outcome with a median survival of <1 year. 1 Furthermore, novel agents rarely result in durable complete remission of RT of DLBCL-type, suggesting an unmet therapeutic need.
Comments on the article: “Withdrawal of low-dose prednisone in SLE patients with a clinically quiescent disease for more than 1 year: a randomised clinical trial”
Authors: Mohammad Reza Mousavi, Erfan Taherifard
Journal: Annals of the Rheumatic Diseases (2020)

We recently have read with great interest the article written by Mathian et al entitled “Withdrawal of low-dose prednisone in SLE patients with a clinically quiescent disease for more than 1 year: a randomised clinical trial” published in 19 December 2019.1 The study assessed development of flares in patients with systemic lupus erythematosus (SLE) with clinically inactive disease course on maintenance versus withdrawal of 5 mg/day prednisone over a 12-month period. This study showed that withdrawal of this low-dose glucocorticoid was associated with a fourfold increase in the risk of flares. Although this study is impressive and provides the strongest evidence regarding the efficacy of low-dose prednisone in the prevention of the disease flares, there are some concerns that may endanger the validity of the study.

First, as this study …
Clinical significances of ErbB family receptors, Myc, and mitogen-activated protein kinase (MAPK) in patients with early-stage non-small cell lung cancer.
Authors: Vienna Ludovini, Guido Bellezza, Fortunato Bianconi, Ivana Ferri, Lorenza Pistola, Antonella Flacco, Elisa Baldelli, Rita Chiari, Vincenzo Minotti, Francesca Romana Tofanetti, Annamaria Siggillino, Mark Ragusa, Jacopo Vannucci, Francesco Puma, Angelo Sidoni, Lucio Crinò
Journal: Journal of Clinical Oncology (2012)

e21094 Background: EGFR deregulation has been extensively studied in non small-cell lung cancer (NSCLC), but less is known about the expression and role of other ErbB receptors and their downstream signal transductions. Myc and MAPK are key downstream components of the EGFR pathway and have significant roles in cell survival, proliferation, and growth. The purpose of this study is to determine the prognostic value of EGFR, ErbB2, ErbB3, ErbB4, Myc and MAPK by immunohistochemistry (IHC) in early stage NSCLC. Methods: 109 NSCLC were evaluated: median age was 67 years (range 40–84); Male/Female:93/16; squamous (SCC)/adenocarcinoma (ADC)/BAC/other: 52/36/3/18; smoker/never smoker:100/9, and stage I/II/III:67/17/25. The tumors with ≥10% positive cells were classified positive, further confirmed by Receiver Operating Characteristic (ROC) analysis. Kaplan-Meier estimates of survival and time to recurrence were calculated for clinical and biologic variables using Cox model for multivariate analysis Results: EGFR and EbrB3 were associated with SCC (p&lt;0.0001 and p=0.004, respectively) whereas ErbB2 and Myc with ADC (p=0.004 and p&lt;0.0001, respectively) . EGFR and ErbB3 were significantly associated (p=0.003), as well as MAPK and ErbB4 (p=0.02). At a median follow-up of 75 months the contemporary overexpression of EGFR, ErbB2 and MAPK was associated with shorter disease free survival (DFS) (HR=5.4, p=0.002) and overall survival (OS) (HR=8.9, p&lt;0.0001). At multivariate analysis adjusting for stage, the co-expression of EGFR, ErbB2 and MAPK was an independent predictor for worse DFS and OS (HR=5.7, p=0.004; HR=8.67, p&lt;0.001, respectively). Conclusions: Our results suggest that in early stage NSCLC, the co-expression of EGFR, ErbB2 and MAPK predicted a worse prognosis. ErbB3, ErbB4 and Myc were not prognostic factors. Such features may have important implications for future targeted therapies. We thank Italian Association for Cancer Research (AIRC) for supporting the study.
Pre-existing inflammatory immune microenvironment predicts the clinical response of vulvar high-grade squamous intraepithelial lesions to therapeutic HPV16 vaccination
Authors: Ziena Abdulrahman, Noel de Miranda, Edith M G van Esch, Peggy J de Vos van Steenwijk, Hans W Nijman, Marij J. P. Welters, Mariette I E van Poelgeest, Sjoerd H van der Burg
Journal: Journal for ImmunoTherapy of Cancer (2020)

Background Vulvar high-grade squamous intraepithelial lesion (vHSIL) is predominantly induced by high-risk human papilloma virus type 16 (HPV16). In two independent trials, therapeutic vaccination against the HPV16 E6 and E7 oncoproteins resulted in objective partial and complete responses (PRs/CRs) in half of the patients with HPV16 + vHSIL at 12-month follow-up. Here, the prevaccination and postvaccination vHSIL immune microenvironment in relation to the vaccine-induced clinical response was investigated. Methods Two novel seven-color multiplex immunofluorescence panels to identify T cells (CD3, CD8, Foxp3, Tim3, Tbet, PD-1, DAPI) and myeloid cells (CD14, CD33, CD68, CD163, CD11c, PD-L1, DAPI) were designed and fully optimized for formalin-fixed paraffin-embedded tissue. 29 prevaccination and 24 postvaccination biopsies of patients with vHSIL, and 27 healthy vulva excisions, were stained, scanned with the Vectra multispectral imaging system, and automatically phenotyped and counted using inForm advanced image analysis software. Results Healthy vulvar tissue is strongly infiltrated by CD4 and CD8 T cells expressing Tbet and/or PD-1 and CD14 + HLA-DR + inflammatory myeloid cells. The presence of such a coordinated pre-existing proinflammatory microenvironment in HPV16 + vHSIL is associated with CR after vaccination. In partial responders, a disconnection between T cell and CD14 + myeloid cell infiltration was observed, whereas clinical non-responders displayed overall lower immune cell infiltration. Vaccination improved the coordination of local immunity, reflected by increased numbers of CD4 + Tbet + T cells and HLA-DR + CD14 + expressing myeloid cells in patients with a PR or CR, but not in patients with no response. CD8 + T cell infiltration was not increased after vaccination. Conclusion A prevaccination inflamed type 1 immune contexture is required for stronger vaccine-induced immune infiltration and is associated with better clinical response. Therapeutic vaccination did not overtly increase immune infiltration of cold lesions.
IMPACT OF CHRONIC KIDNEY DISEASE ON THE SIX-MONTH READMISSION RATE OF PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION: A NATIONWIDE ANALYSIS
Authors: Aaqib H. Malik, Srikanth Yandrapalli, Syed Zaid, Suchith Shetty, Wilbert S. Aronow, Hasan Ahmad, Howard A. Cooper, Julio Panza
Journal: Journal of the American College of Cardiology (2020)
THE ASSOCIATION OF ENDOTHELIAL DYSFUNCTION AND IMPAIRED ARTERIAL WALL PROPERTIES WITH RETINAL VEIN OCCLUSION
Authors: Nikolaos Gouliopoulos, Gerasimos Siasos, Evangelos Oikonomou, Marilita Moschos, Evanthia Bletsa, Panagiota K. Stampouloglou, Dimitrios Athanasiou, Efstathios Dimitropoulos, Georgia Siasou, Georgios Marinos, Dimitris Tousoulis
Journal: Journal of the American College of Cardiology (2020)
Design of anti-inflammatory heparan sulfate to protect against acetaminophen-induced acute liver failure
Authors: Katelyn Arnold, Yongmei Xu, Erica M. Sparkenbaugh, Miaomiao Li, Xiaorui Han, Xing Zhang, Ke Xia, Mark Piegore, Fuming Zhang, Xiaoxiao Zhang, Mike Henderson, Vijayakanth Pagadala, Guowei Su, Lisi Tan, Pyong Woo Park, Richard T. Stravitz, Nigel S. Key, Robert J. Linhardt, Rafal Pawlinski, Ding Xu, Jian Liu
Journal: Science Translational Medicine (2020)

Synthetic heparan sulfate protects against drug-induced acute liver failure by inhibiting the proinflammatory activity of HMGB1/RAGE axis.
US Hospital Type and Proximity to Mass Shooting Events
Authors: Sage R. Myers, Joseph D. DeSimone, Scott A. Lorch, Molly Passarella, Keri M. Cronin, Michael L. Nance
Journal: JAMA Surgery (2020)

This study used data on mass shootings to examine the proximity of adult trauma centers, pediatric trauma centers, and non–trauma center hospitals to such events.
Outcome and determinants of failure to complete primary <scp>R‐CHOP</scp> treatment for reasons other than non‐response among patients with diffuse large B‐cell lymphoma
Authors: Tove Wästerlid, Sara Harrysson, Therese M.‐L. Andersson, Sara Ekberg, Gunilla Enblad, Per‐Ola Andersson, Mats Jerkeman, Sandra Eloranta, Karin E. Smedby
Journal: American Journal of Hematology (2020)

Abstract Patients with diffuse large B‐cell lymphoma (DLBCL) who fail to complete planned treatment with R‐CHOP due to toxicity are sparsely described. We investigated the extent of failure to complete treatment (six cycles or more, or three cycles + RT for patients with stage I disease) with R‐CHOP for reasons unrelated to non‐response, the determinants of such failure and the outcome among these patients. Three thousand one hundred and forty nine adult DLBCL patients who started primary treatment with R‐CHOP were identified through the Swedish lymphoma register 2007‐2014. Of these, 147 (5%) stopped prematurely after 1‐3 cycles of R‐CHOP for reasons unrelated to non‐response, 168 (5%) after 4‐5 cycles and 2639 patients (84%) completed planned treatment. Additionally, 195 (6%) patients did not complete treatment due to non‐response or death before treatment end. In a multivariable logistic regression model, age &gt; 75 years, poor performance status, extranodal disease and Charlson Comorbidity Index ≥1 were significantly associated with failure to complete planned R‐CHOP treatment for other reasons than non‐response. Non‐completion of treatment strongly correlated with survival. Five‐year overall survival for patients who received 1‐3 cycles was 26% (95% CI: 19%‐33%), 49% (95% CI: 41%‐57%) for 4‐5 cycles and 76% (74%‐77%) for patients who completed treatment. Failure to complete planned R‐CHOP treatment is an important clinical issue associated with inferior survival. Old age and poor performance status most strongly predict such failure. These results indicate a need for improved treatment tailoring for patients with certain baseline demographics to improve tolerability and chance for treatment completion.
Association of Dementia Owing to Alzheimer Disease With Mortality Rates Among Adults With Down Syndrome Older Than 35 Years
Authors: Rosalyn Jane Hithersay, Carla Marie Startin, Sarah Hamburg, Kin Y. Mok, John Hardy, Elizabeth M. C. Fisher, Victor L. J. Tybulewicz, Dean Nizetic, Andre Strydom
Journal: JAMA Neurology (2018)
RENAL TRANSPLANTATION REDUCES CARDIOVASCULAR RISK COMPARED TO MAINTENANCE DIALYSIS
Authors: Hiroto Aikawa, Takayuki Yabe, Shingo Matsumoto, Ryo Okubo, Hideo Amano, Rine Nakanishi, Mikihito Toda, Takanori Ikeda
Journal: Journal of the American College of Cardiology (2020)
RGS4 promotes allergen- and aspirin-associated airway hyperresponsiveness by inhibiting PGE2 biosynthesis
Authors: Gordon S. Wong, Jamie L. Redes, Nariman Balenga, Morgan McCullough, Nathalie Fuentes, Ameya Gokhale, Cynthia Koziol-White, Joseph A. Jude, Laura A. Madigan, Eunice C. Chan, William H. Jester, Sabrina Biardel, Nicolas Flamand, Reynold A. Panettieri, Kirk M. Druey
Journal: Journal of Allergy and Clinical Immunology (2020)

Allergens elicit host production of mediators acting on G-protein-coupled receptors to regulate airway tone. Among these is prostaglandin E2 (PGE2), which, in addition to its role as a bronchodilator, has anti-inflammatory actions. Some patients with asthma develop bronchospasm after the ingestion of aspirin and other nonsteroidal anti-inflammatory drugs, a disorder termed aspirin-exacerbated respiratory disease. This condition may result in part from abnormal dependence on the bronchoprotective actions of PGE2.We sought to understand the functions of regulator of G protein signaling 4 (RGS4), a cytoplasmic protein expressed in airway smooth muscle and bronchial epithelium that regulates the activity of G-protein-coupled receptors, in asthma.We examined RGS4 expression in human lung biopsies by immunohistochemistry. We assessed airways hyperresponsiveness (AHR) and lung inflammation in germline and airway smooth muscle-specific Rgs4-/- mice and in mice treated with an RGS4 antagonist after challenge with Aspergillus fumigatus. We examined the role of RGS4 in nonsteroidal anti-inflammatory drug-associated bronchoconstriction by challenging aspirin-exacerbated respiratory disease-like (ptges1-/-) mice with aspirin.RGS4 expression in respiratory epithelium is increased in subjects with severe asthma. Allergen-induced AHR was unexpectedly diminished in Rgs4-/- mice, a finding associated with increased airway PGE2 levels. RGS4 modulated allergen-induced PGE2 secretion in human bronchial epithelial cells and prostanoid-dependent bronchodilation. The RGS4 antagonist CCG203769 attenuated AHR induced by allergen or aspirin challenge of wild-type or ptges1-/- mice, respectively, in association with increased airway PGE2 levels.RGS4 may contribute to the development of AHR by reducing airway PGE2 biosynthesis in allergen- and aspirin-induced asthma.
Endothelium-Targeted Deletion of microRNA-15a/16-1 Promotes Poststroke Angiogenesis and Improves Long-Term Neurological Recovery
Authors: Ping Sun, Kai Zhang, Sulaiman H. Hassan, Xuejing Zhang, Xuelian Tang, Hongjian Pu, R. Anne Stetler, Jun Chen, Ke-Jie Yin
Journal: Circulation Research (2020)

Rationale: Angiogenesis promotes neurological recovery after stroke and is associated with longer survival of stroke patients. Cerebral angiogenesis is tightly controlled by certain microRNAs (miRs), such as the miR-15a/16-1 cluster, among others. However, the function of the miR-15a/16-1 cluster in endothelium on postischemic cerebral angiogenesis is not known. Objective: To investigate the functional significance and molecular mechanism of endothelial miR-15a/16-1 cluster on angiogenesis in the ischemic brain. Methods and Results: Endothelial cell-selective miR-15a/16-1 conditional knockout (EC-miR-15a/16-1 cKO) mice and wild-type littermate controls were subjected to 1 hour middle cerebral artery occlusion followed by 28-day reperfusion. Deletion of miR-15a/16-1 cluster in endothelium attenuates post-stroke brain infarction and atrophy and improves the long-term sensorimotor and cognitive recovery against ischemic stroke. Endothelium-targeted deletion of the miR-15a/16-1 cluster also enhances post-stroke angiogenesis by promoting vascular remodeling and stimulating the generation of newly formed functional vessels, and increases the ipsilateral cerebral blood flow. Endothelial cell-selective deletion of the miR-15a/16-1 cluster up-regulated the protein expression of pro-angiogenic factors VEGFA (vascular endothelial growth factor), FGF2 (fibroblast growth factor 2), and their receptors VEGFR2 (vascular endothelial growth factor receptor 2) and FGFR1 (fibroblast growth factor receptor 1) after ischemic stroke. Consistently, lentiviral knockdown of the miR-15a/16-1 cluster in primary mouse or human brain microvascular endothelial cell cultures enhanced in vitro angiogenesis and up-regulated pro-angiogenic proteins expression after oxygen-glucose deprivation, whereas lentiviral overexpression of the miR-15a/16-1 cluster suppressed in vitro angiogenesis and down-regulated pro-angiogenic proteins expression. Mechanistically, miR-15a/16-1 translationally represses pro-angiogenic factors VEGFA, FGF2, and their receptors VEGFR2 and FGFR1, respectively, by directly binding to the complementary sequences within 3′-untranslated regions of those messenger RNAs. Conclusions: Endothelial miR-15a/16-1 cluster is a negative regulator for postischemic cerebral angiogenesis and long-term neurological recovery. Inhibition of miR-15a/16-1 function in cerebrovascular endothelium may be a legitimate therapeutic approach for stroke recovery.
LEVOSIMENDAN INFUSION AND ACUTE HEART FAILURE PATIENTS: ROLE OF HLM CLASSIFICATION FOR THE IDENTIFICATION OF RESPONDERS AND NON-RESPONDERS
Authors: Andrea D'Amato, Paolo Severino, Mariateresa Pucci, Lucrezia Netti, Fabio Infusino, Marco Valerio Mariani, Rossana Scarpati, Danilo Alunni Fegatelli, Annarita Vestri, Viviana Maestrini, Massimo Mancone, Francesco Fedele
Journal: Journal of the American College of Cardiology (2020)
CORONARY ARTERY CALCIUM SCORE-DIRECTED PRIMARY PREVENTION WITH STATINS BASED ON THE 2018 ACC/AHA MULTISOCIETY CHOLESTEROL GUIDELINES
Authors: Jana Taron, Asya Lyass, Joseph Massaro, Taylor F. Mahoney, Rachel Q. Ehrbar, Vasan S. Ramachandran, D’Agostino B. Ralph, Udo Hoffmann, Michael T. Lu
Journal: Journal of the American College of Cardiology (2020)
EFFECTIVENESS OF CATHETER-BASED PATENT FORAMEN CLOSURE IN DECOMPRESSION SICKNESS PREVENTION: LONG-TERM FOLLOW-UP
Authors: Jakub Honek, Martin Sramek, Ales Tomek, Ludek Sefc, Martin Horvath, Jaroslav Januska, Jiri Fiedler, Tomas Honek, Josef Veselka
Journal: Journal of the American College of Cardiology (2020)
Midterm oncologic outcomes after robotic-assisted laparoscopic radical prostatectomy.
Authors: Edris J Negron, Aria Razmaria, Rodrigo Ledezma, Kyle A Richards, Russell Zelig Szmulewitz, Gregory Zagaja
Journal: Journal of Clinical Oncology (2013)

e16084 Background: The robotic surgery has been extensively adopted in many surgical areas, especially in Urology. It's proven benefits (less blood loss, shorter recovery and reduced complication rates) has made it the most popular method to perform a radical prostatectomy nowadays. However, scarce data exists on the long-term oncologic outcome of robotic assisted laparoscopic prostatectomy (RALP). Since 2003, over 3,000 RALPs have been performed at our institution. We report the midterm oncologic outcome data of 1,054 patients with a median follow up of 60 months after RALP. Methods: From March 2003 to August 2008, 1,054 patients underwent RALP. Prospectively attained clinical data has been stored in an IRB approved database. Follow up has been maintained every 6 months for 2 years, and yearly thereafter. Salvage RALPs were excluded. Biochemical recurrence (BCR) defined as PSA &gt; 0.2ng/ml, disease free survival, cancer specific and overall survival were assessed. Results: Of the 1,054 patients within the database, 1,019 met the criteria for evaluation. Mean age was 60 years (IQR 55-65), and mean BMI 27 kg/m 2 (IQR 25-30). 181 patiemts (17.3%) were African Americans. Pre-operative mean PSA was 5.3 ng/ml (IQR 4.2-7.4). The majority of patient's clinical stage was T1c [ 776 (73.6%)] while 278 were T2. Biopsy Gleason score (GS) was 6, 7, and ≥8, in 666 (63.2%), 324 (30.7%), and 64 patients (6.1%), respectively. 298 patients underwent a bilateral pelvic lymph node dissection (28.3%). Pathologic GS was 6, 7 and ≥8, in 563 (53.5%), 431 (41%), and 58 patients (5.5%), respectively. The pathological tumor stage was T2 in 834 (79.3%), T3a in 164 (15.6%) and T3b in 54 (5.1%). 14 patients (1.3%) had nodal involvement. Positive surgical margins occurred in 205 cases (20%). BCR occurred in 123 patients (12%). 2 deaths due to prostate cancer (0.2%) and 7 due to other causes (0.7%). Cancer specific survival is thus 99.1% at the mean follow up (60months) by Kaplan Meier analysis. Conclusions: Our midterm oncologic outcomes are consistent with those previously reported in open radical prostatectomy series. Ongoing, long term follow up is necessary in order to solidify it's role in prostate cancer managment.