tbuckley/cabot-search huggingface dataset:
Abstract P264: Young Adults, Technology, and Weight Loss: A Focus Group Study
Authors: JannaStephens, JerilynAllen
Journal: Circulation (2015)

Overweight and obesity are major health concerns in young adults. Technology has been integrated into weight loss interventions, however little is known about the effective use of this technology in young adults. The purpose of this study was to explore through focus groups the opinions of young adults on the use of technology and text messaging for weight loss as well knowledge and attitudes towards healthy eating and physical activity. Three focus group sessions were conducted with 17 young adults who wanted to lose weight or maintain weight. One moderator used a single discussion guide with questions to address the topics. Sessions were taped and the discussion was transcribed Two investigators conducted a qualitative analysis using a process of thematic analysis. Categories from each topic were combined to form themes, which provided a comprehensive view of the data. Ages of participants ranged from 18-25 years (mean=21 years). Across all focus groups 59% were female, and 76% were minorities. Five the...
Abstract 11888: Mechanical Circulatory Support Increases Return of Spontaneous Circulation in Patients Receiving Mechanical Chest Compressions for Cardiac Arrest in the Cardiac Catheterization Laboratory
Authors: Joseph M Venturini, Elizabeth Retzer, J Raider Estrada, Janet Friant, David Beiser, Dana Edelson, Jonathan Paul, John Blair, Sandeep Nathan, Atman P Shah
Journal: Circulation (2016)

Introduction: In the cardiac catheterization laboratory (CCL), use of a mechanical chest compression (MCC) device allows acute cardiac life support (ACLS) and percutaneous interventions to occur simultaneously. Use of MCC in the CCL ensures adequate chest compressions without relying on manual compression providers. This is especially important in the context of recent studies that have shown that therapies offered in the CCL increase survival in patients with cardiac arrest. Furthermore, mechanical circulatory support (MCS) has been shown to improve outcomes of patients with cardiac arrest, but it is not known whether emergent, percutaneous MCS initiation provides clinical efficacy in patients undergoing MCC-assisted ACLS in the CCL. Methods: We performed a retrospective analysis of patients who received MCC-assisted ACLS in the CCL at our institution between April 2014 and February 2016. Baseline characteristics, resuscitation characteristics, and clinical outcomes were compared between patients who were treated with MCS and those who were not. Unpaired two-sample t-tests were used to compare continuous variables. Fisher’s exact test was used to compare categorical variables. Results: Thirty-one patients received MCC-assisted ACLS in the CCL. Twenty-two patients (71%) were treated with MCS (14 external cardiac life support (ECLS), 3 Impella, 5 intra-aortic balloon pump (IABP)). Patients who received MCS were significantly more likely to achieve return of spontaneous circulation (ROSC) than those who did not receive MCS (95% v 22%, p = 0.00). Thirty-day survival was more common in the group receiving MCS (Table 1). The majority of patients who received MCS suffered cardiac arrest either outside the hospital or in the emergency department. Conclusions: The addition of percutaneous MCS to MCC-assisted ACLS increased the rate of ROSC. These findings support the use of emergent percutaneous MCS during MCC-assisted ACLS in the CCL.
Abstract 5607: Tissue factor is a novel oncotarget for immunotherapy of triple-negative breast cancer using a second generation ICON in orthotopic mouse models of human and murine TNBC cell line- and patient-derived xenografts
Authors: Zhiwei Hu, Rulong Shen, Amanda Campbell, Elizabeth McMichael, Lianbo Yu, Bhuvaneswari Ramaswamy, Cheryl A. London, Tian Xu, William E. Carson
Journal: Cancer Research (2018)

Abstract Triple-negative breast cancer (TNBC) is often associated with BRCA1 and BRCA2 mutation and is a leading cause of breast cancer death. Due to the lack of validated target molecules, there is currently no approved targeted therapy for TNBC. Tissue factor (TF) is a common yet specific surface target receptor for cancer cells, tumor vascular endothelial cells and cancer stem cells in several types of solid cancers. Here we report evidence supporting the idea that TF is a novel surface target for TNBC patients and cancer lines with BRCA1 and BRCA2 mutations. We showed that TF is over-expressed on TNBC cells and tumor neovasculature in greater than 85% of TNBC patients (n=14) when using standard paraffin-embedded tumor tissues and in nearly 60% of TNBC patients (n=157) when employing tissue microarray slides, but was not detected in adjacent normal breast tissue. We also describe the development of a second-generation TF-targeting immunoconjugate with improved efficacy and higher safety threshold compared to the original immunoconjugate. We showed that L-ICON1 is effective in killing TNBC cells via antibody-dependent cell-mediated cytotoxicity in vitro and in treating human and murine TNBC cell line- and patient-derived xenografts in vivo in preclinical orthotopic mouse models. These results suggest that TF is a novel oncotarget in TNBC and targeting TF may constitute a novel targeted immunotherapy for TNBC patients. The findings in this preclinical study warrant further clinical investigation. Citation Format: Zhiwei Hu, Rulong Shen, Amanda Campbell, Elizabeth McMichael, Lianbo Yu, Bhuvaneswari Ramaswamy, Cheryl A. London, Tian Xu, William E. Carson. Tissue factor is a novel oncotarget for immunotherapy of triple-negative breast cancer using a second generation ICON in orthotopic mouse models of human and murine TNBC cell line- and patient-derived xenografts [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5607.
Abstract 1544: Subcutaneous adiposity is an independent predictor in metastases patients
Authors: Ngan M. Tsang
Journal: Cancer Research (2018)

Abstract Background: The prognostic significance of muscle and adipose tissue in cancer patients provide an appropriate assessment of body composition in recent years. We investigated the independent prognostic significance of visceral and subcutaneous adipose on survival in metastases patients. Methods: We measured visceral adipose tissue index (VATI), subcutaneous adipose tissue index (SATI), and muscle index in 959 metastases patients via computed tomography at L3 level. Univariate and multivariate cox proportional hazards model were used to determine mortality hazard ratio (HR) and were presented in corresponding 95% CI. Result: SATI and gender are independent predictors among patients with metastases disease. High SATI linked to lower mortality (HR:0.749; 95% CI: 0.640-0.877; p&amp;lt;0.001) and longer overall survival (8.38 months; 95% CI, 0.10-137.42) in compared to low SATI patients (4.44 months; 95% CI, 0.03-108.36). Conclusion: The body composition appeared to be true determinants of the prognosis in metastases patients. The research provides an understanding of the association between subcutaneous adipose and the overall survival in metastases patients. Citation Format: Ngan M. Tsang. Subcutaneous adiposity is an independent predictor in metastases patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1544.
Tangier Disease With Continuous Massive and Longitudinal Diffuse Calcification in the Coronary Arteries
Authors: RyutaroKomuro, ShizuyaYamashita, SatoruSumitsuji, Ken-ichiHirano, TakaoMaruyama, MakotoNishida, FumihikoMatsuura, AkifumiMatsuyama, TaizoSugimoto, NoriyukiOuchi, NaohikoSakai, TadashiNakamura, ToruFunahashi, YujiMatsuzawa
Journal: Circulation (2000)
Important Role of Endogenous Erythropoietin System in Recruitment of Endothelial Progenitor Cells in Hypoxia-Induced Pulmonary Hypertension in Mice
Authors: KimioSatoh, YutakaKagaya, MakotoNakano, YoshitakaIto, JunOhta, HirokoTada, AkihikoKaribe, NaokoMinegishi, NorioSuzuki, MasayukiYamamoto, MasaoOno, JunWatanabe, KunioShirato, NaotoIshii, KazuoSugamura, HiroakiShimokawa
Journal: Circulation (2006)

Background— Recent studies have suggested that endogenous erythropoietin (Epo) plays an important role in the mobilization of bone marrow–derived endothelial progenitor cells (EPCs). However, it remains to be elucidated whether the Epo system exerts protective effects on pulmonary hypertension (PH), a fatal disorder encountered in cardiovascular medicine. Methods and Results— A mouse model of hypoxia-induced PH was used for study. We evaluated right ventricular systolic pressure, right ventricular hypertrophy, and pulmonary vascular remodeling in mice lacking the Epo receptor (EpoR) in nonerythroid lineages (EpoR−/− rescued mice) after 3 weeks of exposure to hypoxia. Those mice lack EpoR in the cardiovascular system but not in the hematopoietic system. The development of PH and pulmonary vascular remodeling were accelerated in EpoR−/− rescued mice compared with wild-type mice. The mobilization of EPCs and their recruitment to the pulmonary endothelium were significantly impaired in EpoR−/− rescued mice. B...
Abstract 17607: Impact of Red Cell Distribution Width on Long-term Mortality in Patients Treated With Statin After Percutaneous Coronary Intervention
Authors: Jun Shitara, Shuta Tsuboi, Katsumi Miyauchi, Manabu Ogita, Takatoshi Kasai, Tomotaka Dohi, Hirokazu Konishi, Ryo Naito, Shinichirou Doi, Hideki Wada, Hirohisa Endo, Shinya Okazaki, Kikuo Isoda, Satoru Suwa, Hiroyuki Daida
Journal: Circulation (2016)

Backgrounds: Many RCTs and meta-analysis have demonstrated statins reduce the risk of cardiovascular events in patients who underwent PCI. However, residual risk still remains even after administra...
SAT0741-HPR Cognitive-behavioural and social factors do not predict recurrent secondary health care use in patients with fibromyalgia: a longitudinal study
Authors: J.E. Vriezekolk, V.M. Vervoort, T.C. olde Hartman, T. van Helmond, W.H. van der Laan, R. Geenen, C.H. van den Ende
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> Health care use in fibromyalgia (FM) is relatively high. Besides disease-related variables, cognitive-behavioural factors have been concurrently associated with health care use. It is unknown whether cognitive-behavioural and social factors also predict future health care use. <h3>Objectives</h3> To identify cognitive-behavioural and social factors predicting recurrent secondary health care use in FM. <h3>Methods</h3> Data were drawn from a prospective cohort of recently diagnosed patients with fibromyalgia (n=199), spanning 18 months. Patients were recruited after receiving their diagnosis and protocolled treatment advice by a rheumatologist. Using self-report questionnaires, health care use, cognitive-behavioural (i.e. illness cognitions, pain coping, coping flexibility), social (i.e. invalidation by family, spousal responses to pain and well behaviour), sociodemographic and disease-related variables including comorbidities, severity of FM, and depressive and anxiety symptoms were collected. Primary outcome was recurrent secondary health care use at 18 months follow-up defined as the use or non-use for each of the following four categories of secondary health care: consultation with medical specialists, diagnostic procedures, admission to health care institutions, and multimodal treatment program. A patient was considered a recurrent secondary health care user, if secondary health care from at least one of the four categories was used in the past six months. Univariate and multivariate logistic regression models examined whether and which variables were predictors for recurrent secondary health care use. Internal validation was performed to correct for over-fit of the final multivariate model. <h3>Results</h3> Recurrent secondary health care use was lower than initial secondary health care use. Univariate analysis showed that having at least one comorbidity, depressive feelings, severe consequences of fibromyalgia, low personal control and a high severity of fibromyalgia predicted recurrent secondary health care use. In the multivariate model, having at least one comorbidity was the only remaining predictor for recurrent secondary health care use. <h3>Conclusions</h3> Our results suggest that the existence of comorbidities as communicated by the patient is the strongest warning signal for recurrent secondary health care use in FM. There seems no value in using cognitive-behavioural and social factors for early identification of patients with FM at risk for recurrent secondary health care use. <h3>Disclosure of Interest</h3> None declared
Abstract 57: Impaired Aldehyde Dehydrogenase 2 Activity Contributes To Inhibition Of Mitochondrial Respiration In Hyperglycemic Rats
Authors: VishalMali, MandarDeshpande, JiangXu, ShailendraGiri, Xiao-PingYang, SureshPalaniyandi
Journal: Circulation Research (2014)

Aldehyde dehydrogenase (ALDH) 2 is a mitochondrial isozyme of the heart involved in the metabolism of toxic aldehydes produced from oxidative stress. A decrease in ALDH2 levels and activity was reported in the hearts of experimental hyperglycemia along with an increase in 4-hydroxy-2-nonenal (4HNE). 4HNE is produced in the mitochondria upon lipid peroxidation and known to form adduct with mitochondrial proteins. We hypothesize that reduced ALDH2 activity impairs mitochondrial respiration due to 4HNE adducts formation, ultimately resulting in cardiac damage in hyperglycemia. A single dose (65 mg/kg; i.p.) of streptozotocin in rats resulted in hyperglycemia with a blood glucose level of 443 ± 9 mg/dl versus 121 ± 7 mg/dl in control animals, p<0.0001. N=7-11 in both groups. After 6 months of hyperglycemia, heart function was recorded and the rats were sacrificed. Increases in cardiomyocyte cross sectional area (446 ± 32 μm2 Vs 221 ± 10 μm2; p<0.0001) indicated cardiac hypertrophy in diabetic rats. Both diast...
Bcl-xL Gene Transfer Inhibits Bax Translocation and Prolongs Cardiac Cold Preservation Time in Rats
Authors: JianhuaHuang, KiminoriNakamura, YoshinoriIto, TakeshiUzuka, MasayukiMorikawa, SachieHirai, KeiTomihara, ToshihiroTanaka, YukariMasuta, KeijiIshii, KazunoriKato, HirofumiHamada
Journal: Circulation (2005)

Background— Apoptosis is an important cause of early graft loss after heart transplantation. Bcl-xL was reported to protect the heart against normothermic ischemia and reperfusion injury. In this study, we determined whether overexpression of Bcl-xL could inhibit tissue injury resulting from prolonged cold preservation followed by warm reperfusion of heart transplants. Methods and Results— Lewis rat hearts were transduced with an adenovirus vector harboring Bcl-xL cDNA (AxCAhBclxL) 4 days before collection of tissue. After preservation in University of Wisconsin solution at 4°C for 24 hours, the heart was either perfused with a Langendorff device ex vivo or used for heterotopic heart transplantation in vivo. Bcl-xL gene transfer significantly reduced the infarct size (23.0±2.6% versus 47.7±7.0% in saline control and 48.6±6.1% in vector control, P<0.01) after 2-hour reperfusion at 37°C with the Langendorff device and significantly decreased creatine kinase release (0.82±0.27 IU, versus 1.57±0.33 and 1.50±0...
Activation of gp130 Transduces Hypertrophic Signals via STAT3 in Cardiac Myocytes
Authors: KeitaKunisada, EirohTone, YasushiFujio, HideoMatsui, KeikoYamauchi-Takihara, TadamitsuKishimoto
Journal: Circulation (1998)

Background—gp130, a signal transducer of the IL-6–related cytokines, is expressed ubiquitously, including in the heart. The activation of gp130 in cardiac myocytes was reported to induce myocardial hypertrophy. The downstream side of gp130 consists of two distinct pathways in cardiac myocytes, one a Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway, the other a mitogen-activated protein kinase (MAPK) pathway. In the present study, we examined whether the JAK/STAT pathway, especially the STAT3-mediated pathway, plays a critical role in gp130-dependent myocardial hypertrophy by transfecting wild-type and mutated-type STAT3 cDNA to cardiac myocytes. Methods and Results—We constructed three kinds of replication-defective adenovirus vectors carrying wild-type (AD/WT) or mutated-type (AD/DN) STAT3 cDNA or adenovirus vector itself (AD). Cultured murine cardiac myocytes infected with adenovirus were stimulated with leukemia inhibitory factor (LIF), and the expression of c-fos and at...
Leaflet Escape in a New Bileaflet Mechanical Valve
Authors: TomasoBottio, DinoCasarotto, GaetanoThiene, LucaCaprili, AnnalisaAngelini, GinoGerosa
Journal: Circulation (2003)

Background— Leaflet escape is a mode of structural valve failure for mechanical prostheses. This complication previously has been reported for both monoleaflet and bileaflet valve models. We report 2 leaflet escape occurrences observed in 2 patients who underwent valve replacement with a TRI Technologies valve prosthesis. Methods and Results— At the University of Padua, between November 2000 and February 2002, 36 TRI Technologies valve prostheses (26 aortic and 10 mitral) were implanted in 34 patients (12 women and 22 men) with a mean age of 59.9±10.3 years (range, 30 to 75 years). There were 5 deaths: 3 in hospital, 1 early after discharge, and 1 late. Two patients experienced a catastrophic prosthetic leaflet escape; the first patient was a 52-year-old man who died 10 days after aortic valve and ascending aorta replacement, and the second was a 58-year-old man who underwent a successful emergency reoperation 20 months after mitral valve replacement. Examination of the explanted prostheses showed in both...
Abstract 1745: Inhibition of chemokine receptor 2 (CCR2) with a small molecule antagonist enhances the effectiveness of checkpoint inhibition by altering the tumor microenvironment in mouse colorectal tumors: Reducing tumor size and increasing long term survival
Authors: James J. Campbell, Christine Janson, Linda Ertl, Chris Li, Zhenhua Miao, Antoni Krasinski, Rebecca Lui, Venkat Mali, Jeffrey McMahon, Yibin Zheng, Yu Wang, Xiaoping Zang, Vicky Chhina, Marta Vilalta, Alice Kumamoto, Ton Dang, Shirley Liu, Simon Yao, Penglie Zhang, Thomas J. Schall, Rajinder Singh
Journal: Cancer Research (2018)

Abstract Mouse CT26 colorectal tumors are heavily infiltrated by tumor-specific CD8 T cells, but nevertheless grow rapidly in Balb/c mice. These tumors are partially responsive to anti-PD-1 (α-PD-1) monoclonal antibody therapy, which suggests that an active suppression of the tumor-specific cytotoxic T cells exists in the untreated tumor. As chemokine receptor 2 (CCR2) is expressed by a potentially suppressive leukocyte subset within these tumors (monocytic myeloid derived suppressor cells aka M-MDSCs), we aimed to test whether CCR2 blockade could enhance the anti-tumor effects of α-PD-1. We have found that the therapeutic effects of α-PD-1 therapy are appreciably enhanced by specific blockade of CCR2 via a small molecule antagonist. This combined α-PD-1/CCR2i approach significantly decreases overall tumor size and increases the proportion of long-term survivors, with more than 50% of the mice (up to 73%) showing complete regression of a previously established tumor. The effects of this combined therapy are dependent on the presence of CD8+ T cells, as tumors do not respond to the therapy in CD8-depleted mice. The anti-CT26 tumor response is specific: long term survivors are resistant to re-inoculation with the CT26 tumor (even without further dosing of either drug) but are not resistant to the 4T1 breast tumor. CCR2 antagonism alters the tumor microenvironment by reducing the number of M-MDSC per gram of tumor (a CCR2hi population phenotypically defined as CD11b+/Ly6G-/Ly6Chi). Reduction in tumor size is inversely proportional to the ratio of CD8 T cells to M-MDSC. These data are consistent with a hypothesis that CCR2 antagonism enhances α-PD-1 therapy by preventing M-MDSC from accumulating within the tumor, thus reducing their suppressive effects on cytotoxic T cells. Citation Format: James J. Campbell, Christine Janson, Linda Ertl, Chris Li, Zhenhua Miao, Antoni Krasinski, Rebecca Lui, Venkat Mali, Jeffrey McMahon, Yibin Zheng, Yu Wang, Xiaoping Zang, Vicky Chhina, Marta Vilalta, Alice Kumamoto, Ton Dang, Shirley Liu, Simon Yao, Penglie Zhang, Thomas J. Schall, Rajinder Singh. Inhibition of chemokine receptor 2 (CCR2) with a small molecule antagonist enhances the effectiveness of checkpoint inhibition by altering the tumor microenvironment in mouse colorectal tumors: Reducing tumor size and increasing long term survival [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1745.
Abstract 2621: Genomic determinants of progression and response to therapy in prospectively characterized glioma patients
Authors: Philip Jonsson, Andrew L. Lin, Shahiba L. Ogilvie, Shweta S. Chavan, Andrew T. McKeown, Natalie M. DiStefano, Marc Rosenblum, Lisa M. DeAngelis, Ingo K. Mellinghoff, Barry S. Taylor
Journal: Cancer Research (2018)

Abstract While the genomic landscape of low- and high-grade gliomas has been characterized and incorporated into further disease classification, its relationship to disease progression and treatment response remains poorly understood. To address this question, we integrated prospective clinical sequencing of 1,007 primary and recurrent tumors from 924 glioma patients with clinical and treatment phenotypes. Genomic alterations in effectors of cell cycle progression were a biomarker of aggressive disease in 1p19q intact IDH-mutant disease, arising preferentially in enhancing and recurrent tumors. When present at recurrence, the lesions were associated with rapid disease progression. These alterations were also present in all astrocytic tumors that ultimately relapsed with alkylating therapy-associated hypermutation. Analysis of matched pre-treatment and post-progression tumors indicated that cell cycle alterations preceded the emergence of hypermutation. In total, 391 patients (42%) harbored a potentially therapeutically actionable lesion in their tumor of which 73 patients (19%) received a diversity of targeted therapies. Both the type of mutation and its clonality were associated with therapeutic sensitivity in this cohort. For instance, RAF dimer-dependent BRAF hotspot mutations arose predominantly in IDH-wildtype glioblastomas, were subclonal, and affected patients did not respond to MAPK-directed therapy. In contrast, BRAF V600 hotspot mutations arose clonally in histologically distinct gliomas, both low- and high-grade, and responded to MAPK-directed therapy (either RAF, MEK or ERK inhibition). Collectively, these data reveal previously unrecognized genomic determinants of disease progression and treatment response in diverse types of glioma and serve as a rationale for utilizing genomic information in clinical care of patients with glioma. Citation Format: Philip Jonsson, Andrew L. Lin, Shahiba L. Ogilvie, Shweta S. Chavan, Andrew T. McKeown, Natalie M. DiStefano, Marc Rosenblum, Lisa M. DeAngelis, Ingo K. Mellinghoff, Barry S. Taylor. Genomic determinants of progression and response to therapy in prospectively characterized glioma patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2621.