tbuckley/cabot-search huggingface dataset:
Public Locations of Cardiac Arrest
Authors: LindaBecker, MickeyEisenberg, CarolFahrenbruch, LeonardCobb
Journal: Circulation (1998)

Background—The purpose of this study was to describe the public locations of cardiac arrest and to estimate the annual incidence of cardiac arrest per site to determine optimal placement of automatic external defibrillators (AEDs). This was a retrospective cohort study. Methods and Results—Locations of cardiac arrest were abstracted from data collected by emergency medical service programs in Seattle and King County, Washington, from January 1, 1990, through December 31, 1994. Types of commercial and civic establishments were tallied and grouped into 23 location categories consistent with Standard Industrial Codes, and the number of sites within each location category was determined. With the addition of “public outdoors” and “automobiles” as categories, there were 25 location categories. During the study period, 7185 arrests occurred, 1130 (16%) of which were in public locations. An annual incidence of cardiac arrest per site was calculated. Ten location categories with 172 sites were identified as havin...
Abstract 17518: Good Attendance to Cardiac Rehabilitation is Associated with Achievement of Low C-Reactive Protein Levels in Patients after Acute Myocardial Infarction
Authors: TakahitoDoi, ReonKumasaka, TetsuoArakawa, MichioNakanishi, TeruoNoguchi, TakahiroOhara, ShigefumiFukui, KazuhiroNakao, MasanobuYanase, HiroshiTakaki, MasaharuIshihara, SatoshiYasuda, YoichiGoto
Journal: Circulation (2014)

Backgrounds: Cardiac rehabilitation with exercise training (CR/ET) has been reported to be associated with reduction in C-Reactive Protein (CRP). In patients with acute coronary syndrome receiving statin therapy, achievement of CRP levels below 2mg/L is known to be important for long-term event-free survival. However, the determinants of achieving low CRP after CR/ET are not fully understood. Methods: To address this issue, we studied 490 consecutive acute myocardial infarction (AMI) patients who participated in our CR/ET program and underwent measurements for serum CRP at the beginning and the end of the 3-month CR program. Patients with abnormally high CRP (>= 20mg/L at baseline, >=10mg/L at 3 months) or on hemodialysis were excluded. Patients were divided into 2 groups according to CRP levels at the end of the 3-month CR/ET: Low-CRP group (CRP 2.0mg/dl, n=76). Results: At baseline, there were no significant differences between the two groups in age (Low-CRP gro...
Increased Release of NO During Ischemia Reduces Myocardial Contractility and Improves Metabolic Dysfunction
Authors: KoichiNode, MasafumiKitakaze, HiroakiKosaka, KazuoKomamura, TetsuoMinamino, MichitoshiInoue, MichihikoTada, MasatsuguHori, TakenobuKamada
Journal: Circulation (1996)

Background We have reported that myocardial ischemia increases nitric oxide (NO) production. Several lines of evidence suggest that NO reduces myocardial contraction. Therefore, we tested whether endogenous NO decreases the inotropic response of the ischemic myocardium and whether endogenous NO is beneficial in the metabolic function of ischemic myocardium. Methods and Results The left anterior descending coronary artery was perfused with blood from the left carotid artery in 72 dogs. An infusion of NG-nitro-l-arginine methyl ester (L-NAME), an inhibitor of NO synthase, did not affect fractional shortening (FS) under nonischemic conditions. After reduction of perfusion pressure so that coronary blood flow decreased to 60% of the control value, FS of the perfused area decreased, and intravenous infusion of isoproterenol increased FS. Before and during intravenous infusion of isoproterenol under conditions of coronary hypoperfusion, FS was significantly increased in the L-NAME group compared with the untrea...
The Theory of Kent
Authors: Mauricelev, Ruthlerner
Journal: Circulation (1955)

This is an anatomic study of an alternate theory of conduction, first advanced by Kent, that conduction from atria to ventricles is by way of numerous muscular communications, rather than exclusively through the bundle of His. The entire atrioventricular rings of 22 fetal and newborn hearts, in addition to the A-V node, bundle and bundle branches in five adult hearts, were serially sectioned. No muscular communications outside the conduction system were found. Communications between the A-V node, bundle and left bundle branch with the ventricular musculature were frequently found in the fetus, and less commonly in the adult.
Cardiologist is struck off for sexually assaulting young male armed forces recruits
Authors: Clare Dyer
Journal: BMJ (2018)

A senior consultant cardiologist and former colonel in the British Army has been struck off the UK medical register for sexually assaulting young male service recruits who consulted him for cardiovascular examinations.

Neil Ineson, 62, carried out the assaults at Frimley Park Hospital in Surrey, where he was director of medicine. He also served as an assessor for the General Medical Council for many years.

Ineson, who is currently in prison serving a four year sentence for 11 counts of sexual assault involving seven young RAF airmen and Household Cavalry soldiers,1 did not attend …
Photonic Sensing: Stretchable Optomechanical Fiber Sensors for Pressure Determination in Compressive Medical Textiles (Adv. Healthcare Mater. 15/2018)
Authors: Joseph D. Sandt, Marie Moudio, J. Kenji Clark, James Hardin, Christian Argenti, Matthew Carty, Jennifer A. Lewis, Mathias Kolle
Journal: Advanced Healthcare Materials (2018)

Color-tunable photonic fibers, which reversibly change their vivid reflective coloration upon elongation, derive their functionality from the use of highly stretchable elastomers in familiar photonic structures. In article 1800293, Mathias Kolle and co-workers demonstrate how these devices can substantially improve the efficiency and efficacy of compression therapy, by acting as easily-interpreted indicators of applied pressure when integrated into elastic bandages.
Abstract 3481: Elucidating the metabolic crosstalk between lymphatic endothelial cells and breast cancer using 1H NMR metabolomics
Authors: Suehelay Acevedo-Acevedo, Douglas C. Millar, Sean P. Palecek
Journal: Cancer Research (2018)

Abstract Breast cancer is the second most commonly diagnosed cancer among women worldwide. Patient death is typically caused by metastasis development rather than the primary tumor. Metastasis in breast cancer has been shown to occur via blood and lymphatic vessels. Research shows that breast cancer cells ‘educate' lymphatic and blood endothelial cells to support tumor growth by stimulating growth factor secretion and directing tumor dissemination. In addition, cell metabolism is altered during malignant transformation. Cancer cells have increased energy and macromolecule biosynthesis requirements to sustain rapid proliferation. However, it remains unclear how tumor endothelial cell metabolism is altered and how metabolism contributes to tumor metastasis. Therefore, this study aims to use 1H NMR metabolomics to identify breast cancer-endothelial cell metabolic interactions in a high-throughput manner. Firstly, we studied if in vitro co-culture with breast cancer altered endothelial cell metabolism. We identified distinct metabolic profiles for lymphatic endothelial cells (LECs) grown in monoculture or co-culture with three different breast cancer cell lines. Principal component analysis revealed LECs co-cultured with breast cancer cells clustered separately from control LECs. Interestingly, LECs co-cultured with triple negative breast cancer cells clustered together with LECs co-cultured with HER2+ breast cancer cell lines indicating that the metabolic changes occurring in these LECs were similar. One-way ANOVA with Tukey's HSD post-hoc analysis revealed 17 significantly different metabolites between all five conditions analyzed including: lactate, glucose, phosphocholine, aspartate, acetate, glycerophosphocholine, lysine and methionine. Quantitative metabolite set enrichment analysis revealed 13 metabolic pathways that were significantly enriched between control LECs and LECs co-cultured with breast cancer cell lines. Enriched pathways included: glycolysis, gluconeogenesis, pyruvate metabolism and protein biosynthesis. Together, these results indicate that culturing LECs with certain breast cancer lines causes significant changes in endothelial metabolism. Alterations in endothelial cell metabolism in response to breast cancer co-culture can further our understanding of tumor-vascular interactions and may lead to identification of metabolic biomarkers and a better understanding of breast cancer metastasis. Citation Format: Suehelay Acevedo-Acevedo, Douglas C. Millar, Sean P. Palecek. Elucidating the metabolic crosstalk between lymphatic endothelial cells and breast cancer using 1H NMR metabolomics [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 3481.
Abstract 559: Development of a novel approach to identify cancer drivers for hepatitis B virus-associated hepatocellular carcinoma
Authors: SHIH-CHUN SHEN, Amy Jiaen Lu, John Caleb Shieh, Yih-Ping Su, Bilal Nasir, Ning Ling, Daryl T. Lau, Jamin D. Steffen, Fwu-Shan Shieh, Wei Song, Ying-Hsiu Su
Journal: Cancer Research (2018)

Abstract Infection with Hepatitis B virus (HBV) is a major etiology of hepatocellular carcinoma (HCC), the third leading cause of cancer-related deaths worldwide. Studies have shown that some cells infected with HBV contain integrated viral DNA, and integrated viral DNA has been observed more frequently in HCC than in non-HCC infected liver. Although integration occurs randomly throughout host chromosomes, recurrent integration sites have been reported. Interestingly, these integration sites are located in genes known to be involved in carcinogenesis. During HCC carcinogenesis, tumor cells undergo uncontrolled clonal expansion in which a particular integration junction will become dominant (or a major junction). We have adapted a method known as primer extension capture (PEC) to enrich integrated HBV DNA for next-generation sequencing (NGS) to detect these integration junctions that occur at low frequency. We next developed a novel program, “HccDriverFinder,” to identify major junctions, incorporate PubMed data mining for driver identification, detect HBV mutations (revealing a striking 98.8% HCC-linked mutations identified in cancer), and visualize integration events. By analyzing NGS data generated from 13 matched HCC and adjacent non-HCC tissue samples, we found specific integrations in known targets such as TERT and CCNE1, and uncovered new recurrent HBV integration sites in genes including CSAD and ABCC13 (both of which are reportedly linked with tumorigenesis). We have further optimized the PEC approach to enrich for the whole HBV genome and have applied it to urine DNA from 31 hepatitis, 27 cirrhosis, and 29 HCC patients for the potential of identifying HBV junctions in circulation. Our approach holds the promise of building a driver identification kit for HCC detection, drug development and precision medicine. Citation Format: SHIH-CHUN SHEN, Amy Jiaen Lu, John Caleb Shieh, Yih-Ping Su, Bilal Nasir, Ning Ling, Daryl T. Lau, Jamin D. Steffen, Fwu-Shan Shieh, Wei Song, Ying-Hsiu Su. Development of a novel approach to identify cancer drivers for hepatitis B virus-associated hepatocellular carcinoma [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 559.
Coordinate Control of Proliferation and Migration by the p27Kip1/Cyclin-Dependent Kinase/Retinoblastoma Pathway in Vascular Smooth Muscle Cells and Fibroblasts
Authors: AntonioDíez-Juan, VicenteAndrés
Journal: Circulation Research (2003)

Previous studies have demonstrated a protective effect of the cyclin-dependent kinase (CDK) inhibitor p27Kip1 against atherosclerosis and restenosis, two disorders characterized by abundant proliferation and migration of vascular smooth muscle cells and adventitial fibroblasts. These therapeutic effects might result from p27Kip1-dependent suppression of both cell proliferation and migration. However, the interplay between cell growth and locomotion remains obscure. We show here that p27Kip1 inhibits cellular changes that normally occur during cell locomotion (eg, lamellipodia formation and reorganization of actin filaments and focal adhesions). Importantly, a p27Kip1 mutant lacking CDK inhibitory activity failed to inhibit vascular smooth muscle cell and fibroblast proliferation and migration. Moreover, a constitutively active mutant of the retinoblastoma protein (pRb) insensitive to CDK-dependent hyperphosphorylation inhibited both cell proliferation and migration. In contrast, inactivation of pRb by for...
Comprehensive 4-Dimensional Magnetic Resonance Flow Analysis After Successful Heart Transplantation Resolves Controversial Intraoperative Findings and Reveals Complex Hemodynamic Alterations
Authors: MichaelMarkl, JuliaGeiger, RaoulArnold, AnnaStroh, DomagojDamjanovic, DanielaFöll, FriedhelmBeyersdorf
Journal: Circulation (2011)
Abstract 4872: ONC201 induction of apoptosis in hPheo1 cell line supports use of this oral agent in ongoing phase 2 clinical trial against neuroendocrine tumors (NCT03034200)
Authors: Austin M. Proudfit, Peter M. Anderson, Neetu Gupta
Journal: Cancer Research (2018)

Abstract ONC201 is an imipridone that induces TRAIL and causes apoptosis in cancer cell lines, but not normal cells. Recent data shows the dopamine-like DRD2 receptor binds ONC201 and pheochromocytoma-paragangliomas (PC-PG) have &amp;gt;10x more DRD2 than any other human cancer (TCGA data). We present pre-clinical data on dose response and time course of ONC201 against hPheo1, a PC-PG cell line, that support a recently opened phase 2 clinical trial of weekly oral ONC201 in neuroendocrine tumors (NETs) including PC-PG. The human pheochromocytoma cell line, hPheo1, was treated with ONC201 and studied for in vitro anti-cancer activity. Effects on cell viability/proliferation were measured via cell counting with trypan blue exclusion. Post-treatment target-protein levels were assessed via western blotting. Additionally, cells were stained with Annexin V and analyzed using flow cytometry for markers of apoptosis. Upon treatment with ONC201, hPheo1 cells experienced a dose-dependent decrease in cell viability and proliferation with peak effect at 72 h post-treatment (GI50=3.2 μM). Substantial inhibition of pro-survival kinases, Akt and ERK, were confirmed at 72 hours to further support the drug's efficacy and elucidate on a corresponding mechanism of action. The anti-proliferative effects of the drug were gradual over a 96 h time period, rather than an abrupt, intense response. In addition, apoptosis was confirmed at 24 and 96 h, with Annexin V+ cells detectable by FACS. Pre-clinical data show excellent anti-cancer efficacy of ONC201 against PC-PG cells at concentrations achievable in vivo. These findings suggest both anti-proliferative effects and induction of apoptosis lead to anti-cancer activity. The gradual influence of ONC201 on PC-PG cells, rather than rapid cell destruction argues against a scenario where immediate catecholamine release could result in severe hypertension. These pre-clinical data support safe use of ONC201 against PC-PG in vivo and other NETs in our ongoing Phase 2 clinical trial (NCT03034200; investigator-initiated IND132665). Citation Format: Austin M. Proudfit, Peter M. Anderson, Neetu Gupta. ONC201 induction of apoptosis in hPheo1 cell line supports use of this oral agent in ongoing phase 2 clinical trial against neuroendocrine tumors (NCT03034200) [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 4872.
Increased Angiotensin-Converting Enzyme Activity in Coronary Artery Specimens From Patients With Acute Coronary Syndrome
Authors: ShiroHoshida, JunjiKato, MasamiNishino, YasuyukiEgami, ToshihiroTakeda, MasayoshiKawabata, JunTanouchi, YoshioYamada, TakenobuKamada
Journal: Circulation (2001)

Background—Angiotensin-converting enzyme (ACE) inhibitors are effective in the secondary prevention of ischemic heart disease, but they do not reduce the rate of restenosis. Vascular ACE activity in the culprit coronary lesions of these patients, however, has never been quantified. Methods and Results—We measured the ACE activity of vascular tissue obtained by directional coronary atherectomy in patients with acute coronary syndrome (n=17) and in patients with stable ischemic heart disease (n=36), with and without restenosis. The ACE activity of the culprit coronary lesions was significantly increased in patients with acute coronary syndrome (0.87±0.12 nmol · min–1 · mg protein–1; P<0.01) but not in patients with ischemic heart disease with restenosis (n=11, 0.19±0.05 nmol · min–1 · mg protein–1) when compared with those patients with ischemic heart disease without restenosis (n=25, 0.20±0.05 nmol · min–1 · mg protein–1). There was no difference between the ACE activity of the coronary tissue of the in-st...
Stratification Of Chronic Lung Allograft Dysfunction Phenotypes Using Proteomic Profiling Of Bronchoalveolar Lavage-Fluid
Authors: N. F. Smirnova, H. B. Schiller, N. Kneidmger, J. Behr, M. Mann, O. Eickelberg
Journal: American Journal of Respiratory and Critical Care Medicine (2017)
Abstract 5239: Gli is a primary driver of prostate cancer cell growth
Authors: Na Li, Jackson Moore, Sarah Troung, Mannan Nouri, Jane Foo, Ralph Buttyan
Journal: Cancer Research (2018)

Abstract Canonical Hedgehog signaling is a Smoothened- (Smo-) driven process that activates transcription from Gli proteins. However, we have shown that Hedgehog is activated in prostate cancer (PCa) cells by a non-canonical, non-Smo-dependent process mediated by the binding of transcriptionally active androgen receptors (AR) to the protein processing domain on Gli2/3. This binding competes with β-TrCP, and protects Gli3 (the predominant Gli isoform in PCa cells) from cleavage to its truncated repressor form (Gli3R). Our observations are consistent with the idea that AR transcriptional activity (mediated by liganded full-length AR or by truncated ARs) is effectively coupled to Gli activity in PCa. Here we present our evidence that Gli is the primary driver of PCa cell growth and that suppression of Gli transcriptional activity or interference with AR binding to Gli (using a decoy peptide) is a strong growth suppressor of androgen-dependent (AD) and -independent (AI) PCa cell lines. Gli transcription was inhibited by GANT61 or HPI-1 or by exogenous overexpression of a Gli3R cDNA. Each of these conditions significantly suppressed the growth of LNCaP parental (AD) and LNCaP-AI cells. Knockdown of Gli3 with siRNA decreased growth of a wide variety of PCa cell lines up to 75%. Finally, a decoy peptide (270aa) containing the Gli2 AR binding site displaced Gli3 from AR complexes, increased the levels of Gli3R and significantly suppressed growth of AI cell lines. Collectively, our data supports the idea that androgen-driven growth of PCa is a result of non-canonical activation of Gli and that interference with Gli binding to DNA or with the Gli-AR interaction is a means for suppressing PCa cell growth. Citation Format: Na Li, Jackson Moore, Sarah Troung, Mannan Nouri, Jane Foo, Ralph Buttyan. Gli is a primary driver of prostate cancer cell growth [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 5239.
Abstract 4666: An evaluation of breast cancer cellular membrane lipid-extracted nanoliposomes (CLENs) in relation to formulation design, stability, mechanism of cellular entry and cardioprotective function in vitro
Authors: Hanan M. Alharbi, Robert B. Campbell
Journal: Cancer Research (2018)

Abstract One of the longstanding issues limiting the use of chemotherapeutic agents is the lack of tumor specificity, which leads to systemic toxicity. Therefore, various targeted nanocarriers have been developed to concentrate the cytotoxic drug agents at tumor regions to avoid uptake by normal healthy tissues. Previous studies from our laboratory have demonstrated that cell membrane lipid-extracted nanoliposomes (CLENs) are capable of selective targeting compared to nanoliposomes consisting of mainly conventional lipid materials. Also, CLENs were relatively nontoxic when employed at concentrations traditionally used to evaluate nanoparticles in vitro. However, parameters such as lipid composition, size, and surface charge all have a direct impact on liposomal cellular uptake. In this study, we prepared different CLENs different molar ratios of natural and cellular-derived lipids extracted directly from breast cancer cells (4T1), cholesterol, and DPPE-PEG-5000. The formulations were used to investigate the mechanisms of CLENs uptake and determine the underlying mechanisms regulating cellular entry. In the study, CLENs were used to evaluate cytotoxicity and cellular uptake for both target and off-target cell populations. CLENs containing cholesterol and DPPE-PEG-5000 (70/25/5) were able to retain doxorubicin in relevant therapeutic concentrations. CLEN formulations were able to exert selective cytotoxic drug effects against different target breast cancer cells in vitro. 4T1 CLENs containing cholesterol and DPPE-PEG-5000 (70/25/5) demonstrated greater binding to 4T1 (target) cells compared to CLENs prepared using 4T1 lipid extracts alone. The binding was not only temperature- and time-dependent, but also composition- and cell type-dependent. Off-target effect studies showed that 4T1 CLENs were taken up minimally by off-target cells (including normal breast fibroblasts and normal myocytes), compared to controls. Our studies collectively support the use of lipid extracts derived from target cells for selective drug targeting and enhanced cytotoxicity. Future studies will explore underlying mechanisms of cellular entry and cardioprotective function. Citation Format: Hanan M. Alharbi, Robert B. Campbell. An evaluation of breast cancer cellular membrane lipid-extracted nanoliposomes (CLENs) in relation to formulation design, stability, mechanism of cellular entry and cardioprotective function in vitro [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 4666.