tbuckley/cabot-search huggingface dataset:
Abstract 027: Skeletal Muscle Adipose Tissue Infiltration is Associated with Mortality in Older Men
Authors: Iva Miljkovic, Tanushree Prasad, Jane Cauley, Christine Lee, Kristine Kristine, Peggy Cawthon, Andrew Hoffman, Joseph Zmuda
Journal: Circulation (2013)

Background: Emerging evidence suggests that myosteatosis (adipose tissue (AT) infiltration within skeletal muscle (intra-muscular AT) and within the fascia surrounding skeletal muscle (inter-muscular, visible AT), increases with aging, and is positively associated with cardiovascular disease (CVD) risk factors independent of overall adiposity. Studies examining this important fat depot and mortality are lacking. Methods: We evaluated the association of mortality (all-cause, CVD, and non-CVD) with BMI, peripheral quantitative computed tomography (QCT) measured components of lower leg skeletal muscle adiposity (total, subcutaneous, and intermuscular AT, and muscle attenuation), and dual-energy X-ray absorptiometry (DXA) measured total body and trunk fat in 1155 community-dwelling older men (mean age 77.2 ± 5.1 years). Date and cause of death from death certificates were reviewed by a central physician adjudicator, with cause of death classified by ICD9 codes. Cox proportional hazards models were used to estimate the risk of mortality. Stepwise regression was used to select significant covariates for multivariable models. We tested the following covariates: age, race, study site, lifestyle risk factors, DXA total body fat, skeletal muscle area, height, diabetes, hypertension, stroke, myocardial infarction, renal disease, cancer, lipids, and medications that may influence metabolism. Results: During a mean follow-up of 5.9 years (2005-2012), 246 participants died. Among these, 74 participants died from CVD, and 159 died from non-CVD causes (cancer and other causes). After adjustment for significant covariates, lower intra-muscular AT infiltration, as reflected by greater skeletal muscle attenuation, was associated with decreased all-cause mortality, decreased CVD mortality, and decreased non-CVD mortality (Hazard ratio [95% CI] per SD increase in skeletal muscle attenuation: 0.77 [0.67, 0.90], 0.72 [0.55, 0.94], and 0.81 [0.67, 0.97], respectively; all P-values &lt;0.02). No other measures of peripheral QCT and DXA measured adiposity or generalized obesity (BMI) were associated with mortality, regardless of the degree of adjustment. Conclusion: Our study revealed a previously unreported, independent association between myosteatosis and mortality among older men. Further studies are needed to establish if the association of myosteatosis with mortality is independent of inflammation, insulin resistance, visceral and other ectopic fat depots, and to identify possible biological mechanisms underlying this relationship.
Abstract 13971: Early Up-regulation of Myocardial Cxcr4 Expression is Critical for Cardiac Improvement With Chemical Preconditioning in Acute Myocardial Infarction
Authors: Megan Kamath, Matthew Kiedrowski, Kristal Weber, Farhad Forudi, Marc S Penn, Feng Dong
Journal: Circulation (2013)

Introduction: We have demonstrated the importance of the stromal cell-derived factor (SDF):CXCR4 axis in myocardial repair. Prolonged expression of SDF-1 to a time when cardiac myocytes and cardiac...
Abstract A81: A microRNA signature identified for chemoresistance and mesenchymal phenotype is also found in advanced pancreatic cancer
Authors: James W. Freeman, Alakesh Bera, Venkatasubbarao Kolaparthi
Journal: Cancer Research (2015)

Abstract Recent studies link cancer cells that possess an epithelial to mesenchymal transition (EMT) and cancer stem cell properties with chemoresistance and metastatic potential. Here, we investigated the molecular bases of the chemoresistant mesenchymal phenotype (CRMP) with emphasis on identifying a micro-RNA (miRNA) signature in advanced pancreatic ductal adenocarcinoma (PDAC). We developed a gemcitabine resistant cell model from a PDAC cell line, BxPC3. This gemcitabine resistant cell line (BxPC3-GZR) showed a pronounced mesenchymal phenotype and expressed high levels of CD44 a marker found on stem cells and showed a highly significant increase in expression of nine miRNAs and decrease in eight miRNAs. Based on relevance to cancer and on validation by q-RT-PCR we chose six of the miRNAs (miR-100, miR-125b, miR-21, miR-205, miR-27b and miR-455-3p) as a signature to determine whether they were similarly deregulated in 43 advanced PDAC tumor specimens previously analyzed as part of the Total Cancer Genome Atlas (TCGA). A strong correlation was observed for five of the six miRNAs in the tumor specimens compared to normal pancreas tissue. To assess the functional relevance we initially focused on miRNA-125b, which is over-expressed in both cellular CRMP and advanced PDAC. Knockdown of miRNA-125b in BxPC3-GZR and Panc-1 cells caused a partial reversal of the mesenchymal phenotype and enhanced response to gemcitabine. Moreover, RNA-seq data from each of 40 advanced PDAC tumor specimens from the TCGA data base indicate a negative correlation between expression of miRNA-125b and five of six potential target genes (BAP1, BBC3, NEU1, BCL2, STARD13). Thus far, two of these target genes, BBC3 and NEU1, that are tumor suppressor genes but not yet studied in PDAC, appear to be functional targets of miR-125b since knockdown of miR125b caused their up regulation. The results of this study suggests that CRMP is caused in part by deregulation of a specific set of miRNAs and that these miRNAs are also deregulated in advanced PDAC. These miRNAs and their molecular targets may serve as targets to enhance sensitivity to chemotherapy and reduce metastatic spread. Citation Format: James W. Freeman, Alakesh Bera, Venkatasubbarao Kolaparthi. A microRNA signature identified for chemoresistance and mesenchymal phenotype is also found in advanced pancreatic cancer. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr A81.
Abstract 594: Identification of Cell Cycle Regulatory and Inflammatory Genes as Predominant Targets of p38 MAPK in the Heart
Authors: Jaana Rysa, Olli Tenhunen, Mika Ilves, Ylermi Soini, Heikki Ruskoaho, Hanna Leskinen
Journal: Circulation (2006)

Mitogen-activated protein kinases (MAPKs) regulate cardiomyocyte growth and apoptosis in response to extracellular stimulation, but the downstream effectors that mediate their pathophysiological effects remain poorly understood. We determined the targets and role of p38 MAPK in the heart in vivo by using local adenovirus-mediated gene transfer of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38α in rats. DNA microarray analysis of animals with cardiac-specific overexpression of p38 MAPK revealed that 264 genes were upregulated and 2 genes were down-regulated more than 2-fold. A large number of previously unknown p38 target genes were found, such as cell cycle regulators cyclins A2, and B1 as well as transcription factors Runx1 and Krox20. Many fundamental inflammation-associated genes like interleukin-6 (IL-6) and toll-like receptor-2 as well as cell adhesion genes selectin E and osteopontin were also elevated in p38 MAPK overexpressing hearts. The complete list of 266 differentially expressed genes was loaded into PathwayAssist to build the interaction map showing potential connections among genes regulated by p38 MAPK overexpression in the heart. A central signaling molecule in this pathway was IL-6, which has been implicated in the regulation of 20 genes found to be affected by p38 MAPK. Further, using gel mobility shift assays we identified several cardiac transcription factors including serum response factor (SRF), activator protein-1 (AP-1), nuclear factor κB (NF-κB) that were directly activated by p38 MAPK overexpression. Finally, we determined the functional significance of the altered cardiac gene expression profile by histological analysis and echocardiographic measurements, which indicated that p38 MAPK overexpression induced gene expression results in myocardial cell proliferation, inflammation and fibrosis. In conclusion, we defined the novel target genes and transcription factors as well as the functional effects of p38 MAPK in the heart. Our results demonstrate that the pathophysiological consequence of p38 MAPK overexpression is myocardial cell proliferation and inflammation associated with fibrosis in the adult heart.
Image Quality and Radiation Exposure With a Low Tube Voltage Protocol for Coronary CT Angiography
Authors: Jörg Hausleiter, Stefan Martinoff, Martin Hadamitzky, Eugenio Martuscelli, Iris Pschierer, Gudrun M. Feuchtner, Paz Catalán-Sanz, Benedikt Czermak, Tanja S. Meyer, Franziska Hein, Bernhard Bischoff, Miriam Kuse, Albert Schömig, Stephan Achenbach
Journal: JACC. Cardiovascular imaging (2010)
Use of medication and in vivo exposure in volunteers for panic disorder research
Authors: C B Taylor, R King, J Margraf, A Ehlers, M Telch, W T Roth, W S Agras
Journal: American Journal of Psychiatry (1989)

A survey of 794 subjects volunteering for studies of panic disorder with or without phobic avoidance revealed that fewer than 15% had received imipramine and fewer than 15% had undergone in vivo exposure, although the majority had engaged in some form of counseling and had used benzodiazepines. Subjects with spontaneous panic attacks reported more avoidance than subjects with situational attacks. One-half of the subjects were unemployed. The authors recommend wider use of the available effective treatments for panic disorder and phobic avoidance.
P1233 : Retargeting of bile salt export pump (BSEP) and criteria of favourable outcome in children with progressive familial intrahepatic cholestasis type II (PFIC-II)
Authors: S. Varma, N. Revencu, X. Stephenne, I. Scheers, F. Smets, A. Beleza, C. de Magnée, R. Reding, T. Roskams, E. Sokal
Journal: Journal of Hepatology (2015)
Bovine leukemia virus infection is significantly associated with risk of breast cancer
Authors: Gertrude Buehring, Hua Min Shen, Hanne Jensen, Gladys Block
Journal: Cancer Research (2007)

1747  The purpose of this study is to determine if bovine leukemia virus (BLV) infection of human mammary epithelium is associated with a risk of developing breast cancer. Mammary cancer in mice is caused by a retrovirus, mouse mammary tumor virus, transmitted from mother to nursing pups. Since humans consume more cows milk than human milk, we were interested in determining if a bovine virus might be involved in the etiology of breast cancer. BLV is an oncogenic retrovirus that infects >90% of US dairy herds and >14% of beef herds. Less than 5% of infected cattle develop leukemia and are culled. Most infected cattle remain healthy, are retained in the herd, and are sources of beef and dairy products. Evidence that humans can become infected with BLV is accumulating. Previous studies indicated IgG antibodies to BLV in 39% of volunteers. BLV capsid protein and proviral DNA have been detected in human mammary epithelium. Using a case-control study design, we evaluated 213 samples of formalin-fixed breast tissue sections from 110 women with breast cancer and 103 controls (women with no history of breast cancer). Samples were obtained from 4 catchment areas of the Cooperative Human Tissue Network, and the racial composition of the donors was 26% African American and 74% European American. We tested for the presence of BLV proviral DNA using in situ PCR with primers from the tax region of BLV, which codes for the oncogenic protein and is not homologous to any known region of endogenous human retroviruses. Positive reactions were present only in mammary epithelium. BLV was positive in 59% of cases and 29% of controls. Data were analyzed using unconditional logistic regression with adjustment for donor age, race, catchment area, and length of time in formalin-fixed state. The odds ratio for breast cancer associated with BLV positivity was 3.22, 95% confidence interval = 1.7-6.2, P
Abstract 4117: A Comparison of Cardiac MRI Peri-Infarct Border Zone Quantification Strategies for the Prediction of Ventricular Tachycardia Inducibility
Authors: Jason C Rubenstein, Daniel Lee, Edwin Wu, Alan Kadish, Rod S Passman, Jeffrey J Goldberger
Journal: Circulation (2008)

Peri-infarct border zone (BZ) as quantified by delayed-enhancement cardiac MRI (CMR) has been proposed as a risk stratification tool, and is associated with increased mortality, but has been measured by various methods in the literature. We assessed which BZ analysis best predicts inducible arrhythmia during electrophysiological study (EPS). Methods: CMR was performed in 47 patients with CAD referred for EPS to assess for ventricular tachyarrhythmias (VT). CMR data was analyzed for BZ quantification by three methods. Method I used pixels 2–3 standard deviations over the mean of normal tissue, expressed as % of LV mass. Method II (Yan) used the same pixels but is expressed as % of infarct size. Method III (Schmidt) used a full-width, half-max method. EPS results were classified as negative (non-inducible) or positive (monomorphic VT). Patients with indeterminate EPS outcomes (VF or polymorphic VT, n=9) were not included in this analysis. Results: There were 38 subjects-age 60.2 ± 10.8 yrs, 68% male. During EPS, 20 patients were non-inducible and 18 had induced monomorphic VT (MVT). EF was not significantly different between non-inducible patients and those with MVT (33.4 ± 11.9% vs. 28.1 ± 9.3, p=0.13). Infarct size was significantly different (15.0 ± 11.6% vs. 26.4 ± 12.0%, p = 0.005). BZ by method I was significantly different (1.4 ± 1.3% vs. 3.1 ± 1.5%, p = 0.001), but not by method II (15.2 ± 21.3% vs. 8.0 ± 4.8%, p = 0.17) or method III (4.1 ± 4.5g vs. 3.7 ± 3.7g, p = 0.756). Multivariate analysis demonstrated that BZ by method I was an independent predictor of EPS outcome after controlling for infarct size (OR 1.97 per % change, 95% CI 1.04 to 3.73, p = 0.04). Method I BZ remained an independent predictor when controlling for both infarct size and EF, (OR 2.12 per % change, 95% CI 1.06 to 34.22, p = 0.03). Correlation between techniques was variable (Method I vs. Method II R=0.77, p=0.001; Method I vs. Method III R=0.03, p=0.86; Method II vs. Method III R=0.15, p&lt;0.32). Conclusion: This study demonstrates significant variability between the published methods for measuring BZ. We also show that large BZ by Method I is a stronger predictor of inducible MVT during EPS than EF and infarct size. BZ may be yet another CMR marker of elevated risk of arrhythmia, but requires more rigorous definition.
Anti-CD19 CAR T Cells Administered after Low-Dose Chemotherapy Can Induce Remissions of Chemotherapy-Refractory Diffuse Large B-Cell Lymphoma
Authors: James N Kochenderfer, Robert Somerville, Lily Lu, Alex Iwamoto, James C Yang, Christopher Klebanoff, Udai Kammula, Richard M Sherry, Shi Victoria, Constance Yuan, Steven Feldman, Tatyana Feldman, Andre Goy, Kathleen E Morton, Mary Ann Toomey, Steven A. Rosenberg
Journal: Blood (2014)
Abstract 11353: Value of Real-Time 3D Adenosine Stress Contrast Echocardiography in Patients with Known or Suspected Coronary Artery Disease
Authors: Constantina Aggeli, Ioannis Felekos, Emanouil Poulidakis, Panagiota Pietri, George Roussakis, Konstantinos Toutouzas, Christodoulos Stefanadis
Journal: Circulation (2011)

Aim:  The aim of this study was to evaluate the feasibility of myocardial wall-motion and perfusion assessment using contrast echocardiography during real-time three-dimensional (RT3D) adenosine stress test, and compare its diagnostic accuracy with the two-dimensional (2D) method using coronary angiography as reference.   Methods and results:  Patients with known or suspected coronary artery disease (CAD) have been submitted to adenosine stress contrast echocardiography and coronary angiography, within a one month-period. 2D apical four-, two- and three- chamber, as well as three-dimensional (3D) pyramidal full-volume datasets were acquired at rest and at peak stress. The 17-segment division of the left ventricle was used and each segment was evaluated based on wall motion and perfusion. Sixty patients (age 60.1±8.5 years, 38 men) were enrolled, i.e. 1020 segments were evaluated at rest and at peak stress. Out of the 1020 segments, wall motion analysis was feasible, at rest, in 98% and in 97% of 2D and 3D depicted segments respectively (p=NS). The respective evaluated segments at peak stress were 93% for 2D and 92% for 3D. Perfusion could be evaluated, at rest, in 97% and in 96% of 2D and 3D depicted segments, respectively (p=N;S). At peak stress the evaluated percentages were 92% for 2D and 90% for 3D. Wall motion analysis per patient revealed that the sensitivity and specificity of 2D to detect CAD were 80% and 82% and of RT3D echocardiography were 82% and 64%, respectively, while in the per patient perfusion analysis the respective percentages were 88%, 64% for 2D, and 90%, 73% for RT3D. Regarding left anterior descending artery and right coronary system, there seems to be no statistical significant difference in terms of wall motion and perfusion evaluation between the two modalities.   Conclusions:  Real-time 3D adenosine stress echocardiography is a feasible and valuable technique to evaluate myocardial wall-motion and perfusion in patients with suspected coronary artery disease, despite existing problems concerning lower spatial and temporal resolution as compared with 2D echocardiography.
Irish general practitioners learn immediate cardiac care
Authors: A. Murphy, G. Bury
Journal: BMJ (1995)

and a defibrillator as well as my medical bag up five flights of stairs in a block of flats, where the lift is invariably out of order or its floor swimming in urine?What do I do with the equipment while visiting patients who do not require it?If I leave it in the car the possibility of its being stolen is high.Have the authors considered the practical implications of their advice?
Inhibition of growth of saccharomyces cerevisiae by n SAIDS: Genetic evidence for involvement of the map kinase pathway
Authors: Jae-Ho Lee, Steven J. Shiff
Journal: Cancer Research (2004)

1381   Non-steroidal anti-inflammatory drugs (NSAIDs) exhibit common clinical therapeutic and biochemical effects. Evidence continues to mount that these agents, in addition to their well-known traditional beneficial effects, also reduce the risk of colorectal cancer development. This cancer chemopreventive effect has been hypothesized to result, at least in part, from their ability to inhibit colon cell turnover kinetics, i.e., inhibition of proliferation and induction of apoptosis. This effect may not be wholly dependent upon their inhibitory actions on cyclooxygenase (COX) activity and prostaglandin production, as cells that do not express COX isoenzymes can be inhibited by these compounds. Furthermore, several non COX molecular events have been shown to be altered in mammalian cells by these agents, including signal transduction mediated by NF-κB, PPARs,  ras , and MAP kinases. All have been proposed as fundamentally important mechanisms responsible for the cancer chemopreventive effects of NSAIDs. However, the relative significance of any of these pathways in mediating their inhibitory effects on colonocytes is not clear.  Methods:  In a previous study,  Saccharomyces cerevisiae  was adopted as a model system to identify, impartially, potentially important target molecules or molecular pathways contributing to the inhibitory effects of NSAIDs on cell growth and survival. Using gain of function (over expression cDNA library) and loss of function (targeted deletion library) screening assays encompassing nearly the entire  S. cerevisiae  genome, several genes conferring resistance to growth inhibition on SCP medium supplemented with 75 μM Sulindac sulfide (SS) were identified. To reveal relationships between these various genes, a bioinformatic analysis was performed using the yeast genome database SGD.  Results:  Through searches of the gene interaction databases BIND and GRID, one gene identified in the over-expression screen,  arc40 , and two genes from the deletion library screen,  bro1  and  bul1 , were found to interact with several members of the yeast MAP kinase pathway. To validate this bioinformatic data, haploid strains of yeast created by the gene deletion consortium with targeted deletions of selected MAP kinase pathway genes were grown on plates supplemented with 50 and 75 μM SS to assess their growth characteristics. Strains deficient in BCK1 (MAP kinase kinase kinase) or MPK1 (MAP kinase) were hypersensitive, while an MKK2 (MAP kinase kinase) deficient strain was resistant to SS treatment.  Conclusions:  These data indicate that the growth inhibitory properties of NSAIDs, and perhaps their COX-independent cancer chemoprevention effects, are mediated by effects on the MAP kinase signal transduction pathway in both yeast and mammalian cells.
Incidence and impact outcome of hyperglycaemia in severe scorpion envenomed children requiring intensive care admission
Authors: Kamilia Chtara, Mabrouk Bahloul, Olfa Turki, Najeh Baccouche, Kais Regaieg, Chokri Ben Hamida, Hedi Chelly, Imen Chabchoub, Anis Chaari, Mounir Bouaziz
Journal: Intensive Care Medicine (2015)
Abstract 11042: Heart Failure and Mortality in the Elderly With Impaired Cardiac and Pulmonary Function
Authors: Salman Waheed, John Gottdiener, Paulo H Chaves, Anne B Newman, Jie J Cao
Journal: Circulation (2013)

Background: Both left ventricular systolic dysfunction (LVSD) and impaired pulmonary function (IPF) are prevalent in the elderly, and are associated with increased risk of adverse clinical outcomes...
<i>Falling Stars as Seen From the Balloon</i>
Authors: Thomas B. Cole
Journal: JAMA (2015)

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