tbuckley/cabot-search huggingface dataset:
Abstract 3760: Role of epithelial to mesenchymal transition in response to cisplatin in patient-derived ovarian carcinomas
Authors: Francesca Ricci, Federica Guffanti, Fratelli Maddalena, Patrizia Perego, Robert Fruscio, Romina Baldo, Sonia Magni, Massimo Broggini, Giovanna Damia
Journal: Cancer Research (2014)

Abstract Epithelial ovarian cancer has the highest mortality rate in the western world among gynecological malignancies. Approximately 70% of patients achieve complete remission after first-line cisplatin (DDP)-based therapy, but almost all patients relapse with resistant disease. Understanding the mechanisms at the basis of the resistance to therapy is of pivotal importance and xenografts models are instrumental to address this topic. We have recently been able to stabilize a panel of ovarian cancer xenografts that represent human tumors of origin both at the histological and molecular level. Seven xenografts were characterized for their sensitivity to DDP given once a week for 3 weeks at the dose of 5 mg/kg. A second DDP cycle was given to the regrowing tumors, mimicking clinical conditions. Xenografts were classified as “Responder” (R) or “Non-Responder” (NR) on the basis of their DDP-response. Interestingly, almost all xenografts were less sensitive to the second cycle of DDP. In an attempt to study the role of genes involved in Epithelial-Mesenchymal Transition (EMT), we evaluated by RT-PCR (by the Qiagen RT2 ProfilerTM PCR Array System) in untreated and DDP-treated R and NR xenografts the expression level of 86 EMT genes. By these analysis we wanted to investigate if some EMT genes could be predictive for DDP response, and if DDP treatment could itself induced EMT genes responsible for the observed DDP resistance. 12 genes (KRT14, BMP1, JAG1, PPPDE2, TFPI2, MSN, ITGA5, ITGAV, KRT7, FGFBP1, AHNAK and ESR1) were found to be more expressed in “NR” then “R” xenografts, and few were validated (i.e. AHNAK, JAG1). To address the second point, the fold change of gene expression was considered in DDP-treated versus control samples. 8 genes (ZEB2, TGFB1, WNT5B, MST1R, COL3A1, FN1,PLEK2, FGFBP1) involved in EMT activation were found to be upregulated by the DDP treatment, and are currently under validation. These studies would suggest a predictive role of upregulation of specific EMT genes in response to DDP treatment, and possibly in the development of its resistance. The validation of these genes in patients whose clinical response to a DDP based therapy is known, will help in defining predictive markers to tailor DDP therapy in ovarian cancer patients. Citation Format: Francesca Ricci, Federica Guffanti, Fratelli Maddalena, Patrizia Perego, Robert Fruscio, Romina Baldo, Sonia Magni, Massimo Broggini, Giovanna Damia. Role of epithelial to mesenchymal transition in response to cisplatin in patient-derived ovarian carcinomas. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3760. doi:10.1158/1538-7445.AM2014-3760
Abstract 16610: High Fat Diet-induced Obesity Is Associated With Increased Ischemia Susceptibility Due To Deregulated Activation Of The Rheb/mTORC1 Pathway And Inhibition Of Autophagy
Authors: Sebastiano Sciarretta, Peiyong Zhai, Dan Shao, Yasuhiro Maejima, Jeffrey Robbins, Massimo Volpe, Junichi Sadoshima
Journal: Circulation (2011)

Sebastiano Sciarretta, 2011 Finalist and Presenting Author
Abstract P136: Childhood BMI Associated With Low HDL-c Levels in Adolescence in a Chilean Cohort
Authors: Ann Von Holle, Kari North, Anne Justice, Eastern Kang, Estela Blanco, Sheila Gahagan
Journal: Circulation (2015)

Background: Global prevalence of childhood obesity has reached epidemic proportions. Elevated body mass index (BMI) leads to a cascade of negative health outcomes including hyperlipidemia, hypertension, and diabetes, thus increasing risk for cardiovascular disease (CVD). Some studies have documented an association between early childhood obesity and CVD risk factors. To date, studies have been primarily cross sectional and in European descent populations. Thus, the relationship between childhood obesity and later CVD risk is inadequately understood. To increase our understanding of this complex relationship, this study aims to assess the association between 5-year BMI and HDL-c levels at 17 years in a Chilean longitudinal cohort study. Methods: We used longitudinal data from the Santiago Longitudinal Cohort study. Participants were enrolled as infants between 1991 and 1996. As such, they have experienced Chile’s rapid modernization and dramatic changes in diet, activity, and environment. At 5 years, heigh...
Abstract 5170: Linking tumor evolution and therapy response using diagnostic targeted next generation sequencing in colorectal cancer
Authors: Soulafa Mamlouk, Liam Childs, Thorben Redmer, Pawel Durek, Dirk Schumacher, Hendrik Bläker, Daniela Aust, Moritz von Winterfeld, Volker Heinemann, Dominik Modest, Kerstin Möhr, Markus Morkel, Reinhold Schäfer, Christine Sers
Journal: Cancer Research (2014)

Abstract Complex sets of driver mutations critically control clinical course and treatment response in colorectal cancer (CRC). It is expected that multiple mutations in different signaling pathways interact to establish an individual cancer cell phenotype. Furthermore, mutational patterns can evolve under selective pressure, for instance during tumor metastasis or targeted therapy. Yet only few mutations, such as these in KRAS, NRAS and BRAF, are routinely assessed in the clinic today. With the introduction of next generation sequencing (NGS) many more genes can be simultaneously sequenced, allowing detailed analyses of mutational patterns. We have assembled the CRC5.2 NGS panel for application with Ion Torrent PGM covering 100 frequently mutated genes with 784 amplicons (covering 21,000 COSMIC mutations), going well beyond the scope of commercially available cancer panels. In particular, exon coverage was optimized to embrace all genomic information related to drug sensitivity, using several drug and signaling network databases. The German Consortium for Translational Cancer Research (DKTK) comprises the top cancer centers in Germany. As a part of this group, we employ our custom CRC5.2 panel for the analysis of mutational patterns in CRC. We address several key questions relevant for current diagnostics and treatment in colorectal cancer. In retrospective and prospective clinical studies, we assess mutational heterogeneity in primary tumors, synchronous and metachronous metastases of individual patients. In-depth NGS mutational analyses, transcriptome analysis and methylation studies will identify (epi-)genetic alterations occurring as a consequence of selective pressure during tumor evolution e.g. during metastasis, chemotherapy or targeted tumor therapy. Thus, we will uncover new links between cancer-specific mutations, clinical course and treatment response as well as novel mechanisms of secondary resistance. In addition we aim to identify novel predictive and prognostic mutational markers for the benefit of future CRC patients Citation Format: Soulafa Mamlouk, Liam Childs, Thorben Redmer, Pawel Durek, Dirk Schumacher, Hendrik Bläker, Daniela Aust, Moritz von Winterfeld, Volker Heinemann, Dominik Modest, Kerstin Möhr, Markus Morkel, Reinhold Schäfer, Christine Sers. Linking tumor evolution and therapy response using diagnostic targeted next generation sequencing in colorectal cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5170. doi:10.1158/1538-7445.AM2014-5170
Clinical Ophthalmology. A Systematic Approach
Authors: Jack J. Kanski
Journal: Annals of Internal Medicine (1989)

1. Eyelids 2. Lacrimal Drainage System 3. Orbit 4. Dry Eye Disorders 5. Conjunctiva 6. Cornea 7. Corneal and Refractive Surgery 8. Episclera and Sclera 9. Lens 10. Glaucoma 11. Uveitis 12. Ocular Tumours 13. Retinal Vascular Disease 14. Acquired Macular Disorders 15. Hereditary Fundus Dystrophies 16. Retinal Detachment 17. Vitreous Opacities 18. Strabismus 19. Neuro-ophthalmology 20. Ocular side-effects of systemic medication 21. Trauma Index
Abstract 318: Core Body Temperature Reduction as a Function of Ice-Cold Saline Infusion for the Induction of Hypothermia
Authors: John Freese, Todd Slesinger, Jeffrey Rabrich, Mark Menegus, Robert Silverman, Norma Keller, Judy Dillworth, David Ben-Eli, Doug Isaacs, Glenn Asaeda, Pamela Lai, David Prezant
Journal: Circulation (2014)

Introduction:  The infusion of ice-cold saline (ICS) is often employed for the initiation of therapeutic hypothermia, and many protocols suggest an infusion of up to 30cc/kg in order to achieve one commonly used target temperature range of 32-34 degrees Celcius. We sought to determine if there was any association between ICS volume and core temperature reduction.   Methods:  We analyzed a convenience sample of out-of-hospital cardiac arrest patients for whom therapeutic hypothermia was being inducted via pressurized ICS infusion and for whom core body temperature was being monitored via an esophageal temperature probe.   Results:  Esophageal core temperature data was available for 287 patients. The average patient received 1,136ml (SD 472mL) of ICS via pressure infusion. The average core body temperature upon ED arrival was within the identified target range for all patients (33.2oC, SD 2.3 oC). Among patients who received  1500ml (n=48), average core body temperature achieved target range for all groups (33.34 oC, 33.25 oC, 33.5 oC and 32.87 oC, respectively) though there were patients in each group whose core body temperature was either above or below the target range (SD = 2.64 oC, 2.26 oC, 1.34 oC and 2.11 oC, respectively). No correlation was found between the reduction in core body temperature and the infused volume of ICS (ΔT = -0.95 oC±1.52, -1.51 oC ±1.93, -1.40 oC±1.38, -1.45 oC±1.21, respectively).   Conclusions:  Though perhaps tempered by the disproportionate number of patients in one group, our data would suggest that the relative reduction in and resulting final core body temperature are not a function of the infused volume for patient undergoing the induction of therapeutic hypothermia via ICS infusion. Therefore, if targeted temperature therapy is of clinically important, continuous core temperature monitoring during the induction of cooling is essential to ensure target acquisition.
OBSERVATIONS ON THE SPECIFIC TREATMENT (TYPE A ANTISERUM) OF STAPHYLOCOCCAL SEPTICEMIA; SECOND REPORT
Authors: L. A. Julianelle
Journal: Annals of Internal Medicine (1942)

Article1 February 1942OBSERVATIONS ON THE SPECIFIC TREATMENT (TYPE A ANTISERUM) OF STAPHYLOCOCCAL SEPTICEMIA; SECOND REPORTL. A. JULIANELLEL. A. JULIANELLEAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-16-2-303 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIn an earlier communication1published in this journal, a preliminary account was given of the experimental treatment of staphylococcal septicemia with specific antibacterial serum. Obtained from rabbits following immunization with intact, formalinized organisms, the antiserum was particularly prepared to contain high titers of antibody capable of reacting with the somatic carbohydrate extractable from pathogenic (Type A) staphylococci.2The rationale for the therapeutic expectancy of such an antiserum was based on the theoretical considerations arising from the observation that precipitins for the carbohydrate in question are demonstrable in the sera of those patients only who have recovered from severe, generalized infection.3...References1. JULIANELLE LA: Observations on the specific treatment (Type A antiserum) of staphylococcal septicemia, ANN. INT. MED., 1939, xiii, 308-316. Google Scholar2. JULIANELLEWIEGHARD LACW: The immunological specificity of staphylococci. I. The occurrence of serological types, Jr. Exper. Med., 1935, lxii, 11-21. II. The chemical nature of the soluble specific substances, ibid., lxii, 22-30. CrossrefGoogle Scholar3. JULIANELLEHARTMANN LAAF: The immunological specificity of staphylococci. IV. Cutaneous reactions to the type specific carbohydrates, ibid., 1936, lxiv, 149-159. Google Scholar4. JULIANELLE LA: Determination of staphylococcal types by fermentation of mannite, Proc. Soc. Exper. Biol. and Med., 1937, xxxvi, 117-119. CrossrefGoogle Scholar5. MCNAMEE HG: The treatment of severe staphylococcal infection with specific Type A antibacterial serum, Ann. Surg., 1942, cv, 308-317. CrossrefGoogle Scholar6. TORREYJULIANELLEMCNAMEE RGLAHG: The sulfonamide therapy of staphylococcal septicemia, ANN. INT. MED., 1941, xv, 431-445. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: L. A. JULIANELLEAffiliations: St. Louis, Missouri*Received for publication July 11, 1941.From the Department of Ophthalmology, Washington University School of Medicine, St. Louis.Conducted under a grant from the Commonwealth Fund of New York. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byBACTEREMIA DUE TO COAGULASE-POSITIVE STAPHYLOCOCCUS AUREUS*BURTON A. WAISBREN, M.S., M.D., FRANCOIS ABBOUD, M.D.STAPHYLOCOCCAL BACTEREMIA 1 February 1942Volume 16, Issue 2Page: 303-326KeywordsCarbohydratesOphthalmologyOsteomyelitisPathogensPneumoniaRabbitsSepsisStaphylococcal infectionSurgeonsThrombosis ePublished: 1 December 2008 Issue Published: 1 February 1942 PDF downloadLoading ...
Abstract P321: Coronary Artery Remodeling and Subclinical Atherosclerosis: the CARDIA study
Authors: John J Carr, James G Terry, Joseph Yeboah, Yaorong Ge, James F Lovato, Tamar S Polonsky, Jared Reis, David Goff, Kiang Liu, David Jacobs
Journal: Circulation (2014)

Atherosclerosis related inflammation and plaque result in expansive remodeling of the coronary artery, a finding associated with plaque rupture and clinical events. The extent of expansive coronary remodeling in adults prior to the development of clinical disease is largely unknown. We tested the hypothesis that middle-aged adults who have subclinical coronary artery disease also have larger coronary artery diameters. Methods: Submillimeter thin slice, non-contrast cardiac CT images were obtained in 1197 black and white men and women in the Coronary Artery Risk Development in Young Adults (CARDIA) Study during the year 25 examination (2010-2011, mean age 50 years). Average coronary artery diameter(mm) and cross sectional area (mm2) were measured sequentially along the length of each vessel and averaged for the left main (LM) and proximal circumflex (LCX), left anterior descending (LAD), and right coronary (RCA) arteries. Presence/absence of coronary artery calcifications [CAC (0 versus &gt;0 AU)] was measured independently. Multivariable linear regression models were used to examine the association of CAC with artery size. Results: Coronary diameter was larger in blacks compared to whites (p&lt;0.05) and in men compared to women (p&lt;.0001) following adjustment for age and study center. Presence of CAC was associated with larger diameter coronary arteries after adjustment for age, race, sex, education, height, and study center (Table, model 1). These associations remained following additional adjustment for established cardiovascular risk factors, with the exception of the left main segment (Table, model 2), and were similar for vessel area as for vessel diameter (not shown). Conclusion: Coronary arteries are larger in middle-age individuals with vs without CAC, supporting the hypothesis that atherosclerosis leads to expansive coronary remodeling. Coronary remodeling by non-contrast CT is a measure that may provide new information on cardiovascular risk and prediction of clinical cardiovascular events.
Abstract 4048: GFRα1 is required for GDNF-induced viability, migration, and signaling through RET in breast cancer cells
Authors: Catherine A. Ferrante, Nikki DeAngelis, Raluca Verona
Journal: Cancer Research (2014)

Abstract Hormone resistance is a major challenge in treating breast cancer patients. Although anti-estrogens, such as tamoxifen, are initially successful controlling disease in estrogen receptor alpha positive (ERα+) tumors, patients with metastatic disease and as many as 40 % of patients receiving adjuvant tamoxifen acquire resistance to treatment, relapse, and die. The receptor tyrosine kinase, RET, its co-receptor, GFRα1, and their ligand, GDNF, are proteins that are emerging as potential contributors to hormone resistance in breast cancer. RET and GFRα1 were recently shown to be overexpressed in a subset of ERα+ breast cancer tumors, and GFRα1 expression was associated with lymphovascular invasion. In vitro, silencing RET with siRNA increased MCF7 cells' sensitivity to tamoxifen and, in the absence of estrogens, treatment of MCF7 cells with GDNF induced upregulation of ERα target genes. Additionally, GDNF stimulation of MCF7 cells enhanced proliferation, survival, and cell scattering. Together, clinical and preclinical data suggest that this pathway plays an important role in driving breast cancer invasion, metastasis, and hormone resistance. However, the role of GFRα1 has not been examined in tumor cell invasion and metastasis. In this study we tested the functional consequences of silencing GFRα1 in ERα + MCF7 cells on tumor cell migration, invasion, and RET signaling. We showed that targeted reduction of GFRα1 significantly inhibited GDNF-induced migration in both a transwell (p=&amp;lt;0.001) and scratch wound assay (p=&amp;lt;0.001 at 24 hours). In addition, GDNF-induced increases in viability were significantly decreased when MCF7 cells were treated with neutralizing antibodies against GFRα1 (p=&amp;lt;0.001). Silencing GFRα1 in GDNF-treated MCF7 cells led to reduced invasion through collagen I, although this difference was not significant. Lastly, siRNA targeted reduction of GFRα1 in MCF7 cells inhibited GDNF-induced phosphorylation of RET. Together the data demonstrate that GFRα1 is important in migration and cell viability as well as RET signaling in breast cancer cells. Citation Format: Catherine A. Ferrante, Nikki DeAngelis, Raluca Verona. GFRα1 is required for GDNF-induced viability, migration, and signaling through RET in breast cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4048. doi:10.1158/1538-7445.AM2014-4048
Mechanistic correlations between two itch biomarkers, cytokine interleukin-31 and neuropeptide β-endorphin, via STAT3/calcium axis in atopic dermatitis
Authors: C.-H. Lee, C.-H. Hong, W.-T. Yu, H.-Y. Chuang, S.-K. Huang, G.-S. Chen, T. Yoshioka, M. Sakata, W.-T. Liao, Y.-C. Ko, H.-S. Yu
Journal: British Journal of Dermatology (2012)

Itch is the cardinal symptom of atopic dermatitis (AD). β-Endorphin, a neuropeptide, is increased in both AD skin and sera. Interleukin (IL)-31, an itch-relevant cytokine, activates IL-31 receptors in keratinocytes. However, how IL-31 and β-endorphin interact in AD skin remains elusive.To investigate the mechanistic interaction of IL-31 and β-endorphin in AD.This was a prospective cross-sectional study. We recruited adult patients with AD and controls according to Hanifin's AD criteria. Serum levels of IL-31 and β-endorphin were measured by enzyme-linked immunosorbent assay. Expressions of IL-31 receptor A (IL-31RA) and β-endorphin in the skin were assessed by immunohistochemistry. Their expression in the skin and blood was compared and correlated in patients with AD and in controls. We also treated primary keratinocytes with IL-31 and measured calcium influx, β-endorphin production and signalling pathways to define their mechanistic interactions.β-Endorphin was increased in the supernatant from IL-31-treated keratinocytes. IL-31 receptor activation resulted in calcium influx and STAT3 activation; pretreatment with STAT3 inhibitor stopped the increase of β-endorphin. Notably, either replacement of extracellular calcium or treatment with 2-aminoethoxydiphenyl borate, an inhibitor for the store-operated channel, blocked STAT3 activation. We found higher levels of blood β-endorphin and IL-31, which were significantly correlated, in patients with AD. Moreover, IL-31RA and β-endorphin were increased and colocalized both in AD human skin and TPA-painted mouse skin.IL-31 receptor activation in keratinocytes induces calcium influx and STAT3-dependent production of β-endorphin. These results might contribute to an understanding of the regulatory mechanisms underlying peripheral itch.
High Prevalence of Obesity Among the Poor in MexicoRESEARCH LETTERS
Authors: Lia C Fernald, Juan Pablo Gutierrez, Lynnette M Neufeld, Gustavo Olaiz, Stefano M Bertozzi, Michele Mietus-Snyder, Paul J Gertler
Journal: JAMA (2004)

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Detection of clonotypic IGH and TCR rearrangements in the neonatal blood spots of infants and children with B-cell precursor acute lymphoblastic leukemia
Authors: Tomohito Yagi, Shigeyoshi Hibi, Yasuhiro Tabata, Kikuko Kuriyama, Tomoko Teramura, Tetsuo Hashida, Yoshitaka Shimizu, Tetsuya Takimoto, Shinjiro Todo, Tadashi Sawada, Shinsaku Imashuku
Journal: Blood (2000)