tbuckley/cabot-search huggingface dataset:
TCT-476 Angiographic and clinical analysis of 164 cases of longitudinal stent deformation: comparison of cases from a multicentre case series with cases identified from the MAUDE database
Authors: Nizar Shakhshir, Mohamed Abdel-Wahab, Adel Aminian, Samer Arnous, Antonio L. Bartorelli, Antonio Colombo, Ferrari Cristina, Nicolas Foin, Azeem Latib, Iqbal S. Malik, Mamas Mamas, Gert Richardt, Paul D. Williams, Douglas G. Fraser
Journal: Journal of the American College of Cardiology (2013)
Large differences in survival are not explained
Authors: M. Baum
Journal: BMJ (1996)

EDITOR,—As a specialist breast cancer surgeon it is in my enlightened self interest to accept the findings of Charles R Gillis and David J Hole1; at the same time, as a clinical scientist I cannot allow their conclusions to go unchallenged. From the world overview of trials we now know with statistical confidence that variations in local treatment cannot be associated with any of the differences in survival described in this …
Cardiovascular Manifestations of Proven Coxsackie Infections.
Authors: H. Kurz
Journal: Annals of Internal Medicine (1967)

s1 May 1967Cardiovascular Manifestations of Proven Coxsackie Infections.H. Kurz, M.D., G. Sainani, M.D., E. Krompotic, M.D., S. Slodki, M.D.H. Kurz, M.D.Search for more papers by this author, G. Sainani, M.D.Search for more papers by this author, E. Krompotic, M.D.Search for more papers by this author, S. Slodki, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-66-5-1047_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe coxsackie viruses, particularly group B, have been shown to cause acute pericarditis and myocarditis. The detection in adults of myocarditis or pericarditis caused by the Coxsackie viruses has lagged behind the pediatric experience.Twenty proved cases of Coxsackie infection with cardiovascular involvement have been studied. Eighteen were of adults (12 males and 6 females) between 15 and 66 years of age, and 2 were of children. All patients were closely studied, had routine laboratory investigations, repeated enzyme studies, serial electrocardiograms and chest X rays, phonocardiogram when necessary, and serial viral studies. The infection with Coxsackie virus was proved by... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Chicago, Illinois PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByInfectious diseases. Annual review of significant publications. 1 May 1967Volume 66, Issue 5Page: 1047-1047KeywordsChildrenElectrocardiographyEnzymesMyocarditisResearch laboratoriesThorax Issue Published: 1 May 1967 PDF DownloadLoading ...
Abstract IA2: Network models in oncogene-addicted lung cancer
Authors: Eric B. Haura, Takeshi Yoshida, Bin Fang, Alexey Stukalov, Steven Eschrich, Eric Welsh, Jacques Colinge, John Koomen, Giulio Superti-Furga, Jiannong Li, Uwe Rix, Guolin Zhang, Jae-Young Kim, Keiryn Bennett, Lanxi Song, Ann Chen, Yun Bai
Journal: Clinical Cancer Research (2012)

Abstract Lung cancer is a devastating worldwide disease yet enthusiasm exists for treatment of subsets of the disease with molecularly targeted agents. Mutations in the epidermal growth factor receptor (EGFR) or translocation of echinoderm microtubule associated protein like 4 – anaplastic lymphoma kinase (EML4-ALK) define two unique subsets of lung cancer characterized by sensitivity to tyrosine kinase inhibitors (TKI). Despite striking results with TKI, not all patients respond, the drugs are non-curative, and resistance is universal. Mutations in KRAS also define a group of patients awaiting therapeutic opportunities. We are characterizing signaling networks using tandem affinity purification (TAP) and liquid chromatography-mass spectrometry (LC-MS/MS) to map protein-protein interactions (PPI) and anti-phosphotyrosine immunoprecipitation coupled with LC-MS/MS to map tyrosine phosphorylation. In PC9 cells with mutated EGFR, we characterized a physical EGFR network consisting of 266 proteins by integrating both TAP and pTyr MS data. In H3122 cells harboring EML4-ALK, we identified a PPI network consisting of 113 proteins and using pTyr MS identified changes in tyrosine phosphorylation in 120 proteins (58 decreased, 62 increased) following exposure to ALK tyrosine kinase inhibitor. Functional proteins are being discovered from these networks using siRNA and inhibitor screens. In parallel studies, we have exploited the use of chemical proteomics to discern targets of promiscuous kinase inhibitors and enable optimal combination approaches. In this way, we view network mapping linked to chemical proteomics as one approach to discern novel drug combination studies for in vivo validation and ultimately translation to early phase clinical trials. To translate PPI based mass spectrometry studies to clinic, we are developing in situ assays that identify and quantify PPI using proximal ligation assays (PLA). Pilot studies identify EGFR:Grb2 interactions in formalin fixed human lung cancers. These approaches have the potential to enable ‘network medicine’ by identifying novel combination approaches as well as through identifying subtypes of cancers through network views of cancer.
Bristol Floods 1968. Controlled Survey of Effects on Health of Local Community Disaster
Authors: G. Bennet
Journal: BMJ (1970)

An investigation into the health of people in Bristol flooded in July 1968 was made by means of a controlled survey and a study of mortality rates. There was a 50% increase in the number of deaths among those whose homes had been flooded, with a conspicuous rise in deaths from cancer.Surgery attendances rose by 53%, referrals to hospital and hospital admissions more than doubled. In all respects the men appeared less well able to cope with the experience of disaster than the women.
F-18 FDG PET-CT Findings of Intraperitoneal Carbon Particles-Induced Granulomas Mimicking Peritoneal Carcinomatosis
Authors: Seok Tae Lim, Hwan-Jeong Jeong, Dong Wook Kim, Chang-Yeul Yim, Myung-Hee Sohn
Journal: Clinical Nuclear Medicine (2008)

F-18 FDG PET-CT is a useful modality for monitoring residual or recurrent tumors after surgical resection. We report on 3 patients with intraperitoneal charcoal-induced granulomas mimicking peritoneal carcinomatosis on PET-CT images. Two of them underwent a radical gastrectomy because of advanced gastric cancer, and the other underwent a hemicolectomy because of sigmoid colon cancer. All 3 patients had a history of intraperitoneal chemotherapy using mitomycin C bound to activated carbon particles during surgery. Follow-up PET-CT studies demonstrated increased FDG uptake mimicking peritoneal carcinomatosis on PET images alone. However, the accompanying noncontrast CT showed variously shaped hyperdense nodules in the dependent positions of the peritoneal cavity, including the paracolic gutter and rectovesical space, indicating charcoal-induced granulomas rather than peritoneal carcinomatosis.
Pharmacological Treatment of Early Multiple Sclerosis
Authors: Olaf Stüve, Jeffrey L Bennett, Bernhard Hemmer, Heinz Wiendl, Michael K Racke, Amit Bar-Or, Wei Hu, Robert Zivadinov, Martin S Weber, Scott S Zamvil, Maria F Pacheco, Til Menge, Hans-Peter Hartung, Bernd C Kieseier, Elliot M Frohman
Journal: Drugs (2008)
The Greatest Casualty Is Being Forgotten
Authors: John R. Feussner
Journal: Annals of Internal Medicine (2015)

On Being a Doctor20 January 2015The Greatest Casualty Is Being ForgottenJohn R. Feussner, MD, MPHJohn R. Feussner, MD, MPHFrom Medical University of South Carolina, Charleston, South Carolina.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/M14-1356 Audio Reading - “The Greatest Casualty Is Being Forgotten” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "The Greatest Casualty Is Being Forgotten," by J.R. Feussner. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail The greatest casualty is being forgotten.—Wounded Warrior ProjectI did not serve in the military. I was never drafted (there was one once), and I was not very good at volunteering. After medical school, I completed my training at an academic medical center affiliated with a VA medical center. Some of my earliest rotations were on the VA medical service, and I have been doctoring veterans ever since. Early in my career, I assumed administrative responsibilities at that VA medical center. As part of my duties, I took my turn doing compensation and pension (C & P) examinations, a ... Author, Article, and Disclosure InformationAffiliations: From Medical University of South Carolina, Charleston, South Carolina.Corresponding Author: John R. Feussner, MD, MPH, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 601 CSB, Charleston, SC 29425. PreviousarticleNextarticle Advertisement Audio Reading - “The Greatest Casualty Is Being Forgotten” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "The Greatest Casualty Is Being Forgotten," by J.R. Feussner. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ FiguresReferencesRelatedDetails Metrics 20 January 2015Volume 162, Issue 2Page: 150-151KeywordsArmed forcesChartsEmotionsHomicideMedical conditionsMedical servicesScarsThorax ePublished: 20 January 2015 Issue Published: 20 January 2015 Copyright & PermissionsCopyright © 2015 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
395 SURVIVAL OF PATIENTS RECEIVING YTTRIUM-90 MICROSPHERES VS CHEMOEMBOLIZATION FOR UNRESECTABLE HEPATOCELLULAR CARCINOMA
Authors: L.E. Moreno-Luna, R. Paz-Fumagalli, D.M. Harnois, P.C. de Groen, K.N. Lazaridis, K.V.N. Menon, N.F. La Russo, S.R. Alberts, G.J. Gores, T.M. Therneau, G.A. Wiseman, J.C. Andrews, L.R. Roberts
Journal: Journal of Hepatology (2008)
Reduced sensitivity to pirenzepine-induced blockade of growth hormone responses to arginine, exercise, and growth hormone-releasing hormone in type I diabetic subjects
Authors: V. Coiro, M. Passeri, E. Gardini, L. Capretti, G. Speroni, C. Davoli, M.L. Maffei, F. Fagnoni, L. Bianconi, R. Volpi, P. Chiodera
Journal: Metabolism (1990)
US women asked to pay for epidurals in advance
Authors: J. Ciment
Journal: BMJ (1999)

Responding to reports that certain hospitals are requiring women with Medicaid to pay for epidural analgesia for childbirth in cash and in advance, the director of the Center for Medicaid and State Operations—an agency within the US Department of Health and Human Services—issued a letter to state Medicaid directors across the country reminding them of their responsibilities and demanding that action be taken.

Medicaid—a …
Abstract B28: MicroRNA-641 activates MAPK by targeting NF1 and cooperates with its host gene AKT2 in human cancer
Authors: Edward J. Richards, Marc Coppola, Jianping Guo, William Kong, Jin Q. Cheng
Journal: Cancer Research (2012)

Abstract AKT2 is frequently up-regulated in human cancer. MiR-641 is an uncharacterized microRNA that locates at intron-1 of the AKT2 gene. We hypothesize that miR-641 and AKT2 are co-regulated, and cooperate to promote tumor development. Here we demonstrated that the transcription factors which induce AKT2 also increase miR-641 expression. Further, we identified miR-641 activation of the MAPK pathway by targeting tumor suppressor NF1, a GTPase-activating protein that inhibits RAS. Upon ectopic expression of miR-641, NF1 expression was reduced. As a result, pERK was elevated. Whereas knockdown of miR-641 exhibits opposite effects. In addition, depletion of miR-641 sensitizes tumor cells to cisplatin-induced apoptosis. Knockdown of miR-641 synergized with AKT2 inhibition to induce cell death. These data suggest that miR-641 functions as an oncomiR that co-regulates and cooperates with AKT2 in human cancer. Citation Format: Edward J. Richards, Marc Coppola, Jianping Guo, William Kong, Jin Q. Cheng. MicroRNA-641 activates MAPK by targeting NF1 and cooperates with its host gene AKT2 in human cancer [abstract]. In: Proceedings of the AACR Special Conference on Noncoding RNAs and Cancer; 2012 Jan 8-11; Miami Beach, FL. Philadelphia (PA): AACR; Cancer Res 2012;72(2 Suppl):Abstract nr B28.
Abstract 5293: GSK3β phosphorylation at serine9 by RSK2 enhances calcium-induced stress tolerance and cell survival
Authors: Ji-Young Lee, Cheol-Jung Lee, Mee-Hyun Lee, Ji Hong Song, Yong-Yeon Cho
Journal: Cancer Research (2014)

Abstract Our previous studies demonstrated that RSK2 plays a key role in cell proliferation and transformation induced by tumor promoters such as epidermal growth factor in mouse and human skin cells. However, no direct evidence has been found regarding the relationship between RSK2 and cell survival. In this study, we found that RSK2 interacted and phosphorylated GSK3β at Ser9. Notably, GSK3β phosphorylation at Ser9 was suppressed in RSK2−/− MEFs compared with RSK2+/+ MEFs by stimulation of EGF and calcium ionophore A23187, a cellular calcium stressor. In proliferation, we found that RSK2 deficiency suppressed cell proliferation compared with RSK2+/+ MEFs. In contrast, GSK3β−/− MEFs induced the cell proliferation compared with GSK3β+/+ MEFs. Importantly, RSK2−/− MEFs were induced severe cellular morphology change by A23187 and enhanced G1/G0 and sub-G1 accumulation of the cell cycle phase compared with RSK2+/+ MEFs. The sub-G1 induction in RSK2−/− MEFs by A23187 was correlated with increase of cytochrome c release, caspase-3 cleavage and apoptotic DNA fragmentation compared with RSK2+/+ MEFs. Notably, return back of RSK2 into RSK2−/− MEFs restored A23187-induced morphological change, and decreased apoptosis, apoptotic DNA fragmentation and caspase-3 induction compared with RSK2−/− /mock MEFs. Taken together, our results demonstrated that RSK2 plays an important role in stress-tolerance and cell survival, resulting in cell proliferation and cancer development. Citation Format: Ji-Young Lee, Cheol-Jung Lee, Mee-Hyun Lee, Ji Hong Song, Yong-Yeon Cho. GSK3β phosphorylation at serine9 by RSK2 enhances calcium-induced stress tolerance and cell survival. [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 5293. doi:10.1158/1538-7445.AM2014-5293
A Noncanonical Flt3ITD/NF-κB Signaling Pathway Represses <i>DAPK1</i> in Acute Myeloid Leukemia
Authors: Rajasubramaniam Shanmugam, Padmaja Gade, Annique Wilson-Weekes, Hamid Sayar, Attaya Suvannasankha, Chirayu Goswami, Lang Li, Sushil Gupta, Angelo A. Cardoso, Tareq Al Baghdadi, Katie J. Sargent, Larry D. Cripe, Dhananjaya V. Kalvakolanu, H. Scott Boswell
Journal: Clinical Cancer Research (2011)

Abstract Purpose: Death-associated protein kinase 1 (DAPK1), a tumor suppressor, is a rate-limiting effector in an endoplasmic reticulum (ER) stress-dependent apoptotic pathway. Its expression is epigenetically suppressed in several tumors. A mechanistic basis for epigenetic/transcriptional repression of DAPK1 was investigated in certain forms of acute myeloid leukemia (AML) with poor prognosis, which lacked ER stress-induced apoptosis. Experimental Design: Heterogeneous primary AMLs were screened to identify a subgroup with Flt3ITD in which repression of DAPK1, among NF-κB–and c-Jun–responsive genes, was studied. RNA interference knockdown studies were carried out in an Flt3ITD+ cell line, MV-4-11, to establish genetic epistasis in the pathway Flt3ITD–TAK1–DAPK1 repression, and chromatin immunoprecipitations were carried out to identify proximate effector proteins, including TAK1-activated p52NF-κB, at the DAPK1 locus. Results: AMLs characterized by normal karyotype with Flt3ITD were found to have 10- to 100-fold lower DAPK1 transcripts normalized to the expression of c-Jun, a transcriptional activator of DAPK1, as compared with a heterogeneous cytogenetic category. In addition, Meis1, a c-Jun-responsive adverse AML prognostic gene signature was measured as control. These Flt3ITD+ AMLs overexpress relB, a transcriptional repressor, which forms active heterodimers with p52NF-κB. Chromatin immunoprecipitation assays identified p52NF-κB binding to the DAPK1 promoter together with histone deacetylase 2 (HDAC2) and HDAC6 in the Flt3ITD+ human AML cell line MV-4-11. Knockdown of p52NF-κB or its upstream regulator, NF-κB–inducing kinase (NIK), de-repressed DAPK1. DAPK1-repressed primary Flt3ITD+ AMLs had selective nuclear activation of p52NF-κB. Conclusions: Flt3ITD promotes a noncanonical pathway via TAK1 and p52NF-κB to suppress DAPK1 in association with HDACs, which explains DAPK1 repression in Flt3ITD+ AML. Clin Cancer Res; 18(2); 360–9. ©2011 AACR.
Foamy Virus Vector-mediated Gene Correction of a Mouse Model of Wiskott–Aldrich Syndrome
Authors: Toru Uchiyama, Marsilio Adriani, G Jayashree Jagadeesh, Adam Paine, Fabio Candotti
Journal: Molecular Therapy (2012)

The Wiskott-Aldrich syndrome (WAS) is an X-linked disorder characterized by eczema, thrombocytopenia and immunodeficiency. Hematopoietic cell transplantation can cure the disease and gene therapy is being tested as an alternative treatment option. In this study, we assessed the use of foamy virus (FV) vectors as a gene transfer system for WAS, using a Was knockout (KO) mouse model. Preliminary experiments using FV vectors expressing the green fluorescent protein under the transcriptional control of the endogenous WAS promoter or a ubiquitously acting chromatin opening element allowed us to define transduction conditions resulting in high (>40%) and long-term in-vivo marking of blood cells after transplantation. In following experiments, Was KO mice were treated with FV vectors containing the human WAS complementary DNA (cDNA). Transplanted animals expressed the WAS protein (WASp) in T and B lymphocytes, as well as platelets and showed restoration of both T-cell receptor-mediated responses and B-cell migration. We also observed recovery of platelet adhesion and podosome formation in dendritic cells (DCs) of treated mice. These data demonstrate that FV vectors can be effective for hematopoietic stem cell (HSC)-directed gene correction of WAS.
Gene expression profiling suggests primary central nervous system lymphomas to be derived from a late germinal center B cell
Authors: M Montesinos-Rongen, A Brunn, S Bentink, K Basso, W K Lim, W Klapper, C Schaller, G Reifenberger, J Rubenstein, O D Wiestler, R Spang, R Dalla-Favera, R Siebert, M Deckert
Journal: Leukemia (2007)
Bronchodilator effect of sodium cromoglycate.
Authors: P Helliwell
Journal: BMJ (1979)

ment.We do not agree.Surely it is better to recognise the importance of obstetric anaes- thetic services and improve the services where they are inadequate.Currently the recruitment of doctors into anaesthesia is excellent and the opportunity exists.Unfortunately, medical administrators seeking to save money might misuse the views of Professor Hibbard and his colleagues and block the improvements that are necessary.This is the true importance of the argument.
The Prognostic Role of Detection of Circulating Melanoma Cells in the Blood
Authors: Janice P. Dutcher
Journal: Journal of Clinical Oncology (2003)

Article Tools EDITORIALS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2003.11.020 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 12610168 The Prognostic Role of Detection of Circulating Melanoma Cells in the Blood Janice P. DutcherxJanice P. DutcherSearch for articles by this author Show More Our Lady of Mercy Cancer Center, Bronx, NYNew York Medical College, Valhalla, NY https://doi.org/10.1200/JCO.2003.11.020 First Page Full Text PDF Figures and Tables © 2003 by American Society of Clinical Oncology
Hepatic Disorder and Severe Bleeding Diathesis Following Nitrofurantoin Ingestion
Authors: Kevin J. Murphy
Journal: JAMA (1968)

Severe but transient bleeding disorder and liver dysfunction followed oral ingestion of nitrofurantoin (Furandantin). The patient had prolonged nausea but no other apparent reaction to the drug. The liver disorder appeared to be toxic hepatitis rather than intrahepatic cholestasis, and the bleeding was due to deficiencies of prothrombin and of factor VII, which were in turn attributed to the hepatitis. Spontaneous bleeding into the neck necessitated tracheostomy after exchange transfusion.
Efficient Generation of Hepatoblasts From Human ES Cells and iPS Cells by Transient Overexpression of Homeobox Gene HEX
Authors: Mitsuru Inamura, Kenji Kawabata, Kazuo Takayama, Katsuhisa Tashiro, Fuminori Sakurai, Kazufumi Katayama, Masashi Toyoda, Hidenori Akutsu, Yoshitaka Miyagawa, Hajime Okita, Nobutaka Kiyokawa, Akihiro Umezawa, Takao Hayakawa, Miho K Furue, Hiroyuki Mizuguchi
Journal: Molecular Therapy (2010)

Human embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) have the potential to differentiate into all cell lineages, including hepatocytes, in vitro. Induced hepatocytes have a wide range of potential application in biomedical research, drug discovery, and the treatment of liver disease. However, the existing protocols for hepatic differentiation of PSCs are not very efficient. In this study, we developed an efficient method to induce hepatoblasts, which are progenitors of hepatocytes, from human ESCs and iPSCs by overexpression of the HEX gene, which is a homeotic gene and also essential for hepatic differentiation, using a HEX-expressing adenovirus (Ad) vector under serum/feeder cell-free chemically defined conditions. Ad-HEX-transduced cells expressed α-fetoprotein (AFP) at day 9 and then expressed albumin (ALB) at day 12. Furthermore, the Ad-HEX-transduced cells derived from human iPSCs also produced several cytochrome P450 (CYP) isozymes, and these P450 isozymes were capable of converting the substrates to metabolites and responding to the chemical stimulation. Our differentiation protocol using Ad vector-mediated transient HEX transduction under chemically defined conditions efficiently generates hepatoblasts from human ESCs and iPSCs. Thus, our methods would be useful for not only drug screening but also therapeutic applications. Human embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) have the potential to differentiate into all cell lineages, including hepatocytes, in vitro. Induced hepatocytes have a wide range of potential application in biomedical research, drug discovery, and the treatment of liver disease. However, the existing protocols for hepatic differentiation of PSCs are not very efficient. In this study, we developed an efficient method to induce hepatoblasts, which are progenitors of hepatocytes, from human ESCs and iPSCs by overexpression of the HEX gene, which is a homeotic gene and also essential for hepatic differentiation, using a HEX-expressing adenovirus (Ad) vector under serum/feeder cell-free chemically defined conditions. Ad-HEX-transduced cells expressed α-fetoprotein (AFP) at day 9 and then expressed albumin (ALB) at day 12. Furthermore, the Ad-HEX-transduced cells derived from human iPSCs also produced several cytochrome P450 (CYP) isozymes, and these P450 isozymes were capable of converting the substrates to metabolites and responding to the chemical stimulation. Our differentiation protocol using Ad vector-mediated transient HEX transduction under chemically defined conditions efficiently generates hepatoblasts from human ESCs and iPSCs. Thus, our methods would be useful for not only drug screening but also therapeutic applications.