tbuckley/cabot-search huggingface dataset:
We All Talk Shop.
Authors: J. L. Tracy
Journal: JAMA (1896)

<h3>To the Editor:</h3> —The thought expressed in the words which head this letter was suggested by reading in a secular newspaper an interview of which the following is an extract: "Dr. George F. Shrady, the famous practitioner who was in attendance upon both President Garfield and President Grant, is an advisory physician to the Red Cross Hospital and a conservative man, who is widely quoted upon medical topics. He is editor of the<i>Medical Record</i>of this city, probably the most important medical journal published on the continent. At his home at 8 East Sixty-sixth Street Dr. Shrady thus expressed himself: * * * * * 'It is like a knife—good in its place. There,' said the doctor, pointing to a knife in a glass case, 'is the knife that cut President Garfield, and the knife did him good; but I would not stick it into every sick man in my care.' " The introduction to
Drug therapy for acute myeloid leukemia
Authors: Martin S. Tallman, D. Gary Gilliland, Jacob M. Rowe
Journal: Blood (2005)

Although improvement in outcomes has occurred in younger adults with acute myeloid leukemia (AML) during the past 4 decades, progress in older adults has been much less conspicuous, if at all. Approximately 50% to 75% of adults with AML achieve complete remission (CR) with cytarabine and an anthracycline such as daunorubicin or idarubicin or the anthracenedione mitoxantrone. However, only approximately 20% to 30% of the patients enjoy long-term disease survival. Various postremission strategies have been explored to eliminate minimal residual disease. The optimal dose, schedule, and number of cycles of postremission chemotherapy for most patients are not known. A variety of prognostic factors can predict outcome and include the karyotype of the leukemic cells and the presence of transmembrane transporter proteins, which extrude certain chemotherapy agents from the cell and confer multidrug resistance and mutations in or over expressions of specific genes such as WT1, CEBPA, BAX and the ratio of BCL2 to BAX, BAALC, EVI1, KIT, and FLT3. Most recently, insights into the molecular pathogenesis of AML have led to the development of more specific targeted agents and have ushered in an exciting new era of antileukemia therapy. Such agents include the immunoconjugate gemtuzumab ozogamicin, multidrug resistance inhibitors, farnesyl transferase inhibitors, histone deacetylase and proteosome inhibitors, antiangiogenesis agents, Fms-like tyrosine kinase 3 (FLT3) inhibitors, and apoptosis inhibitors.
Status of Fifty Patients Four and a Half to Seven Years after Mitral Commissurotomy
Authors: O. HENRY JANTON, JULIO C. DAVILA, ROBERT P. GLOVER
Journal: Circulation (1956)

The first 50 consecutive patients undergoing mitral commissurotomy approximately 4½ to 7 years ago have been subjected to a detailed analysis in an attempt to ascertain their present subjective and objective status. Operative mortality was 6 per cent and late mortality was 12 per cent. Forty-one patients (82 per cent) are living and have formed the basis for conclusions. After a comprehensive study of each living patient, including an appraisal of the patient's subjectively reported clinical state, as well as a correlation of the clinical findings, electrocardiographic tracings, teleroentgenograms, and catheterization data, we conclude that 29 patients (71 per cent of those living or 58 per cent of the original 50) are in better condition and living a more nearly normal life than they were prior to surgery.
Tc-99m Red Blood Cell Scintigraphy in Acute Intrahepatic Hematoma
Authors: GERALD W. GROWCOCK, ROBERT R. MURRAY, GREGORY J. GUZLEY
Journal: Clinical Nuclear Medicine (1994)

A focal hot area on Tc-99m blood pool Imaging of the liver is usually indicative of a cavernous hemangioma. This report illustrates the unusual finding of a neoplastic cold area with a coexisting hot area from acute intrahepatic hemorrhage.
WHAT ARE THE CURRENT PRACTICES IN ANTITHROMBOTIC THERAPY AFTER BIOPROSTHETIC AORTIC VALVE REPLACEMENT: A MULTICENTER PATIENT–BASED STUDY
Authors: Claire Bouleti, Alain Leguerrier, Jean–Francois Obadia, Frederic Collart, Emanuelle Florens, Michel Marchand, Laurent Lepage, Genevieve Mulak, Bernard Iung
Journal: Journal of the American College of Cardiology (2013)
Processing demands associated with relational complexity: Testing predictions with dual-task methodologies
Authors: Daniel B. Berch, Elizabeth J. Foley
Journal: Behavioral and Brain Sciences (1998)

We discuss how modified dual-task approaches may be used to verify the degree to which cognitive tasks are capacity demanding. We also delineate some of the complexities associated with the use of the “double easy-to-hard” paradigm for testing claim of Halford, Wilson &amp; Phillips that hierarchical reasoning imposes processing demands equivalent to those of transitive reasoning.
FURTHER STUDIES ON THE SURVIVAL AND DEVELOPMENT IN VITRO OF A MALARIAL PARASITE
Authors: William Trager
Journal: The Journal of Experimental Medicine (1943)

The survival of Plasmodium lophurae in vitro is favored by the presence of calcium pantothenate (0.02 mg. per ml). Survival of about 2 weeks in vitro at 40-41 degrees C. has been obtained under the following conditions: a medium consisting of duck red cell extract in balanced salt solution with glutathione and glucose or glycogen, serum, embryo extract, and calcium pantothenate; daily replacement of about half of the medium with fresh medium; addition of fresh uninfected erythrocytes every 2nd day; gentle agitation of the preparation on a rocking machine. In some of these preparations significant increases in male gametocytes and, more rarely, in total numbers of parasites occurred during the first few days.
Relational priming is to analogy-making as one-ball juggling is to seven-ball juggling
Authors: Robert M. French
Journal: Behavioral and Brain Sciences (2008)

Abstract Relational priming is argued to be a deeply inadequate model of analogy-making because of its intrinsic inability to do analogies where the base and target domains share no common attributes and the mapped relations are different. Leech et al. rely on carefully handcrafted representations to allow their model to make a complex analogy, seemingly unaware of the debate on this issue fifteen years ago. Finally, they incorrectly assume the existence of fixed, context-independent relations between objects.
Special Care Babies and their Developing Relationships
Authors: S. Bourne
Journal: BMJ (1995)

Anne McFadyen Routledge, £12.99, pp 194 ISBN 0 415 10614 1

In Special Care Babies and their Developing Relationships Anne McFadyen first provides a useful review of theoretical perspectives and outcome studies (10 impressive pages of references) and then switches to binocular vision. She differentiates “old science,” with its faith in single measurable objective truths, from “new science” (familiar to physicists), which grapples with uncertainty and accepts that truth is changeable and that the acts of observing and measuring cannot be processed out of knowing the real world.

The heart of this book beats in the middle …
Abstract 2953: Inhibition of calmodulin enhances TRA-8-induced apoptosis in pancreatic cancer cells .
Authors: Kaiyu Yuan, Tong Zhou, Jay McDonald, Yabing Chen
Journal: Cancer Research (2013)

Abstract Current chemotherapy and radiotherapy are not curative for pancreatic cancer. Tumor necrosis factor-related apoptosis-inducing ligand or agonist antibodies for death receptor 4/5 have been shown to be a promising cancer therapy. TRA-8, a humanized activating antibody for the death receptor 5 (DR5), is a potent apoptosis-inducing reagent for cancer cells. However, several pancreatic cell lines are resistant to TRA-8-induced apoptosis. We have previously demonstrated that calmodulin (CaM) antagonists enhance the Fas death receptor-mediated apoptosis pathway. Therefore, we investigated whether inhibition of CaM might affect DR5-induced apoptotic signaling in pancreatic cancer cells. We found that CaM antagonists, trifluoperazine (TFP) and tamoxifen (TMX), dose dependently enhanced TRA-8-induced apoptosis of the TRA-8-resistant PANC-1 pancreatic cells. Consistently, TFP and TMX increased TRA-8-induced activation of caspase 8, caspase 9 and caspase 3. Pretreatment of PANC-1 with Z-IETD-FMK, the caspase-8 inhibitor, decreased TFP-enhanced apoptosis by 2 fold, and markedly decreased caspase 3 activation. Immunoprecipitation analysis of the DR5-induced death inducing signaling complex (DISC) identified the interaction of CaM with DR5. Activation of DR-5 by TRA-8 increased the recruitment of CaM into the DISC, which was inhibited by TFP. In addition, TFP decreased the recruitment of the adaptor protein, FADD, and other DISC proteins that regulate cell survival, including Src and the caspase-8 inhibitory protein FLIP. Collectively, these results support an important role for CaM in DR5-induced DISC formation, thus regulating DR5-mediated survival and apoptotic signaling in pancreatic cancer cells. In summary, we have demonstrated that CaM antagonists sensitize pancreatic cancer cell to TRA 8-induced apoptosis, and that CaM binding to DR5 regulates DR5-induced DISC formation. Defining the function of CaM in regulating DR5-induced signaling pathways may lead to novel therapeutic strategies including the use of CaM antagonists with TRA-8 as combination therapy for pancreatic cancer. Citation Format: Kaiyu Yuan, Tong Zhou, Jay McDonald, Yabing Chen. Inhibition of calmodulin enhances TRA-8-induced apoptosis in pancreatic cancer cells . [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2953. doi:10.1158/1538-7445.AM2013-2953
To perform or not to perform liver biopsy--that is the question
Authors: R W Chapman
Journal: Gut (2002)

Should liver biopsy be performed to determine the cause of abnormal liver biochemical tests in the absence of diagnostic serology?

One of the most difficult management decisions in clinical hepatology, especially for the general gastroenterologist, is whether to perform a liver biopsy in a patient with abnormal liver function tests, particularly in the absence of diagnostic serology, or a history of drug or alcohol use. At first sight the benefits of performing an invasive procedure in such asymptomatic patients are not obvious when balanced against the potential hazards of bile leak or haemorrhage.1

Histological causes of abnormal liver biochemistry have been studied previously in patients with excess alcohol ingestion or advanced liver disease.2,3 However, to date, there have been few published histological data on asymptomatic patients with persistently abnormal liver enzyme abnormalities on which to base management decisions such as liver biopsy. In a recent Scandinavian study, 150 asymptomatic patients with elevated serum transaminases underwent liver biopsy.4 While fibrosis was observed in half of the biopsies, only 2% were cirrhotic, and in the majority a mild …
Cardiac response to pressure overload in the rat: the selective alteration of in vitro directed RNA translation products.
Authors: K R Boheler, W H Dillmann
Journal: Circulation Research (1988)

As cardiac hypertrophy develops, total cardiac RNA and protein synthesis increase significantly. We have identified specific messenger RNAs that change in predominance with the induction of pressure-overload-stimulated cardiac hypertrophy. Total cardiac RNA was isolated from rats either undergoing cardiac hypertrophy secondary to subdiaphragmatic aortic constriction or subjected to sham surgery. The products translated in vitro were separated by two-dimensional gel electrophoresis and quantitated. The translation of four proteins decreased while the translation of four others increased in preparations from hypertrophied hearts compared with those from sham-treated rats. Two isoforms of creatine kinase M were translated in vitro. Only one of these isoforms decreased with cardiac hypertrophy, suggesting that the transcriptional or translational control for creatine kinase is much more complex than previously believed. Finally, since only eight of over 700 different translation products changed in relative predominance with cardiac hypertrophy, we conclude that the accumulation of existing RNA and protein products is the primary adaptive process responsible for cardiac hypertrophy.
Temporal and Mosaic Tsc1 Deletion in the Developing Thalamus Disrupts Thalamocortical Circuitry, Neural Function, and Behavior
Authors: Elizabeth A. Normand, Shane R. Crandall, Catherine A. Thorn, Emily M. Murphy, Bettina Voelcker, Catherine Browning, Jason T. Machan, Christopher I. Moore, Barry W. Connors, Mark Zervas
Journal: Neuron (2013)
Abstract 4973: Telomerase-specific replication-selective oncolytic viruses for adenoid cystic carcinoma cell lines
Authors: Daisuke Sato, Yuji kurihara, Seiji Kondo, Tatsuo shirota, Yasuo Urata, Toshiyoshi Fujiwara, Satoru Shintani
Journal: Cancer Research (2012)

Abstract There is no effective treatment of adenoid cystic carcinoma (ACC) in oral region, which low sensitivity of chemotherapy and radiation therapy. We previously showed that telomerase-specific replication-competent adenovirus (Telomelysin, OBP-301), in which the human telomerase reverse transcriptase (hTERT) promoter controls the adenoviral E1 gene expression, induces a selective antitumor effect in oral squamous cell carcinoma (OSCC) cells in vitro and in vivo orthotopic graft model. We conducted to evaluate the effectiveness of OBP301 against ACC. First, we could confirm that the expression of hTERT in two types of ACC cell lines (ACC2, ACCM) by Western blotting. Then, we examined the antitumor effect of OBP301 in human ACC cells in vitro. OBP-301 infection induced cell death in human ACC cells in a dose-dependent manner. We also examined the expression levels of coxsackievirus and adenovirus receptor (CAR) on the cell surface of each type of cell by flow cytometric analysis. Apparent amounts of CAR expression were detected on human ACC cells. Relative hTERT mRNA expression in ACC was analyzed by real-time RT-PCR, which showed high expression time dependent. In addition, OBP-401 is a genetically engineered adenovirus that expresses GFP by inserting the GFP gene under the control of the cytomegalovirus promoter at the deleted E3 region of OBP-301. Human ACC cells expressed bright GFP fluorescence as early as 12 h after OBP-401 infection. The fluorescence intensity gradually increased in a dose-dependent manner, followed by rapid cell death due to the cytopathic effect of OBP-401, as evidenced by floating, highly light-refractile cells under phase-contrast photomicrographs. In conclusion, our data clearly indicate that telomerase-specific oncolytic adenoviruses have a significant therapeutic potential against human ACC in vitro. These results suggested that treatment of OBP-301 and OBP-401 are possible to improvement of QOL of oral cancer patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4973. doi:1538-7445.AM2012-4973
Upregulation of fibronectin synthesis by interleukin-1 beta in coronary artery smooth muscle cells is associated with the development of the post-cardiac transplant arteriopathy in piglets.
Authors: N Clausell, M Rabinovitch
Journal: Journal of Clinical Investigation (1993)

We previously described in piglets after heterotopic cardiac transplantation the early development of a coronary arteriopathy characterized by increased immunostaining for fibronectin and interleukin-1 beta (IL-1 beta) in the vessel wall. The objective of this study was to culture smooth muscle cells from donor and host coronary arteries in these piglets to determine whether donor cells produce more fibronectin than host cells as judged by increased protein and mRNA levels, and whether IL-1 beta may be regulating this increase by an autocrine mechanism involving increased production of the cytokine. We documented increased donor coronary artery smooth muscle cell fibronectin protein synthesis and mRNA compared to host. By using neutralizing antibodies to IL-1 beta, fibronectin protein synthesis and mRNA levels were reduced in donor cells to the levels observed in the host cells and a similar reduction in synthesis was observed with the IL-1 receptor antagonist. Immunoprecipitation of newly synthesized IL-1 beta revealed increased endogenous levels in donor compared to host cells. We therefore suggest in the coronary arteriopathy a pathophysiologic mechanism whereby IL-1 beta-mediated increased fibronectin synthesis may promote lymphocyte trapping and migration of medial smooth muscle cells leading to progressive intimal thickening associated with the post-cardiac transplant coronary arteriopathy.
Primacy Among the Primates: Killing Chimpanzees to Help Humans
Authors: David M. Warshauer
Journal: JAMA (1985)

<h3>To the Editor.—</h3> Recent work with baboon-to-human heart transplants and impending work with chimpanzee-to-human liver transplants raise serious ethical questions. Certainly, animal products such as insulin, heart valves, and growth hormone, have produced great good for human beings. However, there are essential differences between these products derived from lower domesticated animals and products that will derive from the new and proposed work with the higher primates. First is the philosophical question of consciousness and its implications. There can be little doubt that chimpanzee society rivals our own in awareness, organization, and emotional content.<sup>1</sup>Whether this fact should confer some protection on chimpanzees from being viewed only as reservoirs for spare parts can be debated, although it seems reasonable that it should. The second difference is less debatable. Chimpanzees are an endangered species. Estimated world populations are in the 50,000 range as compared with 4.5 billion humans. Capture techniques to
Dual-Specificity Phosphatase 3 Deficiency or Inhibition Limits Platelet Activation and Arterial Thrombosis
Authors: Lucia Musumeci, Marijke J. Kuijpers, Karen Gilio, Alexandre Hego, Emilie Théâtre, Lisbeth Maurissen, Maud Vandereyken, Catia V Diogo, Christelle Lecut, William Guilmain, Ekaterina V. Bobkova, Johannes A. Eble, Russell Dahl, Pierre Drion, Justin Rascon, Yalda Mostofi, Hongbin Yuan, Eduard Sergienko, Thomas D.Y. Chung, Marc Thiry, Yotis Senis, Michel Moutschen, Tomas Mustelin, Patrizio Lancellotti, Johan W.M. Heemskerk, Lutz Tautz, Cécile Oury, Souad Rahmouni
Journal: Circulation (2014)

A limitation of current antiplatelet therapies is their inability to separate thrombotic events from bleeding occurrences. A better understanding of the molecular mechanisms leading to platelet activation is important for the development of improved therapies. Recently, protein tyrosine phosphatases have emerged as critical regulators of platelet function.This is the first report implicating the dual-specificity phosphatase 3 (DUSP3) in platelet signaling and thrombosis. This phosphatase is highly expressed in human and mouse platelets. Platelets from DUSP3-deficient mice displayed a selective impairment of aggregation and granule secretion mediated by the collagen receptor glycoprotein VI and the C-type lectin-like receptor 2. DUSP3-deficient mice were more resistant to collagen- and epinephrine-induced thromboembolism compared with wild-type mice and showed severely impaired thrombus formation on ferric chloride-induced carotid artery injury. Intriguingly, bleeding times were not altered in DUSP3-deficient mice. At the molecular level, DUSP3 deficiency impaired Syk tyrosine phosphorylation, subsequently reducing phosphorylation of phospholipase Cγ2 and calcium fluxes. To investigate DUSP3 function in human platelets, a novel small-molecule inhibitor of DUSP3 was developed. This compound specifically inhibited collagen- and C-type lectin-like receptor 2-induced human platelet aggregation, thereby phenocopying the effect of DUSP3 deficiency in murine cells.DUSP3 plays a selective and essential role in collagen- and C-type lectin-like receptor 2-mediated platelet activation and thrombus formation in vivo. Inhibition of DUSP3 may prove therapeutic for arterial thrombosis. This is the first time a protein tyrosine phosphatase, implicated in platelet signaling, has been targeted with a small-molecule drug.
Ofatumumab in combination with ICE or DHAP chemotherapy in relapsed or refractory intermediate grade B-cell lymphoma
Authors: Matthew J. Matasar, Myron S. Czuczman, Maria Alma Rodriguez, Michael Fennessy, Thomas C. Shea, Gary Spitzer, Izidore S. Lossos, Mohamed A. Kharfan-Dabaja, Robin Joyce, Luis Fayad, Kristen Henkel, Qiming Liao, Klaus Edvardsen, Roxanne C. Jewell, Doug Fecteau, Rajendra P. Singh, Steen Lisby, Craig H. Moskowitz
Journal: Blood (2013)
EARLY DETECTION OF IMPROVEMENT OF LEFT VENTRICULAR FUNCTION AFTER UNDERSIZED MITRAL ANNULOPLASTY FOR FUNCTIONAL MITRAL REGURGITATION: TWO-DIMENSIONAL SPECKLE TRACKING ECHOCARDIOGRAPHY
Authors: Yasuhiro Shudo, Satoshi Nakatani, Taichi Sakaguchi, Shigeru Miyagawa, Yasushi Yoshikawa, Takashi Yamauchi, Koji Takeda, Shunsuke Saito, Yoshiki Sawa
Journal: Journal of the American College of Cardiology (2010)
CCDC22 deficiency in humans blunts activation of proinflammatory NF-κB signaling
Authors: Petro Starokadomskyy, Nathan Gluck, Haiying Li, Baozhi Chen, Mathew Wallis, Gabriel N. Maine, Xicheng Mao, Iram W. Zaidi, Marco Y. Hein, Fiona J. McDonald, Steffen Lenzner, Agnes Zecha, Hans-Hilger Ropers, Andreas W. Kuss, Julie McGaughran, Jozef Gecz, Ezra Burstein
Journal: Journal of Clinical Investigation (2013)

NF-κB is a master regulator of inflammation and has been implicated in the pathogenesis of immune disorders and cancer. Its regulation involves a variety of steps, including the controlled degradation of inhibitory IκB proteins. In addition, the inactivation of DNA-bound NF-κB is essential for its regulation. This step requires a factor known as copper metabolism Murr1 domain–containing 1 (COMMD1), the prototype member of a conserved gene family. While COMMD proteins have been linked to the ubiquitination pathway, little else is known about other family members. Here we demonstrate that all COMMD proteins bind to CCDC22, a factor recently implicated in X-linked intellectual disability (XLID). We showed that an XLID-associated CCDC22 mutation decreased CCDC22 protein expression and impaired its binding to COMMD proteins. Moreover, some affected individuals displayed ectodermal dysplasia, a congenital condition that can result from developmental NF-κB blockade. Indeed, patient-derived cells demonstrated impaired NF-κB activation due to decreased IκB ubiquitination and degradation. In addition, we found that COMMD8 acted in conjunction with CCDC22 to direct the degradation of IκB proteins. Taken together, our results indicate that CCDC22 participates in NF-κB activation and that its deficiency leads to decreased IκB turnover in humans, highlighting an important regulatory component of this pathway.