tbuckley/cabot-search huggingface dataset:
Abstract C57: The role of the microRNA-200 family in the regulation of tumor cell signaling and metastasis in lung cancer
Authors: Jonathon D. Roybal, David H. Peng, Christin Ungewiss, Pijus K. Mandal, John S. McMurray, Lauren A. Byers, Don L. Gibbons
Journal: Cancer Research (2013)

Abstract Lung cancer is one of the deadliest cancers in the United States due primarily to the development of metastatic disease, resulting in a 16% five year overall survival. Unfortunately response rates are poor with the current modalities used to treat patients, which implies that a greater understanding of the biology of invasion and metastasis is essential. It is thought that the epithelial-mesenchymal transition (EMT) plays a critical role in regulating invasion, migration, and metastasis. The microRNA-200 family (miR-200) is a key maintenance factor for the epithelial phenotype by regulating EMT-inducing transcription factors such as Zeb1, and subsequent metastatic potential, although the mechanistic details of this regulation are incompletely understood. Recent research has demonstrated that miRNAs are capable of regulating the target mRNAs that coordinate intracellular signaling pathways. Using our mutant Kras and p53 murine model of metastatic lung adenocarcinoma, we have shown through reverse phase protein array (RPPA) profiling that in poorly metastatic lung tumor cells, high miR-200 levels can suppress cancer-promoting signaling molecules, such as Signal Transducer and Activator of Transcription 3 (STAT3). In contrast, highly metastatic lung tumor cells with low miR-200 expression have STAT3 activation and increased migratory and invasive properties. Utilizing siRNA approaches or pharmacological inhibition of STAT3 in highly metastatic lung tumor cells decreased their ability to migrate and invade. Our data suggests that the STAT3 pathway is under the control of miR-200/Zeb1 axis and could provide a potential therapeutic target in lung cancer patients. Citation Format: Jonathon D. Roybal, David H. Peng, Christin Ungewiss, Pijus K. Mandal, John S. McMurray, Lauren A. Byers, Don L. Gibbons. The role of the microRNA-200 family in the regulation of tumor cell signaling and metastasis in lung cancer. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Invasion and Metastasis; Jan 20-23, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;73(3 Suppl):Abstract nr C57.
Effects of acetylcholine on electrophysiological properties of rabbit cardiac Purkinje fibers.
Authors: K Mubagwa, E Carmeliet
Journal: Circulation Research (1983)

The action of acetylcholine (10(-9)-10(-4) M) was investigated in isolated rabbit cardiac Purkinje fibers, using standard microelectrode recording of transmembrane potentials and two-microelectrode voltage clamp technique. In nonstimulated fibers, acetylcholine hyperpolarized the diastolic membrane potential and slowed or suppressed spontaneous activity. The hyperpolarization was more pronounced in low potassium solutions and in depolarized fibers; it was less marked in the presence of cesium (2 X 10(-2) M), and was suppressed by barium (3-5 X 10(-3) M). In stimulated fibers, acetylcholine shortened the action potential duration and shifted the plateau level to more negative values; this effect was influenced little by the stimulation frequency and not by chloride removal from the perfusing solution. In voltage-clamped preparations, acetylcholine shifted the holding current in the outward direction at potentials less negative than EK, while it shifted the current in the inward direction at potentials more negative than EK. The changes induced by acetylcholine were concentration-dependent (apparent KM: 1.5 X 10(-7) M); they were mimicked by carbachol (10(-8)-10(-5) M) and blocked by atropine (10(-8)-10(-7) M). The time course of the effects was biphasic: a maximum was reached in the first minute after addition of acetylcholine; thereafter, the effect decayed to a steady value. On removal of acetylcholine, a transient inversion of the changes produced by acetylcholine was observed, the magnitude of which depended on the acetylcholine concentration used and on the duration of exposure to acetylcholine. This time course was not abolished by pretreatment with physostigmine (10(-6) M), manganese ions (2 X 10(-3) M), or with adrenoceptor blockers [propranolol (2 X 10(-7) M) and/or phentolamine (10(-7)-10(-6) M)]. The results show that rabbit Purkinje fibers are as sensitive to acetylcholine as atrial preparations. The changes produced by acetylcholine are suggestive of an increase in an inward rectifying potassium ion conductance and are mediated by muscarinic receptor stimulation. The secondary decay in the effects of acetylcholine and their inversion on washout can be explained by a desensitization mechanism if it is assumed that the acetylcholine-sensitive channel is already functional in the absence of acetylcholine and is modulated in its conductance and/or open state probability by acetylcholine.
High risk infants in Florida to be screened for type 1 diabetes
Authors: F. Charatan
Journal: BMJ (2002)

The American Diabetes Association will create a $10m (£7.1m; €11.4m) endowment over five years to establish the nation's first ongoing state-wide screening programme for infants at risk of developing type 1 diabetes.

The programme will be based at the University of Florida's College of Medicine. The funding, which will be eligible for an equal amount from the state …
P231Molecular and cellular components of human carotid artery plaque related to thrombogenicity
Authors: C Foglieni, P Marchese, M Lombardi, ME Mantione, D Baccellieri, D Ferrara, R Castellano, K Kamami, W Ruf, ZM Ruggeri
Journal: Cardiovascular Research (2014)

Atherosclerosis is a dynamic progressive disease of the large arteries characterized by accumulation of lipids, inflammatory and smooth muscle cells (SMCs) and extracellular matrix. In situ growth or embolization of arterial thrombi following a plaque rupture may lead to acute coronary syndrome and stroke. Fibrous cap rupture may expose thrombogenic material, initiating platelet aggregation and coagulation pathways. These thrombotic changes result from activation of the clotting cascade by tissue factor (TF) and coagulation contact phase. Aim of the project is to study Carotid Plaque (CP) thrombogenicity and the vascular wall components responsible for thrombus formation. CP (n=12) from patients submitted to endoarterectomy for significant stenosis and internal mammary artery fragments (n=4, controls not atherosclerotic) from individuals undergoing coronary artery bypass surgery were snap-frozen and sectioned. Thrombogenesis induced by CP was evaluated ex-vivo under flow conditions using healthy volunteer blood drawn into citrate anticoagulant. Recalcified blood was perfused over CP cryosections at constant flow velocity and 37 °C, and the volume of platelet aggregates and fibrin deposited onto the surface was measured in real time by confocal videomicroscopy. The areas with same XY coordinates than those analyzed in blood flow experiments were relocalized in serial cryosections, to identify by histology (Movat's, Hematoxylin/Eosin) and confocal microscopy the vascular cell phenotypes and wall components involved in thrombus formation. Thrombi formed mainly over endothelium/intima layer (including fibrous cap); were abundant in the media rich in SMC and in foam cells, in the presence of FSP1, collagen type I, proteoglycans, fibrinogen and TF. The fibro-necro-calcific core was quite unreactive, except when TF was present. IMA wall layers were reactive with analogous pattern but showed a different amount of thrombus formation. Addition to blood before perfusion of anti-human TF monoclonal antibody, or antibody blocking factor XI activation, or a combination of them reduced the volume of platelet aggregates, and of fibrin to a different extent in the different vascular layers. These data suggest an in-situ role of vascular cells and matrix, as well as of intra-tissue TF in thrombus formation over CP, involving both TF and contact phase coagulation pathways.
Why public health must contribute to reduce violence
Authors: V. Sivarajasingam, J. P. Shepherd, R. G. Newcombe
Journal: BMJ (2011)

Florence and colleagues found that systematic collection, analysis, and use of anonymised emergency department recorded information on violence significantly reduced violence related hospital admissions. 1 Although violence has long been a public health matter, there is ambivalence in making it a health priority.After all, crime reduction is the responsibility of government departments other than health, and other public services-the police, courts, and probation and prison services-are there to tackle it.
Comparative Analysis of Regulatory Motif Discovery Tools for Transcription Factor Binding Sites
Authors: Wei Wei, Xiao-Dan Yu
Journal: Genomics Proteomics & Bioinformatics (2007)

Abstract In the post-genomic era, identification of specific regulatory motifs or transcription factor binding sites (TFBSs) in non-coding DNA sequences, which is essential to elucidate transcriptional regulatory networks, has emerged as an obstacle that frustrates many researchers. Consequently, numerous motif discovery tools and correlated databases have been applied to solving this problem. However, these existing methods, based on different computational algorithms, show diverse motif prediction efficiency in non-coding DNA sequences. Therefore, understanding the similarities and differences of computational algorithms and enriching the motif discovery literatures are important for users to choose the most appropriate one among the online available tools. Moreover, there still lacks credible criterion to assess motif discovery tools and instructions for researchers to choose the best according to their own projects. Thus integration of the related resources might be a good approach to improve accuracy of the application. Recent studies integrate regulatory motif discovery tools with experimental methods to offer a complementary approach for researchers, and also provide a much-needed model for current researches on transcriptional regulatory networks. Here we present a comparative analysis of regulatory motif discovery tools for TFBSs.
631. Phase 1/2 Trial of Autologous Tumor Mixed with an Allogeneic GVAX® Immunotherapy in Advanced Stage Non-Small Cell Lung Cancer
Authors: John Nemunaitis, Thierry Jahan, Helen Ross, Daniel Sterman, Donald Richards, Bernie Fox, David Jablons, Junko Aimi, Andy Lin, Kristen Hege
Journal: Molecular Therapy (2006)

We have previously demonstrated activity with immunotherapy composed of autologous tumor cells genetically modified to secrete GM-CSF (GVAX®) in advanced stage NSCLC1. In an effort to remove the requirement and variability associated with genetic transduction of individual tumors we developed a "bystander" GVAX® platform composed of autologous tumor cells mixed with an allogeneic GM- CSF secreting cell line. We conducted a phase I/II trial of this immunotherapy (3 to 12 biweekly injections) in advanced stage NSCLC. Tumors were harvested from 86 patients, tumor cell processing was successful in 76, and 49 received study treatment. The most common toxicity was local injection site reactions. Serum GM-CSF pharmacokinetics were consistent with secretion of GM- CSF from the injected cells for up to 4 days with associated transient leukocytosis confirming GM-CSF bioactivity. Evidence of treatment-induced immune activation was demonstrated; however, objective tumor responses were not seen. Compared with autologous GVAX® immunotherapy for lung cancer prepared by transduction of individual tumors with an adenoviral GM-CSF vector, GM-CSF secretion was approximately 25-fold higher with the bystander GVAX® product used in this trial. However, the frequency of injection site reactions, tumor response, time to disease progression, and survival were all less favorable in the current study in comparison to prior results. Follow-up results will be presented. 1. Nemunaitis J, Sterman D, Jablons D, et al. Granulocyte- macrophage colony-stimulating factor gene-modified autologous tumor vaccines in non-small-cell lung cancer. J Natl Cancer Inst 2004;96(4):326–31.
THE SMALL INTESTINE IN VITAMIN B DEFICIENCY
Authors: ROSS GOLDEN
Journal: JAMA (1941)

The association of abnormalities of the small intestine with nutritional disorders in which vitamin deficiency plays a part has been pointed out by a number of writers. Mackie<sup>1</sup>in 1933 mentioned such abnormalities in a case of sprue. In a series of cases of "chronic steatorrhea" Snell and Camp<sup>2</sup>in 1934 described dilatation, hypomotility and smoothing or exaggeration of the mucosal contours in this portion of the digestive tract, changes which were readily demonstrable by the use of a barium sulfate meal. Similar observations were made by Mackie and Pound<sup>3</sup>(1935) in a series of cases of tropical sprue; by Mackie, Miller and Rhoads<sup>4</sup>(1935) in ulcerative colitis; by Pendergrass and Comroe<sup>5</sup>(1935) in a case in which there was chemical and clinical evidence of hypocalcemia, and by Golden<sup>6</sup>(1936) in infantile celiac disease. Snell and Camp expressed the belief that these abnormalities of
Rapid Screening for α<sub>1</sub>-Antitrypsin Deficiency in Patients with Chronic Obstructive Pulmonary Disease Using Dried Blood Specimens
Authors: Francisco Rodriguez, Rosendo Jardí, Xose Costa, Montserrat Cotrina, Roman Galimany, Rafael Vidal, Marc Miravitlles
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

We describe two reliable methods for high-throughput screening of proteinase inhibitor (PI) S and PI Z α1-antitrypsin (α1-AT) deficiency alleles from dried blood spot (DBS) specimens using the LightCycler fluorimetric analyzer. The method was used to study 72 patients with chronic obstructive pulmonary disease. Results were confirmed with DNA sequencing. The α1-AT concentration in DBS was determined with immune nephelometry. Sixteen patients (22%) showed no PI Z or PI S mutations. Five patients (7%) had a heterozygous genotype consisting of a PI S allele and a normal allele for the Z and S positions (non-S non-Z). Twenty-five patients (35%) had a heterozygous genotype consisting of a PI Z and a non-S non-Z allele. Two (3%) had the PI SS genotype, 2 (3%) the PI SZ, and 20 (28%) the PI ZZ. All patients with two normal α1-AT alleles and 10 heterozygous carriers of one normal and one deficient allele had α1-AT levels that fell within the α1-AT DBS normal range (1.8–3.1 mg/dl). Two patients with the rare PI MMmalton- and PI MMheerlen-deficient variants showed deficient α1-AT levels; PI S and PI Z were not detected. Processing 32 samples requires only 40 minutes. This single-step, cost-effective technology is optimal for working with small amounts of DNA, as are present in DBS. The method is suitable for large-scale screening, in cases where PI type is important.
Left Ventricular Hypertrophy With Exercise and ACE Gene Insertion/Deletion Polymorphism
Authors: Saul G. Myerson, Hugh E. Montgomery, Martin Whittingham, Mick Jubb, Michael J. World, Steve E. Humphries, Dudley J. Pennell
Journal: Circulation (2001)

Background —Local cardiac renin-angiotensin systems may regulate left ventricular (LV) hypertrophic responses. The absence (deletion [D]) of a 287-bp marker in the ACE gene is associated with greater myocardial ACE levels and exercise-related LV growth than is its presence (insertion [I]), an effect potentially mediated through either increased activity of the cellular growth factor angiotensin II on the angiotensin type 1 (AT 1 ) receptor or increased degradation of growth-inhibiting kinins. We sought to confirm ACE genotype–associated exertional LV growth and to clarify the role of the AT 1 receptor in this association. Methods and Results —One hundred forty-one British Army recruits homozygous for the ACE gene (79 DD and 62 II) were randomized to receive losartan (25 mg/d, a subhypotensive dose inhibiting tissue AT 1 receptors) or placebo throughout a 10-week physical training program. LV mass, determined by cardiac magnetic resonance, increased with training (8.4 g, P &lt;0.0001 overall; 12.1 versus 4.8 g for DD versus II genotype in the placebo limb, P =0.022). LV growth was similar in the losartan arm: 11.0 versus 3.7 g for DD versus II genotypes ( P =0.034). When indexed to lean body mass, LV growth in the II subjects was abolished, whereas it remained in the DD subjects (−0.022 versus 0.131 g/kg, respectively; P =0.0009). Conclusions —ACE genotype dependence of exercise-induced LV hypertrophy is confirmed. Additionally, LV growth in DD (unlike II) subjects is in excess of the increase in lean body mass. These effects are not influenced by AT 1 receptor antagonism with the use of losartan (25 mg/d). The 2.4-fold greater LV growth in DD men may be due to the effects of angiotensin II on other receptors (eg, angiotensin type 4) or lower degradation of growth-inhibitory kinins.
Credentialing and Public Accountability
Authors: Christine K. Cassel, Eric S. Holmboe
Journal: JAMA (2006)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Treatment of Hyperactive Children
Authors: Aaron Ament
Journal: JAMA (1974)

<h3>To the Editor.—</h3> As a child psychiatrist, I was surprised to note that the article by Sleator et al (<b>229</b>:316, 1974) seemed written solely from the pharmacologic-behavioral standpoint. It has been my experience that very few youngsters are afflicted with a hyperkinetic syndrome free of psychiatric problems. This crucial issue was ignored in the article. The article described a group of 26% of the youngsters in the study who experienced remission and no longer needed medication. The reader had no way of knowing how many of these youngsters underwent remission when psychiatric stress was removed. They may represent potentially symptomatic children who become symptomatic only under stress. They may represent a group whose biochemical immaturity is short-lived. They may constitute a group in which neurochemical defect is corrected permanently by methylphenidate. Or, also, they may represent a group whose symptomatology was almost entirely psychiatric in origin and which cleared
Evaluation of an Algorithm to Guide Patients With Type 1 Diabetes Treated With Continuous Subcutaneous Insulin Infusion on How to Respond to Real-Time Continuous Glucose Levels
Authors: Alicia J. Jenkins, Balasubramanium Krishnamurthy, James D. Best, Fergus J. Cameron, Peter G. Colman, Steven Farish, Peter S. Hamblin, Michele A. O'Connell, Christine Rodda, Kevin Rowley, Helena Teede, David N. O'Neal
Journal: Diabetes Care (2010)

To evaluate an algorithm guiding responses of continuous subcutaneous insulin infusion (CSII)-treated type 1 diabetic patients using real-time continuous glucose monitoring (RT-CGM).Sixty CSII-treated type 1 diabetic participants (aged 13-70 years, including adult and adolescent subgroups, with A1C <or=9.5%) were randomized in age-, sex-, and A1C-matched pairs. Phase 1 was an open 16-week multicenter randomized controlled trial. Group A was treated with CSII/RT-CGM with the algorithm, and group B was treated with CSII/RT-CGM without the algorithm. The primary outcome was the difference in time in target (4-10 mmol/l) glucose range on 6-day masked CGM. Secondary outcomes were differences in A1C, low (<or=3.9 mmol/l) glucose CGM time, and glycemic variability. Phase 2 was the week 16-32 follow-up. Group A was returned to usual care, and group B was provided with the algorithm. Glycemia parameters were as above. Comparisons were made between baseline and 16 weeks and 32 weeks.In phase 1, after withdrawals 29 of 30 subjects were left in group A and 28 of 30 subjects were left in group B. The change in target glucose time did not differ between groups. A1C fell (mean 7.9% [95% CI 7.7-8.2to 7.6% [7.2-8.0]; P < 0.03) in group A but not in group B (7.8% [7.5-8.1] to 7.7 [7.3-8.0]; NS) with no difference between groups. More subjects in group A achieved A1C <or=7% than those in group B (2 of 29 to 14 of 29 vs. 4 of 28 to 7 of 28; P = 0.015). In phase 2, one participant was lost from each group. In group A, A1C returned to baseline with RT-CGM discontinuation but did not change in group B, who continued RT-CGM with addition of the algorithm.Early but not late algorithm provision to type 1 diabetic patients using CSII/RT-CGM did not increase the target glucose time but increased achievement of A1C <or=7%. Upon RT-CGM cessation, A1C returned to baseline.
Reperfusion Injury to Skeletal Muscle on Bone Scan
Authors: Mustafa Kula, Seyhan Karacavus, Kemal Deniz, Huseyin Demir
Journal: Clinical Nuclear Medicine (2009)

We report the bone scan appearance of reperfusion injury involving the muscle groups of the lower extremities in a patient after undergoing thromboembolectomy of the bilaterally femoral artery. The patient was referred to our department with a history of colon adenocarcinoma and widespread bone pain. Bone scan demonstrated extraosseous accumulation of technetium-99m methylene diphosphonate in the muscle groups of the lower extremities, predominantly in the right extremity. Pathologic examination of the gastrocnemius muscle was suggestive of reperfusion injury and atrophic changes. There was no finding of rhabdomyolysis.
Treatment of Pernicious Anaemia
Authors: R. O. Gillhespy
Journal: BMJ (1953)

Thank you for your interest in spreading the word about The BMJ.NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. Username * Your Email * Send To * You are going to email the following Treatment of Pernicious Anaemia Your Personal Message CAPTCHA This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Successful combination treatment of clofarabine, cytarabine, and gemtuzumab‐ozogamicin in adult refractory B‐acute lymphoblastic leukemia
Authors: Cristina Papayannidis, Enrico Derenzini, Ilaria Iacobucci, Antonio Curti, Stefania Paolini, Daniela Cilloni, Michele Baccarani, Giovanni Martinelli
Journal: American Journal of Hematology (2009)

à la diffusion de documents scientifiques de niveau recherche, publiés ou non, émanant des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés.
INCREASED CYSTEINE LEVEL IS ASSOCIATED WITH RECURRENT ATHEROTHROMBOTIC EVENTS AFTER ACUTE CORONARY SYNDROMES
Authors: Jeroen Jaspers Focks, Nick Clappers, Marc A. Brouwer, Etiënne G. Cramer, Eveline G. van Dijk, Martijn G. van Oijen, Jan B. Jansen, Wilbert HM Peters, Freek W. Verheugt
Journal: Journal of the American College of Cardiology (2010)