tbuckley/cabot-search huggingface dataset:
Abstract P3-07-08: Breast cancer in China reveals transcriptomic likeness to Caucasian breast cancer
Authors: X Huang, M Dugo, M Callari, M Sandri, L DeCecco, ML Carcangiu, M Iorio, J Xue, MG Daidone, S Ménard, E Tagliabue, J Wu, R Orlandi
Journal: Cancer Research (2013)

Abstract The incidence of breast cancer among Chinese women has been historically much lower than that of Caucasian women but has increased dramatically over the past 30 years in urban areas of China, an increase likely to continue in the next decades across China with progressive urbanization and economic development. However, it is still unclear whether differences in breast cancer incidence between Chinese and Caucasian women reflect differences in disease biology in addition to environmental factors. To address this question, we compared consecutive cohorts of Chinese and Italian breast cancer patients who underwent surgical resection in the years 2005-2007 at Fudan Cancer Center of Shanghai (China) and Fondazione IRCCS Istituto Tumori of Milan (Italy), respectively, two comprehensive cancer centers with similar inpatients and outpatients recruited in a large area. Analyses of clinico-pathological characteristics of 1563 Chinese and 1052 Italian consecutive breast cancer patients revealed that 50% of patients in the Chinese cohort were younger than 50 years versus 29% of Italian patients, indicating that Chinese women develop breast cancer earlier than Italian patients, with a peak of frequency at 50-60 years. Among Chinese breast tumors, 63% were estrogen receptor (ER)-positive versus 85% of the Italians, and the prevalence of ER-positive tumors was equivalent in pre- and postmenopausal Chinese cases, suggesting the same hormonal features in tumors of younger and older patients, consistent with findings in the Italian cohort. Microarray-based gene and miRNA expression profiling was then conducted on 80 Chinese and 97 Italian samples using Illumina Gene and MicroRNA expression technologies. To minimize potential bias and artifact due to variability in specimen collection, storage, processing and analysis of high-throughput results, samples initially collected in the Chinese and Italian hospitals were all stored, randomly processed and analyzed in the Italian center. Analysis revealed a comparable pattern of gene and miRNA expression in the 2 cohorts with unsupervised hierarchical clustering of 12,338 genes and 858 miRNAs, and similar expression of intrinsic and extracellular matrix (ECM) genes led to a similar partition in intrinsic and ECM subtypes, indicating molecular similarity among Chinese and Caucasian breast cancers. Supported by Ministero Affari Esteri (Italy-China significant bilateral project). Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P3-07-08.
THE NON-TOXICITY OF UREA.
Authors: R. HARVEY COOK
Journal: JAMA (1895)

Urea being the final product of tissue metamorphosis and apparently playing no rôle whatever in our economy, it was natural to consider it a waste material, of which our system should rid itself. Finding this material diminished in various affections it was<i>a priori</i>considered that the system must be overloaded with this effete material, urea. That urea is even yet considered a toxic body by many, is apparent from the numerous articles attributing toxic effects to this substance. The recent article by Dr. J. Nelson Teeter, on "The Relation of Urea to Epilepsy," which appeared in the January number of the<i>American Journal of Insanity</i>, has caused me to write my observations and experiments in regard to the toxicity of urea. Perhaps no one has done more toward fathoming the mysterious depths of auto-intoxication than has Bouchard; to him my experiments are due, nor do my experiments differ from
Medullary Metastasis Causing Impairment of Respiratory Pressure Output with Intact Respiratory Rhythm
Authors: STEPHEN CORNE, KIM WEBSTER, GREGORY McGINN, ST.-JOHN, WALTER, MAGDY YOUNES
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

We present an unusual case of weaning failure. A 67-yr-old man presented with confusion, hyponatremia, and hypercapnic respiratory failure that necessitated mechanical ventilation. CXR revealed a right hilar mass (non-small-cell carcinoma on biopsy). Level of consciousness improved with treatment of his hyponatremia. However, attempts at weaning were complicated by hypercapnia with no overt distress. Resistance and elastance were only slightly abnormal, excluding mechanics as a cause of respiratory failure. Maximal inspiratory pressure (MIP) and vital capacity (VC) were reduced at − 15 cm H2O and 0.97 L, respectively. Limb muscle strength was well preserved, suggesting isolated respiratory muscle weakness. During a weaning trial respiratory rate increased from 7 to 40 breaths/min as Pco 2 increased from 56 to 89 mm Hg, confirming an intact respiratory pacemaker and good response to CO2. However, spontaneous Pdi was only 1 to 2 cm H2O ( < 20% of Pdimax) despite profound hypercapnia. The fact that the patient did not utilize a greater fraction of his pressure-generating capacity suggested preferential impairment of the automatic respiratory centers. MRI showed a large central metastatic lesion in the rostral medulla with only a thin rim of uninvolved tissue. This case illustrates the utility of relating the magnitude of spontaneous efforts to maximal voluntary efforts as a means of localizing the site of involvement in cases of respiratory muscle weakness. It also demonstrates that a large medullary mass lesion may selectively impair brainstem modulation of respiratory pressure output while sparing other medullary functions, and in particular the pacemaking function of the respiratory centers.
Parents' guide to H1N1
Authors: John McConnell
Journal: The Lancet (2009)

Outbreaks of infectious diseases have a way of grabbing the public imagination that outstrips any other medical event. The first decade of the 21st century has seen anthrax spores in the US mail, severe acute respiratory syndrome, avian influenza A H5N1, and now a pandemic of influenza A H1N1 (so called swine flu), which have generated a level of media and public attention that has at times bordered on the hysterical.
Disseminated Intravascular Coagulation in Hypothermia
Authors: Donna L. Carden
Journal: JAMA (1982)

<h3>To the Editor.—</h3> We noted the article by Mahajan et al (1981;246:2517) describing disseminated intravascular coagulation (DIC) in hypothermia. The hematologic workup identifying hypothermia as the primary cause of the DIC was thorough and well documented. However, the association of DIC with hypothermia has been well recognized in the past. Rueler<sup>1</sup>reviewed the subject of hypothermia and pointed out that DIC was a known hematologic complication. Stine<sup>2</sup>reviewed the subject and discussed the complication of intravascular thrombosis. Duguid et al<sup>3</sup>recorded hemorrhagic and thrombotic lesions in the brain, spleen, heart, kidney, and gut during postmortem examination of patients who died of hypothermia. A more recent study<sup>4</sup>evaluated 11 cases of accidental hypothermia and found that seven patients had platelet counts of less than 150,000/cu mm. Furthermore, two of these patients had serum fibrinogen levels of less than 150 mg/dL (normal, &gt;200 mg/ dL) and died of
DOUBLE NASAL ATRESIA DUE TO SMALLPOX.Read before the Mississippi Valley Medical Assoc'ation, at Hot Springs, Nov. 20, 1894.
Authors: HANAU W. LOEB
Journal: JAMA (1895)

One-sided nasal atresia due to smallpox is uncommon enough in rhinologic literature, and as double nasal atresia caused by smallpox must be all the rarer, I am prompted to present the details of this most interesting case to the Association. It is all the more desirable for presentation on account of the success of the treatment, and the great relief which the patient has experienced, for we all know the difficulty of maintaining an opening which nature once has closed. We read, with remarkable monotony, of failure after failure in the treatment of webbed fingers and conditions due to the deposit of scar tissue; we realize quite readily the almost futility of the treatment for the permanent relief of cicatricial contractions and adhesions, resulting from syphilitic lesions of the pharynx, palate and larynx, so that while no great skill is claimed in the management of the case in point, yet
Selective elimination of a chemoresistant side population of B-CLL cells by cytotoxic T lymphocytes in subjects receiving an autologous hCD40L/IL-2 tumor vaccine
Authors: A E Foster, F V Okur, E Biagi, A Lu, G Dotti, E Yvon, B Savoldo, G Carrum, M A Goodell, H E Heslop, M K Brenner
Journal: Leukemia (2010)
Michael Thomas Ward
Authors: Tim Ward
Journal: BMJ (2008)

Michael Thomas Ward (“Mike”) was born in Chesterfield, Derbyshire, to Peter and Winifred on Burns’ night 1935.

A spirited education at St Mary’s propelled Mike, in 1958, into the dragon’s lair under the auspices of Felix Eastcott, who had recently been credited with the first carotid endarterctomy, and the brilliant but irascible cardiologist Jack Litchfield.

This was the era of Richard Gordon’s inspiration, however, and long periods of dedicated continuous duty were peppered with Dunkirk fuelled pockets of hilarity and high …
The effect of intravenous interferon-beta-1a (FP-1201) on lung CD73 expression and on acute respiratory distress syndrome mortality: an open-label study
Authors: Geoff Bellingan, Mikael Maksimow, David C Howell, Martin Stotz, Richard Beale, Monika Beatty, Timothy Walsh, Alexander Binning, Alan Davidson, Martin Kuper, Sanjoy Shah, Jackie Cooper, Matti Waris, Gennady G Yegutkin, Juho Jalkanen, Marko Salmi, Ilse Piippo, Markku Jalkanen, Hugh Montgomery, Sirpa Jalkanen
Journal: The Lancet Respiratory Medicine (2013)
Arterial Hypertension and Renal Allograft Survival
Authors: Kevin C. Mange
Journal: JAMA (2000)

Several observational studies have investigated the significance of hypertension in renal allograft failure; however, these studies have been complicated by the lack of adjustment for baseline renal function, leaving the role of elevated blood pressure in allograft failure unclear.To examine the relationship between blood pressure adjusted for renal function and survival after cadaveric allograft transplantation.Nonconcurrent historical cohort study conducted from 1985 through 1997.University teaching hospital.A total of 277 patients aged 18 years or older who underwent cadaveric renal transplantation without another simultaneous organ transplantation and whose allograft was functioning for a minimum of 1 year. Follow-up continued through 1997 (mean follow-up, 5.7 years).Time to allograft failure (defined as death, return to dialysis, or retransplantation) by systolic, diastolic, and mean arterial blood pressure measurements at 1 year after transplantation.Multivariate Cox proportional hazards modeling demonstrated that nonwhite ethnicity, history of acute rejection, and nondiabetic kidney disease were significant predictors of failure (P = .01 for all). In addition, the calculated creatinine clearance at 1 year had an adjusted rate ratio (RR) for allograft failure per 10 mL/min (0.17 mL/s) of 0.74 (95% confidence interval [CI], 0.62-0.88). The RR per 10-mm Hg increase in blood pressure measured at 1 year after transplantation, after adjustment for creatinine clearance, was 1.15 (95% CI, 1.02-1.30) for systolic pressure, 1.27 (95% CI, 1.01-1.60) for diastolic pressure, and 1.30 (95% CI, 1.05-1.61) for mean arterial pressure. Supplemental analyses that did not include death as a failure event or reduce the minimum allograft survival time for study subjects to 6 months yielded results consistent with the primary analysis. There was no evidence of modification of the blood pressure-allograft failure relationship by ethnicity or diabetes mellitus.Systolic, diastolic, and mean arterial blood pressures at 1 year posttransplantation strongly predict allograft survival adjusted for baseline renal function. More aggressive control of blood pressure may prolong cadaveric allograft survival.
Partner Violence Screening and Women’s Quality of Life—Reply
Authors: Nadine Wathen, Harriet MacMillan
Journal: JAMA (2012)

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
Increased Soluble Form of P-Selectin in Patients With Unstable Angina
Authors: Hisao Ikeda, Yoshinori Takajo, Kazuya Ichiki, Takafumi Ueno, Sanae Maki, Takehiko Noda, Kenzo Sugi, Tsutomu Imaizumi
Journal: Circulation (1995)

Background P-selectin in platelets and endothelial cells mediates adhesive interaction with leukocytes to form thrombi. The purpose of the present study was to investigate the plasma levels of P-selectin in patients with unstable angina and in those with stable effort angina of different pathophysiologies. Methods and Results Plasma P-selectin levels were determined by a monoclonal antibody–based enzyme immunoassay on plasma samples taken from 12 patients with unstable angina, 11 patients with stable effort angina, and 15 healthy volunteers. Patients with unstable angina had angina at rest associated with ECG changes. In patients with unstable angina, plasma P-selectin levels within 1 hour (361±90 ng/mL) and at 3 hours (282±56 ng/mL) after angina were significantly ( P &lt;.05) higher than those in volunteers (177±31 ng/mL). Plasma P-selectin levels at 5 hours after attack (242±46 ng/mL) did not differ from those in volunteers. Although patients with stable effort angina developed angina with ST-segment depressions by treadmill exercise, their plasma P-selectin levels did not change (before, 178±45; immediately after, 186±36; and 1 hour after the exercise, 179±34 ng/mL). Conclusions Plasma P-selectin levels after angina increased significantly in patients with unstable angina but did not in patients with stable effort angina. These findings may contribute to understanding of the pathophysiology of the acute coronary syndrome of unstable angina.
Nonremoval of Dentures During Anesthesia
Authors: Yilmaz Eryasa
Journal: JAMA (1974)

<h3>To the Editor.—</h3> Administration of general anesthesia without removing dentures causes no problems in my practice. It helps to get a better fit with the mask and also maintains a good airway without the insertion of oral or nasal airways. I am concerned, however, that there might be a possibility of aspirating or swallowing dentures in debilitated and deeply sedated patients or during the recovery from anesthesia. Because of this possibility, I order light sedation preoperatively and remove dentures at the end of anesthesia until complete recovery and before the patient is taken to his room.
Eplerenone in Patients With Systolic Heart Failure and Mild Symptoms
Authors: Jennifer K. Rogers, John J.V. McMurray, Stuart J. Pocock, Faiez Zannad, Henry Krum, Dirk J. van Veldhuisen, Karl Swedberg, Harry Shi, John Vincent, Bertram Pitt
Journal: Circulation (2012)

Eplerenone is known to reduce time to first hospitalization for heart failure or cardiovascular death in patients with heart failure and mild symptoms. In chronic diseases such as heart failure, characterized by repeat hospitalizations, analyzing all heart failure hospitalizations, not just the first, should give a more complete picture of treatment benefits.The Eplerenone in Mild Patients Hospitalization and SurvIval Study in Heart Failure (EMPHASIS-HF) trial compared eplerenone with placebo in 2737 patients with mild heart failure, followed for a median 2.08 years (interquartile range, 1.08-3.10 years). Data were collected on all hospitalizations, with a focus on those due to heart failure. Heart failure hospitalization rates in the eplerenone and placebo groups were 10.70 and 16.99 per 100 patient-years, respectively. Allowing for skewness in the frequency of hospitalizations by using the negative binomial generalized linear model, the rate ratio (eplerenone versus placebo) was 0.53 (95% confidence interval, 0.42-0.66; P<0.0001). A plot of cumulative hospitalization rates over time revealed that most of the reduced risk on eplerenone occurred in the first year of follow-up. Several baseline variables strongly predicted the risk of hospitalization. More complex statistical methods, adjusting for mortality (as informative censoring), made a negligible difference in these findings.Eplerenone markedly reduces the risk of heart failure hospitalizations in patients with heart failure and mild symptoms to a greater extent than is captured by only studying the time to first hospitalization. Future clinical trials in heart failure would gain from incorporating repeat hospitalizations into their primary evaluation of treatment effects.URL: http://www.clinicaltrials.gov. Unique identifier: NCT00232180.
Enhancement of TGF-β Signaling Responses by the E3 Ubiquitin Ligase Arkadia Provides Tumor Suppression in Colorectal Cancer
Authors: Vikas Sharma, Anna G. Antonacopoulou, Shinya Tanaka, Alexios A. Panoutsopoulos, Vasiliki Bravou, Haralabos P. Kalofonos, Vasso Episkopou
Journal: Cancer Research (2011)

Abstract TGF-β signaling provides tumor protection against colorectal cancer (CRC). Mechanisms that support its tumor-suppressive properties remain unclear. The ubiquitin ligase Arkadia/RNF111 enhances TGF-β signaling responses by targeting repressors of the pathway for degradation. The corepressors SnoN/Ski, critical substrates of Arkadia, complex with the activated TGF-β signaling effectors Smad2/3 (pSmad2/3) on the promoters of target genes and block their transcription. Arkadia degrades this complex including pSmad2/3 and unblocks the promoter. Here, we report that Arkadia is expressed highly in the mouse colonic epithelium. Heterozygous Akd+/− mice are normal but express less Arkadia. This leads to reduced expression of several TGF-β target genes, suggesting that normal levels of Arkadia are required for efficient signaling responses. Critically, Akd+/− mice exhibit increased susceptibility to azoxymethane/dextran sodium sulfate carcinogen–induced CRC, as they develop four-fold more tumors than wild-type mice. Akd+/− tumors also exhibit a more aggressive pathology, higher proliferation index, and reduced cytostasis. Therefore, Arkadia functions as a tumor suppressor whose peak expression is required to suppress CRC development and progression. The accumulation of nuclear SnoN and pSmad2, along with the downregulation of TGF-β target genes observed in Akd+/− colon and tumors, suggest that tumor-suppressing properties of Arkadia are mediated by its ability to derepress TGF-β signaling. Consistent with this likelihood, we identified mutations in primary colorectal tumors from human patients that reduce Arkadia function and are associated with the accumulation of nuclear SNON. Collectively, our findings reveal that Arkadia enhances TGF-β signaling responses and supports its tumor-suppressing properties in CRC. Cancer Res; 71(20); 6438–49. ©2011 AACR.
Atrioventricular Block, Type II (Mobitz)—Its Nature and Clinical Significance
Authors: RICHARD LANGENDORF, ALFRED PICK
Journal: Circulation (1968)

THE USE OF artificial pacing has greatly intensified interest in chronic A-V block.This interest, in turn, has brought into sharp focus the rare type of A-V block described independently in 1906 by Wenckebach' and by Hay2 and classified by Mobitz in 1924 as type 11.3This type of block is characterized by failure of a ventricular response, without antecedent progressive lengthening of A-V conduction time.Furthermore, in its more advanced form several consecutive atrial im-
Biased use of VH5 IgE-positive B cells in the nasal mucosa in allergic rhinitis
Authors: Heather A. Coker, Helen E. Harries, Graham K. Banfield, Victoria A. Carr, Stephen R. Durham, Elfy Chevretton, Paul Hobby, Brian J. Sutton, Hannah J. Gould
Journal: Journal of Allergy and Clinical Immunology (2005)
Coronary Vasodilation Induced by Angiotensin-Converting Enzyme Inhibition In Vivo
Authors: Krishnankutty Sudhir, Tony M. Chou, Stuart J. Hutchison, Kanu Chatterjee
Journal: Circulation (1996)

Background We studied in coronary conductance and resistance arteries the coronary vasodilator effects of the angiotensin-converting enzyme inhibitor ramiprilat and the contribution of nitric oxide, bradykinin, and prostaglandins to this vasodilation. Methods and Results In seven anesthetized dogs, a Doppler guidewire was placed in the circumflex coronary artery to measure coronary flow velocity, and an ultrasound imaging catheter was introduced over the Doppler wire to measure coronary cross-sectional area. Drugs were infused directly into the left main coronary artery to minimize systemic effects. Ramiprilat increased both epicardial cross-sectional area and coronary blood flow velocity, resulting in an increase in absolute coronary blood flow. Pretreatment with N ω -nitro- l -arginine methyl ester (100 μmol/L intracoronary) to block nitric oxide synthase attenuated ramiprilat-induced increase in epicardial coronary cross-sectional area ( P &lt;.05) but not in coronary flow velocity or coronary blood flow. In contrast, pretreatment with the selective bradykinin antagonist HOE 140 (10 μmol/L) attenuated ramiprilat-induced increase in flow velocity ( P &lt;.025) and coronary blood flow ( P &lt;.05) but not epicardial coronary cross-sectional area. Pretreatment with indomethacin (5 mg/kg body wt IV) did not alter ramiprilat-induced increase in epicardial cross-sectional area, nor did it significantly influence coronary blood flow. Conclusions Other than decreasing angiotensin II production, acute ramiprilat-induced vasodilation in canine coronary conductance arteries is mediated in part by nitric oxide. Ramiprilat-induced vasodilation in resistance arteries is in part mediated by the action of bradykinin.