tbuckley/cabot-search huggingface dataset:
Relationship of Various Factors to the Degree of Coronary Atherosclerosis in Women
Authors: ROBERT F. ACKERMAN, THOMAS J. DRY, JESSE E. EDWARDS
Journal: Circulation (1950)

The degree of coronary artery atherosclerosis present in 600 hearts obtained from women, 100 in each of the decades from 30 through 89 years, was determined by one observer. Coronary atherosclerosis increased with age until the eighth decade when the atherosclerosis tended to level off. Cardiac hypertrophy and diabetes were associated with increased degrees of atherosclerosis. Hearts from the undernourished exhibited less atherosclerosis than did hearts from average weight or overweight individuals. A comparison with data compiled on 600 hearts from men by White and associates has been included.
Data collection system needed for gun injuries
Authors: J. H. Tanne
Journal: BMJ (2000)

Guns have been so tied up with the American myth of the cowboys doing justice with their six shooters and with rights laid down in the Constitution that it has been impossible to discuss the gun control issue in a rational way, a New York seminar was told last week.

Dr Robert Seltzer, executive director of Doctors Against Handgun Injury, said that the Supreme Court had ruled more than 60 years ago that the second amendment of the Constitution, which gives citizens the right to bear arms, applied to state militia, not to individuals. But gun supporters …
Unnatural Death: Confusion of a Medical Examiner
Authors: Milton G. Bohrod
Journal: JAMA (1990)

With the right presentation and push to the general reading public, this book could become a popular best-seller. It is, first of all, a "good read," fascinating and fast flowing and about subjects that interest nearly everyone. Mystery readers will love it. Everyone who has followed newspaper details on the deaths of prominent persons, such as President Kennedy and the Attica victims, will relive the events and, perhaps for the first time, find explanations for puzzling questions. The book, however, should not be mistaken simply for entertainment. In the midst of the fascinating reading, the authors dispense a good deal of reliable and important information about forensic medicine and the role of the medical examiner. The centerpiece of the work is the medicolegal autopsy. The autopsy, once the crown of every pathologist's work, is now—I regret to say—on the decline; the greater number of autopsies are now done in cases
Molecular characterization of transgene-induced immunodeficiency in B-less mice using a novel quantitative limiting dilution polymerase chain reaction method.
Authors: D A Levinson, J Campos-Torres, P Leder
Journal: The Journal of Experimental Medicine (1993)

B-less mice express a human immunoglobulin (Ig) lambda transgene that induces a severe deficiency of both immature pre-B and mature B lymphocytes. To understand this perturbation in B lymphopoiesis, we have devised a sensitive limiting dilution polymerase chain reaction assay that quantitates specific Ig rearrangements and thus quantitates B lineage cells at various stages of differentiation within unfractionated bone marrow. We find that there are significantly reduced frequencies of both VH-to-DJH and VK-to-JK rearrangements in the transgenic strain, whereas the frequency of D-to-JH rearrangements approximates that of wild type. Since Ig gene rearrangements occur in a stepwise fashion in which D-to-JH joining precedes that of VH-to-DJH and VK-to-JK, these results indicate that the major block of B lymphocyte development in the B-less strain occurs after D-to-JH rearrangement. Interestingly, sequence analysis of residual VHDJH junctions from transgenic pre-B lymphocytes reveals that an abnormally high proportion of these are out of frame and therefore nonproductive. Taken together, these data suggest that early expression of the transgenic lambda protein specifically prevents the development of a normal-sized population of precursor B lymphocytes coexpressing functional IgH. The transgene-induced immunodeficiency appears to arise by a precocious maturation process in which precursors bypass a developmental stage associated with cellular expansion.
LECTURES ON INTRACRANIAL SURGERY.IV—ABSCESS OF THE BRAIN.
Authors: EMORY LANPHEAR
Journal: JAMA (1895)

Suppuration in the brain does not differ from abscess in other parts of the body, except in the symptoms which arise from the peculiar location of the pus. Formerly, abscess of the brain and cerebral softening were regarded as synonymous terms; but now we know that softening is the result of the death of brain tissue from interference with the blood supply—a purely passive process, the creamy mass possessing none of the characteristics of pus excepting the resemblance in consistency and color; on the other hand, abscess is the result of an active process, inflammation, and in the broken-down tissues are found the distinctive microörganisms of true pus, and the same rule for the treatment holds good as in abscess elsewhere; let the pus out as soon as its location can be determined. <h3>MORTALITY.</h3> Abscess of the brain, from a surgical standpoint, is more favorable than almost any other form
Reversal of narcotic depression in the neonate by nalozone.
Authors: J M Evans, M I Hogg, M Rosen
Journal: BMJ (1976)

Naloxone 40 mug was administered intravenously one minute after birth to 20 out of 44 neonates whose mother had been given pethidine in labour. These neonates were compared with 20 others whose mothers had had only lumbar epidural block. Alveolar PCO2, alveolar ventilation, and ventilatory rate were measured 10 and 30 minutes after birth. The untreated neonates of mothers who had had pethidine showed significant ventilatory depression compared with infants in the epidural and naloxone-treated groups. The naloxone-treated neonates were comparable with the epidural group, although the effects of naloxone were diminishing at 30 minutes. Naloxone is an effective narcotic antagonist which should be considered to be the drug of choice for treating narcotic depression in the neonate.
The intersection of genetic and chemical genomic screens identifies GSK-3α as a target in human acute myeloid leukemia
Authors: Versha Banerji, Stacey M. Frumm, Kenneth N. Ross, Loretta S. Li, Anna C. Schinzel, Cynthia K. Hahn, Rose M. Kakoza, Kwan T. Chow, Linda Ross, Gabriela Alexe, Nicola Tolliday, Haig Inguilizian, Ilene Galinsky, Richard M. Stone, Daniel J. DeAngelo, Giovanni Roti, Jon C. Aster, William C. Hahn, Andrew L. Kung, Kimberly Stegmaier
Journal: Journal of Clinical Investigation (2012)

Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long-term survival of patients with AML has changed little over the past decade, necessitating the identification and validation of new AML targets. Integration of genomic approaches with small-molecule and genetically based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. Here, we identified a role for glycogen synthase kinase 3α (GSK-3α) in AML by performing 2 independent small-molecule library screens and an shRNA screen for perturbations that induced a differentiation expression signature in AML cells. GSK-3 is a serine-threonine kinase involved in diverse cellular processes, including differentiation, signal transduction, cell cycle regulation, and proliferation. We demonstrated that specific loss of GSK-3α induced differentiation in AML by multiple measurements, including induction of gene expression signatures, morphological changes, and cell surface markers consistent with myeloid maturation. GSK-3α-specific suppression also led to impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in methylcellulose, and anti-AML activity in vivo. Although the role of GSK-3β has been well studied in cancer development, these studies support a role for GSK-3α in AML.
Suspected Monkeypox Outbreak
Authors: Rebecca Voelker
Journal: JAMA (1998)

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
Five futures for academic medicine: the ICRAM scenarios
Authors: Jocalyn Clark
Journal: BMJ (2005)

Various G<sub>q</sub> protein-coupled receptor agonists such as the α<sub>1</sub> adrenoceptor agonist phenylephrine, angiotensin II, and endothe-lin-1 are potent hypertrophic factors. There is evidence of potential cross talk between these agents, particularly in terms of endothelin-1 as playing a central role in mediating the actions of other hypertrophic factors. Using cultured rat neonatal ventricular myocytes, we assessed the potential cross talk between these factors and sought to examine the potential underlying mechanisms. Twenty-four-hour exposure to either agent produced significant hypertrophy as determined by cell size and molecular markers. Although the hypertrophic effects of phenylephrine and angiotensin II were expectedly prevented by α<sub>1</sub> and AT<sub>1</sub> receptor antagonists, respectively, these effects were also blocked by the ET<sub>A</sub> receptor antagonist BQ123 [cyclo(d-Asp-Pro-d-Val-Leu-d-Trp)] but not by the ET<sub>B</sub> antagonist BQ788 (<i>N</i>-<i>cis</i>-2,6-dimethylpiperidinocarbonyl-l-γ-methylleucyl-d-1-methoxycarbonyltryptophanyl-d-norleucine). Both phenylephrine and angiotensin II significantly increased protein expression of both endothelin receptor subtypes. Both phenylephrine and angiotensin II produced significant activation of p38 as well as extracellular signal-regulated protein kinase and c-Jun NH<sub>2</sub>-terminal kinase, although this was unaffected by endothelin receptor blockade. Further studies revealed that the effects of phenylephrine and angiotensin II were mediated by stimulated endothelin-1 production occurring via two separate mechanisms: angiotensin II by increasing the levels of the endothelin-1 precursor prepro endothelin-1 and phenylephrine by upregulating endothelin-converting enzyme 1. Our results indicate that the endothelin-1 system plays an obligatory role in the hypertrophic response to both phenylephrine and angiotensin II in cultured myocytes through a mechanism independent of mitogenactivated protein kinase activation.
Aspirin Induced Suppression of Paget's Disease of Bone.
Authors: P. H. Henneman
Journal: Annals of Internal Medicine (1963)

s1 April 1963Aspirin Induced Suppression of Paget's Disease of Bone.P. H. Henneman, M.D., P. F. Maurice, M.D., L. V. Avioli, M.D., T. A. Dull, M.D., C. H. Bastomsky, M.D., T. N. Lynch, M.D.P. H. Henneman, M.D.Search for more papers by this author, P. F. Maurice, M.D.Search for more papers by this author, L. V. Avioli, M.D.Search for more papers by this author, T. A. Dull, M.D.Search for more papers by this author, C. H. Bastomsky, M.D.Search for more papers by this author, T. N. Lynch, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-58-4-720_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptA has been administered to tolerance for 3 to 27 days during complete balance studies on 6 patients with Paget's disease of bone. Within 3 days, there has occurred a decrease in serum, urinary, and fecal calcium with resultant calcium retention. Phosphorus retention resulted from a decrease in fecal excretion despite a slight increase in urinary phosphorus. Although fasting levels of serum magnesium were unchanged, urinary and fecal magnesium decreased with resultant magnesium retention. Calcium47kinetic analyses in 4 patients revealed increased exchangeable calcium pools, endogenous fecal calcium, and bone resorption and formation rates. Following administration of aspirin, there was... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: P. H. Henneman, M.D.; P. F. Maurice, M.D.; L. V. Avioli, M.D.; T. A. Dull, M.D.; C. H. Bastomsky, M.D.; T. N. Lynch, M.D.Affiliations: Jersey City, N. J. (CI) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1963Volume 58, Issue 4 Page: 720-721 Keywords Aspirin Bone Bone resorption Calcium Excretion Magnesium Phosphorus ePublished: 1 December 2008 Issue Published: 1 April 1963 PDF downloadLoading ...
Research funders agree to increase free access to published research
Authors: I. Torjesen
Journal: BMJ (2011)

<h3>ABSTRACT</h3> The Translocon Associated Protein (TRAP) complex resides in the endoplasmic reticulum (ER) membrane and interacts with the Sec translocon and the translating ribosome to facilitate biogenesis of secretory and membrane proteins<sup>1–4</sup>. TRAP is essential for the secretion of many hormones, and its key role in the production of the hormone peptide insulin has been particularly well established<sup>5,6</sup>. The mechanism by which TRAP engages ribosomes and the translocon to facilitate translocation of protein clients in the secretory pathway is not clear. Here, we reveal the molecular architecture of the mammalian TRAP complex and how it engages the translating ribosome associated with Sec61 translocon on the ER membrane. The TRAP complex is anchored to the ribosome via a long tether and its position relative to the ribosome and the translocon is further stabilized by a finger-like loop. This spatial arrangement positions a cradle-like lumenal domain of TRAP below the protein conducting pore of the translocon for interactions with translocated nascent chains. The biological importance of these key interactions is evident by structure-guided TRAP mutations in <i>C. elegans</i> that lead to growth deficits associated with increased ER stress and defects in insulin secretion. Our findings elucidate the molecular basis of the TRAP complex in the biogenesis and translocation of proteins at the ER.
The Pressure to Withhold or Withdraw Life-sustaining Therapy from Critically Ill Patients in the United States
Authors: John M. Luce, Douglas B. White
Journal: American Journal of Respiratory and Critical Care Medicine (2007)

Section:ChooseTop of pageAbstract <<PROGNOSTIC FACTORSPROFESSIONAL FACTORSSOCIAL FACTORSECONOMIC FACTORSWHEN IS THE PRESSURE APPR...RESOLVING CONFLICTSCONCLUSIONSReferencesCITING ARTICLES
Doctors decry Darfur “genocide”
Authors: Peter Moszynski
Journal: BMJ (2006)

A new report from Physicians for Human Rights has presented detailed evidence of the overwhelming scale of death and suffering in Darfur and contends that “the intense destruction of land holdings, communities, families, as well as the disruption of all means of sustaining livelihoods and procuring basic necessities” amounts to genocide.

This month marks Sudan's 50th anniversary of independence, as well as the first anniversary of the peace deal that officially ended 22 years of civil war. Hence the country was seen as an ideal and symbolic venue for the summit of leaders of the …
1192 HIGH SUSTAINED VIROLOGICAL RESPONSE RATES WITH RESPONSE-GUIDED DANOPREVIR PLUS PEGINTERFERON ALFA-2A (40KD) AND RIBAVIRIN IN TREATMENT-NAIVE, HCV GENOTYPE 1 PATIENTS: ATLAS STUDY FINAL RESULTS
Authors: P. Marcellin, C. Cooper, L.A. Balart, D.G. Larrey, T.D. Box, E. Yoshida, E. Lawitz, P. Buggisch, P. Ferenci, M. Weltman, E. Labriola-Tompkins, S. Le Pogam, I. Nájera, D.N. Thomas, G. Hooper, N. Shulman, Y. Zhang, M.T. Navarro, C.Y. Lim, M. Brunda, E.S. Yetzer, N. Terrault
Journal: Journal of Hepatology (2012)
A Case of Chicken-Pox Pneumonia with X-Ray Findings Suggesting Metastatic Carcinoma
Authors: Herbert G. Levin
Journal: New England Journal of Medicine (1957)

VARICELLA is ordinarily considered to be a benign, self-limited disease of children. That it also occurs in adults is well known. Less well appreciated, however, is the fact that, in adults in particular, the disease may be complicated by pneumonia. Tan, Kaufman and Levene,1 in 1956, reported 16 cases of varicella pneumonia in adults. They noted that before their report only 15 similar cases had been recorded. This paper concerns still another case of pneumonia complicating varicella in an adult. Of added interest is the fact that the x-ray appearance of the lungs caused confusion at first with metastatic cancer. . . .
Liver transplantation for acute liver failure in Europe: Outcomes over 20years from the ELTR database
Authors: Giacomo Germani, Eleni Theocharidou, Renè Adam, Vincent Karam, Julia Wendon, John O’Grady, Patrizia Burra, Marco Senzolo, Darius Mirza, Denis Castaing, Jurgen Klempnauer, Stephen Pollard, Andreas Paul, Jacques Belghiti, Emmanuel Tsochatzis, Andrew K. Burroughs
Journal: Journal of Hepatology (2012)
DC isoketal-modified proteins activate T cells and promote hypertension
Authors: Annet Kirabo, Vanessa Fontana, Ana P.C. de Faria, Roxana Loperena, Cristi L. Galindo, Jing Wu, Alfiya T. Bikineyeva, Sergey Dikalov, Liang Xiao, Wei Chen, Mohamed A. Saleh, Daniel W. Trott, Hana A. Itani, Antony Vinh, Venkataraman Amarnath, Kalyani Amarnath, Tomasz J. Guzik, Kenneth E. Bernstein, Xiao Z. Shen, Yu Shyr, Sheau-chiann Chen, Raymond L. Mernaugh, Cheryl L. Laffer, Fernando Elijovich, Sean S. Davies, Heitor Moreno, Meena S. Madhur, Jackson Roberts, David G. Harrison
Journal: Journal of Clinical Investigation (2014)

Oxidative damage and inflammation are both implicated in the genesis of hypertension; however, the mechanisms by which these stimuli promote hypertension are not fully understood. Here, we have described a pathway in which hypertensive stimuli promote dendritic cell (DC) activation of T cells, ultimately leading to hypertension. Using multiple murine models of hypertension, we determined that proteins oxidatively modified by highly reactive γ-ketoaldehydes (isoketals) are formed in hypertension and accumulate in DCs. Isoketal accumulation was associated with DC production of IL-6, IL-1β, and IL-23 and an increase in costimulatory proteins CD80 and CD86. These activated DCs promoted T cell, particularly CD8+ T cell, proliferation; production of IFN-γ and IL-17A; and hypertension. Moreover, isoketal scavengers prevented these hypertension-associated events. Plasma F2-isoprostanes, which are formed in concert with isoketals, were found to be elevated in humans with treated hypertension and were markedly elevated in patients with resistant hypertension. Isoketal-modified proteins were also markedly elevated in circulating monocytes and DCs from humans with hypertension. Our data reveal that hypertension activates DCs, in large part by promoting the formation of isoketals, and suggest that reducing isoketals has potential as a treatment strategy for this disease.
Uptake of radioiodinated cardiac specific troponin-I antibodies in myocardial infarction
Authors: B. Cummins, G. J Russell, S. T Chandler, D. J Pears, P. Cummins
Journal: Cardiovascular Research (1990)

Journal Article Uptake of radioiodinated cardiac specific troponin-I antibodies in myocardial infarction Get access Bernadette Cummins, Bernadette Cummins Search for other works by this author on: Oxford Academic PubMed Google Scholar Geoffrey J Russell, Geoffrey J Russell Search for other works by this author on: Oxford Academic PubMed Google Scholar Stephen T Chandler, Stephen T Chandler Search for other works by this author on: Oxford Academic PubMed Google Scholar David J Pears, David J Pears Search for other works by this author on: Oxford Academic PubMed Google Scholar Peter Cummins Peter Cummins Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 24, Issue 4, April 1990, Pages 317–327, https://doi.org/10.1093/cvr/24.4.317 Published: 01 April 1990 Article history Received: 06 September 1989 Accepted: 22 November 1989 Published: 01 April 1990
IK1 blockade is unlikely to be a useful antiarrhythmic mechanism
Authors: T. Opthof
Journal: Cardiovascular Research (1994)

Journal Article IK1 blockade is unlikely to be a useful antiarrhythmic mechanism Get access Tobias Opthof Tobias Opthof Laboratorium Experimentele Cardiologie, Academisch Medisch Centrum, Universiteit van Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands: T Opthof. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 28, Issue 3, March 1994, Page 420, https://doi.org/10.1093/cvr/28.3.420 Published: 01 March 1994
Doctors and execution in Turkey
Authors: P Mansour
Journal: BMJ (1994)

EDITOR, - As Tessa Richards points out, the considerable problems besetting the World Medical Association should not mislead us into underestimating the importance of its ethical declarations.1 One of its more important resolutions was that passed in 1981 prohibiting the active participation of physicians in capital punishment other than to certify death. This resolution was in effect adopted in 1992 as one of the recommendations of the BMA's working party on the participation of doctors in abuses of …
Splenic TFH expansion participates in B-cell differentiation and antiplatelet-antibody production during immune thrombocytopenia
Authors: Sylvain Audia, Marzia Rossato, Kim Santegoets, Sanne Spijkers, Catharina Wichers, Cornelis Bekker, Andries Bloem, Louis Boon, Thijs Flinsenberg, Ewoud Compeer, Theo van den Broek, Olivier Facy, Pablo Ortega-Deballon, Sabine Berthier, Vanessa Leguy-Seguin, Laurent Martin, Marion Ciudad, Maxime Samson, Malika Trad, Bernard Lorcerie, Nona Janikashvili, Philippe Saas, Bernard Bonnotte, Timothy R. D. J. Radstake
Journal: Blood (2014)
A Staphylococcus aureus Regulatory System that Responds to Host Heme and Modulates Virulence
Authors: Victor J. Torres, Devin L. Stauff, Gleb Pishchany, Jelena S. Bezbradica, Laura E. Gordy, Juan Iturregui, Kelsi L. Anderson, Paul M. Dunman, Sebastian Joyce, Eric P. Skaar
Journal: Cell Host & Microbe (2007)
How reliable is determination of ulcer size by endoscopy?
Authors: A Sonnenberg, M Giger, L Kern, C Noll, K Study, K B Weber, A L Blum
Journal: BMJ (1979)

The suface areas of 23 artificial ulcers in a rubber manikin and of 35 ulcers in 35 consecutive patients admitted for endoscopy of the upper gastrointestinal tract were estimated by six endoscopists. Of the 138 estimations made in the manikin 80% underestimated the true size of the ulcer: the mean (+/- SD) was -29 +/- 40%. The largest and the smallest estimate of the same ulcer by different endoscopists varied on average by a factor of 4.5 +/- 3.8, and the estimates by the same endoscopists of ulcers with the same size varied by a factor of 2.3 +/- 0.6. In the patients the scatter of the estimates was even larger, the mean factor being 7.8 +/- 6.3. Changes in ulcer size are therefore an unsuitable criterion for assessing ulcer healing. Even if consecutive examinations are performed by the same endoscopist, changes in ulcer area smaller than by a factor of 3 are not discernible.