tbuckley/cabot-search huggingface dataset:
Family of patient who died during a clinical trial receive a six figure settlement
Authors: C. Dyer
Journal: BMJ (2012)

The family of a patient who died during a clinical trial at the Royal Marsden Hospital in London to test a five drug combination for treating testicular cancer has won a six figure sum in an out-of-court settlement.

Gareth Kingdon, 39, was the first patient to die from side effects during the multicentre TE23 trial, which was funded by the Medical Research Council to compare treatment of poor prognosis testicular cancer by five drugs instead of the standard three drug regime.

The family of another patient in the trial, 27-year-old Gary Foster, who was treated at University College London Hospital …
922-55 Transesophageal Echocardiography in Assessing Pulmonary Venous Anastomosis and Flow After Single Lung Transplantation
Authors: Sheri Y. Nottestad, Teresa A. Cronin, John H. Calhoon, J. Kent Trinkle, Edward Sako, Miguel Zabalgoitia
Journal: Journal of the American College of Cardiology (1995)
“No Code” Orders: Clarification in the Aftermath of <i>Saikewicz</i>
Authors: Ronald B. Schram, John C. Kane, Daniel T. Roble
Journal: New England Journal of Medicine (1978)

ON June 30, 1978, the Massachusetts Appeals Court decided, in a case entitled "In the Matter of Shirley Dinnerstein,"1 that the earlier Saikewicz2,3 decision by the Massachusetts Supreme Judicial Court does not require prior judicial review and approval of a "no code" order directing that resuscitative measures be withheld from an irreversibly, terminally ill incompetent patient in the event of cardiac or respiratory failure. Although the Supreme Judicial Court had said in Saikewicz that judicial resolution of questions of life and death do not constitute, in its view, an "encroachment on the domain of medical expertise," the Dinnerstein Court said . . .
Measles immunisation rates and the good practice allowance.
Authors: D Mant, A Phillips, M Knightley
Journal: BMJ (1986)

The recent discussion document on primary health care proposes that a good practice allowance is paid to general practitioners based in part on the uptake of immunisation by patients. The variation between and the validity of practice immunisation rates for measles as determined by one district health authority's child health computer are assessed. In areas of low population mobility district health authority rates may be sufficiently accurate to base a good practice allowance on but should not be used until the social environment of each practice can also be characterised. In areas of high mobility intermittent surveys may be a preferable method of auditing performance.
Hormone-induced bile flow and hepatobiliary calcium fluxes are attenuated in the perfused liver of rats made cholestatic with ethynylestradiol in vivo and with phalloidin in vitro
Authors: Yuhki Hamada, Ari Karjalainen, Fyfe L. Bygravec
Journal: Hepatology (1995)

The actions of vasopressin and glucagon, administered alone or together, were assessed on bile flow in perfused livers from rats made cholestatic by the injection of ethynylestradiol and from those allowed to recover from such treatment. Concomitant measurements were made of biliary calcium output as well as changes in the perfusate Ca2+ concentration, glucose output, and oxygen uptake. Experiments were also conducted where cholestasis was induced in vitro in the perfused liver by the infusion of phalloidin. In each case cholestasis was demonstrated to have occurred by a reduction in bile flow by approximately 50%. The data show that the transient increase in bile flow and bile calcium seen in control rat liver soon after the administration of vasopressin, particularly when coadministered with glucagon, is largely absent in cholestasis induced by ethynylestradiol and attenuated in cholestasis induced by phalloidin. At the same time the pattern of perfusate Ca2+ fluxes in ethynylestradiol-induced cholestasis shifts to one reflecting net efflux of the ion from the liver. The responses to glucagon administration alone contrast with those of vasopressin in that in the perfused liver of ethynylestradiol-treated rats, glucagon induces a pronounced and sustained increase in bile flow. In cholestasis induced by both ethynylestradiol and phalloidin, glucagon fails to induce an initial transient decrease in bile flow. The effects of glucagon, including enhancement of vasopressin-stimulated bile flow in control and in ethynylestradiol-treated rats, can be mimicked by dibutyryl cyclic adenosine monophosphate (cAMP). Changes in glucose output and oxygen uptake induced by both hormones are only slightly attenuated. The data show that the modulation of bile flow that occurs rapidly after the administration of vasopressin and glucagon to control perfused rat liver is altered in conditions of cholestasis induced by either ethynylestradiol or phalloidin.
Abstract 4016: Epigenetic regulation of CXCR3 splicing in prostate cancer cells
Authors: Devi Sharanya Sampath Kumar, Alan Wells
Journal: Cancer Research (2012)

Abstract Prostate cancer is the second leading cause of cancer death among men, with the metastasis of these tumors being the main reason for the high rates of mortality and morbidity. This tumor progression requires epithelial cell dedifferentiation, migration, invasion and growth in an ectopic site. CXCR3 is a G-protein coupled receptor whose splicing was found to be differentially regulated in prostate cancer. We have found over-expression of the CXCR3A splice isoform in prostate cancers and cell lines whereas normal prostate epithelium expresses by and large only the CXCR3B isoform, representing a possible switch in the expression between the CXCR3 splice variants. As these variants link differentially to pro- and anti-invasion signaling pathways, this may explain the relentless progression of the prostate carcinoma cells. The switch is present at both the RNA and the protein level which suggests that the altering factor is at the trancriptional control level. We hypothesized that a mutation in the gene or an epigenetic modification of the genome could possibly be regulating the splicing event and hence the switch in the expression. CXCR3 when scanned for mutations was found to be intact except for a polymorphism in the intronic region which coincided with the normal prostate cells. On the epigenetic regulation side, the CpG dinucleotides in the regulatory regions, the one intron and 5′ upstream region, susceptible to methylation changes were analysed for methylation differences. The upstream sequence does not show a differential methylation pattern whereas the intronic region shows differential methylation between the cancer and normal prostate cells at 3 different nucleotides. A possible explanation is that the methylation in the introns alters the speed of the transcription machinery allowing more time for a particular splice variant to be transcribed more than the other. A bichromatic reporter minigene has been designed for each of the differentially methylated CpG nucleotides, to study its effects on the splicing regulation of the CXCR3 gene. Further studies include expressing the minigene and documenting the splicing differences. 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 4016. doi:1538-7445.AM2012-4016
Activation of caspase-8 in drug-induced apoptosis of B-lymphoid cells is independent of CD95/Fas receptor-ligand interaction and occurs downstream of caspase-3
Authors: Thomas Wieder, Frank Essmann, Aram Prokop, Karin Schmelz, Klaus Schulze-Osthoff, Rudi Beyaert, Bernd Dörken, Peter T. Daniel
Journal: Blood (2001)
"In consequence of enemy action": British medical students in North American medical schools, 1939-45
Authors: S. T. Casper
Journal: BMJ (2010)

Between 1940 and 1945, the Rockefeller Foundation offered fellowships for British medical students to complete their medical training in North America.1 2 3 4 These fellowships arose from the damage caused by the extensive aerial bombardment of medical facilities across Britain and shortages of qualified teachers to train students. To the American committee at the Rockefeller Foundation that provided their fellowships, these medical students became another thread in the enlarging fabric of the “special relationship.” To the British committee charged with selecting them, these students represented a last line of defence, a contingent of students able to fight on should Britain be occupied.5 6



Between two worlds (Jack Vettriano’s On the Border , 1995)

www.jackvettriano.com

Documents from both sides of the Atlantic record the programme that emerged, although the story is chiefly captured by papers held in the Rockefeller Archives (but for a pithy discussion, see Hill7). An early memorandum by Robert Lambert (Rockefeller Foundation) and John Fulton (a Yale physiologist) from September 1940 offers a sense of the origins of the programme: “Fulton has in mind a limited group—not more than a hundred. Thinks US and Canadian medical schools would give free tuition. Yale might take 5, Harvard 10, Columbia 10, etc.”8 

The Rockefeller Foundation subsequently allocated $5000 per student,9 while articles in medical journals justified the programme as a consequence of enemy action and the beginning of a new era of cooperation between British and American medical schools.10 In a letter to the BMJ Henry Dale observed that the interchange of medical personnel was the continuation of international collaborations begun by Anglo-American physiologists.11 By March 1941, a letter between the Rockefeller’s Alan Gregg and Edward Mellanby (secretary of the MRC) reveals that the programme was operational and hailed enthusiastically as a “practicable …
APPENDICITIS WITHOUT PROTECTIVE STIFFENING OF THE ABDOMINAL WALL
Authors: J. D. Malcolm
Journal: BMJ (1920)

ARTIFICIAL PNEUMOTHORAX.intensity, although there was no further rise in temperature.His mind did not become normal again for two days.He made a rapid convalescence, but could not read for any length of time or studv for some months.The focal reaction after the last dose makes it, to my mind, certain that the influenza bacillus was infecting his brain. CASE II.An elderly gentleman when first seen by me had been ill for a week with lethargy and bronchopneumonia.Micrococcuis flavus, streptococci, and influenza bacilli were isolated from his sputum.He was exceedingly ill.The temperature was 1020, the pulse 90 to 100.He was given at once a mixed antigen con- taining the above microbes pending the making of an auto-
Chlordiazepoxide Interaction with Levodopa
Authors: SHIMONA YOSSELSON-SUPERSTINE
Journal: Annals of Internal Medicine (1982)

Letters and Corrections1 February 1982Chlordiazepoxide Interaction with LevodopaSHIMONA YOSSELSON-SUPERSTINE, PHARM.D., ARTHUR G. LIPMAN, PHARM.D.SHIMONA YOSSELSON-SUPERSTINE, PHARM.D.Search for more papers by this author, ARTHUR G. LIPMAN, PHARM.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-96-2-259 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: A possible interaction between benzodiazepine and levodopa has been suggested (1-4) but documentation with challenge and rechallenge has not appeared. We recently observed a profound effect of chlordiazepoxide on the control of parkinsonism; the effect resolved after discontinuation of the benzodiazepine.A 66-year-old woman who had parkinsonism for 15 years had been treated sucessfully with levodopa, 500 mg six times daily; benztropine mesylate (Cogentin, Merck Sharp & Dohme, West Point, Pennsylvania), 1 mg/d; and diphenhydramine HC1 (Benadryl, Parke-Davis; Morris Plains, New Jersey), 25 mg/d. Recently this patient was diagnosed as having metastatic lung carcinoma, but no chemotherapy...References1. SCHWARZFAHN GS. Newer medical treatments in parkinsonism. Med Clin N Amer. 1970;54:773-85. CrossrefMedlineGoogle Scholar2. HUNTERSTERNLAURENCE KGD. Use of levodopa with other drugs. Lancet. 1970;2:1283-5. CrossrefMedlineGoogle Scholar3. MACKIE L. Drug antagonism. Br Med J. 1971;2:651. CrossrefMedlineGoogle Scholar4. WODAKGILLIGANVEALEDOWTY JBJB. Review of 12 months' treatment with levodopa in Parkinson's disease, with remarks on unusual side effects. Med J Aust. 1972;2:1277-82. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: The University of Utah Salt Lake City, UT 84112 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByResponse to 4-month treatment with reboxetine in Parkinson's disease patients with a major depressive episodeInfluence of benzodiazepines on antiparkinsonian drug treatment in levodopa usersParkinson’s DiseaseSubcortical dysrhythmia and catatoniaHypnotics and sedativesDrug Interactions & Reactions Update: Early Reports on Drug Interactions 1 February 1982Volume 96, Issue 2Page: 259-260KeywordsChemotherapyLevodopaLung and intrathoracic tumors Issue Published: 1 February 1982 PDF DownloadLoading ...
Spiegelmer Inhibition of CCL2/MCP-1 Ameliorates Lupus Nephritis in MRL-(Fas)lpr Mice
Authors: Onkar Kulkarni, Rahul D. Pawar, Werner Purschke, Dirk Eulberg, Norma Selve, Klaus Buchner, Volha Ninichuk, Stephan Segerer, Volker Vielhauer, Sven Klussmann, Hans-Joachim Anders
Journal: Journal of the American Society of Nephrology (2007)

The monocyte chemoattractant protein CCL2 is crucial for monocyte and T cell recruitment from the vascular to the extravascular compartment at sites of inflammation. CCL2 is expressed in human lupus nephritis and was shown to mediate experimental lupus; therefore, CCL2 antagonists may be beneficial for therapy. This study describes the l-enantiomeric RNA oligonucleotide mNOX-E36, a so-called Spiegelmer that binds murine CCL2 with high affinity and neutralizes its action in vitro and in vivo. The mirror image configuration of the Spiegelmer confers nuclease resistance and thus excellent biostability. mNOX-E36 does not induce type I IFN via Toll-like receptor-7 or cytosolic RNA receptors, as recently shown for certain synthetic D-RNA. Autoimmune-prone MRL(lpr/lpr) mice that were treated with a polyethylene glycol form of mNOX-E36 from weeks 14 to 24 of age showed prolonged survival associated with a robust improvement of lupus nephritis, peribronchial inflammation, and lupus-like inflammatory skin lesions. Thus, mNOX-E36-based inhibition of CCL2 represents a novel strategy for the treatment of autoimmune tissue injury, such as lupus nephritis.
Quantitative Decision Tools in Medical Education
Authors: Patrick C. Alguire
Journal: JAMA (2010)

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
Bone Metastasis From Thyroid Cancer Diagnosed by I-131 Whole-Body Scan Without Identifiable Lesion in the Thyroid
Authors: Jiantao Wang, Bin Liu, Zhen Zhao, Anren Kuang
Journal: Clinical Nuclear Medicine (2011)

A right chest wall mass was incidentally detected by chest x-ray during routine medical examination in a 38-year-old asymptomatic female patient. Biopsy showed that this mass was a metastatic lesion, while the origin of this malignancy was uncertain. Extensive examinations indicated that the malignancy is from the thyroid. Unexpectedly, pathology results from total thyroidectomy did not reveal any cancer cells. Nonetheless, an iodine-131 scan post-thyroidectomy showed intense activity in the right chest wall mass, and pathology from the second biopsy of the mass confirmed thyroid cancer.
WHO report calls for new approach to substance dependence
Authors: Fiona Fleck
Journal: BMJ (2004)

Scientists have recently gained vital new insights into drug, alcohol, and tobacco dependence, but this knowledge has not been translated effectively into public health policy, the World Health Organization said in a new report published on Thursday.

The report summarises new findings on how psychoactive substances mimic the effects of naturally occurring neurotransmitters and interfere with normal brain functioning by altering storage, release, and removal of these transmitters.

Substance dependence is determined by psychosocial, cultural, and environmental as well as biological and genetic factors and—although …
Media feed on human tragedy
Authors: S. Swafford
Journal: BMJ (1997)

Epidemics change societies. Just look at how Britain reacted to the scares about “mad cow disease” and E coli . Yet not all factions of society see these human tragedies in such grim light. In fact, for the media, epidemics can act like a spotlight, giving them the means to shine. This point was humorously brought home during the re-enactment of an epidemic at the London School of Hygiene and Tropical Medicine last month.

The presentation, meant to be light entertainment for doctors and health officials from around the world, was called Epidemic! Routine investigation or national scandal? It did not take a medical degree to figure out which was the case. The progress of an epidemic was explored through the eyes of a panel composed of a general practitioner, director of the Public Health Laboratory Service, a journalist …
Positive End-Expiratory Pressure after a Recruitment Maneuver Prevents Both Alveolar Collapse and Recruitment/Derecruitment
Authors: Jeffrey M. Halter, Jay M. Steinberg, Henry J. Schiller, Monica DaSilva, Louis A. Gatto, Steve Landas, Gary F. Nieman
Journal: American Journal of Respiratory and Critical Care Medicine (2003)

We tested the hypothesis that collapsed alveoli opened by a recruitment maneuver would be unstable or recollapse without adequate positive end-expiratory pressure (PEEP) after recruitment. Surfactant deactivation was induced in pigs by Tween instillation. An in vivo microscope was placed on a lung area with significant atelectasis and the following parameters measured: (1) the number of alveoli per field and (2) alveolar stability (i.e., the change in alveolar size from peak inspiration to end expiration). We previously demonstrated that unstable alveoli cause lung injury. A recruitment maneuver (peak pressure = 45 cm H2O, PEEP = 35 cm H2O for 1 minute) was applied and alveolar number and stability were measured. Pigs were then separated into two groups with standard ventilation plus (1) 5 PEEP or (2) 10 PEEP and alveolar number and stability were again measured. The recruitment maneuver opened a significant number of alveoli, which were stable during the recruitment maneuver. Although both 5 PEEP and 10 PEEP after recruitment demonstrated improved oxygenation, alveoli ventilated with 10 PEEP were stable, whereas alveoli ventilated with 5 PEEP showed significant instability. This suggests recruitment followed by inadequate PEEP permits unstable alveoli and may result in ventilator-induced lung injury despite improved oxygenation.
Detecting active pulmonary tuberculosis with a breath test using nanomaterial-based sensors
Authors: Morad K. Nakhleh, Raneen Jeries, A'laa Gharra, Anke Binder, Yoav Y. Broza, Mellissa Pascoe, Keertan Dheda, Hossam Haick
Journal: European Respiratory Journal (2014)

To the Editor: 

Detecting active tuberculosis (TB) remains a major global public health challenge [1]. The tuberculin skin test does not distinguish latent from active TB [2]. The interferon-γ release assays have similar limitations [3]. Acid-fast bacilli staining of sputum has a high false-negative rate (up to 50%) [4]. Nucleic acid amplification tests (NAATs), such as GeneXpert MTB/RIF (Cepheid, Sunnyvale, CA, USA), are accurate but require a good infrastructure and the necessity to obtain a good quality sputum sample, which is often unobtainable in more than a third of HIV-infected persons [5, 6].

Given these unmet needs, we explored the use of a novel, rapid, simple and inexpensive point-of-care test for the diagnosis of TB [7]. The approach is based on the detection of volatile organic compounds (VOCs) that are emitted from infected cells and released in exhaled breath [8, 9]. Using gas chromatography linked with mass spectrometry, researchers have previously reported identification of TB-related VOCs in the exhaled breath, though there has been low accuracy in detection (80–85%) [10]. In this study, we explore the possibility of active TB detection via the analysis of exhaled breath using a novel technology of organically modified nanomaterial-based sensors. Such cross-reactive sensors are highly sensitive to the collective changes in the VOCs spectrum [8].

Therefore, we designed a case–control study, in which breath and sputum sampling was performed in 210 adult participants, after informed consent, at three sites in Cape Town, South Africa, between November 2011 and March 2012. The study population consisted of two main subgroups. The first subgroup included those in …
Severe pulmonary pathology after intravenous administration of vectors in cirrhotic rats
Authors: Jeffrey S Smith, Jie Tian, Jay N Lozier, Andrew P Byrnes
Journal: Molecular Therapy (2004)

After an intravascular injection, adenoviral vectors are normally taken up by the reticuloendothelial system in the liver, where they rapidly trigger an innate response. However, we have previously found that the biodistribution of adenoviral vectors is altered in cirrhotic rats due to the presence of pulmonary intravascular macrophages, which cause a shift in vector uptake from the liver to the lungs. We now report that this is correlated with fatal pulmonary hemorrhagic edema in cirrhotic rats. In addition, cirrhotic rats reacted to vector with enormous increases in TNF-α and IL-6 and markedly prolonged coagulation times. Although we also saw fatal reactions to high doses of adenoviral vectors in normal rats, the time course and symptoms were very different, and pulmonary hemorrhagic edema was seen only in cirrhotic rats. Because abnormal pulmonary reticuloendothelial uptake is known to occur in humans during cirrhosis and other diseases, there is the potential that intravascular administration of adenoviral vectors might cause lung pathology in such patients.