tbuckley/cabot-search huggingface dataset:
TV: Super television
Authors: A. Berger
Journal: BMJ (2000)

Superhuman, BBC1, Sundays at 9 pm, 15 October to 19 November

Superlatives may make for a dull review, but I think it would be churlish in this case to hold back. I thoroughly enjoyed both of the episodes of Superhuman that I watched. The first was about traumatic injury to the body, and the second—called “The Enemy Within”—was about cancer. The other four episodes cover other aspects of the power of the human body to heal and regenerate.

In this era of high technology we are presented with both the extraordinary example of engineering that we humans have evolved into and recent scientific advances that tap into these natural resources. Both episodes I watched were beautifully crafted, very accessible from a scientific view, and elegantly presented. Professor Robert Winston is a natural master at explaining, with great clarity, highly complex issues without losing the viewer. The computer imaging used to illustrate his points is stunning.

The material presented tells a range of fascinating stories, but at no point does it feel as if too much is being thrown at us. Much of it is likely to be new to most people, even scientists, so this series is not simply about explaining basic science to non-scientists. In this regard, there really is something foreveryone. I knew something about the benefits of cooling the body, for example, but the programme's anecdotes from the Vietnam and Falklands wars—showing just what this might mean in terms of life and death—were brilliant in illustrating the theory. 

I particularly liked the way Superhuman presented exciting experimental approaches in cancer treatments and introduced us to people who are trying some of them out. It managed to convey the sad fact that sometimes these “human guinea pigs” lose their fight against their disease before they actually start treatment. In this particular programme I was left with just one question. If the bark of bush willow seems such a good candidate for attacking the blood vessels that feed a tumour, why doesn't it attack all the blood vessels in the body? This was a small omission in an otherwise flawless presentation.

Throughout the series the combination of science and optimism is tempered by human reality, and the point is well made that what seems to work in the laboratory does not always translate into the clinic.
Targeting acute myeloid leukemia by dual inhibition of PI3K signaling and Cdk9-mediated Mcl-1 transcription
Authors: Daniel Thomas, Jason A. Powell, Francois Vergez, David H. Segal, Nhu-Y. N. Nguyen, Adele Baker, Tse-Chieh Teh, Emma F. Barry, Jean-Emmanuel Sarry, Erwin M. Lee, Tracy L. Nero, Anissa M. Jabbour, Giovanna Pomilio, Benjamin D. Green, Stéphane Manenti, Stefan P. Glaser, Michael W. Parker, Angel F. Lopez, Paul G. Ekert, Richard B. Lock, David C. S. Huang, Susie K. Nilsson, Christian Récher, Andrew H. Wei, Mark A. Guthridge
Journal: Blood (2013)
President Bush sidesteps critics in stem cell debate
Authors: C. Marwick
Journal: BMJ (2001)

President George Bush took the unusual move of using a nationally televised address last week to announce that he would allow government supported research on existing embryonic cell lines only, not on any new lines that may be developed.

At the same time he announced that he would create a presidential advisory body to oversee the medical and ethical ramifications. It would not review research proposals.

His decision came two days after the US National Academy of Sciences meeting in Washington, where infertility specialists Panayiotis Zavos and Severino Antinori put their case for reproductive cloning to help childless couples to conceive.

The president's statement, however, was specifically about therapeutic cloning, …
Abstract 4406: Clinical efficacious combined chemo/immunotherapy differently activates AKT pathway and functionality of gp100 and Melan-A specific T cell clones
Authors: Belinda Palermo, Cosmo Di Donna, Ornella Franzese, Duilia Del Bello, Novella Gualtieri, Luisa Imberti, Carmen Nuzzo, Enrico Proietti, Caterina Catricalà, Virginia Ferraresi, Paola Nisticò
Journal: Cancer Research (2012)

Abstract A phase II randomized clinical study is ongoing in our Institution to prove the clinical efficacy of dacarbazine (DTIC) one day before peptide-vaccination (Melan-A and NY-ESO-1) in the prevention of melanoma relapse in clinically disease-free HLA-A2 patients. In a previous pilot study, this combination therapy (using Melan-A and gp100 peptides) increased the number of tumor-reactive long-lasting effector-memory CD8+ lymphocytes. To identify the mechanisms enhancing the immune response, induced by DTIC combined with peptide-vaccination, we analyzed the endogenous and treatment-induced antigen specific CD8 T-cell response at the clonal level. We analyzed the sequence of the TCR α-chain of these clones and the molecular results were correlated with the expression of CD27/CD28 co-stimulatory molecule, AKT activation and anti-tumor lytic activity. The combination of chemo/immunotherapy elicited in Melan-A-specific, but not in gp100 clones, a renewal of high-avidity/tumor-reactive T-cell clones, with a broadening TCR diversity in long-surviving patients, suggesting that the selection of immune-resistant tumor variants may be circumvented by this combination, and thus prevent tumor recurrence in melanoma. In gp100 clones, AKT activation (pSer473-AKT) canonically correlates with CD28 and/or CD27 expression, independent of the treatment while in Melan-A clones, lacking CD27 and CD28 expression, non-canonical AKT activation was only observed after the combination therapy. The identification of the extracellular stimuli and signaling pathway responsible for DTIC-mediated activation of the AKT signaling are currently under investigation. 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 4406. doi:1538-7445.AM2012-4406
984 PREDICTION MODELS FOR RISK OF HEPATOCELLULAR CARCINOMA USING SEROMARKERS OF HEPATITIS C VIRUS INFECTION
Authors: M.-H. Lee, H.-I. Yang, S.-N. Lu, C.-L. Jen, S.-L. You, L.Y. Wang, Y. Yuan, G. Litalian, C.-J. Chen
Journal: Journal of Hepatology (2011)
STRUCTURAL RELATIONSHIPS OF SULFAPYRIDINE AND SULFATHIAZOLE
Authors: Emanuel M. Abrahamson
Journal: JAMA (1941)

<h3>To the Editor:—</h3> An explanation for the efficacy of sulfapyridine and sulfathiazole which I have not seen in print is suggested by an examination of their structural formulas: Now, sulfapyridine differs from the parent sulfanilamide by having a pyridine nucleus attached to the amido group. This pyridine nucleus is present in the quinoline alkaloids, such as quinine, and also in the synthetic ethyl hydrocupreine hydrochloride. These are toxic to pneumococci, and the effectiveness of sulfapyridine may possibly be due in some measure to the added pyridine nucleus. If sulfur is substituted for an ethylene linkage in a cyclic compound, the properties are not changed much. Thus, thiopheneand benzenehave properties so close that it is very difficult to separate them. In the same fashion, thiazolediffers little from pyridinein chemical and physical properties. Thus, one would expect sulfathiazole to have about the same chemical properties, and therefore pharmacologic action,
Book: Medical Journalism: Exposing Fact, Fiction, Fraud
Authors: K. Loughlin
Journal: BMJ (2001)

Ragnar Levi Iowa State University Press, $34.95, pp 212 ISBN 0 8138 0303 9 See http://www.isupress.com/ for ordering details Rating: ![Graphic][1]</img>![Graphic][2]</img>![Graphic][3]</img> Answering queries posed by television researchers is part of what an academic historian does these days. This seems to be especially true when your area of interest is the history of medicine and the mass media. One recent programme idea—presented via email—struck me as particularly weak: a series of programmes looking at the way medical advice keeps changing. The researcher had lots of recent examples and wanted me to supply examples from the 1930s, 1940s, and 1950s. I asked what she thought the interest was in documenting such a change? As a historian and keen watcher of medicine on television I hoped to hear something about the way evidence has changed over time: the demand for evidence, what counts as evidence, the rise of randomised controlled trials and of statistical notions of relative … [1]: /embed/inline-graphic-1.gif [2]: /embed/inline-graphic-2.gif [3]: /embed/inline-graphic-3.gif
Ureterolithiasis and Creatine Kinase
Authors: Richard G. Kachel
Journal: Annals of Internal Medicine (1989)

Letters and Corrections15 June 1989Ureterolithiasis and Creatine KinaseRichard G. Kachel, MDRichard G. Kachel, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-110-12-1036_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo The Editor: I have been unable to find any reported association of acute elevation of creatine kinase with the passage of a renal stone. I wish to report the following case documenting this occurrence.A 73-year-old white man developed sudden, severe, left flank pain. He came to the emergency department and a urinalysis showed microhematuria. An intravenous pyelogram showed a calcified stone in the right renal calyx and a second calcified stone partially obstructing the left ureter. The patient was given analgesics and was discharged. Because of intermittent, severe pain in the left flank and vomiting, he returned and...References1. ParrLingemanJordanCoury KJMT. Creatinine kinase concentrations and electrocardiographic changes in extracorporeal shock wave lithotripsy. Urology. 1988;32:21-3. CrossrefMedlineGoogle Scholar2. HoagFranksSmithDeCoteau GCCW. Creatine kinase isoenzyme patterns in normal smooth muscle and smooth muscle neoplasms. Clin Biochem. 1980;13:149-50. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Richard G. Kachel, MD PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 June 1989Volume 110, Issue 12Page: 1036-1036KeywordsAnalgesicsCreatine kinaseEmergency departmentIntravenous pyelographyKidney stonesUreterVomiting ePublished: 1 December 2008 Issue Published: 15 June 1989 PDF downloadLoading ...
1136 ITPA SNPS GENOTYPES AFFECT ANEMIA DEVELOPMENT AT WEEK 4 BUT NOT ON WEEK 12 IN A HCV G1 NAIVE PATIENT'S PROSPECTIVE COHORT
Authors: C.E. Brandào-Mello, M. Patelli, F.J.G. Ruiz, P.R.A. Ferreira, A.F.M. de Souza, G.F. Silva, C.G. Figueiredo-Mendes, A.C. Lyra, M.H. Silva, T.Q. Reuter, R.D.C.M.A. da Silva, M.L.C.G. Ferraz, E.V. Martins Júnior, L.H. Melo, E.G. Marins
Journal: Journal of Hepatology (2012)
In vitro cell-mediated cytotoxicity in primary biliary cirrhosis and chronic hepatitis. Dysfunction of spontaneous cell-mediated cytotoxicity in primary biliary cirrhosis.
Authors: J M Vierling, D L Nelson, W Strober, D M Bundy, E A Jones
Journal: Journal of Clinical Investigation (1977)

The in vitro cytotoxic function and target cell specificity of peripheral blood lymphocytes from selected patients with primary biliary cirrhosis and hepatitis B surface antigen-negative chronic hepatitis were investigated using 51Cr-labeled human Chang and EL-4 mouse sarcoma cell targets in assays of spontaneous cell-mediated cytotoxicity (SCMC) and mitogen-induced cellular cytotoxicity (MICC). In addition, antibody-dependent cellular cytotoxicity (ADCC) against Chang cells was assessed. At an effector-to-target cell ration of 100:1, the mean SCMC against Chang cells was much less in patients with primary biliary cirrhosis than that in either the controls (P less than 0.001) or the patients with chronic hepatitis (P less than 0.005) whereas the value for patients with chronic hepatitis did not differ significantly from that of the controls. The mean SCMC against EL-4 mouse sarcoma cells was also less in patients with primary biliary cirrhosis than in controls (P less than 0.005) whereas the value for chronic hepatitis was not significantly different from that of the controls or patients with primary biliary cirrhosis. In contrast, MICC against both targets and ADCC against Chang cells were similar for each group. Comparison of SCMC and MICC against both target cells, measured simultaneously, showed similar cytotoxic potenital against both target cells for each group. Effector cells capable of mediating cytotoxicity in each assay were defined by testing the cytotoxic function of lymphocyte subpopulations isolated from two representative patients with each disease using techniques of immunoabsorbent affinity chromatography and Fc receptor binding to antigen-antibody complexes. In both primary biliary cirrhosis and chronic hepatitis SCMC and ADCC were mediated by a subpopulation of lymphocytes which lack surface immunoglobulin (sIg-) and bear Fc receptors (Fc+). In contrast, MICC was mediated by sIg- cells which lack Fc receptors. Lymphocytes bearing sIg- were not cytotoxic in any assay. These results establish a difference in cytotoxic function in primary biliary cirrhosis and chronic hepatitis by defining the presence of a defect in spontaneous cytotoxic function of sIg-, Fc+ lymphocytes against Chang cells in primary biliary cirrhosis.
Anti-inflammatory Therapy With Simvastatin Improves Neuroinflammation and CNS Function in a Mouse Model of Metachromatic Leukodystrophy
Authors: Axel Stein, Stijn Stroobants, Volkmar Gieselmann, Rudi D'Hooge, Ulrich Matzner
Journal: Molecular Therapy (2015)

Metachromatic leukodystrophy (MLD) is a lysosomal storage disease caused by a functional deficiency of the lysosomal enzyme arylsulfatase A. The prevailing late-infantile variant of MLD is characterized by widespread and progressive demyelination of the central nervous system (CNS) causing death during childhood. In order to gain insight into the pathomechanism of the disease and to identify novel therapeutic targets, we analyzed neuroinflammation in two mouse models reproducing a mild, nondemyelinating, and a more severe, demyelinating, variant of MLD, respectively. Microgliosis and upregulation of cytokine/chemokine levels were clearly more pronounced in the demyelinating model. The analysis of the temporal cytokine/chemokine profiles revealed that the onset of demyelination is preceded by a sustained elevation of the macrophage inflammatory protein (MIP)-1α followed by an upregulation of MIP-1β, monocyte chemotactic protein (MCP)-1, and several interleukins. The tumor necrosis factor (TNF)-α remains unchanged. Treatment of the demyelinating mouse model with the nonsteroidal anti-inflammatory drug simvastatin reduced neuroinflammation, improved the swimming performance and ataxic gait, and retarded demyelination of the spinal cord. Our data suggest that neuroinflammation is causative for demyelination in MLD mice and that anti-inflammatory treatment might be a novel therapeutic option to improve the CNS function of MLD patients.
The silver lining
Authors: W. A M Cutting
Journal: BMJ (2001)

In August 1998 we celebrated our ruby wedding and took all our family—four children, four spouses, and nine grandchildren—for a holiday in Perthshire. Our happy celebration came to a tragic halt when our son in law, Richard, was knocked off his cycle by an 18 year old driver. Before we could reach him he had been airlifted to the neurosurgical unit at the Southern General Hospital in Glasgow. The senior registrar told us that Richard's intracranial pressure was incompatible with life. The scans showed that cerebral oedema had flattened the ventricles and the blood vessels.

Our daughter Catriona's fortitude and faith were amazing. Within minutes of hearing the sad news she was clear that she wanted Richard's organs donated for transplantation. The transplant coordinator worked hard, but …
Prevention of coronary heart disease
Authors: William C D'Avanzo
Journal: BMJ (2004)

Editor—Marshall seemed not to include the cost to the health system of treatment after a myocardial infarction occurs.1 You could go further and estimate the cost to society of prematurely losing productive members.

Say, for example, one myocardial infarction was prevented with treatment A and two with treatment B in a group of 100. If A costs $1 a year and B, $10, then A would be five times as cost effective as B per event prevented. However, if the cost of treatment after an event occurs is high, B could be more cost effective. If they operate independently A and B together could be the best treatment.

Marshall might have discussed what dosages of statins were used. In the United States the cost is fairly constant with dose, but the effectiveness for a given patient could change and so would the cost effectiveness.

Marshall assumed a patient (pretreatment) had a 10% risk of a coronary event over five years—which seems low for a patient seeing a cardiologist—and then applied a relative risk based on other studies. On the basis of a meta-analysis of other studies, out of 100 people who would have had a coronary event, 69 would have been taking a statin, 72 aspirin, and 50 both.

A 10% risk of a coronary event biases the results towards the lower cost treatment. If you picked a group with an extremely low chance of a coronary event over five years the cheaper treatment would be quite cost effective. Furthermore, were the aspirin and statin groups similar and were they at 10% coronary risk?

To treat patients at lower risk slightly more aggressively is appropriate. Some, however, might conclude from this study that this might have been done at the expense of those at higher risk or by choosing either statins or aspirin but not both.
Acute heart failure patient profiles, management and in‐hospital outcome: results of the Italian Registry on Heart Failure Outcome
Authors: Fabrizio Oliva, Andrea Mortara, Giuseppe Cacciatore, Alessandra Chinaglia, Andrea Di Lenarda, Marco Gorini, Marco Metra, Michele Senni, Aldo P. Maggioni, Luigi Tavazzi
Journal: European Journal of Heart Failure (2012)
Researchers Warm Up to Hypothermia Use After Cardiac and Brain Trauma
Authors: Tracy Hampton
Journal: JAMA (2007)

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
Genetic Defects in Primary Hyperparathyroidism
Authors: Stephen J. Marx
Journal: New England Journal of Medicine (1988)

Primary hyperparathyroidism is a common disorder, and its causes are uncertain. Most patients have overactivity of a single gland, in the form of an adenoma. It has been suggested that parathyroid adenoma may be an expression of parathyroid hyperplasia, because the nonadenomatous glands show subtle features of hyperplasia.1 A previous study supported the theory that parathyroid adenomas are hyperplastic in nature by suggesting that adenomas were not composed of a clone of cells.2 Arnold et al. have reexamined the matter in this issue of the Journal and have concluded that parathyroid adenomas are often, if not always, clonal.3 They used . . .
Early Bronchodilatory Effects of Budesonide/Formoterol Pressurized Metered-Dose Inhaler (pMDI) Compared With Fluticasone Propionate/Salmeterol Dry Powder Inhaler (DPI) and Albuterol pMDI in Adults With Asthma
Authors: F HAMPELJR, P MARTIN, W MEZZANOTTE
Journal: Journal of Allergy and Clinical Immunology (2008)
How Do Phagocytes Eat?
Authors: THOMAS P. STOSSEL
Journal: Annals of Internal Medicine (1978)

Phagocytosis is a cellular function relevant for host defense against infection, tissue turnover, and other aspects of human physiology. Phagocytosis is also representative of functions wherein external stimuli activate motile events in the cell. Recognition of suitable objects by the plasma membrane of the phagocyte initiates phagocytosis. Knowledge of serum proteins that coat objects rendering them recognizable is considerable, but understanding of the chemical basis of recognition is meager. The signals activated by recognition are also not known. The work of phagocytosis that causes pseudopodia to enclose objects in vacuoles is ascribable to metabolic energy-dependent interactions between actin filaments and other contractile proteins in the peripheral cytoplasm. These interactions may also regulate the fusion of lysosomes with phagocytic vacuoles, an event important for the processing of ingested objects after phagocytosis.
Transcription factors and atrial fibrillation
Authors: S. Mahida
Journal: Cardiovascular Research (2013)

Atrial fibrillation (AF) is a prevalent cardiac arrhythmia with a significant genetic component. In recent years, familial and population-based genetic studies in AF have led to the emergence of transcription factors as potentially important contributors to arrhythmia susceptibility. Further evidence to implicate transcription factors in AF has come from studies in animal models, which demonstrate that these proteins play critical roles during AF-related atrial remodelling. Transcription factors have the potential to create a pro-arrhythmogenic substrate in the pulmonary veins and the atrium. However, further research is necessary to fully characterize the mechanistic links between these proteins and AF pathogenesis. In the future, such studies could potentially lead to the development of novel therapies for the arrhythmia. This review focuses on the association between transcription factors and AF.
Liquid Protein Diets and Torsade de Pointes
Authors: Bramah N. Singh
Journal: JAMA (1978)

Three women, aged 27, 33, and 35 years, experienced recurrent syncope five months after losing 36 to 41 kg using liquid protein diets. No abnormalities were noted during physical examination except in one who was hypothyroid. Serum potassium levels varied between 2.9 and 3.9 mEq /liter. The ECGs demonstrated prominent U waves, QU<sub>c</sub>prolongation, and ST and T wave abnormalities, with left axis deviation in two patients. Syncopal episodes were due to ventricular tachycardia and fibrillation, which were not responsive to conventional antiarrhythmic agents used in two patients. Patients using liquid protein diets may thus experience reversible QU<sub>c</sub>prolongation giving rise to serious arrhythmias that are probably best treated with drugs that shorten the QT<sub>c</sub>interval. Caution should be exercised in the use of liquid protein diets for weight reduction in obesity. (<i>JAMA</i>240:115-119, 1978)