tbuckley/cabot-search huggingface dataset:
What can we know about memory?
Authors: J Z Young
Journal: BMJ (1970)

Some glimpse of the possibilities may emerge if we attack the hardest part of the questions that arise from our title.What is it to "know" about memory or indeed about any other matter?There are many definitions of "knowledge" in dic- tionaries, encyclopaedias, and philosophical treatises.I prefer to try to extract one from the works of someone who has Baruu
Reperfusion alters the relation between blood flow and the remaining myocardial infarction.
Authors: A Chu, F R Cobb
Journal: Circulation (1989)

This study evaluated whether or not reperfusion of ischemic myocardium 2 hours after occlusion alters the basic relation between myocardial blood flow and infarction occurring during permanent occlusion. Awake mongrel dogs chronically instrumented with proximal circumflex coronary occluders were subjected to permanent occlusion (group A, n = 10) or occlusion followed by reperfusion 2 hours later (group B, n = 11). Myocardial blood flow was quantified with radioactive microsphere injections before, 6 hours after occlusion (group A), immediately before release, and 4 hours after reperfusion (group B). Three days later, the dogs were killed, and the heart was sectioned systematically into approximately 80 1-2-g circumferential and transmural samples for radioactive counting and histologic infarct quantification. Epimyocardial and endomyocardial samples from the permanent occlusion group (A) and the reperfused group (B) were separated by infarct range and related to regional myocardial blood flow measurements. In groups A and B, regional myocardial blood flow in endomyocardial and epimyocardial layers were inversely related to the extent of infarction. For given degrees of infarction, myocardial blood flow was significantly higher (greater than twofold) in the reperfused group. Myocardial samples with extensive infarction (51-75%) showed only mild (20-30%) reductions in blood flow when compared with nonischemic regions in the reperfused group. Thus, although early reperfusion may salvage ischemic myocardium, these studies showed that reperfusion causes a new relation between blood flow to the ischemic region and eventual histologic infarct size. When myocardial blood flow is used as an index of myocardial salvage after reperfusion, the basic relation obtained from permanent occlusion studies substantially overestimates the extent of myocardial salvage and underestimates the degree of remaining infarction.
THE GROWTH OF NEUROLOGY.CHAIRMAN'S ADDRESS BEFORE THE SECTION ON NERVOUS AND MENTAL DISEASES, AT THE FIFTY-SEVENTH ANNUAL SESSION OF THE AMERICAN MEDICAL ASSOCIATION, BOSTON, JUNE 5-8, 1906.
Authors: WHARTON SINKLER
Journal: JAMA (1906)

I am very glad to have this opportunity of thanking you for the honor conferred on me in making me chairman of this Section. It is a distinction of which one may justly be proud, for the Section has grown from a small beginning in 1891 to one of the most important and widely known in the American Medical Association. It is interesting to consider the development of the Section. Prior to the year 1891 there was no section devoted to this branch of medical science. In 1887 a new section was formed and this was called the Section on Medical Jurisprudence, Chemistry and Psychiatry, and this by expansion began to include the consideration of nervous diseases. In 1891, the subject of neurology having become so prominent in the discussions of the Section, the title was changed to the Section on Medical Jurisprudence and Neurology. In 1900, the scope of
Unexpected artifacts raise new caution in stem cell culture research
Authors: Hyam L. Leffert, Stewart Sell
Journal: Hepatology (2004)

To the Editor: With this letter, we wish to raise caution about interpretations of results owing to artifacts that may occur when cell lines are derived by culturing on cell-derived feeder layers. We recently reported the apparent derivation of rat liver progenitor cell lines by co-culture of liver cells enriched in periportal oval cells after allyl alcohol injury with γ-irradiated mouse STO (SIM [Sandoz inbred Swiss mouse]) fibroblast feeder layers.1 These reported lines are now undergoing intensive reinvestigation in our laboratories and the results indicate that the cells were actually derived from the STO feeder layers. In a series of first stage RT-PCR and PCR, aimed at extending the key original findings of constitutive and inducible differentiation, we were unable to detect rat genes or rat gene products in any of the 11 reported cell strains and lines, including the clonal "rat" line 3(8)#21, and its clonal derivative 3(8)#21-EGFP, a line transduced with enhanced green fluorescent protein. Instead, only mouse genes were detected in all instances. These results were obtained both with purified and cloned putative "rat liver progenitor" cells grown on or off STO feeder layers (γ-irradiated at UCSD), and with the original frozen "rat" cells obtained from untampered-with vials derived from very early passages at the Albany Medical College. These and other unexpected observations, which tend to eliminate cell fusion as the source of this artifact, are described in detail elsewhere.2 Ongoing observations of hepatocytic functions in these lines suggest that some aspects of the original report may yet be correct. For example, the line best characterized, 3(8)#21-EGFP, expresses several hepatocyte properties in vitro and following transplantation (manuscript in preparation). In conclusion, this surprising and previously unreported type of cell culture artifact should be considered by all investigators of cultured stem cell systems which require co-culture with mitotically "inhibited" feeder layer cell lines.
Redesigning Residency Education in Internal Medicine: A Position Paper from the Association of Program Directors in Internal Medicine
Authors: John P. Fitzgibbons, Donald R. Bordley, Lee R. Berkowitz, Beth W. Miller, Mark C. Henderson
Journal: Annals of Internal Medicine (2006)

There has been considerable change in the practice of internal medicine in the past quarter century, including the rise of specialization, increasing time pressure, the hospitalist movement, and the rapidly changing responsibilities of internists in inpatient and outpatient settings. Training programs have not adequately responded to these trends, and there is a consensus that the residency education system urgently needs redesign.
Surgery of Facial Fractures
Authors: Bromley S. Freeman
Journal: JAMA (1964)

This volume fulfills a need for a definitive and reliable outline of the reconstructive surgery of facial fractures. As one of the esoteric specialties, maxillofacial surgery is ofttimes fogged by the attempts of the associated specialties to repair by gadgets or tricks, to offset a lack of proper surgical training. This book, a synthesis of principles and facts, is a splendid monument to the specialization in this field of reconstruction.  An excellent historical background develops the ideas now current and offers references for further investigation. The general principles of the field are outlined and include a necessary section on diagnosis, by both physical and radiographic examination.  The authors assume a certain fundamental diagnostic ability and surgical dexterity and offer a proper textbook and guide. Excellent photographs, superb drawings, and clear diagrams make the book in part a surgical atlas. Deletion of the usual multiple dental techniques, of little but historical
When Illness Goes Public: Celebrity Patients and How We Look at Medicine
Authors: Janice Hopkins Tanne
Journal: BMJ (2006)

T he most famous celebrity patient of recent years is Lance Armstrong, who survived advanced testicular cancer, returned to cycling, and won the Tour de France seven times. He also became an activist, formed a foundation, spoke widely about the disease, and published a bestselling book about his experience.

   ![][1] 

Barron H Lerner

Johns Hopkins University Press, $25, pp 352 ISBN 0 8018 8462 4 www.press.jhu.edu/

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But the first celebrity patient, says Dr Barron Lerner, was Lou Gehrig, the famous American baseball player, who became ill with amyotrophic lateral sclerosis—still known in the United States as “Lou Gehrig's disease”—in 1938 and died in 1941. Gehrig was a star hitter for the New York Yankees, a tall, strong, shy man nicknamed “the Iron Horse” for his endurance.

During the summer of 1938, he was in a slump, but played better toward the end of the …

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Tissue distribution, quantitation and proliferation kinetics of fat-storing cells in carbon tetrachloride–injured rat liver
Authors: Albert Geerts, Jean-Marc Lazou, Pieter de Bleser, Eddie Wisse
Journal: Hepatology (1991)

In this study, we have investigated the cell population kinetics of fat-storing cells in livers of rats intoxicated with CCl4. Fat-storing cells were identified in cryostat sections by immunoperoxidase staining of desmin. The peroxidase label was visualized using diaminobenzidine/hydrogen peroxide containing Ni2+ and Co(2+)-ions (Nico/diaminobenzidine method). In normal rats, we found 12.8 fat-storing cells/0.1 mm2 in periportal areas vs. 9.4 in pericentral fields. After one injection of CCl4, the number of pericentral cells increased gradually to reach a maximum of 39.4 cells/0.1 mm2 96 hr after injection. The desmin staining intensity of the pericentral fat-storing cells increased from 48 hr onward. At 72 to 120 hr, strongly stained cells were observed in pericentral areas and in bands of tissue between adjacent central veins, reminiscent of the connective tissue septa in fibrotic livers. In the periportal areas the number of fat-storing cells was not altered. After a second and third injection of CCl4, the number of cells increased further in the pericentral areas. When more than three injections were given, the pericentral fat-storing cell population reached a new steady state with the cell number being seven times higher than in control animals. Proliferation of fat-storing cells at different stages of CCl4 intoxication was studied by intravenous administration of 3H-thymidine, followed by combined desmin staining and autoradiography. Autoradiographical labeling of fat-storing cells was nearly absent in control animals and at 24 hr after a single CCl4 injection. At 48 to 96 hr, labeling indices of pericentral fat-storing cells were significantly higher than in control animals, with a maximum at 72 hr when 22.9% of the cells were labeled. After multiple injections of CCl4, labeling indices between 4.9% and 8.4% were found. We conclude that fibrogenesis is preceded by a strong expansion of the fat-storing cell population in the pericentral areas of the liver lobules and in bands of tissue between adjacent central veins. Local proliferation is an important mechanism underlying the expansion of this cell population.
Bathing Instructions for Patients With Epilepsy
Authors: Samuel Livingston
Journal: JAMA (1981)

<h3>To the Editor.—</h3> In a recent issue ofThe Journal, Geiger cited the case of "a patient who drowned while taking a bath, as a result of a seizure." His communication is noteworthy because it directs attention to the important subject of water-immersion accidents associated with cleansing activities in patients with seizures. However, his advice that such patients abandon baths in favor of showers does not resolve the problem, since customary showering procedures are not without hazard to persons subject to seizures. Moreover, bathing in bathtubs in accord with specific instructions and limitations has proved to be a relatively safe cleansing activity for patients with epilepsy. Because definitive recommendations relative to baths and showers for seizure patients are essentially, to our knowledge, unavailable in the American literature, we would like to present briefly the instructions routinely given our patients. That bathing in bathtubs may represent a potentially lethal danger for
Proportion of spending on brand name drugs continues to rise in Germany
Authors: N. Stafford
Journal: BMJ (2010)

Brand name drugs accounted for more than 40% of Germany’s public insurance drug budget in 2009, up from 10% in 1993, a new report has shown. 

The report says that patent protected drugs accounted for €13.2bn (£11.2bn, $17.3bn) (41%) of the €32bn drug budget in Germany in 2009. In 1993 they accounted for €1.6bn (10%) of the €16bn budget.

Ulrich Schwabe, co-editor of the report and professor emeritus of pharmacology at the University of Heidelberg, has called on politicians to take legislative action to break the upward trend in German drug costs, which he says are the highest in Europe. 

Speaking at a press briefing in Berlin on 14 September to launch the report, he said that €9.4bn of the total €32.4bn spent on drugs in 2009 could have been avoided if German prices fell to Swedish levels.

Professor Schwabe told the BMJ that he compared German prices with those in Sweden because Swedish prices, which are in the lower third of …
PROGNOSTIC IMPLICATIONS OF SEVERE LESION CALCIFICATION IN PATIENTS UNDERGOING PERCUTANEOUS CORONARY INTERVENTION
Authors: Christos V. Bourantas, Scot Garg, Javaid Iqbal, Yao-jun Zhang, Marco Valgimigli, Stephan Windecker, Friedrich Mohr, Sigmund Silber, Ton de Vries, Yoshinobu Onuma, Hector Garcia-Garcia, Marie-angle Morel, Patrick Serruys
Journal: Journal of the American College of Cardiology (2014)
Hydrogen Sulfide Intoxication
Authors: ROBERT J. STINE
Journal: Annals of Internal Medicine (1976)

The toxicity of hydrogen sulfide is thought to be due primarily to reversible inactivation of the respiratory enzyme, cytochrome oxidase, with resultant inhibition of aerobic metabolism. A patient with severe hydrogen sulfide poisoning and consequent profound metabolic acidosis was treated successfully with nitrites and oxygen. The nitrite-induced methemoglobin, by competitively binding the toxic hydrosulfide anion until detoxified, presumably reactivated and protected cytochrome oxidase and thereby aided the patient's recovery by enhancing aerobic metabolism. His rapid recovery adds clinical support to the efficacy of nitrite therapy in sulfide poisoning. Therefore, we recommend that severe cases of sulfide poisoning be treated with nitrite-induced methemoglobinemia in addition to vigorous supportive care.
Atrial natriuretic peptide suppresses endothelin gene expression and proliferation in cardiac fibroblasts through a GATA4-dependent mechanism
Authors: D. J. Glenn, D. Rahmutula, M. Nishimoto, F. Liang, D. G. Gardner
Journal: Cardiovascular Research (2009)

Atrial natriuretic peptide (ANP) is a hormone that has both antihypertrophic and antifibrotic properties in the heart. We hypothesized that myocyte-derived ANP inhibits endothelin (ET) gene expression in fibroblasts. We have investigated the mechanism(s) involved in the antiproliferative effect of ANP on cardiac fibroblasts in a cell culture model. We found that cardiac myocytes inhibited DNA synthesis in co-cultured cardiac fibroblasts as did treatment with the ET-1 antagonist BQ610. The effect of co-culture was reversed by antibody directed against ANP or the ANP receptor antagonist HS-142-1. ANP inhibited the expression of the ET-1 gene and ET-1 gene promoter activity in cultured fibroblasts. The site of the inhibition was localized to a GATA-binding site positioned between −132 and −135 upstream from the transcription start site. GATA4 expression was demonstrated in cardiac fibroblasts, GATA4 bound the ET-1 promoter both in vitro and in vivo, and siRNA-mediated knockdown of GATA4 inhibited ET-1 expression. ET-1 treatment resulted in increased levels of phospho-serine105 GATA4 in cardiac fibroblasts and this induction was partially suppressed by co-treatment with ANP. Collectively, these findings suggest that locally produced ET-1 serves as an autocrine stimulator of fibroblast proliferation, that ANP produced in neighbouring myocytes serves as a paracrine inhibitor of this proliferation, and that the latter effect operates through a reduction in GATA4 phosphorylation and coincident reduction in GATA4-dependent transcriptional activity.
ACTION OF THE GOLDEN BELT DISTRICT MEDICAL SOCIETY OF KANSAS.
Authors: A. J. Scott
Journal: JAMA (1891)

<h3>To the Editor:</h3> —The American Medical Association acted wisely when it exchanged the annual volume of Transactions for the weeklyJournal; and displayed equal wisdom in locating the plant for its publication in Chicago. The growth ofThe Journalhas been in keeping with the growth of its home, and both bid fair, in the near future, to stand without rivals, the pride of the American people and the admiration of the world. Each member of the Association, may with the writer feel proud that his vote helped to createTHE JOURNALand gave it a home in the grandest city, for its age, that the world has ever seen; while to all, it should be a source of regret, amounting almost to sorrow and shame, that so small a personal matter, a mere whim of a vain and over-selfish brain, should be permitted to cause such a commotion and
CSF-1–dependant donor-derived macrophages mediate chronic graft-versus-host disease
Authors: Kylie A. Alexander, Ryan Flynn, Katie E. Lineburg, Rachel D. Kuns, Bianca E. Teal, Stuart D. Olver, Mary Lor, Neil C. Raffelt, Motoko Koyama, Lucie Leveque, Laetitia Le Texier, Michelle Melino, Kate A. Markey, Antiopi Varelias, Christian Engwerda, Jonathan S. Serody, Baptiste Janela, Florent Ginhoux, Andrew D. Clouston, Bruce R. Blazar, Geoffrey R. Hill, Kelli P.A. MacDonald
Journal: Journal of Clinical Investigation (2014)

Chronic GVHD (cGVHD) is the major cause of late, nonrelapse death following stem cell transplantation and characteristically develops in organs such as skin and lung. Here, we used multiple murine models of cGVHD to investigate the contribution of macrophage populations in the development of cGVHD. Using an established IL-17-dependent sclerodermatous cGVHD model, we confirmed that macrophages infiltrating the skin are derived from donor bone marrow (F4/80+CSF-1R+CD206+iNOS-). Cutaneous cGVHD developed in a CSF-1/CSF-1R-dependent manner, as treatment of recipients after transplantation with CSF-1 exacerbated macrophage infiltration and cutaneous pathology. Additionally, recipients of grafts from Csf1r-/- mice had substantially less macrophage infiltration and cutaneous pathology as compared with those receiving wild-type grafts. Neither CCL2/CCR2 nor GM-CSF/GM-CSFR signaling pathways were required for macrophage infiltration or development of cGVHD. In a different cGVHD model, in which bronchiolitis obliterans is a prominent manifestation, F4/80+ macrophage infiltration was similarly noted in the lungs of recipients after transplantation, and lung cGVHD was also IL-17 and CSF-1/CSF-1R dependent. Importantly, depletion of macrophages using an anti-CSF-1R mAb markedly reduced cutaneous and pulmonary cGVHD. Taken together, these data indicate that donor macrophages mediate the development of cGVHD and suggest that targeting CSF-1 signaling after transplantation may prevent and treat cGVHD.
DIAGNOSTIC ACCURACY OF ATP-STRESS DYNAMIC CT PERFUSION IMAGING AS COMPARED WITH ATP-STRESS CARDIAC MR PERFUSION IMAGING FOR THE ASSESSMENT OF MYOCARDIAL ISCHEMIA
Authors: Teruyoshi Uetani, Akiyoshi Ogimoto, Tamami Kono, Akira Fujii, Takayuki Nagai, Kazuhisa Nishimura, Katsuji Inoue, Jun Suzuki, Takafumi Okura, Jitsuo Higaki
Journal: Journal of the American College of Cardiology (2014)
MANAGING PATIENTS WITH AN INDICATION FOR ANTICOAGULANT THERAPY AFTER TRANSCATHETER AORTIC VALVE IMPLANTATION
Authors: Filippo Figini, Azeem Latib, Alaide Chieffo, Matteo Montorfano, Francesco Maisano, Micaela Cioni, Irene Franzoni, Francesco M. Sacco, Santo Ferrarello, Gill Buchanan, Antonio Grimaldi, Ottavio Alfieri, Antonio Colombo
Journal: Journal of the American College of Cardiology (2012)
A NEW UTERINE SCREEN AND INTRODUCER FOR INSERTING RADON TUBES INTO THE UTERUS
Authors: Frank Edward Simpson
Journal: JAMA (1926)

The screen consists of a hollow cylindric lead tube, which has a lumen just large enough to contain our radon (radium emanation) tubes. It can easily be bent to conform to the curve of the uterine canal, its flexibility being one of the important features. Screens may be made in various lengths and may contain from two to four or more radon tubes placed end to end. The screen containing two radon tubes is 5 cm. long, and each additional tube adds 1.75 cm. to its length. The wall thickness is 0.75 mm., the diameter of the lumen being 2.5 mm., and the outside diameter 4 mm. Each end of the screen is fitted with a nickel plated brass screw cap, which is provided with an eyelet through which a strong silk thread may be passed.  The introducer is 30 cm. long and contains an obturator. One end of the
Diagnosis-Related Groups and Severity of Illness-Reply
Authors: Robert L. Mullin
Journal: JAMA (1986)

<h3>In Reply.—</h3> I am sorry that Dr Thompson missed the point of the article. I did not "try to blame DRGs' shortcomings on the<i>ICD-9-CM</i>coding system"; rather, I was trying to point out the<i>ICD-9-CM</i>shortcomings, which affect a great deal more than the DRGs, as explained in the article. We have, in the New Haven area, used physician profiles, case mix adjusted using DRGs, successfully for about five to six years. Our physicians have accepted these profiles as valid and do not all claim to "treat the sickest ones." Dr Thompson, by overlooking the problems with the current coding system, only reinforces my position that physicians must take the lead in revising this coding system.
Differential dependence of eosinophil chemotactic responses on phosphoinositide 3‐kinase (PI3K)
Authors: R. K. Mishra, J. E. Scaife, Z. Harb, B. C. Gray, R. Djukanovic, G. Dent
Journal: Allergy (2005)

Background: Control of eosinophil migration to sites of inflammatory responses is a potentially therapeutic intervention in diseases such as bronchial asthma. Chemoattractants, their receptors and the associated signalling pathways may, therefore, be important targets for novel therapeutics. While several potentially important chemoattractants have been identified, the signalling pathways mediating their actions are incompletely understood. Aims of the study: The role of phosphoinositide 3‐kinase (PI3K) in responses of human eosinophils to two important eosinophil chemoattractants – platelet‐activating factor (PAF) and eotaxin (CCL11) – was studied to determine whether this enzyme activity might be crucial for eosinophil migration. Methods: Eosinophils were isolated from atopic donor blood by immunomagnetic selection. Chemotaxis was assayed in a 96‐well blind‐chamber cell fluorescence assay. Respiratory burst and leukotriene C 4 secretion were also assayed. Results: Two PI3K inhibitors, wortmannin and LY294002, caused concentration‐dependent inhibition of PAF‐induced eosinophil chemotaxis (IC 50 = 0.54 nM and 0.15 μ M, respectively) but exhibited at least 100‐fold lower potency against eotaxin‐induced responses (IC 50 = 48 nM and &gt;100 μ M, respectively), indicating that these responses were not dependent upon PI3K. Wortmannin and LY294002 also inhibited PAF induced respiratory burst but not PAF‐induced LTC 4 secretion. Conclusions: We conclude that PI3K‐dependence varies with stimulus and response, and that eotaxin‐induced eosinophil migration is not controlled by PI3K. This may indicate a limit to the potential of PI3K inhibitors to suppress tissue eosinophilia in diseases such as asthma.