tbuckley/cabot-search huggingface dataset:
Intramural tracking in esophageal pseudodiverticulosis
Authors: E. Wang, A. Tang, S. Venkatesh, J. So
Journal: Endoscopy (2007)

A 60-year-old man with diabetes mellitus and a long history of alcohol addiction presented with dysphagia and regurgitation of food. An initial endoscopy showed ulcerated lesions, which only yielded inflammatory cells on multiple biopsies, with no signs of malignancy. He subsequently developed a fever, and computed tomography (CT) of the thorax showed mediastinal abscesses and paraesophageal collections ([Fig. 1]). Biopsies grew Candida glabrata, and cultures grew Enterobacter and Klebsiella species. The patient responded well to intravenous imipenem.
P189 Should Screening For Chronic Viral Hepatitis In Patients With Tuberculosis Be Introduced To Nice Guidelines?
Authors: J. Potter, C. Hyams, M. Shaukat, Z. Babiker, V. Macavei, N. Jayasekera, H. Kunst, G. Foster, V. White
Journal: Thorax (2014)

<h3>Background</h3> Screening for viral hepatitis is not routinely recommended in patients diagnosed with tuberculosis (TB). However there are significant similarities in the global distribution of TB and hepatitis B (HBV) and C (HCV). It remains unclear whether co-infection with HBV or HCV is a risk factor for hepatotoxicity in patients receiving anti-tuberculous therapy and significant morbidity and mortality is associated with a late diagnosis. <h3>Objectives</h3> To determine the prevalence of HBV and HCV infection among new cases of active TB across treatment centres in East London and to assess the adverse drug reactions to anti-tuberculous treatment experienced by this population. <h3>Methods</h3> We conducted a retrospective study including all patients diagnosed with active TB during 2013 at two TB clinics in London. Data on demographic characteristics, HBV surface antigen (HBsAg), HCV antibody, human immunodeficiency virus (HIV) and adverse drug reactions were retrospectively analysed. <h3>Results</h3> In total, 472 cases of active TB were notified during 2013. The mean age was 37.7 (+/- 15.3) years (range: 5–92). Males accounted for 62.3% of our cohort. 84.7% of patients were born outside of the UK with the majority of patients being born in either Bangladesh (16.5%), India (27.8%) or Pakistan (15.9%). Overall, 304 patients were screened for HBV, 302 for HCV, and 447 for HIV. Of those screened, HBsAg was detected in 3.3%, HCV antibody in 2.0% and HIV in 3.4%. All patients infected with HBV or HCV were foreign born. Hepatotoxicity was defined as an ALT greater than 5 times the upper limit of normal or requiring a change in treatment. There was no significant difference in rates of hepatotoxicity in either in HepBsAg status (p = 0.371), HCV status (p = 0.597) or HIV status (p = 0.413) but numbers of HBV and HCV infection were small. <h3>Conclusions</h3> The prevalence of HBV and HCV was significantly higher in our cohort of TB patients than the background UK prevalence, which is 0.4% for HCV, 0.3% for HBV and 0.15% for HIV. Routine screening for HBV and HCV on an opt-out basis would be justified in our setting given the high proportion of foreign-born patients. Further research into the magnitude of HBV/HCV co-infection with active or latent TB, any increased risk in drug-induced hepatotoxicity and the cost-effectiveness of routine screening is needed.
The Training of the Internist: Today and Tomorrow
Authors: James V. Warren
Journal: JAMA (1966)

If one out of six of our medical-school graduates were unable to pass his state board examination, there would be great alarm. The fact that almost this many young physicians, having completed acceptable training in internal medicine, are unable, even after several attempts, to pass the examination by the American Board of Internal Medicine should be cause for concern. This fact in itself may have several possible explanations, but I bring it up as only one of the reasons why we should take a fresh, new look at training in internal medicine. In the changing scene of medicine I believe that it is high time we review our methods and goals. With the decline in general practice in the classic and broad sense, there has been a reciprocal rise in specialism in the United States (Fig 1). To me the most impressive fact is the rapid increase in the number
171 MELATONIN IS A SUITABLE THERAPEUTIC STRATEGY TO PROTECTS STEATOTIC LIVERS IN MAJOR HEPATECTOMY UNDER ISCHEMIA-REFERFUSION: A ROLE FOR ER STRESS AND AUTOPHAGY
Authors: M.A. Zaouali, I. Alfany-Fernandez, R.J. Reiter, M. Bejaoui, E. Pantazi, A. Rimola, H. Ben Abdennebi, J. Roselló -Catafau
Journal: Journal of Hepatology (2012)
Ramp abuse. A novel form of patient noncompliance to administration of nasal continuous positive airway pressure for treatment of obstructive sleep apnea.
Authors: M R Pressman, D D Peterson, T J Meyer, J P Harkins, L Gurijala
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

Administration of nasal continuous positive airway pressure (NCPAP) is the treatment of choice for most patients with obstructive sleep apnea. Many patients experience side effects with NCPAP use, and the compliance rate is reported to vary between 46-89%. The ramp is a device found on many NCPAP machines that resets the pressure to 3 cm H2O and then slowly increases the pressure to the prescribed pressure over a period of up to 45 min. The ramp allows patients time to fall asleep before the higher and likely more uncomfortable prescribed pressure is administered. We present a case in which a patient's repeated remote-controlled activation of this ramping feature severely limited effective therapy even when the NCPAP mask was properly in place, the machine was on, and the patient was breathing nasally.
Bradykinin-Induced Vasodilation Is Impaired at the Atherosclerotic Site but Is Preserved at the Spastic Site of Human Coronary Arteries In Vivo
Authors: Takeshi Kuga, Kensuke Egashira, Masahiro Mohri, Hiroyuki Tsutsui, Yasuhiko Harasawa, Yoshitoshi Urabe, Shinichi Ando, Hiroaki Shimokawa, Akira Takeshita
Journal: Circulation (1995)

Background Bradykinin causes endothelium-dependent vasodilation of isolated human coronary arteries in vitro. However, the effect of bradykinin on vasomotion of human coronary arteries in vivo has not been studied. The aim of this study was to examine whether bradykinin-induced vasodilation is altered at the atherosclerotic or spastic site of human coronary arteries in vivo. Methods and Results The effect of bradykinin on vasomotion of epicardial coronary arteries was evaluated in 8 patients with normal coronary arteries (control group), 14 patients with organic coronary stenosis (coronary artery disease [CAD] group), and 8 patients with vasospastic angina (VSA group). Changes in the diameter of epicardial coronary artery were assessed by quantitative coronary arteriography. Intracoronary administration of bradykinin at graded doses (60, 200, and 600 ng) dilated epicardial coronary arteries without altering arterial pressure or heart rate in all patients of either group. In the control group, vasomotor responses of the site where acetylcholine caused dilation were compared with the responses of the site where acetylcholine caused constriction. The magnitudes of bradykinin-induced dilation at the site with acetylcholine-induced dilation (mean±SD: 6±6%, 11±9%, and 15±9%) were comparable to that (3±6%, 8±8%, and 13±9%) at the site with acetylcholine-induced constriction. In the CAD group, vasomotor responses of the stenotic site (% diameter stenosis, 15% to 50%) and nonstenotic site were examined. The bradykinin-induced dilation at the stenotic site (0±4%, 3±8%, and 5±9%) was significantly less ( P &lt;.01) than at the nonstenotic site (3±4%, 8±6%, and 16±11%) and in the control group. Coronary vasodilation with nitrate at the stenotic site (20±11%) was comparable to that at the nonstenotic site (22±16%) and in the control group (21±10%). In the VSA group, vasomotor responses of the site with acetylcholine-induced spasm and the site without spasm were examined. The bradykinin-induced vasodilation at the spastic site (5±5%, 16±15%, and 33±17%) was comparable to that at the nonspastic site (4±8%, 12±14%, and 21±9%). Nitrate-induced dilation was comparable at the spastic site (51±19%) and the nonspastic site (32±13%). The ratio of bradykinin-induced vasodilation to nitrate-induced vasodilation at the spastic site was comparable to the control group. Conclusions These results suggest that bradykinin causes vasodilation of human epicardial coronary arteries in vivo and that bradykinin-induced endothelium-dependent vasodilation is impaired at the stenotic site but is preserved at the angiographically normal site where endothelium-dependent vasodilation by acetylcholine is impaired and at the spastic site.
ABC of clinical haematology: The acute leukaemias
Authors: R J Liesner, A H Goldstone
Journal: BMJ (1997)

Acute leukaemia is a clonal (that is, derived from a single cell) malignant disorder affecting all age groups from infancy to old age.It is characterised by the accumulation of abnormal white blood cells in the bone marrow which replace normal marrow tissue, including haemopoietic precursor cells.This results in bone marrow failure and peripheral blood involvement.Infiltration of various organs is also a feature of some forms of leukaemia.In most cases the aetiology is not obvious, but some constitutional and acquired disorders do predispose to acute leukaemia.In the past 40 years advances in the treatment of acute leukaemia have improved the chance of cure from virtually zero to 20-75%, depending on age and type of leukaemia.This has largely been the result of clinical trials-many of which are still ongoing-and the development and continued improvements in bone marrow transplantation. ClassificationAcute leukaemia is subdivided into (a) acute lymphoblastic leukaemia, in which the abnormal proliferation is in the lymphoid progenitor cells (that is, immature lymphocytes) and (b) acute myeloid leukaemia, which involves the myeloid lineages (that is, cells from which neutrophils, eosinophils, monocytes, basophils, megakaryocytes, etc are derived).The distinction between the two leukaemias is based on morphological, cytochemical, and immunological differences and is of paramount importance as the treatment and prognosis are usually different.Both acute lymphoblastic leukaemia and acute myeloid leukaemia are further subdivided on the basis of morphological criteria: acute lymphoblastic leukaemia into FAB (French-American-British) subtypes L1, L2, and L3 and acute myeloid leukaemia into FAB subtypes M0 to M7.On the basis of surface antigen expression acute lymphoblastic leukaemia is divided into T cell lineage and B cell lineage.B cell lineage is further subdivided: early B precursor acute lymphoblastic leukaemia is the most immature and is negative for the common acute lymphoblastic leukaemia antigen (CD10); common acute lymphoblastic leukaemia and pre-B cell acute lymphoblastic leukaemia are more mature and are CD10 positive; and B cell acute lymphoblastic leukaemia is the most mature and is the only one to express surface immunoglobulin.Little correlation exists between morphological subtype and immunophenotype or prognosis in acute lymphoblastic leukaemia, except that L3 morphology is almost exclusively found in B cell acute lymphoblastic leukaemia.In acute myeloid leukaemia immunophenotyping may not help to distinguish between leukaemias of the myeloid (M0 to M3), the myelomonocytic (M4), and the monocytic (M5) lineages, and special cytochemical stains are usually used to support morphological findings.In erythroleukaemia (M6) and megakaryoblastic leukaemia (M7), however, the surface antigen expression is often diagnostic.
People with partial hearing need to seek hearing potential
Authors: R. A Preiss
Journal: BMJ (2002)

EDITOR—The two deaf mental healthcare professionals who successfully procreated a deaf child by using a deaf sperm donor are reported to have said that a hearing child would be a blessing and a deaf child would be a special blessing.1 Apparently, Mother Nature (or God, if you will) saw fit to provide them with a son with partial or residual hearing. This outcome was predictable (if not poetic) and adds a further dimension to the ethical dilemma.

I believe that …
Attenuation of acetylcholine mediated coronary vasoconstriction with nonvasodilating dose of nitroglycerin in patients with heart failure: evidence for nitroglycerin induced enhancement of endogenous nitric oxide effect?
Authors: U. Elkayam, A. Mehra, J.Y. Kauffman, H. Gogla, S. Bokhari, P.P. Tummala
Journal: Journal of the American College of Cardiology (1998)
Correction: Incorrect Statement in Table of Contents
Authors: B. Cujec
Journal: Annals of Internal Medicine (1994)

Corrections15 April 1994Correction: Incorrect Statement in Table of ContentsFREEB. Cujec, P. Polasek, I. Mayers, and D. JohnsonB. CujecSearch for more papers by this author, P. PolasekSearch for more papers by this author, I. MayersSearch for more papers by this author, and D. JohnsonSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-120-8-199404150-00036 SectionsAboutVisual AbstractPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail In the 1 November 1993 issue of Annals, the Table of Contents summary of the article by Cujec and colleagues [1] incorrectly stated that “acute respiratory failure is a common cause of lack of improvement in oxygenation with the addition of positive end-expiratory pressure (PEEP) in patients who are mechanically ventilated”. The point of the article is that patent foramen ovale, not acute respiratory failure, is a common cause of unresponsiveness to PEEP.REFERENCE1. Cujec B, Polasek P, Mayers I, Johnson D. Positive end-expiratory pressure increases the right-to-left shunt in mechanically ventilated patients with patent foramen ovale. Ann Intern Med. 1993; 119:887-94. Google Scholar Comments0 CommentsSign In to Submit A Comment Author, Article, and Disclosure InformationAuthors: B. Cujec; P. Polasek; I. Mayers; D. Johnson PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 April 1994Volume 120, Issue 8Page: 698KeywordsPositive end expiratory pressureRespiratory failure ePublished: 15 August 2000 Issue Published: 15 April 1994 Copyright & PermissionsCopyright © 1994 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
IFN-α promotes the rapid differentiation of monocytes from patients with chronic myeloid leukemia into activated dendritic cells tuned to undergo full maturation after LPS treatment
Authors: Lucia Gabriele, Paola Borghi, Carmela Rozera, Paola Sestili, Mauro Andreotti, Anna Guarini, Enrico Montefusco, Robert Foà, Filippo Belardelli
Journal: Blood (2003)
Early Treatment of Cystic Fibrosis
Authors: David M. Orenstein
Journal: JAMA (1982)

<h3>To the Editor.—</h3> In the letter by Rosenstein and Langbaum (1982; 247:3313) on diagnostic delay in Duchenne's muscular dystrophy (DMD) and cystic fibrosis (CF), they stated "early intervention has not been associated with improved outcome...." While this may be the case for DMD, it is not so for CF. We studied 16 sibling pairs with CF during a seven-year period<sup>1</sup>and found that the siblings whose conditions were diagnosed before 1 year of age and before the onset of serious pulmonary involvement had substantially better pulmonary function and required notably fewer hospital admissions than their siblings whose conditions were diagnosed after 1 year of age and after the onset of pulmonary compromise. The implication is clear, namely, early intervention is associated with improved outcome (at least during a seven-year follow-up period), and I hope physicians will not delay in the institution of such treatment because of Rosenstein and Langbaum's
Effects of bilirubin and sera from jaundiced patients on osteoblasts: Contribution to the development of osteoporosis in liver diseases
Authors: Silvia Ruiz-Gaspà, Angels Martinez-Ferrer, Nuria Guañabens, Marta Dubreuil, Pilar Peris, Anna Enjuanes, Maria Jesús Martinez de Osaba, Luisa Alvarez, Ana Monegal, Andrés Combalia, Albert Parés
Journal: Hepatology (2010)

Abstract Low bone formation is considered to be the main feature in osteoporosis associated with cholestatic and end-stage liver diseases, although the consequences of retained substances in chronic cholestasis on bone cells have scarcely been studied. Therefore, we analyzed the effects of bilirubin and serum from jaundiced patients on viability, differentiation, mineralization, and gene expression in the cells involved in bone formation. The experiments were performed in human primary osteoblasts and SAOS-2 human osteosarcoma cells. Unconjugated bilirubin or serum from jaundiced patients resulted in a dose-dependent decrease in osteoblast viability. Concentrations of bilirubin or jaundiced serum without effects on cell survival significantly diminished osteoblast differentiation. Mineralization was significantly reduced by exposure to 50 μM bilirubin at all time points (from −32% to −55%) and jaundiced sera resulted in a significant decrease on cell mineralization as well. Furthermore, bilirubin down-regulated RUNX2 (runt-related transcription factor 2) gene expression, a basic osteogenic factor involved in osteoblast differentiation, and serum from jaundiced patients significantly up-regulated the RANKL/OPG (receptor activator of nuclear factor-κB ligand/osteoprotegerin) gene expression ratio, a system closely involved in osteoblast-induced osteoclastogenesis. Conclusion: Besides decreased cell viability, unconjugated bilirubin and serum from jaundiced patients led to defective consequences on osteoblasts. Moreover, jaundiced serum up-regulates the system involved in osteoblast-induced osteoclastogenesis. These results support the deleterious consequences of increased bilirubin in advanced chronic cholestasis and in end-stage liver diseases, resulting in disturbed bone formation related to osteoblast dysfunction. (Hepatology 2011)
GENE DISCOVERY IN<i>DROSOPHILA</i>: New Insights for Learning and Memory
Authors: Josh Dubnau, Tim Tully
Journal: Annual Review of Neuroscience (1998)

▪ Abstract Genetic approaches have been used to investigate increasingly complex biological systems. Here we review the current state of genetic analysis of learning and memory in the fruitfly, Drosophila melanogaster. Emerging findings support two main themes. First, discovery and manipulation of genes involved with behavioral plasticity in genetically accessible systems such as D. melanogaster enables dissection of the biochemical, cellular, anatomical, and behavioral pathways of learning and memory. Second, because core cellular mechanisms of simple forms of learning are evolutionarily conserved, biological pathways discovered in invertebrates are likely to be conserved in vertebrate systems as well.
Role of Brain Disease in Riots and Urban Violence
Authors: V. H. Mark
Journal: JAMA (1967)

<h3>To the Editor:—</h3> That poverty, unemployment, slum housing, and inadequate education underlie the nation's urban riots is well known, but the obviousness of these causes may have blinded us to the more subtle role of other possible factors, including brain dysfunction in the rioters who engaged in arson, sniping, and physical assault. The urgent needs of underprivileged urban centers for jobs, education and better housing should not be minimized, but to believe that these factors are solely responsible for the present urban riots is to overlook some of the newer medical evidence about the personal aspects of violent behavior. It is important to realize that only a small number of the millions of slum dwellers have taken part in the riots, and that only a sub-fraction of these rioters have indulged in arson, sniping, and assault. Yet, if slum conditions alone determined and initiated riots, why are the vast majority
A SIMPLE, ASEPTIC MOUTH-PIECE FOR THE SPIROMETER.
Authors: THOMAS A. STOREY
Journal: JAMA (1907)

So far as I am aware there is no spirometer tip on the market which can be cleaned easily. In view of the thousands of spirometer tests that are made each year in our various gymnasiums, this fact assumes a serious hygienic significance. A recognition of these facts justifies me, I believe, in presenting this device to the medical profession and particularly to those men engaged in anthropometric work. This mouth-piece (A) is made of wood, bevelled on one end to fit easily between the lips. The other end is made to fit snugly in the bore of the rubber tubing (B) which leads to the spirometer. These may be made anywhere. The Narragansett Machine Company of Providence, R. I., has furnished me with tips at the rate of three dollars a thousand. Each mouth-piece is used but once. It is then thrown away. At one-third of a cent apiece
Ethanol and fish oil induce NFκB transactivation of the collagen α2(I) promoter through lipid peroxidation–driven activation of the PKC-PI3K-Akt pathway
Authors: Natalia Nieto
Journal: Hepatology (2007)

To analyze whether fish oil, as a source of polyunsaturated fatty acids from the n-3 series, could synergize with ethanol to promote collagen I upregulation in vivo , collagen α2(I) promoter - βGal ( COL1A2-βGal ) transgenic mice were fed a diet enriched in fish oil in the presence of ethanol (ethanol group) or dextrose (control group). Ethanol-fed mice showed mild steatosis, increased alanine aminotransferase (ALT), aspartate aminotransferase (AST), nonsterified fatty acids, and plasma alcohol levels along with elevated cytochrome P450 2E1 activity, lipid peroxidation end products, and low glutathione (GSH) levels, which suggested enhanced oxidant stress and liver injury. Increased transactivation of the COL1A2 promoter assessed by βGal activity was shown in vivo and by transfection with deletion constructs for the collagen α1(I) promoter ( COL1A1 ) and COL1A2 promoters in vitro . Transcriptional regulation of both COL1A1 and COL1A2 promoters was validated by nuclear in vitro transcription run-on, northern blot analysis, and quantitative polymerase chain reaction, which was followed by the subsequent upregulation of collagen I protein with no changes in matrix metalloproteinase 13 (MMP 13). To further analyze the potential mechanism for collagen I upregulation, an in vitro coculture model was designed with primary stellate cells seeded on the bottom plate of a Boyden chamber and the rest of the liver cells plated on a cell culture insert, and fish oil or fish oil plus ethanol were added. The combination of fish oil plus ethanol increased nuclear factor κB binding to the COL1A2 promoter both in vivo and in the cocultures and also resulted in increased phosphorylation of protein kinase C , activation of PI3 kinase, and phosphorylation of Akt. The in vitro addition of vitamin E prevented such activation and collagen I increase. Furthermore, inhibitors of all 3 kinases blocked the increase in collagen I and NFκB binding to the COL1A2 promoter; the latter was also prevented by vitamin E. Conclusion: These results suggest that fish oil (mainly n-3 polyunsaturated fatty acids [PUFAs]) can synergize with ethanol to induce collagen I, transactivating the COL1A2 promoter through a lipid peroxidation-PKC-PI3K-Akt-NFκB-driven mechanism in the absence of overt steatosis and inflammation. (Hepatology 2007;45:1433–1445.)
In vivo detection of radicals in biological reactions.
Authors: B Chance, G Gao
Journal: Environmental Health Perspectives (1994)

In vivo detection of free radicals on a quantitative basis is essential for an establishment of their role in membrane, protein, and cell and tissue damage. This article compares optical methods, including chemiluminescence, electron paramagnetic resonance (EPR) and NMR methods for the study of free radicals and free radical damage, especially reperfusion injury neutrophil accumulation 6 hr after the ischemia/reperfusion insult. The chemiluminescence method is applied to an evaluation of the improved resistance to free radical stress due to transfection of creatine kinase in the mouse liver.