tbuckley/cabot-search huggingface dataset:
OC-020 Recurrence after radiofrequency ablation for barrett's related high grade dysplasia is due to persistence of epithelial mutations
Authors: S Zeki, L Lovat, R Haidry, H Barr, N Shepherd, M Rodriguez-Justo, N Wright, S McDonald, M Novelli
Journal: Gut (2012)

<h3>Introduction</h3> Radiofrequency ablation (RFA) is a relatively new endoscopic method for ablation of high grade dysplasia (HGD) and intramucosal adenocarcinoma (IMC) in Barrett9s oesophagus. Clinical trials have shown enduring eradication of these pathologies.<sup>1</sup> However, some patients develop recurrent dysplasia or cancer.<sup>1</sup> The reason for this is unknown. The aim of the study was to investigate whether this is related to the persistence of known cancer driving mutations after radiofrequency ablation. <h3>Methods</h3> Patient records were searched for patients with recurrent HGD or IMC after RFA. Biopsies and endoscopic mucosal resection (EMR) specimens were available before and after RFA for each case. Whole biopsies underwent nested polymerase chain reaction (PCR) sequencing for mutations commonly implicated in progression to adenocarcinoma (<i>TP53, CDKN2A, K-ras</i>). <h3>Results</h3> Tissue was obtained for six patients before and after RFA. All patients were male (mean age 67 SD±2). Samples from five patients contained detectable mutations. In 3/5 patients, the same mutation was found in material taken before RFA as after (all TP53 mutations). The indication for RFA in all three patients was HGD; two of the patients developed IMC after RFA. In these two cases laser microdissection was performed on the post-RFA EMR samples. PCR revealed the pre RFA mutation to also be present throughout the IMC specimen. Dysplastic tissue adjacent to the IMC contained a mixture of crypts that were either wild type for the mutation in the IMC or contained the mutation indicating that the IMC was a monoclonal outgrowth and that the persistent mutation was driving the development of the recurrence. Furthermore, in all three cases, PCR of a further specimens (performed at a later time point to the first post-RFA EMR), revealed the same mutation as the initial biopsy before RFA, and the first post-RFA EMR. <h3>Conclusion</h3> The recurrence of dysplasia and cancer after RFA is likely to be due to failure to remove persistent, cancer driving mutations. Further work will need to be done to assess whether this is because of technical errors, or related to specific problems such as “buried Barrett9s”. <h3>Competing interests</h3> None declared. <h3>Reference</h3> 1. <b>Shaheen N</b>, Overholt B, Sampliner RE. Durability of radiofrequency ablation in barrett9s esophagus with dysplasia. <i>Gastroenterology</i> 2011;<b>141</b>:460–8.
Systematic Review: Comparative Effectiveness of Angiotensin-Converting Enzyme Inhibitors or Angiotensin II–Receptor Blockers for Ischemic Heart Disease
Authors: William L. Baker
Journal: Annals of Internal Medicine (2009)

Background: Patients with ischemic heart disease and preserved ventricular function experience considerable morbidity and mortality despite standard medical therapy. Purpose: To compare benefits and harms of using angiotensin-converting enzyme (ACE) inhibitors, angiotensin II–receptor blockers (ARBs), or combination therapy in adults with stable ischemic heart disease and preserved ventricular function. Data Sources: MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, and Cochrane Database of Systematic Reviews (earliest date, July 2009) were searched without language restrictions. Study Selection: Two independent investigators screened citations for trials of at least 6 months' duration that compared ACE inhibitors, ARBs, or combination therapy with placebo or active control and reported any of several clinical outcomes. Data Extraction: Using standardized protocols, 2 independent investigators extracted information about study characteristics and rated the quality and strength of evidence. Disagreement was resolved by consensus. Data Synthesis: 41 studies met eligibility criteria. Moderate- to high-strength evidence (7 trials; 32 559 participants) showed that ACE inhibitors reduce the relative risk (RR) for total mortality (RR, 0.87 [95% CI, 0.81 to 0.94]) and nonfatal myocardial infarction (RR, 0.83 [CI, 0.73 to 0.94]) but increase the RR for syncope (RR, 1.24 [CI, 1.02 to 1.52]) and cough (RR, 1.67 [CI, 1.22 to 2.29]) compared with placebo. Low-strength evidence (1 trial; 5926 participants) suggested that ARBs reduce the RR for the composite end point of cardiovascular mortality, nonfatal myocardial infarction, or stroke (RR, 0.88 [CI, 0.77 to 1.00]) but not for the individual components. Moderate-strength evidence (1 trial; 25 620 participants) showed similar effects on total mortality (RR, 1.07 [CI, 0.98 to 1.16]) and myocardial infarction (RR, 1.08 [CI, 0.94 to 1.23]) but an increased risk for discontinuations because of hypotension (P < 0.001) and syncope (P = 0.035) with combination therapy compared with ACE inhibitors alone. Limitations: Many studies either did not assess or did not report harms in a systematic manner. Many studies did not adequately report benefits or harms by various patient subgroups. Conclusion: Adding an ACE inhibitor to standard medical therapy improves outcomes, including reduced risk for mortality and myocardial infarctions, in some patients with stable ischemic heart disease and preserved ventricular function. Less evidence supports a benefit of ARB therapy, and combination therapy seems no better than ACE inhibitor therapy alone and increases harms. Primary Funding Source: Agency for Healthcare Research and Quality.
Urticaria induced by cetirizine
Authors: D. Calista, S. Schianchi, M. Morri
Journal: British Journal of Dermatology (2001)

Sir, Cetirizine, a second‐generation histamine‐1 receptor antagonist, is widely used to relieve symptoms of allergic rhinitis, conjunctivitis, and urticaria.1 The drug is considered to be safe and only rarely associated with mild and possible dose‐dependent side‐effects, such as somnolence, drowsiness and fatigue.2,3 A 42‐year‐old woman presented with a 3‐day history of acute generalized urticaria. Two hours before onset of the weals, she had taken a 10‐mg tablet of cetirizine for the treatment of allergic rhinitis. The patient’s history was remarkable for recurrent seasonal allergic rhinitis and conjunctivitis that had been treated with loratadine since 1995. She denied any previous history of urticaria, or other drug intake in the weeks prior to the start of her symptoms. Although the patient felt cetirizine was responsible, we were sceptical. However, we recommended discontinuing cetirizine as a precautionary measure. Oral prednisolone was promptly administered and weals gradually regressed over the next 7 days. After a washout period, the patient gave her consent to undergo provocative testing. A placebo challenge gave no response. A skin prick test with cetirizine drops was negative. Intradermal tests to cetirizine dilutions 1%, 0·5%, 0·1% and 0·05% showed no reaction. 5 mg cetirizine drops were given orally without adverse events. Four hours later a double dose of 10 mg was administered in the same way: after 30 min weals developed on the patient’s scalp and then spread over her face, neck, trunk and arms. There were no systemic symptoms. IgE PRIST, C3a and C5a levels tested before and during urticaria, were within normal values. Symptoms regressed with a further course of prednisolone.
The functional CD8 T cell response to HIV becomes type-specific in progressive disease
Authors: Sang Kyung Lee, Zhan Xu, Judy Lieberman, Premlata Shankar
Journal: Journal of Clinical Investigation (2002)

High levels of HIV-specific CD8 T cells are demonstrable throughout HIV disease using laboratory assays that measure responses to consensus epitopes. In acute infection, the dynamics of the antiviral CD8 T cell response correlate well with the decline in viremia. However in chronic infection, although responses are detected against a broader spectrum of epitopes, virus-specific CD8 T cells are apparently unable to control viral replication. To investigate whether CD8 T cells responding to consensus epitopes may have lost their in vivo relevance in the chronic phase because of viral evolution driven by immune pressure, we compared the CD8 T cell response to CD4 T cell targets infected with either lab-adapted HIVIIIB or the patient's own virus. The magnitude of the IFN-γ response declined with disease progression, especially to autologous virus. T cell receptor (TCR) clonotypes of HIVIIIB and autologous virus–responding cells were determined by sequencing TCR β chain variable (TCRBV) genes. In two of three asymptomatic donors, the dominant clonotypes overlapped, whereas in five symptomatic patients, the TCR clonotypes responding to HIVIIIB virus were completely different from those responding to autologous virus. Moreover, in cytolytic assays, T cell lines derived from IFN-γ+ cells responding to lab-adapted or autologous virus cross-recognized target cells infected with either virus in asymptomatic subjects with shared TCR clonotypes but not in progressors with differing clonotypes. Therefore, in advanced-stage patients, viral-specific CD8 T cells recognizing consensus epitopes persist from an earlier response but no longer effectively recognize autologous virus.
Annals of Allergy, St. Paul
Journal: JAMA (1970)

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
The Medical Directory of New York, New Jersey and Connecticut.
Journal: JAMA (1901)

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
Early Recognition of Depressive Illness
Journal: JAMA (1972)

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
Foege resigns CDC directorship for 'first love'
Authors: B. B. Dan
Journal: JAMA (1983)

Although William H. Foege, MD, MPH, has announced his intention to resign as director of the Centers for Disease Control (CDC) when a successor is found, he plans to stay on at the agency to return to his first love: solving international health problems. Scotching rumors that "politics" played a role in his resignation, Foege told<i>JAMA</i>MEDICAL NEWS that he accepted the post fully intending to serve only five or six years. His resignation came exactly six years after his appointment. Finding a replacement with Foege's acknowledged expertise and consummate political skill will not be an easy task for Edward N. Brandt, Jr, MD, assistant secretary for health in the Department of Health and Human Services. Foege has survived the policy shifts of three administrations, serving under three secretaries of health, and has earned respect on Capitol Hill. Brandt accepted Foege's resignation with "regret" but said he was delighted
Vitamin E inhibits CD95 ligand expression and protects T cells from activation-induced cell death
Authors: Min Li-Weber, Markus A. Weigand, Marco Giaisi, Dorothee Süss, Monika K. Treiber, Sven Baumann, Elena Ritsou, Raoul Breitkreutz, Peter H. Krammer
Journal: Journal of Clinical Investigation (2002)

Apoptosis is a morphologically distinct form of cell death involved in many physiological and pathological processes. Expression of the CD95 (APO-1/Fas) ligand (CD95L) is critically involved in activation-induced cell death (AICD) of activated T cells. Here we show that the natural free radical scavenger vitamin E suppresses the activity of the transcription factors NF-κB and AP-1, thus blocking expression of CD95L and preventing T cell AICD. Since AICD is a major cause of T cell depletion in AIDS, we examined 35 HIV-1–positive individuals and found that their T cells are more susceptible to AICD than are T cells isolated from healthy controls. Administration of vitamin E suppresses CD95L mRNA expression and protects T cells of HIV-1–infected individuals from CD95-mediated apoptosis. This evidence that vitamin E can affect T cell survival may merit further clinical investigation.
Cardiomyoplasty and treatment improve left ventricular function and myocardial revascularization after myocardial infarction in rats Katia L. D. De Angelis, Maria Cl�udia Irigoyen, Adolfo A. Leiner, Id�gene A. Cestari. Biengineering Division, Heart Institute (Incor), Medical School, Federal University of S�o Paulo, S�o Paulo, Brazil
Journal: Journal of the American College of Cardiology (2001)
Thrombolysis and Ventricular Tachycardia
Authors: M. Eldar
Journal: Annals of Internal Medicine (1993)

Letters15 January 1993Thrombolysis and Ventricular TachycardiaM. Eldar, MD, S. Behar, MD, and E. Kaplinsky, MDM. Eldar, MDSearch for more papers by this author, S. Behar, MDSearch for more papers by this author, and E. Kaplinsky, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-118-2-199301150-00024 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:The SPRINT study recruited patients between August 1981 and July 1983, before the “thrombolytic era.”The incidence of and the mortality rate associated with primary ventricular fibrillation do not appear to change after thrombolysis [1]. We are not aware of studies examining the effects of thrombolysis on primary ventricular tachycardia.REFERENCE1. Volpi A, Maggioni A, Franzozi G, Pampallona S, Mauri F, Tognoni G. In hospital myocardial infarction. Prognosis of patients with acute myocardial infarction complicated by primary ventricular fibrillation. N Engl J Med. 1987; 317:257-61. Google Scholar Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 January 1993Volume 118, Issue 2Page: 157KeywordsDeath ratesVentricular fibrillationVentricular tachycardia Issue Published: 15 January 1993 Copyright & PermissionsCopyright © 1993 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Sudden death due to coronary atherosclerotic heart disease. Age, smoking habits, and recent thrombi
Authors: D. M. Spain
Journal: JAMA (1969)

A study was made of age, smoking habits, and frequency of recent coronary thrombi in 102 men who died suddenly of a first clinical episode of coronary atherosclerotic heart disease. The average age at time of death was 16 years less in those who smoked cigarettes heavily than it was in the non smokers, while that in the lighter and former smokers was intermediate. The frequency of recent coronary arterial thrombi was 19% and revealed no correlation with smoking habits.
Vancomycin-Resistant Staphylococcus
Journal: New England Journal of Medicine (1987)

Vancomycin has been the most reliable therapeutic agent against infections caused by meticillin-resistantStaphylococcus aureus (MRSA).However, in 1996 the first MRSA to acquire resistance to vancomycin, was isolated from a Japanese patient.The patient had contracted a post-operative wound infection that was refractory to long-term vancomycin therapy.Subsequent isolation of several vancomycin resistant S aureus (VRSA) strains from USA, France, Korea, South Africa, and Brazil has confirmed that emergence of vancomycin resistance in S aureus is a global issue.A certain group of S aureus, designated hetero-VRSA, frequently generate VRSA upon exposure to vancomycin, and are associated with infections that are potentially refractory to vancomycin therapy.Presence of hetero-VRSA may be an important indicator of the insidious decline of the clinical effectiveness of vancomycin in the hospitals.Vancomycin resistance is acquired by mutation and thickening of cell wall due to accumulation of excess amounts of peptidoglycan.This seems to be a common resistance mechanism for all VRSA strains isolated in the world so far.
Imbalanced intrahepatic expression of interleukin 12, interferon gamma, and interleukin 10 in fulminant hepatitis B
Authors: L Leifeld
Journal: Hepatology (2002)

In murine models, overexpression of interleukin (IL)-12 and interferon (IFN)-γ can induce severe liver damage, whereas IL-10 has anti-inflammatory and hepatoprotective properties. To analyze the potential role of these cytokines in human fulminant hepatitis B, we used immunohistochemistry to study expression of IL-12, IFN-γ, and IL-10 in explant livers of 11 patients with fulminant hepatitis B, 5 patients with fulminant hepatitis due to other etiologies, 37 patients with chronic liver disease (CLD; hepatitis B virus, n = 15; hepatitis C virus, n = 10; primary biliary cirrhosis, n = 12), and 10 normal controls (NCs). Furthermore, cytokine messenger RNA (mRNA) levels were determined in the liver specimens by quantitative real-time polymerase chain reaction (PCR). In NCs, faint IL-12 expression was detected in only a few Kupffer cells, whereas sinusoidal endothelial cells, hepatic stellate cells, bile ducts, and lymphocytes expressed IL-12 in CLD and, more conspicuously, in fulminant hepatitis B. In contrast, expression of IFN-γ and IL-10 was restricted to lymphocytes and Kupffer cells, respectively. In fulminant hepatitis B, numbers of IL-12– and IFN-γ–positive cells markedly exceeded those found in CLD and NCs. A close correlation existed between IL-12 and IFN-γ expression (r = 0.68; P < .001). In contrast, IL-10 expression was not significantly different in CLD and fulminant hepatitis. The quantitative differences in immunohistologic cytokine expression closely corresponded to the mRNA levels. In conclusion, our data indicate massive induction of the proinflammatory cytokines IL-12 and IFN-γ in fulminant hepatitis B, which is apparently not counterbalanced by the anti-inflammatory cytokine IL-10. This cytokine imbalance may play an important role in promoting inflammatory reactions leading to massive liver damage in fulminant hepatitis B. (HEPATOLOGY 2002;36:1001-1008.)
Anaphylaxis and stinging insect hypersensitivity
Authors: M. D. Valentine
Journal: JAMA (1987)

<h3>ANAPHYLAXIS</h3> ANAPHYLAXIS as a full-blown medical emergency represents only a fraction of the acute allergic events with systemic manifestations for which this term can be used. The word<i>anaphylaxis</i>(backward protection) was coined by Portier and Richet<sup>1</sup>to describe the increased susceptibility of dogs to repeated injections of sea anemone toxin. Only later was it realized that the reactions of the reinjected dogs were due to hypersensitivity rather than to the loss of a normal protective mechanism. <i>Anaphylaxis</i>is now used to refer generically to the signs and symptoms resulting from the antigen-induced, IgE-mediated release or formation of chemical mediators whose target organs are primarily blood vessels and smooth muscle.<sup>2</sup>This might even include locally restricted, IgE-mediated reactions such as when airborne pollen grains cause allergic rhinoconjunctivitis after deposition on moist conjunctival and nasal membranes. However, it is more customary to regard anaphylaxis as one of several similar