tbuckley/cabot-search huggingface dataset:
Abstract 19859: Reducing Radiation Exposure for Patients also Improves Staff Radiation Exposure in the Cardiac Catheterization Laboratory
Authors: Alina M Robert, Peter N Ver Lee, Barbara Lilieholm, Kevin Morgan, Robert Cunningham, Amina Qazi, Alan Jansujwicz, Matthew S McKay, Rupert Fincke, Guillermo J Crespo, Matthew W Rowe, Paul R vom Eigen, Alan H Wiseman, David J Malenka
Journal: Circulation (2014)

Introduction: As the availability and use of medical imaging has increased, ionizing radiation has become a significant occupational exposure. Staff in the cardiac catheterization laboratory are among those with the highest exposures. Hypothesis: Changing equipment defaults to decrease patient radiation exposure would also decrease staff radiation exposure. Methods: In October 2013 we made equipment adjustments to decrease patient radiation exposure in all 3 cardiac catheterization laboratories at Eastern Maine Medical Center. We changed fluoroscopy defaults to low dose option and low frame rate (7.5 frames/sec from 15 frames/sec) while maintaining the option for operators to use higher settings as needed. We analyzed staff radiation exposure for 8 physicians and 14 nurses by comparing total collar dosimeter dose (in mRem) between the 3 months before and 3 months after the intervention controlling for procedural volume using standard statistical methods. Results: For physician operators, mean dosimeter dose decreased by 41.6% (346.8 ± 264.8 pre vs 202.5 ± 135.9 post intervention, p=0.042). For nurses whose roles are to assist during procedures or to circulate in the room, the mean dosimeter dose decreased by 25% (65.9 ± 49.4 pre vs 50.2 ± 53.5 post intervention, p=0.038). There was no significant difference between the number of cases performed by physicians (p=0.598) and nurses (p= 0.866) before and after the intervention. Procedural success did not decline post-intervention. Compliance with wearing collar dosimeter is required and reported as excellent at our institution. Conclusions: Setting fluoroscopy defaults to low dose and low frame rate to improve patient radiation exposure also significantly decreased radiation exposure for both physician and ancillary staff working in the cardiac catheterization laboratory. If widely adopted this intervention would help to mitigate the long term adverse effects of occupational exposure to ionizing radiation.
IL-21 secreted by APC confers robust expansion of antigen specific CD8+ T cells with distinct phenotype
Authors: Sascha Ansén, Marcus O. Butler, Alla Berezovskaya, Andrew P. Murray, Lee M. Nadler, Naoto Hirano
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

3994 

Adoptive cell therapy with ex vivo expanded CTL is a promising anti-cancer treatment. We previously reported the development of an artificial APC (aAPC), expressing HLA-A2, CD80, and CD83, that can support the priming and expansion of peptide specific CD8+ CTL with potent effector functions. IL-21, a member of the γc cytokine family, is secreted predominantly by activated CD4+ T cells and plays an important role in modulating T, B, and NK cell mediated immunity. In order to gain insight into its function as a mimic of ‘CD4+ T cell help,’ we have studied the function of IL-21 secreting aAPC (aAPC/IL-21). Purified CD8+ T cells from A2+ healthy donors were primed with aAPC pulsed with synthetic natural MART1 (27-35) peptide. After one week, T cells were split and subsequently stimulated three times with either peptide-pulsed aAPC or peptide-pulsed aAPC/IL-21 once a week. Between stimulations, cultures were supplemented with low dose IL-2 and IL-15. The total number of CD8+ T cells generated by aAPC/IL-21 was 12.2 (3.4-24.9, n=4) times the number generated by aAPC. Stimulation with aAPC/IL-21 generated a very high percentage of MART1 tetramer positive CTL, average 71.8% (57.4-86.2%, n=4), which is 3.7 times higher than CTL stimulated by aAPC. As a result, aAPC/IL-21 yielded 43.7 (14.5-90.7, n=4) times more MART1 specific CTL compared to aAPC. Starting with 6.5-11.5 x 106 (n=4) purified CD8+ T cells, we were able to generate 0.2-5.4 x 108 MART1-specific T cells within 5 weeks. Next, we studied the effect of IL-21 exposure on CD8+ T cells during the priming phase. Purified CD8+ T cells obtained from A2+ normal donors were given a single stimulation with either MART1 peptide-pulsed aAPC or aAPC/IL-21. Cultures were supplemented with low dose IL-2 and IL-15 every three days, and phenotypic analysis of MART1 tetramer positive cells was performed 10, 12, and 14 days later. Compared to aAPC, aAPC/IL-21 generated MART1-specific CTL with an increase in the percentage of CD45RA+ and CD28+ cells and a decrease in the percentage of CD45RO+ and CCR7+ cells. Although the effect of IL-21 on the level of CD62L expression was variable, both conditions resulted in similarly high CD27 expression. These results suggest that exposure to IL-21 during the stimulation promotes the expansion of antigen specific CD8+ T cells. Furthermore, IL-21 exposure during the priming phase can modulate the phenotype of expanded antigen specific CD8+ T cells. In conclusion, IL-21 secreting APC may improve our ability to generate mega dose of antigen specific CTL with distinct phenotype for the adoptive cell therapy of cancer.
Risk of skin ulcerations associated with oral nicorandil therapy: a population‐based study
Authors: M.‐T.G. Lee, H.‐Y. Lin, S.‐H. Lee, S.‐H. Lee, S.‐S. Chang, S.‐C. Chen, C.‐C. Lee
Journal: British Journal of Dermatology (2015)

Although healthcare products regulatory agencies have issued warnings on risk of ulceration associated with the use of nicorandil, a population-based study has not been carried out.To determine the relationship between use of nicorandil and skin ulceration.We carried out a population-based study using a cohort of 1 million people assembled from Taiwan's national health insurance database. The association between nicorandil use and skin ulcers was estimated by a Cox proportional hazards regression model adjusting for a nicorandil-specific propensity score (PS) comprising of 86 potential predictors (c-statistic = 0·91).The prospective cohort was longitudinally followed from January 2005 to December 2009, during which 1268 new users of nicorandil and 771 136 nonusers were identified. A higher frequency of skin ulcers (29 of 1268; 2·3%) was observed for users of nicorandil compared with nonusers (3231 of 771 136; 0·4%). Compared with nonusers, the crude hazard ratio (HR) associating nicorandil use with skin ulcers was 5·52 [95% confidence interval (CI) 3·82-7·95] and the PS-adjusted HR was 1·85 (95% CI 1·27-2·69). A risk period analysis showed that the risk of skin ulceration among users of nicorandil was greatest in the first year. Subgroup analysis found that the interaction term reached statistical significance (P < 0·05) for age and diabetes.Use of nicorandil was found to be associated with an increased risk for skin ulceration, especially in the first year after incident exposure. We suggest that regulatory agencies re-evaluate the risk for skin ulceration associated with use of nicorandil.
Patients' assessments of disability in multiple sclerosis
Authors: C. E Selai, M. R Trimble, P. Dorman, P. Rothwell
Journal: BMJ (1997)

More widespread public debate on rationing is essentialEditor-We find it significant that none of the clinicians who contributed to the conference "Rationing in the NHS: Time to Get Real" signed the open letter to Frank Dobson. 1 In the letter, rationing is defined as occurring when not all health services can be provided to everybody who might benefit from them, a definition so broad that it can be said always to have existed.Yet most British clinicians would not recognise the examples given as rationing.A young woman with high cholesterol as a single risk factor for coronary heart disease may be "denied" drug treatment and given dietary advice instead simply because the risks of side effects outweigh the marginal benefit; this is rational, not rationing.Again, "denying" magnetic resonance imaging for uncomplicated migraine in a young person has nothing to do with cost: the risks of iatrogenic anxiety and distress are far greater than any possible benefit from such intervention.The authors do the cause of so called smart rationing a disservice by these examples.This debate is too important to be "dumbed down" in this way.Whenever rationing is discussed there is a tension between those whose professional discipline (health economics, medical ethics, or policy analysis) allows them to work with broad underlying principles and those who are constantly brought face to face with the limitations of these principles through daily contact with patients.The former are much more likely to believe that it is possible and appropriate to base all rationing decisions on a series of well argued principles.Life for the latter is far messier: it is often impossible to apply broad principle to individual cases, let alone find a "currency of comparison" 2 that will enable the claims of, for example, a dying older person on an understaffed geriatric ward to be ranked against those of a patient with multiple sclerosis who might benefit from interferon beta.Struggling to make these sorts of comparisons is painful; the examples given in the open letter tax no one and thereby offer false hope of easy solutions.It is because the choices are difficult that more widespread public debate is essential.Only through such a debate can we all, as citizens, realise what is happening to the NHS, consider if that is the NHS that we want, and decide how much of our taxes an NHS worthy of the name deserves.
A double-blind controlled study of granulocyte colony-stimulating factor started two days before induction chemotherapy in refractory acute myeloid leukemia. Kohseisho Leukemia Study Group [see comments]
Authors: R Ohno, T Naoe, A Kanamaru, M Yoshida, A Hiraoka, T Kobayashi, T Ueda, S Minami, Y Morishima, Y Saito
Journal: Blood (1994)
Abstract ES5-1: Adherence and persistence with adjuvant aromatase inhibitor therapy
Authors: Norah Lynn Henry
Journal: Cancer Research (2015)

Abstract Aromatase inhibitors (AI) are medications that inhibit the aromatase enzyme, which converts androgens to estrogens, resulting in suppression of estrogen production in postmenopausal women. Treatment of postmenopausal women diagnosed with hormone receptor positive breast cancer with adjuvant AI therapy for 5 years has resulted in significant improvements in disease free and overall survival. Despite their proven benefit, however, adherence to and persistence with AI therapy is poor. A key reason for non-persistence with therapy is the development of bothersome side effects that can have a negative impact on quality of life. Retrospective analyses have identified possible predictors of poor tolerance of therapy. Studies have also suggested that development of toxicity may be associated with better response to therapy. Because of the concern about non-persistence with therapy, especially in the setting of prescription of an oral medication for many years, there has been considerable research into understanding the mechanism underlying development of toxicity as well as treatment of these side effects. Ultimately the goal is to improve breast cancer survival outcomes while minimizing the negative impact of therapy on quality of life. Citation Format: Norah Lynn Henry. Adherence and persistence with adjuvant aromatase inhibitor therapy [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr ES5-1.
CAROTID BODY TUMOR
Authors: Robert Schwartz, Leonard J. Abramovitz
Journal: Annals of Internal Medicine (1947)

Case Reports1 May 1947CAROTID BODY TUMORROBERT SCHWARTZ, LEONARD J. ABRAMOVITZROBERT SCHWARTZSearch for more papers by this author, LEONARD J. ABRAMOVITZSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-26-5-784 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe carotid body is an encapsulated, glandular structure located at or near the bifurcation of each common carotid artery. Normally, it is the size of a rice grain or smaller, reaching full development at 20 years. In man, it is difficult to demonstrate the carotid body grossly. Description of the carotid body dates back to 1743, but its functions were not understood until recent years. The carotid bodies (and aortic bodies) are sensory receptors which are stimulated by chemical changes in the arterial blood.1This is in contrast to the receptors of the carotid sinus and aortic arch which respond...Bibliography1. DRIPPSCOMROE RDJH: The clinical significance of the carotid and aortic bodies, Am. Jr. Med. Sci., 1944, ccviii, 681. CrossrefGoogle Scholar2. DELAFIELDPRUDDEN FTM: Textbook of pathology, 13th Ed., p. 413, p. 592. Google Scholar3. EWING J: Neoplastic diseases, 4th Ed., p. 384. Google Scholar4. HARRINGTONCLAGGETTDOCKERTY SWOTMB: Tumors of the carotid body; clinical and pathological considerations of twenty tumors affecting nineteen patients, Ann. Surg., 1941, cxiv, 820. CrossrefGoogle Scholar5. BOYD W: Surgical pathology, 4th Ed., p. 206. Google Scholar6. SOWLES HK: Tumor of the carotid body, New England Jr. Med., 1945, ccxxxiii, 62. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication December 11, 1945.Published with permission of the Medical Director, Veterans Administration, who assumes no responsibility for the opinions expressed or conclusions drawn by the authors. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCarotid body tumor 1 May 1947Volume 26, Issue 5Page: 784-787KeywordsCommon carotid arteries ePublished: 1 December 2008 Issue Published: 1 May 1947 PDF downloadLoading ...
Stem Cells Step Closer to the Clinic
Authors: B Vastag
Journal: JAMA (2001)

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
Soluble CD40 ligand and platelets: self-perpetuating pathogenic loop in thrombosis and inflammation?**Editorials published in the Journal of the American College of Cardiologyreflect the views of the authors and do not necessarily represent the views of JACCor the American College of Cardiology.
Authors: Pȧl Aukrust, Jan Kristian Damȧs, Nils Olav Solum
Journal: Journal of the American College of Cardiology (2004)
Oxidative Stress, T Cell DNA Methylation, and Lupus
Authors: YePeng Li, Gabriela Gorelik, Faith M. Strickland, Bruce C. Richardson
Journal: Arthritis & Rheumatology (2014)

Objective Lupus develops when genetically predisposed people encounter environmental agents, such as ultraviolet light, silica, infections, and cigarette smoke, that cause oxidative stress, but how oxidative damage modifies the immune system to cause lupus flares is unknown. We previously showed that inhibiting DNA methylation in CD4+ T cells by blocking ERK pathway signaling is sufficient to alter gene expression, and that the modified cells cause lupus‐like autoimmunity in mice. We also reported that T cells from patients with active lupus have decreased ERK pathway signaling, have decreased DNA methylation, and overexpress genes normally suppressed by DNA methylation. This study was undertaken to test whether oxidizing agents decrease ERK pathway signaling in T cells, decrease DNA methyltransferase levels, and cause demethylation and overexpression of T cell genes similar to that found in T cells from patients with active lupus. Methods CD4+ T cells were treated with the oxidizers H 2 O 2 or ONOO − . Effects on ERK pathway signaling were measured by immunoblotting, DNA methyltransferase 1 (DNMT‐1) levels were measured by reverse transcriptase–polymerase chain reaction (RT‐PCR), and the methylation and expression of T cell genes were measured using flow cytometry, RT‐PCR, and bisulfite sequencing. Results H 2 O 2 and ONOO − inhibited ERK pathway signaling in T cells by inhibiting the upstream regulator protein kinase Cδ, decreased DNMT‐1 levels, and caused demethylation and overexpression of genes previously shown to be suppressed by DNA methylation in T cells from patients with active lupus. Conclusion Our findings indicate that oxidative stress may contribute to human lupus flares by inhibiting ERK pathway signaling in T cells to decrease DNMT‐1 and cause DNA demethylation.
Abstract 16843: Protease-Activated Receptor 4 Improves Cardiac Function in Models of Viral, Ischemic and Dilated Cardiomyopathy
Authors: Silvio Antoniak, Nigel Mackman
Journal: Circulation (2014)

Introduction: Cardiomyocytes are a major source of protease-activated receptor 4 (PAR4), in the heart. PAR4 activation facilitates a unique signaling pathway in cardiomyocytes through the epidermal growth factor receptor (EGFR) and src kinase in vitro. EGFR signaling is known to mediate survival of cardiomyocytes and enhance antiviral pathways.

Hypothesis: Here, we investigated if cardiac PAR4 mediates protective effects in three different heart failure models in vivo.

Methods: PAR4-/- mice and wild-type (WT) littermates were compared in models of viral, ischemic or dilated cardiomyopathy. Cardiac injury was analyzed by cardiac troponin I (cTnI) ELISA. Gene expression analyses were performed with ELISA and RT-PCR. Changes in heart dimension and function were evaluated by echocardiography.

Results: PAR4 expression was protective in a coxsackievirus B3 (CVB3) viral cardiomyopathy model. PAR4-/- mice had higher cTnI plasma levels compared to WT mice 8d post infection with 10^5 plaque forming units of CVB3 (cTnI: 3.82±0.97 vs. 1.46±0.35ng/mL; P<0.05) and reduced IFNβ and expression of the IFN-response gene CXCL10. The increased injury at day 8 caused more cardiac remodeling leading to increased left ventricular (LV) dilatation and impaired heart function (fractional shortening [FS]: 27.02±1.45 vs. 32.73±2.16%, P<0.05) 28d after CVB3 infection. In cardiac ischemia/reperfusion injury, PAR4-/- mice exhibited higher plasma levels of cTnI after 30min ischemia and 2h reperfusion compared to WT mice (cTnI: 61.2±7.2 vs. 25.3±2.4 ng/mL; P<0.05). The greater injury in PAR4-/- mice led to more pronounced LV dilatation and impaired LV function after 28d of reperfusion compared to WT mice (FS: 30.92±1.02 vs. 38.55±1.32%; P<0.05). Lastly, in a dilated cardiomyopathy model, PAR4 deficiency was associated with increased cardiac injury (cTnI: 1.03±0.38 vs. 0.13±0.01 ng/mL; P<0.05), increased LV dilatation and more pronounced impairment of LV function (FS: 27.02±1.53 vs. 36.12±1.79%; P<0.05) 5d after administration of doxorubicin (20mg/kg).

Conclusions: Our study indicate that PAR4 mediates protective signaling during viral, ischemic and dilated cardiomyopathy progression in the heart, which may be mediated via EGFR transactivation.
Regional left ventricular wall motion.
Authors: H J Gelberg
Journal: Circulation (1980)

The work of Ingelsl represents a serious effort to grapple with the difficult problem of accurately assessing regional left ventricular wall motion.Since the left ventricular wall motion myocardial markers were used as a standard of segmental wall motion, the evaluation of the five methods of wall motion assessment is dependent on the reliability of that standard.I wonder if midmyocardial markers truly reflect endocardial position at end-systole.An echocardiogram showing vigorous posterior left ventricular wall thickening in systole suggests that endocardial and epicardial motion are not necessarily similar.Where along the gradient of motion would one find the midmyocardial marker?Another potential problem with discrete markers aligned in a plane is the inability to distinguish rotational motion from truly contraction generated inward motion.For example, take a cut-out of figure 1 and place pinholes as markers in the manner indicated in that diagram.Shine a bright light toward the silhouette and note the shadows cast on a paper below when the silhouette plane is parallel to the paper on which the shadow is cast.Now rotate the silhouette and note the marker locations on the paper below.The markers appear to have moved inward.The analogy is clear.Rotational motion of the ventricle about its long axis could give an illusion of contraction where none had occurred.If the heart rotates about the long axis, this should be seen in the left anterior oblique projection.Have these investigators viewed the marker placement at systole and diastole in the left anterior oblique view to assess rotation of the markers versus inward contractile motion?
Neutralization of Epstein-Barr Virus by Nonimmune Human Serum
Authors: Glen R. Nemerow, Fred C. Jensen, Neil R. Cooper
Journal: Journal of Clinical Investigation (1982)

These studies were carried out to investigate the mechanism of neutralization of purified Epstein-Barr virus (EBV) by fresh human serum from normal individuals lacking antibody to the EBV viral capsid (VCA) and nuclear antigens (EBNA). Such individuals thus lack serological evidence of immunity to EBV. Although an enzyme-linked immunosorbent assay (ELISA) with highly purified immobilized EBV detected low levels of IgG antibody reactive with EBV in these normal nonimmune sera, this antibody failed to neutralize EBV in the absence of complement. Studies with depleted sera and mixtures of purified complement proteins at physiologic concentrations showed that the IgG antibody and C1, C4, C2, and C3 of the classical pathway were able to fully neutralize EBV. Mixtures of the purified components of the alternative pathway at physiologic concentrations failed to neutralize purified EBV in the presence or absence of the antibody and the alternative pathway did not potentiate classical pathway-mediated neutralization. No evidence for a requirement for C8 was obtained, precluding lysis as the mechanism of neutralization. Since C3 deposition on the viral surface accompanied classical pathway activation, viral neutralization is most likely secondary to the accumulation of complement protein on the viral surface. A coating of protein on the virus could interfere with attachment to, or penetration of potentially susceptible cells.