tbuckley/cabot-search huggingface dataset:
Improving Evidence-Based Practices Through Health Literacy—Reply
Authors: Odette Wegwarth, Gerd Gigerenzer
Journal: JAMA Internal Medicine (2014)

To the Editor The research findings by Wegwarth and Gigerenzer 1 is a sober reminder of the need for better communication between clinicians and patients about the appropriateness of testing and interpretation of results.The inquiries of health literacy have demonstrated poor health outcome when there is a mismatch between patient skills required for the interpretation of health information and the demands clinicians and the health care system imposed on patients. 2When demands exceed the requisite skills, patients may feel overwhelmed and retreat into silence or stop actively participating in their own care.Health literacy is not limited to just the fundamental skills of reading, writing, speaking, and numeracy and simplifying the health information, although these can be part of it.It is a continuum of multidimensional skill sets of competencies acquired over a lifetime that allows an individual to access, participate in, and make informed decisions that directly and indirectly affect health.Studies have shown that even those who have high fundamental literacy skills have poor health literacy and that up to half of US adults are not able to effectively use written material to accomplish healthrelated tasks. 3 The practice of medicine is dynamic with constant shifts to diagnostic and treatment paradigms.The exponential growth of medical knowledge adds to the complexity of medical care, and there is the concern that physicians have difficulties accurately interpreting and translating evidence into clinical practice.Previous studies have shown that physicians have poor comprehension of the concepts used in the medical literature and have difficulty understanding the reported numbers (eg, results) and how to apply them to practice. 4In one study, physicians were asked to determine the probability that someone who tests positive for the fecal occult blood test has colon cancer if they were given the values of the prevalence of the disease and the sensitivity and specificity of the test. 5The answers ranged from 1% to 99%.This lack of numeracy skills clearly has a negative public health impact.It is time that we pay greater attention to the health literacy demands on both physicians and patients and take steps in enhancing medical education to improve physician knowledge and improve communication with patients.We also need to raise the standards of our secondary education so that individuals have better scientific literacy skills to comprehend the cognitive process in how physicians apply medical knowledge to clinical situations.
1044 EVALUATION OF A NOVEL ULTRASOUND METHOD FOR THE DETECTION OF LIVER FIBROSIS – PROSPECTIVE COMPARISON WITH TRANSIENT DYNAMIC ELASTOGRAPHY AND HISTOLOGY
Authors: B. Boozari, A. Potthoff, I. Mederacke, A. Hahn, A. Reising, K. Rifai, H. Wedemeyer, S. Kubicka, M. Manns, M. Gebel
Journal: Journal of Hepatology (2010)
Critique of fundholding study contained errors
Authors: A. Coulter, J. Bradlow
Journal: BMJ (1995)

200 consecutive patients with various malignancies (83 men, mean (SD) age (1-5) years; 117 women, mean age 63-7 (1-3) years). Thiry five of them had lymphoma, nine leukaemia, 15 bronchioalveolar carcinoma, 32 breast cancer, 28 urogenital carcinoma, 19 gastric carcinoma, 22 cancer of the
Mitoxantrone is superior to doxorubicin in a multiagent weekly regimen for patients older than 60 with high-grade lymphoma: results of a BNLI randomized trial of PAdriaCEBO versus PMitCEBO
Authors: Paul N. Mainwaring, David Cunningham, Walter Gregory, Peter Hoskin, Barry Hancock, Andrew J. Norton, Ken MacLennan, Paul Smith, Gillian Vaughan Hudson, David Linch
Journal: Blood (2001)
Cimetidine: an advance in gastric ulcer treatment?
Authors: A G Morgan, W A McAdam, C Pacsoo, B E Walker, A V Simmons
Journal: BMJ (1978)

Sixty patients with endoscopically confirmed gastric ulceration took part in a single-blind trial of cimetidine 1 g daily compared with conventional treatment--namely, carbenoxolone in patients aged under 60 and Caved-(S) in those over 60. Twenty-nine patients received cimetidine: in 12 (41%) ulcer healing was complete after one month, in 26 (90%) healing was complete after two months, and all ulcers were healed after three months of treatment. In the under-60s, ulcers were healed in a greater proportion of patients given cimetidine than in those given carbenoxolone. The difference, however, was significant only at the 5% level, which owing to small numbers was of doubtful clinical validity. In the over-60s cimetidine and Caved-(S) were of similar efficacy. The 54 patients with healed ulcers are being followed up for two years; so far there have been 16 recurrences (30%). Further trials are needed, which should include maintenance treatment aimed at lowering the unacceptably high recurrence rate.
Acute versus chronic alcohol consumption in acetaminophen-induced hepatotoxicity
Authors: Lars E. Schmidt, Kim Dalhoff, Henrik Enghusen Poulsen
Journal: Hepatology (2002)

The aim of this study was to determine by multivariate analysis how alcohol and other factors affect the clinical course and outcome in patients with acetaminophen (paracetamol) poisoning. A total of 645 consecutive patients admitted from 1994 to 2000 with single-dose acetaminophen poisoning were studied, giving special attention to alcohol history, time between overdose and intravenous N-acetylcysteine (NAC) treatment ("time to NAC"), and other data available at the time of admittance. Up until 72 hours after ingestion, time to NAC was the single most important independent risk factor. With a time to NAC less than 12 hours, the mortality rate was 0.42% (95% CI, 0.05-2.7). When time to NAC exceeded 12, 24, and 48 hours, the mortality rate increased to 6.1%, 13%, and 19%, respectively. Chronic alcohol abuse was an independent risk factor of mortality (odds ratio [OR], 3.52; 95% CI, 1.78-6.97). Acute alcohol ingestion was an independent protective factor regarding mortality in alcoholic patients (OR, 0.08; 95% CI, 0.01-0.66) but not in nonalcoholic patients (OR, 0.21; 95% CI, 0.03-1.67). Patient age and quantity of acetaminophen were independent risk factors. In conclusion, time to NAC was confirmed as the major risk factor in acetaminophen-induced hepatotoxicity and mortality. Chronic alcohol abuse was an independent risk factor that could be counteracted by concomitant acute alcohol ingestion. We suggest that patients with chronic alcoholism and suspected acetaminophen poisoning due to an increased risk of developing hepatotoxicity should be treated with NAC regardless of risk estimation.
Interleukin-23 Restrains Regulatory T Cell Activity to Drive T Cell-Dependent Colitis
Authors: Ana Izcue, Sophie Hue, Sofia Buonocore, Carolina V. Arancibia-Cárcamo, Philip P. Ahern, Yoichiro Iwakura, Kevin J. Maloy, Fiona Powrie
Journal: Immunity (2008)

Interleukin-23 (IL-23) is an inflammatory cytokine that plays a key role in the pathogenesis of several autoimmune and inflammatory diseases. It orchestrates innate and T cell-mediated inflammatory pathways and can promote T helper 17 (Th17) cell responses. Utilizing a T cell transfer model, we showed that IL-23-dependent colitis did not require IL-17 secretion by T cells. Furthermore, IL-23-independent intestinal inflammation could develop if immunosuppressive pathways were reduced. The frequency of naive T cell-derived Foxp3+ cells in the colon increased in the absence of IL-23, indicating a role for IL-23 in controlling regulatory T cell induction. Foxp3-deficient T cells induced colitis when transferred into recipients lacking IL-23p19, showing that IL-23 was not essential for intestinal inflammation in the absence of Foxp3. Taken together, our data indicate that overriding immunosuppressive pathways is an important function of IL-23 in the intestine and could influence not only Th17 cell activity but also other types of immune responses.
Don't forget ophthalmic differential diagnoses of cluster headache
Authors: A. S. Litwin, R. Malhotra
Journal: BMJ (2012)

Several treatable ophthalmic conditions were missing from the differential diagnoses of cluster headache in the article by Nesbitt and Goadsby.1 For example, scleritis, uveitis, orbital inflammatory disease (including dacryoadenitis and sino-orbital disease), and intermittent angle closure glaucoma may present with recurrent pain, lacrimation, conjunctival injection, periorbital oedema, ptosis, …
New Program Targets Death Investigator Training
Authors: Rebecca Voelker
Journal: JAMA (1996)

A NEW TRAINING program that is based on an in-depth analysis of job skills may push death investigators closer toward national certification. The Death Investigator Training Program, spearheaded by Milwaukee County (Wisconsin) Medical Examiner Jeffrey Jentzen, MD, is an effort to boost the quality of death investigation throughout the United States. As part of their research in determining what's needed in such a curriculum, Jentzen and his colleagues conducted a national survey. "Only 60% of medical examiners across the country felt they were satisfied with their investigators. So we felt we needed to develop a training curriculum to improve their job performance," Jentzen said at the annual meeting of the American Academy of Forensic Sciences (AAFS) in Nashville, Tenn, where he described the program. <h3>Essential Skills Identified</h3> A recurring theme during the AAFS meetings is the lack of adequate training in death investigation. "Only in seven states is training mandated"
High-density lipoprotein enhancement of anticoagulant activities of plasma protein S and activated protein C
Authors: John H. Griffin, Kazuhisa Kojima, Carole L. Banka, Linda K. Curtiss, José A. Fernández
Journal: Journal of Clinical Investigation (1999)

Low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels are associated, respectively, with either increased risk or apparent protective effects for atherothrombosis. The ability of purified LDL and HDL to downregulate thrombin formation, a contributor to atherothrombotic processes, was assessed. Purified HDL, but not LDL, significantly enhanced inactivation of coagulation factor Va by activated protein C (APC) and protein S, and HDL stimulated protein S–dependent proteolytic inactivation of Va by APC, apparently due to cleavage at Arg306 in Va. In normal plasma, added HDL enhanced APC/protein S anticoagulant activity in modified prothrombin-time clotting assays. When the anticoagulant potency of HDL was compared with phospholipid (PL) vesicles of well-defined composition using this assay, HDL appeared qualitatively different from PL vesicles because HDL showed only good anticoagulant activity, whereas PL vesicles were rather procoagulant. When 20 normal plasmas were tested using this clotting assay, apoA-I levels correlated with anticoagulant response to APC/protein S (r = 0.47, P = 0.035), but not with activated partial thromboplastin time–based APC resistance ratios. Because HDL enhances the anticoagulant protein C pathway in vitro, we speculate that HDL may help downregulate thrombin generation in vivo and that this anticoagulant action is one of HDL's beneficial activities.
Trends in Obesity and Extreme Obesity Among US Adults—Reply
Authors: Katherine M. Flegal
Journal: JAMA (2010)

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
Myocardial infarction size from serial CPK: variability of CPK serum entry ratio with size and model of infarction.
Authors: J A Cairns, E Missirlis, E L Fallen
Journal: Circulation (1978)

To study the variability of the fraction of CPK released from the infarcted heart which enters the serum (serum entry ratio, or SER) with size and model of infarction, nine dogs underwent homogeneous infarctions (LAD ligation) of varying sizes, and 10 dogs underwent scattered infarctions (left coronary embolization). In homogeneous infarcts there was an inverse linear relationship of SER to infarct size (IS) (SER = -0.8514% LV + 0.345, r = 0.98). No such relationship was found for scattered infarcts. CPK Kd (exponential disappearance constant for CPK) was not significantly different in homogeneous (-0.00178 min-1) vs scattered infarcts (-0.00195 min-1). Although similar IS was produced in each (homogeneous 19.9% LV, scattered 18.4% LV) cumulative CPK serum entry (CPKr) was much lower in homogeneous (4175 mlU/ml) vs scattered infarcts (7,296 mlU/ml). SER was also much lower in homogeneous (17.7%) vs scattered infarcts (29.0%) (P less than 0.025). Cumulative CPK plateau occurred significantly later in homogeneous (15.8 hours) vs scattered infarcts (11.7 hours) (P less than 0.01). Further corrections to the serial CPK equations for IS determination are indicated. The method may not be applicable in some infarct situations, e.g., scattered infarction.
IMPACT OF BETA-BLOCKER THERAPY AFTER PRIMARY PERCUTANEOUS CORONARY INTERVENTION IN ACUTE MYOCARDIAL INFARCTION WITHOUT HEART FAILURE: SUB-ANALYSIS OF ALPS-AMI STUDY
Authors: Hioki Hirofumi, Takashi Miura, Atsushi Izawa, Soichiro Ebisawa, Hirohiko Motoki, Takeshi Tomita, Yusuke Miyashita, Jun Koyama, Uichi Ikeda
Journal: Journal of the American College of Cardiology (2014)
Abstract A39: A newly defined role of clusterin in the formation of exosomes derived from prostate cancer cells
Authors: Elham Hosseini-Beheshti, Amina Zoubeidi, Ka Mun Nip, Martin E. Gleave, Emma S. Guns
Journal: Clinical Cancer Research (2010)

Abstract Introduction: Molecular chaperones, including heat-shock proteins (Hsps), help cells cope with stress-induced protein misfolding and aggregation and play prominent roles in cellular signaling and transcriptional regulatory networks asscociated with cancer progression and treatment resistance. Clusterin (CLU) is a stress-activated cytoprotective chaperone, up-regulated in Castration Resistant Prostate Cancer (CPRC), that confers hormone and chemo-resistance. Targeting inhibition of CLU using OGX-011 enhances treatment-induced cell death therapeutic response as is currently in clinical trials of men with advanced prostate cancer. Recent studies have linked cancer with exosome formation; exosomes are 30–100 nm membrane-bound compartments secreted from normal and tumor cells. The mechanisms underlying exosome formation and secretion are not fully understood. Factors such as stage of cancer, cell type and cell cycle could affect the amount and composition of exosomes formed and secreted. Since CLU has chaperone activity with a potent ability to inhibit amorphous and fibrillar aggregation of many different proteins, we hypothesize that it can influence exosome formation and release from androgen independent PCa cells. Methods-Results: PC3 cells were seeded and grown in DMEM with 5% FBS until 70% confluency. Media was changed to 5% charcoal strip serum DMEM and finally to a serum free media for 72 hours before exosome isolation. Exosomes were purified from the conditioned media using differential centrifugation after remove cell debris and protein aggregates. Further analysis by transmission electron microscopy detected the integrity of purified exosomes and their concentration. Western blot analysis was also used to probe for different exosome markers including Actin, Tubulin, TSG 101, HSP70 and CD36. In this study, we functionally analyzed the role of Clusterin in relation to exosome formation from PC-3 PCa cells. Clusterin was knocked down in PC3 cells using siRNA, and confirmed with western blot analysis. The content of Clusterin in exosomes after knockdown remains unchanged while, in contrast, cells become Clusterin depleted. Upon Clusterin knockdown in PC3 cells we also observe a dramatic reduction in the amount of exosomes formed. Conclusion: We have found high levels of CLU in exosomes derived from PCa cells. Our data suggests that CLU may serve a role in exosome formation since knocking it down by siRNA dramatically inhibits the quantity of exosomes formed. Citation Information: Clin Cancer Res 2010;16(7 Suppl):A39
Orthopaedic surgeons: as strong as an ox and almost twice as clever? Multicentre prospective comparative study
Authors: P. Subramanian, S. Kantharuban, V. Subramanian, S. A. G. Willis-Owen, C. A. Willis-Owen
Journal: BMJ (2011)

<b>Objective</b> To compare the intelligence and grip strength of orthopaedic surgeons and anaesthetists. <b>Design</b> Multicentre prospective comparative study. <b>Setting</b> Three UK district general hospitals in 2011. <b>Participants</b> 36 male orthopaedic surgeons and 40 male anaesthetists at consultant or specialist registrar grade. <b>Main outcome measures</b> Intelligence test score and dominant hand grip strength. <b>Results</b> Orthopaedic surgeons had a statistically significantly greater mean grip strength (47.25 (SD 6.95) kg) than anaesthetists (43.83 (7.57) kg). The mean intelligence test score of orthopaedic surgeons was also statistically significantly greater at 105.19 (10.85) compared with 98.38 (14.45) for anaesthetists. <b>Conclusions</b> Male orthopaedic surgeons have greater intelligence and grip strength than their male anaesthetic colleagues, who should find new ways to make fun of their orthopaedic friends.
Abstract LB-303: A hypusine-eIF5A-PEAK1 switch regulates the pathogenesis of pancreatic ductal adenocarcinoma
Authors: Ken Fujimura, Tracy Wright, Jan Strnadel, Jonathan Kelber, Sharmeela Kaushal, Cristina Metildi, Andrew Lowy, Michael Bouvet, Richard Klemke
Journal: Cancer Research (2014)

Abstract Deregulation of mRNA translation and protein synthesis is a hallmark of cancer cell proliferation, survival, and metastatic progression. eIF5A1, and its highly related isoform eIF5A2, are critical translation initiation factors implicated in several human malignancies. Interestingly, eIF5A proteins are the only known proteins in nature that are regulated by a distinct posttranslational modification termed hypusination. This unique lysine modification ([N-(4-amino-2-hydroxybutyl)lysine]) involves polyamine biosynthesis and is catalyzed by two enzymes, deoxyhypusine synthase (DHPS) and deoxyhypusine hydroxylase (DOHH). The highly selective nature of the hypusine modification and its amenability to pharmacological and genetic inhibition make the eIF5A-hypusine pathway an attractive therapeutic target to combat human cancers. Here, we investigated the role of eIF5A1/A2-hypusine pathway in pancreatic ductal adenocarcinoma (PDAC) pathogenesis. Hypusinated eIF5A1/A2 are upregulated in human PDAC tissues and in early stage PanIN tissues isolated from genetically engineered Pdx-Cre:LSL-KRASG12D mice. RNAi-mediated knockdown of eIF5A1/A2 in human PDAC cell lines inhibited cancer cell growth in vitro and inhibited tumor growth orthotopically in mice. In contrast, amplification of eIF5A1/A2 in PDAC cells increased orthotopic growth and tumor formation in mice. The deoxyhypusine hydroxylase inhibitor, CPX, and the deoxyhypusine synthase inhibitor, GC7, inhibited eIF5A1/A2 hypusination, preventing PDAC cell growth. Interestingly, we find that eIF5A1/A2 regulates cancer cell expansion by modulating the expression level of PEAK1, a non-receptor tyrosine kinase essential for PDAC cell growth. Our findings suggest that eIF5A1/A2 utilizes PEAK1 tyrosine kinase as a downstream effector to drive PDAC pathogenesis, and that pharmacological inhibition of the eIF5A1/A2 hypusination-PEAK1 axis may provide a novel therapeutic strategy to combat this deadly disease. Citation Format: Ken Fujimura, Tracy Wright, Jan Strnadel, Jonathan Kelber, Sharmeela Kaushal, Cristina Metildi, Andrew Lowy, Michael Bouvet, Richard Klemke. A hypusine-eIF5A-PEAK1 switch regulates the pathogenesis of pancreatic ductal adenocarcinoma. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr LB-303. doi:10.1158/1538-7445.AM2014-LB-303
Air pollution: the "classical" pollutants.
Authors: D Gloag
Journal: BMJ (1981)

Few disasters can have led to such great good as  four-day London smog of December 1952. Though its extreme concentrations of smoke and sulphur dioxide appear to have caused up to 4000 extra deaths,1 it provided  impetus for  Clean Air Act 1956. Many lines of evidence suggest that  pollution so strikingly reduced by this Act was associated with both acute and chronic illness.2 Air pollution has many components (see box) and may be of different types in different places.3 In this article I deal with smoke and sulphur dioxide pollution,4 mainly in Britain, and in  next I will touch on other pollutants. Severe fogs had occurred before in Britain and elsewhere; and smoke had polluted cities for centuries?in fact,  problem was past its worst well before 1952.5 In  eighteenth century Benjamin Taylor lectured about the clouds of Smoke, Vapour, and corrupted Effluvia, correctly pointing to  importance of temperature inversions,  incomplete com? bustion of coal, and all  Sooty particles . . . and cloud of Smoke, which if continued, ... its caustic quality would seize upon our lungs, restrain their vigour, and at last, render them totally incapable of their office.6 A century earlier  more famous John Evelyn ascribed  ill health of Londoners to  fuliginous and filthy vapour7; while a commission was set up to punish those who burnt coal in  City of London as long ago as 1307. Only in  present century, however, could air pollution become an important cause of illness and death: earlier its effects, though suspected, were overwhelmed by those of infectious diseases.5 Moreover, potentially lethal effects of intense fog would not be so apparent until there was a large population of susceptible people: by 1952 antibiotics enabled many people to survive with precarious respiratory and cardio? vascular systems; and it was these apparently, not  fit, who were killed by  fog.1
Sulfasalazine inhibits the synthesis of chemotactic lipids by neutrophils.
Authors: W F Stenson, E Lobos
Journal: Journal of Clinical Investigation (1982)

Neutrophils metabolize arachidonic acid through the liposygenase pathway to 5-hydroxy-6,8,11,14-eicosatetrenoic acid (5-HETE) and 5,12-dihydroxy-6,8,10,14-eicosatraenoic acid (5,12 diHETE). 5-HETE and 5,12diHETE are potent chemotactic agents and are thought to have important roles in the inflammatory response. In this study we demonstrate the sulfasalazine, at concentrations found in the stool of patients being treated for ulcerative colitis, blocks the synthesis of both 5-HETE and 5,12 diHETE by human neutrophils. A sulfasalazine metabolite, 5-aminosalicylate, also blocks the synthesis of 5,12 diHETE.
AP-1 elements and TCL1 protein regulate expression of the gene encoding protein tyrosine phosphatase PTPROt in leukemia
Authors: Tasneem Motiwala, Nicola Zanesi, Jharna Datta, Satavisha Roy, Huban Kutay, Allyn M. Checovich, Mohamed Kaou, Yiming Zhong, Amy J. Johnson, David M. Lucas, Nyla A. Heerema, John Hagan, Xiaokui Mo, David Jarjoura, John C. Byrd, Carlo M. Croce, Samson T. Jacob
Journal: Blood (2011)