tbuckley/cabot-search huggingface dataset:
The Hitchhiker's Guide to Tobacco Control: A Global Assessment of Harms, Remedies, and Controversies
Authors: Ronald M. Davis, Melanie Wakefield, Amanda Amos, Prakash C. Gupta
Journal: Annual Review of Public Health (2007)

One in three adults worldwide (&gt;1.1 billion people) smokes; 80% live in low- and middle-income countries. Tobacco use causes five million deaths each year and, if current smoking patterns continue, will kill 10 million persons annually by 2020. From 1970 to 2000, tobacco leaf production decreased by 36% in developed countries but more than doubled in developing countries. China is the world's leading producer and consumer of tobacco. Seven multinational tobacco companies dominate the world cigarette market, led by Altria, British American Tobacco, and Japan Tobacco, which collectively manufacture more than 2 trillion cigarettes per year. Extensive knowledge exists about effective tobacco control interventions. However, dissemination of best practices and adoption and implementation of recommended policies are fragmentary. The Framework Convention on Tobacco Control (ratified by 140 countries as of October 1, 2006) provides a template outlining the ingredients for a comprehensive tobacco control campaign.
Impact energy attenuation performance of football headgear
Authors: Andrew S McIntosh, Paul McCrory
Journal: British Journal of Sports Medicine (2000)

Objectives —Commercially available football head protectors were tested to determine their impact energy attenuation performance and ability to reduce the likelihood of concussion. Methods —Prospective study using standardised impact test methods with both rigid (magnesium) and Hybrid III headforms. Results —Eight commercially available head protectors from six manufacturers were tested. The magnitude of the headform accelerations increased as the drop height was increased, ranging from a minimum of 64 g from a height of 0.2 m to a maximum of 1132 g from a height of 0.6 m. The head injury criterion and maximum headform acceleration values followed a similar trend. A steep increase was noted in the magnitude of maximum headform acceleration and head injury criterion when the drop height was increased from 0.4 to 0.5 m. This indicates that the foam material was completely compressed at an impact energy above about 20 J and therefore offers little protection against impacts of greater severity. Repeated tests using a drop height of 0.3 m showed that some helmets exhibit a “memory” effect, whereby impact performance is reduced by up to 50% with repeated impacts. Conclusions —Laboratory tests indicate that current commercially available football headgear performance will not reduce the likelihood of concussion. The absence of internationally recognised standards for soft headgear designed to ameliorate concussion is a major deficiency in sports injury prevention.
Mobilisation of mesenchymal cells in cardiac patients: is intense exercise necessary?
Authors: A Lucia, A De La Rosa, M Avila Silván, L M López-Mojares, A Boraita, M Pérez, C Foster, J García-Castro, M Ramirez
Journal: British Journal of Sports Medicine (2008)

Circulating mesenchymal cells (cMCs) have a potential for regenerating damaged tissue, e.g., ischaemic myocardium. In patients (age range: 53-76 years) with stable coronary artery disease cMCs were determined before and after dynamic exercise of moderate (< respiratory compensation threshold (RCT)) (n = 9 patients) or high intensity (>RCT) (n = 11). Only high-intensity exercise (i.e., provoking signs of myocardial ischaemia in 3 patients and ventricular extrasystoles in another) induced a significant increase in cMCs (p = 0.009). These results support the hypothesis that intense exercise (near or at the point of myocardial ischaemia) is a potent stimulus for MC mobilisation.
Turning the Disability Tide
Authors: Lisa I. Iezzoni, Vicki A. Freedman
Journal: JAMA (2008)

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
Cross-protective efficacy of HPV-16/18 AS04-adjuvanted vaccine against cervical infection and precancer caused by non-vaccine oncogenic HPV types: 4-year end-of-study analysis of the randomised, double-blind PATRICIA trial
Authors: Cosette M Wheeler, Xavier Castellsagué, Suzanne M Garland, Anne Szarewski, Jorma Paavonen, Paulo Naud, Jorge Salmerón, Song-Nan Chow, Dan Apter, Henry Kitchener, Júlio C Teixeira, S Rachel Skinner, Unnop Jaisamrarn, Genara Limson, Barbara Romanowski, Fred Y Aoki, Tino F Schwarz, Willy A J Poppe, F Xavier Bosch, Diane M Harper, Warner Huh, Karin Hardt, Toufik Zahaf, Dominique Descamps, Frank Struyf, Gary Dubin, Matti Lehtinen
Journal: The Lancet Oncology (2011)
Endothelium-dependent relaxation of rat aorta and main pulmonary artery by the phytoestrogens genistein and daidzein
Authors: S Mishra
Journal: Cardiovascular Research (2000)

Objective: The dietary phytoestrogens genistein and daidzein have been shown to relax agonist-preconstricted arteries in vitro; the mechanisms of relaxation remain incompletely understood. This study aimed to determine whether the relaxation of phenylephrine (PE)-constricted rat aorta and main pulmonary artery by genistein and daidzein was endothelium-dependent. Methods: Effects of endothelial-denudation, and pretreatment with with 100 μM l-NG-nitroarginine methyl ester (l-NAME) and/or 10 μM indomethacin on relaxation of PE (1 μM)-preconstricted contractures by genistein (1–100 μM) and daidzein (3–100 μM) were assessed by measuring isometric force development by rat arterial rings. The effect of l-NAME on relaxation to 17β-estradiol (10 μM) was also measured in aorta. Results and conclusions: Genistein and daidzein caused concentration-dependent relaxation of aorta rings preconstricted with PE (1 μM). The IC50 values were 5.7 μM (n=8, 95% confidence limits 4.3–7.7 μM) and 36.7 μM (n=12, 95% confidence limits 25.7–44.1 μM), respectively. Removal of the endothelium and pretreatment with l-NAME (100 μM) significantly inhibited relaxation at 3, 10 and 30 μM genistein and 10 and 30 μM daidzein. The contracture evoked in rat aorta by depolarization with 75 mM K+ solution was similarly relaxed by genistein in a partially endothelium-dependent manner. 17β-Estradiol (10 μM) caused a 48.7±5.0% (n=11) relaxation of the PE contracture, which was significantly reduced to 25.1±5.3% (n=7) by l-NAME. Relaxations brought about by 17β-estradiol, genistein, and daidzein were not significantly affected by the genomic estrogen receptor antagonist ICI 182,780 (10 μM). Similar endothelium-dependent effects of genistein were observed in the main pulmonary artery. The results show that the relaxation of these rat arteries by concentrations of genistein and daidzein which overlap those present in human plasma after ingestion of soybean-containing meals is largely endothelium dependent
Increased Detection Sensitivity for <i>KRAS</i> Mutations Enhances the Prediction of Anti-EGFR Monoclonal Antibody Resistance in Metastatic Colorectal Cancer
Authors: Francesca Molinari, Lara Felicioni, Michela Buscarino, Sara De Dosso, Fiamma Buttitta, Sara Malatesta, Alessandra Movilia, Marco Luoni, Renzo Boldorini, Oscar Alabiso, Salvatore Girlando, Barbara Soini, Alessandra Spitale, Federica Di Nicolantonio, Piercarlo Saletti, Stefano Crippa, Luca Mazzucchelli, Antonio Marchetti, Alberto Bardelli, Milo Frattini
Journal: Clinical Cancer Research (2011)

KRAS mutations represent the main cause of resistance to anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (MoAbs) in metastatic colorectal cancer (mCRC). We evaluated whether highly sensitive methods for KRAS investigation improve the accuracy of predictions of anti-EGFR MoAbs efficacy.We retrospectively evaluated objective tumor responses in mCRC patients treated with cetuximab or panitumumab. KRAS codons 12 and 13 were examined by direct sequencing, MALDI-TOF MS, mutant-enriched PCR, and engineered mutant-enriched PCR, which have a sensitivity of 20%, 10%, 0.1%, and 0.1%, respectively. In addition, we analyzed KRAS codon 61, BRAF, and PIK3CA by direct sequencing and PTEN expression by immunohistochemistry.In total, 111 patients were considered. Direct sequencing revealed mutations in codons 12 and 13 of KRAS in 43/111 patients (39%) and BRAF mutations in 9/111 (8%), with almost all of these occurring in nonresponder patients. Using highly sensitive methods, we identified up to 13 additional KRAS mutations compared with direct sequencing, all occurring in nonresponders. By analyzing PIK3CA and PTEN, we found that of these 13 patients, 7 did not show any additional alteration in the PI3K pathway.The application of highly sensitive methods for the detection of KRAS mutations significantly improves the identification of mCRC patients resistant to anti-EGFR MoAbs.
Dexmedetomidine vs Midazolam for Sedation of Critically Ill Patients&lt;subtitle&gt;A Randomized Trial&lt;/subtitle&gt;
Authors: Richard R. Riker
Journal: JAMA (2009)

<h3>Context</h3>γ-Aminobutyric acid receptor agonist medications are the most commonly used sedatives for intensive care unit (ICU) patients, yet preliminary evidence indicates that the α<sub>2</sub> agonist dexmedetomidine may have distinct advantages.<h3>Objective</h3>To compare the efficacy and safety of prolonged sedation with dexmedetomidine vs midazolam for mechanically ventilated patients.<h3>Design, Setting, and Patients</h3>Prospective, double-blind, randomized trial conducted in 68 centers in 5 countries between March 2005 and August 2007 among 375 medical/surgical ICU patients with expected mechanical ventilation for more than 24 hours. Sedation level and delirium were assessed using the Richmond Agitation-Sedation Scale (RASS) and the Confusion Assessment Method for the ICU.<h3>Interventions</h3>Dexmedetomidine (0.2-1.4 μg/kg per hour [n = 244]) or midazolam (0.02-0.1 mg/kg per hour [n = 122]) titrated to achieve light sedation (RASS scores between −2 and +1) from enrollment until extubation or 30 days.<h3>Main Outcome Measures</h3>Percentage of time within target RASS range. Secondary end points included prevalence and duration of delirium, use of fentanyl and open-label midazolam, and nursing assessments. Additional outcomes included duration of mechanical ventilation, ICU length of stay, and adverse events.<h3>Results</h3>There was no difference in percentage of time within the target RASS range (77.3% for dexmedetomidine group vs 75.1% for midazolam group; difference, 2.2% [95% confidence interval {CI}, −3.2% to 7.5%]; P = .18). The prevalence of delirium during treatment was 54% (n = 132/244) in dexmedetomidine-treated patients vs 76.6% (n = 93/122) in midazolam-treated patients (difference, 22.6% [95% CI, 14% to 33%]; P &lt; .001). Median time to extubation was 1.9 days shorter in dexmedetomidine-treated patients (3.7 days [95% CI, 3.1 to 4.0] vs 5.6 days [95% CI, 4.6 to 5.9]; P = .01), and ICU length of stay was similar (5.9 days [95% CI, 5.7 to 7.0] vs 7.6 days [95% CI, 6.7 to 8.6]; P = .24). Dexmedetomidine-treated patients were more likely to develop bradycardia (42.2% [103/244] vs 18.9% [23/122]; P &lt; .001), with a nonsignificant increase in the proportion requiring treatment (4.9% [12/244] vs 0.8% [1/122]; P = .07), but had a lower likelihood of tachycardia (25.4% [62/244] vs 44.3% [54/122]; P &lt; .001) or hypertension requiring treatment (18.9% [46/244] vs 29.5% [36/122]; P = .02).<h3>Conclusions</h3>There was no difference between dexmedetomidine and midazolam in time at targeted sedation level in mechanically ventilated ICU patients. At comparable sedation levels, dexmedetomidine-treated patients spent less time on the ventilator, experienced less delirium, and developed less tachycardia and hypertension. The most notable adverse effect of dexmedetomidine was bradycardia.<h3>Trial Registration</h3>clinicaltrials.gov Identifier: NCT00216190Published online February 2, 2009 (doi:10.1001/jama.2009.56).
Functional and autoradiographic evidence for endothelin 1 receptors on human and rat cardiac myocytes. Comparison with single smooth muscle cells.
Authors: C J Moody, M R Dashwood, R M Sykes, M Chester, S M Jones, M H Yacoub, S E Harding
Journal: Circulation Research (1990)

This study aimed to determine whether receptors for endothelin were present on the cardiac myocyte as well as on vascular smooth muscle cells. Low- and high-resolution autoradiography was performed using 125I-endothelin 1 on intact rat myocardium and samples of human ventricle obtained from explanted hearts at the time of transplant. In addition to specific binding to the smooth muscle of the blood vessel lumen, there was considerable binding associated with cardiac myocytes. To discover whether there was any functional correlate for this binding, muscle cells were isolated enzymatically from human and rat ventricle and from rat femoral artery, and their contractile characteristics were studied. Single cardiac cells were superfused with physiological saline at 32 degrees C, and their length change was displayed continuously on a chart recorder. Endothelin 1 had a pronounced effect on shortening in both rat and human myocytes. The contraction amplitude was approximately doubled in both cases, from 4.1 +/- 0.8% cell length to 8.1 +/- 1.3% for rat (mean +/- SEM, n = 9, p less than 0.001), and from 2.1 +/- 0.5% to 4.0 +/- 0.5% in human (n = 10, p less than 0.001). In rat, the magnitude of the effect was comparable to that of the alpha-adrenoceptor agonist phenylephrine. The maximum contraction amplitude of the human cells, produced by raising extracellular calcium to greater than 10 mM, was 11.4 +/- 1.1% cell length (n = 9), significantly greater than that produced by endothelin (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Systemic and local antibody responses to gastric Campylobacter pyloridis in non-ulcer dyspepsia.
Authors: B J Rathbone, J I Wyatt, B W Worsley, S E Shires, L K Trejdosiewicz, R V Heatley, M S Losowsky
Journal: Gut (1986)

Antibody titres to Campylobacter pyloridis in serum and gastric juice were estimated by an enzyme linked immunosorbent assay (ELISA) to whole organisms obtained from bacterial culture in 39 patients with non-ulcer dyspepsia. Whereas 20 of the 21 patients with chronic gastritis had gastric C pyloridis, 17 patients with no C pyloridis had normal histology in the gastric antrum and body. Significantly raised serum IgG and IgA antibody titres to C pyloridis were found in colonised patients with gastritis. Patients with raised IgG antibody to C pyloridis were also shown to have significantly raised titres to other Campylobacter species, suggesting antigenic cross reactivity. Gastric juice antibodies were also studied and IgA titres to C pyloridis were detected in a proportion of patients with gastritis, together with low levels of IgM, but no IgG.
Response to: ‘Is there a need for new thresholds to define remission and low disease activity by Disease Activity Score 28 calculated with C reactive protein? Real life data from a local registry’ by Favalli <i>et al</i>
Authors: Roy Fleischmann, Eustratios Bananis
Journal: Annals of the Rheumatic Diseases (2014)

Response to: 'Is there a need for new thresholds to define remission and low disease activity by Disease Activity Score 28 calculated with C reactive protein?Real life data from a local registry' by Favalli et alWe are delighted that the new cut-offs proposed for Disease Activity Score in 28 joints using CRP method (DAS28(CRP)) 1 have been tested and validated in another cohort. 2We hope that these validations change how DAS28(CRP) is currently being used in daily clinical practice and in clinical trials to determine low disease activity and remission.Furthermore, in our publication, 1 we also proposed new cut-offs for Disease Activity Score in 28 joints using ESR method (DAS28(ESR)) that correspond to Simplified Disease Activity Index (SDAI) because we found that DAS28(ESR) underestimates the disease activity compared with SDAI. 1 We hope that these new DAS28(ESR) cut-offs can also be tested in other cohorts as well.
Poor prognostic factors in advanced pulmonary adenocarcinoma patients receiving first-line gefitinib
Authors: Tzu-Yu Kuo, Ming-Ju Tsai, Yi-Hsuan Tsai, Chia-Min Chen, Wei-An Chang, Po-Ju Wei, Chih-Jen Yang, Ming-Shyan Huang
Journal: European Respiratory Journal (2013)

Introduction:  Gefitinib, an EGFR tyrosine kinase inhibitor, has been widely used as a first-line target therapy in advanced lung adenocarcinoma (adenoCa) with susceptible gene mutation, whereas some patients still have poor response. We tried to identify the factors predicting poor prognosis in patients of stage IV lung adenoCa, with susceptible gene mutation, receiving first-line Gefitinib.  Method:  Between Oct., 2009 and Dec., 2012, 47 patients of stage IV lung adenoCa were enrolled. Genetic testing of tumor or effusion samples confirmed presence of susceptible EGFR mutation in all patients. Patients who received no treatment or were lost to follow-up were excluded. Correlation between various clinical features was analyzed by Fisher9s exact test. The relationship between progression-free survival (PFS) and various clinical features was investigated by survival analysis.  Result:  We enrolled 21 and 24 patients with mutation in exon 19 and 21, respectively. Two patients with exon 18 mutation were excluded due to small sample size. No significant difference in PFS was noted between patients with exon 19 and 21 mutations. Patients with pleural effusion or liver metastasis had significantly shorter PFS, whereas other factors, including smoking history, or metastasis to bone, lung, pleural, brain or adrenal gland, did not significantly affect PFS.  Conclusion:  Liver metastasis and pleural effusion suggested poorer PFS in patients receiving gefitinib for their stage IV lung adenoCA with susceptible gene mutations. Our findings demonstrated poor prognostic clinical factors and provided clues to investigate the underlying mechanism of treatment failure in those with susceptible gene mutation.
Consent for Biobanking: Assessing the Understanding and Views of Cancer Patients
Authors: Julien Mancini, Isabelle Pellegrini, Frédéric Viret, Norbert Vey, Lise-Marie Daufresne, Christian Chabannon, Claire Julian-Reynier
Journal: JNCI Journal of the National Cancer Institute (2010)

Cancer patients were questioned about the consent process in a context in which they were routinely requested to donate tumor samples to research. After in-depth interviews of 19 patients, a 12-page questionnaire was designed and mailed to 745 patients who had been recently treated for colorectal cancer, breast cancer, or a hematological malignancy at a French Regional Cancer Center at which an opt-in biobanking system has existed since 2002. The response rate was 77.0% (N = 574). Among responding patients, 349 (60.8%) of the 574 were in favor of a formal and signed consent. Concordance was low (kappa = 0.23) between the number of patients who declared in the survey that they had given consent (213 of 574 [37.1%]) vs the number for whom registered consent had been recorded (267 of 574 [46.5%]). Only 2 (0.3%) of the 574 patients stated that they had signed a refusal, and only 88 (41.3%) of the 213 patients who remembered giving consent understood that their consent for biobanking also covered authorization to use their clinical data. We conclude that the opt-in consent procedure is positively perceived by most patients but should be improved for a better understanding and possibly an even better adherence to the consent process.
Risk of embolization after institution of antibiotic therapy for infective endocarditis
Authors: Isidre Vilacosta, Catherine Graupner, JoséAlberto SanRomán, Cristina Sarriá, Ricardo Ronderos, Cristina Fernández, Leonardo Mancini, Olga Sanz, JuanVictor Sanmartín, Walter Stoermann
Journal: Journal of the American College of Cardiology (2002)
Phosphoinositide 3-Kinase γ–Deficient Mice Are Protected From Isoproterenol-Induced Heart Failure
Authors: Gavin Y. Oudit, Michael A. Crackower, Urs Eriksson, Renu Sarao, Ivona Kozieradzki, Takehiko Sasaki, Junko Irie-Sasaki, Dominica Gidrewicz, Vitalyi O. Rybin, Teiji Wada, Susan F. Steinberg, Peter H. Backx, Josef M. Penninger
Journal: Circulation (2003)

We have recently shown that genetic inactivation of phosphoinositide 3-kinase gamma (PI3Kgamma), the isoform linked to G-protein-coupled receptors, results in increased cardiac contractility with no effect on basal cell size. Signaling via the G-protein-coupled beta-adrenergic receptors has been implicated in cardiac hypertrophy and heart failure, suggesting that PI3Kgamma might play a role in the pathogenesis of heart disease.To determine the role for PI3Kgamma in hypertrophy induced by G-protein-coupled receptors and cardiomyopathy, we infused isoproterenol, a beta-adrenergic receptor agonist, into PI3Kgamma-deficient mice. Compared with controls, isoproterenol infusion in PI3Kgamma-deficient mice resulted in an attenuated cardiac hypertrophic response and markedly reduced interstitial fibrosis. Intriguingly, chronic beta-adrenergic receptor stimulation triggered impaired heart functions in wild-type mice, whereas PI3Kgamma-deficient mice retained their increased heart function and did not develop heart failure. The lack of PI3Kgamma attenuated the activation of Akt/protein kinase B and extracellular signal-regulated kinase 1/2 signaling pathways in cardiac myocytes in response to isoproterenol. beta1- and beta2-adrenergic receptor densities were decreased by similar amounts in PI3Kgamma-deficient and control mice, suggesting that PI3Kgamma isoform plays no role in the downregulation of beta-adrenergic receptors after chronic beta-adrenergic stimulation.Our data show that PI3Kgamma is critical for the induction of hypertrophy, fibrosis, and cardiac dysfunction function in response to beta-adrenergic receptor stimulation in vivo. Thus, PI3Kgamma may represent a novel therapeutic target for the treatment of decreased cardiac function in heart failure.