tbuckley/cabot-search huggingface dataset:
Muscular strength in male adolescents and premature death: cohort study of one million participants
Authors: F. B. Ortega, K. Silventoinen, P. Tynelius, F. Rasmussen
Journal: BMJ (2012)

<b>Objectives</b> To explore the extent to which muscular strength in adolescence is associated with all cause and cause specific premature mortality (&lt;55 years). <b>Design</b> Prospective cohort study. <b>Setting</b> Sweden. <b>Participants</b> 1 142 599 Swedish male adolescents aged 16-19 years were followed over a period of 24 years. <b>Main outcome measures</b> Baseline examinations included knee extension, handgrip, and elbow flexion strength tests, as well as measures of diastolic and systolic blood pressure and body mass index. Cox regression was used to estimate hazard ratios for mortality according to muscular strength categories (tenths). <b>Results</b> During a median follow-up period of 24 years, 26 145 participants died. Suicide was a more frequent cause of death in young adulthood (22.3%) than was cardiovascular diseases (7.8%) or cancer (14.9%). High muscular strength in adolescence, as assessed by knee extension and handgrip tests, was associated with a 20-35% lower risk of premature mortality due to any cause or cardiovascular disease, independently of body mass index or blood pressure; no association was observed with mortality due to cancer. Stronger adolescents had a 20-30% lower risk of death from suicide and were 15-65% less likely to have any psychiatric diagnosis (such as schizophrenia and mood disorders). Adolescents in the lowest tenth of muscular strength showed by far the highest risk of mortality for different causes. All cause mortality rates (per 100 000 person years) ranged between 122.3 and 86.9 for the weakest and strongest adolescents; corresponding figures were 9.5 and 5.6 for mortality due to cardiovascular diseases and 24.6 and 16.9 for mortality due to suicide. <b>Conclusions</b> Low muscular strength in adolescents is an emerging risk factor for major causes of death in young adulthood, such as suicide and cardiovascular diseases. The effect size observed for all cause mortality was equivalent to that for well established risk factors such as elevated body mass index or blood pressure.
Effect of acute hypoxia and hypercapnic acidosis on the development of acetylstrophanthidin-induced arrhythmias
Authors: John F. Williams, Daniel L. Boyd, John F. Border
Journal: Journal of Clinical Investigation (1968)

The effect of acutely induced hypoxia, hypercapnic acidosis, and the combination of the two on the amount of acetylstrophanthidin (AS) required to produce cardiac arrhythmias was determined in anesthetized dogs. Each animal was studied during ventilation with room air and again during ventilation with gas mixtures of appropriate concentrations; 24 hr separated the study periods. AS was infused intravenously at a rate of 5 mug/kg per min. Significantly less AS was required to produce arrhythmias during hypoxia and hypercapnic acidosis together than during the period with normal arterial Po(2), Pco(2), and pH (10 animals). Included in this group were two animals which had undergone previous bilateral adrenalectomy and four animals in which heart rate was maintained at the same frequency during both study periods. A significant reduction in the toxic dose of AS also was demonstrated in eight animals, two with constant heart rate, during hypoxia with normal arterial Pco(2) and pH. Hypercapnic acidosis alone (eight animals) did not significantly alter the toxic dose of AS. After the administration of propranolol (six animals) or hexamethionium (six animals), no significant difference was observed between the toxic dose of AS during hypoxia and that during ventilation with room air. Thus although hypoxia and hypercapnic acidosis together do reduce the amount of AS required to produce arrhythmias, it is the hypoxia which exerts the predominant effect on the development of this increased sensitivity to AS. Furthermore, this effect of hypoxia occurs primarily as a result of reflexly augmented sympathetic stimulation of the heart.
Air pollution and biomarkers of systemic inflammation and tissue repair in COPD patients
Authors: Payam Dadvand, Mark J. Nieuwenhuijsen, Àlvar Agustí, Jordi de Batlle, Marta Benet, Rob Beelen, Marta Cirach, David Martinez, Gerard Hoek, Xavier Basagaña, Antoni Ferrer, Jaume Ferrer, Robert Rodriguez-Roisin, Jaume Sauleda, Stefano Guerra, Josep M. Antó, Judith Garcia-Aymerich
Journal: European Respiratory Journal (2014)

The origin(s) of systemic inflammation in patients with chronic obstructive pulmonary disease (COPD) is unclear. We investigated the impact of exposure to ambient air pollution on systemic biomarkers of inflammation (C-reactive protein (CRP), tumour necrosis factor-α, interleukin (IL)-6, IL-8 and fibrinogen) and tissue repair (hepatocyte growth factor (HGF)) in 242 clinically stable COPD patients (mean age 67.8 years and forced expiratory volume in 1 s 71.3% predicted) in Barcelona, Spain, in 2004–2006. A spatiotemporal exposure assessment framework was applied to predict ambient nitrogen dioxide (NO 2 ) and levels of particles with a 50% cut-off aerodynamic diameter of 2.5 μm (PM 2.5 ) at each participant’s home address during 10 periods of 24 h (lags 1–10) and 1 year prior to the blood sampling date. We used linear regression models to estimate associations between biomarkers and exposure levels. An interquartile range (IQR) increase in NO 2 exposure in lag 5 was associated with 51%, 10% and 9% increases in CRP, fibrinogen and HGF levels respectively. We also observed 12% and 8% increases in IL-8 associated with an IQR increase in NO 2 exposure in lag 3 and over the year before sampling, respectively. These increases were larger in former smokers. The results for PM 2.5 were not conclusive. These results show that exposure to ambient NO 2 increases systemic inflammation in COPD patients, especially in former smokers.
A sensorimotor account of vision and visual consciousness
Authors: J. Kevin O'Regan, Alva Noë
Journal: Behavioral and Brain Sciences (2001)

Many current neurophysiological, psychophysical, and psychological approaches to vision rest on the idea that when we see, the brain produces an internal representation of the world. The activation of this internal representation is assumed to give rise to the experience of seeing. The problem with this kind of approach is that it leaves unexplained how the existence of such a detailed internal representation might produce visual consciousness. An alternative proposal is made here. We propose that seeing is a way of acting. It is a particular way of exploring the environment. Activity in internal representations does not generate the experience of seeing. The outside world serves as its own, external, representation. The experience of seeing occurs when the organism masters what we call the governing laws of sensorimotor contingency. The advantage of this approach is that it provides a natural and principled way of accounting for visual consciousness, and for the differences in the perceived quality of sensory experience in the different sensory modalities. Several lines of empirical evidence are brought forward in support of the theory, in particular: evidence from experiments in sensorimotor adaptation, visual “filling in,” visual stability despite eye movements, change blindness, sensory substitution, and color perception.
LACK OF DISTINCTIVE SURFACE ANTIGEN ON CELLS TRANSFORMED BY MURINE SARCOMA VIRUS
Authors: Vladimir Strouk, Gertrud Grundner, Eva Maria Fenyö, Ed Lamon, Henryk Skurzak, George Klein
Journal: The Journal of Experimental Medicine (1972)

Some murine sarcoma virus (MSV)-transformed mouse 3T3 cells contain the MSV genome in the absence of infectious helper murine leukemia virus (MuLV) and MSV production. These cells, designated S+L- (sarcoma positive, leukemia negative), were analyzed for the presence of a possible MSV-determined membrane antigen by the mixed hemadsorption test and in vitro lymphocyte cytotoxicity assay. Two different serological approaches were used: (a) isoantibody-free sera were obtained by immunizing with MSV of syngeneic origin or by allowing primary, autologous MSV sarcomas to regress, or (b) alloantisera obtained by immunizing C57BL mice with S+L- cells were absorbed with the corresponding nontransformed 3T3 cells until all activity against 3T3 had been removed. While MuLV-superinfected S+L- cells and a culture line of an MSV sarcoma known to produce both MSV and MLV were highly reactive, normal 3T3 and S+L- cells were negative. Similarly, lymph node cells from MSV immune mice or rats did not kill S+L- cells, although they were cytotoxic against target cells known to carry MuLV-associated antigens. Thus, the present study gives no positive evidence for the existence of any MSV-induced new surface antigen in the transformed target cell, known to carry the viral genome.
Cardiovascular Disease Mortality in Europeans in Relation to Fasting and 2-h Plasma Glucose Levels Within a Normoglycemic Range
Authors: Feng Ning, Jaakko Tuomilehto, Kalevi Pyörälä, Altan Onat, Stefan Söderberg, Qing Qiao
Journal: Diabetes Care (2010)

To study mortality in relation to fasting plasma glucose (FPG) and 2-h plasma glucose levels within the normoglycemic range.Data from 19 European cohorts comprising 12,566 men and 10,874 women who had FPG <6.1 mmol/l and 2-h plasma glucose <7.8 mmol/l at baseline examination were analyzed. Multivariate-adjusted hazard ratios (HRs) and 95% CIs for deaths from cardiovascular disease (CVD), non-CVD, and all causes were estimated for individuals whose 2-h plasma glucose > FPG (group II) compared with those whose 2-h plasma glucose ≤ FPG (group I).A total of 827 (246) CVD and 611 (351) non-CVD and 1,438 (597) all-cause deaths occurred in men (women). Group II was older and had higher BMI, blood pressure, and fasting insulin than group I. The multivariate-adjusted HRs (95% CIs) for CVD, non-CVD, and all-cause mortality were 1.22 (1.05-1.41), 1.09 (0.92-1.29), and 1.16 (1.04-1.30) in men and 1.40 (1.03-1.89), 0.99 (0.79-1.25), and 1.13 (0.94-1.35) in women, respectively, for group II as compared with group I. HRs were 1.25 (1.05-1.50), 1.09 (0.89-1.34), and 1.18 (1.03-1.35) in men and 1.60 (1.03-2.48), 1.05 (0.78-1.42), and 1.18 (0.93-1.51) in women, respectively, after additional adjustment for fasting insulin in a subgroup of individuals.In individuals with both FPG and 2-h plasma glucose within the normoglycemic range, high 2-h plasma glucose was associated with insulin resistance and increased CVD mortality.
Optimizing the size variation threshold for the CT evaluation of response in metastatic renal cell carcinoma treated with sunitinib
Authors: R. Thiam, L.S. Fournier, L. Trinquart, J. Medioni, G. Chatellier, D. Balvay, B. Escudier, C. Dromain, C.A. Cuenod, S. Oudard
Journal: Annals of Oncology (2009)
Preventing Adverse Events
Authors: Alan M. Berg
Journal: Annals of Internal Medicine (1995)

Letters15 June 1995Preventing Adverse EventsAlan M. BergAlan M. BergSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-122-12-199506150-00021 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:The article by Petersen and colleagues [1] contains several flaws that raise serious doubts about its conclusion. First, internal medicine residents in a competitive academic center were asked to report adverse events that occurred during hospitalization of patients with whom they were familiar. It is only natural that they would tend to report events that occurred during another team's supervision and to minimize any errors committed either by themselves or the team they were supervising. To do otherwise would put themselves at risk for censure, or at least unwelcome attention.Second, working conditions experienced by housestaff during ...REFERENCE1. Petersen LA, Brennan TA, O'Neill AC, Cook EF, Lee TH. Does housestaff discontinuity of care increase the risk for preventable adverse events? Ann Intern Med. 1994; 121:866-72. Google Scholar Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 June 1995Volume 122, Issue 12Page: 962-964KeywordsAcademic medicineAdverse eventsHospitalizationsSuicide Issue Published: 15 June 1995 Copyright & PermissionsCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Optimal Evidence in Difficult Settings: Improving Health Interventions and Decision Making in Disasters
Authors: Martin Gerdin, Mike Clarke, Claire Allen, Bonnix Kayabu, William Summerskill, Declan Devane, Malcolm MacLachlan, Paul Spiegel, Anjan Ghosh, Rony Zachariah, Saurabh Gupta, Virginia Barbour, Virginia Murray, Johan von Schreeb
Journal: PLoS Medicine (2014)

PointsN As for any type of health care, decisions about interventions in the context of natural disasters, conflict, and other major healthcare emergencies must be guided by the best possible evidence.N Disaster health interventions and decision making can benefit from an evidence-based approach.N We outline how systematic reviews and methodologically sound research can build a much-needed evidence base.N We do this from the standpoint of Evidence Aid, an initiative that aims to improve access to evidence on the effects of interventions, actions, and policies before, during, and after disasters and other humanitarian emergencies, so as to improve health-related outcomes.
Failure of aldosterone suppression despite angiotensin-converting enzyme (ACE) inhibitor administration in chronic heart failure is associated with ACE DD genotype
Authors: Mariantonietta Cicoira, Luisa Zanolla, Andrea Rossi, Giorgio Golia, Lorenzo Franceschini, Giulio Cabrini, Alberto Bonizzato, Maristella Graziani, Stefan D Anker, Andrew J.S Coats, Piero Zardini
Journal: Journal of the American College of Cardiology (2001)
Association Between Polymorphism in the Chemokine Receptor CX3CR1 and Coronary Vascular Endothelial Dysfunction and Atherosclerosis
Authors: David H. McDermott, Julian P.J. Halcox, William H. Schenke, Myron A. Waclawiw, Maya N. Merrell, Neal Epstein, Arshed A. Quyyumi, Philip M. Murphy
Journal: Circulation Research (2001)

Fractalkine, a chemokine expressed by inflamed endothelium, induces leukocyte adhesion and migration via the receptor CX3CR1, and the CX3CR1 polymorphism V249I affects receptor expression and function. Here we show that this polymorphism is an independent risk factor for atherosclerotic coronary artery disease (CAD). Genotyping of the CX3CR1-V249I polymorphism was performed in a cohort of 339 white individuals who underwent cardiac catheterization (n=197 with and n=142 without CAD, respectively). In 203 patients, intracoronary acetylcholine 15 microg/min) and sodium nitroprusside (20 microg/min) were administered to test endothelium-dependent and -independent coronary vascular function, respectively. Change in coronary vascular resistance (DeltaCVR) was measured as an index of microvascular dilation. An association was observed between presence of the CX3CR1 I249 allele and reduced prevalence of CAD, independent of established CAD risk factors (odds ratio=0.54 [95% confidence interval, 0.30 to 0.96], P=0.03). Angiographic severity of CAD was also lower in these subjects (P=0.01). Furthermore, endothelium-dependent vasodilation was greater in these individuals compared with individuals homozygous for the CX3CR1-V249 allele (DeltaCVR during acetylcholine = -46+/-3% versus -36+/-3%, respectively, P=0.02), whereas DeltaCVR with sodium nitroprusside was similar in both groups (-55+/-2% versus -53+/-2%, P=0.45). The association between CX3CR1 genotype and endothelial function was independent of established risk factors and presence of CAD by multivariate analysis (P=0.02). Thus, the CX3CR1 I249 allele is associated with decreased risk of CAD and improved endothelium-dependent vasodilation. This suggests that CX3CR1 may be involved in the pathogenesis of CAD.
Higher autoantibody levels and recognition of a linear NH2-terminal epitope in the autoantigen GAD65, distinguish stiff-man syndrome from insulin-dependent diabetes mellitus.
Authors: J Kim, M Namchuk, T Bugawan, Q Fu, M Jaffe, Y Shi, H J Aanstoot, C W Turck, H Erlich, V Lennon, S Baekkeskov
Journal: The Journal of Experimental Medicine (1994)

The smaller form of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD65) is a major autoantigen in two human diseases that affect its principal sites of expression. Thus, destruction of pancreatic beta cells, which results in insulin-dependent diabetes mellitus (IDDM), and impairment of GABA-ergic synaptic transmission in Stiff-Man syndrome (SMS) are both characterized by circulating autoantibodies to GAD65. Anti-GAD65 autoantibodies in IDDM are predominantly directed to conformational epitopes. Here we report the characterization of humoral autoimmune responses to GAD65 in 35 SMS patients, of whom 13 (37%) also had IDDM. All SMS patients immunoprecipitated native GAD65 and the main titers were orders of magnitude higher than in IDDM patients. Furthermore, in contrast to the situation in IDDM, autoantibodies in 35 of 35 (100%) of SMS patients recognized denatured GAD65 on Western blots. Two major patterns of epitope specificity were identified on Western blots. The first pattern, detected in 25 of 35 SMS patients (71%), of whom 11 had IDDM (44%), was predominantly reactive with a linear NH2-terminal epitope residing in the first eight amino acids of GAD65. Nine of nine individuals who were HLA-haplotyped in this group carried an IDDM susceptibility haplotype and HLA-DR3, DQw2 was particularly abundant. The second pattern, detected in 10 of 35 patients (29%) of whom two had IDDM (20%), included reactivity with the NH2-terminal epitope plus strong reactivity with one or more additional epitope(s) residing COOH-terminal to amino acid 101. The second epitope pattern may represent epitope spreading in the GAD65 molecule, but may also include some cases of epitope recognition associated with IDDM resistant HLA-haplotypes. The principal NH2-terminal linear epitope in GAD65 distinguishes the reactivity of SMS and IDDM autoantibodies and may be a determinant of pathogenicity for GABA-ergic neurons. The greater magnitude and distinct specificity of the humoral response to GAD65 in SMS may reflect a biased involvement of the T helper cell type 2 (Th2) subset of CD4+ T cells and antibody responses, whereas IDDM is likely mediated by the Th1 subset of CD4+ T cells and cytotoxic T cell responses.
Annual Report to the Nation on the Status of Cancer, 1975-2011, Featuring Incidence of Breast Cancer Subtypes by Race/Ethnicity, Poverty, and State
Authors: Betsy A. Kohler, Recinda L. Sherman, Nadia Howlader, Ahmedin Jemal, A. Blythe Ryerson, Kevin A. Henry, Francis P. Boscoe, Kathleen A. Cronin, Andrew Lake, Anne-Michelle Noone, S. Jane Henley, Christie R. Eheman, Robert N. Anderson, Lynne Penberthy
Journal: JNCI Journal of the National Cancer Institute (2015)

The American Cancer Society (ACS), Centers for Disease Control and Prevention (CDC), National Cancer Institute (NCI), and North American Association of Central Cancer Registries (NAACCR) collaborate annually to produce updated, national cancer statistics. This Annual Report includes a focus on breast cancer incidence by subtype using new, national-level data.Population-based cancer trends and breast cancer incidence by molecular subtype were calculated. Breast cancer subtypes were classified using tumor biomarkers for hormone receptor (HR) and human growth factor-neu receptor (HER2) expression.Overall cancer incidence decreased for men by 1.8% annually from 2007 to 2011 [corrected]. Rates for women were stable from 1998 to 2011. Within these trends there was racial/ethnic variation, and some sites have increasing rates. Among children, incidence rates continued to increase by 0.8% per year over the past decade while, like adults, mortality declined. HR+/HER2- breast cancers, the subtype with the best prognosis, were the most common for all races/ethnicities with highest rates among non-Hispanic white women, local stage cases, and low poverty areas (92.7, 63.51, and 98.69 per 100000 non-Hispanic white women, respectively). HR+/HER2- breast cancer incidence rates were strongly, positively correlated with mammography use, particularly for non-Hispanic white women (Pearson 0.57, two-sided P < .001). Triple-negative breast cancers, the subtype with the worst prognosis, were highest among non-Hispanic black women (27.2 per 100000 non-Hispanic black women), which is reflected in high rates in southeastern states.Progress continues in reducing the burden of cancer in the United States. There are unique racial/ethnic-specific incidence patterns for breast cancer subtypes; likely because of both biologic and social risk factors, including variation in mammography use. Breast cancer subtype analysis confirms the capacity of cancer registries to adjust national collection standards to produce clinically relevant data based on evolving medical knowledge.
P06.09 * LONG TERM VISUAL OUTCOME AFTER RADIOSURGERY IN 97 PATIENTS AFFECTED BY ANTERIOR SKULL BASE BENIGN MENINGIOMAS
Authors: M. Marchetti, L. Schembri, S. Bianchi, V. Pinzi, I. Milanesi, L. Fumagalli, P. Ciasca, A. Bergantin, F. Di Meco, L. Fariselli
Journal: Neuro-Oncology (2014)

INTRODUCTION. The concern about radiation induced optic neuropathy (RION) strongly characterized the recent past. This has probably been the main limit to a wider diffusion of radiotherapy and radiosurgery as treatment of meningiomas involving the anterior optic pathways. In spite of this consideration, during the last few years the radiotherapy activity for such lesions is continuously increasing. The aim of the present study is to define the risk of RION on a medium to long term follow-up period in a large series of patients treated by radiosurgery. The efficacy of the treatment is also investigated. MATERIALS AND METHODS: The visual outcome of 97 patients which underwent radiosurgery due to a meningioma involving the anterior optic pathways has been retrospectively evaluated. Patients with a minimum follow-up period longer than 12 months were included. Sixteen patients had a single session radiosurgery (sSRS) with a mean dose of 12 Gy (range 8-13 Gy; median 13 Gy). In these cases the mean tumour volume was 4,9 cc (range 0,3-10,5 cc; median 3.6 cc) Eighty-one patients underwent a multi-session radiosurgery (mSRS). The mean prescription dose was 24 Gy (range 15-30Gy; median 25Gy), the mean tumour volume was 9,5 cc (range 0,5-65 cc; median 6,5 cc) The visual outcome was evaluated in all cases. All the included patients had at least a pre-treatment and a last follow-up visual function assessment. Furthermore local control has been analyzed. RESULTS: The mean follow-up is 43 months (range 12-96 months; 56 patients f-up ≥ 36 monts; 23 patients f-up ≥ 60 months) Compared to the baseline the visual function improved in 24 patients (24 %) and was unchanged in 65 (68 %). Seven patients worsened 8 (8 %). Three out of these experienced a tumour progression. Only two patients with no progression disease developed a “de novo” visual deficit. At the analysis time, the overall local control was 94 %. Eighteen lesions (18%) showed a partial shrinkage, seventy-three (72%) were stable and 6 patients (6%) experienced a progression of the disease. When observed, the tumour progression always occurred later than 36 months post-treatment. CONCLUSIONS: The study confirms the low risk of radiation induced optic neuropathy both in case of sSRS and mSRS. Multisession radiosurgery makes also the larger lesions manageable. The high local control rate and the low toxicity suggest that radiosurgery could be proposed also as a primary treatment.