tbuckley/cabot-search huggingface dataset:
When will we treat physical activity as a legitimate medical therapy…even though it does not come in a pill?
Authors: Timothy S Church, Steven N Blair
Journal: British Journal of Sports Medicine (2008)

A recent highly publicised report claimed that an exercise pill has been discovered.1 A mystical substance was found to increase endurance in mice without exercise training. By the way, this is not the first time such an observation has been made. Nonetheless, it was widely reported that this may be the end of the need to get off the couch and soon all the benefits of exercise will be delivered by a pill. Sound too good to be true? It probably is, as mimicking the multiple health benefits of exercise with a pill would be the equivalent of creating a cancer-free cigarette. If exercise could be put in a pill form, the world as we know it would be radically changed forever, with healthcare and financial implications too large to quantify. We would have a new powerful therapeutic option for the prevention and treatment of cardiovascular disease (CVD), diabetes, dementia, osteoporosis, depression, old age, certain types of cancer and many other ailments, some of which are not typically considered “exercise related”.2

In 2007 the Milken Institute, estimated that the top seven chronic diseases which include CVD, cancer, diabetes, mental disorders and lung disease are estimated to cost the US$1.3 billion annually; with the shift in age of the population this cost is expected to increase dramatically in coming years.3 If exercise came in a pill we could dramatically reduce the prevalence as well as the morbidity and mortality associated with these conditions creating a much healthier, happier and more productive world. Many doctors would be out of work and hospitals would have to be downsized. But creating an exercise pill is no easy task; and as indicated by the list above, the pill would have to simultaneously benefit numerous complex physiological systems, not just improve exercise capacity …
Who funded excellence articles in smoking? Comparison of the overall articles with Spanish articles
Authors: José Ignacio de Granda-Orive, Adolfo Alonso-Arroyo, Francisco Garcia-Rio, Segismundo Solano-Reina, Carlos Andrés Jiménez-Ruiz, Javier Jareño-Esteban, Rafael Aleixandre-Benavent
Journal: European Respiratory Journal (2013)

Objetive: Analyze the funding received by those excellence articles (Global and Spanish) about smoking (2009 to 2011) through Science Citation Index (SCI). Method : Bibliographic search was conducted in SCI-E and in SSCI-E on February 16, 2013, (2009 to 2011). We selected “articles” that had the index h of the overall sample of strategy (number of articles that have at least that number of citations). We have used “smok*” OR “tobac*” as descriptors. Descriptive. Results : Of overall articles, 3,227 were recovered in 2009, of which 37 were at least 37 citations. In 2010 were 3,324 articles (26), and in 2011 were 3,374 (13). About Spanish articles; 98 (16) in 2009, 109 (14) in 2010, and 109 (7) in 2011. We have found more that one financial entity in 63% of the overall articles by and 78.37% in Spanish articles.

View this table:

Entities that have funded excellence smoking articles





Conclusions : 80% of the global articles and the 89.19% of the Spanish have received funding, this articles received more than one funding both overall and Spanish articles. No differences found between the finance to Spanish articles and global.
Cardiac outflow tract malformations in chick embryos exposed to homocysteine
Authors: M BOOT, R STEEGERSTHEUNISSEN, R POELMANN, L VANIPEREN, A GITTENBERGERDEGROOT
Journal: Cardiovascular Research (2004)

Increased homocysteine concentrations have been associated with cardiac outflow tract defects. It has been hypothesized that cardiac neural crest cells were the target cells in these malformations. Cardiac neural crest cells migrate from the neural tube and contribute to the condensed mesenchyme of the aorticopulmonary septum and outflow tract cushions of the heart. The aim of this study is to investigate the effects of homocysteine on cardiac neural crest cells in relation to heart malformations.Homocysteine was injected either into the neural tube lumen (30 micromol/l), or into the circulatory system (30 or 300 micromol/l) of chick embryos. LacZ-retroviral labeling was used to study cardiac neural crest cell migratory pathways after exposure to homocysteine.Cardiac neural crest cells contributed to the aorticopulmonary septum of both control and homocysteine-treated embryos. However, the outflow tract of homocysteine-neural tube injected embryos displayed 60% less apoptosis and 25% reduced myocardialization. A subarterial ventricular septal defect was observed in 83% of the embryos. None of these abnormalities were observed in homcysteine-circulatory system injected embryos.This study demonstrates that homocysteine disturbs apoptosis and myocardialization of the outflow tract, probably by affecting the cardiac neural crest cells.
Epirubicin, oxaliplatin, and capecitabine with or without panitumumab for patients with previously untreated advanced oesophagogastric cancer (REAL3): a randomised, open-label phase 3 trial
Authors: Tom Waddell, Ian Chau, David Cunningham, David Gonzalez, Alicia Frances Clare Okines, Andrew Wotherspoon, Claire Saffery, Gary Middleton, Jonathan Wadsley, David Ferry, Wasat Mansoor, Tom Crosby, Fareeda Coxon, David Smith, Justin Waters, Timothy Iveson, Stephen Falk, Sarah Slater, Clare Peckitt, Yolanda Barbachano
Journal: The Lancet Oncology (2013)
Letter to the editor: Treatment of thrombotic thrombocytopenic purpura using vincristine and factor VIII plasma free
Authors: José Luis Delgado‐Lamas, Fernando Romero‐García, José Rodriguez‐Carrillo
Journal: American Journal of Hematology (1991)

Thrombocytopenic Purpura Using Vincristine and Factor Vlll Plasma FreeWe read with interest the recent reports about TTP treatment, of Byrnes et al. [ 11 and Welborn et al. [2].We would like to comment our experience on this subject.Taking the best approaches of two papers above mentioned, we proposed using only vinca alkaloids in weekly infusion and factor VIII plasma free.During the past 3 years, we have seen four patients with TTP with a severity score above 6 points [3].As we do not have facilities to perform plasmapheresis, we have treated these patients basically with high doses of intravenous steroids, transfusion support with red cells and platelets, weekly infusion of vincristine during two hours for six times and factor VIII plasma free.Two patients were splenectomized.All patients received the medical treatment described.They have remained well and alive up to this communication, without clinical or laboratory evidence of disease activity during 36, 32, 12, and 2 months, respectively.We suggest that is possible to treat this catastrophic disease more specifically, because today knowing that the factor VIII-VW plasma free contain substances that transform the unusually large polymers of VW factors to small polymers, although the original event of generalized vasculitis remain unknown [4].
Non-HDL Cholesterol Is Less Informative Than the Total-to-HDL Cholesterol Ratio in Predicting Cardiovascular Risk in Type 2 Diabetes
Authors: Rury R. Holman, Ruth L. Coleman, Brian S.F. Shine, Richard J. Stevens
Journal: Diabetes Care (2005)

It has been suggested by some authors that non-HDL cholesterol, defined as total cholesterol minus HDL cholesterol, may be a particularly useful predictor of cardiovascular risk (1) and easier to calculate than the commonly used total-to-HDL cholesterol ratio. We have examined whether the U.K. Prospective Diabetes Study (UKPDS) Risk Engine (2), a coronary heart disease (CHD) risk calculator developed specifically for type 2 diabetes that uses the total-to-HDL cholesterol ratio, could be improved by substituting non-HDL cholesterol.

The UKPDS Risk Engine encapsulates a parametric model to estimate the risk of CHD, defined as myocardial infarction or sudden cardiac death, derived from the UKPDS, with 53,000 patient-years of follow-up data (3). For this analysis, 4,540 of the 5,102 UKPDS patients were included, for whom sufficient data were available and whose characteristics have been previously reported (2). Briefly, the UKPDS recruited patients with newly diagnosed type 2 diabetes but no recent myocardial infarction or stroke. They were mean age 53 years (range 25–65), 58% male, 83% white-Caucasian, 10% Indian-Asian, 8% Afro-Caribbean, and 30% were smokers at study entry. Mean (±SD) HbA1c, 1–2 years after study entry, was 6.7 ± 1.4%, systolic blood pressure was 136 ± 20 mmHg, total cholesterol was 5.4 ± 1.0 mmol/l, and HDL cholesterol was …
Asthma and airway hyperresponsiveness among Belgian conscripts, 1978-91.
Authors: P Dubois, E Degrave, O Vandenplas
Journal: Thorax (1998)

Although there is convincing evidence that the prevalence of asthma among children has increased over the last three decades, it remains uncertain whether such an upward trend has occurred in adults. The aim of this study was to assess whether the prevalence of asthma has changed in young Belgian adults in recent years.A retrospective analysis was conducted of available statistics from the Belgian Armed Forces for the period 1978-91 because conscripts who reported a history of past or current asthma at call-up examination underwent standardised assessment of non-specific airway responsiveness by military chest physicians. Exemption from military service due to asthma was strictly based on the objective evidence of airway hyperresponsiveness.A mean of 48,331 conscripts aged 17-31 years were examined annually from 1978 to 1991. The prevalence of reported asthma rose from 2.4% in 1978 to 7.2% in 1991, while the proportion of asthmatics with airway hyperresponsiveness remained little changed at 48.4% in 1978 and 51.4% in 1991.The observed increase in prevalence of reported asthma was not accompanied by a decrease in the proportion of conscripts with objectively measured airway hyperresponsiveness. These observations provide supporting evidence that the increase in asthma symptoms was not simply due to reporting bias.
Effect of lipid-lowering therapy on early mortality after acute coronary syndromes: an observational study
Authors: Herbert D Aronow, Eric J Topol, Matthew T Roe, Penny L Houghtaling, Katherine E Wolski, A Michael Lincoff, Robert A Harrington, Robert M Califf, E Magnus Ohman, Neal S Kleiman, Matyas Keltai, Robert G Wilcox, Alec Vahanian, Paul W Armstrong, Michael S Lauer
Journal: The Lancet (2001)
Long term duration of protective effect for HPV negative women: follow-up of primary HPV screening randomised controlled trial
Authors: K. M. Elfstrom, V. Smelov, A. L. V. Johansson, C. Eklund, P. Naucler, L. Arnheim-Dahlstrom, J. Dillner
Journal: BMJ (2014)

<b>Objectives</b> To assess whether the increased sensitivity of screening for human papillomavirus (HPV) may represent overdiagnosis and to compare the long term duration of protective effect against cervical intraepithelial neoplasia grade 2 or worse (CIN2+) in HPV based and cytology based screening. <b>Design</b> 13 year follow-up of the Swedescreen randomised controlled trial of primary HPV screening. <b>Setting</b> Organised cervical screening programme in Sweden. <b>Participants</b> 12 527 women aged 32-38 attending organised screening were enrolled and randomised to HPV and cytology double testing (intervention arm, n=6257) or to cytology only, with samples frozen for future HPV testing (control arm, n=6270). <b>Main outcome measures</b> Cumulative incidence of CIN2+ and CIN3+ (Kaplan Meier curves). Longitudinal test characteristics were calculated for cytology only, HPV testing only, and cytology and HPV testing combined, adjusting for censoring. <b>Results</b> The increased detection of CIN2+ in the intervention arm decreased over time. After six years, the cumulative incidence of CIN3+ was similar in both trial arms, and after 11 years the cumulative incidence of CIN2+ became similar in both arms. The longitudinal sensitivity of cytology for CIN2+ in the control arm at three years was similar to the sensitivity of HPV testing in the intervention arm at five years of follow-up: 85.94% (95% confidence interval 76.85% to 91.84%) <i>v</i> 86.40% (79.21% to 91.37%). The sensitivity of HPV screening for CIN3+after five years was 89.34% (80.10% to 94.58%) and for cytology after three years was 92.02% (80.59% to 96.97%). <b>Conclusions</b> Over long term follow-up, the cumulative incidence of CIN2+ was the same for HPV screening and for cytology, implying that the increased sensitivity of HPV screening for CIN2+ reflects earlier detection rather than overdiagnosis. The low long term risks of CIN3+ among women who tested negative in HPV screening, support screening intervals of five years for such women. <b>Trial registration</b> Clinicaltrials.gov NCT00479375.
Lnk Inhibits Tpo–mpl Signaling and Tpo-mediated Megakaryocytopoiesis
Authors: Wei Tong, Harvey F. Lodish
Journal: The Journal of Experimental Medicine (2004)

Thrombopoietin (Tpo) is the primary cytokine regulating megakaryocyte development and platelet production. Tpo signaling through its receptor, c-mpl, activates multiple pathways including signal transducer and activator of transcription (STAT)3, STAT5, phosphoinositide 3-kinase–Akt, and p42/44 mitogen-activated protein kinase (MAPK). The adaptor protein Lnk is implicated in cytokine receptor and immunoreceptor signaling. Here, we show that Lnk overexpression negatively regulates Tpo-mediated cell proliferation and endomitosis in hematopoietic cell lines and primary hematopoietic cells. Lnk attenuates Tpo-induced S-phase progression in 32D cells expressing mpl, and Lnk decreases Tpo-dependent megakaryocyte growth in bone marrow (BM)–derived megakaryocyte culture. Consistent with this result, we found that in both BM and spleen, Lnk-deficient mice exhibited increased numbers of megakaryocytes with increased ploidy compared with wild-type mice. In addition, Lnk-deficient megakaryocytes derived from BM and spleen showed enhanced sensitivity to Tpo during culture. The absence of Lnk caused enhanced and prolonged Tpo induction of STAT3, STAT5, Akt, and MAPK signaling pathways in CD41+ megakaryocytes. Furthermore, the Src homology 2 domain of Lnk is essential for Lnk's inhibitory function. In contrast, the conserved tyrosine near the COOH terminus is dispensable and the pleckstrin homology domain of Lnk contributes to, but is not essential for, inhibiting Tpo-dependent 32D cell growth or megakaryocyte development. Thus, Lnk negatively modulates mpl signaling pathways and is important for Tpo-mediated megakaryocytopoiesis in vivo.
Cold water immersion and recovery from strenuous exercise: a meta-analysis
Authors: Jonathan Leeder, Conor Gissane, Ken van Someren, Warren Gregson, Glyn Howatson
Journal: British Journal of Sports Medicine (2011)

Elite-level athletic training and competition is accompanied by the recovery of a series of physiological stressors. The physiological stress will vary considerably depending upon the specific exercise type, duration and intensity and also on the athletes' familiarisation to the exercise insult. It is well documented that when the exercise stress incorporates a novel eccentric component or the exercise is of considerable intensity or duration,1 athletes will likely experience numerous signs and symptoms of fatigue and cellular disturbance that have the potential to reduce performance.

Physiological stress induced by intense exercise is associated with energy substrate depletion, hyperthermia, mechanical muscle damage, oxidative stress, inflammation and nervous system fatigue. The resulting symptoms manifest as reduced performance potential, likely due to increased muscle soreness and decreased muscle function,2 disturbed muscle position sense and reaction time3 as well as increased stiffness and swelling that can last for several days.4 The aetiology of reduced performance potential will vary depending upon the exact physiological stress being recovered from. For example, eccentric exercise is associated with a large mechanical stress and relatively low metabolic cost,5 whereas intermittent sprint exercise may involve both a large mechanical stress and a heightened metabolic cost.6 It is possible that the underlying time course of recovery between different exercise stressors is different, and this consequently may influence how recovery strategies could be implemented. For the purpose of this review, exercise will be subdivided into two categories: ‘eccentric exercise’ that refers to the stress caused from exercise incorporating high mechanical stress (eg, eccentric contractions) and ‘high-intensity exercise’ that refers to stress caused from exercise with a high metabolic cost as well as some elements of eccentric muscle contractions (eg, repeat sprint sports).

Given the potential for physiological stress to compromise training and/or competition performance, there has been …
Oesophageal clearance of small amounts of equal or less than one millilitre of acid.
Authors: R Shaker, P J Kahrilas, W J Dodds, W J Hogan
Journal: Gut (1992)

The oesophageal acid clearance time was evaluated in 10 healthy volunteers of 9small9 boluses of 0.5 and 1 ml and 9minute9 boluses of 0.05 and 0.1 ml 0.1 N HCl, as well as 0.1 and 1 ml 0.01 and 0.001 N HCl. Swallow rate was normalised at q 60 seconds. For 0.1 ml 0.1 N HCl, acid clearance time was also measured for swallow intervals of q 30 and 120 seconds. Acid clearance time to restore pH to 4.0 was significantly longer (p less than 0.01) for the 0.5 and 1 ml 0.1 N HCl (210 and 273 seconds, respectively) than for the 0.05 and 0.01 ml acid boluses (83 and 94 seconds, respectively). The minimum acid clearance time was 18 seconds (0.05 ml 0.1 N HCl). Acid clearance time for 0.1 N HCl was less than one minute on only two occasions. The acid clearance times were comparable when the subjects sat upright. A longer interswallow interval--that is, 120 seconds, resulted in a significantly longer acid clearance time than shorter swallow intervals (p less than 0.05). Oesophageal acid clearance time for small acid volumes averaged more than three minutes and for minute acid volumes was generally more than one minute; and acid clearance times were comparable for the supine and upright postures, while gastrooesophageal reflux episodes causing pH drops to 3-4 may last for less than 15 seconds, substantial oesophageal pH drops to less than or equal to 1.5 that persists less than 15 seconds are difficult to be attributed to true gastrooesophageal reflux.
Discussing Prognosis: “How Much Do You Want to Know?” Talking to Patients Who Do Not Want Information or Who Are Ambivalent
Authors: Anthony L. Back, Robert M. Arnold
Journal: Journal of Clinical Oncology (2006)

Dr D had decided to try to ask patients how much they wanted to know about prognosis. Mr X, a 44-year-old man with large B-cell lymphoma, who had relapsed less than 1 year after receiving cyclophosphamide, doxorubicin, vincristine, and prednisone and rituximab, said he did not want to talk about prognosis at all. He said, “The numbers don’t really matter—I have to do what you tell me gives me the best chance.” Mrs Y, a 68-year-old woman with stage III breast cancer coming for her first visit after starting adjuvant chemotherapy, could not seem to decide whether she wanted prognostic information. “I’m worried about knowing, and I’m worried about not knowing,” she said. “What do you think I should do?” A description of a patient-centered approach for discussing prognosis rather than the commonly used strategies of realism, optimism, and avoidance has been published in this issue of the Journal of Clinical Oncology. This approach recommended that oncologists start by asking patients a straightforward opening question, “How much do you want to know about prognosis?” and the approach was illustrated for a patient who was prepared to have an explicit discussion. However, approximately 20% of patients do not want to discuss prognostic information or only want to hear good news. How should an oncologist, like Dr D, handle that situation? This article describes how to approach patients who either do not want to discuss prognostic information or who are ambivalent—who simultaneously want to know and do not want to know.
Epstein - Barr virus - associated Diseases in Allogeneic Hematopoietic Stem Cell Transplantation
Authors: Xiu-li Wu, Qi-fa Liu
Journal: Journal of Hematology & Oncology (2012)

Epstein -Barr virus (EBV) is a gamma -herpes virus that infects more 90% of humans.Most EBV primary infections and reactivations are subclinical and require no therapy in immunocompetent people.However, EBV infection or reactivation may result in life-threatening diseases in immunocompromised people [1][2][3][4][5].EBV infection and reactivation might be associated with a spectrum of clinical presentations ranging from fever to post-transplant lymphoproliferative diseases (PTLD), including viremia, pneumonia, encephalitis/ myelitis, PTLD, and so on, in recipients of allogeneic hematopoietic stem cell transplantation (allo-HSCT), which arise as a consequence of infected B/T lymphocytes, epithelial cells and neural cells, and they are sustained by EBV latency products [2,3,6].EBV-associated PTLD were only the tip of the iceberg of post-transplant EBV-associated diseases [2], but there is short of large sample data about the incidence of EBVassociated other diseases other than PTLD in recipients of transplants.Kinch et al. reported that 7 of 16 patients with EBV-DNA-emia developed EBV-associated diseases in 39 recipients of allo-HSCT, including 3 PTLD, 1 myelitis, 1 encephalitis and 2 reactivations with fever [7].In one of our prospective study, 16 of 64 patients with EBV-DNAemia developed PTLD and 11 patients developed EBVassociated other diseases, including 6 fever, 1 encephalitis, 1 myelitis, 1 pneumonia, 1 encephalitis accompanying pneumonia and 1 enteritis accompanying hepatitis, in 172 recipients of allo-HSCT.The incidence of PTLD in a large study varied from 0.5% to 22% after allo-HSCT, depending on the number of risk factors including T-depleted graft, the use of ATG, unrelated donor, HLA-mismatched,
Comparative Carcinogenicity of &lt;italic&gt;N&lt;/italic&gt;-Isopropyl-α-(2-Methylhydrazino)-&lt;italic&gt;p&lt;/italic&gt;-Toluamide · HCI (Procarbazine Hydrochloride), Its Degradation Products, Other Hydrazines, and Isonicotinic Acid Hydrazide
Authors: M G Kelly, R W O'Gara, S T Yancey, K Gadekar, C Botkin, V T Oliverio
Journal: JNCI Journal of the National Cancer Institute (1969)