tbuckley/cabot-search huggingface dataset:
Methodologic Guidelines for Review Papers
Authors: D. L. Weed
Journal: JNCI Journal of the National Cancer Institute (1997)

Reading a good review paper is one of the most efficient ways of becoming familiar with state-of-the-art research and practice on any topic in cancer biology, epidemiology, prevention, or treatment.Yet, what constitutes a good review?It must be clearly organized, recently written by a knowledgeable (expert) scientist, and describe a topic appropriate to the general readership of the Journal of the National Cancer Institute.A 10-year methodologic discussion, however, suggests that there is more to the quality of reviews than judgments about writing style, author's expertise, and choice of topic (1-18).Review papers are sources of scientific information and should be read (and written) with specific methodologic considerations in mind.The purpose of this editorial is to propose a set of guidelines for reviews submitted to the Journal, a general oncology journal. BackgroundMethodologic guidelines for review papers (and the related issue of quality) have been discussed in several journals, including in alphabetical order:
Relapse-Free Survival (Rfs) As a Surrogate Endpoint for Overall Survival (Os) in Adjuvant Interferon Trials in Patients (Pts) with Resectable Cutaneous Melanoma: an Individual Patient Data (Ipd) Meta-Analysis
Authors: S. Suciu, A.M.M. Eggermont, P. Lorigan, J. Kirkwood, S. Markovic, C. Garbe, D. Cameron, S. Kotapati, C. Konto, T. Chen, K. Wheatley, N. Ives, G. De Schaetzen, A. Efendi, M. Buyse
Journal: Annals of Oncology (2014)
Dose–Response Relationship of Prenatal Mercury Exposure and IQ: An Integrative Analysis of Epidemiologic Data
Authors: Daniel A. Axelrad, David C. Bellinger, Louise M. Ryan, Tracey J. Woodruff
Journal: Environmental Health Perspectives (2007)

Prenatal exposure to mercury has been associated with adverse childhood neurologic outcomes in epidemiologic studies. Dose-response information for this relationship is useful for estimating benefits of reduced mercury exposure.We estimated a dose-response relationship between maternal mercury body burden and subsequent childhood decrements in intelligence quotient (IQ), using a Bayesian hierarchical model to integrate data from three epidemiologic studies.Inputs to the model consist of dose-response coefficients from studies conducted in the Faroe Islands, New Zealand, and the Seychelles Islands. IQ coefficients were available from previous work for the latter two studies, and a coefficient for the Faroe Islands study was estimated from three IQ subtests. Other tests of cognition/achievement were included in the hierarchical model to obtain more accurate estimates of study-to-study and end point-to-end point variability.We find a central estimate of -0.18 IQ points (95% confidence interval, -0.378 to -0.009) for each parts per million increase of maternal hair mercury, similar to the estimates for both the Faroe Islands and Seychelles studies, and lower in magnitude than the estimate for the New Zealand study. Sensitivity analyses produce similar results, with the IQ coefficient central estimate ranging from -0.13 to -0.25.IQ is a useful end point for estimating neurodevelopmental effects, but may not fully represent cognitive deficits associated with mercury exposure, and does not represent deficits related to attention and motor skills. Nevertheless, the integrated IQ coefficient provides a more robust description of the dose-response relationship for prenatal mercury exposure and cognitive functioning than results of any single study.
Pak1 Kinase Links ErbB2 to β-Catenin in Transformation of Breast Epithelial Cells
Authors: Luis E. Arias-Romero, Olga Villamar-Cruz, Min Huang, Klaus P. Hoeflich, Jonathan Chernoff
Journal: Cancer Research (2013)

Abstract p21-Activated kinase-1 (Pak1) is frequently upregulated in human breast cancer and is required for transformation of mammary epithelial cells by ErbB2. Here, we show that loss of Pak1, but not the closely related Pak2, leads to diminished expression of β-catenin and its target genes. In MMTV-ErbB2 transgenic mice, loss of Pak1 prolonged survival, and mammary tissues of such mice showed loss of β-catenin. Expression of a β-catenin mutant bearing a phospho-mimetic mutation at Ser 675, a specific Pak1 phosphorylation site, restored transformation to ErbB2-positive, Pak1-deficient mammary epithelial cells. Mice bearing xenografts of ErbB2-positive breast cancer cells showed tumor regression when treated with small-molecule inhibitors of Pak or β-catenin, and combined inhibition by both agents was synergistic. These data delineate a signaling pathway from ErbB2 to Pak to β-catenin that is required for efficient transformation of mammary epithelial cells, and suggest new therapeutic strategies in ErbB2-positive breast cancer. Cancer Res; 73(12); 3671–82. ©2013 AACR.
Reduced oxygen uptake efficiency slope in patients with cardiac sarcoidosis
Authors: Wilhelm Ammenwerth, Mark A. Klemens, Catharina Crolow, Nicolas Schönfeld, Roland C. Bittner, Jeanette Schulz-Menger, Torsten T. Bauer
Journal: European Respiratory Journal (2012)

Background: The non-invasive diagnosis of cardiac sarcoidosis (CS) is difficult. Cardiovascular magnetic resonance (CMR) has become a very valuable diagnostic tool in patients with suspected CS, but usually a combination of different tests is used. Oxygen uptake efficiency slope (OUES) is a parameter of cardiopulmonary exercise testing (CPET), which is used as an indicator for cardiovascular impairment. We investigated the predictive value of OUES for the diagnosis of myocardial involvement in sarcoid patients.

Methods: Retrospectively 37 consecutive patients (44.9 ± 13.8 years) with histologically confirmed sarcoidosis and clinical suspicion of heart involvement underwent noninvasive diagnostic testing including CMR. CS was diagnosed according to the guidelines from the Japanese Society of Sarcoidosis and other Granulomatous Disorders with additional consideration of CMR findings. Furthermore, CPET with calculation of predicted OUES according to equations by Hollenberg et al. was carried out.

Results: Patients with CS (11/37; 30%) had a worse cardiovascular response to exercise. OUES was significantly lower in CS-group compared to non-CS-group (59.3 ± 19.1 vs 88.0 ± 15.4 %pred., p < 0.0001). ROC curve method identified 70 %pred. as the OUES cut-off point, which maximized sensitivity and specificity for detection of CS (96% sensitivity, 82% specificity, 89% overall accuracy). OUES < 70 %pred. was the single best predictor of CS (OR: 67, 95% CI: 6.05 to 734.27, p < 0.001) even in multivariate analyses.

Conclusion: Cardiac involvement of sarcoidosis can be predicted by CPET using OUES. Patient selection for CMR can probably be guided by CPET findings in patients with sarcoidosis.
1029-184 The clinical significance of a common, functional, X-linked angiotensin II type 2-receptor gene polymorphism (-1322 G/A) in a cohort of 509 families with premature coronary artery disease
Authors: Khaled Alfakih, Richard Lawrance, Azhar Maqbool, Kevin Walters, Stephen Ball, Anthony Balmforth, Alistair Hall
Journal: Journal of the American College of Cardiology (2004)
Multiple forms of gastroenteropancreatic hormones.
Authors: G B Irvine, R F Murphy
Journal: Gut (1981)

Progress reportMultiple forms of gastroenteropancreatic hormones The isolation and characterisation of many hormones has been facilitated by their secretion from and localisation in specific endocrine glands.Although it is now well established that the gut and pancreas produce a large number of polypeptide hormones, these organs form a diffuse system in which different types of endocrine cells are interspersed among a pre- dominance of non-endocrine tissue.This arrangement, while ideal for regulating the digestion of a varied diet as it transverses the length of the gastrointestinal tract, makes it difficult to isolate the tiny quantities of polypeptide hormones, typically present at concentrations of 100 pmol/g wet weight of tissue.In addition, whereas most endocrine glands can be extirpated and the resulting physiological changes observed, the diffuse anatomical location of endocrine cells in the gut precludes this approach.Consequently, the biological effects of some gut hormones remain uncertain.Traditionally, physiological effects have been used to monitor hormones during their purification.The classical gut hormones gastrin, secretin, and cholecystokinin were characterised after identification of a biological ac- tivity and isolation of the active component by fractionations in which the biological effect was used to assay each fraction.Complications in the interpretation of bioassays can arise, however, when different hormones have a common biological activity.Gastric inhibitory polypeptide, secretin, and glucagon, for example, have insulin-releasing activities and their immu- noreactivities can be detected in the same region of the gut.The advent of radioimmunoassay' some 20 years ago heralded an era of realisation that peptide hormones are present in the circulation and in their tissues of origin in a variety of molecular forms.Consequently, it may be difficult to assign hormonal status to just one of these forms.Normally, this would accrue to the most abundant and most active form present in the circulation.Such a definition may be simplistic, however, as in the case with gastrin, where the 17 amino acid peptide (G-1 7), although present in lower concentration than the 34 amino acid form (G-34), accounts for most of the postprandial circulating gastrin activity in man because of its greater potency.2In contrast, G-34 is not released into the circulation in the cat even though it is detectable in extracts of feline antral mucosa.3When immunoreactive peptides smaller than the active hormone are detected in the circulation they are usually regarded as degradation products.These forms, however, may also be biologically active as is again illustrated by gastrin; the 14 amino acid form (G-14) is nearly as potent as G-17 but is present in much lower amounts.4Indeed, the smallest peptide which exhibits gastrin activity is the tetrapeptide amide that constitutes the C-terminus of both gastrin and 1048on July 14,
Melatonin: a novel protective agent against oxidative injury of the ischemic/reperfused heart
Authors: R REITER, D TAN
Journal: Cardiovascular Research (2003)

This brief review summarizes the recently obtained evidence which illustrates the beneficial effects of the endogenously produced antioxidant, melatonin, in reducing tissue damage and reversing cardiac pathophysiology in models of experimental ischemia/reperfusion. The report also describes the actions of other antioxidants, especially vitamin E and antioxidative enzymes, in altering the degree of ischemia/reperfusion damage in the heart. Based on the data available, melatonin seems to have advantages over other antioxidants tested in terms of ameliorating the hypoxia and reoxygenation-induced damage. While the bulk of the studies that have used melatonin to overcome cardiac injury following transient arterial occlusion and subsequent reperfusion have used pharmacological doses to achieve protection, two recent reports have further shown that merely reducing endogenous circulating concentrations of melatonin (by surgical removal of a source of melatonin, i.e. the pineal gland) exaggerates the degree of injury and reduces survival of animals as a result of induced ischemia/reperfusion of the heart. These findings are consistent with observations in other organs where the loss of physiological concentrations of melatonin results in increased oxidative damage during hypoxia and reoxygenation. These findings have implications for the elderly since in the aged endogenous levels of melatonin are naturally reduced thereby possibly predisposing them to more severe cardiac damage during a heart attack. To date, the bulk of the studies relating to the protective actions of melatonin in reducing cardiac ischemia/reperfusion injury have used the rat as the experimental model. Considering the high efficacy of melatonin in limiting ischemia/reperfusion damage as well as melatonin's low toxicity, the studies should be expanded to include other species and models of cardiac ischemia/reperfusion. The results of these investigations would help to clarify the potential importance of the use of melatonin in situations of oxidative damage to the heart in humans.
Patterns of failure in a randomized trial of adjuvant chemotherapy in postmenopausal patients with early breast cancer treated with tamoxifen
Authors: R. Arriagada, M. Spielmann, S. Koscielny, T. Le Chevalier, T. Delozier, M. Ducourtieux, T. Tursz, C. Hill
Journal: Annals of Oncology (2002)
STUDIES ON THE PATHOGENESIS OF ACUTE INFLAMMATION
Authors: Fred Allison, Margie G. Lancaster
Journal: The Journal of Experimental Medicine (1960)

The relation of intravascular fibrin to the leucocytic sticking reaction in ear chambers of rabbits injured by heat was investigated in two ways. First, attempts were made to destroy the thin layer of fibrin believed to coat the surfaces of cells involved in the sticking reaction. Second, white cell sticking was studied after fibrinogen had been removed from the blood stream. The results of these experiments were as follows:- 1. Activation of fibrinolysin in vivo by streptokinase did not impair sticking of white blood cells. 2. Administration of streptokinase parenterally did not lower fibrinogen blood levels appreciably even when the amount used was large. 3. Thromboplastin infusions alone reduced circulating fibrinogen to low levels but leucocytic sticking was not prevented. Furthermore, frequent death of animals due to pulmonary embolism made such experiments prohibitive. 4. Addition of streptokinase to thromboplastin infusions protected against embolic deaths but did not influence sticking even though the fibrinogen levels achieved were quite low. 5. Finally, when thrombin was added to infusions of thromboplastin and streptokinase, no circulating fibrinogen could be detected. Under such circumstances leucocytic sticking following heat injury occurred without reduction. These findings were interpreted as evidence against a primary role of the blood clotting mechanism in causing the sticking of white blood cells to injured endothelium. Alternative explanations were discussed.
Cost-effectiveness of Prostate Cancer Screening: A Simulation Study Based on ERSPC Data
Authors: E. A. M. Heijnsdijk, T. M. de Carvalho, A. Auvinen, M. Zappa, V. Nelen, M. Kwiatkowski, A. Villers, A. Páez, S. M. Moss, T. L. J. Tammela, F. Recker, L. Denis, S.V. Carlsson, E. M. Wever, C. H. Bangma, F. H. Schröder, M. J. Roobol, J. Hugosson, H. J. de Koning
Journal: JNCI Journal of the National Cancer Institute (2014)

The results of the European Randomized Study of Screening for Prostate Cancer (ERSPC) trial showed a statistically significant 29% prostate cancer mortality reduction for the men screened in the intervention arm and a 23% negative impact on the life-years gained because of quality of life. However, alternative prostate-specific antigen (PSA) screening strategies for the population may exist, optimizing the effects on mortality reduction, quality of life, overdiagnosis, and costs.Based on data of the ERSPC trial, we predicted the numbers of prostate cancers diagnosed, prostate cancer deaths averted, life-years and quality-adjusted life-years (QALY) gained, and cost-effectiveness of 68 screening strategies starting at age 55 years, with a PSA threshold of 3, using microsimulation modeling. The screening strategies varied by age to stop screening and screening interval (one to 14 years or once in a lifetime screens), and therefore number of tests.Screening at short intervals of three years or less was more cost-effective than using longer intervals. Screening at ages 55 to 59 years with two-year intervals had an incremental cost-effectiveness ratio of $73000 per QALY gained and was considered optimal. With this strategy, lifetime prostate cancer mortality reduction was predicted as 13%, and 33% of the screen-detected cancers were overdiagnosed. When better quality of life for the post-treatment period could be achieved, an older age of 65 to 72 years for ending screening was obtained.Prostate cancer screening can be cost-effective when it is limited to two or three screens between ages 55 to 59 years. Screening above age 63 years is less cost-effective because of loss of QALYs because of overdiagnosis.
Frequency of venous thromboembolism in low to moderate risk long distance air travellers: the New Zealand Air Traveller's Thrombosis (NZATT) study
Authors: RJ Hughes, RJ Hopkins, S Hill, M Weatherall, N Van de Water, M Nowitz, D Milne, J Ayling, M Wilsher, R Beasley
Journal: The Lancet (2003)
Experimental Autoimmune Encephalomyelitis Induction in Genetically B Cell–deficient Mice
Authors: Susan D. Wolf, Bonnie N. Dittel, Fridrika Hardardottir, Charles A. Janeway
Journal: The Journal of Experimental Medicine (1996)

Experimental autoimmune encephalomyelitis (EAE) is an animal model for autoimmune central nervous system disease mediated by CD4 T cells. To examine the role of B cells in the induction of EAE, we used B10.PL (I-Au) mice rendered deficient in B cells by deletion of their μ chain transmembrane region (B10.PLμMT). By immunizing B10.PL and B10.PLμMT mice with the NH-terminal myelin basic protein encephalitogenic peptide Ac1-11, we observed no difference in the onset or severity of disease in the absence of mature B cells. There was, however, a greater variation in disease onset, severity, and especially of recovery in the B cell–deficient mice compared to controls. B10.PLμMT mice rarely returned to normal in the absence of B cells. Taken together, our data suggest that B cells do not play a role in the activation of encephalitogenic T cells, but may contribute to the immune modulation of acute EAE. The mechanisms to explain these effects are discussed.
Prognostic value of mechanical efficiency in ambulatory patients with idiopathic dilated cardiomyopathy in sinus rhythm
Authors: I.l Sung Kim, Hideo Izawa, Toshikazu Sobue, Hitoshi Ishihara, Fuji Somura, Takao Nishizawa, Kohzo Nagata, Mitsunori Iwase, Mitsuhiro Yokota
Journal: Journal of the American College of Cardiology (2002)
Proteinase 3 Interacts with a 111-kD Membrane Molecule of Human Umbilical Vein Endothelial Cells
Authors: MIRIAM E. J. TAEKEMA-ROELVINK, CEES VAN KOOTEN, EVERT HEEMSKERK, WILLEKE SCHROEIJERS, MOHAMED R. DAHA
Journal: Journal of the American Society of Nephrology (2000)

Abstract. Proteinase 3 (PR3) is the major autoantigen of antineutrophil cytoplasmic antibodies in Wegener's granulomatosis. Previously, it was demonstrated that PR3 induces apoptosis of human endothelial cells and that PR3 contributes to endothelial cell activation by enhancing interleukin-8 production. The present study demonstrates that PR3 binds specifically to human umbilical vein endothelial cells (HUVEC). Digoxigenin (DIG)-labeled PR3 bound readily to HUVEC cultured on coverslips. By fluorescence-activated cell sorter analysis, a homogeneous binding of PR3 to HUVEC, using either DIG-labeled or unlabeled PR3, was observed. No detectable membrane expression of PR3 was observed after either tumor necrosis factor-α stimulation or in nonstimulated HUVEC. The binding of PR3-DIG to HUVEC was dose-dependent and was inhibited by unlabeled PR3. Scatchard analysis revealed 2000 binding sites per cell, with a K d of 0.1 μM. Affinity precipitation of biotin-labeled HUVEC membrane proteins with protein G-Sepharose bearing PR3 resulted in specific precipitation of a membrane molecule with a molecular weight of 111 kD under nonreducing conditions and 52 and 63 kD under reducing conditions. It is hypothesized that PR3, either released systemically or locally at inflammatory sites following activation of primed polymorphonuclear neutrophils, may lead to endothelial cell injury and activation of endothelial cells.
Variations on a Gene: Rare and Common Variants in <i>ABCA1</i> and Their Impact on HDL Cholesterol Levels and Atherosclerosis
Authors: Liam R. Brunham, Roshni R. Singaraja, Michael R. Hayden
Journal: Annual Review of Nutrition (2006)

Cholesterol and its metabolites play a variety of essential roles in living systems. Virtually all animal cells require cholesterol, which they acquire through synthesis or uptake, but only the liver can degrade cholesterol. The ABCA1 gene product regulates the rate-controlling step in the removal of cellular cholesterol: the efflux of cellular cholesterol and phospholipids to an apolipoprotein acceptor. Mutations in ABCA1, as seen in Tangier disease, result in accumulation of cellular cholesterol, reduced plasma high-density lipoprotein cholesterol, and increased risk for coronary artery disease. To date, more than 100 coding variants have been identified in ABCA1, and these variants result in a broad spectrum of biochemical and clinical phenotypes. Here we review genetic variation in ABCA1 and its critical role in cholesterol metabolism and atherosclerosis in the general population.
Anterior Chordal Transection Impairs Not Only Regional Left Ventricular Function But Also Regional Right Ventricular Function in Mitral Regurgitation
Authors: Thierry Le Tourneau, Daniel Grandmougin, Claude Foucher, Eugene P. McFadden, Pascal de Groote, Alain Prat, Henri Warembourg, Ghislaine Deklunder
Journal: Circulation (2001)

Preservation of annuloventricular continuity through the chordae tendinae aims to maintain left ventricular (LV) function and thus improve postoperative prognosis. This study was designed to prospectively investigate the effect of anterior chordal transection on global and regional LV and right ventricular (RV) function in mitral regurgitation (MR).Sixty-five patients with severe MR underwent radionuclide angiography before and after either mitral valve (MV) repair (42 patients) or replacement with anterior chordal transection (23 patients). LV and RV ejection fractions (EF) were determined at rest. Both ventricles were divided into 9 regions to analyze regional EF and the effect of anteromedial translation related to surgery. After surgery there was a significant decrease in LVEF (P=0.038) and an increase in RVEF (P=0.036). However, LVEF did not change after MV repair (63.8+/-9.9% to 62.6+/-10.3%), whereas RVEF improved (40.7+/-10.1% to 44.5+/-8.1%, P=0.027). In contrast, LVEF decreased after MV replacement (61.7+/-10.1% to 57.2+/-9.9%, P=0.03), and RVEF was unchanged (40.9+/-10.9% to 41.3+/-9.1%). LVEF 4 and 5, in the area of anterior papillary muscle insertion, were impaired after MV replacement compared with MV repair (region 4, 77.6+/-16.7% versus 87.7+/-10.8%, P=0.005, and region 5, 73.9+/-19.3% versus 89.9+/-13.1%, P<0.001). Moreover, anterior chordal transection led to a significant impairment in the apicoseptal region of the RV (RVEF 4, 50.3+/-15.6% versus 59.3+/-13.8%, P=0.02).Anterior chordal transection during MV replacement for MR impairs not only regional LV function but also regional RV function.