tbuckley/cabot-search huggingface dataset:
Strong reciprocity is real, but there is no evidence that uncoordinated costly punishment sustains cooperation in the wild
Authors: Francesco Guala
Journal: Behavioral and Brain Sciences (2012)

Abstract I argue in my target article that field evidence does not support the costly punishment hypothesis. Some commentators object to my reading of the evidence, while others agree that evidence in favour of costly punishment is scant. Most importantly, no rigorous measurement of cost-benefit ratios in the field has been attempted so far. This lack of evidence does not rule out costly punishment as a cause of human cooperation, but it does pre-empt some overconfident claims made in the past. Other commentators have interpreted my article as an anti-experimental pamphlet or as a flat denial of the existence of pro-social motives – which it was not intended to be. While we have enough data to establish the existence (and theoretical relevance) of strong reciprocity motives, I argue in this response that their efficacy (and policy relevance) has not been demonstrated.
Ablation and Mutation of Nonmuscle Myosin Heavy Chain II-B Results in a Defect in Cardiac Myocyte Cytokinesis
Authors: Kazuyo Takeda, Hiroko Kishi, Xuefei Ma, Zu-Xi Yu, Robert S. Adelstein
Journal: Circulation Research (2003)

We have identified a novel form of cardiac myocyte enlargement in nonmuscle myosin heavy chain II-B (NMHC II-B) ablated mice, based on a partial failure in cytokinesis. In contrast to most cells, cardiac myocytes lack NMHC II-A, and ablation of NMHC II-B results in a heart with 70% fewer myocytes at embryonic day 14.5 (E14.5) than control mice (B+/B- and B+/B+). In addition, B-/B- cardiac myocytes show a marked increase in binucleation at E12.5, reflecting the occurrence of karyokinesis in the absence of cytokinesis. An increase in binucleation and cell size is also found in hypomorphic, homozygous mice harboring a single amino acid mutation (R709C) in the gene encoding NMHC II-B. The nonmyocytes in B-/B- hearts and homozygous mutant hearts, all of which contain NMHC II-A, do not show either of these abnormalities. B-/B- cardiac myocytes at E14.5 show a decreased bromodeoxyuridine (BrdU) labeling index compared with controls, consistent with the decrease in myocyte proliferation. This decreased BrdU labeling is not seen in nonmyocyte cells in the heart. In addition to these changes, both B-/B- mice as well as homozygous mutated mice show an increase in cyclin D2 and D3 reflecting an abnormality in earlier steps in the cell cycle. Whereas cardiac myocytes completely ablated for NMHC II-B show enlargement and binucleation, mice expressing as little as 6% of the normal amount of wild-type NMHC II-B in the heart do not show these abnormalities.
Increased levels of cysteinyl-leukotrienes in saliva, induced sputum, urine and blood from patients with aspirin-intolerant asthma
Authors: F Gaber, K Daham, A Higashi, N Higashi, A Gulich, I Delin, A James, M Skedinger, P Gyllfors, M Nord, S-E Dahlen, M Kumlin, B Dahlen
Journal: Thorax (2008)

A diagnosis of aspirin-intolerant asthma requires aspirin provocation in specialist clinics. Urinary leukotriene E(4) (LTE(4)) is increased in aspirin-intolerant asthma. A study was undertaken to investigate new biomarkers of aspirin intolerance by comparing basal levels of cysteinyl-leukotrienes (CysLTs) and leukotriene B(4) (LTB(4)) in saliva, sputum and ex vivo stimulated blood in subjects with aspirin-intolerant and aspirin-tolerant asthma. The effects of aspirin- and allergen-induced bronchoconstriction on leukotriene levels in saliva and ex vivo stimulated blood were also compared with the effects of the provocations on urinary mediators.Induced sputum, saliva, urine and blood were obtained at baseline from 21 subjects with asthma. At a separate visit, 11 subjects showed a positive response to lysine-aspirin inhalation and 10 were aspirin tolerant. Saliva, blood and urine were also collected on the provocation day. Analyses of CysLTs and LTB(4) and the prostaglandin D(2) metabolite 9alpha,11beta-prostaglandin F(2) were performed and the fraction of exhaled nitric oxide was measured.Subjects with aspirin-intolerant asthma had higher exhaled nitric oxide levels and higher baseline levels of CysLTs in saliva, sputum, blood ex vivo and urine than subjects with aspirin-tolerant asthma. There were no differences in LTB(4) levels between the groups. Levels of urinary LTE(4) and 9alpha,11beta-prostaglandin F(2) increased after aspirin provocation whereas leukotriene levels in saliva and ex vivo stimulated blood did not increase.These findings support a global and specific increase in CysLT production in aspirin-intolerant asthma. Measurement of CysLTs in saliva has the potential to be a new and convenient non-invasive biomarker of aspirin-intolerant asthma.
Evidence for association between sarcoidosis and pulmonary embolism from 35-year record linkage study
Authors: A. P. Crawshaw, C. J. Wotton, D. G. R. Yeates, M. J. Goldacre, L.-P. Ho
Journal: Thorax (2010)

In the last year, we have observed large pulmonary embolisms (PEs) in four of 85 patients that attended the Oxford Sarcoidosis Clinic. In addition, we note a few case reports of PEs and unprovoked thrombotic events in patients with sarcoidosis (only one referenced here),1 leading us to question if, compared with normal populations, patients with sarcoidosis have a higher risk of developing PE.

To explore this possibility, we performed a retrospective cohort analysis using data from the well-established Oxford Record Linkage Study.2 This is a database of statistical records, spanning 35 years, of all hospital admissions (including day cases) to National Health Service (NHS) hospitals, and all deaths, regardless of where they occurred, in defined populations within the former Oxfordshire NHS region. The database and methods used for studying disease associations have been described2 and can also be found in the Supplementary data. The sarcoidosis cohort (n=1002) was assembled by identifying admissions during the study period where sarcoidosis was recorded as the principal diagnostic reason for admission. The reference …
Clinical and molecular characterization of diffuse large B-cell lymphomas with 13q14.3 deletion
Authors: M. Mian, M. Scandurra, E. Chigrinova, Y. Shen, G. Inghirami, T.C. Greiner, W.C. Chan, J.M. Vose, M. Testoni, A. Chiappella, L. Baldini, M. Ponzoni, A.J.M. Ferreri, S. Franceschetti, G. Gaidano, S. Montes-Moreno, M.A. Piris, F. Facchetti, A. Tucci, J.Fr. Nomdedeu, T. Lazure, S. Uccella, M.G. Tibiletti, E. Zucca, I. Kwee, F. Bertoni
Journal: Annals of Oncology (2011)
Altered calcium handling in experimental pressure-overload hypertrophy in the ferret.
Authors: J K Gwathmey, J P Morgan
Journal: Circulation Research (1985)

The purpose of this study was to evaluate the relationship between changes in the intracellular handling of free, ionized calcium and the functional alterations that occur in cardiac hypertrophy. We developed a model of right ventricular pressure-overload hypertrophy in the ferret by critical banding of the pulmonary artery; this method produced significant degrees of hypertrophy within 1-3 months of surgery. We removed papillary muscles, 1 mm or less in diameter, from ferrets with cardiac hypertrophy and their age- and weight-matched controls, and loaded them with the bioluminescent calcium indicator, aequorin, in order to record intracellular calcium transients. Compared to the controls, the hypertrophied muscles demonstrated a prolonged duration of isometric contraction but a marked decrease in peak isometric tension development. The increased duration of isometric contraction in the hypertrophied muscles correlated with a similar prolongation of the calcium transient; we interpret this to mean that the rate of sequestration and perhaps release of calcium by intracellular stores is decreased in hypertrophy. In contrast, the amplitudes of the calcium transients were similar in muscles from both groups of ferrets, indicating that the diminution in peak tension developed by the hypertrophied muscles was not due to decreased availability of activator calcium. We conclude that the prolonged time course of tension development, but not the diminished peak isometric tension response, may be related to changes in intracellular calcium handling.
Are you getting the most out of<i>BJSM</i>Education?
Authors: Babette M Pluim
Journal: British Journal of Sports Medicine (2014)

BJSM is a multimedia portal for original research, critical reviews and timely debate in sport and exercise medicine (SEM). Education is a cornerstone of our service, and we therefore have a dedicated BJSM Education website: http://bjsm.bmj.com/site/education/

BJSM Education offers high-quality, peer-reviewed educational material for clinicians whose practice relates to sport, exercise and physical activity promotion. It is designed to support the entire readership from established consultants in sports and exercise medicine (physiotherapists and physicians) to those in training and professionals from other disciplines with an interest in SEM.

The most popular features on the BJSM Education website are 

1.  Educational videos …
Rare diseases bullet 13: Non-neoplastic pulmonary lymphoid lesions
Authors: W D Travis
Journal: Thorax (2001)

Pulmonary lymphoid lesions encompass a spectrum of inflammatory and reactive lesions that are often diYcult to diagnose since they are diYcult to diVerentiate from other reactive and neoplastic entities (box 1).Understanding these lymphoid lesions is complicated by the evolution of concepts, criteria, and terminology over the past few decades.This review will attempt to summarise a historical perspective on this subject and present the current concepts of pulmonary lymphoid lesions.2][3] The terms "lymphocytic interstitial pneumonia" or "diVuse lymphoid hyperplasia" have sometimes been used for both lymphocytic interstitial pneumonia and follicular bronchiolitis.However, in this review lymphocytic interstitial pneumonia and follicular bronchiolitis are regarded separately.
Control of cell proliferation in atherosclerosis: insights from animal models and human studies
Authors: J. J. Fuster, P. Fernandez, H. Gonzalez-Navarro, C. Silvestre, Y. N. A. Nabah, V. Andres
Journal: Cardiovascular Research (2009)

Excessive hyperplastic cell growth within occlusive vascular lesions has been recognized as a key component of the inflammatory response associated with atherosclerosis, restenosis post-angioplasty, and graft atherosclerosis after coronary artery bypass. Understanding the molecular mechanisms that regulate arterial cell proliferation is therefore essential for the development of new tools for the treatment of these diseases. Mammalian cell proliferation is controlled by a large number of proteins that modulate the mitotic cell cycle, including cyclin-dependent kinases, cyclins, and tumour suppressors. The purpose of this review is to summarize current knowledge about the role of these cell cycle regulators in the development of native and graft atherosclerosis that has arisen from animal studies, histological examination of specimens from human patients, and genetic studies.
Nephrin Mutations Can Cause Childhood-Onset Steroid-Resistant Nephrotic Syndrome
Authors: Aure[Combining Acute Accent]lie Philippe, Fabien Nevo, Ernie L. Esquivel, Dalia Reklaityte, Olivier Gribouval, Marie-Jose[Combining Grave Accent]phe Te[Combining Circumflex Accent]te, Chantal Loirat, Jacques Dantal, Michel Fischbach, Claire Pouteil-Noble, Ste[Combining Acute Accent]phane Decramer, Martin Hoehne, Thomas Benzing, Marina Charbit, Patrick Niaudet, Corinne Antignac
Journal: Journal of the American Society of Nephrology (2008)

Classically, infants with mutations in NPHS1, which encodes nephrin, present with nephrotic syndrome within the first 3 mo of life (congenital nephrotic syndrome of the Finnish-type), and children with mutations in NPHS2, which encodes podocin, present later with steroid-resistant nephrotic syndrome. Recently, however, NPHS2 mutations have been identified in children with congenital nephrotic syndrome. Whether NPHS1 mutations similarly account for some cases of childhood steroid-resistant nephrotic syndrome is unknown. In this study, 160 patients who belonged to 142 unrelated families and presented with nephrotic syndrome at least 3 mo after birth were screened for NPHS1 variants once mutations in NPHS2 had been excluded. Compound heterozygous NPHS1 mutations were identified in one familial case and nine sporadic cases. Mutations included protein-truncating nonsense and frameshift mutations, as well as splice-site and missense variants. Mutations were classified as "severe" or "mild" using prediction algorithms and functional assays. Most missense variants trafficked normally to the plasma membrane and maintained the ability to form nephrin homodimers and to heterodimerize with NEPH1, suggesting retained function. The presence of at least one "mild" mutation in these patients likely explains the later onset and milder course of disease. These results broaden the spectrum of renal disease related to nephrin mutations.
Linking Public Health, Housing, and Indoor Environmental Policy: Successes and Challenges at Local and Federal Agencies in the United States
Authors: David E. Jacobs, Tom Kelly, John Sobolewski
Journal: Environmental Health Perspectives (2007)

We describe the successes and challenges faced by federal and local government agencies in the United States as they have attempted in recent years to connect public and environmental health, housing, community development, and building design with environmental, housing, and building laws, codes, and policies. These policies can either contribute to or adversely affect human physical and mental health, with important implications for economic viability, research, policy development, and overall social stability and progress. Policy impediments include tension between housing affordability and health investment that causes inefficient cost-shifting, privacy issues, unclear statutory authority, and resulting gaps in responsibility for housing, indoor air, and the built environment. We contrast this with other environmental frameworks such as ambient air and water quality statutes where the concept of "shared commons" and the "polluter pays" is more robust. The U.S. experiences in childhood lead poisoning prevention, indoor air, and mold provide useful policy insights. Local programs can effectively build healthy homes capacity through local laws and housing codes. The experience of coordinating remediation for mold, asthma triggers, weatherization, and other healthy housing improvements in Cuyahoga County, Ohio, is highlighted. The U.S. experience shows that policymakers should adopt a prevention-oriented, comprehensive multi-disciplinary approach at all levels of government to prevent unhealthy buildings, houses, and communities.
PM-23 * EXPLORATION OF BASIC AND THERAPEUTIC MECHANISMS IN NOVEL MODELS OF RTK/RAS-NETWORK-DRIVEN GLIOBLASTOMA
Authors: N. Zhang, L. Lu, T. Van Dyke
Journal: Neuro-Oncology (2014)

Glioblastoma (GBM) remains fatal despite intensive treatments including standard-of-care surgery, radiation, and chemotherapy. Modern targeted therapies have also failed to produce effective results in clinical trials, possibly due to a lack of relevant preclinical models for drug discovery/assessment. Approximately 90% GBMs harbor aberrations in RTK/RAS-signaling, including EGFR amplification/gain-of-function mutations (57%), PDGFRa amplification (10%), and NF1 deletion/loss-of-function mutations (10%). KRAS mutations also occur, but at low frequency (1%). Frequent alteration of RTK/RAS-signaling emphasizes a great need for several distinct RTK/RAS-network-driven preclinical GBM models that mirror the range of human GBM lesions, since therapeutic responses may differ depending on the major network driver in a given tumor. We have recently generated a genetically-engineered mouse model of GBM via adult-inducible astrocyte-specific perturbation of RB, KRAS and PTEN. The triple mutant mice develop GBMs that faithfully recapitulate the histopathology and molecular characteristics of human primary GBMs. Interestingly, without RAS activation, only low-grade disease is induced. We established astrocytes from the triple mutant mouse model [RB-inactivated/KRASG12D/+/PTEN+/-; RKP astrocytes)] that elicit GBM upon intracranial transplantation, as well as the RB/PTEN double mutant mice [RB-inactivated/PTEN+/-; RP astrocytes], which do not produce GBM. Thus, the RP cells provide an ideal platform for evaluation of multiple RAS-activating events in causation of GBM. We are currently introducing the most frequent events found in human GBMs, including EGFR, ERFRvIII and PDGFRa activation and NF1 deficiency, into RP cells in vitro. The ability of each event to convert the RP cells into GBM-forming astrocytes by orthotopic transplantation is being assessed. This novel in vitro-to-allograft approach provides direct comparisons of etiologies driven by various RAS-activating events in the same genetic background and will potentially lead to basic discovery of distinct mechanisms in GBM tumorigenesis. Furthermore, this approach will generate relevant panels of RTK/RAS-network-driven GBM models for robust preclinical therapeutic discovery and biomarker development.
Noninvasive Communication Systems
Authors: Dennis J. McFarland
Journal: Brain-Computer Interfaces (2008)

Conditions such as amyotrophic lateral sclerosis (ALS), brainstem stroke, and severe brain or spinal cord injury can impair the neural pathways that control muscles or impair the muscles themselves. Individuals most severely affected may lose all voluntary muscle control, including eye movements and respiration, and may be completely locked in to their bodies, unable to communicate in any way. A variety of studies over the past 15 years have shown that the scalp-recorded electroencephalogram (EEG) can be used as the basis for a brain-computer interface (Wolpaw et al., 2002). BCI can provide an alternative method of communication and control for those severely affected individuals.
Pregnancy Outcome After Treatment for Wilms Tumor: A Report From the National Wilms Tumor Long-Term Follow-Up Study
Authors: Daniel M. Green, Jane M. Lange, Eve M. Peabody, Natalia N. Grigorieva, Susan M. Peterson, John A. Kalapurakal, Norman E. Breslow
Journal: Journal of Clinical Oncology (2010)

Purpose This study was undertaken to evaluate the effect of prior treatment with radiation therapy or chemotherapy for unilateral Wilms tumor (WT) diagnosed during childhood on pregnancy complications, birth weight, and the frequency of congenital malformations in live-born offspring. Patients and Methods We reviewed pregnancy outcomes among female survivors and partners of male survivors of WT treated on National Wilms Tumor Studies 1, 2, 3, and 4 by using a maternal questionnaire and a review of both maternal and offspring medical records. Results We received reports of 1,021 pregnancies with duration of 20 weeks or longer, including 955 live-born singletons, for whom 700 sets of maternal and offspring medical records were reviewed. Rates of hypertension complicating pregnancy (International Classification of Diseases [ICD] code 642), early or threatened labor (ICD-644) and malposition of the fetus (ICD-652) increased with increasing radiation dose in female patients. The percentages of offspring weighing less than 2,500 g at birth and of those having less than 37 weeks of gestation also increased with dose. There was no significant trend with radiation dose in the number of congenital anomalies recorded in offspring of female patients. Conclusion Women who receive flank radiation therapy as part of the treatment for unilateral WT are at increased risk of hypertension complicating pregnancy, fetal malposition, and premature labor. The offspring of these women are at risk for low birth weight and premature (ie, &lt; 37 weeks gestation) birth. These risks must be considered in the obstetrical management of female survivors of WT.
The 148M allele of the PNPLA3 gene is associated with indices of liver damage early in life
Authors: Stefano Romeo, Federica Sentinelli, Valentina M Cambuli, Michela Incani, Tiziana Congiu, Vanessa Matta, Sabrina Pilia, Isabel Huang-Doran, Efisio Cossu, Sandro Loche, Marco G Baroni
Journal: Journal of Hepatology (2010)
Podocyte-Specific VEGF-A Gain of Function Induces Nodular Glomerulosclerosis in eNOS Null Mice
Authors: Delma Veron, Pardeep K. Aggarwal, Heino Velazquez, Michael Kashgarian, Gilbert Moeckel, Alda Tufro
Journal: Journal of the American Society of Nephrology (2014)

VEGF-A and nitric oxide are essential for glomerular filtration barrier homeostasis and are dysregulated in diabetic nephropathy. Here, we examined the effect of excess podocyte VEGF-A on the renal phenotype of endothelial nitric oxide synthase (eNOS) knockout mice. Podocyte-specific VEGF(164) gain of function in eNOS(-/-) mice resulted in nodular glomerulosclerosis, mesangiolysis, microaneurysms, and arteriolar hyalinosis associated with massive proteinuria and renal failure in the absence of diabetic milieu or hypertension. In contrast, podocyte-specific VEGF(164) gain of function in wild-type mice resulted in less pronounced albuminuria and increased creatinine clearance. Transmission electron microscopy revealed glomerular basement membrane thickening and podocyte effacement in eNOS(-/-) mice with podocyte-specific VEGF(164) gain of function. Furthermore, glomerular nodules overexpressed collagen IV and laminin extensively. Biotin-switch and proximity ligation assays demonstrated that podocyte-specific VEGF(164) gain of function decreased glomerular S-nitrosylation of laminin in eNOS(-/-) mice. In addition, treatment with VEGF-A decreased S-nitrosylated laminin in cultured podocytes. Collectively, these data indicate that excess glomerular VEGF-A and eNOS deficiency is necessary and sufficient to induce Kimmelstiel-Wilson-like nodular glomerulosclerosis in mice through a process that involves deposition of laminin and collagen IV and de-nitrosylation of laminin.
Alterations in bone mineral density and bone turnover markers in newly diagnosed adults with lymphoma receiving chemotherapy: a 1-year prospective pilot study
Authors: J. Paccou, L. Merlusca, I. Henry-Desailly, A. Parcelier, B. Gruson, B. Royer, A. Charbonnier, D. Ursu, R. Desailloud, R. Garidi, S. Kamel, H. Sevestre, J.P. Marolleau, P. Fardellone, G. Damaj
Journal: Annals of Oncology (2014)