tbuckley/cabot-search huggingface dataset:
Bidirectional erosion of cartilage in the rheumatoid knee joint.
Authors: M Bromley, H Bertfield, J M Evanson, D E Woolley
Journal: Annals of the Rheumatic Diseases (1985)

Specimens of cartilage with contiguous bone and overlying synovial pannus were obtained from 22 rheumatoid knee joints and examined histologically using specific histochemical staining techniques. All showed significant erosions of cartilage by synovial cells, but seven specimens also showed substantial cartilage erosion by cells from the subchondral bone region. This bidirectional attack on rheumatoid knee cartilage did not represent an 'underpinning' of cartilage by synovial pannus, as judged by serial sectioning and the identification of specific cells. Whereas cartilage-pannus junctions had mainly macrophagic or fibroblastic cells, cartilage-bone lesions were usually characterised by chondroclasts and blood vessels. Lymphocytes were generally absent from all sites of cartilage erosion. The bidirectional attack on articular knee cartilage suggests that changes have occurred within the cartilage that make it vulnerable to cellular invasion and erosion. Such changes might reflect a deficiency in 'anti-invasion factors', or the exposure of hidden epitopes and subsequent immunogenicity, or a combination of both.
12(S)-hydroxyheptadeca-5Z, 8E, 10E–trienoic acid is a natural ligand for leukotriene B4 receptor 2
Authors: Toshiaki Okuno, Yoshiko Iizuka, Hiroshi Okazaki, Takehiko Yokomizo, Ryo Taguchi, Takao Shimizu
Journal: The Journal of Experimental Medicine (2008)

Activated blood platelets and macrophages metabolize prostaglandin H(2) into thromboxane A(2) and 12(S)-hydroxyheptadeca-5Z, 8E, 10E-trienoic acid (12-HHT) in an equimolar ratio through the action of thromboxane synthase. Although it has been shown that 12-HHT is abundant in tissues and bodily fluids, this compound has long been viewed as a by-product lacking any specific function. We show that 12-HHT is a natural ligand for leukotriene B(4) (LTB(4)) receptor-2 (BLT2), a G protein-coupled receptor that was originally identified as a low-affinity receptor for LTB(4). BLT2 agonistic activity in lipid fractions from rat small intestine was identified as 12-HHT using high-performance liquid chromatography and mass spectrometry. Exogenously expressed BLT2 in mammalian cells was activated by synthetic 12-HHT, as assessed by guanosine 5'-O-(3-thio) triphosphate binding, the activation of intracellular signaling pathways, and chemotaxis assay. Displacement analysis using [(3)H]LTB(4) showed that 12-HHT binds to BLT2 with a higher affinity than LTB(4). Lipid extracts from cyclooxygenase 1-deficient mice failed to activate BLT2. Bone marrow-derived mast cells (BMMCs) isolated from wild-type mice migrated toward a low concentration of 12-HHT, whereas BMMCs from BLT2-deficient mice did not. We conclude that 12-HHT is a natural lipid agonist of BLT2 in vivo and induces chemotaxis of mast cells.
International retrospective study of over 1000 adults with anaplastic oligodendroglial tumors
Authors: A. B. Lassman, F. M. Iwamoto, T. F. Cloughesy, K. D. Aldape, A. L. Rivera, A. F. Eichler, D. N. Louis, N. A. Paleologos, B. J. Fisher, L. S. Ashby, J. G. Cairncross, G. B. Roldan, P. Y. Wen, K. L. Ligon, D. Schiff, H. I. Robins, B. G. Rocque, M. C. Chamberlain, W. P. Mason, S. A. Weaver, R. M. Green, F. G. Kamar, L. E. Abrey, L. M. DeAngelis, S. C. Jhanwar, M. K. Rosenblum, K. S. Panageas
Journal: Neuro-Oncology (2011)

Treatment for newly diagnosed anaplastic oligodendroglial tumors is controversial. Radiotherapy (RT) alone and in combination with chemotherapy (CT) are the most well studied strategies. However, CT alone is often advocated, especially in cases with 1p19q codeletion. We retrospectively identified 1013 adults diagnosed from 1981–2007 treated initially with RT alone (n = 200), CT + RT (n = 528), CT alone (n = 201), or other strategies (n = 84). Median overall survival (OS) was 6.3 years and time to progression (TTP) was 3.1 years. 1p19q codeletion correlated with longer OS and TTP than no 1p or 19q deletion. In codeleted cases, median TTP was longer following CT + RT (7.2 y) than following CT (3.9 y, P = .003) or RT (2.5 y, P < .001) alone but without improved OS; median TTP was longer following treatment with PCV alone than temozolomide alone (7.6 vs. 3.3 y, P = .019). In cases with no deletion, median TTP was longer following CT + RT (3.1 y) than CT (0.9 y, P = .0124) or RT (1.1 y, P < .0001) alone; OS also favored CT + RT (median 5.0 y) over CT (2.2 y, P = .02) or RT (1.9 y, P < .0001) alone. In codeleted cases, CT alone did not appear to shorten OS in comparison with CT + RT, and PCV appeared to offer longer disease control than temozolomide but without a clear survival advantage. Combined CT + RT led to longer disease control and survival than did CT or RT alone in cases with no 1p19q deletion. Ongoing trials will address these issues prospectively.
Proton Magnetic Resonance Spectroscopy of the Medial Prefrontal Cortex in Patients With Deficit Schizophrenia: Preliminary Report
Authors: Pascal Delamillieure, Jè²µs Fernandez, Jean-Marc Constans, Perrine Brazo, Karim Benali, Pascale Abadie, Thierry Vasse, Florence Thibaut, Patrick Courthè®µx, Michel Petit, Sonia Dollfus
Journal: American Journal of Psychiatry (2000)

Proton magnetic resonance spectroscopy (1H-MRS) was used to study medial prefrontal metabolic impairments in schizophrenic patients with the deficit syndrome.The subjects were 22 schizophrenic patients categorized as deficit (N=5) or nondeficit (N=17) and 21 healthy subjects. (1)H-MRS was performed for the right and the left medial prefrontal cortex.The patients with the deficit syndrome had significantly lower ratios of N-acetylaspartate to creatine plus phosphocreatine than did the healthy subjects or nondeficit patients.As N-acetylaspartate levels could reflect neuronal density and/or viability, this finding suggests a neuronal loss in the medial prefrontal cortex of deficit patients.
Productivity costs among patients with rheumatoid arthritis: the influence of methods and sources to value loss of productivity
Authors: S M M Verstappen
Journal: Annals of the Rheumatic Diseases (2005)

To assess productivity costs incurred by rheumatoid arthritis, comprising paid as well as household productivity costs, from a societal perspective, using different methods.A questionnaire on productivity, including items of the Health and Labour Questionnaire, was completed by 576 patients with rheumatoid arthritis (mean disease duration seven years). The friction cost (FC) method using the gross national wage per hour was applied to estimate paid productivity, and the market equivalent was used to value loss of household productivity. Sensitivity analyses to estimate paid productivity costs among patients of working age included the human capital (HC) method and an alternative source, namely the "added value", to value loss of paid productivity.In the total study population, mean (SD) annual costs from loss of paid productivity according to the FC method were estimated to be 278 (1,559) and mean annual household productivity costs were 2,045 (3,882). When using the HC method, mean annual costs increased to an average of 4,434 (9,957). When using the added value of production, average FC costs increased from 455 to 540 among patients of working age.Costs from loss of household productivity in rheumatoid arthritis were seven times higher than costs from loss of paid productivity, assessed by the FC method. The high paid productivity costs when using the HC method reflect the high work disability rate in rheumatoid arthritis. As the method of measuring and source of valuing productivity loss has an important influence on the costs, a consensus to standardise these issues is desirable.
Platelet-Derived Endothelial Cell Growth Factor in Human Colon Cancer Angiogenesis: Role of Infiltrating Cells
Authors: Y. Takahashi, C. D. Bucana, W. Liu, J. Yoneda, Y. Kitadai, K. R. Cleary, L. M. Ellis
Journal: JNCI Journal of the National Cancer Institute (1996)

Development of new blood vessels is essential for tumor growth and metastasis and depends on the production of angiogenic factors by tumor and/or infiltrating cells. We previously showed that vascular endothelial growth factor (VEGF) expression and vessel count correlate with metastasis in human colon cancer. Although most tumors with high vessel counts express high levels of VEGF, some do not. Recently, platelet-derived endothelial cell growth factor (PD-ECGF), another potent angiogenic factor, has been reported to be expressed in colon cancer.In this study, we examined the role of PD-ECGF in colon cancer angiogenesis and whether PD-ECGF is derived from the tumor or infiltrating cells.Immunostaining for PD-ECGF was performed on 96 colon cancer specimens, some of which were previously stained for VEGF and factor VIII, a marker that is specific for endothelial cells. Double staining was done by using antibodies to PD-ECGF and to CD68 (macrophage specific) or CD3 (lymphocyte specific) to confirm which infiltrating cells produce PD-ECGF. Northern blot analysis for PD-ECGF messenger RNA (mRNA) was performed on four colon cancer specimens and corresponding normal colon mucosae (same patients) and four human colon cancer cell lines (KM12SM, SW620, HT29, and NCI-H508) to determine whether colon cancer epithelium expresses PD-ECGF.Immunohistochemical analysis demonstrated that PD-ECGF was expressed in infiltrating cells in most of the colon cancer specimens (80 [83%] of 96) but rarely in tumor epithelium (five [5%] of 96). Double staining demonstrated that infiltrating cells staining positive for both PD-ECGF and CD68 were more predominant than those staining positive for both PD-ECGF and CD3. The intensity of staining for PD-ECGF in infiltrating cells correlated with vessel counts (Spearman's rank correlation coefficient (R) = .29; P = .004), but did not correlate with the intensity of VEGF staining (R = .176, P = .086) or metastasis (Mann-Whitney U test, P = .253). PD-ECGF staining intensity was higher in specimens with a high vessel count (> 50 at high magnification) and low VEGF-staining intensity (< or = 2+) than in specimens with a high vessel count (again, > 50) and high VEGF-staining intensity (3+). Northern blot analysis revealed that colon cancer specimens and normal mucosae expressed relatively high levels of PD-ECGF mRNA, whereas PD-ECGF mRNA transcripts were not detectable in colon cancer cell lines.PD-ECGF expression in human colon cancer specimens is associated with vessel count and may be responsible for tumor vascularity in those tumors with low VEGF expression. Infiltrating cells expressing PD-ECGF may contribute to angiogenesis, thus providing an additional mechanism for tumor neovascularization.
Sequential responses of mouse spleen T cells in mixed lymphocyte culture-induced cytolysis.
Authors: P Häyry, L C Andersson
Journal: The Journal of Experimental Medicine (1975)

T cells triggered to blast transformation and proliferation by histoincompatible cells have the capacity of reverting "back" to lymphocytes. These "secondary" lymphocytes and their progeny cells are able to respond repeatedly to the same allogeneic stimulus in vitro.
Class I–restricted Cross-Presentation of Exogenous Self-Antigens Leads to Deletion of Autoreactive CD8+ T Cells
Authors: Christian Kurts, Hiroshi Kosaka, Francis R. Carbone, Jacques F.A.P. Miller, William R. Heath
Journal: The Journal of Experimental Medicine (1997)

In this report, we show that cross-presentation of self-antigens can lead to the peripheral deletion of autoreactive CD8+ T cells. We had previously shown that transfer of ovalbumin (OVA)-specific CD8+ T cells (OT-I cells) into rat insulin promoter–membrane-bound form of OVA transgenic mice, which express the model autoantigen OVA in the proximal tubular cells of the kidneys, the β cells of the pancreas, the thymus, and the testis of male mice, led to the activation of OT-I cells in the draining lymph nodes. This was due to class I–restricted cross-presentation of exogenous OVA on a bone marrow–derived antigen presenting cell (APC) population. Here, we show that adoptively transferred or thymically derived OT-I cells activated by cross-presentation are deleted from the peripheral pool of recirculating lymphocytes. Such deletion only required antigen recognition on a bone marrow–derived population, suggesting that cells of the professional APC class may be tolerogenic under these circumstances. Our results provide a mechanism by which the immune system can induce CD8+ T cell tolerance to autoantigens that are expressed outside the recirculation pathway of naive T cells.
Effect of Postdiagnosis Weight Change on Hot Flash Status Among Early-Stage Breast Cancer Survivors
Authors: Bette J. Caan, Jennifer A. Emond, H. Irene Su, Ruth E. Patterson, Shirley W. Flatt, Ellen B. Gold, Vicky A. Newman, Cheryl L. Rock, Cynthia A. Thomson, John P. Pierce
Journal: Journal of Clinical Oncology (2012)

Hot flashes (HF) affect a large proportion of breast cancer (BC) survivors and can negatively affect their quality of life. Treatments other than estrogen replacement to alleviate HF are needed. Body weight is related to hot flashes, but little is known about the effect of weight change on HF.
International Union of Basic and Clinical Pharmacology. LXXXIV: Leukotriene Receptor Nomenclature, Distribution, and Pathophysiological Functions
Authors: Magnus Bäck, Sven-Erik Dahlén, Jeffrey M. Drazen, Jilly F. Evans, Charles N. Serhan, Takao Shimizu, Takehiko Yokomizo, G. Enrico Rovati
Journal: Pharmacological Reviews (2011)

The seven-transmembrane G protein-coupled receptors activated by leukotrienes are divided into two subclasses based on their ligand specificity for either leukotriene B<sub>4</sub> or the cysteinyl leukotrienes (LTC<sub>4</sub>, LTD<sub>4</sub>, and LTE<sub>4</sub>). These receptors have been designated BLT and CysLT receptors, respectively, and a subdivision into BLT<sub>1</sub> and BLT<sub>2</sub> receptors and CysLT<sub>1</sub> and CysLT<sub>2</sub> receptors has been established. However, recent findings have also indicated the existence of putative additional leukotriene receptor subtypes. Furthermore, other ligands interact with the leukotriene receptors. Finally, leukotrienes may also activate other receptor classes, such as purinergic receptors. The aim of this review is to provide an update on the pharmacology, expression patterns, and pathophysiological roles of the leukotriene receptors as well as the therapeutic developments in this area of research.
Ischemic preconditioning limits infarct size following regional ischemia–reperfusion in in situ mouse hearts
Authors: D Miller
Journal: Cardiovascular Research (1999)

Objective: Ischemic preconditioning has been demonstrated in a wide variety of animals, from dogs to rats. Experimentally-induced murine myocardial ischemia–reperfusion has been described, but ischemic preconditioning has not been reported in mouse hearts. To test the hypothesis that mouse hearts exhibit preconditioning-induced protection, experiments were conducted in anesthetized open chest mice subjected to regional myocardial ischemia–reperfusion. Methods: Following barbiturate anesthesia the FVB and C57BL/6J mice underwent a tracheostomy and were mechanically ventilated. The heart was exposed via a left thoracotomy performed with the aid of a dissecting microscope. A 7-0 silk suture on a curved taper needle was passed under the proximal left anterior descending coronary artery to form a snare. Mice were then randomly assigned to receive either no preconditioning or preconditioning. All mice were subjected to 60 min regional myocardial ischemia followed by 2.5 h of reperfusion. Ischemic preconditioning (IP) was induced with two (FVB mice) or three (C57BL/6J mice) cycles of 5 min coronary occlusion and 5 min reperfusion. Control animals did not receive preconditioning ischemia. Area-at-risk was assessed with fluorescent particles. Infarct size was assessed with triphenyl tetrazolium chloride, and is expressed below as a percentage of the area-at-risk. Results: In FVB mice preconditioning reduced infarct size 49%, from 36.7±4.5% to 18.9±2.8% (P<0.05). In C57BL/6J mice preconditioning reduced infarct size by 66%, from 56.4±8.3% to 18.9±4.2% (P<0.05). Conclusion: From these data we conclude that the infarct limiting effect of ischemic preconditioning is demonstrable in murine hearts.
Sports participation increased in Spain: a population-based time trend study of 21 381 adults in the years 2000, 2005 and 2010
Authors: Domingo Palacios-Ceña, Cesar Fernandez-de-las-Peñas, Valentín Hernández-Barrera, Rodrigo Jiménez-Garcia, Cristina Alonso-Blanco, Pilar Carrasco-Garrido
Journal: British Journal of Sports Medicine (2012)

To assess the trend in prevalence of Spanish adults who engaged in sports activities from 2000 to 2010.Retrospective analysis of three population-based cross-sectional surveys conducted on a representative sample of Spanish adults: 2000 (N=5160), 2005 (N=8170) and 2010 (N=8925).The overall prevalence of sport-active men increased from 45.8% to 52.12% between 2000 and 2010. Among women the prevalence also increased from 27.26% to 33.27% (adjusted OR 1.03 95% CI 1.02 to 1.04). A significant decrease in the prevalence of sport-active subjects was found as the age increases. Adjusted time trends analysis showed that the prevalence of sport-active women and men increased over time in all age groups, with exception of women aged 15-25 years (adjusted OR 0.99, 0.97 to 1.01). Higher educational level was associated with more sport activity. The first reason for not practising sport was 'I have no time due to working or studying'. Less than 10% of women and men reported health problems as the reason for not practising any sport.Sports participation in Spain has increased between 2000 and 2010 among young-aged and middle-aged adults and decreased among older people. Women showed lower prevalence of sport activity as compared to men.
Experimental Studies on the Facilitation of AV Conduction by Ectopic Beats in Dogs and Rabbits
Authors: E. Neil Moore, Joseph F. Spear
Journal: Circulation Research (1971)

Experiments were performed on the hearts of open-chest anesthetized dogs and on isolated rabbit hearts. Intracellular microelectrodes and bipolar surface electrodes were used for recording from and for stimulating the atria, AV node, bundle of His, bundle branches and ventricles. Atrial or ventricular premature beats which were usually blocked or delayed within the AV node were facilitated when ectopic activity caused preexcitation and early recovery of the site of block or delay. Ectopic atrial, ventricular, nodal, and bundle of His responses allowed previously blocked or delayed antegrade and retrograde beats to be conducted only when the ectopic activity arrived at an appropriate time at the site of block within the AV node. Therefore, apparent supernormal AV conduction may occur in the human heart by this mechanism, and some reported cases of supernormal conduction may be due to the preexcitation and early recovery of a refractory barrier by ectopic activity.
Adult height in patients with early onset of Crohn's disease
Authors: A Sawczenko
Journal: Gut (2003)

Alemzadeh et al ( Gut2002;51;26–9 [OpenUrl][1][Abstract/FREE Full Text][2] ) reported that adult height, compared with the general Dutch population, was reduced by a mean of −0.9 SDS (95% confidence interval −1.55 to −0.28) in 15 Crohn's patients with prepubertal onset of symptoms. However, the calculated deviation from "target" height (based on parental height) did not reach statistical significance and the authors have speculated that familial short stature, and not Crohn's disease, may be a factor in this group. Furthermore, no height deficit was found in those with postpubertal onset of symptoms. We are currently undertaking a review of those with childhood onset diseases attending our paediatric and adult IBD clinics. In the majority of cases parental height was measured by trained auxologists, although in some, details were not available in the case notes to discern the method of measurement and may therefore have included self reported parental heights. We calculated SDS scores from the revised British Longitudinal standards1 using the method described by … [1]: {openurl}?query=rft.jtitle%253DGut%26rft.stitle%253DGut%26rft.issn%253D0017-5749%26rft.aulast%253DAlemzadeh%26rft.auinit1%253DN%26rft.volume%253D51%26rft.issue%253D1%26rft.spage%253D26%26rft.epage%253D29%26rft.atitle%253DAdult%2Bheight%2Bin%2Bpatients%2Bwith%2Bearly%2Bonset%2Bof%2BCrohn%2527s%2Bdisease%26rft_id%253Dinfo%253Adoi%252F10.1136%252Fgut.51.1.26%26rft_id%253Dinfo%253Apmid%252F12077087%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/ijlink?linkType=ABST&journalCode=gutjnl&resid=51/1/26&atom=%2Fgutjnl%2F52%2F3%2F454.atom
Excitation–Contraction Coupling in Na <sup>+</sup> –Ca <sup>2+</sup> Exchanger Knockout Mice
Authors: Christian Pott, Kenneth D. Philipson, Joshua I. Goldhaber
Journal: Circulation Research (2005)

Cardiac-specific Na + –Ca 2+ exchanger (NCX) knockout (KO) mice surprisingly survive into adulthood without compensatory changes in protein expression levels. To determine how cardiac function is maintained in the absence of NCX, we investigated membrane currents, intracellular Ca 2+ , and action potentials (APs) in whole cell patch-clamped myocytes from wild-type (WT) and NCX knockout mice. There was no difference in resting Ca 2+ or sarcoplasmic reticular Ca 2+ load between KO and WT. During prolonged caffeine exposure, the decrease of the Ca 2+ transient was drastically slowed in KO versus WT myocytes, indicating that no alternative Ca 2+ -extrusion mechanism is upregulated to compensate for the absence of NCX. Peak L-type Ca 2+ current ( I Ca ) was reduced by 62% in KO myocytes compared with WT. Nevertheless, the corresponding Ca 2+ transients were similar, implying an increase in the gain of excitation–contraction coupling in KO cells. APs recorded from KO cells repolarized more rapidly than in WT. In WT myocytes, applying a KO AP waveform voltage clamp reduced Ca 2+ influx via I Ca by 59% compared with WT AP waveform clamps. Again, the corresponding Ca 2+ transients remained similar. Our findings indicate that NCX KO myocytes limit Ca 2+ influx to &amp;20% of that in WT by reducing I Ca and by abbreviating the AP. Contractility is maintained by an increase in the gain of excitation–contraction coupling resulting from both a more rapid repolarization of the AP and an as yet unidentified AP-independent mechanism.
Does the concurrent use of anthracycline and granulocyte colony-stimulating factor influence the risk of secondary leukaemia in breast cancer women?
Authors: S. Di Cosimo, G. Ferretti, P. Papaldo, P. Carlini, A. Fabi, E.M. Ruggeri, A. Alimonti, C. Nardoni, F. Cognetti
Journal: Annals of Oncology (2005)