tbuckley/cabot-search huggingface dataset:
The danger of wearing an anorak
Authors: C. M G Cheung, O. M Durrani, M. S Lim, M. Ramchandani, S. Banerjee, P. I Murray
Journal: Journal of the Royal Society of Medicine (2002)

Campaigns to reduce road traffic accidents have paid little attention to the way headgear could interfere with vision. Binocular visual field measurement was undertaken in six healthy volunteers wearing four different types of anorak. All four anoraks greatly reduced the horizontal and superior field of vision. The anorak producing the worst reduction resulted in a width of vision of 99° and only 15° of vision above eye level, versus 167° and 52° respectively without an anorak.
Problems in health management of professional boxers in Japan
Authors: G Ohhashi, S Tani, S Murakami, M Kamio, T Abe, J Ohtuki
Journal: British Journal of Sports Medicine (2002)

Objective: To investigate whether the incidence of boxing accidents is higher in Japan than in other countries. Method: A nationwide survey of boxers was conducted. Results: A total of 632 boxers responded. Most Japanese boxers were relatively mature when they started boxing (mean starting age of 19.2 years). A high percentage of boxers was found three weight divisions higher than previously reported. Many boxers stated that losing weight was not a big problem. It was found that a punch that turns the head can cause serious physical damage, and it was clarified that only a simple punch, rather than accumulated damage from multiple punches, can cause cerebral concussion. Severe shock causing retrograde amnesia is very rare after a fight and disappears relatively quickly. Many additional symptoms are related to damage to the hearing organs, such as hearing difficulties, tinnitus, and vertigo, but these symptoms also resolve quickly. Many boxers experience memory disturbance, not just after a fight but in daily life. Conclusion: The approach to boxing has become more oriented towards the method of practice and scientific training, rather than psychological factors, which used to be emphasised.
Epigenetic and cultural evolution are non-Darwinian
Authors: Liane Gabora
Journal: Behavioral and Brain Sciences (2007)

Abstract The argument that heritable epigenetic change plays a distinct role in evolution would be strengthened through recognition that it is what bootstrapped the origin and early evolution of life, and that, like behavioral and symbolic change, it is non-Darwinian. The mathematics of natural selection, a population-level process, is limited to replication with negligible individual-level change that uses a self-assembly code.
PET Study of the Effects of Valproate on Dopamine D<sub>2</sub> Receptors in Neuroleptic- and Mood-Stabilizer-Naive Patients With Nonpsychotic Mania
Authors: Lakshmi N. Yatham, Peter F. Liddle, Raymond W. Lam, I-Shin Shiah, Carol Lane, A. Jon Stoessl, Vesna Sossi, Thomas J. Ruth
Journal: American Journal of Psychiatry (2002)

OBJECTIVE: A previous study reported a higher than normal density of dopamine D2 receptors in psychotic mania but not in nonpsychotic mania. The purpose of this study was to further examine D2 receptor density in a larger sample of nonpsychotic manic patients by using positron emission tomography (PET) and [11C]raclopride. METHOD: Thirteen neuroleptic- and mood- stabilizer-naive patients with DSM-IV mania without psychotic features and 14 healthy comparison subjects underwent [11C]raclopride PET scans. Of the 13 patients, 10 were treated with divalproex sodium monotherapy. PET scans were repeated 2–6 weeks after commencement of divalproex sodium. D2 receptor binding potential was calculated by using a ratio method with the cerebellum as the reference region. RESULTS: The [11C]raclopride D2 binding potential was not significantly different in manic patients than in the comparison subjects in the striatum. Treatment with divalproex sodium had no significant effect on the [11C]raclopride D2 binding potential in manic patients. There was no correlation between the D2 binding potential and manic symptoms before or after treatment. CONCLUSIONS: These results suggest that D2 receptor density is not altered in nonpsychotic mania and that divalproex sodium treatment does not affect D2 receptor availability.
Abnormal electrocardiographic findings in athletes: recognising changes suggestive of primary electrical disease
Authors: Jonathan A Drezner, Michael J Ackerman, Bryan C Cannon, Domenico Corrado, Hein Heidbuchel, Jordan M Prutkin, Jack C Salerno, Jeffrey Anderson, Euan Ashley, Chad A Asplund, Aaron L Baggish, Mats Börjesson, John P DiFiori, Peter Fischbach, Victor Froelicher, Kimberly G Harmon, Joseph Marek, David S Owens, Stephen Paul, Antonio Pelliccia, Christian M Schmied, Sanjay Sharma, Ricardo Stein, Victoria L Vetter, Mathew G Wilson
Journal: British Journal of Sports Medicine (2013)

Cardiac channelopathies are potentially lethal inherited arrhythmia syndromes and an important cause of sudden cardiac death (SCD) in young athletes. Other cardiac rhythm and conduction disturbances also may indicate the presence of an underlying cardiac disorder. The 12-lead ECG is utilised as both a screening and a diagnostic tool for detecting conditions associated with SCD. Fundamental to the appropriate evaluation of athletes undergoing ECG is an understanding of the ECG findings that may indicate the presence of a pathological cardiac disease. This article describes ECG findings present in primary electrical diseases afflicting young athletes and outlines appropriate steps for further evaluation of these ECG abnormalities. The ECG findings defined as abnormal in athletes were established by an international consensus panel of experts in sports cardiology and sports medicine.
Presymptomatic DNA testing and prophylactic surgery in families with a BRCA1 or BRCA2 mutation
Authors: EJ Meijers-Heijboer, LC Verhoog, CTM Brekelmans, C Seynaeve, MMA Tilanus-Linthorst, A Wagner, L Dukel, P Devilee, AMW van den Ouweland, AN van Geel, JGM Klijn
Journal: The Lancet (2000)
Airways Inflammation, Atopy, and (1 → 3)- β -<scp>d</scp>-Glucan Exposures in Two Schools
Authors: RAGNAR RYLANDER, MARIA NORRHALL, ULLA ENGDAHL, ALF TUNSÄTER, PATRICK G. HOLT
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

This study investigated two schools, one of which had previous mold problems. Pupils aged 6 to 13 yr were investigated using a questionnaire on symptoms and a skin prick test. The amount of airborne (1 → 3)- β -d-glucan was measured in the classrooms. The levels were significantly higher in the problem school than in the control school (15.3 versus 2.9 ng/m3). The extent of respiratory as well as general symptoms was higher among the pupils in the problem school. Among the atopics, the extent of symptoms of dry cough, cough with phlegm, and hoarseness was similar to the nonatopics in the control school, but significantly higher in the problem school. The results suggest that (1 → 3)- β -d-glucan, either by itself or as an indicator of molds, is a risk indicator of airways inflammation.
Shh Pathway Activity Is Down-Regulated in Cultured Medulloblastoma Cells: Implications for Preclinical Studies
Authors: Ken Sasai, Justyna T. Romer, Youngsoo Lee, David Finkelstein, Christine Fuller, Peter J. McKinnon, Tom Curran
Journal: Cancer Research (2006)

Abstract Gene expression profiling indicates that the Sonic Hedgehog (Shh) pathway is active in ∼30% of human medulloblastomas, suggesting that it could provide a useful therapeutic target. Previously, we showed that spontaneous medulloblastomas in Ptc1+/−p53−/− mice could be eradicated by treatment with a small-molecule inhibitor (HhAntag) of Smoothened (Smo). Here, we compared the responses of mouse medulloblastoma cells propagated in flank allografts, either directly or after culture in vitro, to HhAntag. We found that Shh pathway activity was suppressed in medulloblastoma cells cultured in vitro and it was not restored when these cells were transplanted into the flank of nude mice. The growth of these transplanted tumor cells was not inhibited by treatment of mice with doses of HhAntag that completely suppressed Smo activity. Interestingly, tumor cells transplanted directly into the flank maintained Smo activity and were sensitive to treatment with HhAntag. These findings indicate that propagation of tumor cells in culture inhibits Smo activity in a way that cannot be reversed by transplantation in vivo, and they raise concerns about the use of cultured tumor cells to test the efficacy of Shh pathway inhibitors as anticancer therapies. (Cancer Res 2006; 66(8): 4215-22)
Erythropoietic protoporphyria: evidence for multiple sites of excess protoporphyrin formation
Authors: Perry Scholnick, Harvey S. Marver, Rudi Schmid
Journal: Journal of Clinical Investigation (1971)

A patient with erythropoietic protoporphyria was studied to determine the sites of excess protoporphyrin formation. The patient's protoporphyrin was pulse labeled by the simultaneous administration of the precursors 2-glycine-(14)C and 3,5-delta-aminolevulinic acid-(3)H; delta-aminolevulinic acid preferentially labels the hepatic pool. Blood and feces were studied at intervals for the next 14 days. Protoporphyrin was extracted from erythrocytes, plasma, and feces, identified by thin-layer chromatography, and quantitated spectrophotometrically, and its specific activity was determined by liquid scintillation spectrometry. Analysis of the kinetic and isotopic data indicated at least two sources of protoporphyrin, one localized in the erythroid cells, a second in the liver. The liver was responsible for the majority of the excess protoporphyrin. This report thus provides evidence of a genetic porphyria exhibiting an abnormality of porphyrin biosynthesis in at least two tissues. We propose that the disease, erythropoietic protoporphyria, be renamed erythrohepatic protoporphyria.
QUEST-RA: quantitative clinical assessment of patients with rheumatoid arthritis seen in standard rheumatology care in 15 countries
Authors: T. Sokka, H. Kautiainen, S. Toloza, H. Makinen, S. M M Verstappen, M. Lund Hetland, A. Naranjo, E. Baecklund, G. Herborn, R. Rau, M. Cazzato, L. Gossec, V. Skakic, F. Gogus, S. Sierakowski, B. Bresnihan, P. Taylor, C. McClinton, T. Pincus
Journal: Annals of the Rheumatic Diseases (2007)

To conduct a cross-sectional review of non-selected consecutive outpatients with rheumatoid arthritis (RA) as part of standard clinical care in 15 countries for an overview of the characteristics of patients with RA.
Stromal Cell–Derived Factor-1α in Unstable Angina
Authors: Jan K. Damås, Torgun Wæhre, Arne Yndestad, Thor Ueland, Fredrik Müller, Hans Geir Eiken, Are M. Holm, Bente Halvorsen, Stig S. Frøland, Lars Gullestad, Pål Aukrust
Journal: Circulation (2002)

Chemokines play a pathogenic role in atherogenesis and plaque destabilization by activating and directing leukocytes into the atherosclerotic plaque. However, stromal cell-derived factor (SDF)-1 was recently found to have antiinflammatory effects, and we hypothesized that this chemokine could play a beneficial role in coronary artery disease.Plasma levels of SDF-1alpha were significantly decreased in patients with stable (n=30) and unstable angina (n=30) compared with healthy control subjects (n=20), particularly in those with unstable disease. By flow cytometry and RNase protection assay, we found decreased surface expression but increased gene expression of the SDF-1alpha receptor CXCR-4 in peripheral blood mononuclear cells (PBMC) from patients with stable angina and patients with unstable angina. In vitro, SDF-1alpha (500 ng/mL) reduced both unstimulated and endotoxin/mitogen-stimulated mRNA and protein levels of monocyte chemoattractant protein-1, interleukin-8, matrix metalloproteinase-9, and tissue factor while increasing tissue inhibitor of metalloproteinases-1 in PBMC from patients with unstable angina. The SDF-1alpha-mediated suppression of monocyte chemoattractant protein-1 and interleukin-8 appears to involve cAMP/protein kinase A type I-dependent pathways. Finally, although SDF-1alpha suppressed the spontaneous release of these inflammatory mediators in unstable angina, enhancing effects were seen in unstimulated PBMC from healthy control subjects, possibly reflecting that PBMC in unstable angina are preactivated in vivo.In contrast to several other chemokines, our findings suggest that SDF-1alpha, at least in high concentrations, may mediate antiinflammatory and matrix-stabilizing effects in unstable angina. These effects may promote plaque stabilization, and therapeutic intervention that enhances SDF-1alpha activity could potentially be beneficial in acute coronary syndromes.
Chronic actinic dermatitis treated with mycophenolate mofetil
Authors: M.A. Thomson, D.G. Stewart, H.M. Lewis
Journal: British Journal of Dermatology (2005)

Chronic actinic dermatitis (CAD) is a persistent photodermatosis that usually affects elderly men. We report two male patients, aged 55 years (patient A) and 49 years (patient B), who presented with an eczematous eruption on sun‐exposed skin. Phototesting revealed a markedly reduced 24‐h minimal erythema dose (MED). Both patients had refractory disease and developed significant side‐effects to conventional therapies, including topical steroids, prednisolone, psoralen with ultraviolet A, azathioprine and ciclosporin. They had each received at least 6 years of treatment prior to commencing mycophenolate mofetil (MMF). Each noted a significant improvement in symptoms within 6 weeks and subsequent clearing of the eczematous lesions. Patient A still requires continuous treatment with MMF 500 mg twice daily to prevent relapses. Patient B maintains remission by using MMF 1 g twice daily only during the spring and summer months. Both patients have tolerated the treatment well with no abnormalities in blood cell counts or liver biochemistry. Since commencing MMF, their quality of life has significantly improved. These observations suggests that MMF should be considered as an alternative treatment to conventional therapies for refractory CAD.
Endothelial Differentiation of Hematopoietic Stem and Progenitor Cells from Patients with Multiple Myeloma
Authors: Roberto Ria, Claudia Piccoli, Teresa Cirulli, Franca Falzetti, Giuseppe Mangialardi, Diego Guidolin, Antonio Tabilio, Nicola Di Renzo, Attilio Guarini, Domenico Ribatti, Franco Dammacco, Angelo Vacca
Journal: Clinical Cancer Research (2008)

Abstract Purpose: Vasculogenesis is a physiologic process typical of fetal development in which new blood vessels develop from undifferentiated precursors (or angioblasts). In tumors, near angiogenesis, vasculogenesis contributes to the formation of the microvascular plexus that is important for diffusion. Here, we show that hematopoietic stem and progenitor cells (HSPC) of multiple myeloma (MM) patients are able to differentiate into cells with endothelial phenotype on exposure to angiogenic cytokines. Experimental Design: Circulating HSPCs were purified with an anti-CD133 antibody from patients with newly diagnosed MM before autologous transplantation and exposed to vascular endothelial growth factor (VEGF), fibroblast growth factor-2 and insulin-like growth factor in a 3-week culture. Results: HSPCs gradually lost CD133 expression and acquired VEGF receptor-2, factor VIII–related antigen, and vascular endothelial-cadherin expression. The expression pattern overlapped with paired MM endothelial cells (MMEC). During culture, cells adhered to fibronectin, spread, and acquired an endothelial cell shape. Differentiated HSPCs also became capillarogenic in the Matrigel assay with maximal activity at the third week of culture. Bone marrow biopsies revealed HSPCs inside the neovessel wall in patients with MM but not in those with monoclonal gammopathy of undetermined significance. Conclusions: In patients with MM, but not in those with monoclonal gammopathy of undetermined significance, HSPCs contribute to the neovessel wall building together with MMECs. Therefore, besides angiogenesis, HSPC-linked vasculogenesis contributes to neovascularization in MM patients. Tentatively, we hypothesize that in HSPC cultures a multipotent cell population expressing low VEGF receptor-2 levels corresponds to the endothelial progenitor cell precursor and seems to be the MMEC precursor.
Sustained radiographic and clinical response in patient with bifrontal recurrent glioblastoma multiforme with intracerebral infusion of the recombinant targeted toxin TP-38: Case study
Authors: John H. Sampson, David A. Reardon, Allan H. Friedman, Henry S. Friedman, R. Edward Coleman, Roger E. McLendon, Ira Pastan, Darell D. Bigner
Journal: Neuro-Oncology (2005)

Glioblastoma multiforme remains refractory to conventional therapy, and novel therapeutic modalities are desperately needed. TP-38 is a recombinant chimeric protein containing a genetically engineered form of the cytotoxic Pseudomonas exotoxin fused to transforming growth factor (TGF)-α. TGF-α binds with high affinity to the epidermal growth factor receptor, which is uniformly overexpressed in malignant gliomas, often because of gene amplification. Prior to therapy with TP-38, the patient described here was completely refractory to multiple other therapies, with radiographic and pathologic evidence of tumor progression. After therapy, she improved clinically, was weaned off steroids and anticonvulsants, and experienced a progressive decrease in enhancing tumor volume. Despite multiple prior recurrences, she has not progressed for >43 months after TP-38 therapy. Small remaining areas of enhancement demonstrate no evidence of tumor histologically and are hypometabolic on positron emission tomography. This report describes a dramatic and sustained clinical and radiographic response in a patient with a bifrontal glioblastoma multiforme treated with intratumoral infusion of a novel targeted toxin, TP-38.
Cell death upon epigenetic genome methylation: a novel function of methyl-specific deoxyribonucleases
Authors: Eri Fukuda, Katarzyna H Kaminska, Janusz M Bujnicki, Ichizo Kobayashi
Journal: Genome biology (2008)

Abstract Background Alteration in epigenetic methylation can affect gene expression and other processes. In Prokaryota, DNA methyltransferase genes frequently move between genomes and present a potential threat. A methyl-specific deoxyribonuclease, McrBC, of Escherichia coli cuts invading methylated DNAs. Here we examined whether McrBC competes with genome methylation systems through host killing by chromosome cleavage. Results McrBC inhibited the establishment of a plasmid carrying a PvuII methyltransferase gene but lacking its recognition sites, likely through the lethal cleavage of chromosomes that became methylated. Indeed, its phage-mediated transfer caused McrBC-dependent chromosome cleavage. Its induction led to cell death accompanied by chromosome methylation, cleavage and degradation. RecA/RecBCD functions affect chromosome processing and, together with the SOS response, reduce lethality. Our evolutionary/genomic analyses of McrBC homologs revealed: a wide distribution in Prokaryota; frequent distant horizontal transfer and linkage with mobility-related genes; and diversification in the DNA binding domain. In these features, McrBCs resemble type II restriction-modification systems, which behave as selfish mobile elements, maintaining their frequency by host killing. McrBCs are frequently found linked with a methyltransferase homolog, which suggests a functional association. Conclusions Our experiments indicate McrBC can respond to genome methylation systems by host killing. Combined with our evolutionary/genomic analyses, they support our hypothesis that McrBCs have evolved as mobile elements competing with specific genome methylation systems through host killing. To our knowledge, this represents the first report of a defense system against epigenetic systems through cell death.
Relation of human papilloma virus status to cervical lesions and consequences for cervical-cancer screening: a prospective study
Authors: Mariëlle AE Nobbenhuis, Jan MM Walboomers, Theo JM Helmerhorst, Lawrence Rozendaal, Ans J Remmink, Elle KJ Risse, Hans C van der Linden, Feja J Voorhorst, Peter Kenemans, Chris JLM Meijer
Journal: The Lancet (1999)
Recurrence patterns across medulloblastoma subgroups: an integrated clinical and molecular analysis
Authors: Vijay Ramaswamy, Marc Remke, Eric Bouffet, Claudia C Faria, Sebastien Perreault, Yoon-Jae Cho, David J Shih, Betty Luu, Adrian M Dubuc, Paul A Northcott, Ulrich Schüller, Sridharan Gururangan, Roger McLendon, Darell Bigner, Maryam Fouladi, Keith L Ligon, Scott L Pomeroy, Sandra Dunn, Joanna Triscott, Nada Jabado, Adam Fontebasso, David T W Jones, Marcel Kool, Matthias A Karajannis, Sharon L Gardner, David Zagzag, Sofia Nunes, José Pimentel, Jaume Mora, Eric Lipp, Andrew W Walter, Marina Ryzhova, Olga Zheludkova, Ella Kumirova, Jad Alshami, Sidney E Croul, James T Rutka, Cynthia Hawkins, Uri Tabori, Kari-Elise T Codispoti, Roger J Packer, Stefan M Pfister, Andrey Korshunov, Michael D Taylor
Journal: The Lancet Oncology (2013)
Patients with anaphylaxis to pea can have peanut allergy caused by cross-reactive IgE to vicilin (Ara h 1)
Authors: Marjolein Wensing, André C. Knulst, Sander Piersma, Francesca O'Kane, Edward F. Knol, Stef J. Koppelman
Journal: Journal of Allergy and Clinical Immunology (2003)
Aurora-A Is Essential for the Tumorigenic Capacity and Chemoresistance of Colorectal Cancer Stem Cells
Authors: Patrizia Cammareri, Alessandro Scopelliti, Matilde Todaro, Vincenzo Eterno, Federica Francescangeli, Mary Pat Moyer, Antonino Agrusa, Francesco Dieli, Ann Zeuner, Giorgio Stassi
Journal: Cancer Research (2010)

Colorectal cancer stem cells (CR-CSC) are responsible for the generation and maintenance of intestinal tumors and are highly resistant to conventional chemotherapeutic agents. Aurora-A, a serine-threonine kinase involved in mitosis regulation, plays multiple key functions in tumor initiation and progression. We found that Aurora-A is overexpressed in primary colorectal tumor cells, in the CR-CSC fraction, and in stem cell-derived differentiated cells, compared with normal colon tissue. Aurora-A expression was functionally linked to centrosome amplification in CR-CSC, as indicated by the decrease in cells with multiple centrosomes that followed Aurora-A silencing. Knockdown of Aurora-A resulted in growth inhibition of CR-CSC, alteration of cell cycle kinetics, and downregulation of the expression levels of antiapoptotic Bcl-2 family members, strongly sensitizing to chemotherapy-induced cell death. Moreover, Aurora-A silencing compromised the ability to form tumor xenografts in immunocompromised mice and reduced the migratory capacity of CR-CSC. Altogether, these results indicate that Aurora-A is essential for CR-CSC regeneration and resistance to cytotoxic stimuli and suggest that therapies directed against Aurora-A may effectively target the stem cell population in colorectal cancer.