tbuckley/cabot-search huggingface dataset:
Diagnostic criteria for exercise dependence in women
Authors: D J Bamber, I M Cockerill, S Rodgers, D Carroll
Journal: British Journal of Sports Medicine (2003)

To formulate diagnostic criteria for exercise dependence.Fifty six adult female exercisers were interviewed about their exercise behaviour and attitudes. The eating disorders examination, a semistructured clinical interview, was used to diagnose eating disorders. Interviews were taped, transcribed verbatim, and analysed from a social constructionist perspective using QSR NUD*IST. Participants also completed the exercise dependence questionnaire.Two diagnostic criteria emerged from analysis of the interview data: impaired functioning and withdrawal. Impaired functioning was manifest in four areas: psychological, social and occupational, physical, and behavioural. Impairment in at least two areas was considered necessary for diagnosis. Withdrawal was evident as either an adverse reaction to the interruption of exercise or unsuccessful attempts at exercise control. Either sufficed for diagnosis. The absence or presence of an eating disorder was used to distinguish between primary and secondary exercise dependence. Ten women met these criteria for exercise dependence. All 10 also exhibited eating disorders and, accordingly, should be regarded as showing secondary, rather than primary, exercise dependence. Exercise dependent women had significantly higher scores on the exercise dependence questionnaire than non-dependent women.These new diagnostic criteria should now be adopted and explored further, particularly among men and individuals with possible primary exercise dependence.
Abstract 365: Autocrine vascular endothelial growth factor signaling mediates survival and chemoresistance of human colorectal cancer cells
Authors: Shaija Samuel, Fan Fan, Long H. Dang, Puja Gaur, Ling Xia, Yunfei Zhou, Jia Liu, Federico Tozzi, Eric Sceusi, Xiang-Cang Ye, Lee M. Ellis
Journal: Cancer Research (2010)

Abstract Introduction. Although the effects of VEGF on angiogenesis and vascular function are well known, the autocrine effects of VEGF on tumor cell function remain to be elucidated. We studied phenotypic changes in human colorectal cancer (CRC) cells with homologous deletion of VEGF alleles to determine any potential autocrine/intracrine role of VEGF on tumor cell function. Methods. The human CRC cell lines HCT116 and LS174T with homologous recombination-mediated deletion of VEGF alleles were generated previously (Dang et al, Can Res 2006). To exclude the effect of exogenous VEGF, the cells were grown in low serum condition for all assays. MTT assay was used to detect changes in cell growth. Migration and invasion were determined using modified Boyden chamber assays. Cell death and apoptosis were assessed by FACS analysis following PI and Annexin V/PI staining respectively. Changes in protein levels of VEGF signaling intermediates and mediators of apoptosis were evaluated by Western blotting. Chemosensitivity was determined by FACS analysis following 5-FU treatment and PI staining of cells. Results. Loss of VEGF expression decreased cell growth and increased spontaneous apoptosis in CRC cells. Cells null for VEGF demonstrated increases in migration and invasion. Loss of VEGF expression also increased the sensitivity of cells to the cytotoxic effects of the chemotherapeutic drug, 5-FU, as shown by increased cell death and apoptosis. These effects are mediated via upregulation of the pro-apoptotic mediators cleaved caspase-3 and PARP and, downregulation of the anti-apoptotic mediator survivin. In addition, loss of VEGF led to increased levels of PlGF, SDF-1 and phosphorylated VEGFR-1 in CRC cells. Conclusion. Loss of autocrine/intracrine VEGF signaling leads to an increase in spontaneous apoptosis and chemosensitivity of colon cancer cells. In addition, loss of VEGF signaling led to increases in PlGF and SDF-1, suggesting that loss of VEGF signaling can lead to induction of compensatory pathways that may be mediated by numerous cell types in the tumor microenvironment. These findings have implications for a better understanding of mechanisms of action for VEGF targeted therapies when combined with chemotherapy in patients with metastatic CRC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 365.
The EUTOS prognostic score: review and validation in 1288 patients with CML treated frontline with imatinib
Authors: V S Hoffmann, M Baccarani, D Lindoerfer, F Castagnetti, A Turkina, A Zaritsky, A Hellmann, W Prejzner, J-L Steegmann, J Mayer, K Indrak, A Colita, G Rosti, M Pfirrmann
Journal: Leukemia (2013)
Correlation of the topographical arrangement and the functional pattern of tissue-infiltrating macrophages in giant cell arteritis.
Authors: C M Weyand, A D Wagner, J Björnsson, J J Goronzy
Journal: Journal of Clinical Investigation (1996)

End organ ischemia, fragmentation of elastic membranes, and aneurysm formation in patients with giant cell vasculitis results from an inflammation destroying the mural layers of large and medium sized arteries. Although the inflammatory infiltrate extends through all layers of the affected blood vessel, the most pronounced changes involve the intima and the internal elastic lamina. Analysis of the functional profile of tissue infiltrating CD68+ cells demonstrates that different subsets of macrophages can be distinguished. TGFbeta1-expressing CD68+ cells coproduce IL-1beta and IL-6, are negative for inducible nitric oxide synthase (iNOS), and exhibit a strong preference for localization in the adventitia. The adventitial homing of TGFbeta1+ CD68+ cells places them in the vicinity of IFN-gamma secreting CD4+ T cells which also accumulate in the exterior layer of the artery. Conversely, iNOS expressing CD68+ cells are negative for TGFbeta and are almost exclusively found in the intimal layer of the inflamed artery. The intimal-medial junction is the preferred site for 72-kD collagenase expressing CD68+ cells. Thus, TGFbeta1-producing macrophages colocalize with activated CD4+ T cells and home to an area of inflammation which is distant from the site of tissue damage but critical in regulating cellular influx, suggesting that TGFbeta1 functions as a proinflammatory mediator in this disease. iNOS- and 72-kD collagenase-producing macrophages accumulate at the center of pathology implying a role of these products in tissue destruction. These data indicate that the microenvironment controls the topographical arrangement as well as the functional commitment of macrophages.
Fratricide among CD8+ T Lymphocytes Naturally Infected with Human T Cell Lymphotropic Virus Type I
Authors: Emmanuel Hanon, Jane C Stinchcombe, Mineki Saito, Becca E Asquith, Graham P Taylor, Yuetsu Tanaka, Jonathan N Weber, Gillian M Griffiths, Charles R.M Bangham
Journal: Immunity (2000)
HIV in the Middle East
Authors: Carla Makhlouf Obermeyer
Journal: BMJ (2006)

x Summer caravans toured Morocco distributing 15 000 condoms and providing voluntary and confidential HIV testing and counselling to 7000 young people 21 The way forwardSensitivity surrounding young people's sexual and reproductive health has limited the knowledge base, particularly on young people's perspectives and needs, that could inform legislation, policy, and programmes.Appropriate sex education could be strengthened through working with teachers and parents.Special attention is needed in designing programmes that reach the most vulnerable young people.Above all, government commitment is required to translate the small scale models in the region to national programmes that improve the welfare of all young people.The statements in this article are the views of the authors and do not necessarily reflect the policies or the views of Unicef.Contributors and sources: This article draws on a larger study based on a literature review and interviews with 51 informants supported by Unicef 's Middle East and North Africa office. 1 Bonnie Shepard was responsible for the overall design of the study, gave numerous comments
Pressure Wave Transmission along the Human Aorta
Authors: MICHAEL F. O'ROURKE, James V. Blazek, Charles L. Morreels, L. Jerome Krovetz
Journal: Circulation Research (1968)

Pressure waves were recorded in the proximal aorta, iliac artery, and intermediate sites in 39 patients, aged 6 to 69 years, during diagnostic catheterization. In children, amplitude of the pressure wave increased progressively along the aorta, and a prominent diastolic wave appeared in the distal aorta and iliac artery. These changes in contour were associated with fluctuations in modulus and phase of the pressure wave harmonics. Alterations in the pressure wave during transmission became progressively less with increasing age, and the wave was transmitted virtually unchanged in the older patients with arterial degenerative disease. Percentage amplification (A) of the wave between aortic arch and iliac artery and age (x) were inversely related (A = 58.9 - 0.90x; P &lt;0.001). Transmission time (T, msec) from diaphragm to iliac artery shortened with age (T = 63.5 - 0.62x; P &lt;0.001) indicating a decrease in arterial distensibility. The relationship between amplification and transmission time in the abdominal aorta and iliac artery was A = 1.04T - 16.7 (P&lt; 0.001). Findings are attributed to a decline in peripheral reflection coefficient resulting from decreased distensibility of peripheral arteries with age and in arterial degenerative disease. The functional effects of decreased distensibility are to impair the efficiency of the arterial system in accepting pulsatile flow, and so to increase the load presented to the left ventricle.
Abstract 2989: Integrin-linked kinase regulates mitotic spindle dynamics and its overexpression leads to resistance to paclitaxel-induced cell death
Authors: Simin Lim, Andrew B. Fielding, Eiko Kawamura, Shoukat Dedhar
Journal: Cancer Research (2011)

Abstract Dysregulated mitosis is a hallmark of cancer. Many centrosomal proteins, including the integrin-linked kinase (ILK), that regulate microtubule organization and mitotic spindle assembly have been implicated in cancers. Inhibition or depletion of ILK result in a mitotic spindle defect that has not been well characterized and while ILK is overexpressed in many cancers, the effect of ILK overexpression on mitotic spindle function is unknown. In this study, we have characterized the defective spindle phenotype, and also looked at the effect of ILK overexpression on mitotic spindle function. HeLa cells stably over-expressing wild-type ILK were used for overexpression studies while parental HeLa cells were treated with QLT-0267, an ILK-specific inhibitor, to study the defective spindle phenotype. While ILK inhibition led to an abnormal mitotic spindle phenotype, the spindle contained bona fide kinetochore-microtubules that persisted after cold- or calcium-treatment. ILK inhibition, however, led to higher sister-centromere stretch in chromosomes aligned between two spindle poles, suggesting that kinetochores were under abnormally high tension, likely due to inhibition of microtubule polymerization. Microtubule regrowth in mitotic cells after cold depolymerization was significantly slower with ILK inhibition. In the context of ILK overexpression in cancers, we first measured the duration of mitosis and showed that ILK-overexpressing cells completed mitosis at a faster rate and also required shorter durations between metaphase and anaphase. ILK overexpression also resulted in increased resistance to paclitaxel-induced cell death. Collectively, our data suggest that ILK regulates microtubule dynamics, which is the focus of ongoing investigations in our laboratory, and ILK overexpression has clinical implications by inducing resistance to paclitaxel, possibly through increased microtubule dynamics. This work was supported by funding from the Canadian Institutes of Health Research. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2989. doi:10.1158/1538-7445.AM2011-2989
Jeannette M. Smith, MD, Comes to JAMA as 11th Fishbein Fellow in Medical Journalism
Authors: Marsha F. Goldsmith
Journal: JAMA (1989)

HCFA's LOSS will be<i>JAMA</i>'s gain when Jeannette M. Smith, MD, MPH, leaves her position as an analyst in the Office of Research, Health Care Financing Administration (HCFA), to become the 11th Morris Fishbein Fellow in Medical Journalism. The yearlong fellowship honors Morris Fishbein, MD, editor of<i>JAMA</i>for a quarter century (1924 to 1949). Smith received her bachelor of science degree, with honors in biology, from Andrews University, Berrien Springs, Mich, in 1977, and her MD degree from Loma Linda (Calif) University School of Medicine in 1981. She completed the residency program in anatomic and clinical pathology and an internship in internal medicine at Kettering Medical Center, Dayton, Ohio, before graduate study at Johns Hopkins University School of Hygiene and Public Health, Baltimore, Md, from which she received the MPH degree in 1986. <h3>Active in Ohio</h3> During her 4 years in Dayton, Smith held various positions. She spent
CROSSED RENAL ECTOPIA
Authors: Tom R. Barry
Journal: JAMA (1930)

In 1925, Kretschmer<sup>1</sup>reviewed the literature on crossed renal ectopia and found eighty-seven previously reported cases. In his article he mentions four additional ones, bringing the total to ninety-one. The cases of Beebee,<sup>2</sup>Compton<sup>3</sup>and Smith<sup>4</sup>were not included in this publication, which would bring the previously reported cases to ninety-four, to which I am adding an additional case referred through the courtesy of Dr. R. H. Newman. <h3>REPORT OF CASE</h3> A white woman, aged 28, single, consulted an ophthalmologist on account of some visual disturbance. The examination at this time showed a low grade hyperopic astigmatism associated with an exudate almost filling the entire right disk and extending to the nasal side of the disk. The details of the fundus could not be made out. There were several dark detached opacities in the vitreous. The left fundus was normal. On account of these observations, together
An Evaluation of Diagnostic Techniques Utilized in the Initial Workup of Pediatric Patients with Acute Lymphocytic Leukemia
Authors: D J KUNTZ, J C LEONARD, R M NITSCHKE, J J VANHOUTTE, D A WILSON, G P BASMADJIAN
Journal: Clinical Nuclear Medicine (1984)

The records of 32 pediatric patients with acute lymphocytic leukemia (ALL) were reviewed to evaluate the role of various diagnostic techniques used to assess the extent of extramedullary disease. Our findings indicate that adequate screening for hepatosplenomegaly is obtained by clinical assessment and for bone and renal involvement by bone scintigraphy including concomitant renal imaging. We recommend that radiographs be restricted to scintigraphically abnormal areas and/or sites of bone pain. Liver-spleen scintigraphy, gallium studies, intravenous pyelography, and ultrasound studies of the abdomen and pelvis should be utilized only to answer specific clinical questions. Evaluation in this manner reduces both radiation exposure and patient expense, while it adequately defines the extent of disease in these organs.
Oral 2, Silver hair in a 3-year-old child
Authors: R. Batchelor, S.M. Clark
Journal: British Journal of Dermatology (2007)

A 32‐month‐old girl of Pakistani origin presented to the paediatricians with a short history of abdominal pain, decreased appetite and lethargy and a history of developmental delay. She was referred to us when it was noted that her hair and eyebrows were silver in colour. While in hospital, she became progressively more unwell, developed neck stiffness and refused to walk. A diagnosis of acute meningitis was made and a prelumbar puncture computed tomographic scan showed hydrocephalus with enlarged third and lateral ventricles. She underwent a third ventriculostomy and insertion of a reservoir. Magnetic resonance imaging showed multiple focal ill‐defined enhancement with larger enhancing masses in the cerebellum. These appearances were initially thought suggestive of widely disseminated lymphoma or leukaemia. Surgical biopsy of these lesions was performed and histology showed some evidence of histiocytic tumour with a degree of erythrophagocytosis and lymphophagocytosis. In view of the histology and the phenotypic features, Griscelli syndrome was considered. Blood and hair from the patient were analysed and she was confirmed to be homozygous for a mutation in the RAB27A gene, which has been described in Griscelli syndrome. She has subsequently undergone bone marrow transplantation. Griscelli syndrome is a rare autosomal recessive disorder resulting in partial albinism and a combined immunodeficiency.1 Our case is unusual in that the presentation was neurological with no evidence of cytopenia. 1 Mancini AJ, Chan LS, Paller AS. Partial albinism with immunodeficiency: Griscelli syndrome: report of a case and review of the literature. J Am Acad Dermatol 1998; 38:295–300.
Endothelin-1–Induced Cardiac Hypertrophy Is Inhibited by Activation of Peroxisome Proliferator–Activated Receptor-α Partly Via Blockade of c-Jun NH <sub>2</sub> -Terminal Kinase Pathway
Authors: Yoko Irukayama-Tomobe, Takashi Miyauchi, Satoshi Sakai, Yoshitoshi Kasuya, Takehiro Ogata, Masakatsu Takanashi, Motoyuki Iemitsu, Tatsuhiko Sudo, Katsutoshi Goto, Iwao Yamaguchi
Journal: Circulation (2004)

Peroxisome proliferator-activated receptor-alpha (PPAR-alpha) is a lipid-activated nuclear receptor that negatively regulates the vascular inflammatory gene response by interacting with transcription factors, nuclear factor-kappaB, and AP-1. However, the roles of PPAR-alpha activators in endothelin (ET)-1-induced cardiac hypertrophy are not yet known.First, in cultured neonatal rat cardiomyocytes, a PPAR-alpha activator, fenofibrate (10 micromol/L), and PPAR-alpha overexpression markedly inhibited the ET-1-induced increase in protein synthesis. Second, fenofibrate markedly inhibited ET-1-induced increase in c-Jun gene expression and phosphorylation of c-Jun and JNK. These results suggest that this PPAR-alpha activator interferes with the formation and activation of AP-1 protein induced by ET-1 in cardiomyocytes. Third, fenofibrate significantly inhibited the increase of ET-1 mRNA level by ET-1, which was also confirmed by luciferase assay. Electrophoretic mobility shift assay revealed that fenofibrate significantly decreased the ET-1-stimulated or phorbol 12-myristate 13-acetate-stimulated AP-1 DNA binding activity, and the nuclear extract probe complex was supershifted by anti-c-Jun antibody. Fourth, 24 hours after aortic banding (AB) operation, fenofibrate treatment significantly inhibited left ventricular hypertrophy and hypertrophy-related gene expression pattern (ET-1, brain natriuretic peptide, and beta-myosin heavy chain mRNA) in AB rats.These results suggest that PPAR-alpha activation interferes with the signaling pathway of ET-1-induced cardiac hypertrophy through negative regulation of AP-1 binding activity, partly via inhibition of the JNK pathway in cultured cardiomyocytes. We also revealed that fenofibrate treatment inhibited left ventricle hypertrophy and phenotypic changes in cardiac gene expression in AB rats in vivo.
Election of Republican senator derails US healthcare reform
Authors: J. H. Tanne
Journal: BMJ (2010)

The election of Scott Brown, a Republican, to fill the Massachusetts Senate seat held for 46 years by the Democrat Ted Kennedy has disrupted President Barack Obama’s plan for healthcare reform.

Mr Kennedy, who died in August, had made health care for all Americans one of his lifelong goals.

The House of Representatives and the Senate had both passed healthcare reform bills extending care to at least 30 million of America’s 46 million uninsured citizens. The next step would have been to reconcile the two bills and then have the reconciled bill passed by the House and Senate and signed by the president ( BMJ 2010;340:c173, doi:10.1136/bmj.c173).

That will not …
Monoclonal antibody therapy for prevention of acute coxsackievirus B3 myocarditis in mice.
Authors: C Kishimoto, W H Abelmann
Journal: Circulation (1989)

The efficacy of monoclonal antibodies against T cell subsets in the therapy of experimental myocarditis caused by coxsackievirus B3 (CB3) was investigated. Two-week-old male C3H/He mice were inoculated with CB3 virus. Treatment was begun in the viremic stage (starting on the day of inoculation) in experiment 1 and in the later aviremic stage (starting on day 10) in experiment 2. Rat anti-mouse monoclonal antibodies, Lyt 1 (helper/inducer T) at 1 microgram/mouse (group 2 in experiment 1; group 6 in experiment 2), Lyt 2 (suppressor/cytotoxic T) at 1 microgram/mouse (group 3 in experiment 1; group 7 in experiment 2), and Lyt 1 at 1 microgram plus Lyt 2 at 1 microgram/mouse (group 4 in experiment 1; group 8 in experiment 2), were administered subcutaneously daily for 2 weeks. The treatment groups were compared with infected controls (group 1 in experiment 1; group 5 in experiment 2). In experiment 1, the survival rate in group 4 was higher (p less than 0.01) than in group 1. In experiment 2, mice treated with Lyt 1 plus Lyt 2 (group 8) survived significantly longer (p less than 0.05) than did controls (group 5). In experiment 1, myocardial virus titers on days 5 and 6 did not show any significant differences among the four groups. Serum-neutralizing antibody titers between group 1 and group 4 in experiment 1 or between group 5 and group 8 in experiment 2 did not differ significantly. Histologic examination showed extensive myocardial necrosis and cellular infiltration in untreated groups: there was less infiltration in group 4 and in group 8 and less severe necrosis in group 8.(ABSTRACT TRUNCATED AT 250 WORDS)
Semi-quantification of pneumothorax volume by lung ultrasound
Authors: Giovanni Volpicelli, Enrico Boero, Nicola Sverzellati, Luciano Cardinale, Marco Busso, Francesco Boccuzzi, Mattia Tullio, Alessandro Lamorte, Valerio Stefanone, Giovanni Ferrari, Andrea Veltri, Mauro F. Frascisco
Journal: Intensive Care Medicine (2014)