tbuckley/cabot-search huggingface dataset:
Statins Have Biphasic Effects on Angiogenesis
Authors: Michael Weis, Christopher Heeschen, Alec J. Glassford, John P. Cooke
Journal: Circulation (2002)

Statins inhibit HMG-CoA reductase to reduce the synthesis of cholesterol and isoprenoids that modulate diverse cell functions. We investigated the effect of the statins cerivastatin and atorvastatin on angiogenesis in vitro and in vivo.Endothelial cell proliferation, migration, and differentiation were enhanced at low concentrations (0.005 to 0.01 micromol/L) but significantly inhibited at high statin concentrations (0.05 to 1 micromol/L). Antiangiogenic effects at high concentrations were associated with decreased endothelial release of vascular endothelial growth factor and increased endothelial apoptosis and were reversed by geranylgeranyl pyrophosphate. In murine models, inflammation-induced angiogenesis was enhanced with low-dose statin therapy (0.5 mg x kg(-1) x d(-1)) but significantly inhibited with high concentrations of cerivastatin or atorvastatin (2.5 mg x kg(-1) x d(-1)). Despite the fact that high-dose statin treatment was effective at reducing lipid levels in hyperlipidemic apolipoprotein E-deficient mice, it impaired rather than enhanced angiogenesis. Finally, high-dose cerivastatin decreased tumor growth and tumor vascularization in a murine Lewis lung cancer model.HMG-CoA reductase inhibition has a biphasic dose-dependent effect on angiogenesis that is lipid independent and associated with alterations in endothelial apoptosis and vascular endothelial growth factor signaling. Statins have proangiogenic effects at low therapeutic concentrations but angiostatic effects at high concentrations that are reversed by geranylgeranyl pyrophosphate. At clinically relevant doses, statins may modulate angiogenesis in humans via effects on geranylated proteins.
P223 End of life discussion in pulmonary rehabilitation: too scary or worth a try?
Authors: S. Robinson, L. Wilson, M. Qayoom, S. Dawson, L. Killeen, T. Shturova, I. S. Patel
Journal: Thorax (2011)

<h3>Background</h3> End of life is a topic which may be included in pulmonary rehabilitation (PR) education sessions. Patient expectations from such a session, its optimal content, and who should deliver it is unknown. <h3>Method</h3> The community PR programme in Hammersmith and Fulham has included a session entitled “Managing the Final Stages of COPD” since April 2010. Apprehensions and training needs around this subject were identified in respiratory staff running PR and therefore a community matron with an interest in palliative and end of life care led the sessions. Twelve–sixty min end of life discussion sessions were delivered from April 2010 to June 2011. The content was based around the eponymous British Lung Foundation (BLF) leaflet. Discussions focused principally on making a will, arranging a funeral and considering a Power of Attorney or Advance Decision. Participants were given advance notice and an opportunity to “opt out”. <h3>Results</h3> 72 patients attended these sessions (average number 6). None opted out. One patient asked for more information afterwards. Two partcipants became upset during the session; one opted to attend in spite of a recent bereavement and the other reported “feeling relieved”. Evaluation responses are shown in Abstract P223 table 1. <h3>Conclusion</h3> Advanced care planning is well received and can be delivered as part of community PR education. Respiratory staff leading PR are now confident about delivering this themselves. However this setting is not able to address the advanced care planning needs of specific patients with adverse prognostic indicators and this needs separate planning.
Proceedings: On the relationship between inflammatory joint disease and the foregut hormones, gastrin and secretin.
Authors: P J Rooney, J Millar, J R Hayes, K D Buchanan, W C Dick
Journal: Annals of the Rheumatic Diseases (1974)

This year marks the 40th anniversary of the initial identification of p53 as a transformation-related Ag, which was the result of our effort to identify an antigenically distinct tumor Ag of a chemically induced mouse tumor and develop a cancer vaccine. Many researchers at the time viewed this effort as folly. Since then, its characterization has progressed from being an attractive cancer vaccine candidate to recognition as a key player in regulating critical pathways controlling the cell cycle and oncogenesis. Advances in molecular immunology and oncology have enhanced the role of p53 in both fields. It is now apparent that p53 plays a critical role in controlling immune recognition and responses in normal tissues as well as the tumor microenvironment. Together with the advances in clinical implementation of p53-based cancer immunotherapy, they highlight the importance of p53 in many areas of basic and translational cancer research.
The role of cytogenetic abnormalities as a prognostic marker in primary myelofibrosis: applicability at the time of diagnosis and later during disease course
Authors: Constantine S. Tam, Lynne V. Abruzzo, Katherine I. Lin, Jorge Cortes, Alice Lynn, Michael J. Keating, Deborah A. Thomas, Sherry Pierce, Hagop Kantarjian, Srdan Verstovsek
Journal: Blood (2009)
Abstract P1-02-05: EPLIN? Can Negatively Impact on Angiogenesis and Is Associated with ERK Signalling
Authors: AJ Sanders, L Ye, WG Jiang, MD. Mason
Journal: Cancer Research (2010)

Abstract Background: EPLIN (epithelial protein lost in neoplasm) is a cytoskeletal associated protein involved in regulating actin dynamics and cell motility. EPLIN expression is frequently lost in cells as they progress to a cancer state and this loss may account for enhanced cancer cell motility. EPLIN has also been shown to be lost in clinical breast cancer, which is associated with patients clinical outcome. Recently, EPLIN has been linked to ERK signalling. This study examined the potential of EPLIN to influence the angiogenesis process and its links to ERK in endothelial cells Methods: Over-expression of EPLIN α was achieved through transfection of the vascular endothelial cell, HECV, with a mammalian expression construct containing the full coding sequence of EPLINα. Enhanced levels of EPLINα were verified through RT-PCR, Q-PCR and Western blot analysis before assessing the angiogenic potential of control and transfected cells using angiogenesis and cell migration models. Treatment of transfected and control cells with ERK inhibitor was used to assess the potential interaction between EPLINα and ERK in endothelial cells. Results: Substantial enhancement in EPLINα expression was seen in transfected cells compared to control cells at both transcript and protein level. Over-expression of EPLINα in HECV endothelial cells resulted in a reduced capacity, compared to control, of these cells to form tubule like structures in an in vitro angiogenesis tubule formation assay (6566 +/− 856µm tubule perimeter of control cells vs 2881 +/− 546µm EPLINα overexpressing HECV cells, p = 0.007). This was seen together with a reduced cell migration following overexpression of EPLINα in the cells. Treatment of control cells with ERK inhibitor significantly reduced tubule formation (3537 +/− 277µm tubule perimeter of ERK inhibitor treated control cells vs 6566 +/− 856µm total perimeter of untreated control cells, p = 0.01), however treatment of HECV cells transfected with EPLINα expression construct caused tubule formation levels to return to control levels (6566 +/− 856µm tubule perimeter of untreated control cells vs 5326 +/− 784µm tubule perimeter of ERK inhibitor treated EPLINα overexpressing HECV cells, p = 0.317). Discussion: EPLINα can negatively influence tubule formation in vitro and thus may impact on the angiogenesis process. Furthermore, its impact on tubule formation appears to be linked to ERK signalling. Together, this study suggests a role for EPLINα in angiogenesis, which may be linked with ERK signalling. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P1-02-05.
Social environments and health: cross sectional national survey
Authors: A. McCulloch
Journal: BMJ (2001)

supported.The child protection system does not cause the deaths-none of the children died as a result of abuse or violence by parents or foster parents.However, the system fails to protect adolescents from self endangering behaviour both within the system and during adaptation to independent living.The results indicate the need for continuing attention to be paid to the transition period from foster care to independence.We thank the Ministry of Social Welfare and
UNITED STATES GENERAL HOSPITAL FOR TUBERCLOSIS AT FORT BAYARD, N. M.
Authors: D. M. APPEL
Journal: JAMA (1900)

An order issued by the War Department, August 28, 1899, authorized the surgeon-general to establish a general hospital at Fort Bayard, N. M., as a sanitarium for the treatment of officers and enlisted men of the army suffering from pulmonary tuberculosis, and also to provide therein for the care and treatment of discharged soldiers entitled to the benefits of the U. S. Soldiers' Home, at Washington, D. C. Under the latter clause patients are enabled to remain under treatment indefinitely, even after their discharge from the army by reason of their physical disability or from expiration of their term of enlistment. Fort Bayard was selected by the surgeon-general not only for its admirably suited climate but also because it was immediately available, its abandonment as a military post having been contemplated for some years, and, excepting for its isolation and difficulty of access, no better locality could have been chosen.
Seroconversion of GAD Antibody in “Unclassified” Diabetes With Long Duration of Disease
Authors: Toshikatsu Shigihara, Akira Shimada, Yoshihumi Saisho, Toshihide Kawai, Hiroshi Maruyama, Takao Saruta
Journal: Diabetes Care (2004)

Latent autoimmune diabetes in adults (LADA) (1), or slowly progressive insulin-dependent diabetes mellitus (SPIDDM) (2), is a subtype of type 1 diabetes with a slowly progressive course. LADA, or SPIDDM, is diagnosed by the detection of islet-associated autoantibodies such as islet cell antibody (ICA) or GAD antibody (GADA) in the serum; moreover, patients with LADA are usually originally diagnosed as having type 2 diabetes. If islet-associated autoantibodies are not detected in the serum, these patients who are originally diagnosed as having type 2 diabetes cannot be diagnosed as having LADA and are followed as “unclassified” diabetes at present.

In clinical situations, if islet-associated autoantibodies are not initially detected in the serum, these cases are usually followed as type 2 diabetes or …
Ischaemia and reperfusion induced transient QRS vector changes: relationship to size of the ischaemic territory
Authors: U. Naslund, S. Haggmark, G. Johansson, S. Reiz
Journal: Cardiovascular Research (1993)

Objective: The aim was to investigate QRS vector changes during the first 30 min of coronary occlusion or the early phase of reperfusion with special reference to location and size of myocardium at risk. Methods: 24 h experiments were performed in closed chest anaesthetised pigs. QRS vectors were studied by computerised vectorcardiography via Frank leads. Occlusion of the left anterior descending coronary artery followed by reperfusion was induced in 23 pigs and a sustained occlusion in 20 pigs: left anterior descending coronary artery in seven, right coronary artery in eight, and left circumflex coronary artery in five. Myocardium at risk was measured in postmortem autoradiograms. Eight animals were excluded. Results: Four minutes after occlusion, QRSmcan deviated towards the ischaemic region in 34/35 animals and returned thereafter at varying speeds. In half of the reperfused animals, deviation of QRS vectors towards the ischaemic territory was also observed during the first minutes of reperfusion. A paradoxical increase in QRS vector changes, “reperfusion peak”, was recorded during the initial minutes of reperfusion in 12/19 animals. Maximum spatial QRS vector magnitude increased in all right coronary or left circumflex coronary occlusion animals compared to 6/25 in left anterior descending coronary occlusion animals. QRS vector difference, change in spatial QRS vector angle, and maximum change in QRS azimuth 4 min after occlusion correlated significantly with extent of myocardium at risk. Conclusions: Marked directional and quantitative QRS vector changes, with significant relation to size and location of myocardium at risk, were recorded during the initial minutes of ischaemia. The transient increase in QRS vector changes during the first minutes of reperfusion deserves further exploration as a new indicator of reperfusion. Cardiovascular Research 1993;27:327-333
Homologous sensitisation of embryonic chick atrial myocytes to adenosine: mediation by adenosine A1 receptor and guanine nucleotide binding protein
Authors: B. T Liang, A. J Hirsch
Journal: Cardiovascular Research (1993)

Objective: The aim was to characterise the process and the mechanisms of sensitisation of the atrial myocyte to adenosine receptor agonist. Methods: The ability of adenosine A1 receptor to mediate inhibition of adenylyl cyclase activity and myocyte contractility was determined in atrial myocytes cultured from 14 d chick embryos. Under conditions in which the myocytes were sensitised to the effects of A1 agonist, changes in the levels of adenosine A1 receptor and pertussis toxin sensitive G proteins were determined and correlated with alterations in the adenylyl cyclase activity and contractile responses of the myocyte to the A1 agonist. Results: Removal of adenosine from the culture medium with adenosine deaminase resulted in an enhanced ability of the adenosine A1 receptor agonist R-N6-(2-phenylisopropyl)-adenosine to exert a direct, negative inotropic effect and to inhibit isoprenaline stimulated adenylyl cyclase activity. The increase in the extent of maximum inhibition of adenylyl cyclase activity and of myocyte contractility was 215(30), n=5, and 90(10)%, n=14, respectively. Binding of the antagonist radioligand [3H]-8-cyclopentyl-1,3-dipropylxanthine in membranes from myocytes pre-exposed to adenosine deaminase showed a 70% increase in the adenosine A1 receptor density and a 54% increase in the proportion of the high affinity adenosine A1 receptor: control 33(5)%, n=5, versus sensitised 49(3)%, n=5, p<0.01. The increase in the total number of adenosine receptors and the proportion of the high affinity form was associated with a similar increase in the level of pertussis toxin sensitive G protein(s), as determined by pertussis toxin mediated 32P-ADP ribosylation and by immunoblotting. Prior exposure of the culture to the adenosine receptor antagonist 8-(p-sulphophenyl) theophylline also led to similar results. Conclusions: The data indicate that the increased level of pertussis toxin sensitive G protein(s) results in an enhanced coupling to form the high affinity adenosine A1 receptor, that newly formed high affinity receptors are linked to an enhanced sensitivity of atrial myocytes to A1 adenosine agonist stimulation, and that upregulation of the G protein is a mechanism mediating the homologous sensitisation of cardiac adenosine A1 receptor pathway. Cardiovascular Research 1993;27:102-110
The use of epcs (endothelial progenitor cells) for the regeneration of the musculoskeletal system and the spine
Authors: N C Keramaris, E Tsiridis, N Malliaropoulos, A Kostakos, A Topkas, S Pnevmatikos, P J Papagellopoulos, G Sapkas
Journal: British Journal of Sports Medicine (2011)

Introduction Endothelial progenitor cells (EPCs) are cells that can differentiate into endothelial cells in vitro. Their importance lies on the fact that vasculature has a cornerstone role in the healing process after injury of the musculoskeletal system and of the spine. The main target of this review is to clarify whether EPCs could be a viable alternative of mesenchymal stem cells for musculoskeletal regeneration. Methods The literature search was performed via the internet using the Medline, Scopus and Cochrane database. The key words which were searched in the abstracts were the terms ‘EPCs’, ‘bone’, ‘spine cord’, ‘cartilage’, ‘menisci’, ‘ligament’, ‘tendon’ and ‘healing’. Results Three papers reported that EPCs can differentiate into osteoblasts in vitro. In a fourth paper, EPCs were used in an in vivo model in order to enhance the fracture healing in a non-union animal model. A fifth paper implies that fracture may induce mobilisation of EPCs and recruitment of the mobilised EPCs into fracture sites. Another two papers showed that local transplantation of EPCs with atelocollagen scaffold is a feasible strategy for therapeutic vasculogenesis and osteogenesis needed for fracture and ligament healing. Another paper suggested that co-transplantation of hematopoietic and mesenchymal stem/progenitor cells may improve the regeneration of vascular dependent tissues such as bone, adipose, muscle and dermal grafts. Two papers reported stimulating results for the use of EPCs for spine cord regeneration. Discussion The importance of EPCs for the healing of both musculoskeletal tissue and spine is based on the advantages of this cell population for regeneration purposes: (1) relative abundance, (2) isolation by the circulation, (3) new insight revealing new mechanisms
Hepatitis Associated with Myocarditis
Authors: Nelson C. Sun, Vernon M. Smith
Journal: New England Journal of Medicine (1966)

INFECTION with Coxsackie virus Group B has been shown to cause varying combinations of pleuritis, meningitis, encephalitis, pericarditis, myocarditis, epididymitis, orchitis and pancreatitis.1 2 3 It may result in severe illness and death in newborn and infant children. The uncomplicated disease runs a more benign course in adults.Despite the demonstratedly widespread organ involvement in this disease, associated hepatitis in adult patients has been suggested in only 2 previously published reports.4 , 5 Furthermore, there has been no published report of the pathologic changes occurring in the livers of adult patients with proved infection with Coxsackie virus Group B.Recently, a nineteen-year-old female patient, . . .
Mobile genetic elements of the human gastrointestinal tract
Authors: Eileen Broaders, Cormac G.M. Gahan, Julian R. Marchesi
Journal: Gut Microbes (2013)

The human intestine is an important location for horizontal gene transfer (HGT) due to the presence of a densely populated community of microorganisms which are essential to the health of the human superorganism. HGT in this niche has the potential to influence the evolution of members of this microbial community and to mediate the spread of antibiotic resistance genes from commensal organisms to potential pathogens. Recent culture-independent techniques and metagenomic studies have provided an insight into the distribution of mobile genetic elements (MGEs) and the extent of HGT in the human gastrointestinal tract. In this mini-review, we explore the current knowledge of mobile genetic elements in the gastrointestinal tract, the progress of research into the distribution of antibiotic resistance genes in the gut and the potential role of MGEs in the spread of antibiotic resistance. In the face of reduced treatment options for many clinical infections, understanding environmental and commensal antibiotic resistance and spread is critical to the future development of meaningful and long lasting anti-microbial therapies.
Discrepancy between Clinical and Pathologic Stage: Impact on Prognosis after Radical Cystectomy
Authors: Shahrokh F. Shariat, Ganesh S. Palapattu, Pierre I. Karakiewicz, Craig G. Rogers, Amnon Vazina, Patrick J. Bastian, Mark P. Schoenberg, Seth P. Lerner, Arthur I. Sagalowsky, Yair Lotan
Journal: European Urology (2006)
Review of <i>Contemporary Bioethics: A Reader With Cases</i>
Authors: Ernlé W. D. Young
Journal: JAMA (2011)

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Senators question Medtronic about unreported side effects of spinal protein
Authors: Z. Kmietowicz
Journal: BMJ (2011)

US senators have given a medical device manufacturer until 11 July to explain media reports that researchers studying a product commonly used in spinal surgery failed to mention important side effects. The senators are also concerned that some surgeons who conducted the trials received payments from the company amounting to as much as $26m (£16m; €18m) to perform a study and failed to declare them.

Members of the Senate Committee on Finance, which has jurisdiction over the Medicare and Medicaid health insurance programmes and responsibility to ensure that treatments used are safe and effective, say that they are “extremely troubled” by the reports.

The committee has asked the chairman and chief executive officer of Medtronic to provide it with a number of documents, including all communications with medical journals and investigators who took part in trials relating to the use of morphogenetic protein 2 (rhBMP-2), a recombinant human bone protein …