tbuckley/cabot-search huggingface dataset:
Identification of novel biomarkers in plasma for prediction of treatment response in patients with heart failure
Authors: Thong Huy Cao, Paulene A Quinn, Jatinderpal K Sandhu, Adriaan A Voors, Chim C Lang, Helen M Parry, Mohapradeep Mohan, Donald J L Jones, Leong Loke Ng
Journal: The Lancet (2015)
1149-162 Sinus rhythm restoration after the maze operation and relationship between pre- and postoperative left atrial volume
Authors: Hyelim Oh, Jinho Choi, Sangcheol Lee, Jidong Sung, Hyeoncheol Gwon, Junesoo Kim, Eunseok Jeon, Dukkyung Kim, Sanghoon Lee, Pyowon Park, Kyungpyo Hong, Jeongeuy Park, Jungdon Seo
Journal: Journal of the American College of Cardiology (2004)
Antithrombotic Potency of Hirudin Is Increased in Nonhuman Primates by Fibrin Targeting
Authors: Christoph Bode, Stephen R. Hanson, John F. Schmedtje, Edgar Haber, Petra Mehwald, Andrew B. Kelly, Laurence A. Harker, Marschall S. Runge
Journal: Circulation (1997)

Background Inhibition of thrombin by either the indirect thrombin inhibitor heparin or by more potent direct thrombin inhibitors such as hirudin reduces thrombus formation after arterial injury. The present study was designed to determine if a fibrin-specific thrombin inhibitor could, by local thrombin inhibition, prevent thrombosis more effectively. Methods and Results We first studied antithrombotic potency in vitro, comparing fibrin-targeted hirudin (recombinant hirudin covalently linked to the Fab′ fragment of the anti-fibrin monoclonal antibody 59D8) to recombinant hirudin in baboon plasma. Fibrin-targeted hirudin was nine times more effective than recombinant hirudin in inhibiting fibrin deposition on experimental clot surfaces in baboon plasma ( P &lt;.01). The potency of fibrin-targeted hirudin was then compared with that of recombinant hirudin in a baboon model of thrombus formation. 111 In-labeled platelet deposition was measured in a synthetic graft segment of an extracorporeal arteriovenous shunt in control animals and in animals receiving either fibrin-targeted hirudin or hirudin. In these experiments, fibrin-targeted hirudin was 10-fold more potent than hirudin in inhibiting platelet deposition and thrombus formation ( P &lt;.05). Conclusions These data indicate that targeting a thrombin inhibitor such as hirudin to an epitope present in thrombi results in increased antithrombotic potency.
Technique for Locating Kidney for Needle Biopsy
Authors: W. H. Tu
Journal: JAMA (1965)

<h3>To the Editor:—</h3> Although the technique of percutaneous renal biopsy described by Iversen and Brun<sup>1</sup>was improved by placing the patient in the prone position and locating the kidney in advance with the aid of a fine exploratory needle,<sup>2</sup>a satisfactory specimen may not always be obtained.<sup>3,4</sup>Various methods have been used in attempts to improve location of the kidney for biopsy, including direct fluoroscopic visualization during the procedure,<sup>5</sup>radioactive mercury scan,<sup>6</sup>use of an ultrasonic device,<sup>7</sup>and use of radiopaque skin markers in conjunction with a urogram taken in the prone position.<sup>8</sup>Further refinement of the ultrasonic technique may simplify accurate three-dimensional location of the kidney. Without entailing the use of special devices, the simple technique described in this communication yielded a high incidence of successful renal biopsy. The method adjusts for geometric distortion on the roentgenogram. The spinous processes, which are always
Characterization of in vivo expression of the human papillomavirus type 16 E4 protein in cervical biopsy tissues.
Authors: J M Palefsky, B Winkler, J P Rabanus, C Clark, S Chan, V Nizet, G K Schoolnik
Journal: Journal of Clinical Investigation (1991)

The role of human papillomavirus (HPV) proteins in the pathogenesis of cervical intra-epithelial neoplasia (CIN) and invasive cervical cancer is poorly understood. To characterize E4 protein expression in 49 paraffin-embedded cervical biopsies representing different histopathologic grades of disease, antibodies were elicited to a synthetic peptide corresponding to amino acids 20-34 of a protein predicted to be encoded by the HPV 16 E4 open reading frame. The E4 protein was detected throughout the spectrum of CIN, from CIN1 to CIN3. Expression was localized to the cell nucleus, primarily in the superficial layers of the squamous cervical epithelium. Ultrastructural studies showed that the E4 protein was organized into compact, intranuclear arrays 25-35 nm in diameter. E4 protein expression was also demonstrated in some histologically normal tissues containing HPV 16 DNA, but not in any of five cervical cancers containing HPV 16 DNA. These results suggest that E4 protein expression may precede development of light microscopic tissue abnormalities, that it may continue through the spectrum of CIN, and that expression of this protein may be reduced or terminated in invasive cancer. The function of this protein remains unknown, but its nuclear localization may be consistent with a role in viral maturation.
THE PROPORTION OF CERTAIN IMPORTANT INORGANIC CONSTITUENTS IN THE DYING HEART MUSCLE
Authors: L. C. Scott
Journal: Journal of Clinical Investigation (1930)

Careful survey of the literature does not reveal many examinations of the cardiac muscle for inorganic elements.As a matter of fact I have only been able to discover one analysis of the human heart which makes any pretension to a detailed series of determinations, by Le- matte et al. (1) and this apparently was only on one heart.These investigators determined the percentages of alkali and alkaline earth metals, phosphoric acid, iron, and dry residue, and reported their results in the form of the hydroxides of sodium, potassium, calcium, and magnesium.Determinations of potassium and sodium have been recently made on human heart and skeletal muscle by Harrison, Pllcher, and Ewing (2).Norn (3) also gives a series of potassium and sodium determinations made on the human dog and ox heart.Matthews (4) presents some
Welsh Office to review consultant's lengthy suspension
Authors: R. Dobson
Journal: BMJ (1999)

Two orphan leucine-rich repeat-containing G protein-coupled receptors were recently identified as targets for the relaxin family peptides relaxin and insulin-like peptide (INSL) 3. Human gene 2 relaxin is the cognate ligand for relaxin family peptide receptor (RXFP) 1, whereas INSL3 is the ligand for RXFP2. Constitutively active mutants of both receptors when expressed in human embryonic kidney (HEK) 293T cells signal through Gα<sub>s</sub> to increase cAMP. However, recent studies using cells that endogenously express the receptors revealed greater complexity: cAMP accumulation after activation of RXFP1 involves a time-dependent biphasic pathway with a delayed phase involving phosphoinositide 3-kinase (PI3K) and protein kinase C (PKC) ζ, whereas the RXFP2 response involves inhibition of adenylate cyclase via pertussis toxin-sensitive G proteins. The aim of this study was to compare and contrast the cAMP signaling pathways used by these two related receptors. In HEK293T cells stably transfected with RXFP1, preliminary studies confirmed the biphasic cAMP response, with an initial Gα<sub>s</sub> component and a delayed response involving PI3K and PKCζ. This delayed pathway was dependent upon G-βγ subunits derived from Gα<sub>i3</sub>. An additional inhibitory pathway involving Gα<sub>oB</sub> affecting cAMP accumulation was also identified. In HEK293T cells stably transfected with RXFP2, the cAMP response involved Gα<sub>s</sub> and was modulated by inhibition mediated by Gα<sub>oB</sub> and release of inhibitory G-βγ subunits. Thus, initially both RXFP1 and RXFP2 couple to Gα<sub>s</sub> and an inhibitory Gα<sub>oB</sub> pathway. Differences in cAMP accumulation stem from the ability of RXFP1 to recruit coupling to Gα<sub>i3</sub>, release G-βγ subunits and thus activate a delayed PI3K-PKCζ pathway to further increase cAMP accumulation.
Procainamide and Neutropenia
Authors: R.M. GABRIELSON
Journal: Annals of Internal Medicine (1984)

Letters and Corrections1 May 1984Procainamide and NeutropeniaR.M. GABRIELSON, M.D.R.M. GABRIELSON, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-100-5-766_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Ellrodt and coworkers (1) have performed an important service by calling attention to the problem of neutropenia (granulocytopenia), a known adverse effect of procainamide therapy. Although their article emphasizes an apparent increase in incidence of neutropenia, no explanation is offered. Perhaps the rate of occurrence merits discussion.Patient compliance with the newer sustained-release procainamide dosage (every 6 h) is undoubtedly far greater than with the former conventional dosage (every 3 h). It has been suggested that procainamide prescribing is becoming more aggressive; daily dosages of 4 g, or more are not uncommon. The most important point, however,...References1. ELLRODT A, MURATA G, RIEDINGER M, STEWART M, MOCHIZUKI C, and GRAY R. Severe neutropenia associated with sustained-release procainamide. Ann Intern Med. 1984;100:197-201. LinkGoogle Scholar2. MEYERS J. Cytomegalovirus infections (cytomegalic inclusion disease). In: PETERSDORF RG, ed. Harrison's Principles of Internal Medicine. New York: McGraw-Hill Book Company; 1983:1167-70. Google Scholar3. FELMAN Y and NIKITAS J. Cytomegalovirus infection. Cutis. 1981;27:562-71. MedlineGoogle Scholar4. RUBIN R, COSIMI A, TOLKOFF-RUBIN N, RUSSEL P, and HIRSCH M. Infectious disease syndromes attributable to cytomegalovirus and their significance among renal transplant recipients. Transplantation. 1977;24:458-64. CrossrefMedlineGoogle Scholar5. BETTS R. Syndromes of cytomegalovirus infection. In: STOLLERMAN GH, ed. Advances in Internal Medicine. Chicago: Year Book Medical Publishers; 1980:447-66. MedlineGoogle Scholar1. ELLRODT A, MURATA G, REIDINGER M, STEWART M, MOCHIZUKI C, and GRAY R. Severe neutropenia associated with sustained-release procainamide. Ann Intern Med. 1984;100:197-21. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: R.M. GABRIELSON, M.D.Affiliations: Parke-Davis Morris Plains, NJ 07950 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCardiac glycosides and drugs used in dysrhythmias 1 May 1984Volume 100, Issue 5Page: 766-767KeywordsNeutropenia ePublished: 1 December 2008 Issue Published: 1 May 1984 PDF downloadLoading ...
An apolipoprotein E synthetic peptide targets to lipoproteins in plasma and mediates both cellular lipoprotein interactions in vitro and acute clearance of cholesterol-rich lipoproteins in vivo.
Authors: I R Nikoulin, L K Curtiss
Journal: Journal of Clinical Investigation (1998)

Apolipoprotein (apo) E mediates lipoprotein binding to cellular lipoprotein receptors. Previously we reported that a synthetic peptide representing a linear dimeric repeat of amino acids 141-155 binds cellular LDL receptors. To prepare an apoE peptide that bound to both cholesterol-rich lipoproteins and lipoprotein receptors, an NH2-terminal acetylated apoE dimer peptide was synthesized. This acetylated peptide preferentially associated with lipoproteins in plasma, whereas nonacylated peptides were poor lipid binders. Acetylated peptide/LDL complexes (molar ratios of 4-5:1) enhanced the interaction of LDL with cultured human fibroblasts by 7-12-fold. Participation by both receptors and cell surface heparin sulfate proteoglycans was observed. When a preformed peptide/125I-LDL complex was injected intravenously into C57BL/6J apoE-deficient mice, its rate of removal was threefold higher than that of 125I-LDL alone. The liver and the spleen were major tissue distribution sites. Intravenous administration of free acetylated peptide resulted in a 30% reduction in total plasma cholesterol within 3-30 min, which reflected a 40-50% and 20-26% reduction in very low density lipoproteins and intermediate density lipoproteins, respectively. Therefore, this peptide selectively associated with cholesterol-rich lipoproteins and mediated their acute clearance in vivo.
Highly effective SNP-based association mapping and management of recessive defects in livestock
Authors: Carole Charlier, Wouter Coppieters, Frédéric Rollin, Daniel Desmecht, Jorgen S Agerholm, Nadine Cambisano, Eloisa Carta, Sabrina Dardano, Marc Dive, Corinne Fasquelle, Jean-Claude Frennet, Roger Hanset, Xavier Hubin, Claus Jorgensen, Latifa Karim, Matthew Kent, Kirsten Harvey, Brian R Pearce, Patricia Simon, Nico Tama, Haisheng Nie, Sébastien Vandeputte, Sigbjorn Lien, Maria Longeri, Merete Fredholm, Robert J Harvey, Michel Georges
Journal: Nature Genetics (2008)
The clinical and financial burden of emergency readmissions following elective endoscopy in a teaching hospital practice
Authors: A. Moore, J. Taylor, S. Sarkar
Journal: Gut (2011)

<h3>Introduction</h3> Endoscopy is a profitable day case service for most trusts through it9s income generation potential from PBR. Although on the whole, endoscopy is safe, it does potentially carry small but significant risk which can result in patient morbidity and even mortality. Readmission is monitored quality indicator within the NHS, but following elective endoscopy, is not only a safety concern but can potentially offset the income generation of the service. <h3>Aims</h3> To explore the clinical and financial impact of emergency hospital readmission following elective endoscopy. <h3>Methods</h3> Over 1 financial year (2008–2009), all emergency readmissions within 6 days of an elective GI endoscopy at the Royal Liverpool University Hospital – (provided by clinical information department from Dr Foster Intelligent Systems) were audited for clinical relevance and outcomes. The PBR income generation via the HRG4 grouper for the readmission (hospital Income) and the true cost (reference) of the hospital admission (ie, hospital expenditure) were independently calculated. A deficit between the two indicated either a net loss for a (−ve) or a net profit (+ve) for the trust. <h3>Results</h3> Of the 8365 day-case GI endoscopies performed, 96 were CODED as readmission (1.4%). However, 26 were coding anomalies and were not readmissions making a REAL readmission rate of 0.83%. Of the remainder only 29 were related to endoscopy making and endoscopy related readmission rate of 0.34%. In these patients, the mean length of stay was 5.5 days (7.6 SD), with an overall surgical intervention rate 0.024% but 8.6% in the readmissions. The overall 30-day mortality was 0.012%, but in the readmission only group 4.3%. The cost of readmissions for the all coded readmissions (CODED), actual readmission (REAL) and the endoscopic related readmissions (ENDO) are shown in table 1. The hospital costs from our clinical information services were suggested at £94, 015, but the true figure was 55% lower (£41 528). <h3>Conclusion</h3> The clinical burden of emergency readmissions following elective endoscopy carries a significant LOS, surgical intervention rate and mortality. There are marked discrepancies within the data for readmissions attributed to elective endoscopy mainly through coding errors and unrelated causes. Despite PBR reimbursement the hospital always makes a loss in these cases. With the current financial climate it is ever more important for clinicians to engage with audit, coding and finance to improve not only quality of clinical information but also identify potential areas for optimising service safety and efficiency.
Proatherogenic and Antiatherogenic Effects of Probucol and Phytosterols in Apolipoprotein E–Deficient Mice
Authors: Mohammed H. Moghadasian, Bruce M. McManus, David V. Godin, Brian Rodrigues, Jiri J. Frohlich
Journal: Circulation (1999)

Background —The effects of probucol and a phytosterol mixture (FCP-3PI) on atherosclerotic lesion formation, plasma lipoproteins, hepatic and lipoprotein lipase activities, antioxidant enzyme activities, and plasma fibrinogen were investigated in apolipoprotein E–knockout (apoE-KO) mice. Methods and Results —Three groups of 8 mice were fed a diet containing 9% (wt/wt) fat (controls) or the foregoing diet supplemented with either 1% (wt/wt) probucol (the probucol group) or 2% (wt/wt) FCP-3PI (the FCP-3PI group) for 20 weeks. Compared with controls, atherosclerotic lesion size was 3 times greater in the probucol group, whereas it was decreased by half in the FCP-3PI group. Probucol treatment resulted in high plasma probucol concentrations, which correlated ( r =0.69) with the lesion area. HDL cholesterol was reduced (&gt;75%) in the probucol group and slightly increased (14%) in the FCP-3PI–treated group. Postheparin lipoprotein lipase (LPL) activity was significantly reduced in both treatment groups, but only FCP-3PI significantly decreased hepatic lipase activity. Plasma fibrinogen was increased 42% by probucol and decreased 19% by FCP-3PI relative to controls. Probucol significantly increased plasma glutathione reductase, glutathione peroxidase, and superoxide dismutase activities ( P &lt;0.05). In contrast to findings in apoE-KO mice, there was no probucol-induced atherosclerosis in their wild-type counterparts fed the same dose for the same period of time. Conclusions —Antiatherogenic activity of FCP-3PI in apoE-KO mice is associated with an increase in HDL cholesterol concentration along with decreases in hepatic lipase activity and plasma fibrinogen concentrations. Proatherogenic effects of probucol may be related to increased plasma fibrinogen, decreased HDL cholesterol concentrations along with decreased LPL activity, or its direct “toxicity” due to very high plasma concentration. Our studies demonstrate that the antioxidant and cholesterol-lowering properties of probucol do not prevent atherogenesis in this particular animal model.
The Debt and the Cash Flow of Residents: I. The Grim Present
Authors: Edward J. Stanford
Journal: JAMA (1990)

<h3>To the Editor.—</h3> The article on resident physician indebtedness<sup>1</sup>should be praised for bringing forth, in print, the dilemma facing those with educational loans. I accepted medical school loans after the grants I would have received were discontinued under President Reagan's administration. At graduation from medical school I had accumulated approximately $85 000 in loans. I have nearly paid off my undergraduate loans yet had to defer nearly $75 000. The only way I could pay what I have was to moonlight during residency. I am now receiving payment schedules estimating my accrued interest and the total worth of the loans after the 300 scheduled payments (25 years). My loans have accrued about 120% of their initial value ($165 000). If interest rates do not change, the total payments will be about $560 000, or approximately $2000 per month. If interest increases, this sum will also increase. I agree
Obstacles to conducting epidemiological research in the UK general population
Authors: Hester J T Ward, Simon N Cousens, Blaire Smith-Bathgate, Margaret Leitch, Dawn Everington, Robert G Will, Peter G Smith
Journal: BMJ (2004)

<i>Experiences from a national case-control study of Creutzfeldt-Jakob disease show the tensions between protecting individual patients9 confidentiality and the access required for the benefit of public health</i>
The role of the renin-angiotensin-aldosterone system in cardiovascular homeostasis in normal human subjects.
Authors: J Sancho, R Re, J Burton, A C Barger, E Haber
Journal: Circulation (1976)

To examine the role of angiotensin II in the maintenance of blood pressure and the control of aldosterone secretion in man, eight normal subjects were studied on a tilt table in sodium replete and sodium depleted states prior to and subsequent to the intravenous infusion of an angiotensin converting enzyme inhibitor (CEI). In both the sodium replete or sodium depleted state, upright tilting resulted in an increase in heart rate and a narrowing of pulse pressure. None of the sodium replete or depleted subjects fainted. Tilting was accompanied by a rise in plasma renin activity with an associated rise in plasma aldosterone concentration. When converting enzyme inhibitor was administered, which blocked the generation of angiotensin II, sodium replete subjects were able to compensate for an upright tilt, despite the absence of angiotensin II, without significant hemodynamic change when compared to control state. In sodium depleted subjects, after the administration of converting enzyme inhibitor, there was a sharp and significant decrease in systolic and diastolic blood pressure associated with a significant rise in heart rate. All but one sodium depleted subject fainted within seven minutes. Both plasma aldosterone concentration and plasma renin activity rose on tilting in both sodium replete and sodium depleted subjects. After the administration of converting enzyme inhibitor, plasma aldosterone failed to rise in association with a rise in plasma renin activity. In supine subjects, after the administration of converting enzyme inhibitor, plasma renin activity rose but plasma aldosterone concentration fell. In sodium depleted subjects, after the administration of CEI, aldosterone fell to a level significantly lower than that in supine controls and to a level no different from the supine sodium replete subject. These results indicate that angiotensin II is essential for blood pressure maintenance in sodium depleted individuals, that angiotensin II exerts a direct feedback control on renin secretion, and that angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and to posture.
Viral hepatitis: chairman's introduction
Authors: J-P Benhamou
Journal: Gut (1993)

Five viruses (A, B, D, C, and E) have been identified as agents of acute or chronic hepatitis.For most experts, this list of viruses inducing hepatitis is complete.For a few, however, the existence of additional viruses is a distinct possibility, but the importance of these additional viruses, if indeed they exist, is very limited. Hepatitis A virus (HAV)HAV is an RNA virus.Viraemia is of short duration (two to four weeks) and acute infection is clinically silent in approximately 90% of infected individuals.In approximately 10% of patients, acute HAV infection results in jaundice.In these patients the risk of fulminant liver failure is very low, probably less than 1:1000, and there is no risk of chronic hepatitis.
Effect of nitroglycerin on aortic impedance, diameter, and pulse-wave velocity.
Authors: T W Latson, W C Hunter, N Katoh, K Sagawa
Journal: Circulation Research (1988)

The effects of an intravenous infusion of 1 microgram/kg/min nitroglycerin were studied on systemic arterial properties in nine acutely instrumented dogs. Aortic impedance and pulse-wave velocity were calculated from measured pressure and flow signals collected during random ventricular pacing. Central aortic diameter was simultaneously determined with ultrasonic dimension crystals. Mean blood pressure was maintained constant to avoid the confounding effects of passive, pressure-induced changes in vascular properties. Nitroglycerin both reduced the amplitude of peripheral vascular reflections and delayed the return of these reflections to the aortic root. This reflection delay was manifested as a consistent leftward shift in both impedance modulus and phase. The magnitude of this reflection delay could not be entirely accounted for on the basis of the measured changes in average pulse-wave velocity along the aorta.
Histamine N-methyltransferase inhibitor potentiates histamine- and antigen-induced airway microvascular leakage in guinea pigs
Authors: Kiyohisa Sekizawa, Hideki Nakazawa, Masatoshi Morikawa, Kohei Yamauchi, Kazutaka Maeyama, Takehiko Watanabe, Hidetada Sasaki
Journal: Journal of Allergy and Clinical Immunology (1995)