tbuckley/cabot-search huggingface dataset:
Haemodynamic effects of arterial compliance, total peripheral resistance, and glyceryl trinitrate on regurgitant volume in aortic regurgitation
Authors: S. A Slordahl, H. Piene
Journal: Cardiovascular Research (1991)

Study objective — Afterload reduction is known to reduce regurgitant flow in patients with aortic regurgitation. Both arterial compliance and total peripheral resistance are determinants of afterload. The aim of this study was to evaluate the influence of arterial compliance and total peripheral resistance on the regurgitant volume. Design — The values of arterial compliance and total peripheral resistance were assessed during aortic regurgitation at different regurgitant orifice areas in eight pigs before and after a bolus of glyceryl trinitrate. In a computer model the importance of arterial compliance and total peripheral resistance on the regurgitant volume was assessed by keeping each of them constant while the other variable was changed. Measurements and main results — In both the experimental and computer models a very strong correlation was found between decreased total peripheral resistance and decreased regurgitant volume. Arterial compliance was of hardly any importance. A bolus of glyceryl trinitrate reduced regurgitant volumes and regurgitant fractions significantly. Conclusions — Total peripheral resistance is an important factor in influencing the regurgitant volumes at a given regurgitant orifice area in aortic regurgitation, while arterial compliance is of less importance. Glyceryl trinitrate effectively reduces the regurgitant volumes by its effect on peripheral resistance.
The Proteasome Inhibitor Bortezomib in Combination with Gemcitabine and Carboplatin in Advanced Non-small Cell Lung Cancer: A California Cancer Consortium Phase I Study
Authors: Angela M. Davies, Christopher Ruel, Primo N. Lara, Derick H. Lau, Paul H. Gumerlock, Richard Bold, Stephen Shibata, Heinz-Josef Lenz, David P. Schenkein, David R. Gandara
Journal: Journal of Thoracic Oncology (2008)
Impact of lesion length on vascular brachytherapy failure: a comparison of beta (b) versus gamma (g) irradiation in 990 patients
Authors: Kazuyuki Shirai, Alexandra J. Lansky, Roxana Mehran, Kartik Desai, Costantino Costantini-Ortiz, Brian Proctor, Teraza Conway, Martin Fahy, Maria Corral, Christina Brestowski, George Dangas, Gregg W. Stone, Paul Teirstein, Jeffrey Moses, Martin B. Leon
Journal: Journal of the American College of Cardiology (2002)
Regulator of G-Protein Signaling 5 Controls Blood Pressure Homeostasis and Vessel Wall Remodeling
Authors: Vasyl Holobotovskyy, Mitali Manzur, Marianne Tare, Jennifer Burchell, Erin Bolitho, Helena Viola, Livia C. Hool, Leonard F. Arnolda, Douglas J. McKitrick, Ruth Ganss
Journal: Circulation Research (2013)

Rationale: Regulator of G-protein signaling 5 (RGS5) modulates G-protein-coupled receptor signaling and is prominently expressed in arterial smooth muscle cells. Our group first reported that RGS5 is important in vascular remodeling during tumor angiogenesis. We hypothesized that RGS5 may play an important role in vessel wall remodeling and blood pressure regulation. Objective: To demonstrate that RGS5 has a unique and nonredundant role in the pathogenesis of hypertension and to identify crucial RGS5-regulated signaling pathways. Methods and Results: We observed that arterial RGS5 expression is downregulated with chronically elevated blood pressure after angiotensin II infusion. Using a knockout mouse model, radiotelemetry, and pharmacological inhibition, we subsequently showed that loss of RGS5 results in profound hypertension. RGS5 signaling is linked to the renin–angiotensin system and directly controls vascular resistance, vessel contractility, and remodeling. RGS5 deficiency aggravates pathophysiological features of hypertension, such as medial hypertrophy and fibrosis. Moreover, we demonstrate that protein kinase C, mitogen-activated protein kinase/extracellular signal–regulated kinase, and Rho kinase signaling pathways are major effectors of RGS5-mediated hypertension. Conclusions: Loss of RGS5 results in hypertension. Loss of RGS5 signaling also correlates with hyper-responsiveness to vasoconstrictors and vascular stiffening. This establishes a significant, distinct, and causal role of RGS5 in vascular homeostasis. RGS5 modulates signaling through the angiotensin II receptor 1 and major Gα q -coupled downstream pathways, including Rho kinase. So far, activation of RhoA/Rho kinase has not been associated with RGS molecules. Thus, RGS5 is a crucial regulator of blood pressure homeostasis with significant clinical implications for vascular pathologies, such as hypertension.
Ryanodine, acidosis, and short term mechanical restitution in ferret papillary muscles
Authors: E McCALL, C H ORCHARD, M R BOYETT
Journal: Cardiovascular Research (1988)

Journal Article Ryanodine, acidosis, and short term mechanical restitution in ferret papillary muscles Get access E McCALL, E McCALL From the Department of Physiology, University of Leeds, Leeds, LS2 9JT Search for other works by this author on: Oxford Academic PubMed Google Scholar C H ORCHARD, C H ORCHARD From the Department of Physiology, University of Leeds, Leeds, LS2 9JT Search for other works by this author on: Oxford Academic PubMed Google Scholar M R BOYETT M R BOYETT From the Department of Physiology, University of Leeds, Leeds, LS2 9JT Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 22, Issue 8, August 1988, Page 602, https://doi.org/10.1093/cvr/22.8.602 Published: 01 August 1988
Semiparametric modeling of age at achieving developmental milestones after prenatal exposure to methylmercury in the Seychelles child development study.
Authors: C D Axtell, G J Myers, P W Davidson, A L Choi, E Cernichiari, J Sloane-Reeves, C Cox, C Shamlaye, T W Clarkson
Journal: Environmental Health Perspectives (1998)

Controversy exists concerning the fetal risk associated with exposure to low-dose methylmercury from maternal fish consumption. Previous studies of the effects of acute prenatal mercury exposure identified delays in achieving developmental milestones among exposed children. This led to public health concern that prenatal low-dose exposure from fish consumption could adversely affect the fetus. We evaluated the effects of prenatal methylmercury exposure (through maternal fish consumption) on the age that children walked and first said words in the main study cohort of the Seychelles Child Development Study. We used semiparametric generalized additive models to identify nonlinearities in the relationships between prenatal exposure and developmental outcomes, after adjusting for covariates, and to evaluate their importance. Very slight delays (&lt;1 day) in walking were seen as mercury levels increased from 0 to 7 ppm, but this effect did not persist at the higher exposure levels represented by the cohort, making it difficult to conclude that a cause and effect relationship existed at the exposure levels seen in this cohort. There was no evidence for any association between prenatal exposure and age at talking.
Tilarginine in Patients With Acute Myocardial Infarction and Cardiogenic Shock—Reply
Authors: Robert A. Harrington, John H. Alexander, Judith S. Hochman, Harmony R. Reynolds, Vladimir Dzavik, Frans J. Van de Werf
Journal: JAMA (2007)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Objective Evidence for the Reversibility of Nerve Injury in Diabetic Neuropathic Cachexia
Authors: Jaspreet Grewal, Vera Bril, Gary F. Lewis, Bruce A. Perkins
Journal: Diabetes Care (2006)

Diabetic neuropathic cachexia is an acute complication of diabetes marked by such extreme pain and weight loss that, although exceptionally rare, it imparts major challenges in management and diagnosis. Little is known of the fundamental pathophysiologic features of the peripheral nervous system in this condition; for example, the symptomatic resolution that is classically observed may arise from either complete destruction of pain-transmitting nerve fibers or from their repair. To reconcile this issue, we report the first case to our knowledge that the nerve dysfunction is reversible. A 36-year-old woman presented with subacute hyperglycemic symptoms. Soon after initiation of insulin therapy …
Native Low-Density Lipoprotein Increases Endothelial Cell Nitric Oxide Synthase Generation of Superoxide Anion
Authors: Kirkwood A. Pritchard, Laura Groszek, David M. Smalley, William C. Sessa, Mingdan Wu, Patricio Villalon, Michael S. Wolin, Michael B. Stemerman
Journal: Circulation Research (1995)

Abstract To examine mechanisms by which native low-density lipoprotein (n-LDL) perturbs endothelial cell (EC) release of superoxide anion (O 2 − ) and nitric oxide (NO), ECs were incubated with n-LDL at 240 mg cholesterol per deciliter for 4 days with media changes every 24 hours. n-LDL increases EC release of O 2 − by more than fourfold and increases nitrite production by 57%. In the conditioned media from day-4 incubations, n-LDL increases total nitrogen oxides 20 times control EC (C-EC) levels. However, n-LDL did not alter EC NO synthase (eNOS) enzyme activity as measured by the [ 3 H]citrulline assay. N ω -Nitro- l -arginine methyl ester, a specific inhibitor of eNOS activity, increases C-EC release of O 2 − by &gt;300% but decreases LDL-treated EC (LDL-EC) release by &gt;95%. l -Arginine inhibits the release of O 2 − from LDL-ECs by &gt;95% but did not effect C-EC release of O 2 − . Indomethacin and SKF 525A partially attenuate LDL-induced increases in O 2 − production by ≈50% and 30%, respectively. Thus, n-LDL increases O 2 − and NO production, which increases the likelihood of the formation of peroxynitrite (ONOO − ), a potent oxidant. n-LDL increases the levels of nitrotyrosine, a stable oxidation product of ONOO − , and tyrosine by ≈50%. In spite of this increase in oxidative metabolism, analysis of thiobarbituric acid substances reveals that no significant changes in the oxidation of n-LDL occur during the 24-hour incubations with ECs. These data indicate that n-LDL directly perturbs endothelial oxidative metabolism and uncouples l -arginine metabolism from NO release to increase eNOS generation of O 2 − . Such changes may represent one of the earliest EC perturbations in atherogenesis.
Xylene Poisoning: A Report on One Fatal Case and Two Cases of Recovery after Prolonged Unconsciousness
Authors: R. Morley, D. W. Eccleston, C. P. Douglas, W. E. J. Greville, D. J. Scott, J. Anderson
Journal: BMJ (1970)

Three cases of xylene poisoning occurred after prolonged inhalation of paint fumes. Analysis showed that xylene comprised more than 90% of the solvent in the paint, the total solvent comprising 34% of the paint by weight. One patient was dead on admission, while the other two recovered after at least 15 hours9 loss of consciousness. Both patients had transient liver cell damage, and one temporary impairment of renal function.
A common genetic variant within SCN10A modulates cardiac SCN5A expression
Authors: Malou van den Boogaard, Scott Smemo, Ozanna Burnicka-Turek, David E. Arnolds, Harmen J.G. van de Werken, Petra Klous, David McKean, Jochen D. Muehlschlegel, Julia Moosmann, Okan Toka, Xinan H. Yang, Tamara T. Koopmann, Michiel E. Adriaens, Connie R. Bezzina, Wouter de Laat, Christine Seidman, J.G. Seidman, Vincent M. Christoffels, Marcelo A. Nobrega, Phil Barnett, Ivan P. Moskowitz
Journal: Journal of Clinical Investigation (2014)

Variants in SCN10A, which encodes a voltage-gated sodium channel, are associated with alterations of cardiac conduction parameters and the cardiac rhythm disorder Brugada syndrome; however, it is unclear how SCN10A variants promote dysfunctional cardiac conduction. Here we showed by high-resolution 4C-seq analysis of the Scn10a-Scn5a locus in murine heart tissue that a cardiac enhancer located in Scn10a, encompassing SCN10A functional variant rs6801957, interacts with the promoter of Scn5a, a sodium channel–encoding gene that is critical for cardiac conduction. We observed that SCN5A transcript levels were several orders of magnitude higher than SCN10A transcript levels in both adult human and mouse heart tissue. Analysis of BAC transgenic mouse strains harboring an engineered deletion of the enhancer within Scn10a revealed that the enhancer was essential for Scn5a expression in cardiac tissue. Furthermore, the common SCN10A variant rs6801957 modulated Scn5a expression in the heart. In humans, the SCN10A variant rs6801957, which correlated with slowed conduction, was associated with reduced SCN5A expression. These observations establish a genomic mechanism for how a common genetic variation at SCN10A influences cardiac physiology and predisposes to arrhythmia.
High result in prostate specific antigen test: Repeated testing and free tests might help
Authors: A. M Davis
Journal: BMJ (2003)

Editor—The case of a 52 year old man with a total prostate specific antigen (PSA) of 5.7 ng/ml raises at least three other key considerations.1

The first is the issue of year to year fluctuation, with a careful longitudinal series showing that over 30% of PSA tests in the 4-10 range returned to normal in following years.2 The authors suggested repeating the PSA test, perhaps in four to six weeks, before considering biopsy.

The second issue is what constitutes a “high” total PSA value, and whether a PSA threshold for biopsy of above 4.0 is adequate for a man under 60. A recent study found a sensitivity of only 18% using a total PSA > 4.0 in the diagnosis of prostate cancer in this age range,3 and suggested a threshold of 2.5 in younger men.

Finally, interest is increasing in assaying free PSA to inform the need for biopsy, both for total PSA values above and below 4.0 ng/ml.4,5
Combined therapy with human cord blood cell transplantation and basic fibroblast growth factor delivery for treatment of myocardial infarction
Authors: Seung‐Woo Cho, Il‐Kwon Kim, Suk Ho Bhang, Boyoung Joung, Young Jin Kim, Kyung Jong Yoo, Yoon‐Sun Yang, Cha Yong Choi, Byung‐Soo Kim
Journal: European Journal of Heart Failure (2007)
The role of iron in an acute model of skin inflammation induced by reactive oxygen species (ROS)
Authors: C.W. TRENAM, A.J. DABBAGH, D.R. BLAKE, C.J. MORRIS
Journal: British Journal of Dermatology (1992)

The effect of iron was studied in rats in a ROS-initiated model of acute skin inflammation. Iron dextran was administered i.v. 24 h before the induction of the inflammatory response by intradermal injection of glucose oxidase attached to polyethylene glycol (GOD-PEG). Iron exacerbated the response at 24 and 48 h (P greater than 0.001). Histologically, a similar picture was seen to that without iron except for an increase in tissue oedema and matrix destruction including the skin glands. Associated with iron loading was an increase in Perls stainable iron in the skin (P greater than 0.025) and liver (P greater than 0.001). However, skin inflammation without iron loading also increased skin iron levels (P greater than 0.025). Total serum iron was decreased in iron-loaded and GOD-PEG animals (P greater than 0.01) and the unbound iron binding capacity (UIBC) increased (P greater than 0.01).
"ORIENTAL SORE (CUTANEOUS LEISHMANIASIS) IN THE UNITED STATES"
Authors: Samuel T. Darling
Journal: JAMA (1923)

<h3>To the Editor:</h3> —The illustrations in Dr. Lambert's paper on Oriental Sore (The Journal, April 7, p. 986) show very well the location of the lesions on the back of the elbow and ankle in certain types of the sore. Curiously, these are the favorite sites of the bites of<i>Stegomyia fasciatus</i>(<i>Aedes argenteus</i>), and it is not unlikely that<i>Stegomyia</i>may under certain circumstances impart this infection when infected with a flagellate of this class (<i>Herpetomonas</i>). The diagnosis of dermal leishmaniasis in America is usually confined to communities in which laboratories for diagnosis are available and routine examinations with the microscope practiced. No doubt this infection will be encountered in the warmer southern tier of states when it is thoroughly searched for. The nature of the lesion—its specific character—has been overlooked because of its polymorphous appearance. Aleppo button is perhaps the classical type, but lesions spreading like lupus, or
DIFFERENCE OF NEOINTIMAL CONDITION AFTER BARE-METAL STENT IMPLANTATION BETWEEN ACUTE CORONARY SYNDROME AND STABLE ANGINA: OPTICAL COHERENCE TOMOGRAPHIC STUDY
Authors: Atsushi Kikuchi, Masami Nishino, Takeshi Masaki, Naoki Mori, Daisuke Nakamura, Takahiro Yoshimura, Yasuharu Lee, Masayuki Taniike, Nobuhiko Makino, Hiroyasu KATO, Yasuyuki Egami, Ryu Shutta, Hisaki Morita, Jun Tanouchi, Yoshio Yamada
Journal: Journal of the American College of Cardiology (2012)
DeltaGraph Pro 3 for Macintosh: Presentation Quality Charts and Graphs
Authors: G. Tetrault
Journal: JAMA (1994)

<i>DeltaGraph Pro 3</i>is the most recent version of the premier Apple Macintosh charting application. The first version of<i>DeltaGraph</i>filled an important niche by providing better and more numerous charting options compared with existing spreadsheet and statistics applications. This endeared<i>DeltaGraph</i>to users who needed Microsoft<i>Excel</i>'s data analysis and manipulation features but were dissatisfied with its limited charting capabilities. Current versions of<i>Excel</i>and other Macintosh spreadsheet and statistics programs offer charting features that rival those in the original version of<i>DeltaGraph</i>.<i>DeltaGraph</i>has advanced as well, and the current version has more types of charts and graphs than any other application, including its direct competitor<i>CA-Cricket Graph III 1.5</i>(Computer Associates). <i>DeltaGraph Pro 3</i>has moved beyond charting and graphing, and it now competes with presentation programs such as<i>PowerPoint 3.0</i>(Microsoft),<i>Aldus Persuasion 2.1</i>,<i>More 3.1</i>(Symmantec), and<i>Clarislmpact</i>(Claris).<i>DeltaGraph</i>has an outliner and
Effects of systemic hypertension on ischemic and nonischemic regional left ventricular function in awake, unsedated dogs after experimental coronary occlusion.
Authors: P G Roan, M Buja, S Saffer, C Izquierdo, H Hagler, B Duke, L D Hillis, J T Willerson
Journal: Circulation (1982)

Hypertension and atherosclerotic coronary arterial obstruction frequently coexist in patients. However, the effect of increased aortic pressure on ischemic segmental dysfunction is not well understood. We studied the effects of aortic pressure increases on segmental left ventricular function during myocardial ischemia. Eighty-two dogs instrumented with three to six pairs of pulse-transit piezoelectric crystals were studied in an awake, unsedated state to measure segmental wall thickness. A pneumatic balloon occluder was positioned around the proximal left anterior descending artery (LAD). Thirty-three dogs underwent LAD occlusion and served as normotensive controls (group A). Group B dogs (n = 23) received a 6-hour infusion of phenylephrine (PE) beginning 5 minutes after LAD occlusion to increase aortic diastolic arterial pressure to 120-130 mm Hg; aortic pressure was then allowed to return to normal for the subsequent 18 hours. The eight dogs in group C received a 6-hour infusion of PE, but no coronary arterial occlusion was produced. In group D (n = 12), distal constriction of the thoracic aorta was maintained for 24 hours after LAD occlusion. Regional myocardial blood flow (RMBF) was measured with radioactive microspheres in six conscious dogs and both RMBF and intramyocardial PCO2 were measured in seven open-chest dogs to assess alterations in regional myocardial oxygen supply and demand. Segments of myocardium were arbitrarily grouped according to the amount of net systolic thickening (NET) present 5 minutes after LAD occlusion and before increasing aortic pressure: group 1 retained 67-100+% of control NET, group 2 0-67%, and group 3 less than 0% (paradoxic motion). In dogs receiving PE plus LAD occlusion and in dogs with aortic constriction and LAD occlusion, NET was transiently depressed in groups 1 and 2 compared with the normotensive cohort; 24 hours after occlusion, NET in groups 1, 2 and 3 did not differ significantly from that in the normotensive dogs. Systemic hypertension resulted in a significant increase in endocardial and midwall RMBF and, in seven open-chest dogs, decreased the intramyocardial accumulation of carbon dioxide after LAD occlusion. Increased aortic pressure in dogs without coronary occlusion produced reversible decreases in end-diastolic wall thickness, NET and LV dP/dt. Thus, the production of systemic hypertension with diastolic pressures of 110-120 mm Hg acutely or for 6 hours during evolving canine myocardial infarction does not appear to exert an important deleterious effect on myocardial oxygen supply and demand. However, 24 hours of mildly increased aortic pressure accentuates end-diastolic wall thinning in segments with paradoxic systolic motion and results in a failure of their return to control values at this period.
Use of Modeling to Evaluate the Cost-Effectiveness of Cancer Screening Programs
Authors: Amy B. Knudsen, Pamela M. McMahon, G. Scott Gazelle
Journal: Journal of Clinical Oncology (2007)

Cost-effectiveness analysis (CEA) is an analytic tool that provides a framework for comparing the health benefits and resource expenditures associated with competing medical and public health interventions, thereby allowing decision makers to identify interventions that yield the greatest amount of health, given their resource constraints. Models are important components of most, if not all, CEAs, and they play a key role in evaluating the cost-effectiveness of cancer screening programs, in particular. In this article, we describe the basic types of models used to evaluate cancer screening programs and provide examples of the use of models in CEAs and to guide cancer screening policy. Finally, we offer some suggestions for important concepts to consider when interpreting model results.