tbuckley/cabot-search huggingface dataset:
Abstract 15172: Quantitative Changes in High-Density Lipoprotein Underlie Impaired SR-B1 Mediated Efflux in Obese Individuals
Authors: Kiyoko Uno, My-Ngan Duong, Kathy Wolski, Xing Chen, Ruliang Li, Yu Kataoka, Rishi Puri, Andrea J Lavoie, Stephen J Nicholls
Journal: Circulation (2011)

Background: Obesity is associated with an adverse cardiovascular outcome. While high-density lipoprotein cholesterol (HDL-C) is often decreased in the setting of obesity, little is known regarding ...
Hormones and cardiovascular health in women
Authors: P.G. Crosignani
Journal: Human Reproduction Update (2006)

Cardiovascular diseases (CVDs) may have their origin before birth: the combination of being small at birth and having an overly rich post-natal diet increases the likelihood of obesity and of acquiring a specific metabolic syndrome in adulthood that carries an increased risk of CVD. The incidence of CVD and mortality is very low in women of reproductive age but rises to a significant level in older women. In this article, we discuss CVD in relation to hormonal contraception, pregnancy and polycystic ovarian syndrome (PCOS) in younger women and menopause in older women. Women with PCOS have a higher risk of diabetes and hypertension, but studies to date have not shown an effect on CVD events. Use of combined hormonal contraception has only small effects on CVD because of the low baseline incidence of myocardial infarction (MI), stroke and venous thromboembolism (VTE) among young women. Women with existing risk factors or existing CVD, however, should consider alternative contraception. In pregnancy, CVD is rare, although, in the West, it now accounts for a significant proportion of maternal mortality as the frequency of obstetrical causes of mortality has substantially declined. The frequency of VTE is 15 per 10 000 during pregnancy and the post-partum period. In older women, menopause causes a slightly higher risk of MI after allowing for age, although there is substantial heterogeneity in the results of studies on menopause and age at menopause and MI. A larger effect might have been expected, because estrogen reduces the risk of developing atherosclerosis in premenopausal women, whereas in post-menopausal women who may have established atherosclerotic disease, estrogen increases the risk of myocardial disease through the effects on plaque stability and clot formation. Recent trial results indicate that hormone treatment in menopause does not favourably affect the risk of MI, stroke or other vascular disease. Thus, prevention of CVD should rely on diet and fitness, low-dose aspirin and treatment of hypertension, hyperglycaemia and hyperlipidaemia.
THE RESPONSIBILITIES OF THE FELLOWS OF THE AMERICAN COLLEGE OF PHYSICIANS
Authors: T G MILLER
Journal: Annals of Internal Medicine (1953)

Article1 July 1953THE RESPONSIBILITIES OF THE FELLOWS OF THE AMERICAN COLLEGE OF PHYSICIANST. GRIER MILLER, F.A.C.P.T. GRIER MILLER, F.A.C.P.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-39-1-1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAt this time I have the obligation, as well as the pleasure, of addressing you on some subject that I believe to be of interest to our College. My remarks will be addressed primarily to its younger members, especially to those of you who are being admitted to Fellowship at this Convocation. The future of our organization is in your hands. Soon you will be its officers, its regents and its governors. Each of you is a potential factor in its progress. Although, as physicians, all of you are members of other medical organizations, none of them presents to you,... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Philadelphia, Pennsylvania*Convocation Address, Thirty-fourth Annual Session, American College of Physicians, Atlantic City, New Jersey, April 15, 1953. Nextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTransient Cerebral Circulatory Arrest Coincides With Fainting in Cough Syncope 1 July 1953Volume 39, Issue 1Page: 1-6KeywordsFellowshipsForecasting ePublished: 1 December 2008 Issue Published: 1 July 1953 Copyright & PermissionsCopyright, 1953, by The American College of PhysiciansPDF downloadLoading ...
Polyclonal B-Cell Lymphocytosis With Features Resembling Hairy Cell Leukemia-Japanese Variant
Authors: Takashi Machii, Mitsuhiro Yamaguchi, Ryoichi Inoue, Yukihiro Tokumine, Hirohiko Kuratsune, Hiroshi Nagai, Shunichi Fukuda, Kazumichi Furuyama, Osamu Yamada, Yoshito Yahata, Teruo Kitani
Journal: Blood (1997)
Abstract 13173: Nondipping Pulse Rate was Associated with a High Level of Brain Natriuretic Peptide in Treated Hypertensive Patients
Authors: Yusuke Oba, Tomoyuki Kabutoya, Satoshi Hoshide, Kazuo Eguchi, Kazuomi Kario
Journal: Circulation (2014)

Introduction:  There have been several reports on the relationship between nondipper pulse rate (PR) pattern and cardiovascular events in hypertensive patients. However, it remains unclear whether there is a relationship between a nondipper PR and hypertensive target organ damage.   Hypothesis:  We hypothesized nondipping PR in treated hypertensive patients is associated with target organ damage.   Methods:  Ambulatory blood pressure (BP) monitoring (ABPM) was conducted in 1003 hypertensive patients enrolled in the Japan Morning Surge Home Blood Pressure Study. BP nondipper status was defined as (Awake SBP - Sleep SBP)/Awake SBP    Results:  The subjects with a nondipper PR status (N=247) were older(67.8±10.4 vs. 64.9±11.4 years, p=0.001)and had a higher level of BNP (mean BNP: 26.7 vs. 18.9 pg/dL, p   Conclusions:  PR nondipping was independently associated with a higher level of BNP, but was not associated with UACR in treated hypertensive patients. The association between PR nondipping status and cardiac damage might explain subsequent cardiovascular events.
Hypercatabolism of IgG, IgA, IgM, and albumin in the Wiskott-Aldrich syndrome
Authors: R. Michael Blaese, Warren Strober, Arthur L. Levy, Thomas A. Waldmann
Journal: Journal of Clinical Investigation (1971)

The Wiskott-Aldrich syndrome is an immune deficiency disorder with an impairment of both humoral and cellular immune responses. Metabolic turnover studies of IgG, IgA, IgM, and albumin were conducted in seven patients with the Wiskott-Aldrich syndrome using purified radioiodinated proteins. The survival of each of the proteins studied was significantly shortened with a half-time of 7.5 days for IgG (normal 22.9 +/-4 SD), 3.0 days for IgA (normal 5.8 +/-1), 5.0 days for IgM (normal 10.1 +/-2.1), and 8.6 days for albumin (normal 17, range 13-20); the fractional catabolic rates were correspondingly elevated and the distribution of protein among the body compartments was normal. For three of the four proteins. IgG, IgA, and albumin, the steady-state synthetic rates were generally elevated leading to normal or even elevated serum proteins levels. Thus, in the case of IgA, the synthetic rate averaged five times normal while the fractional degradative rate was twice normal. The resulting serum concentration was, therefore, significantly elevated, IgM represented an exception to this pattern in that the increased rate of degradation was not counterbalanced by an increased synthetic rate and, therefore, the serum levels were low. Albumin clearance studies using albumin-(51)Cr showed gastrointestinal protein loss in these patients to be slightly greater than normal, but this could account for only a small fraction of the hypercatabolism observed. There was no proteinuria or abnormalities of thyroid, adrenal, renal, or liver function. Thus, none of the previously recognized causes of increased serum protein catabolism were present. Patients with the Wiskott-Aldrich syndrome, therefore, have a unique disorder of serum protein metabolism characterized by endogenous hypercatabolism of at least four major serum proteins. This phenomenon may be related to reticuloendothelial hyperfunction since the Wiskott-Aldrich syndrome is associated with reticuloendothelial hyperplasia and accelerated clearance of colloidal materials from the plasma.
Human immunodeficiency virus (HIV) phenotype and interleukin-2/ interleukin-10 ratio are associated markers of protection and progression in HIV infection
Authors: M Clerici, C Balotta, A Salvaggio, C Riva, D Trabattoni, L Papagno, A Berlusconi, S Rusconi, ML Villa, M Moroni, M Galli
Journal: Blood (1996)
Abstract 5009: Exposure Time And Cardiovascular Risk Of NSAID Treatment In Patients With Acute Myocardial Infarction Or Heart Failure
Authors: Gunnar H Gislason, Emil L Fosbol, Steen Z Abildstrom, Tina K Schramm, Morten L Hansen, Fredrik Folke, Lars Kober, Christian Torp-Pedersen
Journal: Circulation (2008)

To analyze the effect of duration of exposure to NSAID treatment on cardiovascular risk in two separate patient-populations of patients with previous acute myocardial infarction (MI) or diagnosis o...
Abstract 17633: Erythropoeitin Rescues Perivascular Adipose Function Which is Lost Following Hypoxia Through Endothelium Dependent Mechanisms
Authors: Sarah B Withers, Neha Passi, Alfred S Williams, Declan De Freitas, Anthony M Heagerty
Journal: Circulation (2010)

Erythropoietin (EPO) has a number of effects which may be beneficial in the treatment of inflammatory diseases including type 2 diabetes and obesity. We hypothesise erythropoietin can restore norma...
SURVIVAL IN UNTREATED AND TREATED CANCER
Authors: Michael B. Shimkin, Matthew H. Griswold, Sidney J. Cutler
Journal: Annals of Internal Medicine (1956)

ExcerptThe most obvious manifestation of cancer is that it kills. In 1878 Winiwarter1published a detailed analysis of Billroth's surgical experience in cancer. Approximately 10% of 548 patients were alive and were stated to be clinically free of cancer following treatment. The follow-up period for many of the patients was less than three years. Nevertheless, the demonstration that the fatal course of cancer could be interrupted in some patients by treatment had great influence and served as an important stimulus to the development of surgery in cancer. It was also taken as evidence for the concept of the unifocal origin...
Highly cytotoxic CD56+CD8+ NK cells as potential novel candidates for cancer cellular therapy
Authors: Garnet Suck, Sixian Chu, Madelaine Niam, Tsyr Lim, Kam Hui, Mickey Koh
Journal: Clinical Cancer Research (2007)

AACR Centennial Conference: Translational Cancer Medicine-- Nov 4-8, 2007; Singapore

B13 

Natural killer (NK) cells are promising candidates for adoptive immunotherapy (AIT) against cancer. However, clinical effectiveness has been limited so far, mainly due to insufficient cytolytic potential of the effectors. A favorable concept could be the application of the highly cytolytic transformed NK cell line KHYG-1, yet application of non-malignant cells to patients is preferable. In this context, we are studying cytotoxic potential and mechanism of action of long term IL-2 stimulated highly purified CD56+CD3- NK cells, which express the CD8 α/α glycoprotein, like KHYG-1. Indeed, this subset has been previously described as highly cytolytic and was implicated in autologous tumour rejection in leukaemia patients. We compared long term expansion of either magnetically enriched CD56+CD3- NK cells or lymphokine activated killer (LAK) cells for subsequent separation into CD8+ and CD8- NK subsets. We found that AIM V media enriched with 5% human AB serum, 5% fetal bovine serum, and high dose IL-2 (1000-2000U) biased NK expansion. Monitoring CD56 and CD3 markers in NK and LAK cultures from 4 healthy donors up to 25 days showed that NK cultures remained pure over time, starting from 94%-98% to 91%-96% NK cells in culture after expansion. Cell numbers increased 1.3 to 3 fold, (from Day 4-7 after sorting, to allow cells to recover), dependent on the donor. NK expansion within LAK cultures was also feasible, however ranged from 16% to 78% NK cells after expansion from starting cultures that comprised 13% to 24% NK cells, reflecting great donor variability. Magnetic separation of NK cells into CD8+ and CD8- subsets was achieved from freshly isolated, long term expanded purified CD56+CD3- NK cells or LAK cultures, and furthermore from long term LAK cultures that were started from revived frozen PBMCs. Intriguingly, The CD56+CD3- CD8+ subset exceeded cytotoxicity of the CD56+CD3-CD8- subset and also KHYG-1 against several tumour target cell lines, including K562 (Chronic myelogenous leukaemia), Daudi (Burkitt's lymphoma), THP-1 (Acute monocytic leukaemia) and Jurkat (Acute T-cell leukaemia). KHYG-1 was in fact in most cases even less cytotoxic then the CD8- subset under these conditions. To reveal molecules that are involved in enhanced cytotoxicity CD8+/CD8- NK subsets are planned to be generated from frozen PBMC 'backups' from well expanding cultures and compared to KHYG-1 in microarray studies exploiting differential target cell killing. Our study is envisaged to be translated into clinics in the future involving our Good manufacturing Practices (GMP) facility at the Health Sciences Authority in Singapore.
Geographical Differences in the Rates of Angiographic Restenosis and Ischemia-Driven Target Vessel Revascularization After Percutaneous Coronary Interventions
Authors: Mandeep Singh, Brent A. Williams, Bernard J. Gersh, Robyn L. McClelland, Kalon K.L. Ho, James T. Willerson, William F. Penny, Donald E. Cutlip, David R. Holmes
Journal: Journal of the American College of Cardiology (2005)
Abstract 519: The Early Decrease of Plasma ADAMTS13 Antigen Levels is a Significant Predictor of Future Thrombotic Events in Patients with Acute Myocardial Infarction
Authors: Masakazu Matsukawa, Koichi Kaikita, Kenji Soejima, Shunichirou Fuchigami, Yoshinori Nakamura, Tsuyoshi Honda, Kenichi Tsujita, Yasuhiro Nagayoshi, Sunao Kojima, Hideki Shimomura, Seigo Sugiyama, Kazuteru Fujimoto, Tomohiro Nakagaki, Ogawa Hisao
Journal: Circulation (2007)

Von WilIebrand factor (VWF) is an important cofactor in platelet adhesion and aggregation. Generally, it is known that multimer of VWF is closely associated with strong platelet adherence and aggregation. The early increase of VWF has been reported to be a risk factor for adverse outcome in acute coronary syndrome. Recently, a metalloprotease that cleaves VWF multimers has been identified, namely, ADAMTS13. We previously reported that ADAMTS13 antigen was localized in coronary thrombi obtained from patients with acute myocardial infarction (AMI). The aim of this study was to investigate serial changes in plasma VWF and ADAMTS13 antigen levels and the detailed analysis of the relationship between these plasma levels and prognosis after AMI. We measured serial changes of plasma VWF and ADAMTS13 antigen levels in 92 AMI patients (after admission, one, three, seven, and 14 days after AMI) and 40 control subjects. Plasma VWF antigen levels were significantly higher in AMI patients compared with controls (P &lt; 0.001) on admission, peaked at three days, and gradually decreased afterward. Plasma VWF antigen levels at one day in the AMI patients accompanied with subsequent thrombosis (thrombosis group), including myocardial infarction, unstable angina pectoris, cerebral infarction, subacute thrombosis, and ischemic cardiac death, were significantly increased compared with non-thrombosis group. On the other hand, the plasma ADAMTS13 antigen levels were significantly decreased in AMI patients compared with controls (P &lt; 0.0001) on admission and remained decreased for 14 days. The ADAMTS13 antigen levels in the thrombosis group decreased until three days and gradually increased afterward. Kaplan-Meier analysis and Cox hazards analysis demonstrated that patients with low ΔADAMTS13 levels (Δ = the value at day 3 - value at admission) had significantly higher probabilities of developing thrombosis during one-year follow-up period (P = 0.0104). These findings suggested that monitoring the changes of VWF and ADAMTS13 antigen levels in the early phase of AMI might be valuable for predicting and preventing thrombosis during one-year follow-up in patients with AMI.
A Study of the Variable Factors in the Use of the Wright's Stain
Authors: Roy F. Feemster
Journal: Annals of Internal Medicine (1928)

Article1 September 1928A Study of the Variable Factors in the Use of the Wright's StainROY F. FEEMSTER, M.D., D.P.H.ROY F. FEEMSTER, M.D., D.P.H.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-2-3-289 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDuring the last three years, while engaged in collecting and staining blood smears in quantity to be used in demonstrating to students the various pathological conditions of the blood, we have experienced considerable difficulty in obtaining constant results with the Wright's Stain as employed in the usual way. In trying to eliminate these variations we have studied the results obtained from various aspects and the following outline will illustrate most of the factors responsible for our failure to obtain uniform stains.DIFFICULTIES WHICH MUST BE CONTROLLEDIn a large number of cases defects in staining are due to lack of... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New Orleans Department of Bacteriology and Pathology Tulane University*Presented before the American College of Physicians at the Annual Clinical Session, March 8, 1928, New Orleans, La. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1928Volume 2, Issue 3Page: 289-293KeywordsBloodStaining Issue Published: 1 September 1928 PDF downloadLoading ...
Abstract 5839: Living Tissue Engineered Heart Valves Based On A Composite Self-Expandable Sandwich-Structured Scaffold And Autolgous Adult Stem Cells: First In Vivo Experiences Towards A Complete Minimally Invasive Approach
Authors: Doerthe Schmidt, Christine Mariani, Arja Puolakka, Marja Rissanen, Jens Kelm, Thorsten Deichmann, Gregor Zund, Simon P Hoerstrup
Journal: Circulation (2008)

Background : A clinically relevant heart valve tissue engineering concept requires minimally invasive techniques for both cell harvest and valve implantation. Here, we present first experiences with autologous tissue engineered heart valves fabricated from composite self-expandable biodegradable scaffolds and adult stem cells implanted by minimally invasive procedures in a sheep model. Methods : Sandwich-structured heart valve scaffolds (n= 12) were fabricated from non-woven PLDLA meshes coated with electrospun PLDLA nanofibers and integrated in self-expanding nitinol stents. Scaffolds were seeded with either autologous ovine bone marrow (BMC; n= 4) or jugular vein-derived cells (JVC; n= 8) and cultured in bioreactors. After 9d, heart valves were endothelialized with autologous peripheral blood-derived endothelial progenitor cells and jugular vein-derived endothelial cells, respectively. After additional 3d, heart valves (n= 6) were implanted trans-apically in pulmonary position. Controls were analysed (n= 6) as to tissue formation and composition (histology, biochemical assays). Mechanical properties were determined by tensile tests. In vivo performance was assessed by echocardiography up to 4 weeks. Results : Histology revealed cell attachment and ingrowth into the scaffold material resulting in layered tissues with endothelialized, eNOS positive surfaces. Amounts of GAG and cell number were similar in all heart valves, comparable to native tissues. Collagen production was higher in BMC based heart valves compared to JVC-derived tissues (Hydroyproline amount 34% vs. 20% of native tissues). Mechanical profiles demonstrated physiological tissue strength (max. tensile stress 0.41± 0.21 MPa) but less elasticity (E-Moduli 1.89± 0.79 MPa) independent of the cell source. Echocardiography displayed in vivo functionality (transvalvular mean pressure gradient 10.36± 3.17 mm/Hg) with more flexibility of BMC based heart valves leaflets. Conclusions : These results demonstrate that heart valve tissue engineering based on a minimally invasive technique for both cell harvest and valve implantation is feasible. This clinically relevant approach is currently investigated in long-term animal studies.
Abstract 14807: Atrioventricular Conduction Intervals Before and After Transcatheter Aortic Valve Implantation
Authors: Miguel Romero, Jose Segura, Javier Suarez de Lezo, Manuel Pan, Soledad Ojeda, Francisco Mazuelos, Jose Suarez de Lezo
Journal: Circulation (2011)

The percutaneous implantation of a CoreValve prosthesis in high risk patients (pts) with severe aortic stenosis may induce or worsen atrivoventricular (AV) conduction disturbances. However, there i...
Abstract 12879: Concordance and Reproducibility between M-mode, Tissue Doppler Imaging and Two-Dimensional Strain Imaging in the Assessment of Mitral Annular Displacement and Velocity in Patients with Various Heart Conditions
Authors: Martina C de Knegt, Tor Biering-Sorensen, Peter Sogaard, Jacob Sivertsen, Jan Skov Jensen, Rasmus Mogelvang
Journal: Circulation (2012)

Introduction: Mitral annular (MA) displacement reflects longitudinal left ventricular (LV) deformation and systolic velocity measurements reflect the rate of contraction. These are important parame...
Abstract 1073: Cardiac Voltage-gated Nav channel Na <sub>v</sub> 1.5 Requires An AnkyrinG-dependent Pathway For Targeting in Cardiomyocytes
Authors: John S Lowe, Oleg Palygin, Patrick Wright, Erwin Shibata, Peter Mohler
Journal: Circulation (2007)

Membrane localization of ion channels is very important for normal function in excitable cells. In heart, voltage-gated Na + channels are necessary for the rapid upstroke of the cardiomyocyte action potential, and variants in SCN5A (encodes Na v 1.5) are associated with fatal arrhythmias. We have identified ankyrin family proteins as critical components for normal ion channel and transporter targeting in cardiomyocytes. Humans with ANK2 (encodes ankyrin-B) loss of function variants display abnormal cardiac phenotypes and risk for sudden cardiac death. Mice that lack ankyrin-B expression display a similar phenotype. Our most recent results demonstrate that a second ankyrin gene product, ankyrin-G (encoded by ANK 3) is critical for targeting Na v 1.5 to specific cardiomyocyte membrane domains. We assessed the hypothesis that Na v 1.5 membrane expression and localization is controlled by an ankyrin-G-dependent pathway and disruption of ankyrin-G/Na v 1.5 interactions lead to human cardiac disease in this study. We used a combination of techniques including biochemistry, confocal microscopy, lentiviral expression, and electrophysiology to evaluate the functional relationship between ankyrin-G and Na v 1.5. We defined the structural elements on ankyrin-G and Na v 1.5 for their interaction using site-directed mutagenesis and in vitro binding assays. Lentiviral expression of shRNA targeted to rat 190 kD ankyrin-G effectively reduced the expression of ankyrin-G with a concomitant reduction of Na v 1.5 in immunofluorescence and immunoblot assays. Further-more, primary cardiomyocytes with reduced ankyrin-G expression have a significant reduction in Na + current density with no evident biophysical effects on Ca 2+ current or inactivation-gating of Na v 1.5 These results confirm the importance of ankyrin polypeptides for normal cardiac function and shed new light on the importance of intracellular trafficking pathways for the delivery and stability of critical ion channels and transporters in excitable cells.