tbuckley/cabot-search huggingface dataset:
Entrainment of reentrant ventricular tachycardia in anisotropic rings of rabbit myocardium. Mechanisms of termination, changes in morphology, and acceleration.
Authors: L Boersma, J Brugada, C Kirchhof, M Allessie
Journal: Circulation (1993)

Entrainment of ventricular tachycardia can either terminate or change the rate and/or morphology of ventricular tachycardia. The purpose of this study was to elucidate the underlying mechanisms by mapping of entrainment of ventricular tachycardia.In 10 Langendorff-perfused rings of anisotropic rabbit left ventricular epicardium created by a cryoprocedure, ventricular tachycardia with a cycle length of 167 +/- 17 milliseconds was induced by incremental pacing. During transient entrainment (10 stimuli), the circulating wave was extinguished by collision with the paced antidromic wave, whereas ventricular tachycardia was reset by the paced orthodromic wave. At shorter pacing intervals, the site of collision shifted deeper into the circuit. Entrainment at high rates (104 +/- 11 milliseconds) resulted in either termination (n = 54), a change in morphology (n = 8), or acceleration (n = 6) of ventricular tachycardia. Termination of ventricular tachycardia was due to complete (84%) or partial (16%) block of the paced orthodromic wave. Partial block induced microreentry within the circuit, resulting in a reflected echo wave that terminated ventricular tachycardia. A change in morphology of ventricular tachycardia was due to reversion of the direction of propagation of the circulating wave around the obstacle. Acceleration of ventricular tachycardia was caused by double-wave reentry induced by block of the paced antidromic wave. In 28 cases, the sequence of activation during entrainment was not stable but changed from beat to beat due to varying arcs of conduction block. Block occurred predominantly (86%) during slow transverse propagation. Before termination, local oscillations in interval occurred, resulting in a shortening of the last local interval at the site of block by 10 +/- 6 milliseconds.Termination of ventricular tachycardia by entrainment was due either to complete orthodromic block or to a reflected echo wave. A change in morphology occurred when the direction of the circulating wave reversed. Acceleration of ventricular tachycardia was due to initiation of double-wave reentry. All changes were preceded by conduction block during one or more stimuli at one or multiple sites in the circuit. Block occurred predominantly during slow transverse propagation and was preceded by local oscillations in interval at the site of block.
Efalizumab in the treatment of chronic plaque psoriasis: experiences from the largest psoriasis treatment centre in Denmark
Authors: Knud Kragballe
Journal: British Journal of Dermatology (2007)

About 20-30% of patients with chronic plaque psoriasis have severe forms of the disease and require systemic treatment. The long-term use of conventional systemic therapies is limited by toxicity, and many patients are resistant to these treatments. New biological agents, such as efalizumab and infliximab, offer a more targeted approach than conventional therapies and are more suitable for long-term, continuous treatment. At our hospital, we started treating patients with efalizumab in 2003 as part of a clinical trial programme and report here our experiences with this agent in 31 patients we have treated over the last 3 years. Here we share our standard procedures for patient selection, screening and treatment initiation, and report the efficacy and safety of efalizumab in our patients. Several case studies are presented to illustrate specific points of interest, such as the use of efalizumab in unstable psoriasis and management of arthropathy events. Finally, we suggest a number of approaches that may help to maximize the chances of long-term success in patients receiving efalizumab. In our hands, efalizumab has proven to be an effective therapy in the majority of patients (> 70%). The majority of these patients move to continuous efalizumab therapy (77%), the longest duration of which is currently 18 months. The main advantage of efalizumab over tumour necrosis factor-blockers is the lower risk of serious side-effects. By devising and disseminating effective strategies for the management of patients receiving efalizumab therapy, we hope this treatment will offer patients a truly continuous, long-term solution to their disease.
Monosomal karyotype in primary myelofibrosis is detrimental to both overall and leukemia-free survival
Authors: Rakhee Vaidya, Domenica Caramazza, Kebede H. Begna, Naseema Gangat, Daniel L. Van Dyke, Curtis A. Hanson, Animesh Pardanani, Ayalew Tefferi
Journal: Blood (2011)
Potter’s Pathology of the Fetus, Infant and Child
Authors: Ramen Chmait, Linda Randolph
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
Accumulation of lodine-131 and Technetium-99m Pertechnetate in Thyroid Carcinoma
Authors: MAKOTO KATAGIRI, SHINJI SUZUKI, SOHTARO SADAHIRO, KOICHI KUBOUCHI, TOSHIROH OHMURA, OSAMU TSUMURA, SEIYA AKATSUKA
Journal: Clinical Nuclear Medicine (1988)

Carcinoma of the thyroid is usually delineated as a cold delect on images with radioiodine and Tc-99m pertechnetate. However, several cases that showed an accumulation of Tc-99m pertechnetate in thyroid carcinoma or in their metastases, but did not show any accumulation of radioiodine, have been reported. This paper presents a rare case of an advanced follicular adenocarcinoma of the thyroid that accumulated both Tc-99m pertechnetate and I-131. In this 41-year-old male patient, there were two primary foci in the thyroid; one occupied the whole left lobe with extension to the mediastinum and the other located in the lower part of the right lobe. In addition, there was a lymph node metastasis in the upper mediastinum adjacent to the left lobe. On images with both I-131 and Tc-99m pertechnetate, the tumor in the left lobe and the metastatlc lymph node were delineated, but the tumor in the right lobe was not. Accumulation of Tc-99m pertechnetate in the lower part of the tumor of the left lobe was more distinct than that of I-131. Therefore, it is considered that despite similar histologic findings the trapping ability of the cancerous tissue differed from area to area.
Japan bans shingles drug after deaths
Authors: H Gurdon
Journal: BMJ (1994)

Nippon Shoji, a Japanese pharmaceutical company that marketed a drug for shingles but hid the fact that three people had died in clinical trials, has been shut down for three months by the government in Tokyo. Fifteen patients are alleged to have died within weeks of taking the drug when it first went on sale last autumn. The case has focused attention on Japan's lax system of testing drugs and on a medical profession that has been accused of sacrificing safety in the pursuit of profit.

No criminal charges have been brought against Nippon Shoji's executives, and the drug, sorivudine, will still be available to those hospitals equipped to deal with its side effects. Sorivudine, which was marketed under the name Usevir, …
LRBA Causes Immunodeficiency and Autoimmunity By Deregulating NFkB-Mediated Multiple Immune Effectors Critical For B Cell Activation
Authors: Jia-Wang Wang, Michelle A. Reiser, Kunyu Li, Eileen Rifkin, Bangmei Wang, Narasaiah Kolliputi, Richard F. Lockey
Journal: Journal of Allergy and Clinical Immunology (2014)
Abrogation of apoptosis in atherosclerotic plaques: Feasibility of noninvasive detection by radionuclide imaging with Annexin-V
Authors: Dagmar Hartung, Artiom Petrov, Frank Kolodgie, Navneet Narula, Andrew Kohut, Nezam Haider, Herman K. Gold, Renu Virmani, Jagat Narula
Journal: Journal of the American College of Cardiology (2003)
RETROGRADE CORONARY VEIN INFUSION OF COMBINED BASIC FIBROBLAST GROWTH FACTOR AND BONE MARROW MESENCHYMAL STEM CELLS RESTORES CARDIAC FUNCTION VIA ENHANCED ANGIOMYOGENESIS IN A CANINE INFARCT MODEL
Authors: Shao-Ping Nie, Xiao Wang, Lei Zhen, Huang-Tai Miao, Hong-Mei Ren, Shu-Tian Shi, Xing-Xin Wu
Journal: Journal of the American College of Cardiology (2014)
Effect of strenuous exercise on platelet activation state and reactivity.
Authors: A S Kestin, P A Ellis, M R Barnard, A Errichetti, B A Rosner, A D Michelson
Journal: Circulation (1993)

BACKGROUND It has been hypothesized that platelets are activated, or made more activatible, by strenuous exercise and that these changes may play a role in the genesis of exercise-induced coronary ischemia. Previous studies have yielded conflicting results but have used assays (eg, platelet aggregation, plasma platelet factor 4, and plasma beta-thromboglobulin) that are subject to methodological problems. METHODS AND RESULTS In the present study, a whole blood flow cytometric method was used to study the platelet activation state and reactivity of 12 physically active and 12 sedentary individuals before and after standardized treadmill exercise testing. The peptide gly-pro-arg-pro (GPRP) was included in this assay to prevent fibrin polymerization and platelet aggregation, thus allowing the measurement of the reactivity to thrombin of individual platelets in the physiological milieu of whole blood. A panel of fluorescent-labeled monoclonal antibodies was used to monitor activation-dependent platelet surface changes: downregulation of glycoprotein (GP) Ib (6D1) and upregulation of GMP-140 (S12), the GPIIb-IIIa complex (PAC1), and GPIV (OKM5). In samples obtained before exercise, platelets not exposed to thrombin showed no evidence of in vitro activation. In the sedentary subjects, exercise caused a consistent and significant augmentation of the platelet activation state and reactivity as judged by the binding of 6D1 in the presence of thrombin 0.05 U/mL (P &lt; .001), 0.005 U/mL (P = .001), and 0 U/mL (P = .004) and by the binding of OKM5 in the presence of thrombin 0.05 U/mL (P &lt; .001), 0.005 U/mL (P = .029), and 0 U/mL (P = .035). Exercise increased the binding of PAC1 at only a single thrombin concentration (0.005 U/mL, P = .027) and did not alter the binding of S12 at any thrombin concentration. In contrast, in the physically active subjects, exercise failed to cause a consistent alteration in either platelet activation state or platelet reactivity. No significant differences were found between the 12 male and 12 female volunteers. CONCLUSIONS Strenuous exercise in sedentary subjects but not physically active subjects resulted in both platelet activation and platelet hyperreactivity. These changes were more readily detected with monoclonal antibodies directed against GPIb (6D1) and, to a lesser extent, GPIV (OKM5) rather than those directed against the GPIIb-IIIa complex (PAC1) and GMP-140 (S12). Platelet activation by thrombin, generally regarded as the most physiologically important agonist, can be studied in whole blood in a clinical setting through the use of the peptide GPRP.
Why twin studies really don't tell us much about human heritability
Authors: Sidney J. Segalowitz
Journal: Behavioral and Brain Sciences (1999)

The derivation of heritability from human twin studies involves serious methodological flaws. Heritability is consistently overestimated because of biological confounds of twinning, consistent and often gross underestimation of the environmental variance, and nonadditive genetic influences that can hugely exaggerate heritability values. Despite this bad research design, behaviour geneticists continue to publish results implying that their heritability results are valid.
ROLE OF GREEN-FLUORESCENT-PROTEIN-EXPRESSING T CELLS IN EXPERIMENTAL AUTOIMMUNE MYOCARDITIS
Authors: Tomoyoshi Yanagisawa, Takayuki Inomata, Ichiro Watanabe, Emi Maekawa, Tomohiro Mizutani, Hisahito Shingawa, Ichiro Takeuchi, Mototugu Nishii, Hitoshi Takehana, Tohru Izumi
Journal: Journal of the American College of Cardiology (2011)
Mechanism of anthralin inflammation 2. Effect of pretreatment with glucocorticoids, anthralin and removal of stratum corneum
Authors: C.M. LAWRENCE, S. SHUSTER
Journal: British Journal of Dermatology (1985)

The inflammatory dose‐response to anthralin was measured in human skin 24 h after pretreatment with topical corticosteroids and anthralin, and 48 h after removal of the stratum eorneum with adhesive tape. Anthralin inflammation was increased after 1% hydrocortisone application and decreased by 0.1% betamethasone valerate and 0.05% clobetasol propionate; although the difference between these effects was not significant, the difference between the effect of hydrocortisone and clobetasol propionate was. Anthralin inflammation was not significantly affected by pretreatment with anthralin and was reduced, although not significantly by removal of the stratum corneum. The finding that anthralin inflammation is not altered in skin in which aryl hydrocarbon hydroxylase (AHH) activity is increased and that anthralin inflammation may be altered in situations in which AHH activity is unchanged, excludes a direct relationship between anthralin inflammation and AHH activity.
Lack of association of CPT1A polymorphisms or haplotypes on hepatic lipid content or insulin resistance in Japanese individuals with type 2 diabetes mellitus
Authors: Yushi Hirota, Takeshi Ohara, Masako Zenibayashi, Shin-ichi Kuno, Keiko Fukuyama, Tetsuya Teranishi, Kunichi Kouyama, Kazuaki Miyake, Eiichi Maeda, Masato Kasuga
Journal: Metabolism (2007)
Lung Function in Patients Receiving Busulphan
Authors: W. A. Littler, C. Ogilvie
Journal: BMJ (1970)

An attempt was made to achieve earlier detection of busulphan lung (fibrosing alveolitis) and to determine its incidence by means of serial studies during life, including measurement of the gas transfer factor. Twenty-three patients were investigated over an average period of nearly two years of busulphan treatment. One case of busulphan lung was detected and subsequently confirmed at necropsy, but in the remainder there was no clinical, radiological, or physiological evidence of fibrosing alveolitis. It is concluded that the development of fibrosing alveolitis may be related to individual genetic or immunological factors rather than to busulphan dosage.
Exercise capacity in patients with severe left ventricular dysfunction.
Authors: W Benge, R L Litchfield, M L Marcus
Journal: Circulation (1980)

Normal or near-normal exercise capacity has been thought to reflect normal left ventricular function. Many compensatory mechanisms could preserve exercise capacity in patients with severe left ventricular dysfunction. We evaluated exercise capacity using a treadmill exercise test in 26 patients with severe left ventricular dysfunction defined by a left ventricular ejection fraction of 30% or less by isotope ventriculography. One half of the patients had normal exercise capacity and a normal cardiothoracic ratio on chest x-ray. This study indicates that traditional predictors of left ventricular function that have been widely used in clinical evaluation of the patients with cardiac disease (cardiothoracic ratio and exercise capacity) can be normal in a significant number of patients with severe left ventricular dysfunction. Thus, left ventricular function cannot be accurately estimated using these traditional predictors and should be assessed quantitatively. The isotope ventriculogram appears to be ideal for this purpose.
Clinical investigation of implantable antitachycardia devices: Report of the policy conference of the North American Society of Pacing and Electrophysiology
Authors: Sanjeev Saksena, A. John Camm, Michael Bilitch, John D. Fisher, Seymour Furman, Jerry C. Griffin, Robert G. Hauser, Mark E. Josephson, Helmut Klein, Samuel Levy, Michel Mirowski, Jeremy N. Ruskin, Melvin M. Scheinman, Albert L. Waldo, David E. Ward, Hein J.J. Wellens, Douglas P. Zipes
Journal: Journal of the American College of Cardiology (1987)
Abstract 1561: Guaiacol glyceryl ether, a novel agent to reduce MUC1 expression in breast cancer cells
Authors: Joshua S. Smith, Jimmie Colon, Rafael Madero-Visbal, Santhi Konduri, Cheryl H. Baker
Journal: Cancer Research (2010)

Abstract Purpose: The overexpression and loss of polarity of Mucin1 (MUC1) has been documented in aggressive breast cancer. We have identified guaifenesin as a novel treatment to reduce or eliminate MUC1 expression on human breast cancer cells. Methods: MCF-7 and ZR-75-1 human breast cancer cells were grown for 48 hours in varying concentrations of guaifenesin to determine if a dose dependent effect on MUC1 protein expression resulted with treatment. In addition, cells were also harvested, RNA isolated, reverse transcribed and PCR was performed using ABI quantitative real time PCR machine. In another set of experiments, MCF-7 cells were plated and grown for 72 hours in the absence or presence of 12.5 mM guaifenesin and the cells were harvested and stained with propidium iodine for analysis by flow cytometry. The Cell-Titer Glo assay was performed on MCF-7 and ZR-75-1 cells incubated for 48 hours in the presence of guaifenesin at varying concentrations and the LD50 was determined. In a final set of experiments, MCF-7 cells, incubated in the presence or absence of guaifenesin, were analyzed for their ability to migrate /proliferate in vitro by using a standard scratch assay. For in vivo studies ovarectomized female nude mice were injected with MCF-7-luciferase tagged cells into the mammary fat pad 24 hours after an estrogen pellet was implanted into the right flank. Treatment (vehicle or 400 mg/kg/daily) was initiated after 10 days and tumor growth was monitored through Kodak imaging system. Six weeks after the treatment tumors were isolated, measured and processed for immunohistochemistry to analyze the expression of MUC1, TUNEL and CD31. Results: Initially, MUC1 gene expression was confirmed in MCF-7 and ZR-75-1 human breast cancer cell lines. Following confirmation, the LD50 was determined to be 12.5 mM. MUC1 gene expression was successfully decreased in a dose-dependent manner in both MCF-7 and ZR-75-1 cell lines when treated with guaifenesin. When MCF-7 cells are treated with 12.5mM guaifenesin, G1 arrest occurs within 24 hours and by 72 hours, 94.2% of cells are in G1 compared to 76.2% in control (drug free) conditions. In addition, there was a significant decrease in the ability of guaifenesin treated MCF-7 cells to migrate into the scratch compared to the control (untreated) cells. In vivo studies revealed that guaifenesin significantly decreased the breast tumor weight and volume which was associated with a low expression of MUC1 in tumor sections as evaluated by immunohistochemistry. Conclusion: These findings suggest that guaifenesin may provide a novel approach to inhibit breast cancer growth. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1561.
Impact of Glucose Intolerance and Insulin Resistance on Cardiac Structure and Function
Authors: Martin K. Rutter, Helen Parise, Emelia J. Benjamin, Daniel Levy, Martin G. Larson, James B. Meigs, Richard W. Nesto, Peter W.F. Wilson, Ramachandran S. Vasan
Journal: Circulation (2003)

Background— Although insulin resistance has been implicated in the pathogenesis of left ventricular (LV) hypertrophy, previous studies have yielded inconsistent results and are limited by referral bias. Methods and Results— We examined the relations between echocardiographic LV measurements and glucose tolerance status in 2623 Framingham Study subjects (1514 women, mean age 53 years) free of myocardial infarction and heart failure. We also evaluated the relations of insulin resistance (homeostasis model, HOMA-IR) and LV and left atrial (LA) measures within the normal and abnormal glucose tolerance categories (the latter included impaired glucose tolerance, impaired fasting glucose, and newly diagnosed diabetes). LV mass (adjusted for age, height, heart rate, and systolic blood pressure) increased across categories of worsening glucose tolerance; the trend was more striking in women ( P &lt;0.001) compared with men ( P =0.054). In subjects with normal (n=2022) and abnormal glucose tolerance (n=327), covariate-adjusted LV mass and LV wall thickness increased across HOMA-IR quartiles in women ( P &lt;0.001) but not men. In contrast, covariate-adjusted LA size increased with worsening glucose tolerance and across HOMA-IR quartiles in the normal and abnormal glucose tolerance groups in both sexes. Adjustment for body mass index considerably attenuated the relations of LV/LA measures and HOMA-IR, rendering them statistically nonsignificant in the normal glucose tolerance group. Conclusions— In our large community-based sample, LV mass and wall thickness increased with worsening glucose intolerance, an effect that was more striking in women compared with men. Insulin resistance was associated with increased LV mass in women alone, but this relation was largely accounted for by obesity.
A single amino acid substitution in the alpha 3 domain of an H-2 class I molecule abrogates reactivity with CTL.
Authors: T A Potter, J A Bluestone, T V Rajan
Journal: The Journal of Experimental Medicine (1987)

We previously described a somatic cell expressing a variant H-2Dd molecule that did not serve as a target for alloreactive anti-Dd CTL. The mutant cell line had been isolated by its failure to express a serological epitope present on the H-2Dd alpha 3 domain. In the present study the alpha 3 domain of the Dd molecule of this somatic cell variant was sequenced and a single nucleotide change resulting in a glutamic acid to lysine substitution at residue 227 was identified. This change was reproduced in the cloned H-2Dd gene by oligonucleotide-directed mutagenesis. Cells transfected with this mutant gene were not killed by anti-H-2Dd CTL. Because previous studies using hybrid H-2 class I molecules had established that the alpha 3 domain does not express allele-specific determinants recognized by CTL, our results raise the possibility that residues in the alpha 3 domain of H-2 class I molecules are critical for CTL recognition and constitute a conserved (or monomorphic) determinant recognized by CTL.