tbuckley/cabot-search huggingface dataset:
Psychodynamic Aspects of Breast Cancer
Authors: H. Becker
Journal: Psychotherapy and Psychosomatics (1979)

We looked into possible differences in the life history and reaction to illness to be observed in younger and older breast cancer patients. The patients, 49 in number, are between 29 and 69 years of age, average age 50. A semi-structured interview took place mostly in the final third of the post-irradiation phase. In the group of women, who developed cancer before the age of 48, some common aspects could be shown in their biography. These women lost an emotionally important person (e.g., a parent) more often in their early childhood. These patients describe an emotionally cold atmosphere in their families along with a missing pronounced basic trust. Also they were overstrained with responsibility too early for their age. The ideals of these patients are somewhat like those of the 'Amazons': they negate the typical female role and its consequences on the bodily, psychic and social level. They seem quite combative, achieving and to the point. As far as sexual responsiveness is concerned only 12% of the younger groups express a consistently positive attitude towards sexuality. Pregnancy, childbirth and breast-feeding are frequently accompanied by serious complications, but they have, in the majority of cases, children. When regarding the multi-causal genesis of cancer, it may be that psychic factors have less influence on the immune system in older patients than the overall ageing process with its weakening of the immunological defence system. The psychic component, if it exists, plays a greater role with the younger patients. The older patients in their life history and pre-morbid behaviour are nearer to what passes for the psychic norm. Other carcinogen factors play a more significant role in older patients: the cancer may have achieved greater autonomy from psychic factors.
Ventricular defibrillation with single and multiple half sinusoidal pulses of current
Authors: J. McFarlane, L. A. Geddes, W. Milnor, W. A. Tacker, J. Bourland, T. W. Coulter
Journal: Cardiovascular Research (1971)

There are three criteria (energy, peak current, and charge) for describing the electrical parameters used for ventricular defibrillation. In this investigation, which deals with defibrillation using single and multiple pulses of half-sinusoidal current, it was found that these three criteria are different. Although slightly less current was required with multiple current pulses, more energy and charge were employed. The least energy and charge were required with a single half-sinusoidal pulse of current.
Left Atrial Transport in Mitral Stenosis
Authors: FRED P. HEIDENREICH, MARK E. THOMPSON, JAMES A. SHAVER, JAMES J. LEONARD
Journal: Circulation (1969)

Active left atrial transport was examined acutely in five patients with mitral stenosis and sinus rhythm. To observe the effect of active left atrial contraction on subsequent left ventricular output, the timing of atrial contraction with respect to ventricular contraction was varied. Atrioventricular (A-V) dissociation produced by right ventricular pacing was used to change continually the relationship of left atrial (LA) to left ventricular (LV) contraction. Measurements of each beat included mitral valve gradient, left ventricular ejection time (LVET), and left ventricular peak-systolic pressure (LVPSP). The diastolic gradient was used to calculate diastolic flow per beat after the area of the stenotic mitral orifice had been previously determined. Calculated diastolic flow increased significantly (24%) as did the parameters of left ventricular output, LVPSP and LVET ( P &lt; 0.005 for both), when atrial contraction was optimally timed. Cumulative effects were observed when a series of well-placed or poorly placed atrial contractions occurred. The method documents change in LV output which depends on appropriate timing of LA contraction that may not have been seen with a steady-state approach.
Loss of Methyl-CpG–Binding Domain Protein 2 Enhances Endothelial Angiogenesis and Protects Mice Against Hind-Limb Ischemic Injury
Authors: Xiaoquan Rao, Jixin Zhong, Shu Zhang, Yushan Zhang, Qilin Yu, Ping Yang, Mong-Heng Wang, David J. Fulton, Huidong Shi, Zheng Dong, Daowen Wang, Cong-Yi Wang
Journal: Circulation (2011)

Background— Despite intensive investigation, how DNA methylation influences endothelial function remains poorly understood. We used methyl-CpG–binding domain protein 2 (MBD2), an interpreter for DNA methylome–encoded information, to dissect the impact of DNA methylation on endothelial function in both physiological and pathophysiological states. Methods and Results— Human umbilical vein endothelial cells under normal conditions express moderate levels of MBD2, but knockdown of MBD2 by siRNA significantly enhanced angiogenesis and provided protection against H 2 O 2 -induced apoptosis. Remarkably, Mbd2 −/− mice were protected against hind-limb ischemia evidenced by the significant improvement in perfusion recovery, along with increased capillary and arteriole formation. Loss of MBD2 activated endothelial survival and proangiogenic signals downstream of vascular endothelial growth factor signaling characterized by an increase in endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor receptor 2 expression, along with enhanced extracellular signal-regulated kinase 1/2 activation and BCL-2 expression. Mechanistic studies confirmed the methylation of CpG elements in the eNOS and vascular endothelial growth factor receptor 2 promoter. MBD2 binds to these methylated CpG elements and suppresses eNOS promoter activity. On ischemic insult, key endothelial genes such as eNOS and vascular endothelial growth factor receptor 2 undergo a DNA methylation turnover, and MBD2 interprets the changes of DNA methylation to suppress their expressions. Moreover, MBD2 modulation of eNOS expression is likely confined to endothelial cells because nonendothelial cells such as splenocytes fail to express eNOS after loss of MBD2. Conclusions— We provided direct evidence supporting that DNA methylation regulates endothelial function, which forms the molecular basis for understanding how environmental insults (epigenetic factor) affect the genome to modify disease susceptibility. Because MBD2 itself does not affect the methylation of DNA and is dispensable for normal physiology in mice, it could be a viable epigenetic target for modulating endothelial function in disease states.
A1.77 Interferon regulatory factor 5 (<i>IRF5</i>) gene variant RS2004640 is associated with carotid intima media thickness in rheumatoid arthritis patients
Authors: S Vosslamber, A van Sijl, C L Bos, J Lubbers, S de Ridder, A E Voskuyl, M T Nurmohamed, C L Verweij
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background and Objectives</h3> Rheumatoid arthritis (RA) is a chronic inflammatory joint disease and is associated with an increased cardiovascular (CV) risk. Interferons (IFNs), especially IFNβ, might play a role in atherosclerosis as they are known inhibitors of vascular smooth muscle cell proliferation and intimal hyperplasia. We studied whether functional relevant SNPs in the interferon regulatory factor 5 (<i>IRF5)</i> gene are associated with carotid intima media thickness (cIMT), a surrogate maker for CV disease. <h3>Materials and Methods</h3> In 353 RA patients of the CARRÉ study, <i>IRF5</i> SNPs rs2004640 and rs4728142 were determined using Taqman Genotyping assay. cIMT was determined in a subgroup of 101 patients by B-mode ultrasonography. Linear regression analyses were used to investigate the association between cIMT and <i>IRF5 </i>genotypes, adjusting for demographic and cardiovascular risk factors. <h3>Results</h3> Patients homozygous for rs2004640 G-allele have higher cIMT compared to those homozygote for the T-allele (p = 0.019) and a trend towards a higher cIMT was observed (p = 0.103) for patients homozygous for the rs4728142 G-allele versus patients with the AA-genotype. Age was an effect-modifier for this association. Linear regression analysis in patients older than 60 years showed that the rs2004640 GG-genotype was associated with higher cIMT (regression coefficient 0.107 (C. I. 0.008; 0.205), p = 0.035) compared to the TT-genotype. This remained significant after adjustment for traditional risk factors (regression coefficient 0.111 (C. I.0.02; 0.202), p = 0.020). <h3>Conclusion</h3> We demonstrate that the <i>IRF5</i> gene variant rs2004640 is associated with preclinical atherosclerosis in RA patients, independent of traditional cardiovascular risk factors. These results might implicate a role for type I IFN in modulating CV disease features in RA.
Evidence that fibroblasts derive from epithelium during tissue fibrosis
Authors: Masayuki Iwano, David Plieth, Theodore M. Danoff, Chengsen Xue, Hirokazu Okada, Eric G. Neilson
Journal: Journal of Clinical Investigation (2002)

Interstitial fibroblasts are principal effector cells of organ fibrosis in kidneys, lungs, and liver. While some view fibroblasts in adult tissues as nothing more than primitive mesenchymal cells surviving embryologic development, they differ from mesenchymal cells in their unique expression of fibroblast-specific protein-1 (FSP1). This difference raises questions about their origin. Using bone marrow chimeras and transgenic reporter mice, we show here that interstitial kidney fibroblasts derive from two sources. A small number of FSP1(+), CD34(-) fibroblasts migrate to normal interstitial spaces from bone marrow. More surprisingly, however, FSP1(+) fibroblasts also arise in large numbers by local epithelial-mesenchymal transition (EMT) during renal fibrogenesis. Both populations of fibroblasts express collagen type I and expand by cell division during tissue fibrosis. Our findings suggest that a substantial number of organ fibroblasts appear through a novel reversal in the direction of epithelial cell fate. As a general mechanism, this change in fate highlights the potential plasticity of differentiated cells in adult tissues under pathologic conditions.
In memoriam: Samuel Vaisrub, MD, FRCP(C), MRCP(Lond) 1906--1980
Authors: W. R. Barclay
Journal: JAMA (1981)

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
Nonbronchodilator effects of inhaled beta 2 agonists. Greater protection against adenosine monophosphate- than methacholine-induced bronchoconstriction in asthma.
Authors: B J O'Connor, R W Fuller, P J Barnes
Journal: American Journal of Respiratory and Critical Care Medicine (1994)

There has been controversy about possible beneficial effects of beta agonists on airway function in asthma, in addition to their effects on airway smooth muscle. We compared the protective effects of terbutaline on bronchoconstrictor responses to methacholine, which constricts smooth muscle directly, adenosine 5'-monophosphate (AMP), which acts indirectly by mast cell activation, and sodium metabisulfite (MBS), which stimulates sensory nerves, in 15 mild asthmatic subjects in a randomized double-blind study carried out in two phases. In the first phase 12 subjects inhaled two doses of 0.5 and 2.5 mg terbutaline or placebo administered as a dry power (Tubohaler) 20 min before challenge with methacholine and AMP. Each subject received increasing doubling doses of methacholine and AMP nebulized from a dosimeter. Challenges were terminated when FEV1 fell by 20% from baseline (PC20). In the second phase 10 subjects (seven of whom had participated in Phase 1) inhaled 0.5 mg terbutaline or placebo before similar challenge with methacholine and MBS. In Phase 1 terbutaline inhibited the bronchoconstrictor response to methacholine by 2.1 and 3.3 doubling doses but caused a significantly greater inhibition of the response to AMP of 3.4 and 4.8 doubling doses after 0.5 and 2.5 mg, respectively. In the second phase 0.5 mg terbutaline had equivalent effects on responses to both methacholine and MBS of 2.6 and 2.2 doubling dilutions, respectively. This effect on methacholine and MBS implies functional antagonism of airway smooth muscle. The enhanced effect on AMP implies an additional non-smooth muscle action that may involve suppression of airway mast cell function.
Direct-to-Consumer Genomics, Social Networking, and Confidentiality
Authors: David B. Resnik
Journal: The American Journal of Bioethics (2009)

Click to increase image sizeClick to decrease image size Acknowledgments This research was supported by the intramural program of the National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH). It does not represent the opinions of the NIEHS, NIH, or the United States government. This open peer commentary by David B. Resnik is not subject to U.S. Copyright law.
Improving Access to Primary Care-Reply
Authors: Eli Ginzberg
Journal: JAMA (1993)

<h3>In Reply.</h3> —Dr Alper raises important issues about the relationships between primary care physicians and managed-care organizations that will have substantial influence on patients' choice and treatment modalities. His warning that patients under managed-care arrangements may change carriers frequently is a fear that warrants attention and evaluation. He implies that the present lowly state of primary care medicine is likely to worsen before it improves. Frankly, I don't have as much faith in health economists as does Dr Alper. Dr Gibb's communication is a useful reminder that the Washington-Alaska-Montana-Idaho program in the Northwest should be reviewed to pinpoint useful lessons about how to organize and provide primary care services more efficiently to underserved populations. I was intrigued by his suggestions that the National Health Service Corps should permit physicians to work part-time to work off their educational debt. And I can see that more attention to the needs of spouses
CHEMICAL FINDINGS IN THE BLOOD OF THE DOG AFTER CLOSED-LOOP OBSTRUCTION OF THE JEJUNUM
Authors: Russell L. Haden, Thomas G. Orr
Journal: The Journal of Experimental Medicine (1929)

The chemical findings in the blood of 6 dogs with closed-loop obstruction of the upper jejunum are reported. The duration of life with closed loops is less than with simple obstruction. All animals showed a marked rise in non-protein nitrogen and urea nitrogen, and fall in chlorides. Usually the C02 combining power of the plasma is increased. The findings in closed-loop obstruction are essentially the same as in simple intestinal obstruction.
Intravenous Urea as a Diuretic in Prostatectomy
Authors: G. B. McKelvie
Journal: BMJ (1962)

ULCERATIVE COLITISsBRiTsH 1711-~~~~~~EIA ORA assessed after two weeks.Clinical "success " was defined as complete freedom from symptoms, and sigmoidoscopic " success" was defined as a definite improvement in the sigmoidoscopic appearances.By both these criteria, combined corticosteroid treat- ment emerged as superior to sulphasalazine for the limited purpose which this therapeutic trial was designed to test.'" polythene" catheter of the " intracath " type was found to be satisfactory in keeping the intravenous transfusion running for 72 hours with the minimum of trouble, and when fitted with a "'plexitron " adaptor allowed blood tranusfusion to be given simultaneously.The transfusion of urea was started in the theatre as soon as the prostate gland had been removed.The urethral catheter used was a Foley self-retaining type made of plastic, and at the end of operation, after washing the bladder with a weak solution of chlor- hexidine, this was connected to a gamma-ray sterilized disposable plastic bag of 1,500-ml.capacity, thereby
Comparison of Ascending Aorta Versus Femoral Artery Cannulation for Acute Aortic Dissection Type A
Authors: Hiroyuki Kamiya, Klaus Kallenbach, Dominique Halmer, Merve Özsöz, Kathrin Ilg, Artur Lichtenberg, Matthias Karck
Journal: Circulation (2009)

Background— The site of cannulation for repair of ascending aortic dissection remains controversial. We present our experience with ascending aortic cannulation for acute aortic dissection type A. Methods and Results— From January 1988 to September 2007, we operated on 242 patients for acute aortic dissection type A. Medical records of 235 patients who received ascending aortic cannulation or femoral cannulation were retrospectively reviewed. Long-term follow-up was complete in 97% of patients. Cannulation was accomplished in 82 patients through the ascending aorta and in 153 patients through the femoral artery. Preoperative patient characteristics were almost comparable between groups. Similarly, there were no differences in preoperative patient characteristics and intraoperative parameters including operation time, bypass time, cross-clamp time, hypothermic circulatory arrest time, and percentage of total arch replacement. The 30-day mortality rate was 14% in the aortic group and 23% in the femoral group ( P =0.07), and incidence of stroke was 4.9% in the aortic group and 4.5% in the femoral group ( P =0.86). During follow-up (mean, 5.5 years), survival at 5 years and 10 years was 65% and 41% in the aortic group and 64% and 46% in the femoral group, respectively ( P =0.97). Conclusions— The cannulation site should be chosen according to the patient’s pathology and status, and the present study suggests that ascending cannulation in patients with acute aortic dissection type A can be a safe alternative, offering acceptable early and long-term outcomes.
Endothelial Cytotoxicity Mediated by Serum Antibodies to Heat Shock Proteins of <i>Escherichia coli</i> and <i>Chlamydia pneumoniae</i>
Authors: Manuel Mayr, Bernhard Metzler, Stefan Kiechl, Johann Willeit, Georg Schett, Qingbo Xu, Georg Wick
Journal: Circulation (1999)

Background —Growing evidence suggests that an immunological reaction against heat shock proteins (HSPs) may be involved in atherogenesis. Because HSPs show a high degree of amino acid sequence homology between different species, from prokaryotes to humans, we investigated the possibility of “antigenic mimicry” caused by an immunological cross-reaction between microorganisms and autoantigens. Methods and Results —Serum antibodies against the Escherichia coli HSP (GroEL) and the 60-kDa chlamydial HSP (cHSP60) from subjects with atherosclerosis were purified by use of affinity chromatography. Western blot analyses and competitive ELISAs confirmed the cross-reaction of the eluted antibodies with human HSP60 and the bacterial counterparts. The cytotoxicity of anti-GroEL and anti-cHSP60 antibodies was determined on human endothelial cells labeled with 51 Cr. A significant difference (40% versus 8%) was observed in the specific 51 Cr release of heat-treated (42°C for 30 minutes) and untreated cells, respectively, in the presence of these anti-HSP antibodies and complement. This effect was blocked by addition of 100 μg/mL recombinant GroEL. In addition, seropositivity against specific non-HSP60 Chlamydia pneumoniae antigens is more prominent among high–anti-HSP titer sera than low-titer sera. Conclusions —Serum antibodies against HSP65/60 cross-react with human HSP60, cHSP60, and GroEL; correlate with the presence of antibodies to C pneumoniae and endotoxin; and mediate endothelial cytotoxicity. These findings suggest that humoral immune reactions to bacterial HSPs, such as cHSP60 and GroEL, may play an important role in the process of vascular endothelial injury, which is believed to be a key event in the pathogenesis of atherosclerosis.
Abstract PD09-08: The potential role of TLK2 as a therapeutic target in breast cancer.
Authors: J-A Kim, X Cao, Y Tan, R Schiff, X Wang
Journal: Cancer Research (2012)

Abstract Invasive breast cancer (IBC) is a heterogeneous disease with distinct molecular and histological features as well as diverse biological behaviors. It is thus critical to find specific gene aberrations that can drive breast cancer initiation and progression as potential therapeutic targets. Our lab has established bioinformatics workflows to identify therapeutic oncogene targets. We have nominated Tousled-Like Kinase 2 (TLK2) as a candidate therapeutic target from 44,932 human genes based on integrative copy number data from The Cancer Genome Atlas (TCGA). TLK2 is a nuclear serine/threonine kinase that serves as a cell cycle checkpoint regulating chromosome assembly, and is inactivated by phosphorylation through the ATM dependent manner in the response to the double strand breaks during the S-phase. Interestingly, we observed 12–14% of focal TLK2 gene amplifications and translocations in invasive breast cancers, which are more frequent in luminal B tumors. Chromosomal aberrations may leads the deregulation of TLK2 kinase activity and results in overcoming the cell cycle checkpoint upon DNA damage such as IR or chemotherapeutic drugs treatments in breast cancer, thus destabilizing the cancer genome. Indeed, our preliminary data show that TLK2 knockdown substantially inhibits cell proliferation in breast cancer cells overexpressing TLK2. Further, this response is sustained in their derivative strains resistant to hormone or anti-Her2 therapies, suggesting the potential of TLK2 inhibition to sensitize these therapies as well. Overall, I expect that this study will provide compelling evidence regarding the role of TLK2 in breast cancer tumorigenesis and genomic instability, and establish its potential as a therapeutic target. The possibility of developing specific TLK2 inhibitors can be well demonstrated by the previous success of drugs against other cell cycle checkpoint kinases that are currently under clinical trials. In addition, molecular assays detecting TLK2 derangements may be applied in the clinics to identify patients who might benefit from future TLK2 inhibitor. If TLK2 endows resistance or sensitivity to other therapies, assays detecting TLK2 aberrations may also have important predictive value for personalization of these treatments. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr PD09-08.
923-3 Fluosol Reduces Myocardial Reperfusion Injury by Prolonged Suppression of Neutrophils by its Detergent Component (RheothRx) and not by Enhancing O 2 Delivery
Authors: João V. Vitola, David A. Ingram, John P. Holsinger, James B. Atkinson, Mervyn B. Forman, John J. Murray
Journal: Journal of the American College of Cardiology (1995)