tbuckley/cabot-search huggingface dataset:
Subcostal two-dimensional echocardiographic identification of anomalous attachment of septum primum in patients with left atrioventricular valve underdevelopment
Authors: Alvin J. Chin, Paul M. Weinberg, Gerald Barber
Journal: Journal of the American College of Cardiology (1990)

Five variations of atrial septal morphology occur in hypoplastic left heart syndrome. One variety, termed anomalous attachment of septum primum, has been described only in necropsy series. Two-dimensional echocardiography was utilized to determine the incidence of this anomaly in patients with left atrioventricular (AV) valve underdevelopment, including those with other ventriculoarterial alignments, such as transposition of the great arteries. Forty-eight (37%) of 129 patients with normally aligned great arteries (and two ventricles) had anomalous attachment of septum primum. Ten (34%) of 29 patients with double outlet right ventricle and left AV valve underdevelopment had this anomaly. Four (50%) of eight patients with single ventricle exhibited this atrial septal variant. The most reliable view to identify anomalous attachment was the subcostal left oblique-equivalent cut. Recognition of atrial septal morphology has implications for preoperative and intraoperative management of patients with left AV valve underdevelopment. The similar prevalence of this atrial septal variant in patients with normally aligned great arteries, double outlet right ventricle and transposed great arteries suggests that there may be a common mechanism for left AV valve underdevelopment that is independent of the development of the arterial portion of the heart.
Acute hypoxic pulmonary vasoconstriction in man is attenuated by type I angiotensin II receptor blockade
Authors: D. G. Kiely, R. I. Cargill, B. J. Lipworth
Journal: Cardiovascular Research (1995)

Objectives: We examined the hypothesis that angiotensin II (ANG II) is a modulator of acute hypoxic pulmonary vasoconstriction (HPV) by looking at the effect of losartan, a selective type 1 ANG II receptor antagonist, on acute HPV in man. Methods: Ten normal volunteers were studied on two separate days. They either received pre-treatment with losartan 25, 50, 100, 100 mg respectively on four consecutive days or matched placebo. They were then rendered hypoxaemic, by breathing an N2/O2 mixture for 20 min to achieve an SaO2 of 85–90% adjusted for a further 20 min to achieve an SaO2 of 75–80%. Pulsed wave Doppler echocardiography was used to measure mean pulmonary artery pressure (MPAP), cardiac output and hence pulmonary vascular resistance (PVR). Results: Baseline MPAP and PVR (during normoxaemia) were unaffected by losartan pre-treatment compared with placebo. However, losartan significantly reduced MPAP at both levels of hypoxaemia compared with placebo: 14.7 ± 0.7 vs 19.0 ± 0.7 mmHg at an SaO2 85–90% (P < 0.01) and 20.0 ± 0.7 vs 25.7 ± 0.8 mmHg at an SaO2 75–80% (P < 0.05) respectively. Similarly losartan significantly reduced PVR compared to placebo: 191 ± 9 vs 246 ± 10 dyne · s · cm−5 at an SaO2 85–90% (P < 0.005) and 233 ± 12 vs 293 ± 18 dyne · s · cm−5 at an SaO2 75–80% (P < 0.05), respectively. Pre-treatment with losartan, however, had no significant effect on systemic vascular resistance although losartan compared to placebo resulted in a significant (P < 0.05) reduction in mean arterial pressure at an SaO2 75–80%: 78 ± 2 vs 87 ± 2 mmHg. Conclusions: Losartan had no effect on baseline pulmonary haemodynamics but significantly attenuated acute hypoxic pulmonary vasoconstriction, suggesting that angiotensin II plays a role in modulating this response in man via its effects on the type 1 angiotensin II receptor.
THE ADDITION OF BEVACIZUMAB IN THE TREATMENT OF PATIENTS WITH METASTASTIC CANCER, INCREASES THE INCIDENCE OF CARDIOVASCULAR EVENTS: A PROSPECTIVE STUDY
Authors: Archontoula Michelongona, Konstantinos Toutouzas, Andreas Synetos, Flora Zagouri, Aristotle Bamias, Meletios Athanasios Dimopoulos, Stella Kyvelou, Ioannis Kapelakis, Dimitris Tousoulis, Christodoulos Stefanadis
Journal: Journal of the American College of Cardiology (2012)
Safety of oral peanut immunotherapy for peanut allergic patients
Authors: A.M. Scurlock, P.H. Steele, S.S. Andrzejewski, L.A. Pons, K.A. Althage, L. Christie, S.K. Carlisle, A.D. Buchanan, S.M. Jones, A.W. Burks
Journal: Journal of Allergy and Clinical Immunology (2005)
The acute-phase response protects mice from D-galactosamine sensitization to endotoxin and tumor necrosis factor-α
Authors: Joseph M. Alcorn, Joshua Fierer, Mario Chojkier
Journal: Hepatology (1992)

D-Galactosamine is an hepatocyte-specific inhibitor of RNA synthesis. It has been used to sensitize animals both to the lethal effects of bacterial endotoxin (lipopolysaccharide) and to a principal lipopolysaccharide-induced mediator of shock, tumor necrosis factor-α. The mechanism by which this sensitization occurs is unknown. Because lipopolysaccharide, acting through a network of cytokines, provokes the transcription of a number of hepatic acute-phase proteins, we postulated that the lipopolysaccharide-sensitizing effect of D-galactosamine could be caused by its inhibition of acute-phase product transcription. We confirmed that the acute-phase response to lipopolysaccharide was attenuated by simultaneous administration of D-galactosamine. However, when the acute-phase response was induced by subcutaneous turpentine 24 hr before D-galactosamine administration, the effect of D-galactosamine on circulating acute-phase reactants was negligible. Furthermore, induction of an a priori acute-phase response protected mice from both D-galactosamine/lipopolysaccharide and D-galactosamine/tumor necrosis factor-α-induced death. The turpentine-induced acute-phase response did not decrease endogenous tumor necrosis factor-α production after lipopolysaccharide, nor did it affect the clearance of larger doses of injected tumor necrosis factor-α. Thus we suggest that the acute-phase response protects against death in D-galactosamine—sensitized mice through an interaction with mediators of shock subsequent to tumor necrosis factor-α release. (Hepatology 1992;15:122-129).
Psychosocial Stress as a Risk for Breast Cancer
Authors: Alf Forsén
Journal: Psychotherapy and Psychosomatics (1991)

Life events, important emotional losses, difficult life situations, and psychological characteristics were investigated in a case-control study of 87 breast cancer patients and their controls. In a second part, the effect of stressful life events preceding cancer diagnosis on survival was studied in an 8-year follow-up of the breast cancer group. The control group was selected from the general female population and matched for sex, age, number of child-births, and language. The findings showed that breast cancer patients had significantly more life events, important losses, and difficult life situations prior to the discovery of the breast tumor than controls. The analysis indicated that important losses during a 6-year prodromal period and life event scores prior to examination on both the 12-month and modified 6-year Social Readjustment Rating Scale were associated with subsequent development of breast cancer. The association persisted after adjustment for marital status, education, and social class. The findings of the survival analyses indicated that life events in the 12 months preceding the onset of breast cancer and lower social class were associated with a smaller chance of disease-free and overall survival after controlling for clinical factors.
Protein Kinase C Isoform Activation and Endothelin-1 Mediated Defects in Myocyte Contractility After Cardioplegic Arrest and Reperfusion
Authors: Rupak Mukherjee, Kimberly A. Apple, Christina E. Squires, Brooke S. Kaplan, Julie E. McLean, Stuart M. Saunders, Robert E. Stroud, Francis G. Spinale
Journal: Circulation (2006)

Background— Endothelin-1 (ET-1) is released after hyperkalemic cardioplegic arrest (CA) and reperfusion and may contribute to contractile dysfunction. ET-1 receptor transduction causes activation of protein kinase C (PKC) isoforms, which can cause differential intracellular events. The goal of this study was to determine which PKC isoforms contribute to myocyte contractile dysfunction with ET-1 and CA. Methods and Results— Percent shortening (PERSHORT) and the time to 50% relaxation (T50) were measured in porcine (n =22) left ventricular myocytes, randomized (minimum: 30 cells/group) to normothermia: (cell media for 2 hours/37°C), and CA: (2 hours/4°C, 24 mEq K + solution followed by reperfusion in cell media), ET-1/CA: (100 pM ET-1 during CA). Studies were performed in the presence and absence of PKC inhibitors (500 nM) against the classical (Beta-I, Beta-II, Gamma) and novel (Epsilon, Eta) isoforms (myocytes from a minimum of 3 pigs per inhibitor). CA reduced PERSHORT by &amp;35% from normothermia ( P &lt;0.05), which was further reduced with ET-1. PKC-Beta-II or PKC-Gamma inhibition increased PERSHORT from ET-1/CA as well as CA only ( P &lt;0.05). CA prolonged T50 by &amp;19% from normothermia ( P &lt;0.05) and was further prolonged with ET-1. Inhibition of the classical PKC isoforms reduced T50 from ET-1/CA ( P &lt;0.05). Inhibition of novel PKC isoforms did not yield similar effects on either PERSHORT or T50 with ET-1/CA. Conclusions— Inhibition of the classical PKC isoforms relieved the negative inotropic and lusitropic effects of ET-1 after CA. These findings provide mechanistic support for developing targeted inhibitory strategies with respect to ET-1 signaling and myocyte contractile dysfunction with cardioplegic arrest and reperfusion.
Abstract 1195: A molecular characterization of the anaplastic prostate carcinomas.
Authors: Ana M. Aparicio, Sankar Maity, Xuemei Wang, Anh G. Hoang, Eleni Efstathiou, Patricia Troncoso, Christopher J. Logothetis
Journal: Cancer Research (2013)

Abstract Molecular markers that identify clinically meaningful, biologically based, subsets of PC are lacking. This results in inefficient clinical trial designs and suboptimal therapy selection off-protocol. The androgen receptor (AR)-negative small cell PC (SCPC) is an often-unrecognized morphological variant of the disease found on repeat biopsies during the castrate-resistant (CR) progression of PC. Its presence predicts for a poor response to hormonal therapies, a distinct clinical behavior and a short survival. Characteristic clinical features of SCPC are frequently present in patients with CRPC, constituting a clinical syndrome termed anaplastic PC. We hypothesized that the anaplastic PC share underlying biology with SCPC, irrespective of morphology. Preclinical studies show that SCPC are characterized by loss of tumor suppressors and AR signaling, as well as overexpression of mitotic genes and proneural transcription factors. To test our hypothesis we used immunohistochemistry to analyze the expression of markers in these pathways, in tumor biopsies from chemotherapy-naïve men with anaplastic PC participating in a prospective phase II clinical trial. To date we have analyzed 6 markers in 25 samples (6 with pure or mixed SCPC morphology) from prostate biopsies (n=10), transurethral resections of prostate tumors (n=4), bone marrow or bone biopsies (n=9), lymph node (n=1) or brain (n=1). Results are shown in Table 1. Table 1. Immunohistochemistry Anaplastic PC % Positive Cells AR RB1 p53 UBE2C Ki67 CYP17A1 0 8 11 11 5 1 0 &amp;lt; or = 10% 3 6 9 9 8 1 &amp;gt; 10% 14 8 5 11 16 24 Of the 17 samples that had ≤10% RB1+ cells, 10 had ≤10% AR+ cells and 9 had &amp;gt;10% UBE2C+ cells. Of the 11 samples that had ≤10% AR+ cells, 10 also had ≤10% RB1+ cells and 6 had &amp;gt;10% UBE2C+ cells. These data support our hypothesis that the anaplastic prostate carcinomas are characterized by loss of tumor suppressors and overexpression of mitotic genes. Updated results in additional samples and of additional markers will be presented. Citation Format: Ana M. Aparicio, Sankar Maity, Xuemei Wang, Anh G. Hoang, Eleni Efstathiou, Patricia Troncoso, Christopher J. Logothetis. A molecular characterization of the anaplastic prostate carcinomas. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1195. doi:10.1158/1538-7445.AM2013-1195
Bichloride of Methylene before the Academy of Medicine of Paris
Authors: F. E. Junker
Journal: BMJ (1884)

The disappearance of the second so6und at the left of the apeX, which, with the shorlt sharp character of the first sound, marks the second stage.ofmitral stenosis, is probably explained by the follOwing considerations.In the normal heart, a second sound is always audible at and to the feft of the apex; and repeated careful examinations have convinced me that it is tlhe aortic second sound which is'here heard and not the pulmonary, even when accentuated and unduly loud.In mitral stenosis, there are two influences tending to prevent the aortic second sound from reaching the surface of the chest.First, the left ventricle, not undergoing dilatation and hypertrophy, while the right enlarges greatly, is overlapped by the latter, which usurps the positiot of the apex, and thius the left ventricle cannot conduct the aortic sound to the chest-wall.Again, the aortic second sound will'be weak, because the diminished amount of blood entering the ventricle, in con- s'euence of the nalTowed mitral orifice, will not distend the aorta, and wvill, therefore, fail to provoke a powerful recoil, such as is necessary for the production of a loud second sound.The presystolic murmur itself often undergoes a modification in this stage.As commonly heard, it occupies the end of the diastolic in- terval, running up to the first sound, and corresponding therefore with the auricular systole.But it may be a long or a short murmur, and may indeed occupy the entire diastolic interval, when it will corres- pond not only with the auricular systolic but also with the active diastolic rebound of the ventricle from contraction; i.e., murmur is produced by the current of blood sucked into the ventricle as it dilates, as well as by that driven into it by the systule of the auricle.This
APA Targets Unnecessary Antipsychotic Use
Authors: Bridget M. Kuehn
Journal: JAMA (2013)

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
Air Travel–Related Deep Vein Thrombosis and Pulmonary Embolism
Authors: Harvey J. Sugerman, Bo G. Eklöf, William D. Toff, Alison E. Burke, Edward H. Livingston
Journal: JAMA (2012)

D eep vein thrombosis occurs when a blood clot forms in the deep veins of the leg and obstructs the flow of blood back to the heart.This can lead to swelling of the leg and pain in the calf muscle, although sometimes there are no symptoms.Pulmonary embolism occurs when blood clots leave the veins where they developed, travel through the right side of the heart, and lodge in the small or large branches of the blood vessels going to the lung (pulmonary arteries).This can cause symptoms such as chest pain, difficulty breathing, or coughing up blood.In severe cases, it may result in collapse and sudden death.Long airplane flights or multiple flights in a short period can cause deep vein thrombosis and pulmonary embolism.Any situation in which the leg is bent at the knee for prolonged periods without much active motion may lead to a reduction of blood flow and increase the risk of blood clots.Other factors can increase this risk, such as recent surgery, taking oral contraceptives or hormone therapy, pregnancy, cancer, heart problems, and older age.Inherited genetic factors may also play a role.
Langerhans' cell histiocytosis: A case history
Authors: J.L. Craze, J. Pritchard
Journal: Annals of Oncology (1996)

Langerhans’ cell histiocytosis (LCH) is a rare condition of uncertain aetiology characterised by the infiltration of certain organs by cells of Langerhans’ cell phenotype (‘LCH cells’), together with inflammatory cells. Tissue damage and fibrosis may ensue, perhaps mediated by cytokines produced by the ‘LCH cells’ or inflammatory cells (or both) and sometimes leading to long term sequelae after the disease has ‘burnt out’. LCH may present to a variety of specialists since many different organs can be involved but the oncologist has traditionally played a major part in management because cytotoxic agents are used for many patients with the disorder. However LCH is not at the present time regarded as a true malignancy.
Abstract 868: HER2-targeted engineered toxin body demonstrates selective binding and cell kill of HER2-overexpressing breast cancer.
Authors: Sangeetha Rajagopalan, Erin Willert, Rachel Wirth, William Null, Jen-Sing Liu, Jack P. Higgins
Journal: Cancer Research (2013)

Abstract The HER2 receptor is overexpressed in 20-30% of breast cancers. HER2 overexpression in breast cancer has been successfully targeted by both antibody and antibody-drug conjugate approaches. Trastuzumab, a humanized monoclonal antibody is approved for the treatment of HER2 positive metastatic breast cancer. More recently, trastuzumab-DM1, an antibody drug conjugate (ADC), has shown promising clinical results in patients refractory to trastuzumab. Because DM1 is a chemotherapeutic and refractory breast cancer patients have typically progressed through several rounds of chemotherapy, we were interested in developing a new ADC approach with trastuzumab that utilized a novel mechanism of action. 5G2 is an engineered toxin body comprised of the trastuzumab scFv and a modified ribosome-inhibiting protein derived from Shiga-like toxin 1 A. 5G2 has exhibited high binding affinity to HER2 protein and HER2-expressing cells. 5G2 exerts a potent HER2-specific cytotoxic effect on HER2-expressing cells, but little activity on various HER2 negative cells. These results demonstrate that 5G2 is a promising HER2-targeted therapeutic agent against breast carcinomas and is currently under further development. Citation Format: Sangeetha Rajagopalan, Erin Willert, Rachel Wirth, William Null, Jen-Sing Liu, Jack P. Higgins. HER2-targeted engineered toxin body demonstrates selective binding and cell kill of HER2-overexpressing breast cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 868. doi:10.1158/1538-7445.AM2013-868
Cervical screening laboratories should be accredited
Authors: L. Beecham
Journal: BMJ (1998)

Guidance on standards and a monitoring procedure for cervical testing laboratories in Britain have been introduced to help to eradicate errors in testing procedures.

Health Services Accreditation, an NHS body set up in 1997 to improve quality of care by monitoring clinical and organisational standards, has announced a series of safety and quality control indicators for cervical …
Experimental Model for an Ectopic Focus Coupled to Ventricular Cells
Authors: Rajiv Kumar, Ronald Wilders, Ronald W. Joyner, Habo J. Jongsma, E. Etienne Verheijck, David A. Golod, Antoni C.G. van Ginneken, William N. Goolsby
Journal: Circulation (1996)

Background We used a mathematical model of a sinoatrial nodal cell (SAN model) electrically coupled to real ventricular cells (VCs) to investigate action potential conduction from an automatic focus. Methods and Results Since input resistance of a VC is less than that of an SAN cell, coupling of the SAN model, with a size factor of 1, to a VC produced either (1) spontaneous pacing at the slower rate of the SAN model but without driving (activation) of the VC for lower values of coupling conductance (G j ) or (2) inhibition of pacing of the SAN model by electrical coupling to the VC for higher values of G j . When the SAN model was adjusted in size to be 3 to 5 times larger than a sinoatrial nodal cell, thus making effective SAN model capacitance 3 to 5 times larger and input resistance 3 to 5 times smaller, the SAN model propagated activity to the coupled VC for G j above a critical value. When the VC was paced at 1 Hz, the coupled cell pair demonstrated a stable rhythm of alternating cycle lengths and alternating conduction directions. By increasing pacing frequency to 2 Hz, we converted this rhythm to a regular 2-Hz frequency in which each action potential originated in the VC. More complex periodic interactions were observed at intermediate cycle lengths and lower or higher values of G j . Conclusions The phenomena we observed demonstrate the critical role of the size of an automatic focus as well as the coupling in the propagation of activity from the focus into surrounding myocardium.
406-5 Oxidized low-density lipoprotein-stimulated smooth muscle cell growth is mediated by the helix loop helix factor Id3: A novel mechanism contributing to atherosclerotic lesion formation
Authors: Angela M Taylor, Feng Li, Ross Gerrity, Richard L Birnbaum, Martin Matsumura, Sarah Rutherford, Puspha-Rekha Thimmalapura, Coleen A McNamara
Journal: Journal of the American College of Cardiology (2004)
Risk factors for severe delayed postpolypectomy bleeding
Authors: M. Sawhney, N. Salfiti, D. Nelson, F. Lederle, J. Bond
Journal: Endoscopy (2008)

Postpolypectomy bleeding is a rare but serious adverse event. The aim of this study was to identify factors associated with the risk of severe delayed postpolypectomy bleeding.This was a case-control study, comparing cases who developed hematochezia and required medical evaluation 6 hours to 14 days after colonoscopic polypectomy, and control patients who underwent polypectomy without delayed bleeding, and who were selected in approximately a 3 : 1 ratio. The following risk factors were specified a priori: resuming anticoagulation (within 1 week following polypectomy), aspirin use, hypertension, and polyp diameter.Of the 4592 patients who underwent colonoscopy with polypectomy, 41 patients (0.9 %) developed delayed postpolypectomy bleeding (cases), and 132 patients were selected as controls. The mean age was 64.3 years for cases and 65.4 years for controls. Cases presented on average 6 days after polypectomy (range 1 - 14 days), and 48 % required blood transfusion (average 4.2 units, range 0 - 17). Two patients required surgery. Anticoagulation was resumed following polypectomy in 34 % of cases compared with 9 % of controls (OR 5.2; 95 % CI 2.2 - 12.5; P < 0.001). For every 1 mm increase in polyp diameter, the risk of hemorrhage increased by 9 % (OR 1.09; 95 % CI 1.0 - 1.2; P = 0.008). Hypertension (OR 1.1) and aspirin use (OR 1.1) did not increase the risk of postpolypectomy bleeding. In exploratory analysis, diabetes (OR 2.5) and coronary artery disease (OR 3.0) were associated with postpolypectomy hemorrhage, but the association was no longer statistically significant once adjusted for the use of anticoagulation.Resuming anticoagulation following polypectomy and polyp diameter were strongly associated with increased risk of severe delayed postpolypectomy bleeding.