tbuckley/cabot-search huggingface dataset:
Diagnosis of common dermatophyte infections by a novel multiplex real-time PCR detection/identification scheme
Authors: M. Arabatzis, L.E.S. Bruijnesteijn van Coppenraet, E.J. Kuijper, G.S. de Hoog, A.P.M. Lavrijsen, K. Templeton, E.M.H. van der Raaij-Helmer, A. Velegraki, Y. Graser, R.C. Summerbell
Journal: British Journal of Dermatology (2007)
Medroxyprogesterone Attenuates Estrogen-Mediated Inhibition of Neointima Formation After Balloon Injury of the Rat Carotid Artery
Authors: Ronald L. Levine, Shi-Juan Chen, Joan Durand, Yiu-Fai Chen, Suzanne Oparil
Journal: Circulation (1996)

Background Estrogen blunts the neointimal proliferative response to balloon injury of the carotid artery in intact female rats and gonadectomized rats of both sexes. This study tested whether, in gonadectomized rats of both sexes, (1) progestin (medroxyprogesterone acetate, MPA) alters neointima formation in injured carotid arteries, (2) addition of MPA alters the antiproliferative effects of estrogen, and (3) an interaction between MPA and estrogen can be accounted for by MPA-induced alterations in serum 17β-estradiol levels. Methods and Results Male and female Sprague-Dawley rats were subjected to gonadectomy, then were randomly divided into four subgroups and treated with either (1) 17β-estradiol, (2) MPA, (3) 17β-estradiol+MPA, or (4) vehicle, and balloon injury of the right common carotid artery was carried out. Two weeks later, rats were killed by overdose of pentobarbital, and the carotid arteries were subjected to morphometric analysis for evaluation of myointimal thickening. Estradiol inhibited myointimal proliferation after vascular injury in gonadectomized rats of both sexes ( P &lt;.05). MPA alone did not alter neointima formation, but addition of MPA to estradiol completely blocked the antiproliferative effects of estrogen without altering serum 17β-estradiol levels. Conclusions These data indicate that exogenous progestin given alone does not alter the vascular injury response in the rat carotid injury model but that addition of a progestin blocks the antiproliferative effects of estrogen in this model. These effects are seen in gonadectomized rats of both sexes. These findings have direct implications for postmenopausal hormone replacement therapy in humans.
Introduction to the Cardio-Oncology Miniseries
Authors: Ravin Davidoff, Michael Fifer, Sanjeev Francis
Journal: Circulation (2015)

The intersection of cancer and cardiovascular disease occurs on several levels.The present miniseries, within Circulation's Contemporary Reviews in Cardiovascular Medicine series, will highlight important areas within the emerging discipline of cardio-oncology.The miniseries will straddle a number of topics, as outlined below.1.The relationship of traditional cardiovascular risk factors with the development of cancer.This is a unique area within cardio-oncology that has not been fully covered in the current literature.2. The link between targeted chemotherapeutics and cardiac, vascular, and metabolic diseases with an emphasis on the molecular mechanisms.This has become an increasingly relevant area, given the rapid development and growth of this class of therapies.3. The clinically important area of cardioprotection during chemotherapy and the current data and areas that require additional research.4. A comprehensive review of the cardiovascular risks faced by cancer survivors and a concise review of current guidelines and areas of uncertainty for the practicing clinician.This miniseries will provide an in-depth review for the practicing clinician (cardiologist, oncologist, and internist) and provide insights, for the physician-scientist and scientist, into the mechanistic link between cancer and cardiovascular biology afforded by examining the cardiovascular impact of targeted cancer therapies and the impact of cardiovascular risk factors and medications in cancer biology.
Anxiety Disorder Comorbidity in Bipolar Disorder Patients: Data From the First 500 Participants in the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD)
Authors: Naomi M. Simon, Michael W. Otto, Stephen R. Wisniewski, Mark Fossey, Kemal Sagduyu, Ellen Frank, Gary S. Sachs, Andrew A. Nierenberg, Michael E. Thase, Mark H. Pollack
Journal: American Journal of Psychiatry (2004)

The authors provide a detailed perspective on the correlates of comorbid anxiety in a large, well-characterized sample of bipolar disorder patients.Anxiety and its correlates were examined in a cross-sectional sample from the first 500 patients with bipolar I or bipolar II disorder enrolled in the Systematic Treatment Enhancement Program for Bipolar Disorder, a multicenter project funded by the National Institute of Mental Health designed to evaluate the longitudinal outcome of patients with bipolar disorder.Lifetime comorbid anxiety disorders were common, occurring in over one-half of the sample, and were associated with younger age at onset, decreased likelihood of recovery, poorer role functioning and quality of life, less time euthymic, and greater likelihood of suicide attempts. Although substance abuse disorders were particularly prevalent among patients with anxiety disorders, comorbid anxiety appeared to exert an independent, deleterious effect on functioning, including history of suicide attempts (odds ratio=2.45, 95% CI=1.4-4.2).An independent association of comorbid anxiety with greater severity and impairment in bipolar disorder patients was demonstrated, highlighting the need for greater clinical attention to anxiety in this population, particularly for enhanced clinical monitoring of suicidality. In addition, it is important to determine whether effective treatment of anxiety symptoms can lessen bipolar disorder severity, improve response to treatment of manic or depressive symptoms, or reduce suicidality.
Clinical Decision Making in Patients With Thyroid Nodules
Authors: Jorge Luiz Gross, Caroline K. Kramer, Luciana Reck Remonti
Journal: JAMA Internal Medicine (2014)

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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Internal Medicine journal
Assessment of atherosclerotic plaque burden with an elastin-specific magnetic resonance contrast agent
Authors: Marcus R Makowski, Andrea J Wiethoff, Ulrike Blume, Friederike Cuello, Alice Warley, Christian H P Jansen, Eike Nagel, Reza Razavi, David C Onthank, Richard R Cesati, Michael S Marber, Tobias Schaeffter, Alberto Smith, Simon P Robinson, René M Botnar
Journal: Nature Medicine (2011)
Cancer Stem Cell Marker Phenotypes Are Reversible and Functionally Homogeneous in a Preclinical Model of Pancreatic Cancer
Authors: Joseph S. Dosch, Elizabeth K. Ziemke, Amrith Shettigar, Alnawaz Rehemtulla, Judith S. Sebolt-Leopold
Journal: Cancer Research (2015)

Survival rates associated with pancreatic cancer remain dismal despite advancements in detection and experimental treatment strategies. Genetically engineered mouse models of pancreatic tumorigenesis have gained considerable attention based on their ability to recapitulate key clinical features of human disease including chemotherapeutic resistance and fibrosis. However, it is unclear if transgenic systems exemplified by the Kras(G12D)/Trp53(R172H)/Pdx-1-Cre (KPC) mouse model recapitulate the functional heterogeneity of human pancreatic tumors harboring distinct cells with tumorigenic properties. To facilitate tracking of heterogeneous tumor cell populations, we incorporated a luciferase-based tag into the genetic background of the KPC mouse model. We isolated pancreatic cancer cells from multiple independent tumor lines and found that roughly 1 out of 87 cells exhibited tumorigenic capability. Notably, this frequency is significantly higher than reported for human pancreatic adenocarcinomas. Cancer stem cell (CSC) markers, including CD133, CD24, Sca-1, and functional Aldefluor activity, were unable to discriminate tumorigenic from nontumorigenic cells in syngeneic transplants. Furthermore, three-dimensional spheroid cultures originating from KPC tumors did not enrich for cells with stem-like characteristics and were not significantly more tumorigenic than cells cultured as monolayers. Additionally, we did not observe significant differences in response to gemcitabine or salinomycin in several isolated subpopulations. Taken together, these studies show that the hierarchical organization of CSCs in human disease is not recapitulated in a commonly used mouse model of pancreatic cancer and therefore provide a new view of the phenotypic and functional heterogeneity of tumor cells.
The 6-month safety and efficacy of abatacept in patients with rheumatoid arthritis who underwent a washout after anti-tumour necrosis factor therapy or were directly switched to abatacept: the ARRIVE trial
Authors: M Schiff, C Pritchard, J E Huffstutter, V Rodriguez-Valverde, P Durez, X Zhou, T Li, K Bahrt, S Kelly, M Le Bars, M C Genovese
Journal: Annals of the Rheumatic Diseases (2008)

<h3>Objective:</h3> To assess the safety, tolerability and efficacy of abatacept in patients with rheumatoid arthritis (RA) who had failed anti-tumour necrosis factor (TNF) therapy and were switched to abatacept directly or after completing washout. <h3>Methods:</h3> In this international, 6-month, open-label trial, patients had active RA, an inadequate response to anti-TNF therapy for 3 months or longer and a disease activity score in 28 joints (DAS28 (C-reactive protein; CRP) of 5.1 or greater. "Washout" patients discontinued anti-TNF therapy 2 months or longer pre-screening; "direct-switch" patients began abatacept (∼10 mg/kg) at their next scheduled anti-TNF therapy dose. <h3>Results:</h3> 1046 patients were treated (449 washout, 597 direct-switch; baseline characteristics were similar between groups). At 6 months, adverse events (AE; 78.0% vs 79.2%), serious AE (11.1% vs 9.9%) and discontinuations due to AE (3.8% vs 4.0%) and serious AE (2.0% vs 1.3%) were comparable in washout versus direct-switch patients. There were no opportunistic infections. At 6 months, in washout versus direct-switch patients, similar clinically meaningful improvements were seen in DAS28 (CRP) (⩾1.2 unit improvement, 59.5% vs 53.6%, respectively; low disease activity state, 22.5% vs 22.3%; DAS28-defined remission, 12.0% vs 13.7%), physical function (health assessment questionnaire disability index ⩾0.22 improvement; 46.3% vs 47.1%) and health-related quality of life (mean change in short-form 36 scores: physical component summary, 5.5 vs 6.1; mental component summary, 4.8 vs 5.4). <h3>Conclusion:</h3> Abatacept demonstrated acceptable safety and tolerability and clinically meaningful efficacy over 6 months in patients with inadequate response to anti-TNF therapy. Results were comparable with or without a washout, supporting direct switching from anti-TNF therapy to abatacept as an option in clinical practice. <h3>Trial registration number:</h3> NCT00124982.
Identification of a Gal/GalNAc Lectin in the Protozoan <i>Hartmannella vermiformis</i> as a Potential Receptor for Attachment and Invasion by the Legionnaires' Disease Bacterium
Authors: Chandrasekar Venkataraman, Bradley J. Haack, Subbarao Bondada, Yousef Abu Kwaik
Journal: The Journal of Experimental Medicine (1997)

The Legionnaire's disease bacterium, Legionella pneumophila, is a facultative intracellular pathogen which invades and replicates within two evolutionarily distant hosts, free-living protozoa and mammalian cells. Invasion and intracellular replication within protozoa are thought to be major factors in the transmission of Legionnaire's disease. Although attachment and invasion of human macrophages by L. pneumophila is mediated in part by the complement receptors CR1 and CR3, the protozoan receptor involved in bacterial attachment and invasion has not been identified. To define the molecular events involved in invasion of protozoa by L. pneumophila, we examined the role of protein tyrosine phosphorylation of the protozoan host Hartmannella vermiformis upon attachment and invasion by L. pneumophila. Bacterial attachment and invasion were associated with a time-dependent tyrosine dephosphorylation of multiple host cell proteins. This host cell response was highly specific for live L. pneumophila, required contact with viable bacteria, and was completely reversible following washing off the bacteria from the host cell surface. Tyrosine dephosphorylation of host proteins was blocked by a tyrosine phosphatase inhibitor but not by tyrosine kinase inhibitors. One of the tyrosine dephosphorylated proteins was identified as the 170-kD galactose/N-acetylgalactosamine–inhibitable lectin (Gal/GalNAc) using immunoprecipitation and immunoblotting by antibodies generated against the Gal/GalNAc lectin of the protozoan Entamoeba histolytica. This Gal/GalNAc–inhibitable lectin has been shown previously to mediate adherence of E. histolytica to mammalian epithelial cells. Uptake of L. pneumophila by H. vermiformis was specifically inhibited by two monovalent sugars, Gal and GalNAc, and by mABs generated against the 170-kD lectin of E. histolytica. Interestingly, inhibition of invasion by Gal and GalNAc was associated with inhibition of bacterial-induced tyrosine dephosphorylation of H. vermiformis proteins. High stringency DNA hybridization confirmed the presence of the 170-kD lectin gene in H. vermiformis. We conclude that attachment of L. pneumophila to the H. vermiformis 170-kD lectin is required for invasion and is associated with tyrosine dephosphorylation of the Gal lectin and other host proteins. This is the first demonstration of a potential receptor used by L. pneumophila to invade protozoa.
Deleterious Role of TLR3 during Hyperoxia-induced Acute Lung Injury
Authors: Lynne A. Murray, Darryl A. Knight, Laura McAlonan, Rochelle Argentieri, Amrita Joshi, Furquan Shaheen, Mark Cunningham, Lena Alexopolou, Richard A. Flavell, Robert T. Sarisky, Cory M. Hogaboam
Journal: American Journal of Respiratory and Critical Care Medicine (2008)

Rationale: Acute respiratory distress syndrome (ARDS) manifests clinically as a consequence of septic and/or traumatic injury in the lung. Oxygen therapy remains a major therapeutic intervention in ARDS, but this can contribute further to lung damage. Patients with ARDS are highly susceptible to viral infection and it may be due to altered Toll-like receptor (TLR) expression.Objectives: To evaluate the role of TLR3 in ARDS.Methods: TLR3 expression and signaling was determined in airway epithelial cells after in vitro hyperoxia challenge. Using a murine model of hyperoxia-induced lung injury, the role of TLR3 was determined using either TLR3-gene deficient mice or a specific neutralizing antibody directed to TLR3.Measurements and Main Results: Increased TLR3 expression was observed in airway epithelial cells from patients with ARDS. Further, hyperoxic conditions alone were a major stimulus for increased TLR3 expression and activation in cultured human epithelial cells. Interestingly, TLR3−/− mice exhibited less acute lung injury, activation of apoptotic cascades, and extracellular matrix deposition after 5 days of 80% oxygen compared with wild-type (TLR3+/+) mice under the same conditions. Administration of a monoclonal anti-TLR3 antibody to TLR3+/+ mice exposed to hyperoxic conditions likewise protected these mice from lung injury and inflammation.Conclusions: The potential for redundancy in function as well as cross-talk between distinct TLRs may indeed contribute to whether the inflammatory cascade can be effectively disrupted once signaling has been initiated. Together, these data show that TLR3 has a major role in the development of ARDS-like pathology in the absence of a viral pathogen.
A review of immune cells and molecules in women with recurrent miscarriage
Authors: S. M. Laird
Journal: Human Reproduction Update (2003)

Immunological rejection of the fetus due to recognition of paternal antigens by the maternal immune system, resulting in abnormal immune cells and cytokine production, is postulated to be one cause of unexplained pregnancy loss. Although there is evidence for this in rodents, there is less evidence in humans. This article focuses on studies in humans, and reviews the recent literature on the differences in immune cells and molecules in normal fertile women and women with recurrent miscarriage (RM). Although much of the evidence is contradictory, these studies do suggest differences in the expression of some immune cells and molecules in women with RM. Differences in the CD56+ population of cells are seen, and there is some evidence for an alteration in the ratio of Th1 and Th2 cytokines produced by peripheral blood monocytes (PBMCs) and clones of decidual CD4+ cells. There is also some evidence for differences in endometrial cytokine production, and in particular decreased production of pro-inflammatory cytokines such as interleukin-6. Possible reasons for the variations in data are discussed, and the importance of compartment (peripheral blood, endometrium or decidua) in which the cells and molecules are measured and the timing of the sampling, both with respect to the menstrual cycle and pregnancy (at the time or just after miscarriage) is emphasized.
Survival Outcomes After Contralateral Prophylactic Mastectomy: A Decision Analysis
Authors: P. R. Portschy, K. M. Kuntz, T. M. Tuttle
Journal: JNCI Journal of the National Cancer Institute (2014)

Contralateral prophylactic mastectomy (CPM) rates have substantially increased in recent years and may reflect an exaggerated perceived benefit from the procedure. The objective of this study was to evaluate the magnitude of the survival benefit of CPM for women with unilateral breast cancer.We developed a Markov model to simulate survival outcomes after CPM and no CPM among women with stage I or II breast cancer without a BRCA mutation. Probabilities for developing contralateral breast cancer (CBC), dying from CBC, dying from primary breast cancer, and age-specific mortality rates were estimated from published studies. We estimated life expectancy (LE) gain, 20-year overall survival, and disease-free survival with each intervention strategy among cohorts of women defined by age, estrogen receptor (ER) status, and stage of cancer.Predicted LE gain from CPM ranged from 0.13 to 0.59 years for women with stage I breast cancer and 0.08 to 0.29 years for those with stage II breast cancer. Absolute 20-year survival differences ranged from 0.56% to 0.94% for women with stage I breast cancer and 0.36% to 0.61% for women with stage II breast cancer. CPM was more beneficial among younger women, stage I, and ER-negative breast cancer. Sensitivity analyses yielded a maximum 20-year survival difference with CPM of only 1.45%.The absolute 20-year survival benefit from CPM was less than 1% among all age, ER status, and cancer stage groups. Estimates of LE gains and survival differences derived from decision models may provide more realistic expectations of CPM.
Measuring cell-type specific differential methylation in human brain tissue
Authors: Carolina M Montaño, Rafael A Irizarry, Walter E Kaufmann, Konrad Talbot, Raquel E Gur, Andrew P Feinberg, Margaret A Taub
Journal: Genome biology (2013)

The behavior of epigenetic mechanisms in the brain is obscured by tissue heterogeneity and disease-related histological changes. Not accounting for these confounders leads to biased results. We develop a statistical methodology that estimates and adjusts for celltype composition by decomposing neuronal and non-neuronal differential signal. This method provides a conceptual framework for deconvolving heterogeneous epigenetic data from postmortem brain studies. We apply it to find cell-specific differentially methylated regions between prefrontal cortex and hippocampus. We demonstrate the utility of the method on both Infinium 450k and CHARM data.
Eukaryotic transcriptional control
Authors: Roger D Kornberg
Journal: Trends in Genetics (1999)

Some 30 years ago, following the elucidation of transcriptional control in prokaryotes, attention turned to the corresponding problem in eukaryotes: how are so many genes transcribed in a cell-type-specific, developmentally regulated manner? The answer has been found in two modes of regulation, one involving chromatin and the other the chief transcribing enzyme, RNA polymerase II. Although basic features of the prokaryotic mechanism have been preserved, the demands of eukaryotic transcription control are met by a huge increase in complexity and by the addition of new layers to the transcription apparatus. Discovering the components of this apparatus has been a major theme of research over the past three decades; unravelling the mechanisms is a challenge for the future.
EXPERIMENTAL EPIDEMIOLOGY OF TUBERCULOSIS
Authors: Max B. Lurie
Journal: The Journal of Experimental Medicine (1930)

1. If normal guinea pigs are confined with an equal number of tuberculous cage mates the incidence of "contact" tuberculosis is increased by crowding. This is probably due largely to an increase in the amount of tubercle bacilli available in the more crowded cages, although no constant relationship could be established between the intensity of the exposure and the incidence of tuberculosis acquired by contagion. Other factors must be determined. 2. If guinea pigs are inoculated intraperitoneally with a given quantity of human tubercle bacilli and distributed in different degrees of crowding, the duration of survival is shortened in the more crowded animals, and the incidence of chronic types of tuberculosis is greater among the less crowded animals.