tbuckley/cabot-search huggingface dataset:
Undermeasuring Overuse—An Examination of National Clinical Performance Measures
Authors: Erika H. Newton, Erin A. Zazzera, Guillaume Van Moorsel, Brenda E. Sirovich
Journal: JAMA Internal Medicine (2015)

most vulnerable times in their lives-as in any other specialty.Not only are minority physicians more likely to work in underserved areas when their training is complete, but the quality of health care may be better when clinicians and patients are of the same race or ethnicity. 5,6he findings also raise questions, however.For example, it is not clear what makes obstetrics and gynecology so attractive to black and Hispanic trainees.I am unaware of any organized program to attract students or retain trainees who are underrepresented minorities.Data from the Association of American Medical Colleges show that between 1980 and 2012, the number of black women graduates of US medical schools increased 4-fold while the number of black men graduating declined. 7Most of the gains for underrepresented minorities in obstetrics and gynecology are likely among black women, partly owing to the high percentage of women entering the specialty.We lack data on the number of black and Hispanic trainees who complete the 4-year obstetrics and gynecology residency or further subspecialty training in urogynecology, maternal fetal medicine, gynecologic oncology, reproductive endocrinology, and infertility or family planning.These subspecialists account for the majority of researchers and medical school faculty and care for many underserved women with complex medical needs.Not only are black and Hispanic physicians underrepresented among medical school faculty, but they are less likely to be promoted, less likely to hold senior faculty and administrative positions, and less likely to be funded by the National Institutes of Health. 8,9imilarly, the number of women in leadership positions within academic institutions is low when compared with the increasing number of women in obstetrics and gynecology and other specialties.It is important to learn what factors contributed to the increase in numbers of women, blacks, and Hispanics in obstetrics and gynecology and whether those factors could improve representation in other specialties.It is also important, however, for obstetrics and gynecology and other specialties in which diversity is improving to monitor their workforce, the quality of postgraduate training, and the advancement of women, blacks, and Hispanics to senior and leadership roles.Progress will stall if women or underrepresented minorities do not advance.Ensuring a diverse physician workforce will require the continuing attention of medic al school leadership and health c are systems, and interventions to provide opportunities for diverse physicians to join the leadership ranks.Increasing physician diversity is yet another opportunity to improve the quality of care for all of our patients, particularly the most disadvantaged and those with a disproportionate burden of disease.
Abstract 20527: Nrf2 Signaling Modulates Human Endothelial Cell Barrier Regulation by S1P
Authors: Tao Jiang, Joseph B Mascarenhas, Venkateswaran Ramamoorthi Elangovan, Ting Wang, Donna D Zhang, Joe G Garcia
Journal: Circulation (2014)

Endothelial cell (EC) barrier dysfunction results in increased vascular permeability observed in inflammation, tumor angiogenesis, and atherosclerosis. The platelet-derived phospholipid, sphingosine-1-phosphate (S1P), decreases EC permeability in vitro and in vivo, features of obvious therapeutic potential. Oxidative stress is a common primary or secondary cause of vascular hyperpermeability in multiple pathological conditions, including inflammation, and exposure to excessive mechanical stress. Thus it is important to understand the relationship between S1P-mediated vascular protection and oxidative stress-induced barrier disruption. We examined the interaction of S1P and human pulmonary artery EC signaling and barrier regulation by the oxidative stress signaling mediator, Nrf2. Human pulmonary ECs pre-treated with either tBHQ (Nrf2 inducer) or Brusatol (Nrf2 inhibitor), were evaluated by transendothelial electric resistance (TER) in response to S1P or thrombin. tBHQ clearly augmented S1P-mediated endothelial barrier enhancement. In parallel, brusatol reduced the S1P-mediated endothelial barrier enhancement. In addition, neither tBHQ or brusatol modified the peak effects of thrombin-induced endothelial barrier disruption. However, tBHQ accelerated the recovery of endothelial barrier disruption induced by thrombin, whereas brusatol retarded EC recovery process. Furthermore, we demonstrated that tBHQ enhanced S1P mediated cortical actin polymerization and barrier enhancement, whereas Brusotal enhanced stress fiber formation in endothelial cells and inhibited S1P-mediated cortical actin formation confirming the active role of Nrf2 signaling in S1P-mediated endothelial barrier regulation. The effect of Brusatol on endothelial barrier function was confirmed by Nrf2 siRNA. These functional analyses confirm the importance of Nrf2 signaling in EC barrier restoration, a highly relevant response in acute lung inflammation resolution and lung fluid balance and further define a novel role of Nrf2-dependent signaling in vascular barrier regulation and cytoskeleton rearrangements
POLYRADICULONEURITIS, WITH REPORT OF CASE
Authors: Patrick S. Madigan, S. U. Marietta
Journal: Annals of Internal Medicine (1938)

Case Reports1 November 1938POLYRADICULONEURITIS, WITH REPORT OF CASEPATRICK S. MADIGAN, M.D., F.A.C.P., S. U. MARIETTA, M.D., F.A.C.P.PATRICK S. MADIGAN, M.D., F.A.C.P.Search for more papers by this author, S. U. MARIETTA, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-12-5-719 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe condition, variously known as infectious neuronitis, polyradiculoneuritis, polyneuritis, myeloradiculitis and polyneuritis pseudomyopathic, undoubtedly occurs more frequently than it is recognized. It appears to have been first discussed by Osler in 1892 under the designation of acute afebrile polyneuritis. Mills mentioned it in 1898 at the time the neuron theory was adopted. In 1916 Patrick noted the occurrence of facial diplegia in the syndrome of polyneuritis. In 1927 Viets mentioned the high total protein content of the spinal fluid as a diagnostic factor.1There has been considerable discussion at times regarding its terminology, especially directed against the use of the...References1. GILPINMOERSCHKERNOHAN SFFPJW: Polyneuritis, a clinical and pathological study of a special group of cases frequently referred to as instances of neuronitis, Arch. Neurol. and Psych., 1936, xxxv, 937-963. CrossrefGoogle Scholar2. COBBCOGGESHALL SHC: Neuritis, Jr. Am. Med. Assoc., 1934, ciii, 1608-1610. CrossrefGoogle Scholar3. ABADIEBERGOUIGNANVERGER : Polyneuritis pseudo-myopathic, Jr. Med. Bordeau, 1936, xxxii, 785. Google Scholar4. MCINTYRE HD: Infective neuronitis, Ohio State Med. Jr., 1937, xxxiii, 875-883. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Fort Sam Houston, Texas*Received for publication July 23, 1938. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byZur Ätiologie und Nosologie der Polyradiculoneuritiden 1 November 1938Volume 12, Issue 5Page: 719-724KeywordsGuillain-Barre syndromeNeuronsProteins ePublished: 1 December 2008 Issue Published: 1 November 1938 PDF downloadLoading ...
Randomized, Double‐Blind, Dose‐Escalation Trial of Triptorelin for Ovary Protection in Childhood‐Onset Systemic Lupus Erythematosus
Authors: Hermine I. Brunner, Clovis A. Silva, Andreas Reiff, Gloria C. Higgins, Lisa Imundo, Calvin B. Williams, Carol A. Wallace, Nadia E. Aikawa, Shannen Nelson, Marisa S. Klein‐Gitelman, Susan R. Rose
Journal: Arthritis & Rheumatology (2015)

Objective To determine the dose of triptorelin that is sufficient to maintain complete ovarian suppression in female patients with childhood‐onset systemic lupus erythematosus (SLE) who require cyclophosphamide therapy, to determine the length of time needed to achieve ovarian suppression after initiation of triptorelin treatment, and to investigate the safety of triptorelin. Methods In this randomized, double‐blind, placebo‐controlled, dose‐escalation study, female patients ages &lt;21 years were randomized 4:1 to receive triptorelin (n = 25) or placebo (n = 6). The starting doses of triptorelin were 25, 50, 75, and 100 μg/kg, and the dose was escalated until complete ovarian suppression was maintained. The primary outcome was the weight‐adjusted dose of triptorelin that provided complete ovarian suppression in at least 90% of the patients, as determined by gonadotropin‐releasing hormone agonist stimulation testing. The secondary outcome was the period of time required to achieve ovarian suppression, as measured by unstimulated follicle‐stimulating hormone and luteinizing hormone levels after the initiation of triptorelin treatment. Results Treatment with triptorelin at a weight‐adjusted dose of 120 μg/kg body weight provided sustained complete ovarian suppression in 90% of the patients. After administration of the initial dose of triptorelin, 22 days were required to achieve complete ovarian suppression. The rates of adverse events (AEs) and serious adverse events (SAEs) per 100 patient‐months of followup were not higher in the triptorelin group compared with the placebo group (for AEs, 189 versus 362; for SAEs, 2.1 versus 8.5). Conclusion High doses of triptorelin are needed to achieve and maintain complete ovarian suppression, but such doses appear to be well tolerated in adolescent female patients with childhood‐onset SLE. Our data suggest that a lag time of 22 days after initiation of triptorelin treatment is required before cyclophosphamide therapy is started or continued.
Abstract 16308: Non-Invasive Three Dimensional Cardiac Electrical Imaging: A Clinical Study
Authors: Long Yu, Qi Jin, Zhaoye Zhou, Liqun Wu, Bin He
Journal: Circulation (2014)

Introduction: Ventricular arrhythmias have been a major threat to human health in developed countries. Each year, more than 300,000 sudden cardiac death cases have been reported in the U.S. alone. The aim of this study is to evaluate a novel Cardiac Electrical Sparse Imaging technique (CESI) for noninvasive mapping and localizing the origin of ventricular arrhythmias in patients undergoing cardiac catheter ablation. Method: Pre-surgical ECG mapping and CT scans were performed in patients (n=13) with symptomatic Premature Ventricular Contraction (PVC, &gt;10,000 beats /24h). Data analysis was performed upon the ectopic beats (n=130) to image the foci and propagation pattern. The imaged activation patterns were compared with the Local Activation Time (LAT) determined from CARTO 3 system and the CESI imaged initiation sites were compared with the last ablation sites. Results: Good correlation was obtained between the CESI imaged activation and the measured LAT with an averaged Correlation Coefficient of 0.79±0.04 and Relative Error of 0.23±0.05 over 130 beats analyzed. The Relative Temporal Shrinkage was as low as 0.01±0.01, indicating 99% of the temporal resolution was preserved. PVCs were found to originate from RV, RVOT and LV. The focal mechanism was well captured with the foci localized 8±0.9 mm away from the last successful ablation sites. In each individual patient, the activation sequence could be imaged with only one beat and the propagation pattern remained stable among all recorded beats. Conclusion: The present results indicate that CESI is feasible to image the activation pattern and localize the ectopic foci in both RV and LV. The imaged activation patterns are in good agreement with the intra-cardiac measured ones over the endocardial surface, and the localized initiators showed concordance with the real ablation outcome. The present promising results suggest the CESI technique can potentially assist clinical management of ventricular arrhythmias.
Echocardiography for Hemodynamic Assessment of Patients With Advanced Heart Failure and Potential Heart Transplant Recipients 11To discuss this article on line, visit the ACC Home Page at www.acc.org/membersand click on the JACC Forum
Authors: James H Stein, Alex Neumann, Lynn M Preston, Maria Rosa Costanzo, Joseph E Parrillo, Maryl R Johnson, Richard H Marcus
Journal: Journal of the American College of Cardiology (1997)
Metastasis suppressors in human benign prostate, intraepithelial neoplasia, and invasive cancer: their prospects as therapeutic agents
Authors: Zahraa I. Khamis, Kenneth A. Iczkowski, Qing‐Xiang Amy Sang
Journal: Medicinal Research Reviews (2011)

Abstract Despite advances in diagnosis and treatment of prostate cancer, development of metastases remains a major clinical challenge. Research efforts are dedicated to overcome this problem by understanding the molecular basis of the transition from benign cells to prostatic intraepithelial neoplasia (PIN), localized carcinoma, and metastatic cancer. Identification of proteins that inhibit dissemination of cancer cells will provide new perspectives to define novel therapeutics. Development of antimetastatic drugs that trigger or mimic the effect of metastasis suppressors represents new therapeutic approaches to improve patient survival. This review focuses on different biochemical and cellular functions of metastasis suppressors known to play a role in prostate carcinogenesis and progression. Ten putative metastasis suppressors implicated in prostate cancer are discussed. CD44s is decreased in both PIN and cancer; Drg‐1, E‐cadherin, KAI‐1, RKIP, and SSeCKS show similar expression between benign epithelia and PIN, but are downregulated in invasive cancer; whereas, maspin, MKK4, Nm23 and PTEN are upregulated in PIN and downregulated in cancer. Moreover, the potential role of microRNA in prostate cancer progression, the understanding of the cellular distribution and localization of metastasis suppressors, their mechanism of action, their effect on prostate invasion and metastasis, and their potential use as therapeutics are addressed.
Development Of Minimal Residual Disease (MRD) Analysis In Childhood Acute Lymphoblastic Leukaemia (ALL) By Next Generation Sequencing (NGS)
Authors: Helen Williamson, Edward Mountjoy, Hashem Shihab, Jack Bartram, Mike Hubank, Nicholas Goulden, Ian Day, Eileen Roberts, John Moppett, Jeremy Hancock
Journal: Blood (2013)
Exercise tests and ST changes.
Authors: P Brown, L Schwartz
Journal: Circulation (1978)

To the Editor:We were interested in the article by Martins and colleagues on cardiac size and function in acromegaly,' because of our recent observations on left ventricular dynamics in this disease.Using echocardiography, we have studied a series of 24 patients, of whom seven were studied one year after elective surgery.All patients had markedly elevated growth hormone levels (16-380 ng/ml without suppression after glucose loading) in the preoperative assessment, with a normalization with postoperative data.Every case exhibited a marked concentric left ventricular hypertrophy (LVH) with a mean LV free wall thickness of 16 mm and absolute LV mass of 484 g, according to the ellipse approximation calculations.None had signs of asymmetric septal hypertrophy.In the postoperative group of seven patients the LV wall thickness was smaller (13 mm, P < 0.001) but the mean LV mass did not differ from the preoperative data (477 g; NS).The mean LV transversal diameter was 51.7 ± 5.1 mm in the preoperative studies and 57.4 ± 4.5 mm in the postoperative studies (P < 0.05).Asynergy was detected by multidirectional contraction cinetics analysis2 in only two patients.They also exhibited ischemic ST segment depressions upon exercise testing.The data suggest that the acromegalic heart disease consists of concentric hypertrophy without other structural or functional ab- normalities.It appears that normalization of the growth hormone levels postoperatively initiates dilatation with persistence of the in- creased LV mass.
Abstract A23: Epigenetic Cis-regulatory interactions in HIF1a-activated melanocytes
Authors: Stacie Loftus, Julie Cronin, Temesgen Fufa, Andrew McCallion, Gregory Crawford, William Pavan
Journal: Cancer Research (2015)

Abstract Melanoma tumors are heterogeneous lesions that progress through distinct cellular phenotypes exhibiting either highly proliferative or invasive cell state gene expression signatures (SOX10+ vs. TGFB+ pathways, respectively) as disease progression occurs. It is appreciated that even within a single tumor, individual cells respond to hypoxic conditions through Hypoxia Inducible Factor 1a (HIF1a) activation, leading to gene expression that promotes invasive cell properties. Regulation of gene expression integrates the binding of intrinsic cell lineage factors and general transcription machinery to key cis-regulatory DNA sequences that are epigenetically defined. In order to identify the cis-regulatory sequences that are utilized in a cell's response to HIF1a activation, we have established an integrated regulatory dataset from melan-Ink4a-ARF-/- immortalized mouse melanocytes. This dataset includes Dnase1 HS regions, enhancer regions marked by H3K4me1 and EP300 co-binding, ChIP-Seq for the transcription factors HIF1a and SOX10, and RNA-SEQ datasets under proliferative and HIF1a-activated growth conditions. We are evaluating HIF1a binding regions in order to identify the cis-regulatory sequences utilized to regulate gene expression, identify the key factors engaged at these sites, and assess the role that DNA variation has in modulating factor binding and gene transcription in the switch from proliferative to hypoxic cell signaling conditions. By identifying the epigenetic cis-regulatory interactions that occur as a result of HIF1a activation, we hypothesize that we will highlight pathways important for melanoma progression that may be relevant to future therapeutics. Citation Format: Stacie Loftus, Julie Cronin, Temesgen Fufa, Andrew McCallion, Gregory Crawford, William Pavan. Epigenetic Cis-regulatory interactions in HIF1a-activated melanocytes. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Melanoma: From Biology to Therapy; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(14 Suppl):Abstract nr A23.
Behavioural counselling in general practice for the promotion of healthy behaviour among adults at increased risk of coronary heart disease: randomised trial Commentary: Treatment allocation by the method of minimisation
Authors: A. Steptoe, S. Doherty, E. Rink, S. Kerry, T. Kendrick, S. Hilton, S. Day
Journal: BMJ (1999)

<h3>Abstract</h3> <b>Objective:</b> To measure the effect of behaviourally oriented counselling in general practice on healthy behaviour and biological risk factors in patients at increased risk of coronary heart disease. <b>Design:</b> Cluster randomised controlled trial. <b>Participants:</b> 883 men and women selected for the presence of one or more modifiable risk factors: regular cigarette smoking, high serum cholesterol concentration (6.5-9.0 mmol/l), and high body mass index (25-35) combined with low physical activity. <b>Intervention:</b> Brief behavioural counselling, on the basis of the stage of change model, carried out by practice nurses to reduce smoking and dietary fat intake and to increase regular physical activity. <b>Main outcome measures:</b> Questionnaire measures of diet, exercise, and smoking habits, and blood pressure, serum total cholesterol concentration, weight, body mass index, and smoking cessation (with biochemical validation) at 4 and 12 months. <b>Results:</b> Favourable differences were recorded in the intervention group for dietary fat intake, regular exercise, and cigarettes smoked per day at 4 and 12 months. Systolic blood pressure was reduced to a greater extent in the intervention group at 4 but not at 12 months No differences were found between groups in changes in total serum cholesterol concentration, weight, body mass index, diastolic pressure, or smoking cessation. <b>Conclusions:</b> Brief behavioural counselling by practice nurses led to improvements in healthy behaviour. More extended counselling to help patients sustain and build on behaviour changes may be required before differences in biological risk factors emerge.
User fees
Authors: A. Creese
Journal: BMJ (1997)

# User fees {#article-title-2}

If user fees for health care are the solution, what exactly is the problem? Proponents of user fees recommend them in two situations. The first is when health spending in total is low or falling—fees are recommended as a way to mobilise more money for health care than existing sources provide. The second, paradoxically, is when health expenditure is high or rising quickly, when fees are recommended as a way of improving efficiency by moderating demand and containing costs.1 2 Opponents of user fees attack them as a political strategy for shifting healthcare costs from the better off to the poor and the sick, pointing to the trade off between this method of raising revenue and maintaining access to care based on need rather than ability to pay.3

Dramatic differences exist between countries. Levels of and trends in national income and the condition of health systems vary widely among countries, and local context needs to be considered when making comparisons. In many “transition” economies such as China, Kyrgyzstan, Georgia, and Vietnam formal and informal charging at “subsidised” (government) health facilities has been used to replace sharply declining public sector funds. In most of the very poor …
Butyrophilin 3A1 binds phosphorylated antigens and stimulates human γδ T cells
Authors: Stefano Vavassori, Anil Kumar, Gan Siok Wan, Gundimeda S Ramanjaneyulu, Marco Cavallari, Sary El Daker, Travis Beddoe, Alex Theodossis, Neal K Williams, Emma Gostick, David A Price, Dinish U Soudamini, Kong Kien Voon, Malini Olivo, Jamie Rossjohn, Lucia Mori, Gennaro De Libero
Journal: Nature Immunology (2013)