tbuckley/cabot-search huggingface dataset:
Why cardiovascular screening in young athletes can save lives: a critical review
Authors: Jonathan A Drezner, Kimberly G Harmon, Irfan M Asif, Joseph C Marek
Journal: British Journal of Sports Medicine (2016)

Cardiovascular (CV) screening in young athletes remains challenging and a topic of considerable debate. Recent criticisms of ECG screening have perpetuated arguments that ECG screening is neither indicated nor effective by applying outdated incidence data and flawed methodology. In response, this article provides a critical review of the arguments in favour of ECG screening in athletes and the early detection of CV disorders at elevated risk of sudden cardiac death (SCD). Importantly, no study to date has demonstrated that screening by history and physical examination alone is effective in detecting athletes at risk or in preventing SCD. ECG screening using current athlete-specific interpretation standards provides a low false-positive rate and improves detection of potentially lethal CV conditions. Further, risk reduction in athletes identified with CV disorders can be effectively achieved through modern strategies for risk stratification and disease-specific management. By every definition of the purpose of CV screening, ECG-inclusive programmes will better meet the stated objective of early detection when proper ECG interpretation and adequate cardiology resources are available. Less debate on screening protocols and more emphasis on advancing physician skills and infrastructure in sports cardiology is needed to more effectively screen targeted athlete populations.
Case 51-1965
Authors: Thomas B. Fitzpatrick, Wallace H. Clark
Journal: New England Journal of Medicine (1965)

Presentation of Case First admission. An eighteen-year-old boy entered the hospital because of stiffness of the joints.He had been well until eight months previously, when mild fatigue developed, and he noticed that his fingers and toes turned bluish white on exposure to cold. Five months before admission the pallor of the fingers became persistent, and he had difficulty in bending them. One month later a biopsy of the skin, performed at another hospital, was interpreted as showing scleroderma. The hematocrit was 44 per cent, the glutamic oxalacetic transaminase (SGOT) 31 units, and the antistreptolysin-O titer 250 Todd units; a . . .
Photosensitizer enhanced disassembly of amphiphilic micelle for ROS-response targeted tumor therapy in vivo
Authors: Liangliang Dai, Yonglin Yu, Zhong Luo, Menghuan Li, Weizhen Chen, Xinkun Shen, Feng Chen, Qiang Sun, Qingfeng Zhang, Hao Gu, Kaiyong Cai
Journal: Biomaterials (2016)
Case 53-1963
Authors: Edward F. Rabe, Benjamin Castleman
Journal: New England Journal of Medicine (1963)

Presentation of CaseA twenty-seven-day-old female premature infant was admitted to the hospital because of persistent vomiting.The child was the product of the third pregnancy of a thirty-two-year-old mother. Two siblings were well. Except for a "cold" persisting for several weeks early in the pregnancy the mother had been well; she had taken an appetite depressant and sedative (Dexamyl) daily, and the total gain in weight was 18 pounds. In the eighth month of pregnancy the membranes ruptured, with subsequent brief but profuse bleeding requiring blood transfusion. On cesarean section placenta praevia was found; the baby breathed and cried . . .
A Track Record on SHOX: From Basic Research to Complex Models and Therapy
Authors: Antonio Marchini, Tsutomu Ogata, Gudrun A. Rappold
Journal: Endocrine Reviews (2016)

SHOX deficiency is the most frequent genetic growth disorder associated with isolated and syndromic forms of short stature. Caused by mutations in the homeobox gene SHOX, its varied clinical manifestations include isolated short stature, Léri-Weill dyschondrosteosis, and Langer mesomelic dysplasia. In addition, SHOX deficiency contributes to the skeletal features in Turner syndrome. Causative SHOX mutations have allowed downstream pathology to be linked to defined molecular lesions. Expression levels of SHOX are tightly regulated, and almost half of the pathogenic mutations have affected enhancers. Clinical severity of SHOX deficiency varies between genders and ranges from normal stature to profound mesomelic skeletal dysplasia. Treatment options for children with SHOX deficiency are available. Two decades of research support the concept of SHOX as a transcription factor that integrates diverse aspects of bone development, growth plate biology, and apoptosis. Due to its absence in mouse, the animal models of choice have become chicken and zebrafish. These models, therefore, together with micromass cultures and primary cell lines, have been used to address SHOX function. Pathway and network analyses have identified interactors, target genes, and regulators. Here, we summarize recent data and give insight into the critical molecular and cellular functions of SHOX in the etiopathogenesis of short stature and limb development.
Therapeutic regulatory T-cell adoptive transfer ameliorates established murine chronic GVHD in a CXCR5-dependent manner
Authors: Cameron McDonald-Hyman, Ryan Flynn, Angela Panoskaltsis-Mortari, Nicholas Peterson, Kelli P. A. MacDonald, Geoffrey R. Hill, Leo Luznik, Jonathan S. Serody, William J. Murphy, Ivan Maillard, David H. Munn, Laurence A. Turka, John Koreth, Corey S. Cutler, Robert J. Soiffer, Joseph H. Antin, Jerome Ritz, Bruce R. Blazar
Journal: Blood (2016)
Reply
Authors: Jian‐Gao Fan, Fu‐Sheng Wang
Journal: Hepatology (2014)

Potential conflict of interest: Nothing to report. Author names in bold designate shared co‐first authorship. We thank Dr. Qi et al. for their positive comments about our special article in Hepatology.1 Beyond the contents discussed in our paper, these authors mentioned the discrepancy and similarity in diagnosis and treatment of Budd‐Chiari syndrome (BCS) between Western countries and China. In particular, Qi et al. suggested that the difference in clinical characteristics and etiology may be associated with the choice of suitable treatment options for BCS. To better recognize how the discrepancy influences the outcome of disease progression and treatment efficacy, there is an urgent need to strengthen translational study on liver diseases including BCS between China and Western countries. Budd‐Chiari syndrome is a rare, heterogeneous, and potentially fatal disease associated with the occlusion of hepatic veins and/or the suprahepatic inferior vena cava.2 There is a distinct geographic variation in BCS incidence between Asia and Western countries, being only lower than 1 to 2 per million inhabitants in Western countries.3 Over the past decades BCS has been frequently reported in China; however, national data on incidence and prevalence of BCS in the Chinese population are not available. The literature reports that BCS is more frequent in Henan, Shandong, Jiangsu, and Anhui Provinces in the Yellow River valley compared to other regions in China.5 The clinical characteristics and etiology of BCS patients in China are similar to those of patients in India and Nepal but significantly different from those of Western patients.3 Idiopathic forms, combined membranous occlusion of the inferior vena cava and the hepatic veins, and higher incidence of hepatocellular carcinoma are typical features of most Chinese BCS patients.5 In addition, selection of treatment modalities for BCS patients is different between China and Western countries.3 Chinese patients with BCS are usually treated using percutaneous transluminal angioplasty and have a similar good clinical outcome to Western patients, who often are treated with transjugular intrahepatic portosystemic shunt plus long‐term anticoagulants.9 As an update, there have been around 3000 articles on BCS in China, but the real prevalence might be higher than estimated due to increased awareness and improved diagnostic methods in China. However, duplicate publications about BCS in China both in English‐language journals and in Chinese‐language journals are relatively common.11 We should pay more attention to this situation in meta‐analyses and systemic reviews of this syndrome.
HER3 Targeting Sensitizes HNSCC to Cetuximab by Reducing HER3 Activity and HER2/HER3 Dimerization: Evidence from Cell Line and Patient-Derived Xenograft Models
Authors: Dongsheng Wang, Guoqing Qian, Hongzheng Zhang, Kelly R. Magliocca, Sreenivas Nannapaneni, A.R.M. Ruhul Amin, Michael Rossi, Mihir Patel, Mark El-Deiry, J. Trad Wadsworth, Zhengjia Chen, Fadlo R. Khuri, Dong M. Shin, Nabil F. Saba, Zhuo G. Chen
Journal: Clinical Cancer Research (2016)

Abstract Purpose: Our previous work suggested that HER3 inhibition sensitizes head and neck squamous cell carcinoma (HNSCC) to EGFR inhibition with cetuximab. This study aimed to define the role of HER3 in cetuximab resistance and the antitumor mechanisms of EGFR/HER3 dual targeting in HNSCC. Experimental Design: We treated cetuximab-resistant HNSCC UMSCC1-C and parental UMSCC1-P cell lines with anti-EGFR antibody cetuximab, anti-HER3 antibody MM-121, and their combination. We assessed activities of HER2, HER3, and downstream signaling pathways by Western blotting and cell growth by sulforhodamine B (SRB) and colony formation assays. HER3-specific shRNA was used to confirm the role of HER3 in cetuximab response. The combined efficacy and alterations in biomarkers were evaluated in UMSCC1-C xenograft and patient-derived xenograft (PDX) models. Results: Cetuximab treatment induced HER3 activation and HER2/HER3 dimerization in HNSCC cell lines. Combined treatment with cetuximab and MM-121 blocked EGFR and HER3 activities and inhibited the PI3K/AKT and ERK signaling pathways and HNSCC cell growth more effectively than each antibody alone. HER3 knockdown reduced HER2 activation and resensitized cells to cetuximab. Cetuximab-resistant xenografts and PDX models revealed greater efficacy of dual EGFR and HER3 inhibition compared with single antibodies. In PDX tissue samples, cetuximab induced HER3 expression and MM-121 reduced AKT activity. Conclusions: Clinically relevant PDX models demonstrate that dual targeting of EGFR and HER3 is superior to EGFR targeting alone in HNSCC. Our study illustrates the upregulation of HER3 by cetuximab as one mechanism underlying resistance to EGFR inhibition in HNSCC, supporting further clinical investigations using multiple targeting strategies in patients who have failed cetuximab-based therapy. Clin Cancer Res; 23(3); 677–86. ©2016 AACR.
Prevention of Congenital Disorders and Care of Affected Children
Authors: Gary L. Darmstadt, Christopher P. Howson, Gijs Walraven, Robert W. Armstrong, Hannah K. Blencowe, Arnold L. Christianson, Alastair Kent, Helen Malherbe, Jeffrey C. Murray, Carmencita D. Padilla, Salimah R. Walani
Journal: JAMA Pediatrics (2016)

As the Sustainable Development Goals are adopted by United Nations member states, children with congenital disorders remain left behind in policies, programs, research, and funding. Although this finding was recognized by the creation and endorsement of the 63rd World Health Assembly Resolution in 2010 calling on United Nations member states to strengthen prevention of congenital disorders and the improvement of care of those affected, there has been little to no action since then. The Sustainable Development Goals call for the global health and development community to focus first and foremost on the most vulnerable and those left behind in the Millennium Development Goal era. To maximize the opportunity for every woman and couple to have a healthy child and to reduce the mortality and severe disability associated with potentially avoidable congenital disorders and their consequences for the children affected, their families and communities, and national health care systems, we propose priority measures that should be taken urgently to address this issue.
Mast cells regulate myofilament calcium sensitization and heart function after myocardial infarction
Authors: Anta Ngkelo, Adèle Richart, Jonathan A. Kirk, Philippe Bonnin, Jose Vilar, Mathilde Lemitre, Pauline Marck, Maxime Branchereau, Sylvain Le Gall, Nisa Renault, Coralie Guerin, Mark J. Ranek, Anaïs Kervadec, Luca Danelli, Gregory Gautier, Ulrich Blank, Pierre Launay, Eric Camerer, Patrick Bruneval, Philippe Menasche, Christophe Heymes, Elodie Luche, Louis Casteilla, Béatrice Cousin, Hans-Reimer Rodewald, David A. Kass, Jean-Sébastien Silvestre
Journal: The Journal of Experimental Medicine (2016)

Acute myocardial infarction (MI) is a severe ischemic disease responsible for heart failure and sudden death. Inflammatory cells orchestrate postischemic cardiac remodeling after MI. Studies using mice with defective mast/stem cell growth factor receptor c-Kit have suggested key roles for mast cells (MCs) in postischemic cardiac remodeling. Because c-Kit mutations affect multiple cell types of both immune and nonimmune origin, we addressed the impact of MCs on cardiac function after MI, using the c-Kit-independent MC-deficient (Cpa3(Cre/+)) mice. In response to MI, MC progenitors originated primarily from white adipose tissue, infiltrated the heart, and differentiated into mature MCs. MC deficiency led to reduced postischemic cardiac function and depressed cardiomyocyte contractility caused by myofilament Ca(2+) desensitization. This effect correlated with increased protein kinase A (PKA) activity and hyperphosphorylation of its targets, troponin I and myosin-binding protein C. MC-specific tryptase was identified to regulate PKA activity in cardiomyocytes via protease-activated receptor 2 proteolysis. This work reveals a novel function for cardiac MCs modulating cardiomyocyte contractility via alteration of PKA-regulated force-Ca(2+) interactions in response to MI. Identification of this MC-cardiomyocyte cross-talk provides new insights on the cellular and molecular mechanisms regulating the cardiac contractile machinery and a novel platform for therapeutically addressable regulators.
Error in Reference List
Authors:  Kurian,  Ford
Journal: JAMA Oncology (2015)

lationship of this depth be fostered?I am still learning how to answer this difficult question, as I imagine most physicians are.Medicine is becoming a field governed by the standard of care and guidelines, but standards and guidelines will never allow us to perfectly predict the outcome of an individual patient.The role of a physician in medicine is no longer as a gatekeeper of therapy: "giving" treatment to some and "refusing" it to others, with patients trusting every word that we say.Rather, a physician is now a gatekeeper of knowledge: a fortune teller with prescriptions as tarot cards and a stethoscope as a crystal ball, with patients looking for the wizard behind the curtain.When discussing treatment options with patients, we need to recognize trust as a necessary component and evaluate its extent early in the discussion of treatment options.Patients want us to be honest and clear.Certainly my family would want that if I treated them.
How Society Subsidizes Big Food and Poor Health
Authors: Raj Patel
Journal: JAMA Internal Medicine (2016)

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
Abnormal Monocyte Chemotactic Response in Cancer Patients
Authors: David A. Boetcher, Edward J. Leonard
Journal: JNCI Journal of the National Cancer Institute (1974)

The in vitro monocyte chemotactic response (MCR) was used to measure effector cell function in 44 cancer patients. Twenty-four of the 44 cancer patients had decreased MCR's, compared to 3 ot 22 normal individuals and 2 of 24 control patients with valvular heart disease. There was a significantly higher incidence of local infection and/or previous granulomatous disease in the cancer patient group with normal MCR's compared to those with low MCR's. This suggests that infection in cancer patients may raise a low MCR to the normal range. Many common medications had no effect on the MCR, with the possible exception of dipyridamole. Abnormal MCR's occurred rarely in patients with minimal disease (stage I), but were found at all other stages. In melanoma patients with recurrent metastatic disease, the appearance of nodal metastases was delayed in patients with normal MCR. Thus decreased MCR is an abnormality that can appear early in the natural history of cancer in humans and may be one indicator ot the effectiveness of host response to the disease.
Assessment of senior medical students in the field of bronchial asthma
Authors: Roman Bontsevich, Kristina Vlasova, Galina Ketova, Valeriya Barysheva, Elena Luchinina, Margarita Malkina, Natalya Goncharova, Yulia Feoktistova
Journal: European Respiratory Journal (2014)

The aim of study is to estimate the knowledge of medical students at the senior courses of higher schools in the key aspect of bronchial asthma (BA).

Materials and methods . The multicentre study was conducted in the Russian Federation in 6 cities (Belgorod, Chelyabinsk, Saratov, Samara, Voronezh & Vladivostok), 139 of higher grade (4th-6th grade) medical students were tested. Knowledge of key aspects of bronchial asthma such as definition, pathogenesis, diagnostics and treatment was evaluated through the means of a questionnaire consisting of 12 questions. These questions were a mix of multi choice and anecdotal.

Results . The average level of correct answers totaled 72.4% and varied from 58.6% to 88.2% in different centers. The most difficult questions were the following: BA definition (43.2% of correct answers), key factor of BA pathogenesis (63.3%), peak flowmetry as the main method of BA self-control (61.9%), fixed combinations of drugs (62.6%).

The best results were shown when defining the following: trigger in the development of an asthmatic attack (89.2%), the main method of BA diagnosis (89.2%), variants of BA severity (87.1%), status asthmaticus (94.2%).

Conclusion . Despite the availability of plenty training and scientific literature in bronchial asthma field the level of knowledge in this area cannot be admitted as satisfactory. The level of incorrect answers to basic questions reaches 41.4% in the certain centers. Thus bronchial asthma subject should be studied more thoroughly in the medical higher schools.
Government rejects BMA’s call to invest extra £350m a week in NHS
Authors: Gareth Iacobucci
Journal: BMJ (2016)

The government has rejected a call from the BMA to invest an additional £350m (€420m; $460m) a week in the NHS, after the association’s chairman of council, Mark Porter, had urged ministers to fulfil the pledge made by the Leave campaign during the recent European Union referendum.

The contentious pledge formed a central plank of the campaign run by politicians wishing the United Kingdom to leave the EU, but prominent campaigners quickly distanced …
TCIRG1 Associated Congenital Neutropenia
Authors: Vahagn Makaryan, Elisabeth Rosenthal, Audrey Anna Bolyard, Merideth L. Kelley, Jennifer Below, Michael Bamshad, Kathryn M. Bofferding, Joshua D. Smith, Kati Buckingham, Laurence A. Boxer, Julia Skokowa, Karl Welte, Deborah A. Nickerson, Gail P. Jarvik, David C. Dale
Journal: Blood (2013)
Melanoma and Non-Melanoma Skin Cancer in Patients with Chronic Lymphocytic Leukemia.
Authors: Timothy G Call, Kari G Rabe, Brewer D Jerry, Neil E. Kay, Clive S. Zent, Susan M Schwager, Deborah A Bowen, Jose F Leis, Han Tun, Svetomir N Markovic, Susan L Slager, Tait D. Shanafelt
Journal: Blood (2009)
Development of Tumors in Fetal and Adult Lung Transplants
Authors: W. E. Heston, C. H. Steffee
Journal: JNCI Journal of the National Cancer Institute (1957)

Development of Tumors in Fetal and Adult Lung Transplants Get access W. E. Heston, W. E. Heston National Cancer Institute,3Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar C. H. Steffee C. H. Steffee National Cancer Institute,3Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 18, Issue 6, June 1957, Pages 779–793, https://doi.org/10.1093/jnci/18.6.779 Published: 01 June 1957 Article history Received: 18 February 1957 Published: 01 June 1957
A randomized phase III study of carfilzomib vs low-dose corticosteroids with optional cyclophosphamide in relapsed and refractory multiple myeloma (FOCUS)
Authors: R Hájek, T Masszi, M T Petrucci, A Palumbo, L Rosiñol, A Nagler, K L Yong, A Oriol, J Minarik, L Pour, M A Dimopoulos, V Maisnar, D Rossi, H Kasparu, J Van Droogenbroeck, D B Yehuda, I Hardan, M Jenner, M Calbecka, M Dávid, J de la Rubia, J Drach, Z Gasztonyi, S Górnik, X Leleu, M Munder, M Offidani, N Zojer, K Rajangam, Y-L Chang, J F San-Miguel, H Ludwig
Journal: Leukemia (2016)

This randomized, phase III, open-label, multicenter study compared carfilzomib monotherapy against low-dose corticosteroids and optional cyclophosphamide in relapsed and refractory multiple myeloma (RRMM). Relapsed and refractory multiple myeloma patients were randomized (1:1) to receive carfilzomib (10-min intravenous infusion; 20 mg/m2 on days 1 and 2 of cycle 1; 27 mg/m2 thereafter) or a control regimen of low-dose corticosteroids (84 mg of dexamethasone or equivalent corticosteroid) with optional cyclophosphamide (1400 mg) for 28-day cycles. The primary endpoint was overall survival (OS). Three-hundred and fifteen patients were randomized to carfilzomib (n=157) or control (n=158). Both groups had a median of five prior regimens. In the control group, 95% of patients received cyclophosphamide. Median OS was 10.2 (95% confidence interval (CI) 8.4–14.4) vs 10.0 months (95% CI 7.7–12.0) with carfilzomib vs control (hazard ratio=0.975; 95% CI 0.760–1.249; P=0.4172). Progression-free survival was similar between groups; overall response rate was higher with carfilzomib (19.1 vs 11.4%). The most common grade ⩾3 adverse events were anemia (25.5 vs 30.7%), thrombocytopenia (24.2 vs 22.2%) and neutropenia (7.6 vs 12.4%) with carfilzomib vs control. Median OS for single-agent carfilzomib was similar to that for an active doublet control regimen in heavily pretreated RRMM patients.
PD2-3-2: Amplification Of Epidermal Growth Factor Receptor Gene And Its Prognostic Implication In Surgically Resected Adenocarcinoma Of The Lung
Authors: Young T. Kim, Moon C. Kang, Yoon K. Jeon, Jee Y. Song, Chang H. Kang, Sook W. Sung, Joo H. Kim
Journal: Journal of Thoracic Oncology (2007)