tbuckley/cabot-search huggingface dataset:
Diagnosis in Locomotor Disorders
Authors: Robert B. Aird
Journal: JAMA (1960)

The purpose of this small volume, as stated by the author, is to consider the principal differential diagnostic possibilities "in a number of prominent symptoms and signs in disorders of the locomotor system." The author adds that it is "a short book, restricted to essentials, for quick reference," written for those in physical medicine departments and rheumatic units of general hospitals and others dealing with the problems of the locomotor system, including general practitioners. A careful review of this volume attests to the success the author has achieved in his purpose. It is clearly and succinctly written. The symptoms and signs considered are arranged in convenient alphabetical order. This arrangement, plus an excellent index, fulfills the author's aim of making the volume useful for quick reference. The book cuts across specialty lines and presents the main entities to be considered for each principal sign and symptom related to the locomotor
Abstract 135: MicroRNA repression of BIRC4/XIAP in lung cancer
Authors: Yili Xie, Jordi Camps, Keytam S. Awad, Danny Wangsa, Jianhui Yang, Nina Yoo, Thomas Ried, King F. Kwong
Journal: Cancer Research (2011)

Abstract Background: MicroRNAs (miRNAs, miR) are short ∼22 nucleotide (nt) noncoding RNA molecules capable of regulating gene expression by targeting mRNA. Baculovirus IAP repeat containing protein-4 (BIRC4/XIAP) is the most potent member of the Inhibitor of apoptosis family of proteins (IAP) and an important cellular pro-survival stimulus. BIRC4 mRNA contains a long 3’ untranslated region (UTR) and its function remains unclear. Previously, we have shown that 17 candidate miRNAs can be identified that potentially interacted with BIRC4's 3’ UTR by using a computerized heuristic algorithm. An inverse relationship was discovered between miR-24 and BIRC4 in non-small cell lung cancers (NSCLC). The objective of this study is to determine whether miR-24 can directly target BIRC4 and consequently regulate apoptosis in NSCLC. Methods: miRNA precursors and anti-miRNA inhibitors were transfected in NSCLC cells and their effect on BIRC4 protein expression was evaluated by western blot and their interaction with the BIRC4 3’UTR was detected by using luciferase reporter plasmids containing the BIRC4 3’UTR (wild type &amp; mutant). Lentiviral p-Receiver-lv19-BIRC4 was transduced into A549 cells to generate stable clones overexpressing BIRC4 in order to examine miR-24's effects on a transcript devoid of the native 3’-UTR. The effects of miRNA on cell apoptosis signaling was determined by MTT cell viability assay, TdT apoptosis assay and Western blot for caspase-3 activation and PARP cleavage. Cytogenetic analyses (SKY &amp;CGH) were performed to detect chromosomal abnormalities that may account for reduced expression of miRNA. Results: miR-24 transfection down-regulates BIRC4 expression in NSCLC cells. Luciferase assay confirmed that miR-24 targets the BIRC4 3’ UTR at nucleotide positions 2294-2310. miR-24 also sensitizes intrinsically TRAIL-resistant A549 cells to TRAIL-induced cell apoptosis, which can be reversed by ectopic expression of miR-24-insensitive BIRC4. miR-24 sensitized-apoptosis is modulated via the canonical apoptosis pathway. Genomic deletion in the miR-24 coding region was found in NSCLC cells with corresponding low levels of miR-24. NSCLC or normal lung cells with normal/high levels of miR-24 did not exhibit cytogenetic deletion in the miR-24 coding region. Conclusions: miR-24 down-regulates BIRC4 expression by directly targeting the BIRC4 3’UTR and can sensitize NSCLC cells to TRAIL-induced apoptosis. Genomic deletion contributes to the reduced expression of miR-24 in NSCLC. This finding raises the possibility that miR-24 mimetics may be of value in combination with TRAIL or other therapeutic strategies in the future treatment of lung cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 135. doi:10.1158/1538-7445.AM2011-135
GMC strikes off GP who arranged late abortion for her daughter
Authors: C. Dyer
Journal: BMJ (2010)

A British GP who arranged a late abortion in Spain for her teenage daughter has been struck off the medical register by the General Medical Council for “multiple instances of deceit, lack of probity, and dishonesty.”

Saroj Adlakha, who ran the Shilpa medical centre in Kings Heath, Birmingham, paid €3200 (£2800; $4400) for her 18 year old student daughter, who was 31 weeks pregnant, to have the abortion at the Ginemedex clinic in Barcelona ( BMJ 2010;340:c175, doi:10.1136/bmj.c175). Her daughter would not have been …
Pickwickian Syndrome? The Dickens!
Authors: Samuel Vaisrub
Journal: JAMA (1978)

The link between Charles Dickens and the syndrome that relates to one of his characters was first mentioned 60 years ago by William Osier, MD, who noted that "a remarkable phenomenon associated with excessive fat in young persons is an uncontrollable tendency to sleep—like the fat boy in Pickwick." The Dickensian connection, which was missed or ignored by Auchincloss et al<sup>1</sup>who first described a typical case, was picked up by Burwell et al<sup>2</sup>in 1956 when they labeled the syndrome Pickwickian. They ascribed the somnolence, cyanosis, polycythemia, alveolar hypoventilation, and right ventricular failure, which characterize the syndrome, to obesity with its attendant increase in the work of breathing. As is often the case with eponymous syndromes, the monolithic structure of the Pickwickian syndrome soon began to crack. Gastaut et al<sup>3</sup>(1965) split off a syndrome that does not conform to type. Its genesis is not in
Platelet Function Testing in Cardiovascular Diseases
Authors: Alan D. Michelson
Journal: Circulation (2004)

ase presentation 1: Mr F. is a 60-year-old man with unstable angina who takes aspirin, 81 mg/day.A platelet function test demonstrates that his platelets are "resistant" to aspirin.Should his treatment be changed?Case presentation 2: Mr K. is a 60year-old man with unstable angina who takes aspirin, 81 mg/day, and clopidogrel, 75 mg/day.A platelet function test demonstrates that his platelets are "resistant" to clopidogrel.Should his treatment be changed? Normal Platelet FunctionPlatelets are small cells of great importance in thrombosis, hemorrhage, and inflammation. 1Formation of the hemostatic plug at sites of vascular injury is described in Figure 1.Platelets localize, amplify, and sustain the coagulant response at the injury site and release procoagulant platelet-derived microparticles.Platelets contain a variety of inflammatory modulators (eg, CD40 ligand [CD40L]) that are released on platelet activation. Platelet Function Testing in Cardiovascular DiseasesPlatelets have an increasingly welldefined critical role in coronary artery thrombosis 3 and in other common car-diovascular diseases, including stroke, peripheral vascular disease, and diabetes mellitus. 1Although the role of platelets in thrombosis is well characterized, platelets may also have a role in the pathogenesis of the underlying atherosclerotic process. 3Platelet function tests have been studied in cardiovascular disease as a means to predict clinical outcomes and to monitor antiplatelet drugs.Table 1 summarizes these tests. Use of Platelet Function Tests to Monitor Antiplatelet DrugsAspirin reduces the odds of a serious arterial thrombotic event in high-risk patients by Ϸ25%. 14However, 10% to
Thyroid cancer in the United States since accident at Chernobyl
Authors: W. Reid, J. Mangano
Journal: BMJ (1995)

ways, one would, strictly speaking, need hundreds of thousands of randomised trials to arrive at conclusive answers about the efficacy of this form of treatment.Clearly, this is not practical.The Centre for Complementary Health Studies is therefore planning a trial designed to answer the much broader question, "does homoeopathy work (regardless of remedy, dose, etc)?"I would be delighted to hear from potential participants in this multicentre study.EERNST
Deficiency of heme oxygenase-1 impairs renal hemodynamics and exaggerates systemic inflammatory responses to renal ischemia
Authors: M.J. Tracz, J.P. Juncos, A.J. Croatt, A.W. Ackerman, J.P. Grande, K.L. Knutson, G.C. Kane, A. Terzic, M.D. Griffin, K.A. Nath
Journal: Kidney International (2007)
Cigarette Smoking: Medical Costs vs Tax Receipts
Authors: W. F. Forbes
Journal: JAMA (1978)

To the Editor.—  The recent dramatic increases in the quality and availability of medical services in many Western countries have led to attempts to identify areas where the rise in costs may be slowed down without diminishing substantially the quality of services.  One area of possible government intervention is the use of tobacco products, and particularly of cigarettes. If the purpose of such intervention is to help to keep health care costs at a manageable level and to prevent other economic losses caused by smoking, it becomes necessary to assess all the economic side effects as well.  However, estimates of the economic costs of cigarette smoking in the United States vary widely, 1-5 partly because no two studies appear to have taken the same items into account, and partly because of the many difficulties inherent in arriving at such estimates. For example, even when only the direct costs of health
617 E1 therapeutic vaccination in patients with chronic HCV genotype 1 infection: Results of a 15-month, placebo-controlled trial
Authors: H. Wedemeyer, H. Van Vlierberghe, H. Blum, E. Nevens, M. Gschwantler, S. Zeuzem, T. Roskams, V. Desmet, S. Dincg, C. Vander Stichele, H. De Winter, G. Maertens, Y. Horsmans
Journal: Journal of Hepatology (2006)
Abstract 1000: Inactivation of notch1 signaling suppresses FGFR1 knockdown-dependent growth inhibition of MDA-MB-231 breast cancer cells
Authors: Andreas I. Evangelou, Irene L. Andrulis
Journal: Cancer Research (2011)

Abstract Breast cancer is a very heterogeneous disease as an array of expressed genes can be detected in individual tumors with varying phenotypic cellular morphology. However, despite this heterogeneity, two main histological subgroups predominate, basal-like and luminal-like tumors. Ongoing efforts aim to identify and target additional genetic alterations in breast tumors. One of the widely known and clinical distinctive markers between these tumor phenotypes for example is the transmembrane protein E-cadherin. Factors involved in the repression of E-cadherin are also involved in breast cancer progression. We have recently (Bane et al., Breast Cancer Research and Treatment 117:183-191, 2009) identified a set of differentially expressed and potentially additional distinctive markers between basal- and luminal-like breast tumors that have suggested an important role for Notch and FGF signaling in the development and maintenance of these breast cancer phenotypes. Other studies have also demonstrated gene amplifications in Notch and FGF receptors that can predispose in breast cancer pathophysiology. In the present study we have determined that downregulation of FGFR1 in the basal breast cancer cell line MDA-MB-231 decreased cell proliferation and survival. Interestingly, when Notch1 was also concomitantly repressed with siRNA, normal MDA-MB-231 cell proliferation and survival was restored. The current findings suggest and define a novel interplay between FGFR and Notch signaling in breast cancer patients that may be associated with poor prognosis due to ongoing and sustained basal-like phenotype in breast tumors. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1000. doi:10.1158/1538-7445.AM2011-1000
Multicentric dermatofibrosarcoma protuberans in patients with adenosine deaminase–deficient severe combined immune deficiency
Authors: Chimene Kesserwan, Robert Sokolic, Edward W. Cowen, Elizabeth Garabedian, Kerstin Heselmeyer-Haddad, Chyi-Chia Richard Lee, Stefania Pittaluga, Clarymar Ortiz, Kristin Baird, Dolores Lopez-Terrada, Julia Bridge, Alan S. Wayne, Fabio Candotti
Journal: Journal of Allergy and Clinical Immunology (2011)
Identification of microRNA-221/222 and microRNA-323-3p association with rheumatoid arthritis via predictions using the human tumour necrosis factor transgenic mouse model
Authors: Ioannis Pandis, Caroline Ospelt, Niki Karagianni, Maria C Denis, Martin Reczko, Carme Camps, Artemis G Hatzigeorgiou, Jiannis Ragoussis, Steffen Gay, George Kollias
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Objective</h3> To identify novel microRNA (miR) associations in synovial fibroblasts (SF), by performing miR expression profiling on cells isolated from the human tumour necrosis factor (TNF) transgenic mouse model (TghuTNF, Tg197) and patients biopsies. <h3>Methods</h3> miR expression in SF from TghuTNF and wild-type (WT) control mice were determined by miR deep sequencing (miR-seq) and the arthritic profile was established by pairwise comparisons. Quantitative PCR analysis was utilised for profile validation, miR and gene quantitation in patient SF. Dysregulated miR target genes and pathways were predicted via bioinformatic algorithms and validated using gain-of-function coupled with reporter assay experiments. <h3>Results</h3> miR-seq demonstrated that TghuTNF-SF exhibit a distinct pathogenic profile with 22 significantly upregulated and 30 significantly downregulated miR. Validation assays confirmed the dysregulation of miR-223, miR-146a and miR-155 previously associated with human rheumatoid arthritis (RA) pathology, as well as that of miR-221/222 and miR-323-3p. Notably, the latter were also found significantly upregulated in patient RA SF, suggesting for the first time their association with RA pathology. Bioinformatic analysis suggested Wnt/cadherin signalling as a putative pathway target. miR-323-3p overexpression was shown to enhance Wnt pathway activation and decrease the levels of its predicted target β-transducin repeat containing, an inhibitor of β-catenin. <h3>Conclusions</h3> Using miR-seq-based profiling in SF from the TghuTNF mouse model and validations in RA patient biopsies, the authors identified miR-221/222 and miR-323-3p as novel dysregulated miR in RA SF. Furthermore, the authors show that miR-323-3p is a positive regulator of WNT/cadherin signalling in RA SF suggesting its potential pathogenic involvement and future use as a therapeutic target in RA.
Abstract 2392: The role of ATM in lytic infection of EBV in nasopharyngeal epithelial cells
Authors: George Sai-Wah Tsao, Pok Man Hau
Journal: Cancer Research (2014)

Abstract Epstein-Barr virus (EBV), a type of oncogenic herpesvirus, is associated with human malignancies. Previous studies have shown that reactivation of EBV in infected cells induces ATM-dependent DNA damage response (DDR). The functional role and involvement of ATM activation during lytic induction remains obscure. In this study, the essential role of ATM for viral DNA replication was examined in EBV-infected nasopharyngeal epithelial cells. Induction of lytic EBV infection triggers ATM activation and localization of DDR proteins at the viral replication compartments. Suppression of ATM activity using siRNA approach or specific chemical inhibitor diminished EBV DNA replication and production of infectious virion in EBV-infected cells induced to undergo lytic infection. Phosphorylation of Sp1 is a downstream event of ATM activation. The phosphorylation of Sp1 at serine 101 residue is crucial in promoting the accretion of EBV replication proteins at the replication compartment to facilitate viral DNA replication. Depletion of Sp1 suppresses viral DNA replication and localization of EBV replication proteins to the replication compartments. Our studies support an important role of ATM activation in lytic infection of EBV. Phosphorylation of Sp1 is an essential process mediating the recruitment of EBV replication protein to replication compartments. Our study highlights the importance of DDR pathway in lytic infection of EBV and suggests the potential application of specific DDR inhibitors to control the EBV replication in infected cells. Funding support: Research Grant Council of Hong Kong (GRF #779312 &amp; 779713; AoE/M-06/08). Note: This abstract was not presented at the meeting. Citation Format: George Sai-Wah Tsao, Pok Man Hau. The role of ATM in lytic infection of EBV in nasopharyngeal epithelial cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2392. doi:10.1158/1538-7445.AM2014-2392
Multiple Biomarker Panels for Cardiovascular Risk Assessment
Authors: James A. de Lemos, Donald M. Lloyd-Jones
Journal: New England Journal of Medicine (2008)

Guidelines for the assessment of cardiovascular risk remain focused squarely on established risk factors.1 Although it is known that tools based on these risk factors, such as the Framingham Risk Score, have a number of limitations when applied in clinical practice — performing reasonably well for groups but not necessarily for individuals and underestimating long-term risk among younger persons2 — it has proved surprisingly difficult to improve on established risk factors for the prediction of cardiovascular disease. Of the many strategies that have been proposed to improve risk stratification, the measurement of plasma biomarkers is particularly attractive as compared with . . .
Traumatic Lung Cysts
Authors: Richard Ellis
Journal: JAMA (1976)

MANY physicians are not aware that an acute lung cyst may occur almost immediately following closed-chest trauma. Failure to arrive at a correct diagnosis will cause confusion and may lead to unnecessary studies and even unwarranted surgery. <h3>Report of Cases</h3><h3>Case 1.—</h3> A 6-year-old boy was brought to the emergency room on Sept 27, 1973, one hour after falling against the edge of a table and striking the right upper chest. Physical examination showed slight swelling and abrasion of the right chest that measured approximately 2 cm in diameter, with surrounding tenderness and some subcutaneous crepitus. There was some pain on the right side that increased with inspiration, but there was no dyspnea nor cough. Examination of the heart and lungs detected no abnormalities. Chest roentgenograms taken less than two hours after the injury showed a traumatic right lung cyst with an air-fluid level and considerable surrounding hemorrhage but no
HIV infection--induced posttranslational modification of T cell signaling molecules associated with disease progression.
Authors: I Stefanová, M W Saville, C Peters, F R Cleghorn, D Schwartz, D J Venzon, K J Weinhold, N Jack, C Bartholomew, W A Blattner, R Yarchoan, J B Bolen, I D Horak
Journal: Journal of Clinical Investigation (1996)

In attempt to elucidate the mechanism of the HIV infection induced T cell unresponsiveness, we studied signal-transducing molecules proximal to the T cell receptor (TCR) in T lymphocytes of HIV-infected individuals. Total amounts of protein tyrosine kinases (PTKs) Lck, Fyn, and ZAP-70 and the zeta chain of the TCR were found significantly decreased in T cells of symptomatic/AIDS patients as well as in T cells of individuals in acute and early asymptomatic stages of HIV infection. Unexpectedly, the detection of Lck, Fyn, and ZAP-70 was reversed after the treatment of cell lysates with dithiothreitol. This suggests that PTKs Lck, Fyn, and ZAP-70 were modified by a mechanism altering the status of sulfhydryl groups. Moreover, this mechanism seems to affect selectively T cells of HIV infected patients since B cell PTKs Syk and Lyn were detected structurally and functionally intact. Interestingly, similar alterations of signaling molecules were not detected in T cells of HIV-infected long-term asymptomatic individuals. Modification of T cell PTKs may thus underlie the HIV-induced impairment of lymphocyte function and may potentially predict disease progression.
THE LABORATORY IN A SCHEME OF PREVENTIVE MEDICINE
Authors: W. G. Willoughby
Journal: BMJ (1930)

THE use of the laboratory in the diagnosis, prognosis, and treatment of disease, and in investigations of circumstances, sich as food and water supplies, involving the health and comnfort of the individual and of the public, has steadily increased in recent years.Chemical and bacteriological worli in connexion with examinations of milk and other foods, water, rivers, sewage effluents, etc., has become a regular part of the scheme of preventive medicine, and public analysts are among the regular officials of a Public Health Authority.The position with regard to human pathology is not so defined, and varies very much in different localities.From its earliest days, and even then in its limited range, the Public Health Service has been particularly concerned with the prevention of infectious disease.It was natural, therefore, that with successive discoveries in the bacteriology and pathology of the infectious diseases, an increasing need for laboratory work in connexion with the Public Health Department should have been felt.The Public Health Service has developed from being concerned mainly with the environment of the public into a more personal relationship with the individual in all forms of ill-health-not merely in a limited number of infectious illnesses.The need for the frequent and systematic aid supplied by the laboratory has grown correspondingly, and there are no Public Health Departments in this country without some arranigements more or less complete for this important purpose.In the interest of individual and public health laboratory assistance should be systematized and made available for all persons for whom it may be required, not merely for those coming directly within the province of the Public Health Department in other ways.It is difficult to see how this could be arranged without the aid of the Public Health Department.This is shown by the frequent applications made to the department by medical practitioners for laboratory assistance, especially in the case of those patients
Clinical Immunity after Neonatal Rotavirus Infection
Authors: Ruth F. Bishop, Graeme L. Barnes, Elizabeth Cipriani, Jennifer S. Lund
Journal: New England Journal of Medicine (1983)

To determine whether rotavirus infection in newborn babies conferred immunity to postneonatal rotavirus infection, we studied 81 babies at birth and kept them under clinical and serologic study for three years. During the first 14 days of life, 44 of the infants excreted rotavirus, and 37 did not. Fifty-five per cent of those with neonatal infection and 54 per cent of those without it had rotavirus infection during the next three years. Symptoms associated with postneonatal rotavirus infection were significantly less frequent and less severe in the infants who had had neonatal infection (P = 0.003) than in those who had not. Thirty-eight per cent of the former group (9 of 24 infants) had symptoms of mild (3 infants) or moderate (6) severity during the first postneonatal infection. In contrast, 85 per cent of the latter group (17 of 20 infants) had mild (3), moderate (6), or severe (8) symptoms. We conclude that neonatal rotavirus infection does not confer immunity against reinfection but does protect against the development of clinically severe disease during reinfection. (N Engl J Med 1983; 309:72–6.)