tbuckley/cabot-search huggingface dataset:
Pandemic influenza A(H1N1)2009: molecular characterisation and duration of viral shedding in intensive care patients in Bordeaux, south-west France, May 2009 to January 2010
Authors: L Malato, V Llavador, E Marmier, J Youssef, C Balick Weber, H Rozé, E Bessede, H J Fleury
Journal: Eurosurveillance (2011)

From May 2009 to January 2010, the Virology Laboratory at the University Hospital of Bordeaux received more than 4,000 nasopharyngeal samples from the Aquitaine region (south-west France) for the diagnosis of pandemic influenza A(H1N1)2009. Eighty-three infected patients deteriorated and were admitted to intensive care units. Our study focused on 24 of these patients. Positivity for influenza A(H1N1)2009 was monitored by realtime PCR and duration of viral shedding was determined. The first available sample of each patient was analysed for bacterial, fungal and viral co-infection. We observed six bacterial (or bacterial/fungal) co-infections and one viral co-infection with respiratory syncytial virus. The samples were analysed for the presence of the neuraminidase H275Y (N1 numbering) mutation, which confers resistance to oseltamivir, by realtime PCR of the neuraminidase gene. No H275Y mutation was observed in any of the viral strains screened in this study. In parallel, a fragment of the haemagglutinin gene encoding amino acid residues 173 to 362 was sequenced to detect mutations that had been reported to increase the severity of the disease. Two patients were infected by strains bearing the D222G (H3 numbering) mutation. The viral shedding of A(H1N1)2009 in this study ranged from four to 28 days with a median of 11 days.
Abstract 919: Clinical Significance of Post-Procedural Thrombolysis in Myocardial Infarction Flow in Patients with Cardiogenic Shock Undergoing Primary Percutaneous Coronary Intervention
Authors: Rajendra H Mehta, Fang-Shu Ou, Eric D Peterson, Richard E Shaw, William B Hillegass, John S Rumsfeld, Matthew T Roe
Journal: Circulation (2008)
Fortnightly Review: Ten years of natriuretic peptide research: a new dawn for their diagnostic and therapeutic use?
Authors: A D Struthers
Journal: BMJ (1994)

In 1981 de Bold et al found that atrial extracts contained a substance which caused natriuresis and vasodilatation.1 Three years later the amino acid structure of atrial natriuretic peptide was identified.2 This was followed by a period of fervent research activity to define its role and therapeutic potential. In 1988, just as the initial flush of research activity was wearing off, a second related compound was identified.3 This was called brain natriuretic peptide because it was first identified in porcine brain. It soon became clear, however, that the main source of this peptide was the cardiac ventricle rather than the brain, and brain natriuretic peptide is now sometimes called B type natriuretic peptide. In 1990 a third natriuretic peptide was identified, and in order to maintain the alphabetical nomenclature it was called C type natriuretic peptide.4 The amino acid structure of the three peptides is shown in the figure. Though C type natriuretic peptide was, like B type, initially localised to the nervous system, it was later found to be present in high concentration in the vascular tree, especially the endothelium.



Amino acid structure of the three peptides



The biological effects of atrial natriuretic peptide and B type natriuretic peptide are very similar, both peptides causing natriuresis, vasodilatation, and suppression of the renin-angiotensin-aldosterone system. Indeed, atrial natriuretic peptide suppresses the renin-angiotensin-aldosterone system at three separate sites. It reduces renin release, suppresses angiotensin converting enzyme activity, and blocks aldosterone release. Atrial natriuretic peptide and C type natriuretic peptide are cleared from the body by an enzyme called neutral endopeptidase and by binding to clearance receptors (see below). B type natriuretic peptide is also cleared by neutral endopeptidase, though less so by the clearance receptor mechanism. With C type natriuretic peptide the overall picture is less clear, but …
Health care professionals's knowledges of OSAHS's diagnosis
Authors: P.M Prapa, I. Nikolopoulos, P. Kythreotis, Konstantinos Gourgoulianis
Journal: European Respiratory Journal (2011)

Introduction:  Obstructive Sleep Apnea/Hypopnea Syndrome (OSAHS), an increasingly well-recognized disease, requires early diagnosis to improve quality of life and prevent its complications. The aim of this study was to evaluate the knowledge of Health Care Professionals9 in relation to OSAHS.   Methods:  A questionnaire was designed to explore HCPs knowledge to identify OSAHS. It was completed by Respiratory Physicians in a Pulmonary Department, by General Practitioners in Primary Care Center and by Primary Care Physicians.  A panel of Respiratory Physicians evaluated the answers.   Results:  A total of 138 HCPs completed the survey, (53,6% Respiratory Physicians (n=74), 18,8% General Practitioners (n=26), 27,5% Primary Care Physicians (n=38).  The HCP9s education on OSAHS was at University (33,4%), Post graduate (1,4%), Medical literature (66,7%), day-to-day practice (53,6%) and medical residency (60,9%).  The correct answers were for:  Clinical symptoms: Snoring 78,2%, daytime sleepiness 87%, morning headaches 58% and nocturia 20,3%  Complications: hypertension, 73,9%, chronic pulmonary heart disease 43.5% and  Clinical features: obesity 79,7%, large neck circumference 42%.  Logistic regression analysis revealed that physicians who acquired their knowledge in their day-to-day practice on OSAHS were more likely to answer correct question concerning clinical symptoms (OR=13.12,95%CI: 2.94-58.41, p   Conclusion:  Following this study; education sessions must been introduced in all education level in an attempt to improve the identification of this disorder and to allow the Physicians to take part in the management of OSAHS.
Abstract 2817: Degree of Left Ventricular Dyssynchrony in Heart Failure Patients Is Related to QRS Width
Authors: Hideyuki Hara, Hidekazu Tanaka, Olusegun Oyenuga, Han-Na Kim, David Schwartzman, John Gorcsan
Journal: Circulation (2008)

Background Recent narrow QRS cardiac resynchronization therapy (CRT) trials using tissue Doppler imaging (TDI) dyssynchrony criteria have not successfully predicted response. Our objective was to test the hypothesis that differences in degree and pattern of dyssynchony exist in narrow QRS vs. wide QRS pts. Methods We studied 277 heart failure (HF) pts with ejection fraction EF ≤ 35% referred for device therapy: 152 had QRS ≥ 120 ms for CRT and 125 with QRS &lt;120 ms for defibrilator therapy. Ninety % had Class III HF, 59 % had ischemic disease. Dyssychrony was assessed by TDI longitudinal velocity opposing wall delay from 12 sites using 3 apical views and speckle tracking radial strain from 6 mid-ventricular sites using short axis views to assess regional time activation. Results Overall, radial mechanical activation was early in the anteroseptum and late in the posterolateral segments in all pts groups. Anteroseptal activation was significantly earlier (254±116ms*) in pts. with QRS &gt;140 compared to those with QRS 120–140 ms (303±98ms) or QRS &lt; 120ms (329±96ms), *p&lt;0.05 vs other groups. Posteriolateral delay was also significantly later (474±89ms*) in pts. with QRS &gt;140 compared to those with QRS 120–140 ms (449±66ms) or QRS &lt; 120ms (440±75ms), *p&lt;0.05 vs other groups. TDI, however, was just delayed in wide QRS patients. Conclusions The degree of radial dyssynchrony was related to QRS width, although the pattern of early septal and late posterolateral activation was preserved across groups. These findings may explain differences in response to CRT in narrow vs. wide QRS patients and impact future CRT considerations.
UNBS5162: a novel naphthalimide derivative with potent pro-autophagic effects in human cancer cells.
Authors: Tina Mahieu, Tatjana Mijatovic, Patrick P. Dumont, Eric Van Quaquebeke, Florence Lefranc, B Nilsson, Frank Van Vynckt, Francis Darro, Robert Kiss
Journal: Cancer Research (2007)

4831  UNBS5162 (N-{2-[2-(dimethylamino)ethyl]-1,3-dioxo-2,3-dihydro-1H-benzo[de]isoquinolin-5-yl}urea) is a novel naphthalimide with in vitro cytotoxic activity (IC50 range of 0.5-5µM) against a range of human cancer cell lines including glioblastoma (Hs683 and U373MG), colorectal (HCT-15 and LoVo), non-small-cell lung (A549) and breast (MCF-7). UNBS5162 also displays significant anti-tumor activity in mouse leukaemia and human cancer xenograft models in vivo. The compound has been designed to avoid the metabolism which provokes the clinical hematotoxicity of a large number of naphthalimide derivatives such as amonafide. Accordingly in mice, UNBS5162 was found to have a 3-4 fold higher maximum tolerated dose than that of amonafide irrespective of administration route. Additionally, UNBS5162 preclinically was found not to provoke marked hematotoxicity unlike amonafide. The mechanism of action of UNBS5162 is different to that of other naphthalimide derivatives, which exert their anti-tumor activity as DNA intercalating agents poisoning topoisomerase II. UNBS5162 displays no anti-topoisomerase II activity. However, it markedly impairs the cell cycle progression of human prostate cancer PC3 and glioblastoma U373 cells by increasing very significantly the duration of their G2 phase, as revealed by flow cytometry (FCM) analyses. This UNBS5162-induced increase in G2 phase duration is provoked by marked pro-autophagic effects (but not pro-apoptotic ones) as also revealed by FCM analyses of acridine orange staining. This pro-autophagic effect has been confirmed by the fact that UNBS5162 also markedly increased the levels of expression (as revealed by western blotting analyses) of LC3-I and LC3-II in human cancer cells. LC3 is a specific marker for autophagy. All the data observed here for UNBS5162 with doses ranging between 1 an 10 µM were also observed with respect to the pro-autophagic drug temozolomide, but at doses of 100 µM or even higher. UNBS5162 also induced cancer cell death through lysosomal membrane permeabilization (LMP) in PC3 prostate cancer cells but not in U373 glioblastoma cells, with this LMP process occurring as an UNBS5162-induced decrease in Hsp70 expression. UNBS5162 was also found to markedly decrease the expression of HERP, a gene involved in cancer cell chemoresistance, in several types of human cancer cells. Finally, computer-assisted cellular imaging revealed that pre-treatment of human cancer cells with non-cytotoxic doses of UNBS5162 promoted the anti-tumor effects of other pro-apoptotic cytotoxic drugs.
Panel of serum biomarkers to predict benefit from bevacizumab (BEV) in advanced NSCLC patients.
Authors: Eduardo Braun, Mary J. Fidler, Sanjib Basu, Anjali Gangaram, Kelly Kaiser Walters, Reem Karmali, Cristina Fhied, Wen-rong Lie, Jeffrey Allen Borgia, Philip D. Bonomi
Journal: Journal of Clinical Oncology (2012)

e21069 Background: BEV has produced modest benefits in patients (PTS) with advanced NSCLC. Identification of positive predictors for BEV would have important implications for individual PTS and health care costs. Methods: We performed a prospective exploratory analysis to identify serum biomarkers as predictors of improved outcomes with BEV. Pre treatment sera were collected from 93 pts prior to initiation of first line treatment for advanced NSCLC. Treatment drugs, including BEV, were prescribed according to treating physician’s discretion. Seventy two serum biomarkers, relevant to angiogenesis and tumor progression, were recorded using Luminex immunobead platform. Serum levels were correlated with progression free survival (PFS) and overall survival (OS) and compared between patient treated with or without BEV containing regimens, BEV + and BEV- groups respectively. Log-rank and interaction p value tests were used to identify markers associated with longer PFS and OS in the BEV+ group but not in BEV- group. Results: Characteristics for each group were: BEV+ (n=43, median age 65 y/o, 72% smokers, 60% females, 100% non-squamous). BEV– (n=50, median age 64 y/o, 84% smokers, 50% female, 70 % non-squamous). The BEV+ group had longer PFS (5.8 vs. 3.0 mos, log-rank p= 0.039) and OS (13.1 vs. 8.5 mos, log-rank p =0.11) when compared to the BEV- group. High serum levels of these markers resulted in a differential decreased hazard in the BEV+ group: PDGF-AB/BB (interaction p &lt;0.01 for PFS, p=0.04 for OS), FGF (interaction p=0.15 for PFS, p&lt;0.04 for OS), tenascin-c (interaction p=0.18 for PFS, p=0.04 for OS), RANTES (interaction p=0.04 for PFS, p=0.6 for OS), epiregulin (interaction p=0.31 for PFS, p=0.04 for OS) and anti-HGF (interaction p=0.18 for PFS, p=0.03 for OS). In the BEV+ group higher levels of PDGF-AB/BB were associated with a better outcome (log-rank p=0.05 and p=0.01 for PFS and OS respectively). We did not find significant correlations between serum levels of VEGF, anti-VEGF or VEGFR and benefit from BEV. Conclusions: This exploratory analysis suggests that these biomarkers may have predictive value for BEV in NSCLC PTS and should be considered for further studies.
The Lungs in Systemic Diseases.
Authors: Eli Hyman Rubin, Stanley S. Siegelman
Journal: Annals of Internal Medicine (1970)

In their preface to The Lungs in Systemic Diseases, the authors state their aim has been to supplement information on the pulmonary manifestations of certain systemic diseases not readily available in conventional textbooks of medicine. This function they have admirably fulfilled. Although the book is not primarily a roentgenologic text, the various conditions described are well illustrated by appropriate radiographs, and the reproductions are in general good. The authors constantly emphasize the importance of roentgenography as the basic tool in the examination of the chest, pointing out that it often provides the first evidence for the existence of otherwise unsuspected disease. The completeness of descriptions of various conditions is uneven. Some are fully discussed and others only sketchily mentioned. Bibliographic annotations are adequate, and the references are arranged under individual disease headings. This makes their use simple. It is somewhat unfortunate that in several instances the illustrations are separated from their text discussion by several pages, making reference to the illustrations difficult. This reviewer found the organization and order of presentation of the material particularly good. In a book of this type in which the pulmonary manifestations of a large number of diseases, many of them unrelated, are discussed, the order of presentation must have posed a considerable problem for the authors. However, they have handled this admirably, and the book can either be utilized for looking up pulmonary manifestations of a single disease, or it can be read completely through with maintenance of continuity. The work will be exceptionally valuable to medical students. In addition to providing clinical descriptions and radiographic illustrations of pulmonary abnormalities in various systemic diseases, it emphasizes the place of chest radiology in the diagnosis of these pathologic conditions. Two sections at the end of the book (one on systemic manifestations of certain intrathoracic diseases and the other a brief review of the principles of chest diagnosis and description of other diagnostic procedures) will also prove to be of exceptional worth to students. For internists, the book will provide brief descriptions and illustrations of radiographic abnormalities noted in association with systemic diseases, and for radiologists its value primarily will be in the description of clinical symptomatology and laboratory abnormalities in relation to the radiographs. Most important, however, is its function in reminding all physicians that pulmonary symptoms or abnormalities seen on a chest film are frequently manifestations of diseases primarily involving other organ systems. RICHARD H. GREENSPAN, M.D
Meta-analysis of cigarette smoking, bone mineral density, and risk of hip fracture
Authors: D. J Torgerson, D. M Reid, M. K Campbell, M. Law, A. Hackshaw
Journal: BMJ (1998)

Clinical management of meningococcal disease Coning may occur without lumbar puncture being doneEditor-Wylie et al do not give the ages of their 252 patients with meningococcal disease, but their recommendation for fewer lumbar punctures should be interpreted cautiously in children. 1 Four deaths were attributed to lumbar puncture, which was done in 198 patients.Two patients deteriorated after lumbar puncture, and postmortem examination showed brainstem herniation.Even when lumbar puncture is not performed, however, patients with meningococcal disease can deteriorate after admission and can cone secondary to raised intracranial pressure.A causal relation in these two cases is not proved.In two patients antibiotic treatment was delayed because initial examination of cerebrospinal fluid was normal.This is a criticism of clinicians, not a risk of lumbar puncture.The risk of cerebrospinal fluid initially giving false negative results and the difficulty of diagnosing meningitis clinically in young children are both recognised.If an ill child warrants a lumbar puncture then he or she should receive antibiotics for 48 hours pending the results of culture, irrespective of the initial results of microscopy.Lumbar puncture may be dangerous if patients have hypotension, coma, raised intracranial pressure, or focal signs and is unnecessary if there is a typical rash.In a series of 445 children with meningitis, the two children with meningococcal infection and cerebral herniation had contraindications to lumbar puncture. 2Lumbar puncture must be performed more readily in children than adults because of the difficulty of diagnosing meningitis clinically.In 86 children with meningococcal meningitis, only 34 had a typical haemorrhagic rash, and not always at presentation. 3 In Wylie et al's series, lumbar puncture gave a positive result initially in 177 of 198 cases and an overall positive result in 186.In children, a clinical diagnosis of meningitis is unlikely to have a similar sensitivity of 89-94%.Moreover, it is unclear how often a positive culture was obtained from another site in the 120 cases that yielded meningococci; molecular biological techniques give no information on antibiotic sensitivity.If fewer lumbar punctures are done in children with meningitis some will be missed and the start of treatment will be delayed.This increases the risk of death, 4 possibly above the 2% attributable to lumbar puncture in this series.Wylie et al have shown a high sensitivity and low mortality from lumbar puncture.Before recommending that the procedure be used less we need to be reassured that clinical diagnosis alone does not result in worse sensitivity and mortality, particularly in children.
Pulmonary Edema and Salicylates
Authors: Charles K. Tashima, Margaret Rose
Journal: Annals of Internal Medicine (1974)

Comments and Correction1 August 1974Pulmonary Edema and SalicylatesCHARLES K. TASHIMA, M.D., MARGARET ROSE, M.D.CHARLES K. TASHIMA, M.D.Search for more papers by this author, MARGARET ROSE, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-81-2-274_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We agree with Davis and Burch (1) that there are few case reports of pulmonary edema associated with salicylate intoxication, because we searched the literature when we encountered a case in September 1972. Our case is similar to those they reported, but the patient did survive the episode.A 27-year-old woman was lethargic and hyperventilating when admitted. She had a history of schizophrenia and admitted ingesting more than 70 tablets of aspirin (Anacin®*) that morning. Her blood pressure was 100/70 mm Hg; pulse, 96/min; temperature 37.4 °C [99.4 °F]; and respiration, 40/min. She was cyanotic, and numerous...References1. DAVISBURCH PR: Pulmonary edema and salicylate intoxication (letter). Ann Intern Med 80:553-554, 1974 LinkGoogle Scholar2. ROBINCROSSZELIS ECR: Pulmonary edema. N Engl J Med 288:239-246, 292-304, 1973 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Saint Francis Hospital School of Medicine University of Hawaii Honolulu, Hawaii 96817*Whitehall Laboratories, New York, New York.†Merck Sharp & Dohme, West Point, Pennsylvania. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDrug-induced heart failureBibliographySalicylate-Induced Pulmonary Edema Clinical Features and PrognosisJOHN E. HEFFNER, M.D., STEVEN A. SAHN, M.D.PROLAMINE SOLUTION TO BLOCK PANCREATIC DUCTFATAL RESPIRATORY-DISTRESS SYNDROME AND SALICYLATE INTOXICATION IN A TWO-YEAR-OLDAntipyretic analgesicsUnrecognized Adult Salicylate IntoxicationROBERT J. ANDERSON, M.D., DANIEL E. POTTS, M.D., PATRICIA A. GABOW, M.D., BARRY H. RUMACK, M.D., ROBERT W. SCHRIER, M.D., F.A.C.P. 1 August 1974Volume 81, Issue 2Page: 274-275KeywordsAspirinBlood pressureEdemaHeart rateIntoxicationRespirationSalicylatesSchizophreniaTemperature ePublished: 1 December 2008 Issue Published: 1 August 1974 PDF downloadLoading ...
Abstract 9479: Histopathological Validation of Optical Coherence Tomography Analysis for Lipid-Rich Plaque and Thin-Cap Fibroatheroma
Authors: Kenichi Fujii, Hiroyuki Hao, Masashi Fukunaga, Tsuyoshi Nakata, Hisashi Sawada, Masahiko Shibuya, Kojiro Miki, Daizo Kawasaki, Motomaru Masutani, Mitsumasa Ohyanagi, Tohru Masuyama
Journal: Circulation (2011)

Background: Optical coherence tomography (OCT) is a unique imaging modality capable of characterizing important morphological features of vulnerable plaque. However, the histopathological correlation data is limited. This study sought to assess agreement of lipid-rich plaques (LLP) between an OCT system and histology in coronary autopsy specimens Methods: OCT examinations were performed in 52 coronary arteries from 19 autopsy hearts within 6 hours after death. LLP were selected for OCT versus histological comparisons. OCT images of LLP were signal-poor regions with diffuse borders &gt;60° in circumferential extent with fibrous cap thickness &lt;300µm. Thin-cap fibroatheroma (TCFA) was defined as LLP with cap thickness &lt;65µm. Results: OCT identified 211 focal plaques. Of those, 40 plaques (19%) were matched with the OCT criteria of LLP and 17 plaques (8%) with TCFA. OCT LLP highly associated with prevalence of large lipid deposition within plaques (85%). However, 41% of those plaques contained areas of extracellular lipid accumulation but no necrotic core and inflammatory cells, which are known as preatheroma (upper images in Figure). False-positive diagnoses of OCT for LLP often contained histological evidence of microcalcification deposition within smooth muscle cells (lower images in Figure), hemosiderin deposition, or organized thrombus. Although the sensitivity for detecting TCFA was 100%, it should be noted that the positive predictive value was only 59%. The positive predictive value of TCFA is increased if intravascular ultrasound is used in addition to OCT for detecting TCFA. Conclusions: Atherosclerotic lesions are heterogeneous, and OCT light signals are attenuated not only by the lipid component but also by microcalcification and/or hemosiderin within plaques. OCT cannot detect the inflammatory status of atherosclerotic LLP. In this specific population, OCT has a limitation in detecting vulnerable plaques corresponding histological specimen.
Gene expression signatures can predict the efficacy of anthracyclines in HER2-negative and HER2-positive breast cancer (BC) patients: The results of the TOP trial and their validation in the BIG1-00 trial.
Authors: Christine Desmedt, Benjamin Haibe-Kains, Evandro Azambuja, Denis Larsimont, Suzette Delaloge, Caroline Duhem, Angelo Di Leo, Veronique D'Hondt, Martine Piccart-Gebhart, Christos Sotiriou
Journal: Annals of Oncology (2009)