tbuckley/cabot-search huggingface dataset:
Pseudomonas aeruginosa colonisation in an intensive therapy unit: role of cross infection and host factors.
Authors: M R Noone, T L Pitt, M Bedder, A M Hewlett, K B Rogers
Journal: BMJ (1983)

Despite the sparsity of Pseudomonas aeruginosa in the environment colonisation and infection with this organism was found at several sites by selective culture in 20 out of 46 patients in an intensive therapy unit. Three patients developed Ps aeruginosa pneumonia. Serial serogrouping and phage typing identified multiple strains in the unit and in the same patient. Rectal carriage occurred in 16 patients but rectal strains did not subsequently appear in tracheal aspirates; strains varied in their affinity for the upper respiratory tract. Colonisation was not directly related to length of stay and was detected in 16 of those colonised within 24 hours of admission. In intubated patients, who were colonised more frequently than those not intubated, upper respiratory tract colonisation correlated strongly with low initial arterial pH values. Personnel were probably responsible for cross infection among patients when the unit was busy. Strain differences and the susceptibility of patients also influenced colonisation and infection. Elimination of major reservoirs of Ps aeruginosa and compliance with procedures to control cross infection remain essential if patients in hospital are to escape colonisation by the organism.
Prevalence of the sensitization to snails and shrimps in patients allergic to house dust mites (HDM) a prospective European multicenter study
Authors: Jean-Marc Rame, François Lavaud, Maria Staevska, André Dubiez, Brigitte Adessi, Martine Vigan, Pascal Girardin, Dominique A Vuitton
Journal: Journal of Allergy and Clinical Immunology (2002)
Ergasteric Hepatitis from Tissue with Australia Antigen
Authors: Makoto Mayumi, Masao Nakajima
Journal: Annals of Internal Medicine (1973)

Letters1 October 1973Ergasteric Hepatitis from Tissue with Australia AntigenMAKOTO MAYUMI, M.D., MASAO NAKAJIMA, M.D.MAKOTO MAYUMI, M.D.Search for more papers by this author, MASAO NAKAJIMA, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-79-4-606_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The hazard of infection with hepatitis B virus among investigators and technicians who are working with it has been emphasized (1). We have experienced an outbreak in which four out of eight members in our laboratory successively developed hepatic disease. The source of infection was successfully traced by subtyping antigens both in the source and in patient serums.Since the beginning of 1971 our laboratory has been engaged in research on Australia antigen (hepatitis B antigen, HB Ag). Our main activity was the screening of serum samples, some 15 000 specimens per month, for HB Ag by...References1. SUTNICKLONDONMILLMAN AWI: Ergasteric hepatitis: endemic hepatitis associated with Australia antigen in a research laboratory. Ann Intern Med 75:35-40, 1971 LinkGoogle Scholar2. LEBOUVIER G: The heterogeneity of Australia antigen. J Infect Dis 123:671-675, 1971 CrossrefMedlineGoogle Scholar3. BANCROFTMUNDONRUSSEL WFP: Detection of additional antigenic determinants of hepatitis B antigen. J Immunol 109:842-848, 1972 MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: MAKOTO MAYUMI, M.D.; MASAO NAKAJIMA, M.D.Affiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1973Volume 79, Issue 4Page: 606-606KeywordsAntigensHepatitis BResearch laboratories ePublished: 13 March 2020 Issue Published: 1 October 1973 PDF downloadLoading ...
IgG subclass distribution in serum and rectal mucosa of monozygotic twins with or without inflammatory bowel disease.
Authors: L Helgeland, C Tysk, G Jarnerot, K Kett, E Lindberg, D Danielsson, S N Andersen, P Brandtzaeg
Journal: Gut (1992)

Serum samples from 26 monozygotic twin pairs concordant or discordant with regard to inflammatory bowel disease, and rectal biopsies from 42 twins of the same subject group, were examined for IgG subclasses. They were all compared with normal controls. Almost all affected twins were in clinical remission. Paired immunofluorescence staining of the rectal mucosa showed that those with ulcerative colitis had a significantly higher (p &lt; 0.01) proportion of IgG1 producing mucosal immunocytes than normal controls (78.1% v 55.9%). Conversely, the IgG2 cell fraction was significantly reduced (15.9% v 34.6%). Healthy twins from ulcerative colitis pairs tended to show a raised proportion of IgG1 cells and the IgG2 cell fraction was significantly reduced (p &lt; 0.05). In discordant ulcerative colitis twin pairs, no difference appeared in the cellular IgG subclass pattern between healthy and affected twins. Furthermore, the proportion of IgG1 in these healthy and diseased twins showed good correlation (T = 0.867). The results in rectal mucosa of twins with Crohn9s disease were widely scattered and affected twins did not differ significantly from normal controls. Healthy twins, however, showed a marginally raised IgG1 cell proportion, but no correlation was seen between the IgG subclass fractions in discordant Crohn9s disease twin pairs. The serum concentrations of IgG1 and IgG2 did not differ from normal controls in twins of either category. These results suggested that in ulcerative colitis, the aberrant mucosal production of IgG1 and IgG2 does not depend on active disease, but is apparently at least partially explained by a genetic impact. Conversely, the mucosal IgG subclass pattern in Crohn9s disease appears to be determined mainly by exogenous variables.
Interlaboratory comparison of four in vitro assays for assessing androgenic and antiandrogenic activity of environmental chemicals.
Authors: Wolfgang Körner, Anne Marie Vinggaard, Béatrice Térouanne, Risheng Ma, Carise Wieloch, Margret Schlumpf, Charles Sultan, Ana M Soto
Journal: Environmental Health Perspectives (2004)

We evaluated and compared four in vitro assays to detect androgen agonists and antagonists in an international interlaboratory study. Laboratory 1 used a cell proliferation assay (assay 1) with human mammary carcinoma cells stably transfected with human androgen receptor. The other laboratories used reporter gene assays, two based on stably transfected human prostate carcinoma cells (assay 2) or human mammary carcinoma cells (assay 4), and the third based on transient transfection of Chinese hamster ovary cells (assay 3). Four laboratories received four coded compounds and two controls: two steroidal androgens, two antiandrogens, an androgenic control, 5alpha-dihydrotestosterone (DHT), and an antiandrogenic control, bicalutamide (ICI 176,334). All laboratories correctly detected the androgenic activity of 4-androsten-3,17-dione and 17alpha-methyltestosterone. For both compounds, the calculated androgenic potencies relative to the positive control (RAPs) remained within one order of magnitude. However, laboratory 3 calculated a 50-fold higher RAP for 4-androsten-3,17-dione. All assays detected and quantified the antiandrogenic effect of vinclozolin [median inhibitory concentration (IC50) values ranging from 1.1 times symbol 10(-7) M to 4.7 times symbol 10(-7) M]. In assays 2 and 3, vinclozolin showed partial androgenic activity at the highest concentrations tested. For vinclozolin, calculated antiandrogenic potencies relative to bicalutamide (RAAPs) differed no more than a factor of 10, and IC50 values matched those of bicalutamide. Similarly, we found antiandrogenic activity for tris-(4-chlorophenyl)methanol. RAAP values were between 0.086 and 0.37. Three assays showed cytotoxicity for this compound at or above 1 times symbol 10(-5) M. In summary, all assays proved sensitive screening tools to detect and quantify androgen receptor-mediated androgenic and antiandrogenic effects of these chemicals accurately, with coefficients of variation between 8 and 90%.
DEGREE AND DISTRIBUTION OF AORTIC ANNULUS CALCIFICATION AS A PREDICTIVE FACTOR FOR PACEMAKER IMPLANTATION AFTER COREVALVE TAVI. A CT DRIVEN, PROSPECTIVE, SINGLE-CENTER STUDY
Authors: Georg Latsios, Seyrani Yücel, Daniel John, Ralf Mueller, Lutz Buellesfeld, Barthel Sauren, Ulrich Gerckens, Eberhard Grube
Journal: Journal of the American College of Cardiology (2010)
Cost‐effectiveness of omalizumab in patients with severe persistent allergic asthma
Authors: R. Brown, F. Turk, P. Dale, J. Bousquet
Journal: Allergy (2007)

Background: The health, economic and societal burden of asthma is considerable, and is greatest in patients with severe asthma, particularly when inadequately controlled. Real‐life studies that assess the effectiveness of treatment are of particular interest. Methods: We determined the incremental cost‐effectiveness ratio (ICER) of adding omalizumab to standard therapy using data from the real‐life 1‐year randomized open‐label study (ETOPA) and using Canada as a reference country. Only patients receiving high‐dose ICS plus LABA were included in the analysis, reflecting the EU label for omalizumab. Costs and quality‐adjusted life years (QALYs) gained were used to calculate the ICER for omalizumab (cost/QALY). Probabilistic sensitivity analysis was performed to determine the 95% confidence interval and one‐sided sensitivity analyses were performed. Results: The base case lifetime analysis of standard therapy vs standard therapy plus add‐on omalizumab for the first 5 years, gave an ICER of €31 209. Probabilistic sensitivity analysis indicated that the 95% confidence interval around the ICER was €27 739–€40 840. The ICER range for one‐way sensitivity analyses was €23 762 without discounting to €66 443 without inclusion of asthma‐related mortality. Conclusions: This study demonstrates that add‐on omalizumab therapy is cost‐effective in patients with severe persistent allergic asthma.
Osier, 'E. Y. D.,' and Hysteria
Authors: Richard L. Golden
Journal: JAMA (1982)

IN ADDITION to his many other attributes, Sir William Osler (1849-1919) was highly regarded as a neurologist. His books,<i>The Cerebral Palsies of Children</i><sup>1</sup>and<i>On Chorea and Choreiform Affections</i>,<sup>2</sup>elegantly attest to this. He was the author of occasional pseudonymous papers and letters under the nom de plume of Egerton Yorrick Davis, "late US Army Surgeon."<sup>3</sup>E. Y. Davis, often abbreviated as "E. Y. D.," was Osler's alter ego, his fanciful half that expressed the humorous, jesting side of his nature—a quirk that often got him into trouble.<sup>4(pp239-242),5,6</sup>No doubt "Yorrick" was borrowed from Shakespeare's<i>Hamlet</i>—"Alas, poor Yorick! I knew him, Horatio: a fellow of infinite jest, of most excellent fancy." Reproduced in the Figure is a mock consultation note written by Osler while professor of medicine at Johns Hopkins University and signed "E. Y. D." Although undated, the address allows us to place
Physical Activity and Bone Mass
Authors: Muhammad M. Hammami
Journal: Annals of Internal Medicine (1996)

Letters1 April 1996Physical Activity and Bone MassMuhammad M. Hammami, MD, PhD and Bashir A. Khan, PhDMuhammad M. Hammami, MD, PhDKing Faisal Specialist Hospital and Research Centre; Riyadh 11211, Saudi ArabiaSearch for more papers by this author and Bashir A. Khan, PhDKing Faisal Specialist Hospital and Research Centre; Riyadh 11211, Saudi ArabiaSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-124-7-199604010-00012 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:In a cross-sectional study, Kannus and colleagues [1] found that differences in bone mineral content between playing and nonplaying arms were significantly larger in women who played tennis and squash at a national level than in controls. They also found that such differences correlated negatively with the “biological age” at which these women began playing and concluded that “bones of the playing extremity clearly benefit from active tennis and squash training” and that the benefit is greater if training starts at or before menarche.The authors did not comment on two unexpected findings. First, upper-arm and forearm ...REFERENCE1. Kannus P, Haapasalo H, Sankelo M, Sievanen H, Pasanen M, Heinonen A, et al. Effect of starting age of physical activity on bone mass in the dominant arm of tennis and squash players. Ann Intern Med. 1995; 123:27-31. Google Scholar Author, Article, and Disclosure InformationAffiliations: King Faisal Specialist Hospital and Research Centre; Riyadh 11211, Saudi Arabia PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1996Volume 124, Issue 7Page: 692KeywordsBoneBone densityExerciseMenarcheMusclesPhysical activity Issue Published: 1 April 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Usefulness of F-18 FDG PET/CT in a Case of Kaposi Sarcoma With an Unexpected Bone Lesion
Authors: Miyako Morooka, Kimiteru Ito, Kazuo Kubota, Kunio Yanagisawa, Katsuji Teruya, Kahehiro Hasuo, Yoshitaka Shida, Rhogo Minamimoto, Yoshimi Kikuchi, Shinichi Oka
Journal: Clinical Nuclear Medicine (2011)

Bone lesions of Kaposi sarcoma are rare. A 56-year-old man who was HIV positive and was diagnosed with Kaposi sarcoma on the basis of the results of a biopsy of skin lesions, underwent F-18 FDG PET/CT scan for detecting Kaposi sarcoma lesions and other AIDS-related diseases. An abnormal uptake was observed in the lumbar spine. MRI showed a diffuse enhanced spine lesion, and Ga-67 and 201Tl scanning were negative. As a result, the lesion was considered to be a Kaposi sarcoma, and the shrinkage of the lesion was noted after the therapy for Kaposi sarcoma.
Therapeutic Significance of Elevated Tissue Transglutaminase Expression in Pancreatic Cancer
Authors: Amit Verma, Sushovan Guha, Parmeswaran Diagaradjane, Ajaikumar B. Kunnumakkara, Angela M. Sanguino, Gabriel Lopez-Berestein, Anil K. Sood, Bharat B. Aggarwal, Sunil Krishnan, Juri G. Gelovani, Kapil Mehta
Journal: Clinical Cancer Research (2008)

Abstract Purpose: Tissue transglutaminase (TG2) is a multifunctional protein that is implicated in development of drug resistance and metastasis. Therefore, we examined therapeutic targeting of TG2 for inhibiting growth and metastasis of in vivo growing pancreatic ductal adenocarcinoma (PDAC) in nude mice. Experimental Design: We implanted Panc-28 pancreatic cancer cells to induce orthotopic PDAC tumors in nude mice and determined the efficacy of liposomal TG2 small interfering RNA (siRNA) either alone or in combination with gemcitabine. Results: We show that down-regulation of endogenous TG2 by siRNA could effectively block the growth of PDAC. Moreover, down-regulation of TG2 significantly enhanced the therapeutic efficacy of gemcitabine against PDAC and inhibited metastatic spread of the disease. The antitumor activity was related to inhibition of proliferation, angiogenesis, and Akt phosphorylation. Conclusion: siRNA-mediated down-regulation of TG2 represents a promising therapeutic approach for improved treatment of PDAC.
A7.16 Lack of Replication of<i>PTPRC Gene</i>as a Predictor of Response to Anti-Tumour Necrosis Factor Therapy in Patients with Rheumatoid Arthritis
Authors: Helena Canhão, Ana Rodrigues, Maria Jose Santos, Diana Carmona-Fernandes, José Costa, Helena Santos, Jaime Branco, Robert Plenge, Daniel Solomon, Jacome Armas, José António Silva, João Eurico Fonseca, Elizabeth Karlson
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background and Objectives</h3> A genome wide association study (GWAS) with Caucasian Northern European and North American rheumatoid arthritis (RA) patients and a replication study with English patients, pointed out for an association between <i>PTPRC</i> locus and response to anti-TNF drugs in RA. The Aim of our study was to evaluate whether this association is also verified in a population of Southern European (Portuguese) patients. <h3>Materials and Methods</h3> We evaluated 383 RA patients from the Portuguese Rheumatic Diseases Register, Reuma.pt, for association between anti-TNF treatment response assessed by an absolute change in DAS28 at six months as the primary outcome and Rs10919563 <i>PTPRC</i> locus. We also studied the same association using the proportion of EULAR good responders and non responders at six months as the secondary outcome. Additive models were used taking the homozygote for the two major alleles as the reference variable. Univariate and multivariate linear and logistic regression analyses were performed, adjusting for clinical variables that influenced treatment response. <h3>Results</h3> Taking the continuous primary outcome, univariate and multivariate linear regression adjusted for DAS28 and HAQ at baseline showed no association between change in DAS28 at 6 months and <i>PTPRC</i> locus (p-values of 0.72 and 0.69 respectively). Also univariate and multivariate logistic regression (good versus non-responders) did not depict any association with this SNP. <h3>Conclusions</h3> In this replication study with a cohort of RA. Portuguese patients, we did not observe an association between Rs10919563 <i>PTPRC</i> locus and response to anti-TNF treatment.
Twenty years of Polish experience with three consecutive protocols for treatment of childhood acute myelogenous leukemia
Authors: A Dluzniewska, W Balwierz, J Armata, A Balcerska, A Chybicka, J Kowalczyk, M Matysiak, M Ochocka, U Radwanska, R Rokicka-Milewska, D Sonta-Jakimczyk, J Wachowiak, M Wysocki
Journal: Leukemia (2005)
Vitreous Mediators after Intravitreal Bevacizumab or Triamcinolone Acetonide in Eyes with Proliferative Diabetic Retinopathy
Authors: Noboru Arimura, Hiroki Otsuka, Keita Yamakiri, Yasushi Sonoda, Shintaro Nakao, Yoshihiro Noda, Teruto Hashiguchi, Ikuro Maruyama, Taiji Sakamoto
Journal: Ophthalmology (2009)
Abstract 2301: Myeloid cells promote fibroblast invasion and lead mammary adenocarcinoma cell invasion.
Authors: Aubie K. Shaw, Sergey Novitskiy, Lisa M. Coussens, Harold L. Moses
Journal: Cancer Research (2013)

Abstract Myeloid cells localize to invasive edges of solid tumors where they promote invasive tumor growth, intravasation into vasculature and metastasis of malignant cells1,2. Fibroblasts, on the other hand, lead collective cell migration3 of carcinoma cells via fostering extracellular matrix (ECM) remodeling and generating tracks of collagen fibers that act as “highways” for cell migration4,5. To identify soluble molecules mediating these juxtacrine communication mechanisms between myeloid cells and fibroblasts in potentiating metastasis, we conducted pilot studies with subsets of spleen- or tumor-derived myeloid cells, tumor-derived fibroblasts, and mammary adenocarcinoma cells. Whereas spleen-derived CD11b+Ly6ChiLy6G− monocytes promote fibroblast migration ex vivo, two populations of tumor-derived myeloid cells, e.g., CD11b+Gr1+ and CD11b+Gr1− cells possessed this capability. In ex vivo migration assays, fibroblast migration was dependent on myeloid cell-derived factors, e.g., CXCL11, CXCL15, FGF2, IGF-1 and Shh, as well as fibroblast Akt and ERK1/2 phosphorylation. Inhibition of fibroblast MEK reduced myeloid cell-induced fibroblast migration, whereas FGF-RI inhibition completely abolished this capability. These studies indicate a role for myeloid cell-fibroblast communication in fostering migration (and potentially activation) of fibroblasts that lead collective cell migration properties of mammary carcinoma cells. Ongoing studies are identifying specific subpopulations of tumor-associated myeloid cells possessing these activities, as well as the role of FGF receptor signaling pathways in facilitating metastasis. 1. Wyckoff, J.B., et al. Direct visualization of macrophage-assisted tumor cell intravasation in mammary tumors. Cancer Res 67, 2649-2656 (2007). 2. Qian, B.Z. &amp; Pollard, J.W. Macrophage diversity enhances tumor progression and metastasis. Cell 141, 39-51 (2010). 3. Friedl, P., Locker, J., Sahai, E. &amp; Segall, J.E. Classifying collective cancer cell invasion. Nat Cell Biol 14, 777-783 (2012). 4. Khalil, A.A. &amp; Friedl, P. Determinants of leader cells in collective cell migration. Integr Biol (Camb) 2, 568-574 (2010). 5. Gritsenko, P.G., Ilina, O. &amp; Friedl, P. Interstitial guidance of cancer invasion. J Pathol 226, 185-199 (2012). The authors acknowledge generous support from the NIH/NCI, a Dept of Defense (DoD) Breast Cancer Research Program Postdoctoral Fellowship, a DoD Era of Hope Scholar Expansion Award, Susan G. Komen Fndt, and the Breast Cancer Research Fndt. Citation Format: Aubie K. Shaw, Sergey Novitskiy, Lisa M. Coussens, Harold L. Moses. Myeloid cells promote fibroblast invasion and lead mammary adenocarcinoma cell invasion. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2301. doi:10.1158/1538-7445.AM2013-2301
Protection of the Surgical Wound with a New Plastic Film
Authors: Curtis P. Artz
Journal: JAMA (1960)

Infection remains one of the major unsolved problems in surgery.1Many reports attest to the increasing incidence of troublesome surgical infections, particularly those caused by the staphylococci.2It is generally accepted that the most important causes of this increase in the incidence of infection has been the widespread, injudicious use of antibiotics, the greater susceptibility of more severely traumatized and of poor-risk patients, and the tendency of surgeons to de-emphasize the importance of aseptic techniques.3  Thomas Lister, in 1867, first brought forward the concept of asepsis in surgery by saying, in part, Admitting then, the truth of the germ theory, and proceeding in accordance with it, we must, when dealing with any case, destroy in the first instance, once and for all, any septic organisms which may exist in the part concerned and, after this has been done, our efforts must be directed to the prevention of
New Zealand: Campaign falters over bed sharing
Authors: C. Essex
Journal: BMJ (1995)

The fall in the rate of the sudden infant death syndrome in New Zealand has had an appreciable impact on the country's postneonatal mortality. In 1988 postneonatal mortality was 6.1/1000 live births and the rate of the syndrome was 4.4/1000. By 1993 postneonatal mortality had fallen to 3.6/1000 and the rate of the syndrome to 2.1/1000.

Since records of the sudden infant death syndrome have been kept the rate in Maoris has always been higher than the rate in non-Maoris, with Pacific Island babies in New Zealand having a slightly lower rate than babies of European descent. Although the rate in non-Maoris had …