tbuckley/cabot-search huggingface dataset:
Autonomic function in mitral valve prolapse.
Authors: E G Abinader
Journal: Circulation (1979)

Methylprednisolone in AMITo the Editor:I read with interest the article by Welman and colleagues (Cir- culation 59: 730, 1979) on the effects of methylprednisolone in acute myocardial infarction.The authors strongly imply that this is a beneficial effect and that methylprednisolone can delay tissue damage.The implication is that by delaying tissue damage it may prevent it.This conclusion is certainly not warranted from the figures' '2in the article.Judging by the total amount of plasma creatine kinase activity and creatine kinase MB-isoenzyme activity present during a 50-hour period (summation of areas under the respective curves) one might con- clude that while there may be some delay the total amount of myocardial damage is actually greater.The assumption is also made that methylprednisolone does nothing to the "metabolism" of the enzymes measured other than change its rate of release from the myocardium.I don't believe this is proven.
Corrigendum to ‘ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008’ [Eur Heart J 2008;29:2388–2442 and Eur J Heart Fail 2008;10:933–989]
Authors: Kenneth Dickstein, Alain Cohen‐Solal, Gerasimos Filippatos, John J.V. McMurray, Piotr Ponikowski, Philip Alexander Poole‐Wilson, Anna Strömberg, Dirk J. van Veldhuisen, Dan Atar, Arno W. Hoes, Andre Keren, Alexandre Mebazaa, Markku Nieminen, Silvia Giuliana Priori, Karl Swedberg
Journal: European Journal of Heart Failure (2009)
Anticardiolipin Antibodies and the Risk for Ischemic Stroke and Venous Thrombosis
Authors: Katherine S. Ginsburg, Matthew H. Liang, Laura Newcomer, Samuel Z. Goldhaber, Peter H. Schur, Charles H. Hennekens, Meir J. Stampfer
Journal: Annals of Internal Medicine (1992)

Objective: To determine whether the presence of anticardiolipin antibodies is a risk factor for ischemic stroke and venous thrombosis in healthy adult men. Design: A nested, case-control study in a prospective cohort. Setting: A nationwide study of physicians. Participants: The study sample was drawn from the Physicians' Health Study, a randomized, double-blind, placebo-controlled trial of aspirin and beta-carotene in 22 071 male physicians. At entry, 68% of the participants submitted plasma samples that were subsequently frozen at -80 °C. During 60.2 months of follow-up, follow-up for nonfatal outcomes was 99.7% complete and ascertainment of fatal outcomes was 100% complete. We identified men with documented ischemic stroke, deep venous thrombosis of the leg, or pulmonary embolus and for whom a plasma sample was available. A control was matched by age, smoking history, and length of follow-up to each of the 100 patients with ischemic stroke and the 90 patients with deep venous thrombosis or pulmonary embolus. ° Measurements: Plasma samples were assessed for IgG anticardiolipin antibodies by enzyme-linked immunosorbent assay. The mean anticardiolipin antibody titers of the case patients in the two diagnostic groups (ischemic stroke; venous thrombosis or pulmonary embolus) were compared with those of the control groups, and relative risks were calculated for patients in increasing percentile categories of anticardiolipin antibodies by conditional logistic regression. ° Results: The anticardiolipin antibody titers were higher in case patients with deep venous thrombosis and pulmonary embolus than in their matched controls (P = 0.01). Persons with anticardiolipin antibody titers above the 95th percentile had a relative risk for developing deep venous thrombosis or pulmonary embolus of 5.3 (95% Cl, 1.55 to 18.3; P = 0.01). The anticardiolipin antibody titers in case patients with ischemic stroke and controls were not significantly different (P > 0.2), and no clear trend of higher risks among those with elevated levels of anticardiolipin antibodies was observed. Conclusion: An anticardiolipin antibody level above the 95th percentile is an important risk factor for deep venous thrombosis or pulmonary embolus but not for ischemic stroke in healthy adult men.
PULMONARY ALVEOLAR PROTEINOSIS
Authors: W R EDMONDSON, J B GERE
Journal: Annals of Internal Medicine (1960)

Case Reports1 June 1960PULMONARY ALVEOLAR PROTEINOSISWILLIAM R. EDMONDSON, M.D., J. BREWSTER GERE, M.D.WILLIAM R. EDMONDSON, M.D.Search for more papers by this author, J. BREWSTER GERE, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-52-6-1310 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptPulmonary alveolar proteinosis was first described by Rosen et al. in June, 1958.1 We have had the opportunity to observe a patient with this disease, and wish to report the clinical, laboratory, radiographic and histologic findings.CASE REPORTA 53 year old Negro man was admitted to the Orange Memorial Hospital on January 13, 1958. For the preceding six months he had noted mild exertional dyspnea, and a cough productive of moderate amounts of white sputum. He attributed these symptoms to the fracture of a left rib in July, 1957. In November, 1957, he developed symptoms and signs of a...Bibliography1. RosenCastlemanLiebow SHBAA: Pulmonary alveolar proteinosis, New England J. Med. 258: 1123-1142, 1958. CrossrefMedlineGoogle Scholar2. Editorial: Alveolar proteinosis, New England J. Med. 258: 1171, 1958. CrossrefGoogle Scholar3. DickYudellRyanKutzerDelmonicoPriorConnell HJJWJMJEPAA: Pneumocystis carinii infection in New York State: preliminary report, Proc. New York State A. Pub. Health Lab. 37: 3-5, 1957. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication December 9, 1959.From the Orange Memorial Hospital, Orange, New Jersey.Requests for reprints should be addressed to William R. Edmondson, M.D., 503 Central Avenue, East Orange, New Jersey. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySecondary alveolar proteinosis in cancer patientsSekundäre maligne Tumoren der Bronchien und LungenPulmonary alveolar proteinosisBeitrag zur Alveolarproteinose der LungenPulmonary alveolar proteinosisThe Diagnosis of Pulmonary Alveolar Proteinosis by Sputum ExaminationÜber die alveoläre LungenproteinosePulmonary Alveolar Proteinosis: A Review of the LiteratureA Fatal Case of Pulmonary Alveolar Proteinosis 1 June 1960Volume 52, Issue 6Page: 1310-1318KeywordsDyspneaElectrocardiographyFibrosisHemoglobinProteinsPulmonary functionRibsSigns and symptomsSputumTachycardia ePublished: 1 December 2008 Issue Published: 1 June 1960 PDF downloadLoading ...
Memorable patients: High altitude medicine
Authors: S. Almond
Journal: BMJ (1999)

Following medical school finals I decided to spend a few weeks trekking in the Himalayas before the rigours of house jobs. I employed a local guide who, for a reasonable daily rate, saw to all the cooking and overnight accommodation as well as navigation.

On one occasion, after a particularly hard day's walking and in fairly bad weather, we arrived at the Chandrachani Pass, which connects the beautiful Kulu and Parvati valleys in the state of Himachal …
Sialic Acid–Binding Immunoglobulin‐Type Lectin H–Positive Plasmacytoid Dendritic Cells Drive Spontaneous Lupus‐like Disease Development in B6.Nba2 Mice
Authors: Laura M. Davison, Trine N. Jørgensen
Journal: Arthritis & Rheumatology (2014)

Objective Patients with systemic lupus erythematosus (SLE) often present with elevated levels of interferon‐α (IFNα) in serum. Plasmacytoid dendritic cells (pDCs) have been suggested to be the primary source of IFNα in SLE due to their capacity to produce high levels of IFNα. During viral infection, a subset of pDCs expressing sialic acid–binding immunoglobulin‐type lectin H (Siglec H) produces the majority of pDC‐derived IFNα. The aim of this study was to provide evidence that Siglec H–positive pDCs are pathogenic in the IFNα‐dependent B6.Nba2 mouse model of lupus. Methods B6.Nba2 blood dendritic cell antigen 2 (BDCA‐2)–diphtheria toxin receptor (DTR)–transgenic (Tg) mice were treated intraperitoneally with DT 3 times weekly starting at 4 weeks or 12 weeks of age and analyzed at 12 weeks and 18 weeks of age, respectively. Lupus‐like disease development was measured by the presence of elevated levels of autoantibodies in serum (as determined by enzyme‐linked immunosorbent assay), increased expression of IFN‐inducible genes (as determined by real‐time reverse transcription–polymerase chain reaction), increased IgG immune complex deposition in kidney glomeruli (as determined by immunofluorescence staining), spontaneous lymphocyte activation, and differentiation of B cells into antibody‐producing plasma cells (as determined by flow cytometry). Results B6.Nba2 mice in which Siglec H–positive pDCs were depleted for 6–8 weeks displayed reduced levels of IFNα‐induced gene transcripts and decreased anti‐chromatin autoantibody levels in serum, and significantly fewer activated splenic T cells and B cells, germinal center B cells, follicular helper T cells, and splenic plasma cells. In 18‐week‐old mice, IgG immune complex deposition in kidney glomeruli was similarly reduced. Conclusion The development of lupus‐like disease in congenic B6.Nba2 mice depends on Siglec H–positive pDCs. We suggest that depletion of Siglec H–positive pDCs represents a novel cellular target in SLE.
Familial Erythrophagocytic Lymphohistiocytosis
Authors: H E MACMAHON, M BEDIZEL, C A ELLIS
Journal: JAMA (1963)

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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Mutations in the L3 loop of zinc-binding domain of p53 are poor prognostic indicators of Caucasians with colorectal adenocarcinomas
Authors: Venkat R. Katkoori, Chakrapani Chatla, Xu Jia, William E. Grizzle, Upender Manne
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

2548 

Background: We previously reported that abnormalities in p53 have different biologic consequences in colorectal adenocarcinoma (CRC) when analyzed based on patient race. Therefore, in the current study, we assessed the mutational patterns of p53 gene in CRCs collected from Caucasians and African-Americans, and correlated with patient survival. Methods: We collected frozen tissues from 121 Caucasian and 63 African-American CRC patients from the University of Alabama at Birmingham Hospital. The status of p53 gene was assessed by direct sequencing of all coding regions (exons 2 - 11), using exon-specific primers. The DNA binding domain (exons 5 - 8) of p53 includes all important structural motifs like L2 and L3 zinc-binding domains and LSH (loop-sheet-helix) motif. Univariate Kaplan-Meier survival analyses were used to assess the prognostic significance of p53 mutations based on race. Results: The incidence of point mutations in p53 was higher in Caucasian (60 of 121, 50%) than in African-American (23 of 63, 37%) patients. The prevalence of mutations at hotspot codons 175, 245, 248, 273, or 282 (52% vs . 35%), particularly in the L3 loop of zinc-binding domain (28% vs . 9%) was more common in Caucasians than in African-Americans. In contrast, polymorphic mutations at codon 72 (Arginine to Proline) were more frequent in African-Americans (14%) than in Caucasians (4%). Caucasians with mutations in L3 domain had higher mortality than those with wild type p53 (5-year, log-rank, P=0.0377). Conclusions: These findings suggest that the mutational pattern of p53 gene differs in CRCs of Caucasian and African-American patients; specifically, mutations within the L3 loop of zinc-binding domain of p53 are associated with poor clinical outcome of Caucasian patients. Thus, mutations in the L3 loop of p53 may be indicators of aggressive phenotypic behavior of colorectal adenocarcinomas . These studies are supported by NCI/NIH grants RO1-CA98932-01 and RO3-CA097542-01.
Residents and Patients: Telling Stories to Cope With Stress
Authors: E Delwart
Journal: JAMA (1998)

A highly divergent HIV-1 isolate, designated YBF 30, was obtained in 1995 from a 40-year-old Cameroonian woman with AIDS. Depending on the genes studied, phylogenetic analysis showed that YBF30 branched either with SIVcpz-gab or between SIVcpz-gab and HIV-1 group M. The structural genes and tat, vpr, and nef of YBF30 are approximately equidistant from those of HIV-1 group M and SIVcpz-gab. In contrast, vif and rev are closer to HIV-1 group M, and vpu is highly divergent. Using a YBF30 V3 loop peptide enzyme immunoassay, we screened 700 HIV-1-positive sera collected in Cameroon; three reacted strongly with the YBF30 peptides and one was confirmed as being related to YBF30 by genetic analysis of a pol fragment. YBF30 is as distinct from SIVcpz-gab as it is from HIV-1 group M and can thus be considered as the prototype strain of a new human immunodeficiency virus group.
Abstract 161: Activation of mTOR pathway in myeloid-derived suppressor cells with lysosomal acid lipase deficiency stimulates cancer cell proliferation and metastasis
Authors: Ting Zhao, Hong Du, Xinchun Ding, Katlin Walls, Cong Yan
Journal: Cancer Research (2014)

Abstract Inflammation plays crucial roles at all stages of tumor development, from tumor initiation to metastatic progression, during which myeloid-derived suppressor cells (MDSCs) are an important participant. Although MDSCs are known to suppress immune surveillance, their roles in directly stimulating cancer cell proliferation and metastasis currently remains unclear. Lysosomal acid lipase (LAL) deficiency causes systemic expansion and infiltration of MDSCs in multiple organs and subsequent inflammation. In the LAL-deficient (lal-/-) mouse model, we found that melanoma metastasized massively in allogeneic lal-/- mice, which was suppressed in allogeneic lal+/+ mice due to immune rejection. Therefore, we hypothesized that MDSCs with LAL deficiency directly stimulate cancer cell proliferation and metastasis. Bone marrow-derived MDSCs from lal-/- mice directly stimulated B16 melanoma cell proliferation in vitro by co-culture analysis and in vivo by co-implantation in the Matrigel plugs. These tumor cell-stimulatory effects were diminished when myeloid-specific human LAL (hLAL) was expressed in myeloid cells in lal-/- mice. In addition, lal-/- MDSCs facilitated B16 melanoma cell metastasis in the lungs of recipient lal+/+ mice via tail vein injection. Furthermore, the mammalian target of rapamycin (mTOR) and its downstream gene products were significantly up-regulated in lal-/- MDSCs. Knockdown of mTOR in lal-/- MDSCs suppressed their stimulation on B16 melanoma cell proliferation, growth and metastasis, indicating the tumor-promoting function of lal-/- MDSCs is mediated, at least in part, through over-activation of the mTOR pathway. Finally, lal-/- MDSCs stimulated proliferation and growth of Lewis lung carcinoma (LLC), and transgenic mouse prostate cancer (TRAMP-C2) cells, and these effects were impaired after mTOR inhibition. Our results indicate that LAL plays a critical role in regulating MDSCs ability to directly stimulate cancer cell proliferation, and overcome immune rejection of cancer metastasis in allogeneic mice through modulation of the mTOR pathway, which provides a mechanistic basis for targeting MDSCs to reduce the risk of cancer metastasis. Therefore, MDSCs possess dual functions to facilitate cancer metastasis: suppress immune surveillance, and stimulate cancer cell proliferation and growth. Citation Format: Ting Zhao, Hong Du, Xinchun Ding, Katlin Walls, Cong Yan. Activation of mTOR pathway in myeloid-derived suppressor cells with lysosomal acid lipase deficiency stimulates cancer cell proliferation and metastasis. [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 161. doi:10.1158/1538-7445.AM2014-161
Book: Matrons, Medics and Maladies: Edinburgh Royal Infirmary in the 1840s
Authors: P Dileep Kumar
Journal: BMJ (2000)

Bill Yule

Tuckwell Press, £12.99, pp 248

ISBN: 1 86232 091 8

———————

Rating: ★★★

The Edinburgh City Hospital

James A Gray

Tuckwell Press, £20, pp 488

ISBN 1 86232 096 9

———————

Rating: ★★

These two books tell the story of medicine in the city of Edinburgh, spanning about 160 years. Bill Yule's Matrons, Medics and Maladies is pleasantly formatted with boxed case histories and hand drawn caricatures of the late 19th century lifestyle. The notes of the house officers in the 1850s show meticulous documentation of clinical cases. We are reminded repeatedly that hospitals and medicine were glowing edifices of the society and culture. The scenes from 19th century Edinburgh, with its multitude of epidemics of typhus, smallpox, plague, and other mysterious fevers, might still be seen in any part of the developing world. Predictably, leeches, cupping, and blood letting take the centre stage of treatments. How the city and the nation came to grips with these is intriguing.

Yule reveals the faces of men and women behind this crusade. They were real people—doctors, nurses, other hospital workers, and administrators. Modern hospital managers will envy the canniness of their counterparts from the 19th century. The efforts to obtain funding to maintain a teaching hospital seem exactly like a late 20th century saga. In reading this account, we come to realise that the fights and friction between different groups in the hospital setting are universal and ubiquitous.

In The Edinburgh City Hospital James Gray dwells on a more modern time in the history of Edinburgh. His is the story of the City Hospital from 1903 to 1999, the year that it was dismantled. This book contains painstakingly researched data on the year to year happenings in the famed “fever hospital.” Several contributions were made to medical science from this hospital, such as triple therapy for tuberculosis by Sir John Crofton, Dr Flenley's work on obstructive airway disease, and Dr Douglas's work on sarcoidosis. It is interesting to note the evolving microdynamics of a hospital from its inception.

Studded with mundane details, this book may be for the history buff rather than for easy reading. The fate of the City Hospital is nothing new to us across the Atlantic, where market economy dictates the shifting sands of the medical landscape. Still, the City Hospital largely achieved its objectives before fading into oblivion.
Erythropoietin enhances the antitumor efficacy of a cisplatin and gemcitabine chemotherapy regime in a murine model of Lewis lung carcinoma.
Authors: Aoife M. Shannon, David J. Bouchier-Hayes, Deirdre Toomey
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 45, 2004

2210 

Recombinant erythropoietin (Epo) is a glycoprotein hormone stimulator of erythropoiesis, currently used in the treatment of chemotherapy-associated or tumor-associated anaemia. Hypoxia, which may be exacerbated by anaemia, occurs within tumors due to an inefficient vascular supply, leading to chemotherapeutic resistance (1). A novel approach to normalising tumor hypoxia might be to administer Epo, thus increasing the amount of erythrocytes in the blood and allowing more efficient oxygen delivery to the tumor. Epo may also have an effect on angiogenesis and on the immune response. We investigated the ability of Epo to potentiate the effects of an anaemia-inducing chemotherapy regime, in an experimental model of Lewis Lung Carcinoma (LLC). The in vitro chemosensitivity of LLC cells to the chemotherapy drugs, cisplatin and gemcitabine, were assessed under both normoxic and hypoxic (2% oxygen) growth conditions using the colorimetric MTT assay. In vivo, C57/Bl6 mice bearing a LLC flank tumor were randomised into a control group (n=10), a group receiving a weekly dose of Epo (10 μg/kg darbepoetin alfa), a chemotherapy group receiving metronomic doses of cisplatin (3 mg/kg) and gemcitabine (60 mg/kg), and chemotherapy combined with Epo. Tumor volume was determined using calliper measurements, while blood haemoglobin concentration was measured using a Hemocue analyser. Microvessel density (angiogenesis) and T-cell infiltration in the tumors were measured using immunohistochemistry. Tumor cells were more sensitive to the effects of chemotherapies under normoxic growth conditions compared to hypoxic conditions. In vivo, chemotherapy-induced anaemia (haemoglobin <10 g/dl) was prevented using weekly Epo treatment. Epo combined with chemotherapy significantly decreased tumor growth relative to chemotherapy alone (See Figure). Epo had no affect on microvessel density, but there was a significant increase in tumor T-cell infiltration in the Epo-treated mice, relative to controls. In conclusion, cisplatin and gemcitabine have greater efficacy under normoxic conditions. The chemotherapy regime significantly decreased tumor growth in the Epo-treated (non-anaemic) mice, compared to mice treated with chemotherapy alone. We hypothesise that this is either due to the increased activity of the chemotherapy drugs under oxygenated conditions, or to an Epo-induced immune response. (1) Shannon AM, Bouchier-Hayes DJ, Condron CM, Toomey D. Tumour hypoxia, chemotherapeutic resistance and hypoxia-related therapies. Cancer Treatment Reviews, 29, 297-307, 2003.



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Abstract 15298: Most Strokes Occur More Than 48 Hours Following Primary Percutaneous Coronary Intervention in STEMI: the Stroke Experience in APEX-AMI Trial
Authors: Jeffrey T Guptill, Renato D Lopes, Rajendra H Mehta, John Horton, Daniel Laskowitz, Karen S Pieper, Paul W Armstrong, Christopher B Granger
Journal: Circulation (2011)

Background- Stroke is a devastating complication when it occurs in the setting of acute myocardial infarction (AMI). Little is known about stroke timing, characteristics, and associated clinical ou...