tbuckley/cabot-search huggingface dataset:
Review: Aldosterone blockade reduces mortality in patients with left ventricular dysfunction
Authors: Peter Liu
Journal: Annals of Internal Medicine (2009)

ACP Journal Club18 August 2009Review: Aldosterone blockade reduces mortality in patients with left ventricular dysfunctionPeter Liu, MDPeter Liu, MDUniversity of Toronto and Canadian Institutes of Health Research, Toronto, Ontario, Canada (P.L.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-151-4-200908180-02009 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Source CitationEzekowitz JA, McAlister FA. Aldosterone blockade and left ventricular dysfunction: a systematic review of randomized clinical trials. Eur Heart J. 2009;30:469-77. https://pubmed.ncbi.nlm.nih.gov/19066207Clinical Impact RatingsGIM/FP/GP: Hospitalists: Cardiology: References1 Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to update the 2001 guidelines for the evaluation and management of heart failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation. 2005;112:e154-235. [PMID: 16160202] Google Scholar2 Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med. 1999;341:709-17. [PMID: 10471456] Google Scholar3 Struthers A, Krum H, Williams GH. A comparison of the aldosterone-blocking agents eplerenone and spironolactone. Clin Cardiol. 2008;31:153-8. [PMID: 18404673] Google Scholar4 Arnold JM, Liu P, Demers C, et al. Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006: diagnosis and management. Can J Cardiol. 2006;22:23-45. [PMID: 16450016] Google Scholar Author, Article, and Disclosure InformationAffiliations: University of Toronto and Canadian Institutes of Health Research, Toronto, Ontario, Canada (P.L.)This article was published at Annals.org on 4 August 2009. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 18 August 2009Volume 151, Issue 4Page: JC2-9KeywordsACE inhibitorsAldosteroneHeart failureHospitalizationsRenal failureSaltsSystematic reviewsTreatment guidelines ePublished: 18 August 2009 Issue Published: 18 August 2009 Copyright & PermissionsCopyright © 2009 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
706 COMPARISON OF LIVER BIOPSY, ELASTOMETRY AND SERUM MARKERS FOR LIVER FIBROSIS ASSESSMENT IN GENOTYPE 4 HCV-INFECTED PATIENTS IN EGYPT. RESULTS OF THE ANRS12184 STUDY
Authors: P. Bonnard, M. El-Kassas, M. Gamal, A.B. Hassan, L. Le Fouler, A. Elsharkawy, E. Delarocque-Astagneau, M. El-Sayed, A. Abd El Hay, M. Abdel-Hamid, F. Carrat, P. Bedossa, M. Mohamed, A. Fontanet, G. Esmat
Journal: Journal of Hepatology (2013)
Nasal-type T/natural killer cell angiocentric lymphoma, Epstein-Barr virus-associated, and showing clonal T-cell receptor γ gene rearrangement
Authors: None YOON, None LEE, None CHANG
Journal: British Journal of Dermatology (1999)

Nasal-type T/natural killer (NK) cell lymphoma, which often shows an angiocentric growth pattern, is a distinct clinicopathological entity highly associated with the Epstein–Barr virus (EBV). This tumour has a characteristic immunophenotype, whereas the cytological spectrum is broad. It is known that a clonal T-cell receptor (TCR) gene rearrangement is not found in this tumour. However, it is still unresolved as to whether the finding of a clonal TCR gene rearrangement excludes the diagnosis of nasal-type T/NK cell lymphoma. We describe a case of nasal-type T/NK cell angiocentric lymphoma, EBV-associated, and showing clonal TCR γ gene rearrangement. The patient died of sepsis 5 months after diagnosis in spite of aggressive chemotherapy.
Nurse led care: Comment in This week in the BMJ is misleading
Authors: Peter Griffiths
Journal: BMJ (2005)

This week in the BMJ for the paper by Walsh et al are offered the conclusion that investment in intermediate care in community hospitals may be more cost effective than financing nurse led care for post-acute patients in acute hospitals. 1 2But the study itself, which confirms existing evidence on the costs of nurse led intermediate care in acute settings, 3 4 tackles neither the effect nor the cost of intermediate care in community hospitals.How then can such a conclusion be drawn?Walsh et al do not make this assertion.The author of the comment offers no support.Our own review of the evidence on nurse led intermediate care found no quality evidence for either the effect or cost of intermediate care in community settings. 5 The BMJ has been at the forefront of setting standards for the reporting of primary research.However, the editors must be aware that many readers simply pick up a take home message from comment, like this, 1 in the journal.
THE INTOXICATION OF SPLENECTOMIZED MICE BY FEEDING FRESH SPLEEN AND OTHER ORGANS
Authors: Paul A. Lewis, Arthur Georges Margot
Journal: The Journal of Experimental Medicine (1915)

The intoxication which is developed when splenectomized mice are fed with fresh spleen is more regular in occurrence when the feeding experiment is carried out four or five days after splenectomy than when it is done at later periods. The intoxication is easily recognizable even in its less severe forms by a lengthening of the coagulation time of the blood. An intoxication of the same character is produced when splenectomized mice are fed with the mucous membrane of the stomach and upper small intestine. Bone marrow and dried blood probably give the same reaction in a somewhat milder form. The other organs either give no intoxication at all when fed, or in certain instances the thyroid, adrenal, and salivary gland (mouse) give intoxications of a different character which affect intact mice and splenectomized animals equally. The spleen or the gastro-intestinal mucosa is equally effective in producing the intoxication, whether it be derived from heterologous or homologous species. Certain experiments, not reported in detail, indicate that the susceptibility to the intoxication disappears in time and that this time may be shortened by repeated feedings with sublethal amounts of organ substance.
RECENT WORK ON CANCER
Authors: CHARLES F. GESCHICKTER
Journal: JAMA (1930)

A review of the work now in progress in European cancer laboratories, based on a recent tour of investigation in Europe of four months' duration furnishes one of the most reliable means of estimating the present status of cancer research. Work in America and in Europe in the field of malignant disease has become quite diversified but falls readily into the three fields of experimentation as to the cause, the diagnosis and the cure of cancer.  WORK ON THE CAUSE OF CANCER  The elaboration of new experimental methods is responsible for most of the recent advances in regard to the etiology of malignant disease. Experimentation with carcinogenic agents, the use of tumor filtrates and work on the metabolism of tumor cells constitute the major lines along which the problem of the cause of cancer is now being attacked. The oldest method of experimentation with carcinogenic agents is still being
Molecular cloning and expression of inducible nitric oxide synthase in chick embryonic ventricular myocytes
Authors: Tatsuya Shimizu, Koh-ichiro Kinugawa, Yasuyuki Sugishita, Kazuro Sugishita, Kazumasa Harada, Hiroshi Matsui, Osami Kohmoto, Takashi Serizawa, Toshiyuki Takahashi
Journal: Cardiovascular Research (1998)

Objective: Inducible nitric oxide synthase (iNOS) has been implicated to contribute to myocardial dysfunction in various settings, but considerable species differences have been noted in the levels of iNOS expression and its function in several tissues. The aim of this study was to elucidate evolutional changes in myocardial iNOS expression and function. Methods: An iNOS cDNA clone was isolated by RT-PCR from the 10-day old cultured chick embryonic ventricular myocytes stimulated with 10 μg/ml of lipopolysaccharide. Expression of the iNOS mRNA was analyzed with Northern blot analysis and RNase protection assay. The iNOS activity was estimated from conversion rates of l-arginine to l-citrulline and intracellular cGMP contents were measured with radioimmunoassay. Furthermore, both [Ca2+]i (fluorescent dye indo-1) and cell contraction (video motion detector) were simultaneously recorded. Results: Aside from the primer sequences, the insert (1026 bp) of the cDNA clone showed 66.4% identity at the deduced amino acid level to the human iNOS cDNAs. Northern blot analysis revealed that chicken iNOS mRNA of approximately 4.5 kb was induced by lipopolysaccharide within 6 h in the cultured myocytes. RNase protection assay also showed that lipopolysaccharide provoked 14.6±5.1-fold increases (n=6, p<0.05) in the iNOS mRNA signals within 6 h. The iNOS activity (+300%, P<0.05) as well as the intracellular cGMP contents (+75%, P<0.01) were significantly augmented in the lipopolysaccharide-stimulated cells. Both the cell contraction and [Ca2+]i were significantly reduced after the administration of a large amount (10 mM) of l-arginine in the myocytes pretreated with both lipopolysaccharide and NG-monomethyl-l-arginine (100 μM). Conclusion: As like as the nucleotide and amino acid sequences, the myocardial effects of the iNOS may also be evolutionary conserved.
Getting It Right When Things Go Wrong
Authors: Christian M. Pettker
Journal: JAMA (2010)

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
Abstract 1970: SOCS-1,-3 gene delivery in gastric cancer cells induces a potent anti-proliferative effect <i>via</i> the suppression of JAK/STAT and P38 MAPK signaling pathways
Authors: Maiko Urase, Satoshi Serada, Yoshihito Souma, Kouta Iwahori, Kazuki Shimada, Toshirou Nishida, Minoru Fujimoto, Tetsuji Naka
Journal: Cancer Research (2011)

Abstract BACKGROUND:Enhanced activation of inflammatory cytokines signaling transductions have been suggested as a driving force in the development of gastric tumors. The suppressor of cytokine signaling (SOCS) family proteins are important negative regulator of proinflammatory cytokine signals and have been reported to be frequently silenced by DNA methylation of CpG islands in gastric cancer (GC). The aim of this in vitro assessment was to evaluate the role of SOCS-1 and SOCS-3 in the proliferation of GC cell through regulating cytokine signaling pathways. MATERIAL AND METHODS:Six GC cell lines (NUGC3, AGS, MKN45, NUGC4, MKN7, and MKN74) were used in this study. Methylation status of SOCS-1/-3 was assessed by methylation specific PCR. The concentrations of IL-6 in the cell culture supernatant was measured by ELISA. Adenovirus vectors encoding either SOCS-1 or SOCS-3 were constructed for gene delivery to GC cells. The status of activated kinases and downstream proteins were determined by Western blot analysis. Anti-proliferative effects in GC cells were assessed by WST-8 assay. RESULTS: In six GC cell lines used in our study, SOCS-1 and SOCS-3 genes were methylated except one cell line, and two cell lines (NUGC3, AGS) showed elevated endogenous IL-6 production with constitutively phosphorylated STAT3. Unexpectedly, anti-IL-6R antibody did not affect both of the cell proliferation and the status of phosphorylated STAT3 in these two cell lines. In contrast, adenovirus-mediated SOCS-1 /-3 gene delivery markedly reduced cell proliferation of these cells. The anti-proliferative effect of SOCS-1/-3 correlated with decreased levels of the activation of STAT3 and p38 MAPK. Cell proliferation assay confirmed that the blockade of JAK/STAT and p38 MAPK signaling pathways also reduced cell proliferation of these cell lines. CONCLUSIONS: Our results indicated that the DNA methylation of SOCS-1/-3 may be associated with GC proliferation, and highlighted an anti-proliferative potential of SOCS-1/-3 through the inhibition of JAK/STAT and p38 MAPK signaling pathways independently IL-6 signaling. Thus, DNA methylation of SOCS-1/-3 can be a molecular marker of GC progression, and their forced expression may represent a novel therapeutic application as a multi-growth signal inhibitor for GC treatment. 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 1970. doi:10.1158/1538-7445.AM2011-1970
How to Choose a Medical Specialty
Authors: William E. Golden
Journal: JAMA (1986)

Increased competition for residency and clinical practice positions has created anxiety in medical students. There is perceived pressure to choose the "right" specialty while in one's training and to develop strategy early in medical school to obtain an appropriate residency. Many trainees are concerned that they may make the incorrect choice. Traditionally, medical schools have not done well in career counseling, although this situation is slowly changing. Anita D. Taylor's book is a welcome addition to a medical educator's resources. She has attempted to give focus to a medical student's thinking in planning one's career. Her viewpoint is that students should choose careers based on interest and personality traits, and she attempts to provide information that would allow students to assess their potential career choices in terms of those variables. In an era when physician reimbursement and practice structure are liable to undergo great alterations, such career reflection is invaluable.
Abstract LB-143: ErbB2, EphrinB1, Src kinase and PTPN13 signaling complex regulates MAP kinase signaling in human cancers
Authors: Paola D. Vermeer, Megan Bell, Kimberly Lee, Daniel W. Vermeer, Bryant Wieking, Ronny I. Drapkin, Shridar Ganesan, John Lee
Journal: Cancer Research (2012)

Abstract Tyrosine kinases, like the ErbB and Src families, can mediate potent oncogenic growth and are successful therapeutic targets of human cancers. However, many cancer cells overcome or successfully modulate these downstream signaling cascades in the absence of growth factor or kinase over-expression. We have previously identified a cellular phosphatase, PTPN13 that significantly modulates mitogenic signaling and can function as tumor suppressors. Decreased PTPN13 expression enhances ErbB2-mediated MAP Kinase activation, and is also associated with decreased survival in breast cancer. Here we show that PTPN13 regulates a signaling complex consisting of ErbB2, Src, and EphrinB1. To our knowledge, this signaling complex has not been previously described. Co-immunoprecipitation, proximity ligation assay and immunofluoroscence studies demonstrate that EphrinB1, a PTPN13 substrate, interacts with ErbB2. In addition, the oncogenic V660E ErbB2 mutation enhances this interaction, while Src kinase mediates EphrinB1 phosphorylation and subsequent MAP Kinase signaling. Decreased PTPN13 function further potentiates these changes. The association of oncogene kinases (ErbB2, Src), a signaling transmembrane ligand (EphrinB1) and a phosphatase tumor suppressor (PTPN13) suggest that EphrinB1 may be a relevant therapeutic target in cancers harboring ErbB2-activating mutations and decreased PTPN13 expression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-143. doi:1538-7445.AM2012-LB-143
Infectious Diseases of the Central Nervous System: First Annual Symposium of the Barrow Neurological Institute
Authors: G. R. Haase
Journal: JAMA (1976)

<b>Current Reviews of Higher Nervous System Dysfunction,</b>edited by Walter J. Friedlander (Advances in Neurology, vol 7), 195 pp, $16, New York, Raven Press, 1975. <i>Advances in Neurology</i>is one of several series of monographs in the neurological sciences that attempt to bring new knowledge to the reader, with minimal delay. Such publishing efforts frequently take recourse to the fixation-in-print of symposia, against which there is no objection, at least not in principle. There is a risk, however, that published symposia may acquire the reputation of being books of easy virtue. Raven Press has, in recent years, been outstandingly successful in the rapid publication of monographs and transactions in the neurological sciences. Their series,<i>Advances in Neurology</i>, begun in 1973, now numbers nine volumes. Volume 6, edited by R. A. Thompson and J. R. Green is entitled<i>Infectious Diseases of the Cen-</i><i>tral Nervous System</i>. The 21 contributions in this
The eradication of breast cancer cells and stem cells by 8-hydroxyquinoline-loaded hyaluronan modified mesoporous silica nanoparticle-supported lipid bilayers containing docetaxel
Authors: Dong Wang, Jingbin Huang, Xinxia Wang, Yuan Yu, He Zhang, Yan Chen, Junjie Liu, Zhiguo Sun, Hao Zou, Duxin Sun, Guichen Zhou, Guoqing Zhang, Ying Lu, Yanqiang Zhong
Journal: Biomaterials (2013)
Failure to phosphorylate AKT in podocytes from mice with early diabetic nephropathy promotes cell death
Authors: T. Tejada, P. Catanuto, A. Ijaz, J.V. Santos, X. Xia, P. Sanchez, N. Sanabria, O. Lenz, S.J. Elliot, A. Fornoni
Journal: Kidney International (2008)
"Unwarranted survivals" and "anomalous deaths" from coronary heart disease: prospective survey of general population
Authors: A. McConnachie, K. Hunt, C. Emslie, C. Hart, G. Watt
Journal: BMJ (2001)

<h3>Abstract</h3> <b>Objectives:</b> To assess survival in people who are at apparent high risk who do not develop coronary heart disease ("unwarranted survivals") and mortality in people at low risk who die from the disease ("anomalous deaths") and the extent to which these outcomes are explained by other, less visible, risk factors. <b>Design:</b> Prospective general population survey. <b>Setting:</b> Renfrew and Paisley, Scotland. <b>Participants:</b> 6068 men aged 45–64 years at screening in 1972-6, allocated to "visible" risk groups on the basis of body mass index and smoking. <b>Main outcome measures:</b> Survival and death from coronary heart disease by age 70 years. <b>Results:</b> Visible risk was a good predictor of mortality: 13% (45) of men at low risk and 45% (86) of men at high risk had died by age 70 years. Of these deaths, 12 (4%) and 44 (23%), respectively, were from coronary heart disease. In the group at low visible risk other less visible risk factors accounted for increased risk in 83% (10/12) of men who died from coronary heart disease and 29% (84/292) of men who survived. In the high risk group 81/107 who survived (76%) and 19/44 (43%) who died from coronary heart disease had lower risk after other factors were considered. Different risk factors modified risk (beyond smoking and body mass index) in the two groups. Among men at low visible risk, poor respiratory function, diabetes, previous coronary heart disease, and socioeconomic deprivation modified risk. Among men at high visible risk, height and cholesterol concentration modified risk. <b>Conclusions:</b> Differences in survival between these extreme risk groups are dramatic. Health promotion messages would be more credible if they discussed anomalies and the limits of prediction of coronary disease at an individual level. <h3>What is already known on this topic</h3> People pay attention to visible risk factors, such as smoking and weight, in explaining or predicting coronary events but are aware that these behavioural risk factors fail to explain some early deaths from coronary heart disease (in those with "low risk" lifestyles) and long survival (in those with "high risk" lifestyles) Such violations to notions of coronary candidacy undermine people9s belief in the worth of modifying behavioural risk factors for coronary heart disease <h3>What this study adds</h3> Visible risk status was a good marker for other coronary risk factors at the extremes of the risk distribution Most men at low visible risk (slim, never smoked) who died prematurely from coronary heart disease had poorer risk profiles on other less visible risk factors; similarly, men at high visible risk (obese, heavy smokers) who survived often had more favourable profiles on other risk factors
Brittle diabetes: long-term control with a portable, continuous, intravenous insulin infusion system.
Authors: J Bayliss
Journal: BMJ (1981)

A young woman had severe brittle diabetes mellitus that was critically unmanageable with all conventional insulin treatment. Continuous subcutaneous and intramuscular infusions of insulin also failed to control her metabolic instability. Use of a continuous intravenous infusion, however, whereby a portable, variable-rate, battery-operated syringe pump delivered insulin through a subcutaneously tunnelled central venous catheter, resulted in good control. When she was receiving hourly intramuscular insulin injections (a mean of 778 IU daily) mean blood glucose concentrations had been 22.1 +/- 1.4 mmol/l (398 +/- 25 mg/100 microliters). After she had received the intravenous infusion for one month as an outpatient mean blood glucose concentration was 8.2 +/- 0.46 mmol/l (148 +/- 8 mg/100 microliters) and only 80 IU insulin daily was required. Follow-up after over five months of use showed that few complications had occurred. The system is simple to use and safe, and the diabetes had been stabilised such that she could enjoy a near-normal life style.