tbuckley/cabot-search huggingface dataset:
CMA draws criticism for sacking editors
Authors: David Spurgeon
Journal: BMJ (2006)

The firing of two top editors from the CMAJ (the journal of the Canadian Medical Association) has drawn harsh international criticism from the scientific and editorial communities as an assault on editorial independence. But the journal's publisher, Graham Morris, insists that, after 10 years with the same editors, “It was time for a fresh approach.”

John Hoey, the editor in chief, and his deputy editor, Anne Marie Todkill, were both dismissed on 20 February by Mr Morris. Dr Hoey, Ms Todkill, and other staff said that they were told not to comment on the firings. And Mr Morris said, “It's our policy not to comment on staff issues.”

Stephen Choi, the acting editor, and other editorial staff, are understood to be considering their position, depending on how the CMA responds to demands for proper mechanisms to protect editorial freedom.

Mr Morris, the president of CMA Media Incorporated, which owns and publishes the journal, said that Dr Hoey “had done a good job in improving the quality of the journal.” CMA Media is a subsidiary of …
A phase II study of sequential combination chemotherapy with cyclophosphamide, prednisone, and 2-chlorodeoxyadenosine in previously untreated patients with chronic lymphocytic leukemia
Authors: A Tefferi, C-Y Li, CB Reeder, SM Geyer, C Allmer, R Levitt, JC Michalak, F Addo, JE Krook, TE Witzig, PL Schaefer, JA Mailliard
Journal: Leukemia (2001)
People in US have poorer health and die younger than those in other rich countries
Authors: M. McCarthy
Journal: BMJ (2013)

People in the United States are less healthy, have more chronic disease and disability, and die at a younger age than people living in other wealthy nations, concludes a new report by a panel convened by the US National Research Council and the Institute of Medicine.1

The panel found that the US fell short in health outcomes at every age from birth to 75 years and that the deficiencies were found at all levels of society. Even high income, college educated, white Americans tended to be sicker and die younger than their peers in other rich countries.

So many problems were identified in so many areas that it indicated that “something is fundamentally going wrong,” said Stephen Woolf, professor of family medicine at Virginia Commonwealth University in …
1134-200 Myocardial performance index in pediatric patients with primary pulmonary hypertension: Correlation with pulmonary artery pressure and response to vasodilators
Authors: Karrie L Dyer, Linda B Pauliks, Scott K Kirby, Lori Claussen, D Dunbar Ivy, Robin Shandas, Lilliam M Valdes-Cruz
Journal: Journal of the American College of Cardiology (2004)
Stimulation of neoplastic mouse lung cell proliferation by alveolar macrophage-derived, insulin-like growth factor-1 can be blocked by inhibiting MEK and PI3K activation
Authors: Jason M Fritz, Lori D Dwyer-Nield, Alvin M Malkinson
Journal: Molecular Cancer (2011)

Abstract Background Worldwide, lung cancer kills more people than breast, colon and prostate cancer combined. Alterations in macrophage number and function during lung tumorigenesis suggest that these immune effector cells stimulate lung cancer growth. Evidence from cancer models in other tissues suggests that cancer cells actively recruit growth factor-producing macrophages through a reciprocal signaling pathway. While the levels of lung macrophages increase during tumor progression in mouse models of lung cancer, and high pulmonary macrophage content correlates with a poor prognosis in human non-small cell lung cancer, the specific role of alveolar macrophages in lung tumorigenesis is not clear. Methods After culturing either an immortalized lung macrophage cell line or primary murine alveolar macrophages from naïve and lung-tumor bearing mice with primary tumor isolates and immortalized cell lines, the effects on epithelial proliferation and cellular kinase activation were determined. Insulin-like growth factor-1 (IGF-1) was quantified by ELISA, and macrophage conditioned media IGF-1 levels manipulated by IL-4 treatment, immuno-depletion and siRNA transfection. Results Primary macrophages from both naïve and lung-tumor bearing mice stimulated epithelial cell proliferation. The lungs of tumor-bearing mice contained 3.5-times more IGF-1 than naïve littermates, and media conditioned by freshly isolated tumor-educated macrophages contained more IGF-1 than media conditioned by naïve macrophages; IL-4 stimulated IGF-1 production by both macrophage subsets. The ability of macrophage conditioned media to stimulate neoplastic proliferation correlated with media IGF-1 levels, and recombinant IGF-1 alone was sufficient to induce epithelial proliferation in all cell lines evaluated. Macrophage-conditioned media and IGF-1 stimulated lung tumor cell growth in an additive manner, while EGF had no effect. Macrophage-derived factors increased p-Erk1/2, p-Akt and cyclin D1 levels in neoplastic cells, and the combined inhibition of both MEK and PI3K ablated macrophage-mediated increases in epithelial growth. Conclusions Macrophages produce IGF-1 which directly stimulates neoplastic proliferation through Erk and Akt activation. This observation suggests that combining macrophage ablation therapy with IGF-1R, MEK and/or PI3K inhibition could improve therapeutic response in human lung cancer. Exploring macrophage-based intervention could be a fruitful avenue for future research.
The subtle microbe
Authors: D G Colin-Jones
Journal: BMJ (1994)

“Ulcer Wars” described the discovery in 1982 of Helicobacter pylori by Dr Barry Marshall in Perth, Australia, and tried to assess the impact of this organism on human disease. Many stories of medical advances are painstaking and dull, but not this. The programme was colourful, slightly offbeat, even irreverent. These ingredients made a good story with an appreciable educational content along the way, aided by a clear, well pitched narrative. However, like so many documentaries these days, it gave insufficient time for views contrary to those of the film makers.

The programme vividly described how H pylori was discovered through serendipity, when a long public holiday over the Easter period in 1982 led to a four day incubation instead of two days, allowing H pylori to be cultured for the first time after …
Homophobia in medicine
Authors: A. Sheard
Journal: BMJ (1998)

Members of parliament and the bishops at the last Lambeth conference were circulated with an open letter on sexuality signed by 23 doctors. This gives dire warnings about the dangers of anal intercourse, and urges that the age of consent for homosexuals should not be reduced.

At least two of the doctors who signed the statement have written for or been quoted in documents produced by “Christian” organisations in the past year or so. These organisations include the Association of Christian Teachers, Christian Action in Research and Education, the Maranatha Community, Cost of Conscience and Reform (jointly), and the Christian Institute. The documents vary in length, but are all similar in content. They include a medical section, “written by doctors,” which warns of the medical consequences of homosexuality; a social section, which links homosexuality with paedophilia; and a religious section, which says the Bible is against homosexuality.

Well that's life, and religious cranks are always with us. But the medical evidence that …
Increased Expression of Leukotriene C4 Synthase Is a Feature of Circulating CD34+ Hematopoietic Stem Cells but Not Circulating Eosinophils in Aspirin-Exacerbated Respiratory Disease (AERD)
Authors: Mary Grace Baker, Julie Negri, John W. Steinke, Larry Borish
Journal: Journal of Allergy and Clinical Immunology (2015)
Courses in Psychiatry
Authors: R. J. Aspinal, S. Beacon, H. F. Bugler, R. Clark, C. S. E. Gifford, J. Greenwood, B. K. Howells, T. Iskander, J. Lambourn, M. E. Rope, I. A. J. Ross-Smith, F. Smith, D. D. Stephens, F. A. Thompson
Journal: BMJ (1970)
Government acts on gifts from drug companies
Authors: L Beecham
Journal: BMJ (1994)

Expensive gifts, such as medical equipment and expenses paid foreign trips, from drug companies to doctors will be banned under parliamentary regulations laid last week. Drug companies have failed to abide by rules laid down by the Association of the British Pharmaceutical Industry, and drug company staff who offer sales inducements to doctors could face criminal charges. Doctors could also be found guilty of accepting inducements. Doctors have been criticised for accepting free air tickets to conferences to cover holiday travel costs and for accepting luxury trips to Venice and Monte …
Cumulative Meta-analyses and the Problem of Multiple Drug Effects-Reply
Authors: Elliott M. Antman
Journal: JAMA (1993)

<h3>In Reply.</h3> —We appreciate the interest of Drs Borzak and Rosman in our recent article comparing the results of cumulative meta-analyses of randomized controlled trials for acute myocardial infarction and the recommendations of clinical experts. We agree that meta-analysis can permit more expeditious identification of the effectiveness of individual interventions. Furthermore, as suggested by some authorities,<sup>1</sup>cumulative meta-analysis may aid investigators in determining whether continued study of a particular clinical problem is warranted. Borzak and Rosman rightly point out that the complexities of clinical medicine, as exemplified by the treatment of a patient with acute myocardial infarction, necessitate skilled clinical judgment. This requires a synthesis not only of the emerging data in the medical literature but also of the particular clinical features of the patient in question with respect to whether he or she is representative of the individuals enrolled in the randomized controlled trials reported in the literature.
Re: Medical Pests
Authors: Wayne Allgaier
Journal: JAMA (1976)

<h3>To the Editor.—</h3> While I sympathize with Dr Harnes' disillusionment in trying to convert the world to the ways of preventive medicine (235:157, 1976), I'm not quite ready to throw in the towel myself. I shall continue to preach nonsmoking, avoidance of alcohol and unnecessary drugs, proper diet and exercise, and other concepts known to promote better physical and emotional health—to the young and healthy as well as to those already suffering from the consequences of the abuse of such principles. I have certain serious shortcomings myself, but I will not allow these imperfections to prevent me from sharing what I know to be true with my patients. My position is not to foist my beliefs, religious or medical, on anyone, but rather to advise them of the facts and let them make the choice.
Neuroconstructivism: Evidence for later maturation of prefrontally mediated executive functioning
Authors: Jonathan Foster, Anke van Eekelen, Eugen Mattes
Journal: Behavioral and Brain Sciences (2008)

Abstract The authors of this commentary concur with the viewpoint presented by Mareschal et al. (2007a; 2007b) concerning the relevance of neurological data when theorizing about cognitive development. However, we argue here that Mareschal et al. fail to consider adequately the relevance of reorganizational brain events occurring through adolescence and early adulthood, especially regarding the prefrontal cortex and the ontogeny of executive functioning. In addition, evidence from the lifespan neurodevelopmental literature indicates that increased activity of neural networks may signify less efficient processing. This observation is of potential relevance when considering the neurological changes associated with cognitive development during childhood and adolescence.
Microparticle-loaded neonatal porcine Sertoli cells for cell-based therapeutic and drug delivery system
Authors: S Giovagnoli, F Mancuso, S Vannini, M Calvitti, M Piroddi, D Pietrella, I Arato, G Falabella, F Galli, M Moretti, L M Neri, M Bodo, S Capitani, D F Cameron, M Ricci, G Luca, R Calafiore
Journal: Journal of Controlled Release (2014)
Searching for Non-coding RNAs in Genomic Sequences Using ncRNAscout
Authors: Michael Bao, Miguel Cervantes Cervantes, Ling Zhong, Jason T.L. Wang
Journal: Genomics Proteomics & Bioinformatics (2012)

Abstract Recently non-coding RNA (ncRNA) genes have been found to serve many important functions in the cell such as regulation of gene expression at the transcriptional level. Potentially there are more ncRNA molecules yet to be found and their possible functions are to be revealed. The discovery of ncRNAs is a difficult task because they lack sequence indicators such as the start and stop codons displayed by protein-coding RNAs. Current methods utilize either sequence motifs or structural parameters to detect novel ncRNAs within genomes. Here, we present an ab initio ncRNA finder, named ncRNAscout, by utilizing both sequence motifs and structural parameters. Specifically, our method has three components: (i) a measure of the frequency of a sequence, (ii) a measure of the structural stability of a sequence contained in a t-score, and (iii) a measure of the frequency of certain patterns within a sequence that may indicate the presence of ncRNA. Experimental results show that, given a genome and a set of known ncRNAs, our method is able to accurately identify and locate a significant number of ncRNA sequences in the genome. The ncRNAscout tool is available for downloading at http://bioinformatics.njit.edu/ncRNAscout.
Steroid Inhibition of Adrenal Corticosteroid Production—A Mitochondrial Effect.
Authors: Gerard N. Burrow
Journal: Annals of Internal Medicine (1969)

s1 May 1969Steroid Inhibition of Adrenal Corticosteroid Production—A Mitochondrial Effect.Gerard N. Burrow, M.D., F.A.C.P.Gerard N. Burrow, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-70-5-1060_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThere is evidence to suggest that certain steroids are capable of inhibiting corticoid production as well as protein and ribonucleic acid (RNA) synthesis in rat adrenal glands in vitro. The data suggest the possibility of local feedback inhibition of steroidogenesis by adrenal steroids, but the mechanism of the inhibition is not clear. The finding that the addition of adenine triphosphate (ATP) and an ATP-generating system overcame corticosterone inhibition of14C-leucine incorporation into rat adrenal protein in vitro suggested an inhibitory effect on cellular energy processes. To study this further, rat adrenal mitochondria were prepared by differential centrifugation, and the effect... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New Haven, Connecticut PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1969Volume 70, Issue 5Page: 1060-1061KeywordsAdenineAdenosine triphosphateAdrenal glandsMitochondriaProtein synthesisProteinsRNASteroidogenesis Issue Published: 1 May 1969 PDF downloadLoading ...
Transcription factor 7–like 2 polymorphism modulates glucose and lipid homeostasis, adipokine profile, and hepatocyte apoptosis in NASH #
Authors: Giovanni Musso, Roberto Gambino, Giovanni Pacini, Gianfranco Pagano, Marilena Durazzo, Maurizio Cassader
Journal: Hepatology (2008)

Abstract Genetic factors underlying the association of NAFLD with diabetes and atherosclerosis are unknown. Recent human studies suggest transcription factor 7–like 2 (TCF7L2) polymorphism predisposes to diabetes through modulation of β-cell function and modulates lipid levels in familial dyslipidemia. Emerging experimental evidence connects TCF7L2 to adipocyte metabolism and lipid homeostasis, as well. We tested if TCF7L2 polymorphism is a risk factor for nonalcoholic fatty liver disease (NAFLD) and if it modulates liver injury, glucose homeostasis, lipoprotein, and adipokine profiles in NASH. TCF7L2 genotype and dietary habits of 78 nondiabetic normolipidemic NAFLD subjects and 156 age-, body mass index–, sex-matched healthy controls were assessed. In 39 biopsy-proven nonalcoholic steatohepatitis (NASH) and matched controls TCF7L2 polymorphism was correlated to liver histology and oral glucose tolerance test–derived parameters of glucose homeostasis. Patients with NASH and controls consumed a high-fat meal and TCF7L2 genotype was correlated to postprandial circulating lipoproteins, adipokines, and cytokeratin-18 fragments. The TCF7L2 CT/TT genotype was more frequent in NAFLD and predicted the presence and severity of liver disease, of β-cell dysfunction, of reduced incretin effect and hepatic insulin resistance in NASH; it also modulated postprandial hepatocyte apoptosis, lipoproteins, and adipokine profiles in both groups. Conclusion: TCF7L2 polymorphism predisposes to NAFLD and significantly impacts liver injury, glucose homeostasis, and postprandial lipoprotein and adipokine responses to fat ingestion. This polymorphism also modulates a fat-induced increase in circulating markers of hepatocyte apoptosis in NASH. Targeting postprandial lipemia, at least in at-risk TCF7L2 genotypes, may improve liver disease and glucose dysmetabolism in these patients. (Hepatology 2008.)
A comprehensive genetic and histopathologic analysis identifies two subgroups of B-cell malignancies carrying a t(14;19)(q32;q13) or variant BCL3-translocation
Authors: J I Martín-Subero, R Ibbotson, W Klapper, L Michaux, E Callet-Bauchu, F Berger, M J Calasanz, C De Wolf-Peeters, M J Dyer, P Felman, A Gardiner, R D Gascoyne, S Gesk, L Harder, D E Horsman, M Kneba, R Küppers, A Majid, N Parry-Jones, M Ritgen, M Salido, F Solé, G Thiel, H-H Wacker, D Oscier, I Wlodarska, R Siebert
Journal: Leukemia (2007)
Tests for HIV in Lupus
Authors: Vicenc Soriano, Josep Ordi, Josep Grau
Journal: New England Journal of Medicine (1994)

To the Editor: Jindal et al1 described a woman with systemic lupus erythematosus who was receiving hemodialysis and was seropositive for the human immunodeficiency virus type 1 (HIV-1) by both enzyme-linked immunosorbent assay (ELISA) and Western blotting, with a low CD4+ cell count but no evidence of HIV-1 infection by viral culture, antigen testing, and the polymerase-chain-reaction test. The authors concluded that false positive serologic results may occur in people with lupus and end-stage renal disease, perhaps related to the presence of autoantibodies. However, the authors did not explain the patient's low CD4+ cell count (130 per cubic millimeter). We . . .
Tumor-Initiating Function of Nucleostemin-Enriched Mammary Tumor Cells
Authors: Tao Lin, Lingjun Meng, Yi Li, Robert Y.L. Tsai
Journal: Cancer Research (2010)

Abstract Nucleostemin (NS) is highly expressed in normal stem cells and tumors and is upregulated by estradiol in MCF7 breast cancer cells. To investigate the role of NS in mammary tumorigenesis, we established first that NS is expressed at higher levels in the basal cell type than in the luminal cell type in mouse mammary tumors and human breast cancer cells. NS expression was also increased during progression of mammary tumors in MMTV-Wnt1 and MMTV-PyMT transgenic mice and by the tumor sphere culture. To determine the function of NS-enriched tumor cells, we generated a bacterial artificial chromosome transgenic mouse line expressing green fluorescent protein (GFP) from the NS promoter and bred it to MMTV-Wnt1 mice, so that NS-expressing cells can be prospectively isolated based on their GFP levels. Notably, NS-enriched mammary tumor cells exhibited stronger in vitro and in vivo tumorigenic activities and expressed higher levels of K5, CD133, Oct4, telomerase reverse transcriptase, and C-X-C chemokine ligand 12 compared with NS-deficient mammary tumor cells. Furthermore, knockdown of NS dramatically reduced the sphere-forming activity of MDA-MB-231 and MCF7 human breast cancer cells. Our findings establish the tumor-initiating and molecular features of NS-enriched mammary tumor cells, suggesting that NS may offer a valuable therapeutic target. Cancer Res; 70(22); 9444–52. ©2010 AACR.
Chimerically fused antigen rich of overlapped epitopes from latent membrane protein 2 (LMP2) of Epstein–Barr virus as a potential vaccine and diagnostic agent
Authors: Xiaoyun Lin, Shao Chen, Xiangyang Xue, Lijun Lu, Shanli Zhu, Wenshu Li, Xiangmin Chen, Xiaozhi Zhong, Pengfei Jiang, Torsoo Sophia Sename, Yi Zheng, Lifang Zhang
Journal: Cellular and Molecular Immunology (2015)
Histological Changes in the Urothelium and Suburothelium of Human Overactive Bladder following Intradetrusor Injections of Botulinum Neurotoxin Type A for the Treatment of Neurogenic or Idiopathic Detrusor Overactivity
Authors: Apostolos Apostolidis, Thomas S. Jacques, Alex Freeman, Vinay Kalsi, Roshni Popat, Gwendoline Gonzales, Soumendra N. Datta, Shabnam Ghazi-Noori, Sohier Elneil, Prokar Dasgupta, Clare J. Fowler
Journal: European Urology (2008)
Abstract B14: The novel function and trafficking mechanism of nuclear ErbB-2
Authors: Long-Yuan Li, Hsiuyi Chen, Yi-Hsien Hsieh, Ying-Nai Wang, Hsiao-Ju Chu, Mien-Chie Hung
Journal: Cancer Research (2009)

We have demonstrated that ErbB‐2 translocates into the nucleus through importin β1—mediated nuclear import by endosomal sorting, and transactivates transcription of cyclooxygenase‐2 which has been known to be involved in tumor progression and metastasis, suggesting nuclear ErbB‐2 may also contribute to the tumor malignancy. However, how the membranebound ErbB‐2 can be released from the lipid bilayer and translocates into the nucleus; and the biological functions of the nuclear ErbB‐2 are not yet completely understood. Here, we have identified novel ErbB‐2‐interacting nuclear proteins. The interplay between nuclear ErbB‐2 and interacting protein was investigated, which may elucidate a novel function of nuclear ErbB‐2 in contributing to tumorigenesis. In addition, ErbB‐2 interacts with endoplasmic reticulum (ER) proteins, Sec61α, a subunit of Sec61 channel, and EDEM. Sec61α and EDEM are known to mediate retrotranslocation of misfolded proteins in the ER to the cytosol (called ER‐associated degradation pathway). We have demonstrated that Sec61α and EDEM also play important roles in retrotranslocation of ErbB‐2 to the cytosol and to the nucleus, suggesting part of ER retrotranslocation pathway is likely involved in nuclear trafficking of ErbB‐2. [This work was supported by National Health Research Institutes NHRI‐EX98‐9603BC, National Science Council NSC952311‐B‐039‐002 and NSC 97‐3111‐B‐039‐004 and Department of Health DOH97‐TD‐I‐111‐TM003 and DOH98‐TD‐I‐111‐TM002 (to LYL)].Citation Information: Cancer Res 2009;69(23 Suppl):B14.