tbuckley/cabot-search huggingface dataset:
The risk of asthma exacerbation after reducing inhaled corticosteroids: a systematic review and meta‐analysis of randomized controlled trials
Authors: J. B. Hagan, S. A. Samant, G. W. Volcheck, J. T. Li, C. R. Hagan, P. J. Erwin, M. A. Rank
Journal: Allergy (2014)

Abstract Background Asthma guidelines suggest reducing controller medications when asthma is stable. Methods The purpose of the study is to estimate the risk of asthma exacerbation in stable asthmatics who reduce inhaled corticosteroids ( ICS ) compared to those who maintain a stable ICS dose. We identified articles from a systematic review of E nglish and non‐ E nglish articles using MEDLINE , EMBASE , Web of Science, and CENTRAL (inception to M ay 25, 2013). We included randomized controlled trials ( RCT s) with a stable asthma run‐in period of 4 weeks or more, an intervention to reduce ICS , and a follow‐up period of at least 3 months. Results The search strategy identified 2253 potential articles, of which 206 were reviewed at the full‐text level and 6 met criteria for inclusion. The relative risk of an asthma exacerbation in individuals who reduced ICS compared to those who maintained the same ICS dose was 1.25 (95% CI 0.96, 1.62; P = 0.10; I 2 = 0%) in studies with a mean follow‐up of 22 weeks. Individuals who reduced ICS had a decreased% predicted FEV 1 of 0.87% (95% CI −1.58%,3.33%; P = 0.49, I 2 = 58%) and a decreased mean morning peak expiratory flow of 9.57 l/min (95% CI 1.25, 17.90; P = 0.02; I 2 = 74%) compared to those individuals who maintained a stable ICS dose. Conclusions Asthma exacerbations were statistically no more likely among individuals who reduced ICS compared to those who maintained their ICS dose, supporting current guidelines which recommend decreasing ICS by 50% after a period of asthma stability.
Reply to the Letter to the Editor by Watanabe et al.
Authors: Diego Arango, Pia Alhopuro, Lauri A. Aaltonen
Journal: Clinical Cancer Research (2006)

In Response: We appreciate the attention given by Watanabe et al. to our recent publication “SMAD4 levels and response to 5-fluorouracil in colorectal cancer” ([1][1]). In this article, we described the potential value of SMAD4 tumor levels to predict the prognosis of Dukes C colorectal cancer
Incidence of bleeding complications associated with abciximab huse in conjunction with thrombolytic therapy in patients requiring angioplasty
Authors: D.W. Sundlof, P. Reprkpattanapitat, N. Wongpraparut, P. Pathi, M.N. Kotler, L.E. Jacobs, S. Yazdanfar
Journal: Journal of the American College of Cardiology (1998)
Is research into ethnicity and health racist, unsound, or important science?
Authors: R. Bhopal
Journal: BMJ (1997)

From January to October 2015, U.S. brands published 35 million posts across Facebook, Twitter, and Instagram, sparking 65 billion actions with social audiences (<i>i.e.</i>, comments, shares, re-Tweets, etc.). Yet just 7 percent of these actions involved sharing of a brand9s content.<sup>1</sup> Despite what is increasingly recognized as the value of shared content for building brand equity, to the author9s knowledge there has been scant study on what actually makes content shareable and the psychological drivers that prompt sharing. Replicating an earlier framework that outlined ways to increase virality of content, the author tracked the 2,000 most-shared social posts over a 12-month period on Facebook and then surveyed more than 10,000 social-media users about what might drive them to share that content online.
The Mallory-Weiss Syndrome
Authors: D. J. B. St. John, J. P. Masterton, N. D. Yeomans, H. A. F. Dudley
Journal: BMJ (1974)

A policy of immediate investigation of patients with haematemesis or melaena or both led to the diagnosis of the Mallory-Weiss syndrome in 16 out of 121 patients admitted to a combined medical-surgical unit over three and a half years. A typical history suggestive of the diagnosis was obtainable in only nine of the 16 patients, though recent alcohol intake was high in another four. All patients survived the episode. Establishment of the diagnosis by oesophagogastroscopy was of special benefit when surgery was needed for control of continuing blood loss, but it also simplified the subsequent medical management of those patients in whom bleeding stopped spontaneously. The incidence of 13.2% in this series suggests that the Mallory-Weiss syndrome may be a relatively common cause of upper gastrointestinal bleeding.
Direct Exposure of Mouse Ovaries and Oocytes to High Doses of an Adenovirus Gene Therapy Vector Fails to Lead to Germ Cell Transduction
Authors: Jon W. Gordon
Journal: Molecular Therapy (2001)

The risk of insertion of adenovirus gene therapy DNA into female germ cells during the course of somatic gene therapy was stringently tested in the mouse by injecting up to 1010 infectious particles directly into the ovary and by incubating naked oocytes in a solution of 2 × 108 particles/ml for 1 h prior to in vitro fertilization (IVF). The vector used was a recombinant adenovirus carrying the bacterial lacZ gene driven by the cytomegalovirus promoter (Adβ-gal). Ovaries were stained for LacZ activity, or immunochemically for LacZ, 5–7 days after injection. Although very large amounts of LacZ activity and protein were detected, all positive staining was in the thecal portion of the ovary, with no staining seen in oocytes. In another series of experiments, mice with injected ovaries were mated, and preimplantation embryos or fetuses were analyzed either for LacZ expression or by PCR for lacZ DNA. None of 202 preimplantation embryos stained positively for LacZ and none of 58 fetuses were positive for DNA by PCR analysis. Finally, more than 1400 eggs were fertilized after exposure to the vector prior to IVF and stained as morulae for LacZ activity. Fewer than 2% of the embryos stained positively for LacZ, and experiments indicated that the staining was due to incomplete washing of the eggs prior to IVF. These data provide strong evidence that adenoviruses cannot infect oocytes and that the risk of female germ-line transduction with such vectors is very low.
Effect of Oestrogens on Myometrial Contractions
Authors: A. I. Klopper, K. J. Dennis
Journal: BMJ (1962)

Some observations by Jeffcoate (1938) originally suggested that oestrogens stimulated uterine contractions in women who developed secondary inertia during labour.From this the belief grew among some British obstetricians that the exhibition of oestrogens would in some way facilitate the onset of labour.In connexion with a survey of perinatal mortality undertaken by the National Birthday Trust we recently had the opportunity to examine a sample of obstetric records from all over the country.It was evident that the practice of giving oestrogens, either as a form of medical induction or as a preliminary to surgical induction, is widespread.It is unlikely that oestrogens will of themselves cause the onset of labour, but there is some evidence to suggest that they may increase uterine contractility, making the muscle more responsive to mechanical stimuli such as rupture of the membranes (Reynolds, 1949).The work of Csapo (1956) shows that during pregnancy progesterone reduces myometrial contrac- tility.Short and Moore (1959) have shown that at the onset of labour there is no fall in blood progesterone, nor according to Shearman (1959) does the output of urinary pregnanediol decline in the weeks before the onset of labour.It is possible that toward the end of pregnancy some endocrine factor which overcomes the progesterone block on myometrial contractility comes into play.During pregnancy large amounts of oestriol are excreted, and in a recent study it was shown that a sharp rise in oestriol excretion occurs toward the end of pregnancy (Klopper et al., 1961).It seemed possible,
Acceptability of a modular, community-informed disaster risk reduction training programme in Delmas, Haiti
Authors: Janet Lin, Alyssa Budoff, Ashley Dyer
Journal: The Lancet Global Health (2014)

BackgroundHaiti experienced an Earthquake that killed 230 000 and injured 300 000 people. National disaster plans were developed; however, little is known about how to translate national policies to the community. The aim of this study was to examine the acceptability of a modular Disaster Risk Reduction (DRR) curriculum implemented with community leaders.MethodsIn 2012, a disaster preparedness community assessment (N=144 households) and key informant interviews were held. In 2013, DRR activities were piloted and outcomes informed curriculum development, which consisted of three content domains: definition of hazards, risks, and vulnerabilities; identification of protective factors and community assets; and development of community engagement strategies to assess, mitigate, and manage environmental threats. Participants were identified during the pilot study as those interested in taking a leadership role. A pre-test and post-test research design was used to assess knowledge acquisition, and questionnaires were administered to determine acceptability of methods.FindingsParticipants (n=16) showed improved ability in defining disaster terms: hazards (pre-test 0; post-test 11; 68% improvement), disaster (2; 10; 50%), vulnerability (7; 14; 44%), and risk (8; 12; 25%). 81·25% of participants correctly identified community assets; 100% proposed strategies for engaging others in DRR activities. Participants found the training acceptable and beneficial: 93·75% enjoyed training activities; 100% found the topics relevant and useful; and 81·25% felt comfortable sharing activities with others.InterpretationCommunity-based activities are acceptable methods for developing local capacity to mitigate risk to future hazards and disasters. A modular format supports the ability of the curriculum to be adapted and applied in other communities in Haiti.FundingThe Douglass Passaro Global Horizons Scholarship.
Check Your References
Authors: B. Leggett
Journal: BMJ (1945)

<h3>Abstract</h3> Epigenetic variation can alter transcription and promote phenotypic divergence between populations facing different environmental challenges. Here we assess the epigenetic basis of diversification during the early stages of speciation. We focus on the extent and functional relevance of DNA methylome divergence between two <i>Astatotilapia calliptera</i> ecomorphs in crater Lake Masoko, southern Tanzania. We report extensive genome-wide methylome divergence between populations linked to key biological processes, including transcriptional activity of ecologically-relevant genes. These include genes involved in steroid metabolism, haemoglobin composition and erythropoiesis, consistent with divergent habitat occupancy of the ecomorphs. Using a common garden experiment, we found that global methylation profiles are rapidly remodelled across generations, but ecomorph-specific differences can be inherited. Collectively, our study suggests an epigenetic contribution to early stages of vertebrate speciation. <h3>One sentence summary</h3> Inheritance and plasticity of epigenetic divergence characterise early stages of speciation in an incipient cichlid species of an African crater lake.
Characterization of large rearrangements in autosomal dominant polycystic kidney disease and the PKD1/TSC2 contiguous gene syndrome
Authors: Mark B. Consugar, Wai C. Wong, Patrick A. Lundquist, Sandro Rossetti, Vickie J. Kubly, Denise L. Walker, Laureano J. Rangel, Richard Aspinwall, W. Patrick Niaudet, Seza Özen, Albert David, Milen Velinov, Eric J. Bergstralh, Kyongtae T. Bae, Arlene B. Chapman, Lisa M. Guay-Woodford, Jared J. Grantham, Vicente E. Torres, Julian R. Sampson, Brian D. Dawson, Peter C. Harris, None for the CRISP Consortium
Journal: Kidney International (2008)
Abstract 179: Impact of diet-induced obesity on inflamatory pathways during prostate cancer progression in Hi-Myc mice.
Authors: Jorge M. Blando, Kaoru Kiguchi, Irina Fernandez, John DiGiovanni
Journal: Cancer Research (2013)

Abstract We have previously reported that diet induced obesity (DIO) enhanced prostate cancer progression and associated inflammation in the ventral prostate of the Hi-Myc mice (Blando et al, CAPR, 2011). Here, we further investigated changes in inflammatory genes as well as cellular changes associated with DIO effects on prostate cancer progression in the Hi-myc mouse model. Initial studies were conducted to look at specific cell populations that are present in the ventral prostate (VP) of Hi-Myc mice on the 30% CR, overweight control (AIN76A) and DIO diets (60 Kcal% fat). Staining for perilipin revealed that adipocytes were restricted to the periphery of the VP of Hi-Myc mice on the 30% CR diet. In contrast, adipocytes could be seen infiltrating the VP of Hi-Myc mice on the overweight control diet and especially in mice on the DIO diet. In this regard, many of the glands in the VP were completely surrounded by adipocytes. Double IF staining was performed for both perilipin and CD3 (T-lymphocytes) or perilipin and RM0029-11H3 (macrophages). Few if any inflammatory cells were seen in VP of Hi-Myc mice on the 30% CR diet. In contrast, adipocytes and inflammatory cells (both T-cells and macrophages) were seen in close proximity to adipocytes that had infiltrated into the VP in the overweight control group and this was particularly prominent in the DIO diet group. Aditionally, staining for B-cells also showed an increased number in the DIO groups as compared to the control and CR diet groups. Sections of VP from Hi-Myc mice on the different diets were also stained for both the IL-23 receptor (IL-23R) and Cox-2. IL-23R expression was dramatically upregulated in the epithelial cells of the VP from Hi-Myc mice on the DIO compared to the other diet groups. Cox-2 expression was also dramatically upregulated in VP of Hi-Myc on the DIO diet. This finding is consistent with the high level of NFκB activation seen in prostate tissues for the same mice and diet group. The VP from mice on DIO diets also showed an increase in the staining of tissue specific cancer stem cell (CSC) markers (SCA-1 and CD49f) when compared to VP from mice on the overweight control and 30% CR diets. In summary, changes in the levels of IL-23R and COX-2 and the increased presence of inflammatory cells together with changes in the adipose tissue, suggest that the tumor microenvironment may play an important role in DIO effects on prostate cancer progression in Hi-Myc mice. Citation Format: Jorge M. Blando, Kaoru Kiguchi, Irina Fernandez, John DiGiovanni. Impact of diet-induced obesity on inflamatory pathways during prostate cancer progression in Hi-Myc mice. [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 179. doi:10.1158/1538-7445.AM2013-179
Why We Should Ban Human Cloning
Authors: G J Annas
Journal: New England Journal of Medicine (1998)

In February the U.S. Senate voted 54 to 42 against bringing an anticloning bill directly to the floor for a vote.1 During the debate, more than 16 scientific and medical organizations, including the American Society of Reproductive Medicine and the Federation of American Societies for Experimental Biology, and 27 Nobel prize–winning scientists, agreed that there should be a moratorium on the creation of a human being by somatic nuclear transplants. What the groups objected to was legislation that went beyond this prohibition to include cloning human cells, genes, and tissues. An alternative proposal was introduced by Senator Edward M. Kennedy . . .
Abstract C11: Molecular mechanism driving BMI1-induced melanoma metastasis
Authors: Roberta Ferretti, Jacqueline A. Lees
Journal: Cancer Research (2013)

Abstract Malignant melanoma is one of the most aggressive human cancers, with a high potential for lethal metastasis and therapeutic resistance. The epigenetic chromatin regulator Bmi1 acts as a key component of the Polycomb Repressor Complex 1 (PRC1) and is a known oncogene. Various studies shown that BMI1 is highly expressed in many human hematopoietic malignancies and in different solid tumor types including prostate, breast, ovarian, colon, brain and lung cancer. Importantly, high Bmi1 expression is an excellent predictor of both metastatic progression and poor therapeutic response. Bmi1's role in tumor onset has been assessed using germline mutant mice showing that Bmi1 ablation efficiently suppress tumor development. This impaired tumorigenicity correlates with an impairment of the self-renewal and proliferative properties of tumor initiating cells, mainly due to Bmi1's repressive activity on the Ink4a/Arf tumor suppressor locus. Nevertheless, this function does not explain why Bmi1 is frequently upregulated in tumors nor Bmi1's role in tumor progression. To evaluate Bmi1's contribution to melanoma progression, we upregulated Bmi1 in two different melanoma cell lines, a murine metastatic cell line and a poorly metastatic human cell line. We found that Bmi1 overexpression activates or increases invasive behavior of both cell lines, without enhancing their proliferative capacity. This finding allowed us to dissect Bmi1's oncogenic activity at later stages of tumorigenesis, in the absence of Bmi1's deregulation of cell proliferation. Our data show that Bmi1 significantly enhances in vitro cell movement and modulates adhesion. Bmi1 also protects cells from apoptosis induced by different stimuli and increases lung metastasis formation in vivo. To characterize Bmi1-induced changes in gene expression, we have performed comparative deep sequencing of total RNA libraries generated from Bmi1 or GFP overexpressing cells. Gene ontology analysis revealed enrichment in cancer-relevant pathways that seem to be controlled by Bmi1, including cell movement, cell death and survival, tissue development and cell morphology. In particular, Bmi1 expression modulates the gene regulatory programs associated with EMT, TGFβ and the non-canonical Wnt pathways. We have identified a new Bmi1 target gene, poorly characterized, that seems to be responsible for Bmi1-induced melanoma progression. These data determine a causal role for Bmi1 in melanoma cell migration and establishment of distant melanoma metastasis. Citation Format: Roberta Ferretti, Jacqueline A. Lees. Molecular mechanism driving BMI1-induced melanoma metastasis. [abstract]. In: Proceedings of the Third AACR International Conference on Frontiers in Basic Cancer Research; Sep 18-22, 2013; National Harbor, MD. Philadelphia (PA): AACR; Cancer Res 2013;73(19 Suppl):Abstract nr C11.
Prevalence Rates of Uterine Cervical Carcinoma in situ for Women Using the Diaphragm or Contraceptive Oral Steroids
Authors: M. R. Melamed, L. G. Koss, B. J. Flehinger, R. P. Kelisky, H. Dubrow
Journal: BMJ (1969)

Study of the prevalence rates of uterine cervical carcinoma in situ among women attending centres of Planned Parenthood of New York City, Inc., showed a small but statistically significant difference between the population choosing and using the diaphragm and the population choosing and using oral steroids for contraception. This can be attributed either to a decreased prevalence rate for women using the diaphragm or to an increased rate for women using oral steroids. The reason for the difference is not apparent from these data.
Decitabine priming enhances the antileukemic effects of exportin 1 (XPO1) selective inhibitor selinexor in acute myeloid leukemia
Authors: Parvathi Ranganathan, Xueyan Yu, Ramasamy Santhanam, Jessica Hofstetter, Alison Walker, Katherine Walsh, Bhavana Bhatnagar, Rebecca Klisovic, Sumithira Vasu, Mitch A. Phelps, Steven Devine, Sharon Shacham, Michael Kauffman, Guido Marcucci, William Blum, Ramiro Garzon
Journal: Blood (2015)
Effects of an enteric anaerobic bacterial culture supernatant and deoxycholate on intestinal calcium absorption and disaccharidase activity.
Authors: K Walshe, M J Healy, A B Speekenbrink, C T Keane, D G Weir, R R O'Moore
Journal: Gut (1990)

Fifty two strains of anaerobic bacteria isolated from the upper gut of patients with small intestinal bacterial overgrowth were screened for phospholipase activity. Bacteroides melaninogenicus spp intermedius had the greatest activity. The effects of culture supernatants of this organism and deoxycholate on intestinal calcium absorption and disaccharidase activity were studied using a rat closed loop model. The supernatant decreased the in vitro uptake of calcium by 15% (p less than 0.001). Deoxycholate reduced calcium uptake by 16% (p less than 0.001). Combined culture supernatant and deoxycholate reduced calcium uptake by 39% (p less than 0.001) suggesting a potentiation of supernatant activity by deoxycholate. Culture supernatant and deoxycholate, both alone and combined, significantly reduced lactase, sucrase, and maltase activity. Electron microscopic evidence showed degeneration of microvilli, disruption of mitochondrial structure, and swelling of the endoplasmic reticulum after exposure of the intestinal loops to the supernatant or deoxycholate.
Changing Diagnosis Codes
Authors: Paul H. Farseth
Journal: New England Journal of Medicine (1978)

Standard Disease ClassificationsData on diseases, disabilities and causes of death are commonly indexed and analyzed by use of standard norms for classification and coding. This process allows comparison of data collected by different researchers and the sharing of raw data from one epidemiologic or health-services investigation to another. The use of codes as short tags for more elaborate narrative descriptions of diseases simplifies the recording and storage of data and allows it to be manipulated in computers.The standard guide to classifying and coding diseases and other medical conditions is the International Classification of Diseases (ICD), published by . . .
Structural Molecular Components of Septate Junctions in Cnidarians Point to the Origin of Epithelial Junctions in Eukaryotes
Authors: Philippe Ganot, Didier Zoccola, Eric Tambutté, Christian R Voolstra, Manuel Aranda, Denis Allemand, Sylvie Tambutté
Journal: Molecular Biology and Evolution (2014)

Septate junctions (SJs) insure barrier properties and control paracellular diffusion of solutes across epithelia in invertebrates. However, the origin and evolution of their molecular constituents in Metazoa have not been firmly established. Here, we investigated the genomes of early branching metazoan representatives to reconstruct the phylogeny of the molecular components of SJs. Although Claudins and SJ cytoplasmic adaptor components appeared successively throughout metazoan evolution, the structural components of SJs arose at the time of Placozoa/Cnidaria/Bilateria radiation. We also show that in the scleractinian coral Stylophora pistillata, the structural SJ component Neurexin IV colocalizes with the cortical actin network at the apical border of the cells, at the place of SJs. We propose a model for SJ components in Cnidaria. Moreover, our study reveals an unanticipated diversity of SJ structural component variants in cnidarians. This diversity correlates with gene-specific expression in calcifying and noncalcifying tissues, suggesting specific paracellular pathways across the cell layers of these diploblastic animals.
Expression of the leukemia oncogene Lmo2 is controlled by an array of tissue-specific elements dispersed over 100 kb and bound by Tal1/Lmo2, Ets, and Gata factors
Authors: Josette-Renée Landry, Nicolas Bonadies, Sarah Kinston, Kathy Knezevic, Nicola K. Wilson, S. Helen Oram, Mary Janes, Sandie Piltz, Michelle Hammett, Jacinta Carter, Tina Hamilton, Ian J. Donaldson, Georges Lacaud, Jonathan Frampton, George Follows, Valerie Kouskoff, Berthold Göttgens
Journal: Blood (2009)