tbuckley/cabot-search huggingface dataset:
Ureaplasma urealyticum colonization, prematurity and bronchopulmonary dysplasia
Authors: WM van Waarde, F Brus, A Okken, JL Kimpen
Journal: European Respiratory Journal (1997)

The aim of the present study was to determine the association between the presence of Ureaplasma urealyticum in endotracheal aspirates and bronchopulmonary dysplasia (BPD). In addition, a review of similar studies from the English literature is presented. During the period February 1990 until March 1991, 108 mechanically-ventilated infants were included in a prospective study. Endotracheal aspirates were cultured for U. urealyticum. Birth weight, gestational age and development of BPD was recorded. Cultures were positive in 23 infants, resulting in a 21% colonization. The infants with positive cultures had a significantly lower gestational age (mean 28.9 vs 31.5 weeks; range 25-40 vs 25-42 weeks; p=0.0014). A positive U. urealyticum culture was not associated with a low birth weight (mean 1,390 vs 1,690 g; range 675-4,090 vs 700-3,600 g; p=0.0712). A positive U. urealyticum culture was significantly associated with BPD (p=0.0373). However, after correction for gestational age by logistic regression analysis, BPD failed to correlate with the presence of positive U. urealyticum cultures. A MEDLINE search of the English language literature was performed to identify all studies having the association of U. urealyticum colonization and BPD. Fourteen controlled studies were found. Five studies found no significant association between U. urealyticum colonization and BPD. In two studies, after correction for gestational age, the association between U. urealyticum colonization and BPD did not remain significant. In five studies with a significant association between U. urealyticum colonization and BPD, no correction for gestational age had taken place. In conclusion, U. urealyticum colonization is not associated with the development of bronchopulmonary dysplasia. U. urealyticum is often associated with gestational age and/or low birth weight; to investigate the association between U. urealyticum and bronchopulmonary dysplasia correction for both parameters should be made.
THE EARLY DIAGNOSIS OF CANCER OF THE STOMACH BY MEANS OF GASTRIC ANALYSIS
Authors: T. I. Bennett
Journal: BMJ (1923)

rTMHE:A&ML 275 gastrogenous diarrhoea, only a few cubic centimetres of mucoid juice like white of egg might be obtained.The presence of blood in leucocytes in ellronic gastritis, and food debris in pyloric growth obstruction, afforded further useful information.The rate of emptying might be very accurately ascertained by the fractional method, and was closely comparable with the rate of emptying as estimated radiographically.The amount of the supernatant fluid and the regurgitation of bile in subsequent specimens were further simple macroscopic observ-ations of contributory importance.The fractional test meal could really be regarded as a diagnostic test ini one condition, and that was pyloric obstruction.In this condition it might give definite evidence as to the cause of the obstruction.Nevertheless as a gastric efficiency test it was of distinct value in duodenal ulcer, Addison's anaemia, and chronic gastrogenious diarrhoea.In other reflex dyspepsias, due to disease of the gall bladder and appendix, hyperchlorhydria 'and achlorhydria both occurred more fre- quently than in normal series, and probably depended respectively on reflex pyloric hypertonus and chroniie infec- tion in the upper gastro-intestinal tract.It should be clearly understood that the fractionial test meal was a rough test and that it could only be regarded as accessory to careful clinical investigations.With these provisos it was a test of real utility.-Dr.IZOD BENNETT made remarks which are embodied in the paper printed below.
Death, where is thy sting?
Authors: L. Farrell
Journal: BMJ (2003)

I'm an old fashioned general practitioner; Dr Finlay and I would have got on famously, gone out drinking together, maybe clubbing in Ibiza, etc. I still enjoy home visits, and value the precious insights gained from enjoying cups of tea and big slices of home made apple pie in the kitchen with Granny Arbuckle, before drinking quarts of cider and sneaking off for a quick shag with her buxom niece Sally amid the fields of barley (OK, I made …
Personal genome testing in medical education: student experiences with genotyping in the classroom
Authors: Simone Lucia Vernez, Keyan Salari, Kelly E Ormond, Sandra Soo-Jin Lee
Journal: Genome Medicine (2013)

Direct-to-consumer (DTC) personal genotyping services are beginning to be adopted by educational institutions as pedagogical tools for learning about human genetics. However, there is little known about student reactions to such testing. This study investigated student experiences and attitudes towards DTC personal genome testing.Individual interviews were conducted with students who chose to undergo personal genotyping in the context of an elective genetics course. Ten medical and graduate students were interviewed before genotyping occurred, and at 2 weeks and 6 months after receiving their genotype results. Qualitative analysis of interview transcripts assessed the expectations and experiences of students who underwent personal genotyping, how they interpreted and applied their results; how the testing affected the quality of their learning during the course, and what were their perceived needs for support.Students stated that personal genotyping enhanced their engagement with the course content. Although students expressed skepticism over the clinical utility of some test results, they expressed significant enthusiasm immediately after receiving their personal genetic analysis, and were particularly interested in results such as drug response and carrier testing. However, few reported making behavioral changes or following up on specific results through a healthcare provider. Students did not report utilizing genetic counseling, despite feeling strongly that the 'general public' would need these services. In follow-up interviews, students exhibited poor recall on details of the consent and biobanking agreements, but expressed little regret over their decision to undergo genotyping. Students reported mining their raw genetic data, and conveyed a need for further consultation support in their exploration of genetic variants.Personal genotyping may improve students' self-reported motivation and engagement with course material. However, consultative support that is different from traditional genetic counseling will be necessary to support students. Before incorporating personal genotyping into coursework, institutions should lead multi-disciplinary discussion to anticipate issues and incorporate teaching mechanisms that engage the ethical, legal, and social implications of personal genotyping, including addressing those found in this study, to go beyond what is offered by commercial providers.
Piroxicam and Cisplatin in a Mouse Model of Peritoneal Mesothelioma
Authors: Enrico P. Spugnini, Irene Cardillo, Alessandra Verdina, Stefania Crispi, Silvia Saviozzi, Raffaele Calogero, Angela Nebbioso, Lucia Altucci, Giancarlo Cortese, Rossella Galati, Jeremy Chien, Viji Shridhar, Bruno Vincenzi, Gennaro Citro, Francesco Cognetti, Ada Sacchi, Alfonso Baldi
Journal: Clinical Cancer Research (2006)

Abstract Purpose: The aim of the present study was to evaluate the effects of piroxicam, a widely used nonsteroidal anti-inflammatory drug, alone and in combination with cisplatin (CDDP), on cell growth of mesothelioma cells. Experimental Design: Cell proliferation, cell cycle analysis, and microarray technology were done on MSTO-211H and NCI-H2452 cells treated with piroxicam. Moreover, the effects of piroxicam and CDDP on tumor growth and survival of mouse xenograft models of mesothelioma were determined. Results: Piroxicam treatment of MSTO-211H and NCI-H2452 cells resulted in a significant inhibition of proliferation. Cell cycle analysis revealed that there was an increase in the rate of apoptosis in MSTO-211H cells and an increase in the cells accumulating in G2-M in NCI-H2452. Moreover, a marked tumor growth inhibition and an extended survival of mice treated with a combination of piroxicam and CDDP in MSTO-211H cell–induced peritoneal mesotheliomas was observed. Last, GeneChip array analysis of MSTO-211H mesothelioma cell line revealed that piroxicam treatment caused up-regulation of metabolic pathway–associated genes and down-regulation of genes related to RNA processing apparatus. Of note, epidermal growth factor receptor, one of the new biological targets of chemotherapy for mesothelioma, was down-regulated and HtrA1, a serine protease recently shown to be an endogenous mediator of CDDP cytotoxicity, was up-regulated following piroxicam treatment both in vitro and in vivo. Conclusion: These data suggest that piroxicam sensitizes mesothelioma cells to CDDP-induced cytotoxicity by modulating the expression of several target genes. Therefore, piroxicam in combination with CDDP might potentially be useful in the treatment of patients with mesothelioma.
Duration of the Inhibition of Histamine- and Allergen-Induced Wheal-and-Flare Responses After Discontinuation of Desloratadine and Levocetirizine
Authors: P DEVILLIER, I DREYFUS, N SAUVAGE, K MESBAH, J COUGNARD, S ROUANET, S GELUMANTOULET, A RIMAILHO
Journal: Journal of Allergy and Clinical Immunology (2008)
Identification of a human TFPI-2 splice variant that is upregulated in human tumor tissues
Authors: Prakasha Kempaiah, Hitendra S Chand, Walter Kisiel
Journal: Molecular Cancer (2007)

Abstract Background Previous studies have shown that the expression of tissue factor pathway inhibitor-2 (TFPI-2), a matrix-associated Kunitz-type serine proteinase inhibitor, is markedly down-regulated in several tumor cells through hypermethylation of the TFPI-2 gene promoter. In the present study, RT-PCR analysis of total RNA from both human normal and tumor cells revealed a novel 289 nucleotide splice variant of the TFPI-2 transcript designated as aberrantly-spliced TFPI-2 (asTFPI-2). Results Nucleotide sequence analyses indicated that asTFPI-2 consists of complete exons II and V, fused with several nucleotides derived from exons III and IV, as well as six nucleotides derived from intron C. 5'- and 3'-RACE analyses of total RNA amplified exclusively the wild-type TFPI-2 transcript, indicating that asTFPI-2 lacks either a 5'-untranslated region (UTR) or a 3'-poly (A) + tail. Quantitative real-time RT-PCR analyses revealed that several human tumor cells contain 4 to 50-fold more copies of asTFPI-2 in comparison to normal cells. In spite of the absence of a 5'-UTR or poly (A) + tail, the asTFPI-2 variant exhibited a half-life of ~16 h in tumor cells. Conclusion Our studies reveal the existence of a novel, aberrantly-spliced TFPI-2 transcript predominantly expressed in tumor cells and provides suggestive evidence for an additional mechanism for tumor cells to down-regulate TFPI-2 protein expression enhancing their ability to degrade the extracellular matrix.
The Thr300Ala variant in ATG16L1 is associated with improved survival in human colorectal cancer and enhanced production of type I interferon
Authors: Wesley A Grimm, Jeannette S Messer, Stephen F Murphy, Thomas Nero, James P Lodolce, Christopher R Weber, Mark F Logsdon, Sarah Bartulis, Brooke E Sylvester, Amanda Springer, Urszula Dougherty, Timothy B Niewold, Sonia S Kupfer, Nathan Ellis, Dezheng Huo, Marc Bissonnette, David L Boone
Journal: Gut (2015)

<h3>Objective</h3> ATG16L1 is an autophagy gene known to control host immune responses to viruses and bacteria. Recently, a non-synonymous single-nucleotide polymorphism in ATG16L1 (Thr300Ala), previously identified as a risk factor in Crohn9s disease (CD), was associated with more favourable clinical outcomes in thyroid cancer. Mechanisms underlying this observation have not been proposed, nor is it clear whether an association between Thr300Ala and clinical outcomes will be observed in other cancers. We hypothesised that Thr300Ala influences clinical outcome in human colorectal cancer (CRC) and controls innate antiviral pathways in colon cancer cells. <h3>Design</h3> We genotyped 460 patients with CRC and assessed for an association between ATG16L1 Thr300Ala and overall survival and clinical stage. Human CRC cell lines were targeted by homologous recombination to examine the functional consequence of loss of ATG16L1, or introduction of the Thr300Ala variant. <h3>Results</h3> We found an association between longer overall survival, reduced metastasis and the ATG16L1 Ala/Ala genotype. Tumour sections from ATG16L1 Ala/Ala patients expressed elevated type I interferons (IFN-I)-inducible, MxA, suggesting that differences in cytokine production may influence disease progression. When introduced into human CRC cells by homologous recombination, the Thr300Ala variant did not affect bulk autophagy, but increased basal production of type I IFN. Introduction of Thr300Ala resulted in increased sensitivity to the dsRNA mimic poly(I:C) through a mitochondrial antiviral signalling (MAVS)-dependent pathway. <h3>Conclusions</h3> The CD-risk allele, Thr300Ala, in ATG16L1 is associated with improved overall survival in human CRC, generating a rationale to genotype ATG16L1 Thr300Ala in patients with CRC. We found that Thr300A alters production of MAVS-dependent type I IFN in CRC cells, providing a mechanism that may influence clinical outcomes.
Postmortem survey of diverticular disease of the colon. II. The muscular abnormality of the sigmoid colon.
Authors: L E Hughes
Journal: Gut (1969)

The relationship of bowel symptoms to diverti- cular disease.To be published.(1969c).The muscle abnormality of diverticular disease of the sigmoid colon.A functional study using the polysiloxane foam enema.To be published.
TR-01 * Ezh2, A NOVEL TARGET IN TREATMENT OF MEDULLOBLASTOMA
Authors: B. Ricke, K. Shah, M. Salacz, P. Camarata, D. Lovick, W. Peng, R. Dolatkhah, Z. Sanaat, K. Kimura, D. Bi, S. Taylor, T. Esfandyari, F. Farassati
Journal: Neuro-Oncology (2015)

Ezh2(enhancer of zeste homolog 2) is a member of the Polycomb-group (PcG) family. PcG family members form multimeric protein complexes that act as suppressors of the transcriptional state of genes over successive cell generations. Ezh2 acts mainly as a gene expression suppressor as it performs this role by the addition of three methyl groups to Lysine 27 of histone 3, a modification leading to chromatin condensation. Ezh2 is overexpressed in a number of human malignancies and its overproduction causes cancer due to silencing the expression of tumor suppressor genes. Overexpression of Ezh2 in medulloblastomas (MDB) has been shown in a number of studies while inhibition of its expression results in loss of viability cancer cells. Therefore targeting Ezh2+ MDB cells has the potential to result in a significant tumor regression. We have developed the first prototype of a mutated Herpes Simplex Virus-1, which is programmed to specifically replicate in cells that overexpress Ezh2 such as MDB cells resulting in their destruction. This oncolytic virus is called as “Signal-Smart 3 or SS3” virus. Normal tissues are not affected by this virus because of low or minimal expression of Ezh2. Oncolytic viruses are a novel family of anti-cancer agents capable of targeting cancer cells in a specific manner with different mechanisms. Many older members of this family are now in advanced phases of clinical trials. In this presentation, we explain our data about the effects of SS3 virus on the viability and tumorigenesis of MDB cells in-vitro and in-vivo.
Adenovirus-mediated In Utero Expression of CFTR Does Not Improve Survival of CFTR Knockout Mice
Authors: Lee A Davies, Anusha Varathalingam, Hazel Painter, Anna E Lawton, Stephanie G Sumner-Jones, Graciela A Nunez-Alonso, Mario Chan, Felix Munkonge, Eric WFW Alton, Stephen C Hyde, Deborah R Gill
Journal: Molecular Therapy (2008)

Gene therapy is being investigated in the treatment of lung-related aspects of the genetic disease, Cystic fibrosis (CF). Clinical studies have demonstrated CF transmembrane conductance regulator (CFTR) expression in the airways of adults with CF using a variety of gene transfer agents. In utero gene therapy is an alternative approach that facilitates vector transduction of rapidly expanding populations of target cells while avoiding immune recognition of the vector. In CF, in utero gene transfer could potentially delay the onset of disease symptoms in childhood and compensate for the role, if any, that CFTR plays in the developing organs. Previously published studies have suggested that transient expression of CFTR in utero was sufficient to rescue the fatal intestinal defect in S489X Cftr(tm1Unc)/Cftr(tm1Unc) knockout mice. We replicated these studies using an identical CFTR-expressing adenoviral vector and CF mouse strain in sufficiently large numbers to provide robust Kaplan-Meier survival data. Although each step of the procedure was carefully controlled and vector-specific CFTR expression was confirmed in the fetal organs after treatment, there was statistically no significant improvement in the survival of mice treated in utero with AdCFTR, compared with contemporaneous control animals.
Pulsatile flow in pulmonary artery, capillary, and vein in the dog
Authors: W. G. GUNTHEROTH, R. GOULD, J. BUTLER, E. KINNEN
Journal: Cardiovascular Research (1974)

Journal Article Pulsatile flow in pulmonary artery, capillary, and vein in the dog Get access WARREN G. GUNTHEROTH, WARREN G. GUNTHEROTH From the Departments of Pediatrics and Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar RICHARD GOULD, RICHARD GOULD From the Departments of Pediatrics and Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar JOHN BUTLER, JOHN BUTLER From the Departments of Pediatrics and Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar EDWIN KINNEN EDWIN KINNEN 2 From the Departments of Pediatrics and Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA 2Present address: Department of Electrical Engineering, University of Rochester, Rochester, New York. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 8, Issue 3, May 1974, Pages 330–337, https://doi.org/10.1093/cvr/8.3.330 Published: 01 May 1974
A Prospective Study of the Efficacy of Influenza Vaccination for Cancer Patients Receiving Chemotherapy
Authors: Yukinari Sanada, Kimikazu Yakushijin, Katsuya Yamamoto, Meiko Nishimura, Yohei Funakoshi, Naoko Chayahara, Masanori Toyoda, Naomi Kiyota, Toru Mukohara, Hironobu Minami
Journal: Annals of Oncology (2014)
<i>Tbx1</i> Regulates Proliferation and Differentiation of Multipotent Heart Progenitors
Authors: Li Chen, Filomena Gabriella Fulcoli, Susan Tang, Antonio Baldini
Journal: Circulation Research (2009)

Rationale : TBX1 encodes a T-box transcription factor implicated in DiGeorge syndrome, which affects the development of many organs, including the heart. Loss of Tbx1 results into hypoplasia of heart regions derived from the second heart field, a population of cardiac progenitors cells (CPCs). Thus, we hypothesized that Tbx1 is an important player in the biology of CPCs. Objective : We asked whether Tbx1 is expressed in multipotent CPCs and, if so, what role it may play in them. Methods and Results : We used clonal analysis of Tbx1 -expressing cells and loss and gain of function models, in vivo and in vitro, to define the role of Tbx1 in CPCs. We found that Tbx1 is expressed in multipotent heart progenitors that, in clonal assays, can give rise to 3 heart lineages expressing endothelial, smooth muscle and cardiomyocyte markers. In multipotent cells, Tbx1 stimulates proliferation, explaining why Tbx1 −/− embryos have reduced proliferation in the second heart field. In this population, Tbx1 is expressed while cells are undifferentiated and it disappears with the onset of muscle markers. Loss of Tbx1 results in premature differentiation, whereas gain results in reduced differentiation in vivo. We found that Tbx1 binds serum response factor, a master regulator of muscle differentiation, and negatively regulates its level. Conclusions : The Tbx1 protein marks CPCs, supports their proliferation, and inhibits their differentiation. We propose that Tbx1 is a key regulator of CPC homeostasis as it modulates positively their proliferation and negatively their differentiation.
Inhibition of tumour necrosis factor and IL-17 production by leflunomide involves the JAK/STAT pathway
Authors: I Gonzalez-Alvaro, A M Ortiz, C Dominguez-Jimenez, A Aragon-Bodi, B D. Sanchez, F Sanchez-Madrid
Journal: Annals of the Rheumatic Diseases (2008)

<h3>Objective:</h3> To study the effects of different disease-modifying antirheumatic drugs (DMARD) on different events mediated by IL-15-activated lymphocytes. <h3>Methods:</h3> Peripheral blood lymphocytes (PBL) were isolated from healthy donors and activated with IL-15 after exposure to different DMARD: leflunomide, cyclosporin A, methotrexate, mycophenolic acid, FK-506, sulphasalazine and sodium aurothiomalate. The expression of different surface molecules on the PBL was then determined by flow cytometry. Cells were also co-cultured with the monocytic cell line THP-1 and the tumour necrosis factor (TNF) concentration in the supernatant was measured after 24 h using an immunoenzyme assay. The effect of the aforementioned drugs on IL-17 production by IL-15-activated PBL was also studied. <h3>Results:</h3> Treatment of PBL with leflunomide, cyclosporin A and FK-506 inhibited the IL-15-induced expression of both CD54 and CD69 by PBL, as well as TNF production in co-cultures of activated PBL and THP-1 cells. The downregulation of CD54 and CD69 in PBL was correlated with the inhibition of TNF production. Likewise, leflunomide, cyclosporin A and FK-506 all inhibited IL-17 production in IL-15-activated PBL. Interestingly, the effect of leflunomide was not reverted by the presence of uridine in the medium. In addition, leflunomide inhibited the phosphorylation of STAT6 in vitro. <h3>Conclusion:</h3> Inhibition of the JAK/STAT pathway may represent an additional effect of leflunomide in chronic polyarthritis because it impairs certain events that control proinflammatory TNF and IL-17 cytokine production.
Perforin pores in the endosomal membrane trigger the release of endocytosed granzyme B into the cytosol of target cells
Authors: Jerome Thiery, Dennis Keefe, Steeve Boulant, Emmanuel Boucrot, Michael Walch, Denis Martinvalet, Ing Swie Goping, R Chris Bleackley, Tomas Kirchhausen, Judy Lieberman
Journal: Nature Immunology (2011)
Dietary modulation of peroxisome proliferator-activated receptor gamma
Authors: R Marion-Letellier, P Dechelotte, M Iacucci, S Ghosh
Journal: Gut (2008)

Peroxisome proliferator-activated receptor gamma (PPARγ) is a nuclear receptor that regulates intestinal inflammation. PPARγ is highly expressed in the colon and can be activated by various dietary ligands. A number of fatty acids such as polyunsaturated fatty acids or eicosanoids are considered as endogenous PPARγ activators. Nevertheless, other nutrients such as glutamine, spicy food or flavonoids are also able to activate PPARγ. As PPARγ plays a key role in bacterial induced inflammation, anti-inflammatory properties of probiotics may be mediated through PPARγ. The aims of the present review are to discuss of the potential roles of dietary compounds in modulating intestinal inflammation through PPARγ.