tbuckley/cabot-search huggingface dataset:
H pylori/Upper GI/Oesophagus Free Papers
Authors: M. Woodward, H. Tunstall-Pedoe, K.E.L. McColl
Journal: Gut (2001)

patients (8%), 6 in each group, having a normal QOL.Mean PIS score for the patients was 7.04 ± 0.1.53% of the UC patients and 75% of the CD patients (p=0.006) were considered well informed (ie.PIQ scores of 7 or more).The mean PIS for UC patients was 6.5 ± 0.4 vs 7.5 ± 0.2 for the CD group (p=0.001).There was however no correlation seen between the QOL and PIS scores, both for UC and CD patients (r=0.3). Conclusion:Most patients with IBD have impaired QOL, inspite of having inactive disease.The level of disease related knowledge appears to be better in patients with CD, though that does not seem to aVect QOL.
Abstract 482: Recurrent glioma with lineage conversion from oligodendroglioma to astrocytoma: Another facet of glioma evolution during recurrence
Authors: Kyung-Hwa Lee, Tae-Young Jung, Shin Jung, Jae-Hyuk Lee, Kyung-Keun Kim, Hangun Kim, Kyung-Sub Moon
Journal: Cancer Research (2019)

Abstract Background: Following the introduction of the molecular classification of gliomas by the WHO in 2016, molecularly-proven lineage conversion during glioma recurrence has never been reported. Methods: We analyzed two cases of recurrent glioma that began as oligodendroglioma, both histologically and molecularly, but converted to astrocytoma over episodes of recurrence. Results: The cases were initially diagnosed as oligodendroglioma with 1p/19q-codeletion and mutation of isocitrate dehydrogenase 1 (IDH1)-R132H. The recurrent tumors showed loss of alpha-thalassemia/mental retardation X-linked (ATRX) expression, strong P53 positivity, and 1p/19q-nondeletion. Next generation sequencing (NGS) analysis performed on the first case confirmed the transition of molecular traits from oligodendroglioma to astrocytoma. An IDH mutation of R132H was preserved in the episodes of recurrence, but ATRX and TP53 mutations were newly acquired and TERT promoter mutation C228T was lost at the most recent recurrence. Conclusions: The issue in question for the presented cases is whether the original tumors were pure oligodendrogliomas that then transdifferentiated into astrocytomas, or whether the original tumor was an oligoastrocytoma having oligodendroglioma cells that outnumbered the astrocytoma cells and where the astrocytoma cells becoming more dominant over the episodes of recurrence. With the recognition of the possibility of lineage conversion, our study suggests that molecular examination should be performed to adjust therapeutic strategies in recurrent gliomas. Indeed, our observation of lineage conversion in glioma recurrence calls into question the current distinction drawn between oligodendroglioma, astrocytoma and oligoastrocytoma, rather than simply bidding “farewell to oligoastrocytoma”. Citation Format: Kyung-Hwa Lee, Tae-Young Jung, Shin Jung, Jae-Hyuk Lee, Kyung-Keun Kim, Hangun Kim, Kyung-Sub Moon. Recurrent glioma with lineage conversion from oligodendroglioma to astrocytoma: Another facet of glioma evolution during recurrence [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 482.
CULTIVATION OF ADULT TISSUES AND ORGANS OUTSIDE OF THE BODY*
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
BOOK REVIEWS
Authors: D. R. BRILL
Journal: JNCI Journal of the National Cancer Institute (1988)

Journal Article BOOK REVIEWS Get access Low-Level Radioactive Waste Regulation: Science, Politics and Fear. Michael E. Burns, ed. chelsea, MI: Lewis Publishers, 1988, 311 pp. $39.00. DAVID R. BRILL DAVID R. BRILL Nuclear Medicine Section, Department of Special, Imaging-Radiology, Geisinger Medical CenterDanville, PA 17822 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 80, Issue 12, 17 August 1988, Pages 971–972, https://doi.org/10.1093/jnci/80.12.971-a Published: 17 August 1988
Casting Light on DIM
Journal: JAMA (1969)

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 5361: PDK1 Plays Crucial Roles in β-Adrenergic Response and Cell Survival in the Heart
Authors: Kaoru Ito, Hiroshi Akazawa, Noritaka Yasuda, Haruaki Nakaya, Issei Komuro
Journal: Circulation (2008)

Background: The 3-phosphoinositide-dependent protein kinase-1 (PDK1) plays a homeostatic role in the regulation of cellular function in multiple organs, by working downstream of phosphatidylinositol-3 kinase (PI3-K) through activating several kinases including Akt and p70 S6 kinase. We found that myocardial expression of PDK1 was decreased in murine models of heart failure. Although previous studies have reported that PDK1 is important for the regulation of cardiomyocyte size, the precise role of PDK1 in the heart remains to be fully characterized. Methods and Results: To elucidate the roles of PDK1 in the postnatal heart, we generated tamoxifen-inducible heart specific PDK1 knockout (PDK1-KO) mice. Deletion of PDK1 at the age of 10 weeks caused severe heart failure. At 1 week after Pdk1 gene disruption, left ventricular systolic function was already deteriorated without reduction in cardiomyocyte size. Langendorff-perfused hearts from PDK1-KO mice exhibited impaired responsiveness to isoproterenol in spite of preserved responsiveness to forskolin. In PDK1-KO hearts, PI3-K γ activity was enhanced and the expression levels of β1-adrenergic receptor (β1AR) in membrane fraction were decreased. Overexpression of PIK-domain of PI3-K γ blocked β1AR internalization by competitively inhibiting the association between PI3-K γ and G-protein coupled receptor kinase 2, and improved cardiac function in PDK1-KO hearts. In addition, we found that cardiomyocyte apoptosis was significantly increased 1 week after Pdk1 gene disruption. PDK1-KO hearts showed reduction of Akt and SGK activities, upregulation of Bax protein and endoplasmic reticulum stress signals, which were the potential causes of cardiomyocyte apoptosis. Overexpression of Bcl-2 in PDK1-KO hearts prevented cardiomyocyte apoptosis and partially improved cardiac function in PDK1-KO mice. Conclusions : These results suggest that PDK1 is essential for normal cardiac function by not only preserving responsiveness to β-adrenergic stimulation but also preventing cardiomyocyte apoptosis. Since PDK1-KO mice reproduces many aspects of human heart failure, we propose that PDK1 may be a promising molecule targeted for the treatment of heart failure.
Effect of Gastric Distension on Duodenal Aspirates in Man
Journal: JAMA (1963)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
The anaphylatoxin C3a downregulates the Th2 response to epicutaneously introduced antigen
Authors: Seiji Kawamoto, Ali Yalcindag, Dhafer Laouini, Scott Brodeur, Paul Bryce, Bao Lu, Alison A. Humbles, Hans Oettgen, Craig Gerard, Raif S. Geha
Journal: Journal of Clinical Investigation (2004)

Mechanical injury to the skin results in activation of the complement component C3 and release of the anaphylatoxin C3a.C3a binds to a seven-transmembrane G protein-coupled receptor, C3aR.We used C3aR -/- mice to examine the role of C3a in a mouse model of allergic inflammation induced by epicutaneous sensitization with OVA.C3aR -/-mice exhibited an exaggerated Th2 response to epicutaneous but not to intraperitoneal sensitization with OVA, as evidenced by significantly elevated levels of serum OVA-specific IgG1 and significantly increased secretion of the Th2 cytokines IL-4, IL-5, and IL-10 by antigen-stimulated splenocytes.Presentation of OVA peptide by C3aR -/-APCs caused significantly more IL-4 and IL-5 secretion by T cells from OVA-T cell receptor (OVA-TCR) transgenic mice compared with presentation by WT APCs.C3a inhibited the ability of splenocytes, but not of highly purified T cells, to secrete Th2 cytokines in response to TCR ligation.This inhibition was mediated by IL-12 secreted by APCs in response to C3a.These results suggest that C3a-C3aR interactions inhibit the ability of APCs to drive Th2 cell differentiation in response to epicutaneously introduced antigen and may have important implications for allergic skin diseases.Nonstandard abbreviations used: atopic dermatitis (AD); epicutaneous (EC); intraperitoneal (i.p.); T cell receptor (TCR).
A rare mutation [IVS-I-130 (G-A)] in a Turkish β-thalassemia major patient
Authors: G.O. Tadmouri, O. Bilenoğlu, S. Kantarcı, H. Kayserili, P. Perrin, A.N. Başak
Journal: American Journal of Hematology (2000)

Here we describe the identification of the rare β-thalassemia mutation IVS-I-130 (G-A) for the first time in Turkey. The hematological evaluation of the patient showed classical signs of β-thalassemia major requiring regular blood transfusions every 30–35 days. DNA analysis was carried out using reverse dot-blot hybridization and restriction endonuclease digestion, as well as genomic sequencing. The patient was found to be heterozygous for the IVS-I-6 (T-C) and IVS-I-130 (G-A) mutations. In order to deduce a possible origin for the IVS-I-130 (G-A) mutation, the sequence polymorphisms in the DNA of the patient and her family were characterized. The method included the analysis of nine polymorphic nucleotides and the hypervariable microsatellite of composite sequence (AT)xTy 5′ to the β-globin gene by DNA sequencing. The sequence haplotype (HT4) carrying the IVS-I-130 (G-A) mutation is also observed in Algeria. This favors a Northeastern African origin for this allele. The observed results agree well with a recent introduction of this mutation to Turkey from Egypt toward the end of the 19th century. Am. J. Hematol. 63:223–225, 2000. © 2000 Wiley-Liss, Inc.
Sulindac hepatotoxicity
Authors: S J Whittaker, J N Amar, I R Wanless, J. Heathcote
Journal: Gut (1982)

Two patients who developed painless jaundice while taking sulindac are described. Rechallenge in one case confirmed the association of hepatic damage with sulindac administration. Laboratory data and liver biopsy findings suggested a hepatitis with cholestatic features.
Garden State
Authors: Daniel Engber
Journal: BMJ (2004)

Directed by Zach Braff On general release in the United States UK release date: 26 November www2.foxsearchlight.com/gardenstate Rating: ![Graphic][1]</img> I t has been more than 40 years since Ken Kesey, in One Flew Over the Cuckoo's Nest , described electroconvulsive therapy (ECT) as a trip to “that filthy brain-murdering room that the black boys call the ‘Shock Shop,’” and almost 30 since Milos Forman's film adaptation of Kesey's novel swept the American Academy Awards. Yet despite decades of evidence that ECT is both safe and effective, its public image has never fully recovered. And now, with the treatment of depression under renewed scrutiny, we have Garden State —an independent film from first time director Zach Braff that dramatises the dangers of prescribing antidepressant drugs to children. Perhaps profiting from the ongoing … [1]: /embed/inline-graphic-1.gif
Avocado hypersensitivity
Authors: C. Blanco, T. Carrillo, R. Castillo, J. Quiralte, M. Cuevas
Journal: Allergy (1994)

The avocado (Av) is a fruit that belongs to the Lauraceae family. We report 17 patients with immediate hypersensitivity to avocado. Clinical manifestations in relation to avocado ingestion were as follows: systemic anaphylaxis in seven patients, angioedema/urticaria in six, vomiting in two, bronchial asthma in one, and rhinoconjunctivitis in one. Skin prick test (SPT) with fresh avocado was positive in all patients with the Strong avocado variety (SAv) and in 14 patients with the Hass avocado variety (HAv). Our patient-associated sensitizations were as follows: 10 to latex, eight to chestnut, eight to banana, four to kiwi, and four to walnut. Avocado-sensitized patients with latex allergy were typically middle-aged women, professionally exposed to latex, who also exhibited frequent associated sensitizations to chestnut, banana, and other fruits. Specific IgE against avocado was demonstrated in 11 of our patients, by both commercial CAP and RAST with avocado extract coupled to nitrocellulose disks. Despite its lower protein content, SAv seems to be more allergenic than HAv, both in vivo and in vitro. On incubating a pool of sera from our patients with avocado, latex, chestnut, and banana extracts, a progressive RAST inhibition was obtained, with SAv- and chestnut-marked disks. This suggests the existence of common antigenic determinants among these allergens.
U.S.S.R.
Journal: JAMA (1962)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Phase II study of transarterial embolization in European patients with hepatocellular carcinoma: Need for controlled trials
Authors: J Bruix
Journal: Hepatology (1994)

Our uncontrolled phase II study was aimed at assessing the efficacy of transarterial embolization in patients with hepatocellular carcinoma and to determine the parameters associated with a favorable response to treatment, improved survival or both. Fifty consecutive patients (25 corresponding to Okuda's stage I and 25 to stage II) with hepatocellular carcinoma (41 being multinodular or massive) were included. Transarterial embolization induced a self-limited postembolization syndrome that was well tolerated. Nevertheless, three patients died shortly after the procedure because of tumor progression (two cases) or progressive liver failure. A favorable response (extensive necrosis with reduction of tumor area greater than 50%) was achieved in 81% of the cases, and this result was independently (p < 0.05) related to a preserved performance status and to a lower alphafetoprotein concentration. The survival of the patients at 1 and 2 yr was 65% and 38%, respectively, better than the expected survival according to a mathematical model obtained from a historical series of untreated cases (42% and 20%, respectively). Cox regression analysis disclosed that both a favorable therapeutic response and a preserved physical condition (reflected by performance status of 0 or 1) were independently associated with better survival (regression coefficient -2.248 and 0.869, respectively). These data indicate that transarterial embolization has a marked antitumoral effect in patients with inoperable hepatocellular carcinoma and that the therapeutic success is associated with improved survival. Nevertheless, because the potential benefit for survival observed in this uncontrolled study appears to be moderate, prospective controlled trials to ascertain the real usefulness of this therapeutic approach are mandatory. (HEPATOLOGY 1994;20:643-650).
The Impact Of Thymoglobulin Prior To Pediatric Unrelated Umbilical Cord Blood Transplantation On Immune-Reconstitution and Clinical Outcome
Authors: Caroline A Lindemans, Robert Chiesa, Persis J Amrolia, Kanchan Rao, Olga Nikolajeva, Arianne de Wildt, Corinne E Gerhardt, Kimberley Gilmour, Marc Bierings, Paul Veys, Jaap Jan Boelens
Journal: Blood (2013)
Practitioner, London
Journal: JAMA (1966)

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 934: Contributory Role of VEGF Overexpression in Endothelin-1-induced Cardiomyocyte Hypertrophy: Involvement of Hyopoxia Inducible Factor
Authors: Nobutake Shimojo, Subrina Jesmin, Yuichi Hattori, Seiji Maeda, Takashi Miyauchi, Kazutaka Aonuma
Journal: Circulation (2007)

Although endothelin-1 (ET-1) stimulates vascular endothelial growth factor (VEGF) expression in a variety of cells, including endothelial cells and vascular smooth muscle cells, the effect of ET-1 on expression of VEGF and its receptors in cardiomyocytes is unknown. In the present study, we found that treatment of neonatal rat cardiomyocytes with ET-1 for 24 h resulted in upregulation of VEGF and its two principle receptors, fetal liver kinase (flk)-1 and fms-like tyrosine kinase (flt)-1, in a concentration-dependent manner (10 −12 -10 −6 M). ET-1 treatment also caused significant cardiomyocyte hypertrophy, as indicated by increases in cell surface area (2.0-fold compared to control) and 14 C-leucine uptake (1.8 fold) by cardiomyocytes. And this ET-1 mediated upregulation of VEGF in cardiomyocytes was associated with the induction of hypoxia inducible factor (HIF)-1β and HIF-2α, not HIF-1α. Treatment with TA-0201 (10 −6 M), an ET A selective blocker, eliminated ET-1-induced overexpression of VEGF and its receptors as well as cardiomyocyte hypertrophy. Treatment with VEGF neutralizing peptides (5–10 μg/ml) partially but significantly inhibited ET-1-induced cardiomyocyte hypertrophy. Both TA-0201 and VEGF neutralizing peptides also significantly prevented the increase of phosphorylated KDR, which implies the activation of VEGF system in ET-1 induced hypertrophied cardiomyocyte. These results suggest that ET-1 treatment of cardiomyocytes promotes overexpression of VEGF and its receptors via activation of ET A receptors, and consequently the upregulated VEGF signaling system appears to contribute, at least in part, to ET-1-induced cardiomyocyte hypertrophy.
One Morning
Journal: JAMA (2002)

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