tbuckley/cabot-search huggingface dataset:
Abstract 11703: Adipose Angiotensinogen Inactivation Reduces Adipose Tissue Inflammation and Increases Metabolic Activity in Adipose Stroma Vascular cells
Authors: Monique J LeMieux, Latha Ramalingam, Randall Mynatt, Nishan S Kalupahana, Jung Han Kim, Naima Moustaid-Moussa
Journal: Circulation (2015)

The adipose renin-angiotensin system (RAS) is an important regulator of blood pressure and fluid balance and has been linked to obesity-induced inflammation, though mechanisms are not completely understood. Previously, we showed that overexpression of the RAS protein precursor, angiotensinogen (Agt) in adipose tissue increases adiposity, insulin resistance, adipose and systemic inflammation in mice fed a low-fat diet (LFD). Accordingly, we hypothesized that Agt inactivation in adipose tissue will protect against obesity-associated inflammation. To test this hypothesis, we generated adipose tissue Agt knockout (Agt-KO) mice using the aP2-Cre-LoxP system. Agt-KO and wild-type (WT) littermates were each fed a LFD or high-fat diet (HFD) to assess metabolic changes. Our results demonstrate that while no significant differences were observed in body weight or fat mass between the two genotypes on either diet, glucose tolerance was improved in the Agt-KO compared to the WT littermates. This was consistent with higher expression of genes involved in insulin signaling, glucose transport and fatty acid metabolism in white adipose tissue from Agt-KO mice. Moreover, Agt inactivation reduced total adipose macrophage infiltration,and gene/protein expression of MCP-1 and other proinflammatory adipokines in Agt-KO mice compared to WT. Lastly, extracellular flux analyses (using Seahorse Xfe) in both differentiated and non-differentiated stromal vascular cells revealed higher glycolytic activity and mitochondrial respiration in Agt-KO compared to WT mice. Overall, our findings indicate that adipose Agt inactivation reduced adipose inflammation and improved glucose tolerance in part via increased metabolic activity of adipose cells. The cellular and molecular changes observed are consistent with previously reported functions of RAS in insulin resistance, and inflammation. Funded by a GIA from the American Heart Association Southwest Affiliate (NMM)
Emergence of third-generation cephalosporin-resistant Escherichia coli from bloodstream infections in Denmark: this is due to both clonal and non-clonal spread of CTX-M-15
Authors: Frank Hansen, C Lester, S.S Olsen, Ole Heltberg, Ulrik Stenz Justesen, T Højbjerg, J Knudsen, A.M. Hammerum
Journal: Clinical Microbiology and Infection (2011)
Gentamicin induces functional type VII collagen in recessive dystrophic epidermolysis bullosa patients
Authors: David T. Woodley, Jon Cogan, Yingping Hou, Chao Lyu, M. Peter Marinkovich, Douglas Keene, Mei Chen
Journal: Journal of Clinical Investigation (2017)

Recessive dystrophic epidermolysis bullosa (RDEB) is an incurable disease caused by mutations in the gene encoding type VII collagen, the major component of anchoring fibrils (AF). We previously demonstrated that gentamicin produced functional type VII collagen in RDEB cells harboring nonsense mutations. Herein, we determined whether topical or intradermal gentamicin administration induces type VII collagen and AFs in RDEB patients.A double-blind, placebo-controlled pilot trial assessed safety and efficacy of topical and intradermal gentamicin in 5 RDEB patients with nonsense mutations. The topical arm tested 0.1% gentamicin ointment or placebo application 3 times daily at 2 open erosion sites for 2 weeks. The intradermal arm tested daily intradermal injection of gentamicin solution (8 mg) or placebo into 2 intact skin sites for 2 days in 4 of 5 patients. Primary outcomes were induction of type VII collagen and AFs at the test sites and safety assessment. A secondary outcome assessed wound closure of topically treated erosions.Both topical and intradermal gentamicin administration induced type VII collagen and AFs at the dermal-epidermal junction of treatment sites. Newly created type VII collagen varied from 20% to 165% of that expressed in normal human skin and persisted for 3 months. Topical gentamicin corrected dermal-epidermal separation, improved wound closure, and reduced blister formation. There were no untoward side effects from gentamicin treatments. Type VII collagen induction did not generate anti-type VII collagen autoantibodies in patients' blood or skin.Topical and intradermal gentamicin suppresses nonsense mutations and induces type VII collagen and AFs in RDEB patients. Gentamicin therapy may provide a readily available treatment for RDEB patients with nonsense mutations.ClinicalTrials.gov NCT02698735.Epidermolysis Bullosa Research Partnership, Epidermolysis Bullosa Medical Research Foundation, NIH, and VA Merit Award.
Spirometry Reference Equations from the HCHS/SOL (Hispanic Community Health Study/Study of Latinos)
Authors: Lisa LaVange, Sonia M. Davis, John Hankinson, Paul Enright, Rebbecca Wilson, R. Graham Barr, Thomas K. Aldrich, Ravi Kalhan, Hector Lemus, Ai Ni, Lewis J. Smith, Gregory A. Talavera
Journal: American Journal of Respiratory and Critical Care Medicine (2017)

Rationale: Accurate reference values for spirometry are important because the results are used for diagnosing common chronic lung diseases such as asthma and chronic obstructive pulmonary disease, estimating physiologic impairment, and predicting all-cause mortality. Reference equations have been established for Mexican Americans but not for others with Hispanic/Latino backgrounds.Objectives: To develop spirometry reference equations for adult Hispanic/Latino background groups in the United States.Methods: The HCHS/SOL (Hispanic Community Health Study/Study of Latinos) recruited a population-based probability sample of 16,415 Hispanics/Latinos aged 18–74 years living in the Bronx, Chicago, Miami, and San Diego. Participants self-identified as being of Puerto Rican, Cuban, Dominican, Mexican, or Central or South American background. Spirometry was performed using standardized methods with central quality control monitoring. Spirometric measures from a subset of 6,425 never-smoking participants without respiratory symptoms or disease were modeled as a function of sex, age, height, and Hispanic/Latino background to produce background-specific reference equations for the predicted value and lower limit of normal.Measurements and Main Results: Dominican and Puerto Rican Americans had substantially lower predicted and lower limit of normal values for FVC and FEV1 than those in other Hispanic/Latino background groups and also than Mexican American values from NHANES III (Third National Health and Nutrition Examination Survey).Conclusions: For patients of Dominican and Puerto Rican background who present with pulmonary symptoms in clinical practice, use of background-specific spirometry reference equations may provide more appropriate predicted and lower limit of normal values, enabling more accurate diagnoses of abnormality and physiologic impairment.
Response to: ’Umbilical-cord messenchymal stem cells for the treatment of automimmune diseases: beware of cell to cell contact' by Alunno <i>et al</i>
Authors: Teck Onn Lim, DanQi Deng, Peilian Zhang, Yun Guo
Journal: Annals of the Rheumatic Diseases (2017)

We thank the authors of the eLetter1 for comments on the possible pitfall in the design of trial of umbilical cord derived mesenchymal stem cell (UC-MSC) for the treatment for lupus nephritis or other autoimmune diseases. It is worth bearing in mind that our trial …
Cancer deaths and cases attributable to lifestyle factors and infections in China, 2013
Authors: F. Islami, W. Chen, X.Q. Yu, J. Lortet-Tieulent, R. Zheng, W.D. Flanders, C. Xia, M.J. Thun, S.M. Gapstur, M. Ezzati, A. Jemal
Journal: Annals of Oncology (2017)
Molecular signatures and responses to targeted therapies in over 300 relapsed and therapy-refractory young adult (AYA) and childhood cancers.
Authors: Erin Haag Breese, Brian Turpin, Phillip Dexheimer, Benjamin Mizukawa, Laura Agresta, Arun Gurunathan, Thomas Pfeiffer, Jeremy Rubinstein, Luke Smart, Garrett Michael Frampton, Mayur Sarangdhar, Brian D. Weiss, Joseph Gerald Pressey, James I. Geller, Maureen Megan O'Brien, Maryam Fouladi, John Peter Perentesis
Journal: Journal of Clinical Oncology (2017)

11514 Background: Contemporary chemotherapy-based regimens provide cures for most pediatric &amp; AYA cancers. However, for patients with relapsed/refractory malignancies, outcomes are poor &amp; imply a distinct and aggressive biology. Identifying common themes in the molecular architecture &amp; oncogenic mechanisms in these patients is a critical priority for drug development. We hypothesized that the molecular signature of cancers in these patients would be independent of histology. We also assessed the response to molecular alteration (MA)-targeted therapies. Methods: IRB-approved analysis of MAs in 306 relapsed/refractory pediatric &amp; AYA malignancies (116 hematologic malignancies, 68 sarcomas, 46 neuroblastomas, 36 CNS, 14 liver, 9 renal, 17 other) was performed. DNA was analyzed for MAs (Foundation Medicine, Cambridge, MA; Univ of Washington, Seattle, WA); additional MAs were identified by cytogenetic &amp; fluorescent in situ hybridization analyses. Results: Median age was 8 years (range birth - 44 yrs). MAs were identified in 90.1% of patients &amp; included a median of 2 mutations (range 0-18) in 133 cancer-related genes. In contrast to genomic analyses of de novo malignancies in children, a high frequency of TP53 MAs was identified (20.4% of patients) and was associated with inferior survival. MAs were identified in targetable pathways including cell cycle regulation (32.6%), DNA repair (7.2%), epigenetic (28.6%), RAS/RAF/MEK (24%), tyrosine kinase (TK; 18.4%), PI3K/AKT/mTOR (11.8%), and NOTCH/WNT (8.9%). A higher number of MAs was associated with inferior survival. Patients with alterations in epigenetic &amp; TK pathways also had inferior outcomes. MAs were frequently independent of histology &amp; the spectrum of mutations was similar to adult cancers. Exceptional responses were observed with MA-based assignment of therapies (epigenetic, NTRK, RAS/RAF/MEK &amp; ALK). Conclusions: Relapsed/refractory pediatric &amp; AYA cancers have frequent MAs independent of histology. The spectrum of MAs is distinct from de novo disease &amp; potentially reflects tumor evolution &amp; resistance mechanisms. These findings support MA-guided approaches to new drug development paired with adult trials.
Evaluation of Chest Pain in the Emergency Department
Authors: Arthur L. Kellermann
Journal: Annals of Internal Medicine (1995)

Letters15 August 1995Evaluation of Chest Pain in the Emergency DepartmentArthur L. KellermannArthur L. KellermannSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-123-4-199508150-00014 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:In their editorial, Drs. Kaul and Abbott [1] assert that emergency physicians are less adept than cardiologists at differentiating chest pain of ischemic origin. No literature is cited to support this claim. The authors also recommend that emergency physicians consult a cardiologist whenever they are confronted with chest pain of uncertain origin. If this advice were followed, emergency physicians would generate millions of additional consultation requests each year. The authors also assert that patients with evolving myocardial infarction are more likely to have early reperfusion if care is delayed until the arrival of a cardiologist. This position ...References1. Kaul S, Abbott RD. Evaluation of chest pain in the emergency department (Editorial). Ann Intern Med. 1994; 121:976-8. Google Scholar2. American Heart Association. Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC). JAMA. 1992; 268:2171-242. Google Scholar3. National Heart Attack Alert Program Coordinating Committee 60 Minutes to Treatment Working Group. Emergency department: rapid identification and treatment of patients with acute myocardial infarction. Ann Emerg Med. 1994; 23:311-29. Google Scholar4. Sabia P, Abbott RD, Afrookteh A, Keller MW, Touchstone DA, Kaul S. The importance of two-dimensional echocardiographic assessment of left ventricular systolic function in patients presenting to the emergency room with cardiac-related symptoms. Circulation. 1991; 84:1615-24. Google Scholar5. Kasman DL. When a heart stops. Ann Intern Med. 1994; 120:432-3. Google Scholar Author, Article, and Disclosure InformationAuthors: Arthur L. Kellermann PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 August 1995Volume 123, Issue 4 Page: 314-318 Keywords Emergency department Emergency medicine Heart Hospital medicine Ischemia Myocardial infarction Reperfusion Residency ePublished: 15 August 2000 Issue Published: 15 August 1995 Copyright & PermissionsCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Reduced need for surgery in severe nasal polyposis with mepolizumab: Randomized trial
Authors: Claus Bachert, Ana R. Sousa, Valerie J. Lund, Glenis K. Scadding, Philippe Gevaert, Shuaib Nasser, Stephen R. Durham, Marjolein E. Cornet, Harsha H. Kariyawasam, Jane Gilbert, Daren Austin, Aoife C. Maxwell, Richard P. Marshall, Wytske J. Fokkens
Journal: Journal of Allergy and Clinical Immunology (2017)
Use of Instrumental Variables Methods in Examining Psychiatric Readmissions
Authors: Anthony T. Lo Sasso
Journal: JAMA Psychiatry (2017)

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 Psychiatry HomeNew OnlineCurrent IssueFor Authors Podcast 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 Psychiatry journal
Two Doses of Antithymocyteglobulin As Graft-Versus-Host Disease Prophylaxis in Haploidentical Allogeneic Stem Cell Transplantation: A Multicenter Prospective Study
Authors: Ren Lin, Yu Wang, Fen Huang, Zhiping Fan, Shen Zhang, Ting Yang, Yajing Xu, Xinquan Liang, Yu Ji, Na Xu, Li Xuan, Jieyu Ye, Jing Sun, Xiaojun Huang, Qifa Liu
Journal: Blood (2016)
Two Types of Mucous Cells in the Colon Crypt?: Reply
Authors: A. K. M. Shamsuddin, B. F. Trump
Journal: JNCI Journal of the National Cancer Institute (1981)

Journal Article Two Types of Mucous Cells in the Colon Crypt?: Reply Get access A. K. M. Shamsuddin, A. K. M. Shamsuddin Department of Pathology University of Maryland School of Medicine22 South Greene St. Baltimore, Maryland 21201 Search for other works by this author on: Oxford Academic PubMed Google Scholar B. F. Trump B. F. Trump Department of Pathology University of Maryland School of Medicine22 South Greene St. Baltimore, Maryland 21201 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 67, Issue 4, October 1981, Pages 747–749, https://doi.org/10.1093/jnci/67.4.747 Published: 01 October 1981
Impact in prognosis of circulating tumor DNA mutant allele fraction (MAF) in RAS mutant metastatic colorectal cancer (mCRC)
Authors: Sanz-García Enrique, Elena Elez, Ginevra Caratu, Judit Matito, Ariadna Garcia, Julieta Grasselli, Mercedes Martínez-Villacampa, Cristina Santos, Nuria Mulet, Joana Vidal, Guillem Argiles, Teresa Macarulla, Jaume Capdevila, Tamara Sauri, Ignacio Matos, Enrique Aranda, Frederick Jones, Rodrigo Dientsmann, Clara Montagut, Josep Tabernero, Ramon Salazar, Ana Vivancos
Journal: Annals of Oncology (2017)
Understanding mechanism of estrogen receptor mediated gene regulation in MCF7 and Ishikawa cell lines
Authors: YouFu Pan, SayLi Kong, YewKok Lee, HaiXia Li, Krishna Murthy, Premila Hirubala, Gary Loh, Edison Liu, Kartiki Desai, Jane Thomsen, Edwin Cheung
Journal: Clinical Cancer Research (2007)

C54  Estrogen receptors (ERs) are members of the steroid hormone receptor superfamily and are ligand-inducible DNA binding transcription factors. The ligand can be estrogen (17β-estradiol, E2), or other selective estrogen receptor modulators (SERMs) such as tamoxifen, raloxifene, or Faslodex (ICI 182780). SERMs are currently used as antagonists for ER positive breast cancer treatments. However, some SERMs such as tamoxifen have been shown to harbor agonistic effects (such as in the uterus) and thus long term exposure to it has been shown to increase the risk of endometrial cancer. How these ligands work in regulating gene expression in different tissues or cell types (such as in MCF7 cells and Ishikawa cells) remains unclear. To gain better understanding in the actions of estrogen and SERMs in different cell context, we have performed extensive global gene expression analyses comparing the effects of different SERMs (by themselves and in various combinations) in MCF7 and Ishikawa cells. Our microarray results show that E2, Tamoxifen, and Faslodex stimulate unique sets of genes in these two cell lines. We have also performed chromatin immunoprecipitation (ChIP) assays for ER in MCF 7 and Ishikawa cells and we found that there are major differences in ER occupancy between the two different cell lines. Taken together, our results demonstrate that differential recruitment of ER to the regulatory regions of genes may contribute to the cell type specific actions of SERMs.
Synergistic cytotoxic effects of selinexor and chloroquine phosphate in mantle cell lymphoma.
Authors: Yongyi Zhang, Kejie Zhang, Yuhan Chen, Daibo Zhang, Qin Yao, Huiqin Zhuo
Journal: Journal of Clinical Oncology (2016)

e19069 Background: Although the cytotoxic effects of novel CRM1 inhibitor, small molecule selective inhibitors of nuclear export (SINE) on Mantle Cell Lymphoma (MCL) cells have now been established, the mechanism of cell death is still not fully understood. The objective of our study was to elucidate the mechanism of Selinexor, a SINE compound, mediated cytotoxic effects and Synergistic cytotoxic effects of Selinexor and Chloroquine phosphate (CQ) in MCL. Methods: CCK-8 assay was used to detect the growth of 4 established MCL cell lines treated with Selinexor and CQ; CalcuSyn 2.0 software was used to detected the Combination index (CI) of Selinexor combined CQ; Apoptosis were detected with Annexin V FITC assay, and Caspase3 activation and PARP cleavage were detected with Western blotting; Senescence associated beta-galactosidase (SA-β-gal) were detected with β-gal staining kit; The extent of autophagic flux were determined by evaluation of fluorescent LC3 puncta under a confocal laser scanning microscope by transduction MCL cells with Tandem fluorescent mRFP-GFP-LC3 (tf-LC3) and the autophagic features were also detected with LC3-II expression assessed by Western blotting. Results: Selinexor resulted in a significant growth inhibition in all the MCL cell lines studied, with IC50 values ranging between 0.64 µM to 2.53 µM; Annexin V FITC assay showed that MCL cells apoptosis were induced by Selinexor, the apoptosis were confirmed by caspase3 activation and PARP cleavage; SA-β-gal positive cells were not detected; Selinexor increased MCL cells autophagic flux. Selinexor combination with CQ produced the synergistic effects on cell growth inhibition (CI 0.81-0.99). CQ inhabited Selinexor induced autophagy in Grsnt-519 cells were confirmed by tf-LC3 staining and LC3-II expression assessed by Western blotting. Conclusions: Selinexor inhibited growth, induced apoptosis and autophagy of MCL cells in vitro. Selinexor induced autophagy acted as a cellular protective role. The combination of Selinexor and CQ, an autophagic inhibitor, produced the synergistic effects on MCL cells growth inhibition. Our data suggest that Selinexor combination with CQ provides a potential therapy for patients with MCL.
Orthotopic Liver Transplantation for Hepatocellular Cancer
Authors: DD Houlihan, F Donnellan, D Maguire, J Geogheogan, O Traynor, PA McCormick, JE Hegarty
Journal: Endoscopy (2006)

Aims: Studies investigating the early follow up survival rates of patients with hepatocellular cancer (HCC) treated with orthotopic liver transplantation (OLT) have yielded conflicting results. The aim of this study is to determine the characteristics and survival curve of patients who have undergone OLT for HCC over a five year period in a single centre.
Abstract 10119: Cardio-respiratory Fitness and Incident Heart Failure
Authors: Hassan Khan, Setor Kunutsor, Rainer Rauramaa, Kai Savonen, Andreas P Kalogeropoulos, Vasiliki V Georgiopoulou, Javed Butler, Jari A Laukkanen
Journal: Circulation (2013)

Aims: To asses the association between cardiorespiratory fitness (CRF) and risk of incident heart failure (HF). Methods: Cardiorespiratory fitness, as measured by maximal oxygen uptake (VO2max), wa...
Predicting survival in gastric cancer patients randomized to docetaxel with mass spectrometric quantitation of TUBB3
Authors: Fabiola Cecchi, Daniel Catenacci, Sarit Schwartz, Yuan Tian, Rosalba Miceli, Filippo Pietrantonio, Antonia Martinetti, Maria Di Bartolomeo, Todd Hembrough, alessandro pellegrinelli
Journal: Annals of Oncology (2017)
Dose- r esponse s tudies of s odium a rsenite in the s kin of K6/ODC t ransgenic m ouse
Authors: William Ward, Gene Ahlborn, Gail Nelson, Geremy Knapp, James Allen, Barbara Roop, Kirk Kitchin, Don Delker, Ming Ouyang, Yan Chen, Thomas O'Brien
Journal: Cancer Research (2007)

3061   It has previously been observed that chronic exposure to inorganic arsenic and/or its metabolites increase(s) tumor frequency in the skin of K6/ODC transgenic mice. To identify potential biomarkers and modes of action for this skin tumorigenicity, gene expression profiles were characterized from analysis of mouse skin RNA taken from K6/ODC mice administered 0, 0.05, 0.25, 1.0 and 10 ppm sodium arsenite in their drinking water for 4 weeks. Skin gene expression was measured with Affymetrix Mouse Genome 430A 2.0 GeneChips® and statistical analysis included GC-RMA normalization followed by a Bayesian regularized t-test. Pathway analysis was conducted with DAVID (NIH) and MetaCore GeneGo. Only the highest dose (10 ppm) resulted in significantly altered KEGG pathways, including MAPK, regulation of actin cytoskeleton, Wnt, Jak-Stat, Tight junction, Toll-like, phosphatidylinositol, and insulin signaling pathways. Approximately 20 genes exhibited a dose response, some known to be associated with carcinogenesis or tumor progression including Cyclin D1, CLIC4, Ephrin A1, Hmox1, and STAT3. Although transcription changes in all these genes have not previously been linked to arsenic carcinogenesis, their association with carcinogenesis in other animal models suggests that these genes may play a role in the early stages of arsenic-induced carcinogenesis. [ Although this work was reviewed by EPA and approved for publication, it may not necessarily reflect official Agency policy ]