tbuckley/cabot-search huggingface dataset:
Abstract P081: Neighborhood Social Environments and Incident Obesity: the Multi-Ethnic Study of Atherosclerosis (MESA)
Authors: Mahasin Mujahid, Amy Auchincloss, Emon Elboudwarej, Mercedes Carnethon, Tonatiuh Barrientos-Gutierrez, Tiffany Powell-Wiley, Ana Diez Roux
Journal: Circulation (2015)

Introduction: The public health burden of obesity in the United States is well documented and obesogenic environments, including the neighborhoods in which individuals live, have emerged as important determinants of obesity risk. Studies examining the association between neighborhood context and obesity have primarily focused on the socioeconomic and built/physical environment and have been mostly cross-sectional. Objective: To investigate associations between neighborhood social environment and incident obesity and to determine if these associations are modified by gender. Methods: Study participants were enrolled in MESA from 2000-2002 and followed for an average of 9.5 years. Obesity was defined as body mass index of ≥30 kg/m 2 using weight and height measurement obtained at baseline and 4 follow-up examinations. Neighborhood social environment was assessed using a survey of area residents and MESA participants that asked them to rate their neighborhood (1-mile area surrounding the home) across dimensions of safety, social cohesion, and aesthetic quality. Cox proportional hazards models, with a robust covariance matrix estimator to adjust for clustering within neighborhoods, were used to test study hypotheses. Results: Among the 3965 participants free from obesity at baseline and with complete data on study covariates, the mean age was 62 (SD=10) and 508 participants developed obesity over the study follow-up. In multivariable models, there were significant associations between neighborhood social environment indicators (Table 1) and incident obesity among men, independent of individual and neighborhood-level confounders (age, gender, race/ethnicity, education, income, neighborhood socioeconomic factors, and neighborhood physical environment). No associations were present among women. Conclusion: Neighborhood-level risk factors are complex and future research is necessary to better understand the increased risk of obesity among men living in better neighborhood social environments.
Fundamentals of Dairy Science.
Authors: Lore Alford Rogers
Journal: JAMA (1928)

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
Patient Preference and Validity of Randomized Controlled Trials
Authors: David Torgerson, Jennifer Klaber Moffett
Journal: JAMA (2005)

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
TGF-β-MAPK signaling enhances metastases by stimulating tumor cell invasion and changes in tumor microenvironment
Authors: Alfiya F. Safina, Erika Vandette, Andrea E. Varga, Andrei V. Bakin
Journal: Cancer Research (2006)

3524   TGF-β is a potent regulator of tumor invasion, immune response, and inflammation, the processes that critically contribute to cancer progression. TGF-β functions as tumor suppressor but can also promote metastasis. This duality of TGF-β creates a major problem for targeting TGF-β signaling in cancer. The current study is aimed to the development of TGF-β therapeutics by identifying specific effectors of the TGF-β pathway contributing to alterations in tumor microenvironment and formation of breast cancer metastases. We show that three mitogen activated pro tein kinase (MAPK) signaling cascades mediated by JNK, p38 MAPK, and ERK contribute to TGF-β-enhanced tumor cell migration, invasion, and changes in tumor microenvironment. Constitutive signaling in breast cancer MDA-MB-231 cells by Alk5-T204D mutant of TGF-β type I receptor (TβRI/Alk5) significantly enhanced migration and invasion, and pulmonary metastases from orthotopic xenografts in SCID mice. Alk5-T204D increased tumor vascularization and reduced cell death as assessed by TUNEL staining but did not affect Ki67 index. TGF-β-mediated cell migration was blocked by inhibitors of JNK, p38, and ERK signaling indicating that all three kinases contribute to cell migration. TGF-β-mediated tumor invasion was associated with a specific up-regulation of matrix metalloproteinase 9 (MMP9) without an effect on MMP1 and MMP2. TGF-β increased secretion and matrix degradation at focal contacts. Studies with kinase inhibitors and dominant negative (dn) MKK6, an upstream kinase for p38 and JNK, showed that ERK and p38 but not JNK contribute to the MMP9 induction. Silencing of MMP9 by RNA interference (RNAi) significantly reduced tumor cell invasion but not migration. Importantly, siRNA to MMP9 reduced TGF-β-mediated tumor vascularization and lung metastases. Thus, MAPK signaling may represent a marker of breast cancer progression and an important therapeutic target against pro-metastatic function of TGF-β.
Cerebrospinal Fluid in Diseases of the Nervous System.
Authors: Robert A. Fishman
Journal: Annals of Internal Medicine (1980)

Historical introduction anatomical aspects of the cerebrospinal fluid physiology of the cerebrospinal fluid blood-brain barrier intracranial pressure - physiology and pathophysiology disorders of intracranial pressure - hydrocephalus, brain oedema, pseudotumour, intracranial hypotension, and related disorders examination of the cerebrospinal fluid - techniques and complications composition of the cerebrospinal fluid CSF findings in diseases of the nervous system lumbar puncture in clinical practice.
A Text-Book of Legal Medicine.
Authors: Frank Winthrop Draper
Journal: JAMA (1906)

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
Gene mutations differently impact the prognosis of the myelodysplastic and myeloproliferative classes of chronic myelomonocytic leukemia
Authors: Nathalie Cervera, Raphael Itzykson, Emilie Coppin, Thomas Prebet, Anne Murati, Stevan Legall, Norbert Vey, Eric Solary, Daniel Birnbaum, Véronique Gelsi‐Boyer
Journal: American Journal of Hematology (2014)

Initially classified in the myelodysplastic syndromes (MDSs), chronic myelomonocytic leukemia (CMML) is currently considered as a MDS/myeloproliferative neoplasm. Two classes-myelodysplastic and myeloproliferative-have been distinguished upon the level of the white blood cell count (threshold 13 G/L). We analyzed mutations in 19 genes reported in CMML to determine if and how these mutations impacted the respective prognosis of the two classes. We defined four major mutated pathways (DNA methylation, ASXL1, splicing, and signaling) and determined their prognostic impact. The number of mutated pathways impacted overall survival in the myelodysplastic class but not in the myeloproliferative class. The myeloproliferative class had a worse prognosis than the myelodysplastic class and was impacted by RUNX1 mutations only. Our results argue for a reclassification of CMML based on the myelodysplastic/myeloproliferative status.
202. Using RNA To Inhibit Intimal Hperplasia by Blocking E2F Function
Authors: Alice K. Tanner, Joseph Nevins, Bruce Sullenger
Journal: Molecular Therapy (2004)

Top of pageAbstract
The six members of the E2F family of transcription factors are key players in the Rb tumor suppressor pathway leading to DNA replication and cell cycle control. The family members have both distinct and overlapping functions, and gaining an understanding of the roles each factor plays in the cell cycle will lead to a more precise understanding of the Rb pathway. This, in turn, will lead to ways to control the pathway in proliferative disorders such as restenosis after angioplasty and cancer.

Using a large combinatorial library of RNA molecules, called aptamers, and an interative in vitro selection technique, the few aptamers that can bind to and inhibit a protein's function can be isolated. This technique was previously employed to isolate RNA aptamers that bind to E2F1 with Kd's of 2nM. These aptamers were able to block cell cycle progression when microinjected into cell nuclei. The same technique has been used here to isolate modified, nuclease resistant RNA aptamers that bind to E2F3 with Kd's of < 1 nM, and that are able to block DNA binding to E2F. One family of aptamers has been shown to bind preferentially to E2F3, while another family has been shown to bind E2F1-5 equally, yielding two very different tools with which to study E2F function.

Another method of using RNA to inhibit E2F function is to use siRNA to individual E2F members. Both the aptamers and the siRNA have been shown to inhibit function of overexpressed E2Fs in NIH/3T3 cells, and are currently being tested for their ability to inhibit intimal hyperplasia in mouse vein graft models using a variety of delivery methods including naked nucleic acid, a pleuronic gel, and viral vectors.
Ruby Green Singing
Authors: M. Therese Southgate
Journal: JAMA (2001)

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 1528: Identification of FGFR3 as a potential therapeutic target gene for human clear cell ovarian cancer by global genomic analysis
Authors: Tsun Yee Tsang, Gayatry Mohapatra, Hiroaki Itamochi, Samuel C. Mok, Michael J. Birrer
Journal: Cancer Research (2014)

Abstract Clear cell ovarian cancer (CCOC) is the second most common subtype of ovarian cancer after serous ovarian cancer. CCOC is more resistant to standard chemotherapy and has a poorer prognosis than serous and endometrioid histotypes. We attempted to identify genes that are responsible for the aggressive behavior of CCOC and could be potential therapeutic targets using genomic and expression profilings. To identify gene amplification, genome-wide DNA copy number alterations were measured in 13 CCOC cell lines using high-resolution oligonucleotide array CGH (Agilent 105k Human Genome CGH Microarray). GISTIC analysis identified 16 amplified regions containing 391 genes. After comparison to our database of differentially expressed genes between human CCOC specimens and normal ovarian surface epithelium specimen (Affymetrix U133 Plus 2.0 microarrays), 45 of the amplified genes showed mRNA overexpression in CCOC specimens. Among the 45 genes, fibroblast growth factor receptor 3 (FGFR3) was amplified in 9/13 CCOC cell lines and was overexpressed (12.9 folds) in CCOC specimens. Analysis using PathwayStudio software identified FGFR3 mediated pathways for cell migration and cell proliferation. Knockdown of FGFR3 by transfection with FGFR3 specific shRNAs suppressed cell migration in KOC-7c and HAC-2 cells. Moreover, knockdown of FGFR3 also suppressed anchorage-dependent cell proliferation of KOC-7c and HAC-2 cells. The results from the present study therefore suggested that FGFR3 may promote metastasis and growth of cancer cells and may serve as a potential target gene for treatment of human clear cell ovarian cancer. Citation Format: Tsun Yee Tsang, Gayatry Mohapatra, Hiroaki Itamochi, Samuel C. Mok, Michael J. Birrer. Identification of FGFR3 as a potential therapeutic target gene for human clear cell ovarian cancer by global genomic analysis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1528. doi:10.1158/1538-7445.AM2014-1528
Abstract #5668: Identification of primary cilia in human breast tissue and cell lines
Authors: Kun Yuan, Natalya Frolova, Yi Xie, Yeon-Jin Kwon, Adam Steg, Lusheng Xu, Rosa Serra, Andra Frost
Journal: Cancer Research (2009)

Primary Cilia (PC), solitary microtubule-based structures present in various types of eukaryotic cells, were recently found to be critical platforms for several signal transduction pathways. Alterations in PC-associated genes were reported to be related to certain congenital and acquired diseases. The functions of PC are cell type specific and are just beginning to be understood. Their presence and roles in the human breast are largely unknown. We sought to examine the occurrence of PC in several human breast cell lines, as well as in normal and malignant human breast tissues. Our results revealed different patterns of PC expression among human breast cell lines. By using a computer-aided quantification approach of immunofluorescence for acetylated tubulin, a marker of PC, we found a relatively high expression of PC in fibroblasts isolated from normal breast (PC present in 55% of cells) and epithelial cell lines derived from normal breast including human mammary epithelial cells (HMEC) and MCF-10A cells (in 8 -16% of cells); a much lower occurrence in MDA-MB-435 cells (in 0.7% of cells), MDA-MB-231 (in 0.2% of cells), and T-47D cells (in 0.2 % of cells); and virtually absent in other breast cancer cell lines including MDA-MB-468, SK-BR-3, ZR-75-1, BT-474 and MCF-7. We also explored the presence of PC in formalin-fixed, paraffin-embedded benign and cancerous human breast tissues by immunofluorescence. PC were readily found in benign, histological normal breast tissues, primarily in fibroblasts and mammary myoepithelial cells (identified by immunostaining for keratin 14), while rarely in luminal epithelial cells (identified by pancytokeratin staining and location). In the cancer tissues examined thus far, no primary cilia have been definitively identified in cancerous epithelial cells by immunofluorescence. These observations indicate that PC are normally present in stromal and epithelial cells of the human breast. However, their occurrence is lower in breast cancer epithelial cells, raising the possibility that loss of PC is associated with carcinogenesis.   Citation Information:  In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 5668.
Establishment of a gene-trap sequence tag library to generate mutant mice from embryonic stem cells
Authors: M. V. Wiles, F. Vauti, J. Otte, E.-M. Füchtbauer, P. Ruiz, A. Füchtbauer, H.-H. Arnold, H. Lehrach, T. Metz, H. von Melchner, W. Wurst
Journal: Nature Genetics (2000)
eps15 and eps15R are essential components of the endocytic pathway.
Authors: Roberta Carbone, Silvia Fré, Gioacchin Iannolo, Francesca Belleudi, Patrizia Mancini, Pier Giuseppe Pelicci, Maria Rosaria Torrisi, Pier Paolo Di Fiore
Journal: Cancer Research (1997)

eps15 and eps1SR are substrates of the epidermal growth factor (EGF) receptor kinase that are characterized by the presence of a protein:protein interaction domain, the EH domain, and by their ability to bind to the clathrin adaptor protein complex adaptor protein 2. Indirect evidence suggests that eps15 and eps15R are involved in endocytosis. Here we show that microinjection of antibodies against eps15 and eps15R inhibits internalization of EGF and transferrin. In addition, fragments of eps15 (encompassing its EH domains or the COOH-terminal region that binds to adaptor protein 2) inhibit EGF internalization or endocytosis of Sindbis virus. These results demonstrate that eps15 and eps15R are essential components of the endocytic machinery.
Control of Cellular Division and Development. Proceedings of the ICN-UCLA Symposium held in Keystone, Colorado, March 2-8, 1980. Edited by Dennis Cunningham, Eugene Goldwasser, James Watson, and C. Fred Fox. In 2 volumes, 1044 pp., illustrated. New York:
Authors: Charles S. Davidson, Nancy L.R. Bucher
Journal: Hepatology (1982)
Dilated cardiomyopathy and atrioventricular conduction blocks induced by heart-specific inactivation of mitochondrial DNA gene expression
Authors: Jianming Wang, Hans Wilhelmsson, Caroline Graff, Hong Li, Anders Oldfors, Pierre Rustin, Jens C. Brüning, C. Ronald Kahn, David A. Clayton, Gregory S. Barsh, Peter Thorén, Nils-Göran Larsson
Journal: Nature Genetics (1999)
BRAF mutation analysis of only one metastatic lesion can restrict the treatment of melanoma: a case report
Authors: E. Richtig, D. Schrama, S. Ugurel, I. Fried, A. Niederkorn, C. Massone, J.C. Becker
Journal: British Journal of Dermatology (2012)

Funding sources: none. Conflicts of interest: J.C.B. is on the ad board and speakers' bureau for Roche and GlaxoSmithKline. Madam, The RAS‐RAF‐MEK‐ERK‐mitogen activated protein kinase (MAPK) pathway is a crucial signalling pathway for the growth of malignant cells. BRAF (v‐raf murine sarcoma viral oncogene homolog B1) mutations, especially V600E1 and to a lesser extend V600K, are frequently present in melanoma.2, 3 Consequently, therapeutic inhibition of this pathway has become an attractive approach for the treatment of patients with melanoma. Indeed, several investigational drugs have been shown to block this pathway to a more or less significant extent.4 For example, vemurafenib (Zelboraf™; Roche Pharma AG, Grenzach‐Wyhlen, Germany), an orally available selective inhibitor of the oncogenic BRAF V600E kinase, has demonstrated impressive clinical efficacy even in advanced disease.5 As a result, Zelboraf™ received approval from the U.S. Food and Drug Administration for the treatment of the corresponding patients in August 2011.6 In contrast to vemurafenib, MEK 1/2 inhibitors targeting the downstream molecules of BRAF signalling should allow the treatment of patients harbouring activating mutations in any of the upstream molecules of MEK. Notably, the combination of the MEK 1/2 inhibitor GSK 1120212 with the mutation‐specific BRAF inhibitor GSK 2118436 has demonstrated encouraging antitumour activity in patients with mutated V600.7 Currently, clinical trials that are testing inhibitors of the respective MAPK pathways are based on the identification of a mutation in one selected melanoma lesion, either primary or metastasized. Once the respective drugs are approved, clinical practice will likely follow this standard as well. However, the following case report raises concerns associated with this current practice.