tbuckley/cabot-search huggingface dataset:
Raynaud's Phenomenon
Journal: JAMA (1963)

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THE SPECIFICITY OF THE BODY-CELL TOXINS.
Journal: JAMA (1904)

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MEDICAL LITERATURE ABSTRACTS
Journal: JAMA (1952)

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
The role of organized medicine in correctional health care
Authors: B. J. Anno
Journal: JAMA (1982)

In the early 1970s, the American Medical Association initiated a program to improve health care in the nation's correctional institutions. The AMA's involvement in such an effort was a surprise to those who viewed organized medicine as one of the "last bastions of conservatism." To them, it was difficult to reconcile the image of the AMA with a program designed to improve the plight of inmates of jails and prisons. After all, prisoners didn't vote, and correctional institutions were at the bottom rung of everybody's ladder. So why should physicians be concerned with the welfare of those who have been charged with transgressing society's laws? In other words, what was in it for physicians? The skepticism of some segments of the public was matched by some members of the Association. There were state societies and individual physicians who wondered whether the image of organized medicine might not be tarnished rather
Health Legislation and the 95th Congress
Journal: JAMA (1979)

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Abstract 1852: Down-regulation of PRMT6 drives Warburg effect through ERK induced relocalization of PKM2 to promote tumorigenicity and sorafenib resistance in hepatocellular carcinoma
Authors: Tin-Lok Wong, Lok-Hei Chan, Stephanie Ma
Journal: Cancer Research (2019)

Abstract Cancer cells have a high dependence of glycolysis for ATP production, especially under hypoxic environment. Metabolic reprogramming in cancer drives an increased glycolytic rate that supports maximal production of nutrients for tumorigenesis. Our group has recently identified the post-translational modification enzyme, protein arginine methyltransferase 6 (PRMT6) to be frequently down-regulated and to exhibit a tumour suppressive effect in maintenance of cancer stemness in hepatocellular carcinoma (HCC) (Chan LH et al. Cell Reports 2018). Our current study finds transcriptome and metabolome profiling of HCC cells with PRMT6 repressed to exhibit enrichment of genes and metabolites involved in glycolysis. In vitro, PRMT6 negatively regulates glycolysis, glucose uptake, lactate production and pyruvate kinase activity in HCC cell lines and patient-derived organoids. Our previous work found PRMT6 to interfere with RAS/RAF binding by directly binding to CRAF and methylating arginine100 residue. Supporting the importance of PRMT6-mediated CRAF methylation, we find overexpression of catalytic inactive PRMT6 to exhibit no effect on glycolysis. MEK/ERK, known downstream effectors of RAS/RAF signalling, has been shown to induce nuclear PKM2 localization. Consistently, we find modulation of PRMT6 to negatively regulate ERK and PKM2 expression and localization. Rescue experiments involving the ERK inhibitor U0126 and shPKM2 further substantiate the importance of ERK/PKM2-mediated glucose metabolic reprogramming in HCC cells with PRMT6 suppressed. Functionally, inhibition of glycolysis by 2-deoxyglucose sensitized PRMT6 knockdown cells to sorafenib treatment in vitro and attenuated tumor growth in vivo. In addition, we also find PRMT6 expression to be regulated via hypoxia by binding of RE1-silencing transcription factor to the promoter region. Rescue experiments by re-expressing PRMT6 under hypoxic conditions further support the involvement of PRMT6 in driving glycolysis in oxygen deprived environments. Our work uncovers a critical function for PRMT6 in driving Warburg effect through regulating expression and localization of PKM2 via post-translational modification of CRAF, thereby promoting HCC initiation and sorafenib resistance. Citation Format: Tin-Lok Wong, Lok-Hei Chan, Stephanie Ma. Down-regulation of PRMT6 drives Warburg effect through ERK induced relocalization of PKM2 to promote tumorigenicity and sorafenib resistance in hepatocellular carcinoma [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 1852.
Diminished Tuberculin Reaction After Oral Administration of Vitamin D2
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
Thoracic Splenosis
Authors: VIRGIL M. HARDIN, M E MORGAN
Journal: Clinical Nuclear Medicine (1994)

The authors present a case that demonstrates the continued high sensitivity of Tc-99m SC liver-spleen imaging for thoracic splenosis. A patient with profound weight loss, positive PPD and left upper lobe lung density on a chest radiograph was felt to have a strong clinical suspicion of a malignant pulmonary lesion. Two needle biopsies of the lesion were consistent with splenic tissue. Transbronchial biopsy of the right lower lobe lung revealed metastatic adenocarcinoma of an unknown origin. A Tc-99m SC liver-spleen scan of the abdomen and thorax indicated the lung density was consistent with thoracic splenosis.
OUR GREAT MEN.
Journal: JAMA (1891)

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
A Mechanism of Haloalkene-Induced Renal Carcinogenesis
Authors: Wolfgang Dekant, Spyridon Vamvakas, Michael Koob, Andreas Kochling, Wolfgang Kanhai, Dirk Muller, Dietrich Henschler
Journal: Environmental Health Perspectives (1990)

Several halogenated alkenes are nephrotoxic; some others induce renal tubular adenocarcinomas in rodents after lifelong administration. A bioactivation mechanism accounting for the organ-selective tumor induction has been elucidated: conjugation of the parent compounds with glutathione (GSH), catalyzed by hepatic GSH S-transferases, results in the formation of haloalkyl and halovinyl glutathione S-conjugates. Formation of S-conjugates (identified by NMR and mass spectrometry) could be demonstrated with trichloroethene, tetrachloroethene, hexachlorobutadiene, perfluoropropene, trichlorotrifluoropropene, and dichloroacetylene in incubations with rat liver microsomes and in the isolated perfused rat liver. The GSH conjugates formed are eliminated from the rat liver with the bile and may be translocated to the kidney, intact or after metabolism to the corresponding cysteine S-conjugates that are metabolized in the kidney by renal tubular cysteine conjugate beta-lyase (beta-lyase) to reactive intermediates, most likely thioacylchlorides and thioketenes. Interaction of these potent electrophiles with DNA [demonstrated for intermediates formed from S-(1,2,3,4,4-pentachlorobutadienyl)-L-cysteine] causes mutagenicity in bacteria, genotoxicity in cultured renal cells, and cytotoxicity in kidney cells. As an alternative to beta-lyase-catalyzed cleavage, the cysteine S-conjugates may be acetylated to the corresponding mercapturic acids, which have been identified in urine. The ability of the kidney to concentrate GSH and cysteine S-conjugates and the intensive metabolism of GSH S-conjugates to cysteine S-conjugates in this organ are evidently responsible for the organotropic carcinogenicity.
The surgical attack in invasive bladder cancer
Authors: D. M. Wallace
Journal: JAMA (1969)

The role of surgical treatment of infiltrating tumors will be affected by two factors: (1) the depth of infiltration<sup>22</sup>and (2) the extent of surface spread. Although it may well be that they represent merely the two extremes of the same disease, it is necessary, for practical purposes, to consider them as two separate forms of neoplasia—the single, infiltrating, localized lesion with which the problem may be one of lymphatic spread, or the lesion associated with widespread mucosal changes in the bladder, prostatic ducts, urethra, renal pelvis, or ureter. Localized but infiltrating lesions can be treated by endoscopic resection, by open resection with or without supplementary radioactive implant, by segmental resection, and by radical cystectomy. <h3>The Endoscopic Approach</h3> The endoscopic approach depends for its success on the capability and experience of the surgeon. There are few resectionists capable of completely resecting a tumor more than 6 cm in diameter,
Senior Author
Journal: JAMA (1977)

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
Manuscripts Approved for JNCI, January 1 to February 1, 1968
Journal: JNCI Journal of the National Cancer Institute (1968)

Journal Article Manuscripts Approved for JNCI, January 1 to February 1, 1968 Get access JNCI: Journal of the National Cancer Institute, Volume 40, Issue 3, March 1968, Page 649, https://doi.org/10.1093/jnci/40.3.649 Published: 01 March 1968
Biological Effects of Short-Term, High-Concentration Exposure to Methyl Isocyanate. V. Morphologic Evaluation of Rat and Guinea Pig Lungs
Authors: Edward H. Fowler, Darol E. Dodd, Catherine M. Troup
Journal: Environmental Health Perspectives (1987)

The morphologic changes induced in the lungs of rats and guinea pigs exposed to high concentrations of MIC vapor (100, 600, and 1000 ppm in the rat and 25, 125, 225, and 675 ppm in the guinea pig) for a short time (15 min) in a static exposure chamber were evaluated at varying postexposure periods (0, 1, 2, 4, and 16 hr). The 675 ppm-exposed guinea pigs were evaluated only immediately following removal from the chamber. Attention was primarily focused on the intrapulmonary conducting airways and the parenchyma (gas exchange region) of the lungs. The severity of morphologic changes observed by light microscopy was directly correlated with exposure concentration and time postexposure in both species. Specifically, degenerative changes were observed in the bronchial, bronchiolar, and alveolar epithelium in both species. Quantitative differences were observed; 100 ppm of MIC in the rat resulted in much less damage than did 125 ppm of MIC in the guinea pig. Morphologic evidence of sloughing of large sheets of conducting airway epithelium with fibrin buildup and increased mucus production resulted in plugging of major airways and atelectasis. These observations support the hypothesis that tissue hypoxia was a major contributing factor resulting in death.
THE PAN-AMERICAN MEDICAL CONGRESS IN THE WEST INDIES.
Journal: JAMA (1892)

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
Clinical Perspectives
Authors: Lawrence D. Grouse
Journal: JAMA (1981)

In this issue we introduce a new section ofThe Journalthat will present the points of view of distinguished clinicians and researchers on topics of general medical interest. Since the articles in this section will express the personal perspectives of these clinicians, we call it CLINICAL PERSPECTIVES (p 689). In the interviews that will constitute CLINICAL PERSPECTIVES, we have invited comments and speculations concerning the future directions of medicine. Experts will present unpublished data and describe new technologies. It is an unfortunate feature of the current medical literature that many research advances are either buried or fragmented in ways that make them difficult to locate, let alone to synthesize into a unified picture. It is also difficult for practitioners who are unacquainted with the arcane details of specialized medical research areas to assess the relative importance of published findings. Yet, such assessments are important to keep one's practice current.
Abstract LB-299: A comprehensive platform of patient-derived xenografts and matched cell lines mirrors the genomic landscape of colorectal cancer
Authors: Luca Lazzari, Giorgio Corti, Claudio Isella, Monica Montone, Pamela Arcella, Eugenia Zanella, Luca Novara, Fabiane Barbosa, Andrea Cassingena, Carlotta Cancelliere, Enzo Medico, Andrea Sartore-Bianchi, Salvatore Siena, Andrea Bertotti, Livio Trusolino, Federica Di Nicolantonio, Michael Linnebacher, Alberto Bardelli, Sabrina Arena
Journal: Cancer Research (2019)

Abstract Preclinical models that accurately reflect patients’ tumor with regards to histopathology, genomics, and therapeutic response represent a compelling need to fuel the progress of effective cancer treatments. Patient-derived tumor xenografts (PDXs) have significantly accelerated this process, but, although they closely mirror structural and molecular features of the tumor of origin, they still retain important restrictions related to maintenance costs and large-scale screening. To overcome this issue, we have established a novel platform of 2D-cell lines (xeno-cell lines, XL) derived from PDXs of colorectal cancer (CRC) from which patient’s germline gDNA was available. We have characterized XL-cells at multiple levels to confirm their proximity to the PDXs of origin and to assess their suitability as patient avatars in vitro to interrogate functional networks in colorectal cancer. All XL-cells showed an epithelial-like morphology and phenotype, as also confirmed by EMT biomarker transcriptomic analysis. Whole exome and RNA-seq analyses showed that genomic features were consistently preserved between PDXs and matched cell models. Expression analysis revealed the XL-line collection as a significant representative of all CRC subtypes (CMS and CRIS subgroups). Furthermore, genomic analysis allowed the identification of molecular biomarkers of response and resistance to targeted therapies, including EGFR and HER2 blockade. In particular, molecular determinants of resistance to dual-HER2 blockade previously reported in the Heracles-A trial were validated in XL-cells. In conclusion, the XL-cell line and PDX platform represents a unique and comprehensive preclinical tool to validate gene function e to identify novel pharmacological vulnerabilities in colorectal cancer. Citation Format: Luca Lazzari, Giorgio Corti, Claudio Isella, Monica Montone, Pamela Arcella, Eugenia Zanella, Luca Novara, Fabiane Barbosa, Andrea Cassingena, Carlotta Cancelliere, Enzo Medico, Andrea Sartore-Bianchi, Salvatore Siena, Andrea Bertotti, Livio Trusolino, Federica Di Nicolantonio, Michael Linnebacher, Alberto Bardelli, Sabrina Arena. A comprehensive platform of patient-derived xenografts and matched cell lines mirrors the genomic landscape of colorectal cancer [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 LB-299.