tbuckley/cabot-search huggingface dataset:
American Heart Journal, St. Louis
Journal: JAMA (1964)

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 4737: Case report: Preclinical testing of NEDD8 and proteasome inhibitors for a treatment-refractory, metastatic high-grade mucinous colorectal cancer
Authors: Erica Torchiaro, Consalvo Petti, Claudio Isella, Enzo Medico
Journal: Cancer Research (2019)

Abstract Colorectal cancer (CRC) is the third leading cause of death in the world. CRC shows variable phenotypic make-ups; among them, a particularly aggressive histological subtype is the “high grade mucinous” (HGM) adenocarcinoma, highly mucinous, prone to metastasis and typically refractory to treatments. In some cases, HGM is accompanied by a peculiar “signet ring” phenotype of cancer cells. Early stage diagnosis of signet ring HGM is rare, since clinical symptoms tend to occur late and most cases are usually detected at an advanced stage, with a poor overall survival. We previously demonstrated that a transcriptional signature of HGM displays negative prognosis and sensitivity to the NEDD-8 inhibitor pevonedistat, suggesting the involvement of neddylation- and ubiquitination-based mechanisms in these cases (Picco et al., JNCI 2017 djw209). To assess the clinical potential of colorectal cancer HGM identification and targeting by pevonedistat or other inhibitor of proteasome pathway, we recently propagated cells and PDXs from a case of early onset, metastatic CRC in a Lynch syndrome patient, refractory to standard care (FOLFOX6, FOLFIRI-Panitumumab) and, surprisingly, also to nivolumab. The tumor was highly mucinous, with signet ring undifferentiated cells. Mutational analysis on tumor tissue from the first surgery highlighted PIK3CA H1047R mutation and no mutations in KRAS, NRAS or BRAF. Surprisingly, exome analysis on two lesions from a subsequent surgery displayed a different scenario: KRAS G13D but not PIK3CA mutation. Probably these discording results suggest a strong tumor heterogeneity and evolution. Considering the failure of all previous therapies, the lack of actionable genetic alterations and the peculiarity of the phenotypic features, patient-derived models (organoids and 2D cell cultures) were derived from the two latter lesions and tested for sensitivity to the NEDD8 pathway inhibitor pevonedistat and the proteasome inhibitors bortezomib and carfilzomib. Interestingly, all models showed a strong sensitivity to both drugs, in particular to bortezomib. This is an example of a rare case of high-grade mucinous colorectal cancer where the integration of several approaches proves useful to identify possible therapeutic strategies for a patient without further standard treatment options. Citation Format: Erica Torchiaro, Consalvo Petti, Claudio Isella, Enzo Medico. Case report: Preclinical testing of NEDD8 and proteasome inhibitors for a treatment-refractory, metastatic high-grade mucinous 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 4737.
Obesity.
Authors: W. Parson
Journal: Annals of Internal Medicine (1963)

s1 April 1963Obesity.W. Parson, M.D., F.A.C.P.W. Parson, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-58-4-720_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThere is dissatisfaction with the current concept of obesity, primarily because the management tends to be ineffectual. Excessive fat is deposited because more calories are ingested than are required. Caloric homeostasis is thought to be disrupted primarily as a psychosomatic disorder, wherein food intake is geared to emotional needs rather than metabolic requirements. However, psychotherapy, diet, anorexigenic pills, et cetera, achieve poor long-term results.The problem needs to be re-examined. In recent years, considerable information has accumulated concerning: (a) the factors controlling feeding behavior in animals, and (b) the metabolic activity of adipose tissue. Genetically obese mice with "regulatory" or... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Charlottesville, Va. (ML) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1963Volume 58, Issue 4Page: 720-720KeywordsAdipose tissueDietEatingEating habitsEmotionsFatsObesityOverweight Issue Published: 1 April 1963 PDF downloadLoading ...
Effects of Decision Aids for Menorrhagia on Treatment Choices, Health Outcomes, and Costs: A Randomized Controlled Trial—Correction
Journal: JAMA (2003)

Andrew D. M. Kennedy, BSc; Mark J. Sculpher, PhD; Angela Coulter, PhD; Nuala Dwyer, FRCOG; Margaret Rees, FRCOG; Keith R. Abrams, PhD; Susan Horsley, RN; Deborah Cowley, RN; Christine Kidson, RN; Catherine Kirwin, RN; Caroline Naish, RN; Gordon Stirrat, FRCOG
Combined Text-Book of Obstetrics and Gynæcology for Students and Medical Practitioners.
Journal: JAMA (1933)

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
Letter: Phosphorus poisoning
Authors: Frank A. Simon, Larry K. Pickering, William B. Jackson
Journal: JAMA (1976)

Jackson's letter discusses several divergent opinions in relation to our original article. There is a marked disagreement between EPA labeling regulations, National Pest Control Association good conduct practice statement, and the instructions printed on the label of a readily available paste. The instructions state: "apply rat paste on bread, cheese, or other food they (rodents) will eat." Cautions are recommended on the label but are not always followed by the public. A survey of multiple supermarkets, which are members of various local and national chains in the Houston area, showed that rat paste containing yellow phosphorus was available for purchase by the general public in all the stores that were contacted. This current public availability of toxic rat paste is supported by the occurrence of our reported cases during the spring of 1975. We appreciate Dr Jackson's differentiation of zinc phosphide from yellow phosphorus; however, both compounds manifest
Identification of bipotential progenitor cells in human liver development
Authors: Y HARUNA
Journal: Hepatology (1996)

Intermediate filament proteins have been reported to be expressed in a cell lineage-specific manner during morphogenesis. We studied the expression of cytokeratin (CK)14, CK19, and vimentin and of the hepatocyte-specific HepPar1 antigen during the development of human liver. Nineteen fetal livers (gestational ages 4 to 40 weeks), 3 normal infant livers, and 3 normal adult livers were studied by immunoperoxidase staining of paraffin sections with monoclonal anti-CK19, anti-vimentin, and HepPar1 antibodies and polyclonal anti-CK14 antibodies. Double-immunostaining for CK14 and CK19 as well as bile duct cytokeratin and HepPar1 antigen was also done. CK19 and HepPar1 antigen were the first markers detected in immature progenitor cells of the liver primordium at 4 weeks' gestation. During subsequent liver development, the progenitor cells expressed HepPar1 antigen, CK14, and CK19, from 8 to 14 weeks' gestation. As hepatocyte differentiation progressed, expression of HepPar1 antigen increased, and CK14 and CK19 were abrogated from hepatoblasts at 14 to 16 weeks' gestation. In contrast, as progenitor cells transformed into ductal plate cells, CK19 expression increased and persisted in differentiated bile ducts, whereas CK14 and HepPar1 antigen were lost. Vimentin was detected in ductal plate and biliary epithelial cells from 9 to 36 weeks' gestation, but not in hepatoblasts or hepatocytes. Double-immunostaining confirmed coexpression of CK14 and CK19 in the progenitor cells for a short time (8 to 14 weeks' gestation) during early development. Double immunostaining for bile duct CK and HepPar1 antigen clearly demonstrated the divergence of the hepatocyte and bile duct epithelial cell lineages. Our findings suggest that hepatic progenitor cells differentiate in steps marked by the acquisition or loss of specific phenotypic characteristics. Commitment of the HepPar1+CK19+ progenitor cells to either hepatocyte or bile duct epithelial cell lineages results in increased expression of one marker and loss of the other marker. These characteristics clearly identify bipotential hepatic progenitor cells in the developing human liver.
The Vital Statistics of Massachusetts, 1856-95.
Journal: JAMA (1897)

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
Acronymity
Authors: Henry T. Ricketts
Journal: JAMA (1974)

The endemic disease that I call acronymia continues to spread exponentially. New governmental agencies sprout at an alarming rate, and for a long time only their minions know the meaning of the alphabetical nomenclature with which they live. Equally prolific are the trains of capital letters that frustrate the reader of medical science. For the most part, we just learn to live with it. There is, however, a special class of acronyms that, although easy to learn, gray the hairs of writers, speakers, and grammarians. These are the invented words that end in "x." I am thinking of Xerox, for example. It is primarily the name of a company, but it is also the name of a product. How do you ask for, or indeed spell, two of them? Since x is pronounced with a sibilant at the end, maybe "two Xerox" would get you two machines, but most would
A prospective study of cigarette smoking and risk of cataract surgery in women
Authors: S. E. Hankinson
Journal: JAMA (1992)

<h3>Objective.</h3> —To examine prospectively the association between cigarette smoking and the risk of cataract extraction in women. <h3>Design.</h3> —Prospective cohort study beginning in 1980 with 8 years of follow-up. <h3>Setting.</h3> —United States, multistate. <h3>Participants.</h3> —Registered nurses 45 to 67 years of age and free of diagnosed cancer. There were 50 828 women included in 1980 and others were added as they became 45 years of age. <h3>Main Outcome Measure.</h3> —Incidence of senile cataract extraction. <h3>Results.</h3> —We documented 493 incident senile cataracts diagnosed and extracted during 470302 person-years of follow-up. The age-adjusted relative risk (RR) among women who smoked at least 65 pack-years was 1.63(95% confidence interval [Cl], 1.18 to 2.26; Pfor trend,.02). A similar increase in RR was noted when smoking was assessed in terms of number of cigarettes currently smoked or number of cigarettes smoked by past smokers. Results were also similar after adjusting for other potential risk factors for cataract. Smoking was also strongly associated with posterior subcapsular cataract specifically (RR, 2.59; 95% Cl, 1.49 to 4.50 for ≥65-pack-year smokers relative to nonsmokers). <h3>Conclusion.</h3> —Smoking appears to increase the risk of cataract extraction. (<i>JAMA</i>. 1992;268:994-998)
A9.3 Deletion of mPGES-1 affects Fatty Acid Composition and Eicosanoid Profiles in Mice
Authors: Helena Idborg, Petter Olsson, Patrick Leclerc, Joan Raouf, Per-Johan Jakobsson, Marina Korotkova
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> mPGES-1 is considered an attractive alternative target for anti-inflammatory treatment with improved selectivity and safety compared to NSAIDs. Genetic deletion or pharmacological inhibition of mPGES-1 activity or expression down-regulate inflammation and pain in experimental models of arthritis. However, a detailed understanding of the molecular mechanisms and pathways affected by deletion/inhibition of mPGES-1 is essential before mPGES-1 inhibitors can safely be applied in the clinics. <h3>Objectives</h3> To investigate the effect of mPGES-1 deletion on the levels of bioactive lipid mediators such as the eicosanoids (down-stream cascade) and fatty acids (up-stream cascade). <h3>Methods</h3> Peritoneal macrophages (PM) from wild type (WT) and knock-out (mPGES-1<sup>-/-</sup>, KO) mice were induced with LPS for 16 h. Cells were harvested for gene expression analysis and supernatants were collected for eicosanoid analysis. Gene expression profiling in WT and KO macrophages was performed using the microarray analysis (Applied Biosystems). Eicosanoid profiling of approximately 30 compounds was performed using LC-MS/MS. Fatty acid composition of total lipids in spleen and brain homogenates of WT and KO mice were determined using GC/FID. <h3>Results</h3> Microarray analysis revealed that genetic deletion of mPGES-1 affected expression of genes related to lipid metabolism and mainly associated with eicosanoid, fatty acid and phospho- lipid metabolism, (e.g., Pla1A, Ptgis, Fabp3, Cept1, Comt etc). Compared to WT, mPGES-1 deficient PM displayed a markedly attenuated increase in PGE<sub>2</sub> production upon LPS stimulation, and exhibited significantly increased levels of PGD<sub>2</sub> metabolites such as 15-deoxy-∆<sup>12,14</sup> PGJ<sub>2</sub> and 15-deoxy-∆<sup>12,14</sup> PGD<sub>2</sub> (p &lt; 0.05). There were significant differences in the fatty acid composition in spleen (e.g., palmitoleic acid decreased in KO, p &lt; 0.05) and brain (e.g., myristic acid decreased in KO, p &lt; 0.05) of KO and WT mice, suggesting that feed-back mechanisms are alternated by the deletion of m-PGES-1. <h3>Conclusions</h3> Data reveals that mPGES-1 deficient PMs displayed shunting towards PGD2 pathway, i.e., towards anti-inflammatory metabolites, upon LPS stimulation compared to WT PMs. Moreover, mPGES-1 depletion alters the fatty acid composition of tissue lipids. These effects of inducible PGE<sub>2</sub> on lipid metabolism have important implications for future mPGES-1 inhibitors and deserve further investigation.
MENTAL HYGIENE IN THE COLLEGES
Journal: JAMA (1929)

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
INDIGESTION AND SIN.
Journal: JAMA (1901)

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
WILLIAM SOMERSET MAUGHAM (1874-1965) PLAYWRIGHT, NOVELIST, TRAVELLER
Journal: JAMA (1968)

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
Glucagon Deficiency Reduces Hepatic Glucose Production and Improves Glucose Tolerance In Adult Mice
Authors: Aidan S. Hancock, Aiping Du, Jingxuan Liu, Mayumi Miller, Catherine L. May
Journal: Endocrine Reviews (2010)

Abstract The major role of glucagon is to promote hepatic gluconeogenesis and glycogenolysis to raise blood glucose levels during hypoglycemic conditions. Several animal models have been established to examine the in vivo function of glucagon in the liver through attenuation of glucagon via glucagon receptor knockout animals and pharmacological interventions. To investigate the consequences of glucagon loss to hepatic glucose production and glucose homeostasis, we derived mice with a pancreas specific ablation of the α-cell transcription factor, Arx, resulting in a complete loss of the glucagon-producing pancreatic α-cell. Using this model, we found that glucagon is not required for the general health of mice but is essential for total hepatic glucose production. Our data clarifies the importance of glucagon during the regulation of fasting and postprandial glucose homeostasis.
THE NAMING OF DISEASES
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