tbuckley/cabot-search huggingface dataset:
Clinicians Accept Hektoen Gold Medal
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
Introduction
Authors: P. Michael Conn
Journal: Endocrine Reviews (1986)

IT IS a novel undertaking that Endocrine Reviews should devote an entire issue to a single subject area. In committing to this project, the Editor-in-Chief and Editorial Board have recognized both the rapid advances made in this area and the potential of GnRH and its analogs to benefit mankind. To date, thousands of GnRH analogs have been synthesized—perhaps more than for any other peptide. Virtually all areas of medicine are being affected by this peptide. The broad interest in GnRH explains why the authors in this volume come from government, industry, and University sources. Several drug companies now market GnRH and its analogs. In April 1985, the first GnRH analog [Leuprolide, D-Leu6-Pro9-GnRH-ethylamide (NEt)] received Food and Drug Administration approval in the United States. Others are marketed worldwide. Other analogs, both agonists and antagonists, will likely be available soon.
Reactivity Parameters in Structure-Activity Relationship-Based Risk Assessment of Chemicals
Authors: James D. McKinney
Journal: Environmental Health Perspectives (1996)

New approaches to the risk assessment process are needed that might be more definitive and satisfying to the scientific community, interest groups, and the public at large. This commentary examines an alternative approach that is based on understanding the relationships of chemical structure and reactivity properties to the toxicokinetic behavior of chemicals in biological systems. This approach is based on the likelihood that there is a limited number of triggering (reactivity) mechanisms by which chemicals can express their toxicity at the molecular level. The fundamental importance of electrophilic character of chemicals as a determinant of their critical molecular reactivities and interactions with biological material in the expression of toxicity is supported. Such an approach also takes advantage of the maturing field of theoretical/computational chemistry in understanding important molecular recognition and reactivity processes (both qualitatively and quantitatively) for chemicals that can underlie their biological/toxicological activity. A process that permits assessment of reaction equivalents delivered to biological systems may hold promise for grouping chemicals by common triggering mechanisms with clearly delineated toxicological endpoints.
Editor's Note: Prevention of Ultraviolet Radiation–Induced Immunosuppression by (−)-Epigallocatechin-3-Gallate in Mice Is Mediated through Interleukin 12–Dependent DNA Repair
Authors: Syed M. Meeran, Sudheer K. Mantena, Santosh K. Katiyar
Journal: Clinical Cancer Research (2018)

The editors are publishing this note to alert readers to a concern about this article (1): Fig. 2A (panel labeled "UV 1/2h", "IL12 KO treated with EGCG") and Fig. 3A (panel labeled "UV alone") are from overlapping sections of the same image. Original data are not available for review.
Cholera
Authors: J. Bird
Journal: BMJ (1849)

SOME writers on Cholera would establish a difference between cases of endemic and epidemic origin; distinguishing varieties of serous diar- rhoea, attended by depression of nervous energy, feebleness of the cir- culation, and low animal heat, as forms of pseudo-Cholern.There is no foundation, however, for this distinction; cases of diarrhoeal Cholera, caused by functional blood lesions, may be converted by neglect, or the employment of purgatives, into well-marked attacks of Cholera.In such, as I shall clinically illustrate, languor, lassitude, nausea, and diarrhoea, accompanied by alternating chills and heats, may precede, even for seve- ral days, the appearance of purely serous, rice-water-like stools, and the algide stage.During the epidemic of 1818, I frequently witnessed cases of this kind, and have good ground for belief, derived from per- sonal observation, that between these and the endemic Cholera attacks,
Mixed reception for myocardial revascularization
Journal: JAMA (1970)

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
Endothelium-specific loss of murine thrombomodulin disrupts the protein C anticoagulant pathway and causes juvenile-onset thrombosis
Authors: Berend Isermann, Sara B. Hendrickson, Mark Zogg, Mark Wing, Marjorie Cummiskey, Yaz Y. Kisanuki, Masashi Yanagisawa, Hartmut Weiler
Journal: Journal of Clinical Investigation (2001)

The thrombomodulin (TM) gene was ablated in mice in a cell type–restricted manner from vascular endothelium by Cre-recombinase–mediated excision controlled by the endothelial cell lineage–specific Tie2 promoter. Forty percent of mutant (TMLox-) mice display a distinct lethal embryonic phenotype not observed in completely TM-deficient embryos. The remaining 60% of TMLox mice survive beyond birth, but invariably succumb to a severe hypercoagulable state and massive thrombosis after 3 weeks, terminating in a lethal consumptive coagulopathy. The progression of thrombosis was age- and sex-dependent. Disruption of the TM/protein C pathway was not associated with a latent proinflammatory state. Disease onset and progression could be prevented by warfarin anticoagulation. These results show that in mice, loss of endothelial cell TM function causes spontaneous and fatal thrombosis in the arterial and venous circulation, resulting from unfettered activation of the coagulation system. The combination of complete disease penetrance, uniform disease onset at young age, large vessel thrombosis of the extremities and multiple organ systems, and consumptive coagulopathy as the disease end-point provides a unique mouse model of human thrombotic disease.
Persistent Vegetative State and the Decision to Withdraw or Withhold Life Support
Journal: JAMA (1990)

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
In This Issue
Journal: Journal of Clinical Investigation (2007)

Leptin gives itself some negative feedbackLeptin is a regulator of energy homeostasis that acts in the CNS to tell the body that energy stores have been restocked and that it can stop feeding.Many individuals who are obese exhibit leptin resistance (an inappropriately small response to high leptin levels), and one possible cause of this is that leptin might poorly activate its receptor (LRb).To gain insight into the physiologic function of a specific leptin-stimulated LRb signal, Björnholm and colleagues generated mice in which one of the LRb tyrosine residues (Tyr985) that is phosphorylated following leptin binding was mutated (pages 1354-1360).Female but not male mice expressing two mutant LRb molecules weighed less than normal mice, did not become obese when fed a high-fat diet, and exhibited decreased feeding and decreased production of neuropeptides that stimulate appetite.In addition, these female mice were more sensitive to leptin administration than wild-type female mice.These data indicate that leptin-mediated phosphorylation of Tyr985 inhibits leptin-mediated LRb signaling in female mice.The authors therefore propose that this negative-feedback pathway might contribute to leptin resistance in some obese individuals, in particular, females.
Sedating Drugs and Neuromuscular Blockade During Mechanical Ventilation
Authors: George Benzing
Journal: JAMA (1992)

<h3>To the Editor.</h3> —In a recent report, Hansen-Flaschen et al<sup>1</sup>discussed the results of their survey of 164 hospitals regarding the "Use of Sedating Drugs and Neuromuscular Blocking Agents in Patients Requiring Mechanical Ventilation for Respiratory Failure." They reported that neuromuscular blocking agents were used in the treatment of respiratory failure in 98% of the hospitals surveyed. The authors expressed concerns about "how little guidance" can be found in the current literature. We and others have described<sup>2,3</sup>terminal motor axonal neuropathy, motor end-plate changes, and muscle atrophy following prolonged use of neuromuscular-blocking agents. We observed a prolonged myasthenic syndrome after 1 week of neuromuscular blockade in a 28-month-old boy. He required brief additional respirator support because of muscular weakness. Electrodiagnostic studies showed a presynaptic disorder similar to what is seen in myasthenic syndromes. Ultrastructural study of an intercostal muscle biopsy specimen obtained 17 days after the onset of weakness
IMMUNITY FROM TUBERCULOSIS
Journal: JAMA (1927)

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
Cervical Osteomyelitis
Authors: John A. D'Elia
Journal: JAMA (1979)

<h3>To the Editor.—</h3> Drs Parker and Tuazon have succinctly described two patients with vertebral osteomyelitis acquired in association with chronic hemodialysis (240:50, 1978). Other reports have suggested urinary tract disease,<sup>1</sup>intravenous drug abuse,<sup>2</sup>and indwelling intravenous catheters<sup>3</sup>as the route of entry. In a review of our experience with vertebral osteomyelitis among insulin-dependent diabetics,<sup>4</sup>we uncovered only one with chronic bacteriuria and one with prior osteomyelitis as potential portals of entry. Subsequently, we have observed vertebral osteomyelitis in an immunosuppressed patient following successful renal transplantation at a time when glucocorticoid-induced diabetes had developed. We have not found vertebral osteomyelitis in our dialysis patients. Thus, we would emphasize the importance of underlying systemic disease in predisposition to vertebral osteomyelitis, as well as the probability of an increased incidence with the use of immunosuppressive drugs. The absence of an obvious portal of entry reinforces the concept of a diagnostic
Nontherapeutic problems of generic drugs lead to call for FDA, legislative diagnosis and cure
Authors: C. Marwick
Journal: JAMA (1989)

GENERIC DRUGS, the favored child of medical care cost cutters, have come under suspicion following revelations that some manufacturers may have engaged in dubious manufacturing and testing practices and about the bribing of Food and Drug Administration (FDA) employees. The Inspector General's Office in the Department of Health and Human Services investigated these allegations under the auspices of the US Attorney's Office. Subsequently criminal charges were lodged. To date, three FDA employees, three drug company employees, and two companies have pleaded guilty to charges of corruption, says a report by Richard Kusserow, the department's inspector general. At the same time, "there is no evidence to date to suggest the quality of generic drug products has been compromised," says Louis W. Sullivan, MD, secretary of the Department of Health and Human Services. Frank E. Young, MD, FDA commissioner, agrees, and the two officials have announced steps to put tighter controls on
Archives of Physical Medicine, Chicago
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 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
Barbara Starfield
Authors: N. Stafford
Journal: BMJ (2011)

<h3>Abstract</h3> Iron superoxide dismutase 1 (FSD1) was recently characterized as a plastidial, cytoplasmic, and nuclear superoxide dismutase with osmoprotective and antioxidative functions. However, its role in oxidative stress tolerance is not well understood. Here, we characterized the role of FSD1 in response to methyl viologen (MV)-induced oxidative stress in <i>Arabidopsis thaliana</i>. The findings demonstrated that the antioxidative function of FSD1 depends on the availability of Cu<sup>2+</sup> in growth media. Prolonged MV exposure led to a decreased accumulation rate of superoxide, higher levels of hydrogen peroxide production, and higher protein carbonylation in the <i>fsd1</i> mutants and transgenic plants lacking a plastidial pool of FSD1, compared to the wild type. MV led to a rapid increase in FSD1 activity, followed by a decrease. Chloroplastic localization of FSD1 is necessary for these changes. Proteomic analysis showed that the sensitivity of the <i>fsd1</i> mutants coincided with decreased abundance of ferredoxin and light PSII harvesting complex proteins, with altered levels of signaling proteins. Collectively, the study provides evidence for the conditional antioxidative function of FSD1 and its possible role in signaling.
THE PROBLEM OF A SATISFACTORY MILK SUPPLY.
Journal: JAMA (1904)

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
Otto Meyerhof (1884-1951)
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 3541: Significance of osteopontin in the sensitivity of malignant pleural mesothelioma cells to pemetrexed.
Authors: Masahiro Seike, Susumu Takeuchi, Chie Soeno, Rintaro Noro, Yuji Minegishi, Akihiko Gemma
Journal: Cancer Research (2013)

Abstract Introduction: Malignant pleural mesothelioma (MPM) is one of the fatal cancers associated with asbestos exposure.Pemetrexed (PEM) is currently recommended as one of the antitumor drugs consisted of standard therapies for MPM.However, the mechanism of the sensitivity of MPM to PEM remains unclear. Methods: We analyzed the antitumor effects of PEM in six MPM cell lines by MTS assay. To identify genes associated with drug sensitivity,we conducted gene expression profiling on the same set of cell lines using Affymetrix HG-U133A GeneChips. Pathway analysis was performed to provide a viewpoint of the biological function of the genes. Results: Three cell lines were sensitive to PEM. Eighteen transcripts and fourteen genes identified by Gene-chips were significantly correlated with sensitivity to PEM. Pathway analysis revealed that SPP1/OPN was an important target in PEM sensitivity. Overexpression of SPP1 was observed in the sensitive cells by Western blotting. Introduction of SPP1 by lentiviral vector significantly enhanced the invasion activities of MPM cells. Expression of SPP1/OPN and AKT phosphorylation were significantly decreased after PEM treatment of the PEM-sensitive cells. PEM treatment with SPP1/OPN knockdown inhibited the PEM-induced cell growth inhibitory effect in PEM-sensitive cells. Conclusions: Our results suggest that SPP1 may be used as a single predictive biomarker of the effectiveness of PEM treatment in MPM. Patient selection based on SPP1/OPN expression may be useful for future clinical development of PEM therapy for MPM. Citation Format: Masahiro Seike, Susumu Takeuchi, Chie Soeno, Rintaro Noro, Yuji Minegishi, Akihiko Gemma. Significance of osteopontin in the sensitivity of malignant pleural mesothelioma cells to pemetrexed. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3541. doi:10.1158/1538-7445.AM2013-3541