tbuckley/cabot-search huggingface dataset:
Plasma phospholipid n-3 polyunsaturated fatty acids, fatal ischemic heart disease, and non-fatal myocardial infarction in older adults.
Authors: Rozenn N Lemaitre, David S Siscovick, Irena B King, Lewis H Kuller, Russell P Tracy
Journal: Circulation (2001)

0013 BACKGROUND. Studies in middle-aged populations suggest that the intake of both long-chain and intermediate chain n-3 polyunsaturated fatty acids (PUFAs) is associated with a reduction in fatal ischemic heart disease (IHD) but not with non-fatal myocardial infarction (MI). OBJECTIVES. To assess the associations of plasma phospholipid n-3 PUFAs, a biomarker of n-3 PUFA intake, with both incident fatal IHD and incident non-fatal MI in older adults. METHODS. We conducted a nested case-control study using data from the Cardiovascular Health Study, a prospective cohort study of adults 65 and older. We identified 54 incident cases of fatal IHD (fatal MI and coronary heart disease death) and 130 incident cases of non-fatal MI. Controls, randomly selected, were matched to the cases on age, gender, clinic, and month of blood draw at a ratio of 1:1. Sampled cases and controls were free of IHD or stroke at the time of the blood draw. Bloods were collected at the baseline CHS examination. Plasma phospholipid PUFAs were measured using gas chromatography. RESULTS. An increase of one standard deviation in plasma phospholipid levels of combined docosahexaenoic acid (22:6n3) and eicosapentaneoic acid (20:5n3) (1% of total fatty acids) was associated with a decreased risk of fatal IHD (Odds ratio: 0.38, 95% CI [0.18-0.82]) but was not associated with non-fatal MI (Odds ratio: 1.01, 95% CI [0.78-1.30]) after adjustment for age, education, systolic blood pressure, weight, and fasting plasma glucose levels. Similarly, an increase of one standard deviation in plasma phospholipid levels of linolenic acid (0.06% of total fatty acids) was associated with a decreased risk of fatal IHD (Odds ratio: 0.46, 95% CI [0.22-0.95]) but was not associated with non-fatal MI (Odds ratio: 1.00, 95% CI [0.76-1.31]). CONCLUSIONS. Higher plasma phospholipid levels of long-chain and intermediate chain n-3 PUFAs are associated with a decreased risk of incident fatal IHD but are not associated with incident non-fatal MI in older adults. These findings are consistent with studies suggesting an anti-arrhythmic effect of n-3 fatty acids.
Methadone maintenance patients in general medical practice. A preliminary report
Authors: D. M. Novick
Journal: JAMA (1988)

Medical maintenance is the treatment by primary care physicians of rehabilitated methadone maintenance patients who are stable, employed, not abusing drugs, and not in need of supportive services. In this research project, physicians with experience in drug abuse treatment provided both the pharmacologic treatment of addiction as well as therapy for other medical problems, as needed. Decisions regarding treatment were based on the individual needs of the patient and on currently accepted medical practice rather than on explicit regulations. We studied the first 40 former heroin addicts who were transferred to this program from more conventional methadone clinics. At a follow-up visit at 12 to 55 months, 33 (82.5%) of 40 patients had remained in treatment; five (12.5%) had been discharged because of cocaine abuse and two (5%) had been voluntarily discharged. Personal benefits of medical maintenance include the dignity of a standard professional atmosphere and a more flexible reporting schedule. This program has the potential for improving treatment of selected methadone maintenance patients. (<i>JAMA</i>1988;259:3299-3302)
Health Politics
Journal: JAMA (2002)

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
Journal of Clinical Investigation, Boston
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 A59: A novel bispecific FAP-DR5 antibody inducing potent and tumor-specific death receptor 5 (DR5) activation by fibroblast activation protein (FAP) dependent crosslinking
Authors: Katharina Wartha, Barbara Weiser, Thomas Friess, Meher Majety, Valeria Runza, Frank Herting, Thomas Weber, Werner Scheuer, Suzana Vega Harring, Hadassah Sade, Huifeng Niu
Journal: Cancer Research (2015)

Abstract Background: Activation of the extrinsic apoptosis pathway in tumor cells through agonistic death receptor 5 (DR5) antibodies has been evaluated in the clinic with limited success so far. In this context, several reports show that DR5 activation is strongly dependent on receptor hyperclustering on the cell surface. Therefore a therapeutic principle that induces DR5 hyperclustering specifically at the tumor site may provide superior efficacy, potency and safety compared to conventional DR5 agonistic antibodies. Fibroblast activation protein (FAP) is a marker for activated fibroblasts and abundantly expressed in cancer associated fibroblasts of various epithelial tumor indications and as a tumor antigen on tumors of mesenchymal origin. Due to its relative absence from normal tissues, FAP can be used as a tumor targeting antigen. Here, we are using the broad expression of FAP in tumor stroma for crosslinking of DR5 by a bispecific antibody. Aim: In order to achieve superior tumor targeting and tumor located DR5 hyperclustering we have generated a bispecific antibody, RG7386, comprised of an agonistic DR5 binder and a FAP targeting moiety. Results: RG7386 shows potent and selective binding to FAP and DR5 and can simultaneously bind to both targets. In in vitro co-culture assays, using human DLD1 colon tumor cells and FAP expressing fibroblasts, RG7386 induces potent, FAP dependent DR5 hyperclustering and apoptosis induction in DR5 positive tumor cells (IC50: 0.05 nM). In preclinical in vivo models with co-injection of DLD-1 tumor cells and fibroblasts as well as patient-derived colorectal cancer models, RG7386 shows FAP dependent efficacy and apoptosis induction superior to conventional DR5 antibodies. Furthermore the superior induction of apoptosis could be confirmed by in vivo and ex vivo analysis of cleaved Caspase-3 with imaging, Luminex and histopathology. Conclusion: RG7386 is a promising novel therapeutic entity for the treatment of solid tumors with FAP positive tumor stroma inducing DR5 activation by FAP dependent DR5 hypercrosslinking which results in potent anti-tumor activity. Citation Format: Katharina Wartha, Barbara Weiser, Thomas Friess, Meher Majety, Valeria Runza, Frank Herting, Thomas Weber, Werner Scheuer, Suzana Vega Harring, Hadassah Sade, Huifeng Niu. A novel bispecific FAP-DR5 antibody inducing potent and tumor-specific death receptor 5 (DR5) activation by fibroblast activation protein (FAP) dependent crosslinking. [abstract]. In: Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; 2014 Feb 26-Mar 1; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(1 Suppl):Abstract nr A59. doi:10.1158/1538-7445.CHTME14-A59
Critique and cavil
Authors: G. X. Trimble
Journal: JAMA (1974)

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
The role of major histocompatibility complex and non-major histocompatibility complex encoded antigens in generation of bile duct lesions during hepatic graft-vs.-host responses mediated by helper or cytotoxic T cells
Authors: F Williams
Journal: Hepatology (1994)

In these studies, we examined the role of discrete classes of alloantigen differences in generating nonsuppurative cholangitis during graft-vs.-host disease. Transfer of C57BL/6J (B6) splenocytes to class I major histocompatibility complex-disparate bm1 × B6 F1, class II major histocompatibility complex-disparate B6 × bm12 F1, or multiple non-major histocompatibility complex antigen-disparate Balb,B × B6 F1 mice led to the development of periportal inflammatory infiltrates and lymphocyte invasion of bile duct walls. However, frank destruction of bile duct walls was observed only in strain combinations with class I majorhistocompatibility complex or multiple non-major histocompatibility complex-encoded disparities. The concomitant presence of class II major histocompatibility complex differences and class I major histocompatibility complex or multiple non-major histocompatibility complex differences did not increase and in some cases was associated with less severe bile duct disease than was observed in strain combinations with discrete histocompatibility antigen differences. Depletion of L-leucyl-L-leucine methyl ester-sensitive cytotoxic T lymphocytes from donor inocula reduced the incidence of destructive bile duct lesions observed early in the course of graft-vs.-host disease in B6→Balb.B × B6 F1 or B6→bm1 × B6 F1 mice. However, transfer of CD8-negative, L-leucyl-L-leucine methyl ester-resistant T helper cells alone was sufficient to generate destructive cholangitis in class I + II major histocompatibility complex-disparate or multiple non-major histocompatibility complex antigen-disparate strain combinations. These findings demonstrate that histologically similar patterns of destructive nonsuppurative cholangitis can be generated by diverse T effector mechanisms directed at class I major histocompatibility complex or non-major histocompatibility complex-encoded antigen differences. However, in this murine graft-vs.-host disease model, the presence of class II major histocompatibility complex-encoded alloantigen differences provided neither a direct nor an additive stimulus for generation of destructive duct lesions. (HEPATOLOGY 1994;19:980–988.)
Immune complexes initiate RSV pathology
Authors: M. L. Zoler
Journal: JAMA (1983)

The American College of Radiology (ACR) has recommended that chest roentgenograms of asymptomatic persons be discontinued as a part of routine prenatal examinations, hospital admissions, tuberculosis screening, and pre-employment examinations. The recommendation is based on studies (<i>N Engl J Med</i>1974;291:1001-1004 and<i>South Med J</i>1977; 70:579-580) indicating that such examinations do not detect a high enough incidence of occult disease to justify the inconvenience, cost, and radiation exposure to the patient. However, the ACR says that chest roentgenograms should still be taken if indicated by the patient's history, results of physical examination or diagnostic tests, or his inclusion in a high risk population. To this end, it recommends that roentgenograms of persons with occupational exposure to substances implicated in pulmonary diseases be taken at intervals appropriate to the latency of the disease. According to Reynold Brown, MD, clinical professor of radiology, University of California Medical School, San Francisco, who
HGCSG1301: A multicenter, double-blind, randomized control phase II trial comparing Hange-shashin-to versus placebo to prevent diarrhea in patients with metastatic colorectal cancer under IRIS/Bev second-line treatment
Authors: M. Dazai, S. Yuki, K. Sawada, T. Muranaka, Y. Kawamoto, H. Nakatsumi, S. Nakano, A. Ishiguro, M. Tateyama, A. Sato, Y. Kobayashi, M. Nakamura, H. Okuda, Y. Takahashi, K. Eto, S. Muto, K. Hatanaka, T. Amano, Y. Sakata, Y. Komatsu
Journal: Annals of Oncology (2018)
Epithelial-Fibroblast Interactions in Bleomycin-Induced Lung Injury and Repair
Authors: Linda Young, Ian Y. R. Adamson
Journal: Environmental Health Perspectives (1993)

Intercellular communication between epithelial cells and fibroblasts of the alveolar wall contributes to regulatory control of each cell type. We examined whether lung injury and subsequent fibrosis are associated with disturbance of this mutual control system. Rats received bleomycin intratracheally, and after 10 days, when acute epithelial injury occurs, and at 6 weeks, when repair with fibrosis is found, pure populations of type 2 epithelial cells and lung fibroblasts were prepared to study interactions with respect to growth control. Epithelial cells were cultured alone, on a permeable filter over fibroblasts, and in co-culture with fibroblasts. The results showed that the low growth rate of normal epithelial cells increased when cells were exposed to fibroblast supernatants. This effect was also seen using cells from the 10-day bleomycin group, but it was diminished in the group treated for 6 weeks. However, epithelial cells from exposed or control rats did not show increased DNA synthesis when grown in contact with fibroblasts in co-culture. In contrast, fibroblast growth was inhibited when exposed to epithelial cell secretions in control cultures and when using cells from the 10-day bleomycin group. No inhibition of fibroblast growth by epithelial cells was found using cells from the fibrotic lungs. These results suggest that after lung injury by bleomycin, a fibroblast-secreted factor promotes epithelial growth; however, during repair, regenerating epithelial cells lose the ability to inhibit fibro-blast proliferation. These local changes in cellular control at the alveolar wall may be sufficient to produce pulmonary fibrosis.
Clinical Lectures on Diseases of the Eye. Including the Conjunctiva, Cornea Sclerotic, Iris and Ciliary body.
Journal: JAMA (1885)

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
THE ORAL Diuretics
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
Ventilator-Associated Pneumonia in Critically Ill Patients
Authors: Deborah Cook
Journal: Annals of Internal Medicine (1999)

Letters15 June 1999Ventilator-Associated Pneumonia in Critically Ill PatientsDeborah Cook, MDDeborah Cook, MDSt. Joseph's Hospital; Hamilton, Ontario L8N 4A6, Canada (Cook)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-130-12-199906150-00011 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Dr. Kramer correctly describes the patients in our study as receiving mechanical ventilation for at least 48 hours. All patients required an endotracheal tube, and noninvasive ventilation was not used.We share Dr. Kramer's interest in using precise language to describe research methods and results. As use of noninvasive ventilation increases, particularly as a strategy for liberating patients from conventional mechanical ventilation (1), new constructs may be useful to more clearly distinguish the temporal and etiologic relations between different life support technologies and nosocomial lung infection. We look forward to the evolution of this lexicon.Reference1. Nava S, Ambrosino N, Clini E, Prato M, Orlando G, Vitacca M, et al . Noninvasive mechanical ventilation in the weaning of patients with respiratory failure due to chronic obstructive pulmonary disease. A randomized, controlled trial. Ann Intern Med. 1998;128:721-8. LinkGoogle Scholar Author, Article, and Disclosure InformationAuthors: Deborah Cook, MDAffiliations: St. Joseph's Hospital; Hamilton, Ontario L8N 4A6, Canada (Cook) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoIncidence of and Risk Factors for Ventilator-Associated Pneumonia in Critically Ill Patients Deborah J. Cook , Stephen D. Walter , Richard J. Cook , Lauren E. Griffith , Gordon H. Guyatt , David Leasa , Roman Z. Jaeschke , and Christian Brun-Buisson Ventilator-Associated Pneumonia in Critically Ill Patients Bruce Kramer Metrics Cited byWhat to Learn from Decision Analysis of Diagnosis and Treatment of Ventilator-associated Pneumonia? 15 June 1999Volume 130, Issue 12Page: 1028KeywordsLungsNoninvasive ventilationNosocomial infectionsVentilator associated pneumoniaVentilators ePublished: 15 August 2000 Issue Published: 15 June 1999 Copyright & PermissionsCopyright © 1999 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
A reluctant surgeon at sea
Authors: A. G. Foraker
Journal: JAMA (1981)

I was a lousy surgeon. A basic lack of manual dexterity plus a profound disinterest in the subject made me reluctant to wield the knife. During my internship in Pittsburgh, and subsequently as a junior medical officer at the US Marine Hospital, Key West, Fla, I assisted at many operations. My nose itched, my back ached, my feet hurt—and I was bored. Finally, I acquired sufficient surgical skill to do a passable appendectomy or hernia repair. But my heart was not in it. In January 1942 I was assigned as medical officer of the icebreaker<i>North Star</i>for duty in Greenland and the North Atlantic. I considered various possible situations that might require surgery at sea. I decided not to do appendectomies except in dire circumstances. My ability as a surgeon was limited. My surgical assistants would be pharmacist's mates, with little operating experience. No professional anesthetist was available. The
Aseptic Meningitis, Trimethoprim, and Sjögren's Syndrome
Authors: Suzanne M. DE la Monte
Journal: JAMA (1985)

<h3>To the Editor.—</h3> The CASE REPORT, "Trimethoprim-Induced Aseptic Meningitis," by Dr Derbes<sup>1</sup>published recently inThe Journaldescribes a patient with Sjörgen's syndrome who, on several well-documented occasions, exhibited an allergic response or hypersensitivity to trimethoprimsulfamethoxazole. While the patient clearly manifested central nervous system (CNS) signs and symptoms after taking sulfa drugs, the author does not demonstrate that the exudate in the cerebrospinal fluid (CSF) was related to or caused by its administration. The abruptness and rapidity of onset of neurologic symptoms following the use of trimethoprim strongly suggest that her response was probably vascular in origin. In contrast to Dr Derbes' statement, our recent studies demonstrated that aseptic meningitis occurs commonly in patients with Sjögren's syndrome.<sup>2,3</sup>Patients with Sjögren's syndrome frequently have polymorphous inflammatory infiltrates in the leptomeninges, and characteristic atypical mononuclear cells are usually present in CSF. The neurologic symptoms associated with the polymorphous meningitis of