tbuckley/cabot-search huggingface dataset:
Obituaries
Journal: JAMA (1979)

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Current Medical Literature.
Journal: JAMA (1901)

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Research brief
Authors: Dara Mohammadi
Journal: The Lancet Infectious Diseases (2020)

Bats, thought to be the ancestral hosts of coronaviruses that cause disease in people, do not themselves become ill when infected, and nobody knows why. Findings from an in-vitro study show that the Middle East respiratory syndrome coronavirus persists in bat cells thanks to a delicate immunological interplay between cell and virus. Bat cells seem able to upregulate type I interferon, which suppresses viral replication to avoids the cell death seen in infected human cells. The virus also adapts by rapidly mutating a specific gene in the viral open reading frame 5.
Economics
Authors: John M. Eisenberg
Journal: JAMA (1992)

In the election year of 1992, health insurance has been a central issue in the campaigns of politicians of every stripe. As the old saying goes, "Politics makes strange bedfellows," and so it is with health insurance. The business community is concerned that the cost of medical care makes the price of doing business in the United States too high. Middle-income Americans are worried that they cannot afford adequate health insurance. The poor are convinced that their medical care is excessively and unjustly rationed because they cannot buy access to it and because public programs are insufficient for them to gain entry to mainstream medical care. Recent health services research has investigated the economics of access to care and has demonstrated that the problem is real and serious. Physician visits for low-income Americans decreased 8% during the middle 1980s, while visits for others, even controlling for the lower use expected
Cytoplasmic RNA quality control failure engages mTORC1-mediated autoinflammatory disease
Authors: Kun Yang, Jie Han, Mayumi Asada, Jennifer G. Gill, Jason Y. Park, Meghana N. Sathe, Jyothsna Gattineni, Tracey Wright, Christian A. Wysocki, M. Teresa de la Morena, Luis A. Garza, Nan Yan
Journal: Journal of Clinical Investigation (2022)

Inborn errors of nucleic acid metabolism often cause aberrant activation of nucleic acid sensing pathways, leading to autoimmune or autoinflammatory diseases. The SKIV2L RNA exosome is cytoplasmic RNA degradation machinery that was thought to be essential for preventing the self-RNA-mediated interferon (IFN) response. Here, we demonstrate the physiological function of SKIV2L in mammals. We found that Skiv2l deficiency in mice disrupted epidermal and T cell homeostasis in a cell-intrinsic manner independently of IFN. Skiv2l-deficient mice developed skin inflammation and hair abnormality, which were also observed in a SKIV2L-deficient patient. Epidermis-specific deletion of Skiv2l caused hyperproliferation of keratinocytes and disrupted epidermal stratification, leading to impaired skin barrier with no appreciable IFN activation. Moreover, Skiv2l-deficient T cells were chronically hyperactivated and these T cells attacked lesional skin as well as hair follicles. Mechanistically, SKIV2L loss activated the mTORC1 pathway in both keratinocytes and T cells. Both systemic and topical rapamycin treatment of Skiv2l-deficient mice ameliorated epidermal hyperplasia and skin inflammation. Together, we demonstrate that mTORC1, a classical nutrient sensor, also senses cytoplasmic RNA quality control failure and drives autoinflammatory disease. We also propose SKIV2L-associated trichohepatoenteric syndrome (THES) as a new mTORopathy for which sirolimus may be a promising therapy.
American Journal of Ophthalmology, Chicago
Journal: JAMA (1966)

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Walter Bradford Cannon (1871-1945) Harvard physiologist
Journal: JAMA (1968)

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Hypoglycemia Subtypes in Type 1 Diabetes: An Exploration of the Hypoglycemia Fear Survey-II
Authors: Rory H. Maclean, Peter Jacob, Pratik Choudhary, Simon R. Heller, Elena Toschi, Dulmini Kariyawasam, Augustin Brooks, Mike Kendall, Nicole de Zoysa, Linda A. Gonder-Frederick, Stephanie A. Amiel
Journal: Diabetes Care (2022)

The Hypoglycemia Fear Survey-II (HFS-II) is a well-validated measure of fear of hypoglycemia in people with type 1 diabetes. The aim of this study was to explore the relationships between hypoglycemia worries, behaviors, and cognitive barriers to hypoglycemia avoidance and hypoglycemia awareness status, severe hypoglycemia, and HbA1c.
Arsenic Exposure
Authors: Edward P. Horvath
Journal: JAMA (1985)

<h3>To the Editor.—</h3> Peters et al<sup>1</sup>reported on a family exposed to arsenic in their home from burning plywood treated with copper-chromium-arsenate (CCA). The authors deserve to be commended for describing an unusual form of arsenic exposure and for highlighting the potential hazards of burning treated wood in the home environment. For years the lay literature has issued warnings against burning anything but untreated wood, but this episode underscores the apparent need to repeat this message periodically. The family experienced a variety of diverse and nonspecific complaints, and it seems plausible that at least some of them may have been due to the irritant effects of arsenic-containing dust. The authors admit being puzzled by at least one finding (alopecia). We are likewise puzzled, but by the inference that persons with prolonged environmental exposure to arsenic supposedly causing systemic symptoms would not have detectable levels in the urine. The authors
GERMANY
Journal: JAMA (1962)

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Index
Journal: Cardiovascular Research (1999)

abciximab (43) 183 Autonomic nervous system (43) 237, (43) 437, (43) 739, (43) ACE (43) 549 762, (43) 901, (44) 185 ACE inhibitors (43) 77, (43) 148, (44) 252, (44) 407, (44) 416, Autonomous nervous system (43) 219 (44) 518 AV-node (43) 974, (44) 344 Acetylcholine (43) 364, (43) 607, (43) 762, (44) 390 Biochemistry (43) 909 ACE-gene polymorphism (43) 192 Bioenergetics (43) 248 Acidosis (43) 32 Blood flow (44) 595 Action potential (43) 135, (43) 364 Blood pressure (43) 237, (43) 437, (43) 471, (44) 543, (44) 579 Adenosine (43) 32, (43) 200, (43) 228, (43) 860, (43) 909, (43) 974, (44) 113, (44) 333 Calcium (43) 157, (43) 1029, (44) 101, (44) 146, (44) 381 Adenosine triphosphate (43) 219 Calcium (cellular) (43) 408, (44) 398, (44) 556, (44) 623 Adenoviral vector (43) 788 Calcium channels (43) 1018, (44) 477 Adrenergic (43) 762, (44) 113 Calcium paradox (43) 417 Adrenergic agonists (43) 607, (43) 901 Calcium sensitivity (43) 1018 a -Adrenoceptors (43) 755, (43) 755 1 Cancer chemotherapy (43) 248 Adrenomedullin (43) 958 Canine (43) 901 Adriamycin (43) 248 Canine atrium (43) 364 Afterload (43) 344 Cardiac development (43) 165 Aging (43) 985 Cardiac function (43) 892 Aldehydes (43) 892 Cardiac hypertrophy (43) 838 Aldosterone (43) 7 Cardiac innervation (43) 930 4-Aminopyridine (43) 364 Angiogenesis (43) 44 Cardiac myocytes (43) 666 Angioplasty (43) 731, (43) 808, (44) 156 Cardiac remodeling (43) 192 Angiotensin (43) 148, (43) 300, (43) 879, (44) 166, (44) 252, Cardiomyopathy (43) 58, (43) 77, (43) 96, (43) 354, (43) 382, (44) 407, (44) 527 (43) 398, (43) 492, (43) 884, (44) 20, (44) 91, (44) 266, (44) Angiotensin II (44) 215, (44) 579 549 Anthracyclines (43) 248 Cardiovascular risk factors (43) 192, (43) 658 Antiarrhythmic agents (43) 135, (44) 60, (44) 303 Cardiovascular surgery (44) 47, (44) 81, (44) 436 Antioxidants (43) 248 Cardiovascular system (43) 509 Apo E deficient mice (44) 579 Ca-channel (44) 121, (44) 381, (44) 390 Apoptosis (43) 252, (43) 254, (43) 398, (43) 947, (44) 436, (44) Ca-pump (43) 323 536 Cell adhesion molecules (43) 1003 L-Arginine (43) 712 Cell communication (43) 968 Arrhythmia (mechanisms) (43) 332, (44) 60, (44) 121, (44) 283, Cell culture (43) 675 (44) 303 Cell culture / isolation (44) 370, (44) 398 Arrhythmias (43) 879, (44) 132, (44) 356 Cellular (44) 121 Arteries (43) 471, (43) 481, (43) 1003, (43) 1040, (44) 156, (44) K-channels (43) 135, (44) 121, (44) 283, (44) 356 274, (44) 608 Cholesterol (43) 721, (43) 744, (44) 601 Aspirin (43) 25 Chronotropic agents (43) 712 Atherosclerosis (43) 457, (43) 471, (43) 492, (43) 744, (43) 850, Circulatory physiology (44) 176 (43) 985, (43) 1003, (44) 498, (44) 579, (44) 588 Circulatory physiology arteries (43) 731 ATP (43) 117 Clinical (43) 595 ATP sensitive potassium channels (43) 125 Coenzyme Q (43) 248 10 AT receptors (43) 77 Collateral circulation (44) 294 1 Atrial fibrillation (44) 60 Computer modeling (44) 333 Atrial function (43) 67, (43)
Heme oxygenase-1 expression and apoptosis colocalize in a rat myocardial infarction model P�ivi Lakkisto, Eeva Palojoki, Antti Saraste, Tom B�cklund, Liisa-Maria Voipio-Pulkki, Ilkka Tikkanen, Kari Pulkki. University of Turku, Turku, Finland, Helsinki University Hospital, Helsinki, Finland
Journal: Journal of the American College of Cardiology (2001)
LONDON
Journal: JAMA (1926)

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
Case of Adult Metastatic Medulloblastoma Demonstrated on 18F-DOPA PET/CT
Authors: Fahad Marafi, Alyaa Sadeq, Abdulredha Esmail, Sharjeel Usmani
Journal: Clinical Nuclear Medicine (2022)

Abstract 18 F-DOPA is a promising radiotracer used for both staging and restaging of primary brain tumors based on increased transport via the L-type large neutral amino acid transport system in tumor cells. Adult medulloblastoma is extremely rare. We present a case of 25-year-old man with posterior fossa medulloblastoma treated with surgery followed by chemotherapy and radiotherapy 5 years back, which later developed metastasis to left cerebral lobe treated with gamma knife followed by surgical debulking. Recent 18 F-DOPA PET/CT demonstrates recurrence and disease progression on follow-up scan. 18 F-DOPA PET/CT is extremely useful for characterizing brain tumors, response assessment, and prognosis.
RECEIVED
Journal: JAMA (2003)

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Abstract 17389: The Role of Arterial Stiffness in Mediating the Association Between Grip Strength and Cardiovascular Events: The Korean Genome and Epidemiology Study
Authors: Cheol Ung Choi, Woohyeun Kim, Chol Shin, Jong-il Choi, Seong Hwan Kim, Hong Seog Seo, Chang Gyu Park, Seung-Woon Rha, Eung Ju Kim, Jin Oh Na, Jin Won Kim, Soon Young Suh, Won Young Jang, Yoonjee Park, Eun Jin Park, Dong Oh Kang
Journal: Circulation (2018)

Introduction: Grip strength has been associated with cardiovascular events. However, there have been no exact mechanisms explaining the association between grip strength and cardiovascular events. Hypothesis: The aim of this study was to assess whether arterial stiffness or endothelial function could mediate the association between grip strength and cardiovascular events. Methods: We studied 1508 participants (Age; 60 ± 7, Men; 47.5 %) from the Ansan cohort of the Korean Genome Epidemiology Study. Participants were assessed for grip strength, measured using a Jamar dynamometer. The central blood pressure, the augmentation index, and the pulse wave velocity were evaluated by using an applanation tonometer. Intima medial thickness was measured by B-mode ultrasonogram with a 7.5 MHz linear array transducer. Results: With increasing the grip strength, augmentation index decreased (r= -0.445, p&lt;0.001). Pulse wave velocity (r= -0.044, p=0.109) and carotid intima medial thickness (r= -0.004, p=0.881) had no significant correlation with grip strength. Conclusions: Grip strength was inversely correlated with augmentation index. This result suggests that systemic arterial stiffness could mediate the association between grip strength and cardiovascular events.
Summaries of Key Journal Articles
Authors: Kim A. Eagle, Christopher P. Cannon, William F. Armstrong, David S. Bach, Ragavendra R. Baliga, Anna M. Booher, Timothy B. Cotts, Jennifer Cowger, Daniel T. Eitzman, James B. Froehlich, Caren S. Goldberg, Hitinder S. Gurm, Jennifer C. Hirsch, Elizabeth Anne Jackson, Fred Morady, Debabrata Mukherjee, Himanshu J. Patel, John E. Rectenwald, Melvyn Rubenfire
Journal: Journal of the American College of Cardiology (2011)
The molecular genetics of autoimmune liver disease
Authors: Peter Donaldson, Derek Doherty, James Underhill, Roger Williams
Journal: Hepatology (1994)

ABSTRACT The dual observations that human leukocyte antigens have an antigen–binding groove and that the polymorphism we study as human leukocyte antigen types is largely related to amino acid substitutions in and around that groove have provided a new focus for immunogenetic studies. In autoimmune liver disease, recent studies have described specific amino acid substitutions in the antigen–binding groove of human leukocyte antigen DR molecules that may determine both disease susceptibility, through their direct influence on antigen binding, and the severity of the disease. In autoimmune hepatitis, lysine residues at DRβ position 71 in European subjects and arginine or histidine residues at DRβ position 13 in Japanese subjects may be responsible for much human leukocyte antigen—encoded disease susceptibility. Similar claims have been made for leucine residues at DRβ 38 in primary sclerosing cholangitis and for leucine residues at DPβ 35 in Japanese patients with primary biliary cirrhosis. To date, our knowledge of genetic susceptibility to autoimmune liver disease is incomplete. Other genes may contribute to susceptibility to autoimmune liver disease—for example the contribution of TAP genes, upstream promoter sequences and class III genes on chromosome 6 and the T–cell receptor genes and complement genes elsewhere in the human genome is currently unclear. Additional information concerning the immunogenetic contribution to disease severity is needed to complete the picture. (Hepatology 1994;20:225-239.)