tbuckley/cabot-search huggingface dataset:
QUININ IN CHOLERA.
Journal: JAMA (1894)

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
Continuing Medical Education: D Is for Delay
Authors: Elisabeth Sanchez-Padilla, Matthias Merker, Frauke Jochims, Themba Dlamini, Patricia Kahn, Maryline Bonnet, Stefan Niemann, Drs Sanchez-Padilla, Mr Beckert
Journal: New England Journal of Medicine (2015)

unreliable in Swaziland, since it can miss a substantial percentage of strains that may be resistant to rifampin.
Abstract 5276: Sumoylation Of Klf5 Is A Molecular Switch Regulating Ppar-δ-containing Transcriptional Programs Of Lipid Metabolism
Authors: Yumiko Oishi, Ichiro Manabe, Kazuyuki Tobe, Takashi Kadowaki, Ryozo Nagai
Journal: Circulation (2008)

Metabolic syndrome is increasingly recognized as a major risk factor for cardiovascular disease. We have previously shown that a zinc finger transcription factor, Krüppel-like factor 5 (KLF5), plays an important role in cardiovascular diseases, such as atherosclerosis and cardiac hypertrophy. Interestingly, KLF5 is also expressed in metabolic tissues, such as adipose tissue, skeletal muscle and pancreatic β-cells. Moreover, we found that KLF5 is crucial for adipocyte differentiation. Therefore, it is very likely that KLF5 plays multiple roles in development and progression of metabolic syndrome and its cardiovascular and metabolic consequences including atherosclerotic cardiovascular disease. Indeed, KLF5 heterozygous knockout ( KLF5 +/− ) mice were resistant to high-fat-induced obesity and metabolic syndrome, despite consuming more food than wild-type mice. This appears to in part reflect their enhanced energy expenditure. Expression of the genes involved in lipid oxidation and energy uncoupling, including uncoupling protein (UCP) and carnitine-palmitoyl transferase 1b (CPT1b) was upregulated in the soleus muscles of KLF5 +/− mice. KLF5 could be reversibly modified by small ubiquitin-like modifier 1 (SUMO1), after which SUMOylated KLF5 strongly inhibited CPT1b , UCP3 and UCP2 promoter activity. Results of chromatin immunoprecipitation, two-hybrid, and reporter assays showed that under basal conditions SUMOylated KLF5 associated with transcriptionally repressive regulatory complexes containing unliganded PPARδ and corepressors. However, upon agonist stimulation of PPARδ, the deSUMOylating enzyme was recruited and KLF5 was deSUMOylated. The unSUMOylated KLF5 now formed transactivating complexes with liganded PPARδ and CBP. Thus, SUMOylation appears to be a molecular switch affecting function of KLF5 and the transcriptional regulatory programs governing lipid metabolism. Moreover, KLF5 is essential for the PPARδ agonist-dependent transcriptional control. Results of the present study have established KLF5 as a novel key molecule in lipid metabolism and suggest that the posttranscriptional modification of KLF5 is an attractive novel therapeutic target for both metabolic and cardiovascular diseases.
Reports of Problems With Use of Liquid-Dosing Devices
Journal: JAMA (1994)

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
Effects of Ozone Exposure on Lipid Metabolism in Human Alveolar Macrophages
Authors: Mitchell Friedman, Michael C. Madden, James M. Samet, Hillel S. Koren
Journal: Environmental Health Perspectives (1992)

Alveolar macrophages (AM) store arachidonic acid (AA), which is esterified in cellular phospholipids until liberated by phospholipase A2 or C after exposure to inflammatory stimuli. After release, there can be subsequent metabolism of AA into various potent, biologically active mediators including prostaglandins and platelet-activating factor (PAF). To examine the possibility that these mediators may account for some of the pathophysiologic alterations seen in the lung after ozone (O3) exposure, human AM were collected by bronchoalveolar lavage of normal subjects, plated into tissue culture dishes, and the adherent cells were incubated with [3H]AA or [3H]lysoPAF. Human AM exposed to 1.0 ppm O3 for 2 hr released 65 +/- 12% more tritium, derived from [3H]AA, than paired, air-exposed controls into media supernatants. In other studies using a similar O3 exposure protocol, there was also a significant increase in human AM prostaglandin E2 production (2.0 +/- 0.5-fold increase above air-exposure values, p less than 0.01, n = 17). In additional studies, using a similar O3 exposure protocol (1.0 ppm for 1 hr), there was also a significant increase in human AM PAF content (1.7 +/- 0.2-fold increase above air-exposure values, p less than 0.02, n = 5). These potent lipid mediators, originally derived from human AM, may play an important role in the mechanisms of O3 lung toxicity.
New approach to treatment of recent stroke?
Authors: G D Perkin
Journal: BMJ (1979)

patients with severe depressions, and the expectation is that those patients with elevated 2-7 patterns will show more antidepressant responses to lithium than those with lower 2-7 patterns, our findings suggest that obsessional thinking might be as important as depression as a discriminator variable of antidepressant responses to lithium.For example, when scale 7 was used alone, our results approximated the 2-7 hit rate found by House and Martin (74",, v 8000 respectively) for the responders, suggesting that response to lithium is almost equally dependent on high scores on obsessional thinking almost as much as on depression.These suggestions from several studies seem worthy of further investigation, given the interest being taken in attempts to find patient subgroups and potential responders prior to the weeks of treatment usually required to evaluate response or non-response to psychoactive drugs.
WHISKY PREFERENCES.
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
Success Shown for Hand-in-Hand
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Success Shown for Hand-in-Hand Get access JNCI: Journal of the National Cancer Institute, Volume 85, Issue 10, 19 May 1993, Page 779, https://doi.org/10.1093/jnci/85.10.779 Published: 19 May 1993
Insomnia
Authors: Daniel J. Buysse
Journal: JAMA (2013)

<h3>Importance</h3>Insomnia is one of the most prevalent health concerns in the population and in clinical practice. Clinicians may be reluctant to address insomnia because of its many potential causes, unfamiliarity with behavioral treatments, and concerns about pharmacologic treatments.<h3>Objective</h3>To review the assessment, diagnosis, and treatment of insomnia in adults.<h3>Evidence Review</h3>Systematic review to identify and summarize previously published quantitative reviews (meta-analyses) of behavioral and pharmacologic treatments for insomnia.<h3>Findings</h3>Insomnia is a common clinical condition characterized by difficulty initiating or maintaining sleep, accompanied by symptoms such as irritability or fatigue during wakefulness. The prevalence of insomnia disorder is approximately 10% to 20%, with approximately 50% having a chronic course. Insomnia is a risk factor for impaired function, development of other medical and mental disorders, and increased health care costs. The etiology and pathophysiology of insomnia involve genetic, environmental, behavioral, and physiological factors culminating in hyperarousal. The diagnosis of insomnia is established by a thorough history of sleep behaviors, medical and psychiatric problems, and medications, supplemented by a prospective record of sleep patterns (sleep diary). Quantitative literature reviews (meta-analyses) support the efficacy of behavioral, cognitive, and pharmacologic interventions for insomnia. Brief behavioral interventions and Internet-based cognitive-behavioral therapy both show promise for use in primary care settings. Among pharmacologic interventions, the most evidence exists for benzodiazepine receptor agonist drugs, although persistent concerns focus on their safety relative to modest efficacy. Behavioral treatments should be used whenever possible, and medications should be limited to the lowest necessary dose and shortest necessary duration.<h3>Conclusions and Relevance</h3>Clinicians should recognize insomnia because of its effects on function and health. A thorough clinical history is often sufficient to identify factors that contribute to insomnia. Behavioral treatments should be used when possible. Hypnotic medications are also efficacious but must be carefully monitored for adverse effects.
Regional Anesthesia
Authors: Joseph M. Dondanville, Morris J. Nicholson
Journal: New England Journal of Medicine (1948)

THE war and the following years witnessed a widespread increase of interest in regional anesthesia. This was a natural sequence to the emphasis placed upon the role of anesthesia in war surgery. Many of the young physicians who received training in anesthesiology during the war have chosen to complete their training in that specialty. Their enthusiasm has added to the magnitude of experimental and clinical investigation of the postwar period. Differential spinal block has furnished new evidence of the mechanism of nerve block. New diagnostic and therapeutic sympathetic blocks have broadened the field of the anesthesiologist. Segmental spinal anesthesia invites . . .
Genetic Aspects of Toxicity during Development
Authors: Daniel W. Nebert, Snorri S. Thorgeirsson, George H. Lambert
Journal: Environmental Health Perspectives (1976)

The Ah locus in the mouse controls the induction of cytochrome P1-450 and at least eleven associated monooxygenase activities. These enzyme systems metabolically potentiate and detoxify drugs, environmental pollutants, and other foreign chemicals, as well as numerous endogenous substrates. For certain substrates, it is known that cytochrome P1-450 produces different reactive intermediates and products that other forms of P-450. Alleles at the Ah locus can be identified in utero. Development toxicity (in the form of stillborns, resorptions, and malformations of the fetus) by 3-methylcholanthrene and 7,12-dimethylbenz[a]anthracene given to the pregnant mother is associated with genetically mediated aromatic hydrocarbon responsiveness in C5BL/6N mice, compared with that in nonresponsive AKR/N mice. Acetaminiphen-produced hepatic necrosis is associated with glutathione depletion in the liver, covalent binding of metabolite(s) of the drug to cellular macromolecules, and P1-450 induction controlled by the Ah locus. For reasons not known, the fetus and mice 10 days of age or less are relatively resistant to glutathione depletion and therefore hepatic necrosis by acetaminophen.
DUPLICATE TWINS AND DOUBLE MONSTERS.
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
Gene Therapy
Authors: Eric D. Albright
Journal: JAMA (1995)

<b>Cancer Gene Therapy</b>, edited by R. E. Sobol and K. J. Scanlon, quarterly, $175 (institutions), $80 (individuals), Norwalk, Conn, Appleton &amp; Lange, March 1994-. Despite the phenomenal growth in research and clinical trials of gene therapy, until recently the only journal devoted exclusively to the topic was<i>Human Gene Therapy</i>(New York, NY: Mary Ann Liebert; 1990- ). Last year, two new journals,<i>Gene Therapy and Cancer Gene Therapy</i>, were founded to help carry the rising publication load. <i>Human Gene Therapy</i>continues to be the dominant journal in the field in terms of number and quality of articles. Yet, the two new entries seem well positioned to compete effectively, each taking a slightly different approach. Both of the new journals are peer-reviewed publications that present articles for clinicians as well as basic researchers. Both new journals contain primarily research articles along with some reports of current clinical trials. They present their
The Barton First-Aid Text-Book. A Manual for the Student in First-Aid.
Journal: JAMA (1906)

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
A formula for calculating the dosages of drugs in emergencies
Authors: D. Chen
Journal: JAMA (1987)

<h3>In Reply.—</h3> Dr Chen is correct to point out that "minute" need not appear in the final two versions of the universal drip formula. The formula and its use do not change, however, and a practitioner need only choose the dosage rate of the drug (in micrograms per kilogram per minute), roughly estimate the patient's weight (in kilograms), and multiply by a constant (0.5) to derive the milligrams of drug needed for a standard volume (250 mL) and drip rate (30 mL/h). The recommendation by Dr Chen to start an intravenous infusion with a drip rate of 3 or 6 mL/h and to increase the rate every ten minutes to avoid volume overload in infants raises precisely the same concerns addressed previously about slow drip rates.<sup>1</sup>If Dr Chen's recommendations are followed, then an inordinately long time (more than 30 minutes) would elapse before intermediate and efficacious dosage rates
Reinstituting warfarin in patients who develop warfarin skin necrosis
Authors: Anand P. Jillella, Charles L. Lutcher
Journal: American Journal of Hematology (1996)

Skin necrosis is a rare but serious complication of oral anticoagulation with coumarin derivatives. Frequently, the necrosis can be extensive and may result in major morbidity and mortality. The majority of these patients require prolonged anticoagulation for life-threatening conditions such as deep venous thrombosis and pulmonary embolism. Resuming oral anticoagulants in the face of skin necrosis is a difficult decision for both the patient and the physician. Because long-term heparin therapy is inconvenient and is associated with significant side effects, we reviewed the literature to find alternative treatment strategies. A Medline search was done, and all papers published in English since 1967 were reviewed. Of 58 cases with skin necrosis attributed to oral anticoagulants, oral anticoagulation was resumed in 7 patients with no resulting adverse effects. Warfarin is the most widely used coumarin derivative in the United States. Based on our review, we make recommendations for resuming warfarin in patients who have developed skin necrosis when the clinical condition absolutely requires prolonged anticoagulation. © 1996 Wiley-Liss, Inc.
PTU-074 Low-Dose Thiopurine and Allopurinol Co-Therapy Results in Significant Cost Savings at a District General Hospital
Authors: H E Johnson, H M Dewhurst, S A Weaver, S D McLaughlin
Journal: Gut (2013)

<h3>Introduction</h3> Thiopurines are used for maintenance of remission in IBD. In England and Wales biologics are approved by NICE (National institute for health and clinical excellence) for Crohn’s disease (CD) but not ulcerative colitis. Adalimumab is recommended in preference to infliximab in patients over 65kg due to cost. Published data report &gt; 50% of patients stop thiopurines due to theraputic failure, hepatitis or side effects. In this situation most UK clinicians start biologics in CD patients. This has significant cost implications. An alternative treatment strategy is low dose thiopurine and allopurinol (LDTA) co-therapy which is effective in most patients who fail standard dose thiopurines. Some patients require liquid thiopurine to achieve the correct (low) dose -this formulation is significantly more costly than tablets. We report the annual cost savings from adopting this strategy at our centre. <h3>Methods</h3> We maintain a prospective IBD database. Patients with CD treated with LDTA in preference to biologic therapy were identified. The annual drug costs of their treatment with LDTA compared with biologic therapy (adalimumab for patients over 65kg, infliximab for patients &lt; 65kg) were calculated including the cost for the formulation of thiopurine used (liquid/capsule/tablets) and the dose prescribed. Costs of attending the day unit for an infusion were not included. <h3>Results</h3> 17 CD patients who failed standard thiopurine and were eligible for biologics were identified over a 1 year period (Sept 2011-Sept 2012). Of these 4 (24%) failed LDTA and progressed to biologics, 13 (76%) entered a sustained clinical remission. Mean weight of patients = 77.3kg (range: 53.5–105), 6 (46%) patients required a liquid thiopurine. Mean calculated costs were: thiopurine £451.95 (range: £48.48-£1345.44). biologic: £11,331 (range: £10,560-£16,081). Mean cost saving per patient: £10,879 (range: £9,215-£15,146). Total cost saving: £141,427. <h3>Conclusion</h3> We have previously reported that low dose thiopurine and allopurinol co-therapy is safe and effective. In the present study we have identified significant annual cost savings can be made when this treatment strategy is used to prevent escalation to biologics. These cost savings are likely to be even more significant in the long term since a significant proportion of patients treated with biologic therapy require dose escalation. We believe adopting this strategy more widely could lead to significant health-care savings. <h3>Disclosure of Interest</h3> None Declared