tbuckley/cabot-search huggingface dataset:
The Consult Guys - Hyperglycemia: Am I a Control Freak?
Authors: Geno J. Merli, Howard H. Weitz
Journal: Annals of Internal Medicine (2013)

Web Exclusives17 December 2013The Consult Guys - Hyperglycemia: Am I a Control Freak?FREEGeno J. Merli, MD and Howard H. Weitz, MDGeno J. Merli, MDSearch for more papers by this author and Howard H. Weitz, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/G13-3005 SectionsSupplemental MaterialAboutVisual Abstract ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail The Consult Guys bring a new perspective to the art and science of medicine with lively discussion and analysis of real-world cases and situations.For more videos from and information on The Consult Guys, visit www.annals.org/ConsultGuys. Comments0 CommentsSign In to Submit A Comment Paola Palomino GuillenJencareMed1 March 2021 The Consult Guys - Hyperglycemia: Am I a Control Freak? I loved this presentation. Fun, concise, with punctual information about articles reviewed. Highly appreciated! Author, Article, and Disclosure InformationAuthors: Geno J. Merli, MD; Howard H. Weitz, MDDisclosures: Geno J. Merli, MD, reports the following: Research grants/contracts: Bristol-Myers Squibb, Bayer, sanofi-aventis; Consultancies: Bristol-Myers Squibb, Bayer, sanofi-aventis. Howard H. Weitz, MD, reports that he has no financial relationships or interests to disclose. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 17 December 2013Volume 159, Issue 12Page: CG5KeywordsHyperglycemia ePublished: 17 December 2013 Issue Published: 17 December 2013 Copyright & PermissionsCopyright © 2013 by American College of Physicians. All Rights Reserved.Loading ...
PLA2R1 Mediates Tumor Suppression by Activating JAK2
Authors: David Vindrieux, Arnaud Augert, Christophe A. Girard, Delphine Gitenay, Helene Lallet-Daher, Clotilde Wiel, Benjamin Le Calvé, Baptiste Gras, Mylène Ferrand, Stéphanie Verbeke, Yvan de Launoit, Xavier Leroy, Alain Puisieux, Sébastien Aubert, Michael Perrais, Michael Gelb, Hélène Simonnet, Gérard Lambeau, David Bernard
Journal: Cancer Research (2013)

Abstract Little is known about the physiological role of the phospholipase A2 receptor (PLA2R1). PLA2R1 has been described as regulating the replicative senescence, a telomerase-dependent proliferation arrest. The downstream PLA2R1 signaling and its role in cancer are currently unknown. Senescence induction in response to activated oncogenes is a failsafe program of tumor suppression that must be bypassed for tumorigenesis. We now present evidence that PLA2R1 functions in vitro as a tumor suppressor, the depletion of which is sufficient to escape oncogene-induced senescence (OIS), thereby facilitating oncogenic cell transformation. Furthermore, mice that are genetically deficient in PLA2R1 display increased sensitivity to RAS-induced tumorigenesis by facilitating OIS escape, highlighting its physiological role as a tumor suppressor. Unexpectedly, PLA2R1 activated JAK2 and its effector signaling, with PLA2R1-mediated inhibition of cell transformation largely reverted in JAK2-depleted cells. This finding was unexpected as the JAK2 pathway has been associated mainly with protumoral functions and several inhibitors are currently in clinical trials. Taken together, our findings uncover an unanticipated tumor suppressive role for PLA2R1 that is mediated by targeting downstream JAK2 effector signaling. Cancer Res; 73(20); 6334–45. ©2013 AACR.
AN AIR-DRIVEN ULTRACENTRIFUGE FOR MOLECULAR SEDIMENTATION
Authors: J. Biscoe, E. G. Pickels, Ralph W. G. Wyckoff
Journal: The Journal of Experimental Medicine (1936)

Details of construction are given for an air-driven ultracentrifuge for molecular sedimentation. This instrument, like the standard oil-driven machine of Svedberg, uses rotors giving a 6.50 cm. radius of rotation and has cameras of great depth of focus.
Plasminogen activator inhibitor-1: A novel biochemical of coronary reperfusion
Authors: Felicilta Andreotti, David R. Hackett, M.Carla Roneaglioni, Agha W. Haidier, Graham J. Davies, Mohamed I. Khan, Tessa Regan, Cornelis Kluft, Attilio Maseri
Journal: Journal of the American College of Cardiology (1990)
VIDEO-TO-PAPER DIGITAL GREY SCALE IMAGE FORMATTER
Authors: J. H. Trueblood, R. D. Jeffcoat, J. H. Powell, J. D. Allison, M. E. Morgan
Journal: Clinical Nuclear Medicine (1983)

Trueblood, J. H.; Jeffcoat, R. D.; Powell, J. H.; Allison, J. D.; Morgan, M. E. Author Information
The PI3K/Akt/mTOR pathway in innate immune cells: emerging therapeutic applications
Authors: T Weichhart, M D Saemann
Journal: Annals of the Rheumatic Diseases (2008)

The phosphatidylinositol-3 kinases (PI3Ks) and the mammalian target of rapamycin (mTOR) pathway have long been recognised as critically regulating metabolism, growth or survival. Recent data indicate that these molecules are also integral players in coordinating defence mechanisms in the innate immune system. In this respect, PI3K and mTOR positively regulate immune cell activation in neutrophils and mast cells. In plasmacytoid dendritic cells, these pathways have recently emerged as important regulators for type I interferon production via activation of the interferon-regulatory factor 7. Interestingly, in myeloid immune cells, PI3K and mTOR seem to constrain full immune cell activation by upregulation of the key anti-inflammatory cytokine interleukin 10 and inhibition of proinflammatory cytokines. These new insights into innate immune cell regulation may pave the way for manipulating distinct features of the innate immune system for therapeutic treatment of various inflammatory diseases and for implementation of improved vaccination strategies.
MERCUROCHROME-220 SOLUBLE IN ROCKY MOUNTAIN SPOTTED FEVER
Authors: H. P. Greeley
Journal: JAMA (1924)

I am reporting this case of a disease which has never responded to any method of treatment, because the treatment given was apparently of value. Such a statement is made with the full appreciation of the fact that no one case report can mean much. A woman, aged 28, married, was referred by Dr. Vogel of Elroy, who made the diagnosis. She entered the Madison General Hospital, May 5. Sixteen days before, she had been bitten by a tick while in southeastern Montana. Five days before, on the train coming East, she had a chill followed by vomiting and fever ranging between 102 and 104 F. She had suffered constantly from a splitting headache and acute generalized pains in the muscles, accompanied by exquisite tenderness. The stools for some days before entrance were tarry. Soon after the onset, a generalized spotted rash appeared. She was quarantined for smallpox, but released
Relative importance of thrombin compared with plasmin-mediated platelet activation in response to plasminogen activation with streptokinase.
Authors: K J Winters, S A Santoro, J P Miletich, P R Eisenberg
Journal: Circulation (1991)

BACKGROUND Platelet activation occurs in vivo during pharmacologic thrombolysis and may contribute to recurrent thrombosis. Plasmin does not directly activate platelets except at high concentrations; thus, the mechanisms for platelet activation during thrombolysis remain undefined. Increases in thrombin activity also occur in patients treated with fibrinolytic agents and may contribute to activation of platelets. We have shown that one mechanism for increased thrombin activity is activation of the coagulation system by plasmin. METHODS AND RESULTS In the present study we sought to determine whether activation of platelets in response to pharmacologic activation of plasminogen in plasma is due primarily to plasmin or mediated by increased thrombin activity. Platelet-rich citrated plasma (PRP) was recalcified and incubated with 1,000 IU/ml of streptokinase or 1.0 caseinolytic units/ml of plasmin. Concentrations of fibrinopeptide A, a marker of thrombin activity, increased markedly over 10 minutes in plasma incubated with streptokinase or plasmin, but not in PRP incubated without plasminogen activator. Platelet activation characterized by the secretion of 14C-serotonin occurred within 2-4 minutes after thrombin activity increased. In stirred recalcified PRP, platelet aggregation was accelerated from 3.6 +/- 0.5 to 2.5 +/- 0.3 minutes (p less than 0.01) when incubated with 1,000 IU/ml of streptokinase. Leupeptin and aprotinin, inhibitors of plasmin activity, markedly attenuated platelet activation in response to pharmacologic activation of plasminogen. However, inhibition of thrombin with heparin, hirudin, or D-Phe-D-Pro-L-Arg-chloromethylketone was more effective in inhibiting the acceleration of platelet activation induced by plasminogen activation, despite the elaboration of plasmin activity. CONCLUSIONS Activation of platelets during coronary thrombolysis may be due in part to increased procoagulant activity induced by plasminogen activation as well as other factors that promote platelet activation in vivo.
Hospital Infection: From Miasmas to MRSA
Authors: L. Sanai
Journal: BMJ (2003)

Graham A J Ayliffe, Mary P English Cambridge University Press, £24.95/$38, pp 274 ISBN 0 521 53178 0 Rating: ![Graphic][1]</img>![Graphic][2]</img>![Graphic][3]</img> Next time you wash your hands before or after examining a patient, stop and consider how your action would have been viewed 150 years ago. Your colleagues would have looked at you askance; although a few would have been familiar with the work of various doctors—including John Pringle, James Lind, Alexander Gordon, Oliver Wendell Holmes, and Ignaz Semmelweis—who advocated washing yourself before contact with patients, most would have told you derisively that washing would not affect the miasmas, or … [1]: /embed/inline-graphic-1.gif [2]: /embed/inline-graphic-2.gif [3]: /embed/inline-graphic-3.gif
Digital Doctoring—Opportunities and Challenges in Electronic Patient-Physician Communication
Authors: Tom Ferguson
Journal: JAMA (1998)

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
RECOMMENDATIONS OF THE ALLERGY RESEARCH COUNCIL OF THE ASSOCIATION FOR THE STUDY OF ALLERGY
Authors: Joseph L. Miller
Journal: JAMA (1930)

To the Editor:  —The following report from the Research Council is endorsed for publication by the Executive Council of the Association for the Study of Allergy.  Ray M. Balyeat, M.D., Oklahoma City.  Harry S. Bernton, M.D., Washington, D. C.  William W. Duke, M.D., Kansas City, Mo.  Richard A. Kern, M.D., Philadelphia.  Albert H. Rowe, M.D., San Francisco.  George Piness, M.D., Los Angeles, Chairman.  Warren T. Vaughan, M.D., Richmond, Va.,  Secretary.  Antiallergic therapy is a carefully thought out and conscientious attempt to apply current immunologic theories to the prevention, alleviation and cure of hereditary and acquired hypersensitiveness and allied clinical conditions.  Statistics show that no immunologic theory of the past three decades has been more than 5 per cent clinically efficient (Manwaring, W. H., and Krueger, A. P.: Laboratory-Endorsed Therapeutic Agents,The
Effect of l-arginine on acetylcholine-induced endothelium-dependent vasodilation differs between the coronary and forearm vasculatures in humans
Authors: Yoshitaka Hirooka, Kensuke Egashira, Tsutomu Imaizumi, Tatsuya Tagawa, Hisashi Kai, Masaru Sugimachi, Akira Takeshita
Journal: Journal of the American College of Cardiology (1994)
Plasma level and gene polymorphism of angiotensin-converting enzyme in relation to myocardial infarction.
Authors: F Cambien, O Costerousse, L Tiret, O Poirier, L Lecerf, M F Gonzales, A Evans, D Arveiler, J P Cambou, G Luc
Journal: Circulation (1994)

BACKGROUND The angiotensin-converting enzyme (ACE) plays an important role in the production of angiotensin II and the degradation of bradykinin, two peptides involved in cardiovascular homeostasy. Presence of a polymorphism in the ACE gene (ACE Ss) has been postulated from segregation analysis of plasma ACE in families. This putative polymorphism, which strongly affects the plasma and cellular levels of ACE, probably by modulating ACE gene transcription, has not yet been identified at the molecular level; however, an insertion/deletion polymorphism is present in the 16th intron of the ACE gene (ACE I/D) and appears to be a very good marker for ACE Ss. The biological role of ACE suggests that the ACE gene polymorphism could affect the predisposition to myocardial infarction (MI). METHODS AND RESULTS We have recently shown, in a large case-control study (ECTIM), that the marker allele D of the ACE gene, which is associated with higher levels of ACE in plasma and cells, was more frequent in male patients with MI than in control subjects, especially in patients considered at low risk. ACE activity has now been measured from frozen aliquots of plasma in a large subsample of the ECTIM study (n = 1086). Plasma ACE level did not differ between patients and control subjects in the older age group (&gt; or = 55 years) but was higher in patients than in control subjects in the younger age group (&lt; 55 years); P &lt; .005 after adjustment on ACE I/D and other risk factors. In patients, plasma ACE levels decreased with age (R = -.225, P &lt; 10(-4)), but in control subjects no such trend was observed. In the low-risk group (ApoB &lt; 1.25 mg/dL, body mass index &lt; 26 kg/m2, and not treated with hypolipidemic drugs), plasma ACE level was increased in patients when compared with control subjects among homozygotes and heterozygotes for the ACE I allele (P &lt; .015). Analysis of the distribution of plasma ACE by using commingling analysis conditional on the marker genotype ACE I/D enabled us to infer the frequencies and effects of the postulated ACE Ss genotypes. The results suggest that the higher plasma ACE levels in patients than in control subjects in the younger age group were due to a difference in frequency of the postulated S allele (.47 versus .36). CONCLUSIONS These results extend our previous findings and indicate that plasma ACE level may be a risk factor for MI, independent of the ACE I/D polymorphism.
Heritability of Behcet's disease
Authors: A. Sensi, O.R. Bariocordi
Journal: British Journal of Dermatology (1986)

Journal Article Heritability of Behçet's disease Get access A. Sensi, A. Sensi Istituto de Genetica Medica, Universita di Ferrara, Ferrara, Italy Search for other works by this author on: Oxford Academic Google Scholar O.R. Bariocordi O.R. Bariocordi Istituto de Genetica Medica, Universita di Ferrara, Ferrara, Italy Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 114, Issue 6, 1 June 1986, Pages 748–749, https://doi.org/10.1111/j.1365-2133.1986.tb04889.x Published: 01 June 1986
Rates of Solid-Organ Wait-listing, Transplantation, and Survival Among Residents of Rural and Urban Areas
Authors: David A. Axelrod, Mary K. Guidinger, Samuel Finlayson, Douglas E. Schaubel, David C. Goodman, Michael Chobanian, Robert M. Merion
Journal: JAMA (2008)

Disparities in access to organ transplantation exist for racial minorities, women, and patients with lower socioeconomic status or inadequate insurance. Rural residents represent another group that may have impaired access to transplant services.To assess the association of rural residence with waiting list registration for heart, liver, and kidney transplant and rates of transplantation among wait-listed candidates.Five-year US cohort of 174,630 patients who were wait-listed and who underwent heart, liver, or kidney transplantation between 1999 and 2004.Rates of new waiting list registrations and transplants per million population for residents of 3 residential classifications (rural/small town population, <10,000; micropolitan, 10,000-50,000; and metropolitan >50,000 or suburb of major city).Compared with urban residents, waiting list registration rates for rural/small town residents were significantly lower for heart (covariate-adjusted rate ratio [RR] = 0.91; 95% confidence interval [CI], 0.86-0.96; P<.002), liver (RR = 0.86; 95% CI, 0.83-0.89; P<.001), and kidney transplants (RR = 0.92; 95% CI, 0.90-0.95; P<.001). Compared with residents in urban areas, rural/small town residents had lower relative transplant rates for heart (RR = 0.88; 95% CI, 0.81-0.94; P = .004), liver (RR = 0.80; 95% CI, 0.77-0.84; P<.001), and kidney transplantation (covariate-adjusted RR = 0.90; 95% CI, 0.88-0.93; P<.001). These disparities were consistent across national organ allocation regions. Significantly longer waiting times among rural patients wait-listed for heart transplantation were observed but not for liver and kidney transplantation. There were no significant differences in posttransplantation outcomes between groups.Patients living in rural areas had a lower rate of wait-lisiting and transplant of solid organs, but did not experience significantly different outcomes following transplant. Differences in rates of wait-listing and transplant may be due to variations in the burden of disease between different patient groups or barriers to evaluation and waiting list entry for rural residents with organ failure.
Influence of MER-29 on Experimental Atherosclerosis of Cholesterol-Fed Cockerels
Authors: Harry Y. C. Wong, Frank B. Johnson, francet farrow, ftosa Shim, David VonEndt
Journal: Circulation Research (1962)

The effects of MER-29 were studied to determine whether this drug will lower the blood lipids as well as the severity of aortic and coronary atherosclerosis of ten-week-old cockerels on a regimen of plain mash or on an atherogenic diet consisting of 2 per cent cholesterol plus 5 per cent cottonseed oil added to plain mash. After ten weeks of treatment with 12.5 mg. or 25.0 mg. per Kg. of MER-29, it was observed that the drug had no significant influence on the blood cholesterol or phospholipid levels. It was interesting to note that cockerels treated with 25.0 mg. of MER-29 per Kg. body weight, whether on plain mash or on an atherogenic diet, demonstrated an increase of aortic-atherosclerosis. The drug did not seem to lower the incidence of coronary atherosclerosis of the group fed an atherogenic diet. It appears that MER-29 causes aortic atherosclerosis of cockerels fed plain mash primarily by blocking the conversion of 24-dehydrocholesterol to cholesterol, thus increasing the amount of 24-dehydrocholesterol which was found in the aortae, as compared with little or none in the aortae of cockerels on plain mash.
Reproducibility of βCell Function Estimates in Non-Insulin-Dependent Diabetes Mellitus
Authors: Hans J Gjessing, Else M Damsgaard, Lars E Matzen, Anders Frøland, Ole K Faber
Journal: Diabetes Care (1987)

We evaluated the reproducibility of different estimates of endogenous insulin secretion in 30 patients with non-insulin-dependent diabetes mellitus (NIDDM). Fasting blood glucose concentration was similar on the 2 days of study. The coefficients of variation of fasting plasma C-peptide, plasma C-peptide 6 min after the injection of 1 mg i.v. glucagon, and the increment in plasma C-peptide after glucagon were 16.0, 14.8 and 24.1%, respectively. The coefficients of variation of the corresponding plasma insulin values were 19.2, 24.8, and 34.8%, respectively. The coefficient of variation of 24-h urinary C-peptide excretion was 22.1%. Because fasting plasma C-peptide correlated closely with plasma C-peptide 6 min after glucagon (test 1: r = .70, P less than .01; test 2: r = .76, P less than .01), it seems that these two values can be used equally well as assessment of beta-cell function in NIDDM. In conclusion, fasting plasma insulin, fasting plasma C-peptide, and plasma C-peptide 6 min after glucagon stimulation showed a similar and acceptable degree of reproducibility. Plasma insulin 6 min after glucagon and increments in plasma insulin and C-peptide, as well as urinary C-peptide, seem to be less reproducible.
Observations on the optimum time for operative intervention for aortic regurgitation. I. Evaluation of the results of aortic valve replacement in symptomatic patients.
Authors: W L Henry, R O Bonow, J S Borer, J H Ware, K M Kent, D R Redwood, C L McIntosh, A G Morrow, S E Epstein
Journal: Circulation (1980)

Fifty consecutive patients undergoing aortic valve replacement for isolated aortic regurgitation were studied prospectively by echocardiography, electrocardiography and cardiac catheterization. Good quality echocardiograms were obtained in 49 of the 50 patients. Left ventricular (LV) dilatation was present in all 49 patients. LV systolic function, as assessed by echocardiographic percent fractional shortening, was normal in many patients but was moderately to severely reduced (less than 25%) in 14 patients (29%). Echocardiographic studies 6 months postoperatively revealed significant reductions in LV end-diastolic dimension (73.8 mm vs 58.7 mm; p less than 0.01), and serial echocardiographic studies early and late after operation revealed that the decrease in LV size had occurred by the time of the early study (8-22 days postoperatively), with little additional change thereafter. Operative deaths occurred in three of the 49 patients (6%). Eight of the 49 patients (16%) died of congestive heart failure (CHF) after hospital discharge at times ranging from 5-43 months after operation. Preoperative echocardiographic measurements of the LV end-systolic dimension and percent fractional shortening were strongly associated (p less than 0.01) with these late CHF deaths. Preoperative LV end-systolic dimension greater than 55 mm and fractional shortening less than 25% identified the high-risk group: nine of 13 patients (69%) in this group died either at operation or subsequently from CHF. In contrast, of 32 patients with LV end-systolic dimension less than 55 mm, only one died at operation and one died late from CHF. Thus, the population at high risk of late death from CHF was identified before operation by echocardiography.
Final planned overall survival (OS) from OPTiM, a randomized Phase III trial of talimogene laherparepvec (T-VEC) versus GM-CSF for the treatment of unresected stage IIIB/C/IV melanoma (NCT00769704)
Authors: Robert HI Andtbacka, Frances A Collichio, Thomas Amatruda, Neil Senzer, Jason Chesney, Keith Delman, Lynn Spitler, Igor Puzanov, Sanjiv Agarwala, Mohammed Milhem, Kevin Harrington, Mark Middleton, Ai Li, Mark Shilkrut, Robert Coffin, Howard Kaufman
Journal: Journal for ImmunoTherapy of Cancer (2014)

Meeting abstracts T-VEC is an oncolytic immunotherapy derived from herpes simplex virus type-1 designed to selectively replicate within tumors and to produce GM-CSF to enhance systemic antitumor immune responses. OPTiM, a randomized Phase III trial of T-VEC vs GM-CSF in patients with unresected