tbuckley/cabot-search huggingface dataset:
Miscellanea Medica
Journal: JAMA (1988)

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
Abstracts of the “8<sup>th</sup> Int. Luebeck Conference Pathophysiology and Pharmacology of Erythropoietin and Other Hemopoietic Growth Factors”
Journal: American Journal of Hematology (2009)

Hypoxia-inducible factors are crucial in the regulatory process of oxygen homeostasis of vertebrate cells.Initiated by leads to transcription of a greater number of hypoxia responsive genes (e.g.vegf, epo) to avoid cellular damages or dysfunctions.We aimed to investigate subcellular distribution and molecular mechanisms regulating the protein topogenesis of HIFs and PHDs.Vector constructs encoding GST-tagged importins, EGFP-tagged HIFs and PHDs PHDs site directed mutants and deletions were generated.Interaction of target protein with importins was analyzed that nuclear import of PHD1 occur importin dependent and relies on an intact nuclear localisation signal (NLS).By contrast, PHD2 is shuttling between the nucleus and the cytoplasm.This shuttling seems to be independent of the of HIFs and PHDs, which mediate the expression regulation of oxygen sensitive genes like Erythropoietin.Intracellular localisation of HIFs and PHD1 on the one hand and PHD2 on the other hand is mediated by different nucleocytoplasmic transport factors.
Starvation: stress or satisfaction?
Authors: E. Crumpton
Journal: JAMA (1966)

After prolonged fasting, obese men showed no significant impairment of memorization of nonsense syllables, repetition of digits forward and backward, mental control, or hand steadiness. The trend, if any, was toward improvement rather than impairment. Irritability, depression, and resistance to testing increased, but also increased was overall satisfaction with self. The typical behavioral reaction appeared to be a reversion to immature, dependent modes of living, which, however, did not represent any real threat to the psychological health of emotionally stable subjects. It appears that fasting for long periods is not especially stressful when it results in an extreme weight loss and consequent increase in self-esteem.
Screening
Authors: P. Boyle
Journal: European Respiratory Journal (2003)

Screening for cancer is currently entering a very promising period as new technologies become available for assessment. However, this great opportunity also presents significant problems, starting with how do you select the likeliest method for evaluation? How do you do trials where the technology will be out-moded by the time the result is known? Indeed, how can all promising technologies be evaluated? There is a need for a renewal of methodological thinking on this topic at present. Randomised trials, which currently rely on death as the primary outcome, are very long and very complicated to undertake and run. There is an urgent need for biological markers, which are true surrogate end-points, to help reduce sample size and make trials more feasible, so that more trials can be done. For those screening modalities of demonstrated effectiveness, the key issue at present is how to maximise the outcome in population screening when the technology is transferred from the research setting to the public health setting. It is essential to remember that screening, per se, has never prevented a cancer nor prevented a cancer death. It is impossible to separate the issues of screening with those of adequate treatment: the best results in a screening programme will come when treatment is excellent. Screening is the first, and sometimes key, stage in a global management programme for the cancer in question. As the aim at present is to strive to maximise the effectiveness of population-based programmes, this aspect should be foremost in all thought processes.
Abstract PR11: CD4+ T lymphocyte ablation prevents pancreatic carcinogenesis in mice
Authors: Yaqing Zhang, Wei Yan, Esha Mathew, Filip Bednar, Shanshan Wan, Meredith A. Collins, Rebecca A. Evans, Theodore H. Welling, Robert H. Vonderheide, Marina Pasca di Magliano
Journal: Cancer Research (2015)

Abstract Pancreatic cancer, one of the deadliest human malignancies, is associated with oncogenic Kras and is most commonly preceded by precursor lesions known as Pancreatic Intraepithelial Neoplasias (PanINs). PanIN formation is accompanied by the establishment of an immune-tolerant microenvironment. However, the immune contribution to the initiation of pancreatic cancer is currently poorly understood. Here, we show that oncogenic Kras-expressing epithelial cells drive the establishment of an immunosuppressive microenvironment through the recruitment and activity of CD4+ T cells. We further show that CD4+ T cells functionally repress the activity of CD8+ T cells. Elimination of CD4+ T cells uncovers CD8+ T cells anti-neoplastic function, and blocks the onset of pancreatic carcinogenesis. Thus, our studies uncover essential and opposing roles of immune cells during PanIN formation, and provide rationale to explore immune-modulatory approaches in pancreatic cancer. This abstract is also presented as Poster A48. Citation Format: Yaqing Zhang, Wei Yan, Esha Mathew, Filip Bednar, Shanshan Wan, Meredith A. Collins, Rebecca A. Evans, Theodore H. Welling, Robert H. Vonderheide, Marina Pasca di Magliano. CD4+ T lymphocyte ablation prevents pancreatic carcinogenesis in mice. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr PR11.
THE CAUSES OF OLD AGE.
Journal: JAMA (1895)

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 12008: Nos1 Adapter Protein Nos1ap Overexpression Alters Qtc Intervals in Transgenic Mice
Authors: Tatjana Williams, Anahi P Arias-Loza, Marco Abeßer, Joachim Schmitt, Kai Schuh, Oliver Ritter
Journal: Circulation (2014)

Background: Congenital long- or short-QT syndrome may lead to life-threatening ventricular tachycardia and sudden cardiac death. Apart from rare disease-causing mutations in ion channels, common genetic variations in the neuronal nitric oxide synthase (NOS1) regulator NOS1AP, have recently been associated with QT interval variations in a human whole-genome association study. In fact, NOS1AP SNPs have been linked to increases in QTc intervals and sudden cardiac death. We therefore speculate that myocardial NOS1AP overexpression may lead to a decrease of the QTc interval and an increased susceptibility to rhythm disorders. Methods and Results: We generated transgenic mice (TG) with a conditional myocardial NOS1AP overexpression and focused on electrical alterations. Conditional overexpression of NOS1AP resulted in a 147% ventricular increase in TG mice compared to WT littermates. NOS1AP was mainly located at the sarcolemma where it interacted with NOS1 and the L-type Ca2+- channel. HW/BW ratio, ventricular ANP expression, ventricular cross-sectional area and collagen deposition were not altered in NOS1AP mice under baseline conditions. However, NOS1AP overexpressing mice showed a clear decrease of QTc intervals (33 vs. 48 ms). They were more prone to bradycardia (resting heart rate 467 bpm vs. 666 bpm). Atrial programmed stimulation repeatedly caused atrial tachycardia. Ventricular programmed stimulation caused VT in some mice with NOS1AP overexpression. We also investigated the functional effect of the human rs16847548 (T/C). We found that this SNP decreased NOS1AP promoter activity in a viral NOS1AP luciferase assay, suggesting that this SNP downregulates NOS1AP expression in humans. Conclusion: Myocardial overexpression of NOS1AP leads to a significant shortening of the QTc interval with an increased susceptibility to atrial and ventricular rhythm disorders. SNP rs16847548 in NOS1AP resulted in downregulation of NOS1AP expression which provides an explanation for elongation of QTc intervals. In summary, not only a mutation in ion channels itself but also genetic alterations in expression of ion channel modifiers, such as NOS1AP, have an impact on QTc intervals.
Altered regulation of IL-2 production in systemic lupus erythematosus: an evolving paradigm
Authors: Gary M. Kammer
Journal: Journal of Clinical Investigation (2005)

In systemic lupus erythematosus (SLE), IL-2 production by T lymphocytes in vitro is impaired. Deficient IL-2 production may be an outcome of a primary SLE T cell disorder that is due to impaired signal transduction. In this issue of the JCI, evidence is presented that an anti-TCR/CD3 complex autoantibody present in SLE sera can bind to T cells and activate the Ca2+-calmodulin kinase IV (CaMKIV) signaling cascade, resulting in downregulation of IL-2 transcription and IL-2 production. Because IL-2 may contribute to the maintenance of T cell tolerance, deficient IL-2 production could promote a breach of T cell tolerance that results in autoantibody production in SLE.
In Comment
Authors: Milton M. Howell
Journal: JAMA (1974)

THIS IS a timely discussion of a remediable problem in present-day practice. It appears to be more an editorial than a scientific paper. As such, I am willing to concede the authors some editorial prerogative and poetic license, since I can agree from experience with most of their conclusions. I do believe that they have indulged in "overkill," and that their reasoning and quotations stretch extrapolative gymnastics to their ultimate. Their quotation from McCabe in the<i>New England Journal of Medicine</i>article, which takes a reported incidence of Gram-negative bacteremia of 1/100 in several major centers and projects 100,000 fatalities a year nationwide, approaches a journalistic quality usually reserved for medical articles in lay magazines. In another instance they suggest, without producing substantiating evidence, that the rate of adverse antibiotic reactions may be the same in ambulatory patients as that already documented in hospitalized populations. As a physician who has
Detection of vulnerable atherosclerotic plaques using super paramagnetic iron oxide (SPIO), mice and rabbit studies Mitra rajabi, Daniel Chen, Mohammed Asif, Michael Quast, Jingna Wei, Mohammad Madjid, Khawar Gul, Ward Casscells, James T. Willerson, Morteza Naghavi. University of Texas-Houston, Houston, TX, University of Texas-Medical Branch at Galveston, Galveston, TX
Journal: Journal of the American College of Cardiology (2001)
Oral Sessions_Tuesday_13 October 2009
Authors: A Guerrini, G Roudillon, O Gontier, L Rebaı, M.-A Isorni, P Mutinelli-Szymanski, M Sorine, P Kalfon, T Strøm, P Toft, K Kloecker, N Schindler, A Schindler, D Vagts, M Dura, F Merino, R Abajas, I De Horra, S Gonza ´lez, L Lo ´pez, A Suescun, M Ballesteros Sanz, J Rodrı ´guez-Paz, F Buro ´n Mediavilla, E Rodrı ´guez
Journal: Intensive Care Medicine (2009)

INTRODUCTION.Acute hyperglycaemia associated with insulin resistance is common in critically ill patients.Glycemic control with insulin is considered important although the blood glucose target is very controversial.Recently, clinical studies have highlighted the potential negative effects of the variability of the blood glucose concentration in several different cohorts of ICU patients.The aim of the study is to evaluate the glycemic variability induced by the use of the lower range (tight arm) of the NICE-SUGAR (NS) algorithm [1] in comparison with a Proportional-Integral-Derivative controller (PID).METHODS.We used the minimal model for glycemic control in ICU patients (MM-ICU) developed by van Herpe et al. [2] in order to simulate a virtual ICU patient characterized by the following parameters G b basal glucose = 101 mg/dL, I b basal plasma insulin = 20 lUI/ml, body weight BW = 80 kg, ratio to ideal body weight IBW R = 150%, carbohydrates rate = 150 mg/min, insulin sensitivity index = 2,1 E-3 during 48 h spent in ICU.The lower range of the NS algorithm was set to[80-110 mg/dL] and the target for the PID was 100 mg/dL.All calculations were performed with the MATLAB software.The interval between 2 consecutive measurements resulted from the strict application of the time (without delay) for the next glucose measurement given by the NS algorithm.RESULTS.Although the strict application of NS requires more blood glucose measurements than PID in these experimental conditions, fluctuations of blood glucose are present during the analysed period with the NS algorithm, whereas blood glucose stabilizes in the target range after only 6 h with the PID.CONCLUSION.The algorithm used for the patients assigned to undergo intensive glycemic control during the NICE-SUGAR study may induce high variability for some patients.Whether this intrinsic property of the algorithm has contributed to the outcome in the intensive control group of the NICE-SUGAR requires further studies and particularly in respect of the stability margins related to changes in insulin sensitivity during the ICU stay and delays to measure blood glucose in the real life.1.
RECENT ITALIAN INVESTIGATIONS ON MALARIA.
Journal: JAMA (1901)

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 17358: Stenting of Atherosclerotic Renal Artery Stenosis Does Not Prevent Congestive Heart Failure, an Analysis of the Coral Trial
Authors: Kaili Ren, Yanmei Xie, Steven Haller, Mark Yu, Wencan He, Jingning Mei, Hanh Nguyen, Emily Cooper, Kenneth Jamerson, Timothy P Murphy, Donald E Cutlip, Lance Dworkin, Michael R Jaff, Michael Steffes, Joseph I Shapiro, William Henrich, Jiang Tian, Pamela Brewster, Christopher J Cooper
Journal: Circulation (2015)

Introduction: In current guidelines congestive heart failure (CHF) is an indication for renal artery stenting, however there is no data on the utility of stenting for the prevention of CHF. We sought to determine the effect of renal artery stenting in patients with atherosclerotic renal artery stenosis (ARAS) without a history of CHF. Hypothesis: In ARAS renal artery stenting does not prevent incident CHF in patients with no history of CHF. Design and method: The Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) trial is a prospective, international, multicenter clinical trial that randomized participants with ARAS, who received optimal medical therapy plus stenting versus no stenting. Optimal medical therapy included treating blood pressure and diabetes to goal, use of an angiotensin receptor-blocking drug, statin, and anti-platelet therapy. Glomerular filtration (eGFR) was estimated using the MDRD-GFR equation. Patients were followed for a median of 43 months (IQR, 31 to 55). Results: At enrollment, there were 795 out of 931 patients without a history of CHF, 395 were in the medical therapy group and 400 were in the medical therapy plus stenting group. In this group 117/795 had global renal ischemia. The rate of CHF admission (7% vs. 6%. p=0.74) and the pulmonary edema rate within those admitted for CHF were not different (82% vs. 64%, p=0.21). The rate of incident CHF was not different in patients with global renal ischemia and renal stenting did not prevent CHF events in this subgroup. Neither the composite event rate (35% vs. 34%, p=0.72), nor the rate of cardiovascular death (8% vs. 8%, p=0.96) differed between the two groups. At 3-year follow-up no differences were observed between medical therapy and medical therapy plus stenting for systolic blood pressure (SBP) (135±19 vs. 134±21 mmHg, p=0.74) or eGFR (56±22 vs. 55±23 ml/min, p=0.50). Conclusions: Renal artery stenting and optimal medical therapy, when compared to optimal medical therapy only, did not reduce the risk of CHF, or other cardio-renal events in patients that were enrolled without history of CHF in the CORAL trial.
Is Everybody Happy?
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
The relationship between the development of rash and clinical and quality of life outcomes by Kras mutation status in patients with colorectal cancer treated with cetuximab in NCIC CTG CO.17.
Authors: C. J. O'Callaghan, D. Tu, C. S. Karapetis, H. Au, M. J. Moore, N. C. Tebbutt, M. G. Trudeau, T. J. Price, D. Yip, D. J. Jonker
Journal: Journal of Clinical Oncology (2011)

481 Background: The NCIC Clinical Trials Group CO.17 trial, conducted with the Australasian Gastrointestinal Trials Group, showed cetuximab monotherapy (CET vs. best supportive care [BSC]) improved overall (OS) and progression-free survival (PFS) and maintained quality of life (QoL) in patients previously treated for advanced colorectal cancer. Correlative analyses showed strong relationships between CET benefits and both rash development and Kras mutation status. Association between rash and CET benefits is now presented by Kras mutation status. Methods: Rash was graded weekly by NCI CTC 2.0 criteria. Landmark-type analyses (LTA) were performed by excluding patients who died within 28 days and then grouping by rash severity (gr 2+ vs. gr 0/1) based both on worst grade ever developed (LTA1) and worst grade on or before day 28 (LTA2). Multivariate Cox models were conducted separately for wild-type (WT) and mutated (MUT) Kras tumors. Results: More rash of severity gr 2+ was observed in WT than MUT patients treated with CET (57.3% vs. 44.4%; p = 0.08). The median OS, PFS, and HRs from LTA2 are presented for WT and MUT groups (see Table). Conclusions: Rash severity was positively correlated with PFS and OS in Kras WT patients who received CET, although only for gr 2+ rash did OS significantly exceed that of BSC patients. In Kras MUT patients, neither gr 0/1 nor gr 2+ rash was associated with either improved PFS or OS vs. BSC patients. Quality of life outcomes will also be reported by Kras mutation status. [Table: see text] [Table: see text]
Tropical Gastroenterology
Authors: Arthur B. French
Journal: JAMA (1981)

<i>Tropical Gastroenterology</i>is an unusual book—indeed it seems unusual that it was published. It appears to be based on the assumption that the basic facts about gastroenterological diseases are available in standard texts for nontropical gastroenterology, and that there is a need for a series of "pearls" on how these diseases are the same or different in the tropics and on the distribution of the diseases in the tropics. The book might indeed be subtitled "A Compendium of Pearls" in contrast to a systematic text. The variety of topics is such that the book does cover in a systematic manner considerations of geographic distribution of disease, variations in disease, and practical aspects of patient care in the tropics. The quality of the pearls naturally varies, and the book could certainly have been made more concise, but it is full of gems that are fascinating to anyone interested in geographic aspects
ST. THOMAS'S HOSPITAL.
Authors: T.A. Barker, JasR. Bennett, R. Goolden, T.B. Peacock, J.S. Bristowe, William Brinton, E. Clapton, JohnF. South, Gilbert Mackmurdo, Samuel Solly, F. le Gros Clark, John Simon, Sydney Jones
Journal: The Lancet (1862)