tbuckley/cabot-search huggingface dataset:
CYSTIC FIBROSIS
Authors: G J BARBERO
Journal: Annals of Internal Medicine (1961)

Editorials1 March 1961CYSTIC FIBROSISGIULIO J. BARBERO, M.D.GIULIO J. BARBERO, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-54-3-586 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIt is very appropriate that the clinical staff conference of the National Institutes of Health, which is published in this issue of the ANNALS, considers the problem of cystic fibrosis of the pancreas by contrasting the classical picture seen in a young child with the more unusual clinical history of an adult who shows definite findings in keeping with this disease picture. The observation of this disease in the adult has become a reality now that more children with the traditional picture are growing into the adult age group, presumably as the result of prolonging their lives with more effective...1 SibingaBarbero MSGJ: Observations on spontaneous sweating; elevated night sweating rates in cystic fibrosis. To be published. Google Scholar2 SibingaBarbero MSGJ: Studies in the physiology of sweating in cystic fibrosis. I. Experimental sweat gland fatigue. Pediatrics (in press). Google Scholar3 KwartShashoua HVE: The structure and constitution of mucus. Trans. N. Y. Acad. Sci. 19: 595, 1957. CrossrefMedlineGoogle Scholar4 ChernickBarbero WSGJ: Composition of tracheobronchial secretions in cytic fibrosis of the pancreas and bronchiectasis. Pediatrics 24: 739, 1959. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *From the Research Department, The Children's Hospital of Philadelphia, 1740 Bainbridge St., Philadelphia 46, Pa. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 March 1961Volume 54, Issue 3Page: 586-587KeywordsAge groupsChild healthChildrenCystic fibrosisPancreasYoung adults ePublished: 1 December 2008 Issue Published: 1 March 1961 PDF downloadLoading ...
Chickenpox
Authors: Sharon Parmet
Journal: JAMA (2005)

Chickenpox Chickenpox is a highly contagious and common childhood disease caused by a virus in the herpes family of viruses called the varicella virus.The varicella virus can remain in the body for decades and become active again, usually in adults, causing herpes zoster (shingles).Shingles involves the occurrence of painful skin sores along the distribution of nerves across the trunk or face.The August 17, 2005, issue of JAMA includes an article reporting that use of the varicella vaccine to prevent chickenpox has greatly reduced medical expenses related to chickenpox.This Patient Page is based on one published in the February 18, 2004, issue of JAMA.
BUENOS AIRES
Journal: JAMA (1920)

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 19906: Evaluation of Approximate Entropy as a CPR Quality Measure
Authors: David D Salcido, Allison C Koller, Matthew L Sundermann, James J Menegazzi
Journal: Circulation (2015)

Introduction: The majority of standard cardiopulmonary resuscitation (CPR) quality metrics are based on univariate, linear measures of CPR process. Non-linear measures, such as approximate entropy (ApEn), which characterizes the disorder of a signal, have been utilized in other areas, such as heart rate analysis, to capture phenomena that elude standard linear measures. Objective: To provide a preliminary evaluation of the performance of ApEn as a CPR-quality metric. Methods: Case data for non-traumatic, EMS-treated out-of-hospital cardiac arrests were obtained from the Pittsburgh site of the Resuscitation Outcomes Consortium for the period spanning the years 2010 to 2014. Cases with at least 1 available defibrillator data file containing an accelerometer-derived chest compression (CC) depth channel were included. CC depth data traces were extracted with custom software created in MATLAB (2014b, The Mathworks, Nattick, MA). Individual CC for the entire length of each available file were located with a calibrated peak finding function and used to calculate individual CC depth (mm), rate (compressions/minute) and flow fraction time series, which were reported in averages over 1-minute epochs. Data from cases with multiple data files were merged to reflect the order of recordings. ApEn was calculated for each 1-minute epoch of depth and rate. Correlation coefficients were calculated to assess the relationship between ApEn, CC rate, CC depth and flow fraction overall and stratified by pre/post 5 minutes of CPR. Results: Of a total of 1,278 cases with defibrillator downloads, a subset of 1,266 cases had analyzable CC depth channels. A total of 1,875,209 individual CC were detected and analyzed, covering 18,719 minutes of CPR. Mean (SD) ApEn of CC rate was 0.92 (0.34) and of CC depth was 0.79 (0.23). ApEn of CC depth was weakly correlated with flow fraction (r = 0.22) and ApEn of CC rate (r = 0.27), but not CC rate or CC depth. Both before and after the 5-minute mark, ApEn correlated weakly with flow fraction (r = 0.14 vs. r = 0.24) and ApEn of CC rate ( r = 0.30 vs 0.26). Conclusion: ApEn was only weakly correlated with CC flow fraction, a common CPR quality measurement. Additionally, ApEn of rate and depth were not correlated with the absolute magnitude of CC rate or depth.
Thromboembolism
Authors: Hugh H. Hussey
Journal: JAMA (1976)

Clinicians generally agree that early recognition of pulmonary embolism is vital to a patient's welfare since it makes possible prompt treatment to meet the exigencies of the case, whatever they may be. The direct treatment will vary according to individual needs and may entail anticoagulant therapy, ligation or placement of an umbrella filter in the inferior vena cava, pulmonary embolectomy, or a combination of the foregoing methods. Supportive measures may be needed to relieve pain, to treat infection in the case of septic pulmonary infarction, or to treat shock or congestive heart failure. The problem of recognizing pulmonary embolism or infarction has been alluded to in an earlier editorial (226: 1351, 1973). The problem exists because the disorder is a great mimicker and its manifestations are often subtly misleading. Thus, it may appear as an otherwise unexplained fever following a surgical operation or in a patient with congestive heart failure;
Abstract 11228: The Endothelial Nitric Oxide Synthase Gene -786T/C Polymorphism is a Significant Predictive Factor for Myocardial Lactate Production During Acetylcholine-Provoked Coronary Spasm
Authors: Koichi Kaikita, Koji Sato, Masafumi Nakayama, Kenichi Tsujita, Sunao Kojima, Seiji Hokimoto, Hisao Ogawa
Journal: Circulation (2014)

Myocardial lactate production (MLP) in the coronary circulation is a supporting diagnostic marker useful in the evaluation of coronary spasm-induced myocardial ischemia during acetylcholine (ACh)-provocation test. We previously found a -786T/C polymorphism in the 5’-flanking region of the endothelial nitric oxide synthase (eNOS) gene and reported that this polymorphism is strongly associated with coronary spasm. However, there is no report showing the relation between MLP induced by ACh-provocation test and eNOS gene -786T/C polymorphism in the large study population. We examined 712 consecutive patients who underwent myocardial lactate measurement during ACh-provocation test and agreed with genetic screening test of eNOS gene -786T/C polymorphism between January 1991 and December 2010. ACh-provoked MLP was observed in 252 out of 712 patients included in the present analysis [252 MLP-positive and 460 MLP-negative patients]. MLP-positive patients were more likely to be female, diabetic, non-smokers, had epicardial, multivessel and diffuse spasm pattern, with eNOS-786T/C polymorphism (60% vs. 44%, p&lt;0.001, 25% vs. 19%, p=0.047, 61% vs. 46%, p&lt;0.001, 83% vs. 36%, p&lt;0.001, 37% vs. 11%, p&lt;0.001, 39% vs. 12%, p&lt;0.001, and 23% vs. 15%, p=0.011, respectively). Multiple logistic regression analysis identified female gender, epicardial spasm and -786T/C polymorphism to correlate with the MLP-positive finding (OR: 0.327; 95% CI: 0.226-0.475; p&lt;0.001, OR: 10.137; 95% CI: 6.767-15.187; p&lt;0.001, and OR: 1.621; 95% CI: 1.025-2.564; p= 0.039). In the analysis of patients with epicardial coronary spasm, Kaplan-Meier survival curve showed no difference in 5-year survival rates free from major adverse cardiac events between MLP-positive and MLP-negative patients with epicardial coronary spasm (p=NS). In conclusion, multiple predictors including female gender and eNOS gene -786T/C polymorphism were the significant predictors for the MLP induced by ACh-provocation test, highlighting the close relation between the genetic factors and ACh-induced myocardial ischemia in Japanese patients with coronary vasospastic angina.
Book: The Cambridge Illustrated History of Medicine * The Oxford Illustrated Companion to Medicine
Authors: M. Powlson
Journal: BMJ (2002)

Ed Roy Porter Cambridge University Press, £19.95, pp 400 ISBN 0 521 00252 4 Third edition Eds Stephen Lock, John M Last, George Dunea Oxford University Press, £39.50, pp 891 ISBN 0 19 262950 6 Rating: ![Graphic][1]</img>![Graphic][2]</img>![Graphic][3]</img>; ![Graphic][4]</img>![Graphic][5]</img>![Graphic][6]</img>![Graphic][7]</img> Rarely does the BMJ publish reviews of reprints or new editions, and rarer still entrust something edited by one of its former editors to a former reviews editor of the Lancet . However, the quality of both of these books shines through. Comparisons of two such worthy works are invidious, but here (although not quite so evident in recent years in the Boat Race) the dark blues—Oxford—have it over the light blues—Cambridge—although, strictly speaking, they are … [1]: /embed/inline-graphic-1.gif [2]: /embed/inline-graphic-2.gif [3]: /embed/inline-graphic-3.gif [4]: /embed/inline-graphic-4.gif [5]: /embed/inline-graphic-5.gif [6]: /embed/inline-graphic-6.gif [7]: /embed/inline-graphic-7.gif
Identification of the thromboxane A2 receptor in hepatic sinusoidal endothelial cells and its role in endotoxin-induced liver injury in rats
Authors: S Ishiguro
Journal: Hepatology (1994)

The presence of the thromboxane A2 receptor in sinusoidal endothelial cells was investigated and its pathogenic role in endotoxin-induced liver injury examined. The receptor was measured with a binding assay using a specific thromboxane A2 receptor antagonist, [3H]S-145. Scatchard analysis of the binding indicated the presence of a single class of high-affinity binding sites with a dissociation constant of 5.00 ± 0.96 nmol/L, a maximal binding of 22.85 ± 2.71 fmol/106 cells and 13.80 ± 1.60 × 103 binding sites per cell. The addition of a cyclooxygenase inhibitor, indomethacin, during the cell preparation increased the maximal binding value and the number of binding sites of 37.34 ± 3.01 and 22.50 ± 1.80 × 103 sites/cell, respectively. The binding was displaced by various thromboxane A2 analogs such as ONO-3708 and STA2 but was not effectively competed for by other prostaglandins. Endotoxin injection reduced dissociation constant, maximal binding and the number of binding sites in sinusoidal endothelial cells to 3.49 ± 0.87 nmol/L, 6.03 ± 0.64 fmol/106 cells and 3.65 ± 0.39 × 103 sites/cell, respectively. A cyclooxygenase inhibitor and a Kupffer cell inhibitor added before endotoxin treatment significantly prevented the reduction in the number of thromboxane A2 receptors. It is possible that these effects were due to a reduction in the agonist-induced internalization of the thromboxane A2 receptor brought about by the prevention of thromboxane A2 production. Preadministration of both a cyclooxygenase inhibitor and a thromboxane A2 receptor antagonist attenuated the degree of endotoxininduced liver injury. These findings indicated that the thromboxane A2—thromboxane A2 receptor system in the hepatic sinusoids plays a significant role in the pathogenesis of endotoxin-dependent liver damage. (Hepatology 1994;20:1281–1286).
To-day's Drugs
Journal: BMJ (1958)

pressure must be reached.In general the former is better suited to the sports car or rally driver who wants to be able to lock all four wheels at speed and the latter to the more sedate driver with a large heavy cat.The Cape Asbestos Company market their "Capasco" HF32, which comes into the first category for use on faster cars; it has a high coefficient of friction, with exceptional resistance to fade."Capasco " HF33 -is smoother and wears better, being more suited to the normal car; "Capasco" BR20 is ideal where medium friction linings are needed and where servo assistance is available.Ferodo MR19 is a solid woven non-metallic material suitable for medium-sized cars; DM7, moulded, is better for light to medium models and has a high friction value, while DM8, also moulded, has alloy chippings for better heat dispersal and is designed for hgh-performance cars.Small and Parkes Ltd. offer Don R14, an entirely satisfactory lining for nornal use, giving a smooth and progressive action at *the brake pedal.Don 24, 424,
Phase IV head-to-head randomized controlled trial comparing ingenol mebutate 0·015% gel with diclofenac sodium 3% gel for the treatment of actinic keratosis on the face or scalp
Authors: E. Stockfleth, C.A. Harwood, C. Serra-Guillén, T. Larsson, M.L. Østerdal, T. Skov
Journal: British Journal of Dermatology (2018)

This study from Germany, Spain and the U.K. compared the effectiveness of two gel treatments for actinic keratosis (AK) on the face or scalp. An AK is a small, spiky, scaly or sandpaper‐like area of sun damage on the skin surface. A very small proportion progress to squamous cell skin cancer. Creams or gels rubbed into the skin are recommended when a large area such as the entire scalp is affected by multiple AKs. Ingenol mebutate 0·015% gel (IngMeb) and diclofenac sodium 3% gel (DS) were compared in 502 patients, mostly male and almost all white‐skinned. IngMeb was applied once daily for three consecutive days and DS twice daily for 90 days (the normal recommendations for use). Patients using IngMeb were allowed to apply it for a second three‐day period if they had new or residual AKs at week 8, which meant that more than half this group used IngMeb twice. Looking at the treated area at week 17 ‐ approximately four weeks after finishing the course of DS, nine weeks after the second course of IngMeb (if used), and 17 weeks after the first (or only) course of IngMeb ‐ almost twice as many patients in the IngMeb group were completely clear of AKs than in the DS group. Even if they had not disappeared completely, more AKs had partially cleared up, and the total number had decreased significantly more, in the IngMeb group. Side effects were mild or moderate, most commonly redness where either gel was applied.
Correction
Authors: MICHAEL A. JENIKE, LEE BAER
Journal: American Journal of Psychiatry (1990)

In the article "Sertraline in Obsessive-Compulsive Disorder: A Double-Blind Comparison With Placebo," by Michael A. Jenike, M.D., et al. (July 1990 issue, pp. 923-928), there are a number of errors that resulted from incorrect computer entry of the randomization code. The final conclusions of the study are not changed, but a stronger trend toward usefulness of the drug is exhibited. In view of positive data from the multicenter trial of sertraline of which this was one center (G. Chouinard, W. Goodman, J. Greist, et al.: Results of a double-blind placebo controlled trial using a new serotonin uptake inhibitor, sertraline, in obsessive-compulsive disorder. Psychopharmacol Bull [in press]), it is likely that the nonsignificant differences from placebo are due to small sample size. Patients in the placebo and sertraline groups were still similar in clinical characteristics (table 1 in the original paper), and there were few side effects in either group (table 2). The corrected table 3 below summarizes the corrected data analyses, which were done by means of analysis of covariance. All comparisons were nonsignificant beyond p> 0.10. On the Yale-Brown scale, the Maudsley questionnaire, and the global scale, the interaction effect was nonsignificant, so main effects can be unambiguously interpreted. On the NIMH scale, the interaction effect was significant, so main effects could not be unambiguously interpreted; thus, tests of simple main effects were carried out between drug and placebo at each of the five trials. None of the resuls of the tests of simple main effects was significant (all p> O.lO). Also, to clarify a point in the paper, the new drug application requesting that obsessive-compulsive disorder be included as an indication for sertraline will not be submitted for some time, but an application was filed for depression as an indication in 1988 (personal communication, Pfizer Pharmaceutical Company). [See table in the PDF file]
MAGAZINE AND TELEVISION REPORT
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
VITAL STATISTICS FOR 1908
Journal: JAMA (2009)

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
P102 Sweat chloride is not a useful marker of clinical response to Ivacaftor
Authors: PJ Barry, WG Flight, J Biesty, D Clough, I Small, S Johnson, AL Brennan, RJ Bright-Thomas, AK Webb, AM Jones, AR Horsley
Journal: Thorax (2013)

<h3>Introduction and Objectives</h3> The development of the targeted CFTR potentiator Ivacaftor has significantly altered the landscape for cystic fibrosis (CF) therapeutics, and heralds the arrival of personalised medicine in this condition. Data from Phase III clinical trials have been encouraging and suggested that the use of Ivacaftor results in a normalisation of sweat chloride and significant increases in pulmonary function and weight in suitable patients. As part of the commissioning requirements for Ivacaftor in the UK, sweat chloride changes represent the major criteria for continuing prescription, with a reduction of 30% or reduction below 60 mmol/L proposed as cut-offs for continuation of therapy. We aimed to assess the relationship of sweat chloride to clinical outcomes in patients receiving Ivacaftor treatment. <h3>Methods</h3> All Ivacaftor naïve patients who carried the G551D mutation were contacted to enable the commencement of the medication. Baseline sweat chloride was recorded, and repeated at 2 months. Baseline pulmonary function, height and weight were recorded and repeated at monthly visits for 3 months. <h3>Results</h3> To date 24 of 27 suitable subjects have commenced Ivacaftor. Mean FEV<sub>1</sub>% predicted was 64.3% predicted at Ivacaftor commencement and mean BMI was 22.1 kg/m<sup>2</sup>. Mean FEV<sub>1</sub> percent predicted increased in absolute terms by 8.9% at 1 month and 8.7% at 3 months (p &lt; 0.001 at both time points). Mean BMI improved to 22.7 kg/m<sup>2</sup> at 1 month and 23.0 kg/m<sup>2</sup> at 3 months (p = 0.002, 0.003 respectively). There was a significant fall in sweat chloride at 2 months (median 114 to 51 mmol/L, p &lt; 0.001). Improvement in sweat chloride was not correlated in absolute or relative terms with improvements in pulmonary function or BMI. Four subjects with a mean absolute FEV<sub>1</sub> improvement of 14.5% had sweat chloride responses not meeting pre-specified criteria at 2 months. Two of these subjects had a subsequent repeat test meeting continuation criteria. In one subject a suboptimal response was attributed to the omission of a single dose. <h3>Conclusions</h3> The use of sweat chloride as a surrogate for clinical efficacy and a criterion for drug continuation is not supported by this data. Sweat chloride may be a marker of 100% adherence to therapy.