tbuckley/cabot-search huggingface dataset:
Correction
Journal: BMJ (1957)

Clicking Jaw Q.-A girl of 16 has in the past three months developed a persistent and very audible clicking on the right side of the jaw, which occurs when her mouth is about half open.What treatment is advised and what is the prognosis ?A.-This patient would be well advised not to seek treat- ment.A clicking jaw can be cured by operative removal of the cartilaginous meniscus of the temporo-mandibular joint, but an operation of this severity is hardly indicated for so trivial a symptom as a click.I gather that there is no limitation of movement of the jaw.Such patients are sometimes helped by manipulation under an anaesthetic, but if there is no limitation of movement of the joint then manipulation would be only a form of sug- gestion therapy.The patient should be reassured, told that there is nothing seriously wrong with the joint, and that many people have clicking jaws.It is very likely that the click will disappear in time.
A consumer's guide to computerized arrhythmia monitoring
Authors: W. J. Sanders
Journal: JAMA (1982)

THE IMPORTANCE of arrhythmia monitoring in the care of the cardiac patient is now well established.<sup>1,2,3</sup>The use of computers in arrhythmia monitoring is also well established, with more than 1,000 hospital-based computerized arrhythmia monitoring systems currently in use throughout the world.<sup>4,5</sup>Arrhythmia monitoring can be broadly divided into two distinct types—inpatient and ambulatory. Ambulatory arrhythmia monitoring is typically performed using a portable battery-operated tape recorder that records the patient's ECG during a 24-hour period. The tape recording is later scanned at high speed to detect cardiac arrhythmias for purposes of diagnosis and for documenting the efficacy of therapy with antiarrhythmic drugs. The patient typically is not hospitalized, and the detection and quantitation of arrhythmias are only useful for documentation purposes. The purpose of inpatient arrhythmia monitoring is to detect and document cardiac arrhythmias as they happen so that appropriate treatment can be initiated. Thus, the inpatient arrhythmia
Errata
Journal: BMJ (1902)

The army medical officer is indeed practical]y deterred from original research through want of scope.means, and encouragement.The handicapping mainly arises from the severe ordeal which senior officers ,ass through as to expenditure.Everything is audited down to a decimal point; no margin is allowed.Until some better system is in- augurated the efficiency of the service in the directions here indicated is not likely to be attained."Y Our correspondent undoubtedly touches upon points which deserve careful consideration in the promotion of efficiency in the direction indicated.
"Just Words"
Authors: Alexander Gode
Journal: JAMA (1963)

<h3>To the Editor:</h3> —I owe the readers of my "Just Words" an apology. I misquoted Paul Verlaine. In a discussion of the impersonal "it" I played with the line "Il pleut dans mon coeur" not remembering that Verlaine's words really were "Il pleure dans mon coeur." The irony of this inexcusable gaffe is that for many years whenever the line (in its mistaken form) ran through my mind I always thought that the poem from which it comes would be still more beautiful if "il pleut" were "il pleure." Since it<i>is</i>"il pleure," I now must conclude, and do so with joy, that the poem is more beautiful than anything I ever deemed possible. Several readers of "Just Words" have accused me of not knowing that "il pleut" is not a form of "pleurer." If that accusation were justified, I would resign from my teaching and editorial positions and
Comparative genomic analysis of primary versus metastasis in colorectal carcinomas.
Authors: E. Vakiani, M. Janakiraman, R. Shen, Z. Zeng, A. Cercek, N. E. Kemeny, A. Heguy, P. Paty, T. A. Chan, L. Saltz, M. R. Weiser, D. B. Solit
Journal: Journal of Clinical Oncology (2011)

10500 Background: Activating mutations in exon 2 of KRAS are routinely used to exclude colorectal cancer (CRC) patients from treatment with EGFR inhibitors. Retrospective studies have also shown a lack of response among patients with BRAF and NRAS mutations, whereas preliminary studies of PIK3CA have been conflicting. As most testing is done on primary tumor tissue, while metastatic disease is what is treated with anti-EGFR agents, we compared the mutational and copy number profiles of primary and metastatic CRCs. Methods: 736 fresh frozen tumors from 613 patients were analyzed for mutations in KRAS, NRAS, BRAF, PIK3CA and TP53 using a Sequenom MALDI-TOF mass spectrometry-based genotyping assay and Sanger sequencing. The cohort included 84 matched primary and metastases and 30 matched metastases. Formalin-fixed paraffin embedded tissue was also subjected to Sanger sequencing in cases showing discrepant results in their mutational profile. All tumors were checked for misidentification using a multiplexed PCR/MS-based genetic fingerprinting assay and a subset of matched pairs was analyzed by comparative genomic hybridization (Agilent, 1M array). Results: We identified 259 (42%) KRAS (219 in exon 2, 12 in exon 3 and 28 in exon 4), 18 (3%) NRAS, 40 (6%) BRAF, 72 (12 %) PIK3CA and 247 (40%) TP53 mutations in the 613 cases. BRAF mutations were significantly less frequent in metastatic CRC tumors, compared to primary tumors (3.8% vs. 7.3%, p=0.01), while TP53 mutations were significantly more frequent (55.6% vs. 30.2%, p<0.001). Mutational analysis of 84 matched pairs of primary and metastatic CRC revealed a concordance rate of 98%, 98% and 95% for RAS/BRAF, PIK3CA and TP53 mutations, respectively. Unsuperivised clustering of array CGH data from 22 matched pairs of primary and metastatic CRC showed that all pairs clustered together. Conclusions: In regards to RAS/BRAF/PIK3CA and TP53 mutational status, primary and metastatic CRC tumors show an extremely high degree of concordance. The results suggest that genomic characterization of the primary tumor for RAS/BRAF/PIK3CA and TP53 mutations can correctly characterize the mutational status of these genes in the patients with metastatic disease.
Deaths
Journal: JAMA (1962)

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
CHRONIC PELVIC PERITONITIS OF UNKNOWN ETIOLOGY OCCURRING IN WOMEN
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 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
Animal Models For The Study Of Drugs In Ischemic Stroke
Authors: S. Karpiak
Journal: The Annual Review of Pharmacology and Toxicology (1989)

Heme oxygenases (HO) catabolize free heme, that is, iron (Fe) protoporphyrin (IX), into equimolar amounts of Fe2+, carbon monoxide (CO), and biliverdin. The stress-responsive HO-1 isoenzyme affords protection against programmed cell death. The mechanism ...Read More
Abstract 5118: TIDE-E: an online evaluator of tumor immune-suppressive function of gene sets
Authors: Jingxin Fu, Wubing Zhang, Peng Jiang, Xiaole S. Liu
Journal: Cancer Research (2019)

Abstract Recent immunotherapy studies have generated a diverse collection of datasets, covering different aspects of cancer immune evasion. However, to the best of our knowledge, there are no public tools that can systematically rank genes regarding their function on tumor immune evasion and comprehensively evaluate biomarkers across multiple clinical cohorts. Therefore, we presented the TIDE-E (evaluator) website for users to evaluate their gene sets across a large panel of data cohorts (http://tide.dfci.harvard.edu). The website integrated two categories of data resources, human clinical datasets from public immunotherapy studies, TCGA, PRECOG, and METABRIC databases, as well as functional genomics datasets from CRISPR screens in preclinical models. For a user-defined gene set, the web application can test its performance as immunotherapy response biomarkers across multiple clinical studies, and rank the gene members according to their relevance in promoting tumor immune evasion. Citation Format: Jingxin Fu, Wubing Zhang, Peng Jiang, Xiaole S. Liu. TIDE-E: an online evaluator of tumor immune-suppressive function of gene sets [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 5118.
THU0080 Professor
Authors: NF Soroka, NP Mitkovskaya, AB Cheschevik
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Lipid profils in patients with rheumatoid arthritis. <h3>Objectives</h3> To investigate lipid profiles in patients with active and inactive rheumatoid arthritis (RA) and to assess the relationship of the inflammatory condition of RA with lipid profiles. <h3>Methods</h3> Seventy-two patients with RA and 25 age and sex matched healthy controls were studied. Patients with RA had not been treated with corticosteroid drugs prior to the study. Forty patients had active disease, and 32 had inactive disease. Plasma lipoproteins were fractionated by gradient ultracentrifugation into subfractions, and their chemical composition and mass were determined. Total cholesterol, triglyceride, LDL-cholesterol, HDL-cholesterol apolipoprotein AI (apo Al)/apolipoprotein B (apo B), lipoprotein (a) [Lp (a)], lipoprotein-associated platelet-activating factor acetylhydrolase (PAF-AH) activity and C-reactive protein (CRP) were measured in both groups. <h3>Results</h3> Patients with active RA had significantly lower plasma total cholesterol and high-density lipoprotein (HDL) cholesterol (42.9 vs. 56.1 mg/dl) levels as compared with controls, due to the decrease in the mass of both the HDL2 and HDL3 subfractions. Patients with active RA also had higher plasma triglyceride levels, mainly due to the higher triglyceride content of the very low-density lipoprotein plus the intermediate-density lipoprotein subfraction. The plasma PAF-AH activity in patients with active RA was lower than that in controls, mainly due to the decrease in PAF-AH activity associated with the intermediate and dense low-density lipoprotein subclasses. The levels of apo Al and HDL-cholesterol were significantly lower in patients than in controls (121.4 vs. 147.4 mg/dl,). The level of Lp (a) was significantly higher in patients than in controls (29.2 vs. 19.2 mg/dl). The ratios of apo B/apo Al, total cholesterol/HDL-cholesterol, and LDL-cholesterol/HDL-cholesterol were significantly higher in patients than in controls (0.89 vs. 0.61, 4.6 vs. 3.2, 2.7 vs. 1.7, respectively). CRP showed a significant correlation with apo Al (r = -0.47, p &lt; 0.05). <h3>Conclusion</h3> This study suggests that patients with active RA have altered lipoprotein and apolipoprotein pattems that may possibly expose them to higher risk of atherosclerosis. The inflammatory condition of RA may affect the metabolism of HDL-cholesterol and apo A1. Our study to show that patients with active RA exhibit low levels of HDL2 and HDL3 and are deficient in plasma PAF-AH activity. These alterations suggest that active RA is associated with partial loss of the antiinflammatory activity of plasma Apo B- and Apo A-I-containing lipoproteins.
Epilepsy
Authors: Douglas T. Davidson, Cesare Lombroso
Journal: New England Journal of Medicine (1954)

Acetylcholine. The presence of acetylcholine within nerve cells is generally accepted as essential for the propagation and synaptic transmission of nerve impulse in most of the peripheral nervous system. Also, many accept this role for acetylcholine in the brain. The chemical is thought to affect the permeability of the cell membrane separating the high intracellular potassium concentrations from the high extracellular sodium concentrations. More specifically, free acetylcholine is thought to foster membrane repolarization and to restore the intracellular and extracellular ionic concentration gradients that have been neutralized during the transmission of a nerve impulse.17 Excessive amounts of free acetylcholine applied . . .
Preventing Physician Suicide
Authors: Douglas A. Sargent
Journal: JAMA (1977)

Psychological barriers in the minds of the failing physician, his family, and colleagues may thwart prevention of physician-suicide. The failing physician may be shunned by colleagues for his disturbed behavior. He denies illness, resorts to self-medication, and avoids treatment. Recognition and rational handling of this presuicidal state may be hindered by the need of the doctor, family, and colleagues to preserve a fantasy of the doctor's omnipotence. Treatment also may be impeded by the failing physician's reluctance to form a therapeutic relationship with the treating psychiatrist. The psychiatrist must help his doctor-patient to determine if he should continue practicing. The key to successful intervention may depend solely on our awareness and handling of these problems. (<i>JAMA</i>237:143-145, 1977)
Bedside aids to auscultation of the heart
Authors: P. T. Cochran
Journal: JAMA (1978)

WITH THE PROFUSION of cardiac diagnostic tools that have appeared in the past few years, the continued importance of careful physical examination of the heart must be emphasized. In spite of the great benefits that have been reaped from invasive and noninvasive studies of the cardiovascular system, all too frequently the decision to obtain such studies and the interpretation of their results are not firmly based on careful assessment of the physical findings. Heart disease is sometimes diagnosed where none exists and is missed where it does because of too great a reliance on the infallibility of technologic tools of cardiac diagnosis. The pathophysiologic lessons learned from echocardiography, cardiac catheterization, and angiocardiography have been especially helpful in extending our understanding of heart sounds and murmurs. Noting the changes in auscultatory findings that result from physical maneuvers and vasoactive drugs administered at the bedside has been recently emphasized by deLeon and
Abstract A45: The prolyl isomerase Pin1 interacts with a ribosomal protein S6 kinase to enhance insulin-induced AP-1 activity and cellular transformation
Authors: Hong Seok Choi, Gwang Mo Namgoog, Hae-Gook Cho
Journal: Cancer Research (2009)

Abstract Phosphorylation of proteins on serine or threonine residues that immediately precede proline (pSer/Thr-Pro) is specifically catalyzed by the peptidyl-prolyl cis/trans isomerase Pin1 and is a central signaling mechanism in cell proliferation and transformation. Although Pin1 is frequently overexpressed in hepatocellular carcinoma (HCC), the molecular mechanism of Pin1 in HCC has not been completely elucidated. Here, we show that Pin1 interacts with p70S6K in vitro and ex vivo. Overexpression of Pin1 resulted in enhanced p70S6K phosphorylation induced by insulin in SK-HEP-1 cells. In contrast, Pin1−/− mouse embryonic fibroblasts (MEFs) exhibited significantly decreased insulin-induced p70S6K phosphorylation compared to Pin1+/+ MEFs. Furthermore, Pin1 enhanced the insulin-induced ERK1/2 phosphorylation through its interaction with p70S6K, whereas the inhibition of p70S6K activity by rapamycin suppressed insulin-induced ERK1/2 phosphorylation in SK-HEP-1 cells. Hence, Pin1 affected AP-1 activity through p70S6K-ERK1/2 signaling in SK-HEP-1 cells. Most importantly, Pin1-overexpressing JB6 Cl41 cells enhanced neoplastic cell transformation promoted by insulin much more than GFP-overexpressing JB6 Cl41 control cells. These results imply that Pin1 amplifies insulin signaling in hepatocarcinoma cells through its interaction with p70S6K, suggesting that Pin1 plays an important role in insulin-induced tumorigenesis and is a potential therapeutic target in hepatocarcinoma. Citation Information: Cancer Res 2009;69(23 Suppl):A45.
ATHEROMATOUS EMBOLIZATION TO THE BRAIN
Journal: JAMA (1965)

Spontaneous avulsion of an atheromatous plaque, as a mechanism for the production of emboli, was proposed more than 100 years ago.<sup>1</sup>It would appear from subsequent pathologic surveys that such emboli are likely to be of minor clinical significance except when they lodge in the vessels of the heart, lower limbs, or brain. The ascending aorta is assumed to be the source of atheromatous emboli to the brain. The great majority of patients with atheromatous emboli in the cerebral circulation are of advanced age and are shown to have severe, often erosive, aortic atherosclerosis. The frequency of factors which have an augmenting influence upon generalized atherosclerosis, such as diabetes mellitus or hypertension, is predictably high in these cases. Severe sclerosis of the coronary arteries is also common. In over half of the patients with verified cerebral infarcts caused by atheromatous emboli, myocardial infarction is demonstrated. The elevated frequency of
Do the American Society of Clinical Oncology (ASCO) Value Framework and the European Society of Medical Oncology (ESMO) Magnitude of Clinical Benefit Scale measure the same construct of clinical benefit?
Authors: Sierra Cheng, Erica McDonald, Matthew C. Cheung, Vanessa Sarah Arciero, Mahin Iqbal Qureshi, Di Maria Jiang, Doreen Anuli Ezeife, Mona Sabharwal, Alexandra Chambers, Dolly Han, Natasha B. Leighl, Kelley-Anne Sabarre, Kelvin K. Chan
Journal: Journal of Clinical Oncology (2017)

6509 Background: Whether the American Society of Clinical Oncology (ASCO) Value Framework and the European Society for Medical Oncology Magnitude of Clinical Benefit Scale (ESMO-MCBS) measure similar constructs of clinical benefit is unclear. It is also unclear how they relate to quality-adjusted life-years (QALYs) and funding recommendations in the UK and Canada. Methods: Randomized clinical trials (RCTs) of oncology drug approvals by the Food and Drug Administration, European Medicines Agency and Health Canada between January 2006 and August 2015 were identified and scored using the ASCO version 1 (v1) framework (August 10, 2015), ASCO version 2 (v2) framework (May 31, 2016) and ESMO-MCBS (May 30, 2015) by at least two independent reviewers. Spearman correlation coefficients were calculated to assess construct (between frameworks) and criterion validity (against incremental QALYs from the National Institute of Clinical Excellence (NICE) and the pan-Canadian Oncology Drug Review (pCODR)). Associations between scores and NICE/pCODR recommendations were examined by logistic regression models. Inter-rater reliability was assessed using intra-class correlation coefficients. Results: From 109 included RCTs, 108 ASCOv1, 111 ASCOv2 and 83 ESMO scores were determined. Correlation coefficients for ASCOv1 vs. ESMO, ASCOv2 vs. ESMO, and ASCOv1 vs. ASCOv2 were 0.36 (95% CI 0.15-0.54), 0.17 (95% CI -0.06-0.37) and 0.50 (95% CI 0.35-0.63), respectively. Compared with NICE QALYs, correlation coefficients were 0.45 (ASCOv1), 0.53 (ASCOv2) and 0.46 (ESMO); with pCODR QALYs, coefficients were 0.19 (ASCOv1), 0.20 (ASCOv2) and 0.36 (ESMO). None of the frameworks were significantly associated with NICE/pCODR recommendations. Inter-rater reliability was good for all frameworks. Conclusions: The weak-to-moderate correlations between the ASCO frameworks and ESMO-MCBS, with QALYs, and with NICE/pCODR funding recommendations suggest different constructs of clinical benefit measured. Construct convergent validity with the ESMO-MCBS in fact did not increase with the updated ASCO framework.
Recombinant Activated Factor VII for Acute Intracerebral Hemorrhage
Authors: Stephan A. Mayer, Nikolai C. Brun, Kamilla Begtrup, Joseph Broderick, Stephen Davis, Michael N. Diringer, Brett E. Skolnick, Thorsten Steiner
Journal: New England Journal of Medicine (2005)

Intracerebral hemorrhage is the least treatable form of stroke and is associated with high mortality. Among patients who undergo computed tomography (CT) within three hours after the onset of intracerebral hemorrhage, one third have an increase in the volume of the hematoma related to subsequent bleeding. We sought to determine whether recombinant activated factor VII (rFVIIa) can reduce hematoma growth after intracerebral hemorrhage.We randomly assigned 399 patients with intracerebral hemorrhage diagnosed by CT within three hours after onset to receive placebo (96 patients) or 40 microg of rFVIIa per kilogram of body weight (108 patients), 80 microg per kilogram (92 patients), or 160 microg per kilogram (103 patients) within one hour after the baseline scan. The primary outcome measure was the percent change in the volume of the intracerebral hemorrhage at 24 hours. Clinical outcomes were assessed at 90 days.Hematoma volume increased more in the placebo group than in the rFVIIa groups. The mean increase was 29 percent in the placebo group, as compared with 16 percent, 14 percent, and 11 percent in the groups given 40 microg, 80 microg, and 160 microg of rFVIIa per kilogram, respectively (P=0.01 for the comparison of the three rFVIIa groups with the placebo group). Growth in the volume of intracerebral hemorrhage was reduced by 3.3 ml, 4.5 ml, and 5.8 ml in the three treatment groups, as compared with that in the placebo group (P=0.01). Sixty-nine percent of placebo-treated patients died or were severely disabled (as defined by a modified Rankin Scale score of 4 to 6), as compared with 55 percent, 49 percent, and 54 percent of the patients who were given 40, 80, and 160 microg of rFVIIa, respectively (P=0.004 for the comparison of the three rFVIIa groups with the placebo group). Mortality at 90 days was 29 percent for patients who received placebo, as compared with 18 percent in the three rFVIIa groups combined (P=0.02). Serious thromboembolic adverse events, mainly myocardial or cerebral infarction, occurred in 7 percent of rFVIIa-treated patients, as compared with 2 percent of those given placebo (P=0.12).Treatment with rFVIIa within four hours after the onset of intracerebral hemorrhage limits the growth of the hematoma, reduces mortality, and improves functional outcomes at 90 days, despite a small increase in the frequency of thromboembolic adverse events.