tbuckley/cabot-search huggingface dataset:
Quadratic discriminant analysis as an aid to interpretive reporting of clinical laboratory tests
Authors: R. S. Ryback
Journal: JAMA (1982)

PHYSICIANS order more laboratory tests today than ever before. Because of the increasing likelihood of clinically spurious values with the increasing number of tests, the difficulty of detecting many medical conditions in early stages, and the difficulty in differentiating among certain medical conditions, interpretive reporting of laboratory results can be of diagnostic value. See also p 2261. A number of sophisticated mathematical approaches have been applied to the analysis of clinical laboratory data.<sup>1-3</sup>One of the more commonly used approaches is discriminant analysis (DA),<sup>4,5</sup>which is a complex mathematical form of pattern recognition, wherein it is determined whether two or more defined medical conditions can be differentiated on the basis of variables other than those used to define the medical conditions. Quadratic discriminant analysis (QDA) is a nonlinear form of DA that does not assume that the variability present in the discriminating variables (eg, clinical laboratory tests) is
Letter by Bisdas et al Regarding Article, “Aspirin Plus Clopidogrel Versus Aspirin Alone After Coronary Artery Bypass Grafting: The Clopidogrel After Surgery for Coronary Artery Disease (CASCADE) Trial”
Authors: Theodosios Bisdas, Axel Haverich, Omke E. Teebken
Journal: Circulation (2011)
INFESTATION WITH FLAGELLATE PROTOZOA
Journal: JAMA (1924)

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
Prostatic Hypertrophy, from Every Surgical Standpoint.
Journal: JAMA (1904)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Acetaminophen Hepatotoxicity
Authors: Alan H. Hall
Journal: JAMA (1986)

<h3>To the Editor.—</h3> The article by O'Dell et al<sup>1</sup>proposing an increased sensitivity to acetaminophen-induced hepatotoxicity in an alcoholic patient requires comment. This patient first developed right upper quadrant pain, nausea, and vomiting and then began taking 6 g of acetaminophen daily (the manufacturer's recommended maximum daily dose is 4 g) to alleviate the pain. Centrilobular hepatic necrosis was subsequently documented on liver biopsy. The patient recovered spontaneously after discontinuing use of acetaminophen (and presumably alcohol) while hospitalized. Acetaminophen plasma levels were not determined. The authors did not report that other possible etiologies (ie, carbon tetrachloride and isoniazid) were investigated. The patient developed a similar illness eight months later, apparently having symptoms first and then taking 6 g of acetaminophen daily. Again, no acetaminophen plasma levels were documented. There was again no reported attempt to exclude exposure to other possible hepatotoxins. On repeated liver biopsy, centrilobular fibrosis was found.
Reply
Authors: Marcello Bianchini, Lesley De Pietri, Guadalupe Garcia‐Tsao, Erica Villa
Journal: Hepatology (2016)

Potential conflict of interest: Nothing to report. We read with interest the correspondence from Amarapurkar and Lo. We thank Dr. Amarapurkar et al. for their comments. We certainly agree that, based on the evidence, there is no need to correct coagulopathy in patients with liver cirrhosis undergoing invasive procedures. Dr. Amarapurkar's correspondence states that correction of coagulopathy is not considered standard of care, when previous guidelines (referenced in our article1) and current guidelines2 recommend such correction. This is the reason why we sought to compare whether thromboelastography (TEG)‐guided correction was associated with a lower transfusion of blood products than correction based on international normalized ratio (INR) and platelet count (PLT). We were surprised to find that even in our cohort of patients with severe coagulopathy (INR, >1.8; PLT, <50,000/mm3) and with a median Model for End‐Stage Liver Disease score of 21, bleeding occurred in only 1 of 60 (2%) patients. It was until we completed the study that we realized that this level of coagulopathy does not define bleeding risk in patients with cirrhosis and should not be corrected.1 In the study mentioned in the correspondence3 where coagulopathy was more conservatively defined (INR, >1.5; PLT, <50,000/mm3), 3 of 128 (2%) that had had a high‐risk procedure developed bleeding, but this bleeding risk was not significantly higher than patients without coagulopathy. Interestingly, compared to patients with coagulopathy who did not bleed, those who bled also had acute kidney injury and/or sepsis as comorbidities and this may represent the difference. Whether correction of coagulopathy in these settings leads to lower bleeding complications remains to be determined.3 These results, together with ours, suggest that, in the absence of comorbidities, the risk of bleeding associated with invasive procedures is quite low and that prophylactic correction of coagulopathy is not warranted. It may be more cost‐effective to correct coagulopathy during or after the procedure if and when bleeding occurs. In our opinion, there is no need to perform a study without prophylactic correction of routine coagulation tests as was suggested by Intagliata et al.,4 because the TEG‐guided transfusion policy in our study required transfusion in only 5 of 30 patients. In our view, there is instead a strong need of prospective, well‐designed studies analyzing predictors of bleeding beyond coagulation tests and the effect of correction of blood products in high‐risk patients. In conclusion, we agree with Dr. Amarapukar on avoiding the widespread use of prophylactic blood products transfusion based solely on INR and PLT count.
ABSTRACTS
Authors: None &NA;
Journal: Clinical Nuclear Medicine (1994)

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Posttranscriptional m6A Editing of HIV-1 mRNAs Enhances Viral Gene Expression
Authors: Edward M. Kennedy, Hal P. Bogerd, Anand V.R. Kornepati, Dong Kang, Delta Ghoshal, Joy B. Marshall, Brigid C. Poling, Kevin Tsai, Nandan S. Gokhale, Stacy M. Horner, Bryan R. Cullen
Journal: Cell Host & Microbe (2017)
Macroangiopathic hemolytic anemia due to congenital cardiovascular anomalies
Authors: R. G. Westphal
Journal: JAMA (1971)

Hemolytic anemia due to vascular trauma occurred in a boy with congenital cardiovascular anomalies that included aortic coarctation and bicuspid aortic valve. Turbulent stress of red blood cells passing through deformed orifices is deemed responsible for the traumatic damage and ensuing hemolysis in this patient.
THE BENEFICENT MICROBE.
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
Jarman index.
Authors: B Jarman
Journal: BMJ (1991)

suffer from greater underascertainment than we estimated the incidence of childhood diabetes would be correspondingly increased throughout the British Isles, indicating an even greater dif- ference between the incidence in 1988 compared with that reported by Bloom et al for 1973-4.2The cause for public concern remains: urgency is added to the case for further national studies such as ours and multinational studies such as EURODIAB.
The road not taken. Tarrasch and Cajal
Authors: A. M. Potts
Journal: JAMA (1972)

In this poem (<i>from Mountain Interval</i>, Henry Holt &amp; Co., 1916), Robert Frost is saying what anyone will say who believes in the validity of history: there are events in the lives of men that "make all the difference" and on occasion they influence not only individual lives but also our cultural future. A curious instance of this is the parallel but divergent course of two physicians. They were essentially contemporaries; each had exceptional mental ability; each was deeply involved in medicine and deeply involved in the game of chess. One of them won a Nobel prize in medical science, the other became not only a world chess master but the preeminent chess player of his day and a formulator of chess knowledge. Obviously I do not know precisely all the various elements that directed Ramon y Cajal away from chess toward the Nobel prize or those, in turn, which
Lectures upon the Nursing of Infectious Diseases.
Journal: JAMA (1931)

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
Successful treatment of refractory anemia by high‐dose methylprednisolone associated with an increment in CD68‐positive cells in bone marrow
Authors: Sayuri Motomura, Toshiko Motoji, Keiko Okutomi, Toshio Nishikawa, Takeshi Kasajima, Hideaki Mizoguchi
Journal: American Journal of Hematology (2001)

Refractory anemia has a relatively low incidence of the subsequent development of acute leukemia and a relatively long survival among the myelodysplastic syndromes (MDS). We observed hematological improvement due to high-dose methylprednisolone in 9 of 18 patients with refractory anemia. The patients' age range was from 28 to 78 years old (mean age: 54), including 14 male and 4 females. A complete response was obtained in 5 patients, minimal response in 4 patients, and no response in 9 patients. Laboratory data of peripheral blood counts and differential counts of bone marrow aspirates were not different, except that fewer chromosomal abnormalities (P = 0.086) were observed in the responder group. Side effects were seen in two patients but were controllable. Overall survival was significantly longer in the responder group (Log-rank P = 0.040, Wilcoxon P = 0.045). The overall survival of responders did not reach the median and 85% of the patients were alive after 180 months, while the median overall survival of the non-responders was 61.8 months. Disease progression was more frequently seen in the non-responder group (P = 0.045). Furthermore, we investigated retrospectively immunohistochemical bone marrow staining, and a significantly higher percentage of CD68-positive (22.6% ± 7.1%) and CD45RA-positive cells was observed in the responder group compared to the non-responder group (6.5% ± 1.3%). Our present results indicate that high-dose methylprednisolone is valuable as a primary treatment before other immunosuppressive treatments, because of its ease of use. High efficacy with high-dose methylprednisolone is expected, especially in patients in which increments in CD68-positive cells in bone marrow are observed. Am. J. Hematol. 66:80–84, 2001. © 2001 Wiley-Liss, Inc.
MURDER AND SCIENCE.
Journal: JAMA (1900)

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
Plasma Concentration of Cystatin-C and Mannose Binding Protein and the Risk of Developing Peripheral Vascular Disease
Authors: Michelle A Albert, Nader Rifai, Paul M Ridker
Journal: Circulation (2001)

P05 Background- Cystatin-C, a cysteine protease inhibitor, and mannose binding lectin, an innate defense protein involved in microbial clearance, have both been hypothesized to mediate atherosclerotic plaque progression. However, little prospective data are available evaluating whether levels of these proteins in healthy individuals are associated with incident cardiovascular disease. Methods and Results-Employing a prospective, nested, case control study design, baseline levels of cystatin-C and mannose binding protein were evaluated among 133 apparently healthy men who subsequently developed symptomatic peripheral arterial disease (cases) and among 133 age and smoking matched controls who remained free of reported vascular disease during a 5 year follow-up period. Overall, median baseline levels of cystatin-C were virtually identical among case and control subjects (0.83mg/L, p=0.84). Similarly, median baseline levels of mannose binding protein among cases and controls were 2.32mg/L and 2.2mg/L,(p=0.69). We found no evidence of association between either cystatin-C or mannose binding protein and the development of peripheral vascular disease in analyses evaluating for linear trends or for threshold effects (all p values &gt;0.05). Conclusion-In contrast to prior retrospective and cross-sectional studies, we found no evidence in this prospective evaluation that baseline levels of cystatin-C or mannose binding protein are associated with increased risk of future vascular disease.
The Rat. Data and Reference Tables for the Albino Rat (Mus Norvegicus Albinus) and the Norway Rat (Mus Norvegicus).
Journal: JAMA (1925)

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
ANGINA PECTORIS.
Authors: AUGUSTUS A. ESHNER
Journal: JAMA (1900)

While the use of the Greek prefix "pseudo," or its English equivalent "false" in medical nomenclature is at times a matter of convenience, it may become a source of confusion or misunderstanding. This is exemplified in the use of the term "pseudo-angina pectoris." Although the question of the pathology of angina pectoris is not definitely settled, it seems not unreasonable to attribute the symptoms of the affection to derangement in the function of the cardiac plexus of nerves, usually induced through interference with the circulation in the coronary arteries, or through disease of the myocardium. In addition, however, to cases in which such vascular or myocardial disease is present, there are other cases in which similar symptoms arise, in the absence of appreciable organic disease referable to the heart. To this latter condition, the designation "pseudo-angina pectoris" has been applied, and among the etiologic factors, toxic and neurotic states have
The problem of physician self-referral under the Medicare and Medicaid antikickback statute. The Hanlester Network case and the safe harbor regulation
Authors: T S Crane
Journal: JAMA (1992)

Dramatic changes have taken place in the legal and ethical status of physician self-referral. In July 1991, the US Department of Health and Human Services issued the "safe harbor" regulation, which permits self-referral only under very narrow constraints. In September 1991, the Department of Health and Human Services Departmental Appeals Board ruled in the landmark<i>Hanlester Network</i>case that joint venture profit distributions are illegal under the antikickback statute when intended to influence investors' reason or judgment in referring Medicare or Medicaid patients. Following this principle on remand in March 1992, the Administrative Law Judge precedentially held that profit distributions violated the statute. Before this remand decision, the Departmental Appeals Board ruling and the safe harbor regulation started the pendulum swinging against self-referral as seen, for example, in the December 1991 revised American Medical Association ethical guidelines. To help providers operate in this new legal and ethical climate, legislation is needed to authorize case-by-case safe harbors. (<i>JAMA</i>. 1992;268:85-91)