tbuckley/cabot-search huggingface dataset:
Acute Renal Failure and Open Heart Surgery
Authors: E. D. Yeboah, A. Petrie, J. L. Pead
Journal: BMJ (1972)

A retrospective study of 428 open heart operations showed the incidence of mild and severe renal failure to be 26% and 4.7% respectively. The mortality rate was 38% in the mild cases and 70% in the severe cases. Only half of the patients whose death was associated with renal failure showed macroscopic or microscopic renal lesions at necropsy. The patients who developed renal impairment had significantly higher mean preoperative blood urea (40 mg/100 ml) than the non-renal-failure cases (33 mg/100 ml). Periods of perfusion over 60 minutes, mean perfusion pressures below 80 mm Hg, and multiple valve replacement operations also increased the incidence of renal failure. There was no statistical correlation between the age of individual patients, the degree of cooling, and postoperative blood urea values. There was no evidence to suggest that frusemide or mannitol separately or together influenced the development of renal failure. Peritoneal dialysis was preferred for initial treatment of patients with severe renal failure, and haemodialysis was required only in special cases.
FDG PET/CT Findings in Purely Cutaneous Rosai-Dorfman Disease
Authors: Jei-Yie Huang, Ching-Chu Lu, Cheng-Hsiang Hsiao, Kai-Yuan Tzen
Journal: Clinical Nuclear Medicine (2011)

Rosai-Dorfman disease or “sinus histiocytosis with massive lymphadenopathy” is a benign systemic proliferative disorder of histiocytes first which was described in 1969. The disease usually presented with bilateral painless lymphadenopathy, fever, leukocytosis, high erythrocyte sedimentation rate, and polyclonal hypergammaglobulinemia. About half of the patients may present with extranodal involvement. Although skin involvement is the most common form of extranodal diseases, purely cutaneous Rosai-Dorfman diseases with no nodal or other extranodal lesions accounting is rare. We presented a 41-year-old man with purely cutaneous Rosai-Dorfman, who underwent FDG PET/CT for detection of disease extension. PET/CT showed accurate localization of increased glucose metabolism.
Direct detection of Mycobacterium tuberculosis using polymerase chain reaction assay among patients with hepatic granuloma
Authors: Diana E. Alcantara-Payawal, Masayuki Matsumura, Yasushi Shiratori, Takehito Okudaira, Roy Gonzalez, Roland A. Lopez, Jose D. Sollano, Masao Omata
Journal: Journal of Hepatology (1997)
A genome-wide association meta-analysis of self-reported allergy identifies shared and allergy-specific susceptibility loci
Authors: David A Hinds, George McMahon, Amy K Kiefer, Chuong B Do, Nicholas Eriksson, David M Evans, Beate St Pourcain, Susan M Ring, Joanna L Mountain, Uta Francke, George Davey-Smith, Nicholas J Timpson, Joyce Y Tung
Journal: Nature Genetics (2013)
Cost-Effectiveness of Diagnostic Strategies for Patients with Chest Pain
Authors: Karen M. Kuntz
Journal: Annals of Internal Medicine (1999)

Background: Many noninvasive tests exist to determine whether patients should undergo coronary angiography. The routine use of coronary angiography without previous noninvasive testing is typically not advocated. Objective: To determine the cost-effectiveness of diagnostic strategies for patients with chest pain. Design: Cost-effectiveness analysis. Data Sources: Published data. Target Population: Patients who present with chest pain, have no history of myocardial infarction, and are able to perform an exercise stress test. Time Horizon: Lifetime. Perspective: Societal. Interventions: No testing, exercise electrocardiography, exercise echocardiography, exercise single-photon emission computed tomography (SPECT), and coronary angiography alone. Outcome Measures: Quality-adjusted life expectancy, lifetime cost, and incremental cost-effectiveness. Results of Base-Case Analysis: The incremental cost-effectiveness ratio of routine coronary angiography compared with exercise echocardiography was $36 400 per quality-adjusted life-year (QALY) saved for 55-year-old men with typical angina. For 55-year-old men with atypical angina, exercise echocardiography compared with exercise electrocardiography cost $41 900 per QALY saved. If adequate exercise echocardiography was not available, exercise SPECT cost $54 800 per QALY saved compared with exercise electrocardiography for these patients. For 55-year-old men with nonspecific chest pain, the incremental cost-effectiveness ratio of exercise electrocardiography compared with no testing was $57 700 per QALY saved. Results of Sensitivity Analysis: On the basis of a probabilistic sensitivity analysis, there is a 75% chance that exercise echocardiography costs less than $50 900 per QALY saved for 55-year-old men with atypical angina. Conclusions: Exercise electrocardiography or exercise echocardiography resulted in reasonable cost-effectiveness ratios for patients at mild to moderate risk for coronary artery disease in terms of age, sex, and type of chest pain. Coronary angiography without previous noninvasive testing resulted in reasonable cost-effectiveness ratios for patients with a high pretest probability of coronary artery disease.
Lack of durable disease control with chemotherapy for mycosis fungoides and Sézary syndrome: a comparative study of systemic therapy
Authors: Charlotte F. M. Hughes, Amit Khot, Christopher McCormack, Stephen Lade, David A. Westerman, Robert Twigger, Odette Buelens, Kate Newland, Constantine Tam, Michael Dickinson, Gail Ryan, David Ritchie, Colin Wood, H. Miles Prince
Journal: Blood (2014)
In vitro studies on cellular and humoral chemotaxis in Crohn's disease using the under agarose gel technique.
Authors: R D'Amelio, P Rossi, S Le Moli, R Ricci, S Montano, F Pallone
Journal: Gut (1981)

The locomotor function of polymorphonuclear cells (cellular chemotaxis) and serum chemotactic activity (humoral chemotaxis) were studied in 51 patients with Crohn9s disease using a method of migration under agarose gel. To study cellular chemotaxis patient9s polymorphonuclear cells were challenged against normal Zymosan activated serum and humoral chemotaxis was evaluated testing the patient9s Zymosan activated serum against normal polymorphonuclear cells. Cellular chemotaxis in the Crohn9s disease group was normal (although 30% of the 51 patients had migration values out of the normal range), while humoral chemotaxis was significantly lower in Crohn9s disease patients than in the control group. However, the value of humoral chemotaxis in the group of Crohn9s disease patients treated with steroids was lower than that of patients not treated, thus accounting for the low mean value observed inthe Crohn9s disease-group as a whole. The present results suggest that a defective chemotactic response may occur in some Crohn9s disease patients, particularly during steroid treatment. These findings might be related either to a defective generation of complement derived chemotactic factors or to the presence of circulating inhibitors.
The expression pattern of small nucleolar and small Cajal body-specific RNAs characterizes distinct molecular subtypes of multiple myeloma
Authors: D Ronchetti, K Todoerti, G Tuana, L Agnelli, L Mosca, M Lionetti, S Fabris, P Colapietro, M Miozzo, M Ferrarini, P Tassone, A Neri
Journal: Blood Cancer Journal (2012)

Small nucleolar RNAs (snoRNAs) and small Cajal body-specific RNAs (scaRNAs) are non-coding RNAs involved in the maturation of other RNA molecules and generally located in the introns of host genes. It is now emerging that altered sno/scaRNAs expression may have a pathological role in cancer. This study elucidates the patterns of sno/scaRNAs expression in multiple myeloma (MM) by profiling purified malignant plasma cells from 55 MMs, 8 secondary plasma cell leukemias (sPCLs) and 4 normal controls. Overall, a global sno/scaRNAs downregulation was found in MMs and, even more, in sPCLs compared with normal plasma cells. Whereas SCARNA22 resulted the only sno/scaRNA characterizing the translocation/cyclin D4 (TC4) MM, TC2 group displayed a distinct sno/scaRNA signature overexpressing members of SNORD115 and SNORD116 families located in a region finely regulated by an imprinting center at 15q11, which, however, resulted overall hypomethylated in MMs independently of the SNORD115 and SNORD116 expression levels. Finally, integrative analyses with available gene expression and genome-wide data revealed the occurrence of significant sno/scaRNAs/host genes co-expression and the putative influence of allelic imbalances on specific snoRNAs expression. Our data extend the current view of sno/scaRNAs deregulation in cancer and add novel information to the bio-molecular complexity of plasma cell dyscrasias.
Septic Shock in Humans
Authors: J E Parrillo, M M Parker, C Natanson, A F Suffredini, R L Danner, R E Cunnion, F P Ognibene
Journal: Annals of Internal Medicine (1990)

Septic shock is the commonest cause of death in intensive care units. Although sepsis usually produces a low systemic vascular resistance and elevated cardiac output, strong evidence (decreased ejection fraction and reduced response to fluid administration) suggests that the ventricular myocardium is depressed and the ventricle dilated. In survivors, these abnormalities are reversible. Failure to develop ventricular dilatation in nonsurvivors suggests that dilatation is a compensatory mechanism needed to maintain adequate cardiac output. With a canine model of septic shock that is very similar to human sepsis, myocardial depression was confirmed using load-independent measures of ventricular performance. Endotoxin administration to humans simulates the qualitative, cardiovascular abnormalities of sepsis. The pathogenesis of septic shock is extraordinarily complex. Diverse microorganisms can generate toxins, stimulating release of potent mediators that act on vasculature and myocardium. A circulating myocardial depressant substance has been closely associated with the myocardial depression of human septic shock. Therapy has emphasized early use of antibiotics, critical care monitoring, aggressive volume resuscitation, and, if shock continues, use of inotropic agents and vasopressors. Pharmacologic or immunologic antagonism of endotoxin or other mediators may prove to enhance survival in this highly lethal syndrome.
Degarelix: A Novel Gonadotropin-Releasing Hormone (GnRH) Receptor Blocker—Results from a 1-yr, Multicentre, Randomised, Phase 2 Dosage-Finding Study in the Treatment of Prostate Cancer
Authors: Hendrik Van Poppel, Bertrand Tombal, Jean J. de la Rosette, Bo-Eric Persson, Jens-Kristian Jensen, Tine Kold Olesen
Journal: European Urology (2008)
Denial and Silent Ischemia: Which Comes First?-Reply
Authors: Arthur J. Barsky
Journal: JAMA (1991)

In Reply. —  We thank Drs Janne, Reynaert, and Decoster for directing our attention to their work on denial; more such research is needed. The phenomenon of denial is particularly knotty to conceptualize and especially difficult to study. Does denial refer to the disavowal of perceptions, eg, pain, or to the disavowal of knowledge and information, eg, the fact that one is ill? How are we to measure denial, and how do we distinguish it from simply refusing to admit something to an interviewer or researcher?  If patients with silent ischemia show more denial than symptomatic patients, how do we know whether they're denying their illness because they experience no symptoms of it, or whether they report no symptoms because they are denying that they feel them? The work of Dr Janne and colleagues suggests that patients with silent myocardial ischemia do indeed exhibit more denial of serious disease, and
Pharmacogenomics of bortezomib test-dosing identifies hyperexpression of proteasome genes, especially PSMD4, as novel high-risk feature in myeloma treated with Total Therapy 3
Authors: John D. Shaughnessy, Pingping Qu, Saad Usmani, Christoph J. Heuck, Qing Zhang, Yiming Zhou, Erming Tian, Ichiro Hanamura, Frits van Rhee, Elias Anaissie, Joshua Epstein, Bijay Nair, Owen Stephens, Ryan Williams, Sarah Waheed, Yazan Alsayed, John Crowley, Bart Barlogie
Journal: Blood (2011)
The Public Health Implications of Global Warming
Authors: John F. Staropoli
Journal: JAMA (2002)

IN 1861 THE NATURAL PHILOSOPHER JOHN TYNDALL MADE THE PREDICtion, little noted at the time, that anthropogenic emissions of carbon dioxide would trap the radiative energy of the sun within the earth’s atmosphere and raise surface temperatures. An early investigation of this “greenhouse effect” concluded that a “large-scale geophysical experiment” began ever since the Industrial Revolution wed civilization to fossil fuels. The recent data of several international consortia show that global warming is accelerating at a rate far greater than that predicted a century ago and is due in large part to combustion of fossil fuels. This issue of MSJAMA brings together several lines of published evidence that global warming has emerged as a public health challenge requiring serious, concerted action. Jonathan Patz and Mahmooda Khaliq survey the immediate threats posed by climate change as well as some of the more insidious ones. Kent Bransford and Janet Lai find grounds for a common approach to both climate change and air pollution. Stephen Liang and colleagues describe technologies that can help track the spread of climate-sensitive infectious disease vectors. Finally, William Burns discusses public policy tools to respond and adapt to these challenges. Unfounded alarmism has no place either in clinical practice or in the legislative process. On the other hand, we cannot simply ignore extensive, peer-reviewed data on the causes and impacts of climate change. Lending a sense of urgency to this seemingly distant and abstract threat may well require us to link its consequences to our quality of life. In the absence of domestic leadership on global warming, one way to accomplish this goal might be to summon health care professionals to nontraditional advocacy roles. A similar approach helped give birth to the Montreal Protocol of 1987. Parties to the convention that produced the treaty identified depletion of the UV-absorbing ozone layer by chlorofluorocarbons (CFCs) as a public health threat of potentially catastrophic proportions requiring immediate action, namely, the phasing out of CFCs and related compounds. A role for health care professionals in global environmental policy is a natural extension of a growing ethos of preventive medicine, the sort that has, for instance, reduced the prevalence of smoking in the United States and led to improvements in food, highway, and gun safety. Similarly, it is not too late and none too soon for the health care community to advocate policies that wean us from fossil fuels and ultimately mitigate the extent of human-induced climate change.
Acetaminophen and Liver Disease
Authors: DAVID M. ROSENBERG
Journal: Annals of Internal Medicine (1978)

Letters and Corrections1 January 1978Acetaminophen and Liver DiseaseDAVID M. ROSENBERG, M.D., FRANCIS A. NEELON, M.D.DAVID M. ROSENBERG, M.D.Search for more papers by this author, FRANCIS A. NEELON, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-88-1-129_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The recent reports in your journal (1, 2) that modest dosages of acetaminophen can cause liver damage in individuals are interesting. Both Barker, de Carle, and Anuras (1) and Johnson and Tolman (2) speculate that patients with underlying liver disease may be unusually susceptible to the toxic manifestations of acetaminophen.We recently observed (3) severe liver dysfunction in two family members who took acetaminophen (3.6 g/day) for symptoms of infectious mononucleosis. Both of our patients had severe disturbance of hepatic function (husband: bilirubin 14.0 mg/dl (76% direct), serum glutamic oxalacetic transaminase (SGOT) 188 IU, lactic dehydrogenase (LDH)...References1. BARKERDE CARLEANURAS JDS: Chronic excessive acetaminophen use and liver damage. Ann Intern Med 87:299-301, 1977 LinkGoogle Scholar2. JOHNSONTOLMAN GK: Chronic liver disease and acetaminophen. Ann Intern Med 87:302-304, 1977 LinkGoogle Scholar3. ROSENBERGMEYERMANNINGNEELON DAIF: Acetaminophen and hepatic dysfunction in infectious mononucleosis. South Med J 70:660-661, 1977 CrossrefMedlineGoogle Scholar4. GELBWESTZIMMERMAN DMH: Serum enzymes in disease. Am J Med 33:249-261, 1962 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: DAVID M. ROSENBERG, M.D.; FRANCIS A. NEELON, M.D.Affiliations: Duke University Medical Center Durham, NC 27710 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byACETAMINOPHEN HEPATOTOXICITYPrediction of organ system toxicity with antirheumatic drug therapyAcetaminophen Chronic ToxicitySevere hepatic damage after acetaminophen use in psittacosisHepatic reactions to drugs.Antipyretic analgesics 1 January 1978Volume 88, Issue 1Page: 129-129KeywordsAminotransferasesBilirubinDehydrogenasesLactate dehydrogenaseLiverLiver diseasesSerum glutamic oxaloacetic transaminase ePublished: 1 December 2008 Issue Published: 1 January 1978 PDF downloadLoading ...
The characteristic site-specific reactivation phenotypes of HSV-1 and HSV-2 depend upon the latency-associated transcript region.
Authors: T Yoshikawa, J M Hill, L R Stanberry, N Bourne, J F Kurawadwala, P R Krause
Journal: The Journal of Experimental Medicine (1996)

After replication at sites of initial inoculation, herpes simplex virus type 1 and 2 (HSV-1 and HSV-2) establish lifelong latent infections of the sensory and autonomic neurons of the ganglia serving those sites. Periodically, the virus reactivates from these neurons, and travels centripetally along the neuronal axon to cause recurrent epithelial infection. The major clinically observed difference between infections with herpes simplex virus type 1 and type 2 is the anatomic site specificity of recurrence. HSV-1 reactivates most efficiently and frequently from trigeminal ganglia, causing recurrent ocular and oral-facial lesions, while HSV-2 reactivates primarily from sacral ganglia causing recurrent genital lesions. An intertypic recombinant virus was constructed and evaluated in animal models of recurrent ocular and genital herpes. Substitution of a 2.8-kbp region from the HSV-1 latency-associated transcript (LAT) for native HSV-2 sequences caused HSV-2 to reactivate with an HSV-1 phenotype in both animal models. The HSV-2 phenotype was restored by replacing the mutated sequences with wild-type HSV-2 LAT-region sequences. These sequences or their products must act specifically in the cellular environments of trigeminal and sacral neurons to promote the reactivation patterns characteristic of each virus.
The Management of Eating Disorders and Obesity
Authors: Karen M. Freund
Journal: Annals of Internal Medicine (2000)

Medical Writings: Book Notes21 November 2000The Management of Eating Disorders and ObesityKaren M. Freund, MD, MPHKaren M. Freund, MD, MPHBoston University Medical Center, Boston, Massachusetts. (Freund)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-133-10-200011210-00027 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Goldstein DJ, ed. 388 pages. Totowa, NJ: Humana Pr; 1999. $125.00. ISBN 0896034070. Order phone 973-256-1699.Field of medicine: Internal medicine, psychiatry, and nutrition.Format: Hardcover book.Audience: Health professionals who specialize in management of obesity and eating disorders and primary care providers.Purpose: To provide an update on prevention and treatment of eating disorders and obesity.Content: The 23 chapters in the book are divided into three sections on bulimia nervosa, anorexia nervosa, and obesity. More than two thirds of the chapters focus on obesity. Several chapters are revisions of preexisting publications.Highlights: The editor's decision to cover eating ... Author, Article, and Disclosure InformationAffiliations: Boston University Medical Center, Boston, Massachusetts. (Freund) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 21 November 2000Volume 133, Issue 10Page: 840KeywordsAnorexia nervosaBulimia nervosaEatingEating disordersHealth care providersNutritionObesityOverweightSoftware toolsWeight loss ePublished: 21 November 2000 Issue Published: 21 November 2000 Copyright & PermissionsCopyright © 2000 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Ductal carcinoma in situ of breast needs to be stratified further according to risk of progressing
Authors: S. Mayor
Journal: BMJ (2010)

<h3>Objectives:</h3> To validate a simple bedside test battery designed to detect mild dementia and differentiate AD from frontotemporal dementia (FTD). <h3>Methods:</h3> Addenbrooke9s Cognitive Examination (ACE) is a 100-point test battery that assesses six cognitive domains. Of 210 new patients attending a memory clinic, 139 fulfilled inclusion criteria and comprised dementia (n = 115) and nondementia (n = 24) groups. The composite and the component scores on the ACE for the two groups were compared with those of 127 age- and education-matched controls. Norms and the probability of diagnosing dementia at different prevalence rates were calculated. To evaluate the ACE9s ability to differentiate early AD from FTD, scores of the cases diagnosed with dementia with a Clinical Dementia Rating &lt; 1 (AD = 56, FTD = 24, others = 20) were compared. <h3>Results:</h3> Two cut-off values for the ACE composite score (88 and 83) were of optimal utility depending on the target population. The ACE had high reliability, construct validity, and sensitivity (93%, using 88 as cut-off). Using the lower cut-off of 83, the ACE had a higher sensitivity (82%) and predictive value than the Mini-Mental State Examination for a wide range of dementia prevalence. The ACE differentiated AD from FTD, and the VLOM ratio (derived using component scores: [verbal fluency + language]/[orientation + memory]) of &lt;2.2 for FTD and &gt;3.2 for AD was highly discriminating. <h3>Conclusion:</h3> The ACE is a brief and reliable bedside instrument for early detection of dementia, and offers a simple objective index to differentiate AD and FTD in mildly demented patients.
Leukotrienes as Mediators of Airway Obstruction
Authors: JEFFREY M. DRAZEN
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

Section:ChooseTop of pageAbstract <<LEUKOTRIENE BIOCHEMISTRYLEUKOTRIENE RECEPTORSLEUKOTRIENE PHARMACOLOGYRECOVERY OF LEUKOTRIENES ...EFFECTS OF AGENTS THAT IN...SUMMARYReferencesCITING ARTICLES