tbuckley/cabot-search huggingface dataset:
Diagnosis and Treatment of Seborrheic Keratosis
Authors: Vincent R. Hunt
Journal: JAMA (1991)

<h3>To the Editor.—</h3> Stern et al<sup>1</sup>suggest that a cost-effective method of quality assurance can be developed by analyzing the records of pathological specimens stored in computer databases. They point out pitfalls with their study, such as the potential for selection bias, because of their inability to ascertain the universe from which specimens were obtained or the number of patients with seborrheic keratoses who were treated appropriately. Also, information supplied by the referring physician on the pathology reporting form was not standardized, and the diverse specialties represented by the physician participants makes it difficult to characterize the nature of the patient population studied. The authors dealt with issues of selection bias by conducting an "informal poll," from which they concluded that the direction of the bias for dermatologists would understate the accuracy calculated in their study. For other specialties, they imply that there is less potential for bias because
Dysregulation of innate immunity in hepatitis C virus genotype 1 IL28B -unfavorable genotype patients: Impaired viral kinetics and therapeutic response
Authors: Susanna Naggie, Anu Osinusi, Antonios Katsounas, Richard Lempicki, Eva Herrmann, Alexander J. Thompson, Paul J. Clark, Keyur Patel, Andrew J. Muir, John G. McHutchison, Joerg F. Schlaak, Martin Trippler, Bhavana Shivakumar, Henry Masur, Michael A. Polis, Shyam Kottilil
Journal: Hepatology (2012)

Recent studies have shown that a single-nucleotide polymorphism upstream of the interleukin-28B ( IL28B ) gene plays a major role in predicting therapeutic response in hepatitis C virus (HCV)-infected patients treated with pegylated interferon (PEG-IFN)/ribavirin. We sought to investigate the mechanism of the IL28B polymorphism, specifically as it relates to early HCV viral kinetics, IFN pharmacokinetics, IFN pharmacodynamics, and gene expression profiles. Two prospective cohorts (human immunodeficiency virus [HIV]/HCV-coinfected and HCV-monoinfected) completing treatment with IFN/ribavirin were enrolled. Patients were genotyped at the polymorphic site rs12979860. In the HIV/HCV cohort, frequent serum sampling was completed for HCV RNA and IFN levels. DNA microarray of peripheral blood mononuclear cells and individual expression of IFN-stimulated genes (ISGs) were quantified on IFN therapy. The IL28B -favorable (CC) genotype was associated with improved therapeutic response compared with unfavorable (CT or TT) genotypes. Patients with a favorable genotype had greater first- and second-phase viral kinetics ( P = 0.004 and P = 0.036, respectively), IFN maximum antiviral efficiency ( P = 0.007) and infected cell death loss ( P = 0.009) compared with unfavorable genotypes. Functional annotation analysis of DNA microarray data was consistent with depressed innate immune function, particularly of natural killer cells, from patients with unfavorable genotypes ( P &lt;0.004). Induction of innate immunity genes was also lower in unfavorable genotypes. ISG expression at baseline and induction with IFN was independent of IL28B genotype. Conclusion: Carriers of the IL28B -favorable genotype were more likely to have superior innate immune response to IFN therapy compared with unfavorable genotypes, suggesting that the unfavorable genotype has aberrant baseline induction of innate immune response pathways resulting in impaired virologic response. IL28B genotype is associated with more rapid viral kinetics and improved treatment response outcomes independent of ISG expression. (HEPATOLOGY 2012)
Red Cell Survival after Heterograft Valve Surgery
Authors: W. H. P. Roeser, L. W. Powell, M. F. O'Brien
Journal: BMJ (1968)

Intravascular haemolysis was studied in 24 patients three to nine months after calf or pig valve heterografts had been inserted for severe valvular heart disease. No patient had haemolytic anaemia. In five of the 24 patients there was subclinical haemolysis, and in these five the haemolysis appeared to be related to residual aortic regurgitation or to the presence of other foreign material such as a Dacron aortic graft. The extent of postoperative haemolysis in these five patients was comparable to that observed preoperatively in patients with valvular heart disease.The results support the belief that, in contrast to artificial valve prostheses, heterograft valves behave similarly to human valves as regards haemolysis.
IMMUNOLOGICAL UNRESPONSIVENESS IN RABBITS PRODUCED BY NEONATAL INJECTION OF DEFINED ANTIGENS
Authors: Richard T. Smith, Robert A. Bridges
Journal: The Journal of Experimental Medicine (1958)

The phenomenon of immunological unresponsiveness induced in the neonatal rabbit by a single injection of a defined protein antigen, has been characterized semiquantitatively, and studies bearing upon the mechanism of such unresponsiveness have been presented. A single intraperitoneal injection at birth of 10 to 100 mg. BSA, HGG, ovalbumin, or a human macroglobulin, or an oral feeding of 100 mg. BSA, induced a state of unresponsiveness lasting at least 90 to 120 days. 100 mg. BSA given from birth to 17 days of age, but not later, produced unresponsiveness of 90 to 120 days' duration. Data are presented which show that the duration of unresponsiveness is finite and related to the amount of antigen given at birth, and that it may be indefinitely prolonged by repeated injections of antigen. Disappearance of injected antigen in the unresponsive animal was exponential with time, with no accelerated or immune phase. Administration of the antigen in adjuvants resulted in significant shortening of the duration of unresponsiveness. The transfer of immune cells to the unresponsive host while resulting in vicarious antibody formation, did not affect the underlying unresponsive state. Negative results of attempts to produce unresponsiveness to a variety of bacterial antigens are presented. The implications of the data are discussed, particularly in reference to the other experimental models of immunological tolerance, and to the various theories of acquired immunity. It is clear that any satisfactory theoretical explanation of acquired immunity will have to account simultaneously for the phenomena of immune tolerance.
Optic Neuritis and Multiple Sclerosis
Authors: Barry G. W. Arnason
Journal: New England Journal of Medicine (1973)

The relation that optic neuritis (ON) bears to multiple sclerosis (MS) remains controversial. Approximately 40 per cent of patients with MS manifest ON at some point during their illness, and epidemiologic studies have shown that ON and MS patients share features that distinguish them from a peer control group. For these reasons the notion that the two entities represent different manifestations of a single disease has gained wide support.There are problems with such an interpretation, however. Although the proportion of patients presenting with isolated ON who will go on to development of MS has been variously reported, most recent . . .
Letter from Ex-President Hibberd—His Return Trip from San Francisco.
Authors: J. F. Hibberd
Journal: JAMA (1894)

<h3>To the Editor:</h3> —On June 11 some of the members of theAmerican Medical Associationwho had return tickets via the Northern Pacific deemed it prudent to accept the arrangement by which their tickets would be honored over the Southern Pacific to Ogden and the Union Pacific to Butte, and on June 12 a larger number availed themselves of the same privileges. This was done for the reason that they discredited the statement that the flood damage to the Northern Pacific would be repaired by the time they arrived at Portland. With more faith about fifty of us took the evening train on June 12 for Portland, which we found still largely under water, but by a long steamer ride down the Willamette and Columbia Rivers—or where the rivers ought to be for the whole country was covered with water— the boat ran into what was usually a creek, and
Acquired von Willebrand Syndrome in Patients With a Centrifugal or Axial Continuous Flow Left Ventricular Assist Device
Authors: Anna L. Meyer, Doris Malehsa, Ulrich Budde, Christoph Bara, Axel Haverich, Martin Strueber
Journal: JACC Heart Failure (2014)

The aim of this study was to determine whether differences in continuous flow left ventricular assist devices (LVADs) may lead to differences in the von Willebrand profile and the occurrence of bleeding and thromboembolic events. The HeartMate II (Thoratec Corp., Pleasanton, California) and HeartWare Ventricular Assist Device (HVAD) (HeartWare, Inc., Framingham, Massachusetts) systems are the most frequently implanted LVADs worldwide. In all patients with an axial-flow HeartMate II, acquired von Willebrand syndrome (AvWS) due to the loss of large molecular weight multimers was found. The large molecular weight multimers of the von Willebrand factor (vWF) play a key role in primary hemostasis through interactions with platelets. This was a retrospective study of the vWF profile and incidence of bleeding and thromboembolic events in 102 patients receiving the HeartMate II (n = 51) and HVAD (n = 51). Between January 2003 and December 2010, vWF testing was performed in 102 of 175 consecutive patients after LVAD implantation. AvWS was found in all patients, demonstrated by a decrease in the high molecular weight multimers of vWF to 30 ± 14% in HeartMate II patients and 34 ± 13% in patients with an HVAD. Significant predictors of vWF antigen included age (p = 0.011), number of days on the device (p = 0.035), C-reactive protein (p < 0.001), and blood group (p = 0.007). Bleeding and thromboembolic event rates were similar. However, lower fractions of vWF antigen and high molecular weight multimers did not correlate with the rate of bleeding complications or thromboembolic events. AvWS developed in all patients after centrifugal or axial flow pump implantation. Different patterns of AvWS were seen between the devices as well as individually. However, the complication rates after implantation were similar.
Coexpression of liver-specific and growth-induced genes in perinatal and regenerating liver: Attainment and maintenance of the differentiated state during rapid proliferation
Authors: Barbara Haber, Leyla Naji, Drew Chessman, Rebecca Taub
Journal: Hepatology (1995)

The liver shows maximal cellular growth during fetal development and after partial hepatectomy. Exploring overlaps in gene expression patterns in these two types of hepatic growth may provide insight into common regulatory pathways. The expression of a large number of growth-induced and liver-specific genes induced in liver regeneration has been examined in the perinatal liver from several days prenatal to 4 weeks postnatal when the major growth phase of the liver ceases. As in liver regeneration, many growth-induced genes, such as PRL-1 and beta-actin, are expressed at a high level throughout the temporal course of liver development and correlate with the proliferative state. The level of fetal liver expression of these genes is similar to peak expression found in the regenerating liver, suggesting that common pathways of transcriptional regulation exist in the two types of proliferation. A subset of liver-restricted immediate-early genes including, IGFBP-1, CL-6, and glucose-6-phosphatase (G6Pase) are induced in regenerating liver and may be important in maintaining hepatic metabolism during regeneration. In developing liver, these genes are expressed primarily in the perinatal period but, unlike the regenerating liver, are not coinduced. For instance, at birth, G6Pase is induced, whereas CL-6 is downregulated. In situ analyses confirm that a proliferation associated gene PRL-1 is expressed in multiple cell types throughout the developing liver, whereas the expression of liver-specific genes is confined to hepatocytes. Taken together, these findings imply that significant similarities and differences in transcriptional regulation and hormonal milieu exist in liver during regeneration and development.(ABSTRACT TRUNCATED AT 250 WORDS)
THE TRAUMATIC FEVERS.
Authors: EDMUND W. HOLMES
Journal: JAMA (1897)

One of the earlier theories of disease was that it came from without, as a direct visitation from God; later, that it originated in the humors of the blood; in modern times the cell doctrine has had its sway, to be supplanted as the microscope increased in power by the bacterial origin of disease, rapidly supplemented by the hypothesis that the products of the bacteria, the ptomains and leucomains, are in many cases the active media, while the more recent investigations of serum therapy seem to foreshadow a partial return to the humoralistic theories. It was only in 1851 that Meigs declared that puerperal fever was a fatality of God's providence; so that whatever the actual truth of our modern speculations may be, there is no pathologic process upon which they have had a greater effect in modifying our methods of treatment, in teaching us how to avoid their transmission,
German junior doctors in Britain
Authors: H-J Bartz, W Kahlke
Journal: BMJ (1994)

EDITOR, - The number of German junior doctors holding preregistration with the General Medical Council is steadily increasing. Between 1988, when the training of junior doctors in Germany was reformed, and 1992 the number of German junior house officers working in Britain increased from two to 485 (General Medical Council, personal communication).

Since 1988, after completing the six year course in medical school German junior doctors have had to work for …
Chronobiology of Cardiac Sudden Death in Men
Authors: Simon W. Rabkin
Journal: JAMA (1980)

Daily variation in occurrence of sudden cardiac death was examined in 3,983 men observed since 1948. For men without previous clinical evidence of ischemic heart disease, an excess proportion of sudden cardiac deaths occurred on Mondays. For men with previous clinical evidence of ischemic heart disease, sudden cardiac death occurred more uniformly throughout the week. By comparison there was no significant daily variation in cancer mortality or in day of occurrence of myocardial infarction. Thus, for men without clinically manifest heart disease, the warning "beware on Monday" should stimulate further investigation.
RUNX 3, apoptosis 0: a new gastric tumour suppressor
Authors: S F Moss
Journal: Gut (2002)

There is convincing evidence that Runx 3 is a new and important tumour suppressor in gastric cancer In comparison with our knowledge of the detailed sequence of somatic genetic changes occurring during colon carcinogenesis, relatively few tumour suppressors or oncogenes have been commonly implicated during the multistage progression to cancer in the stomach. Now, in a collaborative venture reminiscent of their countries' successful co-management of the 2002 World Cup, Li and 26 colleagues from South Korea and Japan have convincingly identified Runx 3 as a new and important tumour suppressor in gastric cancer. Li QL, Ito K, Sakakura C, et al . Causal relationship between the loss of RUNX3 expression and gastric cancer. Cell2002;109:113–24. [OpenUrl][1][CrossRef][2][PubMed][3][Web of Science][4] Runx3/Pebp2alphaC null mouse gastric mucosa exhibits hyperplasias due to stimulated proliferation and suppressed apoptosis in epithelial cells, and the cells are resistant to growth-inhibitory and apoptosis-inducing action of TGF-beta, indicating that Runx3 is a major growth regulator of gastric epithelial cells. Between 45% and 60% of human gastric cancer cells do not significantly express RUNX3 due to hemizygous deletion and hypermethylation of the RUNX3 promoter region. Tumorigenicity of human gastric cancer cell lines in nude mice was inversely related to their level of RUNX3 expression, and a mutation (R122C) occurring within the conserved Runt domain abolished … [1]: {openurl}?query=rft.jtitle%253DCell%26rft.stitle%253DCell%26rft.aulast%253DLi%26rft.auinit1%253DQ.%2BL.%26rft.volume%253D109%26rft.issue%253D1%26rft.spage%253D113%26rft.epage%253D124%26rft.atitle%253DCausal%2Brelationship%2Bbetween%2Bthe%2Bloss%2Bof%2BRUNX3%2Bexpression%2Band%2Bgastric%2Bcancer.%26rft_id%253Dinfo%253Adoi%252F10.1016%252FS0092-8674%252802%252900690-6%26rft_id%253Dinfo%253Apmid%252F11955451%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/external-ref?access_num=10.1016/S0092-8674(02)00690-6&link_type=DOI [3]: /lookup/external-ref?access_num=11955451&link_type=MED&atom=%2Fgutjnl%2F52%2F1%2F12.atom [4]: /lookup/external-ref?access_num=000174888300013&link_type=ISI
EFFECT OF ENVIRONMENTAL TEMPERATURE ON EXPERIMENTAL TRAUMATIC SHOCK IN DOGS 1
Authors: Renato A. Ricca, K. Fink, Leonard I. Katzin, Stafford L. Warren
Journal: Journal of Clinical Investigation (1945)

Pulse: 136 15 ml.blood taken Serum protein: 5.9 grams per cent Fibrinogen: 0.32 grams per cent Hematocrit: 42.6 per cent Specific gravity: 1.0227 Clotting time: 7 minutes and 35 seconds 1:20 P.M.-8 ml.Nembutal, intraperitoneally 1:45 P.M.-40 ml.blood taken Serum protein: 5.7 grams per cent Fibrinogen: 0.30 grams per cent Whole blood NPN: 26.4 mgm.per cent Hematocrit: 34.4 per cent Specific gravity: 1.
Are Fashion Models a Group at Risk for Eating Disorders and Substance Abuse?
Authors: Paolo Santonastaso, Silvia Mondini, Angela Favaro
Journal: Psychotherapy and Psychosomatics (2002)

Few studies to date have investigated whether in fact the prevalence of eating disorders (ED) and/or use of illicit drugs is higher among models than among other groups of females.A group of 63 professional fashion models of various nationalities were studied by means of self-reported questionnaires. They were compared with a control group of 126 female subjects recruited from the general population.Fashion models weigh significantly less than controls, but only a small percentage of them uses unhealthy methods to control their weight. The current frequency of full-syndrome ED did not differ between the groups, but partial-syndrome ED were significantly more common among fashion models than among controls. Current substance use or alcohol abuse was reported by 35% of fashion models and 12% of controls.Our findings suggest that fashion models are more at risk for partial ED and use of illicit drugs than females in the general population.
Clinical Assessment and D-Dimer Testing in Deep Venous Thrombosis
Authors: Abel Wakai
Journal: Annals of Internal Medicine (2002)

Letters3 September 2002Clinical Assessment and d-Dimer Testing in Deep Venous ThrombosisAbel Wakai, MDAbel Wakai, MDBeaumont Hospital; Dublin 9, IrelandSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-137-5_Part_1-200209030-00026 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:I would like to congratulate Kearon and colleagues for their well-designed study (1) and for increasing our understanding of the role of d-dimer testing in suspected deep venous thrombosis. However, a major limitation not discussed in the paper is that the applicability of the findings may be poor. The design of the study is such that it does not allow the findings to be confidently applied outside the restricted setting of the evaluation, for two reasons. First, whole-blood d-dimer testing, although quick and simple to perform, is limited because the interpretation is subjective. Although the test is ...References1. Kearon C, Ginsberg JS, Douketis J, Crowther M, Brill-Edwards P, Weitz JI, et al . Management of suspected deep venous thrombosis in outpatients by using clinical assessment and d-dimer testing. Ann Intern Med. 2001;135:108-11. [PMID: 11453710] LinkGoogle Scholar2. Shitrit D, Heyd J, Raveh D, Rudensky B. Diagnostic value of the d-dimer test in deep vein thrombosis: improved results by a new assay method and by using discriminate levels. Thromb Res. 2001;102:125-31. [PMID: 11323023] CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: Beaumont Hospital; Dublin 9, Ireland PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoManagement of Suspected Deep Venous Thrombosis in Outpatients by Using Clinical Assessment and d-dimer Testing Clive Kearon , Jeffrey S. Ginsberg , James Douketis , Mark Crowther , Patrick Brill-Edwards , Jeffrey I. Weitz , and Jack Hirsh Clinical Assessment and d-dimer Testing in Deep Venous Thrombosis Clive Kearon and Jeffrey S. Ginsberg Clinical Assessment and d-dimer Testing in Deep Venous Thrombosis Clive Kearon and Jeffrey S. Ginsberg Metrics 3 September 2002Volume 137, Issue 5_Part_1Page: 371KeywordsD-dimerDeep vein thrombosisEmergency departmentEnzyme linked immunosorbent assayImmunoassaysLearning curvesResearch laboratoriesSpecificity ePublished: 3 September 2002 Issue Published: 3 September 2002 Copyright & PermissionsCopyright © 2002 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Egg's allergy: an experience from Brazilian Food Allergy Reference Center
Authors: C.M.A. Jacob, A.C. Pastorino, D. Munhoz, R.G. Ramos, T. Batelochio, A.C. Brandão, A.K.F. Gushken, G.H. Yonamine, A.P.B.M. Castro
Journal: Journal of Allergy and Clinical Immunology (2007)
Glucagonostatic Actions and Reduction of Fasting Hyperglycemia by Exogenous Glucagon-Like Peptide I(7–36) amide in type I diabetic patients
Authors: Werner O C Creutzfeldt, Nicola Kleine, Berend Willms, Cathrine Ørskov, Jens J Holst, Michael A Nauck
Journal: Diabetes Care (1996)

OBJECTIVE Glucagon-like peptide I(7–36) amide (GLP-1) is a physiological incretin hormone that, in slightly supraphysiological doses, stimulates insulin secretion, lowers glucagon concentrations, and thereby normalizes elevated fasting plasma glucose concentrations in type II diabetic patients. It is not known whether GLP-1 has effects also in fasting type I diabetic patients. RESEARCH DESIGN AND METHODS In 11 type I diabetic patients (HbA1c 9.1 ± 2.1%; normal, 4.2–6.3%), fasting hyperglycemia was provoked by halving their usual evening NPH insulin dose. In random order on two occasions, 1.2 pmol · kg−1 · min−1 GLP-1 or placebo was infused intravenously in the morning (plasma glucose 13.7 ± 0.9 mmol/l; plasma insulin 26 ± 4 pmol/l). Glucose (glucose oxidase method), insulin, C-peptide, glucagon, GLP-1, cortisol, growth hormone (immunoassays), triglycerides, cholesterol, and nonesterified fatty acids (enzymatic tests) were measured. RESULTS Glucagon was reduced from ∼8 to 4 pmol/l, and plasma glucose was lowered from 13.4 ± 1.0 to 10.0 ± 1.2 mmol/l with GLP-1 administration (plasma concentrations ∼100 pmol, P &amp;lt; 0.0001), but not with placebo (14.2 ± 0.7 to 13.2 ± 1.0). Transiently, C-peptide was stimulated from basal 0.09 ± 0.02 to 0.19 ± 0.06 nmol/l by GLP-1 (P &amp;lt; 0.0001), but not by placebo (0.07 ± 0.02 to 0.07 ± 0.02). There was no significant effect on nonesterified fatty acids (P = 0.34), triglycerides (P = 0.57), cholesterol (P = 0.64), cortisol (P = 0.40), or growth hormone (P = 0.53). CONCLUSIONS Therefore, exogenous GLP-1 is able to lower fasting glycemia also in type I diabetic patients, mainly by reducing glucagon concentrations. However, this alone is not sufficient to normalize fasting plasma glucose concentrations, as was previously observed in type II diabetic patients, in whom insulin secretion (C-peptide response) was stimulated 20-fold.