tbuckley/cabot-search huggingface dataset:
Standardizing Criteria for Logistic Regression Models
Authors: Carlos Campillo
Journal: Annals of Internal Medicine (1993)

Letters15 September 1993Standardizing Criteria for Logistic Regression ModelsCarlos Campillo, MDCarlos Campillo, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-119-6-199309150-00036 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Failure to build regression models appropriately may lead to misleading inferences [1]. A recent letter by Palmas and colleagues [2] furnishes a good example of what may be called the tip of an iceberg.This problem can be divided into three major categories. First, some reports do not include enough information to allow the reader to fully assess the logistic model applied. This category encompasses all reports that include odds ratios and confidence intervals but lack information about the sample size or the statistical power of the model, making it unclear whether there is a true absence ...References1. Hosmer DW, Taber S, Lemeshow S. The importance of assessing the fit of logistic regression models: a case study. Am J Public Health. 1991; 81:1630-5. Google Scholar2. Palmas W, Denton TA, Diamond GA. Ann Intern Med. 1993; 118: 231-2. Google Scholar Author, Article, and Disclosure InformationAuthors: Carlos Campillo, MD PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byClassification Methods in Colon Disease Information SystemPrediction equations of forced oscillation technique: the insidious role of collinearityQuality of reporting of multivariable logistic regression models in Chinese clinical medical journalsLogistic Regression Methods in Selected Medical Information SystemsEvaluation of Logistic Regression Reporting in Current Obstetrics and Gynecology LiteratureRegresión logística en la literatura psiquiátrica: evaluación de los artículos publicados entre 2002 y 2005 en una prominente revistaA Clinically Dangerous Flaw in Reporting Statistical SignificanceA review of two journals found that articles using multivariable logistic regression frequently did not report commonly recommended assumptionsSimplified Therapy with Zidovudine, Lamivudine, and Abacavir for Very Nonadherent, Treatment-Failing PatientsClinician or Statistician?An Appraisal of Multivariable Logistic Models in the Pulmonary and Critical Care LiteratureaLogistic regression in the medical literature: 15 September 1993Volume 119, Issue 6Page: 540-541KeywordsBiologicsConfidence intervalsLinear regression analysisOdds ratioRegression analysis ePublished: 15 August 2000 Issue Published: 15 September 1993 Copyright & PermissionsCopyright © 1993 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Beta-thalassaemia minor and porphyria cutanea tarda
Authors: K.E. McKENNA, J.F. DAWSON
Journal: British Journal of Dermatology (1992)

A case of porphyria cutanea tarda occurring in association with beta‐thalassaemia minor is reported in a 33‐year‐old Northern‐Irish woman. Aetiological factors in this case included oral and parenteral iron therapy for refractory anaemia which was subsequently diagnosed as beta‐thalassaemia minor, and the use of an oestrogen‐containing oral contraceptive pill.
1008-192 Atorvastatin affects thrombosis/fibrinolysis system during the acute phase of unstable angina
Authors: Dimitris Tousoulis, Maria Kotsopoulou, Charalambos A Antoniades, Erini Bosinakou, Costas Tentolouris, Kyriaki Marinou, Charalambos Vlachopoulos, Emmanuel Vavuranakis, Christos Pitsavos, Christodoulos Stefanadis
Journal: Journal of the American College of Cardiology (2004)
OUTCOME OF MYOPERICARDITIS AND PERIMYOCARDITIS: RESULTS FROM A MULTICENTER PROSPECTIVE COHORT STUDY
Authors: Massimo Imazio, Antonio Brucato, Andrea Barbieri, Francesca Ferroni, Federica Bonomi, Francesca Mantovani, Alessandra Chinaglia, Paola Di Corato, Roberta Lugli, Paola Valenti, Giovanni Della Casa, Riccardo Belli
Journal: Journal of the American College of Cardiology (2013)
The role of connexin40 in atrial fibrillation
Authors: S.-M. Chaldoupi, P. Loh, R. N.W. Hauer, J. M.T. de Bakker, H. V.M. van Rijen
Journal: Cardiovascular Research (2009)

Connexin40 (Cx40) is a major gap-junction protein in the atrial myocardium. In the heart, gap junctions are responsible for cell-to-cell conduction of the action potential. In several cardiac diseases, the expression of connexins is changed and is associated with increased propensity for arrhythmias. Atrial fibrillation (AF) is the most common arrhythmia in man with a diverse clinical presentation, different underlying mechanisms, and difficult treatment. The vulnerability to arrhythmias of the heart is determined by the combined presence of an arrhythmogenic substrate and initiating triggers. The arrhythmogenic substrate is formed by reduced effective refractory period, enhanced spatial dispersion of refractoriness, or abnormal atrial impulse conduction. Initiating triggers of AF most frequently originate from firing foci in the pulmonary veins and/or superior caval vein. Prolonged episodes of AF result in electrical and structural remodelling that favours the reoccurrence or perpetuation of AF. This electrical remodelling embodies changes in Cx40 expression and distribution, both in the atrial myocardium itself and in the thoracic veins. In addition, Cx40 gene mutations or polymorphisms give an inherited predisposition to AF. This review focuses on the role of Cx40 in AF, showing that abnormal Cx40 expression is correlated with both trigger formation from the thoracic veins as well as enhanced vulnerability of the atrial myocardium to AF.
Comparing Hospital Performance in Door-to-Balloon Time Between the Hospital Quality Alliance and the National Cardiovascular Data Registry
Authors: Brahmajee K. Nallamothu, Yongfei Wang, Elizabeth H. Bradley, Kalon K.L. Ho, Jeptha P. Curtis, John S. Rumsfeld, Frederick A. Masoudi, Harlan M. Krumholz
Journal: Journal of the American College of Cardiology (2007)
Coxsackievirus and adenovirus infection. Association with acute febrile and juvenile rheumatoid arthritis
Authors: J. J. Rahal
Journal: JAMA (1976)

The prearthritic manifestations of juvenile rheumatoid arthritis in a 16-year-old boy were associated with a rise in coxsackievirus B3 and A9 neutralizing antibody titers from 1:16 to larger than or equal to 1:512, and 1:64 to 1:512, respectively. Recurrent polyarthritis followed and has persisted for three years. Adenovirus 7 was isolated from the pericardial fluid of a 9-year-old girl in whom juvenile rheumatoid arthritis then developed. Of 11 patients with acute, nonspecific, febrile arthritis subsequently studied, fourfold or greater antibody elevations occurred against coxsackieviruses in five, and against rubella and varicella-zoster virus in two. Antibody titers against other viral (and Mycoplasma) antigens remained stable. These findings suggest that coxsackieviruses, as well as other common viruses, may cause acute, nonspecific, febrile arthritis. In certain instances, such infection may be related to the development of juvenile rheumatoid arthritis.
Targeted treatment of pyoderma gangrenosum in PAPA (pyogenic arthritis, pyoderma gangrenosum and acne) syndrome with the recombinant human interleukin-1 receptor antagonist anakinra
Authors: M. Brenner, T. Ruzicka, G. Plewig, P. Thomas, P. Herzer
Journal: British Journal of Dermatology (2009)

The triad of sterile pyogenic arthritis, pyoderma gangrenosum and acne is known by the acronym of PAPA syndrome. It is a rare autosomal dominant disease of early onset. The treatment of pyoderma gangrenosum is challenging as there is often only partial response to systemic glucocorticosteroids and immunosuppressive therapies. We report the rapid and lasting response of pyoderma gangrenosum to the targeted treatment with the recombinant human interleukin-1 receptor antagonist (rHuIL-1Ra) anakinra in a patient with PAPA syndrome.
Influence of Rheologic Changes and Platelet–Neutrophil Interactions on Cell Filtration in Sepsis
Authors: LINDA A. KIRSCHENBAUM, MOHAMMED AZIZ, MARK E. ASTIZ, DHANONJOY C. SAHA, ERIC C. RACKOW
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

We examined the role of erythrocyte (red blood cell; RBC) aggregation and deformability, neutrophil (polymorphonuclear neutrophil; PMN) deformability, whole-blood viscosity, and platelet-neutrophil interactions on cell filtration in subjects who were critically ill with sepsis (CIS), critically ill noninfected subjects (CINS), and healthy controls (C). We assessed cell deformability by filtration through filters of 5-microm pore size. Whole blood, RBC, PMN, and combinations of PMN and RBC were studied. Viscometry was done on isolated RBC. Platelet-PMN interactions were assessed with monoclonal antibodies to CD41 and activated CD63 platelet receptors, and to CD66b PMN receptors. Filtration pressure (Pi) for CIS was significantly greater than for C and CINS at both high and low PMN and RBC concentrations. Viscometry confirmed decreases in RBC deformability and demonstrated significant increases in RBC aggregation in CIS. Increments in Pi were significantly greater with PMN and PMN-RBC combinations suspended in platelet rich plasma (PRP) than in platelet poor plasma (PPP) for CIS as compared with CINS or C. Flow cytometry confirmed significantly greater platelet activation in CIS than in CINS or C (mean fluorescence: 39 +/- 9 lfu versus 18.7 +/- 4.0 lfu and 17.1 +/- 2.3 lfu, respectively) and greater platelet-PMN aggregation (mean fluorescence: 44.7 +/- 3.6 lfu versus 23 +/- 4.1 lfu, respectively) in CIS than in C. We conclude that decreased filtration of whole blood in CIS is related to decreases in RBC and PMN deformability, increases in RBC aggregation, and increased platelet-PMN interactions. Of these, the formation of platelet-PMN aggregates appeares to have the greatest effect in impairing cell filtration. These rheologic abnormalities may contribute to impaired microvascular blood flow in patients with sepsis.
Computerized endoscopic balloon manometry to detect esophageal variceal pressure
Authors: D.-R. Kong, J.-M. Xu, L. Zhang, C. Zhang, Z.-Q. Fu, B.-B. He, B. Sun, Y. Xie
Journal: Endoscopy (2009)

Background and study aims: Measuring the variceal pressure is important in predicting esophageal variceal bleeding. However, current noninvasive methods of measuring variceal pressure have not gained wide popularity. We have developed a computerized endoscopic balloon manometry (CEBM) system to detect variceal pressure. The aims of the study were to test the in-vitro accuracy of CEBM and to evaluate the clinical reliability and feasibility of this method.
HLA antigens in ankylosing spondylitis with peripheral arthritis.
Authors: D N Glass, S Aaron
Journal: Annals of the Rheumatic Diseases (1988)

CorrespondenceHLA antigens in ankylosing spondylitis with peripheral arthritis SIR, We were much interested in the article by Sanmarti et al on HLA studies involving patients with ankylosing spondylitis and peripheral arthritis reported in the Annals.' We noted some parallels with our own findings of an HLA-DR7 association with peripheral arthritis in a similar population.'Especially noteworthy was the use of an HLA-B27 control population in both studies, an essential step in this instance because of the strong negative linkage disequilibrium between HLA-DR7 and HLA-B27.In Sanmarti's study the HLA-DR7 association was limited to children with an erosive peripheral arthritis in addition to ankylosing spondilitis.Although we did not ascertain the extent of erosive disease in all our patients, they were biased towards those with more severe disease and hence were also likely to be erosive.The inclusion of patients that had already had joint replacement helps support this conclusion.Another similarity was the occur- rence of patients with childhood onset disease in both studies.Five of 25 patients from Spain had an onset below the age of 17, whereas none of the group with ankylosing spondylitis only did so, though the mean age of both groups was approximately the same.In neither study is it possible to separate the earlier age of onset from the presence of peripheral arthritis so that HLA-DR7 may well act as a gene determining severity of disease and thus explain both sets of observations.
alpha-Adrenergic receptors in cerebral microvessels of normotensive and spontaneously hypertensive rats.
Authors: H Kobayashi, A Wada, F Izumi, M S Magnoni, M Trabucchi
Journal: Circulation Research (1985)

In rat cerebral microvessels, we characterized alpha 1- and alpha 2-adrenergic receptors, using [3H]prazosin and [3H]-p-amino-clonidine as radioligands. [3H]Prazosin binding to the cerebral microvessels was saturable and of high affinity (dissociation constant of 78 pM), with a maximum binding of 48 fmol/mg protein. [3H]Prazosin binding reached equilibrium within 15 minutes and was dissociated by the addition of 10 microM phentolamine. The inhibitory effects of isomers of norepinephrine and epinephrine on the binding showed that l-isomers were over 10 times more potent than d-isomers. [3H]-p-Amino-clonidine binding to the cerebral microvessels was saturable and of high affinity (KD = 0.61 nM) with a Bmax of 73 fmol/mg protein. The binding reached equilibrium within 30 minutes, and was dissociated by the addition of 100 microM l-norepinephrine. l-Isomers of norepinephrine and epinephrine were over 10 times more potent than d-isomers in displacing the binding. Thus, both [3H]prazosin and [3H]-p-amino-clonidine bindings to the cerebral microvessels were characterized by saturability, high affinity, reversibility, and stereo-specificity. Furthermore, the specificity of both binding sites was pharmacologically evaluated by the inhibitory effects of various adrenergic agonists and antagonists on the bindings. These data indicate the existence of alpha-adrenergic receptors in the cerebral microvessels and are consistent with the hypothesis that the cerebral microcirculation is regulated by adrenergic innervation. Furthermore, the receptors were measured in cerebral microvessels of spontaneously hypertensive rats and Wistar-Kyoto controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Hepatic phospholipids in alcoholic liver disease assessed by proton-decoupled 31P magnetic resonance spectroscopy
Authors: Heinz-Peter Wilhelm Schlemmer, Tanja Sawatzki, Steffen Sammet, Ines Dornacher, Peter Bachert, Gerhard van Kaick, Rüdiger Waldherr, Helmut Karl Seitz
Journal: Journal of Hepatology (2005)
Reports of Adverse Events From Bone Drugs Prompt Caution
Authors: Bridget M. Kuehn
Journal: JAMA (2006)

IN 2003, CASE REPORTS OF A RARE BUT serious condition occurring in patients taking bisphosphonates to prevent breakdown of bone began surfacing. Since then, reports of more than 2000 cases of this adverse event, osteonecrosis of the jaw, have spurred letters of caution from the manufacturer to physicians and dentists, revisions to the labels of some of the products, and recommendations from the US Food and Drug Administration (FDA). Although most cases have occurred in patients receiving high-dose intravenous formulations of the drugs as part of cancer treatment, some have occurred in patients taking popular oral bisphosphonates to treat or prevent osteoporosis, suggesting that the problem may be a class effect. Scientists from the FDA have also recently identified another type of adverse event, severe bone, joint, or muscle pain associated with oral formulations. Some professional groups of physicians and dentists are taking steps to prevent osteonecrosis of the jaw in patients who take these drugs. But many unanswered questions remain about the role of bisphosphonates in these adverse events, how best to prevent such problems, as well as the degree of risk associated with the drugs.
Integrated Obstetrics and Gynaecology for Postgraduates
Authors: E. J. Quilligan
Journal: JAMA (1973)

This is a multiple-authored textbook covering the entire specialty of obstetrics and gynecology, written for the trainee in obstetrics and gynecology at the postgraduate level. The editor and his authors have undertaken what to me is the most difficult task imaginable. The man taking advanced training in a specialty must be exposed to a myriad of details covering clinical medicine, surgical techniques, and basic science. Furthermore, an individual at this stage of training must be exposed to the pros and cons of perhaps many techniques for managing a given problem. Attempting this in a single textbook is not compatible with a book that is portable, and this book by Dr. Dewhurst is portable. This is not to say they have not made a valiant attempt to accomplish this feat of prestidigitation, but it does not quite come off. The book does cover an amazing amount of material and is written
Slowing the Progression of Diabetic Nephropathy
Authors: Giuseppe Remuzzi, Piero Ruggenenti
Journal: New England Journal of Medicine (1993)

Nephropathy, characterized by proteinuria and a decreasing glomerular filtration rate, develops in about 35 percent of patients with insulin-dependent diabetes mellitus1. The risk of death for patients with nephropathy is nine times that of diabetic patients without this complication. Renal disease in diabetes is predictably progressive in that the glomerular filtration rate declines linearly, at a rate of about 1 ml per minute per month. Thus, most patients reach end-stage renal failure within 10 years after the onset of proteinuria. The problem is so extensive that one third of new dialysis patients in the United States have diabetic nephropathy. . . .
Proteotoxicity in the endoplasmic reticulum: lessons from the Akita diabetic mouse
Authors: David Ron
Journal: Journal of Clinical Investigation (2002)

Mutations that impair polypeptide folding commonly result in an unstable and hypofunctional gene product.Their phenotype reflects this loss of function, and the resulting genetic disorder is usually transmitted as a recessive trait.Common forms of cystic fibrosis, hemophilia, and familial hypercholesterolemia are examples of this genetic mechanism in action.A second class of mutations (so-called gain-of-function mutations) encodes proteins with new functions, whose associated disorders are typically transmitted as dominant traits.Some of these are "dominant negative" alleles whose encoded protein can interact with components of the cellular machinery normally accessed by the wild-type gene product.With varying degrees of specificity, these mutations affect the activities of the wild-type allele, for example by disrupting the assembly of a multisubunit complex.Recent observations suggest that gainof-function mutations that affect protein folding can also impair cellular function by less specific mechanisms related to the ability of the mutant protein to challenge the folding capacity in specific cellular compartments.Such mutant proteins are hypothesized to act as proteotoxins and may play a role in important human diseases (1, 2).The paper by Oyadomari et al. (3) appearing in this issue of the JCI addresses important issues related to proteotoxicity in the endoplasmic reticulum (ER).The Ins2 C96Y mutation found in the Akita diabetic mouse precludes formation of an essential disulfide bond between insulin 2 chains and prevents proper folding and processing of this protein.The mutant, malfolded proinsulin-2 is retained in the pancreatic β cell ER (4), presumably by the
The Nuclear Orphan Receptor NR2F6 Suppresses Lymphocyte Activation and T Helper 17-Dependent Autoimmunity
Authors: Natascha Hermann-Kleiter, Thomas Gruber, Christina Lutz-Nicoladoni, Nikolaus Thuille, Friedrich Fresser, Verena Labi, Natalia Schiefermeier, Marei Warnecke, Lukas Huber, Andreas Villunger, Gregor Eichele, Sandra Kaminski, Gottfried Baier
Journal: Immunity (2008)
Relationship of nervous tissue transketolase to the neuropathy in chronic uremia
Authors: R. B. Sterzel, M. Semar, E. T. Lonergan, G. Treser, K. Lange
Journal: Journal of Clinical Investigation (1971)

Patients with chronic uremia develop neurologic defects which are similar to the demyelinating lesions seen in thiamine deficiency. The present study describes inhibitory effects of uremic material on nervous tissue transketolase, a thiamine-dependent enzyme of the pentose phosphate pathway which has been reported to have functional importance in the metabolism of myelinated nervous structures. Transketolase activity (TKA) of normal human brain and spinal cord was measured by the conversion of ribose-5-phosphate (R5P) to sedoheptulose-7-phosphate (S7P). TKA was significantly inhibited by plasma, cerebrospinal fluid and low molecular weight dialysate fractions obtained from patients with uremic neuropathy, but not by samples from normal subjects. The specific effect on transketolase by uremic material was established by showing suppressed formation of S7P from R5P also in the presence of excess cofactor thiamine pyrophosphate and of the other substrate xylulose-5-phosphate. Uremic plasma likewise inhibited a partially purified transketolase preparation from bakers' yeast.31 of 35 chronic uremic patients with inhibition values between 10 and 84% before or during the early phase of intermittent hemodialysis had evidence of neuropathy. Data of clinical grading of the neurologic deficits and values of motor nerve conduction velocity revealed a correlation between the extent of uremic neuropathy and the degree of nervous tissue transketolase inhibition. Hemodialysis markedly reduced the inhibitory effects of the patients' plasma and the data indicate that uremic patients who received effective long-term dialysis treatment show a parallel decline of transketolase inhibition and uremic neuropathy.The findings demonstrate that in patients with chronic renal failure, low molecular weight factors accumulate and inhibit nervous tissue transketolase. This biochemical defect-uncorrectable by thiamine but reversible by dialysis-may interfere with the metabolism of myelin-supporting cells, and/or of the axonal metabolism of medullated structures, and may thus contribute to the degeneration of myelinated nerves seen with uremic neuropathy.