tbuckley/cabot-search huggingface dataset:
Lipopolysaccharide inhibits or accelerates biomedical titanium corrosion depending on environmental acidity
Authors: Fei Yu, Owen Addison, Stephen J Baker, Alison J Davenport
Journal: International Journal of Oral Science (2015)

Titanium and its alloys are routinely used as biomedical implants and are usually considered to be corrosion resistant under physiological conditions. However, during inflammation, chemical modifications of the peri-implant environment including acidification occur. In addition certain biomolecules including lipopolysaccharide (LPS), a component of Gram-negative bacterial cell walls and driver of inflammation have been shown to interact strongly with Ti and modify its corrosion resistance. Gram-negative microbes are abundant in biofilms which form on dental implants. The objective was to investigate the influence of LPS on the corrosion properties of relevant biomedical Ti substrates as a function of environmental acidity. Inductively coupled plasma mass spectrometry was used to quantify Ti dissolution following immersion testing in physiological saline for three common biomedical grades of Ti (ASTM Grade 2, Grade 4 and Grade 5). Complementary electrochemical tests including anodic and cathodic polarisation experiments and potentiostatic measurements were also conducted. All three Ti alloys were observed to behave similarly and ion release was sensitive to pH of the immersion solution. However, LPS significantly inhibited Ti release under the most acidic conditions (pH 2), which may develop in localized corrosion sites, but promoted dissolution at pH 4–7, which would be more commonly encountered physiologically. The observed pattern of sensitivity to environmental acidity of the effect of LPS on Ti corrosion has not previously been reported. LPS is found extensively on the surfaces of skin and mucosal penetrating Ti implants and the findings are therefore relevant when considering the chemical stability of Ti implant surfaces in vivo. Bacterial lipopolysaccharide (LPS) can accelerate or inhibit the corrosion of titanium implants depending on the acidity of the environment. These contrasting effects were demonstrated by Owen Addison and colleagues from Birmingham University, UK. Titanium and its alloys are used in biomedical implants and are generally resistant to corrosion under normal physiological conditions. Inflammation and bacterial activity can, however, modify the local environment in the biofilms around dental implants. The researchers therefore investigated the effects of LPS from bacterial cell walls on corrosion. At normal acidity levels corrosion increased in the presence of LPS, but in the more acidic conditions associated with inflammation corrosion was inhibited. Increased acidity in the absence of LPS increases corrosion. The effects of LPS may influence the long-term stability of many implants.
TCT-443 Multiplug Paravalvular Leak Closure Using Amplatzer Vascular Plug III – Prospective Registry (Wizzard I)
Authors: Grzegorz A. Smolka, Piotr Pysz, Tomasz Roleder, Wojciech M. Wanha, Ewa Peszek-Przybyla, Marek Jasiński, Andrzej J. Ochala, Zbigniew Gasior, Wojciech Wojakowski
Journal: Journal of the American College of Cardiology (2014)
Cardiac Screening With Electrocardiography, Stress Echocardiography, or Myocardial Perfusion Imaging: Advice for High-Value Care From the American College of Physicians
Authors: Roger Chou
Journal: Annals of Internal Medicine (2015)

Background: Cardiac screening in adults with resting or stress electrocardiography, stress echocardiography, or myocardial perfusion imaging can reveal findings associated with increased risk for coronary heart disease events, but inappropriate cardiac testing of low-risk adults has been identified as an important area of overuse by several professional societies. Methods: Narrative review based on published systematic reviews; guidelines; and articles on the yield, benefits, and harms of cardiac screening in low-risk adults. Results: Cardiac screening has not been shown to improve patient outcomes. It is also associated with potential harms due to false-positive results because they can lead to subsequent, potentially unnecessary tests and procedures. Cardiac screening is likely to be particularly inefficient in adults at low risk for coronary heart disease given the low prevalence and predictive values of testing in this population and the low likelihood that positive findings will affect treatment decisions. In this patient population, clinicians should focus on strategies for mitigating cardiovascular risk by treating modifiable risk factors (such as smoking, diabetes, hypertension, hyperlipidemia, and overweight) and encouraging healthy levels of exercise. High-Value Care Advice: Clinicians should not screen for cardiac disease in asymptomatic, low-risk adults with resting or stress electrocardiography, stress echocardiography, or stress myocardial perfusion imaging.
Effect of sotalol on human atrial action potential duration and refractoriness: cycle length dependency of class III activity
Authors: R. P HAYWARD, P. TAGGART
Journal: Cardiovascular Research (1986)

Using intracardiac electrophysiological techniques the effects of sotalol hydrochloride were studied in the right atrium in eight patients with paroxysmal supraventricular atrial arrhythmias. Atrial action potential duration was recorded from two well separated standard sites via endocardial contact electrodes before and for 30 minutes after intravenous sotalol (1 mg X kg-1). Atrial effective refractory period and vulnerability to atrial arrhythmia initiation were assessed by premature extrastimulation. All patients developed a prolonged action potential duration (mean +6%, p less than 0.01 in high atrial site; +8%, p less than 0.01 in low atrial site), with similar increases in atrial effective refractory period (mean +9%, p less than 0.01). The small regional difference in action potential duration detected between these well separated recording sites was minimally decreased, indicating no tendency towards increased regional inhomogeneity of repolarisation. The relatively refractory zone as denoted by the gap between atrial effective refractory period and action potential duration was slightly reduced, and transient repetitive atrial depolarisations, initially provoked by extrastimuli in two patients, were abolished. The relation between atrial interval and duration, investigated using two modes of paced cycle length modification, showed that a gradual reduction in pacing cycle length was more potent in shortening action potential duration than was isolated premature extrastimulation. Sotalol was significantly more effective in opposing shortening of the action potential duration caused by progressive cycle length reduction than that caused by isolated extrastimulation. The class III antiarrhythmic activity of sotalol, confirmed in the atrium, is dependent on cycle length and mode of cycle length alteration. Under study conditions, there was no tendency to increase atrial vulnerability or regional non-uniformity of repolarisation.
"Ramsay Hunt, Ramsay-Hunt, or Hunt's Syndrome?"
Authors: Jerome Z. Litt
Journal: JAMA (1976)

<h3>To the Editor.—</h3> In the course of treating a patient in whom herpes zoster of the geniculate ganglion had developed, I had occasion to investigate her illness rather thoroughly, and in doing so had gone to numerous sources in some of the available dermatologic and neurologic texts. Who among us has not known this condition under the eponym "Ramsay Hunt syndrome?" And who does not look it up in the indices of these texts under the letter "R"? Investigating the matter further, I learned that the well-known American neurologist and neuropsychiatrist, James Ramsay Hunt was responsible for describing this condition in 1907. But in various scientific journal articles and textbooks, there is no unanimity of opinion regarding the spelling, the hyphenation, or the indexing of this good physician's name. Along the way, I found such discrepancies as Ramsey-Hunt, Ramsey Hunt, Ramsay-Hunt, Ramsay Hunt, and other variations of the same syndrome—all
THE TREATMENT OF TYPHOID BACILLUSCARRIERS
Authors: WILLARD J. STONE
Journal: JAMA (1910)

<h3>TYPHOID IMMUNITY</h3> One year ago, before another Section of this Association,<sup>1</sup>I presented the results of a study of typhoid immunity and anti-typhoid inoculation. It was shown at that time that the factors of acquired immunity in typhoid were largely concerned with the process of phagocytosis, and those antibacterial elements which make phagocytosis possible;<i>i. e.</i>, the opsonins and stimulins. The other antibacterial elements, the bacteriolysins, bactericidins and agglutinins, while possessed of certain powers antagonistic to the infection during and immediately subsequent to the attack, were considered, according to work so far done, of lesser value in the perpetuation of such immunity. In this disease, as in many others accompanied by leukopenia, the problem of active immunization seems to resolve itself into a study of these measures which primarily augment the number of leukocytes, with secondary augmentation of those antitropic substances which render the leukocytes capable of phagocytosis. After
First-Trimester Use of Selective Serotonin-Reuptake Inhibitors and the Risk of Birth Defects
Authors: Carol Louik, Angela E. Lin, Martha M. Werler, Sonia Hernández-Díaz, Allen A. Mitchell
Journal: New England Journal of Medicine (2007)

The risk of birth defects after antenatal exposure to selective serotonin-reuptake inhibitors (SSRIs) remains controversial.We assessed associations between first-trimester maternal use of SSRIs and the risk of birth defects among 9849 infants with and 5860 infants without birth defects participating in the Slone Epidemiology Center Birth Defects Study.In analyses of defects previously associated with SSRI use (involving 42 comparisons), overall use of SSRIs was not associated with significantly increased risks of craniosynostosis (115 subjects, 2 exposed to SSRIs; odds ratio, 0.8; 95% confidence interval [CI], 0.2 to 3.5), omphalocele (127 subjects, 3 exposed; odds ratio, 1.4; 95% CI, 0.4 to 4.5), or heart defects overall (3724 subjects, 100 exposed; odds ratio, 1.2; 95% CI, 0.9 to 1.6). Analyses of the associations between individual SSRIs and specific defects showed significant associations between the use of sertraline and omphalocele (odds ratio, 5.7; 95% CI, 1.6 to 20.7; 3 exposed subjects) and septal defects (odds ratio, 2.0; 95% CI, 1.2 to 4.0; 13 exposed subjects) and between the use of paroxetine and right ventricular outflow tract obstruction defects (odds ratio, 3.3; 95% CI, 1.3 to 8.8; 6 exposed subjects). The risks were not appreciably or significantly increased for other defects or other SSRIs or non-SSRI antidepressants. Exploratory analyses involving 66 comparisons showed possible associations of paroxetine and sertraline with other specific defects.Our findings do not show that there are significantly increased risks of craniosynostosis, omphalocele, or heart defects associated with SSRI use overall. They suggest that individual SSRIs may confer increased risks for some specific defects, but it should be recognized that the specific defects implicated are rare and the absolute risks are small.
Abstract 1608: rAAV-Mediated Cyclooxygenase-2 Gene Therapy Affords Permanent (1 year) Cardioprotection Without Adverse Functional Consequences
Authors: Qianhong Li, Qinghui Ou, Santosh K SanganalMath, Buddhadeb Dawn, Chuanjue Cui, Wen-Jian Wu, Xiaoping Zhu, Wei Tan, Yiru Guo, Roberto Bolli
Journal: Circulation (2006)

Although COX-2 is known to play an obligatory role in the infarct-sparing effects of late preconditioning, the long-term effects of COX-2 gene therapy on myocardial ischemic injury and function are...
THE OCCURRENCE DURING ACUTE INFECTIONS OF A PROTEIN NOT NORMALLY PRESENT IN THE BLOOD
Authors: Theodore J. Abernethy, Oswald T. Avery
Journal: The Journal of Experimental Medicine (1941)

The serum obtained from human beings and monkeys during the acute phase of diverse infections contains a protein which is precipitable by the C polysaccharide of pneumococcus. The distribution of this protein in acute phase serum has been studied, and the effect of calcium on the precipitation reaction with the C polysaccharide is described. Other distinctive features of this reaction are discussed. 1. When heated above 65 degrees C., serum obtained from patients during certain acute infections loses the property of reacting in precipitation tests with the C polysaccharide of pneumococcus. The loss of activity under these conditions occurs at temperatures known to denature many proteins. 2. The reactive component in "acute phase" serum which precipitates with the C polysaccharide is tentatively regarded as a protein. 3. The reactive substance is associated with the albumin fraction of serum. 4. In the reaction between patients' serum and C polysaccharide, flocculation is conditioned by the presence of calcium ions. 5. The following distinctive features of the C-reaction are discussed with reference to known characteristics of antigen-antibody phenomena: (a) the occurrence of the reactive component in blood only during the acute stage of the infection; (b) the lack of specificity of the reaction with respect to the inciting cause of the disease; (c) the presence of the active substance in the albumin fraction of the serum; (d) the action of calcium in producing flocculation.
557. Unraveling the Molecular Mechanisms Responsible for Episomal Transgene Silencing In Vivo
Authors: Zhi-Ying Chen, Cheng-Yi He, Hui Xu, Mark A. Kay
Journal: Molecular Therapy (2005)

We previously demonstrated that plasmid bacterial DNA sequences transcriptionally inactivate transgene expression while minicircle DNA vector free of plasmid bacterial backbone is persistently active in vivo. To further elucidate the underlying molecular mechanism, we studied the conditions required for the plasmid bacterial backbone to suppress transgene expression. We found that when circular or linearized minicircle encoding the RSV.hAAT.bpA expression cassette co-injected with circular or linear pBlueScript to mouse liver via hydrodynamic technique, transgene silencing occurred when 2 linear DNAs were infused together, but not when either one or both DNA elements were in circular form, or if the linear expression cassette was injected alone. Southern analyses confirmed that linear DNA but not circular DNA molecules formed random concatemers. This further confirmed our earlier findings that transcriptional silencing occurred only when the bacterial plasmid sequences were covalently attached to the expression cassette, and bacterium-derived plasmid DNA molecules, either in circular or in concatemer form, present in the same cells will not silence DNA expression cassettes in trans-. Furthermore, we found that after injection of a mixture of linear DNA expression cassettes and plasmid bacterial DNAs into normal or SCID mice, silencing was observed in both strains of mouse. These observations strongly suggest that toxic, and probably immunogenic, signaling from plasmid derived DNAs is not responsible for DNA silencing. To determine if DNA methylation was associated with silencing, both transgene and bacterial backbone DNAs were generated from the cytosine methylation-deficient bacterial strain, SCS110. Southern analyses using methylation sensitive restriction enzymes, showed no in vivo cytosine methylation in the CpG motif. This suggests that DNA methylation is not responsible for transcriptional silencing. Interestingly, transgene silencing was alleviated when the RSV.hAAT.bpA expression cassette was flanked with 2 tandem copies of the chicken SH4 insulator at each end. Taken together our results support our hypothesis that the transcriptional suppression is due to differential nucleosome formation and/or histone modifications that are formed in the presence of plasmid bacterial DNA sequences, and then spread to suppress the transgene promoter in cis-.
Interobserver Reproducibility in the Interpretation of Captopril Renograms From Patients Suspected of Having Renovascular Hypertension
Authors: Marianne Tondeur, Alain Sand, Hamphrey Ham
Journal: Clinical Nuclear Medicine (2004)

This work was undertaken to identify, in hypertensive patients suspected of having renovascular hypertension (RVH), scintigraphic images and curves whose interpretation could be difficult. The baseline and postcaptopril Tc-99m MAG 3 images and curves from 10 patients clinically suspected of having RVH were retrospectively selected to have a wide sample of images and curves. The data and a multiple-choice questionnaire were presented as a PowerPoint file, which was sent electronically to Belgian nuclear medicine physicians; they had to answer if the images and curves were or were not suggestive of the diagnosis of RVH or if it was impossible to answer. There was near-complete interobserver agreement for normal baseline and postcaptopril data, for unilateral postcaptopril delayed transit and/or impaired uptake. Agreement was not as good for bilateral and symmetrical changes, for mild changes, or in cases of impaired function. This study shows that the analysis by the Internet of interobserver agreement is an easy and rapid method allowing one to identify difficult to interpret pre- and postcaptopril renographic data.
Mutation of Perinatal Myosin Heavy Chain Associated with a Carney Complex Variant
Authors: Mark Veugelers, Michael Bressan, Deborah A. McDermott, Stanislawa Weremowicz, Cynthia C. Morton, C. Charlton Mabry, Jean-François Lefaivre, Alan Zunamon, Anne Destree, Jean-Marie Chaudron, Craig T. Basson
Journal: New England Journal of Medicine (2004)

Familial cardiac myxomas occur in the hereditary syndrome Carney complex. Although PRKAR1A mutations can cause the Carney complex, the disorder is genetically heterogeneous. To identify the cause of a Carney complex variant associated with distal arthrogryposis (the trismus-pseudocamptodactyly syndrome), we performed clinical and genetic studies.A large family with familial cardiac myxomas and the trismus-pseudocamptodactyly syndrome (Family 1) was identified and clinically evaluated along with two families with trismus and pseudocamptodactyly. Genetic linkage analyses were performed with the use of microsatellite polymorphisms to determine a locus for this Carney complex variant. Positional cloning and mutational analyses of candidate genes were performed to identify the genetic cause of disease in the family with the Carney complex as well as in the families with the trismus-pseudocamptodactyly syndrome.Clinical evaluations demonstrated that the Carney complex cosegregated with the trismus-pseudocamptodactyly syndrome in Family 1, and genetic analyses demonstrated linkage of the disease to chromosome 17p12-p13.1 (maximum multipoint lod score, 4.39). Sequence analysis revealed a missense mutation (Arg674Gln) in the perinatal myosin heavy-chain gene (MYH8). The same mutation was also found in the two families with the trismus-pseudocamptodactyly syndrome. Arg674 is highly conserved evolutionarily, localizes to the actin-binding domain of the perinatal myosin head, and is close to the ATP-binding site. We identified nonsynonymous MYH8 polymorphisms in patients with cardiac myxoma syndromes but without arthrogryposis.We describe a novel heart-hand syndrome involving familial cardiac myxomas and distal arthrogryposis and demonstrate that these disorders are caused by a founder mutation in the MYH8 gene. Our findings demonstrate novel roles for perinatal myosin in both the development of skeletal muscle and cardiac tumorigenesis.
Textbook of Otolaryngology.
Authors: David D. (David Downs) DeWeese, William H. Saunders
Journal: Annals of Internal Medicine (1982)

Since its first publication in 1961, this book has earned a place as one of the leading otolaryngologic texts written for the medical student and the general practitioner. Although the format has remained unchanged, the second edition has expanded by 50 pages, and some figures have been replaced by better ones in addition to 50 new illustrations. The book pans the broad field of otolaryngology, covering it well and in good balance without burdening the reader with exotic diseases and esoteric detail, yet it accentuates the important practical clinical information on common ear, nose, and throat disorders. It indeed reflects the broad clinical experience of the authors. The least palatable parts of any textbook are the sections on dry basic sciences. Sufficient anatomy and physiology has been included to insure a foundation for understanding the regional pathology, yet care has been taken to avoid belaboring detail. The otologie section has
884. Integration of a Helper-Dependent Adenovirus Mediated by the Phage ΦC31 Integrase
Authors: Rénald Gilbert, Laurie Desfossé, Émilie Mairey, Benoît Raymond, Michele P. Calos, Jacques P. Tremblay, Bernard Massie
Journal: Molecular Therapy (2005)

Adenoviral vectors (Ad) deleted of all viral genes, known as helper-dependent Ad (HD) or gutted Ad, possess a linear genomic DNA that remains as a non-integrated episome in the nucleus of the infected cells. Because HD can be grown to very high titers, are weakly immunogenic and can carry up to 35-kb of foreign DNA, they are very attractive vectors for gene therapy applications. Under certain circumstances (for example to stably express large cDNAs such as dystrophin into stem cells or myoblasts) it could be valuable to promote integration of HD into the cell chromosomes. The phage C31 integrase normally mediates integration of a phage DNA containing an attP site into the attB site of the bacterial chromosome. Interestingly, when the C31 integrase is expressed in mammalian cells, it can mediate integration of a circular DNA containing an attB site into pseudo attP sites of the cell chromosomes. In the present study, we tested whether the C31 integrase could promote integration of an HD into mammalian cells. We have thus constructed an HD containing an attB site, which carries as a gene reporter, a green fluorescent protein (GFP) expression cassette. In addition, the GFP expression cassette was flanked by two loxP sites to permit its circularization upon expression of the Cre recombinase. HeLa cells were transfected with plasmids expressing Cre and the C31 integrase. The next day, the cells were transduced with HD-GFPattB and at selected time points, without any selective pressure, the expression of GFP was quantified by flow cytometry. At twelve days post-transduction, the fluorescence index ([% of GFP positive cells] X [intensity of fluorescence]) was significantly higher in cells transfected with Cre and the C31 integrase. This observation suggests these two enzymes are able to promote integration of HD-GFPattB. Experiments are in progress to optimize the integration efficiency and to test if Cre expression is essential for this process to occur.