tbuckley/cabot-search huggingface dataset:
Reduction of neointimal proliferation after implantation of a beta particle emitting gold Au 198 coated stent
Authors: E. Alt, R.A. Herrmann, A. Rybnikar, J.B. Knebel, G. Ritscher, B. Märkl, J. Hausleiter, I. Wolf, W. Erhardt, M. Schwaiger, A. Schörnig
Journal: Journal of the American College of Cardiology (1998)
New ways in respiratory genetics
Authors: M. Kabesch, F. Kauffmann, E. von Mutius
Journal: European Respiratory Journal (2006)

Ever since the first reports on a genetic background for asthma, our knowledge about the role of genetic susceptibility in the development of respiratory diseases has increased steadily, as reviewed recently 1. However, expectations of a fast victory in discovering the important genes for asthma and chronic obstructive pulmonary disease (COPD), respectively, and thereby find the true mechanisms underlying the development of these conditions, have faltered. At the same time, a sobering process has taken place allowing for a more realistic view on the status, the potential and the future of respiratory genetics. It cannot be disputed that significant progress has been achieved in this field. However, it is also true that with this increasing knowledge new scientific questions have arisen and that the transfer of genetic progress into clinical application is still awaited.

A highly stimulating European Respiratory Society meeting of leading groups in respiratory genetics and epidemiology from Europe and the USA, which took place in France in 2002 2, eventually triggered a new European Respiratory Journal series “Respiratory genetics in the post-genome era”, which aims to disseminate new concepts and ideas. Intentionally, this series does not provide another state-of-the-art review. Instead, leaders in the field were asked to communicate their personal views on some of the burning questions in respiratory genetics. A series of essays has emerged from this request in which selected authors present their personal interpretation of the available data on respiratory genomics and …
Bloodletting Ameliorates Insulin Sensitivity and Secretion in Parallel to Reducing Liver Iron in Carriers of <i>HFE</i> Gene Mutations
Authors: Francesco Equitani, Josè Manuel Fernandez-Real, Giacomo Menichella, Maurizio Koch, Menotti Calvani, Valerio Nobili, Geltrude Mingrone, Melania Manco
Journal: Diabetes Care (2007)

To clarify the pathogenesis of diabetes associated with mutations of the hemochromatosis (HFE) gene, 17 carriers, 9 normal glucose tolerant (NGT) and 8 diabetic, were evaluated in an interventional trial.At enrollment and after a 2-year bloodletting period, euglycemic-hyperinsulinemic clamp, oral glucose tolerance test (OGTT), liver histology (nonalcoholic fatty liver disease activity score [NAS]), and liver iron content (LIC) were assessed.NGT subjects had significantly higher baseline insulin sensitivity (P <or= 0.001), secretion, and insulinogenic index (calculated from the OGTT) (P <or= 0.0001 for both) and lower LIC (P = 0.004) and NAS (P = 0.02) than diabetic patients. Baseline LIC correlated negatively with insulin secretion (NGT r(0) = -0.676, P <or= 0.0001; diabetes r(0) = -0.589, P = 0.02) and insulin sensitivity (M value) (NGT r(0) = -0.597, P = 0.009; diabetes r(0) = -0.535, P = 0.03) and positively with NAS (diabetes r(0) = 0.649, P = 0.007) and triglycerides (NGT r(0) = 0.563, P = 0.015). At month 24, circulating iron was reduced by 179 +/- 26% in NGT and 284 +/- 54% in diabetic subjects. Insulin secretion (NGT 20 +/- 4%; diabetes 33 +/- 7%) and insulin sensitivity (NGT 25 +/- 5%; diabetes 18 +/- 3%) increased. LIC decreased in both groups (NGT 126 +/- 42%; diabetes 61 +/- 13%), and NAS ameliorated (NGT 65.1 +/- 6.5 vs. 38.1 +/- 6.83; P <or= 0.0001; diabetes 2.1 +/- 10.7 vs. 69.9 +/- 10; P <or= 0.0001).Iron depletion ameliorates insulin secretion and sensitivity in NGT and diabetic carriers of HFE gene mutations. This amelioration occurs in parallel with decreased LIC and improved NAS. These results justify glucose tolerance testing and prophylactic iron depletion in asymptomatic carriers as well.
Measuring cognitive universals and cultural particulars
Authors: A. Kimball Romney
Journal: Behavioral and Brain Sciences (1998)

A reanalysis of Atran's data is presented in which the comparison between Itzaj and Michigan animal names is represented in spatial rather than taxonomic form. Similarity among all subjects is also represented in spatial terms. Finally, culturally shared knowledge between the two cultures is shown to be about ten times larger than the culture-specific component unique to each culture.
Shear Stress–Dependent Regulation of the Human β-Tubulin Folding Cofactor D Gene
Authors: Andreas Schubert, Marco Cattaruzza, Markus Hecker, Dorothea Darmer, Juergen Holtz, Henning Morawietz
Journal: Circulation Research (2000)

Abstract —The flowing blood generates shear stress at the endothelial cell surface. The endothelial cells modify their phenotype by alterations in gene expression in response to different levels of fluid shear stress. To identify genes involved in this process, human umbilical vein endothelial cells were exposed to laminar shear stress (venous or arterial levels) in a cone-and-plate apparatus for 24 hours. Using the method of RNA arbitrarily primed polymerase chain reaction, we cloned a polymerase chain reaction fragment representing an mRNA species downregulated by arterial compared with venous shear stress (shear stress downregulated gene-1, SSD-1). According to Northern blot analysis, corresponding SSD-1 cDNA clones revealed a similar, time-dependent downregulation after 24 hours of arterial shear stress compared with venous shear stress or static controls. Three SSD-1 mRNA species of 2.8, 4.1, and 4.6 kb were expressed in a tissue-specific manner. The encoded amino acid sequence of the human endothelial SSD-1 isoform (4.1-kb mRNA species) revealed 80.4% identity and 90.9% homology to the bovine β-tubulin folding cofactor D (tfcD) gene. Downregulation of tfcD mRNA expression by shear stress was defined at the level of transcription by nuclear run-on assays. The tfcD protein was downregulated by arterial shear stress. The shear stress–dependent downregulation of tfcD mRNA and protein was attenuated by the NO synthase inhibitor Nω -nitro- l -arginine methyl ester. Furthermore, the NO donor DETA-NO downregulated tfcD mRNA. Because tfcD was shown to be a microtubule-destabilizing protein, our data suggest a shear stress–dependent regulation of the microtubular dynamics in human endothelial cells.
Increased circulating levels of neuropeptide Y (NPY) in hepatorenalsyndrome (HRS). A possible role in the pathogenesis of renalvasoconstriction
Authors: J. Uriz, P. Ginès, A. Cárdenas, P. Sort, W. Jiménez, V. Arroyo, F. Rivera, J. Rodés
Journal: Journal of Hepatology (2000)
Feasibility of Long-Term Patient Self-Reporting of Toxicities From Home via the Internet During Routine Chemotherapy
Authors: Timothy J. Judson, Antonia V. Bennett, Lauren J. Rogak, Laura Sit, Allison Barz, Mark G. Kris, CliffordA. Hudis, Howard I. Scher, Paul Sabattini, Deborah Schrag, Ethan Basch
Journal: Journal of Clinical Oncology (2013)

Patient-reported outcomes are increasingly used in routine outpatient cancer care to guide clinical decisions and enhance communication. Prior evidence suggests good patient compliance with reporting at scheduled clinic visits, but there is limited evidence about compliance with long-term longitudinal reporting between visits.
Ankyrin-G Coordinates Intercalated Disc Signaling Platform to Regulate Cardiac Excitability In Vivo
Authors: Michael A. Makara, Jerry Curran, Sean C. Little, Hassan Musa, Iuliia Polina, Sakima A. Smith, Patrick J. Wright, Sathya D. Unudurthi, Jed Snyder, Vann Bennett, Thomas J. Hund, Peter J. Mohler
Journal: Circulation Research (2014)

Rationale: Na v 1.5 ( SCN5A ) is the primary cardiac voltage-gated Na v channel. Na v 1.5 is critical for cardiac excitability and conduction, and human SCN5A mutations cause sinus node dysfunction, atrial fibrillation, conductional abnormalities, and ventricular arrhythmias. Further, defects in Na v 1.5 regulation are linked with malignant arrhythmias associated with human heart failure. Consequently, therapies to target select Na v 1.5 properties have remained at the forefront of cardiovascular medicine. However, despite years of investigation, the fundamental pathways governing Na v 1.5 membrane targeting, assembly, and regulation are still largely undefined. Objective: Define the in vivo mechanisms underlying Na v 1.5 membrane regulation. Methods and Results: Here, we define the molecular basis of an Na v channel regulatory platform in heart. Using new cardiac-selective ankyrin-G -/- mice (conditional knock-out mouse), we report that ankyrin-G targets Na v 1.5 and its regulatory protein calcium/calmodulin–dependent kinase II to the intercalated disc. Mechanistically, β IV -spectrin is requisite for ankyrin-dependent targeting of calcium/calmodulin–dependent kinase II-δ; however, β IV -spectrin is not essential for ankyrin-G expression. Ankyrin-G conditional knock-out mouse myocytes display decreased Na v 1.5 expression/membrane localization and reduced I Na associated with pronounced bradycardia, conduction abnormalities, and ventricular arrhythmia in response to Na v channel antagonists. Moreover, we report that ankyrin-G links Na v channels with broader intercalated disc signaling/structural nodes, as ankyrin-G loss results in reorganization of plakophilin-2 and lethal arrhythmias in response to β-adrenergic stimulation. Conclusions: Our findings provide the first in vivo data for the molecular pathway required for intercalated disc Na v 1.5 targeting/regulation in heart. Further, these new data identify the basis of an in vivo cellular platform critical for membrane recruitment and regulation of Na v 1.5.
Efficacy of non-steroidal anti-inflammatory drugs for low back pain: a systematic review of randomised clinical trials
Authors: B. W Koes, R. J P M Scholten, J. M A Mens, L. M Bouter
Journal: Annals of the Rheumatic Diseases (1997)

<h3>PURPOSE</h3> To assess the efficacy of non-steroidal anti-inflammatory drugs (NSAIDs) for low back pain. <h3>DATA SOURCES</h3> Computer aided search of published randomised clinical trials and assessment of the methods of the studies. <h3>STUDY SELECTION</h3> 26 randomised clinical trials evaluating NSAIDs for low back pain were identified. <h3>DATA EXTRACTION</h3> Score for quality (maximum = 100 points) of the methods based on four categories: study population; interventions; effect measurement; data presentation and analysis. Determination of success rate per study group and evaluation of different contrasts. Statistical pooling of placebo controlled trials in similar patient groups and using similar outcome measures. <h3>RESULTS</h3> The methods scores of the trials ranged from 27 to 83 points. NSAIDs were compared with placebo treatment in 10 studies. The pooled odds ratio in four trials comparing NSAIDs with placebo after one week was 0.53 (95% confidence intervals 0.32 to 0.89) using the fixed effect model, indicating a significant effect in favour of NSAIDs compared with placebo. In nine studies NSAIDs were compared with other (drug) therapies. Of these, only two studies reported better results of NSAIDs compared with paracetamol with and without dextropropoxyphene. In the other trials NSAIDs were not better than the reference treatment. In 11 studies different NSAIDs were compared, of which seven studies reported no differences in effect. <h3>CONCLUSIONS</h3> There are flaws in the design of most studies. The pooled odds ratio must be interpreted with caution because the trials at issue, including the high quality trials, did not use identical outcome measures. The results of the 26 randomised trials that have been carried out to date, suggest that NSAIDs might be effective for short-term symptomatic relief in patients with uncomplicated low back pain, but are less effective or ineffective in patients with low back pain with sciatica and patients with sciatica with nerve root symptoms.
A Novel Gene Expression Profile in Lymphatics Associated with Tumor Growth and Nodal Metastasis
Authors: Steven Clasper, Daniel Royston, Dilair Baban, Yihai Cao, Stephan Ewers, Stefan Butz, Dietmar Vestweber, David G. Jackson
Journal: Cancer Research (2008)

Invasion of lymphatic vessels is a key step in the metastasis of primary tumors to draining lymph nodes. Although the process is enhanced by tumor lymphangiogenesis, it is unclear whether this is a consequence of increased lymphatic vessel number, altered lymphatic vessel properties, or both. Here we have addressed the question by comparing the RNA profiles of primary lymphatic endothelial cells (LEC) isolated from the vasculature of normal tissue and from highly metastatic T-241/vascular endothelial growth factor (VEGF)-C fibrosarcomas implanted in C57BL/6 mice. Our findings reveal significant differences in expression of some 792 genes (i.e., >or=2-fold up- or down-regulated, P <or= 0.05) that code for a variety of proteins including components of endothelial junctions, subendothelial matrix, and vessel growth/patterning. The tumor LEC profile, validated by immunohistochemical staining, is distinct from that of normal, inflammatory cytokine, or mitogen-activated LEC, characterized by elevated expression of such functionally significant molecules as the tight junction regulatory protein endothelial specific adhesion molecule (ESAM), the transforming growth factor-beta coreceptor Endoglin (CD105), the angiogenesis-associated leptin receptor, and the immunoinhibitory receptor CD200, and reduced expression of subendothelial matrix proteins including collagens, fibrillin, and biglycan. Moreover, we show similar induction of ESAM, Endoglin, and leptin receptor within tumor lymphatics in a series of human head and neck and colorectal carcinomas, and uncover a dramatic correlation between ESAM expression and nodal metastasis that identifies this marker as a possible prognostic indicator. These findings reveal a remarkable degree of phenotypic plasticity in cancer lymphatics and provide new insight into the processes of lymphatic invasion and lymph node metastasis.
Transfusion Medicine
Authors: H G Klein
Journal: JAMA (1987)

<i>BLOOD banking</i>is an archaic term. It should be discarded. If this seems too radical a step to take in the 50th anniversary year of the American blood bank, perhaps the term should be given a gold watch and nudged into an honorable retirement. The bank analogy, connoting a place to deposit, store, and withdraw blood, no longer suits the scope of services and direct patient care responsibilities offered by present-day transfusion centers. During the past quarter of a century, a complex clinical and research discipline has quietly emerged from blood banking. This new discipline projects a different image and deservedly has acquired a new name—<i>transfusion medicine</i>. Blood banking was an American innovation and one that revolutionized medicine. When Bernard Fantus established the first blood bank at Cook County Hospital in Chicago in 1937, the scientific principles for rudimentary blood storage had already been described<sup>1</sup>; however, practical guidelines
ICSBP/IRF-8 differentially regulates antigen uptake during dendritic-cell development and affects antigen presentation to CD4+ T cells
Authors: Fabrizio Mattei, Giovanna Schiavoni, Paola Borghi, Massimo Venditti, Irene Canini, Paola Sestili, Immacolata Pietraforte, Herbert C. Morse, Carlo Ramoni, Filippo Belardelli, Lucia Gabriele
Journal: Blood (2006)
Phylogenetically widespread alternative splicing at unusual GYNGYN donors.
Authors: Michael Hiller, Klaus Huse, Karol Szafranski, Philip Rosenstiel, Stefan Schreiber, Rolf Backofen, Matthias Platzer
Journal: Genome biology (2006)

Splice donor sites have a highly conserved GT or GC dinucleotide and an extended intronic consensus sequence GTRAGT that reflects the sequence complementarity to the U1 snRNA. Here, we focus on unusual donor sites with the motif GYNGYN (Y stands for C or T; N stands for A, C, G, or T).While only one GY functions as a splice donor for the majority of these splice sites in human, we provide computational and experimental evidence that 110 (1.3%) allow alternative splicing at both GY donors. The resulting splice forms differ in only three nucleotides, which results mostly in the insertion/deletion of one amino acid. However, we also report the insertion of a stop codon in four cases. Investigating what distinguishes alternatively from not alternatively spliced GYNGYN donors, we found differences in the binding to U1 snRNA, a strong correlation between U1 snRNA binding strength and the preferred donor, over-represented sequence motifs in the adjacent introns, and a higher conservation of the exonic and intronic flanks between human and mouse. Extending our genome-wide analysis to seven other eukaryotic species, we found alternatively spliced GYNGYN donors in all species from mouse to Caenorhabditis elegans and even in Arabidopsis thaliana. Experimental verification of a conserved GTAGTT donor of the STAT3 gene in human and mouse reveals a remarkably similar ratio of alternatively spliced transcripts in both species.In contrast to alternative splicing in general, GYNGYN donors in addition to NAGNAG acceptors enable subtle protein variations.
Insuring Latinos Against the Costs of Illness
Authors: R B Valdez, H Morgenstern, R Brown, R Wyn, C Wang, W Cumberland
Journal: JAMA (1993)

<h3>Objective.</h3> —To examine the determinants of health insurance coverage for Latinos in the United States and how different targeted strategies for health care reform differentially affect the country's major ethnic groups, focusing on the implications for the Latino population. <h3>Design.</h3> —Data from the 1980 and 1990 Current Population Surveys were used to compare the insurance status of nonelderly (&lt;65 years) Latinos with the Anglo (non-Hispanic white), black, and Asian and other populations by estimating the attributable fraction for selected covariates. The effects of health care reform strategies on the coverage of the major ethnic groups were simulated from these data. <h3>Main Outcome Measures.</h3> —Percentage uninsured, percentage insured by Medicaid, and attributable fraction for covariates. <h3>Results.</h3> —Latinos have the worst health insurance coverage of any ethnic group in the country. Approximately 39% of Latinos are uninsured compared with 13.8% for the Anglo and 24% for the black population. Providing coverage to all the poor could reduce the uninsured rate for Anglos by about 23%, whereas the reduction among Latinos could be about 37% and among blacks about 42%. Similar reductions could be achieved by covering all workers and their minor dependents. Regardless of the approach to reform, however, Latinos would remain with high absolute rates of uninsured. <h3>Conclusions.</h3> —Differences in Medicaid eligibility, labor force characteristics, and family composition between Latinos and other ethnic groups suggest that policy initiatives may affect Latinos differently. Targeted strategies, such as employer mandates, "pay-or-play" programs, or Medicaid expansions, can improve coverage, but many Latinos could still remain uninsured. (<i>JAMA</i>. 1993;269:889-894)
Is inflammatory bowel disease an independent and disease specific risk factor for thromboembolism?
Authors: W Miehsler
Journal: Gut (2004)

<b>Background:</b> Patients with inflammatory bowel disease (IBD) are thought to be at increased risk of venous thromboembolism (TE). However, the extent of this risk is not known. Furthermore, it is not known if this risk is specific for IBD or if it is shared by other chronic inflammatory diseases or other chronic bowel diseases. <b>Aims:</b> To compare the risk of TE in patients with IBD, rheumatoid arthritis, and coeliac disease with matched control subjects. <b>Patients and methods:</b> Study subjects answered a questionnaire assessing the history of TE, any cases of which had to be confirmed radiologically. A total of 618 patients with IBD, 243 with rheumatoid arthritis, 207 with coeliac disease, and 707 control subjects were consecutively included. All three patient groups were compared with control subjects matched to the respective group by age and sex. <b>Results:</b> Thirty eight IBD patients (6.2%) had suffered TE. This was significantly higher compared with the matched control population with only 10 cases reported (1.6%) (p&lt;0.001; odds ratio (OR) 3.6 (95% confidence interval (CI) 1.7–7.8)). Five patients with rheumatoid arthritis (2.1%) had suffered TE compared with six subjects (2.5%) in the control population matched to patients with rheumatoid arthritis (NS; OR 0.7 (95% CI 0.2–2.9)). TE had occurred in two patients with coeliac disease (1%) compared with four subjects (1.9%) in the control population matched to the coeliac disease group (NS; OR 0.4 (95% CI 0.1–2.5)). In 60% of TE cases in the IBD group, at least one IBD specific factor (active disease, stenosis, fistula, abscess) was present at the time TE occurred. <b>Conclusions:</b> IBD is a risk factor for TE. It seems that TE is a specific feature of IBD as neither rheumatoid arthritis, another chronic inflammatory disease, nor coeliac disease, another chronic bowel disease, had an increased risk of TE.
A candidate genetic risk factor for vascular disease: a common mutation in methylenetetrahydrofolate reductase
Authors: P. Frosst, H.J. Blom, R. Milos, P. Goyette, C.A. Sheppard, R.G. Matthews, G.J.H. Boers, M. den Heijer, L.A.J. Kluijtmans, L.P. van den Heuve, R. Rozen
Journal: Nature Genetics (1995)
Randomised trial of interferon α2b plus ribavirin for 48 weeks or for 24 weeks versus interferon α2b plus placebo for 48 weeks for treatment of chronic infection with hepatitis C virus
Authors: Thierry Poynard, Patrick Marcellin, Samuel S Lee, Christian Niederau, Gerald S Minuk, Gaetano Ideo, Vincent Bain, Jenny Heathcote, Stefan Zeuzem, Christian Trepo, Janice Albrecht
Journal: The Lancet (1998)
Reduced activity of 11β-hydroxysteroid dehydrogenase in patients with cholestasis
Authors: Cristiana Quattropani, Bruno Vogt, Alex Odermatt, Bernhard Dick, Brigitte M. Frey, Felix J. Frey
Journal: Journal of Clinical Investigation (2001)

Enhanced renal sodium retention and potassium loss in patients with cirrhosis is due to activation of mineralocorticoid receptors (MRs). Increased aldosterone concentrations, however, do not entirely explain the activation of MR in cirrhosis. Here, we hypothesize that cortisol activates MRs in patients with cholestasis. We present evidence that access of cortisol to MRs is a result of bile acid−mediated inhibition of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), an MR-protecting enzyme that converts cortisol to cortisone. Twelve patients with biliary obstruction and high plasma bile acid levels were studied before and after removal of the obstruction. The urinary ratio of (tetrahydrocortisol + 5α-tetrahydrocortisol)/tetrahydrocortisone, a measure of 11β-HSD2 activity, decreased from a median of 1.91 during biliary obstruction to 0.78 at 4 and 8 weeks after removal of the obstruction and normalization of plasma bile acid concentrations. In order to demonstrate that bile acids facilitate access of cortisol to the MR by inhibiting 11β-HSD2, an MR translocation assay was performed in HEK-293 cells transfected with human 11β-HSD2 and tagged MR. Increasing concentrations of chenodeoxycholic acid led to cortisol-induced nuclear translocation of MR. In conclusion, 11β-HSD2 activity is reduced in cholestasis, which results in MR activation by cortisol.