tbuckley/cabot-search huggingface dataset:
Multiple eruptive myxoid dermatofibromas: report of first case and review of literature
Authors: A. Antal, B. Zelger, J. Reifenberger, T. Niehues, O. Feyen, M. Megahed, T. Ruzicka, B. Homey
Journal: British Journal of Dermatology (2007)

Journal Article Multiple eruptive myxoid dermatofibromas: report of first case and review of literature Get access A. Antal, A. Antal Department of Dermatology and Correspondence: Attila Antal. E‐mail: attila.antal@uni‐duesseldorf.de Search for other works by this author on: Oxford Academic Google Scholar B. Zelger, B. Zelger Department of Dermatology, Innsbruck Medical University, Innsbruck, Austria Search for other works by this author on: Oxford Academic Google Scholar J. Reifenberger, J. Reifenberger Department of Dermatology and Search for other works by this author on: Oxford Academic Google Scholar T. Niehues, T. Niehues Department of Paediatric Oncology, Haematology and Immunology, Heinrich Heine University, Moorenstr. 5, 40225 Düsseldorf, Germany Search for other works by this author on: Oxford Academic Google Scholar O. Feyen, O. Feyen Department of Paediatric Oncology, Haematology and Immunology, Heinrich Heine University, Moorenstr. 5, 40225 Düsseldorf, Germany Search for other works by this author on: Oxford Academic Google Scholar M. Megahed, M. Megahed Department of Dermatology, University of Aachen, Aachen, Germany Search for other works by this author on: Oxford Academic Google Scholar T. Ruzicka, T. Ruzicka Department of Dermatology and Allergology, Ludwig Maximilians University, Munich, Germany Search for other works by this author on: Oxford Academic Google Scholar B. Homey B. Homey Department of Dermatology and Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 157, Issue 2, 1 August 2007, Pages 382–385, https://doi.org/10.1111/j.1365-2133.2007.08032.x Published: 01 August 2007
TCT-588 2-Year Clinical Outcome of the Randomized, Multicenter DUTCH PEERS (TWENTE II) Trial, Comparing Cobalt-Chromium Zotarolimus-Eluting Resolute Integrity Stents and Platinum-Chromium Everolimus-Eluting Promus Element Stents in “All-Comer” Patients
Authors: Clemens von Birgelen, Ming Kai Lam, Liefke van der Heijden, Peter W. Danse, Gillian A. Jessurun, Melvyn Tjon Joe Gin, Rutger Anthonio, Gert van Houwelingen, Frits H. de Man, Martin G. Stoel, Hans W. Louwerenburg, Gerard C. Linssen, Marc Hartmann, Marije M. Löwik, Kenneth Tandjung, Maarten J. Ijzerman, Carine J. Doggen, Hanim Sen
Journal: Journal of the American College of Cardiology (2014)
Body Mass, Fat Free Body Mass and Prognosis in COPD Patients from a Random Population Sample.
Authors: Vestbo J, Prescott E, Almdal T, Dahl M, Nordestgaard Bg, Andersen T, Sorensen Ti, P Lange
Journal: American Journal of Respiratory and Critical Care Medicine (2005)

Rationale: Low body mass index (BMI) is a marker of poor prognosis in chronic obstructive pulmonary disease (COPD). In the general population the harmful effect of low BMI is due to the deleterious effects of a low fat free mass index (FFMI, fat free mass/weight(2)). Objectives: We explored distribution of low FFMI and its association with prognosis in a population based cohort of COPD patients. Methods: We used data on 1,898 COPD patients identified in a population-based epidemiological study in Copenhagen. Fat free mass was measured using bioelectrical impedance analysis. Patients were followed up for a mean of 7 years and the association between BMI and FFMI and mortality was examined taking age, gender, smoking and lung function into account. Main results: The mean FFMI was 16.0 kg/m(2) for women and 18.7 kg/m(2) for men. Among subjects with normal BMI, 26.1 % had an FFMI lower than the lowest FFMI 10(th) percentile of the general population. BMI and FFMI were significant predictors of mortality, independent of relevant covariates. Being in the lowest FFMI 10(th) percentile of the general population was associated with a hazard ratio of 1.5 (95% confidence interval 1.2-1.8) for overall mortality and 2.4 (1.4-4.0) for COPD-related mortality. FFMI was also a predictor of overall mortality when analyses were restricted to subjects with normal BMI. Conclusions: FFMI provides information in addition to BMI and assessment of fat free mass should be considered in the routine assessment of COPD.
The Cytomegalovirus m155 Gene Product Subverts Natural Killer Cell Antiviral Protection by Disruption of H60–NKG2D Interactions
Authors: Melissa B. Lodoen, Gerardo Abenes, Sean Umamoto, Jeffrey P. Houchins, Fenyong Liu, Lewis L. Lanier
Journal: The Journal of Experimental Medicine (2004)

Natural killer (NK) cells are an important early mediator of host immunity to murine cytomegalovirus (MCMV) infection. However, MCMV has evolved mechanisms to elude recognition and clearance by NK cells. We have identified an MCMV immune evasion protein that impairs NKG2D-mediated NK cell antiviral activity. Infection of BALB/c 3T3 cells with the Smith strain of MCMV resulted in strong down-regulation of H60, a high affinity ligand for NKG2D, from the surface of virus-infected cells. The MCMV m155 protein specifically down-regulated H60 without affecting expression of the other known NKG2D ligands, RAE-1 and MULT-1. Treatment with the proteasome inhibitors lactacystin or epoxomicin reversed m155 down-regulation of H60. An MCMV mutant virus lacking m155 was severely attenuated in BALB/c mice; however, treatment with neutralizing anti-NKG2D monoclonal antibody or with NK-depleting anti-asialo GM1 antisera restored virulence of the mutant virus. Thus, down-regulation of H60 by m155 is a powerful mechanism of inhibiting NKG2D-mediated antiviral function.
Commentaries on this month's Cardiovascular Controversy: the merits and demerits of animal experimentation From D P Zipes
Authors: D. P Zipes
Journal: Cardiovascular Research (1994)

Commentaries on this month's Cardiovascular Controversy: the merits and demerits of animal experimentation From D P Zipes Get access Douglas P Zipes Douglas P Zipes Department of Medicine, Krannert Institute of Cardiology, Indiana University, 11 I 1 West 10th St, Indianapolis, IN, USA. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 28, Issue 7, July 1994, Pages 1117–1118, https://doi.org/10.1093/cvr/28.7.1117 Published: 01 July 1994
Increased leukotriene B4 and 8-isoprostane in exhaled breath condensate of patients with exacerbations of COPD
Authors: W A Biernacki
Journal: Thorax (2003)

<b>Background:</b> Exacerbations are an important feature of chronic obstructive pulmonary disease (COPD), accounting for a large proportion of health care costs. They are associated with increased airway inflammation and oxidative stress. <b>Methods:</b> Concentrations of leukotriene B4 (LTB4), a marker of inflammation, and 8-isoprostane, a marker of oxidative stress, were measured in the exhaled breath condensate of 21 patients (11 M) with COPD during an exacerbation and 2 weeks after treatment with antibiotics. In 12 patients who had no further exacerbations these markers were also measured after 2 months. <b>Results:</b> LTB4 concentrations were raised during the COPD exacerbation (mean (SE) 15.8 (1.1) pg/ml and fell after treatment with antibiotics to 9.9 (0.9) pg/ml (p&lt;0.0001). In 12 patients the level of LTB4 fell further from 10.6 (1.1) pg/ml to 8.5 (0.8) pg/ml (p&lt;0.005) after 2 months. In 12 normal age matched subjects the LTB4 levels were 7.7 (0.5) pg/ml. Concentrations of 8-isoprostane were also increased during the exacerbation (13.0 (0.9) pg/ml) and fell after antibiotic treatment to 9.0 (0.6) pg/ml (p&lt;0.0001). In 12 patients there was a further fall from 9.3 (0.7) pg/ml to 6.0 (0.7) pg/ml (p&lt;0.001) after 2 months compared with normal subjects (6.2 (0.4) pg/ml). <b>Conclusions:</b> Non-invasive markers of inflammation and oxidative stress are increased during an infective exacerbation of COPD and only slowly recover after treatment with antibiotics.
His-Purkinje conduction findings after cardiac surgery in children.
Authors: G S Wolff, D Tamer, O L Garcia, P L Ferrer, A S Pickoff, R J Sung, H Gelband
Journal: Circulation (1980)

Conduction abnormalities of the His-Purkinje (HP) system are common sequelae of surgical repair of heart defects.Standard electrophysiologic recordings may fail to demonstrate abnormalities of the HP system when routine intervals are measured.When the conduction system is stressed, certain HP features that may indicate latent conduction disease within the HP system can be revealed.These features include split His potentials (SH) with spontaneous tachycardia or during rapid atrial pacing (RAP); SH with atrial ex- trastimuli (AES); and long HV intervals with AES associated with block distal to His during RAP.These find- ings may represent pathologic or functional properties of the HP system, and were identified in seven of 35 patients after surgical repair of tetralogy of Fallot (29 patients) or ventricular septal defect (six patients) who had electrophysiologic studies 1-8 years after operation.In five of the seven patients, these findings were revealed only when the conduction system was stressed.This incidence does not represent the true frequency of these features in the 35 patients because they were not evaluated under the same electrophysiologic stresses.Clinically, these patients did not differ from those manifesting these HP findings.The electrocardiographic patterns were as follows: normal QRS duration and normal axis (n = 1), right bundle branch block (RBBB) and normal axis (n = 1), RBBB and right-axis deviation (n = 4) (left anterior fascicular block (LAB] with tachycardia developed in one), RBBB and LAB (n = 1).The LAB was diagnosed on the basis of superior axis shift compared with the preoperative tracings.All had normal PR intervals.HP features may be unmasked by stressing the conduction system.The significance of these elicited conduc- tion findings is unclear because data on the normal electrophysiologic properties of the conduction system in children are limited.Therefore, these features may be functional or pathologic.
Prospective evaluation of methylated<i>SEPT9</i>in plasma for detection of asymptomatic colorectal cancer
Authors: Timothy Robert Church, Michael Wandell, Catherine Lofton-Day, Steven J Mongin, Matthias Burger, Shannon R Payne, Esmeralda Castaños-Vélez, Brent A Blumenstein, Thomas Rösch, Neal Osborn, Dale Snover, Robert W Day, David F Ransohoff
Journal: Gut (2013)

<h3>Background</h3> As screening methods for colorectal cancer (CRC) are limited by uptake and adherence, further options are sought. A blood test might increase both, but none has yet been tested in a screening setting. <h3>Objective</h3> We prospectively assessed the accuracy of circulating methylated <i>SEPT9</i> DNA (mSEPT9) for detecting CRC in a screening population. <h3>Design</h3> Asymptomatic individuals ≥50 years old scheduled for screening colonoscopy at 32 US and German clinics voluntarily gave blood plasma samples before colon preparation. Using a commercially available assay, three independent blinded laboratories assayed plasma DNA of all CRC cases and a stratified random sample of other subjects in duplicate real time PCRs. The primary outcomes measures were standardised for overall sensitivity and specificity estimates. <h3>Results</h3> 7941 men (45%) and women (55%), mean age 60 years, enrolled. Results from 53 CRC cases and from 1457 subjects without CRC yielded a standardised sensitivity of 48.2% (95% CI 32.4% to 63.6%; crude rate 50.9%); for CRC stages I–IV, values were 35.0%, 63.0%, 46.0% and 77.4%, respectively. Specificity was 91.5% (95% CI 89.7% to 93.1%; crude rate 91.4%). Sensitivity for advanced adenomas was low (11.2%). <h3>Conclusions</h3> Our study using the blood based mSEPT9 test showed that CRC signal in blood can be detected in asymptomatic average risk individuals undergoing screening. However, the utility of the test for population screening for CRC will require improved sensitivity for detection of early cancers and advanced adenomas. <h3>Clinical Trial Registration Number:</h3> NCT00855348
Decreased Striatal Dopamine D<sub>1</sub>Receptor- Stimulated Adenylyl Cyclase Activity in Human Methamphetamine Users
Authors: Junchao Tong, Brian M. Ross, Gregory A. Schmunk, Frank J. Peretti, Kathryn S. Kalasinsky, Yoshiaki Furukawa, Lee Cyn Ang, Sally S. Aiken, Dennis J. Wickham, Stephen J. Kish
Journal: American Journal of Psychiatry (2003)

It has been assumed that some behavioral changes associated with repeated exposure to dopaminergic psychostimulant drugs might be explained by changes in activity of dopamine receptors, including the dopamine D(1) receptor, which is linked by a stimulatory G protein to the effector enzyme adenylyl cyclase. To establish whether dopamine D(1) receptor function might be altered in human methamphetamine users, the authors measured dopamine-stimulated adenylyl cyclase activity in the brain of chronic human users of the drug.Adenylyl cyclase activity stimulated by dopamine and by guanylyl-imidodiphosphate (to assess G protein and adenylyl cyclase coupling) was determined in the postmortem brain tissue of 16 methamphetamine users who had used the drug both recently and chronically (i.e., at least 1 year) as well as 21 matched comparison subjects.A 25%-30% decrease in the maximal extent of dopamine stimulation of adenylyl cyclase activity was seen in the striatum (nucleus accumbens, caudate, and putamen) of the methamphetamine users. No changes were found in basal or guanylyl-imidodiphosphate-stimulated enzyme activity.These data suggest that dopamine receptor function linked to adenylyl cyclase is partially desensitized in the striatum of human methamphetamine users. Decreased dopamine D(1) receptor function might underlie part of the known (drug withdrawal syndrome) or expected (drug tolerance) consequences of methamphetamine exposure in humans.
Cellular and Molecular Abnormalities in the Vascular Endothelium of Diabetes Mellitus
Authors: George L. King, Teruo Shiba, Javier Oliver, Toyoshi Inoguchi, Sven-Erik Bursell
Journal: Annual Review of Medicine (1994)

▪ Abstract Diabetic vascular complications affect both micro- and macrovasculature, primarily in the retina, renal glomeruli, and multiple sites in the macrovessels. This review presents a summary of the abnormal function found in vivo and in cultured vascular cells exposed to elevated levels of glucose. We also discuss the various biochemical hypotheses that have been proposed to explain the adverse effects of hyperglycemia on vascular cells.
Mitral Leaflet Adaptation to Ventricular Remodeling
Authors: Miguel Chaput, Mark D. Handschumacher, Francois Tournoux, Lanqi Hua, J. Luis Guerrero, Gus J. Vlahakes, Robert A. Levine
Journal: Circulation (2008)

Background— Functional mitral regurgitation (MR) is caused by systolic traction on the mitral leaflets related to ventricular distortion. Little is known about whether chronic tethering causes the mitral leaflet area to adapt to the geometric needs imposed by tethering, in part because of inability to reconstruct leaflet area in vivo. Our aim was to explore whether adaptive increases in leaflet area occur in patients with functional MR compared with normal subjects and to test the hypothesis that leaflet area influences MR severity. Methods and Results— A new method for 3-dimensional echocardiographic measurement of mitral leaflet area was developed and validated in vivo against 15 sheep heart valves, later excised. This method was then applied in 80 consecutive patients from 3 groups: patients with normal hearts by echocardiography (n=20), patients with functional MR caused by isolated inferior wall-motion abnormality or dilated cardiomyopathy (n=29), and patients with inferior wall-motion abnormality or dilated cardiomyopathy but no MR (n=31). Leaflet area was increased by 35±20% in patients with LV dysfunction compared with normal subjects. The ratio of leaflet to annular area was 1.95±0.40 and was not different among groups, which indicates a surplus leaflet area that adapts to left-heart changes. In contrast, the ratio of total leaflet area to the area required to close the orifice in midsystole was decreased in patients with functional MR compared with those with normal hearts (1.29±0.15 versus 1.78±0.39, P =0.001) and compared with patients with inferior wall-motion abnormality or dilated cardiomyopathy but no MR (1.81±0.38, P =0.001). After adjustment for measures of LV remodeling and tethering, a leaflet-to-closure area ratio &lt;1.7 was associated with significant MR (odds ratio 23.2, 95% confidence interval 2.0 to 49.1, P =0.02). Conclusions— Mitral leaflet area increases in response to chronic tethering in patients with inferior wall-motion abnormality and dilated cardiomyopathy, but the development of significant MR is associated with insufficient leaflet area relative to that demanded by tethering geometry. The varying adequacy of leaflet adaptation may explain in part the heterogeneity of this disease among patients. The results suggest the need to understand the mechanisms that underlie leaflet adaptation and whether leaflet area can potentially be modified as part of the therapeutic approach.
Progress of basic research in Parkinson’s disease in China: data mini-review from the National Natural Science Foundation
Authors: Heqi Cao, Gang Chen, Erdan Dong
Journal: Translational Neurodegeneration (2013)

This review is to analyze the role of National Natural Science Foundation of China (NSFC) on the development of basic research of Parkinson's disease from 1990 to 2012. Data on the total number of projects and funding of NSFC allocated to Parkinson's disease, as well as hotspots in western countries, papers published, awards, personnel training, subject construction were collected, and the role of NSFC on other sources of funding was evaluated. Over the past 23 years, a full range of continuous funding from NSFC has led to fruitful results and a strong impetus to the progress of basic research of Parkinson's disease.
Myeloid Mineralocorticoid Receptor Activation Contributes to Progressive Kidney Disease
Authors: Louis L. Huang, David J. Nikolic-Paterson, Yingjie Han, Elyce Ozols, Frank Y. Ma, Morag J. Young, Greg H. Tesch
Journal: Journal of the American Society of Nephrology (2014)

Clinical and experimental studies have shown that mineralocorticoid receptor (MR) antagonists substantially reduce kidney injury. However, the specific cellular targets and mechanisms by which MR antagonists protect against kidney injury must be identified. We used conditional gene deletion of MR signaling in myeloid cells (MR(flox/flox) LysM(Cre) mice; MyMRKO) or podocytes (MR(flox/flox) Pod(Cre) mice; PodMRKO) to establish the role of MR in these cell types in the development of mouse GN. Accelerated anti-glomerular basement membrane GN was examined in groups of mice: MyMRKO, PodMRKO, wild-type (WT) littermates, and WT mice receiving eplerenone (100 mg/kg twice a day; EPL-treated). At day 15 of disease, WT mice had glomerular crescents (37%±5%), severe proteinuria, and a 6-fold increase in serum cystatin-C. MyMRKO, PodMRKO, and EPL-treated mice with GN displayed proteinuria similar to that in these disease controls. However, MyMRKO and EPL-treated groups had a 35% reduction in serum cystatin-C levels and reduced crescent numbers compared with WT mice, whereas PodMRKO mice were not protected. The protection observed in MyMRKO mice appeared to result predominantly from reduced recruitment of macrophages and neutrophils into the inflamed kidney. Suppression of kidney leukocyte accumulation in MyMRKO mice correlated with reductions in gene expression of proinflammatory molecules (TNF-α, inducible nitric oxide synthase, chemokine (C-C motif) ligand 2, matrix metalloproteinase-12), tubular damage, and renal fibrosis and was similar in EPL-treated mice. In conclusion, MR signaling in myeloid cells, but not podocytes, contributes to the progression of renal injury in mouse GN, and myeloid deficiency of MR provides protection similar to eplerenone in this disease.
Mediators of Chronic Obstructive Pulmonary Disease
Authors: Peter J. Barnes
Journal: Pharmacological Reviews (2004)

Chronic obstructive pulmonary disease (COPD) is a major and increasing global health problem that is now a leading cause of death. COPD is associated with a chronic inflammatory response, predominantly in small airways and lung parenchyma, which is characterized by increased numbers of macrophages, neutrophils, and T lymphocytes. The inflammatory mediators involved in COPD have not been clearly defined, in contrast to asthma, but it is now apparent that many lipid mediators, inflammatory peptides, reactive oxygen and nitrogen species, chemokines, cytokines, and growth factors are involved in orchestrating the complex inflammatory process that results in small airway fibrosis and alveolar destruction. Many proteases are also involved in the inflammatory process and are responsible for the destruction of elastin fibers in the lung parenchyma, which is the hallmark of emphysema. The identification of inflammatory mediators and understanding their interactions is important for the development of anti-inflammatory treatments for this important disease.
Neuronal and glioma-derived stem cell factor induces angiogenesis within the brain
Authors: Lixin Sun, Ai-Min Hui, Qin Su, Alexander Vortmeyer, Yuri Kotliarov, Sandra Pastorino, Antonino Passaniti, Jayant Menon, Jennifer Walling, Rolando Bailey, Marc Rosenblum, Tom Mikkelsen, Howard A. Fine
Journal: Cancer Cell (2006)
In vitro prostacyclin production by ovine uterine and systemic arteries. Effects of angiotensin II.
Authors: R R Magness, K Osei-Boaten, M D Mitchell, C R Rosenfeld
Journal: Journal of Clinical Investigation (1985)

Normal pregnancy is associated with reduced systemic pressor responses to infused angiotensin II (ANG II); furthermore, the uterine vascular bed is even less responsive to vasoconstriction by ANG II than the systemic vasculature overall. The mechanism(s) for this refractoriness remains unknown. To determine if vessel production of prostacyclin may be responsible, uterine and omental artery segments were obtained from four groups of sheep, nonpregnant (NP), pregnant (P; 131 +/- 4 d), early postpartum (2.2 +/- 0.4 d), and late postpartum (16 +/- 2 d), and incubated in Krebs-Henseleit alone or with ANG II in the absence or presence of Saralasin. Prostacyclin was measured as 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). Synthesis of 6-keto-PGF1 alpha was de novo, since aspirin inhibited its formation. P and early uterine arteries produced more 6-keto-PGF1 alpha than NP and late vessels (P less than 0.05): 386 +/- 60 (X +/- SE) and 175 +/- 23 vs. 32 +/- 5 and 18 +/- 4 pg/mg X h, respectively. A similar relationship was observed for omental arteries: 101 +/- 14 and 74 +/- 14 vs. 36 +/- 10 and 22 +/- 4 pg/mg X h, respectively. Furthermore, synthesis by arteries from P and early animals was greater in uterine than omental vessels (P less than 0.05); this was not observed in NP or late vessels. ANG II increased 6-keto-PGF1 alpha production 107 +/- 20% and 92 +/- 16% in P and early uterine arteries only; the threshold dose was between 5 X 10(-11) and 5 X 10(-9) M ANG II. This ANG II-induced increase in 6-keto-PGF1 alpha by uterine arteries was inhibited by Saralasin, which by itself had no effect. During pregnancy, the reduced systemic pressor response to ANG II and the even greater refractoriness of the uterine vascular bed may be reflective of vessel production of the potent vasodilator, prostacyclin. Furthermore, in the uterine vasculature, this antagonism may be potentiated by specific ANG II receptor-mediated increases in prostacyclin.