tbuckley/cabot-search huggingface dataset:
Incomplete Stent Apposition After Implantation of Paclitaxel-Eluting Stents or Bare Metal Stents
Authors: Kengo Tanabe, Patrick W. Serruys, Muzaffer Degertekin, Eberhard Grube, Giulio Guagliumi, Wilhelm Urbaszek, Johannes Bonnier, Jean-Michel Lablanche, Tomasz Siminiak, Jan Nordrehaug, Hans Figulla, Janusz Drzewiecki, Adrian Banning, Karl Hauptmann, Dariusz Dudek, Nico Bruining, Ronald Hamers, Angela Hoye, Jurgen M.R. Ligthart, Clemens Disco, Jörg Koglin, Mary E. Russell, Antonio Colombo
Journal: Circulation (2005)

Background— The clinical impact of late incomplete stent apposition (ISA) for drug-eluting stents is unknown. We sought to prospectively investigate the incidence and extent of ISA after the procedure and at 6-month follow-up of paclitaxel-eluting stents in comparison with bare metal stents (BMS) and survey the clinical significance of ISA over a period of 12 months. Methods and Results— TAXUS II was a randomized, double-blind study with 536 patients in 2 consecutive cohorts comparing slow-release (SR; 131 patients) and moderate-release (MR; 135 patients) paclitaxel-eluting stents with BMS (270 patients). This intravascular ultrasound (IVUS) substudy included patients who underwent serial IVUS examination after the procedure and at 6 months (BMS, 240 patients; SR, 113; MR, 116). The qualitative and quantitative analyses of ISA were performed by an independent, blinded core laboratory. More than half of the instances of ISA observed after the procedure resolved at 6 months in all groups. No difference in the incidence of late-acquired ISA was observed among the 3 groups (BMS, 5.4%; SR, 8.0%; MR, 9.5%; P =0.306), with a similar ISA volume (BMS, 11.4 mm 3 ; SR, 21.7 mm 3 ; MR, 8.5 mm 3 ; P =0.18). Late-acquired ISA was the result of an increase of vessel area without change in plaque behind the stent. Predictive factors of late-acquired ISA were lesion length, unstable angina, and absence of diabetes. No stent thrombosis occurred in the patients diagnosed with ISA over a period of 12 months. Conclusions— The incidence and extent of late-acquired ISA are comparable in paclitaxel-eluting stents and BMS. ISA is a pure IVUS finding without clinical repercussions.
CC chemokine receptor 5 gene polymorphisms in beryllium disease
Authors: H. Sato, L. Silveira, P. Spagnolo, M. Gillespie, E.B. Gottschall, K.I. Welsh, R.M. Du Bois, L.S. Newman, L.A. Maier
Journal: European Respiratory Journal (2010)

CC chemokine receptor 5 (CCR5) is expressed on type-1 T-helper cells, which are involved in the pathogenesis of the granulomatous lung disease chronic beryllium disease (CBD). CCR5 gene ( CCR5 ) polymorphisms are associated with sarcoidosis severity. The present study explores associations between CCR5 polymorphisms and CBD and its disease progression. Eight CCR5 polymorphisms were genotyped in CBD (n = 88), beryllium sensitisation (BeS; n = 86) and beryllium-exposed nondiseased controls (n = 173) using PCR with sequence-specific primers. Pulmonary function and bronchoalveolar lavage data were examined for associations with genotypes. There were no significant differences in genotype and allele frequency between CBD, BeS individuals and controls. In CBD, associations were found with decline in forced expiratory volume in 1 s and forced vital capacity and the CCR5 -3458 thymidine (T)T genotype (p&lt;0.0001), and an increase in alveolar–arterial oxygen tension difference at rest (p = 0.003) and at maximum exercise (p = 0.01) and the -5663 adenine allele. Increased bronchoalveolar lavage lymphocyte numbers were associated with CCR5 -2459 guanine/-2135T (p = 0.01) only in the combined CBD and BeS group. This is the first study showing that CCR5 polymorphisms are associated with worsening pulmonary function over time in CBD, suggesting that CCR5 is important in the progression of pulmonary function in CBD. Further studies would be useful to clarify the mechanism whereby CCR5 polymorphisms affect progression of CBD.
Eccentric training in Achilles tendinopathy: is it harmful to tendon microcirculation?
Authors: Karsten Knobloch
Journal: British Journal of Sports Medicine (2006)

Background: Eccentric training has been shown to reduce pain and gain function in patients with chronic Achilles tendinopathy. However, currently no data are available regarding any potential adverse effects of an eccentric training intervention on Achilles tendon microcirculation. Methods: 59 patients (49 (12) years; body mass index 27 (5); 49 mid-portion, 10 chronic insertional tendinopathy) with 64 symptomatic (54 mid-portion, 10 insertional) Achilles tendons were prospectively enrolled. Baseline tendon microcirculation at four distinct tendon positions from the insertion to the proximal mid-portion area was assessed using a laser Doppler system for capillary blood flow, tissue oxygen saturation and postcapillary venous filling pressure. A 12-week daily painful home-based eccentric training regimen was initiated (3×15 repetitions per tendon and day). Results: Achilles tendon capillary blood flow was significantly reduced at the insertion (by 35%, p = 0.008) and the distal mid-portion area (by 45%, p = 0.015) at 2 mm and by 22% (p = 0.007) and 13% (p = 0.122) at 8 mm tissue depths, respectively. Achilles tendon oxygen saturation was not decreased after the 12-week eccentric training regimen throughout the insertion to the proximal mid-portion area (insertion 72 (13) vs 73 (10), proximal mid-portion 63 (13) vs 62 (11), both NS). Achilles tendon postcapillary venous filling pressures were significantly reduced at the insertion (51 (16) vs 41 (19), p = 0.001) and the distal mid-portion (36 (13) vs 32 (12), p = 0.037) at 2 mm and at the insertion at 8 mm (63 (19) vs 51 (13), p = 0.0001). Pain was reduced from 5.4 (2.1) to 3.6 (2.4; p = 0.001) in the mid-portion and from 6 (2.5) to 3.2 (2.7; p = 0.002) in the insertional tendinopathy group. No Achilles tendon rupture or any interruption during the eccentric training was noted among the 59 patients. Conclusion: Daily eccentric training for Achilles tendinopathy is a safe and easy measure, with beneficial effects on the microcirculatory tendon levels without any evident adverse effects in both mid-portion and insertional Achilles tendinopathy.
Fatty acid binding protein-4 (FABP4) is a hypoxia inducible gene that sensitizes mice to liver ischemia/reperfusion injury
Authors: Bingfang Hu, Yan Guo, Wojciech G. Garbacz, Mengxi Jiang, Meishu Xu, Hai Huang, Allan Tsung, Timothy R. Billiar, Sadeesh K. Ramakrishnan, Yatrik M. Shah, Karen S.L. Lam, Min Huang, Wen Xie
Journal: Journal of Hepatology (2015)
Thoracic high resolution computed tomography may be helpful in the differentiation between the patients with chronic obstructive pulmonary disease and the smoking patients with asthma
Authors: Kursat Epozturk, Serdar Berk, Oznur Abadoglu, Omer Tamer Dogan, Emel Atayik
Journal: European Respiratory Journal (2013)

Introduction: Although several approaches are used for the differentiation of asthma and chronic obstructive pulmonary disease (COPD), it may still be challenging in some cases, especially the smokers.  Objective: This study aimed to determine whether thoracic high-resolution computed tomography (HRCT) could help differentiate between smoker asthma patients and COPD sufferers.  Methods: The results of the patients who underwent thoracic HRCT within the five-year period before January 2010 while being followed up with the diagnoses of asthma (59 smoker, 58 non-smoker) or COPD (n: 87) were retrospectively analyzed.  Results: In the COPD group, male patients were more frequent and the mean age was higher. The age of start of symptoms was lower in smoker asthma patients. Thoracic HRCT result was reported as normal much more frequently in the smoker asthma group (32% vs. 1%) whereas emphysema (45% vs. 12%) was more prevalent in COPD group. The radiological comparison of smoker asthma and non-smoker asthma groups yielded no difference.  Conclusion: Although no innovative method or state-of-the-art technology was used in this retrospective study, it was found that even conventional HRCT might contribute to the differentiation of these two diseases.
Isolation of drug delivery from drug effect: Problems of optimizing drug delivery parameters1
Authors: Mir J. Ali, Yot Navalitloha, Michael W. Vavra, Eric W.-Y. Kang, Andrea C. Itskovich, Peter Molnar, Robert M. Levy, Dennis R. Groothuis
Journal: Neuro-Oncology (2006)

A recurring question in the treatment of malignant brain tumors has been whether treatment failure is due to inadequate delivery or ineffective drugs. To isolate these issues, we tested a paradigm in which the "therapeutic" agent was a toxin about which there could be no question of efficacy, provided it was delivered in adequate amounts; we used 10% formalin. We infused 10% formalin into 5- to 8-mm subcutaneous RG-2 and D54-MG gliomas at increasing rates until we achieved 100% tumor cell kill. In RG-2 gliomas, infusions of 10 μl/h × 7 days, and 2, 4, 6, and 8 μl/min × 2 h failed to kill tumors, although growth was delayed, while infusion rates of 12 μl/min × 60 min and 48 μl/min × 15 min produced 100% tumor kill. In D54-MG tumors, infusions of 4, 8, and 24 μl/min produced 100% tumor kill. 14C-Formalin autoradiographs showed a heterogeneous distribution after infusions of 2 μl/min × 2 h, whereas infusions of 48 μl/min × 15 min showed a homogeneous distribution within the tumor, but more than 95% of tissue radioactivity was found in tissue surrounding tumor. Drug delivery remains a major issue in brain tumor treatment: Distribution inhomogeneity, rapid efflux, and consequent treatment failures are likely due to high interstitial fluid pressure. Because the infusion rates being used in the treatment of human brain tumors are low and the tumors are larger, treatment failures can be expected on the basis of inadequate drug delivery alone, regardless of the effectiveness of the drug.
Effects of Percutaneous Coronary Interventions in Silent Ischemia After Myocardial Infarction
Authors: Paul Erne, Andreas W. Schoenenberger, Dieter Burckhardt, Michel Zuber, Wolfgang Kiowski, Peter T. Buser, Paul Dubach, Therese J. Resink, Matthias Pfisterer
Journal: JAMA (2007)

ContextThe effect of a percutaneous coronary intervention (PCI) on the long-term prognosis of patients with silent ischemia after a myocardial infarction (MI) is not known.ObjectiveTo determine whether PCI compared with drug therapy improves long-term outcome of asymptomatic patients with silent ischemia after an MI.Design, Setting, and ParticipantsRandomized, unblinded, controlled trial (Swiss Interventional Study on Silent Ischemia Type II [SWISSI II]) conducted from May 2, 1991, to February 25, 1997, at 3 public hospitals in Switzerland of 201 patients with a recent MI, silent myocardial ischemia verified by stress imaging, and 1- or 2-vessel coronary artery disease. Follow-up ended on May 23, 2006.InterventionsPercutaneous coronary intervention aimed at full revascularization (n = 96) or intensive anti-ischemic drug therapy (n = 105). All patients received 100 mg/d of aspirin and a statin.Main Outcome MeasuresSurvival free of major adverse cardiac events defined as cardiac death, nonfatal MI, and/or symptom-driven revascularization. Secondary measures included exercise-induced ischemia and resting left ventricular ejection fraction during follow-up.ResultsDuring a mean (SD) follow-up of 10.2 (2.6) years, 27 major adverse cardiac events occurred in the PCI group and 67 events occurred in the anti-ischemic drug therapy group (adjusted hazard ratio, 0.33; 95% confidence interval, 0.20-0.55; P&lt;.001), which corresponds to an absolute event reduction of 6.3% per year (95% confidence interval, 3.7%-8.9%; P&lt;.001). Patients in the PCI group had lower rates of ischemia (11.6% vs 28.9% in patients in the drug therapy group at final follow-up; P = .03) despite fewer drugs. Left ventricular ejection fraction remained preserved in PCI patients (mean [SD] of 53.9% [9.9%] at baseline to 55.6% [8.1%] at final follow-up) and decreased significantly (P&lt;.001) in drug therapy patients (mean [SD] of 59.7% [11.8%] at baseline to 48.8% [7.9%] at final follow-up).ConclusionAmong patients with recent MI, silent myocardial ischemia verified by stress imaging, and 1- or 2-vessel coronary artery disease, PCI compared with anti-ischemic drug therapy reduced the long-term risk of major cardiac events.Trial Registrationclinicaltrials.gov Identifier: NCT00387231
Standardization of flow cytometry in myelodysplastic syndromes: a report from an international consortium and the European LeukemiaNet Working Group
Authors: T M Westers, R Ireland, W Kern, C Alhan, J S Balleisen, P Bettelheim, K Burbury, M Cullen, J A Cutler, M G Della Porta, A M Dräger, J Feuillard, P Font, U Germing, D Haase, U Johansson, S Kordasti, M R Loken, L Malcovati, J G te Marvelde, S Matarraz, T Milne, B Moshaver, G J Mufti, K Ogata, A Orfao, A Porwit, K Psarra, S J Richards, D Subirá, V Tindell, T Vallespi, P Valent, V H J van der Velden, T M de Witte, D A Wells, F Zettl, M C Béné, A A van de Loosdrecht
Journal: Leukemia (2012)
The Rickettsia-like Organisms TATLOCK (1943) and HEBA (1959): Bacteria Phenotypically Similar to but Genetically Distinct from <i>Legionella pneumophila</i> and the WIGA Bacterium
Authors: G. ANN HÉBERT, C. WAYNE MOSS, LINDA KIRVEN McDOUGAL, F. MARILYN BOZEMAN, ROGER M. McKINNEY, DON J. BRENNER
Journal: Annals of Internal Medicine (1980)

Two "rickettsia-like organisms," TATLOCK and HEBA, isolated from human blood via guinea pigs and embryonated eggs in 1943 and 1959, respectively, have been cultured on artificial media (charcoal yeast extract agar) for the first time and characterized. TATLOCK and HEBA have identical cultural, biochemical, and antigenic characteristics, as well as identical cellular fatty-acid composition and antimicrobial susceptibilities. These two bacteria have most of the cultural and biochemical characteristics of Legionella pneumophila, and their gas-liquid chromatography cellular fatty-acid profile is similar to that of WIGA, another bacterium similar to L. pneumophila. Direct fluorescent-antibody reagents prepared for HEBA and TATLOCK gave equal high-titered reciprocal staining and were negative on 220 other bacteria, including L. pneumophila. Deoxyribonucleic acid relatedness studies, however, showed that these bacteria are not genetically related to either L. pneumophila or the WIGA bacterium.
Intratumoral production of interleukin-5 leading to paraneoplastic peripheral eosinophilia in hepatocellular carcinoma
Authors: Axel Balian, Eric Bonte, Sylvie Naveau, Arnaud Foussat, Laurence Bouchet-Delbos, Dominique Berrebi, Corinne Vons, Fredérique Capron, Jean-Claude Chaput, Dominique Emilie
Journal: Journal of Hepatology (2001)
The Assessment of Drug-Dependent and Isoimmune Antiplatelet Antibodies by the Use of Platelet Aggregometry
Authors: Daniel Deykin, Lewis J. Hellerstein
Journal: Journal of Clinical Investigation (1972)

The technique of platelet aggregometry provides a simple, quantitative, and specific method for the detection of drug-dependent and isoimmune antiplatelet antibodies. In the presence of antiquinidine antibody, quinidine causes lysis of normal platelets in platelet-rich plasma. The resulting changes in optical density are readily detected in the aggregometer. The initial rate of lysis is a function of the antibody titer, but is relatively independent of the platelet count. In vitro, quinidine produces platelet swelling and inhibits aggregation of platelets by adenosine diphosphate, epinephrine, and collagen. Isoimmune antibodies cause aggregation of platelets in platelet-rich plasma. In studies of a single family the rate of aggregation is proportional to the number of HL-A antigens present on the normal platelets against which the antibody is directed. The simple technique of platelet aggregometry may be a useful adjunct in the selection of compatible donors for platelet transfusion. Serum derived from patients with idiopathic thromboytopenic purpura did not cause platelet aggregation.
Prevention of obesity in mice by antisense oligonucleotide inhibitors of stearoyl-CoA desaturase–1
Authors: Guoqiang Jiang, Zhihua Li, Franklin Liu, Kenneth Ellsworth, Qing Dallas-Yang, Margaret Wu, John Ronan, Christine Esau, Cain Murphy, Deborah Szalkowski, Raynald Bergeron, Thomas Doebber, Bei B. Zhang
Journal: Journal of Clinical Investigation (2005)

Effective therapies for the treatment of obesity, a key element of metabolic syndrome, are urgently needed but currently lacking. Stearoyl-CoA desaturase-1 (SCD1) is the rate-limiting enzyme catalyzing the conversion of saturated long-chain fatty acids into monounsaturated fatty acids, which are major components of triglycerides. In the current study, we tested the efficacy of pharmacological inhibition of SCD1 in controlling lipogenesis and body weight in mice. SCD1-specific antisense oligonucleotide inhibitors (ASOs) reduced SCD1 expression, reduced fatty acid synthesis and secretion, and increased fatty acid oxidization in primary mouse hepatocytes. Treatment of mice with SCD1 ASOs resulted in prevention of diet-induced obesity with concomitant reductions in SCD1 expression and the ratio of oleate to stearoyl-CoA in tissues and plasma. These changes correlated with reduced body adiposity, hepatomegaly and steatosis, and postprandial plasma insulin and glucose levels. Furthermore, SCD1 ASOs reduced de novo fatty acid synthesis, decreased expression of lipogenic genes, and increased expression of genes promoting energy expenditure in liver and adipose tissues. Thus, SCD1 inhibition represents a new target for the treatment of obesity and related metabolic disorders.
Simultaneous measurement of collagen type-VI-related antigen and procollagen type-III-N-propeptide levels in bronchoalveolar lavage
Authors: T Schaberg, K Orzechowski, C Oesterling, H Lode, D Schuppan
Journal: European Respiratory Journal (1994)

Abnormal collagen metabolism is a hallmark of diffuse lung disease. Biochemical parameters which are correlated with collagen synthesis and degradation may be helpful to monitor fibrosis. In this study, we compared the sensitivity and specificity of procollagen type-III-N-propeptide (PIIINP) and collagen type-VI (C-VI) related antigen levels, as well as a ratio of both parameters (PIIINP/C-VI), in bronchoalveolar lavage fluid (BALF) from patients with diffuse and localized lung disease. We investigated 45 patients with diffuse lung disease (idiopathic pulmonary fibrosis (IPF), n = 21; sarcoidosis, n = 13; and lymphangitic carcinomatosis (LC), n = 11); 58 control subjects; and 92 patients with localized lung disease (bronchial carcinoma, n = 37; pulmonary tuberculosis, n = 31; and pneumonia, n = 24). C-VI and PIIINP were measured by immunoassay in concentrated BALF. Although the PIIINP and C-VI levels were increased in diffuse lung disease, the sensitivity of the individual parameters PIIINP and C-VI was low (IPF: PIIINP = 0.62, C-VI = 0.29; LC: PIIINP = 0.64, C-VI = 0.45; sarcoidosis: PIIINP = 0.69, C-VI = 0.15). When calculating the ratio of PIIINP/C-VI for each individual patient, we found a significant increase in this ratio in IPF (1.28 +/- 0.7), LC (2.34 +/- 1.2), and sarcoidosis (0.26 +/- 0.08) compared to both the controls (0.02 +/- 0.01) and other localized lung diseases (bronchial carcinoma 0.05 +/- 0.01; pulmonary tuberculosis 0.02 +/- 0.01), with the exception of pneumonia (0.18 +/- 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)
β2 integrin mediates hantavirus-induced release of neutrophil extracellular traps
Authors: Martin J. Raftery, Pritesh Lalwani, Ellen Krautkrӓmer, Thorsten Peters, Karin Scharffetter-Kochanek, Renate Krüger, Jörg Hofmann, Karl Seeger, Detlev H. Krüger, Günther Schönrich
Journal: The Journal of Experimental Medicine (2014)

Rodent-borne hantaviruses are emerging human pathogens that cause severe human disease. The underlying mechanisms are not well understood, as hantaviruses replicate in endothelial and epithelial cells without causing any cytopathic effect. We demonstrate that hantaviruses strongly stimulated neutrophils to release neutrophil extracellular traps (NETs). Hantavirus infection induced high systemic levels of circulating NETs in patients and this systemic NET overflow was accompanied by production of autoantibodies to nuclear antigens. Analysis of the responsible mechanism using neutrophils from β2 null mice identified β2 integrin receptors as a master switch for NET induction. Further experiments suggested that β2 integrin receptors such as complement receptor 3 (CR3) and 4 (CR4) may act as novel hantavirus entry receptors. Using adenoviruses, we confirmed that viral interaction with β2 integrin induced strong NET formation. Collectively, β2 integrin–mediated systemic NET overflow is a novel viral mechanism of immunopathology that may be responsible for characteristic aspects of hantavirus-associated disease such as kidney and lung damage.
Falls in older women are not reduced by exercise or vitamin D, study finds
Authors: J. Wise
Journal: BMJ (2015)

The overall rate of falls among older women is not reduced by exercise training or vitamin D supplements, a randomised trial has found. But the study, published in JAMA Internal Medicine , found that strength and balance training cut the number of injurious falls by more than half.1

The two year Finnish study included 409 women aged 70 to 80 who lived at home. They had all fallen at least once during the previous year and were not taking vitamin D supplements before the study. The women were randomised into four groups: vitamin D …
Lin-7C/VELI3/MALS-3: An Essential Component in Metastasis of Human Squamous Cell Carcinoma
Authors: Takeshi Onda, Katsuhiro Uzawa, Dai Nakashima, Kengo Saito, Yasuo Iwadate, Naohiko Seki, Takahiko Shibahara, Hideki Tanzawa
Journal: Cancer Research (2007)

Abstract Using proteomic selection, functional verification, and clinical validation, we identified specific down-regulation of Lin-7C/VELI3/MALS-3 (Lin-7C), which marks oral squamous cell carcinoma (OSCC) metastasis. Despite a rarity of sequence variations in the Lin-7C gene in both primary OSCC and OSCC-derived cells, a high prevalence of hypermethylation was detected in the CpG island region that strongly correlated with its down-regulation. Inducible Lin-7C mRNA by experimental demethylation was found in all OSCC cells tested. Overexpression of the Lin-7C gene in an OSCC cell clone does not contribute to underproliferation but results in a noninvasive phenotype with elevated β-catenin expression. Experimental metastases in multiple organs of immunodeficient mice were inhibited in cells expressing Lin-7C. Finally, the Lin-7C expression status in primary tumors afforded significantly (P &amp;lt; 0.001) high accuracy for predicting lymph node metastasis. These results establish Lin-7C as a novel target of early detection, prevention, and therapy for OSCC metastasis. [Cancer Res 2007;67(20):9643–8]