tbuckley/cabot-search huggingface dataset:
Infective complications from endobronchial ultrasound-transbronchial needle aspiration
Authors: D. P. Steinfort, D. F. Johnson, L. B. Irving
Journal: European Respiratory Journal (2009)

To the Editors: 

We read with significant interest the report from Haas 1 in a recent issue of the European Respiratory Journal , which described two cases of infectious complications following endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA). This technique has been widely adopted for the evaluation of mediastinal and hilar lesions for several reasons, including its high-diagnostic accuracy, minimally invasive nature and excellent safety profile. As stated by Haas 1, no significant complications have previously been reported.

We recently experienced a similar complication in our interventional bronchoscopy centre (Royal Melbourne Hospital, Parkville, Australia). A female with small cell lung cancer and a moderate-sized retrosternal thyroid lesion underwent EBUS-TBNA sampling of the thyroid lesion for the purpose of staging. …
RETRACTED ARTICLE: miR-663 attenuates tumor growth and invasiveness by targeting eEF1A2 in pancreatic cancer
Authors: Wenqiao Zang, Yuanyuan Wang, Tao Wang, Yuwen Du, Xiaonan Chen, Min Li, Guoqiang Zhao
Journal: Molecular Cancer (2015)

miR-663 is associated with many important biologic processes, such as the evolution, development, viral infection, inflammatory response, and carcinogenesis among vertebrates. However, the molecular function and mechanism of miR-663 in pancreatic cancer growth and invasion is still unclear. Western blot and real-time PCR were used to study the expression level of eEF1A2 protein and miR-663 in pancreatic cancer tissues and cell lines. The Pearson χ 2 test was used to determine the correlation between miR-663 expression and clinicopathologic features of patients. Patients’ survival was analyzed using the Kaplan–Meier method, using the log-rank test for comparison. The biological function of miR-663 was examined by measuring cell growth, cell invasion and apoptosis analysis in vitro and in vivo. miR-663 target gene and signaling pathway was identified by luciferase activity assay and western blot. We found that, in pancreatic cancer, eEF1A2 was significantly upregulated but miR-663 was significantly downregulated. Further results showed that the expression level of eEF1A2 and miR-663 was strongly associated with TNM stage and node metastasis status of the patients. miR-663 and eEF1A2 were inversely correlated with each other, and the changes in the expression levels of each can also predict the survival of patients with pancreatic cancer. We identified miR-663 as a tumor attenuate molecular that attenuated the proliferation and invasion of pancreatic cancer cells both in vitro and in vivo. Finally, we confirmed that the expression of eEF1A2 can partially restore the pro-apoptotic and anti-invasion functions of miR-663. miR-663 attenuated the proliferation and invasion of pancreatic cells both in vitro and in vivo by directly targeting eEF1A2. miR-663 and eEF1A2 might be potential targets for the treatment of pancreatic cancer in the future.
Suicide Risk in Placebo-Controlled Studies of Major Depression
Authors: Jitschak G. Storosum, Barbara J. van Zwieten, Wim van den Brink, Berthold P.R. Gersons, André W. Broekmans
Journal: American Journal of Psychiatry (2001)

The purpose of this study was to determine if fear of an increased risk of attempted suicide in placebo groups participating in placebo-controlled studies is an argument against the performance of placebo-controlled trials in studies of major depression.All short-term and long-term, placebo-controlled, double-blind studies that were part of a registration dossier for the indication of major depression that were submitted to the Medicines Evaluation Board, the regulatory authority of the Netherlands, from 1983 to 1997 were reviewed for attempted suicide. In addition, all long-term, placebo-controlled studies from a MEDLINE search that were conducted in the last decade in patients with major depression were assessed for attempted suicide.In 77 short-term studies with 12,246 patients in dossiers from the Medicines Evaluation Board, the incidence of suicide was 0.1% in both placebo groups and active compound groups. The incidence of attempted suicide was 0.4% in both placebo groups and active compound groups. In eight long-term studies with 1,949 patients, the incidence of suicide in the placebo groups was 0.0% and 0.2% in the active compound groups. Attempted suicide occurred in 0.7% of both placebo groups and active compound groups. In seven long-term MEDLINE studies, the incidence of attempted suicide in the placebo groups was not higher than in the groups treated with active compound.Fear of increased risk of attempted suicide in the placebo groups should not be an argument against performing short-term and long-term, placebo-controlled trials in major depression.
Vascular endothelial dysfunction and superoxide anion production in heart failure are p38 MAP kinase-dependent
Authors: J WIDDER, T BEHR, D FRACCAROLLO, K HU, P GALUPPO, P TAS, C ANGERMANN, G ERTL, J BAUERSACHS
Journal: Cardiovascular Research (2004)

The mitogen-activated protein (MAP) kinase system, especially the p38 MAP kinase, is activated in chronic heart failure (CHF). However, the role of vascular p38 MAP kinase in CHF has not been analyzed yet.In aortic rings from rats with CHF 10 weeks after myocardial infarction, acetylcholine-induced relaxation was attenuated (maximum relaxation, Rmax: 54+/-5%) compared to sham-operated animals (Rmax: 77+/-5%, p<0.01), while endothelium-independent relaxation elicited by sodium nitroprusside was not significantly changed. Aortic levels of phosphorylated p38 MAP kinase protein were significantly elevated in rats with CHF. In addition, phosphorylation of MAP kinase-activated protein kinase-2 (MAPKAPK-2), an index of p38 MAP kinase activity, was increased. Aortic superoxide anion generation was significantly enhanced in rats with CHF accompanied by elevation of the NAD(P)H oxidase subunit p47phox protein expression. Inhibition of p38 MAP kinase by treatment with the p38 MAP kinase inhibitor SB239063 (800 ppm in standard rat chow) reduced MAPKAPK-2 phosphorylation, preserved acetylcholine-induced relaxation (Rmax: 80+/-4%, p<0.01), and reduced vascular superoxide formation. SB239063 treatment did not affect blood pressure and left ventricular enddiastolic pressure. In aortic tissue from CHF animals treated with the angiotensin-converting enzyme (ACE) inhibitor trandolapril, p38 MAP kinase phosphorylation was significantly reduced.Vascular p38 MAP kinase is markedly activated in rats with CHF. Chronic p38 MAP kinase inhibition with SB239063 prevented endothelial vasomotor dysfunction through reduction of superoxide anion production.
Lipopolysaccharide (LPS)-induced Macrophage Activation and Signal Transduction in the Absence of Src-Family Kinases Hck, Fgr, and Lyn
Authors: Fanying Meng, Clifford A. Lowell
Journal: The Journal of Experimental Medicine (1997)

Lipopolysaccharide (LPS) stimulates immune responses by interacting with the membrane receptor CD14 to induce the generation of cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6. The mechanism by which the LPS signal is transduced from the extracellular environment to the nuclear compartment is not well defined. Recently, an increasing amount of evidence suggests that protein tyrosine kinases especially the Src-family kinases Hck, Fgr, and Lyn, play important roles in LPS signaling. To directly address the physiological function of Hck, Fgr and Lyn in LPS signaling, a genetic approach has been used to generate null mutations of all three kinases in a single mouse strain. hck−/−fgr−/−lyn−/− mice are moderately healthy and fertile; macrophages cultured from these mice express normal levels of CD14 and no other Src-family kinases were detected. Although the total protein phosphotyrosine level is greatly reduced in macrophages derived from hck−/−fgr−/−lyn−/− mice, functional analyses indicate that both elicited peritoneal (PEMs) and bone marrow–derived macrophages (BMDMs) from triple mutant mice have no major defects in LPS-induced activation. Nitrite production and cytokine secretion (IL-1, IL-6, and TNF-α) are normal or even enhanced in hck−/−fgr−/−lyn−/− macrophages after LPS stimulation. The development of tumor cell cytotoxicity is normal in triple mutant BMDMs and only partially impaired in PEMs after LPS stimulation. Furthermore, the activation of the ERK1/2 and JNK kinases, as well as the transcription factor NF-κB, are the same in normal and mutant macrophages after LPS stimulation. The current study provides direct evidence that three Src-family kinases Hck, Fgr, and Lyn are not obligatory for LPS-initiated signal transduction.
Tumor Endothelial Cells Express Epidermal Growth Factor Receptor (EGFR) but not ErbB3 and Are Responsive to EGF and to EGFR Kinase Inhibitors
Authors: Dhara N. Amin, Kyoko Hida, Diane R. Bielenberg, Michael Klagsbrun
Journal: Cancer Research (2006)

Abstract Epidermal growth factor (EGF) receptor family members are expressed by tumor cells and contribute to tumor progression. The expression and activity of EGF receptors in endothelial cells are less well characterized. Analysis of tumor-derived endothelial cells showed that they express EGFR, ErbB2, and ErbB4, whereas their normal counterparts express ErbB2, ErbB3, and ErbB4. The gain in expression of EGFR and the loss of ErbB3 expression in tumor vasculature was also observed in vivo. As a consequence of their expressing EGFR, tumor endothelial cells responded to EGF and other EGF family members by activating both EGFR and ErbB2, by activating the downstream mitogen-activated protein kinase pathway, and by enhanced proliferation. On the other hand, normal endothelial cells did not respond to EGF but instead were responsive to neuregulin (NRG), a ligand for ErbB3 and ErbB4. NRG activated ErbB3 in normal endothelial cells and inhibited growth of these cells. In contrast, tumor endothelial cells, which do not express ErbB3, were not growth inhibited by NRG. Furthermore, due to their expression of EGFR, tumor endothelial cells, unlike normal endothelial cells, are direct targets for EGFR kinase inhibitors. These low-molecular-weight compounds block EGF-induced EGFR activation and proliferation of tumor endothelial cells. These results suggest that a gain of EGF-induced endothelial cell proliferation, and loss of NRG-induced growth inhibition in tumor endothelial cells constitutes a switch that promotes tumor angiogenesis. In addition, these results suggest that EGFR kinase inhibitors may be effective for antiangiogenesis therapy by specifically targeting the tumor, but not the normal, vasculature. (Cancer Res 2006; 66(4): 2173-80)
Response of pulmonary tuberculomas to anti-tuberculous treatment
Authors: H.S. Lee, J.Y. Oh, J.H. Lee, C.G. Yoo, C‐T. Lee, Y.W. Kim, S.K. Han, Y‐S. Shim, J-J. Yim
Journal: European Respiratory Journal (2004)

Pulmonary tuberculomas are well-circumscribed masses caused by Mycobacterium tuberculosis . However, the response of tuberculomas to anti-tuberculous (TB) treatment has not been well defined as yet. The response of pulmonary tuberculomas to anti‐TB treatment was retrospectively reviewed in 45 patients diagnosed between January 1997 and December 2001. The areas of pulmonary tuberculomas were estimated by calculating products of the longest and their perpendicular short diameters on chest radiographs. The response to anti‐TB treatment was categorised as “decreased” (&gt;25% reduction in area versus its initial area), “increased” (&gt;25% increase) and “no change” (the remainder). The mean of treatment duration was 11.5±3.6 months. Three months after treatment, 18 patients (40.0%) were categorised as decreased, 25 (55.6%) as no change and two (4.4%) as increased. Twelve months after treatment, out of 42 patients available for chest radiographs, 32 patients (76.2%) were categorised as decreased, nine (21.4%) as no change and one patient (2.4%) as increased. At the last follow-up (mean follow-up 27.0±10.2 months), 37 patients (82.2%) were categorised as decreased. The majority of pulmonary tuberculomas were decreased by anti-tuberculosis treatment during and even after treatment, although a transient enlargement during the early period of treatment was observed infrequently.
Fibrates increase human apolipoprotein A-II expression through activation of the peroxisome proliferator-activated receptor.
Authors: N Vu-Dac, K Schoonjans, V Kosykh, J Dallongeville, J C Fruchart, B Staels, J Auwerx
Journal: Journal of Clinical Investigation (1995)

In view of the evidence linking plasma high density lipoprotein (HDL)-cholesterol levels to a protective effect against coronary artery disease and the widespread use of fibrates in the treatment of hyperlipidemia, the goal of this study was to analyze the influence of fibrates on the expression of apolipoprotein (apo) A-II, a major protein constituent of HDL. Administration of fenofibrate (300 mg/d) to 16 patients with coronary artery disease resulted in a marked increase in plasma apo A-II concentrations (0.34 +/- 0.11 to 0.45 +/- 0.17 grams/liter; P < 0.01). This increase in plasma apo A-II was due to a direct effect on hepatic apo A-II production, since fenofibric acid induced apo A-II mRNA levels to 450 and 250% of control levels in primary cultures of human hepatocytes and in human hepatoblastoma HepG2 cells respectively. The induction in apo A-II mRNA levels was followed by an increase in apo A-II secretion in both cell culture systems. Transient transfection experiments of a reporter construct driven by the human apo A-II gene promoter indicated that fenofibrate induced apo A-II gene expression at the transcriptional level. Furthermore, several other peroxisome proliferators, such as the fibrate, Wy-14643, and the fatty acid, eicosatetraynoic acid (ETYA), also induced apo A-II gene transcription. Unilateral deletions and site-directed mutagenesis identified a sequence element located in the J-site of the apo A-II promoter mediating the responsiveness to fibrates and fatty acids. This element contains two imperfect half sites spaced by 1 oligonucleotide similar to a peroxisome proliferator responsive element (PPRE). Cotransfection assays showed that the peroxisome proliferator activated receptor (PPAR) transactivates the apo A-II promoter through this AII-PPRE. Gel retardation assays demonstrated that PPAR binds to the AII-PPRE with an affinity comparable to its binding affinity to the acyl coA oxidase (ACO)-PPRE. In conclusion, in humans fibrates increase plasma apo A-II concentrations by inducing hepatic apo A-II production. Apo A-II expression is regulated at the transcriptional level by fibrates and fatty acids via the interaction of PPAR with the AII-PPRE, thereby demonstrating the pivotal role of PPAR in controlling human lipoprotein metabolism.
Interaction of the selectin ligand PSGL-1 with chemokines CCL21 and CCL19 facilitates efficient homing of T cells to secondary lymphoid organs
Authors: Krystle M Veerman, Michael J Williams, Kenji Uchimura, Mark S Singer, Jasmeen S Merzaban, Silvia Naus, Douglas A Carlow, Philip Owen, Jesús Rivera-Nieves, Steven D Rosen, Hermann J Ziltener
Journal: Nature Immunology (2007)
Lead, Cadmium, Smoking, and Increased Risk of Peripheral Arterial Disease
Authors: Ana Navas-Acien, Elizabeth Selvin, A. Richey Sharrett, Emma Calderon-Aranda, Ellen Silbergeld, Eliseo Guallar
Journal: Circulation (2004)

Background— Lead and cadmium exposure may promote atherosclerosis, although the cardiovascular effects of chronic low-dose exposure are largely unknown. The objective of the present study was to evaluate the association between blood levels of lead and cadmium and peripheral arterial disease. Methods and Results— We analyzed data from 2125 participants who were ≥40 years of age in the 1999 to 2000 National Health and Nutrition Examination Survey (NHANES). Peripheral arterial disease was defined as an ankle brachial index &lt;0.9 in at least 1 leg. Lead and cadmium levels were measured by atomic absorption spectrometry. After adjustment for demographic and cardiovascular risk factors, the ORs of peripheral arterial disease comparing quartiles 2 to 4 of lead with the lowest quartile were 1.63 (95% CI, 0.51 to 5.15), 1.92 (95% CI, 0.62 to 9.47), and 2.88 (95% CI, 0.87 to 9.47), respectively ( P for trend=0.02). The corresponding ORs for cadmium were 1.07 (95% CI, 0.44 to 2.60), 1.30 (95% CI, 0.69 to 2.44), and 2.82 (95% CI, 1.36 to 5.85), respectively ( P for trend=0.01). The OR of peripheral arterial disease for current smokers compared with never smokers was 4.13. Adjustment for lead reduced this OR to 3.38, and adjustment for cadmium reduced it to 1.84. Conclusions— Blood lead and cadmium, at levels well below current safety standards, were associated with an increased prevalence of peripheral arterial disease in the general US population. Cadmium may partially mediate the effect of smoking on peripheral arterial disease.
HLA-B27+ anterior uveitis with or without associated spondyloarthritis: clinical and immunological features
Authors: F. RIVERA-CIVICO, J. JIMENEZ-ALONSO, M. MARTIN-ARMADA, M. T. HERRANZ, J. CASTRO, F. PEREZ-ALVAREZ, J L DEL ARBOL, M. TORIBIO, F. SAMANIEGO
Journal: Annals of the Rheumatic Diseases (1999)

Anterior uveitis (AU) is the most common form of uveitis,1-3 and may be produced by different causes. An aetiological diagnosis is commonly established in approximately half of the patients with AU, being seronegative spondyloarthropathies (SA), and mainly ankylosing spondylitis, the most frequent cause of the disease. Approximately 50% of the patients with AU are HLA-B27 positive; half of them usually presenting with associated SA,4-8 the other half are patients with HLA-B27+ but with no associated articular disease (HLA-B27+ AU). Several clinical features have been described to be common in patients with AU associated with HLA-B27, however, these features are similar either in patients with or without associated SA.9 10 This is why we conducted this clinical and immunological study in patients with AU positive for HLA-B27 with the aim of discovering the differences between …
Patients With Cirrhosis and Denied Liver Transplants Rarely Receive Adequate Palliative Care or Appropriate Management
Authors: Zafrina Poonja, Amanda Brisebois, Sander Veldhuyzen van Zanten, Puneeta Tandon, Glenda Meeberg, Constantine J. Karvellas
Journal: Clinical Gastroenterology and Hepatology (2013)
A Successful Case of Inguinal Colotomy for Absence of Rectum in a Child Five Days Old
Authors: T. A. Helme
Journal: BMJ (1890)

myself justified in again trying a purgative, and gave ol.ricini ^i and ol.tiglii iltj; this produced a scanty evacuation, but there was a slight increase in the pain and no amelioration of any of the other symptoms.Examination of the abdomen gave the same negative result as before, but he still suffered the same dull dragging pain of which he had complained all along.Opium and general treatment by rest continued.October 26th.He seemed so well, with the exception of the comparatively slight pain, that I gave him a calomel and jalap purgative the evening before, followed by a saline in the morning, and a slight action of the bowels resulted; the pain diminished, and I hoped that the obstruction had been overcome.Opium discontinued.October 27th.Allowed to get up a little; but that seemed to cause a return of the pain, and he still was unable to straighten himself properly.October 28th.Pain much worse; face distinctly anxious; recourse again had to opium and confinement to the bunk.October 29th.Vomited for the first time; pain was not so much relieved by opium as formerly.October 31st.Slight vomiting again; there had been no passage
In vivo role of interleukin 4 in T cell tolerance induced by aqueous protein antigen.
Authors: H J Burstein, A K Abbas
Journal: The Journal of Experimental Medicine (1993)

High doses of aqueous protein antigens induce a form of immunological tolerance in which interleukin 2 (IL-2)- and interferon gamma (IFN-gamma)-secreting T helper type 1 (Th1) cells are inhibited, but IL-4-secreting (Th2) cells are not. This is manifested by reduced proliferation of antigen-specific T cells upon in vitro restimulation, and marked suppression of specific antibody responses of the immunoglobulin (Ig)G2a, IgG2b, and IgG3 isotypes, but not of IgG1 and IgE. The role of the immunomodulatory cytokine IL-4 in this model of unresponsiveness to protein antigens has been examined. Administration of tolerizing antigen itself primes splenic CD4+ T cells for secretion of lymphokines, both IL-2 and IL-4. Neutralization of IL-4 in vivo with the anti-IL-4 antibody 11B11 during tolerance induction augments IFN-gamma production by T cells of tolerant mice, and reverses the suppression of IgG2a, IgG2b, and IgG3. This blockade of IL-4 function does not, however, restore the proliferative responses of T cells, suggesting that reduced T cell proliferation is due to direct T cell inactivation or anergy. Inhibiting the activity of IL-4 in vivo also inhibits the expansion of antigen-specific Th2-like cells, which are resistant to the induction of unresponsiveness. Thus, the immunologic consequences of high-dose tolerance are due to a combination of clonal T cell anergy and IL-4-mediated immune regulation.
Blood cholesterol is causally related to atherosclerosis
Authors: J J Frohlich
Journal: Cardiovascular Research (1994)

Journal Article Blood cholesterol is causally related to atherosclerosis Get access J J Frohlich J J Frohlich Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 28, Issue 4, April 1994, Page 574, https://doi.org/10.1093/cvr/28.4.574 Published: 01 April 1994
Inhibition of Intestinal Tumorigenesis in <i>Apc</i>min/+ Mice by (−)-Epigallocatechin-3-Gallate, the Major Catechin in Green Tea
Authors: Jihyeung Ju, Jungil Hong, Jian-nian Zhou, Zui Pan, Mousumi Bose, Jie Liao, Guang-yu Yang, Ying Ying Liu, Zhe Hou, Yong Lin, Jianjie Ma, Weichung Joe Shih, Adelaide M. Carothers, Chung S. Yang
Journal: Cancer Research (2005)

Abstract The present study was designed to investigate the effects of two main constituents of green tea, (−)-epigallocatechin-3-gallate (EGCG) and caffeine, on intestinal tumorigenesis in Apcmin/+ mice, a recognized mouse model for human intestinal cancer, and to elucidate possible mechanisms involved in the inhibitory action of the active constituent. We found that p.o. administration of EGCG at doses of 0.08% or 0.16% in drinking fluid significantly decreased small intestinal tumor formation by 37% or 47%, respectively, whereas caffeine at a dose of 0.044% in drinking fluid had no inhibitory activity against intestinal tumorigenesis. In another experiment, small intestinal tumorigenesis was inhibited in a dose-dependent manner by p.o. administration of EGCG in a dose range of 0.02% to 0.32%. P.o. administration of EGCG resulted in increased levels of E-cadherin and decreased levels of nuclear β-catenin, c-Myc, phospho-Akt, and phospho-extracellular signal–regulated kinase 1/2 (ERK1/2) in small intestinal tumors. Treatment of HT29 human colon cancer cells with EGCG (12.5 or 20 μmol/L at different times) also increased protein levels of E-cadherin by 27% to 58%, induced the translocation of β-catenin from nucleus to cytoplasm and plasma membrane, and decreased c-Myc and cyclin D1 (20 μmol/L EGCG for 24 hours). These results indicate that EGCG effectively inhibited intestinal tumorigenesis in Apcmin/+ mice, possibly through the attenuation of the carcinogenic events, which include aberrant nuclear β-catenin and activated Akt and ERK signaling.