tbuckley/cabot-search huggingface dataset:
Abstract 3409: Monitoring of Changes in Atheroma Volume by 64-Slice Computed Tomography.
Authors: Borja Ibanez, Giovanni Cimmino, Javier Sanz, Walter S Speidl, Carlos G Santos-Gallego, Susanna Prat-Gonzalez, Antonio Pinero, Juan Benezet-Mazuecos, M Urooj Zafar, Valentin Fuster, Mario J Garcia, Juan J Badimon
Journal: Circulation (2007)

Non-invasive assessment of plaque burden by Multislice Computed Tomography (MDCT) has been recently shown to be feasible. However, to date, there is no data on its accuracy to assess changes in atheroma burden We and others have previously shown that apoA-IMilano (apoA-IM) infusion induces a large plaque regression in a very short period of time The aim of our study was to assess the feasibility of MDCT to accurately quantify the changes in atheroma volume induced by apoA-IM infusion Methods Aortic atherosclerotic lesions were induced in New-Zealand-White Rabbits (n=7) by 9-month atherogenic diet and aortic denudation, as previously reported. Animals were then randomized to receive 2 infusions, 4 days apart, of apoA-IM (ETC-216, Pfizer. n=4) or equal volume of placebo (n=3). All animals underwent 2 imaging studies in a 64-Slice MDCT scanner (Sensation 64, Siemens), pre- and post-treatment (Rx). After last MDCT study, animals were sacrificed and the aorta processed for histological atherosclerotic lesions characterization and volume quantification . Axial MDCT images were reconstructed (3 mm thick, no overlap). Display settings were manipulated according to previous validated studies. For lumen delineation: window width (WW) 1 and level (WL) 65% of lumen attenuation . For outer vessel boundaries: WW 155% and WL 65%. Results MDCT showed that plaque burden regressed by 29% in apoA-IM group (418mm 3 pre-Rx vs. 302mm 3 post-Rx, p=0.031). Conversely, no significant change was observed by MDCT studies done pre- and post-placebo administration. MDCT performed post-Rx showed that mean plaque volume in apoA-IM animals was 11.5% smaller than that of placebo animals (p=0.018). Mean plaque volume in histology showed similar results:plaque volume was 10.6% smaller in the apoA-IM group (p=0.005 vs. placebo). The interobserver variability for plaque volume quantification in MDCT was 10±4%. Conclusion MDCT detects the changes in atherosclerotic plaque volume induced by apoA-IM infusion. Furthermore, an excellent correlation was found between MDCT and histological plaque volumes. These results, combined to the short time of scan and the accessibility to the coronary territory suggest that MDCT could be applied in human studies testing changes in coronary plaque volume.
Posttraumatic stress disorder among survivors of Cambodian concentration camps
Authors: J D Kinzie, R H Fredrickson, R Ben, J Fleck, W Karls
Journal: American Journal of Psychiatry (1984)

Thirteen Cambodian refugees who had survived 2-4 years of concentration camp experience met the DSM-III criteria for posttraumatic stress disorder. Their predominant symptoms were avoidance, hyperactive startle reactions, emotional numbness, intrusive thoughts, and nightmares, which had lasted at least 3 years after the imprisonment. The patients' avoidance of thoughts or discussion of the past and the shame they felt about Cambodia's history made diagnosis and treatment difficult. These findings give cross-cultural validation to the diagnosis of posttraumatic stress disorder and should alert clinicians to its existence in a population not previously studied.
Abstract 13034: The L19-Il2 Conjugate Induces Plaque Reduction via Activation of Plaque-Associated Regulatory T Cells
Authors: Thore Dietrich, Thomas Hucko, Joerg Willuda, Hans D Menssen, Dietger Stibenz, Philipp Stawowy, Eckart Fleck, Kristof Graf
Journal: Circulation (2010)

L19-IL2 is a human tumor conjugate composed of a single-chain (scFv) antibody specific to the extra-domain B of fibronectin (ED-B) fused to recombinant human interleukine-2 (rhIL2). L19-IL2 is in clinical development as a treatment for cancer. Since ED-B is also strongly expressed in atherosclerotic plaque tissue and correlates with local inflammation, we investigated the impact of L19-IL2 therapy on aortic plaque tissue in apoE-deficient (apoE-/-) mice.   Methods:  L19-IL2, L19 (scFv alone), D1.3-IL2 (control fusion protein) or saline was injected intravenously on day 1, 3 and 5 to 6-month old apoE−/− mice fed with high fat chow. Animals were sacrificed on day 7 and subjected to detailed analysis of vascular tissues.   Results:  Human rhIL2 was only detected in vascular tissues subjected to L19-IL2 treatment. This conjugate significantly reduced the plaque size at the aortic root by 28.1% ± 0.6% (p   Conclusions:  L19–IL2 delivers functional hIL2 to plaques, subsequently causing activation of intra-plaque regulatory T cells via IL2-receptor activation and microvascular leakage, which was associated with rapid reduction in size of pre-established atherosclerotic plaques in apoE−/− mice.
Conference
Authors: J. W. Hirshfeld, Stephen Ellis, D. P. Faxon, P. C. Block, J. R. Carver, J S Jr Douglas, N. L. Eigler, M. A. Hlatky, D R Jr Holmes, A M Jr Hutter, A. K. Jacobs, W L Jr Johnson, J. G. Jollis, S. E. Kimmel, W. K. Laskey, H. Luft, D. J. Malenka, A. A. Oboler, A. E. Summers, A. S. Taussig, J. S. Forrester, P. S. Douglas, J. D. Fisher, R. J. Gibbons, J. L. Halperin, S. Kaul, D. J. Skorton, W. S. Weintraub, W L Jr Winters, M. J. Wolk
Journal: Journal of the American College of Cardiology (1998)
Reply
Authors: Anders Opdahl, Bharath Ambale Venkatesh, Veronica R.S. Fernandes, Colin O. Wu, Khurram Nasir, Eui-Young Choi, Andre L.C. Almeida, Boaz Rosen, Benilton Carvalho, Thor Edvardsen, David A. Bluemke, João A.C. Lima
Journal: Journal of the American College of Cardiology (2014)
Abstract 3691: Deletion of Suppressor Of Cytokine Signaling-1 in a Murine Model of Atherosclerosis Results in a Lethal Systemic Inflammation
Authors: Christina Grothusen, Harald Schuett, Stefan Lumpe, Andre Bleich, Silke Glage, James N Ihle, Bernhard Schieffer
Journal: Circulation (2008)

Introduction: Atherosclerosis is a chronic inflammatory disease of the cardiovascular system which may result in myocardial infarction and sudden cardiac death. While the role of pro-inflammatory signaling pathways in atherogenesis has been well characterized, the impact of their negative regulators, e.g. suppressor of cytokine signaling (SOCS)-1 remains to be elucidated. Deficiency of SOCS-1 leads to death 3 weeks post-partum due to an overwhelming inflammation caused by an uncontrolled signalling of interferon-gamma (IFNγ). This phenotype can be rescued by generating recombination activating gene (rag)-2, SOCS-1 double knock out (KO) mice lacking mature lymphocytes, the major source of IFNγ. Since the role of SOCS-1 during atherogenesis is unknown, we investigated the impact of a systemic SOCS-1 deficiency in the low-density lipoprotein receptor (ldlr) KO model of atherosclerosis. Material and Methods: socs-1 −/− /rag-2 −/− deficient mice were crossed with ldlr-KO animals. Mice were kept under sterile conditions on a normal chow diet. For in-vitro analyses, murine socs-1 −/− macrophages were stimulated with native low density lipoprotein (nLDL) or oxidized (ox)LDL. SOCS-1 expression was determined by quantitative PCR and western blot. Foam cell formation was determined by Oil red O staining. Results: socs-1 −/− /rag-2 −/− /ldlr −/− mice were born according to mendelian law. Tripel-KO mice showed a reduced weight and size, were more sensitive to bacterial infections and died within 120 days (N=17). Histological analyses revealed a systemic, necrotic, inflammation in Tripel-KO mice. All other genotypes developed no phenotype. In-vitro observations revealed that SOCS-1 mRNA and protein is upregulated in response to stimulation with oxLDL but not with nLDL. Foam cell formation of socs-1 −/− macrophages was increased compared to controls. Conclusion: SOCS-1 seemingly controls critical steps of atherogenesis by modulating foam cell formation in response to stimulation with oxLDL. SOCS-1 deficiency in the ldlr-KO mouse leads to a lethal inflammation. These observations suggest a critical role for SOCS-1 in the regulation of early inflammatory responses in atherogenesis.
Dental Education and Dental Practice
Authors: J R Moore
Journal: Journal of the Royal Society of Medicine (1984)

This paper relates recent modes of dental practice to changes that the public and government are likely to ask the health care professions to make in the future. As usual they are asking for the best of all worlds. First, that we maintain the clinical model to the highest standards of personal dental care based and tested against the best research at our disposal, whilst we ensure there is no reduction in the high technical standards for which british dentists have a reputation. Second, that the profession is required to consider ways of providing care on the medicosocial model for the whole community at an economic level the country will afford. The broad changes in dental education have been reviewed, from the technical apprenticeship to the establishment of strong university departments in teaching hospitals. The importance of a sound biomedical foundation and of research both to education and the credibility of dental practice as a primary health care profession is stressed if the profession is to retain its position as a sister to medicine and not slide down to that of a technical ancillary.
Pilot study of celecoxib in oral premalignant lesions (OPLs): Preliminary results
Authors: L. J. Wirth, A. E. Moran, J. F. Krane, L. Weeks, C. M. Norris, L. A. Goguen, C. A. Sullivan, R. I. Haddad, M. R. Posner, M. M. Bertagnolli
Journal: Journal of Clinical Oncology (2005)

1025 Background: 10–44% of patients with OPLs will be diagnosed with squamous cell carcinomas of the head and neck (SCCHNs) over 5–10 years. Cyclooxygenase-2 (COX-2) is progressively upregulated in SCCHN tumorigenesis, and is associated with the malignant phenotype. Preclinical data shows that COX-2 inhibition suppresses tumorigenesis. Methods: This phase II study investigated effects of celecoxib on surrogate endpoint biomarkers (SEBs) in 20 patients with OPLs. Oral mucosa prostaglandin E2 (PGE2) levels in post- vs. pre-treatment samples is the primary SEB. Other SEBs include Ki67, microvessel density and histology. Eligibility requirements included OPL, no tobacco for ≥ 1 month, and no contraindication to celecoxib. Pre- and post-treatment biopsies after 3 months (mos) of celecoxib (400 mg BID) were done. Half the specimen was frozen at -70° C and half formalin-fixed, paraffin-embedded for H&E and immunohistochemistry. PGE2 levels were determined by enzyme immunoassay. Subjects with ≥ 30% decrease in the OPL, ≥ 30% decrease in PGE2 and/or improvement in histology stayed on celecoxib for 12 mos, when biopsies were repeated. Results: 18 patients are evaluable at 3 mos, 10 at 12 mos. One patient was withdrawn for gr 2 allergic reaction. Celecoxib was otherwise well-tolerated. At 3 mos, 10/17 had ≥ 30% decrease in PGE2, median = -40.8% (p=0.04). 2 patients were taken off study at 3 mos, as criteria for continuation were not met. One patient voluntarily withdrew due to gr 1 dyspepsia. At 12 mos, 6/10 had ≥ 30% decrease in PGE2, median = -41.8% (p>0.05). Table 1 shows other SEB results. No subjects developed invasive carcinoma since enrolling. Conclusions: Treatment with celecoxib was well-tolerated, and appears associated with favorable PGE2 modulation. This appears sustained in some but not all patients at 12 mos. Preliminary data suggest celecoxib has promising activity in suppressing SCCHN tumorigenesis in at-risk patients. No significant financial relationships to disclose.
Adaptive‐Servo Ventilator使用により心不全症状の顕著な改善を示した中枢性無呼吸合併拡張型心筋症の1例
Authors: 村中敦子, 高田明典, 横山豊, 山本均美, 矢野俊之, 下重晋也, 湯田聡, 橋本暁佳, 新谷朋子, 土橋和文, 島本和明
Journal: Circulation (2008)
Abstract 2010: A Pre-hospital Percutaneous Cardiopulmonary Bypass Order Treatment Strategy Significantly Improves Neurological Function in Patients with Out-of-Hospital Cardiogenic Cardiopulmonary Arrest
Authors: Hitoshi Kano, Tomoyuki Satou, Kei Yamazaki, Tomoyo Saitou, Akio Endou, Toshihisa Matsui, Naomi Henzan, Masaki Okada, Hiroshi Makise, Yasumi Igarashi, Takao Makino, Naoki Iwakiri, Hiroyuki Fukuda, Noriyoshi Katou, Masaki Togashi, Tetsunori Yoshida
Journal: Circulation (2007)

Objectives: Percutaneous cardiopulmonary bypass (PCPB) is a powerful tool for rescuing the emergency patients (pts) with out-of-hospital cardiogenic cardiac arrest (OHCCA), who are not responding to advanced cardiovascular life support (ACLS). But the system under which the decision to apply PCPB is made at the hospital and preparations then made could exceed the time limitations imposed for cerebral resuscitation. Thus, we have collaborated with the physician-manned ambulance system, and we introduced a pre-hospital PCPB order treatment strategy for patients with out-of-hospital cardiogenic cardiopulmonary arrest, who do not respond to drug administration or electrical cardioversion. Methods: In 174 pts with OHCA treated with PCPB in a single institution, from April 1991 to May 2007. 135 consecutive pts with cardiogenic cardiac arrest refractory to ACLS, who had been treated with PCPB, were included. 135 Pts were divided into two groups. Pre-hospital order groups (n=42) were treated under the pre-hospital PCPB order system, and in-hospital order groups (n=93) were treated under the decision to initiate PCPB was made at the hospital. Rate of return of spontaneous circulation (ROSC), weaning of PCPB, survival to discharge, and favorable neurological recovery were assessed. Results: Pre-hospital order groups showed increases in ROSC, weaning of PCPB, survival to discharge, and significant increases in favorable neurological recovery compared to in-hospital order groups. Conclusions: These results suggest that a pre-hospital PCPB order treatment strategy for patients after CPA significantly improves the neurological function in pts with OHCCA. Table
Enteric coated aspirin may reduce risk
Authors: C. M Grossman
Journal: BMJ (1995)

its mother so modest matemal fevers may lead to fetal temperatures approaching 40°C, which could be dangerous for the baby.2In addition, maternal raised body temperature leads to fetal tachycardia which may be misinterpreted as fetal distress, leading to intervention.2Unlike normal labour rooms (usually kept at 26-28°C), birthing pools are close to body temperature and can therefore prevent the normal loss of heat that is necessary to maintain maternal isothermia.In our unit the protocol for use of the pool originally suggested keeping the water at 37-38°C.In the light of our audit, we now recommend maintaining the temperature at 36-37°C, with hourly monitoring.Prospective research is urgently needed to determine the optimum water temperature for safe use of the birthing pool.This is particularly important in the light of the surprising length of time some women spend in the pool.
FGF-1-induced matrix metalloproteinase-9 expression in breast cancer cells is mediated by increased activities of NF-kB and activating protein-1
Authors: Gina Lungu, Lina Covaleda, George Stoica
Journal: Cancer Research (2007)

2082   Matrix metalloproteinase-9 (MMP9) plays a critical role in tumor invasion, metastasis angiogenesis, inflammation, and would healing. Here, we investigate the effect of fibroblast growth factors-1 on the expression of MMP-9 in ENU1564, a carcinogen-induced rat mammary adenocarcinoma cell line. Gelatin zymography, and RT-PCR demonstrate that FGF-1 dose dependently increased MMP-9 mRNA level and gelatinolytic activity in conditioned medium. Also, FGF-1 treatment of cancer cells activated phosphorylation of Akt, Erk 1/2, and SPK/JNK. Pretreatment of cells with LY294002, a PI3K inhibitor significantly inhibited FGF-1-dependent activation of MMP-9. Also, pretreatment with SP600125, and JNK inhibitor, and with PD98059, and ERK 1/2 inhibitor, strongly inhibited FGF-1-dependent MMP-9 expression. FGF-1-triggered nuclear translocation of NF-kB p65, c-jun, and enhanced degradation of cytoplasmic IkB-α. Electrophoretic mobility shift assay confirmed increased DNA binding of NF-kB, and AP-1 to the MMP-9 promoter in FGF-1 treated cells. The specificity of DNA binding complex was determined by supershift analysis. To define the transcriptional regulation of MMP-9 by FGF-1 we performed promoter-reporter assays. In the previous studies a number of transcription factor binding sites have been characterized in the upstream region of the MMP-9 gene, including those for AP-1, and NF-kB. Our results indicate that mutation of either response element prevented MMP-9 promoter activation by FGF-1. Taken together, these results demonstrated that FGF-1-upregulates MMP-9 expression by activation of a dual signalling pathway, Akt and MAPK, and contribute to cancer progression.
A microfluidically perfused three dimensional human liver model
Authors: Knut Rennert, Sandra Steinborn, Marko Gröger, Birgit Ungerböck, Anne-Marie Jank, Josef Ehgartner, Sandor Nietzsche, Julia Dinger, Michael Kiehntopf, Harald Funke, Frank T. Peters, Amelie Lupp, Claudia Gärtner, Torsten Mayr, Michael Bauer, Otmar Huber, Alexander S. Mosig
Journal: Biomaterials (2015)
Endemic mycoses in patients with STAT3-mutated hyper-IgE (Job) syndrome
Authors: Camila D. Odio, Ki Lee Milligan, Katherine McGowan, Amanda K. Rudman Spergel, Rachel Bishop, Lisa Boris, Amanda Urban, Pamela Welch, Theo Heller, David Kleiner, Mary Anne Jackson, Steven M. Holland, Alexandra F. Freeman
Journal: Journal of Allergy and Clinical Immunology (2015)
Abstract 14422: Epicardial Fat Tissue Causes the Fibrosis of Rat Atrial Myocardium via the Secretion of Activin A
Authors: Nicolas Venteclef, Valeria Guglielm, Elise Balse, Benedicte Gaborit, Julien Amour, Pascal Leprince, Anne Dutour, Karine Clement, Stephane Hatem
Journal: Circulation (2012)
Abstract 14217: Brain Natriuretic Peptide Levels in Patients With Severe Aortic Stenosis at High Surgical Risk: Clinical, Echocardiographic, and Hemodynamic Correlates and Prognosis
Authors: Itsik Ben-Dor, Israel Barbash, Gabriel Maluenda, Teshome Geleta, Camille Hauville, Ana Laynez, Gabriel Sardi, Michael A. Gaglia, Petros Okubagzi, Rebecca Torguson, Zhenyi Xue, Joseph Lindsay, William O. Suddath, Kenneth M. Kent, Lowell F. Satler, Augusto D. Pichard, Ron Waksman
Journal: Circulation (2011)

Background: Brain natriuretic peptide (BNP) is a marker of systolic and diastolic dysfunction and a strong predictor of mortality in patients with heart failure. The present study aimed to assess t...
Abstract P179: Associations of Early and Contemporary Cardiovascular Risk Factors With Coronary Artery Calcification
Authors: Eliseo Guallar, Di Zhao, Roberto Pastor-Barriuso, Sanjay Rampal, Yoosoo Chang, Seungho Ryu, Yuni Choi, Joao Lima, So Yeon Lim, Miguel Cainzos Achirica, Hocheol Shin, Juhee Cho, Yiyi Zhang
Journal: Circulation (2015)

Objective: Traditional cardiovascular disease (CVD) risk factors are key determinants of atherosclerosis and essential components of preventive interventions. However, it is unclear whether the ass...
Meige's syndrome associated with neuroleptic treatment
Authors: J Ananth, E Edelmuth, B Dargan
Journal: American Journal of Psychiatry (1988)

Meige's syndrome is characterized by blepharospasm and oromandibular dystonia. Three cases are presented; two were associated with long-term neuroleptic administration. This drug-induced syndrome may be a variant of tardive dystonia, and prompt discontinuation of neuroleptic treatment may be therapeutic.
来自前沿 不良医学：慢性肾脏病
Authors: 吴元昊, 顾勇
Journal: BMJ (2010)

曾几一度，英国国家卫生医疗服务系统（NHS）的经费已经多过其本来涵盖的部分。因此，在2006年，慢性肾脏病被添加入了NHS的质量和结果框架（QOF）。大多数全科医生不明所以。我们假定这是一个用来识别肾脏病人群及改善其进展的方法。我们被告知，尽管大部分全科医生手上只有少量的终末期肾病患者，人群中患有该病的人数达到惊人的10％。难道我们真的要治疗这么多患者，以防止极罕见的不良预后吗？之后，
Abstract 15180: Impact of the Everolimus-Eluting Stent on Stent Thrombosis According to Baseline Risk of Study Population
Authors: Usman Baber, Roxana Mehran, Jason Kovacic, Annapoorna S Kini, Samin K Sharma, George Dangas
Journal: Circulation (2011)

Purpose Several studies suggest lower risk for stent thrombosis (ST) with use of the 2nd generation everolimus-eluting stent (EES) compared to non everolimus-eluting drug eluting stents (EE-DES). W...
Abstract 5489: Treatment of ApoE-Deficient Mice with Statin Inhibits the Oxidative Stress-Dependent Lysosomal Protease Cathepsin Activation System: Implication for Plaque Stability
Authors: Xian Wu Cheng, Masafumi Kuzuya, Kenji Okumura, Kae Nakamura, Aiko Inoue, Takeshi Sasaki, Haizhen Song, Kyosuke Takeshita, Weon Kim, Guo-Ping Shi, Toyoaki Murohara
Journal: Circulation (2008)

Lysosomal protease cathepsin (Cat) overexpressed in atherosclerotic lesions has a strong proteolytic activity. Given that reactive oxygen species (ROS) are also implicated in protease activation in atherogenesis, we examined a possible role of the ROS-induced cathepsin activation system in neointima formation and atherosclerotic plaque in stability. Murine vascular injury-induced neointima formation was examined by use of a carotid artery ligation model, which demonstrated that cathepsin K deficiency impaired neointima formation and that cystatin C deficiency enhanced it (9-week-old males; n = 18 for each group, P&lt; 0.01). To examine statin-mediated pleiotropic actions on neointima formation and plaque stability, a mouse plaque disruption model (a combination of ligation and cuff placement treatment) was applied to apoE-deficient mice (9-week-old males). The apoE-deficient mice (n = 24–30 for each group) maintained on a normal diet were treated with (1) vehicle (0.5% carboxymethyl cellulose), pitavastatin (1 mg/kg/d), pitavastatin (10 mg/kg/d) for 10 days (before and after cuff treatment; all given by oral gavage every day). Pitavastatin suppressed not only macrophage infiltration but also levels of NADPH oxidase component mRNAs (p22 phox and gp91 phox ) and O2-production in the atherosclerotic lesions. Moreover, pitavastatin increased the collagen fraction and reduced media elastic lamina fragmentation concomitant with decreases in the levels of cathepsin K mRNA and protein. Among these beneficial effects, high doses of pitavastatin further reduced intraplaque hemorrhage. The pitavastatin-mediated vascular-protective effects were mimicked by cathepsin K deficiency in apoE-deficient mice. Pitavastatin lowered the serum levels of cathepsin K but not plasma lipid profile. Pitavastatin inhibited H 2 O 2 -induced Cat K expression and activity in cultured smooth muscle cells and macrophages. Cathepsin K deficiency suppressed vascular injury-induced neointima formation. The data suggested that short-term administration of statin attenuates neointima formation and atherosclerotic plaque stability at least in part by inhibiting the oxidative stress-dependent Cat activation system.