tbuckley/cabot-search huggingface dataset:
Four Plus: The Management of Nephrosis
Authors: Cecil H. Coggins
Journal: New England Journal of Medicine (1976)

...on placing two pints of the urine over the fire, when one-half was evaporated, the other formed itself into a white mass, like the soft white of an egg when boiled.1 Thus did Domenico Cotugno report the results of his urinalysis when treating a soldier with dropsy in 1765. As two articles in this issue of the Journal indicate, edematous patients with heavy proteinuria continue to vex their physicians well through the 20th century.The dropsical soldier responded to potassium bitartrate therapy. Dr. Cotugno, apparently satisfied with his series of one and secure in his choice of therapy, composed the . . .
A review of<i>Dientamoeba fragilis</i>carriage in humans: Several reasons why this organism should be considered in the diagnosis of gastrointestinal illness
Authors: Joel L. N. Barratt, John Harkness, Deborah Marriott, John T. Ellis, Damien Stark
Journal: Gut Microbes (2011)

Dientamoeba fragilis is a protozoan that inhabits the human gut. It is approximately 100 years since Dientamoeba’s discovery and first description when it was described as a rare and harmless commensal. Since then it has struggled to gain recognition as a pathogen despite the evidence supporting its pathogenicity. Dientamoeba remains neglected, probably due to the misconceptions that it is uncommon and non-pathogenic. Usually, carriage of Dientamoeba is associated with symptoms such as abdominal pain and diarrhea. Moreover, antimicrobial therapy followed by resolution of symptoms coincides with the eradication of Dientamoeba. This manuscript reviews the scientific literature relating to Dientamoeba’s prevalence and pathogenicity. While much of the evidence supporting its pathogenicity is only circumstantial, it is apparent that most researchers agree that Dientamoeba is pathogenic. Therefore, in symptomatic patients who harbor Dientamoeba and no other pathogen, Dientamoeba should be considered as the etiological agent and treated as such.
Serotonin transport by cultured bovine aortic endothelium.
Authors: D Shepro, J C Batbouta, L S Robblee, M P Carson, F A Belamarich
Journal: Circulation Research (1975)

Endothelial cells isolated from bovine aortas without prior treatment with enzymes were cultured in RPMI 1640 medium containing 17% fetal calf serum and antibiotics. The endothelial cells at confluency (7 days) were similar to endothelium in situ or to freshly isolated endothelial cells from blood vessels as seen by light, scanning, and electron microscopy. Cultured and freshly isolated indothelial cells exposed to labeled serotonin, even in the presence of iproniazid (5 x 10-4M), took up approximately 125 and 250 pmoles 14C-serotonin/mg protein, respectively, in 3 hours. Imipramine (10-4M) reduced uptake for both cell groups. Cold (4 degrees C) and metabolic inhibitors sharply reduced serotonin uptake by both freshly isolated and cultured endothelial cells. Ouabain (10-5M) almost completely blocked serotonin transport. Six analogues of serotonin at concentrations ten times above experimental serotonin concentrations did not affect serotonin transport in the cultured endothelial cells but did reduce it in the freshly isolated endothelial cells by 50%. The data on transport suggest that serotonin uptake is not unique to pulmonary endothelium, as has been suggested previously. In addition, using cultured indothelial cells to study serotonin transport is compatible with using other serotonin model systems such as platelets, lung, or brain. Lastly, serotonin uptake by endothelial cells may involve an active transport mechanism similar to that described for the pulmonary circulation, platelets, and insect salivary glands.
Dilating effect of perivascularly applied potassium channel openers cromakalim and pinacidil in rat and cat pial arteries in situ
Authors: M Wahl, A A Parsons, L Schilling
Journal: Cardiovascular Research (1994)

Objective: The aim was to test the vasodilator effect of perivascularly applied potassium channel openers cromakalim and pinacidil in pial arteries of cat and rat. Methods: Using an open cranial window technique the diameter of pial arteries in the parietal cortex of rat and cat was recorded with an image splitting method. Employing micropuncture techniques, test compounds were dissolved in inert cerebrospinal fluid and infused into the perivascular space of individual arteries. Results: Cromakalim (7 × 10−18−7 × 10−13 M) induced concentration dependent dilatation of feline pial arteries with a maximum effect of 26.8(SEM 3.2)% at 7 × 10−15M. In rat arteries, cromakalim had a maximum effect of 32.1(4.97)% at 1015 M, while pinacidil (10−10−107 M) exerted a maximum dilatation of 29.5(3.3)% at 10−8 M. The latter is consistent with previous findings in feline pial arteries. The sulphonylurea glibenclamide (10−8-10−6 M) had no effect on the resting diameter of rat and cat pial arteries, indicating that their resting tone is not influenced by mechanisms involving ATP sensitive potassium channels. However, glibenclamide reduced the dilating effect of cromakalim and pinacidil in rat and cat in a dose dependent manner. Conclusions: A comparison with previously published data obtained in isolated middle cerebral and basilar arteries showed that potassium channel openers of the benzopyrane and cyano- guanidine type are much more potent in pial arteries than in peripheral arteries in situ or in isolated arteries of the circle of Willis and of peripheral vascular beds. Cardiovascular Research 1994;28:1803-1807
Effect of stopping smoking after unstable angina and myocardial infarction
Authors: P R J Burch
Journal: BMJ (1984)

<h3>Abstract</h3> <h3>Background</h3> New endemic disease has been spread across Wuhan City, China on December 2019. Within few weeks, the World Health Organization (WHO) announced a novel coronavirus designated as coronavirus disease 2019 (COVID-19). In late January 2020, WHO declared the outbreak of a “public-health emergency of international concern” due to the rapid and increasing spread of the disease worldwide. Currently, there is no vaccine or approved treatment for this emerging infection; thus the objective of this study is to design a multi epitope peptide vaccine against COVID-19 using immunoinformatics approach. <h3>Method</h3> Several techniques facilitating the combination of immunoinformatics approach and comparative genomic approach were used in order to determine the potential peptides for designing the T cell epitopes-based peptide vaccine using the envelope protein of 2019-nCoV as a target. <h3>Results</h3> Extensive mutations, insertion and deletion were discovered with comparative sequencing in COVID-19 strain. Additionally, ten peptides binding to MHC class I and MHC class II were found to be promising candidates for vaccine design with adequate world population coverage of 88.5% and 99.99%, respectively. <h3>Conclusion</h3> T cell epitopes-based peptide vaccine was designed for COVID-19 using envelope protein as an immunogenic target. Nevertheless, the proposed vaccine is rapidly needed to be validated clinically in order to ensure its safety, immunogenic profile and to help on stopping this epidemic before it leads to devastating global outbreaks.
Dual Function MITO-Porter, a Nano Carrier Integrating Both Efficient Cytoplasmic Delivery and Mitochondrial Macromolecule Delivery
Authors: Yuma Yamada, Ryo Furukawa, Yukari Yasuzaki, Hideyoshi Harashima
Journal: Molecular Therapy (2011)

Mitochondrial dysfunction is associated with a variety of human diseases including inherited mitochondrial diseases, neurodegenerative disorders, diabetes mellitus, and cancer. Effective medical therapies for mitochondrial diseases will ultimately require an optimal drug delivery system, which will likely be achieved through innovations in the nanotechnology of intracellular trafficking. To achieve efficient mitochondrial drug delivery, two independent processes, i.e., "cytoplasmic delivery through the cell membrane" and "mitochondrial delivery through the mitochondrial membrane" are required. In previous studies, we developed an octaarginine (R8) modified nano carrier for efficient cytoplasmic delivery, showing that R8-modified liposomes were internalized into cells efficiently. On the other hand, we also constructed MITO-Porter for the mitochondrial delivery of macromolecules, a liposome-based carrier that delivers cargos to mitochondria via membrane fusion. Here, we report the development of a dual function MITO-Porter (DF-MITO-Porter), based on the concept of integrating both R8-modified liposomes and MITO-Porter. We show that the DF-MITO-Porter effectively delivers exogenous macro-biomolecules into the mitochondrial matrix, and provide a demonstration of its potential use in therapies aimed at mitochondrial DNA. Mitochondrial dysfunction is associated with a variety of human diseases including inherited mitochondrial diseases, neurodegenerative disorders, diabetes mellitus, and cancer. Effective medical therapies for mitochondrial diseases will ultimately require an optimal drug delivery system, which will likely be achieved through innovations in the nanotechnology of intracellular trafficking. To achieve efficient mitochondrial drug delivery, two independent processes, i.e., "cytoplasmic delivery through the cell membrane" and "mitochondrial delivery through the mitochondrial membrane" are required. In previous studies, we developed an octaarginine (R8) modified nano carrier for efficient cytoplasmic delivery, showing that R8-modified liposomes were internalized into cells efficiently. On the other hand, we also constructed MITO-Porter for the mitochondrial delivery of macromolecules, a liposome-based carrier that delivers cargos to mitochondria via membrane fusion. Here, we report the development of a dual function MITO-Porter (DF-MITO-Porter), based on the concept of integrating both R8-modified liposomes and MITO-Porter. We show that the DF-MITO-Porter effectively delivers exogenous macro-biomolecules into the mitochondrial matrix, and provide a demonstration of its potential use in therapies aimed at mitochondrial DNA.
The Red-Pigment Factory
Authors: Charles Woernle
Journal: Annals of Internal Medicine (1999)

Ad Libitum4 May 1999The Red-Pigment FactoryCharles Woernle, MDCharles Woernle, MDMontgomery, AL 36116 (Woernle)Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-130-9-199905040-00005 SectionsAboutFull Text ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail The yellow smoke rises from a multitude of stacksAnd delivers to the valley the notice of its source.Beneath the smoke the ground and all it holdsLie red, red from the stuff men spend their lives scurrying to form.Twisted metal and acid liquor give birth to powder Scarlet,Who flows and spills and fills some bags—and other things besides.Onto the walls, onto the men, and into their skin it goes,Carried by the wind that blows the sound of the whistle that rules their lives. Author, Article, and Disclosure InformationAffiliations: Montgomery, AL 36116 (Woernle)Corresponding Author: Charles Woernle, MD, 8871 Old Magnolia Way, Montgomery, AL 36116. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 4 May 1999Volume 130, Issue 9Page: 777KeywordsBirth Issue Published: 4 May 1999 Copyright & PermissionsCopyright © 1999 by American College of Physicians. All Rights Reserved.Loading ...
Résection muqueuse endoscopique d'une lésion plane gastrique avec un bistouri endoscopique de type Triangle TipKnife
Authors: R Coriat, A Chryssostalis, S Chaussade
Journal: Endoscopy (2008)

Introduction: Les lésions à haut risque de dégénérescence de l'estomac sont le plus souvent planes (type IIa et IIb ou IIc). Leur résection endoscopique est recommandée. Lorsque la lésion est de grande taille (>2cm), la mucosectomie à l'anse ou au capuchon ne permet pas une exérèse en 1 seul fragment. L'utilisation d'un bistouri endoscopique de type triangle Tip Knife développé par la société Olympus permet de réaliser une dissection en monobloc de ces lésions.
TCT-583 Longest available clinical follow-up of a cohort of “real-world” patients treated exclusively with drug-eluting stents: Results of 12 years of the DESIRE (Drug-Eluting Stents In the REal world) Registry
Authors: Jose d Costa, Amanda Sousa, Adriana Moreira, RICARDO A. COSTA, Manuel N. Cano, Galo Maldonado, cantidio campos neto, Lucas P. Damiani, Dimytri A. Siqueira, J. Eduardo Sousa
Journal: Journal of the American College of Cardiology (2014)
TCT-690 Safety and Clinical Efficacy of Sideguard® Stent for Treatment of Bifurcation Lesions: Interim Results from the European Sideguard® Bifurcation Registry Study
Authors: Farzin Fath-Ordoubadi, Karl-Eugen Hauptmann, Azeem Latib, Simon Eccleshall, Ian Menown, Mohaned Egred, Nicos Spyrou, Mohan Sivananthan, Mamas Mamas, Sanjay Sastry, Javed Iqbal, Fraser Witherow, Ever Grech, Joseph Mills
Journal: Journal of the American College of Cardiology (2012)
Focal expression of interleukin-2 does not break unresponsiveness to "self" (viral) antigen expressed in beta cells but enhances development of autoimmune disease (diabetes) after initiation of an anti-self immune response.
Authors: M G von Herrath, J Allison, J F Miller, M B Oldstone
Journal: Journal of Clinical Investigation (1995)

The participation of IL-2 in insulin-dependent (type 1) diabetes (IDDM) was analyzed in transgenic (tg) mice expressing the nucleoprotein (NP) of lymphocytic choriomeningitis virus and IL-2 under control of the rat insulin promoter focally in beta cells of the islets of Langerhans. Insertion and expression of the viral (self) gene or of the IL-2 gene alone did not lead to IDDM. Infiltration primarily of CD4 and B lymphocytes and increased expression of MHC class I and II molecules occurred in islets where IL-2 was expressed. By contrast, neither cellular infiltrates nor expression of MHC class I or II glycoproteins above base levels was noted in tgs expressing the viral protein alone. Double tg mice expressing both the viral protein and IL-2 in their islets displayed a modest increase in incidence of spontaneous diabetes compared with that of single transgenic mice expressing IL-2 alone. Breaking of immunological unresponsiveness or sensitization to self antigens did not occur. Neither cytotoxic T lymphocytes (CTL) nor antibodies directed against the viral tg (NP) were generated. However, after challenge with lymphocytic choriomeningitis virus, double tg mice developed anti-self (viral) CTL and IDDM (incidence > 95%) within 2 mo. The generation of virus ("self")-specific MHC-restricted CTL was dependent on CD4+ help. In contrast, viral inoculum to single tg mice expressing either the viral protein or IL-2 failed to enhance the incidence of IDDM over 30% for viral protein or 10% for IL-2 after an 8-mo observation period. Hence, in this autoimmune model in situ expression of IL-2 did not break unresponsiveness but markedly enhanced ongoing disease.
Abstract 2597: PLA2G7 associates with aggressive prostate cancer in vivo and regulates prostate cancer cell migration and adhesion in vitro
Authors: Paula Vainio, Mika Hilvo, Tiina Vesterinen, Santosh Gupta, Ville Härmä, Matthias Nees, Juha P. Turunen, Johan Lundin, Antti Rannikko, Matej Orešič, Olli Kallioniemi, Kristiina Iljin
Journal: Cancer Research (2011)

Abstract There is an urgent need for more efficient and more targeted methods of prostate cancer treatment. We have previously shown PLA2G7 (also known as lipoprotein-associated phospholipase A2, Lp-PLA2) to be a possible biomarker and drug target especially in ERG positive prostate cancers by combining gene expression data from prostate cancer tissues in vivo and functional RNAi studies in vitro. To further study the potential of PLA2G7 in prostate cancer management immunohistochemical staining of 119 clinical prostate cancer samples and 112 adjacent normal prostate samples were performed. In addition, a global lipidomic, eicosanoid and gene expression analysis was utilized to study the effect of PLA2G7 silencing in ERG oncogene positive prostate cancer cells. The results emphasized high expression of PLA2G7 in 66 % of the cancer samples, whereas less than 4 % of the adjacent normal tissues showed positive staining. Furthermore, PLA2G7 expression significantly correlated with high Gleason score. PLA2G7 silencing in vitro induced a reduction in the amount of lysophosphatidyl choline and leukotriene E4, as well as in the expression of multiple genes and signaling pathways involved in cell adhesion and motility. In accordance, knock-down of PLA2G7 in 3D prostate cancer cell culture model lead to decreased invasion to extracellular matrix. Interestingly, PLA2G7 silencing also reduced the expression of ALDH1A1, a marker for malignant prostate stem cells and predictor of poor prostate cancer outcome. In conclusion, these novel findings suggest an oncogenic role for PLA2G7 in aggressive prostate cancers and support the rationale for PLA2G7 targeted therapy in these cancers. A novel PLA2G7 inhibitor is currently under clinical evaluation for cardiovascular diseases, presenting thus an interesting opportunity for drug repositioning to other indications, such as prostate cancer. In addition, lipid-lowering statins are known to lower PLA2G7 mass and activity, therefore PLA2G7 may also represent a target of lipid-lowering therapy in reducing the risk of aggressive prostate cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2597. doi:10.1158/1538-7445.AM2011-2597
Chronic aspirin is effective---if data are massaged sufficiently
Authors: J. G F Cleland
Journal: BMJ (2002)

EDITOR—Baigent et al argue passionately for the effectiveness of aspirin but also warn against the power of prejudice.1 Perhaps there is more than one reasonable perspective on the aspirin meta-analyses, which they should have the courage to admit.

So to arithmetic—250 patients were reported lost to follow up on aspirin in the original ISIS-2 report, more than the 216 deaths' difference between aspirin and placebo.2 This was subsequently revised.3 Which figure should we believe? However, my real concern is about the long term efficacy and risks of aspirin. Should aspirin be a short term intervention after a vascular event or …
M138 Do Standard Cardiovascular Risk Scores Identify Risk In Patients With Copd?
Authors: M. John, S. Hussain, M. A. Haddad, C. Bolton
Journal: Thorax (2014)

<h3>Introduction</h3> Patients with COPD have increased risk of cardiovascular (CV) disease compared to smokers without COPD,<sup>1</sup> with over 25% of deaths CV related.<sup>2</sup> Several CV risk calculators for the general population exist but it is unclear whether they are applicable for COPD. Hypothesis <h3>Standard</h3> CV risk calculators do not identify the increased risk in patients with COPD. <h3>Methods</h3> Subjects with a smoking history &gt;10 pack years, with and without COPD, were assessed at clinical stability, COPD n = 191 and controls n = 106. Post-bronchodilator spirometry and blood pressure were performed, blood taken for lipids and self-reported medical and smoking history recorded. In those without documented established CV disease or diabetes (COPD n = 135 and controls n = 88), 10 year CV risk was calculated using ACC/AHA<sup>3</sup> and NHLBI[4] calculators. <h3>Results</h3> Both groups were well matched for gender and mean arterial blood pressure (MAP), with the COPD group slightly older, Table 1. Mean CV risk scores were similar between patients with COPD and controls, Table 1, ACC/AHA p = 0.16 and NHLBI p = 0.59. When using an established cut-off point of 20% for high 10 year CV risk, similar proportions were identified as high risk: the ACC/AHA calculator - 37% of the patients with COPD and 33% of controls; and with the NHLBI calculator 15% of the patients with COPD and 10% of controls were identified as high-risk. <h3>Discussion</h3> Although nearly double the proportion of patients with COPD compared to controls with a smoking history have current CV disease or diabetes in this cross-sectional study, the increased risk of future incident CV disease in patients with COPD was not identified using standard calculators. Supported by a NIHR BRF Fellowship. <h3>References</h3> Feary, JR, <i>et al</i>. Thorax, 2010;65(11): p. 956-62 McGarvey, LP, <i>et al</i>. Thorax, 2007;62(5): p. 411-5 ACC/AHA Available from: http://my.americanheart.org/professional/StatementsGuidelines/Prevention-Guidelines_UCM_457698_SubHomePage.jsp NHLBI Available from: http://cvdrisk.nhlbi.nih.gov/
Incidence of hepatocellular carcinoma in hepatitis C carriers with normal alanine aminotransferase levels
Authors: Takashi Kumada, Hidenori Toyoda, Seiki Kiriyama, Yasuhiro Sone, Makoto Tanikawa, Yasuhiro Hisanaga, Akira Kanamori, Hiroyuki Atsumi, Makiko Takagi, Satoshi Nakano, Takahiro Arakawa, Masashi Fujimori
Journal: Journal of Hepatology (2009)
Red Puffy Ears
Authors: Hiromichi Kawai, Atsusi Nakajima
Journal: New England Journal of Medicine (2010)

A 63-year-old man with a history of recurrent aseptic meningitis presented with fever and headache. The physical examination showed scleral injection and mild nuchal rigidity. Analysis of the cerebrospinal fluid revealed a mild monocytic pleocytosis indicative of aseptic meningitis. Despite supportive care, the patient had persistent fevers, anorexia, and headache. During treatment, marked bilateral auricular swelling and redness developed (Panel A). Auricular biopsy showed inflammatory changes that are seen in relapsing polychondritis. The administration of a corticosteroid improved the meningeal symptoms and reduced the auricular swelling (Panel B) within a few days. Relapsing polychondritis is a rare rheumatologic disorder that . . .
The ethics of research ethics committees
Authors: J. Nicholl
Journal: BMJ (2000)

Our health service research unit has been carrying out primary evaluative studies for over 30 years. Much of what we do is designed to help improve health care and health services and inform NHS decisions. It may not be fundamental science but it feels worthwhile, sometimes has an important impact, and we know that it is valued, particularly if the studies are done in a timely and nationally representative manner.

But as well as our ever shortening deadlines and increasing workloads we now find that we cannot do our jobs because of research ethics committees. I do not mean that our studies are unethical. Far from it, our studies are nearly always approved—eventually—but the time taken to get approval from several local research ethics committees (LRECs)and in overcoming bureaucratic and practical obstacles, rather than ethical problems, has become a barrier to our research.

> For ethics committees to have become barriers to ethical research … is certainly immoral 

The difficulties of …