tbuckley/cabot-search huggingface dataset:
ON A CASE OF PARAKERATOSIS VARIEGATA
Authors: T. COLCOTT FOX, J. M. H. MACLEOD
Journal: British Journal of Dermatology (1901)

WITHIN recent years a number of cases of psoriasiform and lichenlike eruptions have been reported which do not conform to any of the ordinary recognized types.These cases have been chiefly observed on the Continent.A few months ago a case of this nature presented itself at the Skin Department of the Westminster Hospital, in which the appearances of the skin so strongly suggested the class of case which Unna has named Parakeratosis variegate, that we have been forced to regard it as another example of that rare form of dermatitis.Since this case is one of the first which has been recognized in London, we considered that a clinical and histological description of it, and a reference to the subject of these eruptions in general, might prove of interest and might be of some value in helping to reduce order out of the present chaos which surrounds the subject.* This case was shown by Dr.
Antiphospholipid antibodies associated with alcoholic liver disease specifically recognise oxidised phospholipids
Authors: R Rolla
Journal: Gut (2001)

<h3>BACKGROUND</h3> Circulating antiphospholipid antibodies (aPL) are often detected in patients with alcoholic liver disease (ALD) but little is known about the causes of their formation. <h3>AIMS</h3> We have evaluated whether ethanol mediated oxidative injury might promote the development of aPL in ALD. <h3>PATIENTS AND METHODS</h3> IgG against β<sub>2</sub> glycoprotein 1 (β<sub>2</sub>-GP1), cardiolipin, and human serum albumin (HSA) complexed with either oxidised arachidonic acid (HSA-APP) or malondialdehyde (HSA-MDA) were assayed by ELISA in heavy drinkers with or without ALD and in healthy subjects. <h3>RESULTS</h3> Circulating IgG recognising cardiolipin were significantly higher in ALD patients than in controls. However, anticardiolipin reactivity of ALD sera was only evident using, as the antigen, oxidised cardiolipin but not oxidation protected cardiolipin. In ALD patients, individual values of IgG antioxidised cardiolipin were associated with the titres of antibodies against HSA-MDA and HSA-APP (<i>r</i>=0.68 and 0.72, respectively; p&lt;0.0001) used as markers of oxidative stress. ALD patients also displayed increased levels of antibodies against phospholipid binding protein β<sub>2</sub>-GP1, and individual reactivity towards oxidised cardiolipin and β<sub>2</sub>-GP1 were highly correlated (<i>r</i>=0.85; p&lt;0.0001). IgG binding to oxidised cardiolipin, HSA-MDA, and HSA-APP was also significantly higher in β<sub>2</sub>-GP1 positive than in β<sub>2</sub>-GP1 negative sera. However, preadsorption of β<sub>2</sub>-GP1 positive sera on β<sub>2</sub>-GP1 coated ELISA plates reduced reactivity to oxidised cardiolipin by 80%, without affecting that to HSA-APP or HSA-MDA. <h3>CONCLUSIONS</h3> Ethanol induced oxidative injury is associated with the development of antibodies targeting complexes between oxidised cardiolipin and β<sub>2</sub>-GP1. These antibodies might account for high aPL titres observed in patients with severe ALD.
Artemisinin versus Nonartemisinin Combination Therapy for Uncomplicated Malaria: Randomized Clinical Trials from Four Sites in Uganda
Authors: Adoke Yeka, Kristin Banek, Nathan Bakyaita, Sarah G Staedke, Moses R Kamya, Ambrose Talisuna, Fred Kironde, Samuel L Nsobya, Albert Kilian, Madeline Slater, Arthur Reingold, Philip J Rosenthal, Fred Wabwire-Mangen, Grant Dorsey
Journal: PLoS Medicine (2005)

Background Drug resistance in Plasmodium falciparum poses a major threat to malaria control. Combination antimalarial therapy including artemisinins has been advocated recently to improve efficacy and limit the spread of resistance, but artemisinins are expensive and relatively untested in highly endemic areas. We compared artemisinin-based and other combination therapies in four districts in Uganda with varying transmission intensity. Methods and Findings We enrolled 2,160 patients aged 6 mo or greater with uncomplicated falciparum malaria. Patients were randomized to receive chloroquine (CQ) + sulfadoxine-pyrimethamine (SP); amodiaquine (AQ) + SP; or AQ + artesunate (AS). Primary endpoints were the 28-d risks of parasitological failure either unadjusted or adjusted by genotyping to distinguish recrudescence from new infections. A total of 2,081 patients completed follow-up, of which 1,749 (84%) were under the age of 5 y. The risk of recrudescence after treatment with CQ + SP was high, ranging from 22% to 46% at the four sites. This risk was significantly lower (p < 0.01) after AQ + SP or AQ + AS (7%–18% and 4%–12%, respectively). Compared to AQ + SP, AQ + AS was associated with a lower risk of recrudescence but a higher risk of new infection. The overall risk of repeat therapy due to any recurrent infection (recrudescence or new infection) was similar at two sites and significantly higher for AQ + AS at the two highest transmission sites (risk differences = 15% and 16%, p< 0.003). Conclusion AQ + AS was the most efficacious regimen for preventing recrudescence, but this benefit was outweighed by an increased risk of new infection. Considering all recurrent infections, the efficacy of AQ + SP was at least as efficacious at all sites and superior to AQ + AS at the highest transmission sites. The high endemicity of malaria in Africa may impact on the efficacy of artemisinin-based combination therapy. The registration number for this trial is ISRCTN67520427 (http://www.controlled-trials.com/isrctn/trial/|/0/67520427.html).
Experience with intraperitoneal cisplatin and etoposide and i.v. sodium thiosulphate protection in ovarian cancer patients with either pathologically complete response or minimal residual disease
Authors: R.E.N. van Rijswijk, K. Hoekman, C.W. Burger, R.H.M. Verheijen, J.B. Vermorken
Journal: Annals of Oncology (1997)
Theoretical and Practical Requirements for the Valid Measurement by Indicator-Dilution of Regurgitant Flow Across Incompetent Valves
Authors: WILLIAM W. LACY, WILLIAM H. GOODSON, WILLIAM G. WHEELER, ELLIOT V. NEWMAN
Journal: Circulation Research (1959)

A theory is presented for the measurement of regurgitant flow across an incompetent valve by injection of indicator distal to the valve and recording of time concentration curves proximal and distal to the valve. The conditions which must be met for valid measurements are examined and demonstrated by a functioning mechanical model of the heart. The method is valid regardless of the size of the residual volumes or degree of mixing with these volumes if a representative sample of the concentration of indicator in the blood moving across the valve in both directions is obtained.
Ischaemic preconditioning and mitochondrial permeability transition: a long-lasting relationship: EXPERT'S PERSPECTIVE
Authors: M. Ruiz-Meana
Journal: Cardiovascular Research (2012)

This editorial refers to an article by D.J. Hausenloy et al .[25][1] published in Cardiovascular Research in 2002. It is accompanied by a retrospective editorial by the authors of that original article, D.J. Hausenloy et al ., pp. 160–164, this issue, as part of this Spotlight on Landmark Papers in Cardiovascular Research . 

Since its first description 25 years ago,1 ischaemic preconditioning has become one of the most studied protective interventions in the cardiovascular field, in part due to its universality (it is effective in all animal species tested, including humans, and in different organs) and reproducibility (it has only a weak dependence on the ischaemic protocol applied before sustained ischaemia or on the duration and severity of the ischaemic insult). The identification of the involved signalling pathways and end-effectors was expected to have important therapeutic implications. However, despite the enormous amount of experimental data, our understanding of the cellular mechanisms responsible for preconditioning protection remains incomplete and at some points controversial. The reason for this failure is demonstrated by the large number of publications describing different molecular pathways involved in protection, some of them acting in parallel or being redundant or dispensable, whereas others appear to be additive or to operate in series, making it very difficult to integrate them into a comprehensive survival pathway. No less important was the lack of understanding of the ultimate mechanisms (end-effectors) by which these signalling pathways reduce cell death. End-effectors of preconditioning have to be molecules downstream the signalling pathway directly involved in cell death. They have the greatest therapeutic interest for obvious reasons; however, their identification has proved not to be a trivial task, and multiple candidates …

 [1]: #ref-25
Biology of Cultured Nerve and Muscle
Authors: J. Patrick, S. Heinemann, D. Schubert
Journal: Annual Review of Neuroscience (1978)

Cells from the nervous system can be grown in culture and exhibit many of the biophysical, biochemical, and morphological properties found in vivo. They can be induced to differentiate in culture and perform some of the interactions that occur in the nervous system, including synaptogenesis. A number of important questions relating to nervous system development and function have been approached in culture in ways that cannot be done in vivo. The use of clonal cell lines should lead to rapid progress in the analysis of the nervous system at the chemical level.
Effect of the GABAB agonist baclofen in patients with symptoms and duodeno-gastro-oesophageal reflux refractory to proton pump inhibitors
Authors: G H Koek
Journal: Gut (2003)

<b>Background and aims:</b> A subset of patients with gastro-oesophageal reflux disease (GORD) with refractory symptoms during therapy with proton pump inhibitors (PPIs), have persistent non-acid duodeno-gastro-oesophageal reflux (duodenal reflux). The aim of the present study was to investigate the effect of the GABA<sub>B</sub> receptor agonist baclofen, which was shown to inhibit the occurrence of transient lower oesophageal sphincter relaxations (TLOSRs) in patients with persistent non-acid duodenal reflux during PPI therapy. <b>Methods:</b> Patients were eligible for the study if they had persistent reflux symptoms, normal pH monitoring, and pathological Bilitec monitoring during PPI treatment. Upper gastrointestinal endoscopy and reflux symptom score were performed at the beginning of the study. Baclofen 5 mg three times daily was associated with treatment, and was increased by 5 mg every fourth day until a maintenance dose of 20 mg three times daily was reached. A reflux symptom questionnaire, ambulatory pH monitoring, and Bilitec monitoring were repeated four days later while PPI and baclofen were continued. All data are given as mean (SEM) or median (interquartile range) and were compared using the Student's <i>t</i> test or the Mann-Whitney U test. <b>Results:</b> Sixteen patients (11 women, mean age 46 (3) years) with persistent heartburn or regurgitation for at least three months, in spite of PPI therapy, were included in the study. Erosive oesophagitis was present in seven patients (five with grade 1, two with grade 2). Under PPI therapy alone, all patients had normal acid exposure (0.3 (0.05; 2.2)% of the time) but pathological duodenal reflux exposure (13.8 (11.8; 15.5)% of the time). After addition of baclofen 20 mg three times daily, acid exposure was similar (0.4 (0.15; 2.3)% of the time; NS) but duodenal reflux had significantly decreased (6.1 (0.8; 10.3)% of the time; p&lt;0.05). The number of duodenal reflux episodes and the number of longlasting duodenal reflux episodes (&gt;5 minutes) was decreased, respectively, from 23 (14.5; 34) to 12 (5; 21) (p = 0.06) and from 5 (3; 8) to 2 (0.5;4.5) (p&lt;0.05). The cumulative severity score for 14 reflux symptoms decreased from 10.3 (1.7) to 5.8 (1.3) (p&lt;0.01). Four patients reported mild side effects of nausea or drowsiness. <b>Conclusions:</b> The GABA<sub>B</sub> receptor agonist baclofen improves duodenal reflux and associated reflux symptoms that persist during PPI therapy.
Randomised crossover trial of tripotassium dicitrato bismuthate versus high dose cimetidine for duodenal ulcers resistant to standard dose of cimetidine.
Authors: S K Lam, N W Lee, J Koo, W M Hui, K H Fok, M Ng
Journal: Gut (1984)

Of 212 patients with duodenal ulcer treated with four weeks of one gram daily cimetidine, 25 had ulcers which underwent no reduction in size despite treatment. The effects of tripotassium dicitrato bismuthate (TDB) tablet four times a day or cimetidine 1.6 g daily on the healing of these cimetidine resistant ulcers were compared in a randomised crossover trial. Ten of 12 patients on tripotassium dicitrato bismuthate and five of 13 patients on high dose cimetidine had complete healing (p less than 0.02). On crossing over, seven of the eight ulcers not healed by high dose cimetidine completely healed with TDB in another four weeks, and one of the two ulcers not healed by TDB healed with high dose cimetidine. Overall, TDB healed 85% of cimetidine resistant ulcers, whereas high dose cimetidine healed 40% (p less than 0.006). Tripotassium dicitrato bismuthate is recommended for cimetidine resistant duodenal ulcers.
Metabolic Studies of the Third Component of Complement and the Glycine-Rich Beta Glycoprotein in Patients with Hypocomplementemia
Authors: J. A. Charlesworth, D. Gwyn Williams, E. Sherington, P. J. Lachmann, D. K. Peters
Journal: Journal of Clinical Investigation (1974)

Metabolic studies using radioiodine-labeled third component of complement (C3) and the glycine-rich beta glycoprotein (GBG), a major component of the C3b-feedback pathway, were undertaken in normal subjects, in 22 patients with evidence of complement activation, and in 11 patients with various renal diseases without evidence of complement activation. In seven normal subjects GBG was found to be a rapidly metabolized protein with catabolic rates ranging from 1.7% to 2.2% of the plasma pool/h, synthesis rates from 0.14 to 0.21 mg/kg per h. and extravascular/intravascular distribution ratios from 0.81 to 1.31. In patients with reduced plasma C3, both increased C3 fractional catabolic rates and reduced C3 synthesis rates were observed, and in some patients there was evidence of increased extravascular distribution of the protein. GBG catabolism was usually increased when there was evidence of C3 activation, presumably reflecting activation of the C3b-feedback; but GBG turnover was normal or only slightly accelerated in some patients with accelerated C3 catabolism and profound hypocomplementemia, suggesting that reduced C3 synthesis had limited activation of the C3b-feedback.
Regression of Medial Elastocalcinosis in Rat Aorta
Authors: Rachida Essalihi, Huy Hao Dao, Liz-Ann Gilbert, Céline Bouvet, Yves Semerjian, Marc D. McKee, Pierre Moreau
Journal: Circulation (2005)

Background— We sought to determine whether carbonic anhydrase (CA), which plays an important role in bone resorption, contributes to vascular mineral loss induced by an endothelin receptor antagonist. Methods and Results— Wistar rats were compared with rats receiving warfarin and vitamin K 1 (WVK) for 8 weeks alone or in association with the endothelin receptor antagonist darusentan (30 mg/kg per day), the CA inhibitor acetazolamide (100 mg/kg per day), or both for the last 4 weeks. Rats were also treated with WVK for 5 or 6 weeks, and darusentan was added for the last week or last 2 weeks of treatment, respectively. Treatment with WVK produced medial elastocalcinosis in the aorta and carotid arteries. Immunohistochemistry revealed that CA II was already abundant in the adventitia and in calcified areas of aortic sections from WVK-treated rats. Darusentan did not significantly modify its abundance or distribution. In contrast, CA IV immunostaining, which was weak in WVK-treated rats, became apparent after 1 week of darusentan treatment and declined toward basal levels thereafter. These findings were confirmed by a parallel increase in CA IV protein abundance and activity in the aorta. The mineral loss induced by darusentan was blunted by acetazolamide treatment, confirming the functional relevance of the biochemical findings. Moreover, CA IV immunostaining was enhanced much later in the carotids, where darusentan did not cause regression of elastocalcinosis. Conclusions— Vascular mineral loss induced by the blockade of endothelin receptors seems dependent on the activation of membrane-bound CA IV, suggesting that mineral loss may proceed via local changes in pH similar to that seen in bone resorption.
Genome-wide association study identifies loci influencing concentrations of liver enzymes in plasma
Authors: John C Chambers, Weihua Zhang, Joban Sehmi, Xinzhong Li, Mark N Wass, Pim Van der Harst, Hilma Holm, Serena Sanna, Maryam Kavousi, Sebastian E Baumeister, Lachlan J Coin, Guohong Deng, Christian Gieger, Nancy L Heard-Costa, Jouke-Jan Hottenga, Brigitte Kühnel, Vinod Kumar, Vasiliki Lagou, Liming Liang, Jian'an Luan, Pedro Marques Vidal, Irene Mateo Leach, Paul F O'Reilly, John F Peden, Nilufer Rahmioglu, Pasi Soininen, Elizabeth K Speliotes, Xin Yuan, Gudmar Thorleifsson, Behrooz Z Alizadeh, Larry D Atwood, Ingrid B Borecki, Morris J Brown, Pimphen Charoen, Francesco Cucca, Debashish Das, Eco J C de Geus, Anna L Dixon, Angela Döring, Georg Ehret, Gudmundur I Eyjolfsson, Martin Farrall, Nita G Forouhi, Nele Friedrich, Wolfram Goessling, Daniel F Gudbjartsson, Tamara B Harris, Anna-Liisa Hartikainen, Simon Heath, Gideon M Hirschfield, Albert Hofman, Georg Homuth, Elina Hyppönen, Harry L A Janssen, Toby Johnson, Antti J Kangas, Ido P Kema, Jens P Kühn, Sandra Lai, Mark Lathrop, Markus M Lerch, Yun Li, T Jake Liang, Jing-Ping Lin, Ruth J F Loos, Nicholas G Martin, Miriam F Moffatt, Grant W Montgomery, Patricia B Munroe, Kiran Musunuru, Yusuke Nakamura, Christopher J O'Donnell, Isleifur Olafsson, Brenda W Penninx, Anneli Pouta, Bram P Prins, Inga Prokopenko, Ralf Puls, Aimo Ruokonen, Markku J Savolainen, David Schlessinger, Jeoffrey N L Schouten, Udo Seedorf, Srijita Sen-Chowdhry, Katherine A Siminovitch, Johannes H Smit, Timothy D Spector, Wenting Tan, Tanya M Teslovich, Taru Tukiainen, Andre G Uitterlinden, Melanie M Van der Klauw, Ramachandran S Vasan, Chris Wallace, Henri Wallaschofski, H-Erich Wichmann, Gonneke Willemsen, Peter Würtz, Chun Xu, Laura M Yerges-Armstrong, Goncalo R Abecasis, Kourosh R Ahmadi, Dorret I Boomsma, Mark Caulfield, William O Cookson, Cornelia M van Duijn, Philippe Froguel, Koichi Matsuda, Mark I McCarthy, Christa Meisinger, Vincent Mooser, Kirsi H Pietiläinen, Gunter Schumann, Harold Snieder, Michael J E Sternberg, Ronald P Stolk, Howard C Thomas, Unnur Thorsteinsdottir, Manuela Uda, Gérard Waeber, Nicholas J Wareham, Dawn M Waterworth, Hugh Watkins, John B Whitfield, Jacqueline C M Witteman, Bruce H R Wolffenbuttel, Caroline S Fox, Mika Ala-Korpela, Kari Stefansson, Peter Vollenweider, Henry Völzke, Eric E Schadt, James Scott, Marjo-Riitta Järvelin, Paul Elliott, Jaspal S Kooner
Journal: Nature Genetics (2011)
Activation of the Tumor Suppressor Merlin Modulates Its Interaction with Lipid Rafts
Authors: John T. Stickney, W. Clark Bacon, Meghan Rojas, Nancy Ratner, Wallace Ip
Journal: Cancer Research (2004)

Abstract Neurofibromatosis type 2 (NF2) is a genetic disorder characterized by bilateral schwannomas of the eighth cranial nerve. The NF2 tumor suppressor protein, merlin, is related to the ERM (ezrin, radixin, and moesin) family of membrane/F-actin linkers. Merlin resists solubilization by the detergent Triton X-100 (TX-100), a property commonly attributed to association with the cytoskeleton. Accordingly, NF2 patient mutations that encode merlins with enhanced TX-100 solubility have been explained previously in terms of loss of cytoskeletal attachment. However, here we present data to suggest that the detergent resistance of merlin is a result of its constitutive residence in lipid rafts. Furthermore, when cells are grown to high density, merlin shifts to a more buoyant lipid raft fraction in a density gradient. This shift is mimicked in subconfluent cells treated with cytochalasin D, suggesting that the shift results from merlin dissociation from the actin cytoskeleton, but not from lipid rafts. Intramolecular NH2- and COOH-terminal binding, which occurs when merlin transitions to the growth-suppressive form, also brings about a similar change in buoyant density. Our results suggest that constitutive residence of merlin in lipid rafts is crucial for its function and that as merlin becomes growth suppressive in vivo, one significant molecular event may be the loss of interaction with the actin cytoskeleton. To our knowledge, merlin is the first tumor suppressor known to reside within lipid rafts, and the significance of this finding is underscored by known loss-of-function NF2 patient mutations that encode merlins with enhanced TX-100 solubility.
Randomized Trial of Pterygium Surgery with Mitomycin C Application Using Conjunctival Autograft versus Conjunctival-Limbal Autograft
Authors: Ahmad Kheirkhah, Hassan Hashemi, Mohsen Adelpour, Mojgan Nikdel, Mohammad Bagher Rajabi, Mahmoud Jabbarvand Behrouz
Journal: Ophthalmology (2011)
Colon tumors and colonoscopy
Authors: S. Misra, M. Dwivedi, K. Sharma
Journal: Endoscopy (2011)

A large number of abstracts dealing with colonoscopy were presented at Digestive Disease Week (DDW; 7 – 10 May 2011; Chicago, Illinois, USA). Topics included: new techniques in colonoscopy, recent innovations in endoscopic ultrasonography (EUS), prevention of postpolypectomy bleeding, Raman spectroscopy, bowel preparation during colonoscopy, risk factors for high grade dysplasia (HGD) in colonic adenoma, recent advances in endoscopic treatment of colorectal cancer (CRC), and follow-up of HGD and CRC after endoscopic treatment. This review focuses on the most relevant presentations dealing with colon tumours and colonoscopy.
Cutaneous leishmaniasis. The defect in T cell influx in BALB/c mice.
Authors: M J McElrath, G Kaplan, A Nusrat, Z A Cohn
Journal: The Journal of Experimental Medicine (1987)

Local cellular responses to cutaneous infection with Leishmania mexicana amazonensis were examined in susceptible (BALB/c) and resistant (C57BL/6) mouse strains by immunocytochemical and electron microscopic studies. Infection during the first 8 wk in both animal strains was characterized by progressively enlarging lesions, epidermal thickening and ulceration, and accumulation of eosinophils and Ia+ infected macrophages. Healing of C57BL/6 mouse lesions began after 12 wk of infection and was associated with local influx of both Th (L3T4+) and T cytotoxic/suppressor (Lyt-2+) cells into the dermis, and Ia antigen expression on epidermal keratinocytes. T lymphocyte infiltration was marked and intracellular parasites were scarce by 21 wk of C57BL/6 infection. Similarly, granulomas in C57BL/6 livers contained L3T4+ and Lyt-2+ T lymphocytes and no visible intracellular parasites by 21 wk of infection. In contrast, BALB/c mouse lesions continued to enlarge and never healed. Throughout the entire course of infection, T lymphocyte influx into the heavily infected dermis was minimal. Keratinocyte Ia expression was absent in BALB/c lesions. BALB/c livers were heavily infected by 18 wk of cutaneous infection, with few demonstrable T lymphocytes. A systemic absence of T cells could not be demonstrated in BALB/c mice. Both L3T4+ and Lyt-2+ T cells were found in the peripheral blood in normal numbers in both mouse strains. Our results support the role of T cells as important local effector cells in the healing response of murine cutaneous leishmaniasis. We suggest that local T lymphocyte infiltration may provide lymphokines, particularly IFN-gamma, that can activate infected macrophages to destroy the intracellular parasites. Alternatively, T cells may play a cytotoxic role, killing infected macrophages and allowing local humoral factors to destroy released extracellular parasites.