tbuckley/cabot-search huggingface dataset:
Role of Casein Kinase 1A1 in the Biology and Targeted Therapy of del(5q) MDS
Authors: Rebekka K. Schneider, Vera Ademà, Dirk Heckl, Marcus Järås, Mar Mallo, Allegra M. Lord, Lisa P. Chu, Marie E. McConkey, Rafael Kramann, Ann Mullally, Rafael Bejar, Francesc Solé, Benjamin L. Ebert
Journal: Cancer Cell (2014)
A Decade of Change in Drawings by Black Children
Authors: JEANNE E. FISH, CHARLOTTE J. LARR
Journal: American Journal of Psychiatry (1972)

Comparison of human figure drawings made by black children before 1960 with those made by black children after 1970 indicated that more black racial indicators are included in current drawings. These results suggest that black children are now more positively aware and accepting of their racial and ethnic background than was the case before 1960. The authors offer possible explanations.
Hemolytic activity of five different calcium silicates.
Authors: V Skaug, B Gylseth
Journal: Environmental Health Perspectives (1983)

Mineral characteristics and the in vitro hemolytic activity of three synthetic and two natural calcium silicates (CaSi) are compared. Hemolysis is higher for the synthetic compounds than for the natural ones. The difference is accentuated by weak ultrasonication of the minerals. No variation was observed within the two groups, including both acicular and fibrous forms. Calcium was released from the minerals during storage in Tris-buffered saline. At the same time, hemolysis decreased, and crystallographic alterations occurred in the leached minerals. Treatment of the CaSi with calcium chelators (EGTA and EDTA) did not change hemolytic activity. An increase was observed when 30 mM calcium was added. Hemolysis is related to specific surface areas and the crystalline structure of the minerals. Calcium may also be a contributing factor.
Management of retinal detachment: a guide for non-ophthalmologists
Authors: Hyong Kwon Kang, A J Luff
Journal: BMJ (2008)

Patients with retinal detachment often present to their general practitioner, emergency department, or optometrist after central vision has been compromised. This delay is unfortunate because early repair results in little or no visual loss. Once the detachment extends across the fovea (the central macula), permanent visual impairment is almost inevitable. Thorough examination of the retina needs equipment that is rarely available to non-ophthalmologists. Recognition of symptoms and awareness of the risk factors for retinal detachment may help in making speedy referrals and saving vision.

#### Methods

For an overview in the current management of retinal detachment we consulted textbooks and proceedings of meetings in the field of retinal surgery. We searched Medline and Cochrane Review databases for “retinal detachment”, “retinal break”, “retinal tear”, “retinal hole”, “vitreous detachment”, “lattice”, “retinal tuft”, “vitrectomy”, “scleral buckle”, and “retinopexy”, and we searched the internet for reviews and perspectives on retinal detachment.

Retinal detachment is separation of the neurosensory retina from the underlying retinal pigment epithelium (fig 1)⇓. In health, the potential “subretinal space” between these two layers is closed by the retinal pigment epithelium actively pumping fluid across the retina and into the choroid.1 Cellular interdigitation and extracellular matrix provide additional adhesion. Retinal detachment occurs when the forces of retinal attachment are overcome and fluid accumulates in the subretinal space.



Fig 1 The retina lines the internal surface of the posterior two thirds of the globe. It is thickest around the optic nerve and ends at the ora serrata, 5-7 mm behind the limbus. The macula lies temporal to the optic nerve, bordered by the vascular arcades; the fovea is a depression at its centre that provides fine visual acuity. The outermost layer of the retina contains photoreceptors (rods and cones), loosely attached to the retinal pigment epithelium; they depend on the retinal …
Restoration of the Dystrophin-associated Glycoprotein Complex After Exon Skipping Therapy in Duchenne Muscular Dystrophy
Authors: Sebahattin Cirak, Lucy Feng, Karen Anthony, Virginia Arechavala-Gomeza, Silvia Torelli, Caroline Sewry, Jennifer E Morgan, Francesco Muntoni
Journal: Molecular Therapy (2011)

We previously conducted a proof of principle; dose escalation study in Duchenne muscular dystrophy (DMD) patients using the morpholino splice-switching oligonucleotide AVI-4658 (eteplirsen) that induces skipping of dystrophin exon 51 in patients with relevant deletions, restores the open reading frame and induces dystrophin protein expression after intramuscular (i.m.) injection. We now show that this dystrophin expression was accompanied by an elevated expression of α-sarcoglycan, β-dystroglycan (BDG) and--in relevant cases--neuronal nitric oxide synthase (nNOS) at the sarcolemma, each of which is a component of a different subcomplex of the dystrophin-associated glycoprotein complex (DAPC). As expected, nNOS expression was relocalized to the sarcolemma in Duchenne patients in whom the dystrophin deletion left the nNOS-binding domain (exons 42-45) intact, whereas this did not occur in patients with deletions that involved this domain. Our results indicate that the novel internally deleted and shorter dystrophin induced by skipping exon 51 in patients with amenable deletions, can also restore the dystrophin-associated complex, further suggesting preserved functionality of the newly translated dystrophin.
Book: Women and Schizophrenia Women and Mental Health
Authors: H. Pattison
Journal: BMJ (2001)

Eds David J Castle, John McGrath, Jayashri Kulkarni Cambridge University Press, £18.95, pp 164 ISBN 0 521 78617 7 Dora Kohen Routledge, £16.99, pp 250 ISBN 0 415 18885 7 Rating: ![Graphic][1]</img>![Graphic][2]</img>; ![Graphic][3]</img>![Graphic][4]</img>![Graphic][5]</img> Research in medicine is often, in practice, research in medicine for men. Doing research on people who have regularly fluctuating hormone levels is regarded as too tricky unless, of course, those hormones are themselves seen as the cause of the problem. And those hormones are often regarded as the … [1]: /embed/inline-graphic-1.gif [2]: /embed/inline-graphic-2.gif [3]: /embed/inline-graphic-3.gif [4]: /embed/inline-graphic-4.gif [5]: /embed/inline-graphic-5.gif
Treatment of Diabetic Macular Edema with an Inhibitor of Vascular Endothelial-Protein Tyrosine Phosphatase That Activates Tie2
Authors: Peter A. Campochiaro, Raafay Sophie, Michael Tolentino, Daniel M. Miller, David Browning, David S. Boyer, Jeffrey S. Heier, Laura Gambino, Barbara Withers, Mitchell Brigell, Kevin Peters
Journal: Ophthalmology (2014)
Early dosing practices and effectiveness of recombinant human erythropoietin
Authors: Neil R. Powe, Robert I. Griffiths, Joel W. Greer, Alan J. Watson, Gerard F. Anderson, Gregory de Lissovoy, Robert J. Herbert, Paul W. Eggers, Roger A. Milam, Paul K. Whelton
Journal: Kidney International (1993)

In a national longitudinal-cohort study of 59,462 end-stage renal disease (ESRD) patients, we examined dosing and effectiveness of erythropoietin (EPO) during the first year of its use in clinical practice (July 1989 through June 1990). In unadjusted and multivariate analyses of Medicare claims data, the mean dose of EPO prescribed was: relatively small and similar for initial and maintenance therapy, 2752 (95% confidence interval 2740 to 2764) and 2668 (95% confidence interval 2654 to 2682) units, respectively; lower when initial therapy was started later (591 units lower in September 1989 and 760 units lower in November 1989 vs. July 1989, P < 0.0001); lower by 135 units during initial therapy and by 116 units during maintenance therapy for females (who weigh less) compared to males (P < 0.001); and lower by 400 units for patients treated in for-profit versus not-for-profit centers. In multivariate analysis: hematocrit response was less and mean maintenance dose was 298 units and 621 units greater for patients whose ESRD was due to multiple myeloma and sickle cell disease, respectively, compared to those with hypertension-related ESRD (P < 0.01); and hematocrit response was logarithmically related to dose [hematocrit = 0.97 ln (dose), P < 0.0001]. Forty-four percent of patients had a hematocrit > or = 30 after four months of therapy. The percent of patients transfused during three month periods before and after therapy decreased from 20% to 5%, respectively (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
A COST-EFFECTIVE APPROACH TO RADIOFREQUENCY CATHETER ABLATION OF LEFT-SIDED ACCESSORY PATHWAYS IN YOUNG PATIENTS WITH WOLFF-PARKINSON-WHITE SYNDROME: A NOVEL THREE CATHETER TECHNIQUE
Authors: Christine A. Capone, Scott R. Ceresnak, Lynn Nappo, Gregory J. Gates, Robert H. Pass
Journal: Journal of the American College of Cardiology (2013)
Cerebral air embolism during upper endoscopy
Authors: J. López, X. Pérez, F. Esteve
Journal: Endoscopy (2010)

A 61-year-old woman was admitted due to an episode of hematemesis. Esophagogastroduodenoscopy (EGD) was performed and esophageal varices were described with signs of recent bleeding, for which bands were placed. After the procedure the patient became unresponsive (Glasgow Coma Scale = 3/15) and hypotensive (mean arterial pressure = 40), and thus required intubation and ventilation in the intensive care unit. Neurologic signs such as ocular bobbing were noted. Cerebral computer tomography (CCT) revealed pneumocephalus and ischemic infarction of the right hemisphere ([Figs. 1 3]). The patient became brain dead within 24 hours of admission.
Dietary Sodium and Essential Hypertension: Some Myths, Hopes, and Truths
Authors: JOHN H. LARAGH
Journal: Annals of Internal Medicine (1983)

Rigorous sodium deprivation can lower the blood pressure of some patients with essential hypertension (at best, 30% to 50% of patients). In the rest, sodium depletion is ineffective and, in some instances, can raise the blood pressure and cause adverse clinical effects. In normal persons, it is difficult to affect blood pressure even with drastic changes in salt intake; for the blood pressure to rise even slightly, it may be necessary to consume more than 800 meq/d. There is no evidence to indicate that a widely applied, moderate reduction of salt intake could prevent the development of hypertension. The evidence suggesting that such moderate salt intake would significantly lower blood pressure in the patients with sodium-sensitive essential hypertension is weak. Human hypertension comprises a heterogeneous spectrum of abnormal vasoconstriction-volume interactions. Sodium deprivation, like other forms of therapy, should be applied only to those patients in whom its effectiveness has been established.
Rho Family Small G Proteins Play Critical Roles in Mechanical Stress–Induced Hypertrophic Responses in Cardiac Myocytes
Authors: Ryuichi Aikawa, Issei Komuro, Tsutomu Yamazaki, Yunzeng Zou, Sumiyo Kudoh, Weidong Zhu, Takashi Kadowaki, Yoshio Yazaki
Journal: Circulation Research (1999)

Abstract —Mechanical stress induces a variety of hypertrophic responses, such as activation of protein kinases, reprogramming of gene expression, and an increase in protein synthesis. In the present study, to elucidate how mechanical stress induces such events, we examined the role of Rho family small GTP-binding proteins (G proteins) in mechanical stress–induced cardiac hypertrophy. Treatment of neonatal rat cardiomyocytes with the C3 exoenzyme, which abrogates Rho functions, suppressed stretch-induced activation of extracellular signal–regulated protein kinases (ERKs). Overexpression of the Rho GDP dissociation inhibitor (Rho-GDI), dominant-negative mutants of RhoA (DNRhoA), or DNRac1 significantly inhibited stretch-induced activation of transfected ERK2. Overexpression of constitutively active mutants of RhoA slightly activated ERK2 in cardiac myocytes. Overexpression of C -terminal Src kinase, which inhibits functions of the Src family of tyrosine kinases, or overexpression of DNRas had no effect on stretch-induced activation of transfected ERK2. The promoter activity of skeletal α-actin and c- fos genes was increased by stretch, and these increases were completely inhibited by either cotransfection of Rho-GDI or pretreatment with C3 exoenzyme. Mechanical stretch increased phenylalanine incorporation into cardiac myocytes by ≈1.5-fold compared with control, and this increase was also significantly suppressed by pretreatment with C3 exoenzyme. Overexpression of Rho-GDI or DNRhoA did not affect angiotensin II–induced activation of ERK. ERKs were activated by culture media conditioned by stretch of cardiomyocytes without any treatment, but not of cardiomyocytes with pretreatment by C3 exoenzyme. These results suggest that the Rho family of small G proteins plays critical roles in mechanical stress–induced hypertrophic responses.
Love and Psychotherapy. The Psychotherapeutic Eros
Authors: C.A. Seguin
Journal: Psychotherapy and Psychosomatics (1962)

Research Articles| February 10 2010 Love and Psychotherapy. The Psychotherapeutic Eros Subject Area: Psychiatry and Psychology C.A. Seguin C.A. Seguin Lima Search for other works by this author on: This Site PubMed Google Scholar Acta Psychotherapeutica et Psychosomatica (1962) 10 (3): 173–192. https://doi.org/10.1159/000285630 Article history Published Online: February 10 2010 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation C.A. Seguin; Love and Psychotherapy. The Psychotherapeutic Eros. Acta Psychotherapeutica et Psychosomatica 1 March 1962; 10 (3): 173–192. https://doi.org/10.1159/000285630 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsActa Psychotherapeutica et Psychosomatica Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1962Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
Effects of organometals on cellular signaling. I. Influence of metabolic inhibitors on metal-induced arachidonic acid liberation.
Authors: A Käfer, H F Krug
Journal: Environmental Health Perspectives (1994)

Organic lead and tin compounds stimulate an increase of free arachidonic acid (AA) in HL-60 cells. This fatty acid is involved in numerous health problems and physiological mechanisms. Three major pathways result in a liberation of AA from membrane phospholipids and there is evidence that G-proteins serve as couplers within all three pathways. Therefore we investigated the influence of pertussis toxin (PT) on the organometallic-induced AA liberation. The effect of all studied compounds (organotin and organo-lead) was diminished by PT. We conclude that the organometals activate PLA2 to some extent via a PT-sensitive pathway. The ionophor A 23187 (1-10 microM) led to an increase of free AA by raising the intracellular Ca2+ level. One of the postulated ways of AA release is via Ca2+ channel activation; phospholipases are Ca2+ dependent. Thus, we examined the necessity of free intracellular Ca2+ for the organometallic effect. The Ca2+ chelator EGTA inhibited the increase of free AA induced by organometals. This is true also for verapamil, a Ca2+ channel blocker. Quinacrine, which is thought to be an inhibitor of phospholipase A2 (PLA2), prevented the AA liberation from membrane phospholipids induced by organometals. This could be due to the inhibition of PLA2, but it could also be the result of an inhibited Ca2+ influx.
Buccal delivery of fluorescein isothiocyanate-dextran 4400 and the peptide drug buserelin with glycodeoxycholate as an absorption enhancer in pigs
Authors: A.J. Hoogstraate, J.C. Verhoef, B. Tuk, A. Pijpers, L.A.M.G. van Leengoed, J.H.M. Verheijden, H.E. Junginger, H.E. Boddé
Journal: Journal of Controlled Release (1996)
Characterization of a leukotactic factor derived from psoriatic scale
Authors: HACHIRO TAGAMI, SHIGEO OFUJI
Journal: British Journal of Dermatology (1977)

A study was made on the in vitro characteristics and in vivo biological activities of a leukotactic factor derived from psoriatic scale (PLF). Sephadex G-75 chromatography showed that PLF eluted in the region of the 12,500 dalton protein marker. It resisted heating, lyophilization, acidity (pH 3) and alkalinity (pH 11), but was destroyed by trypsin digestion. The substance attracted polymorphonuclear leukocytes (PMNs) in vitro; this ability was inhibited by antiserum to C3a and was partially reduced by antiserum to C5. Although PLF showed strong chemotactic activity for PMNs, its activity for mononuclear cells was only mild. Intradermal injection of PLF into man or guinea-pig produced an erythematous response with dense tissue neutrophilia, the time course of which was similar to that of the Arthus response. PLF also provoked increased vascular permeability in guinea-pig skin. Moreover, repeated intradermal injection of PLF to the same site in guinea-pigs led to moderate acanthosis of the overlying epidermis. These observations strongly suggest that transepidermal migration of leukocytes in psoriatic lesions is provoked by PLF, whose activity appears to reflect that of complement cleavage products, particularly C3a, presumably produced by complement activation in the subcorneal region of the epidermis. Furthermore, it is postulated that PLF may be a factor which plays a crucial role in the production of typical psoriasiform tissue changes.
Perioperative maintenance of normal temperature
Authors: A. J. Berry
Journal: JAMA (1997)

To the Editor.  —In a randomized clinical trial, Dr Frank and colleagues1assessed the effects of maintenance of normothermia in the operating room on perioperative cardiac events. Using a multivariate logistic regression model, the authors concluded that hypothermia was associated with a 2.2 times greater rate of adverse perioperative cardiac events than was observed in normothermic patients. Although preoperative β-adrenergic blocker use also was significantly associated with fewer perioperative cardiac events, there was minimal discussion of this finding. The authors cite several studies demonstrating that the adverse cardiac effects of hypothermia can be attributed to an increased adrenergic response. This suggests that preoperative β-adrenergic blockade may be an effect modifier on the relationship between hypothermia and cardiac events, although this possibility was not explored.  When logistic regression is used for data analysis, the first step is to assess for effect modification by evaluating interaction terms (product terms) consisting of
The Kidney: Morphology, Biochemistry and Physiology
Authors: Carl F. Anderson
Journal: JAMA (1969)

This book is the first volume of a proposed trilogy concerned with the kidney and its functions. It contains, in fact, six monographs dealing with the embryonic kidney, general anatomy and histology, histochemistry, and ultrastructure of the normal and pathologic glomerulus, tubules, and interstitial tissue. Three of the six chapters have been translated into the English language. Approximately 70% of the references listed in these three chapters are from the Englishlanguage literature. The references are pertinent, numerous, and recent, with the latest published reference dated 1968. Rouiller's chapter concerning general anatomy and histology is outstanding. He includes rather complete references to the classic works dealing with renal structure and thoroughly describes and references the problems and contradictory interpretations concerning the question of intrarenal arteriovenous anastomoses. Simon and Chatelanat's chapter concerning the ultrastructure of the normal and pathologic glomerulus is especially complete, well illustrated, and thought provoking. This book is definitely
A4.13 Evaluation of Histology and Adipokine Expression of Synovial Tissue from Psoriatic Arthritis Patients
Authors: Elisabeth Schmitt, Elena Neumann, Jörg Kriegsmann (Trier), Rainer Straub (Regensburg), U Müller-Ladner
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The pathophysiology of psoriatic arthritis (PsA) has still not been examined in minute detail as has rheumatoid arthritis (RA). As it is often difficult to differentiate between both diseases and there are numerous publications that synovial inflammation and cytokine pattern are different in PsA and RA, we analysed the synovial histological differences with respect to immunomodulatory adipokines resistin, visfatin and adiponectin. <h3>Methods</h3> First, synovial tissues from affected joints with PsA were stained with hematoxylin/eosin to visualise the histology of the synovial membrane. Thereafter, macrophages were detected by immunohistochemistry using an anti-CD16 antibody, fibroblasts using an anti-vimentin antibody. Collagen type IV-antibodies were used to visualise vascular endothelial cells and anti-CD20 antibodies to identify B-lymphocytes. In addition, serial tissue sections were stained for resistin-, visfatin, and adiponectin. <h3>Results</h3> In the majority of patients, the synovial tissue from PsA showed no hyperplasia of the lining layer in comparison to RA (lining thickness in % of PsA patients: 1 cell layer, 64%; 2–3 cell layers, 21%; &gt;4 cell layers, 24%. Vice versa, an increased cellularity in the sublining could be detected. In PsA, a lower number of immune-cell follicles were observed although the number of synovial vessels was increased. In all samples, cellular adipokine signals were detectable. Adiponectin was mainly located in vessels showing a strong expression of this molecule. In contrast to RA, the expression of adiponectin in the lining layer was completely absent in most PsA patients. Resistin was detectable in the sublining but also in the lining layer. A strong expression of visfatin could be found in the sublining, and to a lower extent in the lining layer. There was no association between the localisation of the adipokines and the quantity or of compact inflammatory infiltrates. <h3>Conclusions</h3> The synovial membranes from PsA show clear differences to those of RA-affected joints. Adipokine expression is -in part- also different between RA and PsA patients. Here, specifically adiponectin is more prominent in the RA than in the PsA lining layer. Adipokines may therefore play different roles in inflammatory processes operative in these chronic rheumatic diseases.