tbuckley/cabot-search huggingface dataset:
Increased apoptosis in lymphoid cells may be the initial trigger in the pathogenesis of pristane-induced arthritis
Authors: S. Herman, J. Pfatschbacher, A. Fischer, M. Hoffmann, G. Steiner
Journal: Annals of the Rheumatic Diseases (2011)

<h3>Background</h3> Increased apoptosis/necrosis and/or deficient clearance of apoptotic material may lead to the release of potential autoantigens provoking the break of self-tolerance mechanisms which may eventually lead to autoimmune diseases such as rheumatoid arthritis (RA). To gain more insight in the role of apoptotic processes in the generation of arthritogenic autoantigens the authors are studying autoimmune responses in the pristane-induced arthritis (PIA) model which shows some striking similarities with human RA including the presence of rheumatoid factor and autoantibodies as well as autoreactive T cells against heterogeneous nuclear ribonucleoprotein A2 (RA33). <h3>Objective</h3> To gain more insight in the earliest pathogenetic processes of PIA with special regard to apoptosis/necrosis and consecutive generation of autoantigens and their involvement in arthritis development. <h3>Methods</h3> Pristane (2,6,10,14-tetramethylpentadecane) was injected subcutanously at the base of the tail in DA.1F rats. Apoptosis/necrosis rates in lymph nodes and blood were analysed at various time points after pristane application by immunhistochemistry and flow cytometry. Furthermore, phagocytosis efficiency of peripheral blood cells was analysed using Ig-coupled beads. Pristane-cyclodextrin complexes were used to study the effects of pristane in cultured cells. <h3>Results</h3> 3 days after pristane application the proportion of cells positive for cleaved caspase 3 was highly increased in draining inguinal lymph nodes of DA.1F rats indicating apoptosis. Interestingly, the apoptosis rate decreased to normal levels as seen as in naïve animals within 2 weeks but draining lymph nodes became extremely hypercellular. In peripheral blood both apoptosis and necrosis rates doubled during the first week after pristane injection. In the acute disease phase four times increased apoptosis and necrosis rates were observed which was in contrast to the draining lymph nodes which normalised during the disease course. The authors could not observe any phagoytosis deficiency in pristane-injected animals rather a strongly increased phagocytosis activity was seen in the acute disease phase. In line with this in vivo data, pristane induced pronounced apoptosis and secondary necrosis in a dose dependent manner when added to cultured rat splenocytes. <h3>Conclusion</h3> This data points toward a pronounced apoptosis/necrosis inducing effect of pristane both in vitro and in vivo. This highly increased cell death might be the crucial initial trigger for the development of PIA. Thus, PIA appears to be an excellent model for studying very early immune processes, particularly the generation of neo-autoantigens, which might play a pivotal role in the pathogenesis of RA.
Preliminary observations on genetic alterations in pilocytic astrocytomas associated with neurofibromatosis 1
Authors: Kenji Tada, Masato Kochi, Hideyuki Saya, Jun-ichi Kuratsu, Shoji Shiraishi, Takanori Kamiryo, Naoki Shinojima, Yukitaka Ushio
Journal: Neuro-Oncology (2003)

Neurofibromatosis 1 (NF1) is an autosomal dominant disorder that predisposes sufferers to various forms of neoplasia. Among affected individuals, 15%-20% develop astrocytomas, especially pilocytic astrocytomas (PA), which are benign and classified as grade I by the World Health Organization. They are generally well circumscribed, and their progression is slow. NF1-associated PAs (NF1-PAs) occasionally behave as aggressive tumors. To elucidate underlying genetic events in clinically progressive NF1-PAs, we performed molecular genetic analysis on 12 PAs, including 3 NF1-PAs, for p53, p16, and epidermal growth factor receptor genes, as well as loss of heterozygosity (LOH) on chromosome 1p, 10, 17, and 19q. None of the obvious genetic alterations typically seen in higher grade astrocytomas were found in 9 sporadic PAs. However, in 2 of 3 NF1-PAs, microsatellite analysis showed LOH10, including the PTEN (phosphatase and tensin homolog deleted on chromosome 10) gene locus, despite the diagnosis of pilocytic astrocytoma; one of these also manifested homozygous deletion of the p16 gene. The other NF1-PA harbored only LOH of the NF1 gene locus (17q). Our preliminary results support the hypothesis that some NF1-PAs differ genetically from sporadic PAs.
Penetrance of the Fragile X–Associated Tremor/Ataxia Syndrome in a Premutation Carrier Population
Authors: Sébastien Jacquemont
Journal: JAMA (2004)

Premutation expansions (55-200 CGG repeats) of the fragile X mental retardation 1 (FMR1) gene are frequent in the general population, with estimated prevalences of 1 per 259 females and 1 per 813 males. Several articles have recently described the presence of late-onset neurological symptoms in male carriers of premutation (FMR1) alleles. The main clinical features described in this newly identified syndrome are cerebellar ataxia and intention tremor. Additional documented symptoms include short-term memory loss, executive functional deficits, cognitive decline, parkinsonism, peripheral neuropathy, lower-limb proximal muscle weakness, and autonomic dysfunction.To study the penetrance of the fragile X-associated tremor/ataxia syndrome (FXTAS) among premutation carriers.Family-based study of 192 individuals (premutation carriers and controls) whose families belong to the Northern or Southern California Fragile X Associations. Data were collected (March 2002-April 2003) through a survey and a standardized neurological examination, which was videotaped and subsequently scored in a blinded fashion.Penetrance of intention tremor and ataxia among adult carriers (aged > or =50 years) of premutation expansions of the FMR1 gene.Data from the survey of 192 individuals demonstrated an age-related penetrance of the combination of reported intention tremor and gait ataxia in male carriers (17%, 38%, 47%, and 75% [lower-bound estimates] for participants aged 50-59, 60-69, 70-79, and > or =80 years, respectively). The male carrier group had an age-adjusted 13-fold increased risk (95% confidence interval, 3.9-25.4; P =.003) of combined intention tremor and gait ataxia when compared with male controls. The clinical examination data from 93 individuals demonstrated that male carriers experienced more difficulties on each of 3 standardized neurological rating scales compared with controls (P<.05). Female carrier scores were also higher than those of female controls (P<.05) on 2 of the 3 neurological rating scales, but no participant was identified with probable or definite FXTAS.The study demonstrates that older male carriers of premutation alleles of the FMR1 gene are at high risk of developing FXTAS. Since male premutation carriers are relatively common in the general population, older men with ataxia and intention tremor should be screened for the FMR1 mutation, especially if these signs are accompanied by parkinsonism, autonomic dysfunction, or cognitive decline, regardless of family history.
Model Observers in Medical Imaging Research
Authors: Xin He, Subok Park
Journal: Theranostics (2013)

Model observers play an important role in the optimization and assessment of imaging devices.In this review paper, we first discuss the basic concepts of model observers, which include the mathematical foundations and psychophysical considerations in designing both optimal observers for optimizing imaging systems and anthropomorphic observers for modeling human observers.Second, we survey a few state-of-the-art computational techniques for estimating model observers and the principles of implementing these techniques.Finally, we review a few applications of model observers in medical imaging research.
Differences in aerosol output and airways responsiveness between the DeVilbiss 40 and 45 hand held nebulisers.
Authors: C J Hartley-Sharpe, H Booth, D P Johns, E H Walters
Journal: Thorax (1995)

BACKGROUND--The DeVilbiss 40 glass hand held nebulisers have been widely used for airways responsiveness testing in epidemiological surveys of asthma. These nebulisers have been superseded in some recent studies by the DeVilbiss 45 plastic hand held nebulisers with the assumption that they are interchangeable. This study compared the aerosol outputs of the DeVilbiss 40 and DeVilbiss 45 nebulisers and investigated whether there was any difference in the in vivo measurements of airways responsiveness when using the two nebuliser types. METHODS--The aerosol output of six DeVilbiss 40 and six DeVilbiss 45 nebulisers was calculated by weight loss per actuation, the usual method of calibrating nebuliser output, and compared with the true amount of aerosol obtained measured by a flouride tracer technique. Airways responsiveness was measured twice in 13 asthmatic patients under identical conditions by the Yan protocol using DeVilbiss 40 and 45 nebulisers in random order. RESULTS--Weight loss overestimated the true aerosol output of both types of nebulisers. Weight loss was similar for the DeVilbiss 40 and 45 nebulisers but the true aerosol output of the DeVilbiss 45 was nearly twice that of the DeVilbiss 40 nebuliser. The geometric mean PD20 values with the DeVilbiss 40 nebuliser was a mean 1.7 doubling doses of histamine higher than that obtained with the DeVilbiss 45 nebuliser. CONCLUSIONS--The DeVilbiss 40 and 45 nebulisers should not be used interchangeably for airways responsiveness testing merely because their outputs based on weight loss are similar. Artefactual differences in the prevalence rates of airways responsiveness could occur in longitudinal studies if a change was inadvertently made from using DeVilbiss 40 to DeVilbiss 45 nebulisers.
Psychothérapie conjugate et phases processuelles
Authors: Michel de Boucaud
Journal: Psychotherapy and Psychosomatics (1978)

Research Articles| February 16 2010 Psychothérapie conjugale et phases processuelles Subject Area: Psychiatry and Psychology Michel de Boucaud Michel de Boucaud Bordeaux Search for other works by this author on: This Site PubMed Google Scholar Psychother Psychosom (1978) 29 (1-4): 192–197. https://doi.org/10.1159/000287126 Article history Published Online: February 16 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 Michel de Boucaud; Psychothérapie conjugale et phases processuelles. Psychother Psychosom 31 December 1978; 29 (1-4): 192–197. https://doi.org/10.1159/000287126 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 JournalsPsychotherapy and Psychosomatics Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1978Copyright / 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.
Leaky Ryanodine receptors increases Amyloid-beta load and induces memory impairments in Tg2576 mouse model of Alzheimer disease
Authors: Bénédicte Oulès, Dolores Del Prete, Barbara Greco, Xuexin Zhang, Inger Lauritzen, Mohamed Trebak, Fabio Benfenati, Frédéric Checler, Mounia Chami
Journal: Molecular Neurodegeneration (2013)

Background In Alzheimer disease (AD), the perturbation of the endoplasmic reticulum (ER) calcium (Ca2+) homeostasis has been linked to presenilins (PS) [1], the catalytic core in gamma-secretase complexes cleaving the amyloid precursor protein (APP) thereby generating amyloid beta peptides. Here we investigate whether APP perturbs ER Ca2+ homeostasis and whether ER Ca2+ could in turn influence amyloid beta production.
Two cases of verified clinical failures using internationally recommended first-line cefixime for gonorrhoea treatment, Norway, 2010
Authors: M Unemo, D Golparian, G Syversen, D F Vestrheim, H Moi
Journal: Eurosurveillance (2010)

Neisseria gonorrhoeae has developed resistance to most of the available therapeutic antimicrobials. The susceptibility to extended-spectrum cephalosporins, the last remaining first-line treatment option, is decreasing globally. This report describes the first two cases outside Japan of verified gonorrhoea clinical failures using internationally recommended first-line cefixime treatment. Enhanced awareness and more frequent follow-up examination, test-of-cure and appropriate verification/falsification of presumed clinical treatment failures, involving several clinical and laboratory parameters should be strongly emphasised worldwide.
Comparison of Zotarolimus-Eluting and Everolimus-Eluting Coronary Stents
Authors: Patrick W. Serruys, Sigmund Silber, Scot Garg, Robert Jan van Geuns, Gert Richardt, Pawel E. Buszman, Henning Kelbæk, Adrianus Johannes van Boven, Sjoerd H. Hofma, Axel Linke, Volker Klauss, William Wijns, Carlos Macaya, Philippe Garot, Carlo DiMario, Ganesh Manoharan, Ran Kornowski, Thomas Ischinger, Antonio Bartorelli, Jacintha Ronden, Marco Bressers, Pierre Gobbens, Manuela Negoita, Frank van Leeuwen, Stephan Windecker
Journal: New England Journal of Medicine (2010)

New-generation coronary stents that release zotarolimus or everolimus have been shown to reduce the risk of restenosis. However, it is unclear whether there are differences in efficacy and safety between the two types of stents on the basis of prospectively adjudicated end points endorsed by the Food and Drug Administration.In this multicenter, noninferiority trial with minimal exclusion criteria, we randomly assigned 2292 patients to undergo treatment with coronary stents releasing either zotarolimus or everolimus. Twenty percent of patients were randomly selected for repeat angiography at 13 months. The primary end point was target-lesion failure, defined as a composite of death from cardiac causes, any myocardial infarction (not clearly attributable to a nontarget vessel), or clinically indicated target-lesion revascularization within 12 months. The secondary angiographic end point was the extent of in-stent stenosis at 13 months.At least one off-label criterion for stent placement was present in 66% of patients. The zotarolimus-eluting stent was noninferior to the everolimus-eluting stent with respect to the primary end point, which occurred in 8.2% and 8.3% of patients, respectively (P<0.001 for noninferiority). There were no significant between-group differences in the rate of death from cardiac causes, any myocardial infarction, or revascularization. The rate of stent thrombosis was 2.3% in the zotarolimus-stent group and 1.5% in the everolimus-stent group (P=0.17). The zotarolimus-eluting stent was also noninferior regarding the degree (+/-SD) of in-stent stenosis (21.65+/-14.42% for zotarolimus vs. 19.76+/-14.64% for everolimus, P=0.04 for noninferiority). In-stent late lumen loss was 0.27+/-0.43 mm in the zotarolimus-stent group versus 0.19+/-0.40 mm in the everolimus-stent group (P=0.08). There were no significant between-group differences in the rate of adverse events.At 13 months, the new-generation zotarolimus-eluting stent was found to be noninferior to the everolimus-eluting stent in a population of patients who had minimal exclusion criteria. (ClinicalTrials.gov number, NCT00617084.)
BRAIN TUMORS IN MENTAL HOSPITAL PATIENTS
Authors: SIDNEY LEVIN
Journal: American Journal of Psychiatry (1949)

In a review of 22 cases with brain tumors verified at operation or post-mortem examination at the Boston Psychopathic Hospital during the years 1938-1946, the following observations were made: 1. Glial tumors comprised the majority of cases although there were also meningiomas, craniopharyngiomas, pinealoma, and metastatic tumors. There were no pituitary or posterior fossa neoplasms in the series. 2. In the majority of patients, symptoms which in retrospect gave evidence of the growth of a brain tumor had been present for a period of 6 months or longer prior to admission. 3. In none of the 22 cases was there any history of previous mental illness. 4. The most prominent early manifestations of brain tumor in this series consisted of seizures, depression, and visual impairment. 5. At the time of admission to the hospital most patients showed prominent mental features characteristic of organic brain disease, and some showed clinical pictures resembling those seen in the toxic psychoses. The chief features of the mental status at the time of admission were confusion, memory impairment, and depression. In some cases, due to the prominence of depression, the clinical picture was similar to that often seen in the involutional psychoses. 6. Neurological abnormalities were present in all but 3 cases in which the tumors were confined to the region of the frontal lobes. In one case of olfactory groove meningioma the only positive neurological finding was anosmia. 7. Electroencephalography was of considerable value in preoperative diagnosis and localization of the tumors.
Intragastric acidity as a predictor of the success of Helicobacter pylori eradication: a study in peptic ulcer patients with omeprazole and amoxicillin.
Authors: J Labenz, M Stolte, A L Blum, I Jorias, F Leverkus, M Sollbohmer, J Bertrams, G Borsch
Journal: Gut (1995)

Omeprazole plus amoxicillin cures Helicobacter pylori infection. The hypothesis was tested that low acidity is a predictor of outcome. Fifty patients with relapsing or complicated, or both H pylori positive duodenal (n = 25) or gastric ulcer (n = 25) were randomly treated with either omeprazole 20 mg twice daily plus amoxicillin 1 g twice daily or with omeprazole 40 mg twice daily plus amoxicillin 1 g twice daily over two weeks. After one week of combined treatment, a 24 hour gastric pH measurement was performed in all patients. H pylori cure rate was 67%. Patients who later turned out to be cured had higher pH values during night time and after meals (p &lt; 0.05). In an explorative analysis drug compliance, smoking, location of the ulcer (duodenum versus stomach), age, and grade of body gastritis were additional predictors of the outcome. Smoking (p = 0.006), compliance (p = 0.037), duodenal ulcer disease (p = 0.065), and young age (p = 0.021) were related to high acidity. In conclusion, the success of eradication treatment with omeprazole and amoxicillin in ulcer patients infected with H pylori depends on intragastric pH. Drug compliance, smoking habits, location of ulcer, age, and activity of body gastritis are other predictors and in part related to intragastric acidity.
The Promise and Limitations of Genome-wide Association Studies
Authors: Christine Klein, Katja Lohmann, Andreas Ziegler
Journal: JAMA (2012)

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Transient Mitochondrial Permeability Transition Pore Opening Mediates Preconditioning-Induced Protection
Authors: Derek Hausenloy, Abigail Wynne, Michael Duchen, Derek Yellon
Journal: Circulation (2004)

Background— Transient (low-conductance) opening of the mitochondrial permeability transition pore (mPTP) may limit mitochondrial calcium load and mediate mitochondrial reactive oxygen species (ROS) signaling. We hypothesize that transient mPTP opening and ROS mediate the protection associated with myocardial preconditioning and mitochondrial uncoupling. Methods and Results— Isolated perfused rat hearts were subjected to 35 minutes of ischemia/120 minutes of reperfusion, and the infarct-risk-volume ratio was determined by tetrazolium staining. Inhibiting mPTP opening during the preconditioning phase with cyclosporine-A (CsA, 0.2 μmol/L) or sanglifehrin-A (SfA, 1.0 μmol/L) abolished the protection associated with ischemic preconditioning (IPC) (20.2±3.6% versus 45.9±2.5% with CsA, 49.0±7.1% with SfA; P &lt;0.001); and pharmacological preconditioning with diazoxide (Dzx, 30 μmol/L) (22.1±2.7% versus 46.3±3.0% with CsA, 48.4±5.5% with SfA; P &lt;0.001), CCPA (the adenosine A1-receptor agonist, 200 nmol/L) (24.9±4.5% versus 54.4±6.6% with CsA, 42.6±9.0% with SfA; P &lt;0.001), or 2,4-dinitrophenol (DNP, the mitochondrial uncoupler, 50 μmol/L) (15.7±2.7% versus 40.8±5.5% with CsA, 34.3±3.1% with SfA; P &lt;0.001), suggesting that mPTP opening during the preconditioning phase is required to mediate protection in these settings. Inhibiting ROS during the preconditioning protocols with N -mercaptopropionylglycine (MPG, 1 mmol/L) also abolished the protection associated with IPC (20.2±3.6% versus 47.1±3.8% with MPG; P &lt;0.001), diazoxide (22.1±2.7% versus 56.3±3.8% with MPG; P &lt;0.001), and DNP (15.7±2.7% versus 50.7±6.6% with MPG; P &lt;0.001) but not CCPA (24.9±4.5% versus 26.5±8.4% with MPG; P =NS). Further experiments in adult rat myocytes demonstrated that diazoxide induced CsA-sensitive, low-conductance transient mPTP opening (represented by a 28±3% reduction in mitochondrial calcein fluorescence compared with control; P &lt;0.01). Conclusions— We report that the protection associated with IPC, diazoxide, and mitochondrial uncoupling requires transient mPTP opening and ROS.