gebhart/patrepeval huggingface dataset:
Stimulation of a subset of normal resting T lymphocytes by a monoclonal antibody to a crossreactive determinant of the human T cell antigen receptor. (1985)

A previous study from this laboratory described a monoclonal antibody, S511, that reacted with the T cell antigen receptor on a human T cell leukemia and also on 1-2% of circulating T lymphocytes in all normal individuals tested. The data presented in the present study demonstrate that, when normal T lymphocytes are cultured with or without irradiated non-T cells in the presence of soluble S511 antibody, a concentration- and time-dependent proliferation of the S511-reactive population occurred. Proliferation indices as high as 184 times greater than control were observed, which represents a major stimulatory effect on the initially minor S511+ subset. When S511+ cells were studied for evidence of prior activation, they were shown to be unresponsive to interleukin 2 (IL-2) unless exposed to S511 antibody, and were shown to be in the G0/G1 phase of the cell cycle. Thus, the S511 antibody activated resting normal T cells in a manner analogous to specific antigen binding to the T cell antigen receptor. The leukemic S511 molecule has been shown previously to differ from most other antigen receptors in the mobility of the two chains at 43 and 38 kD and the neutral isoelectric point of each chain. Expansion of reactive normal cells by S511-Sepharose permitted the development of IL-2-dependent T cell lines enriched for S511-bearing cells. The antigen receptor molecules on one such polyclonal S511-enriched T cell line were immunoprecipitated with S511 antibody and shown to have comparable mobility to that present on the leukemic cells, but to possess a greater heterogeneity of mobility. Thus, the leukemic cells and normal cells express similar T cell receptor molecules. The differences in the S511 T cell antigen receptor molecule possibly relate to differences in glycosylation or polypeptide structure.
Disordered macrophage cytokine secretion underlies impaired acute inflammation and bacterial clearance in Crohn's disease (2009)

The cause of Crohn's disease (CD) remains poorly understood. Counterintuitively, these patients possess an impaired acute inflammatory response, which could result in delayed clearance of bacteria penetrating the lining of the bowel and predispose to granuloma formation and chronicity. We tested this hypothesis in human subjects by monitoring responses to killed Escherichia coli injected subcutaneously into the forearm. Accumulation of (111)In-labeled neutrophils at these sites and clearance of (32)P-labeled bacteria from them were markedly impaired in CD. Locally increased blood flow and bacterial clearance were dependent on the numbers of bacteria injected. Secretion of proinflammatory cytokines by CD macrophages was grossly impaired in response to E. coli or specific Toll-like receptor agonists. Despite normal levels and stability of cytokine messenger RNA, intracellular levels of tumor necrosis factor (TNF) were abnormally low in CD macrophages. Coupled with reduced secretion, these findings indicate accelerated intracellular breakdown. Differential transcription profiles identified disease-specific genes, notably including those encoding proteins involved in vesicle trafficking. Intracellular destruction of TNF was decreased by inhibitors of lysosomal function. Together, our findings suggest that in CD macrophages, an abnormal proportion of cytokines are routed to lysosomes and degraded rather than being released through the normal secretory pathway.
Tumor Growth Control by Oral Trofosfamide in Patients with Metastatic Breast Cancer (1998)

Research Articles| March 18 1998 Tumor Growth Control by Oral Trofosfamide in Patients with Metastatic Breast Cancer Subject Area: Oncology K. Mross; K. Mross Search for other works by this author on: This Site PubMed Google Scholar A. Rüther; A. Rüther Search for other works by this author on: This Site PubMed Google Scholar T. Gierlich; T. Gierlich Search for other works by this author on: This Site PubMed Google Scholar C. Unger C. Unger Search for other works by this author on: This Site PubMed Google Scholar Onkologie (1998) 21 (1): 52–56. https://doi.org/10.1159/000026777 Article history Published Online: March 18 1998 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 K. Mross, A. Rüther, T. Gierlich, C. Unger; Tumor Growth Control by Oral Trofosfamide in Patients with Metastatic Breast Cancer. Onkologie 1 February 1998; 21 (1): 52–56. https://doi.org/10.1159/000026777 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 JournalsOnkologie Search Advanced Search This content is only available via PDF. 1998Copyright / 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. Article PDF first page preview Close Modal You do not currently have access to this content.
A Road Map to Comprehensive Androgen Receptor Axis Targeting for Castration-Resistant Prostate Cancer (2013)

Gonadal androgen suppression (castration via orchiectomy or gonadotropin-releasing hormone analogues) suppresses circulating testosterone levels but does not achieve adequate androgen ablation within the prostate cancer microenvironment because it does not address adrenal and intratumoral steroid contributions. These residual extragonadal sources of androgens allow prostate cancer cells to survive, adapt, and evolve into castration-resistant prostate cancer (CRPC). The persistent significance of the androgen receptor (AR) axis in CRPC was recently validated by the clinical efficacy of androgen synthesis inhibitors (abiraterone) and novel, second-generation AR antagonists (enzalutamide). The appreciation that conventional therapeutic approaches achieve a suboptimal ablation of intratumoral androgens and AR axis signaling output opens transformative therapeutic opportunities. A treatment paradigm of comprehensive AR axis targeting at multiple levels (androgen synthesis, metabolism, and action) and at all relevant sites (gonadal, adrenal, intratumoral) simultaneously at the time of initiation of endocrine therapy (instead of the current approach of sequentially adding one agent at a time and only after disease progression) deserves examination in clinical trials to explore whether maximal first-line AR axis suppression via combination therapy can achieve maximal induction of cancer cell apoptosis (before they have the chance to adapt and evolve into CRPC) and thus, improve patient outcomes. Cancer Res; 73(15); 4599-605. ©2013 AACR.
Treatment of Lower Eyelid Fat Pads Using Phosphatidylcholine (2004)

BACKGROUND Injectable phosphatidylcholine, a lecithin-derived phospholipid, has been previously demonstrated to improve the appearance of infraorbital fat pad herniation. Current use internationally has led to a significant interest in this novel substance. OBJECTIVE To evaluate the efficacy and safety of injectable phosphatidylcholine, we conducted an open-label study for the treatment of infraorbital fat pad herniation. METHODS Patients received 0.4-mL phosphatidylcholine (50 mg/mL) injections within infraorbital fat pads every 2 weeks. Patient and physician grading of fat herniation, side effects, digital photographs, and a follow-up questionnaire was recorded. RESULTS Ten of the 13 enrolled patients had three to five treatments. Improvements in fat herniation were reported in 80% and 70% of patients as graded by the physician and patients, respectively. Sixty percent of patients assessed their improvement as equal or greater than 5 points (on a 10-point fat herniation scale); however, the physician judged 40% of patients improving to this degree. Little or no response was seen in three patients. Side effects included burning, erythema, and swelling at the injection site. At follow-up averaging 9 months, 50% of patients reported persistence of benefit, 20% experienced some fading, and 30% were the nonresponders. CONCLUSIONS Injectable phosphatidylcholine is a novel treatment for infraorbital fat herniation that may benefit some patients who are considering blepharoplasty. Larger studies evaluating long-term safety and efficacy of phosphatidylcholine for cosmetic purposes are warranted.
Clinical Evaluation of the Use of the M2A Patency Capsule System Before a Capsule Endoscopy Procedure, in Patients with Known or Suspected Intestinal Stenosis (2005)

The current technical development of the patency capsule limits its use in clinical practice, as it did not detect stenoses undiagnosed by CT or SBFT. The start of dissolution at 40 hours after ingestion is too slow to prevent episodes of intestinal occlusion. Patients with Crohn's disease are most likely to be at risk of blockage of progression of the capsule and should benefit from a CT investigation before VCE. However, a careful interview eliciting the patient's medical history and symptoms remains the most useful indicator with regard to suspicion of an intestinal stenosis.
The potential of mesenchymal stem cells derived from amniotic membrane and amniotic fluid for neuronal regenerative therapy (2014)

The mesenchymal stem cells (MSCs), which are derived from the mesoderm, are considered as a readily available source for tissue engineering. They have multipotent differentiation capacity and can be differentiated into various cell types. Many studies have demonstrated that the MSCs identified from amniotic membrane (AM-MSCs) and amniotic fluid (AF-MSCs) are shows advantages for many reasons, including the possibility of noninvasive isolation, multipotency, self-renewal, low immunogenicity, anti-inflammatory and nontumorigenicity properties, and minimal ethical problem. The AF-MSCs and AM-MSCs may be appropriate sources of mesenchymal stem cells for regenerative medicine, as an alternative to embryonic stem cells (ESCs). Recently, regenerative treatments such as tissue engineering and cell transplantation have shown potential in clinical applications for degenerative diseases. Therefore, amnion and MSCs derived from amnion can be applied to cell therapy in neuro-degeneration diseases. In this review, we will describe the potential of AM-MSCs and AF-MSCs, with particular focus on cures for neuronal degenerative diseases.
Plasma mutant α-galactosidase A protein and globotriaosylsphingosine level in Fabry disease (2014)

Fabry disease is an X-linked genetic disorder characterized by deficient activity of α-galactosidase A (GLA) and accumulation of glycolipids, and various GLA gene mutations lead to a wide range of clinical phenotypes from the classic form to the later-onset one. To investigate the biochemical heterogeneity and elucidate the basis of the disease using available clinical samples, we measured GLA activity, GLA protein and accumulated globotriaosylsphingosine (Lyso-Gb3), a biomarker of this disease, in plasma samples from Fabry patients. The analysis revealed that both the enzyme activity and the protein level were apparently decreased, and the enzyme activity was well correlated with the protein level in many Fabry patients. In these cases, a defect of biosynthesis or excessive degradation of mutant GLAs should be involved in the pathogenesis, and the residual protein level would determine the accumulation of Lyso-Gb3 and the severity of the disease. However, there are some exceptional cases, i.e., ones harboring p.C142Y, p.R112H and p.M296I, who exhibit a considerable amount of GLA protein. Especially, a subset of Fabry patients with p.R112H or p.M296I has been attracted interest because the patients exhibit almost normal plasma Lyso-Gb3 concentration. Structural analysis revealed that C142Y causes a structural change at the entrance of the active site. It will lead to a complete enzyme activity deficiency, resulting in a high level of plasma Lyso-Gb3 and the classic Fabry disease. On the other hand, it is thought that R112H causes a relatively large structural change on the molecular surface, and M296I a small one in a restricted region from the core to the surface, both the structural changes being far from the active site. These changes will cause not only partial degradation but also degeneration of the mutant GLA proteins, and the degenerated enzymes exhibiting small and residual activity remain and probably facilitate degradation of Lyso-Gb3 in plasma, leading to the later-onset phenotype. The results of this comprehensive analysis will be useful for elucidation of the basis of Fabry disease.
Synthesis of (±)-Ambrox from (E)-Nerolidol and β-Ionone via Allylic Alcohol [2,3] Sigmatropic Rearrangement (1996)

ADVERTISEMENT RETURN TO ISSUEPREVNoteNEXTSynthesis of (±)-Ambrox from (E)-Nerolidol and β-Ionone via Allylic Alcohol [2,3] Sigmatropic RearrangementAlejandro F. Barrero, Joaquín Altarejos, Enrique J. Alvarez-Manzaneda, José M. Ramos, and Sofía SalidoView Author Information Departamento de Química Orgánica, Facultad de Ciencias, Universidad de Granada, 18071 Granada, Spain, and Departamento de Química Inorgánica y Orgánica, Facultad de Ciencias Experimentales, Universidad de Jaén, 23071 Jaén, Spain Cite this: J. Org. Chem. 1996, 61, 6, 2215–2218Publication Date (Web):March 22, 1996Publication History Received26 October 1995Published online22 March 1996Published inissue 1 January 1996https://pubs.acs.org/doi/10.1021/jo951908ohttps://doi.org/10.1021/jo951908obrief-reportACS PublicationsCopyright © 1996 American Chemical SocietyRequest reuse permissionsArticle Views1847Altmetric-Citations49LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-AlertscloseSupporting Info (1)»Supporting Information Supporting Information SUBJECTS:Alcohols,Cyclization,Mixtures,Rearrangement,Superacids Get e-Alerts
Obesity and socioeconomic status in adults: United States, 2005-2008. (2010)

Data from the National Health and Nutrition Examination Survey, 2005-2008. Among men, obesity prevalence is generally similar at all income levels, however, among non-Hispanic black and Mexican-American men those with higher income are more likely to be obese than those with low income. Higher income women are less likely to be obese than low income women, but most obese women are not low income. There is no significant trend between obesity and education among men. Among women, however, there is a trend, those with college degrees are less likely to be obese compared with less educated women. Between 1988-1994 and 2007-2008 the prevalence of obesity increased in adults at all income and education levels.
Activation of human B cells: alternate options for initial triggering and effects of nonmitogenic concentrations of anti-IgM antibodies on resting and activated cells. (1987)

The monoclonal antibody 1F5, which is reactive with the CD20 (Bp 35) pan-B cell antigen, was shown to activate resting human peripheral blood B cells into the middle to late G1 phase of the cell cycle. However, in contrast to F(ab')2 fragments of polyclonal anti-mu, 1F5 synergized only weakly with B cell growth factor (BCGF) for DNA synthesis in these cells. We provide evidence that the CD20 molecule and surface immunoglobulin represent two alternative activation pathways in resting B cells. We also show that anti-immunoglobulins, during co-stimulation with BCGF, may play an important role in G1 as well as for the initial cell triggering. Thus, anti-mu in nonmitogenic concentrations was shown to provoke distinct effects on 1F5-pretreated G1 cells, as monitored by increases in cellular volumes as well as in cytoplasmic Ca2+ levels. Moreover, anti-mu could increase c-myc mRNA levels in 1F5-primed cells, implying that c-myc expression can be regulated in G1 as well as during the initial G0 to G1 transition. Partially purified human BCGF neither induced G1 entry in resting peripheral blood cells nor primed the cells for DNA synthesis. The finding that BCGF did not influence c-myc mRNA levels in resting or in activated B cells suggests that its mitogenic action does not involve the c-myc function.
Enhanced Dendritic Cell Maturation by TNF-α or Cytidine-Phosphate-Guanosine DNA Drives T Cell Activation In Vitro and Therapeutic Anti-Tumor Immune Responses In Vivo (2000)

Dendritic cells (DC) manipulated ex vivo can induce tumor immunity in experimental murine tumor models. To improve DC-based tumor vaccination, we studied whether DC maturation affects the T cell-activating potential in vitro and the induction of tumor immunity in vivo. Maturation of murine bone marrow-derived DC was induced by GM-CSF plus IL-4 alone or by further addition of TNF-alpha or a cytidine-phosphate-guanosine (CpG)-containing oligonucleotide (ODN-1826), which mimics the immunostimulatory effect of bacterial DNA. Flow cytometric analysis of costimulatory molecules and MHC class II showed that DC maturation was stimulated most by ODN-1826, whereas TNF-alpha had an intermediate effect. The extent of maturation correlated with the secretion of IL-12 and the induction of alloreactive T cell proliferation. In BALB/c mice, s.c. injection of colon carcinoma cells resulted in rapidly growing tumors. In this model, CpG-ODN-stimulated DC cocultured with irradiated tumor cells also induced prophylactic protection most effectively and were therapeutically effective when administered 3 days after tumor challenge. Thus, CpG-ODN-enhanced DC maturation may represent an efficient means to improve clinical tumor vaccination.
Retinomorphic Event-Based Vision Sensors: Bioinspired Cameras With Spiking Output (2014)

State-of-the-art image sensors suffer from significant limitations imposed by their very principle of operation. These sensors acquire the visual information as a series of “snapshot” images, recorded at discrete points in time. Visual information gets time quantized at a predetermined frame rate which has no relation to the dynamics present in the scene. Furthermore, each recorded frame conveys the information from all pixels, regardless of whether this information, or a part of it, has changed since the last frame had been acquired. This acquisition method limits the temporal resolution, potentially missing important information, and leads to redundancy in the recorded image data, unnecessarily inflating data rate and volume. Biology is leading the way to a more efficient style of image acquisition. Biological vision systems are driven by events happening within the scene in view, and not, like image sensors, by artificially created timing and control signals. Translating the frameless paradigm of biological vision to artificial imaging systems implies that control over the acquisition of visual information is no longer being imposed externally to an array of pixels but the decision making is transferred to the single pixel that handles its own information individually. In this paper, recent developments in bioinspired, neuromorphic optical sensing and artificial vision are presented and discussed. It is suggested that bioinspired vision systems have the potential to outperform conventional, frame-based vision systems in many application fields and to establish new benchmarks in terms of redundancy suppression and data compression, dynamic range, temporal resolution, and power efficiency. Demanding vision tasks such as real-time 3-D mapping, complex multiobject tracking, or fast visual feedback loops for sensory-motor action, tasks that often pose severe, sometimes insurmountable, challenges to conventional artificial vision systems, are in reach using bioinspired vision sensing and processing techniques.
Ultrasensitive Detection of DNA in Diluted Serum Using NaBH4 Electrooxidation Mediated by [Ru(NH3)6]3+ at Indium−Tin Oxide Electrodes (2010)

There is a crucial need for simple and highly sensitive techniques to detect DNA in complicated biological samples such as serum. Here we present an ultrasensitive electrochemical DNA sensor using (i) single DNA hybridization with peptide nucleic acid (PNA), (ii) selective binding of [Ru(NH(3))(6)](3+) to hybridized DNA, (iii) fast NaBH(4) electrooxidation mediated by [Ru(NH(3))(6)](3+), and (iv) low background currents of NaBH(4) at indium-tin oxide (ITO) electrodes. The [Ru(III)(NH(3))(5)NH(2)](2+) formed from [Ru(III)(NH(3))(6)](3+) in borate buffer (pH 11.0) is readily electrooxidized to both [Ru(IV)(NH(3))(5)NH(2)](3+) and Ru complex with a higher oxidation state. In the absence of [Ru(NH(3))(6)](3+) bound to the DNA-sensing ITO electrodes, the oxidation currents of NaBH(4) are very low. However, in the presence of [Ru(NH(3))(6)](3+), the oxidation currents of NaBH(4) are highly enhanced due to electron mediation of the oxidized Ru complexes. The significant enhancement in the electrocatalytic activity of sensing electrodes after [Ru(NH(3))(6)](3+) binding facilitates to obtain high signal-to-background ratios. PNA and ethylenediamine on DNA-sensing electrodes significantly decrease [Ru(NH(3))(6)](3+) binding, also allowing for high signal-to-background ratios. The oxidation charges of NaBH(4) obtained from chronocoulometry are highly reproducible. All combined effects enable the detection of DNA with a detection limit of 1 fM in ten-fold diluted human serum. The simple and fast detection procedure and the ultrasensitivity make this approach highly promising for practical DNA detection.