169,829 research outputs found
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Mitomycin C in highly myopic eyes - Author reply
No full textOphthalmology. 2005 Feb;112(2):208-18; discussion 219.
Mitomycin C modulation of corneal wound healing after photorefractive keratectomy in highly myopic eyes.
Gambato C, Ghirlando A, Moretto E, Busato F, Midena E.
SourceRefractive Surgery Service and Antimetabolite Therapy Research Unit, Department of Ophthalmology, University of Padova, Padova, Italy.
Abstract
PURPOSE: To evaluate the role of topical mitomycin C in corneal wound healing (CWH) after photorefractive keratectomy (PRK) in highly myopic eyes.
DESIGN: Prospective, double-masked, randomized clinical trial.
PARTICIPANTS: Seventy-two eyes of 36 patients affected by high (>7 diopters) myopia.
METHODS: In each patient, one eye was randomly assigned to PRK with intraoperative topical 0.02% mitomycin C application, and the fellow eye was treated with a placebo. Postoperatively, mitomycin C-treated eyes received artificial tears (3 times daily, tapered in 3 months), whereas the fellow eye was treated with fluorometholone sodium 2% and artificial tears (3 times daily, tapered in 3 months).
MAIN OUTCOME MEASURES: Uncorrected visual acuity (UCVA) and best-corrected visual acuity (BCVA), contrast sensitivity, manifest refraction, and biomicroscopy. Contrast sensitivity was determined using the Pelli-Robson chart. Corneal confocal microscopy documented CWH.
RESULTS: Mean follow-up was 18 months (range, 12-36). No side effects or toxic effects were documented. At 12-month follow-up examination, UCVAs (logarithm of the minimum angle of resolution) were 0.4+/-0.48 and 0.5+/-0.53 (P = .03) in mitomycin C-treated eyes and corticosteroid-treated eyes, respectively. At 1 year, corneal haze developed in 20% of corticosteroid-treated eyes, versus 0% of mitomycin C-treated eyes. At 12, 24, and 36 months, corneal confocal microscopy showed activated keratocytes and extracellular matrix significantly more evident in untreated eyes (Ps = 0.004, 0.024, and 0.046, respectively).
CONCLUSION: Topical intraoperative application of 0.02% mitomycin C can reduce haze formation in highly myopic eyes undergoing PRK.
Comment in
Ophthalmology. 2006 Feb;113(2):357; author reply 357-8
Dispelling the Myths Behind First-author Citation Counts
No full textWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
A Multi-Language Comparison of Influences on Author Verification using Character N-Grams
No full textWe create a new multi-language corpus for author verification based on Wikipedia talkpages, and evaluate the influence that differences in topic and time have on character n-gram author profiles. Topic alignment between two texts is found to increase author verification precision, and an authors writing style is found to change over time, but not more significantly after 3 years than after 1 year.Information ArchitectureWISElectrical Engineering, Mathematics and Computer Scienc
A 0.12mm<sup>2</sup> Wien-Bridge Temperature Sensor with 0.1°C (3σ) Inaccuracy from -40°C to 180°C
No full text Resistor-based temperature sensors can achieve much higher resolution and energy efficiency than conventional BJT-based sensors [1], but they typically occupy more area (> 0.25 mm 2 ) and have lower operating temperatures (le 125 {circ} {C}) [2]-[4]. This work describes a 0.12mm 2 resistor-based sensor that uses a Wien-bridge (WB) filter to achieve 0.1 {circ} {C} (3 sigma) inaccuracy from - 40 {circ} {C} to 180 {circ} {C}. Compared to a state-of-the-art WB sensor [4], it occupies 6 × less area and achieves comparable relative accuracy over a 76% wider operating range. Session 10.3 Green Open Access added to TU Delft Institutional Repository ‘You share, we take care!’ – Taverne project https://www.openaccess.nl/en/you-share-we-take-care Otherwise as indicated in the copyright section: the publisher is the copyright holder of this work and the author uses the Dutch legislation to make this work public.Electronic InstrumentationMicroelectronic
A combined "omics" approach identifies N-Myc interactor as a novel cytokine-induced regulator of IRE1 protein and c-Jun N-terminal kinase in pancreatic beta cells.
No full textType 1 diabetes is an autoimmune disease with a strong inflammatory component. The cytokines interleukin-1? and interferon-? contribute to beta cell apoptosis in type 1 diabetes. These cytokines induce endoplasmic reticulum stress and the unfolded protein response (UPR), contributing to the loss of beta cells. IRE1?, one of the UPR mediators, triggers insulin degradation and inflammation in beta cells and is critical for the transition from "physiological" to "pathological" UPR. The mechanisms regulating inositol-requiring protein 1? (IRE1?) activation and its signaling for beta cell "adaptation," "stress response," or "apoptosis" remain to be clarified. To address these questions, we combined mammalian protein-protein interaction trap-based IRE1? interactome and functional genomic analysis of human and rodent beta cells exposed to pro-inflammatory cytokines to identify novel cytokine-induced regulators of IRE1?. Based on this approach, we identified N-Myc interactor (NMI) as an IRE1?-interacting/modulator protein in rodent and human pancreatic beta cells. An increased expression of NMI was detected in islets from nonobese diabetic mice with insulitis and in rodent or human beta cells exposed in vitro to the pro-inflammatory cytokines interleukin-1? and interferon-?. Detailed mechanistic studies demonstrated that NMI negatively modulates IRE1?-dependent activation of JNK and apoptosis in rodent and human pancreatic beta cells. In conclusion, by using a combined omics approach, we identified NMI induction as a novel negative feedback mechanism that decreases IRE1?-dependent activation of JNK and apoptosis in cytokine-exposed beta cells
A ±25A Versatile Shunt-Based Current Sensor with 10kHz Bandwidth and ±0.25% Gain Error from -40°C to 85°C Using 2-Current Calibration
No full textAccurate current sensing is critical in many industrial applications, such as battery management and motor control. Precise shunt-based current sensors have been reported with gain errors of less than 1% over the industrial temperature range (-40°C to 85°C) [1]–[4]. However, since they are intended for coulomb counting, their bandwidth is limited to a few tens of Hz, making them unsuitable for battery impedance or motor-current sensing. This paper presents a current sensor with a wide (10kHz) bandwidth and a tunable temperature compensation scheme (TCS), which allows it to be flexibly used with different types of shunts while maintaining high accuracy. A low-cost room-temperature calibration scheme is proposed to optimize gain flatness over temperature by exploiting the shunt's self-heating at large currents. Over the industrial temperature range and a ±25A current range, it achieves state-of-the-art gain error (±0.25%) with both low-cost PCB and stable metal-alloy shunts.Green Open Access added to TU Delft Institutional Repository 'You share, we take care!' - Taverne project https://www.openaccess.nl/en/you-share-we-take-care Otherwise as indicated in the copyright section: the publisher is the copyright holder of this work and the author uses the Dutch legislation to make this work public.Electronic InstrumentationMicroelectronic
An Article About Albertus C. Van Raalte, Author Unknown, Except for Parts Taken from an Article by Anna C. Post
No full textAn article about Albertus C. Van Raalte, author unknown, except for parts taken from an article by Anna C. Post. The author knew first generation persons in the Holland settlement and therefore, the article has some value.https://digitalcommons.hope.edu/vrp_1890s/1012/thumbnail.jp
Dietary supplementation with high doses of regular vitamin D3 safely reduces Diabetes incidence in nod mice when given early and long-term.
No full textHigh doses of the active form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], prevent diabetes in the NOD mouse but also elicit unwanted calcemic side effects. Because immune cells themselves can convert vitamin D3 into 1,25(OH)2D3 locally, we hypothesized that dietary vitamin D3 can also prevent disease. Thus, we evaluated whether dietary administration of high doses of regular vitamin D3 (800 IU/day) during different periods of life (pregnancy and lactation, early life [3-14 weeks of age], or lifelong [3-35 weeks of age]) safely prevents diabetes in NOD mice. We found that only lifelong treatment raised serum 25-hydroxyvitamin D3 from 173 nmol/L in controls to 290 nmol/L, without inducing signs of calcemic or bone toxicity, and significantly reduced diabetes development in both male and female NOD mice. This diabetes protection by vitamin D3 correlated with preserved pancreatic insulin content and improved insulitis scores. Moreover, vitamin D3 treatment decreased interferon-γ-positive CD8(+) T cells and increased CD4(+)(CD25(+))FoxP3(+) T cells in pancreatic draining lymph nodes. In conclusion, this study shows for the first time that high doses of regular dietary vitamin D3 can safely prevent diabetes in NOD mice when administered lifelong, although caution is warranted with regards to administering equivalently high doses in humans
Understanding the molecular and intracellular function of vitamin D in the immune system: Implications for translation.
No full textVitamin D is a hormone that can be obtained from food (e.g. fatty fish and dairy products), but is mainly made in the skin where sunlight exposure converts it into its biologically active metabolite, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3). The widespread expression of the vitamin D receptor (VDR) and vitamin D3-metabolizing enzymes in almost all cells of the immune system indicates a role for 1,25(OH)2D3 as a modulator of immune responses. In dendritic cells (DCs), 1,25(OH)2D3 interferes with the differentiation and maturation process resulting in the induction of a tolerogenic state. Tolerogenic DCs (tolDCs) are characterized by downregulated antigen-presentation, reduced costimulation and low pro-inflammatory cytokine production. As a result, tolDCs are poor T cell stimulators and induce T cell hyporesponsiveness. In addition, tolDC mediate a shift in T cell polarization from Th1/17 responses to more tolerogenic responses, with the induction of regulatory T cells (Tregs). On the other hand, 1,25(OH)2D3 are also able to directly modulate activated T cells. In these cells, 1,25(OH)2D3 decreases the production of pro-inflammatory cytokines and induces Tregs.
An important role for 1,25(OH)2D3 and its nuclear receptor in the development of type 1 diabetes (T1D) has been suggested by the discrepancy observed between absence of ligand and absence of receptor. Vitamin D3 deficiency in early life is associated with elevated risk for T1D, while the VDR null mouse model, lacking a functional VDR, do not present with aggravated disease. This difference indicates an important role for the unliganded VDR in the immune response. In the first part of this project, we investigated whether an unliganded VDR could affect the phenotype and function of murine bone marrow-derived DCs (BMDCs). Therefore, we studied myeloid BMDCs generated ex vivo from bone marrow precursors of VDR null, with a truncated, non-functional VDR, and VDR ∆AF-2 mice, with a mutated C‑terminal activation factor AF-2 domain thus rendering ligand-induced gene transcription impossible. To our surprise, the unliganded VDR did not affect BMDC phenotype or their T cell stimulatory capacity compared to VDR null BMDCs. These data indicate that an unliganded VDR does not elicit a more inflammatory phenotype in BMDCs.
Currently, no therapies for T1D are established which tackle the underlying immune attack. In general, immunotherapies focus on the inhibition of pathogenic immune cell activation and the (re-)establishment of self-tolerance against autoantigens. Given the interesting characteristics of Tregs and tolDCs to induce antigen-specific protection, cellular immunotherapies like adoptive T cell transfer and tolDC-based vaccines provide promising strategies for autoimmune diseases. In this regard, 1,25(OH)2D3 or its low‑calcemic analog TX527 are ideal for ex vivo modulation of autologous T cells and DCs.
Previously, our group showed successful ex vivo modulation of T cells isolated from healthy donors by 1,25(OH)2D3 as well as its analog TX527. However, for the clinical applicability of autologous adoptive T cell therapy, validation in samples from patients with T1D is required, especially as a defect in Treg function has been shown in T1D. Therefore, we further explored whether autologous T cells obtained from patients with T1D could be ex vivo modulated by 1,25(OH)2D3 and its analog TX527. Indeed, treatment with 1,25(OH)2D3 and TX527 increased the frequency of CD4+CD25highCD127low Tregs, with elevated CTLA-4 expression in this population. Moreover, exposure to 1,25(OH)2D3 and TX527 imprinted a unique homing signature and reduced the production of effector cytokines in the T cells isolated from T1D patients. In addition, both 1,25(OH)2D3 and TX527 promoted the formation of a stable Treg phenotype, which is essential for their possible clinical application as they will be reintroduced in an inflammatory microenvironment.
For the third part of this PhD project, we build further on a previous finding in our lab that demonstrated that the induction of the tolDC profile by 1,25(OH)2D3 is accompanied by an early and transcriptionally mediated metabolic reprogramming. We previously showed that glucose availability and glycolytic metabolism are crucial to induce and maintain tolDCs. This observation strokes with the emerging concept of immunometabolism which states that intracellular metabolism determines the phenotype and function of immune cells. In this regard, we aimed to find a primary target of vitamin D3 that could act as a metabolic switch in tolDCs. We identified the glycolytic enzyme PFKFB4 as strongly and directly upregulated by 1,25(OH)2D3 in differentiating monocytes. Pharmacological inhibition of PFKFB4 activity by the small molecule inhibitor 5-MPN could interfere with the increase in glucose metabolism, and more specifically glucose oxidation, which are hallmark features of tolDC. Moreover, PFKFB4 inhibition altered tolDC phenotype and their ability to induce functional Tregs. A better understanding of the metabolic pathways influenced by 1,25(OH)2D3 in human tolDCs will aid the development and improve the efficacy of tolDC-based immunotherapies.status: Publishe
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