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    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The 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

    Variations on the Author

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    “Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship

    Appropriate Similarity Measures for Author Cocitation Analysis

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    We provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis

    Rosiglitazone promotes AQP-2 translocation in renal cells via a Ca2+ dependent/cAMP independent mechanism (892.9)

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    Preliminary results by our group showed that exposure to Rosiglitazone (RGZ) induces phosphorylation and apical translocation of AQP2 in mouse collecting duct clone 4 (MCD4) cells. Here we studied the effect of short-term exposure to 50 μM RGZ on cAMP- and Ca2+-mediated signaling pathways, both key players for AQP2-mediated water reabsorption in the collecting duct. Cytosolic Ca2+ and cAMP levels were imaged in real-time in MCD4 cells loaded with Fura-2 or transiently transfected with the EPAC-based fluorescent probe H90, respectively. Physiologically, AQP2 phosphorylation/translocation depends on cytosolic cAMP levels. Nonetheless, cAMP measurements showed that RGZ did not induce significant changes in cAMP levels. Conversely, 20 minutes RGZ stimulation of Fura-2 loaded MCD4 cells induced a large, transient cytosolic Ca2+ peak that was not the result of direct blockade of the SERCA pump since the rate of store empting elicited by CPA in the absence of external Ca2+ was not significantly different in the presence of RGZ. Importantly, removal of external Ca2+ and inhibition of Ca2+ channels with ruthenium red prevented the RGZ-induced increase in cytosolic Ca2+ indicating a prominent role for Ca2+ entry at the plasma membrane. In conclusion, RGZ-induced AQP2 phosphorylation/translocation process is likely initiated by a fast, large extracellular Ca2+ influx most likely via Ca2+-dependent transient receptor potential channels. Further studies to ascertain which cascade of kinases is involved in this scenario are in progress

    Dispelling the Myths Behind First-author Citation Counts

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    We 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

    INCREASED URINARY EXCRETION OF AQUAPORIN 2 IN PATIENTS WITH ESSENTIAL HYPERTENSION: GENETIC ASSOCIATION WITH POLYMORPHISM OF THE CYTOSKELE- TAL PROTEIN ALPHA-ADDUCIN

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    Essential hypertension refers to a lasting increase in blood pressure with heterogeneous genetic and environmental causes. In developed countries, essential hypertension affects 25-35% of the adult population. Several studies indicate that the pathophysiology of essential hypertension depends on the primary or secondary inability of the kidney to excrete sodium at a normal blood pressure. In this study we tested the hypothesis that alteration in Aquaporin 2 (AQP2) expression/trafficking may also contribute to the extracellular volume expansion observed in hypertension. To test this hypotesis in humans, we monitored the urinary AQP2 excretion as biomarker of kidney concen- trating ability. Patients with essential hypertension were examined to determine if urinary excretion of AQP2 differed from that of healthy control subjects. Urinary excretion of AQP2 was measured in hyper- tensive patients without medication and in 13 healthy subjects. AQP2 excretion, quantitated by ELISA, was significantly higher in hypertensive patients than in controls (3264±143 vs 1659±191 fmol/mg creatinine; p<0.002). Since abnormalities of tubular sodium reabsorption observed in essential hypertension were previously be shown to be associated with the polymorphism of the cytoskeletal protein alpha-adducin, in a subset of hypertensive pa- tients AQP2 excretion was examined after acute sodium load (2 L of saline (Na+ 310 mEq) infused i.v.) and the genetic association with polymorphism of alpha-adducin was evaluated. Prelimi- nary results suggest that, after two hours of acute sodium load, AQP2 excretion was significantly higher (3216±277 (n=8) vs 2669±277 n=22 fmol/mg creatinine; P<0.01) in patients carrying ad- ducin mutation with respect to hypertensive patient carrying a normal adducin gene. Conclusions: Urinary AQP2 excretion was increased in hypertensive patients. Moreover, higher urinary AQP2 excretion after acute sodium load positively associated with adducin mutation. This suggests that increase in AQP2 expression/trafficking possibly related to alteration of cytoskeleton structure, may contribute to the extracellular volume expansion observed in hypertension

    IMPAIRMENT OF AQP2 TARGETING IN RESPONSE TO VASOPRESSIN IN HYPERCALCI- URIC PATIENTS: EVIDENCE FOR EXTRACELLULAR CALCIUM ACTING AS FIRST MESSENGER

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    Disturbances in renal concentrating ability have been associated with hypercalciuria in humans and experimental animals. In a previous work we have shown that extracellular calcium, possibly acting through Calcium Sensing Receptor (CaR) signaling, antagonizes forskolin-induced AQP2 translocation in renal cells. To test the hypothesis that increased urinary calcium inhibits AQP2 targeting in response to vasopressin in humans, in this study we evaluated AQP2 excretion in hypercalciuric children after 1-deamino-arginin-vasopressin (dDAVP) administration. Normocal- ciuric children served as control. Urine osmolarity and AQP2 excretion were measured in urine samples obtained hourly after 10 mg (if weight 0.2 on 3 separate samples. AQP2 excretion in urine samples was measured by Enzyme-Linked immunosorbent assay (ELISA). In the group of normocalciuric children having normal urinary concentration ability, dDAVP ad- ministration resulted in a significant increase in urine osmolality (1110±32 mOsm/l at peak, n=19) associated with a significant increase in urinary AQP2 excretion (from 250±80 fmol/mg Creat be- fore to 467±113 after dDAVP treatment, P<0.0001). In contrast, in hypercalciuric children AQP2 excretion did not significantly increase in response to dDAVP administration either in the group displaying normal urinary concentration ability (AQP2 excretion from 291±58.9 fmol/mg Creat before to 291±77 after dDAVP treatment, urine osmolarity 1018±32 mOsm/l at peak, n=13). and in the group having poor urinary concentration ability (AQP2 excretion from 432±117 fmol/mg Creat before to 391±80 after dDAVP test, urine osmolality 512±104 mOsm/l at peak, n=12). The obtained data demonstrate that in hypercalciuria AQP2 excretion in response to vasopressin is reduced or abolished. This effect was observed in both normal and poor responders. These data would support the hypothesis that increased urinary calcium levels inhibits AQP2 targeting in re- sponse to vasopressin in humans possibly through activation of CaR signaling. In hypercalciuric patients the impairment of AQP2 targeting observed in response to vasopressin may contribute to reduce the risk of an increased incidence stone formation during antidiuresis

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    Integrin signaling modulates AQP2 trafficking via Arg-Gly-Asp (RGD) motif

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    Aquaporin-2 (AQP2) increases the water permeability of renal collecting ducts in response to vasopressin. Vasopressin stimulation is accompanied by a profound remodeling of actin cytoskeleton whose dynamics are regulated by crosstalk between intracellular and extracellular signals. Here, we report that AQP2 contains a conserved RGD domain in its external C-loop. Co-immunoprecipitation experiments demonstrated that AQP2 binds integrin 1 in renal tissue and in MCD4 cells. To investigate the role of this interaction on AQP2 trafficking, cells were exposed to synthetic RGD-containing peptides, GRGDNP or GRGDSP, able to bind certain integrins. Incubation with these peptides increased the membrane expression of AQP2 in the absence of hormonal stimulation as assessed by confocal analysis and cell surface biotinylation. To identify the signals underlying the effects of peptides on AQP2 trafficking, some possible intracellular messengers were evaluated. Exposure of MCD4 cells to GRGDNP increased intracellular cAMP as assessed by FRET studies while GRGDSP increased intracellular calcium concentration. Taken together, these data propose integrins as new players controlling the cellular localization of AQP2, via two distinct signal transduction pathways dependent on cAMP and calcium respectivel
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