1,720,956 research outputs found
Going Beyond Counting First Authors in Author Co-citation Analysis
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
“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
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
The role of protein ITIH5 in resistance to vemurafenib targeted therapy, proliferation and activity of major signaling pathways in human melanoma cell lines
Vemurafenib je selektivni inhibitor mutiranog proteina BRAF V600E koji se javlja u 60%
melanoma. Unatoč početnim obećavajućim rezultatima, ubrzo nakon liječenja
vemurafenibom dolazi do pojave stečene otpornosti stanica melanoma na ovaj lijek. Stečena
otpornost često je posljedica reaktivacije signalnog puta MAPK (engl. mitogen activated
protein kinase) ili aktivacije alternativnog signalnog puta PI3K/AKT (engl. phosphoinositide3-kinase/Akt). U mnogim je tumorima, uključujući melanom, uočena smanjena ekspresija
gena ITIH5. Unatoč tome, njegova uloga u stečenoj otpornosti stanica melanoma na
vemurafenib još nije istražena. Cilj ovog diplomskog rada bio je istražiti učinak utišavanja
ovoga gena na otpornost na vemurafenib, na signalne puteve MAPK i PI3K/AKT te na
proliferaciju staničnih linija melanoma čovjeka WM793B i A375M. Utišavanje gena ITIH5
provedeno je prolaznom transfekcijom stanica malim interferirajućim RNA koje ciljaju ITIH5
koristeći kalcijev fosfat. Provjera ekspresije i uspješnosti utišavanja provedena je
kvantitativnom polimeraznom lančanom reakcijom (qPCR). Nakon utišavanja ITIH5
provjerena je vijabilnost i proliferacija stanica metodom MTT te razina biljega aktivnosti
istraživanih signalnih puteva i proliferacije metodom Western blot. Navedene su analize
pokazale da tretman vemurafenibom znatno snižava ekspresiju gena ITIH5 te da snižena
ekspresija ITIH5 povećava proliferaciju u navedenim staničnim linijama melanoma čovjeka.Vemurafenib is a selective inhibitor of the mutated protein BRAF V600E, which occurs in
60% of melanomas. Despite initial promising results, shortly after treatment with
vemurafenib, acquired resistance of melanoma cells develops. Acquired resistance is often
the result of the reactivation of the MAPK (mitogen activated protein kinase) signaling
pathway or the activation of the alternative PI3K/AKT (phosphoinositide-3-kinase/Akt)
signaling pathway. Decreased expression of the ITIH5 gene has been observed in many
tumors, including melanoma. However, its role in the acquired resistance of melanoma cells
to vemurafenib has not yet been investigated. The aim of this thesis was to investigate the
effect of ITIH5 silencing on the resistance to vemurafenib, on the activity of MAPK and
PI3K/AKT signaling pathways, and on the proliferation of human melanoma cell lines
WM793B and A375M. ITIH5 silencing was performed by transfecting cells with small
interfering RNA targeting ITIH5 using calcium phosphate. Verification of expression and
success of silencing was performed by quantitative polymerase chain reaction (qPCR). After
the silencing of ITIH5, cell viability and proliferation were checked using the MTT test,
while the levels of specific markers that represent the activity of signaling pathways or the
proliferation was checked using the Western blot method. The results showed that the
reduced expression of the ITIH5 increases the proliferation of the human melanoma cell lines
and is a consequence of vemurafenib treatment
The role of protein ITIH5 in resistance to vemurafenib targeted therapy, proliferation and activity of major signaling pathways in human melanoma cell lines
Vemurafenib je selektivni inhibitor mutiranog proteina BRAF V600E koji se javlja u 60%
melanoma. Unatoč početnim obećavajućim rezultatima, ubrzo nakon liječenja
vemurafenibom dolazi do pojave stečene otpornosti stanica melanoma na ovaj lijek. Stečena
otpornost često je posljedica reaktivacije signalnog puta MAPK (engl. mitogen activated
protein kinase) ili aktivacije alternativnog signalnog puta PI3K/AKT (engl. phosphoinositide3-kinase/Akt). U mnogim je tumorima, uključujući melanom, uočena smanjena ekspresija
gena ITIH5. Unatoč tome, njegova uloga u stečenoj otpornosti stanica melanoma na
vemurafenib još nije istražena. Cilj ovog diplomskog rada bio je istražiti učinak utišavanja
ovoga gena na otpornost na vemurafenib, na signalne puteve MAPK i PI3K/AKT te na
proliferaciju staničnih linija melanoma čovjeka WM793B i A375M. Utišavanje gena ITIH5
provedeno je prolaznom transfekcijom stanica malim interferirajućim RNA koje ciljaju ITIH5
koristeći kalcijev fosfat. Provjera ekspresije i uspješnosti utišavanja provedena je
kvantitativnom polimeraznom lančanom reakcijom (qPCR). Nakon utišavanja ITIH5
provjerena je vijabilnost i proliferacija stanica metodom MTT te razina biljega aktivnosti
istraživanih signalnih puteva i proliferacije metodom Western blot. Navedene su analize
pokazale da tretman vemurafenibom znatno snižava ekspresiju gena ITIH5 te da snižena
ekspresija ITIH5 povećava proliferaciju u navedenim staničnim linijama melanoma čovjeka.Vemurafenib is a selective inhibitor of the mutated protein BRAF V600E, which occurs in
60% of melanomas. Despite initial promising results, shortly after treatment with
vemurafenib, acquired resistance of melanoma cells develops. Acquired resistance is often
the result of the reactivation of the MAPK (mitogen activated protein kinase) signaling
pathway or the activation of the alternative PI3K/AKT (phosphoinositide-3-kinase/Akt)
signaling pathway. Decreased expression of the ITIH5 gene has been observed in many
tumors, including melanoma. However, its role in the acquired resistance of melanoma cells
to vemurafenib has not yet been investigated. The aim of this thesis was to investigate the
effect of ITIH5 silencing on the resistance to vemurafenib, on the activity of MAPK and
PI3K/AKT signaling pathways, and on the proliferation of human melanoma cell lines
WM793B and A375M. ITIH5 silencing was performed by transfecting cells with small
interfering RNA targeting ITIH5 using calcium phosphate. Verification of expression and
success of silencing was performed by quantitative polymerase chain reaction (qPCR). After
the silencing of ITIH5, cell viability and proliferation were checked using the MTT test,
while the levels of specific markers that represent the activity of signaling pathways or the
proliferation was checked using the Western blot method. The results showed that the
reduced expression of the ITIH5 increases the proliferation of the human melanoma cell lines
and is a consequence of vemurafenib treatment
Dispelling the Myths Behind First-author Citation Counts
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
The role of protein ITIH5 in resistance to vemurafenib targeted therapy, proliferation and activity of major signaling pathways in human melanoma cell lines
Vemurafenib je selektivni inhibitor mutiranog proteina BRAF V600E koji se javlja u 60%
melanoma. Unatoč početnim obećavajućim rezultatima, ubrzo nakon liječenja
vemurafenibom dolazi do pojave stečene otpornosti stanica melanoma na ovaj lijek. Stečena
otpornost često je posljedica reaktivacije signalnog puta MAPK (engl. mitogen activated
protein kinase) ili aktivacije alternativnog signalnog puta PI3K/AKT (engl. phosphoinositide3-kinase/Akt). U mnogim je tumorima, uključujući melanom, uočena smanjena ekspresija
gena ITIH5. Unatoč tome, njegova uloga u stečenoj otpornosti stanica melanoma na
vemurafenib još nije istražena. Cilj ovog diplomskog rada bio je istražiti učinak utišavanja
ovoga gena na otpornost na vemurafenib, na signalne puteve MAPK i PI3K/AKT te na
proliferaciju staničnih linija melanoma čovjeka WM793B i A375M. Utišavanje gena ITIH5
provedeno je prolaznom transfekcijom stanica malim interferirajućim RNA koje ciljaju ITIH5
koristeći kalcijev fosfat. Provjera ekspresije i uspješnosti utišavanja provedena je
kvantitativnom polimeraznom lančanom reakcijom (qPCR). Nakon utišavanja ITIH5
provjerena je vijabilnost i proliferacija stanica metodom MTT te razina biljega aktivnosti
istraživanih signalnih puteva i proliferacije metodom Western blot. Navedene su analize
pokazale da tretman vemurafenibom znatno snižava ekspresiju gena ITIH5 te da snižena
ekspresija ITIH5 povećava proliferaciju u navedenim staničnim linijama melanoma čovjeka.Vemurafenib is a selective inhibitor of the mutated protein BRAF V600E, which occurs in
60% of melanomas. Despite initial promising results, shortly after treatment with
vemurafenib, acquired resistance of melanoma cells develops. Acquired resistance is often
the result of the reactivation of the MAPK (mitogen activated protein kinase) signaling
pathway or the activation of the alternative PI3K/AKT (phosphoinositide-3-kinase/Akt)
signaling pathway. Decreased expression of the ITIH5 gene has been observed in many
tumors, including melanoma. However, its role in the acquired resistance of melanoma cells
to vemurafenib has not yet been investigated. The aim of this thesis was to investigate the
effect of ITIH5 silencing on the resistance to vemurafenib, on the activity of MAPK and
PI3K/AKT signaling pathways, and on the proliferation of human melanoma cell lines
WM793B and A375M. ITIH5 silencing was performed by transfecting cells with small
interfering RNA targeting ITIH5 using calcium phosphate. Verification of expression and
success of silencing was performed by quantitative polymerase chain reaction (qPCR). After
the silencing of ITIH5, cell viability and proliferation were checked using the MTT test,
while the levels of specific markers that represent the activity of signaling pathways or the
proliferation was checked using the Western blot method. The results showed that the
reduced expression of the ITIH5 increases the proliferation of the human melanoma cell lines
and is a consequence of vemurafenib treatment
Biodiversity and extinction
Trenutno smanjenje bioraznolikosti ima svoj utjecaj na sve ekosustave i organizme na Zemlji. Čovjek je najviše zaslužan za takvu situaciju i to zahvaljujući svojoj djelatnosti: izlovom, mijenjanjem i smanjenjem staništa divljih organizama, korištenjem raznih toksina, zagađenjem okoliša koje u konačnici dovodi do globalnoga zatopljenja. Izumiranja uzimaju sve više maha i danas se smatra da svijet ulazi u šesto masovno izumiranje, a prvo potaknuto biotičkim čimbenikom. Znanstvenici sve više proučavaju izumiranja i kretanja stope bioraznolikosti u prošlosti kako bi uspješno ekstrapolirali te zaključke na sadašnjost i tako ublažili trenutna kretanja. Od neizmjerne je važnosti obrazovati javnost i tako utjecati na ljudsko razmišljanje kako bi što prije došlo itekako potrebnih promjena.The current biodiversity crisis along with other factors affects every ecosystem and all organisms on Earth. Human beings are protagonists of such changes considering their massive impact on life that has to do with the exploitation of goods, hunting, changing the structure of habitats and pollution, which leads to global warming. Extinction is becoming a serious problem, and there are speculations that the world is on the edge of sixth mass extinction, which would be the first caused by a biotic factor. Scientists all around the globe are trying to collect as much information about past crises as they can so that they can understand present better and help the future faster. It is also very important to educate and engage the public and to change the human mindset because needed changes have to happen as soon as possible
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